CARDIOVASCULAR A&P
Blood flow through the ​RIGHT​ side​: coronary circulation
SVC/IVC: veins of the body carry deoxygenated blood to the heart
a low pressure system)
Into Right atrium
Tricuspid valve
right ventricle(contracts against
pulmonary artery
ascending aorta: brings blood up the thoracic cavity and the brain
Descending aorta:brings the blood to the abdomen and lower organs
Veins- low pressure
Arteries- high pressure
Blood Flow through the ​LEFT ​heart​: systemic circulation
Enter into Pulmonary veins
Left atrium Mitral/bicuspid valve Left ventricle
Aorta (ascending/descending) big artery with lots of pressure- the left ventricle should work very hard to
push the blood all over the body
Left ventricle has to pump blood out the aorta - a damn big boy artery → lots of counter resistance →
works harder → pushing blood toward the systemic system
-Back and forth motion for pumping of the heart not “squishing”
HEART VALVES IN THE HEART PERMIT BLOOD TO FLOW IN ONE DIRECTION.
Cardiac Contraction​:
DIASTOLE: relaxation/filling w. Blood [the atria is relaxing the ventricles is contracting and vice versa]
SYSTOLE: contraction/ejection of blood
left /right heart work simultaneously yet independently because they are doing two different jobs, the
right is receiving and the left side is pushing out into the systemic circulation.
tricuspid/bicuspid​:
During atrial filling (diastole) the tricuspid valves on the right side of the heart and the bicuspid on the left
side (Separates the r.atrium and r. Ventricle) - the valves are ​closed
→ as the atria distend and fill with blood and pressure increases in the atria... the valves are ​forced
open (blast open) and blood drops down into the ventricles
Pulmonic/aortic valves​:
- During ventricular filling (diastole), the pulmonic and aortic valves are closed (shut)
- As the pressure in the ventricles increases, these valves are forced open(blast open the pulmonic
and aortic valve) and eject blood into the aorta/systemic circulation (systole)
Layers of the heart​:
Endocardium: (endocarditis - read in text) inner layer;
- continuous with valves & lining of blood vessels if becomes infected it can lead to an infection of
the valve.. endocarditis
M​yocardium: “​m​uscle” - acts as the pillow/cushion for the heart; middle layer
Epicardium: exterior layer
Pericardium: “double layer” - outer layer; filled w. Pericardial fluid 15ml of serous fluid heart is encased
pillow or cushion for the heart ...pericarditis
Cardiac Conduction ​:starts at the SA node located in the right atrium knows to fire an electrical pulse
- Normal SA node 60 to 100 bpm
Impulse travels down to AV node (thru right atrium)
Impulse travels to ventricles
Through the bundle of his
Bachmann’s bundle (thru left atrium)
AV node - send signals 60 to 100 times in a min ← lol
(R&L) - (thru ventricles) via the bundle of HIS
It's like electricity that travels thru the heart causing it to contract
Better to have a low heart rate than high rate
Want pt to be in sinus rythym
Blood supply ​TO ​the heart​:
- @ least 6 ​coronary arteries​ ​(not tested on which artery supplying which body part)
- Right coronary artery supply the : R ventricle, SA/AV nodes
- If it was obstructed or occluded with plaque these pts may have ...
- Inferior wall MI w. Bradycardia
- Left Coronary artery: MAIN SUPPLIER of left ventricle (anterior wall).
- Lateral wall of left atrium and ventricle
- Massive MI
- High mortality rate
- Left anterior descending: anterior wall left ventricle
- Anteroseptal MI
- Left circumflex: lateral left atrium and ventricle
- Lateral wall MI
Left main coronary artery​- main supplier of the left ventricle.(hardest working part of the heart)
Hardest working part of the heart
→ if obstructed → MI massive MI, high mortality rate
Nickname- left main coronary occlusion - the widow maker (hasta la vista babyyyy)ㅋㅋㅋ
Arteries​:​carry oxygenated blood from the heart to → peripheral organs
- Thick walled & muscular
- High pressure system
Thick walled & muscular
High pressure system
Aorta is the big artery of the body with the highest pressure... If artery is severed(cut) they splash off
burst out bc they are high pressure system pt can die if it isn't stopped
Arterial line?-> measures arterial BP.. We’ll talk
Veins​: ​carry deoxygenated blood from all of the organs back to the heart and lungs where gas exchange
happens
- Thin walls; distensible, expand get bigger that's why iv fluids are given thru veins
- Veins in the lower extremities have valves
- Low pressure system
- IV intravenous fluids can only be put into veins bc they are a low pressure system and can
expand to accommodate the volume of the veins
- If IV falls out the blood drips due to low pressure
-Purpose of veins (VALVES) in legs; prevention of blood backflow → must go back to
superior/inferior VC
-Veins in the lower extremities have valves to counteract the force of gravity helps to make sure the
blood doesn't drop back down the valve keeps the blood moving up thru the SVC into the IVC and
veins low pressure systems.
PAD INCREASES ISCHEMIA
ECHOTRIN 81 MG
PERSANTINE ANTIPLATELET
PAIN MED SIDE EFFECT- MOOD CHANGES, SUICIDAL
IDEATION
12-24 hr post op walking for femoropop. Give diruetics too. No harsh
soap, dressing open
CARDIAC DIAGNOSTIC TESTS
EKG​: electrocardiogram / ECG - test that records electrical currents that are generated by the heart
→ ​info on 2 things- abnormal heart rhythm (sinus rhythm) & any ischemia (damage to the
heart due to lack of oxygen) to the heart
- Painless for pt. It's safe, pt needs to hold still, hairy chest may need to shave chest to get good
contact with the leads of EKG
- Telemetry is wireless continuous EKG, you see 2 electrical views of the heart. You don't know
which views they are it's whatever the tech sets the monitor for.
- Hook pt up to leads - 2 on arms, 2 on legs, 6 on left side of chest → record the electrical
activity of heart
- Typically gives 12 electrical views of the heart (full 12 leads) ??? physics thing - cross section for
checking out the entire heart
- 2 leads foro viewing EKG on a screen (monitor) ? on a telemetry unit
- When pt is having chest pain you don't know where the problem is, must do 12 lead EKG
- Chest pain- ischemia causes heart attack (location of ischemia unknown)
- Must do a ​12 lead EKG​ [12 electrical lead used on the heart] to find the ischemia you
can see every possible part in the heart to figure out where ischemia is
- EKG is more specific than telemetry on finding ischemia
Stress test​: done w. Treadmill / exercise bicycle → ​pt connected to BP, EKG and heart monitor
machines to assess the heart respond to exercise
Is done to reproduce the effects of exercise on the heart while pt has EKG increase oxygen demand of the
heart while exercising
- NPO after midnight/2 hours before the test
- Must get consent
- No caffeine
- No alcohol
- Shouldn’t smoke
- Check with PHCP for meds being taken/shouldn’t be taken
- Tell Pt wear to comfortable rubber sole shoes and clothes
- Must notify HCP during test if experiencing chest pain, SOB, or dizziness
- Typically- either physician/advanced HCP present for a stress test (PA/NP) bc pt can
have heart attack
- Monitor pt after or 10 to 15 mins until HR & BP EKG have returned to baseline
- What we’re looking for on pt EKG- any changes in ​ST segment​ elevation or depression
Pharmacological stress test:
*Some pt’s cannot perform a stress test bc they are unable to perform physical exercise, but they might
need the stress test. Ex. orthopedic surgery, knee replacement, COPD, confused
inject through IV- mimics sympathetic Nervous System stimulation and effects of the heart rate
makes it accelerates it makes it go faster → increases BP - causes vasoconstriction (makes the heart
work harder) increase in (svr) systemic vascular resistance
Effects of sympathetic Nervous System on blood vessels causes vasoconstriction (makes the heart
work harder)
Connected to BP, heart monitor and EKG
-thallium
-dobutamine
-Adenosine
-NPO before the test! No smoking, caffeine, & alcohol
If necessary the effects of the drugs can be reversed with IV Aminophylline.
Holter monitor​ - older test- 24hr EKG reading typically done on an outpatient. device that pt/ wears monitored for 24 hours - ​ambulatory EKG
Pt sent home with Diary - to record symptoms date and time & what they were doing @ the time
- ie. chest pain → right after eating a meal
- Nursing intervention: teach pt the warning signs and symptoms
- Indigestion, pressure, SOB,
- Event monitor: pt hooked up to 3 EKG leads go home with pen and push button on pen and
monitored remotely to see if they have a cardiac problem.
Loop recorder implantation​ - loop inserted under the skin of the chest.
● Used when physician have hard time catching the symptom. The loop is inserted to send the info
to the Doctor for constant monitoring.
Echocardiogram:
Painless, Not invasive
Transducer is placed on pt’s chest
ultrasound/ sound waves
Looking @ structure of the heart
Particularly the valves
● Left ventricle * the hardest working part of the heart, aorta comes out of the left ventricle big
cauona artery in the body with a lot of pressure in it , high pressure system, the left ventricle is
pumping against the aorta to push the blood out to the rest of the body. Echocardiogram looks at
that left ventricle and gives us a number that lets us know how well the left ventricle is working…
number is called
*** ejection fraction - shows how well the left ventricle ejects blood
- normal ejection rate: 50%-70%
Ex. ejection fraction of 20% left ventricle is not pumping properly
If blood in the heart doesn't go forward, particularly the left side, it's going to go backwards first into the
left atrium then dump back into the lungs
TEECG:​ transesophageal echocardiogram pg702
swallow Transducer: passed sits in esoph. Or → stomach → provides views of left atrium, mitral
valve, aortic arch
- NPO 6 to 8hrs with anesthesia- pt has to swallow transducer
CVP reading-​ central venous pressure- cath sits superior vena cava or inferior vena cava sits in
the right atrium
A high CVP indicates a lot of fluid in the heart or body (fluid volume excess) HF.
Can measure pressure in the right side of the heart
Normal: 5-10
Ie: reading of 20?
→ Fluid volume excess in lungs → backing up into the heart! :O → inc. pressure of heart.
→ Crackles? Lungs can be filled w fluid
→ fluid volume deficit with the reading of a negative number ​(hypovolemia) ..dehydration in
elderly, hemorrhage, very low cvp
CVP ​tests right ventricular function.
*****Professor would gave crazy high or low number to determine fluid volume deficit or overload
x-ray​: Checking size of heart
Cardiomegaly: enlarged heart
Fluid in lungs? heart ?
EPS ​studies: (electrophysiology studies)​ cath in to heart to try to reproduce the dysrhythmia that made the
patient sympathetic, figure out the dysrhythmia to fix the problem
Pt → ​cath lab ​- they try to reproduce the dysrhythmia that made pt symptomatic
- Cause found? treat ! with either meds/electricity
Electrical treatment includes: cardioversion, pacemaker, or implanted defibrillator.
Pt needs an implanted defibrillator if they had a serious heart problem idk i wasn’t paying attention?? If a
patient has A-Fib!
IMPORTANT lab values to monitor:
Troponin: protein that is released by a damaged myocardium
- Specific to the heart
-
Normals:​ 0.04-0.39 ​mg/ml
CPK or CK-MB:​ creatine phosphokinase - cardiac enzymes ​ ​[non-specific] indicator of muscle
damage ​enzymes that are released whenever there is muscle damage to the body. If heart is
damaged then CPK/CK can be elevated
Lab level: ​Troponin ​is a protein that is released when there is heart muscle damage, very specific to the
heart, results are available really quickly, helps to tell us if pt is having ischemia (lack of oxygen, damage
to the heart.)
- abnormally high levels of these substances can be detected in serum blood samples.
- Elevated when there is any muscle damage in body
- Car accidents (inc. CK levels) skeletal muscle damage
- Heart damage
- Elderly pt’s who fall and lay in the same position for a long time
- Rhabdomyolysis​ is a serious syndrome due to a direct or indirect muscle injury.
It results from the death of muscle fibers and release of their contents into the
bloodstream. This can lead to serious complications such as renal (kidney) failure.
This means the kidneys cannot remove waste and concentrated urine​ ? when pt lays
on the floor for like 15 hrs.
BNP (Brain Natriuretic Peptide)​: hormone that’s released from a ​dilated left ventricle → a lot of
pressure for a long time → became flopping & dilated flabby when pt is in heart failure → now
cannot pump! ​MARKER FOR HEART FAILURE​ *
***100<​ abnormal ​ / Pt might have edema, crackle on Left lung
> 100 suggest pt is in heart failure
***K+​ is important because? Normal cardiac rhythms/action potential electrolyte
- Electrolyte: CAN BE DANGEROUS; we give it carefully in the clinical setting
- Normal K+ levels: 3.5-5
- Hypokalemia: K+ levels less than 3.5. Causes abnormal heart rhythms, ventricular dysrhythmias
- Hyperkalemia: K+ levels more than 5.1. Causes asystole
- K+ levels above 9-10? ​ASYSTOLE​- no contraction of heart - flatline(deathhhh)
- Kay-exelate given to decrease hyperkalemia
- apnea: no breathing
- Very important to watch out for potassium level
Cholesterol levels​ preferred total under 200. Npo is preferred before drawing the levels
Ischemia occurs when cholesterol is above 200!!
HDL/LDL: high/low density lipids
High HDLs - help transport cholesterol to the liver
Low LDL (the bad kinds of fat): like to stick to the walls of the blood vessels (high LDL cause
atherosclerosis)
HDL: good cholesterol Promotes excretion of cholesterol through the liver
LDL: the bad kind (the bad kinds of fat): like to stick to the walls of the blood vessels with
plaque and fats causing it to narrow
WBC normal : 5,000-10,000
Hgb: norm:12-18g/dl
carry RBC which has oxygen to the heart and to all the organs ← ​no
oxygen to perfuse? With low levels
- If pt for ex has hgb of 6 increasing demands of the heart making the heart work even
harder bc it's not getting perfused with oxygen in the blood cells.
Hct:​ norm:37-52%
** Anemic patients cannot have enough oxygenation because the RBC is not enough to carry o2.
It's important for cardiac pts to not be anemic
PT,PTT,INR​ - Must check for patient with cardiovascular disease for med effectiveness
*​PTT:​ partial thromboplastin time…... partial bc heparin is only given for a short period of time before
warfarin
- Monitors the effectiveness of the IV infusion of he​p​arin (anticoagulant) blood thinner used in
cardiovascular pts
- It's documented as top over bottom number
- 1.5-2 x35= 70-90 ​(therapeutic range) ​/ 35 seconds ​(control)
- Normal people’s blood take 35 seconds to clot using a PTT test
- **antidote for heparin is​ p​rotamine sulfate*​*
- Pts on heparin you want their blood to take longer to clot, we need to anticoagulant them bc the
blood clots are causing a problem. that's how you prevent blood clots
- Pts blood is nice and thin taking a long time for their blood to clot.
- Excreted thru the body very quickly, very short half life can be on heparin in the morning and go
to surgery a few hours later.
PT/INR:​ prothrombin time
Monitors the effectiveness of ​coumadin (warfarin)​ blood thinnerBottom number - control # = ~11 seconds
A normal person’s blood should take ~11 seconds to clot (​control)
-if a person is taking coumadin you want the top number to be ...
1.5-2x the control → 15-22 seconds
See fraction below:
15-22……… ← therapeutic pt range
~11 seconds
INR​:​ international normalized ratio;
Pt’s on coumadin you want INR to be ​2-3 : therapeutic
There are no lab values to monitor the effectiveness of other drugs, just coumadin and heparin
Has a much longer half life takes longer to get out of the body
Antidote for coumadin is vitamin K
Cardiac calcium scoring test : CT scan
Noninvasive
Identifies pt at high risk for heart disease
Cat scan
Info about calcified plaque in the CA
0 IS NO PLAQUE in the arteries
1-10 little minimal
100 some
100-400 moderate
>400 large amount
Angiogram​ can be performed to look at any structure in the body
Angiogram: can be done to look @ blood supply in any organ of the body
Aka cardiac catheterization ​-​ invasive
Artery is accessed w. Catheter by cardiac interventionist
Dye is injected to view the patency of the coronary arteries
Definitive and invasive method of studying the heart
→ pictures are taken to see which blood vessels are occluded
- Consent before,pt needs to know why they are having the test, physician must tell pt the
hazards/complications
- Emboli, bleeding, stroke, & DEATH (Physician need to notify patient, not RN - from 2nd
test) may need to cough when dye is injected
- Pt must stay still, may have palpitations, must feel warm when dye is injected .../feverish?
NPO 6-8 hrs prior
- Take baseline VS before sending pt
- Assess / document heart and lung sounds preprocedure
- Attain allergy info
- iodine/shellfish allergy?
- Assess peripheral pulses prior to procedure
- Femoral artery ( assess pedal pulses) is used may need to shave the site
accessed: mark w SHARPIE: ​mark where the pedal pulses are!!!
ATHEROSCLEROSIS can be anywhere! → plaque can be dislodged →
EMBOLI * prob important lol
-
-
Pt is supine, strpped to xray table, sometimes given mild sedation, femoral or
radial artery is accessed
Cath is floated up thru the artery up to the coronary arteries, dye is injected
and watch dye as it travels thru the coronary artery. Can see which blood
vessels are patent or open... and which vessels are obstructed/ occluded or
closed. If closed then pt may an angioplasty performed with stents. i
If a lot of vessels occluded can go for surgery
Go for pressure reading, blood samples.
Post procedure: if femoral artery site used may be on bed rest 2-6 hrs
- Keep extremity straight
- Assess insertion site for bleeding, swelling, check pressure dressing - weight? (sandbag 5 lbs),
injection of collagen into area; arteries- HPS prone to bleeding! *
- Collagen may be injected into the area to seal off the site that was assessed for the procedure
pressure dressing can be there. Sandbags for trouble for controlling the bleeding
- Encouraging fluids (fluid IV to excrete dye from body)
- Assess peripheral pulses, temp., & color of extremity
- REPORT: any bleeding, hematoma, changes in mental status (dislodgement of a clot?
Embolism); checking for peripheral pulses
- NEW WAY → using the radial artery now instead of femoral artery … so the pt can be
ambulatory more quickly!!! :D
- Coming back w. A bracelet for radial procedure - under the bracelet → little balloon cuff
filled with air plastic piece that comes off the bracelet syringe attached release loosen or put
more air into cuff tighter
- (radial)Hand is feeling numb and becoming pallor cyanosis or cold !*&@^#$%&*
LOOSEN CUFF! So hand circulation is returned
- When there is oozing or bleeding more air added to the cuff
- Goal when pt Will come back w. an order for how much air should be removed every
hour so the cuff can then be removed
- Assess pulse, site, temp.
Check pedal pulses
Reason for getting tested is from the buildup of fat and plaque in the coronary arteries causing
them to narrow isn't just happening in the coronary artery can become systemic cause it to travel
and cause pt to lose pedal pulses.
Post vital signs
Check extremities for temp color
Check for abnormal heart rhythms
Promote fluids to get rid of dye
Report any bleeding, hematoma, change in pulses
Change in mental status after angiogram: plaque went to the brain can cause stroke
HYPERTENSION
Stroke volume: volume pumped by the left ventricle (in the vessel)every beat
Cardiac output: amount of blood that is pumped out with every systole(contraction) from the left
ventricle/ ​major determinant ​of the systolic BP top number
- Systemic vascular resistance (SVR): (aka afterload) force that opposes the movement of blood (diameter
of the blood vessel) its major determinant of diastolic BP\
- If blood vessels are nice and wide open the blood can very nicely throughout the body
SVR ; narrow constricted blood vessels heart must work harder to pump blood SVR is much higher
- Cardiac output refers to volume that is pumped out with every systole and SVR has to do with diameter
of blood vessels
CO= HR x SV
BP = CO x SVR
Volume x diameter
To lower BP: need to lower CO or SVR or BOTH
How to reduce CO or volume: diuretics get rid of volume
Treat vascular resistance with vasodilators - dilate/open up the blood vessels
MAP:​ mean arterial pressure: average bp during an entire cardiac cycle. reflects blood flow to ALL the
vital organs
Reflects the pressure throughout your whole body, away from the core.
Normal 70 to 100
If it's too high too much stress on the heart treated with vasodilators
If it's too low if the pt is hemorrhaging losing a lot of volume
Factors influencing BP​:
Baroreceptors or pressure receptors located in the aortic arch or carotid artery.. When it sense there's not
enough oxygen in the body stimulate Sympathetic NS stimulation- chemicals released: adrenaline(makes
heart beat faster)/ epinephrine (increases HR & causes vasoconstriction)
Renal system affects pt BP (kidneys) control Na/ water excretion and retention, when kidneys don't get
enough oxygen release renin release angiotensin 1 and 2 causes vasoconstriction YOU DO NOT WANT
VASOCONSTRICTION TO HAPPEN
→ Na retained = H2O retained
→ hypoperfused → renin is released → stimulates production of angiotensin
→ angiotensin - vasoconstrictor
→ vascular resistance
Endocrine system: causes release of aldosterone leads to → retention of Na & H2O
Atherosclerosis: build-up of plaque in the walls of the vessels; dec lumen of vessel → inc. pressure →
inc. BP
systolic : 140
Diastolic: 90
Can’t diagnose hypertension w a single measurement:
must be @ least 3 reading at 3 different visits; ​check BP of both arms for measurement - using the higher
reading
Use correct size BP cuff ​- false high/low readings (measure cuff w width of cuff- should be 1/3 around
upper arm
If it goes all around the pts arm the cuff is too big
If it cover only a small part it's too small
Lab values
Measure BUN & creatinine levels for kidney function
Cholesterol
Glucose: diabetics are more prone to vascular disease
White coat syndrome:​ elevated BP when they see the doctor or the nurse
Encourage pt to buy their own for home
Arm should not be up
Should be relaxed
Center the cuff correctly by markings
Two types of hypertension:
Primary hypertension: ​unknown​ underlying cause- look @ risk factors >>>!!
Secondary hypertension: ​known​ underlying cause such as ​kidney disease, endocrine disorders,
medications → causes high BP
Risk Factors​:
Age: more than 50% of individuals over 60 → have hypertension .. Nonmodifiable
Sex: more likely in men young adulthood ; nonmodifiable
Women >55; lose protective effect of estrogen … menopause dec. estrogen ; nonmodifiable
Race: 2x likely if ur black
Family history: 1st degree relative twice the risk non modifiable
Obesity: sorta modiafiable
*​Android​: central ​abdominal​ obesity- inc. heart disease - junk in the front * lol apple, often in
men
Gynoid​: have their ​junk​ in the trunk - more in women pears
Smoking: inhaling nicotine and co2 - causes vasoconstriction → heart works harder → what are we
supposed to be inhaling???? Clean O2 Modifiable
Na intake​: salt pulls water into blood vessels ,increases retention, modifiable - the more salty food u
eat → more water needed → inc. pressure
Lipid levels​: inc. risk of atherosclerosis - plaque narrows the lumen; modifiable bring cholesterol levels
down with diet or meds to treat or prevent hypertension.
Alcohol:​ limit 1 oz./day (30 mL) no more than 3 drinks a day inc. risks for cardiovascular disease, red
wine can be beneficial
Sedentary lifestyle​: inc. risks of cardiovascular disease (modiafable)
Well conditioned body at less risk for cardiovascular disease
→ if you’re well conditioned, your body utilizes O2 more efficiently
Diabetes​: impaired glucose and fat metabolism → contribute. To atherosclerosis * narrows lumen →
inc. in pressure! Higher risk for deposits of the fats and cholesterol in the blood vessel leading to
HTN . if careful they can control diabetes Type 2
Stress: ​modifiable ; ​epinephrine, cortisol, → narrows blood vessel;
→ Not important: TYPE B PERSON - chronically angry - always releasing adrenaline and cortisol
and wears away at the sympathetic nervous system at higher risk for HTN
Hypertension: ​the silent fuckin KILLERRR
Clinical manifestations​:
- “Silent killer”
- angina (heart has to work harder to move blood forward bc it's working so hard it needs more
oxygen, probably not available and it's what gives the pt chest pain or angina ) - inc. in
SVR/afterload of the heart; O2 required (CORONARY ARTERIES)*
- Headache: if HTN is very high all it takes is a little pressure bc of small blood vessels in the
brain)
- blurred vision (retinopathy)
- Dizziness
- epistaxis (nose bleeding)
When treating HTN trying to prevent target organ damage to the Brain, heart, kidneys, eyes*
Long Term untreated HTN can lead to HF takes year for this to happen ​hemorrhagic stroke. .
Untreated HTN blood vessels very tight and constricted the heart has to work harder to pump against that
resistance can cause hemorrhagic stroke
THE HEART IS A MUSCLE​ when your heart is working very hard the heart gets bigger and thicker,
but overtime the heart becomes flabby, dilated and can't pump anymore... called Heart Failure HF if the
heart cant pump it's called HEART FAILURE.
The blood vessels in the brain are tiny if the pressure goes up the blood vessels can burst and develop a
hemorrhagic stroke.
----we try to decrease the secondary affect organ the main vital organs [brain]
Min 38 on the recording
Systemic Effects of HTN​:
- Cardiac: inc in vascular resistance → makes heart work harder
- Cerebral​: Hemorrhagic stroke- burst in the brain
- Embolic stroke- caused by blood clot → anticoagulants!
- SEND FOR ​CAT SCAN!​ To check for embolic/hemorrhagic stroke
- Untreated HTN can cause Peripheral vascular disease : narrows blood vessel can deliver
blood and oxygen to the lower extremities lead to → ischemic muscle pain
- Long term untreated HTN renal arteries constricted not enough O2 going to kidneys.. Lead to
renal failure Renal: look at BUN & Creatinine levels to determine renal failure and decreased
UO
- Retinal: can cause damaged blood vessels in the retina, blurred vision and retinal hemorrhage
...With long term hypertension
- Can be assessed with the ophthalmoscope .. can see damaged retina w. Long Term HTN
*Long standing hypertension can lead to heart failure
Nursing Dx​:
- Altered tissue perfusion: Renal, cerebral, cardiopulmonary, peripheral
- Management of therapeutic regime: ineffective
- Knowledge deficit
Conservative treatment (SENS)​: supportive and educative
- Start off with Dietary approach (DASH) - Dietary Approaches to Stopping Hypertension;
Mediterranean diet (high intakes of olive oil, avocados, fish, olives, nuts, chicken, fresh fruits &
veggies - not celery (​because celery contains high amounts of sodium)​ & others
- Avoided high salted foods: cheese, cold cuts, fast foods, salted nuts, processed foods, canned food
- Whenever you eat high salted food your skin can feel tighter
- Decrease amount of fat
- Exercise: 20-​30 mins at least 3x/week ​Helps body use oxygen more efficiently, help with weight
loss and help with mood
- Cessation of smoking
- Stress management:
Pharmacologic Management: LOOK AT CHART FOR MEDS principle treatment
- Diuretics-​-promotes excretion of sodium and water , decreasing cardiac output. Before giving
monitor Bp, check k levels, IO, monitor for dehydration for elderly, given in the morning
Aldactone or spironolactone diuretics ​it's potassium sparing which can cause the pt to retain potassium
lasix /furosemid​e- careful! You’re depleting K+
- IV push, PO, lasix drip
- Check pt. BP & K+ level
- I&O
- High risk for dehydration * FATIGUE!
Thiazide diuretic: sulfa based - check allergies
Hydrochlorothiazide
-
- Alpha and Beta
Vasodilators (nitrates)​ ​Cause systemic vasodilation blood vessel and arteries, decrease preload
and afterload/SVR, increase blood flow to the heart.
Coronary arteries are dilated with nitrates; it's helping the arteries bring more O2 and blood to the
heart.
- (Renal arteries bring blood to the kidney)
- (Carotid arteries bring blood to the brain)
- Ace inhibitor
- Central acting inhibitor
- Angiotensin receptor blocker, aka: Ace ii
- Alpha adrenergic blockers
- Calcium Channel Blocker
- Beta Blockers
Vasodilator​: nitrates - hypertension (emergency situation) causes systemic vasodilation (all over arteries
& veins) typically to treat chest pain
Can be given IV, Paste, patch
- Dec. preload; inc. afterload
- acute chest pains
- Coronary arteries
no
- PO: isordil/imdoor
- Check BP every time before administering
- patch - put on chest, sustained release, last a long time. (​remove @ night​ to prevent ​tolerance to
medication​- the effect is reduced when the body gets used to it because the body is relaxed.
- Can cause Headache​s, flushing, palpitations
- IV: chest pain and VERY high BP (critical care setting)
Nitro paste - put onto paper → arms, chest, tape it, change it Q6H (nitro ointment) absorbed thru
the skin
Central acting inhibitors:​ working in CNS in brain; older group of drugs - catapres, ​wytensin, aldomet
Sends message to vasodilate and not to constrict → can cause ​orthostasis / orthostatic BP changes
when pt goes to lying to sitting or standing position BP drops drastically
ACE:​ Act right on blood vessel - can cause​ orthostasis
→ capoten vasotec, -pril (ACE inhibitor) ​1st line of therapy to lower BP and used
frequently​!
→ ​can lead to dry cough that may interfere w. Compliance. Monitor BP
ACE II (ARBS​): useful w renal pt; ​check BP & HR
→ can cause dizziness & cough
CCB Calcium channel blockers​:​ relaxes smooth muscle in arterial walls, dilate coronary arteries
→ do not give to pt in heart block *
→ check BP and pulse
When pt doesn't have enough calcium in the body it causes twitching or spasms of muscle
Too much calcium in cells of the blood vessels, causes vessels to contract so this med blocks the
calcium from causing the blood vessels to constrict. So they dilate the arterial walls.
→ ​AVOID EATING GRAPEFRUITS * (avoid grapefruits w/ statins &CCB) interfere with
metabolism of CCB
Beta blockers: ends in ​-lol (think beta adrenergic blockers) too much adrenaline makes the heart beat too
fast.. Make the blood vessels to constrict
→ ​Check BP, HR
→ beta ADRENERGIC blocker - beta adrenaline blockers - block SNS bronchodilation .. blocks the effect of adrenaline/epinephrine on the sympathetic nervous
system helps to keep the heart rate nice and low and dilated.
→ prevents tachycardia, vasoconstriction
→ avoid w resp. Problem bc bronchus will not be able to dilate → acute resp. Episode
→ avoid stopping abruptly ​… rebound HTN , cause increase in O2 demand of the
heart
→ Heart & SNS: needs to be chill mode
Underlying heart/lung issues
Pt with anaphylaxis reaction has to give them epinephrine injection causes bronchodilation
Do not give to people with lung problems, asthma, COPD
- People who take beta blockers have nice slow heart rate.. their heart has a lot of time for their
ventricles to fill with blood
Beta blocks adrenaline
Hypertensive Crisis​:​ rapid rise in BP systolic or diastolic
Give med slowly by IV (beta blockers)
Goal: prevent target organ damage of the heart, brain, or kidneys
Systolic: >240
-Rapid dec. can result in stroke
Diastolic: >120
-the formula to decrease the BP Gradual reduction in BP (MAP) by 10-20% every hour
Etiology​:
Poorly controlled hypertensives BP
pt who have stopped taking their meds.
Substance abuse
Pt having MI
Eclampsia:​ ​high blood pressure and excess protein in the urine during pregnancy or organ dysfunction.
It’s a rare but serious condition where high blood pressure results in seizures during pregnancy. ​Toxemia
pregnancy
Signs and symptoms ​
Related to cerebral edema and spasm of cerebral vessels ​
Headache, nausea, vomiting, seizure, confusion, coma, blurred vision, transient blindness due to
detached retina, have MI​
Angina​ and dyspnea related to increase in SVR
Treatment:
Significantly decrease BP within an hour in order to prevent death or target organ damage to the vital
organs. Brain and heart
Potent & direct IV vasodilators
IV push
Nipride drip, nitroglycerin drip ​, hyperstat, apresoline, labetalol, normodyne
Most common: nipride & nitroglycerin**
Have to be on infusion pump that is adjusted to pt BP
From ppt:
Arterial line for monitoring​→ cath that sits in Radial artery connected to something that looks like
IV Tubing connected to a bag of solution→ transducer that invasively measures pt aterial baseline Bp
→ continuously displays BP on monitor. IV bag has Bp cuff wrapped around with bulb hanging
down squeezed to provide positive pressure against the solution.
High pressure system so need the pressure
Direct measurement of the wall of artery
- Make sure pt still has radial pulse
- Make sure fingers are warm and mobile
- Monitor Bp
- Can draw blood thru them called arterial blood used for ABGs
- Neura checks (smile, tongue midline, pupil, hourly UO)
Nursing considerations​:
BP check every 2-3 mins
Connected to automatic BP cuff connected to heart monitor which is programmed to check every 2-3min
Monitor for hypotension
SUPERLATIVE neuro checks assessing for stroke
hourly urine output
Neura checks, pupil
Goal​: gradual reduction of pt’s BP 10-20% over the first hour.. MAP measurement use ; mean arterial
pressure
Then further gradual reduction in BP
- Can’t reduce BP too quickly →cause decrease cerebral perfusion and stroke
HOURLY OUTPUT SHOULD BE 30ml/HR
FOR THE TEST: READ THE BOOK/ATI BOOK***
Peripheral Arterial Disease (problem with blood supply and oxygen in
the lower extremities)
Accumulation of plaque and fat in peripheral arteries causes the blood vessels to become narrow and
restricts blood flow to the extremities as well as restricting blood flow to the nerve doesn't happen
overnight.
Lumen of vessel is occluded- can be a systemic problem
→ inc in pressure → inc. in BP
Untreated can cause → ischemia and loss of the limb
Treated with meds, exercise, or surgery .
Plaque or fat acts as an irritant and creates platelets there and makes the blood clot form.
If it occurs in the coronary artery the pt can have ischemia in the heart and cause an infarction
If it occurs in the carotid arteries the pt can have a stroke & brain
If it occurs in the legs can have ischemia and gangrene of the lower extremities.
Risk Factors​:
- Elevated lipid levels chronic cholesterol leads to plaque formation not enough oxygen going through
causes the blood to become thicker or viscus and starts to close off
- Cigarette smoking profoundly accelerates atherosclerosis and causes (vasoconstriction)
- Diabetes ​- accelerates atherosclerosis which increases risk for amputation- smaller vessels become
damaged makes it harder to treat
- Hypertension (2x risk for PAD)
- Gender-more common in MEN>women
- Age (50+ yo)
- ​Cholesterol: >200 → inc. risk for atherosclerosis
Subjective assessment
- Intermittent claudication; muscle cramp or muscle weakness triggered by exercise (burning, neuropathy
(weakness numbness, numbness)​- refers to an aching pain in your legs when you walk/exercise
Exercise causes this bc of → lack of O2 going to the extremities that also compromises oxygenation
of the nerves → develop neuropathy type S&S… vessels have plaque and narrowed not enough
oxygen going to the lower extremities.
document this as peripheral neuropathy
neuropathy
- Pain ​(experience pain at rest particularly when extremities elevated)
Pain usually occurs distal to where occlusion is (in particular when extrem. Is elevated)
Ex. femoral popliteal.. they are going to have Calf pain
Aorta leica vessel may have thigh pain
- As disease progresses may also have ischemic pain at rest
- Arterial: Hanging limbs off bed helps return blood flow to extremities via gravity dependent
postison force of gravity helps pull the blood down to their lower extremities.. May be more
comfortable when sleeping sitting up. Feel better symptomatic relief
- ex. pts w venous problems → elevate feet in bed
- ex. if pt has occlusion in popliteal: pain down calf
Objective assessment
● 5 P’s:
○ pain(claudication )
○ pallor (chalky white looking compromised blood flow to lower extremities)
○ Pulselessness (difficult to palpate pedal pulses on these patients)
○ paresthesia: ​numbness, tingling to lower ext.
○ poikilothermia: extremity adjust to the same temp of the room. room cold = pt cold/room
hot = pt hot
*****ALWAYS CHECK PEDAL PULSES TO CHECK FOR PERFUSION .. USE DOPPLER start on
the top of the foot start in middle and go around in tiny concentric pulses and hear pedal pulse be careful
to not push down on the pulse you won't be able hear the little amount of pulse they have
●
●
●
●
●
●
Skin appearance
○ Shiny tight pale skin scaly
○ Thick toenails
○ Dependent rubor- ​dependent position drop legs down (legs dangling) turns bright
red color
○ When put legs back up turn very pale again that chalky white color
Skin temperature
○ Cool or Cold to touch​ - bilaterally assess (w. Back of hand for temp.) always comparing
side to side
○ assess for peripheral pulses using ​doppler ultrasound- gentle touch bc u might diminish
the pulse
Depression, anxiety bc of loss of mobility
○ Diabetic pts also don't feel much pain bc neuropathy
○ Afraid of amputation - anxiety potential loss of their limb
High risk for development of Ulcers:
arterial( mostly on toe or upper aspect of the foot, bed of arterial ulcer very pale bc there's no
oxygen, may not have pulses),
diabetic (found on pressure points , plantar surface , heel more prone to that peripheral neuropathy,
they dont know theres a problem bc they dont feel it
●
venous( look red, bc there's no compromised blood flow there it's going to bleed when dressing is
taken off, should have pulses .)
Dorsalis pedis or pedal pulse very important to check with pt with PAD bc it lets us know the heart
is pumping sufficiently to the most distal part of the body… check on both sides
Diagnosis
- Doppler studies
- ​Ankle brachial index​ - compares BP of arm and ankle. ​anything <1 suggests PAD;​ Divide arterial
ankle pressure by ankle the brachial arterial pressure... should be 0.9 to 1.3
- ​Angiogram: peripheral - same precautions for heart angiogram, consent , assess for allergies,
baseline vitals → searching for occlusions
If pt actually has arterial pulses you have to mark it.
Dye is injected
Divide arterial ankle pressure by ankle the brachial arterial pressure
Conservative treatment
● Engaged in Risk factor modifications: lower cholesterol & saturated fats, smoking cessation,
mediterranean diet, no sodium foods (processed foods like cheese, cold cuts, fast foods, junk
food)
● Exercise: Asking to walk until feeling pain or cramping or neuropathy.. rest and then going a
little further, push themselves, aid in development of → ​collateral circulation. walk
everyday!!! Pt with PAD can help themselves by walking!!!!
○ Collateral circulation is the Branching of blood vessels →to maintain oxygenation and
perfusion.. helps perfusion to the heart (OLD PPL - this takes years to develop)
→ Less ischemic events w these damn miracle branches
● Extremity protection (diabetics): Cotton socks so their feet can breath! Helps to prevent skin
breakdown; no heat/coldness (cant distinguish w. neuropathy); specific closed shoes; linens
preferred - bed cradle and this lets the sheets not be all over pt’s legs, never soak their feet, can
distinguish between heat and cold with neuropathy.
●
Medications: ​Aspirin mainly used,​ Trental, Plavix, persantine, antilipemics, pain meds
antiplatelets
○ Aspirin; antiplatelet: blood thinner works on platelets. When taken everyday Ecotrin
enteric coated aspirin. To reduce GI bleed stomach ulcers (81 mg enteric coated*).. Can
cause ototoxicity, tinnitus, cause bleeding, bruise a lot, bleeding gums,
○ Trental: for claudication (pain commonly in legs, caused by little blood flow flow usually
during exercise.)
○ Aspirin ​(antiplatelet effect) ​- Look out for hematuria, blood in stool, epistaxis, gum
bleeding
○ Plavix: vascular disease (blood vessel anywhere; dec. platelet aggregation double
risk for bleeding and bruising.
○ Persantine: antiplatelet
○
○
Antilipemics: Cholesterol lowering meds
Elavil(older) for neuropathy/nerve pain - lyrica and neurontin
Pain meds​: rlt. To PAD… neuropathy medicine
- Side effects: mood/mental status changes
- antidepressants for neuropathy (elavil-tricyclic antidepressant; cymbalta-SSRI - selective
serotonin receptor inhibitor or some shit)
Endovascular procedures​: procedure room, access femoral artery usually, inject dye, watch dye flow
through open up blood vessels with angioplasty.
- ​Angioplasty ​(balloon is flat and deflated go to where plaque is, open up balloon it compresses the clot
along the blood vessel then deploy a stent that helps the blood vessel maintain patent or open )
- ​Stents(frame in blood vessel) stent is not a cure unless they modify their risk factors. Modify their
cholesterol, take antiplatelet medication.
- ​Atherectomy​ (shave the clot off)
- ​Embolectomy ​(surgical removal of the clot)
Surgical treatment​:to bypass obstruction, and provide/restore blood flow to the affected extremity. (​not a
cure!​) clamp off site where obstruction is and sew in a graft from one end to the other end.
***Performed when pt has pain at rest and danger when they are about to lose their limb
- Aortobifemoral bypass, ​femoropopliteal bypass “fem-pop” most common,​ femorotibial bypass
-​ Pre-op: bacteriostatic shower (Chlorhexidine), ​antibiotics, foley, central venous line CVL, vital signs
and baseline pulses- mark on pt’s extremity with marker, consent
Women → before surgery don’t shave legs for 72 hours prior bc portal of infection if there is a cut ​- - Post-op​: peripheral pulse checks with every vital sign check get doppler, assess for return of blood flow,
pain meds, OOB, ROM, assess suture line/ swollen, suture can be pink or fluffy normal, red, drainage
hard needs to be reported., want pt to cough and deep breath, a
- Check vital signs every 15 mins for the 1st hour
- Then 30 mins for the over 2 hours
- Then every hour for 4 hours
- IMPORTANT TO DO AS SOON AS PT IS BACK ON THE UNIT
- Assess for the return of blood flow. Warm to touch, leg turns pink/red, pedal pulses, edema,
swollen means blood has returned to lower extremities.
→ u HAVE TO assess your patients for S&S - THINK CLINICALLY - checking for signs of
returning blood flow → tingly & itchy throbbing is a GOOD THING! return of blood flow to
the extremity
→ Sharp stabbing discomfort is BAD! Can indicate occlusion of the blood vessel!!! This is
prob ​important lol tell HCP
- You want to get out of bed as soon as possible without bedding or sitting at 90 degrees bc of
bending on the graft site. → when ambulating pt- avoid flexion @ the graft site DON'T WANT
TO OCCLUDE THE GRAFT
-want
30ª to standing in one smooth movement so that u dont fuck up the graft
→ keep close eye on BP - graft sewn into blood vessels ! high BP must be treated - graft can separate
→ nitrates, diuretics (deplete volume);
→ low BP (70/50) graft can collapse → pt needs IV fluids!
Call surgeon immediately - loss of peripheral pulse; 12-24 hrs OOB ambulating; S&S of infection in
incision- warmth redness, drainage, WBC, fever
Diabetics- notorious for poor wound healing - high risk
Avoid using tape, harsh soaps, or peroxide on skin → leave dressing open let air heal it!
If the pt loses their pedal pulse let doctor know
BP 200/100 can be concerning because all that pressure can cause the incision to pop, can
give vasodilators.
BP 70/50 can collapse give fluids, volume to pump that vessel back up
Teaching​:
- Keep incision clean and ​dry​/yes shower no bath tubs
-​ Frequent position change
- Medications (esp blood thinners, antiplatelets)
- Professional foot care podiatrist (no pedicures lol)
- Risk factor modification (STARTS W. U!)
- Surgical follow up
​diagnosis: ​Ineffective tissue perfusion
2 more arterial processes​:
Buerger’s disease​: thromboangiitis obliterans- affects small/medium sized peripheral arteries that
become inflamed, spasm, & are prone/develop to blood clots; ​can affect upper/lower extremities​.;
vast majority of pts w buerger’s are MEN! (>95%) ​BOYS GET BURGERS!!!!! Typically smokers;
often around age of 40 yo; asians and eastern europeans have a higher prevalence; ​as disease
progresses to → tissue ulceration & gangrene
S/S very similar to PAD
Treatment? Stop smoking lol; keep extremity warm; prevent injury to extremity, often given CCB (Ca
channel blockers causes vasodilation)
If the extremity gets necrotic they may lose the disease
Can result in amputation
Raynaud’s syndrome​: vasospasm/ spasm of the blood vessel; ​often related to the cold or to
physical/emotional stress​; most common in young women (15-45 yo); usually affects the palms of
the hands; spasm of the blood vessels. manifestations- red white & blue ​(blue white & red) ​hands
turn kinda dusky, blueish; progression → hands turn chalky white, & as spasm resolve → hands turn
red
Keep hands warm w gloves; stop smoking ; CCB; nitrates
Aortic Aneurysms: Thoracic and Abdominal
Aorta highest pressure vessel in the body, aorta largest artery in the body
-Definition: outpouching of a blood vessel, it occurs when the vessel becomes weakened. Particularly
the middle layer of the artery becomes weakened muscular layer of the blood vessel ;
-Inner lining of the artery is called the Intima , outer part is called the externa, middle is media
-Weakness caused by deposits of fat/plaque that has been deposited along the wall of the blood vessel
that makes it become → vessel loses elasticity and potentially weak → RIGID; if compounded, inc. BP
= tightened blood vessel → POP BITCH!
- high pressure vessel with blood surging through it, the force against this area causes the blood
vessel to bulge and expand and even worse if pt has HTN.
- High pressure system; most often occur @ curved areas/areas where there is no skeletal muscle
supporting the vessel; inc. risk of blood clots
- Cerebral aneurysm
***ALWAYS RISK FOR RUPTURE AT THE ANEURYSM SITE
- Middle layer of an artery is weakened
- Weakened by fat and plaque with a loss of elasticity
- Exacerbated by hypertension
- Occurs where artery is not supported by skeletal muscle and curvatures
- Risk of rupture at site
-​ Risk of thrombus/embolism at site (Blood clot forming)...if the thrombus detaches it can become
an embolism up the ascending aorta or down the ascending aorta.
*IF THE AORTA RUPTURE THE PT IS GOING TO HEMORRHAGE ON THE SPOT AND DIE
Brain aneurysm: u fuckin die bro
Shoulder aneurysm: baseball pitchers!
Risk factors​:
- Atherosclerosis
- Hypertension.. Increases pressure along the wall of the vessel and can makes aneurysm grow faster
- Hyperlipidemia...causes atherosclerosis. High HDL
- Smoking
- Diabetes
- Heredity (familial-aortic)
- Age after 50
- Gender- MEN> aortic
Diagnosis​:
- Abdominal ultrasound using transducer outside of the abdomen, no prep involved
- X-ray
- CT scan
- TEE: transesophageal echocardiogram (Thoracic Aortic Aneurysm) NPO
- Doppler of lower extremities (abdominal aortic aneurysm- shunted into aneurysm and not into lower
extremity.)
Aneurysm Formation​:
- Saccular: Affects only one side of the blood vessel
- Fusiform: affects the entire circumference of the blood vessel
- aortic Dissection: different layers of the artery start to split and blood starts to seep through those layers..
Bc of pressure it starts to look like an aneurysm but it's not a true aneurysm it's called a pseudoaneurysm
Entire circumference of aneurysm
Dissection- layers of arterial wall starts to separate & blood seeps in between the wall and vessel
Assessment of a TAA​: (10%)
- 10 percent of aortic aneurysm are thoracic
- History: Marfan’s syndrome(connective tissue disorder [long thin arms- dangly looking, high forehead
and upper palate, retina problems, aorta and valve problems] ABE FCKIN LINCOLN!! Michael phelps),
hypertension, trauma, infection
-​ Subjective​: may be asymptomatic if it's small, symptoms are not related to aneurysm itself it is related
to the pressure that it's putting on surrounding organs in the thoracic cavity. chest pain, back pain, SOB,
hoarse(pressure on trachea) , difficulty swallowing(pressing on esophagus)
(symptoms related to pressure of adjacent structures of the thoracic cavity); (symptoms around pressure
where aneurysm was not rly bc something ruptured)
- Objective: ptosis (drooping eyelid), unequal BP of upper extremities depending where it's located
(aneurysm is stealing blood), ​deviated trachea, edema of head and neck ← BAD! Prolonged symptoms!
- Rupture of aneurysm: sudden and excruciating back or chest pain
Assessment of an AAA (abdominal aortic aneurysm) ​: (90%) aka triple A!
Can be asymptomatic, it is related to the pressure that it's putting on surrounding organs
Constant steady presence - gnawing discomfort
- Majority of aortic aneurysm are AAA’s
- Subjective: abdominal, back or flank pain, steady, gnawing, may radiate to groin or legs,
pain/discomforts is always there
- Objective: pulsatile area on the abdomen to left of the midline of the xiphoid process and the umbilicus.
A bruit may be auscultated over the AAA..Use a bell gently over the aneurysm to listen for a turbulent
blood flow (bruit)
- DO NOT TOUCH THE aneurysm AAA ***​ IT CAN RUPTURE
Abdominal aortic aneurysm rupture​:
- Sudden severe back pain (ripping/tearing sensation in back/abdomen) or if the pt says that
pain/discomfort is gone that means it has ruptured. Only last about 15 minutes.. then die bc they
hemorrhage to death.
- Resolution of prior discomfort
- High mortality rate &gt; 50 percent
- Hemorrhagic shock: s/s : pale, tachycardia, hypotension, diaphoresis, mottling (purple discoloration) of
lower extremities, umbilical and flank ecchymosis- turner or cullen signs..
(purplish discoloration of legs - poor prognostic sign - aka the end is coming! unless we do something!)
flank and umbilical ecchymosis (turner’s and cullen's sign)
At the end the pt would not have BP for some reason
Medical treatment​: beta adrenergic blockers
- Goal: decrease rate of enlargement and decrease risk of rupture by giving pt antihypertensive as an
outpatient PO or IV. ​ Keep systolic BP around 100.
- PO or IV [ batalol, alpha and beta blocker] antihypertensive BB, CCB,
- Call health care provider for changes of symptoms : abdominal fullness, back or chest pain, or SOB or
911
*** Try to treat with blood pressure medication first bc it's a complicated surgery
Surgery​: performed if the aneurysm is 2x the normal diameter of the aorta in that location
-Long surgery
- Pre-op: bowel prep to prevent infection,​ VERY IMPORTANT TO teach pt how to Cough and deep
breath before sending them to surgery bc of incision​ , type and crossmatch TC( have blood available in
the event if they need to be transfused), mark peripheral pedal pulses, teach how to use Incentive
spirometer
- Surgery: clamps above and below (distal & proximal) aneurysm, aneurysm is removed along with clots,
graft sutured from end to end. Anything under the clamp won't be getting oxygen. Worried about ..
Kidneys are not getting oxygen while it's clamped so pt are at high risk for developing renal
problems after surgery.
-Check BUN ,creatinine, and urine output
*clamp also does not allow oxygen to go down to lower extremities so that's why you mark the pedal
pulses
- High risk for hypovolemia and hypothermia​, Long surgery with exposure of abdominal organs. And
infection.
Post op care for AAA​:
- ICU for 24-48 hrs
- Long abdominal suture line closed with staples all the way down.. Retention suture on top of staples to
help keep suture closed so it doesn't dehiscence. Bc they can look 7 months pregnant
- Assess for signs of hemorrhage.. Hypotension, tachycardia, monitor hemoglobin and hematacrit,
monitor urine output. Any ecchymosis in the perineal area. Monitor hgb/hct , urine output
- assess abdominal dressing for any bleeding
- assess for peripheral pulses
- Assess for graft occlusion (can occur if a blood clot forms there or BP is very low) lose pedal pulses,
pain or numbness, pale mottled in the lower extremities) , by monitoring pedal pulses and the temp of LE
- Assess for renal failure (no kidney perfusion → higher risk [Q24 output monitoring]) BUN,
creatinine, IO
- Post op vital signs. Hooked up to continuous monitoring of VS: EKG,
- MUST give Pain meds bc they have to move and must cough and deep breath
- Elevated HOB 45 degrees​ only cannot have pt flexing or bending at the graft site just until graft has
taken
- Lung sounds q4h, high risk for pneumonia so coughing and deep breathing is important [must listen to
lungs posteriorly]... need to turn pt over to side to listen, can splint the abdomen, give them a pillow
- Assess for bowel sounds
- Maintain fluid replacement so pt BP stays normal
*Pt won't be able to cough and use the spirometer unless you give them a pain med
Assessing for: Tachycardia, hypotension, altered mental status, t positive sign, dec Hgb/Hct, cold temp,
diaphoretic, expanded belly girth,
Assess for graft occlusion: check distal pulses
BUN/creatinine - renal adequacy
Usually NG tube is placed immediately after surgery for a short time - listen for bowel sounds / passing
gas once that comes back NG TUBE can come out...they can then start clear liquids and advance from
there.
Post op ileus high risk - abdominal cavity surgery, organs were manipulated
May avoid open surgery and do...
EVAR: endovascular aneurysm repair: stent is deployed up to the aorta and sent is in the location
where the aneurysm site. Aneurysm is not removed but prevents the blood from making the
aneurysm bigger.
- much less invasive, pt recovers much faster; not open procedure → goes through artery
after procedure:
- monitor peripheral pulses before and after
- monitor access site (femoral artery)
- Can have full activity 3 days after procedure after stent is deployed
Surgical treatment of a TAA​:
- Pre-op: similar to lung surgery (high risk for pneumonia)
- Post-op: assess for hemorrhage via chest tubes, drain blood and serum (water seal chamber so no air
goes into the lung, suction, & drainage)
-Assess for rapid collection of blood hemorrahe maybe
- assess for ischemia of spinal cord bc pt may not move (NEURO CHECKS! Hand grasps, foot
push….motor assessments , PERL, etc.)
-observe for respiratory distress ​(Cough and deep breath very important​ & IS)
- high risk for atelectasis & pneumonia
Cough and deep breath and use the spirometer every hour
Aortic dissection​:
- Tear in the lining of the arterial wall. Blood seeps into the layers of the aorta and dissects or splits the
vessel wall. Causes fake looking aneurysm and causes that pseudoaneurysm
-whenever ventricle goes into Systole increases pressure and worsens the dissection
- Contributing factors include Marfan’s and hypertension
- Diagnosis: CT, and angiogram
S & S aortic dissection​:
- Severe, sudden back, chest, abdominal pain or dyspnea depending on location of dissection
- Aortic arch dissection: neurological changes [not enough blood supply to the brain] confusion, altered
mental status.. Aortic arch sits on top of the heart so If dissection starts to grow... heart sits underneath
and becomes compressed or squished.. the heart can cause cardiac tamponade
- Complications: cardiac tamponade, compromised blood flow to spinal cord, kidneys, & abdominal
organs [depends on the location]
Treatment of dissection​:
- Goal: lower BP
- Nipride potent vasodilator- IV and beta blockers
- Quiet environment to decrease sympathetic nervous system stimulation
- Sedation
- Surgery
Venous disorders
DVT Prophylaxis if pt didn't have an actual cardiac problem
Pt can have when they have an IV, superficial Phlebitis inflammation or infection of the vein:
phle=vein itis=infection red infection
Superficial Phlebitis​ ​
- Often related to intraVENOUS infusions ​
- Typically found on upper extremities
- Characterized by localized warmth, swelling, redness, and pain ​
- IV must be discontinued ​
- Treated with warm applications and elevation
infiltration= ​the catheter is no longer in the vein it's in the tissue causing the arm to become swollen.
Cold to touch and not red. The site is puffy and swollen. The iv needs to come out and need a new one
Fluid is leaking into the subQ tissue- swollen & cold to touch
IV needs to be removed and the pt needs a new IV
DVT: Dx impaired tissue perfusion
Formation of a blood clot in the deep veins of the calves.
Danger: Blood clot dislodges (breaks off) and travels via the entire venous circulation and lodges in the
pulmonary vasculature. Can result in DEATH
CLOT goes into superior/inferior vena cava → right atrium → tricuspid → R ventricle … then
gets lodged in pulmonary vasculature - pulmonary embolism (aka pulm. infarction) →
DEATH!!!
Related to venous stasis - usually forms @ the valve; accumulation of RBCs, platelets & fibrin
Virchow’s Triad (3)​ :etiology (risk factors for pt developing DVT)
1. Stasis of blood flow(blood just stays there) : Immobility, surgery(orthopedic), pregnancy, obesity,
varicose vein, atrial fibrillation, heart failure
2. Vessel injury (something damaged or irritated the blood vessel): Chemotherapy, trauma, central
vein catheterization, sepsis
3. Hypercoagulability (thick viscous clumpy blood) caused by : dehydration, birth control BCP’s,
smoking, blood dyscrasias (abnormal condition or disease of the blood), infection
Ortho: lovenox/heparin - prevention of DVT
If you’re young woman: seeking BC- stop Smoking
S&S DVT​:
- Unilateral leg pain or ​calf tenderness
- - Edema or swollen
- Warmth
- Can become red and hard
- - Homan’s sign​- when pt dorsiflex the foot if pt has pain or discomfort may suggest pt has a DVT
[do not perform . It Might cause PE bc blood clot can dislodge not really valuable can cause false
positive or negative and cause dislodgement]
Example of DVT nursing diagnosis : risk for ineffective tissue perfusion; fluid volume deficit, poor
circulation,
Diagnostic tests​:
- Venous ultrasound
- Venogram (invasive) inject dye to look for where the clot is
- Lung scan (rule out PE)
- Labs: PT/PTT - showing value of heparin drip (IV) or warfarin
- First put pt on heparin drip
Prevention of DVT​: DVT prophalaxis
- Early ambulation- get them out of bed​! ​Immobility number 1 cause - dont need a doctor's
order. Addressing the stasis of the blood flow component from virchow's triad
- Adequate hydration 2-3L a day within cardiac tolerance.. Addressing hypercoagulability
component
- Sequential compression devices SCD (definitely for prophylaxis) helps with circulation of the
blood pushed blood back to venous circulation back to the heart -​ make sure to inspect the skin.
Need physician's order ​if ambulating pt is not possible make sure to apply SCD
- Anticoagulation: lovenox (low molecular weight heparin) [70 mg]SUB Qin love handle--do not
aspirate or add pressure when taking the needle out
- SUB Q injection of low molecular weight heparin, SQ heparin (5000 units/12 hrs (1 mL) ;
DON’T RUB THE SITE AFTER U INJECT! BRUISING
You never want to massage a pt’s lower extremities
-There is no lab value to assess the effectiveness of lovenox
-no risk
Treatment of DVT​:
- Thrombolytics: Help break up the blood clot (streptokinase, urokinase, TPA (tissue
plasminogen activase) -ase → ENZYMES
- Thrombectomy: blood clot removal (surgically)
- Heparin IV (/infusion)/SQ 5000 heparin IV push /
IV heparin drip standard concentration 25000 U/250 mL of IV fluid transition to
- Oral anticoagulant Coumadin (check PT/INR) started while still on heparin drip when PT or INR
is therapeutic then you can stop heparin drip
- Lower extremity elevation to decrease swelling, promote venous control
- Sequential compression devices SCD use on unaffected extremity
- danger of using SCD in affected extremity can dislodge clot and cause it to travel back to the
heart and lungs
- Frequent clot formers: cardiolipin syndrome frequent PE sent to get
- Vena cava filter: sits in SVC or IVC catches the blood clot before it makes their way to the
heart or the lungs. If blot clot travels thru venous circulation and goes into lungs..
- Pulmonary blood vessels become occluded by the blood clot blocks blood flow distal to the
occlusion in the lungs that part of the lungs becomes ischemic and necrotic can result in death
called pulmonary infarction. If pt can still breath the problem is the lung is not perfused bc the
blood clot is blocking blood flow to the lungs.
- Most pulmonary emboli come from DVT of the lower extremities. Can also be result of a fat
embolism from a long bone fracture that can go to the lung
- A.fib can also cause PE
PTT: if its low 35> rebolus w. 5,000 cc; inc. IV rate by 3 mL/hr; repeat in 6 hours
PTT: if its too high normal 70-90 therapeutic range → 2-2.5
Google heparin nomogram??
Rebolus w. 2500 units, then inc. IV rate by 2 mL/hr - repeat in 6 hours
Heparin - rapid onset/short half life
Very short half life
Coumadin - risk for blood clots & Heparin @ same time
- Coumadin has a much longer half life & slow onset
- Watch for bleeding,bruising, nose bleeds, hematuria, nose bleeds
INR & PT are therapeutic - discontinue heparin
Normal PT: 11 seconds
Therapeutic: 1.5-2x control
15-22 PT / INR 2-3 → D/C heparin → pt discharge! Byebye
pt. Prone to blood clots - ​VC filter​: kinda looks like a collapsed (see pic) umbrella in a coconut - traps
whatever before they get to the lungs or wherever else they’re heading - stops them!
Pulmonary embolism​:
-
Occlusion of pulmonary vasculature by foreign substance
Blocks blood flow distal to the occlusion
Can result in sudden death (no gas exchange!)
Lung is ventilated, not perfused
Pulmonary infarction
Source of PE​:
- Majority​ dvt of lower extremities
result in sudden death
- Atrial fib
- ​Fat embolism​ from long bone fracture:can
- Amniotic embolism
Symptoms of a PE​:
-Dyspnea, chest pain, tachycardia, apprehension, cough, hemoptysis[blood in the sputum coughing up
blood] only 10% of pt
-may/not pneumatosis, crackles, wheeze, OR- lung sounds can be clear…
-Sudden onset
-Sudden death
Diagnostics​:
-spiral CT scan
-V/Q (problem of perfusion) inject dye pt inhales a gas and they can look for the distribution of gas in the
lung
-Pulmonary angiogram- the blood flow thru the lungs is abnormal
-ABG’s
-D-dimer looks for the product of fibrin degeneration. It is an indication of clotting abnormality
Collaborative care​: O2 in some way/shape/form... Oxygen mask will be given may need to be ventilated
- oxygen(mechanical intubation) → Non-rebreather O2: 100% high flow O2 . put o@ mask
- Head elevation to help the pt breath better
- Thrombolytics break up that blood clot
- Anticoagulants (watch out for bleeding)
- monitor PT/PTT/INR
Another early intervention that you can implement if u suspect PE?
- Check pulse ox.! And BP
- Put N/C into mouth!!! Crank dat shit up - unleaded O2! Save the patient! Do what you can until
RRT comes and gives pt ​nonrebreather!
Varicose vein​:
Pathology: veins become dilated and tortuous, become large and bulge. Vein enlarged, valves are
stretched and become incompetence.
- Fluid can leak into the capillary bed and leaks out to tissue and can develop lower extremity
edema.
Predisposing factors​: prolonged standing, familial (women), obesity, pregnancy
-Esophageal varices (ppl can hemorrhage to death! Risk- alcohol abuse, liver disease), Blakemore tube
- hemorrhoids (varicose veins in rectal area)
-symptoms:​ lower extremity ache or fatigue, edema, cosmetic disfigurement, can be removed, heat can
be applied, chemical injected that can treat it and help it disappear.
-treatment:​ ligation and stripping, thermal ablation, sclerotherapy
- ​nursing care:​ check extremity for color, movement, sensation, temperature, edema and peripheral
pulses, ambulate, extremity elevated to promote venous return , compression stocking help promote
venous return.
Thallium scan: shows hot spots and cold spots on a scan - lets us know where ischemia might’ve occurred
Precipitates heart failure
If the heart isn’t contracting as much, the blood can back up into the pulmonary vasculature - give beta
blockers cautiously and monitor for HEART FCKIN FAILURE!
→ edema, SOB, weight gain
DIGOXIN inc BPw
Coronary artery disease (acute coronary syndrome ACS)
Coronary artery supply blood to the heart or the myocardium
Pathophysiology​:
- Start off with Plaque formation: deposit of fat and plaque/cholesterol lipids along the walls of the
vessel/ coronary artery... causes the lumen of the artery to narrow and compromising blood flow
and oxygen to the heart eventually the blood vessel cause it to close
- Fat and plaque acts as an irritant to the blood vessel which can open causes Platelet
aggregation to attract to the area: → start to form clots or thrombus can occlude vessel OR
can cause….
- Thrombus dislocation: blood clots dislodge and travel and lodges in the myocardium itself
causing oxygen deprivation and ischemia can occur
- Collateral circulation. Should exercise
- Not as much oxygen can get to the myocardium because the narrowing of the lumen
- Fatty plaque can rupture and form a thrombus, the thrombus will start to get bigger and obstruct
the blood flow and enter into acute coronary syndrome, have unstable angina that is completely
relieved by resting nitroglycerin not helping and MI where the heart muscle can die and become
damage
Collateral circulation​:
- Development of collateral circulation → branching of blood vessel to reestablish
oxygenation to the lower extremities
​→ blood flow to the heart: limit the risk of ischemia and infarction
- Occurs when pt has chronic ischemia, chronic blockage the heart will try to reroute
circulation around that blockage so it can get blood to the heart muscle.. Tiny blood vessels
form to reroute blood around the blocked artery
- Developed by itself over the course of many many years as the vessel gradually starts
to close off branches off of the vessel will start to happen.
- Developed by walking: takes a long time for these branches to grow; present in the older
people will have better collateral circulation helps to keep the blood rich with oxygen and
particularly in the event of the vessel closing off and help maintain perfusion to the
myocardium
- More devastating or severe in young people bc they haven't had time to develop collateral
circulation
- also happens in colon
Diagnostics​:
- cardiac enzymes: troponin (specific to the heart), CK (Creatine kinase); non specific muscle
damage indicator​/C
​ PK, CK-MB/BNP
- Stress test/pharmacological stress test; monitored with EKG
-
Thallium stress: contrast injected during a stress test ,dye; shows hot spot and cold spot that
reflects perfusion to the heart… indicating ischemic area, less invasive
Holter monitor: 24 hr EKG reading; writing diary important to write down s/s
Echocardiogram: uses ultrasound to look at valves and left ventricular walls. Gives us ejection
fraction percentage which is 50 to 70%
TEE echocardiogram; transducer that is swallowed gave a good look of the aortic arch make pt
NPO prior.
MUGA: computerized tests can a computer that looks at the heart and can also give us the
ejection fraction
Cardiac cath/angiogram: assess for allergies to iodine and shellfish , mark pedal pulses,
EKG: abnormal heart rhythm, any ischemic damage to the heart
● P wave: atrial contraction/depolarization/systolic
● QRS complex: Ventricular contraction/depolarization/diastolic
● ST segment (important): where we see ischemic changes; either elevated or​ depressed
when heart experiences​ ischemia
● Depressed ST elevation indicates ischemia
● ST elevation indicated injury
● T wave: ventricular relax/repolarization/diastolic
1 AVR V1 V4
2 AVL V2 V5
3 AVF V3 V6
Lead 2
Sinus rhythm​: normal heart rhythm
Modifiable risk factors​:
- Serum lipids: increase the risk of acute coronary syndrome/disease NPO before levels are drawn
- Less than 200.. ​Greater than 240 increases risk for CAD by 3 times​, and want pt to have
high HDL and low LDL.
- Start to modify lipid levels with dietary approach, start by eliminating high cholesterol food and
high fat foods. if cholesterol levels remain high after 6 months start pt on Statin.
- Mevocor (lovastatin), Lipitor (atorvastatin), Prevachol (prevastatin)
● Statins (large med group most common) inhibit synthesis of cholesterol, can have GI
side effects, elevate ​liver function test, ​Cause opacity of the lens of the eye​, before
pt is started on statin is important to get baseline liver function test and
baseline eye exam and regular eye exams after.
● avoid grapefruit​; interfere with synthesis of this medication,
● Pt can complain of severe muscle pain, feel like they've been hit by a truck→ called
rhabdomyolysis if this happens,.... If this does occur statins need to be stopped and
placed on another medicine. (muscles break down)…→ kidney cannot process all
those proteine → renal failure
-
-
-
Bile acid sequestrant (Questran (cholestryramine) → has a lot of GI side effects, Eliminates
cholesterol by converting to bile acids in the liver. Lowers LDL, raises HDL :Interferes with
absorption of some meds, i.e. Coumadin, diuretics.
Nicotinic Acid; Niacin: ( Increases lipase, the enzyme that breaks down lipids to lower
cholesterol) OTC med; can cause flushing, pruritus, GI symptom, can purchase flush free niacin
lopid (fibric acid):cause GI side effects. Restricts the production of lipoprotein
Another Modifiable risk factor; Hypertension: BP greater than 160/90 significantly increases
SVR, workload of the heart and oxygen demand ; HTN causes blood vessels vasoconstriction
→ heart work harder left ventricle to push blood into SVR → systemic vascular
resistance/afterload and increases oxygen demand to push blood out. Heart needs more
oxygen to push the blood out and if pt had CAD not much O2 is getting to the heart so it's
IMPORTANT TO TREAT HTN WITH MED TO PREVENT long standing
myocardial disease​.
Smoking: increase risk of cad 2-6 times; nicotine → causes vasoconstriction → afterload the
energy the blood has to push againish SVR; inhaling CO2 decreases oxygen available
Sedentary lifestyle. Heart uses oxygen more efficiently when well conditioned, Exercise will
increase collateral circulation to a certain extent.
Obesity: android (apple); all the body fat in the front higher risk, more common in male
Stress: Type B person
Diabetes: impaired glucose metabolism and fat increases risk of fat deposit in the coronary artery
with atherosclerosis and closing of the coronary blood vessel.
Homocysteine; amino acid found in dietary protein; elevated level are found to be associated with
increased risk of coronary artery disease; damages the lining of the blood vessel
- Treated elevated homocysteine levels with B complex vitamin (B6, B12, & folic acid
are important)
Unmodifiable risk factors​:
- Age: the highest incidence in middle age is in white men
- 60-65+ → increase incidence in women develop from the ​lack of estrogen
(menopause)
- Gender … Men
- Race: more common in whites
- Family history: first degree family history in MI, cardiovascular disease, blood vessel disorder
Disease states R/T CAD:
- Angina pectoris (chest pain)
- Acute MI
- Sudden cardiac death
prevent acute MI
Angina pectoris:
- The demand for myocardial oxygen exceeds the ability of the coronary arteries to supply the
oxygen →oxygen deficient/ ischemia is expressed as a symptom which is chest pain (angina!)
-
**Silent ischemia/silent MI - asymptomatic heart disease. most common in pts. w.
chronic htn &​ diabetics ​asymptomatic cardiac ischemia
- The coronary arteries are narrowed due to atherosclerosis - stenosis of 75% or greater if the
vessels are occluded more than ¾ can lead to ischemia. can also result from a coronary artery
spasm Angina chest pain can occur from a blood clot in the coronary arteries or when it's lodged
in the heart itself.
- Ischemia or oxygen deficit to the heart, can also happen in situations where the BP is very high
due to the increased pressure in the artery being constricted and causing the heart to work harder
so it's going to need more oxygen.
- Myocardium becomes cyanotic or dusky/ ischemic within the 1st 10 sec. of coronary
occlusion EKG changes will start to occur (in ST segment)
When the myocardium becomes hypoxic (low oxygen) conversion from aerobic to
anaerobic metabolism.
- Conversion occurs from aerobic → anaerobic metabolism with the
production of ​LACTIC ACID​ (by product) is what's causing the pt to have the
chest pain; if blood flow is restored/resumes within 20 mins aerobic metabolism
will occur…
- If nothing is done to fix the problem and don't get rid of the blood clot
tissue, necrosis of the myocardium is complete in 4-6 hrs. if blood flow isn’t
restored …if heart becomes dead and necrotic it won't pump well
- ER situation: what do u ask? What time did ur chest pain start?!
- 9AM? The tissue is dead there's nothing we can do about it
- Last night around 5pm ? Jump into action! We can stop the ischemia
Three grades of myocardial insult
- Ischemia
- Injury
- Infarct is permanent damage
- The left ventricle is most at risk for ischemia → it’s the hardest working part of the heart bc
pumps against systemic vascular resistance
Left main artery supplies blood to the left ventricle so if it's occluded the left ventricle can be in big
trouble the widow maker bc the L.V needs big oxygen supply
Precipitating factors:
- Physical exertion - increases tachycardia/increases HR; decrease ventricular filling time over long
haul starts to decrease cardiac output
- Strong emotions- stimulate the SNS → increases HR & BP.. When BP is increased makes
heart work harder bc of vasoconstriction
- Large meal- can precipitate chest pain (especially if already have underlying HD); pressing on
diaphragm - further restricting O2 oxygenaton);when a pt eats a large meal blood is shunted down
in the Gut(away from the heart) to aid in digestion making less oxygen and blood available to the
heart. ex .thanksgiving time = ER pts. With full stomachs
- when also eating a large meal it compresses the diaphragm - further restricting O2
oxygenation to the heart.
-
-
Temperature extremes: cold temp? Blood vessels Vasoconstriction which causes it to
work harder SVR is increased; HOT? Blood vessels dilate! → blood is pooling in the
extremities when the pt. Is vasodilated (blood is not going to the heart / coronary
arteries to aid in perfusion to the heart )
Sexual activity; increases SNS
Stimulant: coffee (caffeine), certain drugs, red bull?! Can produce cardiac event
Cigarette smoking: vasoconstriction
Circadian rhythms: normal sleep/wake cycle; cardiac symptoms are more prevalent in the
morning after awakening vs later at night (O2 is dec. - precipitate angina) bc of increase of SNS
in the morning the demands cause vasoconstriction and tachycardia vs at night metabolic
demands are lower
Types of angina​:
- stable: predictable pattern of onset, duration and intensity, occurs infrequently, usually exercise
induced (exertional angina) ex. Climbing a flight of stairs every time
● Patient does not necessarily need to be hospitalized - (not for stable angina)
● Can be controlled by meds nitroglycerin, rest
● Predictable angina can be related to stable blood clot in the coronary artery
-
unstable: (also known as progressive, preinfarction angina) angina, unpredictable, may occur at
rest, during sleep. ​Requires hospitalization, should be on telemetry, can lead to MI, should on
blood thinning and probably start to see changes in EKG.
- Tuff fiber on the outside of the plaque will rupture, *Fat/plaque are leaking into the
bloodstream → platelets try to go to the area to cover the rupture/ control the leaking
and make things worse by causing a blood clot that eventually is going to occlude
the blood vessel all together (more obstruction).
- hospitalized , on telemetry, meds. : aspirin/heparin
- Unstable angina: changes in ST segment
-
prinzmetal’s: “coronary vasospasm” - not related to atherosclerosis!
- Pt have Excessive Calcium in the cells of the walls of the coronary arteries (too much
calcium causes spasm/twitching)→ causing coronary vasospasm to narrow or spasm →
causing chest pain you would give CCB ​.
- Raynaud’s syndrome/disease? spasms of peripheral arteries
Anginal symptoms:
- Pure Chest pain or pressure (constriction/squeezing/heaviness) can be under sternum
- When Pt complains of pain, ask Pt to rate the pain 1 to 10.
- Cardiac pts. Feel elephants standing on their chest kind of pressure.
- Subj.: substernal pain
- Many experience “Severe indigestion” give GI meds: Maalox, Mylanta (Antacid) to distinguish
if they feel better related to GI, but if not relieved then it's a cardiac issue.
-
Pt experiencing chest pain can have Radiation to neck, jaws, shoulders, arms (particularly down
the left arm and back)
- Women have different symptoms when it comes to a CV event - no chest pain, “i feel
exhausted/hit by a fcking TRUCK” & SOB and extremely fatigue *
- Shortness of breath: if the left side of the heart can’t pump the blood, blood is backing up into
the lungs → auscultate crackles - lungs are filling w. Fluid → cardiac crackles
- Pt can have Diaphoresis/ pale
- Arm can feel numb
- A sense of Impending doom and do something bc usually something terrible does happen, you
can call rapid response team RRT
- Some people may have no chest pain, women may not have classic chest pain, can have extreme
fatigue, feel like they have been hit by a truck and feel like they have been hit by a truck can be
dismissed as anxiety while in fact can be having an MI. SOB
- Numbness of arm/abnormal heart rhythm - ischemia
Nursing dx: ineffective/altered tissue perfusion: myocardial
Treatment of angina: given two different ways
- Pt with atherosclerosis, CAD, PAD uses aspirin. First line of treatment Aspirin; ​can be used
prophylactically to prevent clumps/clots (can be systemic),
- Prophylaxis (between 81 to 300 mg/day everyday) further production of atherosclerosis
- PO oral aspirin to prevent atherosclerosis, helps by preventing platelets from accumulating in the
coronary artery/blood vessel. Keep in mind the risk for bleeding
- Already had a heart attack? Administer chewable 325 mg/day in acute chest pain/ situations
works faster to help break up the clots and platelets as an antiplatelet.
- Hazards: GI bleeding/bleeding in general (bruising/bleeding gums/blood in output)
- Give to the patient with GI bleeding; Enteric coated aspirin - ecotrin → saves
irritation to GI ​lining​ (don't crush)
-
PCTA (percutaneous(through the skin) coronary transluminal angioplasty) (aka angioplasty)
Typically done for single or double vessel disease
- 1. Performed @ Cath lab ​with contrast IV to locate obstruction
- Femoral artery is accessed, allergies?, mark pedal pulses, consent
- 2. Angioplasty- performed by floating a catheter with deflated balloon up into affected
coronary artery once it's in they inflate the balloon and plaque is then compressed along
the wall of the blood vessel
- Typically give pt two IV medication infusions during the procedure.. Heparin drips to
prevent more blood clots from happening and nitroglycerin drips because it's a
vasodilator trying to open up the vessel as much as possible so the balloon can be inflated
as much as possible.
- 3. Stent is deployed- is floated up into the vessel to keep it open and patent
- This does not fix anything, it is not a cure, it can continue unless the pt is engaged in
lifestyle modifications.
- Monitor for bleeding at insertion site
-
Stent- is a thrombogenic. Make sure pt is on anticoagulants after stent procedure.
Keep in mind: pt. w . stent → inc. risk of formation of blood clots
Thrombogenic: inc. risk for blood clots
- Goes home on aspirin, plavix, coumadin for at least 3 months
-
Anticoagulants - (coumadin)
Heparin​, platelet aggregation inhibitor, GP)
- IIb/IIIa inhibitors
- Start heparin drip for cad pts admitted to hospital
- Heparin is a vasodilator
- Monitor for PPT
- Antidote protamine
Beta blockers good for dilating coronary arteries
Calcium channel blockers (​prevents spasms due to excess calcium at coronary arteries) ​ good for
dilating coronary arteries
-
Nursing diagnoses:
- Pain
- Anxiety
- Decreased cardiac output
- Altered tissue perfusion myocardium
Heparin- blood thinner (could cause emboli)
Nitrates ​used in the treatment of both chest pain and if they have MI , vasodilators , dilate both arteries
and veins! particularly Effective at dilating coronary arteries
Nitrates vasodilators ,​ dilate both arteries and veins! particularly Effective at dilating coronary arteries
- Acute chest paint can give nitroglycerin sublingual PROTOCOL 1 tablet every 5 mins for a
maximum of three doses.
- Monitor BP before administering everytime
- Very good @ dilating the coronary arteries ********
- S/E: hypotension, headaches, and flushing
- Can also be taken sublingually - dose; 0 .4 - 0.6 mg (1/150) (1/125)
- Brown bottle- photophobia precaution (keep in the dark) light resistant
- 1 pill every 5 mins for maximum of 3 doses
- Check BP every time!
- Warn pt that it can cause a headache and make the pt feel warm and flushed
- Ask pt. Pain scale after every dosage
- If this doesn't work, call 911
-
Nitropaste​ - for HTN - squeeze onto paper (changed every 6 hrs) CHECK BP! Causes lots of
vasodilation. Not used for emergency sitaution
-
Nitro patch​- take off @ bedtime to prevent tolerance to medication Not used for emergency
situation
IV Nitroglycerine​ - potent vasodilator open blood vessel so heart doesn't have to work as hard. Does a
good job at opening the arteries to increase perfusion to the myocardium
- needs special IV tubing solution can be caustic [drug can cause deterioration of regular IV
tubing])
- IV nitroglycerin - critical care setting: dilates coronary arteries; dec. SVR/afterload; heart
doesn't have to pump as hard → doesn’t need more O2 to work
- Need to be on automatic BP cuff and monitor that is frequently cycling to check BP, brown
bag needs to hanging over the IV
- Dec. preload, dec. etc.
- Every 3 mins cycling, or ARTERIAL LINE! But its invasive lol
Fibrinolytics: fibrinic acid- DONT GIVE WITH STATINS; gemfibrozil; LFT, GI, statins →
restricts lipoprotein production
This is a much better alt. ! instead of open heart surgery
Nursing interventions:
- Rate pain (1-10); 10 is crushing chest pain; not everyone has chest pain (sometimes
asymptomatic)
- common med: nitroglycerine - one tablet every 5 mins for max 3 times
- SE: headache, hypotension, flushing
- check BP before administering drug
- Place patient in quiet environment
- → less anxiety (try to keep down sympathetic nervous system; → adrenal(ine?),
epinephrine)
- Administer supplemental oxygen: typically NC (at least 2 to 4L) - mouth breathers due to
hyperventilation? Use an oxygen mask!
- Nitroglycerin (protocol)- headaches/flushing* - give heads up that these side effects may occur
- Monitor vital signs - check frequently every 5-15 min
- Use cardiac monitor EKG
- Obtain EKG- some kind of telemetry only uses 2 electrical views of the heart (so do you
know where the ischemia is happening? No, so you should see ​12 leads EKG ​→ 12 lead
EKG you can look at every area of the heart to where the ischemia is occuring (white to the
right … → Left, pepper is spicy … is black.. Then .. so red goes under … christmas tree
down → green across - brown (middle of chest)
- Assess for ​impaired peripheral perfusion ​(assess for decreased pulses & changes in LOC
[brain O2 deficient, altered level of consciousness meaning pt is not receiving oxygen in the
brain], ​pallor ​( if pt becomes pallor the skin is not receiving enough oxygen it's the largest
organ in the body but it's a low priority organ) , decreased u/o ​kidneys is not receiving
enough blood and oxygen [30 mL @ LEAST/hr]) (the heart isn’t pumping blood to every
part of organs .. diminished peripheral pulses means heart is not pumping); kidney’s not
getting enough blood either → urine output decreases
- decreased UO is not the first thing you will notice when oxygen isn't getting enough
oxygen, something you will notice later on.
- Restalablish perfusion to the brain and the heart itself
- Monitor labs esp. Cardiac enzymes (CK-MB) troponin, baseline PT/PTT
- PT/PTT - going to be placed on heparin drip … for coronary arteries → plaque
builds up and the heart isn’t perfusing
Myocardial infarction​:
- Results from sustained ischemia, resulting in cellular death and necrosis (tissue death) of the
myocardium (gangrene of the heart; tissues are dead); occlusion of the artery (plaque) OR
plaque that dislodges to the myocardium → causes ischemia/tissue death
- Can be ischemic for 20 min before cellular death occurs… ​in about 6 weeks →
the dead necrotic tissue is replaced w scar tissue that is MUCH LESS
COMPLIANT/ELASTIC than healthy tissue which can compromise cardiac output
- ex> burn: tissues are not elastic and tiny
- Transmural MI ​(all 3 layers of the heart are involved) results when the infarction has developed in
the entire thickness of the myocardium is involved
- endo/myo/pericardium
- THIS IS BAD! When all 3 layers have infarcted
- Presence of good collateral circulation can greatly impact/limit the extent of the ischemia
supplying blood to the heart, the MI won’t be as bad
- Subendocardial MI, only the endocardium has become ischemic not as terrible
- Impending doom
- Altered LOC
Diagnosis of an MI​: 3 things to look at (clinical presentation, cardiac enzymes (blood work), & EKG
changes)
1. Clinical Presentation:
- SICK LOOKING PT. with sense of impending doom (Radiating pain in neck, jaw, chest)
- “Chest” pain, NOT relieved by the 3 NitroGlycerin (seek 911 if 3 doses dont work), Pallor,
Nausea and vomiting, Dyspnea, SOB (caused by the left side of heart not moving blood
forward ; blood regurgitates back into lungs; called pulmonary edema); not enough blood to
the brain → alter LOC
- Benefits of nitrates: dilate the coronary arteries and veins; arterial dilation → dec.
SVR/afterload; heart doesn’t have to work as hard; ​MONA​(morphine, oxygen,
nitroglycerine, aspirin)
- Morphine: a good dilator; 2-5 mg IV push
2. Cardiac Enzymes CK/CPK MB(isoenzyme: elevated when positive) elevated Troponin T and I -series
of troponins every 8 hrs → ischemic event
3. EKG CHANGES ST segment depression/elevation; Inverted or “flipped” T wave; any changes in ST
segment are indicative of ischemia
When you look at an EKG strip or telemetry monitor you want to see 3 configurations. You want to see a
bump, skinny spiky complex followed by another bump.. want to see this over and over again with pt
with normal heart rhythm.
- The first bump represents atrial contraction/ systole, or depolarization which is the P Wave
- Following the P wave is the skinny spiky complex called the QRS complex sometimes goes
up, down, up or sometimes down up down or up down ALL YOU WANT TO SEE IS
SKINNY SPIKY COMPLEX FOLLOWING THE P WAVE.
- The QRS complex represents ventricular contraction or ventricular systole, or ventricular
Depolarization
- T wave represents ventricular relaxation , ventricular diastole, ventricular repolarization.
- If you see P QRS AND T over and over again you can say the patient is in sinus rhythm.
- When pt is having ischemia to the heart or myocardium the change you're going to see is in
the ST segment which is between the QRS complex and the T Wave .
- ST segment runs along the isoelectric line
- Pts with ischemia the ST segment is going to be depressed or ST segment will be elevated.
- STEMI: ST Elevation Myocardial Infarction. Any change in the ST segment is an
indication of ischemia
- Not elevated/depressed? NON-STEMI
- inverted/flipped T wave → old ischemic damage (in the past the pt/ has had a MI)
- In order to say the pt actually had an ischemia on a EKG have to see the ST segment
changes on two consecutive leads or two electrical views. See it in lead 1, 2, 3 or AVR
or AVF in roman numerals
- Pts are prone to abnormal heart rhythms, Dysrhythmia and arrhythmia and
sometimes put on prophylaxis antidysrhythmics like amiodarone or lidocaine.
- Pt having a heart attack or MI they are going to look sick , have elevated enzymes,
and note ST segment depression or elevation on two consecutive EKG
- Additional EKG changes?? Abnormal heart rhythms due to myocardium becoming hypoxic
→ causes irritability of the myocardium
- Premature ventricular contractions/PVCs(QRST; wide bizarre looking beat): if the
ventricle contracts before it was supposed to, the ventricle isn’t filled w. Blood →
cardiac output; the more PVC → the worse cardiac output will be
- Normal conduction path
- Conduction through Bundle of His- smooth conduction; if the shit goes
elsewhere → PVCs
- Common causes: Hypokalemia & ​hypoxia​ are common causes of PVCs
- Med. to prevent ischemia? LIDOCAINE - prophylactically - acute care setting;
IV drip to prevent PVCs
Treatment of an MI​:
- Nitrates:​ special tubing; light sensitive (cover w dark bag); continuous BP monitoring (need
fusion pump?)
- Dilating coronary arteries
- Systemic: decrease SVR (afterload); heart doesn’t have to work as hard
-
-
-
Dilates veins - benefits of dilating veins results in less blood going back to the right side
of the heart which is called decrease in preload/ decreases workload of the heart (volume
or the amount of blood before it gets back to the heart)
- If having an MI going to be on that IV nitroglycerin drip
- systolic BP less than 90 will be a contraindication for the use of nitrates
- MONA (morphine(sulfate) oxygen nitrate aspirin) causes venous dilation
- Morphine helps w pain BUT it also causes venous dilation/ vasodilator →
decreases preload/afterload; give 2-5 mg typically IV PUSH* every 5 to 15
mins (cannot delegate, only nurse)
Pain management: aspirin in acute ischemic events for antiplatelet effect considered first line of
defense- CHEW aspirin btw 160-325 mg.
Thrombolytics​: used less now. clot busters; streptokinase/urokinase/TPA (tissue plasminogen
activase); they’re enzymes that break up blood clots! Given IV to help lice or break up clot and
restore myocardial blood flow… must be given within the first 6 hours of cardiac event
- TPA is used a lot for OTHER clotting events →
- Stroke? Hemorrhagic or embolic → CT SCAN OF HEAD! Hemorrhagic stroke?
TPA NO! Embolic? Yes!
- Given IV - must be given within the first 6 hours of onset of chest pain
- Thrombolytics are not used around here anymore.. Except in remote facilities. Why?
Now usually cardiac cath.
- Contraindication: Active internal bleeding; recent brain surgery/brain bleed(ex)
hemorrhagic stroke) - DON’T GIVE TPA
- prolonged CPR → do not give clot busting medicine
- After thrombolytics therapy, Pt. put on heparin drip (bc little clots r
floating around so breaks it up even further) → inc. risk for bleeding
→ monitor PT/PTT, Hgb/Hct, check vital signs, assess urine/stool
colors for blood , internal bleeding, further assess any abd./back pain *
- Put pressure on site if blood is being drawn bc inc. risk for bleeding SO
PRESSURE!
Antidysrhythmics​: because the myocardium becomes hypoxic and ischemic it becomes irritable
and increases risk for abnormal heart rhythm used as prophylaxis.
- Immediately after the Pt has an MI they need to rest, as their enzymes start to normalize and go down
and do frequent serial blood draws every 8 hours for troponin and CK as they become normal and EKG
becomes normal the pain needs to be resolved. First you will dangle them at the edge of the bed to see
how they tolerate it because you don't want to be in bed for too long… they get OOB to the chair monitor
EKG, vital signs and eventually be able to ambulate and assume activities of daily living
-
CABG (coronary artery bypass graft): MIDCAB, LVAD
- OHS: open heart surgery
- AVR/MVR: aortic/mitral valve replacement (different surgery from CABG)
- Some suckers need both (yikes)
-
With CABG surgery there are typically 2,3,4 or more blood vessels that have
become occluded and use vessel/veins from the pt leg to bypass the occluded
vessel.
Pt teaching: is important to teach pt to cough and deep breath due to the incision down the middle
of the chest
- Surgeon opens up the chest by sawing the sternum open and pt is in pain after the
procedure so VERY IMPORTANT TO GIVE PAIN MEDS AND
PREMEDICATE THE PT BEFORE COUGHING AND DEEP BREATHING,
HOLD PILLOW OR SPLINT
- Teach them about the importance of leg exercise after surgery
- Tell them they are going to have an incision down their leg and down their chest,
chest tubes coming out of the chest, might foley to monitor UO, multiple IVs,
endotracheal tube ventilator to help breath sometimes on only for short period of
time.
- CABG: surgeon is only manipulating the outside of the heart; takes veins from legs/arms → sews
them onto aorta and then onto myocardium → re-establish blood flow to heart ; not a cure!
Providing symptomatic relief
- What will help: lifestyle changes & meds (beta blocker and antiplatelets)
- Dissect heart, get rid of old valve, put in new valve (metal valve or biological
valve)
- More invasive: VALVE (AVR/MVR) → higher incidence of arrhythmias
(antiplatelets/BBs)
- double/triple/quadruple CABG (2-4)
- Harvest vessels from arteries in legs, open chest, LOTS of ​pain on sternum
- Implement good pre-op teaching: C & DB, splinting, leg exercise
implementation, taking pain meds, incisions on legs and sternum
- Post op- chest tubes, may have foley, multiple IVs, breathing
tube, ventilator (for a little while usually in a recovery room) we
try to extubate pts. ASAP
-​ During procedure: body temp. Cooled/ decreased to abt. 85ºF to decrease metabolic demands
- Before surgery: pt is placed on a cardiopulmonary bypass machine
shunts the blood away from the body where it's perfused with oxygen
(perfusionist - connects pt to machine) → all of the pt’s blood passes
through machine to keep machine perfused (surgeon has clear field)
- Problems while on the machine: electrolyte imbalances (potassium)
& ***the risk for embolic phenomena (blood clots) put on lots of
anticoagulants to prevent these blood clots from happening.
- (blood clots/emboli) → like to go to brain → post op
STROKE
- The less time the pt. Is on coronary artery bypass machine,
the BETTER
KNOW HOW LONG PT IS ON BYPASS MACHINE
FOR! 3+ hours? O shit…call the other surgeon to check if it is
right... 1.5 hrs → better!
- Blood thinners during procedure to prevent clotting ​- during
procedure they sew PACING WIRES into MYOCARDIUM
used in the event that the pt. needs to be connected to an
external pacemaker​ (heart is edematous after surgery and this is
when these wires are needed) (look for more info. W. heart
blocks**) - comes out before pt. goes home; nursing diagnoses
for these include; decreased cardiac output,
- must access for valve surgery more than cabg surgery
- Risk for infection
- Pacing wires come right out the abdominal cavity
- Not used that often
- Heart is usually paralzyed or stopped to do the procedure , when they see the blood flow thru the
vessel are adequate they warm the pt back up they shock the heart into normal rhythm, they ween
the pt off the coronary bypass machine and sew pacing wires into the pt.
-
-
-
MIDCAB: Single or double vessel disease: thoracotomy approach - pt is not placed on bypass
machine → less risk of consequences of machine side effects…typically Pt is in hospital for
less time, & lower incidence of infection
LVAD: left ventricular assist device- keep heart pumping; typically a **​bridge to a new
heart/​heart transplant (won’t live with LVADs forever)
Rest: - graduated rest; as we treat the pt. and EKG and test results are stabilized , the pt. Starts
to be pain free → inc. activity level
- NPO, clear/full liquids diet [blood needs to go to GI tract to aid in digestion] cardiac
prevention diet [low Na & fat(cholesterol)]
After surgery
*Monitor chest tubes for bleeding, frequent VS checks* chest tubes come out very quickly
*Arterial line? For direct BP measurements
*CABG: BP 80/50 → graft will collapse rlt. To HYPOVOLEMIA → pt need fluid/volume
*Conversely: if pt. Is BP 200/100 → EXPLODE!? → pt needs diuretics or
vasodilators-nipride/nitrates to decrease volume
*Pt should be on heart monitor/ telemetry - monitor HR & Heart rhythm
May need to warm pt back up
*Monitor suture lines initially for bleeding and later for infection
*at risk for embolism phenomenon Observe for changes in LOC - neuro checks (hand grip, foot
push, smile, tongue out PERL)
Assess lung sounds - ARF risk for pneumonia, atelectasis
Be careful - pain meds… helps them to cough and deep breath and ambulate
Monitor electrolytes : K- 3.5-5.1, should potassium of at least 4 or higher bc of diuretics
Diuretics can cause HYPOKALEMIA ! WATCH K levels! Do I have to supplement the lost
K+?
Pts are supine for long time are going to need SCD for leg that is not being used
Continue to monitor vitals, incision, cough and deep breath once they are on the med surg floor
Later on give pt stool softener (Colace): given to prevent vagal stimulation which causes a decrease HR
- When bearing down, watch out the vagus nerve, Vagus nerve is located in several dif. Areas:
carotids, rectal area, put pt.’s face in a bucket of ICE WATER : ​if BP 140/** → check the
rectal temperature → massage → reduce the HR (causes bradycardia [see below])
- Vagal stimulation/massage lead to BRADYCARDIA ​*​ We don't want pts To bear down if
they have constipation bc can cause vagal stimulation and cause profound bradycardia and can
die. (VASOVAGAL) COLACE docusate sodium is given.- this is stool softener to prevent vagal
stimulation which lowers the heart heart
- Physical assessment: ONE carotid artery @ a time when checking bc it can slow Pt.’s HR
Digoxin works by stimulating the vagus nerve in other ways and it slows down the HR.
Discharge teaching​:
- Keep incision clean and dry
- Should shower but should not take baths
- Tell them S&S of infection of suture lines (normal suture line: pink/red/puffy is ok) VERY
RED, drainage, hard, fever, warm to touch → infection*
- keep lower extremities elevated
- can/should walk - AMBULATE!
- Should engage pt. in risk factor modification: diet, smoking, activity bc the CABG is not a cure
- Shouldn’t be doing HEAVY LIFTING (bearing down)
- Teach them about their medicine
- When pt. Can climb 1-2 flights of stairs without chest pain/SOB, THEY CAN HAVE SEX!
(Viagra/cyldenophil/cialis? Erectile dysfunction (ED Meds)…
- pts cant take ED drugs with nitrates/other vasodilators because not only no erection …
THERE WON’T BE A BP! Too much vasodilation (BP too low) should not be taking
any nitrate at the same time
- Vagus nerve- When you’re having sex VAGUS nerve is stimualted in RECTAL AREA!!!!
lowers BP
OFF PUMP BYPASS​:open up chest, heart is lifted out of chest cavity- surgeon can have a clear
view/field to work
SAPHENOUS VEIN GRAFT​: bypass (relisten)
REVASCULARIZED MYOCARDIUM: ​vessel stitched to … to bypass
BLOW UP THE LAST SLIDE FOR THIS PPT AND LOOK @ THIS SHIT
Swan-ganz catheterization- CVP (5-10) inc. → FVE
-assess peripheral pulses
<picture> FUCKING LOOK @ IT !!!!!!!!!!!! GOOD WRAP UP SLIDE. IF I DON’T KNOW THIS
- Less time on N.C. ???????
- Endo- tube: breathing not for a long time
- EKG
- Assess peripheral pulses
- Neurologic assessment
- Epicardial pacing device
- Radial arterial line - ABG checks and BP checks
Left ventricular assist device
Impella
Thermagard set up: Dec. metabolic demands- helps to protect integrity of brain/heart
Sedated continuously (brief to b successful) skin integrity!
YOUTUBE: Medical school therapeutic hypothermia *** video
→ ​(also called targeted temperature management) refers to deliberate reduction of the
core body temperature, typically to a range of about 32° to 34° C (89.6° to 93.2° F) in
patients who don't regain consciousness after return of spontaneous circulation
following a cardiac arrest.
CAD Case study
Case 1.
- Find the location of the pain, scale 1-10
- 8 on scale → vital check
- Med → nitroglycerine, aspirin
- Reassess → pain, vitals
Chest pain for 10 mins… 8/10
Complete vitals!
After 2 administers… 12 lead EKG
CK/MB/troponins
RT- intubate pt./ambu bag
Compensation mechanism - trying to inc. o2 to periphery
Shock → person doesn’t have BP …. (cardiogenic shock!)
MODIFIED TRENDELENBURG - head down and legs up; upside down position to get blood up to brain
ST segment elevation (REPRESENTS MYOCARDIAL ISCHEMIA) → STEMI
Isoelectric - flatline
Angioplasty and stent; get pt’s consent; report and documentations(charting)
Broken call bell; incident report → fix
INCIDENT REPORT - (its a bad thing) anything out of usual circumstances happened → just the
facts; nothing subjective
Valvular disease (Valvular Heart Disease)
-
-
S1: created by closure of the mitral and tricuspid valves. Indicates the beginning of ventricular
systole ventricles are contracting and moving blood forward atrium are filling up with blood
[closure of AV valves]
S2: created by closure of the aortic and pulmonic valves. When these valves are closed they are
filling up with blood
Stenosis: Valves that cannot open fully are stenosed or stenotic “stuck shut”
Regurgitation: valves that cannot close completely are insufficient or regurgitant. Always open a
little bit.
Heart murmur: reflects turbulent blood flow through normal or abnormal valves.
Types of Valvular Disease​:
- Mitral stenosis: mitral valve is “STUCK SHUT” (btw left atrium & ventricle)
- Left ATRIUM works harder → hypertrophy around the left atrium (gets thicker then
gets stretched/floppy [can’t pump anymore]) not enough blood going forward →
instead (dec. CO)/ backs up into LUNGS (backflow) dilation of left atrium and if
untreated → HEART FAILURE ! CHF
- Mitral insufficiency or regurgitation (always little bit open; doesn’t close all the way)the blood is
able go down into the L.V but some of it goes back up into L.a
- Left atrium fills with blood (from the lung and left ventricle) TOO MUCH WORK
FOR THAT LEFT ATRIUM. Backflow of blood into the LA during ventricular
systole, more blood goes into the L.A which causes it to work harder dilate and
hypertrophy Now more blood is going into the left ventricle as well so both will
dilate and hypertrophy(thin out) bc of the change → increase risk for Afib,
symptoms are dyspnea, orthopnea, HF, resp problem,
- Mitral valve prolapse - benign situation not as important
- Related to endocarditis, and rheumatic heart disease (present is healthy individual, often
happens in women), asymptomatic, can lead to mitral insufficiency, atypical chest pain,
palpitation, dizzie, 5x risk for develop bacterial endocarditis.
- Aortic stenosis: found after the left ventricle
- Left ventricle working harder during systole needs more oxygen, leading to hypertrophy.
Pt may develop angina or chest pain due to demand for oxygen by working harder. Back
flow into the lungs can cause dyspnea on exertion. Why pt develop syncope?? If blood
keeps backing up into the lungs and not moving forward to perfuse the rest of the body
which causes the dizziness. Because less blood moving forward b/c of the obstructed
aortic valve.
- Aortic insufficiency or regurgitation (the valve is always open)
- Passive blood backflow. Asymptomatic for a long period. Related to Marfan’s syndrome.
Mitral Stenosis
- Related to previous underlying infection called RHD (rheumatic heart disease) - typically
caused by untreated strep infection. Not seen anymore in this country. When a child has a
-
-
sore throat taken to the doctor and a swab test is taken and treated right away. ( s/s for kid:
sore throat, and strep can cause kidney damage) ; GROIN AREA- BRIGHT RED!
SCARLET FEVER → S&S of rheumatic heart disease
Prevents blood flow from LA to LV, the LA has to work much harder to get the blood through the
obstructed valve
Increased LA pressure since it has to work much harder. When it produces dilation of LA with
eventual HF, CHF (if it is untreated)
When pt goes into Heart failure the lung sound you will hear are crackles, fine crackles, cardiac
crackles. Pt in HF coughing will not clear the fine crackles. You will need to give pt diuretics
Bc of the dilation and growth and change of the atrium, this is what precipitates the arrhythmia
A-fib: anytime the heart changes it shape it can increase the risk for abnormal heart rhythm
S/S:​ DOE(dyspnea on exertion), orthopnea(when the person needs to sit up to breath),
PND(paroxysmal nocturnal dyspnea (when pt wakes up in the middle of the night and cant
breath), pulmonary edema (lungs fill up with fluid) , JVD [jugular vein distention.], peripheral
edema in the lower extremities.
“Rumbling murmur” (NO QUESTIONS ABOUT MURMUR =)
FLUID VOLUME EXCESS IN THE LUNGS!
Mitral insufficiency or regurgitation​: always a little open (LA pays price; gets blood from lungs also gets
blood back from the LV/lungs)
- Related to RHD
- Backflow of blood into LA during systole over the time
- LA and LV dilate and hypertrophy
- Increase risk for Afib
- S/S: DOE, orthopnea (sit up to breath),dyspnea, , HF,
- CHF → respiratory problems
- Sounds like a ​“High-pitched” or “cooing” murmur
Mitral valve prolapse​: BENIGN ..around the valve there are leaflets/tissues that help keep the valve in
place ,When ventricles go into systole push the leaflets back into the atrium it's not a big deal it's benign
- R/T endocarditis, RHD
- Present in healthy individuals (often times women)
- Benign, asymptomatic
- Can lead to mitral insufficiency, regurgitation
- S/S: atypical chest pain, palpitations, dizziness
- 5 times risk for bacterial endocarditis *
- Heard as a “click” after S1
Aortic stenosis​: aorta stuck fuckin SHUT (left ventricle is working harder to eject blood into the aorta so
it can to the systemic circulation needs more oxygen ! ​lead to left ventricular hypertrophy:starts to
thicken ​ )
- R/T RHD
- LV obstruction during systole leads to LV hypertrophy
Hardest working part of heart → has to pump against the most SVR → works even
HARDER
- Needs more O2 (chest pain! → ischemia!)
S/S: DOE, angina, syncope; there is no/less blood moving forward to the brain!
Harsh “crescendo-decrescendo” murmur louder and softer and again all over
-
-
Aortic insufficiency or regurgitation​: the LV doesn't have problem passing blood into the aorta however
some of the blood in the aorta can back splash in the LV, passive splashing of the blood into LV the aortic
valve is always a little open
Not related to any type of infection or bacterial infection
- R/T Marfan’s syndrome (connective tissue disorder) and bacterial endocarditis
- constant Backflow of blood from aorta to the LV (during diastole) leads to Left ventricular
dilation
- Asymptomatic for many years
- S/S: DOE, orthopnea, palpitations, angina (chest pain)
- “High-pitched blowing” murmur
Nursing diagnoses​:
- Decreased cardiac output
- Activity intolerance
- Impaired gas exchange (possibly)
Treatment​:
- Medications:
- Digoxin lanoxin : slows down the heart rate, and it increases the force of myocardial
contraction so the heart can contract harder trying to improve cardiac output.
- monitor K+ levels, hypokalemia → increases digitalis toxicity → yellowish/green
vision, bradycardia, Halos around light (vision), Nausea; serum levels
- (normal digoxin serum level = 0.5-2.0 ng/ml narrow therapeutic window if the
level was 0.2 subtherapeutic can have HR of 100)if levels are 0.5 can cause
digitalis toxicity which can have a HR of 30 ,visual changes, N/V
- Check apical pulse for 1 full minute and do not administer if HR is less 60bpm
- Benefit of digoxin is it gives the heart more time to fill with blood which
increases cardiac output.
- Positive inotropes → inc. demand for myocardial O2
- Apical pulse for 1 FULL minute
- Dose: 0.125 - 0.25 mg PER DOSE (often given PO orally /IV push slowly)
- Inc. vagal tone (particularly @ AV node) → BRADYCARDIA ***
- Often on Coumadin not bc of the valve bc of the atrial fibrillation Pt with valve surgery,
give coumadin. Pts are in A FIB high risk for developing blood clots
- pradaxa, eliquis, … commercial - drug not to be used for heart valve problem →
COUMADIN (blood thinner - PT/INR) 11 seconds
- 1.5-2x control
-
-
-
-
- INR: 2-3
Hazards:
- Vitamin K for antidote coumadin
- Antidote heparin: Protamine
- Amioderone: antidysrhythmic
- Antibiotics:
Surgery​:
Balloon valvuloplasty​:inserted with a catheter undilated then they open balloon to open valve
back up (not a surgical procedure and done through femoral artery)
- need to assess pt afterwards for the development of embolic phenomonen
Aortic Valve replacement (AVR​):similar to CABG care is similar to OHS; incision on
sternum saw open ,retractors put in place to hold open(WATCH FOR INFECTION OF
THE STERNUM! CAN BE DEADLY! The heart is opened/dissected to remove the diseased
valve to replace with synthetic valve or organic valve. Made of tissue from an animal or a
cadaver. Tissues often need to be replaced. Metal valves last longer.
There's a lot more manipulation to the heart with OHS so development of local edema in the
heart increases the risk for abnormal heart rhythm particularly heart blocks increase abnormal
heart rhythm. These are the pts that you would use the pacing wire, hooked up to an
external pacemaker. As edema/swelling goes down their normal rhythm may be stored and
the external pacemaker can be removed. Can require Anticoagulation.
These pt have no leg incision. More concerned with rhythm disturbances than with pts who
have CABG
→ ICU psychosis (o shit they become crazy without windows and whatever when the pt is in
the ICU too long) A-FIB! → coumadin), prosthetic valves are put in
- Metal valves require​ lifetime​ anticoagulation always (Coumadin)
- procense valve (PIG valve), BOVINE VALVE (cow), or metal valve
- Valves made of biological tissue: doesn’t need to be on lifetime anticoagulation, but
metal valve
- Mitral Valve Replacement (MVR)
- Metal valves require​ lifetime​ anticoagulation (Coumadin)
***TVAR: (transcatheter aortic replacement) replace valve through blood vessel - much less invasive!
Float new valve up ​→ ​replace a severely narrowed aortic valve due to aortic stenosis
-
without a conventional chest incision.
Transcatheter Aortic Valve Replacement: TVAR
- High risk populations: CV disease, CKD, chronic respiratory dysfunction, heart failure
- Approach: Percutaneous (90%) or trans apical (small incision)
- Post op assessment: hematomas at insertion site, bleeding (retroperitoneal), arterial occlusion
- Nursing care: Telemetry for arrhythmias (heart block and pacemaker care), neurovascular
- assessment (distal to puncture site), lung sounds, careful I and O, daily weights, 6 hours bed rest,
- no bending at groin, dual antiplatelet 9 (aspirin and Plavix), SCD’s RECOVERY IS MUCH
FASTER, easier
- Assess the femoral artery and float this valve up the new one using a catheter.
- arrhythmias (heart block)
Infectious Heart Disease
Endocarditis​:​inner lining of the heart it's continuous with the valve of the heart important to keep in
mind that this infection can travel to the inner values and eventually alter the function of the valve of the
heart. (can also be referred as SVE subacute bacterial endocarditis)
- Bacterial or viral infection of the endocardium
- Any infective agent can cause it really
- Acute: rapid onset, tends to resolve quickly
- Subacute more insidious onset or sneaks up on the pt less toxic but might last for longer time
- Prosthetic valve endocarditis PVE: Can also develop from insertion of a Prosthetic valve and
becomes infected.
Risk factors​:
- Intravenous drug use
- Underlying valve disease: mitral valve problem, increase the risk for developing endocarditis
- Invasive procedures: catheterization, angiogram, triple bypass surgery, IV insertion, inserting a
foley, Central line dressing change, any kind of dentist work or surgery can be a portal of entry.
Pathophysiology​:
- Eroded or worn away areas in endocardium attract sediment or junk , which attracts bacteria and
forms a lesion or a growth.
- Lesions can grow and eventually destroy the endocardium or the inner lining of the heart and the
valves.
- The growth leads to eventual obstruction of blood flow through the valves
Assessment​: signs and sympotms
- Fever
- Anorexia
- Fatigue
- Weight loss
- Cough (related to the obstructed valves that are not allowing for forward flow of the blood to the
heart so the blood is going to back up into the lungs causing the cough as well as SOB)
- Shortness of breath
- Chills
- Malaise
- Joint pain (depending where this vegetation is or the growth is the vegetation shoots off tiny
blood clots microemboli, if the emboli lodges in the joint cause the joint pain/ discomfort)
- Embolization
- Petechiae:if the emboli lodges underneath the skin it causes this pink purplish spot on the skin,
another manifestation of an embolic phenomenon like a blood dot.
- Splinter hemorrhages: Long black longitudinal lines on the distal half of the nail bed
- Osler’s nodes: red painful growth, on the fingers or toes
-
Janeway lesions: flat purple discoloration, Small purple-red lesions on the palms and soles of the
feet
Diagnostics​:
- Look at pts WBC to see if it's elevated (5,000 to 10,000 normal) and sed rate can be elevated too
- Get blood cultures, shows us what kind of bacteria is growing and what kind of antibiotics is
going to be best to treat the problem
- TEE
- Make sure you do a good job at asking the questions that might lead us to where the portal of
entry was of the acquisition of this infection
Ex. did they have any invasive procedure, were they a substance abuser?
- History of invasive procedures
Nursing diagnoses​:
- Infection:
- Interventions when pt has an infection: check temperature for fever, check WBC count,
administer IV antibiotics as ordered, administer antipyretic tylenol
- Activity intolerance
- Risk for altered tissue perfusion
Treatment
- Must administer Intravenous antibiotics that have to be treated if not can be fatal, can be given for
4 to 6 weeks. HIGH PRIORITY TO CHECK/ASSESS FOR ALLERGIES BEFORE GIVING
ESPECIALLY THE FIRST DOSE BUT CHECK EVERY TIME ANYWAYS.
- May receive IV antibiotics at home through a PICC line (peripherally inserted central catheter)
inserted in the antecubital space a ling catheter, that is put into the SVC OR IVC
- Send home with a PICC line when they have no more fever(afebrile), when WBC is within
normal range, when their lungs are cleared, when their heart sounds normal.
- Often fatigued so do need to Rest, should still be in ROM, bed to chair.
- May need surgical repair or removal of infected valve
- Anticoagulants: bc of all the little blood clot microemboli causing the petechiae, splinter
hemorrhages, janeway lesion can be placed on anticoagulants sometimes.
Pericarditis:​ outermost layer. Pericardium has an inner layer and outer layer. Normally 30 to 50 ml of
serous drainage in pericardial sac that fluid helps cushion the heart every time the heart goes into systole
or diastole. Like a pillow around the heart. Can occur with or without fluid
- Inflammation of the pericardial sac Can occur with or without an increase in fluid in the
pericardial space. If the fluid starts to increase around the heart and fluid collection gets bigger
puts a lot of pressure on the heart (squish or compress the heart).
- Viral( most common),​ bacterial, trauma(car accident), can occur MI, post OHS (Drussler
syndrome)
-
Not given antibiotics to treat viral chest pain
Assessment
Pt with pericarditis makes us nervous bc they often have chest pain bc it can radiate to the neck or back it
makes us think they are having an MI
- Pain radiates to the neck or back, their pain as a pleuritic quality respiratory component, worse
when they take a deep breath in.
- We can do something that really lets us know if they have this condition when laying down in a
supine position. It is very uncomfortable to feel better when you sit up, pain is relieved. When the
patient is laying down the layers are rubbing against each other when the patient sits up the heart
falls more freely in the thoracic cavity less of that rubbing when sitting up makes the patient feel
better. Classic sign to find out.
- “Pericardial friction rub” use stethoscope place at left lower sternal border hear a high
pitched scratching or rubbing sound
Diagnostics
- Elevated WBC and elevated sed rate
- Low grade fever
- Positive blood cultures if it's bacterial often caused by virus doesn't always show on a blood
culture.
- EKG shows an elevated ST segment and inverted/upside down T wave, once you start to treat this
pt the ST segment and T wave will return to normal.
- Echocardiogram shows us the amount of fluid collection in the pericardial space. Fluid collected
in this area is called pericardial effusion meaning fluid collection.
- As the heart gets compressed it will have difficulty going into systole or contracting as it being
swished and difficulty relaxing/ diastole. Systole and diastole starts to look the same number
- “Narrow pulse pressure” difference between systolic and diastolic BP ex. 110/70 =40
- SOB
- Tachycardiac
- Tend to have clear lungs
- Beck's triad consist of muffled heart sounds hard to hear due to the increased fluids, lead to HTN,
jugular vein distention
Treatment
- Analgesics (ASA or high doses of NSAIDs motrin, ibuprofen: monitor risk for bleeding,
irritating to gastric mucosa should be given with food or milk)
- Antibiotics if bacterial
- Steroids- anti inflammatories; prednisone IV, PO
- increase sugar levels
- monitor weight
- PO: give with food or milk can be irritating to the gastric mucosa
- Cause mood swings, euphoria, depression
Cardiac tamponade
- Pericardial space fills with fluid and compresses heart anything over 130 ml
- Threatens normal heart function: heart cant go into systole or diastole
- Can be assessed for “Pulsus Paradoxus” use BP cuff have pt take a deep breath
- Pericardiocentesis: removing fluid from the pericardial space, put anesthetic on pts chest, pt
hooked up to EKG machine, take a big syringe attached to a big needle landmarks that they use
to try and draw back and take fluid out the pericardial space…..
- Keep your eye on the ST segment or the T wave means the needle is up against the wall of the
ventricle and if it punctures the walls of the ventricle that could kill the pt.
- Typically after heart surgery pt can develop recurrent pericardial effusion .Pts pericardium
has become irritated and keep getting pericardiocentesis. Pericardial windows make a little
flap bring a piece down so the fluid can constantly drip into the thoracic cavity to prevent
the build up of fluid in the pericardium.
Congestive Heart Failure
HF
-
Right sided
Left sided
Or both
Definition
- The heart is unable to pump an adequate amount of blood to meet the metabolic needs of the
body’s tissue.
- Can no longer pump blood and move it forward to the perfuse and oxygenate the rest of the
bodies organs
- HF decreases quality of life; carries poor prognosis kinda like the end stage or
terminal heart disease.
- Can't be cured.
- Cause: CAD, HTN, MI, endocarditis and mitral valve problems. Valvular disease (especially
mitral valves)
- CAD,
- MI: tissue becomes Ischemic necrotic, necrosis (tissue death)→ lose elasticity →
replaced with less elastic tissue scar tissue and the heart can't pump anymore.
- Hypertension contributes to HF → increasing SVR/afterload, the workload of the
heart making the heart work harder especially the left ventricle work harder → the
heart gets thicker and floppy, flabby and → can't pump any more
- endocarditis, mitral valve stenosis.
- Most common: L side HF
- Cor pulmonale could cause RIGHT side HF
Left ventricular failure
The heart typically has to pump against an increase in vascular resistance and when that happens the
blood backs up from the left ventricle in the atrium and then the blood backs up and spills back into the
lungs. Eventually these patients get symptoms of pulmonary congestion along with pulmonary edema.
- Decreased cardiac output
Symptoms: decreased pedal pulses, altered LOC blood is not perfusing the rest of the body
properly.
- Blood “backs up” into the lungs
- Eventual symptoms of pulmonary congestion and pulmonary edema
- When studying, ​L​eft side HF, the symptoms are in the ​L​ung: P for pulmonary
- Symptoms
- Orthopnea (need to sit up to breath)
- Hemoptysis (blood tinged sputum)
- Cyanosis (bluish discoloration of the skin from poor circulation)
- Paroxysmal nocturnal dyspnea (pt wakes up in the night needing to breath)
-
Elevated pulmonary capillary wedge pressure (reading that is obtained in a critical care
setting)
- Exertional dyspnea (running out of air during physical activity)
- Cough
- Decreased pedal pulses
- Alter LOC
- Decreased kidney function (low in urine output)
- Can hear fine Crackle(=cardiac crackles) in the lung, lungs will fill from the base up to
the apex of the lungs with fluid.
- need to give diuretics to get rid of the fluid retention
- Check K+ level before administering diuretics they are potassium wasting
- Give PO up to 40 mEq
- If pt K+ level is below 2.5? Give IV 40 mg → RUN (10 mEq in 100 mL/hr )
- have a low ejection fraction less than 50% left ventricle is not pumping properly diagnosed
with an echocardiogram, Cardiac catheterization, nuclear stress test
Right ventricular failure
Right side of the heart gets blood from the venous circulation.
- Non-functioning right ventricle causes backflow of blood into venous circulation
- Where does the right side get blood from? Superior, inferior vena cava blood backs up
into venous circulation Results in peripheral edema (particularly lower extremities).
- veins in the liver becomes congested and engorged with blood , hepatomegaly which is
the liver becomes enlarged( since the liver is infected these patients will change color and
turn jaundice), also develop an enlarged spleen called splenomegaly and JVD: jugular
vein distention.
- PTS CAN BE IN BOTH LEFT AND RIGHT SIDED FAILURE
- Portal (liver) circulation related to liver (hepatomegaly or enlarged liver) →
JAUNDICE/icteric
- Right side problem progress, or untreated, or terminal, color turns to​ jaundice
(liver problem)
- Right side symptoms usually occurs in peripherally;
- How to assess for Jugular vein distention:
- Symptoms
- Fatigue
- increased or elevated peripheral venous pressure
- bc of the hepatomegaly these pts can develop ascites or fluid collection in the
abdomen
- distended jugular vein
- anorexia
- GI distress
- cyanosis
- Dependent edema in whatever is the lowest part of the pts body.
- if pt is out of bed in the chair you might see edema in the legs
-
- if pt is bed ridden the edema is going to be in their sacrum
Sacrum edema; pt with long time in bed, these are the pts that when you turn them over to
your side you can see the dents from the linen and do not resolve quickly.
If male pt is sitting out bed on a chair for a long time and has a history of HF you can
notice a swelling in their scrotum. Scrotal area edema
Jaundice if the liver is affected by the fluid collection in their body/belly they may
develop anorexia and complain of GI distress.
How to assess for Jugular vein distention: ​While you're lying down on an exam table,
with the head of the table at a 45-degree angle and your head turned to the side, your
doctor will measure the highest point at which pulsations can be detected in your internal
jugular vein
Activation of compensatory mechanisms
- Baroreceptors (pressure receptor) located in the carotid artery and aortic arch produce ^ SNS;
- When oxygen levels are low these baroreceptors are low they sense hypoxia they tell the SNS to
start working, SNS stimulation causes the heart to beat faster (tachycardia) to initially try to
increase cardiac output and also tells with the SNS stimulation that epinephrine and adrenaline
are being produced now and causes vasoconstriction.
- This increase in SNS initially leads to an increase in cardiac output bc the heart is beating faster
trying to pump out more blood however with this increase in cardiac output there is now more
blood going back to the heart increase in preload causing the ventricles to be increasingly
stretched out.
- Frank starling Mechanism: as these ventricles get stretched out they lose their elasticity and
ultimately lose the ability to contract or spring back normally. (think of an Old worn out rubber
band → can’t stretch / can’t contract, new rubber band is nice and stretchy and bounces back
nice and quickly. That's what happens to the heart with this chronic increased cardiac
output.
- Why are pressure receptors up to the head? Because the brain has to be perfused and the blood
comes against gravity to the brain.
- Carotid and aortic baroreceptor sense when pt is hypoxic
- When they sensing, ^ SNS → ^ cardiac output; heart beat faster → increase Cardiac
output for oxygen delivery (less time to fill) → vasoconstriction to try to perfuse the
brain! Bad effect… makes the heart pump harder (SVR!/afterload) --> inc. preload…
more blood going into heart → stretccchchhhhhhhh rubber band! Old worn out
rubberband → can’t stretch / can’t contract
- ^ cardiac output > ^ in preload and ventricular stretch; more blood going back to the heart →
make heart stretch hard to increase the volume like ​rubber band​/extra volume → becomes
saggy and loses elasticity; ​beta adrenergic blocker ​to soothe the SNS stimulations (newer
treatment) / long time SNS stimulation is not good
-
decreased cardiac output → kidney becomes hypoxic too is not perfused well when the
kidneys become hypoxic there is a → release of renin (vasoconstriction) from kidney. Causes
release of angiotensin ​which is a powerful vasoconstrictor which is making it worse for the heart
it's going to increase the BP (vasoconstrictor → inc. in SVR/afterload making the heart work
harder powerful vasoconstriction)
- Ultimately going to change the shape of the heart going to start to become floppy/ flappy.
- Also adrenal gland if it's hypoxic (hypoperfused), they release aldosterone which causes sodium
and water retention.
- If it happens for a long time, the ventricle changes their shape, called remodeling. Remodeling of
ventricles looks like an oval or an egg and impairs cardiac contractility. Lose their elasticity
* Frank-Starling mechanism: ultimately hurting the Patient; inc. blood volume → inc. cardiac
muscle like a rubber band → inc. ventricular contraction
The new way of treating pts with HF particularly early on is to abort this SNS stimulation
so you would give ...
​ * Beta-adrenergic Blocker needed to suppress SNS stimulation (block the effect)
- In the past, best treatment were giving digoxin and lasix not now has changed
Systemic effects of CHF
- Neuralogically: Fatigue, restless, confused why? Decreased cardiac output → so the brain is
not perfused, not getting enough oxygen to the brain.
- CV: Chest pain, tachycardia, ​Atrial fibrillation (very common dysrhythmia of a CHF patient)
- As the hearts starts to stretch and change its shape the atrium starts to stretch and change its shape
it knocks out the SA node, all these irritable areas start to compete to initiate conduction
Edema: lower extremities, hepatomegaly( ascites and cause jaundice), sacrum edema, and JVD,
scrotum swelling ALL cardiovascular
- lots of sign of a fluid volume excess, fluid shifted from the vascular space to the
interstitial space; Left ventricle and atrium spills the fluid to the lung from the bottom
to the top: fine crackles, also called cardiac crackles, used to called rales in the past,
rhonchi(coarse crackles: more sign of inflammation or exudate; rhonchi is more hear
pt with bronchitis, pneumonia or respiratory problems → give water and cough and
deep breath)
- To get rid of cardiac crackles, use diuretics, USUALLY DO NOT GIVE WATER OR
RESTRICTED.
- RESP: SOB, dyspnea, ​start off with a dry, hacking cough you will hear those fine crackles
that will start at the base of the lungs ​,poor O2 sats
If we don’t treat these pts, the lungs will fill with blood/fluid or alveoli, called
pulmonary edema( when the pt is drowning in their secretions. With pulmonary edema
you're going to see frothy, bubbling, pink tinged sputum, lungs filled with fluid from the
base to the top of apices of the lungs. Also have poor O2 sats.
- Pt gains weight. Anytime pts gain weight of more than 1LB a day over the course of
3 to 5 days we become very concerned.
- The way we determine if we're successfully treating heart failure is by a patient's
weight loss. They know bc clothes and shoes become tight
-
Sometimes patients know they are gaining weight without weighing themselves They
know bc clothes and shoes become tight
GI: ​weight gain or loss (best parameter for the treatment for the pt w/ heart failure)​,
ascites,bc of that collection they may become anorexic.
- In end stage heart failure the pt can develop anasarca which is generalized body
edema arms, legs,all over the body including ascites.
- poor prognostic sign → sign that pt will not last long. The veins have lost their
ability to keep blood in the blood vessel and it leaking out into the interstitial space/ tissue
-
fluid will move to interstitial space; fluid vol excess → pt may have hypotension; poor prognostic
sign → sign that pt will not last long) Anasarca(generalized body edema) and modelling, what are
you going to say to Pt??????????????????
-
GU: nocturia (urinating a lot at night; fluid shift)
Pt in HF at night the vital organs metabolic demands are decreased so the brain and heart
don't use much blood and oxygen, blood is rerouted/ ​Fluid shift to the kidney,( brain and heart
does not need oxygen as much at night) → blood goes to kidney → to try to better perfuse
the kidneys... kidney functions increase at night → increase urination
-
Skin: pallor, dusky, cyanotic, diaphoresis, with right sided HF there's jaundice, poor cap. refill
* A-fib: knocks SA node out, the upper area of atrium all quivers (fibrill) and AV nodes selectively
conduct.
* Anasarca: generalized body edema / fluid escape from IVF -> ISF / poor prognostic sign (death sign)
* Fine crackles (rale) starting from the bottom of the lungs to the top
Diagnostics
- Chest x-ray: cardiomegaly, pulmonary edema/congestion
- Echocardiogram: show any underlying valve disease, ​ejection fraction: 50 to 70%
- MUGA: ejection fraction
* BNP: over 100 > indicates HF
Nursing diagnoses​:
- Activity intolerance
- Impaired gas exchange (due to all the fluid in the lungs)
- Fluid volume excess
- Decrease cardiac output*
Treatments of CHF
- Diet: low sodium, fluid retention; no processed, canned foods,cheese. (typically 2 g of sodium in
hospital meals); pt teaching planfirst first do a 24 hour history ask the pt. What they like to
normally eat for bfast, lunch, dinner when they’re not in the hospital and help them make healthy
substitutions. (Mediaterrrian diet, DASH diet)
-
Digoxin: pts in heart failure; + inotrope/cardiac glycoside; inc. myocardial contractility;
delays conduction @ AV node; HEART SLOWS! Ventricular rate is slower → more time to
fill → inc. cardiac output
- PO/IV push → heart monitor
- Normal dose 0.125 to 0.25 mg (PO/IV)
- Aka digitalis and LANOXIN
- Check apical pulse for 1 full min.hold if the HR is below 60bpm
- Narrow therapeutic window 0.5 to 2
- Dig Toxicity → pt feel dizziness, visual changes (greenish/haloes) N/V, low K+ levels
→ inc. risk of dig toxicity
- digafab/​digabine - dig toxicity antidote
- Must monitor potassium levels bc hypokalemia low potassium increases the effect of
digoxin lead to dig toxicity.
- Make sure pt has normal potassium more than 4, 3.5 isn't going to really work
- Concerning bc we when we give these pts a lot of diuretics these pts also lose
potassium.
- Not used a much maybe more in elderly pts that have already been using this and
it's been working for them
-
Diuretics: teach pt about foods that are rich in K+ supplement while pt is taking diuretics.
- ex. Bananas, orange juice, avocados, green leafy vegetables
- Restrict fluids; 1500-2000 mL fluid restriction/day (educate pt on how much this is)
- 1 kg = 1 L of fluid.. If pt gained 2Lb mean they gained 1 L of fluid 1000ml
- Placed on I&O (measurements)
- Daily weights → best parameter for treatment of heart failure.
- A pt who is in HF and you notice they have a lot of edema and crackles in their lungs the
nurse can weigh the pt everyday without needing a doctor's order. Implement daily
weights. Nurse, LPN,​ PCT can weigh the pt
- Commonly used to treat pt in HF: used to treat that fluid volume excess.
- DEHYDRATION RISK FOR ELDERLY! Fluid vol. Deficit
- Poor skin turgor/tenting, sunken eyes, dry oral mucosa dry and sticky; flat neck
veins, BP LOWWWWW! Check!
- Can be given PO/IV lasix (furosemide): K+ wasting
- Monitor potassium level
- Check BP before administering it's going to deplete the patient's volume.
- Ideally results in a good diuresis.. Should have a good urine response to this
- Monitor urine output
- Daily weights → best parameter for successful treatment of heart failure.
- when giving diuretics to elderly pts we can easily overshoot the mark and too much
causes dehydration
-
DEHYDRATION RISK FOR ELDERLY! Fluid volume Deficit, hypovolemia
- Poor skin turgor/tenting, sunken eyes, dry oral mucosa dry and sticky; flat neck
veins, BP LOWWWWW! Check!
-
K+ sparing: Aldactone
Shock → urine output * best parameter for treatment
- If these pts gain 3+ lbs over 3-5 days, they NEED TO NOTIFY THE HCP! O
shit retention!
- KCL-potassium chloride (when pts are on diuretics we often put them on this)
- requires a prescription
- can be administered orally or IV
- oral potassium comes in pills called K DUR.
- DUR: stand for duration it's long acting, very big they are like horse pills. Not supposed
to be broken bc they are sustained release however they are scored and can be broken for them if pt has
difficulty swallowing but you’re not supposed to
- Ordered in Meq
- can be given as an elixir 10, 20 Meq (very bitter put little of OJ to mask the taste)
- supplement pts potassium intravenously but has to be done VERY CAREFULLY!
​ - Standard is 10 meq in 100 ml of IV fluid over 1 hour
- ​Potassium is very irritating to veins, keep a close eye on the pt IV site, very painful and
comfortable for pt.
- prepared bags can come from pharmacy with 1000ml
-
Nitrates: also used to treat pts in heart failure
- Nitro Patch or nitropaste
- Benefit: dec. SVR/afterload; makes the heart not work as hard. cause dilation of systemic
circulation -> dec BOTH preload/afterload!
- Decrease resistance in the veins by opening up the veins not as much blood is going back
to the heart decreasing preload very helpful to heart that can't pump
- CHECK BP before adminsitering & can cause headaches/flushing/dizziness
- Sublingual nitro? NO! IV/patch : long-acting/ remove at night for prevent tolerance
-
Ace inhibitors : -pril… are good vasodilators preventing vasoconstriction- often used in
conjunction w diuretics
- decreases vascular resistance so the heart doesn't have to work as hard
- Benefit to pt w HF: dec. pre w/diuretics and afterload
-
Beta ADRENALINE Blockers: ADRENERGIC - new treatment for HF. Prevent SNS
stimulation ; no vasoconstriction → no heart beat faster
- Blocking the heart's response and blocking the SNS from causing that vasoconstriction
and preventing that tachycardia keeping the HR nice and slow so the ventricles can fill with
blood and maintain a good cardiac output preventing vasoconstriction so the heart doesn't
have to work as hard ultimately the beta blockers prevent the remodeling of the ventricles
-
-
-
-
- have to be careful with the beta blockers because it causes a decrease in the contractility
of the heart and decrease demand of oxygen in the heart which is good.
- Good effect if heart ain’t contracting as hard → doesn’t need that much O2
- Digoxin does the opposite it increase contractility of the heart making it work
harder which increases oxygen demands of the heart which is bad
- Do not give in to pt with breathing problems, their lungs need to be able to respond
to adrenaline and epinephrine bronchodilator and beta blockers are blocking that
effect.
- DO NOT STOP ABRUPTLY IN PT WITH HF.. if you do all of sudden the pts
heart is going to have to beat faster the oxygen demand of the heart is going to
increase and that can precipitate many other problems.
- See the compensatory mechanism slide! Go back!
If pt comes into the hospital in acute HF we have to quickly increase the contractility of the
myocardium. We do this through intravenous infusions….
Dobutamine/Dobutrex:
- Iv medicated drip/ weight based administration
- pt cannot stay on this mediation forever it's a bridge to getting the pt symptoms under control.
- also going to be giving them duiretics to decrease that fluid volume excess
- this drug causes SNS stimulation, increases the HR, cause vasoconstriction, given to push BP
back up if pt comes in with very low BP with HF.
- Pts who come in and need to be put on d
peripheral/vasoconstrictor @ HIGH doses;
- inc. myocardial contractility; + inotropes
- Treat end stage HF
- Admin. On infusion pump
- Side effects: headaches, angina(chest pain), palpitations, & tachycardia
Dopamine: - Pts who come in and need to be put on dopamine…. Are in
- end stage heart failure Nickname: no hopamine (lol) they are getting close to the
end. Heart has lost ability to contact independently → gradual tapering; weaning pts
off……..
Often have a problem the pts of these medicines/ weaning them off you'll get an
order to wean them off but to sustain a systolic BP of 100. When you start to turn the
rate down over the course of hours you will notice their BP will drift 90, 80 and then
you will need to bump them back They go back into heart failure end stage HF;
develop peripheral edema; so much ischemia/damage
- primacor/natrecor for HF
***USE OF PACEMAKERS: help improve the pts. ejection fraction and helps arrhythmia ….hmmmm
Acute HF: IV meds. IV nitroglycerine → dec. pre/afterloads; monitor BP, special IV tubing
**Can go into pulmonary edema: manifestation Of severe heart failure.
- Fluid leaks from the alveoli to into the pulmonary tissue
- S/S: Pts in pulmonary edema: are extremely anxious, tachypnic, fast breathing, experience AIR
HUNGER( using their accessory muscle to breath, neck working very hard in trying to breath );;
develop frothy pink tinged sputum; essentially drowning in their own secretions
- cold/clammy, diaphoretic
- CVP: >10 indication of fluid volume excess
- Treatment: Pt needs IV diuretics & 100% non-rebreather mask → eventually possibly
intubation ventilator (worst case scenario)
- LASIX 40 mg or 80 mg slowly
- Put in high fowler position
- Give morphine to decrease preload and afterload.
- Oxygen mask
- Check oxygen saturation
- May need to get arterial blood gasses
Cor pulmonale
**One of the independent causes of right-sided HF: ​cor pulmonale ​→ a phenomenon that occurs
that causes the right ventricle to enlarge bc the pt has some kind of underlying lung problems or
Pulmonary HTN
- The right side of the heart has to push the blood into the lungs and if the pressure/tension is
increased in the lungs the right side of the heart is going to have to work harder to slash/
push the blood into the lungs causes the right side of the heart to enlarge., can be related to
lung disease; most often rlt. To pulmonary HTN (inc. pressure in the lungs)
- Also can be caused by a very large pulmonary embolism/blood clot.
- Develop a lot of respiratory symptoms
- (caused by COPD, long term emphysema;long term asthma)
- Right side will eventually hypertrophy/enlarged- pulmonary embolism
- S/S: dyspnea, SOB/Wheeze, may develop signs of right sided HF
- EKG: since the atrium and the ventricles become enlarged, when the right side of the heart
enlarges that P wave represents conduction from the SA node to the AV node it changes its shape.
The P wave starts to look like the letter M develops a notch in the middle that makes it look like
the letter P can be called P pulmonale or P mitrale
- One of the most common causes for COPD, respiratory problems or pulmonary HTN is smoking.
- Think to yourself… Does this pt have a history of smoking?
- Treat the underlying respiratory problem
- Pt given Oxygen, diuretics, low Na diet, digoxin, beta blockers
Joint commision core measures for HF​: must be done & HAVE DOCUMENTATION
- Left Ventricular function assessment (ejection fraction via echocardiogram)
- ACE or ARB(angiotensin receptor blocker) for moderate or severe HF (poor EF) → (must
doc. That pt is on this med.)
- Smoking cessation counseling: has to be document pt received education not smoking
-
Discharge instructions: diet, symptoms, activity levels, weight monitoring over 3-5 days,
medications
- Also document pt received education weight monitoring and meds instruction
Cardiomyopathy (Idiopathy)​: an abnormal situation or problem with the heart. A group of cardiac disease
that affect the heart’s ability to pump
- Primary: no known cause
- Secondary: has an underlying cause
- 3 types: Dilated, Hypertrophic, Restrictive → all kinda look like heart failure
Dilated Cardiomyopathy​: looks like heart failure except didn't have a heart attack
- Most common
- CMP, >90%
- Pathology:​ Cardiomegaly (enlarged heart), poor systolic function( heart cant contract), decreased
cardiac output
- Secondary causes: ETOH (chronic alcohol use), chemotherapy, heredity, chronic alc. use seen in
younger people than in older people
- S/S: crackles, edema, diminished pedal pulses, a-fib, dyspnea, JVD, embolic phenomena, cough,
orthopnea; blood clotting phenomena
- looks like heart failure except didn't have a heart attack, they are not old, seen more in young ppl.
- Treatment: focus is improving myocardial contractility, digoxin, diuretics, ace, beta blockers, IV
Dobutrex,Dobatmine, transplant (candidate for a HEART TRANSPLANT if they are young !)
- Not going to transplant a patient with underlying medical problems or a poor ejection fraction
● s/s are almost same as CHF but causes are different
Hypertrophic cardiomyopathy
- Pathology: Massive ventricular hypertrophy. Left ventricle becomes very thickened so thickened
that it can obstruct the aortic valve
- If that aortic valve is obstructed the left ventricle is going to have to work even harder to move
that blood out and it's going to grow even more and if the aortic valve is obstructed blood is not
going to move forward you see signs of decreased cardiac output. May obstruct the aortic valve
bc of thickness
- AKA: ​Idiopathic​ (we don't know why) ​hypertrophic​ (thicken) ​subaortic​ (under) ​stenosis
(IHSS)
- Secondary causes: Genetic, aortic stenosis, hypertension
- Common cause of death otherwise in healthy young adults they discover the problem during the
autopsy.
- Bc the left ventricle is so hypertrophy and needs more oxygen to pump is….
- s/s:
- angina (thickness requires increased O2 demand)
- syncope(due to not a lot of blood going in the brain)
- SOB, dyspnea (bc blood is going into the lungs)
- SVT(supraventricular tachycardia)
-
- at risk for A-Fib, V-Fib,
- on the EKG you will see an increase in voltage/duration of QRS
Treatment: Beta blockers and Calcium channel blockers
Sometimes surgery can be performed to resect/cut the ventricle to make it more compliant.
These patients all have of symptoms of difficulty breathing
All present with SOB
Restrictive Cardiomyopathy​ looks like pericarditis
- Pathology: similar to pericarditis. Decreased filling during diastole so the heart can't rest for too
long so it doesn't have time to fill .
- But it does contract, Systole is unaffected
- Least common type
- Primary cause is unknown
- Heart is being squished
- Secondary causes: Neoplasm, radiation, endocardial fibrosis
- S/S: angia, syncope, DOE
- Treatment: avoid situations that decrease ventricular filling (dehydration,tachycardia, increase in
vascular resistance or increase in SNS, ^ SVR)
HF is the terminal illness of heart disease, heart cant be replaced so at this point when someone is in
terminal HF the focus is on comfort and care, Hospice care
***HF is a chronic/TERMINAL ILLNESS OF HEART DISEASE
- Palliative care: pain control, oxygen, repositioning pt, keep them clean and dry, all parts of
ADL’s ( comb their hair, wash denture…), taking care of the family → make them feel
comfortable
- Sign of near death: arrhythmias, mottling( lower ext. Turn purple color; blood leaks from the
vessel) cheyne stoke; tachypnea and apnea continuously
- DO NOT LEAVE DYING PT ALONE.
- Check for DNR order
Cheyne stokes: when a person is about to do you will notice a change in breathing. Fast breathing then
they stop and start breathing again.
Altered mental status when they are about to die
The pt loses their appetite before dying may need to explain to the family
Mottling: pt is dying from their trunk down to their lower extremities, they turn purplish bluish color,
blood is pooling in the lower extremities the blood vessels are unable to keep the blood in the vessels and
starts to leak out.
**All cardiomyopathies have pulmonary symptoms
**Only treat, not cure
Endocarditis & Pericarditis
Infections on the layers of the heart
Endo- : inner most layer
Myocardium: muscle surrounding heart (middle part)
Pericardium: outer
Objective
- Describe etiology and pathophysiology of endocarditis
- Identify major risk factors and preventable measures of endocarditis
- Describe clinical manifestations and complications of endocarditis
- Discuss diagnostic testing regarding endocarditis
- Describe clinical management, prevention and antibiotics for endocarditis
- Discuss implementation of nursing agency including rest and ROM
- Describe etiology and pathophysiology of pericarditis
- Identify risk factors and preventative measures of pericarditis
- Describe clinical manifestations and complications of pericarditis
- Discuss diagnostics regarding pericarditis
- Discuss the clinical management of the patient with pericarditis
- Describe the clinical management of the patient with pericarditis
- Describe nursing management of the patient with pericarditis
Infectious disease of the heart​:
○ Endocarditis: Valves are the most common endocarditis locations. Ex/ mitral valve &
Aortic valve.
○ - Pathogens enter the bloodstream(infection in blood) and enter heart, stick to layer of
heart. When the pathogens damage the valve, bacteria can stick to the damaged part & if
the person’s body is unable to fight (weakness) = endocarditis.)
○ Myocarditis
○ Pericarditis (visceral, fibrous layers with pericardial cavity)
- The ideal management
-Prevention
Infective endocarditis​:
- Microbial infection involving the endocardium
- Risk factors
- IV drug abusers; injecting by oneself; injection without cleaning your skin -> staph.
infection.
- Valve replacement recipients
- Systemic infections (ie, GI, Resp infection spread to blood -> reach to the heart)
- Structural cardiac defects: ex valve disorders. Ex) mitral stenosis, mitral valve prolapse
Invasive procedures involving mucosa: ex dental (lots of bacteria in your mouth)* →
opened gum -> bacteria moves in → travel to the body through blood vessel
*Structural + invasive = in high risk of endocarditis
-
Endocarditis pathophysiology:
- Caused by direct invasion of the endocardium by a microbe; common microbes
- Streptococci(on skin)
- Enterococci
- Pneumococci
- Staphylococci
- The infection usually causes deformity of the valve leaflets or chordae tendineae; (valves are
not smooth anymore!) → valve activities damaged → Valvular destruction
Infective endocarditis
- Possible portals of entry for infectious organisms include
Oral cavity if dental procedures have been performed
Skin rashes, abscesses or lesions
Infections, (cutaneous, genitourinary, GI, Systemic)
Surgery, or invasive procedures; including IV line placement (any catheter is portal of entry for
pathogens ex. Expired IV tubing)
Clinical manifestations of endocarditis
- Murmur: Atrial → ventricular; valve’s not working well; ventricle can't pump blood enough;
decreased cardiac output; risk for heart failure(Nursing Diagnosis)
- Heart failure (caused by decreased cardiac output)
- Arterial embolization (due to bacteria in valve)
Blood+bacteria=emboli will deposit.
- Splenic infarction
- Hematuria (blood in urine)
- Neurologic changes: stroke, TIA(mini stroke), headache
- Roth spot: hemorrhage in the eyes. With pale center.
When the emboli deposit dislodge and travel, it can result Roth spot (eyes) and ulcer nodes
(Oslers nodes, Janeway lesions)
- Petechiae
- Oslers nodes:On palms and soles, small painful
- Janeway lesions: Flat reddened macular on hands and feet (caused by septic emboli)
- Splinter hemorrhages: reddish brown lines under nails
S&S develop from toxic effects of infection, destruction of heart valves, and embolizations of growths on
the heart.
Diagnostics
-
Echocardiogram - for endocardial movement
Positive Blood cultures
Auscultation for murmurs
Prevention of endocarditis
- prophylaxis antibiotic treatment before and after invasive procedure.
- Proper dental hygiene, hand hygiene
- Minimize use of all catheters
Complications
- heart failure (ventricles are not getting enough blood = not good circulation)
- Cerebral vascular complications (TIA,stroke)
- Blood flow obstruction
- Dehiscence of prosthetic valves
- Valvular stenosis or regurgitation(valves are not efficiently working)
- Myocardial damage(heart working harder)
- Sepsis
Management of endocarditis
- Nonsurgical
- Antibiotics (look for allergies before give to Pt)
- ROM activity balanced during adequate bedrest
- Monitor s/s (fluid volume: edema, SOB, etc)
- Surgical
- Removal of infected valve
- Repair or removal of congenital shunts
- Repair of injured valves and chordae tendineae
- Draining of abscesses in heart of elsewhere
Nursing management
- Auscultate heart murmurs
- Monitor for s/s of systemic embolization (EKG)
- Monitor for s/s of organ damage
- Assess invasive lines (infection)
- Educate on activity restrictions & ROM: educate to prevent further development
- Educate on prevention and health promotion (hand hygiene)
Rheumatic endocarditis;​ not common in America anymore. Common in 3rd world countries.
-Acute rheumatic fever
-School-age children
- group A beta-hemolytic streptococcal pharyngitis
- ​Prompt treatment of strep throat with antibiotics can prevent the development of rheumatic
fever​: red blood cell rupturing; immune response: attacking proteins of bacteria and our body cells (skin,
joint, heart, brain)
- Streptococcus is spread by ​direct contact​ with oral or respiratory secretions (better treat strep right
away!!, have more risk for endocarditis when the young pt, with history, gets older)
- malnutrition, overcrowding, and lower socioeconomic status
- Affects all bony joints, producing polyarthritis; pain in the joints
<picture describing how infection happens in processes.>
Pericarditis ​(usually had a trauma to heart before)
- Inflammation / alteration of pericardium
- Dressler's syndrome (immune system response after heart tissue damaged by MI)
- Postpericardiotomy syndrome (had heart surgery before and got infection)
- Chronic constrictive pericarditis (get it again and again chronically) ex. Dialysis, cancer patients.
- Adhesive(dry), serous, purulent, calcific, fibrinosis, sanguineous(bloody)
<picture of pericarditis>
Normal vs abnormal(thicker pericardium, heart has less space) → fluid build up in the cavity →
pericardial effusion → pressure increases → heart barely moves
Pathophysiology of pericarditis
- Can be caused by
- Trauma
- Infection
- MI
- Pneumonia, TB (another reason for chronic pericarditis)
- Connective tissue disorders
- Hypersensitivity (allergic rxt)
- Neoplastic disease (conditions that cause tumor growth)
- Radiation
- Renal failure
- Tumor
- Postpericardiotomy syndrome
- Leads to
- Pericardial effusion
- Accumulation of fluid in the pericardial sac
- Increased pressure on the heart -> heart can barely move -> fluid does not let the
heart pump -> cardiac tamponade
- Constrictive pericarditis: thickening and decreased elasticity that restrict the heart’s
ability to fill properly with blood (lead to blood backflow - ex. of R side: Pulmonary
edema → right sided heart failure)
- If the heart is filled with less blood, the ventricles pump out less blood, causing
decreased cardiac output and symptoms of HF
- Less ventricular filling also causes and increase systemic venous pressure which leads
to peripheral edema and hepatic failure.
Chest pain(common symptom) when you lay down. why? Bc the gravity pulls down heavy heart = gives
more pressure - more pain.
Endo- : bacterial. Peri- : usually viral and no blood culture needed.
NSAID’s use; need to eat before taking NSAID’s (GI protection; med for GI - Maalox(coats the GI))
Pericarditis: Acute and Chronic
- Inflammation or alteration of the pericardium
- Acute pericarditis associated with
- Infection organism
- Post MI (Dressler’s syndrome)
- Acute exacerbation of systemic connective tissue disease
- Chronic constrictive pericarditis: chronic inflammation causes fibrous thickening of the
pericardium. Caused by: TB, radiation, trauma, renal failure, metastatic cancer
Clinical manifestations and diagnostic of pericarditis:
- Substernal precordial pain (chest pain) like heart attack
- Radiating to left side of neck, shoulder or back
- Grating, oppressive pain, aggravated by breathing, (inspiration), coughing, swallowing
- Pain worsened by supine position, deep inhalation
- Pain relieved by sitting up and leaning forward
- Pericardial friction rub (sandpaperish sound. Listen in YouTube)
- Fever with elevated WBC (check blood C/S); whenever one has infections
- Elevated ESR (blood test detects inflammation in body)
- 12 lead ECG: diffuse ST segment depression; (Any A-Fib?) ST-T wave spike
- A fib on the tele
- Echocardiogram to evaluate for a pericardial effusion: ejection fraction: see if the patient has a
heart failure
- Dyspnea and S/S of HF
Complication
- pericardial effusion: pericarditis does not necessarily mean there is pericardial effusion in the
space; but when it can cause the fluids to enter into the cavity. It comes as complication; There is
fluid in cavity normally but when it’s over 40 to 50 mL in the space considered pericardial
effusion.
- Cardiac tamponade: accumulation of fluid and blood so much the heart compromise and leads to
edema, shock -> due to ​increased intrapericardial pressure
Intervention / Clinical Management
- Determine and treat the cause
- Usually viral - NO Antibiotics
- Pain management
- NSAIDs: aspirin, ibuprofen,neproxin
- Corticosteroid - prednisone (needs taper down to discontinue)- if not responding to
NSAIDs
- Assume positions that will relieve discomfort. Sit up, lean forward (lay down - cause
chest pain)
- Colchicine(콜치신) 1-2 mg PO on day 1, then 0.5 - 1mg PO daily for 6 months;
tape-down medicine.
- Monitor for
- Pericardial effusion- Ultrasound, x-ray. doctor needs to drain it →
pericardiocentesis.
- Cardiac tamponade; ultrasound, x-ray
- Pericardiocentesis: Stick the needle on the patient to drain the fluids via catheter.
- Pericardial window: for patients who are chronic and come back with more fluid each time; it’s
like flap that would cut into the pericardial cavity so the fluids can drain to the chest cavity. Or it
can be set up a drain outside of body for long term.
- Pericardiectomy: definitive treatment for chronic constrictive pericarditis
- NSAIDs, nonsteroidal anti- inflammatory drugs
Nursing Management
- Pain relief
- Analgesics: Pain present? Assess the pain scale before and after, check the medicine is
working.
- Positioning
- Recognize symptoms of cardiac tamponade
- Normal BP 120/80, pulse pressure: 40, because of the heart’s atria and ventricles different
functions; pulse deficit gets closer because of the shrink of the heart; blood pressure
drops by 10 (systolic); pulse deficit should be greater than 10; Ex. Bp: 100/90 P:10
- Pulsus paradoxus - During inspiration, the systole is gonna drop more or equal to 10.
ex) expiration bp: 120/80 → inspiration bp: 110/90
- Falling arterial pressure
- Rising venous pressure
- Distant heart sounds: heart sound like far away because it's filled by water. (Muffled
sound)
*Important listening: Endocarditis → murmur. Pericarditis → muffled heart sound, and
friction rub
-
Education: S&S of HF, go to hospital if you have chest pain.
Monitor for HF
Endocarditis (bacterial) VS pericarditis (Viral) - Suggested video to watch at home
Nursing process for pericarditis
- Diagnosis: acute pain related to inflammation of the pericardium, risk for decreased cardiac
output
- Plan: relief of pain, absence of complication
- Interventions: rest, monitor response to pain medicine, auscultation
- Evaluation: expected outcomes?
- Performs ADLs without pain, fatigue, or SOB
- Sustain BP WNL
- Heart sounds are strong and can be auscultated
- Absence of neck vein distention
- (jugular vein)
*** Know the term that vegetation grow in valves
Vegetation grows on bacteria on valves
How to differentiate ischemic change with pericarditis: muffled heart sound, puliric quality(Respiratory
quality gets better when pt sit up), enzyme change? NO (only ischemia will cause enzyme change)
Pt with MI: Look sick, Pain, pallor, diaphoretic, SOB
Pt with pericarditis: does not look sick = less dangerous situation than MI
Changes in ST segment in pericarditis as we treat them.
Pericarditis Hallmark*** patient has jugular vein distention but clear lung sound.
Pulsus paradoxus* (abnormally large decrease in stroke volume, systolic blood pressure and pulse wave
amplitude during inspiration. The normal fall in pressure is less than 10 mmHg)
Case study 1
Michael, 32 yrs, presents to the hospital ER with chest pain of 4 hrs of duration.
Chest pain:
- heart problem such as MI, Lung(PE); describe the pain, EKG, cardiac enzyme, V/S
- Physical assessment: V/S, heart sound, LOC
- Colchicine; expensive, gut gas out, when NSAIDs not working
Case study 2.
- Ceftriaxone (Rocephin) → check penicillin allergy
Understanding EKG’s and Dysrhythmia /arrhythmia Time 39 mins
4 Properties of the cardiac cells
1) Automaticity- ability of cells of heart to sponatenously initiate an electrical impulse
automatically
- starts@ SA node (right atrium; which is pacemaker of the heart) knows to automatically
SPARK/ fire btw 60-100 bpm
2) Excitability - the ability of the myocardial cells to respond to the electrical impulses
- Interferences: scar tissue r/t ischemia;
- Automaticity should start from the SA node , conduction should happen from the
SA node down to the AV node down the bundle of his
3) Conductivity: is the ability to transmit the impulse from cell to cell.; after SA node,
conductivity → AV node (atria/ventricles) → then through ventricles via Bundle of His
4) Contractility: ability of myocardial fibers to shorten in response to the electrical impulse
- Struck by lighting → convulsions
**** The whole point of conduction through the heart is to make the heart
contract. It's like a lightning bulb that goes through the heart that causes it to
contract or pump.
EKG Characteristics​: of a healthy heart
Whenever you see an EKG you want to see a…
● P wave (atrial depolarization/contraction/systole): should always be round and
upright bump
● QRS complex (ventricular depolarization/contraction/systole): narrow skinny
spiky complex
● T wave (ventricular repolarization aka diastole/relaxation): round and upright in healthy heart
● The part of the cardiac cycle that you do not see on the telemetry strip is atrial repolarization,
atrial relaxation/ diastole
● The walls of the atria are so thin that they don't even cause blimp on the radar when you're
relaxing on telemetry.
● You want to see these three happening over and over again
Normal sinus rhythm:
EKG Measurement
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P-R interval​ (0.12-0.20 seconds or 3-5 small boxes): ​measuring
conduction from SA node(up in the R.A) down to the AV node- how
fast conduction is occuring EX. in this PR interval its 4boxes times
0.04= 0.16 seconds which falls in the PR interval of 0.12- 0.20. It's
normal.
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QRS complex (​no greater than 0.12 seconds or 3 small boxes​): measures conduction through
the ventricles through the bundle of his. Measure by either the initial upward deflection or initial
downward deflection to the return of the isoelectric line. Bottom line is You want this line to be
nice and narrow and skinny. EX: this QRS complex is 2 boxes 0.04 times 2= 0.08seconds which
is normal.
T wave should appear upright always
*** each little box equal: 0.04 seconds
*** PRI=0.16 secs it's 4 boxes
***QRS complex=0.08 secs it's 2 boxes
***Inverted T wave → old myocardial damage (heart attack within the past few years)
****Each box is point 0.2 then multiply by 5 boxes which is 1 second, count every 5 box as 1 second, at
the end there are 6 seconds total. This is called a 6 second strip.
Steps for dysrhythmia identification​:
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Calculate heart rate by counting # of R waves in a six second strip and multiply by ten. This
will give you a heart rate for one minute 60
The QRS happen regularly, when you listen to the apical you it will also sound regular
If you see P,QRS and T you know the impulse originates at the SA node.
Only see 4 sinus beats in a 6 second strip multiply the 6 by 10 it's 60seconds. We can
multiply the 4 beasts times 10 it will give us the patients HR for a full minute. HR is 40
Determine regularity of R waves by plotting out the R-R interval
Examine P waves, should be round and upright followed by QRS complex.
Measure the PR interval, from the beginning of the P wave to the beginning of the QRS complex
(represents conduction from atria to the SA node)
Measure the QRS complex from the beginning of the Q wave to the end of the S wave (represents
conduction through the ventricles)
Sinus rhythms
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Sinus Bradycardia
P, QRS, & T happening over and over again
Impulse originates at sinus node
Rate is less than 60 BPM
Usually r/t an increase in vagal tone → valsalva maneuver, carotid massage; bearing down
which can cause this very slow heart rate, causes decrease in cardiac output and causes the
patient to faint. We give these patients Colace so they don't bear down.
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An increase in vagal tone can be caused by ​DIGOXIN​. It slows the heart rate down by
increasing the vagal tone at the @ AV node (it's like pouring cement in the AV node)slows
conduction from the atrium down to the ventricles, to slow the HR!
○ Not treated unless symptomatic…
■ Dizziness​, fatigue r/t dec. cerebral perfusion
■ You would ask the patient if they are seeing halos and their HR is this low you
would ask if they are taking digoxin and you want to find out their dig level.
Normal: 0.5-2.
■ If patient is symptomatic sometimes can be treated with IV ATROPINEtreatment
■ Some people have nice slow steady HR and it's not necessarily a bad thing, well
conditioned athletes, runners, their ventricles have a lot of time to fill with blood.
*** PRI=4 X 0.04= 0.16 secs
***QRS complex=3 X 0.04=0.12 secs
*** 4 QRS X 10= 40 (bradycardia)
The conduction from the SA node to the AV node is normal, conduction to the ventricles is normal the
problem with this strip is that the HR is 40
Sinus rhythms​:
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Sinus Tachycardia​: SNS stimulation: blood loss, infection, pain, stress, anxiety, fever can cause
tachycardia
PR = 0.12(4boxes x 4), QRS=0.04(1 box)
You count the QRS line bc it represents
ventricular contraction rate, that's what you
count when you're counting the patient's apical.
EX. there are 11 QRS in this strip with 6
seconds so you multiply by 10 which is 110.
Impulse originates at sinus node
Rate is greater than 100
Usually related to ​SNS stimulation: ​adrenaline or epinephrine can cause SNS stimualtion, it's an
expected response for your HR to go up when given these meds. Stress, fear, and anxiety release
adrenaline causes this stimulation to increase your HR. Fever, pain can also cause the patient to
have tachycardia and exercise. Sometimes even turning the patient in bed poorly conditioned
people. Usually a vagal maneuver can be done to slow down the HR such as a rectal temperature,
having the patient cough causes the pt to bear down.
Atrial dysrhythmias​: ectopic/abnormal spots in the atria that compete to initiate conduction/common
cause- anything to make the atria enlarge
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Atrial flutter​: not normal; pt loses atrial kick → decreases CO; s/s: hypotension, SOB, altered
LOC, diminished peripheral pulses
Saw-tooth​ shaped flutter waves represent the atria fluttering and if you count them approx….
- There are 19 flutter waves and we’re assuming this is a 6 second strip so multiply by 10
which is 190 flutter waves per minute.
Atrial rate 250-300 / min: AV node: theyre like the fuck? Slow down- they aint havin’ it; too
fast conduction → no CO
Selective AV conduction to ventricles → gna sounds very regular - going to think pt
is experiencing normal sinus but u NEED to do an EKG
○ Can develop S&S (dyspnea etc.)
○ Caused by CAD, change in the atria which are CHF, Valvular disease
(stenosis,regurgitation)
*** ​When you listen to the patient's apical heart rate you are listening to the ventricular rate
This strip looks very regular because of the QRS complex
Ventricular rate is 70 (7 QRS complex x 10) which is normal so you would never know this patient has
atrial flutter
*** Every three flutter waves it is followed by the QRS complex which is the ventricle contracting in this
strip.
This isnt always the case sometimes you can see 2 flutter waves then the QRS or someimtes 4 or 5
*** 19 flutter waves X 10 = 190 atrial flutter rate
Atrial dysrhythmias​:
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Atrial fibrillation: ​very common dysrhythmia in our older population even sometimes in younger
people.
Typically caused by anything that makes the atria change its shape. With long standing HTN,
CAD, HF
The atria are no longer fluttering; they are fibrillating/quivering. loose their atrial kick (as in A
Flutter)
Can no longer count those quivers but if you could...
Atria quiver at rate of 300-600 quiver per minute
If all of those quivers were conducted down to the ventricles then the ventricular rate will also be
the same rate which would be bad because the ventricles will have no time to fill with blood.
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The AV node which is between that shaking quivering atria and the ventricles selectively
conducts some of those quivers down to the ventricles. Very irregular in terms of the conduction
down to the ventricles.
Irregular ventricular response: when counting apical - HARD TIME! Do apical & radial @
same time (no difference in pulse pressure)
When patient is in Afib you are not going to see any P waves
Risk of mural thrombi
Rapid ventricular rate treated with digoxin
17 QRS complex multiply by 10= 170 ventricular HR. pt has very low cardiac output because their heart
doesn't have enough time to fill with blood.
*** No P waves → quivering lines before QRS complex
This rhythm is very irregular and it's very hard to count a patient's ventricular heart rate
when they have Afib.
● Irregular ventricular response: when counting apical - HARD TIME! Do apical & radial @
same time (no difference in pulse pressure) everytime you palpate the radial pulse you
should be hearing apical as well.
EKG Atrial fibrillation
- When pt ventricular HR is greater than 100 bpm is called uncontrolled Afib and needs to be
treated, need to slow ventricular HR down
100+ bpm- uncontrolled afib (gotta do something abt it) → slow the rate
*** when pt is in Afib you need to listen to apical pulse for 1 full minute it cant be less bc in
the moment that you are listening where the complexes are close together and you would be
getting a faster rate than if you were listening to where the complexes are farther apart and
it will be a slower rate.
Ways to slow down the HR
- Pt will become symptomatic very quickly
- We can try to use vagal maneuvers: rectal temp, or ask the pt to cough causing you to bear down
- That drug that works by increasing vagal tone is Digoxin which- slows the heart rate des
ventricular rate, digitalizing the patient means we give the digoxin either PO or IV push every 6
hours for 4 doses. Digoxin works by increasing tone @ the AV node
- Pour some cement into AV node - it's going to be harder for those quivers to get
conducted down into the ventricles not all quivers will be conducted down to ventricles
- Nurse practicinoer, and RN can give med IV push. LPN can not do this.
- The other drug given when the patient is in uncontrolled Afib which means the ventricular rate is
greater than 100: ​Cardizem (gtt)drip ​: CCB* IV drip - Afib to slow ventricular rate
- concentration is 100mg in 100ml NS normal saline
-
- medicated drip needs to be administered in a IV pump to slow the HR won't stay on this
drug forever also put on other meds such Dig, BB, oral CCB to try to bring down that ventricular
rate under 100 so the ventricles have more time to fill with blood
Send pt for procedure - ablation: using heat to cauterize the ectopic areas in order to restore sinus
rhythm
- Problems: ​risk of MURAL THROMBI: blood clots that form on the wall of the atria in Afib (can
also be A flutter)​ * since atria are either fluttering/quivering are NOT CONTRACTING! Blood can
stagnate and pt can develop blood clots in atria bc it collects a long the wall of the atria
- Blood clots in atria adhere to the walls of the atria
Hence the term mural thrombi- walls of the atria (mural → painting on a wall [huge/extensive])
- If the blood clot dislodges and travels through the body it's called a thrombus or embolism
and most commonly goes to the Brain which causes a → stroke. Very common in pt with
Afib.
- Sometimes this can be the presenting symptom when pt comes to the ER, we don't know
why but we hook them up to the telemetry and we see they are in Afib. sometimes can be
found by accident
- Immediately put patient on heparin drip (short half life, PTT, 2 to 2.5 times over the
control is 35 seconds) to help decrease the risk of forming the Mural thrombi in the
hospital.
- Must be placed on oral anticoagulation therapy to be able to send them home- not aspirin →
**​coumadin (most common)
- xarelto, pradaxa, eliquis (Big guns of anticoagulants) need to be on a potent anticoagualnt
used to treat afib
- No lab value that monitors effectiveness of these drugs … no dietary restrictions
- However: still @ risk for bleeding! * the way we know these patients have had too much
of these medicine is that they are bleeding often GI bleeding
- Teaching: hazards of risk of bleeding with these meds: blood in urine/stool and
bruising ​straight edge razors are a no-no
- GI bleeding- melena ; very prone to bleeding
- Coumadin: ​PT/INR; dietary teaching: no green leafy veggies can
decrease the effects of med, avoid vitamin K rich foods- antidote vit. K,
longer onset, longer half life
- Heparin has a very short onset / short half life , antidote: protamine
sulfate, PTT
- Particularly in younger patients you want to get them out of AFIB and back into sinus
rhythm.
- When pts are in Afib and they are not in sinus they lose their atrial kick:​ is normally
when the atria goes into systole (p wave) they squeeze and give one more extra squish at
the end of systole to try and push as much blood down into the ventricles as possible.
Over the long run this can affect cardiac output
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Send pt for a procedure called Cardioversion ​(bring the A-fib back to normal sinus
rhythm): done in cardiac lab *​use low doses of electricity (40-50Juels)​ are used to try to
get pt back into sinus rhythm;
It's synchronized with the patient's own telemetry rhythm. The reason why this is done is
because you never want to cause energy or defib to occur on a T wave, you don't want the
energy to discharge on the T wave.
pt MUST be therapeutically anticoagulated”before attempting cardioversion
(heparin drip) “*** ​Ventricular dysrhythmias
If these patients are not anticoagulated can cause the blood clot on the wall of atria
to dislodge and can cause a stroke
Device used for pt with Afib to help improve cardiac output and ejection fraction.
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Premature ventricular contraction (PVC)
○ 2 common causes: ​hypoxia(low
oxygen)/hypokalemia(this are the abnormal
heart rhythms/ heartbeat that occur - most
common causes; give oxygen to the patient to
solve this problem/give IV KCL; ALSO CAFFEINE! Hypoxia ←→ ischemia
● Characteristic: Wide and distorted QRS complex and T wave is in the opposite direction of QRS
complex
● Ventricles have contracted before it was supposed to, if the ventricles contract before it's
supposed to it didn't have enough time to fill up with blood from the atrium. If this keeps
happening it's going to ultimately decrease cardiac output.
● Typically occur when there's a Irritable focus/area in the ventricle
○ Contraction didn’t happen the way it was supposed to - alt. Path → LONGER
(wider)
○ If the ventricle contracts supposedly faster than its supposed to → dec. filling → dec.
CO
○ All of the PVC look the same, bc it's only coming from one irritable area in the heart
called = Unifocal
*** Regular rhythm: Sinus rhythm even though with irregular wave shapes
***Ventricular trigeminy - every 3 beats
Ventricular bigeminy - every other beat
Ventricular quadrigeminy - every 4 beats …
**the more PVC a pt can have the worse their cardiac output can be
● Treated with IV Lidocaine/amiodarone
● Amiodarone used as first line of treatment
● Lidocaine used as second line of treatment
** can be benign. If this were to happen all of sudden you can put oxygen on the patient and can
also check the pt potassium level.
***Happen a lot with pt in MI because their myocardium is hypoxic or ischemic
Ventricular dysrhythmias
Coming from same irritable areas in the heart .. then 2 of the
same irritable area in the heart ; two PVC in a row called couplet
→ 3 PVCs in a row: salvo/triplet
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Multifocal PVC’s
Runs of PVC’s (couplet(2), salvo(3)(or triplet),
v-tech/ ventricular tachycardia(4)) o fckkkkk~ theres no cardiac output need to do something
about that
● Danger of decreased cardiac output
● SA node intrinsic rate 60 to 100 bpm knows to fire away, but if it fails ischemia, electrical
imbalance… the AV node will take over as the pacemaker of the heart. ​Intrinsic rate of the AV
node is 40 to 60 bpm. If an AV node stops working the ventricles have their own intrinsic
rate also which is 20 to 40bpm in the AV node.
● Anything higher than 40 is going to be called….
● Risk of V-tach can then deteriorate to V-fib → there's no cardiac output. That's lethal
dysrhythmias pt can die.
● Pts who are in Vfib we defibrillate the pt. When pt is in ventricular fibrillation we get those
paddles on the code cart and put jelly on theaddleso we don't burn the pt. one goes under the
right shoulder the other goes under the left breast. So the electricity can restart the heart. Tell
everybody to get out of the way other than the person defibrillating.
● When we defibrillate a pt who is in v-tach it is not synchronized with the EKG. use lots of
energy, use about 300 juels.
● If pt is in vtach and they are still able to talk we can treat it with drugs such as the ​amiodarone
and lidocaine.
● If pt is in vtach and they are unstable and have no BP, LOC has changes treated like Vfib we get
the paddle and defibrillate the patient
- Apnea: pt is not breathing anymore.
- Asystole: is the flatline no systole (when there's a flatline there's no electrical activity in the
heart it's dead, in order to defib the pt there must be some kind of electrical activity so with
vfib there is some kind of electrical activity going on so we can get the paddles to reset the
electricity in the heart and try to the get the pt back in a rhythm.)
-When pt is in asystole we given them epinephrine over and over again and we give it until
they are back in Vfib which is quivering all across the screen now when the is in Vfib you
can NOW use the defibrillator to get them back in dysrhythmia.
- you do CPR on flatline to contract the heart manually, and get blood to the brain and perfuse the
heart itself. Always do systole for both Vfib and vtach.
Heart blocks​:
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First degree heart block; delayed or prolonged PR interval
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PRI greater than 0.20 (5 small boxes): P wave is far away from QRS complex
Conduction delayed at AV node; too much digoxin in the AV node → makes it hard for
impulses to travel
R/t digoxin (too much) or vagal stimulation (Pt bearing down, constipation, carotid artery
massage (don’t do this because emboli in the carotid artery dislodged and travels to the brain),
rectal temperature)
Don't typically do anything for this
*** notch on the down of the QRS wave → bundle branch block
Heart blocks​:
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Second degree heart block​ ​(don't study for test. Not gonna be on exam)
It’s also called ‘Mobitz One’ or ‘Wenckebach’
Progressive lengthening of PRI until a QRS is dropped
“Grouped beating” a.k.a. footprints
*** second and third degree heart block patients need PACE Maker
Heart blocks
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Mobitz two (Not on exam either, this is one of secondary heart block)
Not every beat originating in atria is conducted to ventricle
Occurs in a ratio, 2:1, 3:1 (2 and 3 is P, 1 is QRS)
Biggest danger All heart blocks run risk of progressing to third degree heart block
Heart blocks
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Third degree heart block;​ worst heart block
No impulses from atria are conducted down to
the ventricles (the atrias are doing their thing and
the ventricles are doing their thing and there's no
communication between the two and can
ultimately compromise cardiac output
Often you will see the P wave map out to each other as do the QRS
Atria and ventricles beat independently
Requires pacemaker for second and third
*** no relationship between P wave and QRS complex
*** QRS complex: 4 X 10 = 40 (Intrinsic rate of ventricle: 20-60)
*** P waves: 8 X 10 = 80 (Intrinsic rate of atria (SA node): 60-100)
***impaired cardiac output. Patient needs pacemaker (after open heart surgery and valvular surgery)
Paced rhythms​:
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Internal: permanent (inside of subclavian pocket wire
to atria and ventricles under the skin) .
- nursing considerations​: patient can not be around
any magnetic fields bc magnet is what's used to change
the pts settings to change the rate and change the gain which like the electrical volume. Watch out
at airports with screening, For the first week or 2 pt should not lift their arm up in the air the lead
that's inserted, needs to embed into the myocardium, carry a pacemaker identification card that
indicates the kind of the pacemaker they have and the setting they are on.
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external pacemaker: temporarily (Pacing wire, pace pads (inserted through jugular vein))
Has two jobs Sensing: ability to recognize spontaneous atrial or ventricular activity
-to Sense the presence of spontaneous electrical activity
Capture: pacemaker provides an adequate stimulus/electrical activity to produce ventricular
contraction
ventricular pacing
*** No p wave: underlying rhythm is A-Fib
*** irregular rhythm
The pacemaker sensed that there was nothing happening in the ventricles so it delivered an impulse which
is called a pacemaker spike it's delivered enough energy to cause the ventricles to contract which is called
ventricular capture
*** after 4 beat → no QRS shows up → pacemaker senses pacing spike→ shocks the ventricle →
ventricle capture (ventricular contraction) occurred
***never wanna see a pacing spike on T wave can precipitate ventricular tachycardia the
pacemaker is not sensing correctly. V-tach which is a deadly dysrhythmia.
When the pacemaker fires on T wave → ventricular tachycardia occurs → deteriorate to
V-Fib → Asystole. YOU HAVE TO REPORT cardiologist will come in with the magnets to
reset the setting.
- We can see ventricular capture but we don’t see atrium capture bc atrium wall is
very thin
***When the pt has asystole a pacemaker is not going to help them bc they have no electrical
impulse no heartbeat, these pt need the implanted debiliatrot and it's only going to help them if they
are in VFib .
Pt can be cold and dead and the pacemaker will still be working and can still see spikes can't
assume bc they have a pacemaker that the heart was working so you always have to check the pt to
make sure they are still alive . Pacemaker will still be firing but the pt is not alive
- Pacemaker can also be put on patients with HF; it helps to improve their cardiac output.
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When pt dies there's no urgency to turn the pacemaker off , pt usually doesn't know they have it,
but if a pt has an implanted defib those pts know it they feel like a horse has kicked them in the
chest and when these pt die the defibrillator will keep discharging and it's a lot of energy and the
chest will jump even when they are dead (AISD)- distressing for the family to see.
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*** no ROM or raising arm up after pacemaker set up surgery bc leads have to be in
myocardium.
***Should avoid magnetic field Pt with pacing wire (ie. airport metal detector) bc pacemaker is using
magnetic force to work; it can change rate and wave; more energy is needed because of the scarred tissues
on the heart.
*** FYI: pt has to wear and carry information; what type of pacemaker…
*** lead on wrong place can stimulate diaphragm
***the pacemaker fires even after the patient dies.
*** implanted defib; they go into defib and the machine charges and kicks like a horse → gone into
Asystole → chest keeps jumping → apply magnetic force → decrease the defib machine works
*** sometimes pacemaker inserted to override tachyarrhythmia
MRI not an option; metal detectors - airports;
Pacemakers are programmed with a magnet. Thats y they cant go near magnets
Vame​- amt of energy required to close the ventricle to contract- less energy - better
Scar tissue. An slow conduction
Change the ​rate
Ambulatory care: anesthesia/quartering? Must receive clearance from cardiologist
Must carry w them an identification card- what kind of pacemaker & type of (brand) pacemaker
If pt has a pacemaker: HICCUPS? Means lead is stimulating the diaphragm.
Caution: dying pt… if the pt has a rhythm, they’re fine? NO! Monitor the pt and spend time w the pt.
(palliative/end of life care)
Pacemaker: pacing spikes? Your patient can be dead so check on the pt. Pacemaker pts might have a pulse
but that's the pacemaker! Check the pt!
Myocardial injury
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Elevation or depression of the ST segment
T wave inversion
Deep Q waves
Wide QRS complex(Idio Ventricular Conduction
Defect)
First degree AV heart block-prolonged PRI
Shock
Definition of shock; physiologic shock NOT emotional shock;
Bottom line of shock → pt has no BP; hypotension or very low BP (bottom line)
- Shock is characterized by a decrease in blood flow to body tissue. When the patient's BP is very
low the blood is not getting to the vital organs.
- The absence of oxygen results in a conversion from aerobic to anaerobic metabolism(by
product: lactic acid → these people can go into metabolic acidosis).
- Aerobic metabolism is metabolism with oxygen
- Anaerobic metabolism without oxygen
- Whenever it does this kind of metabolism it produces a waste product called lactic acid
- Eventually cellular and tissue death occurs with widespread organ failure
- If unrecognized and untreated shock will result in death!
- Bottomline patient will not have a BP
Type of shock: watch color! They’re SO pale & cold! → for every shock, except septic!
1. Distributive: problem with the blood vessel, no actual blood loss
- Neurogenic (not on exam)
- Septic
- anaphylactic
2.Hypovolemic: volume problem pt is losing volume
3.Cardiogenic: the pump in the body is broken not ejecting blood into systemic circulation
1. Distributive shock (no actual blood loss, “relative hypovolemia”- problem with blood
vessel → massive vasodilation occurs) the blood vessel has lost the ability to constrict
and can't push the blood to the rest of the organs and cannot maintain perfusion.
- in most types of shocks, they become pale, cold to touch except for septic shocks
- Neurogenic shock​ (Level 4): r/t disease or injury to the spinal cord. (​The brain sends a
message to the blood vessels through the spinal cord telling the blood vessels to
either dilate or constrict.) ​If there's an injury or disease to the spinal cord the message
doesn't get through to the blood vessel which is neurogenic shock.
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Septic shock​: r/t infection; bacteria/virus/invading organism → triggers
inflammatory response with widespread vasodilation. The vasodilation is what's
causing the shock problem, blood vessels are all dilated, blood is pooling and blood is
not being pumped by the blood vessel back to the vital organs.
Typically when a pt is in shock they are cold and clammy, pale…except for septic in
the early stages of septic shock these patients are warm and flushed and may have a
fever and confusion. But eventually turn cold and clammy as they dont receive
perfusion.
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most common in elderly (early sign: confusion) and very young babies under the
development of immune system; ***in the early stages the ​patients are warm, fever,
flushed; no blood loss in septic shock
Anaphylactic shock​: r/t allergic reaction; chemical release when pt goes into
anaphylaxis which is histamine which causes→ ​widespread vasodilation → the
vasodilation is what's causing the BP to drop. no BP. antihistamin is given if its early
on to treat the histamine problem; ​Benadryl*
- Simple allergic reaction: hives, itching and can be treated with antihistamine
** Anaphylaxis is a reaction where the airway is compromised (respiratory involved
ex.Narrow airway, tongue swelling, itching mouth, throat or tongue);
Right away give patient ** Epinephrine pen/ adrenaline- causes bronchodilation (if the
respiratory system is being compromised and causes vasoconstriction which is good bc
bottomline pt doesn't have a BP , reversal of anaphylactic shock.
Some pts will say they have an allergic reaction if they feel that they have a GI problem
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Hypovolemic shock
- Actual loss of intravascular fluid: loss of fluid/blood from the vessel
- Causes include surgery, trauma, hemorrhage, burns (fluid shift from intravascular space
to interstitial (tissue) the body is attempting to hydrate the burned tissue but it's depleting
the volume from the blood vessel that's how burn cause hypovolemic shock), profound
dehydration: losing a lot of volume or blood.
- Dehydration Higher risk: babies and children, the elderly.
- Decreases blood flow, CO, and tissue perfusion → need a lot of IV fluid
- Treatment: lots of IV fluids
Cardiogenic shock
- Heart is unable to pump sufficiently to maintain cardiac output and perfusion
- Causes include MI(ischemia & tissue death especially on left side ventricle, heart
cannot pump → cardiac output decreased), v-fib: ventricles are quivering ,
v-tach(where the ventricles are contracting so fast that there's no cardiac output), HF.
- Decreased CO → fluid back into the lung → pulmonary edema; NO giving additional
fluid
- Treatment: vasodilator, diuretic
Stage of shock
- Initial
- Compensatory
- Progressive
- Irreversible
Initial or early stage: very hard to tell the patient is in shock
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Very Few signs and symptom
BP may be normal or slightly decreased (can't really tell bc of baroreceptor sends a message
to the SNS which produces adrenaline/ epinephrine which causes vasoconstriction to try and
maintain perfusion so it makes the pt tachycardic → increase the heart rate → may decrease
BP)
SNS stimulation maintains perfusion; hard to tell if the pt is having a shock.
Lactic acid builds up in the blood
Compensatory stage:
- Fluid shift occurs (from Interstitial (tissues) to intravascular (blood vessel)) = ​compensation
- SNS stimulation maintains perfusion to vital organs (Brain, heart). The rest of the organs are like
we don't care.
- Patient skin is going to turn pale from not getting enough blood and oxygen (not a vital organ)
- The kidney is not a vital organ, if the kidneys are not getting enough blood and oxygen there will
be a decrease in urine output.
- SNS stimulation maintains perfusion to vital organs but now you will see BP may be decreased,
pts HR is going to get even faster to try to compensate and pump out more blood and oxygen to
the organs( tachycardia)
- tachypnea from trying to breath in more oxygen
- hyperpnea(deeper breathing to try to get more blood and oxygen bc tissue need more O2),
- decreased urine output (because of the low kidney perfusion not being a vital organ; ​not an early
sign occurs after 2 to 3 hours​)
- bc of the fluid shift from the tissue to blood vessel they become thirsty
- hypothermia(cold, drop in temp)
- pale, pallor (see oral mucosa and conjunctiva)
- changes in LOC
- Septic shock​: pt tend to be warm and flushed, ​hyperthermia,​ the body doesn't get perfused in
some way so eventually they become pale and clammy
- Pt is alert enough to feel the thirst → hard to tell if pt is compensatory shock
Progressive stage
- Failure of compensatory mechanisms (SNS stimulation)
- Massive SNS response; sensing that its not working; produces more vasoconstriction →
vasoconstrict lot more since little bit of vasoconstriction didn't work → blood vessels become
very tight and constricted,narrowed blood vessel diameter become clamped down→ not
much is going to get through/come out the clamped down blood vessel) if the pts blood
vessel are clamped down it's going to be very hard to get an IV into this point during the
progessive stage. You want to get the IV in during the compensatory shock before the blood
vessels become constricted and clamped down. Pt is going to start getting worse.
- Compensation is working against the patient
- Conversion from aerobic to anaerobic metabolism with the production of lactic acid
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Pts become Listless, confused, BP less than 80, tachycardia to try to compensate for the low
oxygen, cold, pale, oliguria(very low urine output way less than 30ml/hr), hypothermia,
cyanosis/dusky.
*** Hypovolemic shock/distributive shock→ first treatment: IV fluid (its obvious); is one IV good???
No, two IV’s at least. Due to vasoconstriction
Irreversible stage - refractory
- Patient is near death
- Unconscious, unresponsive, BP is close to 0, a lot of abnormal heart rhythms bc myocardium is
so hypoxic, dysrhythmia or arrhythmias (back and forth), cheyne-stokes, anuria(no urine),
mottled(purple), lungs filled with crackles(particularly in cardiogenic shock)
- Mottling poor prognostic sign
***treatment for all types of shock except cardiogenic shock we give lots of fluids. We need
to have an IV in these pts to give them fluids. If you think it is going into shock 2 IV is
better inserted sooner rather than later.
Nursing assessment
- Neurological assessment​: when pt is not receiving enough oxygen you're going to start seeing
changes in Mental status: early sign in elderly people is confusion particularly septic shock.
- Causes for elderly: stroke, sepsis,pneumonia, UTI
(sepsis in nursing home; take temp → call doctor → blood culture, antibiotics)
- Once the antibiotics are given to them within 48 hours their mental status improves.
- Restless, anxious, if not treated can go into a coma
- You want to reorient these patients frequently
- Observe for lethargy.
- Implement good neuro check
- hand grasp
- foot push
- smile
- stick tongue out should be midline
- assess pupil for reaction to light and accommodation
- Glaucoma scale: independent nursing action that can be implemented to track a pt
neuro status
*** should be done on the patients everyday and all of your patients
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Cardiovascular assessment (cardiogenic shock)
- Frequent vital sign (every 5-15minutes)
- Should have arterial line (most invasive way to monitor a patient's BP) Bottomline when
pt is in shock no matter what they​ have low or no BP
- normal central venous pressure is 5-10​, determines how much pressure is in the right
side of the heart, as well as how much pressure is in the lungs.
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When pt is in hypovolemic shock/hemorrhagic shock CVP is low,
In cardiogenic shock the heart cant pump blood forward CVP is going to be high bc of
the fluid retaining in the heart and backing up into the lungs.
- Connected to heart monitor (telemetry)
- Connected to an arterial line if not, should have BP cuff and monitor that it set to cycle
and checks their BP every 3 to 5 minutes
- Tachycardic with a weak pulse
- Hypertension
- JVD for cardiogenic shock (blood loss = flat JV)
- Eventually become Cold, clammy, cyanotic and can have chest pain
- Make sure to monitor Peripheral Pulses/pedal pulses
- Hemorrhagic shock (hypovolemic shock)
- Lab valve:look for HGB and HCT
- Flat neck veins
- Respiratory assessment
​ - monitor pts respiratory rate, depth and rhythm every 15 minutes
- Lung sound = crackles for cardiogenic shock due to blood backflow into the lungs.
Anaphylactic shock you will hear a wheeze bc bronchus is constricted
- Gastrointestinal tract assessment
- Assess for bowel sounds
- After gastrointestinal surgery assess for hemorrhagic shock, pt will come back with an
NG tube, if they start to hemorrhage you will see it in the NG tube canister.
- Check color in NG tube, look for blood drainage in the ng tube canister
- Can have lower GI bleed in their colon check stool for bleeding
- May need to assess for occult blood if you can't see it. Guaiac card .
** Patients who are in shock we need to implement hourly urine output
Best parameter of treating patients in a shock: for fluid replacement is the patients Hourly urine
output check. Check foley’s urometer. Normal: 30ml/hr ; kidneys not being perfused well.
* SNS can trick us causing the BP to be increased but its not telling is we have replaced
the fluid problem
* The best parameter for the treatment for a patient in Heart failure is the patient's
weight. If they are losing weight we know we’re successfully treating the heart failure.
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Monitor temperature often, keep them warm bc they are becoming cold and clammy
When pt is in septic shock these pts may be febrile .(with temp over 100; give tylenols(600 mg);
no swallowing via IV or suppository,​ give them a hypothermia blanket to cool the body and
bring the temperature down.)
Hazard: Put something in between the pt and the blanket so it's not directly on their skin,
reposition the patient so the blanket isn't just on one side of the patient's body.
Treatment of shock​: should be in critical care, should be on heart monitor, monitored, ideally have an
arterial lines, Need O2 via nasal cannula or mask , intubation put on ventilator, keep them supined with
their head down and put their feet up a little bit to get blood down to their vital organs.
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Hypovolemic​: give lots of IV fluids (hard to put in later bc of vasoconstriction, at least 2 IVs);
N/S, ringers, blood,
hypertonic solutions come in smaller volumes and try to raise the BP (benefits → pulls fluid
from the tissue into the vessel→ BP up again) ex: albumine, plasminaid
Goal: systolic BP over 100 with urine output more than 50 ml/hr. Flood the pt with IV fluid
Helpful if the Pt has a central line (in shock, the benefit of the central line is because blood
vessels are wide and big, more fluid can flow into the central line) if we can't use the femoral
artery.
DO NOT USE FLUIDS WHEN THE PT IS IN CARDIOGENIC SHOCK the pump is
broken and not moving the blood forward its backing up into the lungs called pulmonary
edema.
Cardiogenic​: decrease preload (decreases the volume that is going back to the heart)drugs
that can cause systemic vasodilation we can give nitrate, morphine, diuretic (lasix) to get rid
of the volume that impairs the heart to pump.
Intra-aortic balloon pump (also used in massive left ventricular MI)
A catheter is inserted through the femoral artery and goes up the ascending aorta. At the end
there's a balloon. When the ventricles go into the systole balloon and are collapsed/deflated
the blood can exit the ventricle into systemic circulation and blood can easily go up the
aortic arch blood flow is unimpeded when the balloon is flat. Balloon is going along with
EKG so it knows when to inflate & deflate.
When the ventricles go into diastole/filling → balloon inflates → pushes blood down the
descending aorta and up the ascending aorta, it's like getting systole for the price of one
increase cardiac output;
Balloon is timed with pts EKG so it knows when to inflate & deflate in the instance of left
ventricular ischemia. Put this balloon in to give the heart rest.
As the ventricles start to recover intra aortic balloon pump will inflate with every other
diastole then with every third disystole eventually we can wean the patient off the intra aortic
balloon pump
Do NOT give a lot of fluids
- Goal: decrease preload of the heart with everything mentioned above
- Oxygen may need to be intubated. Heart monitor, Arterial line for BP measurement
Septic​: cornerstone in treating these pts are anti-infectives; requires either antibiotics.
- check for allergies before administering antibiotics
- Monitor lab value: WBC for infection
- Give a lot of fluids in septic shock
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Anaphylactic​: allergic reaction. Use benadryl and steriods (for simple allergic reaction ex. Hives,
itching, Nausea, vomiting, steroids(decreases inflammatory responses)
These drugs can be given to pt in anaphylaxis however if the pt airway is involved MUST GIVE
THE PT EPINEPHRINE.
If patient cant breath must give epinephrine
Benefit of epinephrine pen: causes vasoconstriction to try and help the BP, and also causes
bronchodilation
Give fluids as well
Levophed​,
*** when pt is very very sick without BP (very very hypotensive; BE careful → levophed;
massive/profund vasoconstriction; is administered IV, last attempt to get pt BP up.
- Should be given through a central line or ​Swan ganz catheter​, if it's received through a
peripheral line and if it's infiltrated and goes into surrounding tissues, it can cause the
superficial tissue to die and limb loss. Poor prognostic sign for Pt who take Levophed. Can
cause death
Intra-aortic balloon pump​:
Arterial line monitoring; inserted through radial artery; connected to the BP monitor → check BP in
the artery (​invasive BP monitoring​); connected to IV bag looking N/S bag with a little bit of
heparin in it → puff BP cuff around the bag → provides counter pressure because artery is in a high
pressure system ** can be inserted by a respiratory therapist. has a little hoohaw → drops meds into
the A line toy will see solution run down and its flushing the arterial line so it doesn't clot off; 3 way
stopcock: can rotate, draw ABG here. A line
Check the hand for mobility, warmth, pulse​. You want to see the waveform with the socratic notch
every hour
- Phlebostatic axis: zero reference
- Indication
- hypo/hypertension
- Shock
- vasoactive drugs
- ARDS
- Blood gasses
Blood will back up without the counter pressure
Arterial lines:
- Complication: hemorrhage, thrombus, infection, neurovascular impairment, limb loss
- Nursing: allen test, flush system, neurovascular assessment
***Allen test where you occlude the radial artery and make a fist hand turn pale when you let go, will
return to its normal color.
​Check the hand for mobility, warmth, pulse​.
Pulmonary artery catheter Swan ganz catheter​:
- Calculates cardiac output
- Measures central temp
- O2 saturations
- Administer drugs
- Draw blood
- Pulmonary pressures
- Pacing
Blood transfusions:
- Indications: severe blood loss related to trauma, surgery, severe anemia (hgb<7.0), bleeding
disorders.
- We don’t rush transfusion these days. Mostly bc there's not enough blood available.
- Requirements: order for blood type and volume, consent, pt must be type and
crossmatch (sample of pt blood and donor’s blood mixed together to look for
clumping/clotting/agglutination presents. If the blood clumps or agglutination it is not
compatible
- Blood is observed under microscope for infection or any disease like hepatitis and HIV
Types of blood products:
1. Packed red blood cells(very common in transfusion): used to increase oxygen carrying capacity of
blood. typically given to anemic pt, pts that are hemorrhaging, often have blood available for pt
that have surgery. Typically come in a volume of 250ml and typically transfuse over 2 to 4 hours.
- Transfused over 2 to 4 hours
- Packed RBCs can’t ever hang more than 4 hours. It will expire after 4 hrs
- Usual infused rated: 60 ml/hr (total volume is 250 ml)
2. Platelets: controls or prevents bleeding. (Get Infused quickly)
- Get it from multiple donors (pooled up to 10 donors) hopefully in 1 bag.
3. Plasma: “FFP” (fresh frozen plasma; freezing temp helps preserve clotting factors)given to
expand blood volume however After plasma is donated it's frozen. The freezing component helps
to preserve clotting factor to help control or prevent bleeding.
Nursing consideration:
- Large bore IV (angiocatheter. a smaller bore causes hemolysis so we use a large gauge needle like
17,18,19) the higher the needle size the smaller the lumen of the angiocatheter easier to start with
the higher number gauge. Wanting the needle to be bigger bc if it's too small can cause hemolysis
or breaking up of the blood cells destroy it.
- Blood needs to be retrieved or picked up from the blood bank and you can send a PCT to do this.
- Blood is checked by 2 RN’s always(no delegation) require confirmation process (compare
verbally the pts DOB, type of blood, expiration date, pts name, unit number, etc..) scan the
blood and then scan the patient
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When you hang blood you need a special blood IV tubing. IV blood tubing has a filter with a
mesh that helps trap any matter that's in the blood so it doesn't go into the pt and also has a “Y”
connector ALWAYS start priming blood tubing with normal saline. After nurses have checked
the blood the blood is hung on the other side of the blood tubing, you clamp of the normal saline
and open clamp to allow blood through (clear line; N/S with blood infusion line with a filter on it
that filter out the blood)
- Always before starting a transfusion must take a complete set of Vital signs before starting
infusion with temperature check.​ ​Fever is early signs of transfusion reaction.
- Always Start slowly for the first 15 minutes ex. 35-40ml/hr and increase it to 60ml/hr.
- Stay with the patient for the first 15 minutes to look out for a transfusion reaction
- Packed RBCs must be infused within 4 hours! They expire after 4hours
- Platelets and FFP are infused rapidly
- When transfusion is finished you flush the line with the normal saline
- Monitor for infusion reaction
- Symptom: Fever, warmth, itching, chills, itching, weakness, dyspnea, tachycardia,
hypotension
*** Who can pick up the blood from the blood bank? PCT (can be delegated….)
- Need to document
Transfusion reactions:
- Frequent vital sign checks
- Fever, warmth, itching, chills, itching, weakness, dyspnea, tachycardia,​ hypotension… pt can go
into anaphylactic shock. If pt has any of these symptoms the first thing you should do is
- **** Stop transfusion immediately, close off the roller clamp at the top where the blood is
and open the one where the saline is and flush the line through, check vitals.
- check blood for compatibility, obtain blood and urine samples​ if they have a transfusion
reaction
- Want to make sure you have the RIGHT BLOOD on the RIGHT PT!!!!!
- premedication : when we know a patient has an history of transfusion reaction
- Benadryl; for whom has history of allergic reaction
- Prednisone to prevent that inflammatory response
- Lasix (for cardiac patient lasix can be administered before transfusion to prevent
pulmonary edema and prevent fluid volume excess)
- In a cardiac pt that is being transfused and we were concerned about fluid volume
excess the priority assessment while giving a pt a transfusion you will listen to lung
sounds!! You will not set the infusion pump to 80ml/hr gentle transfuse the pt with
an underlying cardiac problem. Respiratory rate, pulse ox
- You also want to get baseline lung sounds, if pt already has crackles in the lungs,
lasix can be administered before the transfusion.
- SEE THE PICTURE ON THE PPT SLIDES
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CAN DELEGATE:
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Cardiac delegation from RN to PCT
■ Pick up blood from blood bank
■ Measure I&O
■ Vital signs
■ Weight gain/loss check
■ Keep Pt in quiet environment
■ Intake of IVs and liquid
■ Change position of Pt (prevent DVT, ulcer)
■ Gradual activity tolerance
■ Be with Pt for end of life care, Postmortem care
Cardiac delegation from rn to LPN/dietitian/PT..etc
■ Watch telemetry and report to RN
■ Ask dietician or nutritionist to come and educate the patient about diet plan
■ After ischemic event; ROM→ dangling→ OOB
RN only can do
■ Assessment/ monitor normal or abnormal
● VS, neuro, angina pain scale 1 to 10, suture line..
■ Teaching pt who is taking anticoagulant drugs.
● Diet - no leafy veggies
● Lab values