CARDIOVASCULAR
EKG BASICS
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1 large box = 0.20 seconds
5 large boxes = 1 second
1 small box = 0.04 seconds
WAVEFORMS
1.
P wave - upright and rounded; should not be longer than 0.10 seconds
- Represents the SA node sending out an electrical impulse & atrial depolarization (squeeze)
- P wave present = SA node is working & will have regular rhythm
2. QRS complex - tall and pointy, we DO NOT want a wide QRS (means something is wrong)
- Represents ventricular depolarization
- Ventricle contraction (squeeze) (in ST segment)
3. T wave - upright and rounded
- Represents ventricular repolarization (ventricles relaxing/refilling with blood)
- Helpful in monitoring extreme electrolyte imbalances (hypo/hyperkalemia, issues with
myocardial oxygen supply, or other cardiac disturbances such as pericarditis or ventricular
aneurysm)
ABNORMAL:
4. U wave - small, rounded wave after the T wave
- Common with drug toxicities (ex. digoxin) & electrolyte imbalances (hypokalemia)
INTERPRETING EKG’S
1.
2.
Count the HR
Is it regular or irregular?
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Ensure that the strip is 6 seconds long (30 large boxes)
To count HR, count the R’s and multiply by 10 (ex. 6 R’s = 60 bpm)
P wave present = regular rhythm
One P wave for every QRS complex
No wide QRS’s!
MEASURING INTERVALS:
Measures the amount of time it takes for the impulse to travel from one wave to the next
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P-R interval - movement of electrical activity from atria → ventricles
- Beginning of P wave to beginning of QRS complex
- Reflects the time required for atrial depolarization
- Should be between 0.1 and 0.2 seconds (not bigger than 1 large box)
- Most commonly measured
QRS interval - ventricular depolarization
- Beginning of Q to top of S (where it begins to flatten)
- Should be between 0.06 and 0.10 seconds
QT interval - time it takes for the ventricles to depolarize, contract, and repolarize
- Beginning of Q to end of T (bottom of hill)
- Should be less than 0.52 seconds
- Usually measured with magnesium-related issues, not on a regular basis
RHYTHMS
Normal Sinus Rhythm
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Normal sinus rhythm is generated by the SA node (sinus node)
HR: 60-100 bpm
1 consistent P wave for every QRS complex
SINUS DYSRHYTHMIAS
Symptoms:
● Hypotension
● Dizziness
● Lightheadedness
● Fatigue
● Syncope (fainting)/change in LOC
● SOB
● Diaphoresis (sweating)
● Anxiety
● Palpitations/chest pain
● Restlessness
*NOTE: only treat symptomatic patients as it may be their normal for some patients and they might just
require observation
Sinus Bradycardia: the sinus node creates an impulse at a slower-than-normal rate
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HR: < 60 bpm
Rhythm: regular
P wave: upright and rounded
Causes: lower-metabolic needs (sleep, athletic training, hypothyroidism, hypoxia, hypothermia,
hypotension, declining towards death)
Treatment:
- Vitals
- 12-lead EKG
- Obtain IV access
- Oxygen
- Eventually may need pacemaker (TCP) if HR remains too low after medication & Pt can’t tolerate
Meds:
- Atropine → 0.5 mg IV push
- Works on SA node
- After administration, get another BP, watch the HR, and maybe another EKG
*REMEMBER: medication is the LAST treatment option! Need vitals first in order to determine pulse ox for
necessary oxygen, etc.
Sinus Tachycardia: the sinus node creates an impulse at a faster-than-normal rate
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HR: > 100 bpm
Rhythm: regular
P wave: upright and rounded
Causes: anemia, fever, hypovolemic shock, hypotension, PE, MI, pain, anxiety, illicit drugs,
caffeine/stimulants, dehydration, hemorrhaging, sepsis/infection, electrolyte imbalances, stress, HF,
physical activity, fear, cardiac tamponade
Treatment: treat the cause! (tachycardia is a secondary issue from something else)
Meds:
- Maybe beta blockers to slow the HR
ATRIAL DYSRHYTHMIAS
Premature Atrial Contraction (PAC): abnormal contractions caused by pacemaker cells firing too early
-
Rhythm: irregular
P wave: appears prematurely
Treatment:
- Vitals, 12 lead EKG, IV access, oxygen
- Document
- Treat the cause (decrease stress, avoid alcohol and caffeine)
*Not really a whole lot to do
Afib: SA node not working, causing uncoordinated electrical activity in the atria, which causes rapid & disorganized
“fibbing” or “quivering” of the muscles, instead of fully squeezing → decreased cardiac output
*NOTE: this causes blood to collect in the atria, placing the patient at HIGH RISK FOR CLOTS & STROKE
*MEMORY TRICK: when you fib, your lip quivers
- HR: 300-600 bpm (unmeasurable)
- Rhythm: irregular
- P wave: absent (just see waves/quivering)
- Causes: other cardiac/pulmonary conditions (cardiomyopathy, pericarditis, HTN, CAD, HF, open heart
surgery), obesity, CKD, hyperthyroidism, diabetes
- Symptoms: all due to low O2 → fatigue, dizziness, lightheadedness, SOB, chest pain, tachycardia,
palpitations, anxiety, diaphoresis (depending on how high HR is)
- Treatment:
- Controlled (60-80 bpm): vitals, EKG, etc. & continue with their meds
- Uncontrolled (> 140 bpm):
- Vitals, 12 lead EKG, IV access, oxygen
- Meds
- Cardiac ablation (rhythm control)
- Cardioversion → synchronized administration of shock to R wave; stops heart
for about 6 seconds via SA node to restart and get a new, normal rhythm.
- This is NOT defibrillation
*NOTE: VERY UNCOMFORTABLE FOR PATIENT → GIVE PAIN MEDS PRIOR
- Meds:
- Control the HR (PRIORITY after vitals):
- Beta blockers
- Calcium channel blockers
- Digoxin
- Control the rhythm: (antiarrhythmics)
- Amiodarone
- Nicardipine (Cardene) - ???
- Anticoagulants (for life or until resolved)
- Apixaban (Eliquis)
Aflutter: similar to Afib, but not produced by the SA node. The atria are beating too quickly but at a regular
rhythm
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HR: 250-350 bpm
Rhythm: regular
P wave: not distinct, P & T run together; “sawtooth”
Causes: same as Afib
Symptoms: same as Afib
Treatment: same as Afib
Meds: same as Afib
SVT: abnormally fast HR that originates above the ventricles, typically in the atria. Very narrow QRS complex
*MEMORY TRICK: supra=above
- HR: > 100 bpm (typically 150-250)
- Rhythm: regular
- P wave: typically not visible (may be hidden in preceding T wave, check T wave for change in shape)
- Causes: caffeine, stimulants, drugs, sometimes cause is just unknown
- Symptoms: dizzy, lightheadedness, SOB, chest pain, palpitations, anxiety, sweating, “my heart is flopping
like a fish”, hypotensive (BP drops with high HR bc body doesn’t like that your heart is so fast)
- Treatment:
- PRIORITY → vitals, 12 lead EKG, IV access, oxygen
- Vagal maneuvers (bearing down like BM, blow through occluded straw, or bucket of ice in face)
→ want to initiate gasp to restart SA node
- Meds
- Cardiovert
- Meds:
- Adenosine → 6mg, 12mg, 12mg (STOPS THE HEART AND RESTARTS SA NODE = FLATLINE)
- MUST GET BP BEFORE ADMINISTERING -- drops BP very quickly
- Do not give more than 3 times
- Most ideal because it works very quickly (< 6 seconds)
- *NOTE: if Pt is hypotensive (< 100), CANNOT give Adenosine; MUST CARDIOVERT
- If Adenosine doesn’t work → cardioversion
- If cardioversion doesn’t work → Amiodarone (works slower than Adenosine)
- Beta blockers/calcium channel blockers
VENTRICULAR RHYTHMS
Premature Ventricular Contractions (PVC’s): wide and atypical (or bizarre-looking) QRS complexes that fire
earlier than expected. Could be upright or inverted, followed by a short pause
*NOTE: PVC’s can turn into Vtach (> 150 bpm) = deadly → watch for chest pain (notify HCP)
- Rhythm: irregular (or “regular except” with PVC)
- Unifocal: PVC coming from 1 ventricular pacemaker
- Bifocal (or multifocal): PVC coming from 2 (or more) different parts of the ventricle
- Bigeminy: PVC that occurs every other beat (beat, PVC, beat, PVC)
- Trigeminy: PVC falling every third beat (beat, beat, PVC)
- P wave: normal except PVC (no P wave with PVC)
- Causes: increased workload on the heart -- hypoxia, electrolyte imbalances, MI, cardiomyopathy, excessive
stimulant ingestion, HTN, recreational drug use/drug toxicity
- Symptoms: may be asymptomatic
- Treatment:
- Vitals, 12 lead EKG, IV access, oxygen
- Treat the underlying cause (have to figure out why they’re getting PVC’s)
- Stimulant/caffeine → wait until it wears off
- May need to ask -- How big was your coffee? How many cups did you drink? Did you
have chocolate? Sudafed? Etc.
Vtach: three or more PVC’s in a row; wide, consistent, QRS complexes. Can have a pulse or be pulseless.
No cardiac output (= low oxygen) or contractions which may be fatal!
*MEMORY TRICK: looks like tombstones
- HR: > 150 bpm
- Rhythm: regular
- P wave: not visible
- Causes: multiple PVC’s, drug toxicities, caffeine/stimulants, hypoxia, acidosis, hypo/hyperkalemia,
hypothermia, hypoglycemia, cardiac tamponade, PE, MI
- Symptoms:
- PULSE:
- Awake (Vfib is always pulseless)
- C/O chest pain, SOB, palpitations, sweaty, anxious, maybe hypotensive or maybe normal
BP (depending on how long you’re in it)
- PULSELESS:
- Dead, need to be resuscitated
- Treatment:
- PULSE:
- Vitals, 12 lead EKG, IV access, oxygen
- Need to change rhythm → vagal maneuvers, cardioversion, Amiodarone
- PULSELESS:
- CPR + defibrillation
- Epinephrine, Amiodarone
Vfib: rapid, disorganized pattern of multiple sources of electrical activity in the ventricles. Prevents ventricles from
pushing blood out of the heart (no cardiac output = no oxygen in the body). Shaky/quivering line. A lethal
dysrhythmia requiring immediate treatment -- LIFE-THREATENING
- HR: ALWAYS PULSELESS
- Rhythm: cannot assess
- P wave: no P waves, QRS complexes, or T waves
- Causes: illicit drug use, MI (most common rhythm seen with MI’s), same as Vtach
- Symptoms: loss of consciousness, pulseless
- Treatment: CPR + defibrillation
*MEMORY TRICK: defib Vfib
- Meds:
- Vasopressor → epinephrine
- Antiarrhythmic → amiodarone
Idioventricular Rhythm: occurs when the SA and AV nodes fail to function and the rhythm is generated from the
ventricles
- HR: < 40 bpm
- Rhythm: regular
- P wave: no P or T waves; wide QRS
- Causes: MI, post-cardiac arrest, drug toxicity (cocaine, digoxin, anesthetics), severe electrolyte imbalances,
myocarditis, cardiomyopathy, congenital heart disease
- Symptoms:
- Dizzy/lightheadedness
- SOB
- Syncopal episode
- Sweaty
- Anxiety
- Hypotension
- Decreased LOC
- Treatment:
- Vitals, 12 lead EKG, IV access, oxygen
- Treat the cause
- Prepare for pacemaker
Asystole: FLATLINE - no electrical activity in the heart
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Symptoms: no response from patient, pulseless
Treatment:
1. See flatline on monitor → check for pulse (to ensure flatline is not caused by loose ECG
patch/wire)
2. No pulse? → immediately start CPR
*NOTE: NO defibrillation (nothing to defibrillate)
3. Pause compressions briefly (< 10 seconds) to rule out a fine line VFib by placing a second monitor
lead. ONLY if it is VFib → THEN defibrillate
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4.
Meds:
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Ensure IV access for epi
Epinephrine
HEART BLOCKS
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Caused by the delay or blockage of electrical conduction at the AV node
When identifying heart blocks, look at the P-R interval pattern
First Degree: prolonged atrial depolarization in the AV node. Every atrial impulse gets through the AV node; it just
takes longer. It is the same interval each time
*MEMORY TRICK: If the R is far from the P, then you have FIRST DEGREE
- Looks very similar to NSR - only difference is P-R interval is > 0.20 seconds (1 large box)
- Rhythm: regular
- P wave: upright & rounded
- Symptoms: typically asymptomatic
- Treatment: not typically required
- Vitals, 12 lead EKG, IV access, oxygen
- Find/treat underlying cause
Second Degree - Type I (AKA Wenckebach or Mobitz I): occurs when not all atrial impulses get through the
AV node to the ventricles. There are more P waves than QRS complexes
*MEMORY TRICK: longer, longer, longer, DROP. Then you have a WENCKEBACH
- Rhythm: regular
- P wave: upright & rounded; P-R interval gets progressively longer until a QRS is dropped
- Symptoms: dizzy, lightheadedness, diaphoresis, syncope, anxiety, hypotension, SOB
- Treatment:
- Asymptomatic:
- Vitals, 12 lead EKG, IV access, oxygen
- Symptomatic:
- Atropine → stimulates heart to beat faster
- Prepare for temporary pacemaker → Transcutaneous pacing (TCP)
Second Degree - Type II (AKA Mobitz II): sudden failure of impulse conduction from atria to ventricles. Also
drops QRS complexes, however, the P-R intervals are exactly the same length with each complex
*MEMORY TRICK: if some P’s don’t get through, then you have MOBITZ II
- Rhythm: regular
- P wave: upright & rounded; P-R interval stays the same length until QRS is dropped
- Symptoms: same as type I
- Treatment: same as type I
Third Degree (complete heart block): occurs when the AV node is completely blocked and prevents any
impulses from entering or exiting. There is no communication between the atria and ventricles (atria is working
independently). P wave to P wave will be same length apart
*MEMORY TRICK: if P’s and Q’s don’t agree, then you have THIRD DEGREE
- HR: atrial = 60-100 bpm; ventricular = < 60 bpm
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Rhythm: regular
P wave: upright & rounded; P waves are NOT associated with QRS complexes (independent); P waves
may be hidden in T waves or QRS complexes → have to find them
Symptoms: same as type I
Treatment:
- Asymptomatic: very rare
- Vitals, 12 lead EKG, IV access, oxygen
- Figure out cause
- Symptomatic:
- Vitals, 12 lead EKG, IV access, oxygen
- Atropine
- TCP
- If above do not work → permanent pacemaker
TEMPORARY PACEMAKERS
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The energy source is an external battery pack
Transcutaneous (TCP): electrical stimulation used for emergent situations to increase HR
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Pads placed externally on the skin with one pad on the chest and one on the back (like AED pads)
Sends electrical stimulation through the thoracic musculature to the heart → VERY PAINFUL
Pacer spikes seen prior to QRS
CONTINUOUS VITAL SIGNS AND MONITORING REQUIRED
Transvenous (TVP): pacing lead wires are inserted via central line through subclavian vein so that they are in
direct contact with the right atrium (atrial pacing), right ventricle (ventricular pacing), or both chambers (dual
chamber pacing)
- Wire connects to external box where the desired rate is set
- More invasive = increased infection risk (vs. TCP) but lasts longer than TCP
- May be used temporarily until Pt can go to OR for permanent pacemaker & for emergent situations
- Pacer spike seen prior to QRS
- CONTINUOUS VITAL SIGNS AND MONITORING REQUIRED + monitor central venous site for signs of
infection
Transthoracic (TTP): pacer wire is surgically placed in the atrium or ventricle and fed out through the skin to
connect to external box/pacemaker (bascially same as TVP except wires are surgically placed)
CONTINUOUS VITAL SIGNS AND MONITORING REQUIRED
PERMANENT PACEMAKERS
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Wires are placed in the atria, ventricle, or both and the wires are placed in an internal pacing unit housed
under the skin near the clavicle
Atrial: wire in atria
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Pacer spike prior to P wave
Used with SA node failure
Ventricular: wire in ventricle
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Pacer spike prior to QRS complex
Used with a complete AV block
Biventricular: pacer lead in each ventricle
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Two pacer spikes prior to QRS
Dual Chamber: one wire in atria, one wire in ventricle
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Two pacer spikes: one before P wave and one before QRS
CARDIAC DISORDERS
Infective Endocarditis (IE): infection/inflammation of the endometrium (innermost layer of the heart), typically
affecting heart valves
- Platelet and fibrin deposit onto the injured area, forming a nonbacterial thrombotic endocardial lesion,
then microogransims get stuck under lesions, forming vegetation (looks like plaque build up), which can
severely damage the valves
- Common microorganisms: streptococcus, staph aureus (MRSA)
- Risk factors:
- Age (> 60)
- Immunodeficiency (can’t fight off bacteria)
- IV drug use (creating a port of entry!)
- Diabetes mellitus
- Prosthetic heart valves
- Prior history of IE
- Congenital or structural heart disease
- Presence of IV access or an implanted cardiac device
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Symptoms:
- Osler’s nodes (lymph nodes) - red, painful nodes in pads of finger & toes
- Janeway lesions - painless spots on palms and soles
- Splinter hemorrhages - vertical red lines under nail beds
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- ELDERLY: confusion, fever, fatigue (think S/S of infection)
Labs & Diagnostics:
- LABS: CBC (elevated WBCs), BMP, BNP, sed rate, blood cultures (two sets from different sites)
- DX: transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE) → these
show what the heart/valves look like and can identify any growth or abscesses
Treatment/INT:
- IV antibiotics for 4-6 weeks → will need PICC line
- Valve repair/replacement
- Assessments: cardiac history (previous valve replacement or invasive procedures), IV drug user,
neuro, skin, lab/dx results
Teaching:
- Will be in hospital for a longer period of time because of abx
- Once you have a valve replacement → MUST INFORM DENTIST! Bacteria will go straight to valves
- Don’t create new portal of entry → be careful with brushing teeth, use soft toothbrush
- Finish full course of abx
*MEMORY TRICK: think endo(carditis) like endodontist
Nursing Diagnosis:
- Ineffective tissue perfusion
- Decreased cardiac output
Complications:
- Embolization: those thrombotic lesions can break off and will likely travel to brain → HF &
dysrhythmias
Pericarditis: inflammation of the pericardium; common following an MI
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Causes: can be infectious (viral, bacterial, fungal, or parasitic) or noninfectious (MI, drug-related,
autoimmune, trauma)
Symptoms:
- Radiating chest pain that is relieved by sitting up and leaning forward
- SOB
- Palpitations
- Fatigue/low energy
- Abnormal EKG (ST-segment elevations or PR-segment depression)
- Friction rub upon auscultation (best heard @ left sternal border at the end of expiration. Have
Pt lean forward)
- Decreased appetite
Labs & Diagnostics:
- LABS: CBC (elevated WBC’s), blood cultures (+), C-reactive protein (+), sed rate
- DX: EKG, TEE or TTE, chest x-ray, cardiac CT scan
- Assessments: ABC’s, vitals, heart/lungs auscultation, I&O/daily weights, lab results
*Rule out MI
Treatment/INT:
- Elevate HOB to 30-45 degrees to relieve pressure on organs and decrease orthopnea (SOB when
lying down)
- Meds (pain is usually associated with inflammation)
- Emotional support (may have anxiety bc of fear that pain is r/t MI)
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Meds:
- Antiinflammatory → NSAIDs or ASA; maybe corticosteroids
- Diuretic
- Nitro
- Calcium channel blockers (depending on BP)
Nursing Diagnosis:
- Acute pain
- Risk for decreased cardiac output
Teaching:
- Med compliance!
- S/S of MI vs. S/S of worsening pericarditis → if symptoms continue to get worse or chest pain is
unrelieved with rest, call 911 and get to the hospital
Complications:
- Pericardial effusion: fluid builds and builds in chest putting too much pressure on the heart →
requires pericardiocentesis to drain fluid
- S/S: hypotensive, poor cardiac output
- May need repeat pericardiocentesis as it can come back
- Fluid is sent to lab to be cultured to ensure it’s not infectious
- Can lead to cardiac tamponade
- Cardiac tamponade: worsening of the effusion, too much pressure on the heart
- S/S: Beck’s triad - hypotensive, muffled heart sounds, jugular vein distention (JVD)
- Requires emergency bedside pericardiocentesis
- If pericardiocentesis doesn’t work, they go to OR for pericardial window surgery
VASCULAR DISORDERS
Hypertensive Crisis:
-
-
Hypertensive urgency:
- Diastolic BP > or = 120 mmHg
- No obvious organ damage
Hypertensive emergency: MOST SERIOUS
- Organ damage to VITAL organs - brain, kidneys, heart, lungs
- Symptoms will appear depending on where organ damage is
- Kidneys → renal failure
- Lungs → acute respiratory failure
- Brain → brain damage
- Need to immediately lower their BP in order to prevent total organ damage
- Check albumin levels
- Precipitating factors may include noncompliance with meds
- If it is not treated, they will die
Aortic Artery Disease (aneurysms):
-
Permanent localized dilation of an artery that forms when the layers/walls are weakened. This is due to
plaque build up (high cholesterol), which leads to the aorta getting wider/bulging and weaker
Abdominal Aortic Aneurysms (AAA):
- More common in men and Caucasians
- Below diaphragm
Thoracic Aortic Aneurysms (TAA):
- More common in men (age 40-70)
- Most common site for a dissecting aneurysm (tear in aorta) → HIGH MORTALITY RATE - want to catch
before
- Above diaphragm
*Both AAA and TAA carry high mortality rates
Risk factors:
- Genetics → Marfan’s syndrome is the hereditary disease most closely linked
- Increases with age
- Smoking → important because this a change a patient can control
- Atherosclerosis
- Treated & untreated HTN
- CAD
- High cholesterol
- Blunt trauma (MVA)
Symptoms:
Thoracic Aortic Aneurysms (TAA):
- Constant, severe back/chest pain
- Heart failure
- Dyspnea
- Cough/coarseness in voice
- Dysphasia
Abdominal Aortic Aneurysms (AAA):
- Constant, throbbing pain in abdomen
- Back pain
- Cyanosis
- Pulsating mass in abdomen → DO NOT PALPATE - RISK FOR RUPTURE
Diagnostics:
- CT scan with IV contrast ASAP → GOLD STANDARD. Will show exact location of aneurysm and its size
- Abdominal ultrasound or TTE (issue with ultrasound is that they have to press on abdomen)
- EKG (to rule out MI because of chest pain)
- Cardiac CT
Treatment/INT:
- HTN leads to rupture → need to constantly manage BP w/meds
- Keep them CALM → do not want to increase sympathetic response
- Meds
-
If the aneurysm is small (< 5 cm), they will manage it outpatient from home (antiHTN meds, q 6 month CT
scans)
If the aneurysm is bad, they may need IV antiHTN meds
Surgical management:
- Resection & repair - patch the wall with a mesh graft/lining
- RISK FACTORS: infection, mesh issues (tearing, body rejecting it), puncturing of aorta (hemorrhage, death)
- Can also have an MI as a result of surgery or go into renal failure
Meds:
- antiHTN → probably beta blockers
- Statins → lower cholesterol
- Tetracyclines & macrolides → abx to inhibit AAA progression
- Stool softeners (prevent strain)
Assessments:
- #1 → VITALS (HTN = increased risk of rupture)
- Peripheral pulses, skin color, temperature - lack of flow may indicate dissection
- Abdominal - very gentle abdominal assessment (not anywhere near mass). Will hear bruit with mass
Nursing Diagnosis:
- Risk for aspiration
- Risk for bleeding
- Fear
- Risk for ineffective peripheral tissue perfusion
- Acute pain
Teaching:
Managing from home:
- Monitoring BP
- Low-sodium diet
- Med compliance
- No bearing down (stool softeners, laxatives)
- Regular follow-up (routine CT & ultrasound to assess growth)
- Knowing risks for surgery (given by surgeon)
- Maintain healthy weight/healthy lifestyle (regular exercise)
- Avoid crossing/elevating legs to decrease pressure on aorta
- Smoking cessation if possible
- S/S of aortic dissection
Complication: aortic dissection
Aortic Dissection: sudden tear in aorta that creates a false lumen which could allow blood into the aortic wall.
Can lead to rupture of aortic aneurysm → LIFE-THREATENING
- Primary cause: degeneration of aortic media. HTN is also relevant
- Most common sites: ascending and descending thoracic
- Symptoms:
- Sudden onset of severe and persistent pain
- Feels like someone is tearing/ripping apart inside of your chest or back and extending to the
shoulders, epigastric area, or abdomen
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-
Anything distal to dissection will lose blood flow
Diaphoresis, nausea, vomiting, faintness, and tachycardia
BP is differing from one arm to the other → frequent, MANUAL BP
- Do not delegate BP! Want good, accurate measurements
Symptoms of ruptured aortic aneurysm:
- Similar to dissection
- Pain and then loss of consciousness due to hypovolemic shock from massive blood loss
- Can die if not treated quickly enough -- a lot of patient’s don’t make it to hospital in time
CARDIOVASCULAR DYSFUNCTION
Cardiac Output: total amount of blood pumped per minute
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Dependent upon the HR and stroke volume
Normally, we pump about 4-8 liters/minute
Stroke Volume: amount of blood pumped out of the left ventricle with each heartbeat
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Dependent on 3 factors: preload, afterload, and contractility
Preload: the end diastolic pressure or volume that stretches the right or left ventricle. It reflects fluid volume
status (pressure in the heart before it pumps)
- Can be affected by…
- Body position (different lying down vs. sitting up)
- Meds
- Amount of overall blood volume
Afterload: the force or resistance the ventricles must overcome to eject blood into the aorta or pulmonary circuit
(the resistance it must overcome to circulate blood)
Contractility: force/strength of contraction of heart muscle
- There are meds that affect this (dobutamine, epinephrine)
Hemodynamic Monitoring Systems: provides direct measurement of pressures in the heart and great vessels
(invasive)
- Central venous pressure (CVP)
- Arterial (A-line)
Central Venous Pressure (CVP): measuring pressure from blood returning to right atrium from SVC
- Transducer is secured at the phlebostatic axis, which is the external reference point that ensures accurate
readings
- Pt lays in supine position in order to get to right atrium
- Pressure bag holds saline flush bag to prevent backup of blood
- At risk for infection, hemorrhage
- If this doesn’t work → A-line for accurate BP
Arterial line: inserted into radial artery to ensure accurate BP
-
MAP of 65 mmHg is necessary for end-organ perfusion
Can also draw blood from it so we’re not sticking them again
Prior to insertion → Allen’s test to confirm good blood flow in the ulnar artery in case the radial artery is
damaged as a result of cannulation (color should return in 7-10 seconds)
Complications: bleeding, infection, dislodged line leading to further complications
Central Venous Monitoring: can measure preload & CVP
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Sits in either right atrium or right above it → HUGE INFECTION RISK
Has multiple ports → can give multiple drugs/fluid at one time or TPN
Complications: infection, dislodgment
Myocardial Infarction (MI): destruction of heart muscle from lack of oxygenated blood supply
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Atherosclerosis that ruptures and forms a thrombus in the coronary artery (and occlusion of blood flow to
the heart)
No blood flow → ischemia to the heart muscle which will eventually cause it to die and will not be able to
regenerate → decreased CO
Stable angina: episodes of intermittent chest pain with exercise but is relieved by rest
- Warning sign of potential heart muscle damage
- Can take nitro, but typically don’t
- Nitro: take it first then call 911
Acute Coronary Syndrome: kind of like unstable angina
- NSTEMI: a partial occlusion of a major coronary vessel or a complete occlusion of a minor coronary vessel
causing reversible partial thickness heart muscle damage
- STEMI: a complete occlusion of a major coronary vessel resulting in irreversible full thickness heart
muscle damage
*Will see elevated troponin
- Occlusion of the right coronary artery → HF symptoms
- Left Anterior Descending (LAD) coronary artery: occlusion of this = “widow maker”
- TO DO: look at 12 lead EKG to see where the MI is occurring
Risk factors:
- Males > females
- Female - postmenopausal
- Smoking
- Diabetes
- HTN
- High cholesterol
- Afib
- Stress
- Trauma
- CAD
- Obesity
- Family history
*Identify modifiable risk factors
Symptoms:
- Stable angina (predictable)
- Unstable angina (sudden)
- MEN:
- Jaw pain
- Left arm pain radiating from upper shoulder
- WOMEN:
- Back pain
- GI
- Anxiety
- Diaphoretic
- Fatigue
- ELDERLY:
- Change in mental status
*Depending on which vessel is affected, you may see other symptoms such as hypotension, bradycardia, JVD, HTN,
CHF, tachypnea
Labs & Diagnostics:
- LABS: troponin, CK, CKMP, BMP, BNP
(CK is released from the brain, skeletal tissue, and cardiac tissue; CKMP is specific to the cardiac muscle)
- CKMP is increased at 3 hours and remains elevated for up to 36 hours and then starts to return to
normal
- Troponin elevates within 4 hours and stays elevated for 10 days
- DX: echo, vitals
Treatment:
- Coronary angiography → GOLD STANDARD (thread catheter up through right radial and inject dye to see
what the heart looks like to see where the occlusion is. Once they find it, they can put a stent in and open
it up)
- Oxygen
- Meds
- Reperfusion therapy
- Coronary Artery Bypass Graft (CABG) - surgical
Meds:
- Nitroglycerin → preferred drug. Can give up to 3 times - TAKE BP Q 5 MIN! CANNOT GIVE UNLESS YOU
HAVE BP (BP → NITRO)
- Aspirin
- Morphine → vasodilates - DON’T give right away
-
-
Beta Blocker → given sometimes to bring HR down bc you don’t want heart working too hard. Metoprolol
has antidysrhythmic and antiHTN properties but slow the HR - HOLD med & notify HCP if apical pulse
<60/min
Heparin → given before cath lab to prevent anything from occurring
Coronary Artery Bypass Graft (CABG): surgical revascularization that bypasses blockages in the coronary
arteries that are causing heart muscle damage
- Done when there are multiple vessels (3+) that have blockages
- If a patient is not a candidate for a PCI, sometimes they will go straight to OR for this
- They take a healthy vein or artery, typically the internal thoracic artery (mammary) or saphenous vein, and
it is grafted to the blocked coronary artery so blood can bypass the blockage
- COMPLICATIONS:
- Dysrhythmias (specifically Afib) - may need meds to maintain
- Bleeding
- MI
- Stroke
- Nonunion of sternum
- Sternal infection
- Renal failure (because of bypass machine used during surgery)
- Heart failure - long-term, not curable
- Systemic inflammatory response
Nursing Management:
- Nursing Diagnosis:
- Decreased cardiac output
- Assessments:
- Pain
- Vitals
- Peripheral pulses
AFTER CABG:
- Monitor urine output
- They will be on a hemodynamic monitoring system (R-line)
- Chest tubes for drainage
- Hourly I&O
- Skin color, temp
- Interventions:
- Oxygen
- IV fluids
- Meds
- If femoral approach for PCI → bedrest
- Monitor both sites for bleeding
- Heart-healthy diet
- Up and walk ASAP following surgery - may be just side of bed, chair, etc. but want them up
- Monitor for infection in their incision
- Teaching:
-
Med compliance
Worsening symptoms (MI)
Diet
PT
No lifting > 10 lbs
Do not raise arms above head
No bending at waist
No vigorous activity until cleared by your physician
Cardiac rehab (like PT but for your heart)
Cardiogenic Shock: occurs when the heart muscle is unable to pump adequate CO to meet the body’s needs to
maintain adequate tissue perfusion. Leads to decreased cardiac output (decreased ejection fraction)
- Causes:
- Most common cause → MI
Compensatory mechanisms kick in to try and help but eventually they’re going to stop working because they need
help and if they’re not fixed, you will die. Leads to increased HR
-
-
-
Symptoms: similar to MI
- SOB/chest pain
- Crackles upon auscultation
- Decreased peripheral pulses
- Cool, pale skin/diaphoresis
- Bowel sounds/N/V
- Decreased urine output
- Restlessness
- Confusion
- Increased HR
- Increased lactic acid build up
- ABG’s - metabolic acidosis
- Inadequate organ perfusion → eventually lead to multiple organ systems fail
Labs & Diagnostics:
- LABS: CBC, BMP (assess organ function), cardiac enzymes, lactic level (assess tissue perfusion),
ABG analysis (metabolic acidosis)
Treatment:
- PRIORITY → Oxygen - 100% via non rebreather mask (want to decrease the work of breathing
and improve oxygenation)
- Meds
- PCI
- Intra-aortic balloon pump → used when initial medical management doesn’t improve cardiac
output; goal is to increase oxygen supply and decrease the myocardial oxygen demand
- Mechanical Circulatory Support (MCS) Devices:
- Mechanical pumps to help decrease the workload on the heart
-
-
LVAD: in left ventricle. Used in HF or cardiogenic shock as a bridge to recovery or to
transplantation while they’re waiting. Medically controlled on meds while they’re
waiting
Extracorporeal membrane oxygenator (ECMO) → used at the bedside for those with severe
acute respiratory and/or cardiac failure who have a high mortality risk
Heart transplant → eventually this may be the only option
Meds:
WANT TO INCREASE BP & CARDIAC OUTPUT AND DECREASE CARDIAC WORKLOAD
- Inotropics → dobutamine and epinephrine (improve CO)
- Vasopressors → dopamine, norepinephrine (Levophed), or phenylephrine (support BP &
maintain adequate MAP) - likely will have an A-line
- Nitroglycerin → decreases preload through venous dilation & afterload through arterial dilation
(*NOTE: it will decrease BP - use with caution)
- Nitroprusside → decrease afterload - also decreases BP - CAUTION
- Diuretics → decrease filling volumes by increasing urine output
- Morphine sulfate → may relieve pain due to an MI and decrease venous return & preload
through its action as a venous dilator
Nursing Management:
- Nursing Diagnosis:
- Decreased cardiac output
- Assessments:
- Hemodynamic monitoring
- BP on each arm
- Interventions:
- 100% oxygen non-rebreather mask
- Diet low in sodium
- LVAD - can get up for small periods but with frequent rest periods in between
- Teaching:
- S/S of heart failure
- When to call 911/when to notify physician