02.02 EKG (ECG) Waveforms
Outline
Overview
1. The heart’s electrical activity that stimulates the atria and ventricles to contract produce
a waveform on an EKG
2. These waveforms are broken down into in a P wave, QRS complex and T wave.
Nursing Points
1. P wave
1. Atrial depolarization
1. Positive deflection
2. PR interval
1. Beginning of P wave to beginning of QRS
2. Time it takes for electrical current to reach ventricles
1. 0.12-0.20 seconds
2. QRS Complex
1. Ventricular depolarization
1. Negative and positive deflection
2. QRS interval
1. Beginning of the Q wave to ending of S wave
2. Time it takes for the electrical current to travel through the ventricles
1. 0.06 -012 seconds
3. T wave
1. Ventricular repolarization
1. Positive deflection
2. QT interval
1. Beginning of QRS to the end of T wave
2. Time it takes for the ventricles to contract and relax
1. 0.36-.044 seconds
3. ST segment
1. End of QRS complex to the beginning of T wave
2. Time between ventricular depolarization and repolarization
Assessment
1. Recognize PQRST waveforms on EKG
2. Check pulse if abnormal waveforms are observed
Therapeutic Management
1. Recognize and report abnormal waveforms
1. Long PR interval
2. Prolonged QRS Complex
3. Tall T waves
03.05 Atrial Fibrillation (A Fib)
Outline
Overview
1. Atrial fibrillation
1. Multiple disorganized cells produce additional electrical impulse in atria
1. Causes atria to quiver at a fast rate
1. <300 bpm
2. Unable to effectively contract
1. Pooling of blood in atria
2. High risk for stroke
2. AV node blocks some of the electrical impulses from reaching the
ventricles
1. Rapid irregular ventricular contractions
By J. Heuser – Own work, CC BY-SA 3.0,
https://commons.wikimedia.org/w/index.php?curid=465397
Nursing Points
General
1. Characteristics of Atrial fibrillation
1. Rhythm
1. Irregular
2. Rate
1. Atrial rate
1. >300 bpm
2. Wavy baseline
2. Ventricular rate
1. 60-100 bpm
2. >100 bpm
1. “Rapid Ventricular Response” (RVR)
3. P:QRS ratio
1. No obvious P waves
1. Wavy baseline
2. Not measurable
4. PR interval
1. Not measurable
5. QRS complex
1. 0.06-0.12 seconds
Assessment
1. Patient Presentation
1. Palpitations
2. Fatigue
3. Lightheaded/Syncope
2. Acute or chronic
1. If chronic
1. Monitor rate/meds
2. If acute
1. Convert to NSR
3. Atrial and ventricular rates
1. RVR
4. Decreased Cardiac Output
1. Syncope
2. Hypotension
5. PT/INR
1. If taking Coumadin
Therapeutic Management
1. Nursing Interventions
1. Acute or chronic
2. 12 Lead EKG
3. Restore NSR
4. Assess for s/s of stroke
2. Convert to NSR
3. Control ventricular rate
1. Medications
1. Antiarrhythmics
2. BB
3. Calcium Channel Blockers
2. Transesophageal Echocardiogram (TEE) or Cardioversion (CV)
3. Ablations
4. Decreased risk for stroke
1. Anticoagulants
1. Coumadin (Warfarin)
2. Xarelto (Rivaroxaban)
3. Eliquis (Apixaban)
Nursing Concepts
1. EKG Rhythms
2. Perfusion
3. Clotting
Patient Education
1. Do not miss a dose of on anticoagulants
1. Check PT/INR as instructed
2. Check radial pulse
1. Report if >100
▪
Treatment: blood thinners (esp. if 48 hours or greater), antidysrhythmics (Cardizem,
Amiodarone, Digoxin, etc.) or cardioversion (if hemodynamically unstable AND < 48
hours)
03.06 Premature Atrial Contraction (PAC)
Outline
Overview
1. Premature atrial contraction
1. Additional stimulus initiated in the atria
1. Not originated by SA node
2. Causes a premature contraction by the atria
1. Decreased filling time in atria
2. Common arrhythmia
3. Normal ventricular contraction will follow the early atrial contraction
2. Must have an underlying rhythm
Nursing Points
General
1. Characteristics of PAC
1. Rhythm
1. Regular
2. Irregular with PAC
1. Abnormal P wave
2. Rate
1. Normal
2. Depends on underlying rhythm
3. P:QRS ratio
1. 1:1
4. PR interval
1. 0.12-0.20 seconds
2. Depends on underlying rhythm
5. QRS complex
1. 0.06-0.12 seconds
2. Depends on underlying rhythm
Assessment
1. Patient Presentation
1. Fluttery feeling in chest
2. Feeling of “heart skipping”
3. Dizzy
2. Electrolytes
Therapeutic Management
1. Nursing Interventions
1. Determine underlying rhythm
2. Determine frequency of PACs
2. Determine the cause
1. Caffeine intake
2. Electrolyte imbalance
3. MI
3. Treat the cause
4. Symptomatic
1. Beta blockers
5. Asymptomatic
1. Continue to monitor
Nursing Concepts
1. EKG Rhythms
Patient Education
1. Check radial pulse
1. Report if >100
2. Notify MD if symptomatic
03.07 Supraventricular Tachycardia (SVT)
Outline
Overview
1. Supraventricular tachycardia
1. Increased electrical stimulation in atria or AV node
1. Stimulates ventricles to contract rapidly
1. 150-250 BPM
2. Decreasing cardiac output
Nursing Points
General
1. Characteristics of Supraventricular Tachycardia
1. Rhythm
1. Regular
2. P waves
1. Pointed
2. Hidden in T wave
2. Rate
1. 150-250 BPM
3. P:QRS ratio
1. Visible P waves
1. 1:1
2. Non-visible P waves
1. Not measurable
4. PR Interval
1. Visible P waves
1. <0.20 seconds
2. Non-visible P waves
1. Not measurable
5. QRS complex
1. <0.12 seconds
Assessment
1. Patient Presentation
1. Palpitations
2. Fluttering in chest
3. SOB
4. Lightheaded
5. Chest pain
2. Decreased Cardiac Output
1. Syncope
2. Hypotension
Therapeutic Management
1. Nursing Interventions
1. Stable/Unstable
2. 12 Lead EKG
2. Determine the cause/Treat the cause
3. Control heart rate
1. Vagal Maneuvers
2. Medications
1. BB
2. Calcium Channel Blockers
3. ACLS guidelines
1. Stable
1. Adenosine
2. Unstable
1. Cardioversion (CV)
Nursing Concepts
1. EKG Rhythms
2. Perfusion
Patient Education
1. Check radial pulse
1. Report if >100
Treatment: vasovagal maneuver (mild symptoms, HR 150s up to 170, BP stable), Adenosine
(moderate symptoms, HR 170s-190s, at or just above stable), synchronized cardioversion (HR
190s up to 230 or more, many symptoms, BP unstable) ; depends on symptoms & whether
stable or unstable hemodynamically
03.08 Premature Ventricular Contraction (PVC)
Outline
Overview
1. Premature ventricular contraction
1. Additional stimulus initiated in the ventricle
1. Causes a premature contraction of the ventricles
1. Decreased filling time
1. Decreased cardiac output
2. Ventricles contract before atria can contract (no P wave)
2. Must have underlying rhythm
Nursing Points
General
1. Characteristics of PVC
1. Rhythm
1. Irregular with PVC
2. Regular
1. Depends on underlying rhythm
2. Rate
1. Normal
1. Depends on underlying rhythm
3. P:QRS ratio
1. No P wave during PVC
1. Not measurable
2. 1:1
1. Depends on underlying rhythm
4. PR interval
1. Not measurable during PVC
2. 0.12-0.20 seconds
1. Depends on underlying rhythm
5. QRS complex
1. > 0.12 during PVC
1. Abnormal looking
Assessment
1. Patient Presentation
1. Feeling of “heart skipping a beat”
2. Pounding heart beat
2. Electrolytes
3. VS
4. Oxygen saturation
Therapeutic Management
1. Nursing Interventions
1. Determine underlying rhythm
2. Determine frequency of PVCs
1. Bigeminy
2. Trigeminy
2. Determine/treat the cause
1. Caffeine intake
2. Electrolyte imbalance
3. Hypoxia
4. Medications
5. MI
3. Asymptomatic
1. Continue to monitor
4. Symptomatic/Frequent
1. Medications
1. Antiarrhythmics
2. Beta blockers
3. Calcium channel blockers
2. Implantable Cardioverter Defibrillator
3. Ablations
Nursing Concepts
1. EKG Rhythms
2. Perfusion
Patient Education
1. Notify MD if symptomatic
2. Limit caffeine intake
03.09 Ventricular Tachycardia (V-tach)
Outline
Overview
1. Ventricular Tachycardia
1. Multiple unorganized electrical signals in the ventricles
1. Ventricles contract at a rate of 150-250 bpm
2. May or may not have pulse
3. Significantly reduces CO and perfusion
Nursing Points
General
1. Characteristics of Ventricular tachycardia
1. Rhythm
1. Regular
2. Irregular
2. Rate
1. 150-250 bpm
1. Ventricular rate
3. P:QRS ratio
1. No P waves
1. Not measurable
4. PR interval
1. No P waves
1. Not measurable
5. QRS complex
1. > 0.12 seconds
2. “Wide”
Assessment
1. Patient Presentation
1. Palpitations
2. Chest pain
3. Decreased CO
1. Hypotensive
2. LOC changes
3. Lightheaded
4. Syncope
2. Pulse or pulseless
3. Electrolytes
Therapeutic Management
1. Nursing Interventions
1. Determine if a pulse is present
2. Sustained or Unsustained
1. Monomorphic
2. Polymorphic
2. Determine/Treat the cause
1. Electrolytes
2. MI
3. Abnormal heart conditions
3. Follow ACLS guidelines
1. V-tach with pulse
1. Amiodarone IV
2. Magnesium Sulfate IV
3. Synchronized Cardioversion (CV)
2. Pulseless V-tach
1. CPR
2. Defibrillate
3. Epinephrine
Nursing Concepts
1. EKG Rhythms
2. Perfusion
Patient Education
1. Seek medical help
Treatment: Monomorphic & stable- Amiodarone IV, if polymorphic then Phenytoin or IV
Magnesium
Cardiovert if drug therapy fails
03.10 Ventricular Fibrillation (V Fib)
Outline
Overview
1. Ventricular Fibrillation
1. Multiple unorganized electrical signals in the ventricles
1. Causing the ventricles to quiver
1. Wavy lines
2. Heart not able to pump blood out
1. Zero cardiac output
3. Life threatening emergency
1. Cardiac arrest
Nursing Points
General
1. Characteristics of Ventricular fibrillation
1. Rhythm
1. Irregular
2. Rate
1. Not measurable
3. P:QRS ratio
1. Not measurable
4. PR interval
1. Not measurable
5. QRS complex
1. Not measurable
Assessment
1. Patient Presentation
1. Cardiac arrest
2. Will NEVER have a pulse!
Therapeutic Management
1. Nursing Interventions
1. CPR
2. Follow ACLS guidelines
1. CPR
2. Defibrillate
3. Epinephrine
4. Amiodarone
Nursing Concepts
1. EKG Rhythms
2. Perfusion
03.11 1st Degree AV Heart Block
Outline
Overview
1. 1st degree AV heart block
1. Conduction delay in the AV node
1. Prolonged conduction from the atria to ventricles
2. PR interval >0.20 seconds
Nursing Points
General
1. Characteristics of 1st degree AV heart block
1. Rhythm
1. Regular
2. Irregular
2. Rate
1. Varies
2. Depends on underlying rhythm
3. P:QRS ratio
1. 1:1
4. PR interval
1. >0.20 seconds
5. QRS complex
1. 0.06-0.12 second
Assessment
1. Patient Presentation
1. Asymptomatic
2. VS
Therapeutic Management
1. Nursing Interventions
1. Continue to monitor
2. Determine/treat possible causes
1. Electrolytes
2. Medications
3. MI
3. Symptomatic bradycardia
1. ACLS guidelines
Nursing Concepts
1. EKG Rhythms
Patient Education
1. Count radial pulse
1. Report if <60 or >100 and symptomatic
1st degree is associated with MI, CAD, rheumatic fever, hyperthyroidism, electrolyte
imbalances, & vagal stimulation (this can be as simple as the pt. bearing down to have a bowel
movement). The P wave is the normal shape and rate just longer in duration. These pts are
asymptomatic but this can signal more serious AV blocks. Treatment will be to stop the
offending medication, give stool softeners, correct electrolyte imbalances, etc.
03.12 2nd Degree AV Heart Block Type 1
(Mobitz I, Wenckebach)
Outline
Overview
1. 2nd degree AV heart block type 1
1. Impulse from atria have difficulties reaching ventricles
1. AV node is defective
1. Progressively prolonged PR interval
2. Some QRS are dropped
2. Also called
1. Mobitz Type 1
2. Wenckebach
Nursing Points
General
1. Characteristics of 2nd degree AV heart block type 1
1. Rhythm
1. Regular
2. Irregular
2. Rate
1. Varies
1. Depends on underlying rhythm
3. P:QRS ratio
1. 1:1
1. Except in dropped QRS
4. PR interval
1. Progressively prolonged
1. Then QRS dropped
5. QRS complex
1. 0.06-0.12 seconds
Assessment
1. Patient presentation
1. Asymptomatic
Therapeutic Management
1. Nursing interventions
1. Continue to monitor
2. Know underlying rhythm
2. Determine/treat cause
1. Electrolytes
2. Medications
1. Digoxin
3. MI
3. Treat if symptomatic bradycardia
1. ACLS
Nursing Concepts
1. EKG rhythms
Patient Education
1. Count radial pulse
1. Report if symptomatic
03.13 2nd Degree AV Heart Block Type 2
(Mobitz II)
Outline
Overview
1. 2nd degree AV heart block type 2
1. Impulse from atria have difficulties reaching ventricles
1.
1. Defective AV node
2. Defective conduction system in ventricles
1. Dropped QRS
2. Also called
1. Mobitz Type II
Nursing Points
General
1. Characteristics of 2nd degree AV heart block type 2
1. Rhythm
1. Regular
2. Irregular
2. Rate
1. Varies
1. Usually slow
3. P:QRS ratio
1. 1:1
1. Except in dropped QRS
4. PR interval
1. Normal
1. 0.12-0.20 seconds
2. Prolonged
1. >0.20 seconds
5. QRS complex
1. 0.06-0.12 seconds
Assessment
1. Patient presentation
1. Lightheaded
2. Dizzy/Syncope
3. S/S of decreased CO
Therapeutic Management
1. Nursing interventions
1. Assess patient
2. VS
3. Notify MD
2. ACLS guidelines
1. Atropine
2. Prepare patient for pacemaker
1. Temporary if unstable
1. Transcutaneous
2. Permanent
Nursing Concepts
1. EKG rhythms
2. Perfusion
Patient Education
1. Seek medical help
03.14 3rd Degree AV Heart Block (Complete
Heart Block)
Outline
Overview
1. 3rd degree AV heart block
1. Complete heart block
2. Atria are contracting at own pace
1. Signal unable to get to the ventricles
3. Ventricles are contracting at own slow pace
1. Decreased CO and perfusion
4. Dissociation between P waves and QRS complex
1. NO relationship between the atria and ventricles
Nursing Points
General
1. Characteristics of 3rd degree AV heart block
1. Rhythm
1. Regular
1. P to P
2. Regular
1. R to R
2. Rate
1. Varies
1. Usually slow
1. Ventricular rate
2. More P waves
1. Normal atrial rate
3. P:QRS ratio
1. No relationship between P waves and QRS
1. Not measurable
4. PR interval
1. No relationship between P waves and QRS
1. Not measurable
5. QRS complex
1. Wide
1. >0.12 seconds
Assessment
1. Patient presentation
1. Fatigue
2. Dizzy/Syncope
3. Decreased CO
1. Hypotensive
2. Chest pain
2. Medical emergency
Therapeutic Management
1. Nursing interventions
1. Assess patient
2. Therapeutic management
1. Pacemaker
1. Temporary if unstable/emergent
Nursing Concepts
1. EKG rhythms
2. Perfusion
Patient Education
1. Seek medical help
2.
Defibrillation
▪ Defib for Vfib and pulseless Vtach
▪ Always continue chest compressions when waiting for defibrillator to
charge & resume ASAP after discharge
▪ Monophasic defibrillators send energy in 1 direction so joules are set as high
as 360j, biphasic sends energy in two directions so joules can be from 120-200j
▪ NEVER place pads over a pacemaker or AICD
Asystole is cardiac standstill or “without contractions” there is no ventricular electrical
electricity & no rate or rhythm, no pulse, and no C.O
Some atrial electrical activity may be evident; if atrial electrical activity present, the rhythm is
called P-wave Asystole
The causes & clinical significance of asystole is extensive myocardial damage (from ischema or
infarction), hypoxia, hypo/hyperkalemia, hypothermia, acidosis, drug OD, acute respiratory
failure, ventricular aneurysm, and traumatic cardiac arrest
Treatment is CPR & Epi, this will not be defibrillated because there is no rhythm to convert.
02.05 Nursing Care and Pathophysiology of
Coronary Artery Disease (CAD)
Outline
Overview
Pathophysiology: Coronary arteries are responsible for delivering oxygen to the heart.
CAD occurs when plaque forms in the arteries. This plaque narrows the arterial space
or the lumen. This narrowing causes blood flow to be impaired. When the blood flow is
impaired oxygen delivery is inadequate. Oxygen can not supply the heart
adequately. When oxygen is not sufficiently and adequately supplied to the heart
tissue, ischemia occurs.
1. Coronary artery disease
1. Buildup of plaque in main vessels
2. Primary causes = high blood pressure and cholesterol
3. Sign = chest pain
1.
Nursing Points
General
1. Major vessels
1. Inner walls damaged
2. Inflammation
1. Plaque sticks to walls
2. Clots form
3. Blockage –> loss of blood supply to heart
2. Risk factors
1. Smoking
2. High blood pressure
3. Obesity
4. Diabetes
5. Hyperlipidemia
6. Family history
3. Complications
1. Acute coronary syndrome–>plaque breaks off and occludes coronary artery
1. STEMI (ST segment elevation myocardial infarction)–>”widowmaker”
1. Near or complete blockage
2. NSTEMI (non ST Segment elevation myocardial infarction)
1. Partial blockage
3. Unstable angina
4. Concerned for—>cardiac arrest
Assessment
1. Presentation
1. Chest pain
2. Arrhythmia–>listen to heart
3. Shortness of breath
4. Elevated blood pressure
5. Possibly asymptomatic–>until MI
2. Doctor orders
1. Electrocardiogram (EKG)
2. Cholesterol levels
3. CT scan–>visualize vessel occlusion and stenosis
4. Angiogram–>view inside vessels
5. Stress test–>view blood flow
Therapeutic Management
1. Medications
1. Cholesterol medications–>Statins
1. Decrease plaque in blood
2. Anticoagulants
1. Avoid blood clotting
3. Beta blockers
1. Decrease workload of heart
4. Calcium channel blockers
1. Relax vessels, allow blood through
5. Nitroglycerin
1. Open arteries, allow blood through–>decrease chest pain
2. Procedures
1. Angioplasty–>go in through vein to open vessels
2. Stent placement–>keep vessel open
3. Coronary artery bypass surgery–>new vessel pathway around blockage
Nursing Concepts
1. Clotting
1. Walls damaged, plaque sticks, clots form
2. Perfusion
1. Build-up of plaque and blood clots–>decrease perfusion
3. Oxygenation
1. Decreased perfusion=decreased oxygenation of heart
4. EKG Rhythms
1. Show if heart damaged
Patient Education
1. Quit smoking
2. Stay active
3. Eat healthy diet
4. Control stress
5. Manage diabetes
Major cause of CAD is atherosclerosis
Clinical Manifestations of CAD
Angina
Angina occurs because the myocardial cells are deprived of oxygen and glucose needed for
aerobic metabolism and contractility.
Anaerobic metabolism begins and lactic acid accumulates, this lactic acid irritates myocardial
nerve fibers and transmits pain message to cardiac nerves and upper thoracic posterior nerve
roots which accounts for referred cardiac pain to shoulders, neck, lower jaw, arms
Management
 FIRST:
 Provide O2
 Get ECG to find out if STEMI
 Give Nitrates (to vasodilate for symptomatic relief) & Morphine (to pain that
SNS stimulation & decrease O2 demand)
 Aspirin
THEN:
 Get to cath lab ASAP! If no cath lab then thrombolytic therapy
 Beta blockers (eg, metoprolol): indicated in all patients unless contraindicated
03.02 Nursing Care and Pathophysiology for
Heart Failure (CHF)
Outline
Pathophysiology: In heart failure, the heart does not pump effectively. This can occur because
of many reasons but usually, because there has been damage to the heart tissue. The heart is
not able to pump enough fluid forward so fluid then backs up. This fluid backup increases work
on the heart as it tries to keep up and cannot.
Overview
The heart is a pump, circulates blood throughout the body. Heart failure = pump failure. Heart
failure occurs when the heart cannot pump enough blood to supply the body’s needs.
Nursing Points
General
1. Pump Failure
1. Decreased perfusion forwards
2. Increased congestion backwards
2. Causes
1. Myocardial Infarction
1. Dead muscle can’t pump
2. Hypertension
1. ↑ afterload = ↑ stress on heart muscle
3. Valve Disorders
1. Blood not moving in right direction
2. Inefficient pump
3. Diagnostics
1. BNP (Brain Natriuretic Peptide) – stretch of LV
2. Echocardiogram
1. Ejection Fraction
2. Can diagnose valve disorder
3. Chest X-Ray (CXR
1. Cardiomegaly
2. Pulmonary Edema
4. Complications
1. Volume Overload
1. Pulmonary Edema
2. Exacerbations
2. Decreased Perfusion
1. Heart
1. Angina, MI
2. Arrhythmias
2. Organs
1. Impaired Kidney Function
Assessment
1. Right-Sided Heart Failure
1. Decreased Pulmonary Perfusion
1. ↓ oxygenation
2. ↓ activity tolerance
3.
2. Increased Systematic Congestion
1. Peripheral Edema
2. ↑ JVD
3. ↑ Preload
4. Weight Gain
5. Fatigue
6. Liver / GI Congestion
2. Left Sided Heart Failure
1. Decreased Systemic Perfusion
1. Skin pale or dusky
2. ↓ Peripheral pulses
3. Slow capillary refill
4. ↓ renal perfusion
1. ↓ urine output
2. Kidney Injury / Failure
2. Increased Pulmonary Congestion
1. Pulmonary edema
1. Cough
2. Pink/frothy sputum
3. Crackles
4. Wheezes
5. Tachypnea
6. SOB on Exertion
2. Anxiety/restlessness
Therapeutic Management
Goal is to decrease workload on heart while still increasing cardiac output. Discussed in more
detail in Therapeutic Management Lesson
1. Decrease Preload
2. Decrease Afterload
3. Increase Contractility
Patient Education
Discussed in more detail in Therapeutic Management Lesson
1. Diet & Lifestyle Changes
2. Medication Instructions
3. Activity Restrictions
4. Frequent Follow-Ups
Medications
▪
▪
▪
▪
▪
▪
Vasodilators improves coronary artery blood flow by dilating the coronary arteries.
Reduces preload, afterload (in high doses), & increases myocardial O2 supply
Morphine dilates pulmonary and systemic blood vessels, reducing preload and afterload
Positive inotropes increase myocardial contractility and are used for patients with
evidence of cardiogenic shock or with low CO
Diuretics are the first line for treating patients with volume overload
ACE inhibitors block RAAS by inhibiting the conversion of angiotensin I to II, reduce
afterload & SVR, inhibit ventricular remodeling
Pts unable to tolerate ACE inhibitors are given angiotensin II receptor blockers (ARBs)
promote afterload reduction & vasodilation
Stages of Heart Failure
A
At high risk for HF, but without structural heart disease
B
Structural heart disease, but without signs or symptoms o
C
Structural heart disease with prior or current symptoms o
D
Refractory HF requiring specialized interventions
BNP Heart Failure Guidelines
So there are multiple ways that we can diagnose and classify heart failure, but we just want you
to know these three. The lab value we use is called Brain Natriuretic Peptide or BNP – this is
released whenever the ventricles are stretched. So in Congestive Heart Failure patients when
they’re severely volume overloaded, we can see this number jump into the thousands. In the
labs course we will talk in much more detail about this value, so be sure to check that out.
Clinical Signs of Heart Failure
So let’s look at what this patient looks like when you actually see them in practice…
In the module intro we asked y’all to brainstorm what you thought this patient looked like.
Guys if you get nothing else about Heart Failure, THIS is the part you’ve got to get.
Remember we said that there’s decreased perfusion forward and increased congestion
backwards, right? So in right-sided heart failure we’re going to see some oxygenation problems
because of decreased perfusion to the lungs. They may struggle with activity because they just
don’t have enough blood flow for their lungs!
Then backwards we see that congestion into the system – they are way overloaded in the
systemic circulation – so what does that mean? That means peripheral edema – okay how
would you feel if you swelled up like crazy? You’d be tired, you’d probably gain some weight?
Some of that fluid may even collect in the gut and make you nauseous.
Then because the blood can’t get past the heart from the body, it even backs up into the neck
and you’ll see this crazy jugular venous distention – it looks like a rope on their neck!! So if
you’re seeing these signs of excessive volume out in the body – you gotta think right sided
heart failure!
Okay, so what about the left? Well they actually have decreased perfusion to the body.
Remember your signs of decreased perfusion? They’re gonna be pale, decreased pulses, maybe
slow cap refill, and their skin might even be cold, right? Signs of decreased perfusion. Then, we
see the congestion happening in their lungs – y’all their lungs are full of fluid! How would you
feel? You’d be struggling to breathe, right? They’ll have a cough, and their sputum will be pink
and frothy because there’s just so much blood pumping through the lungs! Imagine if this was
you and had all this fluid in your lungs – what position would you want to be in? You lay down
and you’ll feel like you’re drowning – a lot of these patients sleep with lots of pillows or even in
a recliner. Some of them even lose weight because it becomes a choice to either eat or
breathe! So if you see these severe respiratory issues and fluid on the lungs, you’ve got to think
Left-sided heart failure!
So right sided the classic sign is the systemic overload and left-sided classic sign is pulmonary
edema. If you get this you can pick out any issues they’ll have!
Complications of Heart Failure
Now, there are quite a few other complications of heart failure, but the one I really want y’all to
understand is what happens when the kidneys don’t get perfused. So here’s our heart failure
patient who has decreased perfusion forward and increased congestion backward. They’re
volume overloaded, probably struggling to breathe, and now, they aren’t perfusing their
kidneys.
When the kidneys lose blood flow, it stimulates the Renin-Angiotensin-Aldosterone system
(RAAS). You will learn more about this in pharmacology, but what you need to know is that it
causes three main things to happen in the body.
1. The first is water retention because of aldosterone and ADH. The kidneys see a lack
of flow and think they need to hold onto water! So it is increasing the preload (or
stretch) on ventricles whose preload is already sky-high!
2. The second is vasoconstriction. This is the body trying to pull blood towards the
heart to increase the blood pressure – this increases afterload (the force the heart
has to pump against) – in a patient whose heart is already struggling as it is!
3. And the third is the RAAS activates the Sympathetic Nervous System – it’s basically
telling the heart to work harder and faster – which it cannot do! The end result is
MORE volume overload, MORE stress on the heart muscle, and a perpetuated cycle
that never ends.
That’s why I call it the cycle of death. What you’ll see when we look at therapeutic management
in the next lesson is that the majority of therapy is aimed at breaking this cycle.
So let’s recap – anything that can affect the heart’s ability to pump effectively can cause heart
failure, including an MI, hypertension, and valve disorders. Right-sided heart failure presents
with symptoms of decreased pulmonary perfusion and increased systemic congestion – so
they’re swollen, gain weight, lots of edema. Left-sided is the opposite – decreased systemic
perfusion and increased pulmonary congestion, so these patients are really struggling to
breathe. We diagnose with a BNP, Chest X-ray, and Echocardiogram. And don’t forget that the
impact this has on the kidneys can make the problem worse – we’ll talk about how we work to
break that cycle of death for these patients.
Nursing Care and Pathophysiology of
Myocardial Infarction (MI)
Outline
Overview of Myocardial Infarction (MI)
Sudden restriction of blood supply to a portion of the heart causing ischemia and death to the
muscle tissue
Nursing Points
General
1. Myocardial infarction literally translates into “heart muscle death” and is the result of a
complete loss of blood flow, or perfusion to the heart.
2. Oxygen supply can’t meet oxygen demand
3. Is often caused by atherosclerotic plaque breaking off of the vessel wall and causing
acute loss of blood flow through the coronaries.
Nursing Assessment
1. Chest pain
1. Burning, squeezing, crushing, etc
2. Radiation of pain
2. Shortness of breath
3. Irregular heart rate
4. Altered Vital Signs:
1. Hypertension vs Hypotension (shock)
2. Tachycardia
3. Abnormal EKG
4. Low O2 Saturation
5. Altered Labs:
1. Troponins!
2. Lipid profile
3. CBC/BMP
Myocardial Infarction Therapeutic Management
1. Antiplatelet and Anticoagulant Medications
1. Prevent platelet aggregation and reduce viscosity of blood
2. Aspirin and IV heparin
2. Vasodilatory Agents
1. Nitroglycerin, Morphine
3. Time is Tissue: PCI (Percutaneous Coronary Intervention) should be performed within 90
minutes
1. To cath lab to attempt coronary artery stenting to restore blood flow
4. CABG (Coronary Artery Bypass Grafting)
1. In both emergent or non-emergent situations if PCI is unsuccessful
5. High-dose statin
6. Beta-blockers/ACE-inhibitors
7. Vital Sign and Lab Monitoring
Nursing Concepts
1. Perfusion
2. Oxygenation
Patient Education for Myocardial Infarction
1. Diet/Exercise
2. Smoking Cessation
3. Taking new medications as prescribed
4. Follow up
Nursing Interventions
MONA:
 Morphine

Oxygen
 Nitroglycerin
 Aspirin (ASA)
*note – this is only a mnemonic and not the correct order of administration – see rationale for
details*
RATIONALE
Initial treatment for acute coronary syndrome.
 Morphine: given ONLY if aspirin and nitroglycerin do not relieve chest pain. Initial dose
is 2-4 mg IV.
 Oxygen: helps for you to remember to check oxygenation for chest pain – if under 94%
or if patient is short of breath give 2L NC initially. Administer oxygen only when clinically
relevant.
 Nitroglycerin: This is the initial medication given, along with aspirin. This medication
dilates the blood vessels to help allow any blood flow that might be impeded. Give 0.4
mg sublingual tab, wait 5 minutes, if the chest pain is not relieved administer another
dose. This can happen 3 times total. Monitor a patient’s blood pressure, hold for a
systolic BP of less than 90 mmHg.
 Aspirin: given to thin the blood and decrease mortality risk. A total of 4 baby aspirin (81
mg each) can be given for a total of 324 mg, or a single 325 mg dose.
12-Lead ECG
If initial 12-lead ECG indicates inferior MI, do a right-sided 12-lead ECG.
RATIONALE
Assess a 12 lead ECG immediately on anyone complaining of chest pain to determine if an ST
elevated MI is occurring. If it is-Take the patient to the cath lab STAT! If the ECG is a normal
sinus or otherwise non-concerning rhythm, place them on a 3 or 5 lead cardiac monitor for
frequent re-assessing.
Right sided 12 lead ECG shows the right side of the heart to assess for right ventricular
ischemia. **Inferior MI’s need to be treated differently!**
3 or 5 Lead monitoring
RATIONALE
No matter the outcome of the 12 lead ECG, placing a patient on a form of cardiac monitoring is
key. You are worried about a worsening condition such as cardiac arrest.
Cardiac Catheterization with Percutaneous Coronary Intervention (PCI)
RATIONALE
A patient who has an ST elevated MI (STEMI) will be rushed to the cath lab so they can locate
the clot and place a stent to regain blood flow to the heart.
A patient may also go to the cath lab without having a STEMI, and they may still find a clot.
Most NON-STEMI’s are treated without catheterization.
BP Monitoring
 The measurement is determined by the doctor, who is determining this based on
evidence based research married with patient factors.
 It can be measured by the systolic BP or the Mean Arterial Pressure (MAP).
 This can also be monitored by an arterial line.
RATIONALE
This is important because the higher the blood pressure, the more pressure is on a clot. It isn’t
out of the question for someone to have more than one clot, and increased pressure could
break free a clot lodge itself somewhere else either in the heart, lungs, brain, or extremity.
Heparin
RATIONALE
This is an anticoagulant that breaks up blood clots (as well as prevents them).
 Monitor aPTT or Anti-Xa Q6H to adjust and maintain therapeutic levels.
For STEMI
 Bolus: 60 units/kg (max 4,000 units)
 Continuous infusion: 12 units/kg/hr
 -Adjust according to your organization’s nomogram (Q6H- based on results of aPPT or
Anti-Xa)
For N-STEMI
 Bolus: 60-70 units/kg (max 5,000 units)
 Continuous Infusion: 12-15 units/kg/hr

-Adjust according to your organization’s nomogram (Q6H- based on results of aPPT or
Anti-Xa)
Insert Large Bore IV and draw initial Cardiac Enzymes
RATIONALE
IV access is important for administration of medications, possible interventions if angina
worsens, and any scans that may be needed to rule out thrombosis.
Cardiac enzymes further serve to rule out Myocardial Infarction and can give an indication to
the extent of myocardial damage.
 Troponin I
 CK
 CK-MB
 Myoglobin
Monitor Cardiac Enzymes:
 Troponin I
 Creatine Kinase-MB (CKMB)
RATIONALE
The values of these enzymes are based on your institutional laboratory technique. If they are
elevated it indicates that the cardiac muscle is stressed out or injured.
 Troponin I is an enzyme that helps the interaction of myosin and actin in the cardiac
muscle. When necrosis of the myocyte happens, the contents of the cell eventually will
be released into the bloodstream.
o Troponin can become elevated 2-4 hours after in ischemic cardiac event and can
stay elevated for up to 14 days.
 Creatine Kinase MB: This enzyme is found in the cardiac muscle cells and catalyses the
conversion of ATP into ADP giving your cells energy to contract. When the cardiac
muscle cells are damaged the enzyme is eventually released into the bloodstream.
o CKMB levels should be checked at admission, and then every 8 hours afterwards.
Left coronary artery is called the widow maker
Code Meds
CABG
Coronary artery bypass grafting is a surgery that improves blood flow to heart & is open heart
surgery
A healthy artery or vein from the body is connected, or grafted, to the blocked coronary artery.
This grafted artery or vein bypasses the blocked portion of the coronary artery & creates a new
path for oxygen-rich blood to flow to the heart muscle
The goals of CABG is to improve the pt’s chance of survival, allowing them to resume a more
active lifestyle, improve the pumping action of heart that may be damaged by a heart attack,
lowering the risk of heart attack (in some patients, such as those who have diabetes), improving
quality of life, reducing angina & other coronary heart disease symptoms.
Steps to rhythm analysis
1. Determine rhythm (is it irregular?)
 For atrial rhythm, measure P-P intervals
 For ventricular rhythm, measure R-R intervals
2. Determine rate (How fast?)
 1 lg blk=300, 2 lg blks=150, 3 lg blks=100, 4 lg blks=75, 5 lg blks-60, etc
3. Evaluate P wave – present?, normal size/shape?, one P for every QRS
4. Determine duration of PR interval – 0.12-0.20? Consistent?
5. Determine duration of QRS complex – 0.06-0.10? Same shape & size? Come after every P
wave?
6. Evaluate T waves – present? Normal shape? Normal amplitude?
7. Determine duration of QT interval – duration a normal 0.36 to 0.44 second? As heart rate
increases, QT interval decreases; when QTc is longer than 0.50 men/women, torsades de
pointes likely to develop
8. Evaluate other components - ectopic beats? U wave present? repolarization of the Purkinje
fibers d/t hypokalemia
CPR-BLS (Basic Life Support)
Outline
Nursing Points
General
1. CPR-BLS
1. CPR = Cardiopulmonary Resuscitation
1. Chest compressions
1. For circulation
2. Rescue Breathing
2. BLS = Basic Life Support
2. Assessment
1. Check scene for safety
2. Check for level of consciousness
1. If unconscious
1. Tap or shake shoulder
2. “Are you okay?”
2. If unresponsive
1. If others are around
1. Delegate
1. Bystanders call 911
2. Bystanders get AED
2. Start CPR
2. If alone
1. Call 911
2. Get AED if available
3. Start CPR
3. CPR
1. CAB Acronym
1. Chest compressions
1. Kneel next to shoulders and neck
2. Heel of hand over center of chest
1. Between nipples
3. Place other hand on top
4. Elbows straight
5. Shoulder placement
1. Directly over hands
6. Compressions
1. 2 inches deep
2. Rate = 100-120 per minute
1. Sing “Stayin’ Alive” for rhythm
3. 30 per cycle
2. Airway open
1. Head tilt, chin lift
1. Palm on forehead
2. Tilt head back
3. Lift chin with other hand
3. Breathing
1. Use barrier
1. Make seal
2. Breaths
1. 2 per cycle
2. 1 second each
3. Watch chest for rise and fall
1. Ensures air gets in
4. AED
1. Automated External Defibrillator
2. Analyzes heart rhythm
3. Determines if electric shock needed
4. Step by step voice instructions
5. Visual aids for hearing impaired
6. Placement and maintenance
1. Placement
1. Highly visible
1. Common areas
2. Bright colors
3. Mounted on walls
2. Maintenance
1. Monthly
1. Battery testing
2. Pad inspections
3. Accessory check
4. Calibration
02.05 Nursing Care and Pathophysiology of
Acute Respiratory Distress Syndrome (ARDS)
Outline
Overview
Acute Respiratory Distress Syndrome
1. Causes – anything causing inflammatory response in lungs
1. Bacteremia, Sepsis
2. Trauma, fat embolus
3. Burns + Fluid Resuscitation
4. Massive transfusion
5. Pneumonia, Aspiration
6. Drug overdose
7. Near drowning
Pathophysiology: There are 4 phases within acute respiratory distress syndrome (ARDS). ARDS
occurs rapidly and usually within 90 minutes of the body’s inflammatory response and between
24-48 hours of lung injury. In phase 1 there is an injury to the capillary endothelium of the
pulmonary system. In phase 2 there is an injury to the basement membrane, interstitial space,
alveolar epithelium. The damage to the lungs causes permeability so now fluid fills the alveoli
(where it doesn’t belong) and this will impair gas exchange. In phase 3 there is damage to the
alveoli because of the fluid that causes atelectasis and hypoxemia. In phase 4 the products of
cell damage cause the formation of a hyaline membrane. This membrane is thick and will
further prevent oxygen exchange. In this phase with impaired gas exchange, respiratory
acidosis occurs. The damage to the lungs that occurs can not be reversed.
Nursing Points
General
1. Inflammatory Response
1. Cytokines
1. Alveolar damage
2. Scarring
3. Decreases lung compliance
2. Increased capillary permeability
1. “Floods” alveoli
2. Decreases gas exchange
2. Early recognition improves survival
Assessment
1. Symptoms of underlying condition
2. Chest X-ray → diffuse bilateral infiltrates
1. “White Out”
3. Refractory Hypoxemia
1. P/F Ratio (PaO2 / FiO2)
2. Mild <300
3. Moderate <200
4. Severe <100
Therapeutic Management
1. Treat underlying cause
2. Ventilatory Support
1. High levels of PEEP
2. Prone position – improve flow into lungs
3. Special Vent Modes
1. APRV
2. Oscillator
3. Prevent Complications
1. O2 toxicity – keep sats 85-90%
2. Ventilator Acquired Pneumonia – prevent infection
3. Barotrauma – keep volumes 4-6 mL/kg
1. Damage caused by too much pressure in noncompliant lung
Nursing Concepts
1. Oxygenation
2. Gas Exchange
3. Infection Control
Patient Education
1. Educate family on severity of condition and probable course
2. Possible need for tracheostomy
3. Purpose for endotracheal tube and ventilator
4. Recovery time, may need rehab
5. Infection control precautions
•
•
•
•
Type of pulmonary edema not related to heart failure
Sudden progressive form of acute respiratory failure
Alveolar capillary interface becomes damaged and more permeable to intravascular
fluid
• Alveoli fill with fluid
Hallmark features
•
•
•
Bilateral patchy infiltrates on chest x-ray
No signs or symptoms of heart failure
No improvement in PaO2 despite increasing oxygen delivery
Pulmonary System
Barotrauma
As lung inflation pressures increase, risk for barotrauma increases. Barotrauma results when the
increased airway pressure distends the lungs and possibly ruptures fragile alveoli or
emphysematous blebs. Patients with noncompliant lungs (e.g., COPD) are at greatest risk for
barotrauma.
•
•
•
•
•
•
•
•
•
•
•
•
Ventilator-associated pneumonia
• Strategies for prevention of ventilator-associated pneumonia
• Strict infection control measures
• Elevate HOB 45 degrees or more to prevent aspiration
Barotrauma
• Rupture of overdistended alveoli during mechanical ventilation
• To avoid, ventilate with smaller tidal volumes
• Higher Paco2
• Permissive hypercapnia
Volutrauma
• Occurs when large tidal volumes are used to ventilate noncompliant lungs
• Alveolar fracture and movement of fluids and proteins into alveolar spaces
• Avoid by using smaller tidal volumes or pressure-control ventilation
Stress ulcers
• Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical
ventilation
• Management strategies
• Correction of predisposing conditions
• Prophylactic antiulcer agents
• Early initiation of enteral nutrition
Renal failure
• Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or
hypercapnia
• May also be caused by nephrotoxic drugs used for infection associated with
ARDS
2 kinds of inotropes: positive inotropes & negative inotropes.
Positive inotropes strengthen force of heartbeat. Negative inotropes weaken force of
heartbeat.
Relieve bronchospasm – Albuterol
Reduce airway inflammation – corticosteroids
Reduce pulmonary congestion – Furosemide, Morphine, etc.
Reduce anxiety & pain – Ativan, Fentanyl, etc.
For atrial fibrillation - calcium channel blockers (Cardizem) & β-adrenergic blockers
(Metoprolol)
For infections – Zithromax & Rocephin
•
•
•
•
Ethical considerations-pt’s values
No Living will or DNR then life-saving measures are continued
Closest relative- spouse, parents, siblings, etc.
If disagreement between parents or siblings
Hospital ethics committee
05.05 Nursing Care and Pathophysiology for
Pulmonary Embolism
Outline
Overview
1. A pulmonary embolism is a life-threatening blood clot in the lungs caused by an
embolus (usually blot clot) from a vein in the lower extremity, or from clots that form
after surgery.
2. Causes decreased perfusion, hypoxemia, and if large enough, right-sided heart failure.
3. Management includes stabilizing the cardiopulmonary system and anticoagulant
therapy.
Nursing Points
General
When a blood clot breaks free and travels through the vascular system, it has the potential to
become lodged and block blood flow.
With a pulmonary embolism, this blood clot breaks free and travels through the right side of the
heart and gets lodged in the pulmonary blood vessels, preventing blood from becoming
oxygenated (and thereby decreasing perfusion to lung tissue). This is a life-threatening
emergency and must be handled quickly, and precautions are always indicated.
Assessment
1. Signs/Symptoms
1. Anxiety
2. Dyspnea/Tachypnea
3. Chest pain
4. Hypoxemia
5. Rales
6. Fever
7. Diaphoresis
8. Hemoptysis
2. Diagnostic Testing
1. Vital signs
2. ABG
3. CXR
4. V/Q lung scan
5. D-dimer
1. Negative D-dimer used to rule out PE on patients with a low likelihood of
a DVT.
2. If positive, further testing necessary
6. Imaging with contrast dye
1.
1.
1. Spiral CT
2. Pulmonary angiogram
Therapeutic Management
1. Therapeutic Management
1. Cardiopulmonary stabilization
1. Monitor for hypoxemia
2. Assess vital signs
3. Listen to lung sounds frequently
1. Rales
4. Heart sounds
5. Assess circulation
1. Peripheral edema
2. Distended neck veins
6. Monitor for feelings of anxiety/fear
7. HOB elevated
8. Oxygen as ordered
9. Analgesics
1. Morphine
2. Anticoagulation
1. Baseline labs
1. Platelet count
1. DO NOT administer if <100,000/mm
2. If value drops to half of baseline, consider HIT
2. Hemoglobin/Hematocrit
1. A drop can indicate hemorrhage
3. aPTT
1. Reflects response to treatment for titration of heparin
2. Monitor for bleeding
1. Bruising
2. Bloody stools
3. Hematuria
4. Gums/teeth
5. Flank pain
1.
Nursing Concepts
Clotting, Gas exchange, Oxygenation
Patient Education
1. Oral anticoagulants
1. Side effects
2. Bleeding precautions
3. Follow up appointments
2. Pain management
1. Clot may still exist at discharge
1. ~4 weeks to dissolve
2. Pain medications as ordered
3. Activity
1. As tolerated
4. Some of the typical diagnostic test that you would do our abgs, chest X Ray, an ECG and
this might be to check for atrial fibrillation, troponin levels which may be done to check
for clots in coronary arteries & b/c of the pt’s c/o chest pain. The D dimer is going to be
elevated once that clot starts to degrade, it is possible with the D dimer to get a false
negative though. The CT scan requires a patient to get IV contrast. If the patient cannot
get IV contrast then they will do a ventilation perfusion scan where they will inhale
radioisotopes. A pulmonary angiography is the most sensitive diagnostic test but it is
invasive and expensive. This angiography is considered the gold standard for diagnosing
a pulmonary embolism and advances in medicine and technology have made this
procedure safer.
5. Prevention is the best medicine in this case in order to keep a pulmonary embolism from
happening. That is the reason why hospitals have come up with the VTE protocol that is
the venous thromboembolism protocol that involves anticoagulants like heparin
injections or lovenox injections, sequential compression devices, and Ted hose. If the
patient has already had a PE then you would want to anti coagulate them so that you
could prevent any further emboli. To help with any problem related to that pulmonary
embolism you will want to give them oxygen and if it is significant enough they may
have to go on the mechanical ventilator. Pulmonary toilet refers to any method used to
assist in clearing secretions from the airways. This could be chest physiotherapy,
maintaining hydration status, coughing and deep breathing, or using an incentive
spirometer. This patient may have chest pain or they have been in mobile because of
thoracic or abdominal pain which has compromised the respiratory system even more
6. The goal of anticoagulant therapy is to prevent clots from forming and it takes into
account the patience VTE risk. Once the patient has already had a problem with clots
they will be started on drug therapy to prevent any more clots from forming such as
warfarin, heparin, lovenox, or other coagulation inhibitors. If the patients PE is
significant enough they may want to go ahead and give thrombolytics which will break
up the clot.
7. A patient that is hemodynamically unstable with a massive pulmonary embolism bit is
not able to have thrombolytic therapy maybe a candidate 4 a pulmonary embolectomy. 2
prevent further emboli an IVC filter maybe the treatment for patients that are at high risk.
A catheter in the femoral vein is placed in the inferior vena cava and a filter is deployed
that will prevent clots from going into the pulmonary system complications with this
device can be misplacement, migration, and perforation.
8.
A tracheostomy is a surgically created stoma (opening) in the anterior part of the trachea (Fig.
26.3, A). A tracheostomy may be done to (1) establish a patent airway, (2) bypass an upper
airway obstruction, (3) facilitate removal of secretions, (4) permit long-term mechanical
ventilation, and (5) assist with weaning from mechanical ventilation.
All tracheostomy tubes have a faceplate, or flange, which rests against the neck, and an
obturator, which is used to help insert the tube. Many tracheostomy tubes have an outer cannula
(which keeps the airway patent), and an inner cannula (which can be disposable or non
disposable and removed for cleaning). At a minimum, you must assess the tracheostomy site
every shift. Confirm the patency of the tracheostomy tube. Observe the site for any redness,
inflammation, edema, ulceration, or signs of infection. Sterile dressing changes should be done
every 12 hours. Clean around the stoma with normal saline and apply a sterile pre-cut dressing
around the tracheostomy tube site. You can complete dressing changes more often based on your
assessment. Change the tracheostomy tapes after the first 24 hours and then as needed (Fig. 26.5
and Table 26.9). A 2-person technique, 1 person to stabilize the tracheostomy and the other to
change the tapes, is best practice to ensure that the tracheostomy does not become accidentally
dislodged during the procedure. In some places, the HCP and/or respiratory therapist may
complete this task. At the end of the procedure, place 2 fingers underneath the tapes to ensure
they are not too tight around the neck. When turning and repositioning the patient, take care not
to dislodge the tracheostomy tube. Because tube replacement may be difficult in the immediate
postoperative period, several precautions are required, including (1) keep a replacement tube of
equal or smaller size at the bedside, readily available for emergency reinsertion; (2) do not
change tracheostomy tapes for at least 24 hours after the surgical procedure; and (3) if needed,
the HCP performs the first tube change usually no sooner than 7 days after the tracheostomy.
If the tube is accidentally dislodged, immediately call for help. While waiting for the HCP, a
respiratory therapist, or other designated individual to arrive, several options may be used
(depending on your nursing scope of practice and specific agency policies and procedures). It is
essential that you know and understand your role and scope of practice for care of the patient
with a tracheostomy. mmediately call for help. Quickly assess the patient’s level of
consciousness, ability to breathe, and the presence or absence of any respiratory distress. If
respiratory distress is present, you can quickly use a hemostat to spread the opening where the
tube was displaced. Insert the obturator in the replacement (spare) tracheostomy tube, lubricate
with saline, and insert the tube into the stoma. Once the tube is inserted, remove the obturator at
once so that air can flow through the tube.
TABLE 26.8 Suctioning a Tracheostomy
Assess the need for suctioning hourly. Indications include visible coughing, coarse crackles or
wheezes over large airways, moist cough, increase in peak inspiratory pressure on mechanical
ventilator, and restlessness or agitation. Neurologic patients may not show any signs and/or
symptoms of the need to be suctioned, so suctioning once per shift (at minimum) is
recommended. Do not suction routinely.
1. If suctioning is indicated, explain procedure to patient.
2. Collect necessary sterile equipment: suction catheter (no larger than half the lumen of the
tracheostomy tube), sterile water, cup, and personal protective equipment (PPE). If a closed
tracheal suction system is used, the catheter is enclosed in a plastic sleeve and reused (Fig. 26.4).
No other equipment is needed.
3. Check suction source and regulator. Adjust suction pressure to no greater than 125 mm Hg
pressure with tubing occluded.
4. Assess heart rate and rhythm, respiratory rate and SpO2 to provide baseline for detecting
changes in patient condition during suctioning.
5. Wash hands and put on PPE.
6. Use sterile technique to open package, fill cup with sterile water, put on sterile gloves, and
connect catheter to suction tubing. Designate one hand as contaminated for (1) connecting and
disconnecting the tubing at the suction catheter, (2) using the manual bag-valve-mask (BVM),
and (3) operating the suction control. Suction sterile water through the catheter to test the system.
7. Provide preoxygenation for a minimum of 30 seconds by (1) adjusting ventilator to deliver
100% O2 or (2) using a reservoir-equipped BVM connected to 100% O2. The method chosen
depends on whether the patient is attached to a mechanical ventilator or has a tracheostomy tube
in place but is spontaneously breathing and receiving supplemental O2. The patient who has a
long-term chronic tracheostomy and is not acutely ill may be able to tolerate suctioning without
using a BVM.
8. Gently insert catheter without suction to the point at which the patient coughs. Do not insert
the catheter until you meet resistance (this is the carina, and repeated trauma with suction
catheter can promote bleeding). Apply suction as you slowly begin to withdraw the catheter.
9. Apply continuous suction for no more than 10 to 15 seconds.
10. Observe the patient during the suctioning procedure. Immediately stop suctioning and
remove the suction catheter from the patient’s trachea if the patient becomes bradycardic or
hypotensive, a dysrhythmia occurs, or SpO2 decreases to less than 90%. A vagal response may
have occurred.
11. After each suction pass, wait at least 30 seconds before suctioning again. Always
hyperoxygenate for at least 30 seconds (via mechanical ventilator or BVM with 5 or 6 breaths) in
between each suctioning pass.
12. Repeat procedure until airway is clear. Limit insertion of suction catheter to as few times as
possible. If airway is not clear after 3 suction passes, allow the patient to rest before additional
suctioning.
13. Return O2 concentration to prior setting.
14. Rinse catheter. If using the in-line suction catheter (via mechanical ventilation), ensure that
normal saline used to flush out the suction catheter does not enter the patient’s airway. For
disposable suction catheters, dispose of catheter by wrapping it around fingers of gloved hand
and pulling glove over catheter. Discard equipment in proper waste container.
15. Suction the oropharynx or use mouth suction.
16. Reassess heart rate and rhythm and SpO2. Auscultate to assess changes in lung sounds.
17. Record time, amount, and character of secretions and patient response to suctioning.
TABLE 26.9 Tracheostomy Care
The following are general guidelines for basic tracheostomy care. Become familiar with the
specific policies and/or procedures in your agency:
1. Explain procedure to patient.
2. Use tracheostomy care kit or collect necessary sterile equipment (e.g., suction catheter, 1 pair
sterile gloves, 1 pair nonsterile gloves, water basin, tracheostomy ties, tube brush or pipe
cleaners, 4 × 4–inch gauze pads, sterile water or normal saline, tracheostomy dressing
[optional]). NOTE: Clean rather than sterile technique is used at home.
3. Place patient in semi-Fowler’s position.
4. Assemble needed materials on bedside table next to patient.
5. Wash hands. Put on PPE.
6. Auscultate chest sounds. If wheezes or coarse crackles are present, suction the patient if
unable to cough up secretions (Table 26.8). Remove soiled dressing and clean gloves.
7. Open sterile equipment, pour sterile H2O or normal saline into 2 compartments of sterile
container or 2 basins, and put on sterile gloves. NOTE: Hydrogen peroxide (3%) is only used if
an infection is present. If it is used, rinse the inner cannula and skin with sterile H2O or normal
saline afterward to prevent trauma to tissue.
8. If present, unlock and remove inner cannula. Many tracheostomy tubes do not have inner
cannulas. Care for these tubes includes all steps except for inner cannula care.
9. Replace a disposable inner cannula with a new cannula. With a non disposable cannula:
• Immerse inner cannula in sterile solution and clean inside and outside of cannula using tube
brush or pipe cleaners.
• Rinse cannula in sterile solution. Remove from solution and shake to dry.
• Insert inner cannula into outer cannula with the curved part downward, and lock in place.
10. Remove dried secretions from stoma using 4 × 4–inch gauze pad soaked in sterile water or
saline. Gently pat area around the stoma dry. Be sure to clean under the tracheostomy flange
(faceplate), using cotton swabs to reach this area.
11. Place dressing around tube (Fig. 26.5). Use a pre-cut tracheostomy dressing or unlined gauze.
Do not cut the gauze because threads may be inhaled or wrap around the tracheostomy tube.
Change the dressing as needed. Wet dressings promote infection and stoma irritation.
12. Change tracheostomy tapes, using a 2-person change technique. Tie tracheostomy tapes
securely with room for 2 fingers between tapes and skin (Fig. 26.5). To prevent accidental tube
removal, secure the tracheostomy tube by gently applying pressure to the flange of the tube
during the tape changes. Do not change tracheostomy tapes for 24 hours after the tracheostomy
procedure.
13. Some patients prefer tracheostomy tapes made of Velcro, which are easier to adjust.
14. Repeat care 3 times/day and as needed.
Mechanical ventilation is the process by which the FIO2 (21% [room air] or more) is moved in
and out of the lungs by a mechanical ventilator. Mechanical ventilation is not curative. It is a
means of supporting patients until they recover the ability to breathe independently. It can also
serve as a bridge to long-term mechanical ventilation or until a decision is made to stop
ventilatory support. Indications for mechanical ventilation include (1) apnea, (2) inability to
breathe or protect the airway, (3) acute respiratory failure (see Chapter 67), (4) severe hypoxia,
and (5) respiratory muscle fatigue
Types of Mechanical Ventilation
The 2 major types of mechanical ventilation are negative pressure and positive pressure
ventilation.
Negative Pressure Ventilation
Negative pressure ventilation involves the use of chambers that encase the chest or body and
surround it with intermittent subatmospheric (or negative) pressure. The “iron lung” was the first
form of negative pressure ventilation. It was developed during the polio epidemic. Intermittent
negative pressure around the chest wall pulls the chest outward, reducing intrathoracic pressure.
Air rushes in via the upper airway, which is outside the sealed chamber. Expiration is passive.
The machine cycles off, allowing chest retraction. This type of ventilation is like normal
ventilation in that decreased intrathoracic pressures produce inspiration, and expiration is
passive. Negative pressure ventilation is noninvasive and does not need an artificial airway.
Positive Pressure Ventilation
Positive pressure ventilation (PPV) is the main method used with acutely ill patients (Fig. 65.19).
During inspiration the ventilator pushes air into the lungs under positive pressure. Unlike
spontaneous ventilation, intrathoracic pressure is raised during lung inflation rather than lowered.
Expiration occurs passively as in normal expiration. There are 2 categories of PPV: volume and
pressure ventilation.13
Volume Ventilation
With volume ventilation, a predetermined VT is delivered with each inspiration. The amount of
pressure needed to deliver the breath varies based on compliance and resistance factors of the
patient-ventilator system. So, the VT is consistent from breath to breath, but airway pressures
vary.
Pressure Ventilation
With pressure ventilation, the peak inspiratory pressure is predetermined. The VT delivered to
the patient varies based on the selected pressure and compliance and resistance factors of the
patient-ventilator system. Careful attention must be given to the VT to prevent unplanned
hyperventilation or hypoventilation. For example, when the patient breathes out of synchrony
with the ventilator, the pressure limit may be reached quickly, and the volume of gas delivered
may be small.
Alarm Possible Causes
High-pressure limit
• Secretions, coughing, or gagging
• Patient fighting ventilator (ventilator asynchrony)
• Condensate (water) in tubing
• Kinked or compressed tubing (e.g., patient biting on ET tube)
• ↑ Resistance (e.g., bronchospasm)
• ↓ Compliance (e.g., pulmonary edema, ARDS, tension pneumothorax, atelectasis, pneumonia)
• Improper alarm setting
• ET tube inserted too far (e.g., right mainstem bronchus or carina)
Interventions
• Clear secretions and ↑ sedation
• Reassure patient
• Remove water from ventilator tubing
• Unkink tubing, insert bite block, or reposition patient
• Give bronchodilator
• Assess breath sounds, obtain chest x-ray
• Adjust ET tube
Low-pressure limit
• Total or partial ventilator disconnect
• Loss of airway (e.g., total or partial extubation)
• ET tube or tracheotomy cuff leak (e.g., patient speaking, grunting)
Interventions
• Check connections
• Confirm adequate tidal volume and ET tube position with chest x-ray
• Reinflate cuff
Positive end-expiratory pressure (PEEP) is a ventilatory maneuver, or mechanical ventilator
setting, in which positive pressure is applied to the airway during exhalation. Normally during
exhalation, airway pressure drops to near 0, and exhalation occurs passively. With PEEP,
exhalation is passive but pressure falls to a preset level, often 3 to 20 cm H2O. Lung volume
during expiration and between breaths is greater than normal with PEEP.
Ventricular Assist Devices
A ventricular assist device (VAD) provides short- and long-term support for the failing heart and
allows more mobility than the IABP. VADs are inserted into the path of flowing blood to
augment or replace the action of the ventricle. Some VADs are implanted internally (e.g.,
peritoneum). Others are positioned externally. A typical VAD shunts blood from the left atrium
or ventricle to the device and then to the aorta
Continuous Positive Airway Pressure
Continuous positive airway pressure (CPAP) restores functional residual capacity (FRC) and is
similar to positive end-expiratory pressure (PEEP). However, the pressure in CPAP is delivered
continuously during spontaneous breathing, preventing the patient’s airway pressure from falling
to 0. For example, if CPAP is 5 cm H2O, airway pressure during expiration is 5 cm H2O. During
inspiration, we generate 1 to 2 cm H2O of negative pressure. This reduces airway pressure to 3
or 4 cm H2O. CPAP is often used to treat obstructive sleep apnea.
Bilevel Positive Airway Pressure
In addition to O2, bilevel positive airway pressure (BiPAP) provides 2 levels of positive pressure
support: higher inspiratory positive airway pressure and lower expiratory positive airway
pressure.13 Like CPAP, the patient must be able to spontaneously breathe and cooperate with
this treatment (Fig. 65.14).
BiPAP is used for COPD patients with HF and acute respiratory failure and for patients with
sleep apnea. Its use after extubation can help prevent reintubation. Patients with shock, altered
mental status, or increased airway secretions cannot use BiPAP because of the risk for aspiration
and the inability to remove the mask.
ET intubation is common in ICU patients requiring mechanical ventilation for short periods of
time (e.g., less than 2 weeks). Other indications for intubation include (1) upper airway
obstruction (e.g., burns, tumor, bleeding), (2) apnea, (3) high risk for aspiration, (4) ineffective
clearance of secretions, and (5) respiratory distress
Steps for ET
Begin then bagging them with 100% O2 for at least 3-5 mins, positioning them supine in the
“sniffing” position, rapid sequence intubation (RSI) is a combination of sedation & paralytics to
decrease aspiration & injury. Because RSI intubation needs to happen quickly, so pts with a
difficult airway should not be done this way. Some of the problems related to intubation are
chipping teeth, neck mobility if there is a suspected spinal cord injury, increased salivation, and
difficulty swallowing. A patient may bite down on the tube, so a bite block or sedation may be
necessary. ET tube needs to be secured very well and the nurse needs to ensure that does not
move by frequently assessing position. Mouth care can be difficult, because of the size of the
oral cavity with an ET tube and bite block. Once intubated inflate the cuff & confirm placement
by attaching a CO2 detector, if in the esophagus then CO2 is not detected. Then listen for
bilateral breath sounds & epigastric area for no sounds, watch for symmetric rise & fall. Check
SpO2. If correct placement then hook up to ventilator & secure the ETT. Obtain a chest xray to
confirm placement.
Before intubation is started, preoxygenate the patient using the BVM and 100% O2 for 3 to 5
minutes. Each intubation attempt is limited to less than 30 seconds. Ventilate the patient between
successive attempts using the BVM and 100% O2.
Rapid-sequence intubation (RSI) is the rapid, concurrent administration of both a sedative and a
paralytic drug during emergency airway management to induce unconsciousness for intubation.
A sedative-hypnotic-amnesic (e.g., propofol, etomidate [Amidate]) is given to induce
unconsciousness, along with a rapid-onset opioid (e.g., fentanyl) to blunt the pain of the
procedure. This is followed with a drug (e.g., rocuronium) to produce skeletal muscle
paralysis.17 Monitor the patient’s O2 status during the procedure with pulse oximetry.
After intubation, inflate the cuff. Confirm the placement of the ET tube while continuing to
manually ventilate the patient using the BVM with 100% O2. Use an EtCO2 detector to confirm
proper placement by noting the presence of exhaled CO2 from the lungs (Fig. 65.16). Place the
detector between the BVM and ET tube and look for a color change (indicating the presence of
CO2) or a number. At least 5 or 6 exhalations with a consistent CO2 level must be present to
confirm tube placement in the trachea.13 Auscultate the lungs for bilateral breath sounds and the
epigastrium for the absence of air sounds. Observe the chest for symmetric chest wall movement.
SpO2 should be stable or improve
Obtain a chest x-ray to confirm tube location (2 to 6 cm above the carina in the adult). This
position allows the patient to move the neck without moving the tube or causing it to enter the
right mainstem bronchus. Once proper positioning is confirmed with x-ray, record and mark the
position of the tube at the lip or teeth or nose.
Pulmonary System
Barotrauma
As lung inflation pressures increase, risk for barotrauma increases. Barotrauma results when the
increased airway pressure distends the lungs and possibly ruptures fragile alveoli or
emphysematous blebs. Patients with noncompliant lungs (e.g., COPD) are at greatest risk for
barotrauma.
•
•
Ventilator-associated pneumonia
• Strategies for prevention of ventilator-associated pneumonia
• Strict infection control measures
• Elevate HOB 45 degrees or more to prevent aspiration
Barotrauma
• Rupture of overdistended alveoli during mechanical ventilation
• To avoid, ventilate with smaller tidal volumes
• Higher Paco2
• Permissive hypercapnia
Volutrauma
• Occurs when large tidal volumes are used to ventilate noncompliant lungs
• Alveolar fracture and movement of fluids and proteins into alveolar spaces
• Avoid by using smaller tidal volumes or pressure-control ventilation
Stress ulcers
• Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical
ventilation
• Management strategies
• Correction of predisposing conditions
• Prophylactic antiulcer agents
• Early initiation of enteral nutrition
Renal failure
• Occurs from decreased renal tissue oxygenation from hypotension, hypoxemia, or
hypercapnia
• May also be caused by nephrotoxic drugs used for infection associated with
ARDS
2 kinds of inotropes: positive inotropes & negative inotropes.
Positive inotropes strengthen force of heartbeat. Negative inotropes weaken force of
heartbeat.
Relieve bronchospasm – Albuterol
Reduce airway inflammation – corticosteroids
Reduce pulmonary congestion – Furosemide, Morphine, etc.
Reduce anxiety & pain – Ativan, Fentanyl, etc.
For atrial fibrillation - calcium channel blockers (Cardizem) & β-adrenergic blockers
(Metoprolol)
For infections – Zithromax & Rocephin
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•
•
•
Ethical considerations-pt’s values
No Living will or DNR then life-saving measures are continued
Closest relative- spouse, parents, siblings, etc.
If disagreement between parents or siblings
Hospital ethics committee
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•
•
•
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•
•
•
Artifical airway nursing care
For thick secretions you need to make sure that the pt. is adequately hydrated can add extra water
to tube feedings. Use humidify, just make sure that you are routinely assessing for accumulated
condensation which will increase the pressure in the ventilator tubing. Make sure to empty
excess condensation in the tubing away from the pt. Thick, copious secretions could also indicate
developing pneumonia. Chest percussion and turning every two hours will mobilize secretions.
Oral care- Brush teeth BID, oral swabs with 1.5% hydrogen peroxide every 2-4 hrs,
chlorhexidine oral rinse twice a day, moisturizer to lips, oropharyngeal suctioning & reposition
and retape ET tube every 24 hours.
02.02 EKG (ECG) Waveforms
Outline
Overview
1. The heart’s electrical activity that stimulates the atria and ventricles to contract produce
a waveform on an EKG
2. These waveforms are broken down into in a P wave, QRS complex and T wave.
Nursing Points
1. P wave
1. Atrial depolarization
1. Positive deflection
2. PR interval
1. Beginning of P wave to beginning of QRS
2. Time it takes for electrical current to reach ventricles
1. 0.12-0.20 seconds
2. QRS Complex
1. Ventricular depolarization
1. Negative and positive deflection
2. QRS interval
1. Beginning of the Q wave to ending of S wave
2. Time it takes for the electrical current to travel through the ventricles
1. 0.06 -012 seconds
3. T wave
1. Ventricular repolarization
1. Positive deflection
2. QT interval
1. Beginning of QRS to the end of T wave
2. Time it takes for the ventricles to contract and relax
1. 0.36-.044 seconds
3. ST segment
1. End of QRS complex to the beginning of T wave
2. Time between ventricular depolarization and repolarization
Assessment
1. Recognize PQRST waveforms on EKG
2. Check pulse if abnormal waveforms are observed
Therapeutic Management
1. Recognize and report abnormal waveforms
1. Long PR interval
2. Prolonged QRS Complex
3. Tall T waves
Nursing Concepts
1. EKG Rhythms
ECG
The electrical activity of the heart is measured by electrodes & recorded on the
electrocardiogram. The P wave starts with the firing of the SA node, causing a depolarization of
the atria. The QRS starts with the firing of the AV node causing a depolarization of the
ventricles. The T wave represents the repolarization of the ventricles. The spaces between the
different waves – PR, QRS, & QT intervals – are the time that it takes for impulse to travel from
one area to another. Any delay in the intervals indicates a dysfunction.
0.20-P wave
0.6-.12-qrs
Depolarization represents the mechanical activity of contractions, or systole, which is the
ejection of blood from the ventricles. Relaxation otherwise known as diastole is when the
ventricles get refilled. Stroke volume is the amount of blood ejected from the ventricle with each
heartbeat. To calculate cardiac output you would multiply the heart rate X the stroke
volume. Generally 100mls fill the left ventricle but only 60mls is pushed into circulation.
▪
▪
Stroke volume: Amt of blood ejected with each heart beat
Cardiac output: Amt of blood pumped by each ventricle in 1 minute
▪ Normal 4-8 L/min
•
When cells are injured, they release their contents, including enzymes and other proteins,
into the circulation. These biomarkers are useful in the diagnosis of myocardial injury
and infarction.
Cardiac-specific troponin is a myocardial muscle protein released into circulation after
injury or infarction. Two subtypes, cardiac-specific troponin T (cTnT) and cardiacspecific troponin I (cTnI), are specific to myocardial tissue.
Normally the level in the blood is very low, so a rise in level is diagnostic of myocardial
injury. cTnT and cTnI are detectable within hours (on average of 4 to 6 hours) of
myocardial injury, peak at 10 to 24 hours, and can be detected for up to 10 to 14 days.
Troponin is the biomarker of choice in the diagnosis of MI.
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•
•
 Cardiac Biomarkers
 Creatine kinase (CK) – found in variety of organs, tissues
 Three isoenzymes
 CK-MM – specific to skeletal muscle
 CK- BB – brain & nervous tissue
 CK-MB - cardiac specific - specific for myocardial injury or
infarction
 Rises in 3-6 hours, peaks in 12-24 hours, returns to baseline
within 12-48 hours (level peak & return to normal can be
delayed in one who had large MI)
 Additional blood studies
 C-Reactive protein – found in liver during acute inflammation
 Risk factor for coronary artery disease (CAD)
 Homocysteine (amino acid)
 Elevated levels increased risk for CAD, peripheral vascular disease
(PVD), and stroke
Diagnostic Studies of Cardiovascular System
 Cardiac natriuretic peptide markers
 Three types
 Atrial natriuretic peptide (ANP) - atrium
 B-type natriuretic peptide (BNP) – ventricles (best-cardiac or
respiratory cause of dyspnea)
 C-type natriuretic peptide – endothelial, renal epithelial cells
 Increased levels of BNP levels signify heart failure
Electrocardiogram
• The basic P, QRS, and T waveforms are used to assess cardiac activity. Deviations from
the normal sinus rhythm can indicate problems in heart function.
• There are many types of electrocardiographic monitoring, including a resting 12-lead
ECG, ambulatory ECG monitoring, and exercise or stress testing.
• Continuous ambulatory ECG (Holter monitoring) can provide diagnostic information
over a greater period of time than a resting 12-lead ECG.
• An event monitor or loop recorder is used to document less frequent ECG events. An
event monitor is a portable unit that uses electrodes to store ECG data once triggered by
the patient. A disadvantage of this type of monitoring is that if symptoms occur for only a
brief time, they may be over before the patient puts on the device and triggers it to record.
Likewise, if patients are extremely symptomatic (e.g., syncopal), they may not be
physically able to trigger the ECG recording.
• An implantable loop recorder is used for patients who are suspected to have serious yet
rare dysrhythmias. This small recorder is implanted though a small incision into the chest
wall. It is activated to record either by the patient through a remote device or
automatically if the heart rate exceeds or goes below a set rate. External loop recorders
are worn for a month and require electrodes continually placed on the skin. This device
only records when activated by the patient when symptoms occur.
• Cardiac symptoms frequently occur only with activity due to the demand on the coronary
arteries to provide more oxygen. Exercise testing is used to evaluate the heart’s response
to physical stress. This helps to assess CVD and set limits for exercise programs.
Exercise testing is used for individuals who do not have restrictions related to walking or
using a bicycle.
• The echocardiogram uses ultrasound (US) waves to record the movement of the
structures of the heart. In the normal heart, ultrasonic sound waves directed at the heart
are reflected back in typical configurations.
• A contrast echocardiography involves the addition of an IV contrast agent (e.g., albumin
microbubbles, agitated saline) to assist in defining the images, especially in technically
difficult patients (e.g., obese).
• The echocardiogram provides information about abnormalities of (1) valvular structures
and motion, (2) cardiac chamber size and contents, (3) ventricular and septal motion and
thickness, (4) pericardial sac, and (5) ascending aorta.
• The ejection fraction (EF) or the percentage of end-diastolic blood volume that is
ejected during systole can also be measured. The EF provides information about the
function of the left ventricle during systole.
• Stress echocardiography, a combination of treadmill test and US images, evaluates wall
motion abnormalities. This test provides the information of an exercise stress test with the
information from an echocardiogram. For those individuals unable to exercise, an IV
drug (e.g., dobutamine [Dobutrex], dipyridamole [Persantine]) is used to produce
pharmacologic stress on the heart while the patient is at rest.
• Transesophageal echocardiography (TEE) provides more precise echocardiography of
the heart than surface 2-D echocardiography by removing interference from the chest
wall and lungs. The TEE uses a flexible endoscope probe with an US transducer in the tip
for imaging of the heart and great vessels. The probe is passed into the esophagus to the
level of the heart, and M-mode, 2-D, Doppler, and color-flow imaging can be obtained.
TEE is contraindicated if the patient has a history of esophageal disorders, dysphagia, or
radiation therapy to the chest wall. Patients will require sedation during a TEE.
Cardiac Catheterization
• Cardiac catheterization is a common outpatient procedure. It provides information about
CAD, coronary spasm, congenital and valvular heart disease, and ventricular function.
• Cardiac catheterization is also used to measure intracardiac pressures and O2 levels, as
well as CO and EF.
• With injection of contrast media and fluoroscopy, the coronary arteries can be seen,
chambers of the heart can be outlined, and wall motion can be observed.
• Cardiac catheterization is done by inserting a radiopaque catheter into the right and/or left
side of the heart.
• For the right side of the heart, a catheter is inserted through an arm vein (basilic or
cephalic) or a leg vein (femoral). Pressures are recorded as the catheter is moved into the
vena cava, the right atrium, the right ventricle, and the pulmonary artery. The catheter is
then moved until it is wedged or lodged in position. This blocks the blood flow and
pressure from the right side of the heart and looks ahead through the pulmonary capillary
bed to the pressure in the left side of the heart (pulmonary artery occlusive pressure).
This pressure assesses the function of the left side of the heart.
• The left heart catheterization is done by inserting a catheter into a femoral or brachial
artery. The catheter is passed in a retrograde manner up to the aorta, across the aortic
valve, and into the left ventricle.
Coronary angiography is done with a left-sided heart catheterization.
• The catheter is positioned at the origin of the coronary arteries, and contrast medium is
injected into the arteries. Patients often feel a temporary flushed sensation with dye
injection. The images identify the location and severity of any coronary blockages.
• Complications of cardiac catheterization include bleeding or hematoma at the puncture
site, allergic reactions to the contrast media, looping or kinking of the catheter, infection,
thrombus formation, aortic dissection, dysrhythmias, MI, stroke, and puncture of the
ventricles, cardiac septum, or lung tissue.
END-OF-LIFE CARE
The goals for EOL care are to (1) provide comfort and supportive care during the dying process,
(2) improve the quality of the patient’s remaining life, (3) help ensure a dignified death, and (4)
provide emotional support to the family.
T AB LE 9. 2
Physical Manif estation s at E nd of Lif e
System
Cardiovascular
system
Gastrointestinal
system
Manifestations
• Increased heart rate; later
slowing and weakening of pulse
• Irregular rhythm
• Decreased BP
• Delayed absorption of drugs
given IM or subcutaneously
• Slowing or cessation of GI
function (may be enhanced by
pain-relieving drugs)
• Gas accumulation
• Distention and nausea
• Loss of sphincter control,
producing incontinence
• Bowel movement before
imminent death or at time of
death
System
Integumentary
system
Musculoskeletal
system
Respiratory
system
Sensory system
Manifestations
• Mottling on hands, feet, arms,
and legs
• Cold, clammy skin
• Cyanosis of nose, nail beds,
knees
• “Waxlike” skin when very near
death
• Gradual loss of ability to move
• Sagging of jaw resulting from
loss of facial muscle tone
• Difficulty speaking
• Swallowing becoming more
difficult
• Difficulty maintaining body
posture and alignment
• Loss of gag reflex
• Jerking seen in patients on high
doses of opioids
• Increased respiratory rate
• Cheyne-Stokes respiration
• Inability to cough or clear
secretions resulting in grunting,
gurgling, or noisy congested
breathing (death rattle or
terminal secretions)
• Irregular breathing, gradually
slowing down to terminal gasps
(may be described as guppy
breathing)
System
Manifestations
• Usually last sense to disappear
Hearing
Sight
Taste and smell
• Blurring of vision
• Sinking and glazing of eyes
• Blink reflex absent
• Eyelids stay half-open
• Decreased with disease
progression
Touch
• Decreased sensation
• Decreased sense of pain and
touch
Urinary system
• Gradual decrease in urine output
• Incontinence of urine
• Inability to urinate