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CCRN Exam > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

S1

  1. Sound it makes
  2. Caused by which valves closing
  3. Loudest where on the heart specifically
  4. Systole/diastole: beginning or end?
A
  1. “Lub”
  2. Caused by closure of AV (mitral, tricuspid) valves
  3. Apex (midclavicular, 5th intercostal space)
  4. End of diastole | beginning of systole
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2
Q

S2

  1. Sound it makes
  2. Caused by closure or opening of which valves?
  3. Loudest at which part of the heart?
  4. Systole/diastole: beginning or end of which?
  5. When does S2 split?
  6. What causes S2 wide, fixed splitting?
  7. When is S2 the loudest?
A
  1. “Dub”
  2. Closure of semilunar (aortic, pulmonic) valves
  3. Base (right sternal border, 2nd intercostal space)
  4. End of systole, beginning of diastole*
  5. Splits on inspiration.
  6. Right bundle branch block
  7. Pulmonary embolism*
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3
Q

Name the auscultatory points

A
  1. Aortic
  2. Pulmonic
  3. Erbs
  4. Tricuspid
  5. Mitral (apical)
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4
Q

Which heart sounds are considered normal? Which are considered abnormal?

A

Normal = S1 & S2

Abnormal = S3 & S4

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5
Q

S3

  1. What causes S3 to occur?
  2. When does it occur in systole or diastole?
  3. Where is it heard best with a stethoscope?
  4. What disease is it associated with? Which symptom might it occur before?
  5. Also known as _______
  6. What state name does it sound like?
    *7. What is it caused by?
A
  1. Rapid rush of blood into a dilated ventricle.
  2. Occurs early in diastole, right after S2
  3. Apex
  4. Heart failure. Crackles.
  5. Ventricular Gallup.
  6. Kentucky.
  7. Pulmonary hypertension and cor pulmonale. Mitral, aortic, or tricuspid insufficiency.
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6
Q

S4

  1. What causes it?
  2. Occurs before or after S1, S2, or S3.
  3. Best heard at which location of the heart with the stethoscope?
  4. Associated with which diseases and symptoms?
  5. Also known as what name?
  6. Is associated with which state?
  7. Is it heard in the presence of atrial fibrillation? Why?
A
  1. Atrial contraction of blood into a noncompliant ventricle.
  2. Right before S1
  3. Apex.
  4. Myocardial ischemia, infarction, hypertension, ventricular, hypertrophy, aortic stenosis*
  5. Atrial Gallup.
  6. Tennessee.
  7. No. No atrial contraction.
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7
Q

What condition is due to pericarditis and is associated on pain with deep inspiration and may be positional?

A

Pericardial friction rub

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8
Q

What are murmurs?

A

Turbulent blood flow within the heart. Valvular disease.

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9
Q

Systolic blood pressure is an indirect measurement of what two things?

A

Cardiac output and stroke volume

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10
Q

Diastolic blood pressure is an indirect measurement of what?

A

Systemic vascular resistance (SVR)

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11
Q

How much longer is diastole compared to systole?

A

One-third longer

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12
Q

When are coronary arteries perfused; during systole or diastole?

A

Diastole.

This is known as “the filling” period

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13
Q

What is a necessary tip to learn when learning about valvular heart disease?

A

If you can picture which valves are open, and which are closed during each phase of the cardiac cycle, such as systole and diastole, you’ll be able to decide what problems is being described.

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14
Q

Normal heart sounds in S1 in S2 in adults are due to what occurring with the valves?

A

Valve closure

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15
Q

What causes valves to open and close? Explain what is happening to each specifically.

A

Valves open and closed based on pressure changes. When pressure in the chamber above a valve is higher, the valve opens when pressure drops in the chamber above the valve. The pressure is greater below the valve in the valve closes.

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16
Q

Which is longer SYSTOLE or DIASTOLE?

A

Diastole is 1/3 longer than SYSTOLE, because it needs time for filling.

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17
Q

What are the 7 causes of valvular heart disease?

A
  1. Coronary artery disease, ischemia, and acute MI.
  2. Dilated cardiomyopathy
  3. Degeneration.
  4. Bicuspid, aortic valve; genetic.
  5. Rheumatic fever.
  6. Infection.
  7. Connective tissue diseases
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18
Q

Murmurs of ________ occur when the valve is CLOSED.

A

Insufficiency | regurgitation

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19
Q

Which types of murmurs are acute or chronic?

A

Murmurs of insufficiency/regurgitation

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20
Q

Murmurs of ________ occur when the valve is OPEN.

A

Stenosis

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21
Q

Which types of murmurs are a chronic problem only (not acute) and develop over a period of time?

A

Stenosis

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22
Q

Systolic murmurs
1. Make what type of sound?
2. Which valves are OPEN during systole?
3. Which valves are CLOSED during SYSTOLE? Is this insufficiency or stenosis? Why?
4. If the patient has a pulmonary artery catheter and has mitral insufficiency, what will this cause?
5. What is VSD?

A
  1. Lub… shhhb… dub
  2. Semi-lunar valves (tricuspid & mitral)
  3. AV valves (pulmonary & aortic). Mitral insufficiency.
  4. Will cause large giant V waves on the pulmonary artery occlusion pressure tracking.
  5. Ventricular septal defect.
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23
Q

Diastolic murmurs
1. Make what type of sound?
2. Which valves are closed during diastole?
3. Which valves are open during diastole?

A
  1. Lub… dub… shhhb
  2. Semilunar valves— tricuspid & mitral
  3. AV Valves— pulmonary & aortic
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24
Q

Closed valves are associated with what?

A

Insufficiency or regurgitation. Acute or chronic.

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25
Q

Open valves are associated with what?

A

Stenosis. Occurs overtime. NOT ACUTE.

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26
Q

Explain the differences between the right and left side of the heart.

A

The right side – decreased pressure, thinner walls, deoxygenated blood to the lungs from the vena cava, CO2 is off, O2 is on

The left side dash increased pressure, thicker walls, oxygenated blood through the aorta.

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27
Q

What is mitral insufficiency? What is the valve doing?

A

Occurs when the mitral valve is closed. The mitral valve is closed during SYSTOLE.

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28
Q

What is mitral stenosis? What is the valve doing?

A

Occurs when the mitral valve is open. It is open during diastole.

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29
Q

What is aortic insufficiency? What is the valve doing?

A

Occurs when the aortic valve is closed. The aortic valve is closed during diastole.

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30
Q

What is aortic stenosis? What is the valve doing?

A

Occurs when the aortic valve is open. The aortic valve is open during SYSTOLE.

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31
Q

How can you remember all these valves into figure them out?

A

Picture in your mind what the aortic valve is doing specifically. Remember the pulmonic valve is doing the same thing, such as opening and closing.

Now picture with the mitral valve is doing and remember that the tricuspid valve is doing the same thing as far as opening and closing.

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32
Q

Does a murmur due to a VSD occur during systole or diastole?

A

During ejection = SYSTOLE

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33
Q

Murmur’s associated with an acute MI

  1. If you have myocardial ischemia or infarction, which valve can be affected in what can it lead to?
  2. What muscle in the heart can be affected also?
  3. Papillary muscle dysfunction is considered what grade of injury?
  4. Papillary muscle rupture is considered what grade of injury?
  5. Where is a ventricular septal defect located at?
A
  1. Mitral valve; mitral valve regurgitation.
  2. Papillary muscle. Can be either dysfunction or rupture.
  3. Grade I or II
  4. Grade V or VI
  5. Sternal border, fifth ICS.
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34
Q

What are 4 non-modifiable risk factors for coronary artery disease?

A

Age, sex, family, history, genetics

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35
Q

What are 9 modifiable risk factors for coronary artery disease?

A

Smoking, atherogenic diet, alcohol intake, physical activity, dyslipidemias, hypertension, obesity, diabetes, metabolic syndrome

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36
Q

What is the spectrum of ischemic heart disease?

A

Asymptomatic, coronary artery disease, stable, angina, chest pain with activity, predictable, lesions are usually fixed and calcified

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37
Q

If a patient has an MI, are they required to have chest pain?

A

No. Especially in women in those with diabetes or older than 75 years old.

Signs and symptoms can be nausea, shortness of breath, extreme fatigue, syncope, acute delirium, or falling.

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38
Q

What is acute coronary syndrome due to? What may it result in?

A

Platelet mediated thrombosis.

Sudden Cardiac death

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39
Q

What are the three types of acute coronary syndrome?

A
  1. Unstable angina.
  2. Non-ST elevation myocardial infarction (NSTEMI)
  3. ST elevation myocardial infarction (STEMI)
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40
Q

If you are having chest pain at rest, unpredictable, may be relieved with nitroglycerin, troponins are negative, ST depression, T wave inversions; what type of ACS is this?

A

Unstable angina

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41
Q

Troponin is positive, you have ST depression, T wave inversions, and unrelenting chest pain; what type of ACS is this?

A

NSTEMI

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42
Q

If troponin is positive, ST elevation in two or more continuous leads, and unrelenting chest pain; what ACS is this?

A

STEMI

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43
Q

What is variant or Prinzmetal’s angina?

A

-A type of unstable angina
-Associated with transient ST segment elevation
-Due to coronary artery spasm with or without lesions
-Occurs at rest
-Maybe cyclic (same time of day)
-Maybe precipitated by nicotine, ETOH, cocaine
-troponins are negative
-Nitroglycerin relieves chest pain while ST returns to normal

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44
Q

What is the first thing you do with the management of acute chest pain for a patient?

A

Assess the patient first to determine how they are doing. If necessary, obtain a stat ECG and have it done and read within 10 minutes.

This will determine how high of a risk they are and allow you to categorize them into an STEMI, NSTEMI, or neither.

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45
Q

Let’s say the ECG shows ST elevation, which ACS is this associated with?

A

STEMI

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46
Q

ECG shows ST depression, or T wave inversion… what ACS is this associated with?

A

NSTEMI

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47
Q

Which medication should be given first for chest pain?

A

Aspirin as soon as possible!

Have it chewed. Will improve morbidity and mortality.

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48
Q

If a patient is having chest pain, what is the management process?

A
  1. Assess the patient
  2. Obtain ECG
  3. Give aspirin
  4. Anticoagulant: heparin or lovenox
  5. Anti-Platelets
  6. Beta blockers
  7. Treat pain - nitroglycerin & morphine
  8. History, labs
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49
Q

When should you not use beta blockers for the management of acute chest pain?

A

If the patient has taken cocaine.

if going to use a non-cardio selective betablocker, such as propranolol.

If the patient has hypotension, Brady Cardia, or is using sildenafil (viagra)

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50
Q

Name the leads associated with the right coronary artery and the inferior LV

A

II, III, aVF

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51
Q

Name the leads associated with the left interior descending, and interior LV

A

V1, V2, V3, V4

52
Q

Name the leads associated with the circumflex, and lateral LV

A

V5, V6, I, aVL

53
Q

Name the leads associated with the low lateral LV

A

V5, V6

54
Q

Name the leads associated with the high lateral LV

A

I, aVL

55
Q

Name the leads associated with RCA, posterior LV

A

V1, V2

56
Q

Name the leads associated with RCA, right ventricular infarct

A

V3R, V4R

57
Q

What are the four different places you can have in acute MI?

A
  1. Inferior.
  2. Right ventricular.
  3. Interior.
  4. Lateral.
58
Q

If you’ve had a right coronary artery, occlusion, where in the heart have you had an MI?

A

Inferior MI

59
Q

Inferior MI
1. Associated with occlusion where?
2. ST elevation or depression? And which leads?
3. Reciprocal changes where?
4. Associated with which AV conduction disturbances?
5. Development of what type of murmur?
6. What symptom is associated with inferior MI? What does it eventually lead to?
7. Use which medications with caution?

A
  1. Right coronary artery occlusion.
  2. Elevation. II, III, aVF
  3. Lateral wall (I, aVL)
  4. Second-degree type one AV block, third-degree AV block, sick sinus syndrome, sinus bradycardia.
  5. Systolic — leads to mitral valve regurgitation, and muscle rupture.
  6. Tachycardia. higher mortality.
  7. Beta blockers and NTG.
60
Q

Right ventricular (RV) infarct

  1. Which arteries are involved with the supply?
  2. What are the signs and symptoms?
  3. What’s the treatment?
  4. What should you avoid?
A
  1. The right coronary artery, which supplies the infer wall the left ventricle also supplies the right ventricle; therefore, about 30% of the inferior wall, and my patients also have RV inDarcy
  2. JVD at 45°, high CVP, hypotension, usually clear lungs, Bradyarrhythmias.
  3. Fluids and positive inotrope.
  4. Preload reducers such as nitrates, diuretics. Caution with beta blockers.
61
Q

Anterior MI

  1. Associated with what occlusion?
  2. In what leads does ST elevation occur?
  3. Reciprocal changes are where?
  4. May develop what ominous sign?
  5. Can lead to what defect?
  6. Better or worse to have compared to inferior MI?
A
  1. Left interior descending (LAD) occlusion
  2. V1-V4
  3. ST depression in inferior wall (II, III, aVF)
  4. Seconddegree type II AV block or right bundle branch block.
  5. Ventricular septal defect.
  6. Worse. Higher mortality. Will have heart failure.
62
Q

Lateral MI

  1. ST elevations in which leads?
  2. Involves which artery?
A
  1. V5, V6 (low lateral) and I, aVL (high lateral)
  2. Left circumflex artery
63
Q

What is the treatment of STEMI?

A
  1. Determine onset of infarct. If symptoms occur less than 12 hours — REPERFUSION
  2. Percutaneous coronary intervention (PCI)- within 90 minutes (door to balloon)
    3.
64
Q

How can you be eligible for having a percutaneous coronary intervention?

A
  1. ST elevation into are more continuous leads OR new onset left bundle branch block
  2. Answer to chest pain for more than 12 hours
  3. Chest pain of 30 minutes in duration.
  4. Chest pain unresponsive to sublingual nitroglycerin.
65
Q

What should you monitor for when following reperfusion for a STEMI with PCI?

A
  1. Signs of re-occlusion — chest pain in ST elevation. Also contact physician.
  2. Basal vagal reaction during sheath removal. — give fluids and atropine.
  3. Bleeding —
    a. At sheath site - immediately apply manual pressure above puncture site. Continue manual pressure for 20 minutes to achieve hemostasis.
    b. At retroperioneal - fluids, blood — if sudden hypertension or severe low back pain
  4. Vascular complications — check pulse
66
Q

What is the window for Fibrinolytic therapy?

A

30 minutes door to drug administration

67
Q

What are the contraindications for fibrinolytic therapy?

A
  1. Any prior intracranial hemorrhage.
  2. Any known structural cerebral vascular lesion.
  3. Any known malignant intracranial neoplasm.
  4. Ischemic stroke within three months, except acute ischemic stroke within three hours.
  5. Suspected aortic dissection.
  6. Active bleeding
  7. Significant closed head or facial trauma within three months.
68
Q

What are the four evidence of reperfusion?

A
  1. Chest pain, relief due to fibrinolysis of clot.
  2. Resolution of ST segment deviations due to return of blood flow.
  3. Marked elevation of troponin/CK – MB: due to myocardial stunning when the vessel opens.
  4. Reprovision arrhythmia as such as VTAC or V fib due to myocardial stunning when vessel opens.
69
Q

What is nursing management for evidence of reperfusion?

A
  1. Assess for major and minor bleeding; change in loss of consciousness or brain bleed
  2. Institute bleeding precautions.
  3. Assessed for reperfusion.
  4. Assess for occlusion as evidenced by reoccurring chest pain, ST deviation.
70
Q

What is the most common complication of an acute MI?

A

Arrhythmias

Example, examples include ventricular, tachycardia, or ventricular fibrillation, bradycardia, heart blocks, six sinus syndrome, atrial fibrillation, heart failure, cardiogenic shock, rein function, pericarditis, ventricular, septal, defect, ventricular, aneurysm, popular muscle rupture, cardiac wall rupture

71
Q

What are the five cardiac authorization lab procedures?

A
  1. diagnostics
  2. PCI — most common being intracoronary stunting. Also includes balloon, angioplasty without stent (PTCA)
  3. Percutaneous balloon valvotomy
  4. Pacemaker implants.
  5. Electrophysiology studies — implantable cardio converter defibrillator (ICD) & cardiac ablation therapy
72
Q

What are the five cardiac authorization lab procedures?

A
  1. diagnostics
  2. PCI — most common being intracoronary stunting. Also includes balloon, angioplasty without stent (PTCA)
  3. Percutaneous balloon valvotomy
  4. Pacemaker implants.
  5. Electrophysiology studies — implantable cardio converter defibrillator (ICD) & cardiac ablation therapy
73
Q

What is the goal of PCI with stent?

A

Restoration of blood flow distal to a coronary artery lesion with partial or total occlusion

74
Q

What is the goal of PCI with stent?

A

Restoration of blood flow distal to a coronary artery lesion with partial or total occlusion

75
Q

What are the complications of PCI?

A
  1. Stent thrombosis — most likely occurs within 24 hours of stent placement or within the first 30 days.
  2. Retroperitoneal bleed
76
Q

What should you monitor for during PCI sheath removal?

A

Vasovagal response

— this includes hypotension below, 90 systolic, pallor, nausea, yawning, diaphoresis

77
Q

What qualifies as hypertensive, emergency or crisis?

What is the treatment?

Greatest risk of occurrence?

A

Elevated blood pressure with evidence of end organ damage that can be related to acute hypertension— Needs critical care admission

Treatment— emergent, lowering of blood pressure by using either nitroprusside or labetalol

Nitroprusside— preload AND after load reducer. Assess for cyanide toxicity secondary to drug metabolite unexplained metabolic acidosis.

Labetalol— intermittent IV doses preferred over continuous infusions. Affect will continue 4-6 hours after IV dose has been discontinued.

Greatest risk — STROKE

78
Q

What qualifies as hypertensive urgency?

A

Elevated blood pressure without evidence of acute and organ damage

— no need for critical care admission

79
Q

What is the 6 “Ps” for signs and symptoms of peripheral arterial disease?

A
  1. Pain (activity, rest)
  2. Pallor
  3. Pulse absent or diminished.
  4. Paresthesia.
  5. Paralysis.
  6. Poikilothermia: loss of hair on toes or lower legs; glossy, thin, cool, dry skin (chronic sign of PAD)
80
Q

What test is used to assess for PAD? What does it assess?

A

Ankle-brachial index (ABI)

Assesses the adequacy of lower extremity perfusion.

Normal is above 0.9– divide the ankle pressure by the brachial pressure on the same side

  • you only need to remember what is normal for ABI on the exam
81
Q

What position should you put the bed for treatment of peripheral arterial disease?

A

Reverse Trendelenburg

82
Q

Should you elevate or not elevate an affected extremity that has peripheral arterial disease?

A

Do NOT elevate the affected extremity— it will decrease perfusion

Use medication’s instead — thrombolytics, anticoagulant, antiplatelets, vasodilators

83
Q

What are the four signs and symptoms of acute symptomatic carotid artery disease?

A
  1. Transient ischemic attack (TIA)
  2. Monocular visual disturbances.
  3. Aphasia.
  4. Stroke.
84
Q

What are the four signs and symptoms of acute symptomatic carotid artery disease?

A
  1. Transient ischemic attack (TIA)
  2. Monocular visual disturbances.
  3. Aphasia.
  4. Stroke.
85
Q

What is the gold standard for testing for acute symptomatic carotid artery disease?

A
  1. Angiography — however, risk of stroke during exam.

Can also do a ultrasound, CTA, MRA

86
Q

What is the gold standard for testing for acute symptomatic carotid artery disease?

A
  1. Angiography — however, risk of stroke during exam.

Can also do a ultrasound, CTA, MRA

87
Q

What is the treatment for acute symptomatic carotid artery disease?

A

Carotid endarterectomy, carotid, stenting, aspirin, statin therapy

88
Q

What is Wolff-Parkinson-white syndrome?

A

When somebody goes from tachycardia to supra ventricular tachycardia. Typically seen in those younger than 30 years old.

May also present as pre-excited atrial fibrillation

Treatment if unstable— radio frequency ablation; synchronize, cardioversion, or adenosine administration

Treatment if pre-excited a fib— beta blockers, amiodarone, procainamide IV.

89
Q

What happens if you give adenosine, digoxin, or a calcium channel blocker for pre-excited atrial fibrillation?

A

You may enhance the conduction and result with the patient getting ventricular fibrillation. Do not do this!

Give beta blockers, amiodarone or procainamide IV instead

90
Q

Prolongation of the QT interval (must master this)

  1. What does it lead to?
  2. What are the causes?
  3. What is the treatment?
A
  1. Leads to torsades de pointes.
  2. Can be caused from drugs such as— amiodarone, quinine, haloperidol, procainamide
    — can also be caused from electrolyte problems, such as— hypokalemia, hypocalcemia, hypomagnesemia
  3. Treatment— magnesium.
91
Q

What is the pacemaker code? Explain each in detail.

A

A = atria
V = ventricle
D = dual (both)

First initial= chamber is PACED (invented first)

Second initial= chamber is SENSED (function came along second)

Third initial= response to sensing (came last)

I = inhibits
D = inhibits and triggers
O = none

92
Q

What are the three basic pacer malfunctions?

A
  1. Failure to pace (no spike at all)
  2. Failure to capture (spikes without a QRS)
  3. Failure to sense (pacing in native beats)
93
Q

What are the three basic pacer malfunctions?

A
  1. Failure to pace (no spike at all)
  2. Failure to capture (spikes without a QRS)
  3. Failure to sense (pacing in native beats)
94
Q

Implantable cardio converter defibrillators (ICD) provide what tiered therapy?

A

Program to shock, to burst pace, to provide pacing for Brady arrhythmias

Do not place shocking pads directly over the ICD

95
Q

What are the different types of heart failure that exist?

A

Acute, chronic, acute exacerbation of chronic heart failure, systolic or diastolic heart failure, right sided or left sided

Most extreme = cardiogenic shock (all systems failed)

96
Q

What is heart failure?

A

High intracardiac pressures + decreased cardiac output

97
Q

What is acute decompensated heart failure?

A

Abrupt onset of symptoms that are severe enough to merit hospitalization— 75% of these patients have a history of chronic heart failure

98
Q

What is acute decompensated heart failure?

A

Abrupt onset of symptoms that are severe enough to merit hospitalization— 75% of these patients have a history of chronic heart failure

99
Q

What is systolic dysfunction heart failure?

A

Left ventricular systolic dysfunction

EF is 40% or less — problem with ejection

100
Q

What is diastolic dysfunction of heart failure?

A

EF is above 50%— problem with filling, ejection is OK

101
Q

What is BNP? When does it elevate?

A

B-type natriuretic peptide

— released by the ventricle when the ventricle is under wall, stress and attempts to dilate and decrease ventricular pressure

— elevates when the left ventricle is under stress (left ventricular failure) or when the right ventricle is under stress (pulmonary hypertension, pulmonary embolism)

102
Q

Compare & contrast systolic versus diastolic heart failure

A

Systolic — ejection problem, can fill OK. Signs are larger left ventricle, EF below 40%, S3 heart sound, BP is low. Treatment is BB, ARB, diuretics, dilators, positive inotropes, aldosterone antagonist. Do not give calcium channel blockers. Overall, may result in mitral insufficiency as the left ventricular wall and enlarges.

Diastolic— filling problem, can eject OK. Normal size ventricle. Thick walls. Normal EF. S4 heart sound. BP is high. Treatment — Calcium channel blockers, BB, ARB, low-dose diuretics, aldosterone antagonist. Do not give positive inotropes.

103
Q

What might you find on a chest x-ray when looking at systolic verse diastolic heart failure?

A

A shift to the left because of an enlarged heart. Potential left ventricular hypertrophy patterns.

104
Q

What are some of the causes and signs and symptoms of right sided heart failure?

A

Causes— acute RV infarct, pulmonary embolism, pulmonary stenosis/insufficiency, COPD, pulmonary hypertension, left ventricular failure

Signs and symptoms — hepatomegaly, splenomegaly, dependent edema, venous, distention, elevated JVD, tricuspid insufficiency, abdominal pain

105
Q

What are the causes and signs and symptoms of left sided heart failure?

A

Causes— coronary artery disease, MMI, cardiomyopathy, fluid overload, chronic uncontrolled hypertension, aortic stenosis/insufficiency, mitral stenosis/insufficiency, cardiac tamponade

Signs and symptoms — dyspnea, to Kania, hypoxemia, pack of cardio, crackles, cough with pink frothy, sputum, elevated PAOP, diaphoresis, anxiety, confusion

106
Q

What is the main cause of death from heart failure?

A

The development of sudden death arrhythmia

107
Q

What are the two types of heart failure classifications?

What are their stages?

A
  1. American Heart association.
    —4 stages
    A: high risk-no evidence of dysfunction
    B: heart disorder with no symptoms
    C: heart disorder with symptoms
    D: end-stage cardiac disease
  2. NYHA heart failure.
    —4 classes
    I: extraordinary activity, results in HF symptoms
    II: comfortable at rest, but ordinary activity, results in HF symptoms
    III: comfort at rest, but minimal activity causes HF symptoms
    IV: symptoms occur at rest, severe limitation to physical exercise.
108
Q

What question will be asked on the exam about cardiomyopathy?

What is the difference between dilated and hypertrophic cardiomyopathy?

A

It will be either about dilated or hypertrophic cardiomyopathy

Dilated — systolic dysfunction; thinning, enlargement of LV chamber, mitral valve regurgitation. May need ventricular assist device or heart transplant.

Hypertrophic — diastolic dysfunction; increased thickening of heart, muscle, fatigue, dyspnea, chest pain, palpitations, S3 or S4 heart sounds, syncope. Increased risk of sudden cardiac death!

109
Q

What is the clinical presentation of cardiogenic shock in relation to the compensatory stage versus the progressive stage?

A

Compensatory stage— tachycardia, tachypnea, crackles, mild hypoxemia, respiratory alkalosis, or early metabolic acidosis, anxiety, irritability, neck vein distention, S3 Heart sounds, cool skin, urine output is down, NARROW PULSE PRESSURE, BP lower

Progressive stage — hypotension, worsening tachycardia, tachypnea, oliguria, metabolic acidosis, worsening crackles, hypoxemia, clammy, skin, modeled skin, worsening anxiety, lethargy, potential chest pain, or arrhythmias

110
Q

What are the etiologies (or causes) of cardiogenic shock?

A

Acute MI, chronic heart failure, cardiomyopathy, arrhythmias, cardiac tamponade, papillary muscle rupture (life threatening emergency, immediate surgical intervention)

111
Q

What is the treatment of cardiogenic shock?

A
  1. Identify the cause.
  2. Manage arrhythmias (Brady or tachy)
  3. Reperfusion.
  4. Emergent surgery (if mechanical problem, such as papillary muscle or VSD.)
  5. Mechanical support.
112
Q

What will you be tested on in regards to cardiogenic shock support?

A

Intra-aortic balloon pump (IABP) — you need to know it is using management of left ventricular heart failure, cardiogenic, shock, cardiomyopathies, and used for patients who are awaiting a heart transplant.

It does two things — inflates and deflates

Inflation = increases, coronary artery, perfusion

Deflation = decreases after load; deflates right before systole begins; is the R wave of ECG

113
Q

What should you be looking out for regarding cardiac surgery on the exam?

A

Complications and nursing care

114
Q

What are the complications related to CABG?

A

Tamponade, pericarditis

Arrhythmias, electrolyte, abnormalities, bleeding, pain, anxiety, renal failure, endocrine problems, GI problems, infections

115
Q

What is the postop chest tube management of a CABG?

A
  1. Maintain patency — no dependent loops allowed, do not milk or strip chest tubes, if clot appears gently milk, the chest tube
  2. Mediastinal chest tube = remove serosanguineous fluid; pleural chest tube = removes air, blood, or serous fluid from pleural space
  3. Keep chest tubes lower than patients chest
  4. DO NOT CLAMP — unless changing system.
  5. If over 100mL in 2 hours— requires intervention (give blood, give fluids, etc)
116
Q

If a patient has had a post valve repair or replacement, what should you anticipate?

A

Conduction disturbances— temporary, or permanent pacing may be needed

117
Q

Mechanical and biological valves
1. Advantages.
2. Disadvantages.
3. What should you avoid?
4. Which type of medication will be needed for each replacement specifically?

A
  1. Mechanical — relatively easy to insert, reliable, last longer
    Biological — only short term anticoagulation is required (still need aspirin therapy)
  2. Mechanical — high risk of thrombosis, permanent anticoagulation therapy
    Biological — wears down, especially in high-pressure systems
  3. Avoid a drop in preload. May result in hypotension.
  4. Mechanical = anticoagulation
    Biological = antiplatelet (aspirin)
118
Q

Transcatheter Aortic Valve Replacement (TAVR)

  1. What does the procedure involve?
  2. Why is this used over cardio pulmonary bypass?
  3. Where is the insertion point?
  4. What is the ideal candidate?
  5. Who was considered not an ideal candidate?
  6. What type of medication therapy will be required?
A
  1. Placement of a collapsible prosthetic valve over a diseased valve.
  2. Because it avoids cross clamping of the aorta.
  3. Femoral artery.
  4. Those with severe aortic valve disease that is classified as HIGH RISK for open surgery
  5. Extreme high risk/in operatable or low risk.
  6. Dual anti-platelet therapy will be required. Aspirin for life and Plavix for 3 to 6 months post procedure.
119
Q

Cardiac Tamponade
1. Etiologies
2. Signs and symptoms
3. What will you see on an arterial waveform?

A
  1. Surgical related; medical related such as pericarditis and pericardial effusion or trauma.
  2. Narrowed pulse pressure (82/68) and pulsus paradoxus
    Others: restlessness, agitation, hypotension, increased JVD, muffled heart sounds
  3. Pulsus paradoxus— excessive drop greater than 12 mmHg in the systolic blood pressure during what’s up who’s there inspiration, increases intrathoracic pressure, decreases venous return
120
Q

Cardiac trauma

  1. Which valve is most at risk for a rupture due to trauma?
  2. Myocardial contusion has signs and symptoms that are similar to what condition?
A
  1. Aortic valve — because it is most anterior in the chest.
  2. Pericarditis.
121
Q

Pericarditis vs Myocardial Contusion

  1. Etiology of each
  2. Signs and symptoms of each
  3. Treatment of each
A

Pericarditis
—Etiology: trauma (rare), viral, after an MMI, postop, cardiac surgery, radiation, idiopathic, Dressler’s syndrome (immune response after an MI, surgery, or traumatic injury)

—Signs and symptoms: chest pain, pain, worsens with inspiration, dyspnea, low-grade temperature, increase sed rate, ST elevation, cardiac tamponade, Dressler’s syndrome lasting months

—Treatment: symptom relief, analgesic, anti-inflammatory agents, NSAIDs, steroid, anabiotic’s, monitor for worsening symptoms, constructive pericarditis, cardiac tamponade

Trauma
—Etiology: outcome in pericarditis, broken vessels, bleeding into heart, cardiac arrhythmia, death can occur within first 48 hours

—Signs and symptoms: signs of trauma, chest pain, pain worsens with inspiration, dyspnea, low-grade temperature, ST elevation in the AREA OF INJURY

—Treatment: monitor for arrhythmias, analgesic as needed

122
Q

Aneurysms

  1. What are they?
  2. Etiology
  3. Main 2 types?
A
  1. Localized, blood filled outpouching in the wall of an artery, which becomes more likely to rupture the larger it becomes.
  2. Arteriosclerosis, hypertension, smoking, obesity, bacterial infections, congenital abnormalities, trauma, Marfan syndrome.
  3. Abdominal aortic and thoracic aortic.
123
Q

Abdominal aortic aneurysms (AAA)

  1. What percentage of all CV-related aneurysms?
  2. What are the signs and symptoms?
A
  1. 75%
  2. If small— a symptomatic, pulsations in abdominal area, abdominal or low back pain, nausea, vomiting, shock.
124
Q

Thoracic Aortic Aneurysms

  1. What percentage of all CV related aneurysms?
  2. Signs and symptoms?
  3. Treatment if smaller than 5cm? Larger than 5cm?
A
  1. 25%
  2. Sudden tearing, ripping pain in chest that radiates to the shoulders, neck and back; cough, horseless, dysphasia, dyspnea, dizziness, and difficulty, walking and speaking, widening of mediastinum on chest x-ray.
  3. < 5 cm— typically no symptoms. Monitor regularly. Ultrasound or CT scan. Treat the hypertension with beta blockers, which may slow the growth. People with Marfan syndrome are treated sooner.

> 5 cm— typically symptoms are above 6 cm. Surgical repair. Dissection = SURGERY. Aggressive treatment of hypertension and heart rate control with Labetalol drip.

125
Q

Aortic Dissection

  1. What is it?
  2. Appearance?
  3. Occurs suddenly or gradually?
  4. Location?
  5. How emergent?
  6. Treatment?
A
  1. Blood passes through the inner lining in between the layers of the aorta.
  2. The tear is spiral in nature.
  3. Can be either suddenly or gradually.
  4. Ascending aorta or in the aortic arch.
  5. Life-threatening.
  6. Immediate surgical intervention!

CCRN Exam (3 decks)

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