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Cardiology Flashcards

1
Q

What are two types of dysfunction in CHF?

A

Diastolic and Systolic

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2
Q

What is underlying systolic dysfunction and what happens to ejection fraction?

A

Impaired contractility and decreased ejection fraction

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3
Q

What are some causes of systolic HF? (2)

A

Ischemic heart disease, HTN that results in cardiomyopathy

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4
Q

What is underlying diastolic HF?

A

Impaired ventricular filling during diastole (increased stiffness or impaired relaxation of ventricle)

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5
Q

What are the pathological changes behind diastolic and systolic HF?

A

In diastolic HF, there is hypertrophic concentric myocyte remodeling (which is why the ventricle is stiff and can’t relax).

In systolic HF, there is dilated eccentric myocyte remodeling which is why the ventricle can’t contract efficiently

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6
Q

What is seen on Echo in diastolic HF?

A

Impaired relaxation of the left ventricle

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7
Q

What are the causes of diastolic HF? (2)

A

HTN causing myocardial hypertrophy resulting in diastolic dysfunction.

Restrictive cardiomyopathy from amyloidosis, sarcoidosis, and hemochromatosis

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8
Q

What is EF in diastolic HF?

A

Normal or increased

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9
Q

What is NYHA class 3 HF and NYHA class 4 HF?

A

Class 3 = symptoms during activities of daily living

Class 4 = symptoms at rest

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10
Q

What the signs and symptoms of left sided HF?

A

dyspnea, orthopnea, PND, nocturnal cough (due to pulmonary congestion); dullness to percussion at lung bases (also due to pulmonary congestion); S3, S4, displaced PMI, bibasilar crackles

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11
Q

What is the cause of S3? S4?

A 
S3 = rapid filling into a non-compliant left ventricle
S4 = blood ejected into a non-compliant or stiff left ventricle
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12
Q

What are the symptoms of right sided HF?

A

Peripheral pitting edema (non-specific and secondary to venous insufficiency), JVD, hepatomegaly, hepatojugular reflux, ascites.

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13
Q

Draw out the pathophysiology of CHF?

A

Decreased CO output results in 2 things at the same time: 1. RAAS activation 2. Activation of the sympathetic nervous system.

Both of these things result in systemic vasoconstriction and volume retention.

This ultimately results in increased LV end disastolic volume and increased LV end diastolic pressure. This pressure is transmitted back to the pulmonary veins leading to pulmonary congestion

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14
Q

How is CHF diagnosed?

A
  1. CXR (shows cardiomegaly)
  2. EKG
  3. Cardiac enzymes - need to rule out MI
  4. BNP
  5. Echocardiogram - initial test of choice
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15
Q

Why is echo the test of initial choice in Heart Failure?

A

Echo helps estimate EF

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16
Q

What drugs help decrease mortality in systolic CHF? (4)

A
  1. ACEI/ARB
  2. Beta Blockers
  3. Spirnolactone or Eplerenone
  4. Hydralizine Dinitrate (in African Americans)
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17
Q

What drugs help decrease symptoms in systolic CHF? (3)

A
  1. Thiazide Diurectics
  2. Loop Diuretics
  3. Digoxin
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18
Q

What are two important side effects of Spirnolactone?

A
  1. Hyperkalemia

2. Gynecomastia

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19
Q

When should digitalis be used in CHF?

A

For patients with EF < 40% who continue to have symptoms despite optimal medical therapy

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20
Q

What are the signs of digoxin toxicity?

A

Nausea/vomiting, visual disturbances, heart block

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21
Q

What is the treatment for diastolic CHF?

A

No medications have proven mortality benefit. Use diuretics for symptom control and beta blockers

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22
Q

What two classes of medications are contraindicated in diastolic CHF?

A

Digoxin and Spirnolactone

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23
Q

What is flash pulmonary edema?

A

Severe form of heart failure with rapid accumulation of fluid in the lungs

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24
Q

What are the clinical features of acute decompensated HF?

A

Acute dyspnea associated with increased left sided filling pressures with or without pulmonary edema

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25
Q

How is acute decompensated HF managed? (4)

A
  1. Diurectics (help treat volume overload and decrease preload)
  2. Nitrates (vasodilators) in patients who are not hypotensive (decrease afterload)
  3. Dobutamine if above fails (increased contractility) (Digoxin takes several weeks to work)
  4. Oxygen
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26
Q

How are arrhythmias classified?

A

Arrhythmias, tachyarrhythmias, and bradyarrhythmias

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27
Q

What are two types of arrhythmia?

A

premature atrial complexes and premature ventricular complexes

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28
Q

What is the underlying physiology of a premature atrial complex (PAC)?

A

early beat that arises in the atria and fires on its own

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29
Q

What is sign of premature atrial compex on EKG?

A

Early P waves that differ in morphology from regular P waves (because they originate in the atria and not the SA node)

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30
Q

What causes PACs?

A

Adrenergic excess, drugs, alcohol, tabacco, etc

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31
Q

What is the clinical significance of a PAC?

A

No significance in a normal heart; significant as a precursor of ischemia in a diseased heart

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32
Q

What is the treatment for a PAC?

A

If asymptomatic, no treatment. If symptomatic, beta blockers

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33
Q

What is the underlying physiology of premature ventricular contractions?

A

Early beat fires from focus in ventricle, and then this electrical current spreads to the other ventricle.

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34
Q

What is seen on EKG in PVC?

A

wide QRS

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35
Q

True or False: PVC can occur in patients with or without structural heart disease?

A

True

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36
Q

What are some causes of PVCs?

A

Hypoxia, caffeine, stimulants, structural heart disease

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37
Q

When is a PVC significant?

A

When there are frequent PVC, mortality increases; need to get a workup for underlying structural heart issues

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38
Q

How are PVCs managed?

A

If symptoms or if they are frequent refer to cardiology for workup and give beta blockers.

If not symptomatic or if infrequent, don’t do anything

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39
Q

Are primary cardiac tumors more common or metastatic tumors to the heart from elsewhere in the body?

A

Metastatic cardiac tumors from other parts of the body are much more common

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40
Q

What is the most common primary cardiac neoplasm?

A

Atrial myxoma

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41
Q

What is the treatment for atrial myxomas?

A

Surgical excision

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42
Q

What problems do atrial myxomas cause?

A

embolization, valvular dysfunction, or metastatic disease

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43
Q

What are the clinical features of atrial myxomas? (2 are critical sx)

A

Fever,
fatigue

palpitations

low-pitched diastolic murmer that changes character with changing body positions (diastolic polp)

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44
Q

What are the clinical features of typical anginal chest pain?

A
  1. Substernal
  2. Worse with exertion
  3. Better with rest or nitroglycerin
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45
Q

What are the different ways CAD can present?

A
  1. Asymptomatic
  2. Stable angina pectoris
  3. Unstable angina pectoris
  4. MI (NSTEMI or STEMI)
  5. Sudden cardiac death
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46
Q

Describe the pathology of stable angina pectoris?

A

Fixed atherosclerotic lesions that narrow the major coronary arteries and cause an imbalance between blood supply and oxygen demand.

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47
Q

What is the worst and most common risk factors for CAD? (2)

A
  1. Worst: Diabetes Mellitus

2. Most common: Hypertension

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48
Q

Describe the two prognostic factors for CAD?

A
  1. Left ventricular ejection function:
    If <50% associated with increased mortality
  2. Vessels involved:
    LAD or 2 vessel disease is worse prognosis
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49
Q

What is the goal for LDL in patients with CAD?

A

Less than 100 mg/dL

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50
Q

What is metabolic syndrome X

A

Any combination of hypercholesterolemia, hypertriglyceridemia, diabetes, impaired glucose tolerance, HTN.

Caused by insulin resistance

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51
Q

What is syndrome X?

What tests are normal (2), what tests are abnormal (2), and what is the prognosis?

A

Exertional angina with normal coronary arteriogram and coronary catheterization.

Exercise stress testing and nuclear imaging shows evidence of myocardial ischemia

Prognosis is excellent

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52
Q

What do Q waves on EKG mean?

A

Prior MI

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53
Q

When is an exercise EKG considered sensitive?

A

When patients are able to exercise sufficiently to 85% of their maximum heart rate.

Maximum heart rate is (220-age)

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54
Q

What does a positive exercise EKG show? (4)

A

ST segment depression because exercise induced ischemia results in subendocardial ischemia, producing ST segment depression

Chest pain

Significant arrthymia

Hypotension

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55
Q

What should patients with positive stress EKG and stress echocardiography undergo?

A

Should undergo cardiac catherization

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56
Q

Why is stress echocardiogram useful?

A

Can also detect wall motion abnormalities of the heart

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57
Q

In ambulatory setting what is escalation for stable angina?

A

EKG —-> Stress EKG —> Cardiac Cath + Angio

or

EKG —-> Stress Echo —> Cardiac Cath + Angio (if you are a cardiologist)

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58
Q

What does a positive stress mycardial perfusion scan show?

A

Viable myocardial cells will take up radioisotope and therefore light up.

Non-viable cells will not take up radioisotope and therefore will not light up

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59
Q

Areas of reversible ischemia may be rescued with _________ or _______.

A

Percutaneous coronary intervention

or

coronary artery bypass graft

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60
Q

What drugs can be used for pharmacological stress testing and how do they work?

A

Adenosine and Dipyridamole cause coronary vasodilation so normally diseased coronary arteries are already maximally dilated at rest to increase blood flow, they receive less blood flow when all coronary arteries are maximally dilated.

Dobutamine increases myocardial oxygen demand by increasing heart rate, blood pressure, and cardiac contractility.

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61
Q

What is the definitive test for CAD?

A

Coronary catheterization + coronary angiography (done together usually)

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62
Q

What is the standard of care for stable angina?

A

Aspirin + Beta Blocker +/- nitrates for chest pain.

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63
Q

What are some side effects of nitrates?

A

Headache, orthostatic hypotension, syncope

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64
Q

What does the literature say about revascularization for stable angina?

A

Controversy over which is better: medical management (aspirin + beta blocker) vs PCI/CABG. No meaningful difference in treatment. Revascularization does not reduce the incidence of MI, but does improve symptoms.

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65
Q

What are the main indications for CABG? (3)

A
  1. Three vessel disease with >70% stenosis in each vessel.
  2. Left main coronary disease with >50% stenosis
  3. Left ventricular dysfunction
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66
Q

What is the diagnosis difference between NSTEMI and Unstable angina?

A

NSTEMI shows elevation of cardiac enzymes that is not seen in unstable angina.

Both NSTEMI and USA lack ST segment elevation and pathologic Q waves

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67
Q

What are the clinical features of USA?

A

Anginal pain at rest, no ST segment elevation on EKG and no cardiac enzyme elevation

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68
Q

How is USA managed? (5)

A

Admit to the hospital floor and treat similar to MI except for fibrinolysis

  1. Aspirin (continue for 9-12 months)
  2. Beta-blockers
  3. Clopidogrel (CURE trial) (continue for 9-12 months)
  4. LMWH (2 days)
  5. Nitrates for pain
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69
Q

What is role of cardiac catheterization in USA?

A

No studies have shown medical benefits of revascularization compared to medical management of USA.

Many patients with USA that is controlled with medical therapy eventually require revascularization

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70
Q

What is variant prinzmetal angina?

A

Transient coronary artery vasospasm that is usually accompanied by a fixed atherosclerotic plaque but can also occur in normal coronary arteries.

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71
Q

What does prinzmetal angina show on EKG?

A

ST segment elevation (transmural ischemia) that is seen on EKG during chest pain

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72
Q

What is the definitive test for prinzmetal angina?

A

Coronary angiography is the definitive test when patient is given IV ergonovine or acetylcholine (provoke vasoconstriction)

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73
Q

How is prinzmetal angina managed?

A

Calcium channel blockers and nitrates

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74
Q

What is the mortality rate of MI?

A

30%, most deaths occur before the patient reaches the hospital

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75
Q

What are some clinical features of MI?

A
  1. Intense substernal chest pain that is often described as crushing.
  2. Pain radiates to the neck, jaw, arms, commonly on the left side
  3. Pain does NOT respond to angina
  4. Diaphoresis
  5. Vomiting
  6. Can be asymptomatic in some patients
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76
Q

What is the most early change seen on EKG in a patient with MI?

A

Peaked T-waves

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77
Q

What does ST segment elevation indicate?

A

Transmural injury (all layers of heart muscle are affected)

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78
Q

What does ST segment depression indicate?

A

Subendocardial injury (NSTEMI)

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79
Q

Other than elevated cardiac enzymes, what may be diagnostic of on acute infarct?

A

ST segment elevation in 75% of cases

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80
Q

What EKG leads will show an anterior wall infarct?

A

EKG changes in leads V1-V4

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81
Q

What EKG leads will show a posterior wall infarct?

A

EKG changes in leads V1 and V2

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82
Q

What EKG leads will show a lateral wall infarct?

A

EKG changes in leads 1 and aVL

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83
Q

What EKG leads will show a inferior wall infarct?

A

EKG changes in leads 2, 3, avF

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84
Q

What is the current diagnostic gold standard for myocardial injury?

A

Cardiac enzymes

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85
Q

How often should cardiac enzymes be monitored?

A

Every 8 hours after initial draw for 24 hours

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86
Q

When do troponins increase, peak, and return to normal following MI?

A

Increase within 3-5 hours
Peak in 24 hours
Return to normal in 5-14 days

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87
Q

When does CKMB increase, peak, and return to normal following an MI?

A

Increases within 4-8 hours
Peaks within 24 hours
returns to normal in 48-72 hours

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88
Q

In MI, what three medications are the only agents that decrease mortality?

A
  1. Aspirin
  2. Beta Blockers
  3. ACE inhibitors
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89
Q

What should be given to patients with an acute MI? (9)

A
  1. Oxygen
  2. Aspirin
  3. Beta Blockers
  4. ACE inhibitors
  5. Statins
  6. Nitrates (decrease preload)
  7. Morphine
  8. LMWH
  9. Clopidogrel (should be initiated in all patients who undergo PCI)
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90
Q

For an acute MI, what is the time limit for revascularization?

A

Within 90 minutes of Hospital Arrival

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91
Q

What is the go to revascularization technique for acute MI?

A

PCI

Urgent or emergent CABG is typically performed only in the setting of mechanical complications of an acute MI, cardiogenic shock, life threatening arrhythmias, or after failure of PCI. It is almost never performed in the acute setting of a patient that is stable after PCI.

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92
Q

What is the time frame for thrombolytic therapy in acute MI?

A

If patient cannot reach a hospital that has PCI quickly enough, give thrombolytics in the first 24 hours after chest pain, preferably in the first 6 hours

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93
Q

When is free wall rupture more likely post MI?

A

In the first two weeks after an MI, usually 1-4 days after an MI

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94
Q

What complications does a free wall rupture of the heart lead to?

A

Leads to hemopericardium or cardiac tamponade

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95
Q

When is rupture of the interventricular septum most likely post MI?

A

Within 10 days post-MI

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96
Q

What does a papillary muscle rupture cause in patients post-MI?

A

Mitral Regurgitation (get echo if you hear a new murmur)

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97
Q

How is acute pericarditis treated post-MI and what medications are contraindicated?

A

Treat with aspirin. NSAIDs and corticosteroids are contraindicated

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98
Q

What is Dressler syndrome? When does it occur post-MI and how is it treated?

A

Dressler syndrome is a immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis occuring weeks to months post-MI.

Aspirin is the most effective therapy.

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99
Q

What are the different tachyarrhythmias? (7)

A
  1. Afib
  2. Aflutter
  3. Multifocal atrial tachycardia
  4. Paroxysmal Supraventricular Tachycardia
  5. Ventricular tachycardia
  6. Wolf Parkinson White Syndrome
  7. Vfib
100
Q

Describe the pathology of Afib?

A

Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally irregular and rapid ventricular rate. Instead of intermittently contracting, the atria quiver continously

101
Q

What are some causes of Afib?

A
  1. Heart disease
  2. Lung disease
  3. Hyperthyroidism and Hypothyroidism
  4. Systemic illness
102
Q

What are some of the clinical features of Afib?

A

Fatigue, exertional dyspnea, palpitations, angina, syncope

103
Q

What is seen on EKG in patients with AFib?

A

Irregularly irregular rhythm

104
Q

What is the first thing to check for in patients with Afib?

A

Are they hemodynamically stable?

105
Q

If a patient is with Afib is not hemodynamically unstable, what should be done?

A

Immediate electrical cardioversion

106
Q

In a patient with Afib who is hemodynamically stable, what is the next goal?

A

Rate control via Beta Blockers (Calcium channel blockers are an alternative).

Then ascertain the duration of the Afib.

107
Q

If the duration of Afib is less than 48 hours, what should be done?

A

Cardioversion

108
Q

If the duration of Afib is more than 48 hours or unknown what are the next steps?

A

Perform a TEE to see if there is a thrombus in the left atrium. If there isn’t a thrombus, cardiovert the patient.

If there is a thrombus, anticoagulate the patient for 3 weeks, then cardiovert

109
Q

After cardioversion of a patient with Afib what is the next step?

A

Continue anticoagulating the patient for 4 weeks and keep INR between 2-3 range.

110
Q

What is preferred in patients with Afib, electrocardioversion or pharmacological cardioversion?

A

Electrical cardioversion

111
Q

What is the difference between cardioversion and defibrillation and when is each indicated (4 indications for cardioversion and 2 for defib)

A

Cardioversion delivers shock that is in synchrony with the QRS complex. Indications = Afib, aflutter, VT with pulse, and SVT

Defib delivers a shock that is not in synchrony with the QRS complex. Indications = Vfib, and VT without a pulse

112
Q

What is the pathological cause of Aflutter?

A

One irritable automaticity focus in the atria fires at about 250-300 bpm giving rise to regular atrial contractions. However, the long refractory period in the AV node allows only one out of every 2 or 3 flutter waves to conduct to the ventricles.

113
Q

What are some causes of atrial flutter?

A

Heart disease
COPD
Atrial septal defect

114
Q

What is seen on EKG for patients with aflutter?

A

Saw tooth baseline WITH a QRS appearing every 2nd or third “tooth”. These EKG changes are best seen in the inferior leads

115
Q

What is the treatment for AFlutter?

A

Similar to the treatment for Afib

116
Q

What type of patients develop multifocal atrial tachycardia?

A

Patients with severe pulmonary disease (COPD)

117
Q

What are the EKG findings in patients with multifocal atrial tachycardia? (3)

A

Variable p wave morphologies and variable PR and RR intervals.

At least three different P-wave morphologies are required to make an accurate diagnosis

118
Q

Describe two pathological issues that can cause Paroxysmal Supraventricular Tachycardia?

A
  1. Two pathways, one fast and the other slow, within the AV node so the renterent circuit is within the AV node
  2. An accessory pathway between the atria and the ventricles that conducts retrogradely
119
Q

What are the EKG findings in paroxysmal supraventricular tachycardia?

A

Narrow QRS complexes with P waves that may or may not be discernible.

120
Q

What is the most common arrhythmia associated with digoxin toxicity?

A

Paroxysmal supraventricular tachycardia

121
Q

How is paroxysmal supraventricular tachycardia treated?

A
  1. Maneuvers that stimulate the vagus delay (Valsalva maneuver, carotid sinus massage, breath holding, head immersion in cold water).
  2. Acute treatment: IV adenosine
122
Q

What causes Wolf-Parkinson-White Syndrome?

A

Accessory conduction pathway from atria to ventricles through the bundle of kent that causes premature excitation because it lacks the delay seen in the bundle of HIS

123
Q

What are the EKG changes seen in WPW syndrome?

A

Delta wave, narrow complex tachycardia, short PR interval

124
Q

How is WPW syndrome treated?

A

Radiofrequency catheter ablation of one arm of the reentrant loop

Medically can use procainamide or quinidine.

125
Q

Describe the pathology of Ventricular tachycardia

A

Defined as rapid and repetitive firing of three or more PVCs in a row at a rate of 100 and 250 bpm.

AV dissociation is present, so P waves continue with their cycle unaffected by the tachycardia

VT originates below the bundle of HIS

126
Q

What are the two types of ventricular tachycardias?

A

Sustained VT: lasts longer than 30 seconds and is symptomatic. This is a life threatening arrhythmia and can progress to Vfib if untreated.

Nonsustained VT: Brief and self limited runs of VT. Usually asymptomatic

127
Q

What are the symptoms of ventricular tachycardia?

A

Palpitations, dyspnea, lightheadedness, angina, impaired consciousness, sudden cardiac death, cannon A waves in the neck.

128
Q

What is seen on EKG in patients with VTach?

A

Wide and bizarre QRS complexes. Can have identical QRS complexes or polymorphic QRS complexes.

129
Q

Does VTach respond to vagal maneuvers or adenosine?

A

No

130
Q

For patients with sustained VT and patients who are hemodynamically stable, what is the treatment?

A

IV amiodarone, IV procainamide, IV sotalol

131
Q

How are hemodynamically unstable patients with Vtach treated?

A

Immediate synchronous DC cardioversion followed by IV amiodarone to maintain sinus rhythm

132
Q

How is nonsustained Vtach treated?

A

If patients have no underlying heart disease and nonsustained Vtach, they should not be treated.

If they have undelrying heart disease and nonsustained Vtach, they should have an electrophysiologic study done on them. If it is inducible, they should have an ICD placement

133
Q

Describe the pathogenesis of VFib?

A

Multiple foci in the ventricles fire rapidly leading to a chaotic quivering heart with no cardiac output

134
Q

How do most episodes of VFib begin?

A

Begin with VTach which evolves into VFib

135
Q

How is Vfib managed if it associated with an MI?

A

If VFib develops within 48 hours of an acute MI, long-term prognosis is favorable and reoccurance is lwo. Chronic therapy is not necessary.

136
Q

How is Vfib managed if it is not associated with an MI?

A

If VFib is not associated with an acute MI, reoccurance is high. These patients need to be on chronic therapy of antiarrhythmic like amiodarone or have an automatic defibrillator placed

137
Q

Where do narrow complex tachycardias originate?

Where do wide complex tachycardias originate?

Which one is more ominous?

A

Narrow complex tachycardias originate above ventricles. Wide complex tachycardias originate below the ventricles and are more ominous because they are more likely to progress to VFib

138
Q

True or False, Always suspect VTach in patients with wide (>.12 second) QRS tachycardia

A

True

139
Q

VT and VFib make up what % of episodes of cardiac arrest?

A

75%

140
Q

What are the clinical features of VFib?

A

No Blood pressure, no pulse, absent heart sounds

141
Q

What does EKG show in patients with VFib?

A

No atrial P waves, no QRS complex, no waves can be identified, and there is an irregular rhythm

142
Q

How is VFib managed?

A

Immediate defibrillation and CPR.

If three sequential shocks fail to establish rhythm, give 1 mg IV bolus of epinephrine followed by more epinephrine.

143
Q

If cardioversion is successful in VFib, what should you do?

A

Maintain continuous IV infusion of IV amiodarone. In chronic patients, put them on implantable defibrillators.

144
Q

What heart rate is seen in sinus bradycardia?

A

Sinus rate < 60, however usually clinically significant if persistently < 45 bpm

145
Q

What are some causes of sinus bradycardia?

A

increased vagal tone
ischemia
anti-arrhythmic drugs
normal finding in trained athletes

146
Q

What are the symptoms of sinus bradycardia?

A

Can be asymptomatic. Patients may complain of fatigue, inability to exercise, angina or syncope

147
Q

How is sinus bradycardia treated?

A

Atropine can help increase sinus rate, but a cardiac pacemaker may be required if the bradycardia persists.

148
Q

What is sick sinus syndrome?

A

Sinus node dysfunction characterized by a persistent spontaneous sinus bradycardia. Patients are usually elderly

149
Q

Describe the findings of First-degree heart block? (2)

A
  1. PR interval is prolonged (>.2)

2. QRS complex follows each p wave

150
Q

Where is the delay seen in first-degree heart block?

A

At the AV node

151
Q

Where is the delay seen in second-degree heart block Morbitz type 1?

A

Av node

152
Q

Describe morbitz type 1 heart block?

A

A type of second degree heart block characterized by progressive prolongation of the PR interval until a P wave fails to conduct

153
Q

Which of the heart blocks are benign conditions?

A

First Degree Heart Block

Second Degree Heart Block Morbitz Type 1

154
Q

Where does a Morbitz type 2 heart block occur?

A

His-Purkinje System

155
Q

Describe Morbitz type 2 heart block?

A

Second-degree AV block where p wave fails to conduct suddenly, without a preceding PR interval prolongation, therefore QRS drops spontaneously

156
Q

Describe a Third Degree AV block?

A

Absence of conduction between atrial impulses to ventricles, so no correspondence between P waves and QRS complex.

157
Q

What two types of heart blocks require pacemakers?

A

Morbitz type 2 and Third Degree Heart Block

158
Q

What is the most common type of cardiomyopathy?

A

Dilated Cardiomyopathy

159
Q

What is the cause of dilated cardiomyopathy?

A

An insult (ischemia, infection, alcohol) causes dysfunction of the left ventricle impairing contractility

160
Q

What are some clinical features of dilated cardiomyopathy?

A

Symptoms of right sided and left sided heart failure. S3, S4, Tricuspid or Mitral Valve insufficiency murmurs. Cardiomegaly is commonly seen. Sudden death.

161
Q

How is dilated cardiomyopathy treated?

A

Similar to the treatment of congestive heart failure

162
Q

What is the genetics of hypertrophic cardiomyopathy?

A

Autosomal Dominant

163
Q

Describe the pathophysiology of hypertrophic cardiomyopathy?

A

Diastolic dysfunction due to a hypertrophied ventricle (can’t relax)

164
Q

What are the clinical features of hypertrophic cardiomyopathy?

A

Dyspnea on exertion, chest pain, palpitations, sudden cardiac death

165
Q

What are the physical exam findings of hypertrophic cardiomyopathy?

A

Sustained PMI

Loud S4

166
Q

How is hypertrophic cardiomyopathy diagnosed?

A

Echo

167
Q

How is hypertrophic cardiomyopathy treated?

A
  1. Avoid exercise
  2. Beta blockers
  3. Myomectomy
168
Q

What is the pathological cause behind restrictive cardiomyopathy?

A

Infiltration of the myocardium results in impaired diastolic ventricular filling due to decreased ventricular compliance.

169
Q

What are some causes of restrictive cardiomyopathy?

A

Amyloidosis, Sarcoidosis, Hemochromatosis, Scleroderma, Chemotherapy, or Radiation therapy

170
Q

What are the clinical features of restrictive cardiomyopathy?

A

Dyspnea and exercise intolerance

171
Q

How is restrictive cardiomyopathy diagnosed and what are some findings with amyloidosis as the primary cause?

A

Echocardiogram shows increased RA and LA size with normal LV and RV.

In amyloidosis, myocardium appears brighter and has a sparkled appearance.

172
Q

What is diagnostic of restrictive cardiomyopathy?

A

Endomyocardial biopsy

173
Q

What is the treatment for the following causes of restrictive cardiomyopathy?

Hemochromotosis:
Sarcoidosis:
Amyloidosis:

A

Hemochromotosis: Phlebotomy or deferoxamine
Sarcoidosis: Glucocorticoids
Amyloidosis: No treatment available

174
Q

What is the cause of myocarditis?

A

Inflammation of the myocardium with causes including:

Viruses (Coxsackie, Parvovirus B19)
Bacteria (Rheumatic fever, group A strep, Lyme)
SLE, 
medications, 
idopathic
175
Q

How does myocarditis present?

A

Chest pain, fatigue, fever, pericarditis

176
Q

How is myocarditis treated?

A

Treatment is supportive

177
Q

How is myocarditis diagnosed?

A

Look for elevation of cardiac enzymes and ESR

178
Q

How does myocarditis differ from acute pericarditis?

A

Myocarditis is inflammation of the myocardium. Pericarditis is inflammation of the pericardium

179
Q

What are some causes of acute pericarditis?

A 
Idiopathic (post-viral)
Acute MI (first 24 hours after MI)
Uremia
After MI (Dressler syndrome)
Radiation
180
Q

What is the prognosis of acute pericarditis?

A

Majority of patients recover within 1-3 weeks. A minority of patients have a prolonged course of recurrent symptoms

181
Q

What are some complications of acute pericarditis?

A
  1. Pericardial effusion

2. Cardiac tamponade

182
Q

Describe the symptoms of acute pericarditis?

A

Pain is pleuritic, may radiate to the trapezius ridge and neck, Pain is POSITIONAL

Fever and leukocytosis may be present

Pericardial friction rub may or may not be present

183
Q

Describe what relieves acute pericarditis pain and what aggravates it.

A

It is aggravated by lying supine, coughing, swallowing, and deep inspiration. Pain is relieved by sitting up and leaning forward.

184
Q

Describe pericardial friction rub?

A

Scratching high-pitched sound with up to three components.

185
Q

What does EKG show in acute pericarditis?

A

Diffuse ST segment elevation and PR depressions

186
Q

Besides EKG, what other test should be done in patients with acute pericarditis?

A

Echocardiogram (to see if patient has a pericardial effusion)

187
Q

How is pericarditis managed?

A

Give the patient NSAIDs (colchicine). Give glucocorticoids if case is severe, but try to avoid if possible.

188
Q

Describe the pathological cause of constrictive pericarditis?

A

Fibrous scarring of the pericardium leads to rigidity and thickening of the pericardium with obliteration of the pericardial cavity

189
Q

Describe how constrictive pericarditis affects the normal function of the heart?

A

A fibrotic and rigid pericardium restricts the diastolic filling of the heart. In late diastole, ventricle filling is halted abruptly resulting in a pericardial knock

190
Q

What are the different physical exam signs between acute pericarditis and constrictive pericarditis?

A

In acute pericarditis, patients may have a pericardial friction rub which is a scratching high pitched sound.

In constrictive pericarditis, patients may have a pericardial knock, which corresponds to abrupt cessation of ventricular filling

191
Q

What are the clinical features of constrictive pericarditis?

A

Patients have clinical signs of cirrhosis (ascites, hepatomegaly) and distended neck veins.

Patients may or may not have signs of pericardial knock

192
Q

What does cardiac catheterization show in constrictive pericarditis?

A

Elevated and equal diastolic pressures in all chambers of the heart.

193
Q

What is the test of choice for constrictive pericarditis and what does it show?

A

Echocardiogram shows a sharp halt in ventricular diastolic filling.

194
Q

What physical exam signs can help in diagnosing pericardial effusion?

A

All physical exam signs are extremely nonspecific and often do not aid in diagnosis

195
Q

What test is the best test to evaluate for pericardial effsuion and cardiac tamponade?

A

Echocardiogram

196
Q

What is the least amount of fluid that needs to be in the pericardium for it to be detected by a CXR?

A

Fluid has to be greater than 250 ml

197
Q

What is the least amount of fluid that needs to be in the pericardium for it to be detected by an Echo?

A

Fluid has to be greater than 25 ml

198
Q

What does a pericardial effusion fluid analysis help with?

A

Identifying the cause of the fluid.

This looks for protein, glucose content, cell count and differential, cytology, specific gravity, hematocrit, gram stain, acid-fast stains, fungal smear, cultures, LDH content

199
Q

What is important in causing a cardiac tamponade?

A

It is the rate of fluid accumulation in the pericardial sac, not the amount.

200
Q

What is beck’s triad for cardiac tamponade?

A

Hypotension

Muffled heart sounds

JVD

201
Q

What is pulsus paradoxus and what clinical syndrome shows this finding?

A

Pulsus paradoxus is exaggerated decrease in arterial pressure during inspiration (> 10 mm Hg drop) and it is seen in cardiac tamponade

202
Q

What is electrical alternans and what clinical syndrome shows this finding?

A

Alternate beat variation in the direction of EKG waveforms seen in cardiac tamponade because of pendular swinging of the heart within the pericardial sac

203
Q

How is cardiac tamponade treated?

A

Pericardiocentesis followed by surgery if the cause is bleeding

204
Q

How is cardiac tamponade treated if the cause is renal failure?

A

Dialysis works a lot better than pericardiocentesis

205
Q

What is the difference between acute and subacute endocarditis?

A

Acute endocarditis occurs on a normal heart valve and is caused by more virulent bacteria. Subacute endocarditis occurs on damaged heart valves and is caused by less virulent organisms.

206
Q

What is the most common cause of acute endocarditis?

A

S. aureus

207
Q

What is the most common cause of subacute endocarditis? (2)

A

Streptococcus viridans and enterococcus

208
Q

How long does acute endocarditis take to kill someone if it is untreated? What about untreated subacute endocarditis?

A

Untreated acute endocarditis is fatal in less than 6 weeks.

Untreated subacute endocarditis takes much longer than 6 weeks to be fatal.

209
Q

What is the most common causes of native value endocarditis?

A
  1. S. viridans (most common in native valves)
  2. S. aureus, S. epidermidis, and Enterococci
  3. HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella)
210
Q

What is the most common cause of prosthetic value endocarditis?

A

Staphylococci are more common within 60 days of surgery (S. epi more common than S. aureus)

Streptococci are . most common cause of late-onset endocarditis; symptoms appear 60 days after surgery.

211
Q

What is the most common cause of endocarditis in IV drug users and what side of the heart does it affect?

A

S. aureus and it affects the right side of the heart.

212
Q

When should endocarditis be suspected in a patient?

A

Always suspect endocarditis in a patient with a new heart murmur and unexplained fever or bacteremia.

213
Q

True or false, untreated endocarditis is almost always fatal?

A

True

214
Q

What criteria is used to diagnose endocarditis?

A

Duke clinical criteria

215
Q

How is endocarditis treated?

A

Parenteral antibiotics based on culture results for 4-6 weeks.

216
Q

How is endocarditis managed if the patient does not have culture results?

A

Penicillin plus aminoglycoside

217
Q

When should a patient have antibiotic prophylaxis for endocarditis?

A

Patient must have a qualifying cardiac indication AND procedure to warrant antibiotic prophylaxis

218
Q

What are qualifying cardiac indications for endocarditis prophylaxis? (3)

A
  1. Prosthetic values
  2. History of infective endocarditis
  3. Congenital heart disease
219
Q

What are qualifying procedures for endocarditis prophylaxis?

A
  1. Procedure involving biopsy or incision of respiratory mucosa.
  2. Procedures involving infected skin or musculoskeletal tissue.
  3. Dental procedures involving manipulation of gingival mucosa or teeth bleeding
220
Q

What type of endocarditis affects patients with SLE?

A

Libman-sacks endocarditis aka Nonbacterial verrucous endocarditis

221
Q

What type of endocarditis affects cancer patients?

A

Cancer patients get non-bacterial thrombotic endocarditis which is made up of sterile deposits of fibrin and platelets. These may embolize to the brain or the periphery.

222
Q

Define hypertensive emergency?

A

Systolic BP > 220 and/or diastolic BP > 120 in addition to end-organ damage (immediate treatment is indicated)

223
Q

Define hypertensive urgency?

A

Systolic BP > 220 and/or diastolic BP> 120 without end-organ damage.

224
Q

What organs should you check in hypertensive emergency?

A
  1. Eyes: Papilledema
  2. CNS: Altered mental status, intracranial hemorrhage, hypertensive encephalopathy
  3. Kidneys: Renal failure or hematuria
  4. Heart: USA, MI, CHF with pulmonary edema, aortic dissection
  5. Lungs: Pulmonary edema
225
Q

How are hypertensive emergencies treated?

A

If patient has hypertensive encephalopathy or if diastolic blood pressure is greater than 130, give the patient IV hydralazine, IV nitroprusside,

If the patient are in less immediate danger, give oral captopril, clonidine, labetalol (pregnant women)

226
Q

How are hypertensive urgencies treated?

A

Treated using oral agents such as captopril, clonidine, labetalol

227
Q

What are some predisposing factors for aortic dissection?

A
  1. Long-standing systemic hypertension
  2. Cocaine use
  3. Connective tissue diseases such as Marfan and Ehlers-Danos syndrome
228
Q

What are the two types of Stanford classifications of aortic dissections?

A

Type A (proximal) - ANYTHING that involves the ascending aorta (including retrograde extension from descending aorta)

Type B (distal) - distal to take-off of the subclavian artery

229
Q

Describe the pain from aortic dissections?

A

Severe, tearing, ripping, stabbing pain that is abrupt in onset either in the anterior chest or back of the chest

Anterior chest pain is more common in Type A dissection

Posterior chest pain is more common in Type B dissection

230
Q

Describe one key physical exam sign of aortic dissection?

A

Pulse or BP asymmetry between limbs

231
Q

What is the best test for a suspected aortic dissection?

A

TEE (can be done in unstable patients)

232
Q

What is seen on CXR in a patient with aortic dissection?

A

Widened mediastinum

233
Q

How are Type A and Type B aortic dissections treated?

A

Type A is treated by first using IV medications (beta blockers to lower heart rate and nitroprusside to lower systolic blood pressure) to lower systolic blood pressure to below 120 mm Hg.

Then surgery is done

Type B is treated by medical management (pain control and IV beta blockers to lower blood pressure). Unrelenting symptoms may require surgical treatment.

234
Q

Where do most abdominal aortic aneurysms occur?

A

Between the renal arteries and iliac bifurcation

235
Q

What increases the risk for abdominal aortic aneurysms?

A

Age (rare before 50 years old, most are diagnosed at 65-70 years old).

236
Q

What risk factor predisposes to abdominal aortic aneurysm?

A

Atherosclerotic weakening of the aortic wall. Other factors include trauma, HTN, vasculitis, SMOKING, and connective tissue disorders.

237
Q

What are clinical features of abdominal aortic aneurysms?

A
  1. Pulsatile mass on abdominal exam.
  2. Sense of “fullness”
  3. Usually asymptomatic and discovered on abdominal examination or a radiological study for another reason
238
Q

What are the signs of impending rupture of an abdominal aortic aneurysm?

A

Sudden onset of severe pain in the back or lower abdomen that radiates to the legs, groin, buttocks

Grey turner sign (ecchymoses on back and flanks), Cullen sign (ecchymosis around umbilicus)

239
Q

What is the triad for abdominal aortic aneurysm rupture?

A

Abdominal pain, hypotension, and palpable pulsatile abdominal mass - emergent laparotomy

240
Q

How are abdominal aortic aneurysms detected?

A

US or CT

US better because just as sensitive as CT and no radiation.

241
Q

What dictates when AAA should be treated?

A

If abdominal aneurysm is > 5 cm or symptomatic, surgical resection with synthetic graft placement is recommended.

If it is < 5 cm imaging is recommended as follow up. However, size does not dictate if a AAA will bleed.

Patient may be likely to die from other medical issues before a AAA kills them.

242
Q

What is peripheral vascular disease?

A

Occlusive atherosclerotic disease of the lower extremities.

243
Q

What are the three most common sites of PAD occlusion?

A
  1. Superficial femoral artery
  2. Popliteal artery
  3. Aortoiliac occlusive disease
244
Q

What are some risk factors for PAD?

A
  1. Smoking (most important)
  2. CAD, Hyperlipidemia, HTN
  3. Diabetes
245
Q

How should patients with PAD be evaluated?

A
  1. Evaluate cardiovascular system (HTN, carotid bruits, murmurs, AAA)
  2. Check arterial pulses
  3. Inspect lower extremities for color change, ulcers, muscle atrophy, hair loss, thickened toenails
  4. Consider the following tests: CBC, EKG, renal function tests, and coagulation profile
246
Q

What indicates prognosis of PAD?

A

Intermittent claudication patients have a prognosis that is generally good.

Patients with pain at rest or ischemic ulcers have the worst prognosis (especially smokers and diabetics)

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