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EOR Exam - Family Medicine > Cardiovascular Part 1 > Flashcards

Cardiovascular Part 1 Flashcards

1
Q

Summarize the typical signs and symptoms of angina.

A

Non-provokable mid-strenal chest pressure/squeezing, poorly localized and radiating to jaw, arms, back, neck, often brought on by exertion.

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2
Q

Describe some associated symptoms of angina.

A

dyspnea, nausea, diaphoresis, numbness, fatigue

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3
Q

Differentiate stable angina from unstable angina.

A

Stable angina is exacerbated by physical activity and relieved by rest and/or up to 3 doses NTG. Unstable may begin at rest and is not relieved by rest or NTG.

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4
Q

Describe Prinzmetal angina.

A

vasospasm at rest with preservation of exercise capacity.

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5
Q

Describe ECG findings associated with angina.

A

Horizontal or downsloping ST depression, non-specific T wave changes, poor R wave progression

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6
Q

Differentiate a physical stress test from a pharmacological stress test and state which is more beneficial.

A

Physical is usually done on a treadmill and is the most useful and cost effective. STD > 1mm is positive. Pharmacological uses adenosine or dipyridamole with injection of a radioactive tracer that produces computer images of the heart. Used in patients that can’t tolerate exercise.

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7
Q

What is the gold standard test for evaluation of angina?

A

Coronary angiography (cath) –> costly and invasive.

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8
Q

List risk factors for angina

A

CAD, HTN, DM, age > 65, family history, obesity, hyperlipidemia, smoking, alcohol, women > men.

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9
Q

Define metabolic syndrome.

A

3+ of: abdominal obesity, triglycerides > 150, HDL < 40 (men) or < 50 (women), HTN, fasting BGL > 110

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10
Q

Describe the drug of choice for acute management of angina.

A

NTG: decrease preload (mycardial demand) and decreases coronary vasospasm.

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11
Q

List the AEs and contraindications (CI) of NTG.

A

AE: HA, flushing, hypotension, peripheral edema
CI: SBP < 90, RV infarction, PDE-5 inhibitor use

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12
Q

Describe the daily administration of a long acting nitrate.

A

Should include an 8-10 hour treatment free interval to avoid development of tolerance.

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13
Q

List and describe 6 other medications used in the management of angina.

A

Beta-blockers (BBs): prolong filling time and dec myocardial oxygen demand - 1st line for chronic angina
ACEIs: most useful in patient’s with heart failure
CCBs: used when BBs are contraindicated or max’d
Platelet inhibitors (ASA/plavix)): reduce possibility of infarction
Ranolazine: reduces flow of Ca into cells (similar action to CCBs and BBs)
Statins: for patients with increased LDL

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14
Q

Describe the pathophysiology of angina.

A

Insufficient myocardial oxygen supply s/p narrowing (constriction or atherosclerosis) of coronary arteries.

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15
Q

Describe some signs or symptoms that make an arrhythmia unstable.

A

chest pain, dyspnea, altered mental status, hypotension, cool/pale skin, weak pulses.

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16
Q

Differentiate broadly the management of stable vs unstable arrhythmia.

A

Stable: medications
Unstable: electricity (cardioversion or pacing)

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17
Q

List treatment options for sinus bradycardia.

A

Atropine, epinephrine, dopamine, transcutaneous or transvenous pacing.

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18
Q

List some common causes of sinus tachycardia.

A

exercise, emotion, pain, fever, shock, anemia, thyrotoxicosis, heart failure, drugs

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19
Q

What heart rate cut-off generally defines SVT?

A

> 150

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20
Q

What is the most common cause of a regular, narrow complex SVT?

A

AV nodal re-entry

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21
Q

List treatment options for SVT.

A 
If sinus tach, treat underlying cause.
Synchronized cardioversion if unstable.
Valsalva/carotid sinus massage.
Meds: adenosine, amiodarone, CCB, BB, procainamide.
Catheter ablation.
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22
Q

Name and describe the most common chronic arrhythmia.

A

Atrial Fibrillation - characterized by irregularly irregular narrow QRS complexes and no discernible p waves.

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23
Q

What pathology can result from atrial fibrillation?

A

Decreased cardiac output and embolic events.

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24
Q

What is meant by the term “holiday heart”?

A

Atrial fibrillation brought on by excessive alcohol use.

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25
Q

Differentiate ongoing medical management of a-fib in patients with heart failure from those without.

A

HF: digoxin, amiodarone, dronedarone

No HF: metoprolol, esmolol, diltiazem, verapamil

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26
Q

What is an important consideration when determining treatment of a-fib with rapid ventricular response?

A

Ensure anti-coagulation - may consider synchronized cardioversion if unstable.

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27
Q

Describe atrial flutter.

A

Typically regular QRS complexes with saw tooth p wave pattern.

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28
Q

Describe treatment options for atrial flutter.

A

Unstable: synchronized cardioversion at 50J
Stable: anticoagulants and rate control (BB/CCB)
Sustained/recurrent: catheter ablation
Dofetilide (class III) if anti-arrhythmic therapy is chosen

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29
Q

Describe premature ventricular contractions (PVCs).

A

Early, wide and bizarre QRS complexes with no p wave. Common and benign but more frequent with myocardial irritability (ischemia or electrolyte disturbance).

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30
Q

Describe ventricular tachycardia.

A

3+ consecutive PVCs. May be stable, unstable, or pulseless. Frequent complication of acute MI and dilated cardiomyopathy.

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31
Q

Describe the treatment of stable, unstable, and pulseless ventricular tachycardia.

A

Stable: amiodarone, lidocaine, procainamide
Unstable: synchronized cardioversion
Pulseless: defibrillation and CPR

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32
Q

Describe torsades de pointes.

A

Polymorphic V-Tach whose QRSs twist around the baseline. Results from hypoMag, hypoK, or prolonged QT.

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33
Q

Describe treatment for torsades de pointes.

A

Mag, d/c causative med, correct electrolyte abnormality.

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34
Q

Describe Brugada Syndrome.

A

Congenital abnormality of the heart’s conduction system that leads to syncope and sudden cardiac arrest. May require placement of ICD.

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35
Q

Describe sick sinus syndrome and state the definitive treatment.

A

sinus brady, sinus pause, sinus arrest, or episodes of alternating brady/tachy usually found in elderly. Definitive treatment is permanent pacemaker.

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36
Q

Describe the four types of AV Blocks.

A

1: prolonged p-r with no extra p waves.
2-I: progressively lengthening p-r leading to a non-conducted p wave.
2-II: intermittently non-conducted p-waves
3: complete dissociation between p waves and QRSs

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37
Q

Describe the treatment of AV blocks.

A

If symptomatic and unstable, may consider atropine but transcutaneous or transvenous pacing is often required. Permanent pacing is the definitive treatment.

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38
Q

Define CHF.

A

Inability of the heart to pump sufficient blood to meet the metabolic needs of the body at normal filling pressure.

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39
Q

What is the most common cause of heart failure?

A

Coronary artery disease

40
Q

Describe the respiratory sequelae of left sided heart failure.

A

Fluid back up from the LV leads to increased pulmonary venous pressure causing fluid to leak into the alveoli. CHF = most common cause of transudatove pleural effusion.

41
Q

Describe common signs and symptoms associated with left heart failure.

A

exertional dyspnea, orthopnea, PND, cough, fatigue, rales, gallops, HTN, tachycardia, cyanosis, S3 (systolic) and S4 (diastolic) heart sounds, diaphoresis, cold and pale skin, nocturia.

42
Q

Describe the pathophysiology and signs and symptoms of right heart failure.

A

Increased systemic venous pressure leads to pitting edema in legs, JVD, ascites, anorexia, hepatosplenomegaly, nocturia.

43
Q

What is the most common cause of right heart failure?

A

Left heart failure

44
Q

Differentiate heart failure with preserved ejection fraction (HFpEF) from heart failure with reduced ejection fraction (HFrEF).

A

HFpEF: concentric LVH shrinks chamber size leading to diastolic dysfunction and S4 gallop.
HFrEF: eccentric LVH leading to enlarged chamber and weakened LV myocardium with systolic dysfunction and S3 gallop.

45
Q

Describe the four classes of heart failure as defined by limitations in daily activity.

A

I: ordinary activity does not cause fatigue, dyspnea, or anginal pain.
II: slight limitation in physical activity.
III: marked limitation of physical activity - less than ordinary activity causes symptoms.
IV: unable to perform any physical activity without symptoms and symptoms may be present at rest.

46
Q

List chest x-ray findings associated with CHF.

A

kerley B-lines, bat wing pattern, cephalization of vessels, perihilar congestion, peribronchial cuffing, cardiomegaly, pleural effusion.

47
Q

What comorbidities caused by CHF may be found on lab studies?

A

Anemia, renal insufficiency, elevated liver enzymes, hypoNa, hyperK (hypoK if on diuretics)

48
Q

State the ECG changes commonly found in CHF.

A

Low voltage, arrhythmia, IV conduction deficits, LVH

49
Q

What is the most useful diagnostic study in assessing for CHF and why?

A

Echo because it can assess size and function of the chambers. IE, valve abnormalities, pericardial effusion, shunting, wall abnormalities, and EF.

50
Q

What is the most important diagnostic and prognostic indicator of CHF?

A

election fraction

51
Q

Define a normal ejection fraction and differentiate different types of heart failure based on EF.

A

Normal EF = 55% - 60%
HFrEF (systolic): thin vent walls with dilated LV chamber and S3 present
HFpEF (diastolic): thick vent walls, small LV chamber, and S4 present

52
Q

Describe the serum lab BNP and state how it is useful in CHF.

A

Hormone released from cardiac muscle in response to stretch/stress. Its inteded effect is to inc Na/water secretion and vasodilate through dec RAAS activation. BNP > 100 indicates CHF is likely.

53
Q

What comorbidities affect BNP and how is this clinically relevant?

A

Inc BNP: DM, ACS, renal failure
Dec BNP: obesity
More useful to trend individual patient’s BNP than to compare results among patients.

54
Q

How is BNP most commonly used in the emergent setting?

A

To differentiate dyspnea caused by CHF from other causes of dyspnea. BNP < 100 virtually excludes HF as cause of acute dyspnea.

55
Q

Aside from echo and CXR, what other two imaging studies may be useful in CHF?

A

Stress imaging/radionuclide angiography to assess cause and severity.
Cath to assess for CAD and determine CO

56
Q

What non-pharmacological interventions are indicated in the management of CHF?

A

Aerobic exercise, low Na diet (< 2g/day and < 2 L/day fluid intake), smoke cessation, alcohol cessation, stress reduction.

57
Q

What medications are considered first line in the initial treatment of CHF?

A

ACEIs and diuretics

58
Q

Describe the physiologic benefits of prescribing an ACEI in CHF.

A

Shown to dec mortality and hospitalization. Directly reverses pathology by dec renin and sympathetic stimulation which decreases remodeling and fibrosis.

59
Q

What are the AEs and CIs associated with ACEIs?

A

AE: first dose HypoTN, renal insufficiency, hyperK, cough, angioedema
CIs: hypotension and pregnancy

60
Q

If a patient cannot tolerate ACEIs, what medication is an alternative?

A

ARBs - losartan, vlasartan, etc.

61
Q

How have BBs been show to be helpful in CHF and in what HF patients are they not indicated?

A

Decrease mortality through increased EF and decreased ventricular size. Do not use in decompensated CHF.

62
Q

Describe the effects of hydralazine and NTG and when they might be used in CHF.

A

Hydralazine decreases afterload
NTG decreases preload
Used in combo when patients cannot tolerate ACEI or BB. May also be used in pregnancy and shown to work better in African Americans.

63
Q

What other class of medications may be used in combination with ARBs or BBs to vasodilate?

A

Aldosterone receptor antagonists.

64
Q

What is the most common diuretic used in the treatment of CHF and what are its physiologic effects on electrolytes and its AEs?

A

Loop diuretics - inhibit water reabsorption at loop.
Inc secretion of Cl, Na, K
AEs: hyperglycemia, hyperuricemia, sulfa allergies

65
Q

When are K sparing diuretics most commonly used and what are their AEs and CIs?

A

Weak diuretic - used in combo woth loop diuretics.
AEs: hyperK, gynecomastia
CI: renal failure

66
Q

What are the AEs associated with thiazide diuretics?

A

hypoNa, hyperuricemia, hyperglycemia, sulfa allergy

67
Q

What are the physiologic effects of digoxin and how is it used in CHF?

A

Positive inotrope, negative chronotrope

Used short term in severe acute CHF and in patients with A-fib –> decreases hospitalization but no mortality benefit.

68
Q

What are the AEs of digoxin?

A

narrow therapeutic index, arrhythmias, seizures, dizziness, anorexia, N/V/D, gynecomastia, visual disturbances.

69
Q

Which CCB is most likely to be used in CHF and in what circumstance?

A

Amlodipine –> in CHF s/p angina or HTN

Most useful in diastolic HF (HFpEF)

70
Q

Describe the MOA of Ivabradine and how is it useful in CHF?

A

Blocks channel responsible for pacemaker current in SA node –> dec HR and prolongs diastole. Has been shown to slow progression of CHF.

71
Q

What is placement of an ICD or biventricular pacer indicated in CHF?

A

ICD: when EF < 35%
Pacer: when QRS is prolonged

72
Q

What medications have been shown to decrease mortality in CHF?

A

ACEIs, ARBs, BBs, NTG + hydralazine, spironolactone.

73
Q

What is the initial out-patient regimen for treatment of CHF?

A

ACEI and diuretic –> may add BB

74
Q

What are the three pathophysiologic changes that initially occur in congestive heart failure?

A
  1. Increased afterload
  2. Increased preload
  3. Decreased contractility
75
Q

Acute decompensated heart failure always includes one of three broad categories of symptoms. Name the three general findings.

A
  1. Signs of pulmonary edema
  2. Sympathetic activation
  3. Signs of pulmonary congestion on CXR
76
Q

CHF is characterized by abnormal retention of which two substances?

A

Water and sodium

77
Q

Define atherosclerosis.

A

A chronic inflammatory response to lipid accumulation in the arterial wall.

78
Q

Differentiate the pathophysiology of silent atherosclerosis from the development of CAD.

A

Intimal plaques are often present for years without producing symptoms. Fissuring or erosion of the plaque leads to platelet activation and thrombus formation which can occlude the vessel.

79
Q

T/F: Death from CAD has been steadily rising over the past several decades.

A

False: While CAD remains the #1 killer in the US and worldwide, the mortality rate has declined each year since 1968.

80
Q

What organs are mostly affected by atherosclerosis?

A

Heart (CHF, MI), brain (stroke, vascular dementia), peripheral vasculature (especially arms and legs)

81
Q

List 5 risk factors of CAD identified in the landmark Framingham Heart Study.

A
  1. Smoking
  2. Diabetes
  3. Dyslipidemia (inc LDL and dec HDL)
  4. HTN
  5. Family Hx in a male < 55 or a female < 65
82
Q

Are men or women more likely to develop CAD?

A

Men are 4 x more likely at younger age. By age 70, the ratio is 1:1.

83
Q

Which serum lab test gives the best indication of inflammation secondary to CAD?

A

C-reactive protein (CRP)

84
Q

How should a patient at risk of CAD be counseled on reducing their risk (modifiable risk factors)?

A

Smoke cessation, decrease LDL and triglycerides, increase HDL through exercise, control BP, control blood glucose, BMI < 25, waist circumference < 40 (< 35 in women), low fat and high fiber/veg/whole grain diet, start exercising.

85
Q

What pharmacologic agent is the cornerstone in primary prevention of CAD and why?

A

Platelet inhibitors (ASA) because they are cheap and available.

86
Q

What classes of medications are often prescribe as secondary prevention of CAD?

A

Beta blockers, ACEIs, Statins, NTG - relieves symptoms but does not prevent.

87
Q

Differentiate primary prevention from secondary prevention from tertiary prevention.

A

1: Stop someone from getting a disease
2: Detect a disease and prevent it from getting worse
3: Improve quality of life and reduce symptoms of a disease you already have.

88
Q

Describe the basic pathophysiologic process of LDL developing into a plaque.

A

LDL accumulates under the endothelial cell layer of the intima –> LDL particles taken up by macrophages and become foam cells –> fatty streak develops –> fibroblasts from collagen cap over lipid pool.

89
Q

Differentiate a stable plaque from an unstable plaque.

A

Stable: thick and difficult to rupture –> may narrow vessel.
Unstable: fissures develop in endothelium exposing lipids to circulation which triggers a thrombus formation.

90
Q

Describe foam cells and state the age at which they begin to form.

A

Foam cells are macrophages that chew up lipids. Once they die, they remain in place and release cytokines that attract more macrophages to the area. This process begins at about age 10.

91
Q

Describe the heart murmur/heart sounds associated with: aortic stenosis, mitral regurgitation, aortic regurgitation, mitral stenosis

A

AS: crescendo-decrescendo systolic murmur, weak S2
MR: holosystolic murmur, mid-systolic click, wide S2 split, S3
AR: doastolic decrescendo murmur, late diastolic rumble
MS: loud S1, opening snap after S2, diastolic rumble

92
Q

Which valve disease is most likely to result in syncope?

A

Aortic stenosis

93
Q

Which valve is most likely to be affected by rheumatic heart disease?

A

Mitral

94
Q

Differentiate the pharmacological management of mitral stenosis from regurgitation.

A

MS: Diuretics (dec preload) anti-arrhythmics for A-Fib
MR: Vasodilators, prophylactic anticoagulation

95
Q

Differentiate S/S of pulmonic stenosis from tricuspid regurgitation.

A

TR: holosystolic murmur, JVD
PS: midsystolic crescendo-decrescendo murmur, early pulmonic ejection sound

EOR Exam - Family Medicine (15 decks)

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