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A Comprehensive Review for the Certification and Recertification Examination for Physician Asistants > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Hypovolemic shock is caused by what?

A

Hemorrhage, loss of plasma, or loss of fluid and electrolytes, resulting in decreased intravascular volume. This may be caused by obvious loss or by “third-space” sequestration

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2
Q

Causes of cardiogenic shock

A

MI, dysrhythmias, heart failure, defects in the valves or septum, hypertension, myocarditis, cardiac contusion, rupture of the ventricular septum, or cardiomyopathies

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3
Q

Causes of obstructive shock

A

Tension pneumothorax, pericardial tamponade, obstructive valvular disease, and pulmonary problems, including massive pulmonary embolism

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4
Q

Distributive shock includes what?

A

Septic shock, systemic inflammatory response syndrome (SIRS), anaphylaxis, and neurogenic shock

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5
Q

Septic shock has a high mortality rate (30-87%). It is most often associated with what?

A

Gram-negative sepsis

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6
Q

Causes of neurogenic shock

A

Spinal cord injury or adverse effects of spinal or epidural anesthesia

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7
Q

Definition of postural hypotension

A

Greater than 20 mm Hg drop in systolic BP or a drop greater than 10 mm Hg in diastolic BP between supine and sitting and/or standing measurements

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8
Q

In postural hypotension, if there is a rise in pulse of more than 15 bpm, what is the probable cause?

A

Depleted circulating blood volume

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9
Q

In postural hypotension, if there is no change in the pulse rate, what causes should be considered?

A

Medications, central autonomic nervous system disease (e.g., Parkinson disease or Shy-Drager syndrome), or peripheral neuropathies (e.g., diabetic autonomic neuropathy)

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10
Q

New York Heart Association Functional Classification of Heart Disease: Class I

A

No limitation of physical activity; ordinary physical activity does not cause undue fatigue, dyspnea, or anginal pain

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11
Q

New York Heart Association Functional Classification of Heart Disease: Class II

A

Slight limitation of physical activity; ordinary physical activity results in symptoms

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12
Q

New York Heart Association Functional Classification of Heart Disease: Class III

A

Marked limitation of physical activity; comfortable at rest, but less than ordinary activity causes symptoms

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13
Q

New York Heart Association Functional Classification of Heart Disease: Class IV

A

Unable to engage in any physical activity without discomfort; symptoms may be present even at rest

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14
Q

End-organ damage in untreated HTN includes what

A

Heart failure, renal failure, stroke, dementia, aortic dissection, artherosclerosis, and retinal hemorrhage

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15
Q

When is a two-drug regimen started in hypertension?

A

Stage 2 HTN (≥160 mm Hg systolic or ≥100 mm Hg diastolic)

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16
Q

Diuretics help reduce plasma volume and chronically reduce peripheral resistance. Thiazide diuretics are normally the DOC. When would loop diuretics be used?

A

In those with renal dysfunction and when close electrolyte monitoring is assured

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17
Q

Beta blockers tend to be more effective at treating HTN in what patients?

A

Whites

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18
Q

Beta blockers must be used with caution with what patients?

A

In those with pulmonary disease or diabetes

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19
Q

ACEI I becoming increasingly the treatment of choice for what circumstances of HTN?

A
  • For mild to moderate HTN
  • For whites
  • When diuretics are insufficient
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20
Q

Calcium channel blockers cause peripheral vasodilation. They are preferable in what type of patients?

A

In African Americans and elderly patients

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21
Q

What is Aliskiren?

A

It is a renin inhibitor used for refractory cases of HTN or special situations; it is approved for mono- or combination therapy

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22
Q

What are the preferred agents for hypertensive urgencies and emergencies?

A

Sodium nitroprusside and, if myocardial ischemia is present, nitroglycerin or a beta blocker

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23
Q

Other acceptable agents used in hypertensive urgencies and emergencies?

A

Nicardipine, enalaprilat, diazoxide, trimethaphan, and loop diuretics

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24
Q

Aortic dissection usually call for what treatment?

A

Nitroprusside and a beta blocker, usually labetalol or emolol, and urgent surgery

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25
Q

What is the preferred medication for HTN during pregnancy?

A

Hydralazine

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26
Q

What oral agents are used for less severe HTN?

A

Clonidine, captopril, and nifedipine

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27
Q

Metabolic syndrome is a major contributor to coronary heart disease and at least three of the criteria have to be met to diagnose this. What is the criteria?

A
  1. Abdominal obesity
  2. Triglycerides greater than 150 mg/dL
  3. HDL 110 mg/dL
  4. HTN
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28
Q

Patients are considered at high risk for ischemic heart disease if they have which medical conditions?

A

Cerebrovascular disease, peripheral arterial disease, abdominal aortic aneurysm, chronic or end-stage renal disease or diabetes

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29
Q

Prinzmetal (or variant) angina is caused by what?

A

Vasospasm at rest, with preservation of physical activity. These are typically younger patients.

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30
Q

What are the three common patterns of presentation of unstable angina (UA)?

A
  1. Angina at rest
  2. New onset of angina symptoms
  3. Increasing pattern of pain in previously stable patients
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31
Q

The American Heart Association (AHA) report what as the most common presentation of unstable angina?

A

Angina at rest

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32
Q

When is unstable angina suspected?

A

When the pain is less responsive to NTG, lasts longer, and occurs at rest or with less exertion than previous episodes of angina

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33
Q

Stable angina pectoris usually lasts how long?

A

Less than 3 minutes

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34
Q

What ECG changes during an angina attack is among the most sensitive clinical signs?

A

Horizontal or downsloping ST-segment depression on the ECG

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35
Q

What is considered to be a positive test in a stress test?

A

ST-segment depression of 1 mm (0.1 mV)

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36
Q

What is the definitive diagnostic procedure for ischemic heart disease?

A

Coronary angiography

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37
Q

What medication is the first-line therapy for chronic angina?

A

Beta blockers

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38
Q

What antiplatelet medications should be used in all patients with ischemic heart disease unless a contraindication exists?

A

ASA, Clopidogrel (Plavix)

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39
Q

What does Ranolazine (Ranexa) do for angina?

A

It prolongs exercise duration and time to angina and is useful for symptom control

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40
Q

What is the usual cause of death in MI patients?

A

Ventricular fibrillation

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41
Q

What are some atypical symptoms that elderly patients may present with?

A

Altered mental status, generalized weakness, stroke, or syncope

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42
Q

Dressler syndrome (post-MI syndrome) consists of what?

A

Pericarditis, fever, leukocytosis, and pericardial or pleural effusion. Usually comes 1-2 weeks post-MI

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43
Q

A patient who presents with transient ST-segment changes of ≥0.5 mm that develop during a symptomatic episode and resolve when the patient becomes asymptomatic is highly suggestive of what?

A

Acute ischemia and CAD

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44
Q

What on an ECG is highly suspicious for a new MI?

A

New left bundle branch block

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45
Q

Inferior ECG leads

A

II, III, aVF

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46
Q

Posterior ECG leads

A

V1-V2

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47
Q

Anteroseptal ECG leads

A

V1-V2

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48
Q

Anterior ECG leads

A

V1-V3

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49
Q

Anterolateral ECG leads

A

V4-V6

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50
Q

What is the timing of initial elevation (in hours) for myoglobin, cardiac troponin I, cardiac troponin T and CK-MB?

A

Myoglobin: 1-4 hours
Cardiac troponin I: 3-12 hours
Cardiac troponin T: 3-12 hours
CK-MB: 3-12 hours

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51
Q

What is the peak elevation for myoglobin, cardiac troponin I, cardiac troponin T and CK-MB?

A

Myoglobin: 6-7 hours
Cardiac troponin I: 24 hours
Cardiac troponin T: 12-48 hours
CK-MB: 24 hours

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52
Q

When does myoglobin, cardiac troponin I, cardiac troponin T, and CK-MB return to normal?

A

Myoglobin: 24 hours
Cardiac troponin I: 5-10 days
Cardiac troponin T: 5-14 days
CK-MB: 48-72 hours

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53
Q

TIMI (Thrombolysis in Myocardial Infarction) is used for risk stratification in ACS patients. One point is given for certain factors. What are these factors?

A
  • Age 65 and older
  • Three or more risk factors for CAD
  • Use of ASA within the last 7 days
  • Known CAD with stenosis 50% or greater
  • More than one episode of rest angina within the last 24 hours
  • ST segment deviation
  • Elevated cardiac markers
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54
Q

What score is considered high risk when using TIMI?

A

3 or more

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55
Q

What are the most commonly used thrombolytic agents used in STEMI?

A

Alteplase, reteplase, and tenecteplase

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56
Q

Absolute contraindications to thrombolytic agents?

A

Previous hemorrhage or stroke, any stroke within the past year, known intracranial neoplasm, active internal bleeding, or suspected aortic dissection

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57
Q

Relative contraindications to thrombolytic agents?

A

Known bleeding diathesis, trauma within the past 2-4 weeks, major surgery within the past 3 weeks, prolonged or traumatic CPR, recent internal bleeding, noncompressible vascular puncture, active diabetic retinopathy, pregnancy, active PUD, current use of anticoagulants, and BP greater than 180/110

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58
Q

What are the four cyanotic congenital anomalies?

A
  1. Tetralogy of Fallot
  2. Pulmonary atresia
  3. Hypoplastic left heart syndrome
  4. Transposition of the great vessels
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59
Q

Tetralogy of Fallot consists of what?

A

Ventricular septal defect, aortic origination over the defect, right ventricular outflow obstruction, and right ventricular hypertrophy

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60
Q

Pulmonary atresia

A
  • Most often occurs with an intact ventricular septum

- The pulmonary valve is closed; an atrial septal opening and patent ductus arteriosus are present

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61
Q

Hypoplastic left heart syndrome

A

Group of defects with a small left ventricle and normally placed great vessels

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62
Q

Transposition of the great vessels

A

Most commonly a complete transposition of the aorta and pulmonary artery

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63
Q

Tetralogy of Fallot murmur

A

Crescendo-decrescendo holosystolic at LSB, radiating to back

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64
Q

Tetralogy of Fallot physical findings

A

Cyanosis, clubbing, increased RV impulse at LLSB, loud S2

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65
Q

Tetralogy of Fallot important clinical information

A

Polycythemia is usually present; tet (hypercyanotic) spells include extreme cyanosis, hyperpnea, and agitation (this is a medical emergency!!)

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66
Q

Pulmonary atresia murmur

A

Depends on presence of tricuspid regurgitation

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67
Q

Pulmonary atresia physical findings

A

Cyanosis with tachypnea at birth, tachypnea without dyspnea, hyperdynamic apical impulse, single S1 and S2

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68
Q

Pulmonary atresia important clinical information

A

Sudden onset of severe cyanosis and acidosis requires emergency treatment

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69
Q

Hypoplastic left heart syndrome murmur

A

Variable; not diagnostic

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70
Q

Hypoplastic left heart syndrome physical findings

A

Shock, early heart failure, respiratory distress, single S2; presentation varies with specific syndrome

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71
Q

Hypoplastic left heart syndrome important clinical information

A

Occurs more often in males; accounts for 1/4 of cardiac deaths before age 7

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72
Q

Transposition of the great vessels murmur

A

Systolic murmur if associated with VSD; systolic ejection murmur if with pulmonary stenosis

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73
Q

Transposition of the great vessels physical findings

A

Cyanosis in newborn is most common sign; tachypnea without respiratory distress; if large VSD, symptoms of CHF and poor feeding; single loud S2; absent LE pulses if with aortic arch obstruction

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74
Q

What are the 5 noncyanotic congenital heart anomalies?

A
  1. Atrial septal defect
  2. Ventricular septal defect
  3. Atrioventricular septal defect
  4. Patient (persistent) ductus arteriosus
  5. Coarctation of the aorta
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75
Q

Atrial septal defect

A

Opening between the right and left atria. Of the four main types, ostium secundum is the most common

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76
Q

Atrial septal defect murmur

A

Systolic ejection murmur at 2nd LICS; early to middle systolic rumble

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77
Q

Atrial septal defect physical findings

A

Failure to thrive, fatigability, RV heave, wide fixed split S2

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78
Q

Ventricular septal defect

A

May be perimembranous (most common), muscular, or outlet openings between the ventricles

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79
Q

VSD murmur

A

Systolic murmur as LLSB; others depend on severity of defect

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80
Q

VSD physical findings

A

Depends on the size of the defect - from asymptomatic to signs of CHF

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81
Q

VSD important clinical information

A

Outlet VSDs are more common in Japanese and Chinese

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82
Q

Patent ductus arteriosus

A

Failed or delayed closure of the channel bypassing the lungs, which allows placental gas exchange during the fetal state. Unlike other congenital anomalies, surgical treatment is usually not indicated as many patients respond to IV indomethacin

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83
Q

PDA murmur

A

Continuous (machinery) murmur in patients with isolated PDA

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84
Q

PDA physical findings

A

Wide pulse pressure, hyperdynamic apical pulse

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85
Q

Coarctation of the aorta

A

It involves narrowing of the proximal thoracic aorta

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86
Q

Coarctation of the aorta murmur

A

Systolic, LUSB, and left interscapular area; may be continuous

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87
Q

Coarctation of the aorta physical findings

A

Infants may present with CHF; older children may have systolic hypertension or murmur of underdeveloped lower extremities

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88
Q

Coarctation of the aorta important clinical information

A

Differences between arterial pulses and blood pressure in UE and LE pathognomonic

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89
Q

Aortic stenosis

A

Narrows the valve opening, impeding the ejection fraction of the left side of the heart.

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90
Q

What is the most common valvular disease in the U.S. and second most frequent cause for cardiac surgery?

A

Aortic stenosis

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91
Q

Aortic insufficiency (regurgitation)

A

Results in volume overloading due to the retrograde blood flow into the left ventricle

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92
Q

Mitral stenosis

A

Impedes blood flow between the left atrium and ventricle

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93
Q

Mitral insufficiency (regurgitation)

A

Allows retrograde blood flow and volume overload of the left atrium

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94
Q

Mitral valve prolapse

A

Usually is asymptomatic, but it may be associated with mitral regurgitation

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95
Q

Causes of mitral and aortic valve disorders

A

Most frequent causes are congenital defects; other causes include rheumatic heart disease, connective tissue disorders, infection, and senile degeneration

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96
Q

Which valvular disorder presents with thready carotid pulses?

A

Aortic stenosis

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97
Q

Which valvular disorder presents with bounding pulses and widened pulse pressures?

A

Aortic regurgiation

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98
Q

Aortic stenosis murmur location

A

2nd RICS

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99
Q

Aortic stenosis radiation

A

To neck and LSB

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100
Q

Aortic stenosis intensity

A

Often loud with a thrill (grades 4-6)

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101
Q

Aortic stenosis pitch/quality

A

medium pitch; harsh

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102
Q

Aortic stenosis aids to hearing

A

Patient sitting and leaning forward

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103
Q

Aortic stenosis timing

A

midsystolic

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104
Q

Aortic regurgitation murmur location

A

2nd-4th LICS

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105
Q

Aortic regurgitation radiation

A

To apex and RSB

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106
Q

Aortic regurgitation intensity

A

Grades 1-3

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107
Q

Aortic regurgitation pitch/quality

A

High pitch; blowing

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108
Q

Aortic regurgitation aids to hearing

A

Patient sitting and leaning forward; full exhalation

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109
Q

Aortic regurgitation associated findings

A

Midsystolic or Austin Flint murmur suggests large flow; arterial pulses large and bounding

110
Q

Aortic regurgitation timing

A

Systolic (soft) and diastolic decrescendo

111
Q

Mitral stenosis murmur location

A

Apex

112
Q

Mitral stenosis radiation

A

Little or none

113
Q

Mitral stenosis intensity

A

Grades 1-4

114
Q

Mitral stenosis pitch/quality

A

Low pitch

115
Q

Mitral stenosis aids to hearing

A

Patient in left lateral position; full exhalation

116
Q

Mitral stenosis associated findings

A

S1 accentuated; opening snap follows S2

117
Q

Mitral stenosis timing

A

Middiastolic

118
Q

Mitral regurgitation murmur location

A

Apex

119
Q

Mitral regurgitation radiation

A

To left axilla

120
Q

Mitral regurgitation intensity

A

Soft to loud

121
Q

Mitral regurgitation pitch/quality

A

Medium to high pitch; blowing

122
Q

Mitral regurgitation associated findings

A

S2 often decreased; apical impulse prolonged

123
Q

Mitral regurgitation timing

A

Pansystolic

124
Q

Tricuspid regurgitation murmur location

A

LLSB; holosystolic

125
Q

Tricuspid regurgitation radiation

A

To right sternum and xiphoid area

126
Q

Tricuspid regurgitation intensity

A

Variable

127
Q

Tricuspid regurgitation pitch/quality

A

Medium; blowing

128
Q

Tricuspid regurgitation aids to hearing

A

Increases slightly with inspiration

129
Q

Tricuspid regurgitation associated findings

A

JVP often elevated

130
Q

Tricuspid regurgitation timing

A

Pansystolic

131
Q

Pulmonic stenosis murmur location

A

2nd-3rd ICS; mid-systolic crescendo-decrescendo

132
Q

Pulmonic stenosis radiation

A

To left shoulder and neck

133
Q

Pulmonic stenosis intensity

A

Soft to loud, possibly associated with thrill

134
Q

Pulmonic stenosis pitch/quality

A

Medium; harsh

135
Q

Pulmonic stenosis associated findings

A

Early pulmonic ejection sound common

136
Q

Pulmonic stenosis timing

A

Systolic

137
Q

Underlying conditions in pulmonic and tricuspid disorders that cause pulmonary HTN are treated with what?

A

Arterial vasodilators (hydralazine, nitroprusside) or positive inotropric agents (amiodarone, digitalis, digoxin)

138
Q

Class Ia antiarrhythmic drugs action

A

Sodium channel blockers; depress phase 0 depolarization; slow conduction; prolong repolarization

139
Q

Class Ia antiarrhythmic drugs indications

A

Supraventricular tachycardia; V tach; prevention of V fib; symptomatic ventricular premature beats

140
Q

Class Ia antiarrhythmic drugs examples

A

Quinidine, procainamide, dispyramide, moricizine

141
Q

Class Ib antiarrhythmic drugs action

A

Shorten repolarization

142
Q

Class Ib antiarrhythmic drugs indications

A

V tach; prevention of V fib; symptomatic ventricular premature beats

143
Q

Class Ib antiarrhythmic drugs examples

A

Lidocaine, mexiletine

144
Q

Class Ic antiarrhythmic drugs action

A

Depress phase 0 repolarization; slow conduction

145
Q

Class Ic antiarrhythmic drugs indications

A

Life-threatening V tach or V fib, refractory supraventricular tachycardia

146
Q

Class Ic antiarrhythmic drugs examples

A

Flecainide, propafenone

147
Q

Class II antiarrhythmic drugs action

A

Beta blockers; slow AV conduction

148
Q

Class II antiarrhythmic drugs indications

A

Supraventricular tachycardia; may prevent ventricular fibrillation

149
Q

Class II antiarrhythmic drugs examples

A

Esmolol, propranolol, metoprolol

150
Q

Class III antiarrhythmic drugs action

A

Potassium channel blockers; prolong action potential

151
Q

Class III antiarrhythmic drugs indications

A

Refractory V tach; supraventricular tachycardia; individual agents have specific indications

152
Q

Class III antiarrhythmic drugs examples

A

Amiodarone, sotalol, dofetilide, ibutilide

153
Q

Class IV antiarrhythmic drugs action

A

Slow calcium channel blockers

154
Q

Class IV antiarrhythmic drugs indications

A

Supraventricular tachycardia

155
Q

Class IV antiarrhythmic drugs examples

A

Verapamil, diltiazem

156
Q

Class V antiarrhythmic drugs action

A

Adenosine: slows conduction time through AV node, interrupts reentry pathways; digoxin: direct action on cardiovascular system via ANS

157
Q

Class V antiarrhythmic drugs indications

A

supraventricular tachycardia

158
Q

Class V antiarrhythmic drugs examples

A

Adenosine, digoxin

159
Q

What is the holiday heart syndrome?

A

It is an arrhythmia that is caused by alcohol excess or withdrawal; most commonly it is atrial fibrillation

160
Q

Atrial flutter usually occurs in what patients?

A

In those with COPD, heart failure, ASD, or CAD

161
Q

Junctional rhythms occur in what patients?

A

In patients with normal hearts or those with myocarditis, CAD, or digitalis

162
Q

Signs and symptoms of an unstable rhythm

A

Chest pain, dyspnea, altered mental status, and hypotension

163
Q

Patients with unstable bradycardia leading to hypotension, shock, altered mental status, angina, or heart failure should be treated with what?

A

A vagolytic (i.e., atropine) or positive chronotropic (i.e., epinephrine or dopamine). Transcutaneous or transvenous pacing is often indicated and may need to be followed by permanent pacing

164
Q

Treatment of a regular, narrow-complex tachycardia in a stable patient

A
  • First, Valsalva maneuvers may be attempted.
  • The initial medication of choice is adenosine administered via rapid IV push
  • If adenosine is ineffective, beta blockers or CCB can also be used
165
Q

Treatment of a regular, narrow-complex tachycardia in an unstable patient

A

synchronized cardioversion

166
Q

Treatment of sustained or recurrent PSVT

A

Refer for catheter ablative surgery

167
Q

If a patient with significant tachycardia is stable and the QRS complex is wide, what is the treatment of choice?

A

An antiarrhythmic infusion of procainamide, amiodarone, or sotalol

168
Q

Rate control methods for afib in the presence of heart failure

A

Use of digoxin, amiodarone, or dronedarone

169
Q

Rate control methods for afib in the absence of heart failure

A

Beta blockers (i.e., metoprolol or esmolol) or CCB (diltiazem or verapamil)

170
Q

What is the primary antiarrhythmic therapy in chronic atrial flutter?

A

Dofetilide

171
Q

Brugada syndrome

A

Genetic disorder that causes syncope, ventricular fibrillation, and sudden death, often during sleep. It is more common in Asian men.

172
Q

What is the treatment for ventricular premature beats and sustained V tach w/o heart disease or electrolyte abnormalities?

A

Usually not treated. If the patient is having symptoms, can give a beta blocker or CCB

173
Q

Treatment of V tach with severe hypotension or loss of consciousness

A

Synchronized cardioversion; ventricular overdrive pacing may help

174
Q

Pulseless v tach treatment

A

Immediate defibrillation along with CPR

175
Q

Preferred pharmacologic interventions for acute V tach (in order)

A
  1. Amiodarone
  2. Lidocaine
  3. Procainamide
176
Q

An ICD may be indicated for recurrent sustained V tach with what conditions?

A

In patients with structural heart disease or without a reversible cause, for congenital long QT syndrome, and for Brugada syndrome

177
Q

Treatment of acquired long QT syndrome

A

Treatment of electrolyte abnormalities and discontinuation of drugs that prolong the QT interval

178
Q

What is the initial treatment for torsades de pointes?

A

IV magnesium, correction of electrolyte abnormalities (hypokalemia or hypomagnesemia), and withdrawal of drugs that may have precipitated the event

179
Q

What treatment may be indicated after initial treatment of torsades?

A

Isoproterenol infusion and overdrive pacing

180
Q

Treatment for recurrent torsades

A

Permanent pacemaker

181
Q

In sick sinus syndrome, besides scarring of the heart’s conduction system or infants who have had heart surgery, what are other causes or exacerbations?

A

Digitalis, CCB, beta blockers, sympatholytic agents, antiarrhythmic drugs, and aerosol propellant abuse. It may also result from underlying collagen vascular or metastatic disease, surgical injury, or, rarely, coronary disease

182
Q

What are some reversible causes of sick sinus syndrome?

A

Digitalis, quinidine, beta blockers, or aerosol propellants

183
Q

Dilated cardiomyopathies are the most common type of cardiomyopathies (95%). What is is associated with?

A

Reduced strength of ventricular contraction, resulting in dilation of the left ventricle

184
Q

Causes of dilated cardiomyopathies

A

Excessive alcohol consumption, postpartum state, chemotherapy toxicity, endocrinopathies, and myocarditis; it may be idiopathic

185
Q

Hypertrophic cardiomyopathy demonstrates what?

A

Massive hypertrophy (particularly of the septum), small left ventricle, systolic anterior mitral motion, and diastolic dysfunction

186
Q

What in hypertrophic cardiomyopathy promotes the development of an arrhythmia?

A

Microscopic myocardial abnormalities

187
Q

Restrictive cardiomyopathy results from what?

A

From fibrosis or infiltration of the ventricular wall because of collagen-defect diseases, most commonly amyloidosis, radiation, postoperative changes, diabetes, and endomyocardial fibrosis

188
Q

How is the left ventricle in restrictive cardiomyopathy?

A

Small or normal, with mildly reduced function

189
Q

Signs and symptoms of dilated cardiomyopathy

A

It results in signs and symptoms of left or biventricular congestive failure; the most common presentation is dyspnea. Patients may have an S3 gallop, pulmonary crackles (rales), and increased JVP

190
Q

Takotsubo cardiomyopathy presents with what?

A

Retrosternal chest pain indistinguishable from acute MI

191
Q

Patients with hypertrophic cardiomyopathy may present with what symptoms?

A

Dyspnea and angina. Syncope and arrhythmias are common. It may be asymptomatic. Sudden death may be the initial presentation

192
Q

Physical exam in hypertrophic cardiomyopathy

A

Sustained PMI or triple apical impulse, loud S4 gallop, variable systolic murmur, a bisferiens carotid pulse, and jugular venous pulsations with a prominent “a” wave

193
Q

Presentation for restrictive cardiomyopathy

A

Decreased exercise tolerance; in advanced disease, patients develop right-sided congestive failure; pulmonary HTN is usually present

194
Q

What does cardiac catherization reveal in Takotsubo cardiomyopathy?

A

Hypocontractility of the left ventricular apex and patent coronary arteries

195
Q

What does the echocardiogram reveal in hypertrophic obstructive cardiomyopathy?

A

LVH, asymmetric septal hypertrophy, small left ventricle, and diastolic dysfunction

196
Q

What study may be necessary in restrictive cardiomyopathy to differentiate restrictive disease from other forms of cardiomyopathy or pericarditis?

A

Endomyocardial biopsy

197
Q

Treatment of dilated cardiomyopathy

A
  1. Abstinence from alcohol is essential
  2. Underlying disease should be treated
  3. CHF requires supportive treatment
198
Q

Takotsubo cardiomyopathy treatment

A

Usually treated with supportive care. Inotropes should generally be avoided. Most patients return to baseline within 2 months

199
Q

Hypertrophic cardiomyopathy treatment

A
  1. Initial treatment employs beta blockers or CCBs; disopyramide is used for its negative inotropic effects
  2. Surgical or nonsurgical ablation of the hypertrophic septum may be required
  3. Dual chamber pacing, implantable defibrillators, or mitral valve replacement may be indicated
200
Q

What medication may help patients with restrictive cardiomyopathies?

A

Diuretics

201
Q

Pericardial effusion is secondary to what?

A

Pericarditis, uremia, or cardiac trauma

202
Q

Pericardial effusion produces what?

A

Restrictive pressure on the heart

203
Q

What occurs in cardiac tamponade?

A

The fluid that accumulates compromises cardiac filling and impairs cardiac output

204
Q

What is the primary presenting symptom of acute pericarditis?

A

Sharp, pleuritic substernal radiating chest pain often relieved by sitting upright and leaning forward; a cardiac friction rub is characteristic

205
Q

Electrical alternans is pathognomonic of what?

A

Effusion

206
Q

In the presence of hemodynamic compromise, what is the treatment of an effusion?

A

Pericardiocentesis

207
Q

What is the treatment of recurrent effusions?

A

May be treated surgically with a pericardial window

208
Q

Strictly inflammatory conditions in a pericardial effusion may be treated with what?

A

Steroids or NSAIDs

209
Q

Pericardiectomy may be performed when?

A

To relieve constrictive pericarditis

210
Q

Most cases of native valve infective endocarditis (IE) are caused by what pathogens?

A

Streptococcus viridans, Staphylococcus aureus, and enterococci

211
Q

In IV drug users, what is the most common pathogen and what valve is frequently involved?

A

S. aureus and the tricuspid valve is frequently involved

212
Q

Approximately 90% of IE patients have what sign?

A

A stable murmur, but this may be absent in right-sided infections. A changing murmur is rare but diagnostically significant

213
Q

Classic features of IE

A
  1. Palatal, conjunctival or subungal petechiae
  2. Splinter hemorrhages
  3. Osler nodes
  4. Janeway lesions
  5. Roth spots
214
Q

Osler nodes

A

Painful, violaceous, raised lesions of the fingers, toes or feet

215
Q

Janeway lesions

A

Painless red lesions of the palms or soles

216
Q

Roth spots

A

Exudative lesions in the retina

217
Q

What study has no specific diagnostic features in infective endocarditis?

A

ECG

218
Q

Patients must have what in the Duke criteria to be considered “definite” in the diagnosis of IE?

A
  1. Two major criteria
  2. One major and three minor OR
  3. Five minor criteria
219
Q

IE is considered “possible” with what in the Duke criteria?

A
  1. One major and one minor

2. Three minor

220
Q

Major criteria of IE

A
  1. Two positive blood cultures of a typical causative microorganism
  2. Echocardiographic evidence of endocardial involvement including new valvular regurgitation
221
Q

Minor criteria of IE

A
  1. Predisposing factor
  2. Fever higher than 100.4 F (38 C)
  3. Vascular phenomena (e.g., embolic disease or pulmonary infarction)
  4. Immunologic phenomena (e.g., glomerulonephritis, Osler nodes, Roth spots)
  5. Positive blood culture not meeting major criteria
222
Q

What is an appropriate initial therapy for patients with suspected IE?

A

Gentamicin with ceftriaxone OR vancomycin

223
Q

What is an appropriate therapy for acutely ill patients with heart failure pending blood cultures?

A

Gentamicin, vancomycin plus cefepime

224
Q

Antibiotic prophylaxis is recommended in what patients?

A

Prosthetic valves, previous IE, some congenital heart conditions, some acquired valve disorders, hypertrophic cardiomyopathy, and cardiac transplant recipients with valvulopathy. Amoxicillin is the usual drug of choice

225
Q

Valve replacement (especially of the aortic valve) may be necessary in what patients with IE?

A

If the IE does not resolve with antibiotic therapy, if an abscess develops, or if a fungal infection is the cause

226
Q

What systems are most commonly affected in rheumatic heart disease?

A

Heart, joints, skin, and CNS

227
Q

What ages are most commonly affected by rheumatic heart disease?

A

Children from ages 5-15 years

228
Q

What is the typical lesion in rheumatic valve disease?

A

Perivascular granuloma with vasculitis

229
Q

What are the most commonly involved valves in rheumatic heart disease?

A

Mitral valve ( 75-80%) followed by the aortic valve (30%)

230
Q

How many of the Jones criteria is required to make the diagnosis of rheumatic fever?

A

Two major or one major and two minor

231
Q

Major Jones criteria for rheumatic fever

A

Carditis, erythema marginatum, subcutaneous nodules, chorea, and polyarthritis

232
Q

Minor Jones criteria for rheumatic fever

A

Fever, polyarthralgias, reversible prolongation of the PR inteval, rapid ESR, or C-reactive protein

233
Q

What part of treatment is essential in rheumatic fever?

A

Strict bed rest

234
Q

Antibiotic treatment of rheumatic fever

A

IM penicillin is used for documented streptococcal infection; in patients who are allergic to penicillin, erythromycin is appropriate

235
Q

What do salicylates do in rheumatic fever?

A

Reduce fever and relieve joint problems

236
Q

What do corticosteroids do in rheumatic fever?

A

Relieve joint symptoms but do not prevent cardiac disease

237
Q

Prevention of rheumatic fever

A

Early treatment of streptococcal pharyngitis

238
Q

Prevention of the recurrence of rheumatic fever is essential to prevent heart damage. What antibiotic is given for prophylaxis?

A

Benzathine penicillin every 4 weeks

239
Q

What are signs of peripheral arterial disease?

A
  • Femoral and distal pulses will be weak or absent; an aortic, iliac, or femoral bruit may be present.
  • Skin changes to the lower extremity includes loss of hair, shiny atrophic skin, and pallor with dependent rubor
240
Q

What is Leriche syndrome?

A

Iliac artery disease; erectile dysfunction may occur in this syndrome

241
Q

Acute arterial occlusion threatens limb viability and results in what signs and symptoms?

A

Pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis

242
Q

An ABI of what indicates significant PAD?

A

≤0.9

243
Q

What is the gold standard study for PAD?

A

Angiography

244
Q

Although it is not regularly used for screening, an elevation of what has a strong association with incidence and progression of PAD?

A

Homocysteine

245
Q

What aggressive risk factor modification is used for PAD?

A

Tobacco use must be discontinued; DM, HTN, and HLD must be controlled

246
Q

What has been shown to be helpful at reducing symptoms of claudication in PAD?

A

Beta blockers, ACE inhibitors, statins, progressive exercise, and supervised exercise programs

247
Q

What medication(s) should be used in all patients with PAD (unless there is a contraindication)?

A

ASA and/or clopidrogel

248
Q

What medication can be added to help with symptom relief of PAD (primarily improved pain-free walking distances)?

A

Cilostazol (phosphodiesterase 3 inhibitor)

249
Q

What are risk factors for varicose veins?

A

Women who have been pregnant, obesity, family history, prolonged sitting and standing, and history of phlebitis

250
Q

The main mechanisms of varicose veins?

A

Superficial venous insufficiency and valvular incompetence

251
Q

What test differentiates saphenofemoral valve incompetence from perforator vein incompetence?

A

Brodie-Trendelengurg test

252
Q

Small venous ulcers in varicose veins heal with what treatment?

A

Leg elevation and compression bandages

253
Q

Large venous ulcers in varicose veins require what treatment?

A

Compression boot dressing (Unna boot) or skin grafts

254
Q

Interventional techniques for varicose veins

A

Endovenous radiofrequency or laser ablation, compression sclerotherapy, and sometimes surgical stripping of the saphenous tree

255
Q

Virchow triad

A

Stasis, vascular injury, and hypercoagulability

256
Q

What study is the most accurate method for definitive diagnosis of DVT?

A

Venography; however it is associated with increased risk and is rarely needed.

257
Q

Studies used in pulmonary embolism

A
  1. Pulmonary angiography (gold standard)
  2. CT angiography (most commonly used)
  3. V/Q scanning
258
Q

Treatment of superficial thrombophlebitis

A
  1. Bed rest, local heat, elevation of the extremity, and NSAIDs
  2. Antibiotics may be required if evidence of infection exists
  3. More serious disease may require surgical intervention
259
Q

Preferred treatment for DVT

A

Anticoagulation with enoxaparin (a low-molecular-weight heparin) or unfractioned heparin followed by warfarin

260
Q

Skin changes in chronic venous insufficency

A

Shiny, thin, and atrophic with dark pigmentary changes and subcutaneous induration

261
Q

Nonclassic symptoms of giant cell arteritis

A

Respiratory tract problems, mononeuritis complex (peripheral neuropathy), fever of unknown origin, or unexplained neck and head pain

262
Q

What do lab studies show in giant cell arteritis?

A
  • ESR and CRP will be markedy elevated

- Most patients have a normochromic normocytic anemia and thrombocytosis; some have elevated alkaline phosphatase

263
Q

Treatment of giant cell arteritis

A

High dose prednisone (1-2 months before tapering) and low dose ASA. Treatment should be initiated immeidately and not delayed for biopsy results

264
Q

Aortic aneurysm is what?

A

A weakness and subsequent dilation of the vessel wall

265
Q

Causes of aortic aneursym

A

Artherosclerosis is the most common cause, although some exist as congenital defects or as a result of syphilis, giant cell arteritis, vasculitis, trauma, Marfan syndrome, or Ehlers Danlos syndrome

266
Q

Where do the majority of aortic aneurysms occur in?

A

The abdomen (90% compared to 10% in the thoracic area)

267
Q

What is the study of choice for abdominal aneurysms?

A

Abdominal ultrasonography

268
Q

Current recommendation for abdominal aortic aneurysm screening

A

Single abdominal U/S for men older than the age of 65 years who have ever smokes; this may be followed by contrast-enhanced CT

269
Q

Diagnostic studies for thoracic aneursyms

A

It may require aortography for diagnosis; CT and MRI are preferred over U/S

270
Q

Treatment of aortic aneurysm

A
  • The only effective treatment is endovascular or open surgical repair
  • Five year survival after repair is greater than 60%

A Comprehensive Review for the Certification and Recertification Examination for Physician Asistants (8 decks)

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