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Cardio Flashcards

1
Q

What is the normal range for the PR interval?

A

0.12-0.2 seconds

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2
Q

What is the normal duration for a QRS complex?

A

Less than 0.12 seconds

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3
Q

What is the normal QTc?

A

Less than 0.44 seconds

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4
Q

What defines pathological Q waves?

A

More than 0.04 seconds or more than one-third of the QRS amplitude

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5
Q

What are the EKG findings for RAA (P pulmonale)?

A

Increased P wave amplitude

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6
Q

What are the EKG findings for LAA (P Mitrale)?

A

Increased P wave duration (possible biphasic)

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7
Q

How many centimeters above the sternal angle defines JVD?

A

7 cm

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8
Q

What is the hepatojugular reflux?

A

distention of neck veins upon applying pressure to the liver

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9
Q

What is Kussmaul’s sign? What causes it?

A

(↑ in jugular venous pressure [JVP] with inspiration): Often seen in cardiac tamponade and constrictive pericarditis.

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10
Q

What causes the S4 heart sound?

A

Decreased ventricular compliance

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11
Q

What causes the S3 heart sound?

A

Volume overload

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12
Q

What causes bounding peripheral pulses?

A

Compensated aortic regurgitation

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13
Q

What is pulsus paradoxus, and what does it mean?

A

(↓ systolic BP with inspiration): Pericardial tamponade;

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14
Q

What is pulsus alternans, and what does it mean?

A

(alternating weak and strong pulses): Cardiac tamponade or impaired left ventricular function

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15
Q

What is pulsus parvus et tardus, and what does it mean?

A

(weak and delayed pulse): Aortic stenosis.

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16
Q

What are the ABCDs of a-fib management?

A

Anticoagulate
Beta blockers
Cardiovert/CCBs
Digoxin (in refractory cases)

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17
Q

What are the components of the CHA2 DS2 -VASc scoring system to estimate stroke risk in atrial fibrillation

A 
■ CHF (1 point) 
■ HTN (1 point)
■ Age ≥ 75 (2 points) 
■ Diabetes (1 point) 
■ Stroke or TIA history (2 points) 
■ Vascular disease (1 point) 
■ Age 65–74 (1 point) 
■ Sex category (female) (1 point)
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18
Q

What types of drugs can cause first degree or mobitz type I AV blocks?

A

Beta blockers
CCBs
Digoxin

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19
Q

What is the treatment for mobitz type I AV block?

A

Atropine PRN

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20
Q

What is the treatment for mobitz type II AV block?

A

Pacemaker placement

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21
Q

What is the prognosis for mobitz type II AV block?

A

Frequently progresses to third degree AV block

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22
Q

What is the most common indication for a pacemaker placement?

A

Sick sinus syndrome

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23
Q

What are the components of the PIRATES mnemonic for remembering the causes of a-fib?

A 
Pulmonary disease
Ischemia
Rheumatic heart disease
Anemia/atrial myxoma
Thyrotoxicosis
Ethanol
Sepsis
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24
Q

What is the timeframe in which you can cardiovert a patient out of a-fib?

A

Less than 2 days, otherwise may throw a clot

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25
Q

True or false: atrial flutter is treated similarly to a-fib?

A

True

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26
Q

What are the EKG findings of multifocal atrial tachycardia?

A

At least 3 different P-wave morphologies

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27
Q

What is AV nodal reentry tachycardia? How does it appear on EKG

A

A reentry circuit in the AV node depolarizes the atrium and ventricle nearly simultaneously.

Rate 150–250 bpm; P wave is often buried in QRS or shortly after.

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28
Q

What is the treatment for AVNRT?

A

Cardiovert if hemodynamically unstable. Carotid massage, Valsalva, or adenosine can stop the arrhythmia.

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29
Q

What causes AVRT? What are the EKG findings?

A

An ectopic connection between the atrium and ventricle that causes a reentry circuit. Seen in WPW.

A retrograde P wave is often seen after a normal QRS. A preexcitation delta wave is characteristically seen in WPW.

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30
Q

What is the treatment for AVRT?

A

Same as AVNRT

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31
Q

What causes paroxysmal atrial tachycardia? EKG findings?

A

Rapid ectopic pacemaker in the atrium (not sinus node).

Rate > 100 bpm; P wave with an unusual axis before each normal QRS.

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32
Q

What is the treatment for paroxysmal atrial tachycardia?

A

Adenosine can be used to unmask underlying atrial activity by slowing down the rate.

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33
Q

An EF of less than what percent indicates systolic dysfunction?

A

50%

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34
Q

What is the earliest and most common presenting symptom of systolic dysfunction?

A

Exertional dyspnea
Orthopnea
PND

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35
Q

True or false: both digoxin and diuretics confer a mortality benefit with systolic heart dysfunction

A

False–neither do

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36
Q

What is the underlying pathophysiology of systolic heart dysfunction?

A

The heart compensates for ↓ EF and ↑ preload through hypertrophy and ventricular dilation (Frank-Starling law), but the compensation ultimately fails, leading to ↑ myocardial work and worsening systolic function.

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37
Q

What is the treatment for acute systolic heart failure?

A

Aggressive diuresis

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38
Q

SHould Beta blockers be continued or stopped during a CHF exacerbation?

A

Stopped

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39
Q

What are the components of the LMNOP mnemonic for the treatment of acute systolic HF?

A 
Lasix (furosemide)
Morphine
Nitrates
Oxygen
Position (upright)
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40
Q

What are the lifestyle modifications for CHF?

A

Lower Na and fluid intake

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41
Q

What is the pharmacologic therapy for chronic CHF?

A

Beta blockers and ACEIs/ARBs

Diuretics

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42
Q

What is the one diuretic that has been shown to decrease mortalaty in chronic HF patients?

A

Spironolactone

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43
Q

When is daily ASA and a statin indicated in the treatment of chronic HF?

A

If underlying cause is a MI

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44
Q

What are the procedural treatments for HF?

A

ICD

LVAD

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45
Q

When is an ICD indicated in the treatment of HF?

A

If EF is less than 35%

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46
Q

What is the extra heart sound associated with systolic HF? non-systolic?

A 
systolic = S3
Non = S4
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47
Q

What will an EKG and echo typically show with systolic dysfunction?

A

Q waves and a decreased EF

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48
Q

What will an EKG and echo typically show with non-systolic dysfunction?

A 
LVH
Normal EF (more than 55%)
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49
Q

What is the general pathophysiology of non systolic heart dysfunction?

A

Decreased ventricular compliance with normal systolic function

The ventricle has either impaired active relaxation (ischemia) or impaired passive filling (scarring)

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50
Q

What are the s/sx of non-systolic HF?

A 
Unstable angina
SOB
DOE
arrhythmias
MI
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51
Q

What is the treatment for non-systolic HF?

A

Diuretics

Maintain BP

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52
Q

True or false: digoxin is useful for patients with non systolic HF

A

False

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53
Q

What is the most common loop diuretic?

A

Furosemide (lasix)

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54
Q

What are the side effects of loop diuretics?

A

Hypokalemia
Hypocalcemia
Ototoxic

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55
Q

What are the side effects of thiazide diuretics?

A 
Hypokalemic metabolic alkalosis
Hyperglycemia (GLUC)
Hyperlipidemia
Hyperuricemia
Hypercalcemia
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56
Q

What are the three major K sparing diuretics?

A

Spironolactone
Triamterene
Amiloride

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57
Q

What is the classic carbonic anhydrase inhibitor?

A

Acetazolamide

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58
Q

What are the side effects of CAIs?

A

hyperchloremic metabolic acidosis

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59
Q

What are the contraindications to mannitol use?

A

Pulmonary edema

Anuria

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60
Q

What is the most common form of cardiomyopathy?

A

Dilated

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61
Q

What are the physiological characteristics of dilated cardiomyopathy?

A

LV dilation and decreased EF 2/2 impaired contractility

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62
Q

What are the known secondary causes of dilated cardiomyopathy?

A

EtOH
Myocarditis
Postpartum status
Drugs

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63
Q

Which antineoplastic agent classically causes dilated cardiomyopathy?

A

Doxorubicin

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64
Q

What are the three major infectious causes of dilated cardiomyopathy?

A

Coxsackievirus
HIV
Chagas disease

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65
Q

What is the underlying pathophysiology of hypertrophic cardiomyopathy?

A

Impaired relaxation

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66
Q

What is the underlying pathophysiology of restrictive cardiomyopathy?

A

Impaired elasticity

67
Q

What happens to LV cavity size at the end of diastole in the following types of cardiomyopathy:

Dilated
Hypertrophic
Restrictive

A

Dilated - Increased Markedly
Hypertrophic - Decreased
Restrictive - Increased

68
Q

What happens to LV cavity size at the end of systole in the following types of cardiomyopathy:

Dilated
Hypertrophic
Restrictive

A

Dilated - Increased Markedly
Hypertrophic - Decreased markedly
Restrictive - Increased

69
Q

What happens to EF in the following types of cardiomyopathy:

Dilated
Hypertrophic
Restrictive

A

Dilated - Decreased
Hypertrophic - Increased or normal
Restrictive -decreased or normal

70
Q

What happens to heart wall thickness in the following types of cardiomyopathy:

Dilated
Hypertrophic
Restrictive

A

Dilated - Decreased
Hypertrophic - Increased
Restrictive - Increased

71
Q

How do you diagnose cardiomyopathies?

A

Echo

72
Q

What is the treatment for cardiomyopathies?

A

Address underlying etiology if known

Treat CHF

73
Q

What is the inheritance pattern of hypertrophic obstructive cardiomyopathy?

A

AD

74
Q

What is the murmur heard with HOCM? What increases the intensity?

A

a systolic ejection crescendo-decrescendo murmur that ↑ with ↓ preload

75
Q

What is the treatment for HOCM?

A

beta blockers

Myomectomy

76
Q

What is the general cause of restrictive cardiomyopathy?

A

Infiltrative diseases

77
Q

What are the s/sx of restrictive cardiomyopathy?

A

Left and right sided heart failure

78
Q

What is the treatment of restrictive cardiomyopathy?

A

Judicious use of diuretics and vasodilators

79
Q

What are the 4 risk equivalents of CAD

A

DM
AAA
Symptomatic carotid artery disease
PAD

80
Q

Are cardiac enzymes elevated with prinzmetal angina?

A

No

81
Q

What are the only two drugs that have been shown to have a mortality benefit in the treatment of angina?

A

ASA

Beta blockers

82
Q

What defines unstable angina?

A

new onset chest pain that is accelerating or occurs at rest

83
Q

What is the range of scores in the TIMI risk score?

A

0-7

84
Q

When is heparin indicated in the treatment of a NSTEMI?

A

Patients with chest pain refractory to medical therapy, a TIMI score of ≥ 3, a troponin elevation, or ST changes > 1 mm should be given IV heparin and scheduled for angiography and possible revascularization

85
Q

What is the best predictor of survival with an MI?

A

Left ventricular EF

86
Q

What can an EKG show with a STEMI, besides ST elevation?

A

New LBBB

87
Q

What is the progression of EKG changes with a STEMI?

A

Peaked T waves → ST-segment elevation → Q waves → T-wave inversion → ST-segment normalization → T-wave normalization over several hours to days.

88
Q

In inferior wall MI, avoid nitrates. Why?

A

Risk of severe hypotension

89
Q

What are the four indications for a CABG?

A
  • Unable to stent
  • Left main coronary artery disease
  • Triple vessel disease
  • Depressed ventricular function
90
Q

When are thrombolytics indicated in the treatment of a STEMI? (3)

A
  • PCI cannot be performed with 90 mins
  • No contraindications
  • the patient presents within 3 hours of chest pain onset,
91
Q

When does HF usually present post MI?

A

First day

92
Q

When do arrhythmias/pericarditis usually present post MI?

A

2-4 days

93
Q

When does left ventricular free wall rupture present post MI?

A

5-10 days

94
Q

When does ventricular aneurysm present post MI?

A

Weeks to months later

95
Q

What are the s/sx of Dressler syndrome

A 
Fever
Pericarditis
Pleural effusions
Leukocytosis
Increased ESR
96
Q

How often are lipids levels monitored? When does screening start, typically?

A

q 5 years for 35+ males and 45+ females, if not high risk

97
Q

When are high, intermediate, and low intensity statins indicated for the treatment of CAD?

A

■ ≥ 7.5% 10-year risk → high-intensity statin.
■ Between 5% and 7.5% 10-year → moderate-intensity statin.
■ ≤ 5% 10-year risk → no statin.

98
Q

What are the LDL and HDL criteria for dyslipidemia?

A

■ LDL > 130 mg/dL
or
■ HDL < 40 mg/dL

99
Q

What is the first intervention for dyslipidemia?

A

The first intervention should be a 12-week trial of diet and exercise in a patient with no known atherosclerotic vascular disease.

100
Q

What is the effect of fibrates on lipid levels?

A

Decreases triglycerides

Increases HDL

101
Q

What is the effect of statins on lipid levels?

A

Decreases LDL

Decreases Triglycerides

102
Q

What is the effect of cholesterol absorption inhibitors (ezetimibe) on lipid levels?

A

Decreases LDL

103
Q

What is the classic cholesterol absorption inhibitor?

A

Ezetimibe

104
Q

What is the effect of niacin on lipid levels?

A

Increases HDL

Decreases LDL

105
Q

What are the bile acid resins?

A

Cholestyramine
Colestipol
Colesevelam

106
Q

What is the effect of bile acid resins on lipid levels?

A

Decreases LDL

107
Q

What is the BP goal for patients 60+?

A

150/90

108
Q

What is the BP goal for patients less than 60 or with DM/CKD?

A

140/90

109
Q

What are the two HTN drugs that are safe in pregnancy?

A

Labetalol

Hydralazine

110
Q

Why should you not lower the BP more than 25% in the first 2 hours of a HTN emergency?

A

Prevent cerebral hypoperfusion or coronary insufficiency

111
Q

What is the treatment for HTN 2/2 renal disease?

A

ACEIs to slow progression of renal disease

112
Q

What is a common cause of HTN in young women?

A

OCP use

113
Q

What is the metabolic disturbance with Conn syndrome?

A

Hypokalemic alkalosis

114
Q

What are the components of the CARDIAC RIND mnemonic for causes of pericarditis?

A 
Collagen vascular disease
Aortic dissection
Radiation
Drugs
Infections
Acute renal failure
Cardiac (MI)
Rheumatic fever
Injury
Neoplasms
Dressler syndrome
115
Q

Pulsus paradoxus is classically seen in what?

A

Cardiac tamponade

116
Q

What are the EKG changes seen in pericarditis?

A

Diffuse ST segment elevation and/or ST depression

117
Q

What is the treatment for pericarditis?

A

addressing the underlying cause

Corticosteroids and NSAIDs

118
Q

Which is more important in the setting of cardiac tamponade: the rate of filling, or the amount?

A

rate

119
Q

What are the components of Beck’s triad for cardiac tamponade?

A

Hypotension
JVD
Distant heart sounds

120
Q

What is Kussmaul’s sign?

A

Increased JVD on inspiration

121
Q

What is the treatment for tamponade?

A

Aggressive volume expansion with IVFs

Urgent pericardiocentesis

122
Q

Over how many centimeters is repair indicated for AAA?

A

5 cm

123
Q

When can aortic stenosis lead to symptoms in childhood?

A

If bicuspid or unicuspid valve

124
Q

What are the three major s/sx of aortic stenosis?

A

Angina
CHF
Syncope

125
Q

What is pulsus parvus et tardus, and what does it indicate?

A

Weak, delayed carotid upstroke, associated with aortic stenosis

126
Q

Once symptoms appear with aortic stenosis, how long do patients have to live, if untreated?

A

5 years

127
Q

What is the etiology of acute vs chronic aortic regurgitation?

A

Acute: Infective endocarditis, aortic dissection, chest trauma.

Chronic: Valve malformations, rheumatic fever, connective tissue disorders.

128
Q

What are the s/sx of acute aortic regurg?

A

Acute: Rapid onset of pulmonary congestion, cardiogenic shock, and severe dyspnea.

129
Q

What are the s/sx of chronic aortic regurg?

A

Slowly progressive onset of dyspnea on exertion, orthopnea, and PND.

130
Q

What is the treatment for aortic regurgitation?

A

Vasodilator therapy (dihydropyridines or ACEIs) for isolated aortic regurgitation until symptoms become severe enough to warrant valve replacement.

131
Q

What is the most common etiology of mitral valve stenosis?

A

Rheumatic heart disease

132
Q

What are the s/sx of mitral stenosis?

A

Symptoms range from dyspnea, orthopnea, and PND to infective endocarditis and arrhythmias.

133
Q

What is the treatment for aortic stenosis?

A

Antiarrhythmics (β-blockers, digoxin) for symptomatic relief; mitral balloon valvotomy and valve replacement are effective for severe cases.

134
Q

What are the two major etiologies of mitral valve regurgitation?

A

Primarily 2° to rheumatic fever or chordae tendineae rupture after MI.

135
Q

What is the treatment for mitral valve regurgitation?

A

Antiarrhythmics if necessary (AF is common with LAE; nitrates and diuretics to ↓ preload). Valve repair or replacement for severe cases.

136
Q

Aortic aneurysms are most commonly associated with what disease process?

A

Atherosclerosis

137
Q

What are the s/sx of a AAA?

A

Asymptomatic but pulsatile abdominal mass or abdominal bruit

138
Q

What is the screening test for AAA?

A

Screen all men 65–75 years of age with a history of smoking once by ultrasound for AAA (see Figure 2.1-16).

139
Q

Aortic dissections are most commonly associated with what disease process?

A

HTN

140
Q

What are the classic PE findings of aortic dissection?

A

Asymmetric pulses and BP measurements.

141
Q

What is the diagnostic imaging modality of choice for an aortic dissection?

A

CT angio

142
Q

What is the treatment for aortic dissection?

A

Monitor and medically manage BP and heart rate as necessary. Avoid thrombolytics. Begin β-blockade before starting vasodilators to prevent reflex tachycardia.

143
Q

What are the components of virchow’s triad?

A
  • hemostasis
  • Endothelial damage/trauma
  • hypercoagulability
144
Q

What is the treatment for a DVT?

A

IV unfractionated heparin or SQ LMWH, followed by PO warfarin for 3-6 months

145
Q

how can you roughly locate the presence of a clot in the lower extremity?

A

occur at bifurcations distal to the last palpable pulse

146
Q

Pain at rest usually occurs at what ABI?

A

less than 0.4

147
Q

A very high ABI can indicate what pathology?

A

Calcification of the arteries

148
Q

What are the 6 P’s of acute ischemia?

A 
Pain
Pallor
Paralysis
Pulselessness
Paresthesias
Poikilothermia
149
Q

What is the role of exercise in the treatment of claudication?

A

Helps to develop collateral circulation

150
Q

What are the medications that can improve symptoms of claudication?

A

ASA
Cilostazol
Thromboxane inhibitors

151
Q

What is the most common cause of lymphedema in the developed world?

A

Surgical side effect

152
Q

What is the role of diuretics in the treatment of lymphedema?

A

Ineffective, and relatively contraindicated

153
Q

What are the major features that distinguish syncope from a seizure?

A

Unlike syncope, seizures may be characterized by a preceding aura, tonic-clonic activity, tongue-biting, bladder and bowel incontinence, and a postictal phase.

154
Q

Cardiac causes of syncope are typically associated with what symptoms?

A

Very brief or absent prodromal symptoms
h/o exertion
Lack of association with changes in position

155
Q

What should be done to r/o cardiogenic causes of syncope?

A

Holter monitor
ECG
Echo
Stress test

156
Q

What should be done to r/o neurological causes of syncope?

A

Heat CT

EEG

157
Q

When does reinfarction typically occur s/p MI?

A

0-48 hours

158
Q

When does ventricular septal typically occur s/p MI?

A

hours-1 week

159
Q

When does free wall rupture typically occur s/p MI?

A

Hours-2 weeks

160
Q

When does postinfarction angina typically occur s/p MI?

A

hours - 1 month

161
Q

When does papillary muscle rupture occur s/p MI?

A

2 days - 1 week

162
Q

When does pericarditis occur s/p MI?

A

1 day - 3 months

163
Q

When does a left ventricular aneurysm typically occur s/p MI?

A

5 days - 3 months

164
Q

ST/segment elevations and deep Q waves in the same lead as a recent, previous MI = ?

A

free wall rupture

A1 (32 decks)

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