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Cardiology Flashcards

1
Q

What does an S3 gallop denote and define the mechanism

A

Dilated LV

Occurs at beginning of diastole when blood rushes in and splashes within the dilated ventricle

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2
Q

What does the S4 gallop denote and define the mechanism

A

LVH

Occurs at end of diastole when atrial contraction occurs and sound is blood hitting stiff ventricular wall

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3
Q

CP worse on palpation

A

Costochondritis

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4
Q

CP worse with positional change

A

Pericarditis

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5
Q

CP pleuritic

A

PNA, PE, PTX, Pleuritis, Pericarditis

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6
Q

You have a case of very clear myocardial ischemia. What is the next best step, treatment or diagnosis?

A

Treatment (ASA, morphine, nitrates, oxygen)

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7
Q

When do CK-MB and troponin rise? What situations are they useful in?

A

3-6 hrs

CK-MB levels fall after 1-2 days so they’re good for looking for ischemia occurring after an infarct. Troponins stay high for 1-2 wks

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8
Q

What enzyme is one of the earliest to rise in myocardial ischemia?

A

Myoglobin

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9
Q

A patient comes in with chronic chest pain that is exertional and associated with jaw pain. EKG and troponins don’t establish the dx. What is your next diagnostic test?

A

Stress test

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10
Q

In what situations would you want a dipyridamole/adenosine thallium stress test or dobutamine echo for diagnostics?

A

When patients have reduced exercise tolerance and can’t achieve 85% maximum HR (i.e. COPD, obesity, deconditioning, amputation, leg ulcers, previous stroke, dementia)

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11
Q

In what situations would an exercise thallium stress test or stress echo be warranted for diagnostics?

A

When the EKG is unreadable due to ischemia (i.e. LBBB, ST abnormality at baseline, digoxin use, pacemaker in place, LVH)

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12
Q

Your patient comes in with a stress test for CP that demonstrates reversible ischemia. What is the next step in management?

A

Angiogram (do whenever there is reversible ischemia)

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13
Q

Angiogram results of myocardial ischemia demonstrates an infarction in LAD territory. At this juncture what may be the next best step in management?

A

Coronary bypass

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14
Q

What is the most accurate method to determine EF?

A

Nuclear ventriculogram

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15
Q

Your patient is having mild chest pain and presents with signs and symptoms consistent with myocardial ischemia. Should you do stress testing?

A

NO! Don’t do stress testing if the patient has current CP

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16
Q

Which treatment for ACS reduces mortality?

A

Aspirin

Oxygen and morphine do not

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17
Q

What is the mechanism of clopidogrel, ticagrelor, and prasugrel?

A

Inhibit ADP-induced activation P2Y12 receptor that causes aggregation of platelets

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18
Q

What medication is added to aspirin if a patient is having an acute MI?

A

An ADP inhibitor (clopidogrel or ticagrelor)

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19
Q

What medication is specifically provided to patients receiving an angioplasty?

A

Prasugrel

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20
Q

Besides aspirin, which treatments lower mortality in STEMI?

A

Primary angioplasty and thrombolytics

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21
Q

Angioplasty is one type of percutaneous coronary intervention (PCI). How quickly should this be done from arrival at ED?

A

90 minutes

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22
Q

Does angioplasty reduce mortality among patients with stable angina?

A

No

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23
Q

In what situation are thrombolytics given for ACS?

A
  • When catheterization-based therapy is unavailable (i.e. rural hospital or nearest cath hospital is awhile away)
  • Within 30 mins of reaching ED
  • CP of
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24
Q

How do thrombolytics mechanistically work and why do they need to be provided within a certain time window?

A

Activate plasminogen to plasmin which chops fibrin strands of clots into D-dimers. The reason it needs to be given quickly is that with time factor VIII stabilizes fibrin and it cannot be cleaved by plasmin.

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25
Q

What medication reduces mortality in ACS but aren’t urgent?

A

Beta-blockers

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26
Q

ACEi and ARBs reduce mortality of ACS only when ….

A

There is evidence of left ventricular or systolic dysfunction

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27
Q

What medication should be given to all ACS patients regardless of EKG or troponin findings?

A

Statins

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28
Q

Why are beta-blockers helpful in ACS? (think mechanism)

A

Most common cause of death in MI and CHF is arrhythmia. By slowing heart rate they are anti-arrhythmic. They also allow more time for diastolic filling and thus providing oxygen to coronaries.

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29
Q

A patient presents with cocaine-induced chest pain. What medicine do you want to administer for rate control and to prevent arrhythmia?

A

CCB (i.e. verapamil, diltiazem)

*A beta-blocker will cause unopposed adrenergic effects on alpha receptors causing vasocontriction

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30
Q

In what 3 CP situations should you consider CCB for rate-control and anti-arrhythmic effect?

A

Cocaine-induced
Beta-blocker allergy
Coronary vasospasm/Prinzmetal angina

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31
Q

What medications would you want to give if an MI patient went into Vtach or Vfib?

A

Lidocaine or amiodarone

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32
Q

If there is any anatomic complication of an MI (e.g. septal wall rupture, valve rupture, cardiogenic shock, myocardial wall rupture) what is the appropriate means of diagnosis?

A

Echo

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33
Q

What is the management of a myocardial wall rupture post-MI?

A

Pericardiocentesis and urgent repair

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34
Q

How can a right-heart catheter (Swan-Ganz) be helpful in diagnosis of septal wall rupture post-MI?

A

Demonstrates a step-up in oxygen saturation when moving from RA to RV

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35
Q

For any electrical complication of MI (i.e. sinus bradycardia, RV infarction, or 3rd degree block) what is the diagnostic test which is useful?

A

EKG

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36
Q

What is the treatment of right ventricular infarction occurring post-MI?

A

Fluid loading

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37
Q

How long after an MI should a patient wait before having sex again?

A

2-6 weeks

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38
Q

All patients discharged post-MI should go home on what meds?

A

Aspirin, clopidogrel, statin, beta-blocker, ACEi

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39
Q

There are differences between mgmt of STEMI and NSTEMI.
Are thrombolytics used in NSTEMI?
What anticoagulation is used?

A

No thrombolytics

LMWH is used

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40
Q

What is the mechanism of heparin?

A

Potentiates antithrombin which inhibits almost all steps of clotting cascade. Heparin only prevents new clots from forming.

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41
Q

Do nitrates reduce mortality?

A

No

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42
Q

In chronic angina ACEi or ARBs should be used only if …. (3 situations)

A 
CHF
Systolic dysfunction
Low EF (LV dysfunction)
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43
Q

Generally, can you do CABG before angiography?

A

No

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44
Q

What is the main difference in internal mammary artery grafts and saphenous vein grafts during CABG?

A

Internal mammary artery grafts stay open for 10 yrs whereas saphenous vein grafts occlude after 5 years

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45
Q

In a patient with CAD what role does ranolazine play?

A

Anti-angina med used to reduce pain if other meds haven’t reduced pain

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46
Q

What are indications for CABG?

A

1) Three vessel with > 70% stenosis
2) Two stenotic vessels in a diabetic
3) LAD with > 50-70% stenosis
4) Two or three vessels with low EF

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47
Q

What is the LDL goal in a patient with DM?

A
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48
Q

What is the most frequent side effect of statins?

A

Liver toxicity

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49
Q

What is the most common cause of erectile dysfunction?

A

Anxiety

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50
Q

For a patient presenting with acute pulmonary edema what is appropriate management?

A

Oxygen, furosemide, nitrates, morphine

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51
Q

What is the mechanism of carvedilol?

A

Antagonist of B1, B2, and alpha receptors

Thus it is anti-arrhythmic, anti-ischemic, and anti-hypertensive

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52
Q

When evaluating the patient with CHF during the CCS portion of the exam what initial tests do you want to order?

A

CXR
Echo (distinguish systolic vs diastolic dysfunction)
Oximetry
EKG

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53
Q

What is the MOA of imamrinone and milrinone? What effect do they have?

A

PDE inhibitors which decreased afterload by vasodilating and also increase contractility

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54
Q

How does CHF cause a respiratory alkalosis?

A

CHF causes hypoxia

Hypoxia causes hyperventilation

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55
Q

The majority of patients with acute pulmonary edema (which should be taken to ICU) will respond to: preload reduction or afterload reduction? If that doesn’t work then what drugs may be the next management step?

A

Preload reduction

If that doesn’t help (which it should in most) then give contractility increasing agents such as dobutamine, imamrinone, and milrinone

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56
Q

What is the treatment for Vtach associated with acute pulmonary edema?

What about when hemodynamically stable, sustained Vtach?

A

When with acute pulmonary edema: synchronized cardioversion

Stable: lidocaine, amiodarone, or procainamide

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57
Q

What is the management for Vfib or pulseless Vtach?

A

Unsynchronized cardioversion

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58
Q

What is nesiritide?

A

An atrial natriuretic peptide used for acute pulmonary edema preload reduction

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59
Q

What is the utility of measuring the BNP level?

A

If normal it can rule out CHF. BNP goes up in CHF and can see if SOB in a patient is likely from CHF

60
Q

What will happen to cardiac output, RAP, wedge pressure, and systemic vascular resistance in acute pulmonary edema?

A

CO: Decreased
Wedge: Increased
RAP: Increased
SVR: Increased

61
Q

Which three meds have been shown to reduce mortality in the chronic management of CHF from systolic dysfunction?

A

ACEi
Beta-blockers
Spironolactone (in more advanced cases)

*Diuretics may have a role but unclear effect on mortality

62
Q

What role does digoxin have in the chronic mgmt of CHF from systolic dysfunction?

A

Lessens symptoms and frequency of hospitalizations (no mortality effect)

63
Q

Patient with systolic CHF presents with gynecomastia and erectile dysfunction on spironolactone. What med do you want to switch him to?

A

Eplerenone

64
Q

Diastolic dysfunction CHF is treated with …?

A

Beta-blockers and diuretics

65
Q

When are patients with CHF candidates for an implantable defibrillator?

A

EF remaining below 35%

66
Q

At what point is a patient a candidate for a biventricular pacemaker in CHF?

A

When EF 120ms

*QRS >120ms measn ventricles aren’t beating together and forward flow is compromised. The biventricular pacemaker helps gt them on the same page

67
Q

What is an absolute contraindication to beta-blockers?

A

Symptomatic bradycardia

68
Q

In a young patient with SOB worse on exertion and probable valvular heart disease what is the likely cause?

A

Mitral valve prolapse

69
Q

Buzzwords

What valvular disease associated with immigrants and pregnant patients?

A

MItral Stenosis

70
Q

Inhalation increases murmurs on what side of heart and why?

A

Right-side

Inhalation decreases intrathoracic pressure which increases venous return and thus more blood on right side

71
Q

Exhalation increases murmurs on what side of heart?

A

Left-side

72
Q

What effect does squatting and lifting legs in the air do to venous return?

A

Increases venous return

*Squatting will suddenly squeeze veins of legs and cause increased venous return

73
Q

What effect does valsalva and suddenly standing do to venous return?

A

Decrease venous return

*Because Valsalva increases intrathoracic pressure

74
Q

Which murmurs become louder with squatting and lifting legs in the air? Which become softer?

A

Louder: AS, AR, MS, MR, and all right-sided

Softer: HOCM murmur, MVP

75
Q

Valsalva and standing both make which murmurs sound louder?

A

HOCM and MVP

76
Q

What hemodynamic consequence does handgrip have and which murmurs will sound louder? (Hint: 3)

A

Increases afterload (but since veins in arm aren’t as big as in leg then there will be no effect on venous return)

AR, MR, and VSD will become louder

77
Q

What hemodyanmic consequence does amyl nitrate have on murmurs and why?

A

It decreases afterload by vasodilating arteries and thus AR, MR, and VSD will be softer

78
Q

What effect does amyl nitrate have on murmurs of MVP and HOCM? Why?

A

It makes them louder because it allows further emptying of LV which decreases LV size and increases degree of obstruction and prolapse in HOCM and MVP, respectively

79
Q

What effects do handgrip and amyl nitrate have on AS?

A

Handgrip makes it softer

Amyl nitrate makes it louder

80
Q

Where are pulmonic valve murmurs best heard?

A

Second left intercostal space

81
Q

What murmurs are best heard at the lower left sternal border?

A

AR, tricuspid regurgitation, and VSD

82
Q

What is the best initial test for diagnosis valve lesions?

What is the most accurate?

A

Initial: Echo
Accurate: Left heart catheterization

83
Q

Regurgitant lesions are best treated with what meds?

A

Vasodilator therapy such as ACEi and ARBs

84
Q

What is the best treatment for stenotic valvular lesions?

A

Anatomic repair

85
Q

T/F

Diuretics can help any valve lesion which improves with valsalva

A

True

But in cases with stenosis anatoomic repair is still best

86
Q

Anything which makes the LV smaller has what effect on murmurs of HOCM and MVP?

A

Increases intensity

87
Q

Do bioprosthetic valves need anticoagulation?

A

No, but they don;t last as long as the mechanical valves which do require anticoagulation

88
Q

Diastolic decrescendo murmur heard at left sternal border =

A

Aortic regurgitation

89
Q

Quincke pulse, corrigan pulse, musset’s sign, duroziez’s sign, and hill sign are seen with what murmur? What are they each?

A

Quincke pulse: arterial or capillary pulsations in fingernail
Corrigan’s: water-hammer, high-bounding pulses
Musset’s: head bobbing up and down with each pulse
Duroziez: murmur heard over femoral artery
Hill sign: BP gradient much higher in lower extremities

90
Q

What is medical mgmt of AR?

What is mgmt when EF

A

Medical mgmt: ACEi/ARB, nifedipine, or loop diuretic

Low EF: surgical mgmt

91
Q

Rheumatic heart disease, endocarditis, and cystic medial necrosis can all cause what murmur?

A

AR

92
Q

Rheumatic fever in immigrants and pregnant patients are at greater risk for what valvular condition?

A

Mitral stenosis

93
Q

What are common presenting symptoms of mitral stenosis? (Hint: think anatomy)

A

Dysphagia, hoarseness, and afib

94
Q

Opening snap followed by diastolic rumble =

A

Mitral stenosis

95
Q

Based on listening to the murmur of mitral stenosis how can you determine how advanced a case it is?

A

The opening snap occurs earlier (that is, closer to S2)

96
Q

Straightening of the left heart border and elevation of the left mainstem bronchus on CXR may indicate which valvular condition?

A

MS

97
Q

What is the best initial therapy for MS?

What is the most effective therapy?

A

Initial: diuretics
Effective: balloon valvuloplasty

98
Q

A holosystolic murmur heard best at apex and obscuring the S1 and S2 is …

A

MR

99
Q

Ischemic heart disease and conditions which dilate the heart can cause which left heart valvular disorder?

A

MR

100
Q

What is the best initial therapy for MR?

A

ACEi/ARB, nifedipine, loop diuretic

*If EF

101
Q

Fixed S2 splitting is caused by …

A

ASD

102
Q

Explain which types of cardiac conditions cause wide S2 splitting and which cause paradoxical S2 splitting?

A

Normally the aortic valve closes a little before the pulmonic. When inspiring there is increased venous return which causes the pulmonic valve to stay open longer which makes a noticeable split when they close.

Pathologies of right heart that delay pulmonic closure cause wide S2 (e.g. RBBB, pulmonic stenosis, RVH, pulmonoary HTN)

Pathologies that delay closure of aortic valve are often of left heart (e.g. LBBB

103
Q

What are common causes of dilated cardiomyopathy?

A 
Ischemic
Alcohol
Chagas disease
Adriamycin
Radiation
104
Q

What is the treatment for all forms of dilated cardiomyopathy?

A

ACEi/ARB, beta-blockers, spironolactone

*Digoxin decreases symptoms but doesn’t prolong survival

105
Q

What is the mainstem of therapy of hypertrophic cardiomyopathy?

A

Beta blockers and diuretics

106
Q

What is Kussmaul’s sign? Which form of cardiomyopathy is it found in?

A

Increase in jugular venous distension seen on inhalation.

Restrictive cardiomyopathy

107
Q

What is the single most accurate test of etiology of restrictive cardiomyopathy?

A

Endomyocardial biopsy

108
Q

What is the classic presentation of pericarditis?

A

Pleuritic CP better when sitting up and leaning forward

109
Q

Buzzword

Friction rub on exam

A

Pericarditis

110
Q

Buzzwords

ST segment elevation in all leads
PR segment depression in lead II

A

Pericarditis EKG findings (the latter is pathognomonic)

111
Q

What is the best initial therapy for pericarditis?

A

Colchicine combined with an NSAID

112
Q

What is the classic presentation of pericardial tamponade?

A

SOB, hypotension, jugular venous distension (Kussmaul’s sign), muffled heart sounds pulsus paradoxus, electrical alternans

113
Q

Describe the physiology of pulsus paradoxus

A

Inhalation causes increased venous return to right heart which compresses the LV and reduces SBP. In pericardial tamponade the whole heart is compressed so on inhalation it decreases by > 10 mmHg

114
Q

Equalization of all pressures in the heart during diastole seen on right-heart cath should make you suspicious of ….

A

Pericardial tamponade

115
Q

What is the best initial therapy for pericardial tamponade? What is the most effective long-term therapy?

A

Initial: pericardiocentesis

Long-term effectiveness: pericardial window placement

116
Q

A patient presents with SOB, edema, and jugular venous distension. CXR shows calcification encircling the heart. What is the dx?
What is the best initial mgmt? Most effective?

A

Constrictive pericarditis (often with signs of chronic right heart failure)

Initial: diuretic
Most effective: pericardial stripping (surgical removal of pericardium)

117
Q

Buzzword

Difference in BP between left and right arms

A

Aortic dissection

118
Q

In a thoracic aorta dissection case what medicines should you start quickly? What do you order for diagnosis?

A

Beta-blockers and nitroprusside

CTA/MRA/TEE (any are correct)

119
Q

What should you screen for in men >65 yo who have smoker or currently do?

A

Abdominal aortic aneurysm with ultrasound

120
Q

When abdominal aortic aneurysms are greater than ____ they are repaired surgically

A

5 cm

121
Q

What is the best initial test for dx of peripheral arterial disease? Most accurate?

A

Initial: ABI
Accurate: Angiography

122
Q

Cilostazol is a medication used in what condition and why?

A

PAD because it is a vasodilator capable of helping the symptoms of claudification in the legs

123
Q

Do CCBs help in PAD? Why?

A

No. CCBs dilate the muscular layer of the artery but the narrowing in the artery is closer to the lumen of the vessel

124
Q

You find afib on an EKG of a patient who comes in the ED. What additional tests may you want to order?

A

Echo (look for valve function, clots, or LA size)
Thyroid testing
Electrolytes
CK-MB/Troponins

125
Q

Tx of unstable afib

A

Synchronized cardioversion

126
Q

What defines being hemodynamically unstable?

A

SBP

127
Q

Tx stable afib

A

1) Rate control patients with beta-blockers, CCB, or digoxin

2) Anticoagulate if persisted > 2 days or unsure how long its been present

128
Q

Should you heparin bridge patients with afib before placing them on warfarin?

A

No

129
Q

What is the use of CHADS2? What are its components? How does it dictate treatment decision?

A

Estimates the risk of stroke in patients with afib
C= CHF; H = HTN; A = Age >75; D = DM; S = Stroke or TIA (worth two points)
If patients have score of 1 put on ASA
If patients have score 2 or greater than warfarin

130
Q

Tx of unstable aflutter

A

Synchronized cardioversion

131
Q

Tx of stable aflutter

A

Rate control similar to afib and consider anticoagulating

132
Q

Polymorphic P waves in an arrhythmia associated with COPD is ….
What is tx?

A

Multifocal atrial tachycardia (MAT)

Oxygen first then diltiazem (DO NOT GIVE B-BLOCKERS)

133
Q

Tx unstable SVT (initial mgmt)

A

Synchronized cardioversion

134
Q

Tx stable SVT (initial mgmt)

A

Vagal maneuvers. If those don’t work then give IV adenosine

135
Q

Tx SVT (long-term mgmt)

A

Radiofrequency catheter ablation

136
Q

Worsening of SVT after giving CCB or digoxin may actually be what arrhythmia?

A

Wolf-Parkinson-White Syndrome

137
Q

Tx Wolf-Parkinson-White (best initial)

A

Procainamide

138
Q

Tx Wolf-Parkinson-White (best long-term mgmt)

A

Radiofrequency catheter ablation

139
Q

SVT alternating with Vtach may indicate what arrhythmia?

A

WPW

140
Q

Tx unstable Vtach

A

Synchronized cardioversion

141
Q

Tx stable Vtach

A

Amiodarone, lidocaine, procainamide, magnesium

142
Q

What is torsades de pointes and what should always be given?

A

Undulating Vtach often caused by prolonged QT interval

Magnesium should always supplement medical or electrical mgmt

143
Q

Tx Vfib

A

Unsynchronized cardioversion

144
Q

Tx pulseless VTach

A

Unsynchronized cardioversion

145
Q

What should you order for concern of syncope?

A

EKG, Troponins/CK-MB, Echo, Head CT

Step 3 (19 decks)

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