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UWorld Medicine HY > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Key lab findings with cholesterol emboli

A

Eosinophilia, eosinophiluria, and low complement

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2
Q

Skin findings in cholesterol emboli

A
  1. Livedo reticularis (reticulated, mottled, discolored skin due to swollen venules from capillary obstruction)
  2. Blue toe syndrome
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3
Q

Internal organ damage in chiolesterol emboli

A
  1. Acute kidney injury
  2. Pancreatitis
  3. Mesenteric ischemia
  4. Embolic stroke, amaurasis fugax
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4
Q

3 potential triggers of vasovagal syncope

A

Stress, pain, or urination

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5
Q

What, if any, are the warning signs of:

  1. Syncope 2/2 arrhythmia
  2. Syncope 2/2/ orthostatic hypotension
  3. Vasovagal syncope
A
  1. Arrhythmia: no warning
  2. Orthostatic hypotension: lightheadedness when standing up
  3. VasovagaL; nausea, diaphoresis, pallor in response to stress, pain, or urination
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6
Q

What can be done to abort a vasovagal syncope episode when a person starts feeling nauseous, sweaty, and pale?

A

Physical counterpressure measures (PCM: squatting, arm-tensing, leg-crossing, and leg-crossing with lower body muscle tensing)

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7
Q

Treatment of primary Raynaud’s syndrome? Secondary?

A

Primary: Trigger avoidance and CCBs if necessary
Scondary: The same, plus aspirin to patients at risk for digital ischemia

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8
Q

Difference between primary and secondary Raynaud’s in terms of:

  • Demographics
  • Symmetry
  • Risk of tissue injury
A

Demographics: Primary is younger women (<30), secondary is more older men (>40)
Symmetry: Primary is symmetric, secondary may be asymmetric
Risk of tissue injury and ulceration: only in secondary

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9
Q

Causes of secondary Raynaud’s syndrome (6)

A
  1. Connective tissue disease (lupus, scleroderma)
  2. Occlusive vascular disease
  3. Hyperviscosity syndromes
  4. Sympathomimetic drugs
  5. Birth control pills
  6. Smoking
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10
Q

An ICU patient on pressures has necrosis of distal fingers and toes. Likely cause?

A

Norepinephrine-induced vasospasm (can also caused mesenteric ischemia and AKI)

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11
Q

Most common location of cardiac myxoma?

Potential hemodynamic consequence?

Murmur?

A

Mostly in LA.
Can mimic mitral stenosis by blocking LA outflow, may lead to HF
Early diastolic mumor - “tumor plop”

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12
Q

Complications of cardiac myxoma (3)

A
  1. LA outflow obstruction and heart failure
  2. Invasion leading to arrhythmias or heart block (or effusion)
  3. Emboli (e.g. stroke)
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13
Q

Murmurs that get louder with standing and valsalva and quieter when squatting

A

HOCM and MV prolapse

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14
Q

Enlarged “water bottle” cardiac silhouette on CXR

A

Pericardial effusion (may follow URI)

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15
Q

Signs of pericardial effusion on EKG

A
  1. Electrical alternans (in voltage amplitude)

2. Low-voltage QRS complexes

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16
Q

Clinical signs of cardiac tamponade

A

Beck’s triad: hypotension, elevated JVP, muffled/distant heart sounds
Pulsus paradoxus may also be seen (also seen in constrictive pericarditis, sever asthma/COPD)

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17
Q

What may be seen on CXR in constrictive pericarditis?

A

Pericardial calcifications

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18
Q

Heart sounds in constrictive pericarditis

A

Pericardial friction rub: high-pitched grating/squeking sound during systole (most common), diastole, or both

Pericardial knock: high-frequency mid-diastolic sound (due to abrupt cessation of diastolic filling)

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19
Q

JVP increases or stays the same with inspiration. Cause?

A

Kussmaul’s sign due to constrictive pericarditis

(Normally JVP decreases during inspiration due to blood being drawn into the chest and heart, but here it cannot take the extra volume)

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20
Q

Sharp x and y descents on central venous tracing. Cause?

A

Constrictive pericarditis

Sharp X descent (systole): RA cannot relax fully because of pericarditis

Sharp Y descent (diastole): RV filling is limited

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21
Q

Causes of constrictive pericarditis (4)

A
  1. Idiopathic
  2. Viral
  3. Tuberculosis
  4. Iatrogenic (radiation or heart surgery)
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22
Q

Pain of acute pericarditis

A

Sharp, pleuritic, and relieved by leaning forward

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23
Q

EKG in acute pericarditis

A

Diffuse ST elevation and PR depression

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24
Q

First-line treatment for acute pericarditis?

Alternative?

A

First-line: NSAIDs

Alternative: Colchicine

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25
Q

Treatment for Dressler’s syndrome (post-MI autoimmune pericarditis)

A

High-dose aspirin

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26
Q

Type of pericarditis that does not affect the myocardium

A

Uremic pericarditis (no EKG changes)

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27
Q

Treatment for uremic pericarditis

A

Hemodialysis

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28
Q

Most common predisposing valvular anomaly leading to endocarditis

A

Mitral valve prolapse (often with MV regurgitation)

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29
Q

Immunologic phenomena in bacterial endocarditis

A
  1. Osler nodes (painful fingertip nodules)
  2. Roth spots (retinal hemorrhage with pale centers)
  3. Glomerulonephritis
  4. Rheumatoid factor

(Janeway lesions, splinter hemorrhages, etc are embolic)

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30
Q

Embolic phenomena in bacterial endocarditis

A
  1. Septic emboli to brain (stroke), fingers (gangrene),e tc
  2. Renal or splenic infarcts
  3. Splinter hemorrhages
  4. Janeway lesions (painless)
  5. Conjunctival hemorrahge

(Osler nodes, Roth spots, and glomerulonephritis are immunoloigic)

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31
Q

Difference between Osler’s nodes and Janeway lesions

A

Osler’s nodes: painful and palpable (on fingertips, immune mediated)

Janeway lesions: painless

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32
Q

What can cause AV block in bacterial endocarditis?

A

Perivalvular abscess

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33
Q

Effect of inspiration on right-sided murmurs

A

Increased

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34
Q

Clinical triad of splenic abscess in endocarditis

A

Fever, leukocytosis, LUQ pain

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35
Q

Modified Duke criteria for bacterial endocarditis

A

Definite: both major or one major and 3 minor
Possible: one major and one minor or 3 minor
Major:
1. Blood cx with typical organism
2. Valvular vegetation
Minor (6): Predisposing cardiac lesion, IV drug use, fever, embolic phenomena, immunologic phenomena, atypical blood cx organism.

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36
Q

Subacute endocarditis associated with dental procedure or respiratory tract infection

A
  1. Strep viridans: mostly S. mutans and S. anguis (others are S. mitis and S. oralis)
  2. Less commonly, Eikenella corrodens (one of the HACEK)
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37
Q

Endocarditis associated with IBD and colon cancer

A

Strep gallolyticus (formerly named Strep bovis)

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38
Q

Endocarditis associated with prosthetic valves, implanted devices, and intravascular catheters

A

Staph epi

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39
Q

Endocarditis associated with nosocomial UTIs

A

Enterococcus

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40
Q

Right-sided endocarditis associated with IV drug use

Empiric therapy?

A

Staph aureus most commonly (can also be strep or enterococci)

Empirically treat with vancomycin

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41
Q

Medication for hyperlipidemia that leads to flushing and itching?

What can be given to help?

A

Niacin

Can give aspirin to reduce flushing (flushing is prostaglandin mediated)

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42
Q

Who should be on a statin?

A
  1. All diabetics 40-75
  2. Hyperlipidemia (e.g. LDL >190)
  3. Clinically significant atherosclerotic disease (ACS/MI, angina, stroke/TIA, PAD)
  4. ASCVD risk 7.5% or more
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43
Q 
RA and PCWP in cardiogenic shock?
Hypovolemic shock?
Anaphylactic shock?
Tension pneumothorax?
Massive PE?
A

Cardiogenic: Both elevated
Hypovolemic: Both decreased
Anapylactic/septic: Both normal or decreased
Tension pneumothorax: both decreased (decreased venous return)
Massive PE: high RA, decreased PCWP

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44
Q

A ventilated patient has decreased CO and low RA pressure - potential cause?

A

Pneumothorax due to barotrauma on PEEP (high pressure leads to elevated intrathoracic pressure, kinda like a tension pneumothorax)

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45
Q

Effect of large AV fistula on hemodynamics

A
  1. Low diastolic pressure (decreased vascular resistance)
  2. Wide pulse pressure (high venous return)
  3. May lead to high-output heart failure
46
Q

JNC 8 guidelines for target BP

A

<140/90 for all under 60 years and all with CKD or DM

<150/90 in patients over 60 w/o CKD or DM

47
Q

JNC guidelines on initial antihypertensive agent in CKD? DM?

A

CKD or DM: ACEI/ARB

48
Q

JNC 8 guidelines for initial hypertensive agent in those without CKD or DM, by race

A

Black: Thiazide or CCB, not ACEI/ARB

Other race: any of thiazide, CCB, or ACEI/ARB

49
Q

Labs for a new diagnosis of hypertension

A
  1. Urinalysis (for occult hematuria and urine protein/creatinine ratio)
  2. Chemistries
  3. Lipid panel
  4. EKG
50
Q

Most effective lifestyle change in essential hypertension?

Second-most?

A

Most: Weight loss
Next: DASH diet (rich in fruits, vegetables, low-fat dairy)

51
Q

Causes of secondary hypertension (8)

A 
Renal:
1. Renal parenchymal disease
2. Renal artery stenosis
Endocrine
3. Primary aldosteronism
4. Pheochromocytoma
5. Cushing syndrome
6. Hypothyroidism and hyperthyroidism
7. Primary hyperthyroidism
Vascular:
8. Aortic coarctation
52
Q

Treatment-refractory systemic hypertension with recurrent flash pulmonary edema

A

Consider renal artery stenosis

53
Q

Hypertension patient develops hypokalemia after staring a thiazide diuretic

A

Primary aldosteronism

54
Q

Sequence of the work-up for primary aldosteronism

A
  1. Aldosterone / renal ratio (will be >20)
  2. Adrenal suppression test (salt load will not suppress aldosterone level)
  3. CT of adrenals
    4a. If adenoma on CT in a younger patient (<35-40), can go to surgery
    4b. But if it is an older patient (>35-40), do adrenal venous sampling to confirm the adenoma is the source
55
Q

Treatment for primary aldosteronism due to bilateral adrenal production

A

Aldosterone receptor blockers: spironolactone or eplerenone

56
Q

Causes of isolated systolic hypertension (ISH) (3)

A
  1. Stiff aorta and major arteries
  2. Aortic regurgitation
  3. Hyperdynamic states (anemia, hyperthyroid, AV fistula)
57
Q

Key physical exam finding in malignant hypertension

A

Papilledema, retinal hemorrhage, or exudates

58
Q

Hypertensive encephalopathy

A

Severe hypertension with cerebral edema and non-localizing neurologic signs and symptoms

59
Q

Possible kinds of end organ damage in hypertensive emergency (10)

A 
Brain:
1. Hypertensive encephalopathy
2. Ischemic or hemorrhagic stroke
3. Subarachnoid hemorrhage
4. Retinopathy
Cardiac/Vascular
5. Acute heart failure
6. Acute coronary syndrome
7. Acute pulmonary edema
8. Aortic dissection
Other:
9. Acute hypertensive glomerulosclerosis
10. Microangiopathic hemolytic anemia
60
Q

Definition of pulmonary hypertension

A

PA pressure >25 mm Hg

61
Q

Groups of pulmonary hypertension

A

1: Primary PA HTN (idiopathic, genetic, connective tissue disease)
2. Left heart failure
3. Lung disease / hypoxia
4. Thromboembolic (multiple PEs)
5. Mixed/other (sarcoidosis, vasculitis, PV)

62
Q

Treatment options for idiopathic pulmonary hypertension

A
  1. Endothelin receptor blockers like bosentan
  2. PDE5 inhibitors like sildenafil
  3. Prostanoids like epoprostenol
63
Q

Treatment for pulmonary hypertension due to left heart failure

A

Loop diuretics and ACEI/ARB

64
Q

Treatment for pulmonary hypertension due to chronic lung disease

A

Oxygen and potentially bronchodilators

65
Q

Treatment for pulmonary hypertension due to chronic thromboembolic occlusion

A

Long-term anticoagulation

66
Q

Potential EKG changes in mitral stenosis

A
  1. P mitrale: broad notched P wave
  2. Atrial tachyarrhythmias may be seen
  3. RV hypertrophy may be seen: tall R in V1, V2
67
Q

What symptom can mitral stenosis lead to due to compression?

A

Hoarseness due to compression of the recurrent laryngeal nerve, due to LA hypertrophy

68
Q

Arrhythmia that may be seen in mitral stenosis

A

Atrial fibrillation (due to LA dilation) (also seen in mitral regurgitation)

69
Q

Most common cause of mitral regurgitation in the first world? In the developing world?

A

First-world: mitral valve prolapse (myxomatous degeneration)
Developing world: rheumatic heart diase

(Other causes: MI, endocarditis, mitral annular calcification)

70
Q

Holosystolic murmur with accompanying S3

A

Mitral regurgitation

71
Q

Low-pitched diastolic rumble with a loud S1 and opening snap after S2

A

Mitral stenosis

72
Q

Arrhythmia that may be seen in mitral regurgitation

A

Atrial fibrillation (due to LA dilation) (also seen in mitral stenosis)

73
Q

Valve disease following pacemaker placement

A

Tricuspid regurgitation (damage to valve or inadequate leaf coaptation to the wire)

74
Q

Diastolic decrescendo murmur

A

Aortic regurgitation

75
Q

Most common cause of aortic regurgitation in young adults in developed countries

A

Congenital bicuspid valve

Other causes: endocarditis, rheumatic heart disease, Marfan syndrome, syphilitic aortitis

76
Q

Pulsus parvus et tardus

A

Aortic stenosis

77
Q

Mid-to-late peaking systolic murmur with soft single S2

A

Aortic stenosis

78
Q

LV outflow obstruction with left-right asymmetry of carotid pulses and BP between arms

A

Supravalvular aortic stenosis: congenital narrowing the ascending aorta

(Often also have coronary artery stenosis)

79
Q

What is classic angina pectoris?

Atypical angina?

A

Classic angina has all three of:

  1. Typical location, quality, and duration
  2. Provoked by exercise and/or emotional upheaval
  3. Relieved with nitroglycerin or rest

Atypical angina: two out of three

80
Q

First-line treatment of stable angina?

Alternate or adjunct?

A

First-line: Beta-blockers

Alternate/adjunct: CCBs

(May also use sublingual nitroglycerin for acute episodes, and may add long-acting nitrates)

81
Q

When can you go directly to coronary angiography (e.g. no stress test) in the work-up of suspected stable angina pectoris?

A

Classic anginal chest pain in a man over 40 or a woman over 60
(Classic angina has all three of:
1. Typical location, quality, and duration
2. Provoked by exercise / emotional upheaval
3. Relieved by nitroglycerin / rest)

82
Q

When do you not use exercise EKG as the initial stress test?

A
  1. Unable to exercise to target heart rate (85% of maximum, which is 220-age)
  2. Pacemaker or LBBB (difficult to interpret)
83
Q

When does revascularization improve outcomes in chronic stable angina? (4)

A
  1. Angina refractory to medical therapy
  2. Involvement of a large area of myocardium on stress testing
  3. Left-main and 3-vessel disease
  4. Significant CAD w/ reduced LV systolic function
84
Q

What does a fixed perfusion defect represent on technetium-99 myocardial perfusion imaging stress testing?

Variable?

A

Fixed: scar tissue
Reversible: ischemia due to CAD

85
Q

Which of these do you hold and which do you continue prior to cardiac stress testing?

  1. ACEI/ARB
  2. Beta blockers
  3. CCBs
  4. Digoxin
  5. Diuretics
  6. Nitrates
  7. Statins
A

Hold beta-blockers, CCBs, and nitrates (these all immediately impact cardiac dynamics)

Continue others (ACEI/ARB, digoxin, diuretic, statins)

86
Q

Treatment for vasospastic angina

A

CCBs (e.g. diltiazem)

87
Q

Medications to avoid / be cautious with in vasospastic angina

A

Non-selective beta-blockers (e.g. propanolol): loss of beta2 vasodilation can worsen vasospasm

Aspirin: Inhibiting prostacyclin production can worsen vasospasm

88
Q

Medical treatment for acute STEMI

A 
MONABASH + dual antiplatelet:
Morphine prn for pain
Oxygen prn (sat >92%)
Nitroglycerin prn for pain
Aspirin (chewed) + plavix
Beta blocker
ACEI
Statin
Heparin
89
Q

When are beta-blockers CI in acute MI

A

Decompensated HF or bradycardia

90
Q

Treatment of patients with MI who have decompensated HF but normal/high BP?

If they have hypotension?

A

Normal BP: Supplemental O2 and a loop diuretic

Hypotension: Supplemental O2 and a vasopressor (e.g. NE), +/- loop diuretic

91
Q

What does S4 indicate?

A

Stiff LV wall (can be seen with MI, hypertension)

92
Q

Treatment of unstable sinus bradycardia during an acute MI

A

IV atropine

93
Q

Most common arrhythmias within 10 minutes of occlusion in MI?

10-60 minutes after?

A

First 10 minutes: re-entrant ventricular arrhythmias

10-60 minutes: Abnormal automaticity

94
Q

Location and vessel of MI with ST elevation in V1-V4

A

Anterior MI: LAD

95
Q

Location and vessel of MI with ST elevation in I, aVL, V5, and V6, and ST depression in II, III, and aVF

A

Lateral: LCX or diagonal artery

96
Q

Location and vessel of MI with ST depression in V1-V3

A

Posterior: RCA (if right-dominant, 70%) or L circumflex (if left-dominant, 20%)

(Other 10% are co-dominant)

97
Q

Location and vessel of MI with ST elevation in II, III, and aVF

A

Inferior MI: usually RCA (80%), sometimes L circumflex

98
Q

Location and vessel of MI with ST elevation in V1 > V2 and III > II

A

Right ventricle: RCA occlusion

99
Q

What vessel occlusion(s) can lead to SA node block?

A

RCA (60%) or L circumflex (40%)

100
Q

What vessel occlusion(s) can lead to AV node block?

A

RCA (80%), L circumflex 20%

101
Q

Treatment for MI with JVD but clear lungs?

What should not be given?

A

This is an RV MI:

  • Give IV saline to increase preload
  • Avoid vasodilators like nitrates (reduce preload)
102
Q

Treatment of pericarditis shortly after MI

A

Aspirin and/or colchicine

Avoid other NSAIDs

103
Q

Acute mitral regurgitation during MI: Cause? Murmur? Complication?

A

Cause: papillary muscle rupture in inferior MI

Murmur: may be MR murmur, but may be little or no murmur due to early equalization of LA and LV pressures

Complication: acute pulmonary edema

104
Q

MI complicated by chest pain, shock, a new holocystolic murmur, and left and right heart failure?
Type of MI seen in?

A

Intraventricular septum rupture. May be seen with LAD or RCA MI

105
Q

MI complicated by chest pain, shock, and distant heart sounds?

A

Free wall rupture. May be seen with LAD MI (the “widowmaker”)

106
Q

Late complication of MI leading to HF, arrhtyhmia, mitral regurgitation, or mural thrombus

A

Ventricular aneurysm

107
Q

Persistent ST elevation well after MI

A

Ventricular aneurysm

108
Q

Medications shown to improve morbidity and mortality in CAD patients

A
  • Dual antiplatelet therapy
  • Beta-blockers
  • ACEIs/ARBs
  • Statins
  • Aldosterone antagonists (e.g. spironolactone) w/ EF <40% and symptomatic HF or DM)
109
Q

How is treatment of cocaine-induced MI different than a regular MI?

A
  • Give benzodiazepenes
  • Beta-blockers are CI (loss of beta2) - can give CCB instead
  • No fibrinolytics (increased risk of intracerebral hemorrhage)
  • Otherwise similar: aspirin, O2, nitrates, can do PCI
110
Q

Medication that can help prevent pathologic remodeling if started within 24 hours of an MI

111
Q

Molecular target of clopidogrel

A

P2Y12 receptor on platelets

UWorld Medicine HY (7 decks)

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