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EM Board exam > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Cocaine associated chest pain
percentage with AMI

A

6%

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2
Q

Acute myocardial infarction

anatomic difference STEMI vs NSTEMI

prognosis STEMI vs NSTEMI

A

STEMI: trans mural infarction, full thickness of myocardium

NSTEMI: seven the cardio, partial wall thickness

prognosis similar

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3
Q

Acute myocardial infarction
percentage with normal EKG
significant Q wave

A

percentage with normal EKG: 4%
significant Q wave: 1 square wide, 1/3 of height of R wave

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4
Q

Differential diagnosis of ST segment elevation

A

–Acute MI

–Prinzmetal’s angina (vasospasm)

–Pericarditis

–Ventricular wall aneurysm

–Benign early repolarization

–Bundle branch block

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5
Q

Prinzmetal’s angina - EKG diagnostic pearl to distinguish from STEMI (1)

LV aneurysm: EKG diagnostic pearl to distinguish from STEMI (4)

A

Prinzmetal: Usually no reciprocal depression

LV aneurysm:

No reciprocal depression

Qwaves present

Look for old ECGs — no change

No serial changes

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6
Q

Posterior MI EKG description

A

Posterior MI (ST-depression with tall R-waves and upright Ts in V1-2)

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7
Q

Sgarbossa criteria - use and description (2)

A
  • ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
  • ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads (concordant with the QRS).
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8
Q
A

Possible isolated posterior MI

ST-depression + tall R-waves in V1-2 + upright Ts

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9
Q

Diagnosis

A

MI in setting of LBBB - Sgarbossa: concordance in aVL, V5-6

Scarbosa:

  • ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
  • ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads (concordant with the QRS).
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10
Q
A

concordance in V3

MI by Scarbosa

  • ST-segment elevation measuring ≥1 mm concordant with the QRS in any lead.
  • ST-segment depression measuring ≥1 mm in any of the V1 through V3 leads (concordant with the QRS).
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11
Q
A

STE in aVR à acute LMCA occlusion

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12
Q
A

deWinter T-waves acute LAD occlusion

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13
Q

Normalization of ischemia-related ST elevation

Early T wave inversions can be highly specific markers of reperfusion

accelerated idioventricular rhythm (rate 60-120) AIVR

A

Predictors of reperfusion in AMI

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14
Q
A

accelerated idioventricular rhythm (rate 60-120) AIVR

Benign after reperfusion, don’t supress

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15
Q

Troponin rise, peak and normalization

A

•Troponin

–3-6 hours (rises)

–12-24 hours (peaks)

–7-10 days (normalizes)

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16
Q

AMI oral meds

A

•Beta blocker (metoprolol) early IV discouraged

–Give within 24 hours orally but no rush

–Contraindications (asthma, CHF, bradycardia, hypotension; caution in RV MI)

•Addl. platelet inhibitors (in ED or cath lab)

–GP Ilb/IIIa receptor antags IV

–Clopidogrel, ticagrelor: can give oral load

–Prasugrel 60 mg oral load at cath; avoid if history of TIA or stroke

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17
Q

AMI thrombolytic therapy indications (3)

A

symptoms greater than 30 minutes, less than 12 hours

STEMI EKG criteria (STE 2 contig, posterior STEMI, LBBB + Scarbossa)

PCI would be > 90 minutes

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18
Q

absolute contraindications to thrombolytic therapy (6)

A
  • PCI immediately available
  • Active bleeding from any site
  • CVA within 6 months or hemorrhagic CVA at any time in the past
  • Intracranial or intraspinal surgery or trauma within 2 months
  • Intracranial or intraspinal neoplasm, aneurysm or AV malformation
  • Suspected aortic dissection
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19
Q

Early AMI arrhythmias with poor prognosis (5)

A

–2˚ Mobitz II (progress to 3˚)

–3˚ AV block from anterior MI

–Persistent sinus tach, SVT, A-fib

–New BBB, bifascicular block (RBBB (RBBB + hemiblock)

–Left posterior hemiblock (large infarct size)

•Increased risk of pump failure, mortality

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20
Q

AMI valve dysfunction

A

•Acute mitral regurgitation (usually due to ischemic dysfunction of papillary muscles)

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21
Q

chest pain, hypertension, JVD, lungs CTA

A

inferior STEMI with RV infarct

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22
Q

late complications of MI - weeks

systemic (1)

Pericardial and eponym

Myocardial (3) and tx

A

systemic (1): embolism of mural thrombus

Pericardial and eponym: pericarditis, Dressler’s syndrome if approximately 2 to 8 week timeframe

Myocardial (3) and tx: acute mitral regurgitation from papillary muscle rupture, LV free wall rupture, septal wall rupture (acute VSD with CHF)

Tx -> Hemodynamic support, IABP, OR

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23
Q

high-output heart failure causes (5)

A

–Thyrotoxicosis

–Anemia

–A-V fistula

–Paget’s disease of the bone

–Beriberi

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24
Q

ssystolic dysfunction leads to high levels of (2) which in turn leads to (1)

A

renin and anngiotensin, high afterload

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25
Q

heart failure
afterload reduction: 3

preload reduction: 3

hypotension management: 2

A

afterload reduction: nitroglycerin, ACE inhibitor, nitroprusside

preload reduction: nitrates, diuretics, and nesiritdie

hypotension management: dobutamine, IABP

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26
Q

Endocarditis risk factors, less known (two)

valves affected, relative hierarchy

most common infective agent for IVDA and prosthetic valves

A

Endocarditis risk factors, less known (two): mitral valve prolapse, pacemaker

valves affected, relative hierarchy: –Mitral > aortic > tricuspid (IVDA) > pulmonic

most common infective agent for IVDA and prosthetic valves: staph aureus

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27
Q

Endocarditis
most common pathogen for acute and subacute forms

left-sided (2)

right-sided (3)

A

Common pathogen: staph aureus and strep viridans respectively

left-sided (2): –S. viridans, S. aureus

right-sided (3): –S. aureus, S. pneumoniae, gram negatives

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28
Q

Endocarditis, most common pathogens
prosthetic valve, early:
aesthetic valve, late:

A

prosthetic valve, early: •S. epidermidis, S. aureus
aesthetic valve, late: •S. viridans, Serratia, Pseudomonas

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29
Q

Endocarditis, cutaneous stigmata (4)

A

–Osler nodes: tender nodules on the tips of the fingers and toes (Osler = Ow!)

–Janeway lesions: nontender, hemorrhagic plaques on the palms and soles

–Roth spots: retinal hemorrhages with central clearing

–Petechiae and splinter hemorrhages

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30
Q

Endocarditis treatment antibiotics

x or y + z; add this for prosthetic valves

A

•penicillins or vancomycin, and add aminoglycoside

–Add rifampin for prosthetic valves

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31
Q

Endocarditis,

indications for prophylaxis

A

High-risk cardiac conditions + dental procedure

–Prosthetic cardiac valve

–History of infective endocarditis

–Congenital heart disease (CHD)

–Cardiac transplantation recipients with cardiac valvular disease

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32
Q

Endocarditis,

prophylaxis medication, PCN all alternative PO and IV

A
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33
Q

Aortic stenosis
contraindicated medications

A

Nitrates and vasodilators

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34
Q

Aortic regurgitation
acute and chronic etiologies (2 each)

A

–Acute: endocarditis, dissection

–Chronic: RHD; also seen with Marfan’s syndrome

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35
Q

Mitral valve stenosis

Associated arrhythmias

A

•atrial tachyarrhythmias

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36
Q

Etiology of chronic mitral regurgitation (4)

A

•Etiology of chronic MR

–MVP

–Dilated cardiomyopathy

–RHD

–Mitral annulus calcification

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37
Q

Medical management of mitral regurgitation
acute (2)
chronic (3)

A

•Medical management of acute MR

–Afterload reduction

–IABP to temporize until surgery

•Medical management of chronic MR

–Symptomatic treatment of CHF

–Treatment of A-fib

–Endocarditis prophylaxis (s/p replacement)

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38
Q

Mitral valve prolapse

Symptoms (4)

Complications (2)

Endocarditis proph?

A

•Symptoms

–Chest pain (atypical)

–Dyspnea

–Anxiety

–Palpitations (increased incidence of SVT)

complications: rare, arrhythmias, thromboembolic disease, rare endocarditis
prophylaxis: no; anticoagulation and beta blockers as needed

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39
Q

Cardiomyopathy types (3)

A

•Three types

–Dilated cardiomyopathy

–Hypertrophic cardiomyopathy

–Restrictive cardiomyopathy

40
Q

Dilated cardiomyopathy
etiologies (8)

A

–Idiopathic (most common)

–Alcohol

–Peripartum

–Viral (myocarditis)

–End-stage CAD

–Sarcoidosis

–Amyloidosis

–Hypothyroidism

41
Q

Hypertrophic cardiomyopathy

etiology
mechanical pathophysiology (2)
A
  • Often familial autosomal dominant
  • Asymmetric thickening of septum causing two problems

–Noncompliant ventricle with decreased diastolic filling

–Dynamic obstruction of LV outflow (with mitral valve leaflets blocking outflow tract)

Leads to:

–Exertional syncope

–Sudden death

–Cardiac ischemia

–Dysrhythmias

42
Q

Hypertrophic cardiomyopathy

murmur louder with
murmur decreased with

A

murmur louder with: decreased preload (hypovolemia, standing, Valsalva)
murmur decreased with: increased afterload (squatting, Trendelenburg, handgrip, volume expansion)

43
Q

Hypertrophic cardiomyopathy

treatment (3) + contraindication

A

Treatment:

–Avoid exertion
(worsens obstruction and leads to arrhythmias)

–Negative inotropes (beta blockers, calcium channel blockers) to decrease obstruction

–Never use digoxin or positive inotropes (increased obstruction)

–Surgical myomectomy

44
Q
A

Hypertrophic cardiomyopathy with large amplitude QRS complexes, deep, narrow Qs

45
Q

Pericarditis

less common etiologies (4)

A

–Connective tissue disease

–Neoplasm

–Uremia

–Radiation

46
Q

Features

–Chest pain ________ with inspiration and swallowing

–Pain ________ on sitting up, bending forward

  • Rub________ on sitting up, bending forward
A

–Chest pain increases with inspiration and swallowing

–Relief on sitting up, bending forward (and may hear the rub better in this position)

–Rub (increased by leaning forward)

47
Q

Pericarditis

four stages of EKG changes

A

–Stage 1: Diffuse ST elevation (does not correspond to coronary artery distribution) & PR segment depression

–Stage 2: ST-segments and PR return to baseline

–Stage 3: T wave inversions

–Stage 4: Normalization of EKG

48
Q

Pericarditis

treatment (2)

A

ASA, NSAIDs, colchicine

49
Q

Pulsus paradoxus

Definition

A

Fall in systolic blood pressure greater than 10 during inspiration

50
Q

Pericardial Tamponade

ECHO findings (2)

A

•ECHO findings

–Effusion

–RV diastolic collapse (specific for tamponade)

51
Q

Myocarditis

etiologies (4)

A

–Idiopathic

–Infectious (usually viral, especially coxsackie B virus)

–Chemotherapy

–Connective tissue disease

52
Q

Hypertensive emergency

therapeutic goal

A

–rapid reduction in BP (reduce MAP 30%)

53
Q

Hypertensive emergency

agent choices for CNS (non-ischemic stroke), ischemic stroke, pregnancy induced

A

•CNS: encephalopathy, hemorrhagic CVA

–Nitroprusside

–Labetalol

•Ischemic stroke

–Hypertension usually resolves within hours

•Transient and cerebroprotective

–Treatment: observe, labetalol, nicardipine

•Pregnancy-induced hypertension, eclampsia

–Hydralazine

–Labetalol

–Magnesium sulfate for seizures

54
Q
A
55
Q

Hypertensive emergency

agent choices for cardiac ischemia/CHF, aortic dissection

A

cardiac ischemia/CHF: nitroglycerin, nitroprusside/Nicardipine if severe

aortic dissection: BB (esmolol, labetalol, propranolol), then nitroprusside or nicardipine

56
Q

Hypertensive emergency

agent choices for catecholamine crisis (pheochromocytoma, cocaine, MAOI)

A

–Alpha plus beta blocker is best

–Do not use beta blocker alone
(avoid unopposed alpha effect)

–Labetalol plus phentolamine (alpha blocker)

57
Q

Hypertensive emergency medications

nitroprusside
mechanism
half-life
use with
avoid in

A

mechanism: arterial and venous dilation
half-life: minutes
use with: beta-blocker to blunt reflex tachycardia
avoid in: pregnancy and renal patients due to cyanide metabolite

58
Q

Hypertensive emergency medications

labetalol
mechanism
contraindications (3)

A

Mechanism: beta greater than alpha blocker
contraindications: bronchospasm, CHF, AV blocks

59
Q

Hypertensive emergency medications

fenoldopam
mechanism
benefits

A

mechanism: dopamine agonist, no alpha or beta affects
benefits: may increase renal blood flow and sodium excretion

60
Q

Hydralazine
mechanism
side effects, acute and chronic

A

mechanism: arteriolar vasodilator
side effects, acute and chronic: reflex tachycardia, lupus Lake syndrome

61
Q

Aortic dissection

less common risk factors (four)

A
  • Collagen vascular disorders such as Marfan’s
  • Pregnancy (especially third trimester)
  • Bicuspid aortic valve
  • Aortic coarctation
  • Chest trauma, iatrogenic (cardiac catheterization)
62
Q

Aortic dissection

Stanford classification

A

–Type A: any dissection which involves ascending aorta (surgical treatment)

–Type B: descending aorta only (primarily medical management)

63
Q

Aortic dissection

best test

A

Best tests: TEE
alternatives: CT first-line MRI alternative

64
Q

Aortic dissection

treatment (3)

A

–Beta blockers, then nitroprusside for both types

–Stanford A: requires surgery

–Stanford B: 1/3 will require surgery for complics.

65
Q

AAA

location, majority

elective repair > *** cm

A

location, majority: infra renal

elective repair > 5 cm

66
Q

Acute limb ischemia

timing, embolus versus thrombus

A

timing, embolus versus thrombus: symbolic usually much more acute, thrombus most likely secondary to severe underlying atherosclerosis

67
Q

Acute limb ischemia

treatment (4)

A

–Vascular surgery consultation!

–Heparin (unless worried dissection/AAA)

–Embolectomy

–Bypass for atherosclerotic disease

68
Q

Virhow’s triad

what and the significance

A

Risk factors for VTE

–Stasis

–Hypercoagulability

–Endothelial damage

69
Q

Phlegmasia cerulea dolens and phlegmasia alba dolens

what?

A

–Uncommon, severe presentation of DVT

–Massive iliofemoral DVT

–Acute, severe, massive swelling

–Cyanotic, congested extremity (cerulea)

–Pale (alba) if arterial spasm causes “milk leg”

–Increased compartment pressure, ischemia

–May require surgery for compartment syndrome

70
Q

EKG changes, hyperkalemia (5)

A

Flat P wave

–Peaked T waves

–Wide QRS

–Prolonged QT (due to hypoCa) and PR

–Eventual sine wave and Vfib

Arrs:

–Bradydysrhythmias and AV blocks

–Tachydysrhythmias

71
Q

EKG changes, hypokalemia (4)

A

–PVCs

–U waves

–Prolonged QT

–ST segment depression

72
Q
A
73
Q
A

Hypercalcemia

74
Q
A

Hypocalcemia

75
Q

Electrolyte abnormalities that prolong the QT interval

A

– Hypokalemia

– Hypocalcemia

– Hypomagnesemia

76
Q

Torsade de Pointes

treatment (4)

A

–Magnesium (will shorten QT interval)

–Overdrive pacing

–Isoproterenol

–Cardioversion/defibrillation

–Magnesium infusion for prophylaxis after conversion

Do not use procainamide or amiodarone

77
Q

This condition and
other associated findings

A

Osborne wave (J) of hypothermia

Prolonged intervals

  • Sinus bradycardia
  • +/- muscle tremor artifact
  • Slow a. fib
  • V. fib / asystole
78
Q

EKG abnormality and description

A

Digoxin effect

–T wave depression

–ST downsloping (Salvador Dali moustache)

–QT shortened

79
Q

Digoxin arrhythmias at toxic levels (5)

A

–PVCs (most common dysrhythmia)

–Sinus and AV node blocks

–AV dissociation

–SVT (especially with blocks)

–Sinus bradycardia

80
Q

TCA EKG (5)

A
  • Sinus tachycardia (most common)
  • Prolonged QT
  • Right axis deviation
  • QRS width > 100 ms
  • Conduction blocks
81
Q

Multifocal atrial tachycardia

Description (2)

Tx (maybe)

avoid

A

–At least 3 different P wave morphologies

–Variable PR intervals

–Associated with

–Treat underlying condition

MgSO4 may be helpful; no shocks

82
Q
A

Multifocal atrial tachycardia

83
Q

WPW

Treatment caveats: wide complex and afib

A

wide complex: treat as VF

afib: procainamide or cardioversion, NO AV nodal blockade

(can potentiate conduction down the accessory pathway)

84
Q
A

WPW with a fib and variable conduction down accessory pathway

85
Q

Ventricular tachycardia
preferred drug hierarchy

Rate criteria

A

procainamide > amiodarone > lidocaine

rate greater than 120, usually greater than 150

86
Q

Accelerated idioventricular rhythm

what
underlying cause
treatment

A

what: wide complex regular rhythm rate 40 to 120
underlying cause: seen during reperfusion after ischemia
treatment: observation, atrial pacing if slow and hypotensive

87
Q
A

Accelerated idioventricular rhythm

88
Q

2nd° block

Mobitz 1: associated disease, tx (2)

Mobitz 2: associated disease, associated EKG finding, complication, treatment

A

Mobitz 1: inferior MI, atropine, occasionally transcutaneous spacing

Mobitz 2: anterior MI, associated with bundle branch block, progression to complete heart block, pacemaker

89
Q
A

2nd degreee Mobitz 1

90
Q
A

2nd degreee Mobitz 2

91
Q

Third-degree block

treatment caveat

A

Narrow complex may not need treatment, transient
wide complex, pacemaker

92
Q

Brugada

etiology of sudden death
genetics
racial epidemiology
treatment

A

etiology of sudden death: V. fib
genetics: autosomal dominant
racial epidemiology: Southeast Asian male
treatment: implantable defibrillator

93
Q

Diagnosis
EKG description

A

Brugada

  • Pseudo-RBBB pattern
  • ST elevations in V1 and V2
94
Q

Always assume wide complex tachycardia on the boards is

A

Ventricular tachycardia

95
Q

LLSA articles tips

bystander hands only CPR > Standard CPR

Post cardiac arrest

hyperoxia?

Temperature?

PCI?

A

bystander hands only CPR >> Standard CPR

Post cardiac arrest

hyperoxia? bad

Temperature? hypothermia

PCI? good for all STEMI, likely NSTEMI as well

96
Q

Alteplase/thrombolytics in STEMI - absolute contraindications (9)

A

Any PMH ICH, brain tumor, aneurysm, suspected dissection, active bleeding, bleeding, bleeding disorder

3 wks: CPR

6 wks: trauma/surgery, bleeding

3 mo: stroke

6 mo: Head trauma/brain surgery

EM Board exam (18 decks)

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