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Main Deck Step 2 Content Review > First Aid Step 2 CK - Cardiology > Flashcards

First Aid Step 2 CK - Cardiology Flashcards

1
Q

A normal PR interval is between ____________.

A

120 and 200 milliseconds

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2
Q

List two things that can cause a widened QRS complex.

A

•PVC • Bundle-branch block

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3
Q

The QRS complex should be no longer than ___________.

A

120 msec (three small boxes)

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4
Q

How does left bundle-branch block present on an EKG?

A

•QRS greater than 120 msec•Deep S and no R on lead V1• Tall R in I, V5, and V6

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5
Q

In addition to the rabbit ears, list two signs of right bundle-branch block.

A

•Wide R in V1 • Wide S in V6

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6
Q

What does it mean if QRS is positive in I and aVF?

A

Normal axis

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7
Q

What does it mean if QRS is positive in I and negative in aVF?

A

Left axis deviation

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8
Q

What does it mean if QRS is negative in I and positive in aVF?

A

Right axis deviation

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9
Q

The QTc should be no longer than _____________.

A

440 msec

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10
Q

Q waves should not be longer than ____________.

A

1/3 of the QRS amplitude

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11
Q

Go through the progression of ischemia.

A

•T wave inversion•ST depression or elevation•Q waves

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12
Q

What is poor R wave progression?

A

Normally, the R wave amplitude should increase from V1 to V5. If this doesn’t happen, it can be a sign of ischemia.

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13
Q

Go through the formula for determining left- and right-ventricular hypertrophy.

A

• LVH: amplitude of S in V1 + R in V5 or V6 is > 35 mm•RVH: right-axis deviation and an R wavein V1 > 7 mm

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14
Q

Go through the cardiac physical exam.

A

• Heart auscultation: murmurs, rubs, gallops, rate, rhythm•Point of maximum impulse •Jugular venous distension •Kussmaul sign (inspiring worsens JVD) •Hepatojugular distension • Edema•Pulses

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15
Q

An early decrescendo diastolic murmur is a sign of ____________.

A

aortic regurgitation

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16
Q

What is pulsus parvus et tardus?

A

A late and slow pulse that can be a sign of aortic stenosis

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17
Q

List four treatment pillars of atrial fibrillation.

A

•Anticoagulants•Beta-blockers (rate control)•Cardioversion / CCBs (for beta-blocker intolerance)•Digoxin (for refractory atrial fibrillation)

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18
Q

Explain how the CHADVAS system is used to determine when anticoagulation is needed.

A

CHA(2)DS(2) VAS•CHF (1 point)• HTN (1 point)•Age greater than 75 (2 points)•Diabetes (1 point)•Stroke history (2 points)•Vascular disease (1 point)•Age 65 - 74 (1 point)• Sex - female (1 point)Anti-coagulate for score 2+

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19
Q

What drug treats WPW?

A

Procainamide

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20
Q

First-degree AV block is defined as _______________.

A

a PR interval greater than 200 msec

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21
Q

What’s the difference between Mobitz I (Wenckebach) and Mobitz II heart block?

A

• I is progressive PR lengthening until a QRS is missed.•II is static PR with occasional QRS missed.(“ONE by ONE, the PR intervals lengthen in Mobitz ONE.”)

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22
Q

What is sick sinus syndrome?

A

A heterogeneous syndrome in which people develop sporadic bradycardia and tachycardiaThis is the most common indication for pacemaker placement!

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23
Q

Go through the causes of acute and chronic atrial fibrillation.

A

•Acute: PIRATES- Pulmonary disease- Ischemia- Rheumatic heart disease (mitral stenosis - > left atrial enlargement)- Anemia- Thyrotoxicosis- Ethanol- Sepsis•Chronic:- HTN- CHF

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24
Q

Those with atrial fibrillation typically have no _____________ on ECG.

A

P waves

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25
Q

What should you do in new-onset atrial fibrillation?

A

•If it’s unstable and been less than 2 days, then cardiovert.• If it’s been longer than 2 days or unclear, then must get echo to rule out atrial clot.

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26
Q

What is atrial flutter?

A

A circular pattern of electrical activity in the atria that does not involve rapid ventricular response Treat the same as atrial fibrillation.

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27
Q

Differentiate AV-nodal reentrant tachycardia (AVNRT) and AV-reentrant tachycardia (AVRT).

A

• Both involve electrical depolarization passing back into the atria from the ventricles.• AVNRT depolarizes the atria and the ventricles at the same time THROUGH the node.•AVRT depolarizes the atria through a pathway outside the node. This is the pathology of WPW tachycardia.

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28
Q

Describe paroxysmal atrial tachycardia.

A

In PAT, there is an ectopic atrial pacemaker site with a rate of greater than 100 BPM. It can be diagnosed with an EKG showing a P wave before every QRS but with an atypical axis.

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29
Q

What is the classic caveat of diuretics and digoxin use in CHF?

A

They improve symptoms but confer no mortality benefit.

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30
Q

Review CHF.

A

•There is no one test for CHF. It is a clinical syndrome. •History: - Dyspnea (initially exertional and finally at rest) - Chronic cough - Fatigue• Exam: - S3/S4 - Elevated parasternal lift - Pedal edema - Pulmonary edema (if left-sided), JVD/hepatomegaly (if right-sided)•Tests: - Echo: dilated or thickened ventricles -Elevated BNP

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31
Q

These things can precipitate PVCs: ________________.

A

•Hyperthyroidism•Electrolyte abnormalities•Hypoxia

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32
Q

If someone has ventricular tachycardia, what is the “big” question you need to ask to know how serious it is?

A

“Is it sustained (greater than 30 seconds) or non-sustained (less than 30 seconds)?” Non-sustained ventricular tachycardia is often asymptomatic. Sustained ventricular tachycardia can lead to hypotensive shock.

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33
Q

List two treatments for ventricular tachycardia.

A

•If unstable: cardioversion •If stable but symptomatic: amiodarone, lidocaine, procainamide

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34
Q

What is a key difference between ventricular fibrillation and torsades on an EKG?

A

Torsades will have narrow QRS complexes, while ventricular fibrillation will have wide QRS complexes.

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35
Q

What is the difference between cardioversion and defibrillation?

A

• Defibrillation is a non-synchronous shocking of ventricular fibrillation. It is non-synchronous because there is no rhythm in ventricular fibrillation, so it doesn’t matter when in the electrical activity of the heart you defibrillate.• Cardioversion is a synchronous shocking of the heart, used in unstable atrial fibrillation or ventricular tachycardia. The “synchronous” part means that it shocks during the R wave to reset unstable tachycardias.

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36
Q

List two electrolyte abnormalities that predispose to torsades.

A

•Hypokalemia•Hypomagnesemia

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37
Q

What is a good mnemonic for acute CHF treatment?

A

LMNOP•Lasix• Morphine•Nitrates• Oxygen• Position upright

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38
Q

In general, what are the goals of acute CHF treatment?

A

• Diurese to remove fluid overload (furosemide, ACE inhibitor)•Give oxygen to reduce tissue hypoxia•Position upright to reduce pulmonary congestion•Seek to identify the cause of the acute attack for prevention of future cases.Common causes include the following:- Medications: CCB, thiazolidinediones, NSAIDs- Valvular disease- Arrhythmia- Thyrotoxicosis

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39
Q

Review chronic therapy for CHF.

A

• Pharmacologic: - Prevent remodeling: Beta-blockers and ACE inhibitors or ARBs - Diurese: furosemide or hydrochlorothiazide - Reduce mortality: spironolactone - Address CAD risk (if that was the cause of CHF): ASA and statin • Lifestyle: - Decrease sodium and fluid intake • ICD in someone with EF less than 35% • Left-ventricular assist device in those unresponsive to medical therapy

40
Q

Review the signs of left- and right-sided heart failure.

A

•Left-sided: pulmonary edema on CXR, bibasilar rales, paroxysmal nocturnal dyspnea•Right-sided: hepatomegaly, JVD, peripheral edema

41
Q

How can you use an EKG to tease out systolic versus diastolic dysfunction?

A

LVH is a sign of diastolic dysfunction!

42
Q

Which diuretics cause gout?

A

Loop

43
Q

Which diuretic causes metabolic alkalosis?

A

ThiazidesThe extra sodium sent to the collecting tubule gets exchanged for H+ which is then excreted.

44
Q

Acetazolamide causes what pH abnormality?

A

Hyperchloremic metabolic acidosis

45
Q

List the causes of primary dilated cardiomyopathy.

A

• Idiopathic (most common!) • Alcohol• Pregnancy• Myocarditis•Drugs (doxorubicin, cocaine, AZT) • Thyroid dysfunction•Infection (Chagas, Coxsackie) • Beriberi

46
Q

List the causes of secondary dilated cardiomyopathy.

A

•HTN•Ischemia

47
Q

Go through the workup of dilated cardiomyopathy.

A

•Hx: gradual CHF symptoms•PE: JVD, S3, AV regurgitation • Dx: echocardiography

48
Q

How should you treat DCM?

A

• Address the cause: e.g., decrease ETOH, correct thyroid• Treat CHF (described in another two cards)

49
Q

Discuss how you can increase and decrease the HOCM murmur?

A

•It increases with decreased preload (because decreased fluid closes the aortic valve space): Valsalva, standing•It decreases with increased preload (ditto): straight leg raise.

50
Q

How is HOCM treated?

A

•Beta-blockers or CCBs to prevent over-excitation• Ablation/excision for severe cases•Avoid vigorous training

51
Q

List five causes of restrictive cardiomyopathy.

A

•Scarring (from surgery) • Fibrosis (from radiation) • Sarcoidosis• Hemochromatosis• Amyloidosis (from multiple myeloma, for instance)

52
Q

Typically, ________-sided heart failure signs predominate in restrictive cardiomyopathy (although both sides are affected).

A

right

53
Q

Prinzmetal angina classically affects _____________.

A

young women in the morning

54
Q

Again, review the “classic triad” of angina.

A

•Substernal chest pain• Provoked by exertion• Relieved by rest of nitroglycerin

55
Q

The pain of angina is usually described as _____________.

A

dull or pressure-like

56
Q

List four non-cardiac causes of chest pain.

A

• GERD• Anxiety• Pleuritic chest pain (pneumonia) • MSK

57
Q

Only __________ and __________ have been shown to improve mortality in angina.

A

ASA; beta-blockers

58
Q

What is the TIMI scoring system?

A

The Thrombolysis In Myocardial Ischemia scoring system gives the likelihood of benefit from enoxaparin in CAD: •Age greater than 65•ASA use in past 7 days•Known CAD•Three or more risk factors (HLD, HTN, DM, smoking)•Severe angina•ST elevation•Enzymes You get one point for each. Greater than 2 indicates enoxaparin.

59
Q

Go through the workup and treatment of unstable angina.

A

•Admit to hospital• Do ECG (if STEMI, then cath lab) •Take enzymes (if NSTEMI, then cath lab later) •Initiate MOAN (morphine, oxygen, ASA, NTG) •Serial enzymes to rule out MI • Do TIMI scoring and give anticoagulation for greater than 2

60
Q

Go through the ECG changes of an MI.

A

• Peaked T waves•ST elevation•Q waves•ST normalization•T normalization

61
Q

In an MI involving the RCA, you’ll see ST elevation in leads ______________.

A

II, III, and aVF

62
Q

Anterior MIs (from infarction of the LAD) show ST elevation in leads _____________.

A

V1 - V4

63
Q

LCA occlusions cause ST elevation in which leads?

A

I, aVL, V5, and V6

64
Q

Posterior infarctions cause ST elevations in ___________.

A

… trick question: they cause ST depressions in V1 and V2, and they will cause ST elevations in leads put on the back (V7 and V8)

65
Q

Go through the immediate management of MI.

A

• First, perform PCI if within 90 minutes and no contraindications. •Second, give tPA if cannot do PCI and within 3 hours of chest pain onset. •Bypass for (1) triple vessel disease, (2) depressed ventricular function, or (3) left main coronary disease

66
Q

Review the post-MI complications, giving a rough timeline.

A

•Immediate: heart failure, arrhythmia•2-4 days: arrhythmia, pericarditis •5-10 days: LV wall rupture, papillary muscle ruptue•Weeks-months: ventircular aneurysm, thrombi, CHF, Dressler syndrome (pericarditis, leukocytosis, elevated ESR)

67
Q

Review the labs that define dyslipidemia: •Total cholesterol: _______•LDL: ________• Triglycerides: ________• HDL: _________

A

•Total cholesterol: greater than 200•LDL: greater than 130• Triglycerides: greater than 150• HDL: less than 40

68
Q

List some common causes of dyslipidemias.

A

•Obesity• DM•Familial hypercholesterolemia•Alcoholism• Hypothyroidism•OCP use•Nephrotic syndrome• Diuretic use

69
Q

What are the lipid screening guidelines?

A

Lipid panel every 5 years in those older than 35 or older than 20 with risk factors

70
Q

This guideline is in flux now, but it used to be that you would treat for ASCVD risk of ___________ in ten years.

A

7.5% or higher

71
Q

Free wall rupture with pulseless electrical activity should be treated with ________________.

A

ACLS and pericardiocentesis

72
Q

Renal artery stenosis can be diagnosed with what two tests?

A

• Renal artery Doppler• MRA

73
Q

Review the mnemonic for causes of pericarditis.

A

CARDIAC RIND• Collagen disorders • Aortic dissection• Radiation•Drugs • Infection •Acute renal failure (uremia) •Cardiac (MI) •Rheumatic fever• Injury (post-surgical) • Neoplastic •Dressler syndrome

74
Q

What is the mechanism of minoxidil?

A

Like hydralazine, it decreases arterial resistance.

75
Q

A person comes in with a history and exam suspicious for pericarditis (i.e., pleuritic chest pain, fever, dyspnea). What tests should you order?

A

• ECG: rule out MI•CXR: rule out pneumonia

76
Q

The most important determiner of tamponade severity is ________________.

A

the rate of fluid accumulation

77
Q

What is the Kussmaul sign?

A

Increased JVD on inspiration

78
Q

Tamponade should be managed with _____________.

A

aggressive IVF (to maintain preload), pericardiocentesis (to relieve the pressure), and a pericardial window (for further drainage

79
Q

What ECG sign is diagnostic of pericardial effusion?

A

Electric alternans

80
Q

A “water bottle heart” on a CXR of an adult is suggestive of _____________.

A

pericardial effusion

81
Q

An AAA greater than ____ cm requires surgery.

A

5

82
Q

Give the USPSTF recommendation for AAA screening.

A

All men age 65 to 75 with a history of smoking should be screened with US for AAA.

83
Q

Describe the natural history of aortic stenosis.

A

People can be asymptomatic for years with aortic stenosis, but once they become symptomatic, they usually progress to syncope, ACS, CHF, and death within five years.

84
Q

Widened pulse pressure is suggestive of aortic _____________.

A

regurgitation

85
Q

What drugs are given to symptomatically relieve mitral stenosis?

A

Antiarrhythmics (beta-blockers)

86
Q

Aortic dissections are usually secondary to ________________.

A

untreated hypertension

87
Q

The most common sites of aortic dissection are _______________.

A

above the aortic valve and distal to the subclavian artery

88
Q

Explain the Stanford system for classifying aortic dissections.

A

• Stanford A: proximal to the left subclavian • Stanford B: distal to the left subclavian (“B is Beyond!”)

89
Q

How do you medically manage hemodynamically stable aortic dissection?

A

Give beta-blockers first and then vasodilators to treat HTN (important to do it in this order to avoid reflex tachycardia). Note: this would only be in Stanford B dissections, as Stanford A dissections are surgical emergencies.

90
Q

Explain the anticoagulation protocol for DVT.

A

First, give LMWH or unfractionated heparin for 5-7 days. Then, treat with warfarin for 3-6 months at target INR of 2.5.

91
Q

You should only get a D-dimer to ________________.

A

rule out DVT/PE when the pre-test probability is low

92
Q

Give the normal and symptomatic ranges for ankle-brachial indices.

A

•Normal = greater than 0.9• Pain at rest = less than 0.4

93
Q

GIve the 6 Ps of peripheral ischemia.

A

• Painful • Pallor•Paresthesia• Pulses• Poikilothermia• Paralyzed

94
Q

How do you diagnose primary lymphedema?

A

It is a diagnosis of exclusion –you must rule out cardiac and metabolic causes.

95
Q

What history questions are important to ask in assessing syncope versus seizure?

A

• “Did you feel it coming on?” - A positive answer suggests seizure or vasovagal syncope. • “Did you lose bowel/bladder control? - A positive here suggests seizure. • “Did you return to your baseline in under fifteen minutes?” - A positive here suggests vasovagal syncope.

Main Deck Step 2 Content Review (24 decks)

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