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USMLE STEP 1 - OLD > PRCM _ Cardiology cards > Flashcards

PRCM _ Cardiology cards Flashcards

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USMLE® Step 1 flashcards
1
Q

Coronary artery disease (CAD)?

A
  • Stable angina - Acute coronary syndrome
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2
Q

Acute coronary syndrome (3)?

A
  • Unstable angina- NSTEMI- STEMI
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3
Q

Angina pectoris - cardiac causes?

A

Chest pain secondary to myocardial ischemia(1) Stable angina(2) Acute coronary syndromes

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4
Q

Unstable angina v. NSTEMI?

A

NSTEMI - elevated cardiac enzymes (troponin, CK-MB)Both lack ST segment elevations and pathologic Q waves

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5
Q

T/F: Chest pain relief with nitroglycerin is specific for myocardial ischemia and MI

A

False - Sublingual nitroglycerin will relieve chest pain secondary to esophageal motor disorder

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6
Q

ST segment changes at less than ___ METS (metabolic equivalents of oxygen consumption) and at less than ___% of age-predicted maximal heart rate indicates a high probability of myocardial ischemia.

A

6 METS70% of age-predicted maximal heart rate

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7
Q

Angina pectoris: Stable angina v. unstable angina?

A

Stable angina- Chest pain brought on by exertion or emotion that is relieved with rest or nitroglycerinUnstable angina (1) Chest pain at rest(2) New-onset chest pain that is severe and worsening(3) Chronic chest pain with increasing frequency, duration, or intensity

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8
Q

Major risk factors (7) for coronary artery disease (CAD)?

A

(1) Diabetes mellitus(2) Hyperlipidemia - high LDL(3) HTN(4) Cigarette smoking(5) Age - men > 45, women > 55(6) Family history of PREMATURE CAD—> MI/sudden cardiac death in MALE first-degree relative < 55 y/o—> MI/sudden cardiac death in FEMALE first-degree relative < 65 y/o (7) Low HDL (< 35) Note: High HDL (> 60) is a negative risk factor (protective)

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9
Q

Worst risk factor for stable angina?

A

Diabetes mellitus

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10
Q

Most common risk factor for stable angina?

A

HTN

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11
Q

Goal LDL in patients with CAD?

A

< 100 mg/dL

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12
Q

Stable angina:Medical therapy (4)?

A
  • Risk factor modification—> Anti-hypertensive—> HMG-CoA reductase inhibitor (statin)—> DM therapy for glucose control- Aspirin- Beta-blocker- Nitrates
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13
Q

Stable angina:First-line beta blockers (2)?

A

Atenolol, metoprolol

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14
Q

Stable angina:Secondary treatment if symptomatic on beta-blocker and nitrate?

A

Calcium channel blocker

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15
Q

Stable angina:Risk factor modification -Smoking cessation reduces the risk of CAD by ___% in ___year(s) after quitting.

A

Smoking cessation reduces the risk of CAD by 50% in 1 year after quitting.

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16
Q

Cardiac catheterization/revascularization methods (2)?

A

(1) Percutaneous coronary intervention (PCI), also referred to as angioplasty(2) Coronary artery bypass grafting (CABG)

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17
Q

PCI/angioplasty:Complication?

A
  • Re-stenosis is a significant problem, with up to 40% of stents failing within first 6 months- However, if there is no evidence of re-stenosis by 6 months, it usually does not occur
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18
Q

CAD:Poor prognostic indicators (3)?

A

(1) Two- or three-vessel coronary artery disease(2) Left main coronary artery disease- Supplies approximately 2/3 of the heart(3) Left ventricular dysfunction, with EF < 50%

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19
Q

CABG:Indications (3):

A

(1) Three-vessel disease, with >70% stenosis in each vessel (especially in diabetics)(2) Left main coronary artery disease, with >50% stenosis (3) Left ventricular dysfunction

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20
Q

Unstable angina:Medical therapy (7)?

A
  • Risk factor modification- Aspirin -and- clopidogrel - Beta-blocker- Nitrates- LMWH (enoxaparin/Lovenox)- Morphine - Oxygen (if patient hypoxic) * consider cardiac catheterization and revascularization *
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21
Q

Management of unstable angina includes repletion of deficient electrolytes, especially ___ (2)?

A

K+ and Mg2+

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22
Q

Prinzmetal’s angina (coronary artery vasospasm):ECG

A
  • Hallmark is ST segment elevation (not depression) on ECG during chest pain- ST segment elevation resolves when chest pain resolves
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23
Q

Prinzmetal’s angina (coronary artery vasospasm):Definitive test

A

Coronary angiography displays coronary vasospasm with the administration of IV ergonovine (to provoke chest pain)

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24
Q

Prinzmetal’s angina (coronary artery vasospasm):Medical therapy (2)?

A

Calcium channel blockersNitrates

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25
Q

Prinzmetal’s angina (coronary artery vasospasm):First-line CCB?

A

Diltiazem

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26
Q

PCI/angioplasty:Techniques/strategies to reduce high rates of revascularization (2)?

A

(1) Drug-eluting stents(2) Aspirin + clopidogrel + glycoprotein IIa/IIIb inhibitors

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27
Q

T/F: Revascularization (PCI/CABG) decreases the incidence of MI

A

False - Revascularization DOES NOT decrease the incidence of MI, but DOES result in significant improvement in symptoms

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28
Q

Myocardial infarction has a ___% mortality rate. ___% of the deaths are pre-hospital.

A

Myocardial infarction has a 30% mortality rate. 50% of the deaths are pre-hospital.

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29
Q

Chest pain response to nitroglycerin:Stable angina?Unstable angina?NSTEMI/STEMI?

A

Stable angina: YesUnstable angina: YesNSTEMI/STEMI: No

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30
Q

Cause of sudden cardiac death in the setting of MI?

A

Ventricular fibrillation (Vfib)

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31
Q

Evolution of ECG findings in MI?

A

(1) Peaked T waves(2) ST segment elevation(3) Q waves(4) T wave inversion

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32
Q

ST segment:Depression v. elevation?

A

ST segment depression: Sub-endocardial injury ST segment elevation: Transmural injury

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33
Q

Anterior wall MI:ECG changes?Coronary vessel involved?

A

Anterior wall MI - ST segment elevation and/or Q waves in leads V1-V4- Occlusion of left anterior descending (LAD) coronary artery

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34
Q

Anteroseptal wall MI:ECG changes?Coronary vessel involved?

A

Anteroseptal wall MI- ST segment elevation and/or Q waves in leads V1-V2- Occlusion of proximal left anterior descending (LAD) coronary artery

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35
Q

Anterolateral wall MI:ECG changes?Coronary vessel involved?

A

Anterolateral wall MI- ST segment elevation and/or Q waves in leads V4-V6- Occlusion of left circumflex (LCX) coronary artery

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36
Q

Lateral wall MI:ECG changes?Coronary vessel involved?

A

Lateral wall MI- ST segment elevation and/or Q waves in leads I, aVL- Reciprocal ST segment depression in leads II, III, aVF- Occlusion of left circumflex (LCX) coronary artery

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37
Q

Posterior wall MI:ECG changes?Coronary vessel involved?

A

Posterior wall MI - ST segment depression in leads V1 and V2- Prominent R waves in leads V1 and V2- Prominent and upright T waves in leads V1 and V2- ST segment elevation and/or Q waves in POSTERIOR LEADS V7-V9- Occlusion of posterior descending artery (PDA) of right coronary artery (RCA)

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38
Q

Inferior wall MI:ECG changes?Coronary vessel involved?

A

Inferior wall MI- ST segment elevation and/or Q waves in leads II, III, aVF- Reciprocal ST segment depression in leads I, aVL- Occlusion of right coronary artery (RCA)NOTE- Abdominal discomfort is especially common in inferior wall MIs

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39
Q

ECG that exhibits changes consistent with inferior wall infarction:Next clinical step?

A

Right-sided ECG with leads V4R, V5R, and V6R

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40
Q

Inferior wall MI with right ventricular infarct/dysfunction:ECG changes?Coronary vessel involved?

A

Inferior wall MI with right ventricular infarct/dysfunction- ST segment elevation and/or Q waves in leads II, III, aVF- Reciprocal ST segment depression in leads I, aVL- ST segment elevation in leads V3R and V4R on RIGHT-SIDED ECG - Occlusion of right coronary artery (RCA)

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41
Q

Right ventricular infarct:Clinical presentation (4)?

A
  • Hypotension- Clear lungs - Elevated jugular venous pressure- Hepatomegaly
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42
Q

NSTEMI/STEMI:Medical therapy (7)?

A

“MONA BASH”- Morphine - Oxygen- Nitrates- Aspirin and clopidogrel- Beta-blocker- ACE-inhibitor- Statins- Heparin (enoxaparin/Lovenox)

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43
Q

Medical therapies (3) shown to reduce post-MI mortality?

A
  • Aspirin- Beta-blocker- ACE-inhibitor
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44
Q

Medical therapy shown to reduce post-MI mortality in patients with post-MI LV dysfunction?

A

Beta-blockers (carvedilol)

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45
Q

Medical therapy shown to reduce post-MI remodeling of the myocardium?

A

Beta-blockers

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46
Q

Right ventricular infarct:Treatment?

A
  • Generally, RV infarction is treated similarly to STEMIADDITIONS- Volume expansion with IV fluids (usually, normal saline) to increase preload and thereby the blood flow out of the right ventricle SUBTRACTIONS:- NO morphine and NO nitrates, which cause venodilation thereby decreasing preload - NO beta-blockers, which decrease HR and cardiac contractility
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47
Q

Methods of revascularization in STEMI (3)?

A

(1) Percutaneous coronary intervention (PCI)(2) Thrombolytic therapy(3) Coronary artery bypass graft (CABG)

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48
Q

PCI:Timeframe requirements for indication as preferred method of revascularization?

A

PCI performed with a door-to-balloon time less than 90 minutes

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49
Q

Thrombolytic therapy: - Timeframe requirements for therapy to be an available method of revascularization?- Timeframe requirements for optimal therapy outcomes?- First-line agent for therapy?

A

Thrombolytic therapy may be administered up to 24 hours after the onset of angina pectoris (chest pain)Outcomes are best if thrombolytics given within the first 6 hoursFirst-line is alteplase (shown to have best outcomes among thrombolytics)

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50
Q

Post-MI patients should undergo ___ before hospital discharge and should schedule ___ within ___ weeks of discharge.

A

Post-MI patients should undergo MEASUREMENT OF LV EF% before hospital discharge and should schedule EXERCISE STRESS TEST within 4-6 weeks of discharge.

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51
Q

Post-MI patients have a high risk of ___ during the next 5 years.Risk increases in the setting of what 2 factors?

A

Post-MI patients have a high risk of STROKE during the next 5 years.The LOWER the EF% and the OLDER the patient, the higher the 5-year risk of stroke

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52
Q

Treatment of premature ventricular contractions (PVCs) post-MI?

A

None

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53
Q

Treatment of ventricular tachycardia (VT) post-MI in a hemodynamically stable patient?

A

IV amiodarone

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54
Q

Most common cause of death in first few days post-MI?

A

Ventricular arrhythmia, either VT or Vfib

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55
Q

Treatment of second-degree (Mobitz II) or third-degree AV block in the setting of anterior wall MI?

A

Pacemaker

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56
Q

Treatment of second-degree (Mobitz II) or third-degree AV block in the setting of inferior wall MI?

A
  • IV atropine - If conduction is not restored, pacemaker
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57
Q

Post-MI, patients may:- Return to work in?- Resume sexual intercourse in?

A
  • Return to work in 8 weeks - Resume sexual activity in 4-6 weeks
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58
Q

Most common cause of in-hospital death post-MI?

A

CHF (pump failure) Severe CHF leads to cardiogenic shock

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59
Q

New-onset mitral regurgitation (MR) post-MI?

A

Papillary muscle rupture

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60
Q

Dressler syndrome:Treatment?

A

Fever, malaise, fibrinous pericarditis, leukocytosis, and pleuritis weeks to months post-MI (autoimmune etiology)Treatment is aspirin

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61
Q

LDL calculation?

A

LDL = TC - HDL - (TG/5)TC = Total cholesterolTG = Triglycerides (VLDL)LDL accounts for approximately 2/3 of total cholesterol (TC)

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62
Q

Total cholesterol:- Ideal?- Borderline?- High?

A

Total cholesterol:- Ideal < 200 - Borderline 200-240- High > 260

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63
Q

LDL:- Ideal?- Borderline?- High?

A

LDL:- Ideal < 130- Borderline 130-160- High > 160

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64
Q

Triglycerides (VLDL):- Ideal?- Borderline?- High?

A

Triglycerides (VLDL):- Ideal < 125- Borderline 125-250- High > 250

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65
Q

CAD risk is primarily due to the ___ component of cholesterol because it is thought to be the most atherogenic of all lipoproteins.

A

LDL

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66
Q

Coronary artery disease (CAD):- Positive risk factor (lipoprotein)?- Mechanism?

A
  • LDL - LDL is proposed to be the most atherogenic of all lipoproteins
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67
Q

Coronary artery disease (CAD):- Negative risk factor (lipoprotein)?- Mechanism?

A
  • HDL- HDL removes excess cholesterol from arterial walls
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68
Q

HDL cholesterol:- HDL level that corresponds to a “negative risk factor” for CAD?- HDL level that corresponds to a “positive risk factor” for CAD?

A
  • Low HDL < 40 is a risk factor for CAD- High HDL > 60 is a negative risk factor (protective) for CAD
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69
Q

HDL cholesterol:- For every 10 mg/dL increase in HDL levels, CAD risk decreases by ___%

A

For every 10 mg/dL increase in HDL levels, CAD risk decreases by 50%

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70
Q

Total cholesterol-to-HDL ratio:- The lower the TC/HDL ratio, the ___ the risk of CAD

A
  • The lower the total cholesterol-to-HDL ratio, the LOWER the risk of CAD
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71
Q

Total cholesterol-to-HDL ratio and risk of CAD:- Desirable ratio?- Ratio of average (standard) risk?- Ratio of double the risk?- Ratio of triple the risk?

A

TC/HDL RATIO:- Ratio < 4.5 is desirable- Ratio of 5 is average (standard) risk for CAD- Ratio of 10 is double the risk - Ratio of 20 is triple the risk

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72
Q

USPSTF - Lipid Screening,Recommended Ages + Intervals:- Men?- Men at increased CAD risk?- Women?- Women at increased CAD risk?

A

AVERAGE (STANDARD) RISK:- Men 35+ y/o every 5 years- Women 45+ y/o every 5 yearsINCREASED RISK:- Men 20-35 y/o every 5 years- Women 20-45 y/o every 5 years

73
Q

USPSTF - Lipid Screening:- Initial lipid screen?- Follow-up lipid screen if initial screen is abnormal/concerning?

A

Initial lipid screen: - Non-fasting - Total cholesterol (TC) and HDL - Follow-up lipid screen in the setting of an abnormal initial lipid screen: - Fasting - Complete lipid panel: TC, HDL, TG (VLDL), LDL

74
Q

Goal LDL levels:- Patient with average (standard) CAD risk?- Patient with DM?- Patient with established CAD?- Patient with DM and CAD?

A

Average (standard) risk:- LDL < 130 Patient with DM:- LDL < 100Patient with established CAD:- LDL < 100Patient with DM and established CAD:- LDL < 70

75
Q

Diet therapy for hypercholesterolemia (high LDL):- Total calories from fat (%)?- Total calories from saturated fat (%)?- Total cholesterol?

A
  • The treatment of choice for hypercholesterolemia is diet therapy* With an intensive diet, LDL cholesterol can be reduced by an average of 10%:(1) < 30% of total calories from fat(2) < 10% of total calories from saturated fat(3) < 300 mg/day of cholesterol
76
Q

Medications that can cause changes in TC, LDL, HDL, and/or TG (VLDL): - Thiazide diuretics

A

Thiazide diuretics:- Increase TC- Increase LDL- Increase TG (VLDL)

77
Q

Medications that can cause changes in TC, LDL, HDL, and/or TG (VLDL): - Beta-blockers (propranolol)

A

Beta-blockers (propranolol):- Increase TG (VLDL)- Decrease HDL

78
Q

Two medication classes that can increase serum lipids, other than thiazide diuretics and beta-blockers?

A

Corticosteroids and HIV protease inhibitors

79
Q

Medication therapy for hyperlipidemia:- First-line?-Second-line?-Third-line?

A
  • First-line: HMG-CoA reductase inhibitors (statins) - Second-line: Niacin- Third-line: Bile-acid sequestrants
80
Q

Risk factors for CAD:- Most important risk factor?- Second most important risk factor?

A
  • Most important: High LDL- 2nd most important: Low HDL
81
Q

DYSLIPIDEMIA SYNDROMES:* Type I* Exogenous hyperlipidemia - Lipoprotein(s) elevated?- Treatment?

A

Type IExogenous hyperlipidemiaLipoprotein(s) elevated: - Chylomicrons Treatment:- Diet therapy

82
Q

DYSLIPIDEMIA SYNDROMES:* Type IIa* Familial hypercholesterolemia - Lipoprotein(s) elevated?- Treatment?

A

Type IIaFamilial hypercholesterolemia Lipoprotein(s) elevated:- LDL Treatment:- First-line: Statins - Second-line: Niacin - Third-line: Bile-acid sequestrants (cholestyramine)

83
Q

DYSLIPIDEMIA SYNDROMES:* Type IIb* Combined hyperlipoproteinemia - Lipoprotein(s) elevated?- Treatment?

A

Type IIbCombined hyperlipoproteinemia Lipoprotein(s) elevated:- LDL + VLDL (TG)Treatment:- First-line: Statins - Second-line: Niacin - Third-line: Fibrates (gemfibrozil)

84
Q

DYSLIPIDEMIA SYNDROMES:* Type IV* Endogenous hyperlipidemia - Lipoprotein(s) elevated?- Treatment?

A

Type IVEndogenous hyperlipidemia Lipoprotein(s) elevated:- VLDL (TG)Treatment:- First-line: Niacin - Second-line: Fibrates (gemfibrozil) - Third-line: Statins

85
Q

DYSLIPIDEMIA SYNDROMES:* Type V* Familial hypertriglyceridemia - Lipoprotein(s) elevated?- Treatment?

A

Type VFamilial hypertriglyceridemia Lipoprotein(s) elevated:- VLDL (TG) + chylomicrons Treatment:- First-line: Niacin - Second-line: Fibrates (gemfibrozil)

86
Q

Elevated TG (VLDL) levels are associated with?

A

Impaired glycemic control

87
Q

Anti-hypertensive classes (2) that adversely effect plasma lipid levels?

A

Thiazide diuretics and beta-blockers

88
Q

HMG-CoA reductase inhibitors (statins):- Effects on lipids?

A
  • Decreases LDL levels
89
Q

Niacin:- Effects on lipids?

A
  • Decreases LDL levels- Decreases TG (VLDL) levels- Increases HDL levels
90
Q

Bile-acid sequestrants (cholestyramine):- Effects on lipids?

A
  • Decreases LDL levels- INCREASES TG (VLDL) LEVELS
91
Q

Fibrates (gemfibrozil):- Effects on lipids?

A
  • Decreases TG (VLDL) levels- Increases HDL levels
92
Q

Most potent drug for decreasing LDL?

A

HMG-CoA reductase inhibitors (statins)

93
Q

Most potent drug for decreasing TG (VLDL) levels?

A

Niacin

94
Q

Most potent drug for increasing HDL?

A

Niacin

95
Q

Drug for hyperlipidemia contraindicated in diabetic patients?

A

Niacin - may worsen glycemic control

96
Q

HMG-CoA reductase inhibitors (statins):- Side effects (2)?

A
  • AST/ALT elevation- CPK elevation (harmless) in the setting of myositis
97
Q

HMG-CoA reductase inhibitors (statins):LFT monitoring?

A

Monitor LFTs - Monthly for first 3 months- Then every 3-6 months

98
Q

Diastolic heart failure:- Pathophysiologic mechanism?- Causes include (2)?- Heart sound?

A

DIASTOLIC HEART FAILURE- Owing to impaired ventricular filling during diastole in the setting of decreased ventricular distensibility (impaired ventricular relaxation, increased stiffness of the ventricle, or both)- Etiologies include(1) HTN –> Hypertrophic cardiomyopathy(2) Restrictive cardiomyopathy (e.g., amyloidosis, sarcoidosis, hemochromatosis) - S4 atrial gallop

99
Q

Systolic heart failure:- Pathophysiologic mechanism?- Causes include (2)?- Heart sound?

A

SYSTOLIC HEART FAILURE- Owing to impaired ventricular contractility with decreased ejection fraction (EF)- Etiologies include(1) Ischemic heart disease or post-MI—> contractility of infarcted cardiac muscle is impaired, with resultant decreased EF(2) HTN –> Dilated cardiomyopathy- S3 ventricular gallop

100
Q

S3 ventricular gallop:- left-heart S3 best appreciated at ___ on auscultation - right-heart S3 best appreciated at ___ on auscultation - S3 heart sound represents?

A
  • Left-heart S3 best appreciated with bell of stethoscope at cardiac apex - Right-heart S3 best appreciated with bell of stethoscope at LLSB (tricuspid area) - S3 a/w atrial contraction against an overfilled ventricle–> Contraction of blood into an already-overfilled ventricle (increased end-systolic volume) in the setting of decreased EF%
101
Q

S4 atrial gallop:- left-heart S4 best appreciated at ___ on auscultation - right-heart S4 best appreciated at ___ on auscultation - S4 heart sound represents?

A
  • Left-heart S4 best appreciated with bell of stethoscope at cardiac apex - Right-heart S4 best appreciated with bell of stethoscope at LLSB (tricuspid area) - S4 a/w atrial contraction against a non-compliant (stiff) ventricle with increased end-diastolic pressure in the setting of a ventricle with decreased distensibility
102
Q

Signs/symptoms of LEFT-SIDED heart failure (10)?

A

(1) Dyspnea 2/2 pulmonary congestion/edema(2) Orthopnea - Difficulty breathing in the recumbent position(3) Paroxysmal nocturnal dyspnea (PND) - Awakening after 1 to 2 hours of sleep due to acute dyspnea (4) Nocturnal cough(5) Confusion and memory impairment - Occur in advanced CHF 2/2 inadequate brain perfusion(6) Diaphoresis and cool extremities at rest (NYHA IV)(7) Displaced PMI 2/2 cardiomegaly(8) Pathologic S3 and/or S4 heart sounds (9) Crackles/rales at lung bases indicative of pulmonary edema; 2/2 fluid spilling into alveoli (10) Dullness to percussion and decreased tactile fremitus of lower lung bases 2/2 pleural effusion

103
Q

Signs/symptoms of RIGHT-SIDED heart failure (6)?

A

(1) Peripheral pitting edema (2) Nocturia 2/2 increased venous return with elevation of legs (3) Elevated jugular venous pressure (JVP)(4) Hepatomegaly/hepatojugular reflex(5) Ascites(6) Pathologic S3 and/or S4 heart sounds

104
Q

Echocardiogram:- Ejection fraction?- Ventricular chamber dilation?- Ventricular hypertrophy?(1) Systolic heart failure(2) Diastolic heart failure

A

SYSTOLIC HEART FAILURE- EF < 40%- Ventricular chamber dilationDIASTOLIC HEART FAILURE- EF > 40% (preserved ventricular function)- Ventricular hypertrophy

105
Q

CXR:- Pulmonary congestion?- Cardiomegaly?(1) Systolic heart failure(2) Diastolic heart failure

A

SYSTOLIC HEART FAILURE- Pulmonary congestion (Kerley B lines)- Cardiomegaly DIASTOLIC HEART FAILURE- Pulmonary congestion (Kerley B lines)- WITH -or- WITHOUT cardiomegaly

106
Q

New York Heart Association (NYHA) Classification of Heart Failure:- Class I- Class II- Class III- Class IV

A

CLASS I- Symptoms only occur with vigorous activities, such as playing a sport. Patients are nearly asymptomatic.CLASS II- Symptoms occur with prolonged or moderate exertion, such as climbing a flight of stairs or carrying heavy packages. Slight limitation of activities.CLASS III- Symptoms occur with usual activities of daily living, such as walking across the room or getting dressed. Markedly limiting.CLASS IV- Symptoms occur at rest. Incapacitating.

107
Q

Most common cause of death from CHF?

A

Sudden death from ventricular arrhythmias - Cardiac ischemia provokes ventricular arrhythmias

108
Q

SYSTOLIC HEART FAILUREMild CHF (NYHA I to II):- Treatment (3)?

A

(1) Lifestyle modifications, including sodium restriction (4g/day) and physical activity(2) ACE inhibitor (3) Loop diuretic

109
Q

SYSTOLIC HEART FAILUREAce Inhibitor: - Pharmacologic mechanisms (2) involved in the treatment of CHF?

A

(1) Venodilation - Decreases preload(2) Vasodilation - Decreases preload

110
Q

SYSTOLIC HEART FAILUREAce Inhibitor: - Benefits (3) of starting an ACE inhibitor in patients with systolic dysfunction

A

(1) Alleviate symptoms in mild, moderate, and severe CHF(2) Reduce mortality (3) Improve prognosis (prolong survival)

111
Q

SYSTOLIC HEART FAILUREAce Inhibitor: - Clinical/laboratory values to monitor (4)

A
  • Blood pressure- K+- BUN- Cr
112
Q

SYSTOLIC HEART FAILUREAce Inhibitor: - Alternative therapy for patients who experience cough as a side effect of ACE inhibitor therapy?

A

ARB - Angiotensin receptor blocker

113
Q

SYSTOLIC HEART FAILUREMild-to-Moderate CHF (NYHA II to III):- Treatment (3)?

A

(1) ACE inhibitor(2) Loop diuretic(3) Beta-blocker

114
Q

SYSTOLIC HEART FAILUREBeta-blocker: - Proven to reduce mortality in what patient demographic?

A

Post-MI heart failure

115
Q

SYSTOLIC HEART FAILUREBeta-blocker: - First-line agent- Second-line agent

A

First-line: Carvedilol Second-line: Metoprolol

116
Q

SYSTOLIC HEART FAILUREModerate-to-Severe CHF (NYHA III to IV):- Treatment (5)?

A

(1) ACE inhibitor(2) Loop diuretic(3) Beta-blocker (4) Aldosterone antagonist(5) Digoxin

117
Q

SYSTOLIC HEART FAILUREAldosterone antagonist: - RALES trial showed that ___ reduces morbidity and mortality in CHF patients NYHA III to IV

A

Spironolactone

118
Q

SYSTOLIC HEART FAILUREAldosterone antagonist: - Contraindicated in what patient population?

A

Renal failure

119
Q

SYSTOLIC HEART FAILUREAldosterone antagonist: - Clinical/laboratory values to monitor (3)

A
  • K+- BUN- Cr
120
Q

SYSTOLIC HEART FAILUREAldosterone antagonist: Alternative agent in males experiencing gynecomastia on spironolactone?

A

Eplerenone

121
Q

SYSTOLIC HEART FAILUREModerate-to-Severe CHF (NYHA III to IV):- Indication for digoxin therapy?

A

CHF patients who remain symptomatic on ACE inhibitor, loop diuretic, beta-blocker, and aldosterone antagonist * Check serum digoxin levels periodically* DIGOXIN TOXICITY- GI: nausea, vomiting, anorexia- Cardiac: Premature ventricular complexes (PVCs - ectopic ventricular beats), AV block, Afib- CNS: Visual disturbances, disorientation

122
Q

Heart failure medications shown to decrease mortality in CHF patients?

A
  • ACE inhibitors- ARBs - Beta-blockers (carvedilol > metoprolol) - Aldosterone antagonists (spironolactone) NOT- Diuretics - Digoxin
123
Q

DIASTOLIC HEART FAILURE:- Treatment v. systolic heart failure

A
  • Beta-blockers (clear benefit)- Diuretics (loop) for symptom control (volume overload)- ACE inhibitors, ARBs - No clear benefit - Do NOT use aldosterone antagonists (spironolactone) or digoxin
124
Q

The overall 5-year mortality for all patients with CHF is approximately ___%

A

The overall 5-year mortality for all patients with CHF is approximately 50%

125
Q

In CHF, indications (2) for digoxin therapy?

A

(1) EF < 40%(2) Afib with rapid ventricular rate (RVR)

126
Q

HTN:Cardiac complications (4)?

A

(1) CAD(2) MI(3) CHF w/ LVH(4) HTN a/w increased risk of aortic dissection

127
Q

HTN:Renal complications (2)?

A

(1) Nephrosclerosis- Arteriosclerosis of the afferent and efferent arterioles and of the glomerulus (2) Renal failure- Decreased GFR and tubular dysfunction

128
Q

HTN:CNS complications (2)?

A

(1) Intracerebral hemorrhage (stroke)(2) Transient ischemic attack (TIA)

129
Q

HTN:Eye complications (2)?

A

(1) RetinopathyEARLY- Arteriovenous nicking (discontinuity in the retinal vein 2/2 thickened arterial walls)- Cotton wool spots (2/2 infarction of the nerve fiber layer in the retina) LATE- Hemorrhages and exudates(2) Papilledema

130
Q

Most common cause of secondary HTN in young women?

A

Birth control pills (OCPs)

131
Q

Most common cause of renovascular HTN in:- Young women?- Older men?

A

Younger women - Fibromuscular dysplasia Older men - Renal artery stenosis (RAS)

132
Q

NORMAL HYPERTENSION:- Systolic BP- Diastolic BP- Management

A

Systolic BP < 120 Diastolic BP < 80No treatment

133
Q

PRE-HYPERTENSION:- Systolic BP- Diastolic BP- Management

A

Systolic BP 120-139Diastolic BP 80-89Lifestyle modification

134
Q

STAGE I HYPERTENSION:- Systolic BP- Diastolic BP- Management

A

Systolic BP 140-159Diastolic BP 90-99Lifestyle modification + drug therapy

135
Q

STAGE II HYPERTENSION:- Systolic BP- Diastolic BP- Management

A

Systolic BP > 160 Diastolic BP > 100Lifestyle modification + 2-drug combination therapy

136
Q

Definition of HTN in:- General population- Diabetics and patients with renal disease

A

GENERAL POPULATION HTN = BP > 140/90DIABETICS / RENAL DISEASEHTN = BP > 130/80

137
Q

Diagnosis of HTN:- Number of readings- Posture- Caffeine- Smoking - Length of the cuff bladder

A
  • Measurement of 3 blood pressure readings, at least 1 week apart- Upright/supine for 5 minutes before measuring blood pressure- No caffeine in the past 1 hour- No smoking in the past 30 minutes- Length of the cuff bladder should be 80% of the circumference of the upper arm
138
Q

Blood pressure cuff that is too small can report a falsely ___ BP reading, whereas a cuff that is too large can report a falsely ___ reading.

A

BP cuff too small - Report a falsely INCREASED BPBP cuff too large - Report a falsely DECREASED BP

139
Q

EtOH:- Cardioprotective?- Risk factor for CAD?

A
  • An absolute maximum of 2 drinks per day may be cardioprotective- Alcohol intake that exceeds this amount is a risk factor for CAD
140
Q

Anti-hypertensive therapy:- In general population, the minimum goal is to reduce BP to a level of?- In patients with diabetes and/or renal disease, the minimum goal is to reduce BP to a level of?- Ideal goal is to reduce BP to a level of?

A

MINIMUM BP GOALS- General population —>BP BP

141
Q

Black patients “Salt-sensitive” HTN- Anti-hypertensive choices (2)?

A

THIAZIDESCalcium channel blockers

142
Q

White patients “Salt-insensitive” HTN- Anti-hypertensive choices (3)?

A

ACE inhibitorsARBs Beta-blockers

143
Q

Anti-hypertensive agent(s) of choice in ALL patients with diabetes?

A

ACE inhibitor - Protective effect on the kidneys to slow development of diabetic nephropathy

144
Q

Anti-hypertensive agent(s) of choice in ALL patients with renal disease?

A

ACE inhibitor - Protective effect on the kidneys

145
Q

Anti-hypertensive agent(s) of choice in ALL patients with CHF?

A
  • ACE inhibitor / ARB- Thiazide diuretic
146
Q

Anti-hypertensive agent(s) likely to have a favorable effect on osteoporosis? Why?

A

THIAZIDE DIURETICS slow the process of bone demineralization

147
Q

Anti-hypertensive agent(s) likely to have a favorable effect on migraines? Why?

A

BETA-BLOCKERS are typically used as prophylaxis for migraine headaches

148
Q

Hypertensive urgency/emergency drug selection:Pheochromocytoma

A

Phentolamine

149
Q

Hypertensive urgency/emergency drug selection:Eclampsia

A

Magnesium sulfate (MgSO4)

150
Q

Hypertensive urgency/emergency drug selection:Aortic dissection

A

Esmolol

151
Q

Hypertensive urgency/emergency drug selection:Intracranial hemorrhage (stroke)

A

Sodium nitroprusside

152
Q

Anti-hypertensive agent(s) of choice in pregnant patients?

A
  • Methyldopa- Beta-blockers - Hydralazine
153
Q

Anti-hypertensive agent(s) CONTRAINDICATED in pregnant patients?

A
  • ACE inhibitors / ARBs - Thiazide diuretics - Calcium channel blockers * Always obtain a pregnancy test in women of reproductive age before starting anti-hypertensive therapy, as the above agents are teratogenic
154
Q

Anti-hypertensive agent(s) likely to have an adverse effect on gout? Why?

A

THIAZIDE DIURETICS b/c side effects include hyperuricemia (elevated uric acid levels in the blood)

155
Q

ANTI-HYPERTENSIVE SIDE EFFECTS- Thiazide diuretics (6)?

A
  • HYPOKALEMIA - Hypomagnesemia - Hyperuricemia - Hyperglycemia - CHOLESTEROL: Increase TC, LDL, and TG (VLDL)- Metabolic alkalosis
156
Q

ANTI-HYPERTENSIVE SIDE EFFECTS- Beta-blockers (6)?

A
  • Bradycardia- Bronchospasm - Insomnia- Fatigue- Depression- CHOLESTEROL: Decrease HDL, increase TG (VLDL)
157
Q

ANTI-HYPERTENSIVE SIDE EFFECTS- ACE inhibitors (4)?

A
  • Acute renal failure- Hyperkalemia - Dry cough angioedema - Skin rash
158
Q

Anti-hypertensive agent(s) of choice in asthmatics?

A

Calcium channel blocker NOTE: Beta-blockers contraindicated b/c side effects include bronchospasm

159
Q

Supraventricular premature beats occur when there is premature or early activation of the atrial myocardium as a result of an impulse generated by an ectopic focus within the atrial myocardium, rather than the sinus node. Supraventricular premature beats can originate from (2)?

A

(1) Atrial myocardium- Premature atrial complexes (PACs), also called atrial premature beats (APBs) (2) Atrioventricular (AV) node - Premature junctional complexes (PJCs), also called junctional premature beats (JPBs)

160
Q

ECG FINDINGS,Premature atrial complexes (PACs): - P waves - PR intervals - QRS complexes

A

P WAVES- Early P waves that differ in morphology from sinus P waves- The interval b/w the last sinus P wave and the ectopic P wave is shorter than the interval b/w 2 sinus P waves (“premature”)- Usually a pause following PAC QRS complex before next sinus P wave PR INTERVALS- Corresponds to conduction through the AV node - Time interval from atrial depolarization to ventricular depolarization- PAC PR interval may be shorter/longer than sinus PR interval, depending on site of ectopic atrial focus QRS COMPLEXES- Normal QRS complexes b/c conduction of the ventricle is normal

161
Q

TREATMENT,Premature atrial complexes (PACs): - Asymptomatic- Symptomatic

A
  • PACs generally asymptomatic and do NOT require treatment- If PACs cause “skipped beats” or palpitations, treatment w/ beta-blockers may be helpful
162
Q

ECG FINDINGS,Premature ventricular complexes (PVCs): - P waves - RR intervals - QRS complexes

A

P WAVES- Typically, no P wave identified on ECG, b/c P wave us usually buried in the widened QRS complex RR INTERVALS (cycle length) - Typically, a full compensatory pause follows the PVC- RR complex b/w sinus QRS complexes before and after the PVC is TWICE the RR interval b/w 2 successive sinus beats QRS COMPLEXES - Wide QRS complexes identified on ECG 2/2 conduction via abnormal pathways

163
Q

TREATMENT,Premature ventricular complexes (PVCs): - Asymptomatic- Symptomatic

A
  • PVCs generally asymptomatic and do NOT require treatment- If PVCs are symptomatic (e.g., palpitations), treatment w/ beta-blockers may be helpful
164
Q

Premature ventricular complexes (PVCs): - Workup

A
  • PVCs occur in patients WITH AND WITHOUT structural heart disease - If a patient is found to have frequent PVCs, work-up for underlying structural heart disease should be initiated * Patients with frequent, repetitive PVCs AND underlying heart disease are at an increased risk for sudden death 2/2 cardiac arrhythmia, especially Vfib
165
Q

Premature atrial/ventricular complex (PAC, PVC) rhythms:- Couplet- Bigeminy - Trigeminy

A

Couplet - 2 successive PACs/PVCsBigeminy - PAC/PVC every other beatTrigeminy - PAC/PVC every third beat

166
Q

Atrial fibrillation (Afib):- Mechanism

A
  • Multiple foci in the atria fire continuously in a chaotic pattern, causing a totally irregular, rapid ventricular rate - Instead of intermittently contracting, the atria quiver continuously - Most frequent origin for ectopic foci that cause atrial fibrillation is cardiac tissue extending into the pulmonary veins
167
Q

ECG FINDINGS,Atrial fibrillation (Afib): - P waves - RR intervals - QRS complexes

A

P WAVES- Lack of discrete P waves- Replaced with tiny chaotic fibrillatory or f waves RR INTERVALS - irregularly irregular RR intervals QRS COMPLEXES- Narrow QRS complexes

168
Q

Patients with Afib and underlying heart disease are at a markedly increased risk for what 2 adverse events?

A
  • Thromboembolism - Hemodynamic compromise
169
Q

Treatment of Afib in a hemodynamically STABLE patient?

A
  • AFFIRM trial showed that rate control is superior to rhythm control in the treatment of Afib - Rate control with beta-blockers (first-line) or calcium channel blockers if HR > 100 bpm
170
Q

Treatment of Afib in a hemodynamically UNSTABLE patient?

A
  • Afib with rapid ventricular response (RVR) —> Hemodynamic instability - Treatment with synchronized cardioversion to sinus rhythm- Cardioversion energies in succession: 100J to 200J to 300J to 360J
171
Q

Holiday heart syndrome

A

Afib following alcohol ingestion is frequently seen during holidays and weekends

172
Q

ATRIAL FIBRILLATIONACUTE MANAGEMENTAnticoagulation to prevent embolic cerebrovascular accident (CVA):If Afib present > 48 hours (or unknown period of time), risk of embolization during cardioversion is significant (2% to 5%).Management strategies (2)?

A

MANAGEMENT STRATEGY #1- Anticoagulation for 3 weeks before cardioversion - Cardioversion- Anticoagulation for 4 weeks after cardioversion MANAGEMENT STRATEGY #2- Transesophageal echocardiogram (TEE) to image the left atrium IF NO THROMBUS PRESENT- IV heparin- Cardioversion within 24 hours- Anticoagulation for 4 weeks after cardioversion IF THROMBUS PRESENT- Anticoagulation for 3 weeks before cardioversion - Cardioversion- Anticoagulation for 4 weeks after cardioversion

173
Q

Anticoagulation in the management of chronic Afib:- Patients

A

Treatment of patients

174
Q

Deep venous thrombosis (DVT):Virchow’s triad

A

Endothelial injury, venous stasis, and hypercoagulability

175
Q

Deep venous thrombosis (DVT):Symptoms (4)

A
  • Lower extremity pain and swelling that worsens with walking and improves with rest- Homans’ sign = Pain on ankle dorsiflexion- Palpable cord- FeverNOTE- Only 50% of patients with these classic DVT findings have a DVT- Only 50% of patients with documented DVT have these classic findings
176
Q

Deep venous thrombosis (DVT):Diagnostic tools (3)

A
  • Doppler analysis and Duplex ultrasonography (initial test)- Ascending contrast venography (gold standard, yet infrequently used clinically)- D-dimer assay–> Negative D-dimer helps to rule out DVT
177
Q

Deep venous thrombosis (DVT):Treatment options (3)

A
  • Anticoagulation - Thrombolytic therapy- IVC filter NOTE: IVC filter effective only in preventing PE, not DVTs
178
Q

Deep venous thrombosis (DVT):Anticoagulation therapy

A
  • Heparin bolus + constant infusion, titrated to PTT of 1.5 to 2 times aPTT- Once aPTT level is therapeutic, start warfarin (Coumadin) and continue for 3 to 6 months- Anticoagulate to INR 2-3 - Continue heparin until INR has been therapeutic (2-3) for 48 hours

USMLE STEP 1 - OLD (12 decks)

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