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PRCM Clerkship > Adult Medicine _ Cardiology > Flashcards

Adult Medicine _ Cardiology 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 METS

70% 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 nitroglycerin

Unstable 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 blockers

Nitrates

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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: Yes
Unstable angina: Yes
NSTEMI/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 STEMI

ADDITIONS
- 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 hours

First-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 cholesterol
TG = 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 years

INCREASED 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 < 100

Patient with established CAD:
- LDL < 100

Patient 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 I
Exogenous hyperlipidemia

Lipoprotein(s) elevated: - Chylomicrons

Treatment:
- Diet therapy

82
Q

DYSLIPIDEMIA SYNDROMES:

  • Type IIa
  • Familial hypercholesterolemia
  • Lipoprotein(s) elevated?
  • Treatment?
A

Type IIa
Familial 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 IIb
Combined 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 IV
Endogenous 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 V
Familial 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 dilation

DIASTOLIC 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 FAILURE
Mild 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 FAILURE
Ace Inhibitor:
- Pharmacologic mechanisms (2) involved in the treatment of CHF?

A

(1) Venodilation - Decreases preload

(2) Vasodilation - Decreases preload

110
Q

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

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

SYSTOLIC HEART FAILURE
Ace 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 FAILURE
Mild-to-Moderate CHF
(NYHA II to III):
- Treatment (3)?

A

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

114
Q

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

A

Post-MI heart failure

115
Q

SYSTOLIC HEART FAILURE
Beta-blocker:
- First-line agent
- Second-line agent

A

First-line: Carvedilol

Second-line: Metoprolol

116
Q

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

A

Spironolactone

118
Q

SYSTOLIC HEART FAILURE
Aldosterone antagonist:
- Contraindicated in what patient population?

A

Renal failure

119
Q

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

A
  • K+
  • BUN
  • Cr
120
Q

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

A

Eplerenone

121
Q

SYSTOLIC HEART FAILURE
Moderate-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) Retinopathy
EARLY
- 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 < 80
No treatment

133
Q

PRE-HYPERTENSION:

  • Systolic BP
  • Diastolic BP
  • Management
A

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

134
Q

STAGE I HYPERTENSION:

  • Systolic BP
  • Diastolic BP
  • Management
A

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

135
Q

STAGE II HYPERTENSION:

  • Systolic BP
  • Diastolic BP
  • Management
A

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

136
Q

Definition of HTN in:

  • General population
  • Diabetics and patients with renal disease
A

GENERAL POPULATION
HTN = BP > 140/90

DIABETICS / RENAL DISEASE
HTN = 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 BP

BP 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

THIAZIDES

Calcium channel blockers

142
Q

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

A

ACE inhibitors
ARBs
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/PVCs

Bigeminy - PAC/PVC every other beat

Trigeminy - 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 FIBRILLATION
ACUTE MANAGEMENT
Anticoagulation 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
  • Fever

NOTE

  • 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

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