PRCM _ Cardiology cards Flashcards
(178 cards)
1
Q
Coronary artery disease (CAD)?
A
- Stable angina - Acute coronary syndrome
2
Q
Acute coronary syndrome (3)?
A
- Unstable angina- NSTEMI- STEMI
3
Q
Angina pectoris - cardiac causes?
A
Chest pain secondary to myocardial ischemia(1) Stable angina(2) Acute coronary syndromes
4
Q
Unstable angina v. NSTEMI?
A
NSTEMI - elevated cardiac enzymes (troponin, CK-MB)Both lack ST segment elevations and pathologic Q waves
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
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
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
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)
9
Q
Worst risk factor for stable angina?
A
Diabetes mellitus
10
Q
Most common risk factor for stable angina?
A
HTN
11
Q
Goal LDL in patients with CAD?
A
< 100 mg/dL
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
13
Q
Stable angina:First-line beta blockers (2)?
A
Atenolol, metoprolol
14
Q
Stable angina:Secondary treatment if symptomatic on beta-blocker and nitrate?
A
Calcium channel blocker
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.
16
Q
Cardiac catheterization/revascularization methods (2)?
A
(1) Percutaneous coronary intervention (PCI), also referred to as angioplasty(2) Coronary artery bypass grafting (CABG)
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
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%
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
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 *
21
Q
Management of unstable angina includes repletion of deficient electrolytes, especially ___ (2)?
A
K+ and Mg2+
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
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)
24
Q
Prinzmetal’s angina (coronary artery vasospasm):Medical therapy (2)?
A
Calcium channel blockersNitrates
25
Prinzmetal's angina (coronary artery vasospasm):First-line CCB?
Diltiazem
26
PCI/angioplasty:Techniques/strategies to reduce high rates of revascularization (2)?
(1) Drug-eluting stents(2) Aspirin + clopidogrel + glycoprotein IIa/IIIb inhibitors
27
T/F: Revascularization (PCI/CABG) decreases the incidence of MI
False - Revascularization DOES NOT decrease the incidence of MI, but DOES result in significant improvement in symptoms
28
Myocardial infarction has a ___% mortality rate. ___% of the deaths are pre-hospital.
Myocardial infarction has a 30% mortality rate. 50% of the deaths are pre-hospital.
29
Chest pain response to nitroglycerin:Stable angina?Unstable angina?NSTEMI/STEMI?
Stable angina: YesUnstable angina: YesNSTEMI/STEMI: No
30
Cause of sudden cardiac death in the setting of MI?
Ventricular fibrillation (Vfib)
31
Evolution of ECG findings in MI?
(1) Peaked T waves(2) ST segment elevation(3) Q waves(4) T wave inversion
32
ST segment:Depression v. elevation?
ST segment depression: Sub-endocardial injury ST segment elevation: Transmural injury
33
Anterior wall MI:ECG changes?Coronary vessel involved?
Anterior wall MI - ST segment elevation and/or Q waves in leads V1-V4- Occlusion of left anterior descending (LAD) coronary artery
34
Anteroseptal wall MI:ECG changes?Coronary vessel involved?
Anteroseptal wall MI- ST segment elevation and/or Q waves in leads V1-V2- Occlusion of proximal left anterior descending (LAD) coronary artery
35
Anterolateral wall MI:ECG changes?Coronary vessel involved?
Anterolateral wall MI- ST segment elevation and/or Q waves in leads V4-V6- Occlusion of left circumflex (LCX) coronary artery
36
Lateral wall MI:ECG changes?Coronary vessel involved?
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
37
Posterior wall MI:ECG changes?Coronary vessel involved?
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)
38
Inferior wall MI:ECG changes?Coronary vessel involved?
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
39
ECG that exhibits changes consistent with inferior wall infarction:Next clinical step?
Right-sided ECG with leads V4R, V5R, and V6R
40
Inferior wall MI with right ventricular infarct/dysfunction:ECG changes?Coronary vessel involved?
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)
41
Right ventricular infarct:Clinical presentation (4)?
- Hypotension- Clear lungs - Elevated jugular venous pressure- Hepatomegaly
42
NSTEMI/STEMI:Medical therapy (7)?
"MONA BASH"- Morphine - Oxygen- Nitrates- Aspirin and clopidogrel- Beta-blocker- ACE-inhibitor- Statins- Heparin (enoxaparin/Lovenox)
43
Medical therapies (3) shown to reduce post-MI mortality?
- Aspirin- Beta-blocker- ACE-inhibitor
44
Medical therapy shown to reduce post-MI mortality in patients with post-MI LV dysfunction?
Beta-blockers (carvedilol)
45
Medical therapy shown to reduce post-MI remodeling of the myocardium?
Beta-blockers
46
Right ventricular infarct:Treatment?
- 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
47
Methods of revascularization in STEMI (3)?
(1) Percutaneous coronary intervention (PCI)(2) Thrombolytic therapy(3) Coronary artery bypass graft (CABG)
48
PCI:Timeframe requirements for indication as preferred method of revascularization?
PCI performed with a door-to-balloon time less than 90 minutes
49
Thrombolytic therapy: - Timeframe requirements for therapy to be an available method of revascularization?- Timeframe requirements for optimal therapy outcomes?- First-line agent for therapy?
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)
50
Post-MI patients should undergo ___ before hospital discharge and should schedule ___ within ___ weeks of discharge.
Post-MI patients should undergo MEASUREMENT OF LV EF% before hospital discharge and should schedule EXERCISE STRESS TEST within 4-6 weeks of discharge.
51
Post-MI patients have a high risk of ___ during the next 5 years.Risk increases in the setting of what 2 factors?
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
52
Treatment of premature ventricular contractions (PVCs) post-MI?
None
53
Treatment of ventricular tachycardia (VT) post-MI in a hemodynamically stable patient?
IV amiodarone
54
Most common cause of death in first few days post-MI?
Ventricular arrhythmia, either VT or Vfib
55
Treatment of second-degree (Mobitz II) or third-degree AV block in the setting of anterior wall MI?
Pacemaker
56
Treatment of second-degree (Mobitz II) or third-degree AV block in the setting of inferior wall MI?
- IV atropine - If conduction is not restored, pacemaker
57
Post-MI, patients may:- Return to work in?- Resume sexual intercourse in?
- Return to work in 8 weeks - Resume sexual activity in 4-6 weeks
58
Most common cause of in-hospital death post-MI?
CHF (pump failure) Severe CHF leads to cardiogenic shock
59
New-onset mitral regurgitation (MR) post-MI?
Papillary muscle rupture
60
Dressler syndrome:Treatment?
Fever, malaise, fibrinous pericarditis, leukocytosis, and pleuritis weeks to months post-MI (autoimmune etiology)Treatment is aspirin
61
LDL calculation?
LDL = TC - HDL - (TG/5)TC = Total cholesterolTG = Triglycerides (VLDL)LDL accounts for approximately 2/3 of total cholesterol (TC)
62
Total cholesterol:- Ideal?- Borderline?- High?
Total cholesterol:- Ideal < 200 - Borderline 200-240- High > 260
63
LDL:- Ideal?- Borderline?- High?
LDL:- Ideal < 130- Borderline 130-160- High > 160
64
Triglycerides (VLDL):- Ideal?- Borderline?- High?
Triglycerides (VLDL):- Ideal < 125- Borderline 125-250- High > 250
65
CAD risk is primarily due to the ___ component of cholesterol because it is thought to be the most atherogenic of all lipoproteins.
LDL
66
Coronary artery disease (CAD):- Positive risk factor (lipoprotein)?- Mechanism?
- LDL - LDL is proposed to be the most atherogenic of all lipoproteins
67
Coronary artery disease (CAD):- Negative risk factor (lipoprotein)?- Mechanism?
- HDL- HDL removes excess cholesterol from arterial walls
68
HDL cholesterol:- HDL level that corresponds to a "negative risk factor" for CAD?- HDL level that corresponds to a "positive risk factor" for CAD?
- Low HDL < 40 is a risk factor for CAD- High HDL > 60 is a negative risk factor (protective) for CAD
69
HDL cholesterol:- For every 10 mg/dL increase in HDL levels, CAD risk decreases by ___%
For every 10 mg/dL increase in HDL levels, CAD risk decreases by 50%
70
Total cholesterol-to-HDL ratio:- The lower the TC/HDL ratio, the ___ the risk of CAD
- The lower the total cholesterol-to-HDL ratio, the LOWER the risk of CAD
71
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?
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
72
USPSTF - Lipid Screening,Recommended Ages + Intervals:- Men?- Men at increased CAD risk?- Women?- Women at increased CAD risk?
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
USPSTF - Lipid Screening:- Initial lipid screen?- Follow-up lipid screen if initial screen is abnormal/concerning?
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
Goal LDL levels:- Patient with average (standard) CAD risk?- Patient with DM?- Patient with established CAD?- Patient with DM and CAD?
Average (standard) risk:- LDL < 130 Patient with DM:- LDL < 100Patient with established CAD:- LDL < 100Patient with DM and established CAD:- LDL < 70
75
Diet therapy for hypercholesterolemia (high LDL):- Total calories from fat (%)?- Total calories from saturated fat (%)?- Total cholesterol?
* 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
Medications that can cause changes in TC, LDL, HDL, and/or TG (VLDL): - Thiazide diuretics
Thiazide diuretics:- Increase TC- Increase LDL- Increase TG (VLDL)
77
Medications that can cause changes in TC, LDL, HDL, and/or TG (VLDL): - Beta-blockers (propranolol)
Beta-blockers (propranolol):- Increase TG (VLDL)- Decrease HDL
78
Two medication classes that can increase serum lipids, other than thiazide diuretics and beta-blockers?
Corticosteroids and HIV protease inhibitors
79
Medication therapy for hyperlipidemia:- First-line?-Second-line?-Third-line?
- First-line: HMG-CoA reductase inhibitors (statins) - Second-line: Niacin- Third-line: Bile-acid sequestrants
80
Risk factors for CAD:- Most important risk factor?- Second most important risk factor?
- Most important: High LDL- 2nd most important: Low HDL
81
DYSLIPIDEMIA SYNDROMES:* Type I* Exogenous hyperlipidemia - Lipoprotein(s) elevated?- Treatment?
Type IExogenous hyperlipidemiaLipoprotein(s) elevated: - Chylomicrons Treatment:- Diet therapy
82
DYSLIPIDEMIA SYNDROMES:* Type IIa* Familial hypercholesterolemia - Lipoprotein(s) elevated?- Treatment?
Type IIaFamilial hypercholesterolemia Lipoprotein(s) elevated:- LDL Treatment:- First-line: Statins - Second-line: Niacin - Third-line: Bile-acid sequestrants (cholestyramine)
83
DYSLIPIDEMIA SYNDROMES:* Type IIb* Combined hyperlipoproteinemia - Lipoprotein(s) elevated?- Treatment?
Type IIbCombined hyperlipoproteinemia Lipoprotein(s) elevated:- LDL + VLDL (TG)Treatment:- First-line: Statins - Second-line: Niacin - Third-line: Fibrates (gemfibrozil)
84
DYSLIPIDEMIA SYNDROMES:* Type IV* Endogenous hyperlipidemia - Lipoprotein(s) elevated?- Treatment?
Type IVEndogenous hyperlipidemia Lipoprotein(s) elevated:- VLDL (TG)Treatment:- First-line: Niacin - Second-line: Fibrates (gemfibrozil) - Third-line: Statins
85
DYSLIPIDEMIA SYNDROMES:* Type V* Familial hypertriglyceridemia - Lipoprotein(s) elevated?- Treatment?
Type VFamilial hypertriglyceridemia Lipoprotein(s) elevated:- VLDL (TG) + chylomicrons Treatment:- First-line: Niacin - Second-line: Fibrates (gemfibrozil)
86
Elevated TG (VLDL) levels are associated with?
Impaired glycemic control
87
Anti-hypertensive classes (2) that adversely effect plasma lipid levels?
Thiazide diuretics and beta-blockers
88
HMG-CoA reductase inhibitors (statins):- Effects on lipids?
- Decreases LDL levels
89
Niacin:- Effects on lipids?
- Decreases LDL levels- Decreases TG (VLDL) levels- Increases HDL levels
90
Bile-acid sequestrants (cholestyramine):- Effects on lipids?
- Decreases LDL levels- INCREASES TG (VLDL) LEVELS
91
Fibrates (gemfibrozil):- Effects on lipids?
- Decreases TG (VLDL) levels- Increases HDL levels
92
Most potent drug for decreasing LDL?
HMG-CoA reductase inhibitors (statins)
93
Most potent drug for decreasing TG (VLDL) levels?
Niacin
94
Most potent drug for increasing HDL?
Niacin
95
Drug for hyperlipidemia contraindicated in diabetic patients?
Niacin - may worsen glycemic control
96
HMG-CoA reductase inhibitors (statins):- Side effects (2)?
- AST/ALT elevation- CPK elevation (harmless) in the setting of myositis
97
HMG-CoA reductase inhibitors (statins):LFT monitoring?
Monitor LFTs - Monthly for first 3 months- Then every 3-6 months
98
Diastolic heart failure:- Pathophysiologic mechanism?- Causes include (2)?- Heart sound?
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
Systolic heart failure:- Pathophysiologic mechanism?- Causes include (2)?- Heart sound?
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
S3 ventricular gallop:- left-heart S3 best appreciated at ___ on auscultation - right-heart S3 best appreciated at ___ on auscultation - S3 heart sound represents?
- 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
S4 atrial gallop:- left-heart S4 best appreciated at ___ on auscultation - right-heart S4 best appreciated at ___ on auscultation - S4 heart sound represents?
- 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
Signs/symptoms of LEFT-SIDED heart failure (10)?
(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
Signs/symptoms of RIGHT-SIDED heart failure (6)?
(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
Echocardiogram:- Ejection fraction?- Ventricular chamber dilation?- Ventricular hypertrophy?(1) Systolic heart failure(2) Diastolic heart failure
SYSTOLIC HEART FAILURE- EF < 40%- Ventricular chamber dilationDIASTOLIC HEART FAILURE- EF > 40% (preserved ventricular function)- Ventricular hypertrophy
105
CXR:- Pulmonary congestion?- Cardiomegaly?(1) Systolic heart failure(2) Diastolic heart failure
SYSTOLIC HEART FAILURE- Pulmonary congestion (Kerley B lines)- Cardiomegaly DIASTOLIC HEART FAILURE- Pulmonary congestion (Kerley B lines)- WITH -or- WITHOUT cardiomegaly
106
New York Heart Association (NYHA) Classification of Heart Failure:- Class I- Class II- Class III- Class IV
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
Most common cause of death from CHF?
Sudden death from ventricular arrhythmias - Cardiac ischemia provokes ventricular arrhythmias
108
SYSTOLIC HEART FAILUREMild CHF (NYHA I to II):- Treatment (3)?
(1) Lifestyle modifications, including sodium restriction (4g/day) and physical activity(2) ACE inhibitor (3) Loop diuretic
109
SYSTOLIC HEART FAILUREAce Inhibitor: - Pharmacologic mechanisms (2) involved in the treatment of CHF?
(1) Venodilation - Decreases preload(2) Vasodilation - Decreases preload
110
SYSTOLIC HEART FAILUREAce Inhibitor: - Benefits (3) of starting an ACE inhibitor in patients with systolic dysfunction
(1) Alleviate symptoms in mild, moderate, and severe CHF(2) Reduce mortality (3) Improve prognosis (prolong survival)
111
SYSTOLIC HEART FAILUREAce Inhibitor: - Clinical/laboratory values to monitor (4)
- Blood pressure- K+- BUN- Cr
112
SYSTOLIC HEART FAILUREAce Inhibitor: - Alternative therapy for patients who experience cough as a side effect of ACE inhibitor therapy?
ARB - Angiotensin receptor blocker
113
SYSTOLIC HEART FAILUREMild-to-Moderate CHF (NYHA II to III):- Treatment (3)?
(1) ACE inhibitor(2) Loop diuretic(3) Beta-blocker
114
SYSTOLIC HEART FAILUREBeta-blocker: - Proven to reduce mortality in what patient demographic?
Post-MI heart failure
115
SYSTOLIC HEART FAILUREBeta-blocker: - First-line agent- Second-line agent
First-line: Carvedilol Second-line: Metoprolol
116
SYSTOLIC HEART FAILUREModerate-to-Severe CHF (NYHA III to IV):- Treatment (5)?
(1) ACE inhibitor(2) Loop diuretic(3) Beta-blocker (4) Aldosterone antagonist(5) Digoxin
117
SYSTOLIC HEART FAILUREAldosterone antagonist: - RALES trial showed that ___ reduces morbidity and mortality in CHF patients NYHA III to IV
Spironolactone
118
SYSTOLIC HEART FAILUREAldosterone antagonist: - Contraindicated in what patient population?
Renal failure
119
SYSTOLIC HEART FAILUREAldosterone antagonist: - Clinical/laboratory values to monitor (3)
- K+- BUN- Cr
120
SYSTOLIC HEART FAILUREAldosterone antagonist: Alternative agent in males experiencing gynecomastia on spironolactone?
Eplerenone
121
SYSTOLIC HEART FAILUREModerate-to-Severe CHF (NYHA III to IV):- Indication for digoxin therapy?
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
Heart failure medications shown to decrease mortality in CHF patients?
- ACE inhibitors- ARBs - Beta-blockers (carvedilol > metoprolol) - Aldosterone antagonists (spironolactone) NOT- Diuretics - Digoxin
123
DIASTOLIC HEART FAILURE:- Treatment v. systolic heart failure
- 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
The overall 5-year mortality for all patients with CHF is approximately ___%
The overall 5-year mortality for all patients with CHF is approximately 50%
125
In CHF, indications (2) for digoxin therapy?
(1) EF < 40%(2) Afib with rapid ventricular rate (RVR)
126
HTN:Cardiac complications (4)?
(1) CAD(2) MI(3) CHF w/ LVH(4) HTN a/w increased risk of aortic dissection
127
HTN:Renal complications (2)?
(1) Nephrosclerosis- Arteriosclerosis of the afferent and efferent arterioles and of the glomerulus (2) Renal failure- Decreased GFR and tubular dysfunction
128
HTN:CNS complications (2)?
(1) Intracerebral hemorrhage (stroke)(2) Transient ischemic attack (TIA)
129
HTN:Eye complications (2)?
(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
Most common cause of secondary HTN in young women?
Birth control pills (OCPs)
131
Most common cause of renovascular HTN in:- Young women?- Older men?
Younger women - Fibromuscular dysplasia Older men - Renal artery stenosis (RAS)
132
NORMAL HYPERTENSION:- Systolic BP- Diastolic BP- Management
Systolic BP < 120 Diastolic BP < 80No treatment
133
PRE-HYPERTENSION:- Systolic BP- Diastolic BP- Management
Systolic BP 120-139Diastolic BP 80-89Lifestyle modification
134
STAGE I HYPERTENSION:- Systolic BP- Diastolic BP- Management
Systolic BP 140-159Diastolic BP 90-99Lifestyle modification + drug therapy
135
STAGE II HYPERTENSION:- Systolic BP- Diastolic BP- Management
Systolic BP > 160 Diastolic BP > 100Lifestyle modification + 2-drug combination therapy
136
Definition of HTN in:- General population- Diabetics and patients with renal disease
GENERAL POPULATION HTN = BP > 140/90DIABETICS / RENAL DISEASEHTN = BP > 130/80
137
Diagnosis of HTN:- Number of readings- Posture- Caffeine- Smoking - Length of the cuff bladder
- 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
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.
BP cuff too small - Report a falsely INCREASED BPBP cuff too large - Report a falsely DECREASED BP
139
EtOH:- Cardioprotective?- Risk factor for CAD?
- An absolute maximum of 2 drinks per day may be cardioprotective- Alcohol intake that exceeds this amount is a risk factor for CAD
140
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?
MINIMUM BP GOALS- General population --->BP BP
141
Black patients "Salt-sensitive" HTN- Anti-hypertensive choices (2)?
THIAZIDESCalcium channel blockers
142
White patients "Salt-insensitive" HTN- Anti-hypertensive choices (3)?
ACE inhibitorsARBs Beta-blockers
143
Anti-hypertensive agent(s) of choice in ALL patients with diabetes?
ACE inhibitor - Protective effect on the kidneys to slow development of diabetic nephropathy
144
Anti-hypertensive agent(s) of choice in ALL patients with renal disease?
ACE inhibitor - Protective effect on the kidneys
145
Anti-hypertensive agent(s) of choice in ALL patients with CHF?
- ACE inhibitor / ARB- Thiazide diuretic
146
Anti-hypertensive agent(s) likely to have a favorable effect on osteoporosis? Why?
THIAZIDE DIURETICS slow the process of bone demineralization
147
Anti-hypertensive agent(s) likely to have a favorable effect on migraines? Why?
BETA-BLOCKERS are typically used as prophylaxis for migraine headaches
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Hypertensive urgency/emergency drug selection:Pheochromocytoma
Phentolamine
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Hypertensive urgency/emergency drug selection:Eclampsia
Magnesium sulfate (MgSO4)
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Hypertensive urgency/emergency drug selection:Aortic dissection
Esmolol
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Hypertensive urgency/emergency drug selection:Intracranial hemorrhage (stroke)
Sodium nitroprusside
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Anti-hypertensive agent(s) of choice in pregnant patients?
- Methyldopa- Beta-blockers - Hydralazine
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Anti-hypertensive agent(s) CONTRAINDICATED in pregnant patients?
- 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
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Anti-hypertensive agent(s) likely to have an adverse effect on gout? Why?
THIAZIDE DIURETICS b/c side effects include hyperuricemia (elevated uric acid levels in the blood)
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ANTI-HYPERTENSIVE SIDE EFFECTS- Thiazide diuretics (6)?
- HYPOKALEMIA - Hypomagnesemia - Hyperuricemia - Hyperglycemia - CHOLESTEROL: Increase TC, LDL, and TG (VLDL)- Metabolic alkalosis
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ANTI-HYPERTENSIVE SIDE EFFECTS- Beta-blockers (6)?
- Bradycardia- Bronchospasm - Insomnia- Fatigue- Depression- CHOLESTEROL: Decrease HDL, increase TG (VLDL)
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ANTI-HYPERTENSIVE SIDE EFFECTS- ACE inhibitors (4)?
- Acute renal failure- Hyperkalemia - Dry cough angioedema - Skin rash
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Anti-hypertensive agent(s) of choice in asthmatics?
Calcium channel blocker NOTE: Beta-blockers contraindicated b/c side effects include bronchospasm
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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)?
(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)
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ECG FINDINGS,Premature atrial complexes (PACs): - P waves - PR intervals - QRS complexes
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
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TREATMENT,Premature atrial complexes (PACs): - Asymptomatic- Symptomatic
- PACs generally asymptomatic and do NOT require treatment- If PACs cause "skipped beats" or palpitations, treatment w/ beta-blockers may be helpful
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ECG FINDINGS,Premature ventricular complexes (PVCs): - P waves - RR intervals - QRS complexes
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
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TREATMENT,Premature ventricular complexes (PVCs): - Asymptomatic- Symptomatic
- PVCs generally asymptomatic and do NOT require treatment- If PVCs are symptomatic (e.g., palpitations), treatment w/ beta-blockers may be helpful
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Premature ventricular complexes (PVCs): - Workup
- 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
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Premature atrial/ventricular complex (PAC, PVC) rhythms:- Couplet- Bigeminy - Trigeminy
Couplet - 2 successive PACs/PVCsBigeminy - PAC/PVC every other beatTrigeminy - PAC/PVC every third beat
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Atrial fibrillation (Afib):- Mechanism
- 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
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ECG FINDINGS,Atrial fibrillation (Afib): - P waves - RR intervals - QRS complexes
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
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Patients with Afib and underlying heart disease are at a markedly increased risk for what 2 adverse events?
- Thromboembolism - Hemodynamic compromise
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Treatment of Afib in a hemodynamically STABLE patient?
- 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
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Treatment of Afib in a hemodynamically UNSTABLE patient?
- 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*
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Holiday heart syndrome
Afib following alcohol ingestion is frequently seen during holidays and weekends
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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)?
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
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Anticoagulation in the management of chronic Afib:- Patients
Treatment of patients
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Deep venous thrombosis (DVT):Virchow's triad
Endothelial injury, venous stasis, and hypercoagulability
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Deep venous thrombosis (DVT):Symptoms (4)
- 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
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Deep venous thrombosis (DVT):Diagnostic tools (3)
- 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
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Deep venous thrombosis (DVT):Treatment options (3)
- Anticoagulation - Thrombolytic therapy- IVC filter NOTE: IVC filter effective only in preventing PE, not DVTs
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Deep venous thrombosis (DVT):Anticoagulation therapy
- 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
