Unit 4 Textbook: Cardiovascular Flashcards

1
Q

Medications that can cause an increase in BP

A

Oral contraceptives, nicotine, steroids, appetite suppressants, TCA’s, cyclosporine, NSAIDs, some nasal decongestants

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2
Q

Diagnostic criteria for high BP

A

> 140/90 for <60 years old 3+ readings at least 1 week apart

>150/90 for >60 years old

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3
Q

Diagnostic tests to be done at visit for high BP

A

Electrocardiogram, blood glucose, hemoglobin, hematocrit, complete urinarylis, complete chem panel, liver function, BMP, fasting lipid panel

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4
Q

DOC for nonblack hypertension

A

Thiazide diuretic or ARB or ACE alone or in combo

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5
Q

DOC for black hypertension

A

Thiazide diuretic or calcium channel blocker or combo

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6
Q

DOC for all races hypertension with diabetes or chronic kidney disease

A

ACEI or ARB or combo

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7
Q

Diuretics

A

Decrease BP by causing diuresis which causes decreased plasma volume, stroke volume and cardiac output
May cause hypokalemia or hypomagnesia, leading to arrhythmias

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8
Q

Thiazide diuretics

A

Chlorthalidone, hydrochlorothiazide, indapamide, metolazone
Inhibit reabsorption of Na and Cl in proximal tubule
Takes several days to take effect
Cause potassium and bicarb excretion but decreased Ca excretion
Cause uric acid retention
Not recommended for kidney disease

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9
Q

Side effects of thiazide diuretics

A

Hypokalemia, hypomagnesia, hypercalcemia, hyperuricemia, hyperglycemia, tinnitus, paresthesia, N/V, diarrhea, impotence

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10
Q

Loop diuretics

A

Bumetanide, ethacrynic acid, furosemide, torsemide
Indicated in presence of edema
Inhibits reabsorption of Na and Cl in loop
May cause hypocalcemia, hypokalemia, and hypomagnesia
Reserved for patients with renal dysfunction

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11
Q

Potassium sparing diuretic

A

Amiloride, spironolactone, eplerenone, triamterone
Interfere with sodium reabsorption at distal tubule which decreases K+ secretion
True benefit indicated in heart failure
May cause hyperkalemia and hyponatremia

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12
Q

SE of potassium sparing diuretics

A

Gynecomastia, hirsutism, menstrual irregularities

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13
Q

Beta blockers

A

Block central and peripheral beta receptors–results in decreased CO and sympathetic outflow
Can be used in stable CHF to decrease mortality and vascular remodeling

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14
Q

Beta blockers with intrinsic sympathomimetic activity

A

Pindolol and acebutolol

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15
Q

Beta blockers are contraindicated in

A

Sinus bradycardia, asthma, COPD, AV block, cardiac failure

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16
Q

In diabetic patients, beta blockers can

A

Mask all symptoms of hypoglycemia

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17
Q

SE of beta blockers

A

Fatigue, drowsiness, bronchospasm, N/V

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18
Q

ACE inhibitors

A

-Pril
Inhibits ACE enzyme which decreases angiotensin II and blocks aldosterone
Inhibits bradykinin degradation and increases synthesis of vasodilating prostaglandins
Decreased mortality in patients with CHF, post MI and systolic dysfunction

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19
Q

ACE inhibitors are contraindicated in

A

Patients with CHF, bilateral renal stenosis, pregnancy

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20
Q

SE of ACEI

A

Dry cough, rashes, dizziness, angioedema

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21
Q

ARBs

A

-sartan
Block vasoconstriction and aldosterone secreting effects of angiotensin II
Indicated for patients with hypertension, nephropathy in type 2 diabetes, HF and those who can not tolerate ACEI

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22
Q

ARBs contraindicated in

A

pregnancy

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23
Q

SE ARBs

A

Dizziness, upper respiratory infections, cough, viral infection, fatigue, pharyngitis, rhinitis

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24
Q

Renin inhibitors

A

Aliskiren
Block conversion of angiotensinogen to angiotensin I
Avoid in pregnancy

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25
Q

Ca channel blockers

A

Inhibits movement of Ca ions across cell membrane causing CV muscle relaxation and vasodilation
Can also decrease contractility, decrease HR and decrease conduction
Have less effect on veins
Nondihydropyridines and Dihydropyridines

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26
Q

Nondihydropyridines

A

Verapamil + Diltiazem
Decrease HR and slow conduction at AV node
Avoid in patients with heart block

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27
Q

Dihydropyridines

A

-Dipine

Potent vasodilators

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28
Q

CCB’s are recommended specifically for

A

Prinzmetal angina

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29
Q

Peripheral a1 blockers

A

Doxazosin, prazosin, terazosin
Effective for BPH by dilating peripheral arterioles and veins
CI in presence of CV disease
Can cause water and sodium retention in chronic use

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30
Q

Central a2 agonists

A

Decrease sympathetic outflow, CO and peripheral resistance by blocking a1
Clonidine, methyldopa, guanabenz guanfacine

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31
Q

Direct vasodilators

A

Hydralazine + Minoxidil
Cause arteriolar smooth muscle relaxation; reserved for essential or severe hypertension
May cause fluid retention, reflex tachycardia, lupus like syndrome

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32
Q

Recommended drug for hypertension in pregnancy

A

Methyldopa

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33
Q

Recommended drugs for hypertension in diabetics

A

ACEI and ARBs (not in combo)

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34
Q

Commonly used meds in hypertensive emergency

A

Hydralazine, nitrates, CCB’s, beta blockers, alpha 1 blockers, and ACEI

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35
Q

Function of HDL

A

Removes LDL from peripheral cells and transports to liver for metabolism

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36
Q

4 major statin benefit groups

A
  1. Have clinical atherosclerotic CV disease
  2. no ASCVD but LDL>190
  3. no ASCVD, 40-75 years old, type 1 or 2 DM with LDL 70-189
  4. no ASCVD or DM, 40-75 years old, LDL 70-189, 10 year risk of ASCVD of >7.5%
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37
Q

Goals of statin therapy

A

High intensity statin: decrease by 50%
Moderate intensity statin: decrease by 30%
Low intensity statin: decrease by less than 30%

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38
Q

Most common complaint when taking statins

A

muscle related myopathy

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39
Q

MOA of statins

A

Block conversion of HMG-CoA to mevalonate–rate limiting step in production of cholesterol by liver; increases number of LDL receptors on liver so larger amount of LDL can be taken up by liver and decrease in plasma LDL
Max effects seen in 4-6 weeks

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40
Q

Statins CI in

A

Pregnancy, breastfeeding, active liver disease

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41
Q

Ezetimibe

A

Cholesterol absorption inhibitor
Inhibits cholesterol absorption at brush border of small intestine
Can be used alone or in combo with statins

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42
Q

Bile acid resins

A

Cholestyramine and Coleseuelam
Bind bile acids in the intestines, forming an insoluble complex that is excreted in the feces–decreased return of cholesterol to liver causes increased LDL receptors on liver

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43
Q

Bile acid resins CI in

A

biliary obstruction, chronic constipation, triglycerides >300

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44
Q

Niacin

A

Naturally occuring B vitamin that can improve cholesterol when given at 100-300 recommended daily dose
Decreased VLDL synthesis, inhibits lipolysis, increased lipoprotein lipase activity

45
Q

Niacin CI in

A

hepatic dysfunction, severe hypotension, hyperglycemia, gout, A fib, peptic ulcer disease

46
Q

SE of niacin

A

Increased prostaglandins

47
Q

Fibric acid derivatives

A

Gemfibrozil and Fenofibrate
Mainly affect triglycerides and HDL
CI in patients with history of gallstones and severe renal or hepatic dysfunction

48
Q

First line cholesterol meds

A

Statin

49
Q

Second line cholesterol meds

A

Cholesterol absorption inhibitors and niacin and bile acid resins

50
Q

Third line cholesterol meds

A

Fibric acid derivatives

51
Q

Angina

A

Clinical syndrome caused by coronary heart disease, O2 demand greater than O2 supply
Stable angina–provoked by physical exertion or emotional stress; relieved by rest and nitroglycerine

52
Q

Nonpharmacological treatment for angina

A

Decreased weight, smoking cessation, exercise

53
Q

Drugs used to treat angina

A

ACEI, nitrates, beta blockers, Ca channel blockers, antiplatelets

54
Q

ACEI indicated for which angina patients

A

EF<40%, hypertension, diabetes, kidney disease

Monitor renal function and serum K+ (may contribute to hyperkalemia due to decreased aldosterone)

55
Q

Nitrates

A

Cause dilation throughout vasculature
Dilation of veins causes less blood to be returns to heart and decreases preload
Increased blood flow and O2 supply to myocardium due to artery dilation
Sublingual forms are rapid acting

56
Q

First line therapy for acute angina tx

A

Nitrates

57
Q

Long acting nitrates

A

Isosorbide dinitrate, isosorbide mononitrate, nitroglycerine patch
Chronic prophylaxis

58
Q

SE of nitrates

A

Headache, flushing, dizzy, weakness, orthostatic hypotension

59
Q

Antiplatelet therapy for angina

A

inhibits platelet aggregation
Aspirin + Clopidogrel
Decreases chance of MI

60
Q

Aspirin

A

Irreversible enzyme antagonism to block prostaglandin synthesis–blocks TXA 2

61
Q

Clopidogrel

A

Decreased ADP induced platelet activation

62
Q

First line for chronic prophylaxis of angina

A

Beta blockers
Combo therapy of Beta blocker + Ca channel blocker or long acting nitrate is second line
3 drug combo is third line

63
Q

Highest risk factors for heart failure

A

CAD, Htn, cardiomyopathy

64
Q

Drugs that can worsen HF

A

NSAIDs, steroids, hormones, antihypertensives, Na containing drugs, lithium, amphetamines, cocaine, alcohol

65
Q

4 levels of HF

A
  1. no limitation in physical activity
  2. slight limitation in physical activity; comfortable at rest
  3. marked limitation in physical activity; less than ordinary activity causes dyspnea
  4. Unable to carry physical activity without symptoms; symptoms present at rest
66
Q

Goals of HF therapy

A

Improve quality of life, decrease mortality, decrease compensatory mechanisms causing symptoms

67
Q

Drug therapy for HF

A

Usually long term
ACEI + Beta blockers
Diuretics, aldosterone antagonists, hydralazine, nitrates, digoxin can also be used

68
Q

ACEI indicated for HF

A

Captopril, enalopril, fosinopril, lisinopril, quinopril, trandolapril, ramipril, perindopril

69
Q

ACEI in HF MOA

A

Cause dilation on venous and arterial sides, inhibits fluid accumulation and increases blood flow to vital organs without precipitating reflex tachycardia

70
Q

Patients with HF and significant volume overload should be started on

A

Diuretic + ACEI + Beta blocker

Loop diuretics are most potent

71
Q

Most useful approach to see if HF meds are working

A

Daily weight measurements

72
Q

What drugs may decrease effects of diuretics

A

NSAIDs

73
Q

Most studied ARB in HF

A

Losartan

74
Q

Beta blockers for HF

A

Decreased SNS activation decreases the progression of HF even though negative inotropic effect
Add to Diuretics and ACEI for tx of stage 2-4
Primary function: prevent and reverse adrenergically mediated intrinsic myocardial dysfunction and remodeling

75
Q

Beta blockers approved for HF

A

Carvedilol, metoprolol, bisoprolol

76
Q

Beta blockers for HF CI in

A

bronchospastic disease, symptomatic bradycardia, advanced heart block

77
Q

Digoxin

A

Can prevent clinical deterioration but does not decrease mortality
Mild inotropic effect by inhibiting Na/K ATPase thus increasing Ca entry into cell

78
Q

Signs of digitoxin toxicity

A

N/V, anorexia, fatigue, headache, disorientation, confusion, seizures, arrhythmias

79
Q

Drugs that increase digoxin levels

A

Quinidine, amiodarone, flexainide, propaferone, spironolactone, verapamil, antibiotics, anticholinergics

80
Q

Drugs that decrease digoxin levels

A

Antacids, cholestyramine, neomycin

81
Q

Alternative HF drugs for african americans who can not take ACEI

A

Hydralazine

82
Q

First line for HF tx

A

ACEI with or without a diuretic

83
Q

Second line for HF tx

A

ACEI + beta blocker with diuretic

84
Q

Third line for HF tx

A

ACEI, Beta blocker, aldosterone agonist, diuretic, digoxin

85
Q

Conditions that can cause arrhythmias

A

Myocardial ischemia, chronic HF, hypertension, valvular heart disease, hypoxemia, thyroid abnormalities, electrolyte disturbances, drug toxicity, caffeine and alcohol, anxiety, exercise

86
Q

Goals of treatment for arrhthmias

A

Relieve acute episode of irregular rhythm, establish SR, and prevent further episodes

87
Q

Class 1 anti arrhythmic

A

Na channel blockers

88
Q

Class 1a anti arrhythmic

A

Procainamide, quinidine, disopyramide
intermediate onset/offset
Treatment of supraventricular and ventricular arrhythmias
Slows phase 0, prolongs phase 3 and decreases automaticity
Blocks a1 causing vasodilation

89
Q

Specific side effect of quinidine

A

Potent anticholinergic

Same with disopyramide

90
Q

Class 1b anti arrhythmic

A

Lidocaine and mexiletine
Fast onset and offset
Decreased automaticity and conduction velocity and shorter refractoriness
Primarily exerts effects on ventricular myoacrdium
Prolongs AP

91
Q

Lidocaine is specific to

A

Ischemic tissue

92
Q

Class 1c anti arrhythmic

A

Slow onset and offset

Supraventricular usually

93
Q

Class 2 anti arrhythmic

A

Beta blockers
Decrease automaticity and conduction velocity and prolongs refractoriness
Decreased myocardial O2 consumption, decreased HR, decreased BP, decreased myocardial contractility

94
Q

Uses of beta blockers for arrhythmias

A

Paroxysmal supraventricular tachycardia, A fib, arrhythmias due to catecholamines excess, ischemia, mitral valve prolapse, MI, and V tach

95
Q

Class 3 anti arrhythmic

A

K+ channel blockers
Amiodarone, dronedarone, sotalol
Decrease automaticity and conduction velocity and prolongs refractoriness
no negative inotropic effects

96
Q

Amiodarone approved for

A

life threatening recurrent ventricular arrhythmias

Requires a loading dose

97
Q

Dronedarone CI in patients

A

with HF

May increase digoxin levels also

98
Q

Sotalol used for

A

Supraventricular and ventircular arrhythmias

99
Q

Class 4 anti arrhythmic

A

Calcium channel blockers
Used to treat supraventricular arrhythmias
Slow conduction, prolong refractoriness, decrease automaticity
Vascular relaxation
Negatice inotropic effects

100
Q

Digoxin for anti arrhythmic

A

Stimulates PANS which increases vagal tone–slows conduction through AV node + prolongs AV nodal refractory period
Used primarily to slow ventricular rate in supraventricular arrhythmias

101
Q

Adenosine

A

Converts PSVT to SR

Activates potassium channels to decrease intracellular K+– decreases spontaneous SA nodal depolarization

102
Q

Atropine

A

Enhances both sinus nodal automaticity and AV nodal conduction
Blocks ACh
Used exclusively for tx of symptomatic bradycardia

103
Q

A fib 1st line treatment

A

If hemodynamically unstable, immediate DCC
If hemodynamically stable: IV diltiazem, IV verapamil or IV Beta blocker
IV amiodarone used for ventricular rate control

104
Q

First line tx for PSVT

A

Hemodynamically unstable: syncrhonized DCC or vagal maneuvers

105
Q

Second line tx for PSVT

A

DOC is adenosine

If persistent, IV dilitazem, verapamil, or beta blocker

106
Q

Drugs for symptomatic nonsustained VT

A

Beta blockers, nondihydropyridine CCB, class 1C AAD

107
Q

First line drugs for sustained VT

A

Immediate synchronized DCC if unstable; IV amiodarone, IV procainamide or IV sotalol if stable

108
Q

Tx for pulseless VT/VF

A

CPR + AED
If persists, vasopressor therapy (epi)
If persists, IV amiodarone