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
Ca channel blockers
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
26
Nondihydropyridines
Verapamil + Diltiazem Decrease HR and slow conduction at AV node Avoid in patients with heart block
27
Dihydropyridines
-Dipine | Potent vasodilators
28
CCB's are recommended specifically for
Prinzmetal angina
29
Peripheral a1 blockers
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
30
Central a2 agonists
Decrease sympathetic outflow, CO and peripheral resistance by blocking a1 Clonidine, methyldopa, guanabenz guanfacine
31
Direct vasodilators
Hydralazine + Minoxidil Cause arteriolar smooth muscle relaxation; reserved for essential or severe hypertension May cause fluid retention, reflex tachycardia, lupus like syndrome
32
Recommended drug for hypertension in pregnancy
Methyldopa
33
Recommended drugs for hypertension in diabetics
ACEI and ARBs (not in combo)
34
Commonly used meds in hypertensive emergency
Hydralazine, nitrates, CCB's, beta blockers, alpha 1 blockers, and ACEI
35
Function of HDL
Removes LDL from peripheral cells and transports to liver for metabolism
36
4 major statin benefit groups
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%
37
Goals of statin therapy
High intensity statin: decrease by 50% Moderate intensity statin: decrease by 30% Low intensity statin: decrease by less than 30%
38
Most common complaint when taking statins
muscle related myopathy
39
MOA of statins
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
40
Statins CI in
Pregnancy, breastfeeding, active liver disease
41
Ezetimibe
Cholesterol absorption inhibitor Inhibits cholesterol absorption at brush border of small intestine Can be used alone or in combo with statins
42
Bile acid resins
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
43
Bile acid resins CI in
biliary obstruction, chronic constipation, triglycerides >300
44
Niacin
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
Niacin CI in
hepatic dysfunction, severe hypotension, hyperglycemia, gout, A fib, peptic ulcer disease
46
SE of niacin
Increased prostaglandins
47
Fibric acid derivatives
Gemfibrozil and Fenofibrate Mainly affect triglycerides and HDL CI in patients with history of gallstones and severe renal or hepatic dysfunction
48
First line cholesterol meds
Statin
49
Second line cholesterol meds
Cholesterol absorption inhibitors and niacin and bile acid resins
50
Third line cholesterol meds
Fibric acid derivatives
51
Angina
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
Nonpharmacological treatment for angina
Decreased weight, smoking cessation, exercise
53
Drugs used to treat angina
ACEI, nitrates, beta blockers, Ca channel blockers, antiplatelets
54
ACEI indicated for which angina patients
EF<40%, hypertension, diabetes, kidney disease | Monitor renal function and serum K+ (may contribute to hyperkalemia due to decreased aldosterone)
55
Nitrates
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
First line therapy for acute angina tx
Nitrates
57
Long acting nitrates
Isosorbide dinitrate, isosorbide mononitrate, nitroglycerine patch Chronic prophylaxis
58
SE of nitrates
Headache, flushing, dizzy, weakness, orthostatic hypotension
59
Antiplatelet therapy for angina
inhibits platelet aggregation Aspirin + Clopidogrel Decreases chance of MI
60
Aspirin
Irreversible enzyme antagonism to block prostaglandin synthesis--blocks TXA 2
61
Clopidogrel
Decreased ADP induced platelet activation
62
First line for chronic prophylaxis of angina
Beta blockers Combo therapy of Beta blocker + Ca channel blocker or long acting nitrate is second line 3 drug combo is third line
63
Highest risk factors for heart failure
CAD, Htn, cardiomyopathy
64
Drugs that can worsen HF
NSAIDs, steroids, hormones, antihypertensives, Na containing drugs, lithium, amphetamines, cocaine, alcohol
65
4 levels of HF
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
Goals of HF therapy
Improve quality of life, decrease mortality, decrease compensatory mechanisms causing symptoms
67
Drug therapy for HF
Usually long term ACEI + Beta blockers Diuretics, aldosterone antagonists, hydralazine, nitrates, digoxin can also be used
68
ACEI indicated for HF
Captopril, enalopril, fosinopril, lisinopril, quinopril, trandolapril, ramipril, perindopril
69
ACEI in HF MOA
Cause dilation on venous and arterial sides, inhibits fluid accumulation and increases blood flow to vital organs without precipitating reflex tachycardia
70
Patients with HF and significant volume overload should be started on
Diuretic + ACEI + Beta blocker | Loop diuretics are most potent
71
Most useful approach to see if HF meds are working
Daily weight measurements
72
What drugs may decrease effects of diuretics
NSAIDs
73
Most studied ARB in HF
Losartan
74
Beta blockers for HF
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
Beta blockers approved for HF
Carvedilol, metoprolol, bisoprolol
76
Beta blockers for HF CI in
bronchospastic disease, symptomatic bradycardia, advanced heart block
77
Digoxin
Can prevent clinical deterioration but does not decrease mortality Mild inotropic effect by inhibiting Na/K ATPase thus increasing Ca entry into cell
78
Signs of digitoxin toxicity
N/V, anorexia, fatigue, headache, disorientation, confusion, seizures, arrhythmias
79
Drugs that increase digoxin levels
Quinidine, amiodarone, flexainide, propaferone, spironolactone, verapamil, antibiotics, anticholinergics
80
Drugs that decrease digoxin levels
Antacids, cholestyramine, neomycin
81
Alternative HF drugs for african americans who can not take ACEI
Hydralazine
82
First line for HF tx
ACEI with or without a diuretic
83
Second line for HF tx
ACEI + beta blocker with diuretic
84
Third line for HF tx
ACEI, Beta blocker, aldosterone agonist, diuretic, digoxin
85
Conditions that can cause arrhythmias
Myocardial ischemia, chronic HF, hypertension, valvular heart disease, hypoxemia, thyroid abnormalities, electrolyte disturbances, drug toxicity, caffeine and alcohol, anxiety, exercise
86
Goals of treatment for arrhthmias
Relieve acute episode of irregular rhythm, establish SR, and prevent further episodes
87
Class 1 anti arrhythmic
Na channel blockers
88
Class 1a anti arrhythmic
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
Specific side effect of quinidine
Potent anticholinergic | Same with disopyramide
90
Class 1b anti arrhythmic
Lidocaine and mexiletine Fast onset and offset Decreased automaticity and conduction velocity and shorter refractoriness Primarily exerts effects on ventricular myoacrdium Prolongs AP
91
Lidocaine is specific to
Ischemic tissue
92
Class 1c anti arrhythmic
Slow onset and offset | Supraventricular usually
93
Class 2 anti arrhythmic
Beta blockers Decrease automaticity and conduction velocity and prolongs refractoriness Decreased myocardial O2 consumption, decreased HR, decreased BP, decreased myocardial contractility
94
Uses of beta blockers for arrhythmias
Paroxysmal supraventricular tachycardia, A fib, arrhythmias due to catecholamines excess, ischemia, mitral valve prolapse, MI, and V tach
95
Class 3 anti arrhythmic
K+ channel blockers Amiodarone, dronedarone, sotalol Decrease automaticity and conduction velocity and prolongs refractoriness no negative inotropic effects
96
Amiodarone approved for
life threatening recurrent ventricular arrhythmias | Requires a loading dose
97
Dronedarone CI in patients
with HF | May increase digoxin levels also
98
Sotalol used for
Supraventricular and ventircular arrhythmias
99
Class 4 anti arrhythmic
Calcium channel blockers Used to treat supraventricular arrhythmias Slow conduction, prolong refractoriness, decrease automaticity Vascular relaxation Negatice inotropic effects
100
Digoxin for anti arrhythmic
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
Adenosine
Converts PSVT to SR | Activates potassium channels to decrease intracellular K+-- decreases spontaneous SA nodal depolarization
102
Atropine
Enhances both sinus nodal automaticity and AV nodal conduction Blocks ACh Used exclusively for tx of symptomatic bradycardia
103
A fib 1st line treatment
If hemodynamically unstable, immediate DCC If hemodynamically stable: IV diltiazem, IV verapamil or IV Beta blocker IV amiodarone used for ventricular rate control
104
First line tx for PSVT
Hemodynamically unstable: syncrhonized DCC or vagal maneuvers
105
Second line tx for PSVT
DOC is adenosine | If persistent, IV dilitazem, verapamil, or beta blocker
106
Drugs for symptomatic nonsustained VT
Beta blockers, nondihydropyridine CCB, class 1C AAD
107
First line drugs for sustained VT
Immediate synchronized DCC if unstable; IV amiodarone, IV procainamide or IV sotalol if stable
108
Tx for pulseless VT/VF
CPR + AED If persists, vasopressor therapy (epi) If persists, IV amiodarone