Unit 4 Textbook: Cardiovascular Flashcards
Medications that can cause an increase in BP
Oral contraceptives, nicotine, steroids, appetite suppressants, TCA’s, cyclosporine, NSAIDs, some nasal decongestants
Diagnostic criteria for high BP
> 140/90 for <60 years old 3+ readings at least 1 week apart
>150/90 for >60 years old
Diagnostic tests to be done at visit for high BP
Electrocardiogram, blood glucose, hemoglobin, hematocrit, complete urinarylis, complete chem panel, liver function, BMP, fasting lipid panel
DOC for nonblack hypertension
Thiazide diuretic or ARB or ACE alone or in combo
DOC for black hypertension
Thiazide diuretic or calcium channel blocker or combo
DOC for all races hypertension with diabetes or chronic kidney disease
ACEI or ARB or combo
Diuretics
Decrease BP by causing diuresis which causes decreased plasma volume, stroke volume and cardiac output
May cause hypokalemia or hypomagnesia, leading to arrhythmias
Thiazide diuretics
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
Side effects of thiazide diuretics
Hypokalemia, hypomagnesia, hypercalcemia, hyperuricemia, hyperglycemia, tinnitus, paresthesia, N/V, diarrhea, impotence
Loop diuretics
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
Potassium sparing diuretic
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
SE of potassium sparing diuretics
Gynecomastia, hirsutism, menstrual irregularities
Beta blockers
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
Beta blockers with intrinsic sympathomimetic activity
Pindolol and acebutolol
Beta blockers are contraindicated in
Sinus bradycardia, asthma, COPD, AV block, cardiac failure
In diabetic patients, beta blockers can
Mask all symptoms of hypoglycemia
SE of beta blockers
Fatigue, drowsiness, bronchospasm, N/V
ACE inhibitors
-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
ACE inhibitors are contraindicated in
Patients with CHF, bilateral renal stenosis, pregnancy
SE of ACEI
Dry cough, rashes, dizziness, angioedema
ARBs
-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
ARBs contraindicated in
pregnancy
SE ARBs
Dizziness, upper respiratory infections, cough, viral infection, fatigue, pharyngitis, rhinitis
Renin inhibitors
Aliskiren
Block conversion of angiotensinogen to angiotensin I
Avoid in pregnancy
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
Nondihydropyridines
Verapamil + Diltiazem
Decrease HR and slow conduction at AV node
Avoid in patients with heart block
Dihydropyridines
-Dipine
Potent vasodilators
CCB’s are recommended specifically for
Prinzmetal angina
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
Central a2 agonists
Decrease sympathetic outflow, CO and peripheral resistance by blocking a1
Clonidine, methyldopa, guanabenz guanfacine
Direct vasodilators
Hydralazine + Minoxidil
Cause arteriolar smooth muscle relaxation; reserved for essential or severe hypertension
May cause fluid retention, reflex tachycardia, lupus like syndrome
Recommended drug for hypertension in pregnancy
Methyldopa
Recommended drugs for hypertension in diabetics
ACEI and ARBs (not in combo)
Commonly used meds in hypertensive emergency
Hydralazine, nitrates, CCB’s, beta blockers, alpha 1 blockers, and ACEI
Function of HDL
Removes LDL from peripheral cells and transports to liver for metabolism
4 major statin benefit groups
- Have clinical atherosclerotic CV disease
- no ASCVD but LDL>190
- no ASCVD, 40-75 years old, type 1 or 2 DM with LDL 70-189
- no ASCVD or DM, 40-75 years old, LDL 70-189, 10 year risk of ASCVD of >7.5%
Goals of statin therapy
High intensity statin: decrease by 50%
Moderate intensity statin: decrease by 30%
Low intensity statin: decrease by less than 30%
Most common complaint when taking statins
muscle related myopathy
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
Statins CI in
Pregnancy, breastfeeding, active liver disease
Ezetimibe
Cholesterol absorption inhibitor
Inhibits cholesterol absorption at brush border of small intestine
Can be used alone or in combo with statins
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
Bile acid resins CI in
biliary obstruction, chronic constipation, triglycerides >300
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
Niacin CI in
hepatic dysfunction, severe hypotension, hyperglycemia, gout, A fib, peptic ulcer disease
SE of niacin
Increased prostaglandins
Fibric acid derivatives
Gemfibrozil and Fenofibrate
Mainly affect triglycerides and HDL
CI in patients with history of gallstones and severe renal or hepatic dysfunction
First line cholesterol meds
Statin
Second line cholesterol meds
Cholesterol absorption inhibitors and niacin and bile acid resins
Third line cholesterol meds
Fibric acid derivatives
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
Nonpharmacological treatment for angina
Decreased weight, smoking cessation, exercise
Drugs used to treat angina
ACEI, nitrates, beta blockers, Ca channel blockers, antiplatelets
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)
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
First line therapy for acute angina tx
Nitrates
Long acting nitrates
Isosorbide dinitrate, isosorbide mononitrate, nitroglycerine patch
Chronic prophylaxis
SE of nitrates
Headache, flushing, dizzy, weakness, orthostatic hypotension
Antiplatelet therapy for angina
inhibits platelet aggregation
Aspirin + Clopidogrel
Decreases chance of MI
Aspirin
Irreversible enzyme antagonism to block prostaglandin synthesis–blocks TXA 2
Clopidogrel
Decreased ADP induced platelet activation
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
Highest risk factors for heart failure
CAD, Htn, cardiomyopathy
Drugs that can worsen HF
NSAIDs, steroids, hormones, antihypertensives, Na containing drugs, lithium, amphetamines, cocaine, alcohol
4 levels of HF
- no limitation in physical activity
- slight limitation in physical activity; comfortable at rest
- marked limitation in physical activity; less than ordinary activity causes dyspnea
- Unable to carry physical activity without symptoms; symptoms present at rest
Goals of HF therapy
Improve quality of life, decrease mortality, decrease compensatory mechanisms causing symptoms
Drug therapy for HF
Usually long term
ACEI + Beta blockers
Diuretics, aldosterone antagonists, hydralazine, nitrates, digoxin can also be used
ACEI indicated for HF
Captopril, enalopril, fosinopril, lisinopril, quinopril, trandolapril, ramipril, perindopril
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
Patients with HF and significant volume overload should be started on
Diuretic + ACEI + Beta blocker
Loop diuretics are most potent
Most useful approach to see if HF meds are working
Daily weight measurements
What drugs may decrease effects of diuretics
NSAIDs
Most studied ARB in HF
Losartan
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
Beta blockers approved for HF
Carvedilol, metoprolol, bisoprolol
Beta blockers for HF CI in
bronchospastic disease, symptomatic bradycardia, advanced heart block
Digoxin
Can prevent clinical deterioration but does not decrease mortality
Mild inotropic effect by inhibiting Na/K ATPase thus increasing Ca entry into cell
Signs of digitoxin toxicity
N/V, anorexia, fatigue, headache, disorientation, confusion, seizures, arrhythmias
Drugs that increase digoxin levels
Quinidine, amiodarone, flexainide, propaferone, spironolactone, verapamil, antibiotics, anticholinergics
Drugs that decrease digoxin levels
Antacids, cholestyramine, neomycin
Alternative HF drugs for african americans who can not take ACEI
Hydralazine
First line for HF tx
ACEI with or without a diuretic
Second line for HF tx
ACEI + beta blocker with diuretic
Third line for HF tx
ACEI, Beta blocker, aldosterone agonist, diuretic, digoxin
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
Goals of treatment for arrhthmias
Relieve acute episode of irregular rhythm, establish SR, and prevent further episodes
Class 1 anti arrhythmic
Na channel blockers
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
Specific side effect of quinidine
Potent anticholinergic
Same with disopyramide
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
Lidocaine is specific to
Ischemic tissue
Class 1c anti arrhythmic
Slow onset and offset
Supraventricular usually
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
Uses of beta blockers for arrhythmias
Paroxysmal supraventricular tachycardia, A fib, arrhythmias due to catecholamines excess, ischemia, mitral valve prolapse, MI, and V tach
Class 3 anti arrhythmic
K+ channel blockers
Amiodarone, dronedarone, sotalol
Decrease automaticity and conduction velocity and prolongs refractoriness
no negative inotropic effects
Amiodarone approved for
life threatening recurrent ventricular arrhythmias
Requires a loading dose
Dronedarone CI in patients
with HF
May increase digoxin levels also
Sotalol used for
Supraventricular and ventircular arrhythmias
Class 4 anti arrhythmic
Calcium channel blockers
Used to treat supraventricular arrhythmias
Slow conduction, prolong refractoriness, decrease automaticity
Vascular relaxation
Negatice inotropic effects
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
Adenosine
Converts PSVT to SR
Activates potassium channels to decrease intracellular K+– decreases spontaneous SA nodal depolarization
Atropine
Enhances both sinus nodal automaticity and AV nodal conduction
Blocks ACh
Used exclusively for tx of symptomatic bradycardia
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
First line tx for PSVT
Hemodynamically unstable: syncrhonized DCC or vagal maneuvers
Second line tx for PSVT
DOC is adenosine
If persistent, IV dilitazem, verapamil, or beta blocker
Drugs for symptomatic nonsustained VT
Beta blockers, nondihydropyridine CCB, class 1C AAD
First line drugs for sustained VT
Immediate synchronized DCC if unstable; IV amiodarone, IV procainamide or IV sotalol if stable
Tx for pulseless VT/VF
CPR + AED
If persists, vasopressor therapy (epi)
If persists, IV amiodarone
