From Jen: Cardio Flashcards
Hydrochlorothiazide
Diuretic
Adverse: ↓K+ Mild ↑ lipids ↑ uric acid lassitude (lethargy) ↑ Ca2+ hyperglycemia
Loop diuretics
Diuretic
Adverse: K+ wasting hypotension ototoxicity metabolic alkalosis
Clonidine
α2 agonist
Adverse:
dry mouth
sedation
severe rebound HTN
Methyldopa
Adverse: sedation
Positive Coombs test
reserpine
Depletes central and peripheral catecholamines (inhibits VMAT-packaging catecholamines into vesicles)
Adverse: sedation depression nasal stuffiness diarrhea
Guanethidine
Reduces catecholamine release
Adverse: orthostatic and exercise hypotension
sexual dysfunction
diarrhea
Prazosin
α1 antagonist
Adverse:
orthostatic hypotension (1st dose)
dizziness
headache
beta blockers
Adverse: impotence asthma exacerbation bradycardia CHF AV block CNS effects: sedation, sleep alterations
Hydralazine
Vasodilator
Adverse: nausea headache lupus-like syndrome reflex tachycardia (prevent with beta blocker) angina salt retention (prevent with diuretic)
Minoxidil
Vasodilator
Adverse: hypertrichosis
reflex tachycardia (prevent with beta blocker)
angina
salt retention (prevent with diuretic)
Nifedipine
Verapamil
Calcium channel blocker
vasodilator
Adverse: flushing constipation (verapamil) AV block (verapamil) nausea edema
Nitroprusside
vasodilator
cyanide toxicity
Diazoxide
vasodilator
Adverse: hyperglycemia (reduces insulin release, hypotension)
ACE inhibitors
Captopril, enlapril, fosinopril
Adverse: cough hyperkalemia angioedema taste changes hypotension fetal renal damage in pregnancy rash increase renin
Angiotenin II receptor inhibitors
ARB
Losartan
Adverse: fetal renal toxicity, hyperkalemia
Hydralazine
MOA
MOA: increase cGMP; smooth muscle relaxation (arterioles > veins)
***afterload reduction
Use: severe HTN, CHF
First line in pregnancy with methyldopa
Hydralazine
Toxicity
compensatory tachycardia (contraindicated in angina, CAD) fluid retention nausea headache angina lupus-like syndrome
Minoxidil
K+ channel opener- hyperpolarized and relaxes vascular smooth muscle
Use: Severe HTN
toxicity: hypertrichosis pericardial effusion reflex tachycardia angina salt retention
Nifedipine
Diltiazem
Verapamil
Calcium channel blockers
-block voltage dependent L-type calcium channels of cardiac and smooth muscle; reduce muscle contractility
Use: HTN, angina, arrhythmias (not nifedipine), prinzmetal’s angina, Raynaud’s
Toxicity: cardiac depression peripheral edema flushing dizziness constipation
Isosorbide dinitrate
nitroglycerin
Vasodilate by releasing NO in smooth muscle, causing increased cGMP and smooth muscle relaxation
Dilates veins» arteries
**decrease preload
Use: angina, pulmonary edema, erection enhancer
Toxicity: tachycardia, hypotension, flushing, headache
“Monday disease” in industrial exposure: loss of tolerance for vasodilating action during weekend result in in tachycardia, dizziness and headache on reexposure.
Malignant HTN treatment
Nitroprusside- short acting, increase cGMP via direct release of NO
Fenoldopam- D1 receptor agonist: relaxes renal vascular smooth muscle
Diazoxide- K+ channel opener: hyperpolarizes and relaxes vascular smooth muscle
Anti-anginal therapy
GOAL
Reduce myocardial O2 consumption by decreasing one or more of:
- end diastolic volume
- BP
- HR
- contractility
- ejection time
Nitrate use in angina:
EDV BP Contractility HR Ejection time O2 consumption
*Decrease Preload
EDV: ↓ BP: ↓ Contractility: ↑ (reflex) HR: ↑ (reflex) Ejection Time: ↓ O2: ↓
Beta blocker use in angina:
EDV BP Contractility HR Ejection time O2 consumption
EDV ↑ BP ↓ Contractility ↓ HR ↓ Ejection Time ↑ (slower) O2: ↓
Nitrates + beta blocker in angina
EDV BP Contractility HR Ejection time O2 consumption
EDV: no change BP: ↓ Contractility: No change HR: ↓ Ejection Time: No change O2: ↓↓
HMG CoA reductase inhibitors
Statins
MOA: inhibit cholesterol precursor, mevalonate
↓↓↓ LDL
↑HDL
↓Triglycerides
Adverse: reversible increase in LFTs, rhabdomyolysis
Niacin
MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion
↓↓ LDL
↑↑ HDL
↓Triglycerides
Adverse: flushing, decrease in by long term use or ASA
Bile acid resin
Cholestyramine, colestipol, colesevelam
MOA: prevent reabsorption of bile acids
↓↓ LDL
Slightly ↑ HDL
Slightly ↑ Triglycerides
Adverse: GI side effects, fat soluble vitamin deficiency
Ezetimibe
Competitively inhibit cholesterol absorption at brush border
↓↓ LDL
no effect on HDL or triglycerides
Adverse: Rare ↑ LFTs
Fibrates
Gemfibrozil, clofibrate, bezafibrate, fenofibrate
MOA: upregulate lipoprotein lipase, increasing TG clearance
↓ LDL
↑ HDL
↓↓↓ Triglycerides
Adverse: myositis, increased LFTs
Cardiac glycosides
Digoxin: 75% bioavailability
20-40% protein bound
half life: 40hrs
urinary excretion
Digoxin
MOA: direct inhibition of Na/K ATPase leads to inhibition of Na/Ca exchanger; increased intracellular Ca with positive inotropy.
Also stimulates vagus nerve
Use: CHF (↑ contractility) atrial fibrillation (↓ conduction at AV node and depression of SA node)
Digoxin
Toxicity
↑ PR, ↓QT, scooping of ST segment, T wave inversion
↑ parasympathetic activity (SLUDGE)
arrhythmia
toxicity made worse by : renal failure (impaired excretion), hypokalemia (competitively binds K binding site on Na/K ATPase), quinidine (decrease clearance, displaces dig from tissue binding sites)
Antidote: Normalize K+
lidocaine, cardiac pacer, anti-digitoxin Fab fragments, Mg2+
Class I antiarrhythmics
Na+ channel blockers
local anesthetics, slow or block conduction (slow upstroke)
Decrease slop of phase 4 depolarization in pacemaker cells (↑ threshold for firing)
State dependent-selectively depress tissue that is frequently depolarized
Class IA
Drugs/MOA
Quinidine, Procainamide, Disopyramide
MOA: ↑ AP duration, ↑ effective refractory period, ↑ QT interval
Use: Affect atrial and ventricular arrhythmias **esp. rentrant and ectopic SVT, Vtach, WPW
Class IA
Toxicity
Thrombocytopenia, Torsades de pointes (↑ QT interval)
Quinidine: cinchonism (headache/tinnitus)
Desopyramide: heart failure
Procainamide: reversible SLE-like syndrome
Class IB
Drugs/MOA
Lidocaine, Mexiletine, Tocainide
MOA: ↓ AP duration, affect ischemic or depolarized Purkinje and ventricular tissue
Useful in acute ventricular arrhythmias **esp. post-MI or digitalis-induced arrhythmias
Class IB is BEST for post-MI
Class IB
Toxicity
Lidocaine, Mexiletine, Tocainide
local anesthetic, CNS stimulation/depression, CV depression
Class IC
Drugs/MOA
Flecainide, encainide, propafenone
MOA: prolongs refractory period in AV node, no effect on AP duration
Use: SVTs, afib, last resort in refractory VTach
Class IC
Toxicity
Flecainide, encainide, propafenone
Pro-arrhythmic, especially post-MI (Class IC = Contraindicated)
Significantly prolongs the refractory period in AV node
Class II
(beta blockers)
Drugs/MOA
Propranolol, esmolol, metoprolol, atenolol, timolol, carvedilol
MOA: Block beta receptor: ↓ cAMP and Ca2+ currents (↓ slope of phase 4)
Suppress abnormal pacemakers by ↓ slope of phase 4 (AV node particularly sensitive)- ↑ PR interval
Uses:
Vtach, SVT, to slow ventricular rate during atrial flutter/fibrillation
Class II
(beta blockers)
Toxicity
Impotence asthma exacerbation CHF bradycardia AV block sedation/sleep alterations mask hypoglycemia metoprolol: dyslipidemia
Class III (K+ channel blockers)
Drugs/MOA
Sotalol, ibutilide, amiodarone
MOA: ↑ AP duration, ↑ refractory period, ↑ QT interval
Use: when other antiarrhythmic fail
Class III (K+ channel blockers)
Toxicity
Sotalol- torsades de pointes, excessive beta block
ibutilide- torsades
amiodarone- pulmonary fibrosis, hepatotoxicity, corneal deposits, skin deposits, neurologic effects, constipation, CV effects (bradycardia, CHF, heart block), hypo/hyperthyroidism
Class IV (Calcium channel blockers)
Drugs/MOA
verapamil, diltiazem
MOA: primarily affect AV nodal cells, ↓ conduction velocity, ↑ refractory period and PR interval
Use: prevention of nodal arrhythmias
Class IV (Calcium channel blockers)
Toxicity
Verapamil, diltiazem
Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
Adenosine
↑ K+ out of cells, hyperpolarizing the cell and decreasing intracellular Ca
very short acting
Use: drug of choice when abolishing AV nodal arrhythmias
Toxicity: flushing, hypotension, chest pain
K+
Depresses ectopic pacemakers in hypokalemia (digoxin toxicity)
Mg2+
Effective in torsades de pointes and digoxin toxicity
