Cardiovascular Flashcards
Primary (essential) hypertension
Thiazide diuretics
ACE inhibitors
ARBs
Dihydropyridine Ca2+ channel blockers
Hypertension w/ HF
ACE inhibitors/ARBs
Beta blockers (only in compensated HF, contra in cardiogenic shock)
Diuretics
Aldosterone antagonists
Hypertension w/ diabetes mellitus
ACE inhibitors/ARBs (protective against diabetic nephropathy)
Ca2+ channel clockers
Thiazide diuretics
Beta-blockers
Hypertension w/ pregnancy
Hydralazine
Labetalol
Methyldopa
Nidedipine (causes peripheral vasodilation which may cause reflex tachycardia —> useful in ptns w/ bradycardia)
Dihydropyridine Ca2+ channel blockers
Amlodipine, Clevedipine. Nicardipine, Nefedipine, Nimodipine
MOA:
Block voltage-gated L-type calcium channels of cardiac and smooth muscle —> dec. muscle contractility
Vascular smooth muscle > Heart
Use:
All except Nimodipine - Hypertension, Angina (including Prinzmetal), Raynaud phenomenon
Nimodipine - Subarachnoid hemorrhage
Clevidipine - hypertensive emergency
Adv. effects: Peripheral edema Flushing Dizziness Gingival hyperplasia
Increased mortality and risk of MI with short acting DHPs
Non-dihydropyridine Ca2+ channel blockers
Verapamil, Diltiazem
MOA:
Block voltage-gated L-type calcium channels of cardiac and smooth muscle —> dec. muscle contractility
Slow SA and AV nodes
Heart > Vascular smooth muscle
Use:
Hypertension
Angina
Atrial fibrillation/flutter (SVT)
Adv. effects: Cardiac depression AV block Hyperprolactinemia Constipation
Hydrallazine
MOA:
Inc. cGMP —> smooth muscle relaxation
Vasodilates arterioles > veins
Afterload reduction
Use:
Severe HTN (acute) - emergency
HF (w/ organic nitrate for mortality benefit)
Safe to use during pregnancy
Co-admin with beta blocker to prevent reflex tachycardia
Adv. effects: Compensatory tachycardia (contra in angina/CAD) Lupus-like syndrome Fluid retention Headache Angina
Nitroprusside
MOA:
Increase cGMP via direct release of NO
Short acting arterial and venous dilator
Use: Hypertensive emergency
Can cause cyanide toxicity (releases cyanide), modest tachycardia and Na- and H20 retention
Fenoldopam
MOA: Dopamine D1 receptor agonist Coronary , peripheral, RENAL, and splanchnic vasodilation Decrease BP Increase natriuresis
Use: Hypertensive emergency, postoperative antihypertensive
Can cause hypotension and tachycardia
Exceptionally beneficial in hypertensive patients with renal insufficiency
Nitrates
Nitroglycerin, Isosorbide dinitrate, isosorbide mononitrate
MOA:
Vasodilate by increasing NO in vascular smooth muscle —> inc. in cGMP and smooth muscle relaxation
Dilate veins»_space; arteries
Decrease preload, increase peripheral venous capacitance, decrease LVEDP
Use:
Angina
Acute coronary syndrome
Pulmonary edema
Adv. effects: Reflex tachycardia (treat w/ beta blockers) Hypotension Flusing Headaches "Monday disease"
Patients taking daily maintenance nitrates need to have a nitrate free period every day to avoid tolerance of the drug
Ranolazine
MOA:
Inhibits late phase of sodium current –> reducing diastolic wall tension and oxygen consumption
Does not affect HR or contractility
Use:
Angina refractory to other medical therapies
Adv. effects: Constipation Dizziness Headache Nausea QT prolongation
HMG-CoA reductase inhibitors
statins
MOA:
Inhibit conversion of HMG-CoA to mevalonate (a cholesterol precursor)
Causes hepatocytes to increase their LDL receptor density
Lower LDL, Increase HDL, Slightly lower TG
Adv. effects:
Hepatotoxicty (rise in LFTs)
Myopathy (esp. when used with fibrates or niacin)
Do liver function test before starting on a statin
Bile acid resins
Cholestyramine, Colestipol, Colesevelam
MOA:
Prevent intestinal reabsorption of bile acids
Liver must use cholesterol to make more
Lower LDL, Slightly increase HDL, Slightly increase TG
Adv. effects:
GI upset
Decrease absorption of other drugs and fat-soluble vitamins
Ezetimibe
MOA:
Prevent cholesterol absorption at small intestine brush border
Lower LDL
Adv. effects:
Rare increase in LFTs (with statins)
Diarrhea
Fibrates
Gemfibrozil, Bezafibrate, Fenofibrate
MOA:
Upregulate LPL —> Inc. TG clearance
Activates PPAR-a to induce HDL synthesis –> dec. hepatic VLDL production
Lower TG, Slightly increase HDL, Slightly lower LDL
Adv. effects:
Myopathy (inc. risk with statins)
Cholesterol gallstones
mainly used to prevent pancreatitis in patients with very high TG levels
Niacin (vitamin B3)
MOA:
Inhibits lipolysis (hormone sensitive lipase) in adipose tissue
Reduces hepatic VLDL synthesis
Lower LDL, Increase HDL, Slightly lower TG
Adv. effects:
Red, flushed face (decreased by NSAIDs or long term use)
Hyperglycemia
Hyperuricemia
Used in patients who have failed other lipid lowering drugs
Digoxin
MOA:
Direct inhibition of Na+/K+ ATPase –> indirect inhibition of Na+/Ca2+ exchanger.
Increase in intracellular Ca2+ —> positive inotropy
Stimulates vagus nerve —> decrease HR
Use:
HF (increase contractility)
Atrial fibrillation (decrease conduction at AV node, depression of SA node)
Adv. effects:
Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block, fatigue, abdominal pain, confusion and delirium
Hyperkalemia (poor prognosis)
Toxicity due to renal failure (dec. excretion), hypokalemia, drugs that displace digoxin from tissue binding sites and dec. clearance (verapamil, amiodarone, quinidine)
Antidote:
Slowly normalize K+, cardiac pacer, anto-digoxin Fab fragments, Mg2+
Antiarrhythmics (Class IA)
Quinidine, Procainamide, Disopyramide
Na+ channel blockers - state dependent; modest dissoc.
Moderate K+ channel blocking activity*
MOA:
Increase AP duration
Increase effective refractory period in ventricular AP (ERP)
Increase QT interval
Use:
Both atrial and ventricular arrhythmias (esp. re-entrant and ectopic SVT and VT)
Adv. effects:
Torsades de pointes* (due to inc. QT interval)
Thrombocytopenia
HF (disopyramide)
Reversible SLE-like syndrome (procainamide)
Cinchonism (headache, tinnitus) (quinidine)
Antiarrhythmics (Class IB)
Lidocaine, Mexiletime, Phenytoin
Na+ channel blockers - state dependent; fast dissoc.
MOA:
Decrease AP duration
Preferentially affect ischemic or depolarize Purkinje & ventricular tissue.
Use:
Acute ventricular arrhythmias (esp post MI*)
Digitalis-induced arrhythmias
Adv. effects:
CNS stimulation/depression
Cardio depression
Antiarrhythmics (Class IC)
Flecainide, Propafenone
Na+ channel blockers - state dependent; slow dissoc.
MOA:
Sig. prolongs ERP in AV node & accessory bypass tracts
No effect - ERP in purkinje and ventricular tissue
Min. effect on AP duration
Prolong QRS duration to a greater extent at higher heart rates
Use:
SVTs -esp atrial fibrillation
Last resort in refractory VT
Adv. effects:
Proarrhythmic esp post MI
Contraindicated in structural and ischemic heart disease
Antiarrhythmics (Class II)
metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol
Beta-blockers
MOA:
Decrease SA and AV nodal activity (decrease cAMP. decrease Ca2+)
Decrease slope of phase 4 (suppress abnormal pacemakers)
Prolonged repolarization (at AV node)
Esmolol very short acting
Use:
SVT
Atrial fibrillation & atrial flutter ventricle rate control
Adv. effects:
Impotence
Exacerbation of COPD / asthma
Cardio effects - bradycardia, AV block, HF
Dyslipidemia (Metoprolol)
Exacerbate vasospasm in Prinzmetal (Propranolol)
Unopposed alpha agonism in pheochromocytoma or cocaine toxicity if given alone (except carvedilol & labetalol)
Treat overdose w/ saline, atropine, glucagon
Antiarrhythmics (Class III)
Amiodarone, Ibutilide, Dofetilide, Sotalol
K+ channel blockers - markedly prolonged repolarization
MOA:
Increase AP duration
Increase ERP
Increase QT interval
demonstrate reverse use dependence (slower HR, more QT interval is prolonged)
Use:
Atrial fibrillation
Atrial flutter
Ventricular tachycardia (amiodarone, sotalol)
Adv. effects:
Sotalol - torsades de pointes, excessive Beta blockade
Ibutilide - torsades de pointes
Amiodarone - pulmonary fibrosis*, hepatotoxicity, hypo/hyperthyroidism, acts as a hapten (corneal blue/grey deposits resulting in photodermatitis), neurologic effects, constipation, cardio effects (bradycardia, heart block, HF)
Check PFTs, LFTs, and TFTs when using amiodarone
Amiodarone is lipophilic has class I, II, III, IV effects
Antiarrhythmics (class IV)
Verapamil, Diltiazem
Ca2+ channel blockers
MOA:
Decrease conduction velocity
Increase ERP
Increase PR interval
slow rise of action potential prolonged repolarization (at AV node)
Use:
Prevention of nodal arrhythmias (SVT)
Rate control in atrial fibrillation
Adv. effects: Constipation Flushing Edema Cardio effects (HF, AV block, sinus node depression)
Adenosine
MOA:
Increased K+ out of cells —> hyperpolarizing the cell and decreasing Ica
Very short acting
DOC in diagnosing/terminating certain forms of SVT
Used for chemical stress test
Effects blunted by theophylline and caffeine (antagonists)
Adv, effects:
flushing, hypotension, chest pain, sense of impending doom, bronchospasm
Mg2+
Effective in torsades de pointes & digoxin toxicity
