Cardio Pharm

Front 1

Essential HTN

Back 1

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.

Front 2

CHF

Back 2

Diuretics, ACE inhibitors/ARBs, B-blockers (compensated CHF), K+-sparing diuretics (prevent arrhythmias).
B-blockers CI in decompensated CHF
dont use Ca channel blockers bc can cause arrhytmias

Front 3

Diabetes mellitus

Back 3

ACE inhibitors/ARBs, calcium channel blockers, diuretics, B-blockers, a-blockers.
ACE inhibitors are protective against diabetic nephropathy

Front 4

Hydralazine

Back 4

mechanism: increases cGMP, which causes smooth muscle relaxation. Vasodilates arterioles>veins; afterload reduction.
Clinical use: Severe hypertension, CHF. First-line therapy for hypertension in pregnancy, with
methyldopa. Frequently coadministered with a B-blocker to prevent reflex tachycardia.
Toxicity: Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea,
headache, angina. Lupus-like syndrome.

Front 5

Calcium channel blockers

Back 5

Nifedipine, verapamil, diltiazem.
Mechanism: Block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.
Vascular smooth muscle-nifedipine > diltiazem > verapamil (Verapamil = Ventricle).
Heart-verapamil > diltiazem > nifedipine.
Clinical use: Hypertension, angina, arrhythmias (not nifedipine), Prinzmetal's angina, Raynaud's.
Toxicity: Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation.

Front 6

Nitroglycerin
isosorbide dinitrate

Back 6

Mechanism: Vasodilate by releasing nitric oxide in smooth muscle, causing an increase in cGMP and smooth muscle relaxation. Dilate veins >> arteries. Decrease preload.
Clinical use: Angina, pulmonary edema. Also used as an aphrodisiac and erection enhancer.
Toxicity: Reflex tachycardia, hypotension, flushing, headache, "Monday disease" in industrial
exposure; development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend, resulting in tachycardia, dizziness, and headache on reexposure.

Front 7

Nitroprusside

Back 7

clinical use: malignant hypertension
mechanism: Short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity (releases CN).

Front 8

Fenoldopam

Back 8

clinical use: malignant hypertension
mechanism: Dopamine D1 receptor agonist-relaxes renal vascular smooth muscle.

Front 9

Diazoxide

Back 9

clinical use: malignant hypertension
mechanism: K+ channel opener- hyperpolarizes and relaxes vascular smooth muscle. Can cause
hyperglycemia (reduces insulin release).

Front 10

Antianginal therapy

Back 10

Nitrates and Nifedapine (affect preload), B-blockers and verapamil (affect afterload).

Pindolol and acebutolol are partial beta-agonists, and are therefore CI in angina

Front 11

lovastatin
pravastatin
simvastatin
atorvastatin
rosuvastatin

Back 11

HMG-CoA reductase inhibitors
Effect on LDL: decrease the MOST
Effect on HDL: increase
Effect on TGs: decrease
Mechanism of action: inhibit cholesterol precursor, mevalonate
Side effects: hepatotoxicity (increased LFTs), rhabdomyolysis

Front 12

Niacin

Back 12

Effect on LDL: decrease a lot
Effect on HDL: increase a lot
Effect on TGs: decrease
Mechanism of action: Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
Side effects:Red, flushed face, which is decreased by aspirin or long-term use
Hyperglycemia (acanthosis nigricans)
Hyperuricemia (exacerbates gout)

Front 13

cholestyramine
colestipol
colesevelam

Back 13

Bile acid resins
Effect on LDL: decrease a lot
Effect on HDL: slightly increase
Effect on TGs: slightly increase
Mechanism of action: Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more
Side effects: Patients hate it- tastes bad and causes GI discomfort, decreases absorption of fat-soluble vitamins
Cholesterol gallstones

Front 14

ezetimibe

Back 14

cholesterol absorption blocker
Effect on LDL: decrease a lot
Effect on HDL: none
Effect on TGs: none
Mechanism of action: Prevent cholesterol reabsorption at small intestine brush border
Side effects: rare increase in LFTs

Front 15

gemfibrozil, clofibrate, bezafibrate, fenofibrate

Back 15

Fibrates
Effect on LDL: decrease
Effect on HDL: increase
Effect on TGs: decrease the MOST
Mechanism of action: Upregulate LPL, which increases TG clearance
Side effects: Myositis, hepatotoxicity (increase LFTs), cholesterol gallstones

Front 16

Digoxin

Back 16

cardiac glycoside
75% bioavailability, 20-40% protein bound, t1/2 = 40 hours, urinary excretion
Mechanism: Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/
antiport. increases [Ca2+]i; leads to positive inotropy. Stimulates vagus nerve (Resets baroreceptor response which is hypersensitive in people with CHF)
Clinical use: CHF (increases contractility); a. fib (decreases conduction at AV node and depression of SA node).

Toxicity: Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision (think Van Gogh). ECG- increased PR, decreased QT (bc decreased APD. more depolarized Vrest during phase 4 leads to a shorter APD and decreased refractoriness, which can predispose to DADs and arrhythmias), scooping, T-wave inversion, arrhythmia, hyperkalemia.

toxic effects Worsened by renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ATPase), quinidine (decreased digoxin clearance; displaces digoxin from tissue-binding sites)

Antidote: Slowly normalize K+, lidocaine (Na channel blocker - more Na outside the cell allows Na/Ca antiporter to function), cardiac pacer, anti-dig Fab fragments, Mg2+

Front 17

Quinidine
Procainamide
Disopyramide

Back 17

ClassIA
Increase APD (class III effects too at slower rates), increase ERP, increase QT interval.
Affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia. Decreased automaticity.
Toxicity: Toxicity: quinidine (cinchonism - headache, tinnitus); thrombocytopenia; torsades de pointes due to inceased QT interval; procainamide (reversible SLE-like syndrome).
Hyperkalemia increases toxicity

Front 18

Lidocaine
Mexiletine
tocainide

Back 18

Class IB
Decrease APD by blocking phase III sodium window current
Preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Useful in acute ventricular arrhythmias (especially post-MI) and in digitalis-induced arrhythmias.

Toxicity: local anesthetic. CNS stimulation/depression, cardiovascular depression.
Hyperkalemia increases toxicity

phenytoin can also fall into the IB category

Front 19

Flecainide
Encainide
Propafenone

Back 19

Class IC
No effect on AP duration. Useful in V-tachs that progress to VF and in intractable SVT. Usually used only as last resort in refractory tachyarrhythmias. For patients without structural abnormalities (can aggravate ventricular arrhythmias in ppl w heart abnormalities).
Prolongs refractory period in AV node - good for a. fib and PSVT

Toxicity: proarrhythmic, especially post-MI (contraindicated). Significantly prolongs refractory period in AV node.
Hyperkalemia increases toxicity

IB Best post MI
IC Contraindicated post MI

Front 20

propanolol
esmolol
metoprolol
atenolol
timolol

Back 20

Class II - B-blockers
Mechanism: Decrease cAMP, decrease Ca currents. suppress abnormal pacemakers by decreasing the slope of phase 4. AV node particularly sensitive - increased PR interval. Esmolol is very short acting.

Clinical use: V-tach, SVT, slowing ventricular rate during atrial fibrillation and atrial flutter. PACs, PVCs. Suppress DADs bc they are triggered by catecholamines. Does NOT prolong QT.
Toxicity: Impotence, exacerbation of asthma, cardiovascular effects (bradycardia, AV block,
CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia. Metoprolol can cause dyslipidemia. Treat overdose with glucagon.

Front 21

Sotalol
ibutilide
bretylium
dofetilide
amiodarone.

Back 21

Class III - K+ channel blockers
Mechanism: increase APD, increase ERP. Used when others fail. Increase QT interval, PR, QRS.
Toxicity:
sotalol - torsades de point and excessive beta block.
ibutilide-torsades;
bretylium-new arrhythmias, hypotension;
amiodarone - pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF).
Amiodarone has less of a risk for torsades bc it is able to maintain its K channel block at fast heart rates.

Amiodarone has class I, II, III, and IV effects because it alters the lipid membrane.

Front 22

verapamil
diltiazem

Back 22

Class IV - Ca2+ channel blockers
Mechanism: decreased conduction velocity, increased ERP in AV node, increased PR interval. Used in prevention of nodal arrhythmias (like SVT).
Toxicity: Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression).

Front 23

Adenosine

Back 23

increases K+ out of cells --> hyperpolarizing the cell + decreasing ICa (thus slows conduction thru AV node and reduced rate of spontaneous depolarizations). Drug of choice in diagnosing/ abolishing supraventricular tachycardia. Very short acting (~15 sec). Toxicity includes flushing, hypotension, chest pain. Effects blocked by theophylline.

Front 24

K+

Back 24

Depresses ectopic pacemakers in hypokalemia (e.g., digoxin toxicity).

Front 25

Mg2+

Back 25

Effective in torsades de pointes and digoxin toxicity.