First Aid Cardiovascular Pharmacology

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Therapy for primary (essential) hypertension
Diuretics, ACE inhibitors/ARBs, calcium channel blockers

Therapy for hypertension with CHF
Diuretics, ACE inhibitors/ARBs, B-blockers (compensated CHF, NOT decompensated CHF), aldosterone antagonists

Therapy for hypertension with DM
ACE inhibitors/ARBs, calcium channel blockers, diuretics, B-blockers, A-blockers

Contraindicated in cardiogenic shock

Calcium channel blockers: Dihydropyridine
amlodipine, nimodipine, nifedipine

Calcium channel blockers: Non-dihydropyridine
diltiazem, verapamil

Calcium channel blockers: MOA
block VG L-type calcium channels of cardiac and smooth muscle, thereby reducing muscle contractility

Calcium channel blockers (dihydropyridine): Clinical use
(except nimodipine)
hypertension, angina (incl. Prinzmetal), Raynaud phenomenon

Calcium channel blockers (non-dihydropyridine): Clinical use
hypertension, angina, atrial fib/flutter

Nimodipine: Clinical use
(calcium channel blocker)
to prevent cerebral vasospasm in SAH

Calcium channel blockers: Toxicity
cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation

Hydralazine: MOA
increase cGMP for smooth muscle relaxation; vasodilates arterioles > veins; AFTERload reduction

Hydralazine: Clinical use
severe hypertension, CHF;
first-line for HTN during pregnancy, with methyldopa;
frequently co-administered with B-blocker to present reflex tachycardia

Hydralazine: Toxicity
compensatory tachycardia (treat with B-blocker), fluid retention, nausea, headache, angina, lupus-like syndrome

Contraindications for hydralazine therapy
in angina/CAD due to risk of reflex sympathetic stimulation and compensatory tachycardia

Therapy for hypertensive emergency
nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

for hypertensive emergency; short-acting; increased cGMP via direct release of NO

Nitroprusside: Toxicity
cyanide toxicity (nitroprusside releases cyanide)

for hypertensive emergency; dopamine D1 receptor agonist –> coronary, peripheral, renal, and splanchnic vasodilation; decreases BP and increases natriuresis

Therapy for isolated systolic hypertension in NON-diabetic patients
thiazide diuretics, dihydropyridine calcium antagonists

Nitroglycerin and isosorbide dinitrate: MOA
vasodilate by increasing NO in vascular smooth muscle, increase in cGMP and smooth muscle relaxation; vasodilates veins >> arteries; PREload reduction

Nitroglycerin and isosorbide dinitrate: Clinical use
angina, acute coronary syndrome, pulmonary edema

Nitroglycerin and isosorbide dinitrate: Toxicity
Reflex tachycardia (treat with B-blocker), hypotension, flushing, headache, “Monday disease” in industrial exposure — tachycardia, dizziness, headache

Goal of antianginal therapy
reduction of myocardial O2 consumption by decreasing 1 or more determinant: end-diastolic volume, blood pressure, heart rate, and/or contractility;
Nitrates + B-blockers = greatest effect on reduction of myocardial O2 consumption
*see table in FA page 299*

Lipid-lowering agents
Statins (HMG-CoA reductase inhibitors); niacin (vit B3); bile acid resins; cholesterol absorption blockers; fibrates

Statins: MOA
inhibit conversion of HMG-C0A to mevalonate (a cholesterol precursor); upregulate LDL receptors

Statins: most significant effect
decrease LDL levels in circulation

Statins: Side effects/toxicity
hepatotoxicity, rhabdomyolysis (esp. when used with fibrates and niacin)

Niacin: MOA
inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

Niacin: most significant effect
increases HDL

Niacin: Side effects/toxicity
red/flushed face, hyperglycemia (acanthosis nigricans), hyperuricemia

Bile acid resins
cholestyramine, colestipol, colesevelam

Bile acid resins: MOA
prevent intestinal reabsorption of bile acids

Bile acid resins: most significant effect
decrease LDL
but slightly increase triglycerides; also slightly increase HDL

Bile acid resins: Side effects/toxicity
bad taste, GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gallstones

Cholesterol absorption blockers (ezetimibe): MOA
prevent cholesterol absorption at small intestine brush border

Cholesterol absorption blockers (ezetimibe): most significant effect
decrease LDL

Cholesterol absorption blockers (ezetimibe): Side effects/toxicity
rarely increase LFTs, diarrhea

gemfibrozil, clofibrate, bezafibrate, fenofibrate

Fibrates: MOA
upregulate LPL and increase triglyceride clearance; activate PPAR-alpha to induce HDL synthesis

Fibrates: most significant effect
decrease triglycerides

Fibrates: Side effects/toxicity
myositis (when given with statin), hepatotoxicity, cholesterol gallstones

Cardiac glycosides (digoxin): MOA
direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchanger –> increases intracellular calcium –> positive inotropy (contractility);
stimulates vagus nerve –> decreases HR

Cardiac glycosides (digoxin): bioavailability, half-life and excretion
75% bioavailability;
half-life = 40 hours;
urinary excretion

Cardiac glycosides (digoxin): Clinical use
CHF (for increased contractility);
atrial fibrillation (for decreased conduction at AV node and depression of SA node)

Cardiac glycosides (digoxin): Toxicity
cholinergic (N/V/D, blurry yellow vision), increased PR, decreased QT, arrhythmia, AV block; hyperkalemia

Cardiac glycosides (digoxin): Antidote
Slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

Antiarrhythmics: Classes
I: Na+ channel blockers (A, B, and C)
II: Beta-blockers
III: K+ channel blockers
IV: Ca2+ channel blockers
Miscellaneous: adenosine, magnesium

Mnemonic for all Na+ channel blockers
Double Quarter Pounder, Lettuce, Mustard, Pickles, and Fries
(Disopyramide, Quinidine, Procainamide, Lidocaine, Mexiletine, Propafenone, Flecainide)

Na+ channel blockers: MOA
slow or block conduction (esp. in depolarized cells); decrease slope of phase 0 and increase threshold for firing in abnormal pacemaker cells

Na+ channel blockers: Toxicity
Hyperkalemia causes increased toxicty for all class I drugs

Na+ channel blockers, Class IA
Quinidine, Procainamide, Disopyramide

Na+ channel blockers, Class IA: MOA
increase AP duration, increase effective refractory period, increase QT interval

Na+ channel blockers, Class IA: Clinical use
atrial and ventricular arrhythmias, esp. re-entrant and ectopic SVT and VT

Na+ channel blockers, Class IA: Toxicity
thrombocytopenia, torsades de pointes (due to icreased QT interval);
quinidine: cinchonism (headache and tinnitus);
procainamide: reversible SLE-like syndrome;
disopyramide: heart failure

Na+ channel blockers, Class IB
lidocaine, mexiletine
phenytoin can also fall into this category

Na+ channel blockers, Class IB: MOA
decrease AP duration (steepen re-polarization curve)
preferentially affect ischemic or depolarized Purkinje and ventricular tissue

Na+ channel blockers, Class IB: Clinical use
acute ventricular arrhythmias (esp. post-MI), digitalis-induced arrhythmias

Na+ channel blockers, Class IB: Toxicity
CNS stimulation/depression, CV depression

Na+ channel blockers, Class IC
flecainide, propafenone

Na+ channel blockers, Class IC: MOA
significantly prolongs refractory period in AV node; minimal effect on AP duration

Na+ channel blockers, Class IC: Clinical use
SVT, including atrial fibrillation; only as last resort in refractory VT

Na+ channel blockers, Class IC: Toxicity, Contraindications
pro-arrhythmic; contraindicated post-MI and in structural or ischemic heart disease

Beta blockers
metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

Beta blockers: MOA
decrease SA and AV nodal activity by decreasing cAMP and calcium currents; suppress abnormal pacemakers by decreasing slope of phase 4;
AV node particularly sensitive – increase PR interval

Beta blockers: Clinical use
SVT, slowing ventricular rate during atrial fibrillation/flutter

Beta blockers: Toxicity
Lots; impotence, exacerbation of COPD and asthma, bradycardia, AV block, CHF, sedation, sleep alterations;
metoprolol: dyslipidemia
propranolol: exacerbation of Prinzmetal angina

Beta blockers: Contraindications/cautions
diabetes mellitus — beta blockers may mask symptoms of hypoglycemia;
cocaine use — risk of unopposed alpha-adrenergic receptor agonist activity; treat overdose with glucagon to increase intracellular cAMP and increase HR and contractility (independent of adrenergic receptors)

K+ channel blockers
amiodarone, ibutilide, dofetilide, sotalol

K+ channel blockers: MOA
increase AP duration, increase effective refractory period, increase QT interval

K+ channel blockers: Clinical use
when other antiarrhythmics fail; atrial fib/flutter;
amiodarone and sotalol: VT

K+ channel blockers: Toxicity
sotalol: torsades de pointes, excessive B-blockade
ibutilide: torsades de pointe
amiodarone: pulm fibrosis, hepatotoxicty, hypo-/hyper-thyroidism, corneal deposits, blue/gray skin deposits (photodermatitis), neuro effects, constipation, bradycardia, heart blck, CHF

amiodarone important info
check PFTs, LFTs, and TFTs
has class I, II, II and IV effects; alters lipid membrane

Non-dihydropyridine Ca2+ channel blockers
verapamil, diltiazem

Non-dihydropyridine Ca2+ channel blockers: MOA
decrease conduction velocity, increase effective refractory period, increase PR interval

Non-dihydropyridine Ca2+ channel blockers: Clinical use
prevention of nodal arrhymthmias like SVT, rate control in atrial fibrillation

Non-dihydropyridine Ca2+ channel blockers: Toxicity
constipation, flushing, edema, CHF, AV block, sinus node depression

Adenosine: MOA
increase K+ out of cells -> hyperpolarizing the cell, decreasing intracellular Ca2+; very short acting (~15 seconds)

Adenosine: Indications
drug of choice for diagnosing and abolishing SVT

Adenosine: Toxicity
flushing, hypotension, chest pain

Which two substances block the effects of adenosine?
theophylline and caffeine

Magnesium: Indications
Torsades de pointes, digoxin toxicity

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