Cardiac drugs Flashcards

Question

NON-VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS

Answer 1

Digoxin, adenosine (actions are outside of Vaughan-Williams classification)

Answer 2

Local anesthetic agent Class 1B antiarrhythmic drug prototype Is administered IV only Onset of action 45-90 sec Bolus for loading, continuous IV infusion thereafter Half life 15-20 min single dose; 90-120 min with IV infusion Side effects – GI, neurologic, respiratory

Answer 3

Prototype antiarrythmic agent with multiple class effects Primarily a class III antiarrhythmic agent – K+ channel blocker prolonging action potential duration and repolarization. Also has class I, II, and IV antiarrhythmic activity Every 200 mg of amiodarone contains 80 mg of iodine; accounts for many of the side effects Pharmacology – only 50% bioavailable with oral therapy, requires prolonged loading period (up to 3 months) as the drug is highly lipophilic and binds to all adipose tissue and these stores are saturated before therapeutic effect noted. Metabolized by liver to active metabolite. Half life is 26-107 days. Indicated for supraventricular and ventricular arrhythmias

Answer 4

``` Minor and asymptomatic - corneal microdeposits - elevated LFTs - thyroid function abnormalities - blue-gray skin discoloration Minor and symptomatic - skin rash, photosensitivity - CNS – ataxia, temors, headache, paresthesias - GI – nausea, anorexia, constipation - visual complaints - hair loss - epididymitis ```

Answer 5

Major side effects (require dose reduction or drug discontinuation) Hypothyroidism/hyperthyroidism Pulmonary complications Bradycardia – sinus node dysfunction, AV node blockade Arrhythmia aggravation (rare) Hepatic injury Drug interactions – warfarin, digoxin, beta blockers, calcium channel blockers, other drugs that prolong QT interval (eg antibiotics)

Answer 6

Enhances vagal tone (vagal innervation primarily to sinus and AV nodes) - reduces sinus node automaticity and rate - prolongs refractoriness of AV node and slows conduction through this structure At toxic doses also increases sympathetic outputs from central nervous system. The increase in the peripheral vagal tone and central sympathetic outputs results in digoxin toxic arrhythmias

Answer 7

REDUCTION IN VENOUS RETURN Diuretics - thiazide, loop, aldosterone antagonist Venodilation (capacitance vessels) - nitrates (IV, SL, transdermal, oral) - nitroprusside (IV)

Answer 8

Reduce venous congestion improve shortness of breath improve lower extremity edema Reduce preload, reducing end-diastolic volume and wall stress and increasing stroke volume Thiazide vs. loop diuretics Loop diuretics (e.g. furosemide) more efficacious and commonly used in patients with congestive heart failure

Answer 9

Prototypic inotropic drug Increase in intracellular Ca++ Increase in myocardial contractility Increase stroke volume and cardiac output; reduces LV preload Directly and indirectly reduces sympathetic nervous system activity Decrease in heart rate (withdrawal of sympathetic activity and increased vagal tone)

Answer 10

75% of dose rapidly absorbed; rest inactivated in lower gut by bacteria Half life 36 hour Binds to tissue receptors in heart as well as skeletal muscle Is lipid soluble, penetrates the brain Is excreted unchanged in urine Dose adjustment necessary in chronic renal failure Dose reduction in patients with reduced skeletal muscle mass (thin patients, elderly)

Answer 11

Cardiac bradycardia, AV block, asystole, supraventricular arrhythmias, junctional arrhythmias, ventricular arrhythmias Noncardiac - GI (nausea, vomiting, abdominal pain, anorexia) - Neurologic (visual disturbances, abnormal dreams, headache, dizziness, apathy, confusion, mental disturbances, anxiety, depression, delirium, hallucinations) - Weakness

Answer 12

Reduction in arterial vascular tone or resistance (afterload) Reduction in venous tone- increase in venous capacitance, decrease in venous return (preload Reduction in myocardial wall stress Improved ventricular systolic function (inotropy)-increase in stroke volume and cardiac output Enhanced myocardial relaxation (lusitrophy) - improved diastolic function

Answer 13

Direct acting – smooth muscle dilatation Alpha receptor blockade Angiotensin converting enzyme (ACE) inhibition Angiotensin II receptor blockade (ARB) Calcium channel blockade Nitric oxide generation – endothelium derived relaxing factor

Answer 14

Direct smooth muscle relaxation and arterial vasodilation via inhibition of calcium influx Can be administered IV or orally (three times per day) When used for heart failure therapy is combined with long acting nitrate (isosorbide mononitrate or dinitrate)

Answer 15

Cardiovascular – tachycardia (which can precipitate angina), hypotension Drug induced lupus-like syndrome Headache Dizziness Flushing Increased renin secretion- salt and water retention and edema GI – anorexia, nausea, vomiting

Answer 16

``` Hemodynamic effects mediated by: Reduction in angiotensin II levels - reduction in arterial vascular resistance (afterload) Prevention of aldosterone secretion - reduced salt and water retention - reduced preload Blockade of bradykinin metabolism - arterial vasodilation Reduction in sympathetic activity ```

Answer 17

``` Hypotension Weakness Dizziness, lightheadedness Syncope Acute renal failure – primarily in patients with renal artery stenosis, heart failure, chronic renal disease, hypertensive kidney disease Cough Hyperkalemia -for ACEI with sulfhydryl group Neutropenia Altered taste Angioedema ```

Answer 18

Blocks the binding of angiotensin II to the AT1 receptor on the vascular smooth muscle - reduction in arterial vascular resistance (afterload) Reduces sympathetic activity Blocks effect of angiotensin II on adrenal gland- inhibits secretion of aldosterone Has no effect of bradykinin metabolism Primarily used in patients intolerant of ACE inhibitors, as add-on therapy in patients treated with an ACE inhibitor, and in patients with preserved LVEF

Answer 19

Side effect profile generally the same as that for ACE inhibitors Hypotension Dizziness, lightheadedness Syncope Weakness Hyperkalemia Acute renal failure – primarily in patients with renal artery stenosis, heart failure, chronic renal disease, hypertensive kidney disease Less likely to cause cough, neutropenia, angioedema

Answer 20

For undiagnosed patients with symptoms of ischemia, heart failure, or arrhythmia avoid elective care; refer to physician For diagnosed patients with cardiac symptoms Asymptomatic: routine care Mild symptoms with exertion: elective care OK, recommend consultation with physician Symptoms with minimal activity or at rest: avoid elective care; if treatment necessary, manage in consultation with physician; consider referral to a special patient care setting; avoid use of vasoconstrictors or epinephrine