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18 Cards in this Set
- Front
- Back
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In the heart would do Calcium channel do?
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Calcium channel effects are coupled with B1 adrenergic receptors such that their stimulation causes Ca++ influx.
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Calcium channel blockers
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Prevent calcium ions from entering cells. Involves--- Myocardium, SA node, AV nodes.
Classified as: Dihydropyridines (DHP), Phenylalkylamine (non-DHP), Benzothiazepine (non-DHP) |
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CCB- Verapamil (Phenylalkylamine)
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blocks VSM of arteries (vasodilation of peripheral and coronary arteries), decrease heart rate and BP (if no cardiac disease)
ADRs---constipation, vasodilation, bradycardia, heart block |
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CCB- Diltiazem (Benzothiazepine)
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less effects on heart
ADRs--- less constipation and bradycardia |
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CCB- Nifedipine (DHP)
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vasodilation by blocking channels at VSM
EFFECTS-- decrease BP, increase HR and force ADR's--- Vasodilation (edema, flushing, dizziness) |
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CCB----Nimodipine (DHP) & Clevidipine (DHP)
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nimodipine-- not used for HT or angina, helps prevent neurological damage
Clevidipine-- new IV only |
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Heart Failure description and signs/symptoms
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HF- inability to pump enuf blood for metabolic needs, involves cardiac remodeling due to sympathetic stimuli.
S/S---decreased exercise tolerance, fatigue, tachycardia, orthopnea, perpheral edema, weight gain, s3 gallop |
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HF drugs--- 1
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Diuretics- reduce blood volume, decrease venous and arterial pressure. Spironolactone--- (K+ sparing)-decrease cardiac remodeling. Eplerenone does same except few ADRs.
ACEI's-- decrease production of angiotensin II, dilate arteries and veins, decrease release of aldosterone. ARBS-block angiotensin II receptors. |
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HF drugs---2
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Beta blockers- Carvedilol, bisoprolol, metoprolol, ADRS-bradycardia, heart block, decreased BP.
Inotropic-- Cardiac glycosides (digoxin), sympathomimetics (dopamine & dobutamine), phosphodiesterase (inamrinone & milrinone |
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Digoxin --- HF Inotropic drug
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increases cardiac output, myocardial contractility, and urine production. Decrease sympathetic tone.
inhibition of sodium potassium pump Cautions---hypokalemia, heart disease ADR's-- cardiac (dysrhythmia), non-cardiac (GI, fatigue, visual distrubances. |
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Electrocardiogram
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P- wave--depolarization of atria
PR interval- AV nodal conduction QRS- depolarization of ventricles T- Wave-- repolarization of ventricles QT interval- depolarization and repolarization of ventricles |
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Dysrhythmias ---- Types
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Supraventicular- above the ventricles
Venticular- at ventricles and below (most dangerous) |
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Antidysrhythmic drugs
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Ia (quinidine, procainamide, disopyramide)
lb (lidocaine, phenytoin, mexiletine, tocainade ic (flecainide, propafenone) II b-blocker (propranolol, acebutolol, esmolol) III K+ channel blockers (berapamil, diltiazem) others (digoxin, adenosine0 |
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la-----quinidine and procainamide
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quinidine-- blocks NA+ channels, anticholinergic (high HR), well absorbed (sulfate fastest), ADR's-- diarrhea, cinchonism (tinnitus), cardiotoxicity (torsade)
Procainamide-- less anticholinergic, active (NAPA), ADR's-- SLE, blood -dyscrasias, cardiotoxicity |
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lb-----lidocaine, phenytoin, mexiletine and tocainide---None pro-dysrthmias
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Lidocaine- blocks Na+ channels, given IV/IM,
Phentoin- IV, hypotension, same as lidocaine Mexiletine- GI, neurologic Tocainide- serious blood dyscrasias, pulmonary fibrosis |
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II b-blocker--propranolol, acebutolol and esmolol
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Propranolol--Nonselective B adrenergic blocker, use-- tachydysrhthmias (sympathetic stimulation)
Acebutolol-- oral, b specific, causes bronchospasms Esmolol--IV, short acting |
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amiodarone
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uses-- refractory patients, complicated kinetics (lipid soluble), long half life measured in (1-4) months, ADR's-- cardiac (bradycardia), non-cardiac (pulmonary fibrosis)
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III k+ channel blockers---verapamil, diltiazem
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Verapamil---- uses in supraventricular dysrhythmias, ADR's---bradycardia, AV block, HF, Hypotension, peripheral edema, constipation
Diltiazem---less cardiac effects and constipation |
