Term
| What is the main cause of HF |
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Definition
insufficient blood supply to the heart
(70% b/c of CAD (narrrowing of vessles and cardiac myocytes can't pum p as well and 30% b/c of HTN or abnormal valves) |
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Term
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Definition
| left ventricular contractile dysfunction |
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Term
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Definition
| CAD (70%), systemic arterial HTN(preloading), valvular heart disease (volume loading from mitral regurgitation, or aortic regurgitation, pressure loading from aortic stenosis), extrinsic cardiomyopathy, intrinsic cardiomyopathy |
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Definition
| abnormailities of left ventricular relaxation and/or filling (impaired relaxation leads to inc. LV diastolic pressure which leads to inc in left artial and pulmonary capillary pressure which leads to fluid overload in lungs |
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Definition
| acute myocardial ischemia |
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Term
| Frank-starling relationship in heart failure |
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Definition
relation of CO and preload
inc volume returning to heart chamber (preload) determines how much cardiac output occurs [cardiac output on y axis and vent end-diastolic pressure] if pt has HF you can give drug (digoxin) which will increase contractility at any given preload so you have more CO (curve will shift up, but not to normal level) |
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Term
| Cardiac remodeling and hypertrophy (aortic stenosis systemic HTN leads to: |
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Definition
| chronic PRESSURE overload, leads to concentric hypertrophy (new sarcomeres are added parallel to existing myofilaments--> increases wall thickness and decreases cavity size! |
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Term
| cardiac remodeling and hypertrophy. mitrial or aortic regurgitation leads to: |
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Definition
| chronic volume overload--> eccentric hypertrophy (new sarcomeres are added in series to the existing myofilaments. wall thickness inc proportional to cavity size |
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| positively inotropic drug |
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| positively inotropic drug |
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| positively inotropic drug |
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| positively inotropic drug |
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Term
| what does digoxin contain (structure) |
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Definition
| steroid nucleus, lactone ring, and three sugar residues linked by glycosidic bonds |
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Term
| Positively inotropic drugs- digitalis glycosides MOA: |
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Definition
bind and inhibit Na+/K+ATPase pump on the sarcolemma. Increase intracellular[Na+] which increases ca+/na+ exchanger so Ca+ influx increases and contractility increases!!!
INDIRECTLY: inc parasymp tone= dec HR dec conduction velocity (treats arrhythmia). digoxin is unique in that it inc conduction while dec HR
(block Na+/K+ATPase, inc [Na+] in cell=inc Ca+ influx= inc contractility, also inc parasymp tone and dec conduction dec HR) |
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Term
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Definition
too much Ca+ in cell= inc automaticity, tachycardia, ventricular ectopic beats
inc vagal activity= atrial tachycardia with 2:1 AV block
GI: anorexia, nausea, vomiting and diarrhea
neuronal disturbances: fatigue, confusion, vertigo, color vision
gynecomastia |
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Term
| digitalis glycosides and cardiac electrophysiology |
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Definition
increases PR interval, decreases QT interval (hockey stick configuration)
(digoxin slows AV conduction velocity but increases AV refractory period) |
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Term
| digitalis glycosides interactions |
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Definition
antacids and cholestyramine: reduce absorption of digoxin in GI tract
- Diltiazem, quinidine and verapamil reduce digoxin clearance= digoxin toxicity. - Diuretics can precipitate hypokalemia and therefore digitalis toxicity (hypokalemia inc digoxin binding to sodium pump) |
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| antidote for digoxin toxicity |
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Definition
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Term
| indications for digitalis glycosides |
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Definition
| HF, atrial fibrillation and flutter (reduce electrical conduction through AV node= reduction in atrial flutter/fibrillation) |
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Term
| positively inotropic drugs- Adrenergic B- receptor agonists |
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Definition
| dobutamine and isoproterenol |
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Term
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Definition
| B agonist. synthetic DA analogue. racemic mixture (a1 agonist (vasoconstriction) canclled out by b2(vasodilator) isomer) net effect is increased contractiity (B1 receptor) |
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Term
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Definition
| B agonist. Non selective. Inc myocardial contractility (B1) and HR (b1) produces peripheral arterial vasodilation (B2) |
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Term
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Definition
predicted from agonist actions at adrenoreceptors.
-excessive cardiac stimulation- tachycardia, palpitations and arrhythmias |
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Definition
pos. ionotropic drug,binds to B1 receptor. low doses causes vasodilation by stimulating dopaminergic receptors on SM and stim presynaptic D2 receptors (dec NE releasE). intermediate doses- stimulate B1 receptors in heart.
high doses= stimulate a1 receptors |
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Term
| Phosphodiesterase inhib- pos inotropic drugs (milrinone and enoximone) MOA |
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Definition
| PDE type 3 inhibitors (stop conversion of cAMP to 5'AMP)= inc cAMP in cardiac tissues and SM which causes inc cardiac contractility and relax vasc SM. desensitization DOES NOT occur (additive effects w/b-agonists though) |
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Term
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Definition
| tachycardia, palpitation, serious arrhythmias |
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Term
| Vasodilators- ACE inhib MOA |
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Definition
causes venous and arterial dilation
- dec. secretion of ADO and ADH= reduce BV and venous pressure and edema. - inc CO by reducing arterial pressure and afterload!! counteract ADE of ang 2 on cardiac remodeling in pts w/HF
(DEC AFTER LOAD = INCREASED CO WITH LESS WORK) |
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Term
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Definition
| selectively reduce binding of Ang 2 to AT1 receptors. similar to ACE inhib, do not cause chronic cough. |
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Term
| vasodilators- Hydralazine and nitrates |
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Definition
| hydralazine relaxes arterial smooth muscle, isosorbide dinitrate relaxes venous smooth muscle. in combo reduces Cardia preload and after load = reduced venous pressure and edema and inc CO. use in HF pt who can't take ACE inhib. |
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Term
| aldosterone antagonists- spironolactone and eplerenone MOA |
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Definition
compete w/ADO for mineralocorticoid receptors in renal tubules and other tissues. inc Na+ excredtion dec. K+ and H+ excretion. exerte moderate diuretic effect. prevend ADE of excessive ADO levels. additive effects w/ ACE inhib and B-blockers
ADO normally inc BV by inc sodium reabs so block this to dec BV |
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| Carvedilol (b-antagonist) MOA |
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Definition
| negative inotropic effect (used to be contraindictated in HF b/c of it). drugs reduce excessive symp. stim of heart and circualtion in pts w/HF. dec HR and contractility but not function! HF pts have too many catecholamines trying to compensate for the hypotension and inc renin, this can cause tachycardia, give b-blocker to stop this! |
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Term
| Diuretics- furosemide and thiazides MOA |
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Definition
| reduce BV and edema, loop diuretics have more natriuretic activity than other diuretics. use carefully to avoid excessive diuresis, dehydration and electrolyte imbalances. monitor hypokalemia esp if on digoxin. (remove extra blood sittin in heart) |
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Term
| Atrial natriuretic peptide (ANP) |
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Definition
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Term
| Brain natriuretic peptide (BNP) |
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Definition
| released from brain and ventricles, the plasma level of BNP goes UP in pts w/ HF |
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Term
| c-type natriuretic peptide (CNP) |
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Definition
| released from vascular endothelial cells, no effect on nitiuresis (sodium excretion) |
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Term
| Nesiritide (natriuretic peptide) MOA |
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Definition
| mimics actions of ANP. arterial and venous dilation! inc VO and SV w/o inc HR. causes natriuresis and diuresis. binds to NP recept, inc intracellular levels of cGMP and causes SM relazation. no effect on contractility or electrophysiology. |
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Term
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Definition
| hypotension, ventricular tachycardia, HA, nausea |
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Term
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Definition
| (natriuretic peptide) acutely decompendated CHF (HF that's not compensated) |
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