Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
62 Cards in this Set
- Front
- Back
What classes of drugs do you use to reduced preload on the heart?
|
a diuretic, or venodilator
|
|
what class of drug do you use to reduce afterload on the heart?
|
arteriodilator
|
|
what class of drug do you use to increase the contractility of the heart?
|
inotropic drugs
|
|
what class of drug to you use to lower the heart rate, and reduce energy expenditure of the heart?
|
B-adrenergic antagonists
|
|
What are the main effects of digoxin on the heart?
|
contractility is increased
Heart rate is slowed CO is increased only in failing hearts |
|
How does Digoxin increased myocardial contractility and thus stroke volume?
|
This inhibits the Na+, K+, ATPase
this increases Na and Ca inside the cell, and lowers K inside the cell. Due to high Ca+ - actin-myosin interaction is increased. |
|
How do potassium and digoxin interact?
|
K+ and digoxin compete for a binding site on the Na/K ATPase receptor. (so excess K blocks digoxin)- and reduces abnormal cardiac automaticity due to digoxin toxicity
|
|
How does calcium affect digoxin toxicity?
|
this increases the toxic effects
|
|
What do you treat digoxin toxicity with?
|
potassium, as it blocks digoxins binding to the Na/K ATPase
|
|
how does digoxin slow the heart in normal people?
|
the decreases the HR due to vagal stimulation.
(by sensitizing arterial baroreceptors, stimulating central vagal nuceli, and increasing SA node sensitivity to ACh) |
|
How does digoxin slow the HR in failing hearts?
|
digoxin will increase myocardial contractility, and this will reduce the sympathetic tone acting on the heart
|
|
how does digoxin affect CO in failing hearts?
|
this will increase CO in failing hearts- due direct action of the myocardium and in direct action by the PNS
|
|
How is digitialis used in conjunction with Class IA antiarrhythmic drugs?
|
pretreatment with digitalis will prevent paradoxical ventricular tachycardia
|
|
What are the vascular effects of digoxin in CHF pts?
|
increase contractility, and increased CO- results in less baroreceptor activation, and thus a decrease in sympathetic tone on the vasculature. so vasodilation
(it was vasoconstricted in an attempt to bring BP of the failing system up) |
|
When would you expect diuresis to occur in a pt treated with digoxin?
|
only if they have edema. the improved CO will pump more blood to the kidneys, allowing them to filter more fluid out
|
|
How does Digoxin affect the GI system?
|
Anorexia and diarrhea
Vomiting due to chemoreceptor stimulation abdominal pain |
|
What is the lipid solubility of digoxin?
|
medium
|
|
what is the oral availability of digoxin?
|
75%
|
|
what is the half-life in hours for digoxin?
|
40 hours
|
|
what is the plasma protein binding for digoxin?
|
20-40% bound
|
|
what is the renal elimination percentage for digoxin?
|
greater than 80%
|
|
what is the volume of distribution in L/Kg for digoxin?
|
6.3 L/Kg
|
|
How long (in days) will it take digoxin to reach steady state at constant dosing?
|
1 week (7 days)
|
|
What is the dosing regimine for rapid digitalization?
|
3 doses given over 24-36 hours followed by regular maintenance doses
|
|
What is the margin of safety like for digoxin?
|
these have narrow margins of safety- so toxic effects can occur even with therapeutic doses
|
|
What are the early signs of digoxin toxicity?
|
GI symptoms, anorexia, nausea, vomiting, diarrhea, salivation
|
|
What kind of cardiac arrhythmias can digoxin produce?
|
Bradycardia
Ectopic ventricular beats AV block Bigeminy Ventricular Fib |
|
What is the most common cause of death in pts taking digoxin?
|
Ventricular fibrillation
|
|
Why is digoxin toxicity declining?
|
use of serum level monitoring
noting drug interactions |
|
What are the CNS effects of digoxin?
|
headache, fatigue, malaise, drowsiness, disorientation, hallucinations
|
|
What does digoxin do to the skin?
|
causes rashes, eosinophilia, gynecomastia
|
|
What is the treatment of for digitalis toxicity?
|
stop digitalis administration
or potassium (NEVER Ca2+) Lidocaine, phenytoin, propranolol Digitalis Immune Fab (immunotherapy) |
|
How does Quinidine affect digoxin?
|
this displaces it from its binding sites in plasma proteins, while decreasing its renal clearance. this increases its toxicity greatly.
|
|
What types of actions increase digoxin toxicity?
|
decreasing its renal clearance, or decreasing its volume of distribution
Increasing its absorption |
|
How do diuretics that dont spare K affect digoxin?
|
thiazies and loop diuretics will decrease the volume of distribution, as well as dump K+ from the body
this increases digoxin toxicity |
|
How does dosing of Digoxin different for kids and old people?
|
old people are very sensitive to digoxin toxicity (due to hypochlorhydria, or reduced GFR)
Kids require MORE digoxin per Kg than adults |
|
What is the ending both phosphodiesterase inhibitors share?
|
-rinone
|
|
What do phosphodiesterase inhibitors do?
|
these inhibit cAMP phophodiesterase isozyme....which increases diastolic function and mycardial contractility
|
|
What is Inamrinone
|
this is phosphodiesterase inhibitor (bipyridine, or indolator)
|
|
what is milrinone?
|
this is phosphodiesterase inhibitor (bipyridine, or indolator)
|
|
who should be given bipyridines?
|
pts who can be closely monitored, and are not responding to digoxin, diuretics, or vasodilators
|
|
are bipyridines safe for long term?
|
no they are not, they increase mortality and hospitalization risks
|
|
What is low dose dopamine used for?
|
this increases Cardiac output, and improves renal blood flow in low doses
|
|
What disease is Dopamine use indicated for?
|
used in severe refractory congestive heart failure
|
|
What does Dobutamine do?
|
this is a B-1 selective agonist, used for its positive inotropic effect on the heart
|
|
What do calcium sensitizers do?
|
these inhibit phosphodiesterase III and sensitize troponin-C to Ca2+ levels
|
|
What are calcium sensitizers used for?
|
Survive and Revive situations
|
|
How do loop diuretics like furosemide treat CHF?
|
these are used for intensive diuresis, to remove large volumes of edema
|
|
how do thiazides treat CHF?
|
these are used for maintenance therapy
|
|
What kinds of problems come with using triamterene and amiloride in CHF?
|
these can cause hyperkalemia when combined with ACE inhibitors, or angiotensin II receptor antagonists
|
|
What is Nesiritide?
|
this is recombinant human B-type Natriuretic peptide (hBNP)
|
|
What does Nesiritide do?
|
this treats CHF,
reduces global symptoms, including dyspnea, fatigue |
|
How does Nesiritide compare to nitroglycerin?
|
Nesiritide doesnt have the tolerance issues like nitro does
|
|
How does the renin-angiotensin system affect afterload?
|
this increases afterload due to angiotensin induced vasoconstriction
|
|
how does the renin-angiotensin system affect stroke volume?
|
the high afterload impedes ejection, and thus decreases stroke volume
|
|
how does the renin-angiotensin system affect preload?
|
this increases preload by expanding the fluid volume of the body- via aldosterone (from angiotensin)- uptake of Na+ in the collecting duct
|
|
How does the renin-angiotensin system affect cardiac tissue?
|
this promotes remodeling of cardiac tissue
|
|
How do ACE inhibitors help with CHF?
|
these decrease afterload (that angiotensin induced)
and decrease preload (that was induced by aldosterone) |
|
How are beta blockers used in CHF?
|
these are dangerous in severe CHF, but are used in pts with diastolic dysfunction or cardiomyopathies
|
|
What does Sodium Nitroprusside do?
|
this is a vasodilator, used to reduce preload and afterload in CHF
|
|
What does Nitroglycerine and Isosorbide dinitrate do?
|
this lowers preload (VEINS)
more than arteries (afterload) |
|
what does Hydralazine do?
|
this is a peripheral vasodilator,
causes relaxation of Arteries Heart responds to BP drop via autonomics increasing HR, CO, and ejection fraction |