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76 Cards in this Set

  • Front
  • Back

What are the 2 groups of CHF?

people with systolic failure and diastolic failure
What is systolic failure?
reduced mechanical pumping action and reduced ejection fraction
What is diastolic ejection fraction? What may be normal?
stiffening and loss of adequate relaxation reduces filling and cardiac output. The ejection fraction may be normal even though stroke volume is significantly reduced
Are inotropic drugs better for acute or chronic HF?
acute
What type of Ca channel is on the SR of a myocyte? How are they stimulated to open?
ryanodine-sensitive calcium channels open when Ca increases slightly in the cell
What does the drug ryanodine do?
inhibits ryanodine-sensitive calcium channels
What is the channel called that reuptakes Ca from cytoplasm? What type of channel is it?
SERCA is a Ca ATPase
What does phosphlamban do? What inhibits it?
1) inhibits SERCA
2) proteinkinase A phosphorylates and inactivates it
What type of Ca channel allows Ca into cell from extracellular fluid?
L-type Ca channel
How do sympathomimetics affect the duration of L-type channels being open?
They increase it and increase Ca influx
How is Ca removed from cytoplasm to extracellular fluid?
via the antiporter NCX which exchanges Na for Ca
What is typically seen in acute HF?
systolic dysfunction with reduced cardiac output and decreased ejection fraction
High output failure rarely results, however, what conditions would predispose someone to failure from over use? Can it be treated the same?
hyperthyroidism, beriberi, anemia, and arteriovenous shunts

It is generally not responsive to the same drugs
What are the typical signs of cardiac failure?
tachycardia, decreased excercise tolerance, SOB, peripheral and pulmonary edema, and cardiomegaly
The baroreceptor reflex is set to different pressures in HF, how is it changed?
it has a lower sensitivity to arterial pressure which results in decreased sensory input to the vasomotor center even at normal pressures
What does vasoconstriction result in at the heart? What hormone in particular increases this?
increased afterload with decreased ejection fraction and cardiac.
2) Angiotensin II increases afterload
What can excessive beta activation cause in the myocyte? What organic effect does it have?
leakage of Ca from the SR via RyR channels which causes stiff ventricles and arrythmias
What enzymes are activated by excessive beta activation that result in apoptosis?
caspases
What is the effect of angiotensin II on sympthetic stimulation?
+ feedback
If phospholambin is elevated what happens to intracellular Ca?
it increases because SERCA can't take up Ca
Beta agonists cause decreased cytoplasmic Ca through what mechanism?
activate protein kinase A which phosphorylates and inactives phospholamin allowing SERCA to take up Ca
what is the most intrinsic compensatory mechanism in HF?
hypertrophy
What is the general trend of stroke volume to filling pressure? What mechanism is responsible for this? At what pressure does this relationship plateau?
1) as filling pressure increases so does the stroke volume
2) frank starling relation
3) won't work beyond 15mmHg filling pressure
At what filling pressure will pulmonary congestion and edema occur?
1) 20-25mmHg
Why are diuretics given to someone with heart failure in terms of preload?
to reduce the high filling pressure by removing salt
How Does nitroglycerin have an impact on preload?
it reduces preload by redistributing blood away from the heart and into the peripheral veins
How is afterload defined?
it is the resistance (from aorta and sysmtemic arteries) against which the heart must pump blood
What is the first mechanism to compensate for decreased SV and decreased CO?
increased heart rate
Where does digoxin have effects in the body aside from the heart?
CNS and GI
What is the MOA of cardiac glycosides?
inhibit Na, K ATPase in almost all tissues
What are the mechanical effects of cardiac glycosides?
increased free calcium after an increase intracellular Na. This impairs the sodium-Ca exchanger (NCX). The increase Ca is stored in the SR for later release
Is the membrane potential of a myocyte increased or decreased with digoxin? What happens to the duration of the action potential?
1) decreased because of reduced Na excretion and K+ uptake into cell.
2) the AP decreases because less Ca comes in during the plateau phase. This is because there is accumulated Ca in the cytplasm
How do ectopic beats originate in someone taking digoxin?
Afterpotentials or delayed after depolarizations result from oscillations of increased free intracellular Ca. When these afterpotentials are large enough they cause an ectopic beat
If afterpotentials with digoxin occur in the purkinje system what is seen on an EKG?
bigeminy
What does therapeutic digoxin use do to the SA node, atrial refractory period, atrioventricular node, purkinje system and EKG?
1) SA node rate decreases
2) decreased refactory period
3) decreased conduction velocity and increased refactory period
4) slightly decreased refactory period
5) increased PR interval and decreased QT interval
How will toxic digoxin use present? What system predominates?
extrasystoles, tachycardia can go to fibrillation.

Sympathetic effects
Do parasympathetic or sympathetic responses predominate at lower doses of digoxin? What do these responses entail?
1)parasympathetic
2) barorecptors are sensitized, vagal stimulation and muscarinic transmission to cardiac muscle
What are the most common manifestations of digoxin?
AV junctional rhythm, preventricular depolarizations, bigeminal rhythm, second degree AV blockade
What is the most common site of digoxin toxicity next to the heart?
GI
What does therapeutic digoxin use do to the SA node, atrial refractory period, atrioventricular node, purkinje system and EKG?
1) SA node rate decreases
2) decreased refactory period
3) decreased conduction velocity and increased refactory period
4) slightly decreased refactory period
5) increased PR interval and decreased QT interval
How will toxic digoxin use present? What system predominates?
extrasystoles, tachycardia can go to fibrillation.

Sympathetic effects
Do parasympathetic or sympathetic responses predominate at lower doses of digoxin? What do these responses entail?
1)parasympathetic
2) barorecptors are sensitized, vagal stimulation and muscarinic transmission to cardiac muscle
What are the most common manifestations of digoxin?
AV junctional rhythm, preventricular depolarizations, bigeminal rhythm, second degree AV blockade
What is the most common site of digoxin toxicity next to the heart?
What are the symptoms?
1) GI
2) anorexia, nausea, vomiting and diarrhea
Will digoxin be inhibited or potentiated with potassium?
they antagonize each other so that moderately high potassium reduces digoxins toxic effects
Someone taking calcium with digoxin will be predisposed to what?
the toxic effects of digoxin. Note that magnesium may lower effects
What is the MOA of bypyridines? What are two drugs in this group?
1) inhibit phosphodiesterase 3
2) inamrinone and milrinone
What effect does cAMP have on Ca influx? Why are bypyridines given?
1) increases the amount of Ca that enters the cell and has a vasodialator effect
2) bypyridines increase Ach degradation by PDE3
What is the mechanism of phosphodiesterase?
degrade cAMP
What are the side effects of inamrinone?
it is a byprydine that has bone marrow and liver toxicity
What are the side effects of milrinone?
arrythmias
When are bypyridines used?
acute or severe chronic HF
What is dobutamine?
a beta 1 agonist
What beta-adrenoceptor agonist is used most in HF?
dobutamine
What effects does dobutamine have on the heart?
increased CO and decreased ventricular filling pressure
What are the side effects of dobutamine?
1)tachycardia
2) angina or arrythmias in people with CAD,tachyphylaxis
What are examples of aldosterone antagonists?
spirolactone and eplerenone
Do Ace inhibitors reduce preload or afterload?
afterload by decreasing peripheral resistance and reduce preload by decreasing water retention
What are ace inhibitors effects on the autonomic nervous system?
they decrease sympathetic output by decreasing angiotensin which has an effect on presynaptic NE release
What is losartan?
a drug that blocks angiotensin AT1 receptors and has similar effect to ace inhibitors. used in patients intolerant to ace inhibitors
What is a synthetic form of BNP?
nesiritide increases cGMP in smooth muscle and reduces venous and arteriorlar tone
What compounds are competitive inhibitors of endothelin?
bosentan and tezosentan but both have teratogenic and hepatotoxic effects
What beta blockers are generally used in HF?
bisprolol, carvedilol, and metoprolol
What are some effects of beta blockers in HF?
attenuate adverse effects of high concentrations of catecholamines including apoptosis, increase beta receptors, decrease heart rate, decrease cardiac remodeling
What are the stages of HF?
1) stage A: high risk but no signs or symptoms
2) stage B: structural heart disease with no symptoms
3) stage C: structural heart disease and symptoms responsive to ordinary treatment
4) Stage D: heart failure need special interventions (transplant)
Once Stage C of HF is reached there are classes of HF. What are they?
class I: no limitations
class II: slight limitation in ordinary activity
class III: SOB, tachycardia with little excercise
class IV: symptoms at rest
What drugs are given to remove excess sodium in people with mild HF?
thiazide and furosemide
What is the concern with using a diuretic and taking digoxin?
some diuretics cause hypokalemia which can potentiate the adverse effects of digoxin. supplemental potassium can reduce effects
What are examples of potassium sparing diuretics given to people with moderate to severe HF?
spironolactone and eplerenone
Why are beta blockers given?
attenuate the effects of catecholamines
In someone with third heart sounds and dialated ventricles what drug combo should be given?
digitalis and enalapril
What other conditions can digitalis be given for?
atrial arrythmias because it has cardioselective parasympathetic effects
What drug can result in long QT syndrome?
digoxin because of hyperkalemia

what is the most common cause of CHF

coronary artery disease and hypertension

CHF

when compensatory mechnisms fail and teh peripheral and lung tissues are congested

HF

When the heart muscle weakens and enlarges, it loses its ability to pump blood through the heart and into teh systemic circulation