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;
74 Cards in this Set
- Front
- Back
What is the most important cause of CHF?
|
coronary heart disease with hypertension
|
|
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
|