CHF Flashcards
1
Q
differentiate between high output and low output heart failure
A
- high output: heart is performing at maximum, but body needs more oxygen
- ex: hyperthyroidism, anemia
- low output: failure of heart; unable to keep up with normal demands of the body
2
Q
sympathetic stimulation of the heart predisposes the heart to
A
arrhythymias
3
Q
describe the frank starling law
A
- as preload increases -> increased stretch -> increased contractility -> increased stroke volume
4
Q
afterload is determined by
A
- arterial resistance
- aortic impedance
- vascular resistance
5
Q
what function of drugs will reduce preload? afterload? contractility?
A
- preload: venodilators
- afterload: arteriodilator drugs
- contractility: B-blockers
6
Q
why is contractility decreased in CHF
A
myocardial muscle fibers are stretched too far as ventricles become dilated
7
Q
in CHF, what happens if you give a drug that decreases cardiac output
A
- baroreceptor reflex will activate -> increased sympathetic stimulation of heart -> reflex tachycardia
8
Q
list the cardiac contractility determinants
A
- sensitivity of contractile proteins to ca2+
- amount of Ca2+ released from SR
- amount of Ca2+ stored in SR
- amount of trigger Ca2+
- activity of Na-Ca exchanger: (NCX; pumps Ca2+ out)
- intracellular Na+ concentration and activity of Na/K ATPase
9
Q
list other used names of Digitalis
A
- cardiac glycoside
- Digoxin
10
Q
MOA of Digoxin
A
- inhibits membrane sodium pump Na+/K+ ATPase
11
Q
MOA of cardiac effects of digoxin
A
**inhibition of Na/K ATPase
- increased intracellular Na+
- decreased explusion of intracellular Ca2+
- increased intracellular Ca2+ leads to increased SR Ca2+ stores
- increased action-myosin interaction by Ca2+
- increased contractility (positive inotropy)
12
Q
explain how digoxin also slows heart rate in normal and failing hearts
A
- Failing hearts, predominant tone is sympathetic
- as digitalis increases myocardial contractility, sympathetic tone will be reduced
- normal hearts: indirectly stimulates parasympathetics
- Sensitization of arterial baroreceptors
- Stimulation of central vagal nuclei
- Increased SA node sensitivity to acetylcholine
13
Q
is cardiac output increased by digitalis in a failing or normal heart
A
- Cardiac output is increased by digitalis in the failing but not the in normal heart
- Due to increased peripheral vasoconstriction in individuals with normal heart function
14
Q
putting it together, list effects of digoxin
A
- increases contractility
- slows heart rate
15
Q
digoxin
- route of administration?
- where is it excreted
A
- oral
- 80% excreted by kidneys, 20% by liver
16
Q
what is the earliest sign of adverse effects of digoxin
A
- all glycosides are toxic, narrow margin of saftey
- earliest sign of toxicity: GI
- N/V/D
17
Q
adverse effects of Digoxin
A
- CNS
- HA, fatigue, drowsiness, hallucination
- cardiac
- arrhythmias: sinus bradycardia, ectopic ventricular beats, AV block, bigeminy
18
Q
why should you measure K+ when patient is on digitalis
A
K+ and digitalis interact in two ways:
- Both inhibit each other’s binding to Na+ , K+ -ATPase receptor thus K+ counteracts digitalis toxicity
- K+ also reduces abnormal cardiac automaticity
- **Therefore digitalis toxicity is treated with K+
19
Q
intoxication treatment of digoxin
A
- minor (GI): discontinue or reduce digitalis
- moderate (arrhythmias): oral or IV potassium
- severe: digitalis immune fab
20
Q
why is cardioversion not recommended in patients taking digoxin (unless patient is in V-Fib)
A
- it will induce arrhythmias
21
Q
Quinidine has what effect on digoxin
A
- it displaces digoxin from tissue binding sites and enhances its toxicity
22
Q
hypokalemia has what effect on digitalis action
A
- get more action -> increases toxicity
- thiazides, loop diuretics
23
Q
what happens when digoxin is given with B-blocker
A
further decrease of SA or AV node acitivity
24
Q
why is digoxin not given with NE-releasing agents
A
catecholamines sensitize myocardium to digoxin -> increased toxicity
25
List the phosphodiesterase inhibitors
* inamrinone
* milrinone
26
inamrinone and milrinone have what main effect
* positive inotropes
* cause vasodilation
* **inodilators**
27
MOA of inamrinone and milrinone
* inhibit cAMP phosphodiesterase
* cause:
* increase cAMP
* increase in Ca2+ influx
* significant vasodilating effect
28
indication to use phosphodiesterase inhibitors
* acute heart failure (pt is dying)
* goal: increase cardiac output
29
when should phosphodiesterase inhibitors not be used
* long term
* cause decreased survival compared to placebo due to arrhythmias
30
low dose of dopamine has what effect
* D1 receptors in kidney -\> renal vasodilation
31
moderate dose of dopamine has what effect
* acts on B1 receptors in heart -\> inotropic effect
32
high dose of dopamine has what effect
* acts on alpha receptors in vessels -\> vasoconstriction
33
when is dopamine given in heart failure? route of administration?
* only in severe refractory CHF
* IV
34
MOA of dobutamine? route of administration?
* selective B1-agonist
* positive inotropic, less tachycardia
* IV
35
why are diuretics used in CHF
* they decrease salt and water retention -\> decreases venous pressure
* decreased edema
* decreased cardiac size
36
list the drugs that reduce CHF mortality
* aldosterone antagonist
* B-blockers
* ARBs
* ACE inhibitors
37
angiontensin II has what three primary effects
1. direct vasoconstriction: _result_: increases afterload
2. increases Na+ reabsorption in proximal tubule; releases aldosterone: _result_: increases preload
3. alteres cardiovascular strucutre: _result_: increases remodeling
38
which Potassium sparing diuretic action are used in CHF? why
* Spironolactone (Aldactone®), Eplerenone (Inspra®)
* Additional benefit by inhibiting aldosterone receptors
39
ACE inhibitors have what common name ending
end in "**.....pril**"
40
ARBs have what common name ending
end in sartan
41
MOA of ACE-I
* inhibits angiotensin converting enzyme
* thus angiotensin I can't become angiotensin II
42
MOA of ARB
* blocks angiotensin II from binding to the AT1 receptor
43
DOC for treatment of CHF
ACE-inhibitors
* effect: diminish cardiac workload
* decrease afterload: reduce angiotensin II-induced vasoconstriction
* decrease preload: reduce aldosterone release
44
adverse effects of ACE-I
* dry cough and angioedema
* due to reduction in bradykinin metabolism
45
B-blockers are used in what stages of CHF
* effective only in early stages
* dangerous in severe, end stage CHF due to negative inotropic effect
46
List the vasodilators
* sodium nitroprusside (nitropress)
* isosorbide dinitrate
* hydralazine
47
why are vasodilators used in CHF
* reduce preload (venodilation)
* reduce afterload (arteriolar dilation)
* or both
48
MOA of Sacubitril/Valsartan (entresto)
* contains two drugs: ARB and a neprilysin inhibitor
* neprilysin inhibitor: leads to -\> decreased vasoconstriction, decreased sodium retention, and decreased cardiac remodeling
49
adverse effects of Sacubitril/Valsartan (entresto)
* hypotension
* hyperkalemia (ARB)
* cough and angioedema
50
Contraindications of Sacubitril/Valsartan (entresto)
* pregnancy (ARB)
* concurrent use with ACE inhibitor due to serious risk of angioedema
