Treatment of Heart Failure Flashcards
6 categories of drugs that can treat heart failure
diuretics
ACE inhibitors
AT receptor blockers
Vasodilators
Beta-blockers
Cardiac glycosides
what are possible causes of heart failure
myocardial damage
hypertension
genetic/congenital
chemical toxicity
infection
difference between systolic and diastolic heart failure
systolic = reduced contractility
diastolic = reduced filling of the heart
how does the CV system compensate for decreased cardiac output
- increased SNS activity
- increased renin-angiotensin system
- increased force of heart contraction
- ventrivular hypertrophy
how does the SNS play a role in compensating for decreased cardiac output
- baroreceptors dewtect this change and cause reflex machanism
- increased SNS and decreased PSNS
- increases heart rate (force of contraction and PVR)
symptoms of heart failure due to the SNS compensation response
tachycardia
sweating
fluid retention
how does the renin-angiotensin system compensate for decreased cardiac output
- decreased CO means leass bloodflow to the kidneys
- get SNS activation of B1 receptors in kidneys
- Na+ and H2O retention by kidneys heads in increased blood volume and cardiac output
- increased renin released by kidneys leads to Angiotensin II being formed - binds AT1 receptors and nerve terminals to increase NE leading to increased PVR
how does fluid retention and vasoconstriction help compensate for decreased cardiac output
increased BV in veins - increased pressure in blood returning to the heart - stretching of cardiac muscles - increased strength of contraction
structural changes in the heart when we have decreased cardiac output
- have enlarged atria and ventricles
- more blood but not able to efficiently pump it out
ventricular enlargement vs hypertrophy
enlargement: cavities dilate when cardiac muscle is weakened - volume good, strength bad
hypertrophy: cardiac muscle cells increase in size to componsate for stress - strength good, volume bad
what is a compensated heart
heart functions normally at rest but may fail due to exercise or stress - due to compensatory mechanisms
what is a decompensated heart
- severely damaged heart cannot be compensated by the SNS, renin-angiotensin system or ventricular hypertrophy
- excessive stretching of heart muscle weakens the heart further
- edema - excessive fluid in venous system can leak into tissues
a combination of which conditions is termed congestive heart failure
decompensated heart + edema - need intervention!
characteristics of conjestive heart failure
- insufficient CO to supply organs with nutrients and O2
- fluid accumulation in lower limbs or lungs
- reflex mechanisms worsen effects since normal CO cant be reached
- body cannot respond, must regulate heart yo pump blood more efficently
symptoms of conjestive heart failure
tachycardia
shortness of breath
sweating
peripheral/pulmonary edema
decreased exercise tolerance
enlargement of heart
hypertension/hypotension
urine retention
theraputic strategies for conjestive heart failure are aimed at…
reducing workload of the heart
treatment strategies for conjestive heart failure - lifestyle changes
heathy diet
limit salt
limit alcohol and caffiene
decrease stress
exercise (cautious)
quit smoking
treatment strategies for conjestive heart failure - surgical procedures
angioplasty
bypass treatment
transplant
ventricular pacemakers
left ventricular assist device
what drugs are used to treat mild heart failure or patients with left ventricular dysfunction
ACE inhibitors (enalapril)
ARB (losartan)
how do enalapril and losartan work on blood vessels to treat heart failure
- cause vasodilation
- devreased SVR and afterload
- reduce stress on the heart
how do enalapril and losartan work on the heart to treat heart failure
- decrease afterload, preload and edema
- increases ejection fraction
- results on decreased oxygen demand for the heart
how do enalapril and losartan work on the kidney to treat heart failure
- decreases Na/H2O reabsorption
- decreases BV and CO
- decreases preload
- decrease overall stress on the heart (benefit on the heart > difr rffrct of decreased CO)
what drugs are used to treat heart failire in patients with edema
diuretics (furosemide) - first-line treatment for patients woth pulmonary edema
vasodilators (long-acting nitrates)
what drugs are used to treat patients with excessive tachycardia
low dose B-blockets (metoprolol)
- must be cautious becasue we have decreased CO
cardiac glycosides in treating heart failure
- effective but can be toxic so don’t use as first-line treatment
- use in patients who remain symptomatic after treatment
- use in patients who have CHF and atrial fibrilation or enlarged dysfunctional left ventricle
characteristics of Digoxin (cardiac glycoside)
- absorbed and distribited well
- direct effect (heart)
- indirect effect (baroreceptors)
mechanism of cardiac glycosides (e.g. digoxin)
- inhibits Na+/K+ ATPase
- leads to increased force and decrease rate of contraction (heart fills more efficiently and doesnt have to work as hard to pump blood out)
direct effect of digoxin (cardiac muscle cells)
increases Na+ inside cell - decreases Ca2+ efflux out of cell - increases intracellular Ca2+ - increases interaction between actin and myosin - INCREASED CARDIAC CONTRACTILITY
indirect effect of digoxin (baroreceptors)
improved circulation - baroreceptors respond - increased PSNS activity and decreased SNS activity
administration of digoxin
- long half life (40 hours)
- to achieve theraputic doses quickly, patients given large initial dose followed by daily maintenence dose
- maintenence adjusted based on body weight, kidney function and plasma digoxin levels
cardiac toxicities of digoxin
arrhythmias in patients with low K+ levels (from diuretics or diarrhea) which can lead to tachycardia and fibrillation
toxicities of digoxin from drug interactions
interaction with quinidine (anti-arrythmic drug) reduces digoxin clearance - inclreases plasma levels and can lead to toxicity
GI/CNS toxicity of digoxin
anorexia
nausea
vomitting and diarrhea
dizziness
headaches
vision disturbances
what happens when Na+/K+ ATPase enzyme is inhibited in cardiac cells
- reduces the exchange of K+ for Na+ which reduces Na+ and Ca2+
- more Na+ and Ca2+ remains in the cell
- more Ca2+ = increased rate and force of contraction
