Tx of Congestive Heart Failure Flashcards
CHF
Weakened heart which results in backup of blood in heart and lungs
caused by- heart not pumping as strongly (heart attack, CAD, diabetes, etc), too much work for heart (htn, arteriosclerosis, valve defects, etc)
prevalence increases with age
Systolic dysfunction
heart contracts less forcefully and less blood is pumped out (reduced EF)
Diastolic dysfunction
heart is stiff and does not relax- reduced filling
High output HF
- healthy heart, but exhausted by working too hard
- hyperthyroidism, anemia, av shunts, thiamine deficiency
- poor or no response to inotropic drugs
Low output HF
- usual
- heart unable to keep up wtih metabolic demands
- inotropic drugs work
compensatory responses during CHF
- dec CO–> dec RBF–> inc renin release–> inc ang II–> inc preload, afterload, remodeling
- dec carotid sinus firing inc SYM discharge–> inc force and rate
- cardiac performance decreases with time
- b blockers and vasodilators reduce HF mortality by interrupting the compensatory mechanisms
Preload
- forces that act on venous side to affect myocardial contractility
- Venous return increases–> more blood enters heart–> ventricular pressure rises–> ventricular muscle is stretched–> force of contraction increases
-CHF preload elevated by increase in blood volume and venous tone
Venodilators do what
reduce preload by dilating peripheral veins to retain more blood and keep blood away from heart
-nitroglycerin
diuretics and salt reduction
reduce preload by decreasing blood volume
afterload
arterial resistance against which heart pumps
-afterload rises because inc in SYM and renin-ang system which elevate peripheral resistance via arterial constriction
arteriodilators
reduce afterload by decreasing peripheral resistance
myocardial contractility
reduced contractility when myocardial muscle fibers do not function properly or become fewer as in myocardial infarction
-CHF myocardial muscle fibers are stretched beyond their limits as ventricles become dilated
inotropic drugs
increase contractility
heart rate
determinant of cardiac output
CO=HRxSV
-due to reduced CO–> baroreflex activation–> sym overactivity–> reflex tachycardia
b-adrenergic blockers
reduce cardiac work by slowing heart rate
Concentration of Ca inside vs outside of cell
Outside- 2 mM
Inside- .1-10 uM
3 step treatment of CHF
- Use diuretics to correct volume overload. Then:
1) Initiate ACE inhibitor to reduce cardiac workload. Patient with systolic dysfunction- add b blocker
2) persistent symptoms- add aldosterone antagonist (spironolactone)
3) persistent- add digoxin, ARB; AA pts add hydralazine/isosorbide dinitrate instead because ARBs are not as effective
Diuretics in CHF
most common-
furosemide, bumeanide, torsemide
thiazides- mild CHF
ultimate goal- eliminate fluid retention
ethacrynic acid
diuretic reserved for pts allergic to sulfonamides
ACE inh in CHF
diminish cardiac workload by decreasing afterload (red angiotensin) and decreasing preload (reduce aldosterone release)
-captopril, enalapril, lisinopril, ramipril, quinapril
ARB
-sartan
- more specific than ACE inhibitors (do not affect bradykinins)
- more complete inh of angiotensin action
Sodium nitroprusside
vasodilator
-infused IV in acute decompensated CHF as long as cerebral and renal perfusion can be maintained despite reduction in systemic BP
-reduces preload and afterload by working on veins and arteries
-excessive hypotension can occur
-
oral nitroglycerine and isosorbide dinitrate
dilate veins more than arteries- lower preload more than afterload
-can lead to tolerance
CCB
amlodipine or felodipine
- relax arteriolar smooth muscles
- produce vasodilation
Verapamil and diltiazem
inhibit cardiac contraction, SA node impulse gen, AV node conduction
DO NOT USE IN CHF
b blockers
negative inotropic effect- worsen ventricular fxn however studies show that long term tx with certain b blockers improves symptoms of CHF by slowing heart rate and contraction velocity to improve CO, exercise tolerance, ventricular fxn
-bisoprolol, carvedilol, metoprolol
Aldosterone antagonists
spironolactone and aplerenone
-reduce mortality in HF
but can cause hyperkalemia, gynecomastia (switch to eplerenone), renal insufficiency
Inotropic drugs
- digoxin is the only glycoside now used in US for tx of CHF and afib
- inc Na and Ca
- therapeutic concentrations increases cardiac contractility in normal and failing heart
- narrow therapeutic window (50-60% of toxic dose)
Drugs that enhance digoxin toxicity
quinidine, amiodarone, captopril, verapamil, diltiazem, cyclosporine
-abx inc digoxin absorption
digoxin AE
- GI- anorexia, nausea, vomiting, diarrhea
- cardiac- most dangerous, can simulate almost all arrythmias- Vfib,
- K+ counteracts digoxin toxicity because it inhibits binding to Na/K/ATPase and reduces abnormal cardiac automaticity
Tx of digoxin intox
discontinue dig
correction of hypokalemia and hypomagnesemia
lidocaine if arrythmic
digoxin antibodies
PDE inhibitors
inotropes
-PDEs inactivate cAMP and cGMP
Inamrinone (amrinone) and milrinone are given via injection
-inhihbt type III PDE present in cardiac and smooth muscle cells
- increase contractility by increasing cAMP and inward calcium flux in heart
-cause vasodilation
-some intolerable adverse effects long term
-acute hf tx
dopaminergic agonists
dopamine and b1 agonists like dobutamine are infused IV to inc myocardial contractility in acute CHF
b2 agonists
albuterol and pirbuterol relax vascular smooth muscle
-used only for acute failure or failure refractory to oral drugs
