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IC > Tx of Congestive Heart Failure > Flashcards

Tx of Congestive Heart Failure Flashcards

1
Q

CHF

A

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

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2
Q

Systolic dysfunction

A

heart contracts less forcefully and less blood is pumped out (reduced EF)

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3
Q

Diastolic dysfunction

A

heart is stiff and does not relax- reduced filling

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4
Q

High output HF

A
  • healthy heart, but exhausted by working too hard
  • hyperthyroidism, anemia, av shunts, thiamine deficiency
  • poor or no response to inotropic drugs
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5
Q

Low output HF

A
  • usual
  • heart unable to keep up wtih metabolic demands
  • inotropic drugs work
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6
Q

compensatory responses during CHF

A
  • 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
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7
Q

Preload

A
  • 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

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8
Q

Venodilators do what

A

reduce preload by dilating peripheral veins to retain more blood and keep blood away from heart
-nitroglycerin

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9
Q

diuretics and salt reduction

A

reduce preload by decreasing blood volume

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10
Q

afterload

A

arterial resistance against which heart pumps

-afterload rises because inc in SYM and renin-ang system which elevate peripheral resistance via arterial constriction

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11
Q

arteriodilators

A

reduce afterload by decreasing peripheral resistance

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12
Q

myocardial contractility

A

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

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13
Q

inotropic drugs

A

increase contractility

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14
Q

heart rate

A

determinant of cardiac output
CO=HRxSV
-due to reduced CO–> baroreflex activation–> sym overactivity–> reflex tachycardia

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15
Q

b-adrenergic blockers

A

reduce cardiac work by slowing heart rate

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16
Q

Concentration of Ca inside vs outside of cell

A

Outside- 2 mM

Inside- .1-10 uM

17
Q

3 step treatment of CHF

A
  • 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
18
Q

Diuretics in CHF

A

most common-
furosemide, bumeanide, torsemide

thiazides- mild CHF

ultimate goal- eliminate fluid retention

19
Q

ethacrynic acid

A

diuretic reserved for pts allergic to sulfonamides

20
Q

ACE inh in CHF

A

diminish cardiac workload by decreasing afterload (red angiotensin) and decreasing preload (reduce aldosterone release)

-captopril, enalapril, lisinopril, ramipril, quinapril

21
Q

ARB

A

-sartan

  • more specific than ACE inhibitors (do not affect bradykinins)
  • more complete inh of angiotensin action
22
Q

Sodium nitroprusside

A

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
-

23
Q

oral nitroglycerine and isosorbide dinitrate

A

dilate veins more than arteries- lower preload more than afterload
-can lead to tolerance

24
Q

CCB

A

amlodipine or felodipine

  • relax arteriolar smooth muscles
  • produce vasodilation
25
Q

Verapamil and diltiazem

A

inhibit cardiac contraction, SA node impulse gen, AV node conduction
DO NOT USE IN CHF

26
Q

b blockers

A

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

27
Q

Aldosterone antagonists

A

spironolactone and aplerenone
-reduce mortality in HF
but can cause hyperkalemia, gynecomastia (switch to eplerenone), renal insufficiency

28
Q

Inotropic drugs

A
  • 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)
29
Q

Drugs that enhance digoxin toxicity

A

quinidine, amiodarone, captopril, verapamil, diltiazem, cyclosporine

-abx inc digoxin absorption

30
Q

digoxin AE

A
  • 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
31
Q

Tx of digoxin intox

A

discontinue dig
correction of hypokalemia and hypomagnesemia
lidocaine if arrythmic
digoxin antibodies

32
Q

PDE inhibitors

A

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

33
Q

dopaminergic agonists

A

dopamine and b1 agonists like dobutamine are infused IV to inc myocardial contractility in acute CHF

34
Q

b2 agonists

A

albuterol and pirbuterol relax vascular smooth muscle

-used only for acute failure or failure refractory to oral drugs

IC (31 decks)

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