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first-line treatment for Heart Failure (CHF). ( pg 250-254, 273)

**Ace inhibitors **-   captopril (capoten), enalpril ( vasotec), lisinopril ( Prinivil or Zestril), ramipril ( altace), trandolapril ( mavik)should be prescribed to all patients with heart failure unless contraindicated

ARB’s-  candesartan ( atacand), valsartan( diovan) should be used if ACE inhibitors are intolerant to patient

Beta blockers – bisoprolol ( zebeta), carvediol ( coreg), metroprolol (Lopressor),  are the recommended agents ( all patients with stable mild severe HF

Digoxin (lanoxin), hydralazine

Lasix ( furosemide)- fluid overload

Thiazide diuretics (NaCl inhibitors) – hydrochlorthiazide ( hydroDIURIL)

Potassium sparing diuretic- Aldosterone antagonist -spironalctone 9 aldactone), eplerenone (inspra),

 It can be used for NYHA stage I or before any onset of HF symptoms. It regresses ventricular hypertrophy, modify cardiac remodeling, and useful for HFpEF and HFrEF. I also wanted to say diuretics based on several articles.

Also depends on the co morbities

  • treatment of acute heart failure and pulmonary edema. ( pg 250-254, 25, 37, 249)
  • Nitrates, diuretics, morphine:  
    Nitroprusside- vasodilator  
    Nesiritride- atrial peptide , vasodilator and diuretic 
    L – loop 
    M – morphine  
    N -nitrates 
    O – oxygen 
    P – positioning 
    IV loop diuretics 
    – Cause venodilation and diuresis – Reduces pre-load 
    IV opiates (e.g. morphine) 
    – Reduce anxiety 
    – Vasodilates, reducing preload  
    – Reduces sympathetic drive  
    – Not routinely offered 
    IV, buccal or sublingual nitrates (Glyceryl trinitrates “GTN”) 
    – Reduce preload and afterload  
    – vasodilates 
    Oxygen >> maintains O2 sats  
    (Positioning – keep patient upright) 
  • cardiogenic 
    decreased preload, decrease afterload, inc o2 
    inc o2 
    CPAP, BiPAP 
    dec preload 
    nitroglycerin, loop diuretics (furosemide, bumetanide) 
    dec afterload 
    nitroprusside, ACEi/ARB 
    treat underlying cause, mechanical ventilation
  • side effects of ACE inhibitors and mechanism of action of ACE inhibitors. (pg. 279, 274-275)
  • side effectscough (change to an ARB) Angioedema, rash, diaphoresis, angioedema, cough, abdominal pain, leukopenia, myalgia, headache, renal insufficiency. INCREASES creatinine, hyperkalemia, hypotension. Teratogen (fetal renal malformations)
  • MOA- inhibits angiotensin converting enzyme, interfering with conversion of angiotension I to angiotensin II. ACE inhibitors inhibit the breakdown of bradykinin a potent and naturally occurring vasodilator by blocking the enzyme kininase II. This is thought to be the cause of the cough commonly experienced by patients who take this class of drugs.
  • Uses: HTN, Chronic HF, Prevention of renal failure in diabetes

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