In heart failure, the heart fails to pump enough blood to maintain sufficient blood flow throughout the body.
The goal of the heart is to maintain the cardiac output, which is the amount of blood which is pumped by the heart in one minute. Our body tries to compensate by 
  1. Increasing the heart rate. 
  2. Activating the Renin-Angiotensin-Aldosterone-System (RAAS), which cause an increase in blood volume and vasodilatation. 
  3. Sympathetic activation, which causes tachycardia and cardiac remolding. 
  4. The release of BNP, in response to stretch of cardiac muscle which causes natriuresis and inhibition of aldosterone.
These compensatory mechanisms increase the load on the failing heart. Our goal is to inhibit these compensatory mechanisms to decrease the further load on the failing heart which these compensatory mechanisms (especially activation of RAAS and sympathetic system) put. The BNP release is not enough in the presence of activated RAAS. 
Thus, 
  1. we will inhibit the RAAS by an ACEi or ARB (e.g Enalapril, Ramipril, Valsartan or Candesartan). 
  2. Give a maximum tolerated dose of a beta blocker, gradually titrated if there are no signs of fluid overload (that is after management of acute exacerbation with diuretics, but will start as soon as possible) (Carvedilol, Metoprolol or Bisoprolol are preferred)
  3. Give diuretics to manage the fluid overload and acute exacerbation. Thiazide diuretics to manage mild fluid overload and loop diuretics to manage severe heart failure and acute exacerbations. (Hydrochlorothiazide, Furosemide, Torsemide)
  4. An aldosterone antagonist such as spironolactone or eplerenone should be a part of the standard therapy for heart failure i.e, (ACEi/ARB + Beta-blocker + Spironolactone/eplerenone), because it has shown to decrease mortality by 29%. 
  5. If symptoms are not controlled by the above medications then will consider any one of the following, per patient's need.
  6. Give a Neprilysin inhibitor such as sacubitril, which inhibit degradation of BNP, which further decrease the blood volume by counteracting the RAAS, and decrease the mortality by 20% as compared to ACEi (enalapril) alone. Try to switch the ACEi or ARB alone to Valsartan-Sacubitril if a patient can tolerate it.
  7. Decrease the heart rate by (if EF still < 35%) Ivabradine if the maximum tolerated dose of beta-blockers alone not able to control the symptoms and if patient's heart rate is more than 70.  
  8. Consider adding digoxin if rate control is needed, and the patient has atrial fibrillation. 
  9. Hydralazine, Nitrates or their combination is preferred in African-Americans (because ACEi/ARBs are less effective in African-Americans) or if symptoms are not controlled with ARBs/ACEis and the EF is still < 35%. There is high risk of hypotension with these and are difficult to tolerate, Monitor closely. 
  10. Consider adding Cardiac resynchronization therapy if the patient has conduction defects such as LBBB, QRS width > 120msec and EF < 35%.
  11. Consider ICD placement if the patient has a history of MI or arrhythmias with EF < 35
    %.
  12. Anticoagulation has no added benefit, except in patients with acute MI, where it should be given for 3 months if not contraindicated. 
  13. Reassess the symptoms if controlled, consider decreasing the dose of diuretics. 
  14. If nothing from above work consider, palliative care, cardiac transplantation, left ventricular assist device or drugs or devices under investigation.
Date Updated: 31st March 2018 by Dr. Adil Ramzan

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