Heart Failure

Heart failure refers to a condition where the heart is unable to adequately pump blood to the body.  There are many causes of heart failure including but not limited to myocardial infarction, hypertension, diabetes, pulmonary hypertension, stress cardiomyopathy, and valve disorders.  Heart failure generally results in fluid accumulation in the body and/or lungs.  Fluid accumulation in the body results in edema of the extremities or abdomen. Fluid accumulation in the lungs can cause shortness of breath, cough, and low oxygen levels.  

Treatment of heart failure depends on prevention of cardiac remodeling, management of fluid volume, improving contractility, and reducing workload.

Treatment Strategies

Prevention of Cardiac Remodeling

The use of beta-blockers at the surface may seem counterintuitive, but by considering the physiologic effects of beta-blockers, their resulting improvement in survival becomes apparent.  Beta-blockers prevent remodeling of cardiac muscle structure.  This effect is thought to be from blunting of the response to sympathetic nervous system activation.  Norepinephrine causes hypertrophy and remodeling of cardiac muscle. By inhibiting the effects of norepinephrine by blocking beta receptors, beta-blockers reduce remodeling.  In addition, beta-blockers reduce heart rate and release of renin to the kidneys, which also improves long-term survival in patients with heart failure.  

Angiotensin II and aldosterone both cause cardiac remodeling. By lowering angiotensin II and aldosterone levels, cardiac remodeling decreases.  ACE inhibitors are the primary drugs used for this effect.

Reduction of Workload

Increased preload and afterload stress the heart and result in worsening heart failure symptoms.  Increased preload and afterload are the result of sodium and water retention.  In heart failure, decreased renal blood pressure and perfusion results in the increase of renin. Renin release activates the renin-angiotensin-aldosterone system, which results in release of angiotensin II and aldosterone. These hormones promote the retention of sodium and vasoconstriction, which increases preload and afterload on the failing heart.  The failing heart has difficulty compensating for the increased demand.  By reducing the demand induced by the poor renal perfusion, heart failure symptoms improve. Reducing this demand is accomplished through inhibition of the renin-angiotensin-aldosterone system. 

The first line medication in blunting the response to reduced renal perfusion is with ACE inhibitors. ACE inhibitors cause decreased levels of angiotensin II, bradykinin, and aldosterone by decreasing the conversion of angiotensin I to angiotensin II.  Angiotensin receptor blockers are used in patients with intolerance of ACE inhibitors due to angioedema or cough. 

Management of Fluid Volume

Excess fluid places increased demand on the heart and results in fluid accumulation in tissues including the lungs.  Fluid and sodium restriction are mainstays in treatment of heart failure.  Medication management of fluid volume is also important.  Diuretics are used to manage fluid volume. Loop diuretics are commonly used but must be monitored closely to avoid over diuresis.  Vasodilators can also improve preload stress placed on the heart. Vasodilators allow for a fluid sink. Nitrates are used commonly to reduce preload. Hydralazine is an arteriolar dilator, which can help reduce afterload.  

Contractility

Improving the function of cardiac muscle fibers will also improve heart failure symptoms by improving cardiac output.  Digoxin is the only medication aimed at improving heart failure symptoms that is used chronically. All other agents used to treat heart failure by improving contractility have been associated with worsened survival so are only used in the acute setting.  

Digitalis is unique because is allows for increased contractility at low doses (raises intracellular calcium by inhibiting the sodium-potassium-adenosine triphosphatase enzyme exchanger) while slowing heart rate through increased vagal tone and inhibition of sympathetic activation of the heart.  These factors combine to allow for reduced hospitalizations and survivability.  

Dopamine and dobutamine can be used short-term in the hospital setting to improve contractility but must be given IV.