Rush Center for Congenital
and Structural Heart Disease

 

Definition

The inability of the heart to generate enough cardiac output to meet the body's demands.  This could be caused by:

 + Increase workload on an otherwise normal myocardium:


 - Expanded blood volume such as with anemia.
 - Left to right shunting of blood, such as with AV fistula or septal defects (ASD, VSD, PDA and AVC defect).  This will cause already oxygenated blood in the left heart to return to the right heart.  The result is decrease in the left ventricular cardiac output and increase in the right ventricle cardiac output.  The decrease cardiac output from the left ventricle will cause poor blood supply to the body, while the increase cardiac output from the right ventricle will cause work overload of the right ventricular myocardium.  An expanded right ventricle will also cause abnormal leftward deviation of the ventricular septum (flattening) resulting in abnormal left ventricular contour and further reduction of ejection capabilities.
 - Valvar regurgitation, causing volume overload of the ventricle.

Normal blood flow, normal cardiac chambers.
Cardiac Output is measured in liters/minute/M2 of body surface area.  A normal cardiac output is 2.5-3 l/min/M2

Expanded blood volume due to anemia, or AV fistula will result in larger cardiac output.  A cardiac output of 4-5 l/min/M2 will result in dilation and eventually failure of both right and left ventricles.
 + Pressure overload of one or both ventricles

Such as with valvular diseases (pulmonary or artic stenoses), coarctation of the aorta, pulmonary vascular obstructive disease or systemic hypertension.

 + Cardiac myocardial disease such as with myocarditis and cardiomyopathy.

 

Poor LV function, compare with normal LV function below

Normal LV function
 + Coronary arterial insufficiency, such as with Kawaski disease and hyperlipdemia.
 + Abnormal heart rhythm, typically tachycardia.
Rapid heart rate will prevent proper filling of the ventricles as it shortens diastole, thus reducing cardiac output.
 
Atrial flutter with 2:1 block.  Rapid heart rate for prolonged period of time can cause poor heart function as noted in the echo movie clip above.

 

Pathophysiology

Symptoms

Regardless of the cause, children and particularly infants will be short of breath, feed poorly and fail to thrive.  With exertion, such as suckling, they will become pale and sweat profusely.  The heart will eventually dilate and the elevated LV and RV end-diastolic pressures will cause pulmonary edema and hepatomegaly respectively.  Pulmonary edema will result in tachypnea, while GI edema will lead to worsening absorbtion and further failure to thrive.

Signs

Inspection:  Pallor, respiratory distress, elevated JVP (not possible to assess in infants & young children).
Palpation:  edema, poor capillary refill, poor pulses, hepatomegaly, cardiomegaly, increase RV and/or LV impulses.
Auscultation: gallop rhythm, murmur if associated with CHD or AV valve insufficiency due to ventricular dilation. 

 

Treatment

First, attention should be directed to cause and if possible treated.

Supportive therapy: 

Supportive treatment of heart failure is to reduce the workload on the heart and improve myocardial function.  this is done through:

Reduce pre-load: reducing the blood volume through diuretic therapy will reduce the burden on the heart as it will have to pump less blood.
Reduce after-load:  Reducing the systemic vascular resistance (through vasodilation) will reduce the effort needed by the heart to pump blood.
Improve myocardial contractility:  Pharmacological agents such as digoxin, or intravenous agents such as milrinone can improve myocardial contractility as well as reduce the energy needed to perform same function.