CHF includes cardiovascular response to inadequate perfusion and series of neurohormonal response in addition to structural abnormality. The systemic response to compensate for inadequacy is to increase cardiac output. Cardiac output is determined by heart rate and stroke volume. Additionally, stroke volume is influenced by three factors; contractility, preload (the volume of blood in the left ventricle at the end of a diastole), and afterload (pressure of resistance the ventricles must overcome to eject blood during systole).
Preload is assessed by measuring the right atrial pressure and is affected by any restriction. The example that Figueroa & Peters (2006) provides is an increase in positive pleural pressure (seen in COPD or asthma) will reduce ventricular filling. The compensatory mechanism that responds to the decrease preload by decreasing stretch is called the Frank-Starling law. The optimal filling pressure is between 10-12mmHg. The force of ventricular contraction will decrease when the pressure exceeds 12mmHg and the myocardial fibers are overstretched. A prolonged decrease force of contraction will lead to heart failure.
Contractility is the force generated by contracting myocardium and is expressed as the ejection fraction. The contraction of the myocardium depends on the ability of the ventricular muscle fibers. Structure of the heart such as valvular abnormalities can affect contractility. According to Figueroa & Peters (2006),” A heart with normal systolic function will maintain an ejection fraction over 50-55%.” As mentioned before, overstretching the myocardial fibers will lead to heart failure.
Afterload is the pressure or resistance the ventricles need to overcome to eject blood during systole and is assessed by the mean arterial pressure. According to Figueroa & Peters (2006), afterload represents three factors that are impaired in CHF patients; vascular resistance, wall tension, and intrathoracic pressure. (Osborn, 2014 p901-903)
When cardiac output action is compromised, the sympathetic nervous system and renin-angiotensin-aldosterone system is activated. The activation of the sympathetic nervous system releases norepinephrine, which causes vasoconstriction in an attempt to increase ventricular preload. Myocardial contractility and heart rate increases to increase cardiac output. Circulating levels will increase fluid retention by increasing sodium absorption of the kidney. The increased intravascular volume will improve blood pressure and cardiac output. An additional function of norepinephrine allows renal vasoconstriction that maintains the glomerular filtration at a stable rate despite decreased renal perfusion. However, these mechanisms cannot be maintained extensively because it causes cardiac wall stress by constantly increasing pressure. Effects of long term maintenance inclu