Heart Failure, Part 2. Preload

A major function of the heart – pumping blood in the aorta and truncus pulmonalis – can be evaluated by measurement of cardiac output (CO), and it can be done in different ways (discussion of methods of CO calculation is beyond the scope of Pathology). For us, it is enough to understand that CO directly depends on stroke volume (SV) and heart rate (HR). There is another integrated indicator of cardiac function: cardiac index, which is more reflective toward an individual patient and, therefore, more preferable in the clinical settings.

There are three, well known from the course of physiology, primary mechnasims that regulate stroke volume: preload, afterload and contractility.

Preload corresponds to diastolic filling of the chambers and stretching of the cardiac wall. The key factor that affects preload is central venous pressure, which goes up with sympathetic vasoconstriction. According to famous Frank-Starling law, as more stretched the myocardium is, as higher stroke volume will be. In this situation we can find stronger contraction of cardiomyocytes. (Do not confuse stronger contraction with enhanced contractility because, according to definitions, contractility corresponds to changes in the force generated by the myocardium at the non-changing diastolic filling).

Impaired preload. When a chamber cannot accommodate the required amount of blood, stroke volume and cardiac output will decline and, subsequently, heart failure will follow. There are few mechanisms of preload impairment reduction):
- Decreased myocardial compliance (insufficient myocardial relaxation) seen in

   • Ventricular hypertrophy (left or right), because hypertrophied myocardium fails to relax properly during diastole

   • Hypertrophic and restrictive cardiomyopathy due to hypertrophy and sclerosis of the myocardium
- Obstruction of a chamber inflow
   • Valvular stenosis, e.g., mitral stenosis that leads to preload reduction of the left ventricle

- Compression of the heart within the pericardic sac (cardiac tamponade)

   • Pronounced hydropericardium or exudative pericarditis
   • Acute MI with ventricular wall rupture
- Decreased venous blood pressure, usually associated with hypovolemia
- Impaired atrial contraction in atrial fibrillation

Limitations of Frank-Starling law. In the chart below you can see how end diastolic volume affects stroke volume. In healthy people (blue line), EDV increase leads to gradual elevation of SV, which reach plateau at EDV ≈ 200 ml. In patients with heart failure (pink line), we see similar dynamics, but after certain point (EDV ≈ 200 ml) SV goes down (= further EDV increase will reduce SV). Interpretation of these findings will lead us to the conclusion that in patients with an advanced heart failure, when diastolic filling is significantly elevated, Frank-Starling law does not work, and less amount of blood will be pumped out.

To be continued tomorrow