Geert Kleinnibbelink

Chapter 1 16 scenarios. 10 These anatomical differences between ventricles originate fromembryological development and the substantially different haemodynamic loading conditions faced. In addition to anatomical differences, function of the left and right sidemay differ. Function of the ventricles is defined as the ability of the heart to meet the metabolic demands of the body which is reflected by the cardiac output (CO). The CO is defined by the volume of blood which is pumped out per minute by the ventricles and can be calculated by multiplying stroke volume (SV) (the amount of blood ejected by each ventricle every contraction (end-diastolic volume [EDV] minus end-systolic volume [ESV])) by heart rate (HR). Mathematically is this represented by following equations: Cardiac output (CO) = Stroke volume (SV) × Heart rate (HR) Stroke volume (SV) = End-diastolic volume (EDV) – end-systolic volume (ESV) Both ventricles, left and right, serve as the primary pumping chambers of the heart serving both separate, but linked circulations. Under resting conditions, both the RV and LV pump out 5-6 L blood per minute. The RV serves as pump for the pulmonary circulation where it transports blood to and from the lungs to deliver carbon dioxide for exhalation and to pick up oxygen. The LV serves as a pump for the systemic circulation to deliver oxygenated blood to all tissues of the body. Despite the fact that pulmonary and systemic are separate circulations, both RV and LV pump the same amount of blood since both are serially linked. As mentioned above, the CO is the product of HR and SV. The major factors who are influencing SV, and so cardiac function, are preload, afterload and contractility. Preload is defined as end-diastolic ventricular wall stress or stretch which is directly proportional to EDV. The higher EDV, the more cardiac muscle sarcomeres will stretch resulting in proportional increase in contractility until a certain optimum. The relationship between ventricular stretch and contraction is also known as the Frank-Starling mechanism. Preload is mainly driven by the venous return. Although both RV and LV receive the same amount of blood, as the pulmonary and systemic circulation are serially linked, their preload differs due to their different geometry and mass resulting in different end-diastolic wall stress per unit area myocardium.