Cardiac output is the volume of blood ejected by one ventricle during a eriod of 1 min. It depends on both heart rate and stroke volume. A 70-kg adult will have a stroke volume of 70 to 80 ml and a heart rate of 65 to 75 beats/min and so a cardiac output of approximately 5 l/min (75 ml * 70 beats/min). This may vary considerably.
Heart rate is determined both by the intrinsic electrical properties of the heart and cardiac muscle fibres and by extrinsic influences provided mostly by vagal and sympathetic innervation. Stroke volume is also determined by the intrinsic properties of cardiac muscle and by extrinsic influences (neural, hormonal, and chemical).
Two opposing factors determine stroke volume: the energy of contraction of the myocytes and the arterial pressure against which blood must be expelled. The energy of contraction depends on the following:
1. the degree of stretch of the myocytes during diastole;
2. the intrinsic strength of contraction (the contractility) of the myocytes for a given degree of stretch during diastole. Contractility is largely influenced by extrinsic factors (neural, hormonal, and chemical).
The microscopic architecture of actin and myosin in skeletal and cardiac muscle is such that maximum contractile energy is only generated at a length of 2.2 to 2.3 ^m. Under resting conditions, at the end of diastole, sarcomere lengths are suboptimal (usually below 2 ^m). Stretching the sarcomeres will improve their contraction. Sarcomeres are stretched when ventricular filling is increased before systole. Thus force of contraction tends to increase with an increase in end-diastolic volume. This principle has become known as Starling's law of the heart. This can be represented graphically by a Starling curve, also known as a ventricular function curve (Fig 1).
Fig. 1 Ventricular function curve (Starling curve). This is applied to any graph whose ordinate is a measure of contractile energy (e.g. stroke volume or stroke work) and whose abscissa is an index of resting fiber length (e.g. end-diastolic volume, filling pressure, or end-diastolic pressure).
The ventricles are approximately spherical pumps. The internal pressure within a sphere is proportional to wall tension and inversely proportional to its radius (Laplace's law). As the radius increases the curvature of the wall decreases. Less of the wall tension is directed towards the cavity and so less pressure is generated. This contradicts Starling's law of the heart. However, within the normal size range of the ventricles the improved performance of the myocytes induced by stretching them (and reducing the curvature of the sphere) outweighs the mechanical disadvantage of an enlarged ventricle. Beyond a certain limit pathological ventricular distension results in greatly reduced mechanical efficiency and the typical dilated 'failing' heart.
As well as ventricular filling (end-diastolic volume), arterial pressure is an important intrinsic determinant of stroke volume. This can be understood by examining the mechanics of cardiac contraction:
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