Cardiac Output

Cardiac output is the amount of blood ejected by the ventricles per minute. It is the product of stroke volume (the amount of blood ejected by the ventricles per beat) and the heart rate. The cardiac output cannot exceed the rate of venous return to it and therefore factors governing venous return are primarily responsible for cardiac output. Other factors include afterload, contractility, stroke volume and heart rate. Preload or venous return is the force distending the ventricle. The greater the stretch, the greater the force of contraction. This mechanism is known as Frank Starling mechanism. It occurs before stretching the myofibrils results in more efficient creation of cross bridges between the contractile proteins. Thus, an increase in the distension of the ventricle will result in an increase in the force of contraction sufficient to pump the extra volume. An increase in preload will result in an increase in cardiac output. Afterload or total peripheral resistance is the force against which the ventricles must act in order to eject blood. This largely depends on vascular resistance; however; it also contains a component of myocardial stiffening. Increasing afterload increases myocardial oxygen consumption and may decrease stroke volume eventually decreasing cardiac output. Contractility is the strength of the force of myocardial contraction. The degree of contractility is also known as ionotropic state. A positive ionoresponse is an increase in contractility. When contractility is reduced, stroke volume will fall which eventually causes a fall in cardiac output. Stroke volume which is the amount of blood ejected by the ventricles per beat has a direct control on cardiac output. The ejection fraction is the proportion of the stroke volume which s ejected. Stroke volume is determined by volume and pressure of the blood filling the ventricles (preload), resistance to ejection (afterload) and myocell shortening (contractility). volume overload by Valsalva manoeuvre or isotonic exercise learning eventually increases cardiac output. Herat rate is controlled by balance of parasympathetic and sympathetic innervation. An increase in heart rate is known as positive chronotropic state (tachycardia) while a decrease of heart rate id known as negative chronotropic state (bradycardia). When the sympathetic system acts on increasing the heart rate, this eventually increases the cardiac output and vice versa for the parasympathetic system.

The Frank-Starling law of the heart states that stroke volume increases with an increase in the volume of blood in the ventricles before contraction (end diastolic volume) when all other factors remain constant. Increasing afterload or decreasing inotropy (force of contraction) shifts the curve down and to the right whereas decreasing afterload or increasing inotropy shifts the curve up and to the left results in a higher stroke volume. Increased venous return increases the ventricular filling (end diastolic volume) and therefore preload which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increase the sarcomere length, which increase in force generation and enables the heart to eject the additional venous return, thereby increasing the stroke volume. This phenomenon can be described in mechanical terms by length-tension and force- velocity relationships of cardiac muscle. Increasing preload increases the active tension developed by the muscle fibre and increases velocity of fibre shortening at a given afterload and ionotropic state. One mechanism to explain how preload influences contractile force is increasing the sarcomere length increases troponin C calcium sensitivity which increases the rate of cross bridge attachment and detachment and the amount of tension developed by the muscle fibre. The effect is increased sarcomere length on the contractile proteins is termed length- dependent activation.

Oedema occurs when and excessive volume of fluid accumulates in the tissues either within cells (cellular edema) or in the interstitial spaces (interstitial oedema).Interstitial oedema may occur as a result of imbalance between hydrostatic (which may be increased),