VENTRICULAR DILATATION

· Regardless of the initiating factor, dilatation is adaptive as the cardiac muscle stretches:

1. increasing volumes of blood can be accommodated in the stressed chamber

2. the dilated fibres will contract more forcefully than normal myocardial tissue (Frank-Starling law)

· Dilatation is adaptive and beneficial only up to a point. If tissue is stretched excessively, compensation value is lost as contraction force actually declines

· Acute ventricular distension, as seen during CPB, will lead to increased LV end diastolic pressures and subsequent decrease in subendocardial perfusion

· Chronic volume loading leads to eccentric hypertrophy [the heat dilates and, because of increased chamber size, assumes an eccentric position in the chest]

AETIOLOGIES OF VENTRICULAR DILATATION

Causative factor	Pathological mechanisms
Hypertension	Increased arterial blood pressure poses resistance to the ejection of blood from the left ventricle
Left-to-right shunt	Left to right shunt is characterised by abnormal flux of blood from left to right cardiac chambers
Valvular disease	Valvular stenosis/regurgitation (particularly regurgitation: eccentric hypertrophy) causes excessive accumulation of blood in certain cardiac chambers
Hypervolaemia	Excess extracellular fluid increases venous return to right side of heart
Ischaemic	Common, due to impaired functioning of myofibrils reducing contractility and subsequent cardiac output causing fluid retention in an effort to increase venous return and concomitantly cardiac output.
Rheumatic
Idiopathic (largely viral)
Pulmonary disease	Constriction of the blood vessels of the lungs (associated with lung disease) increases resistance to ejection of blood to right side of heart
CPB	i) Inadequate venous drainage ii) Aortic regurgitation ± VF