During a cardiac cycle the cardiac walls change between contracted and relaxed and the valves open and close in response to pressure changes. This master thesis is a study of the changes in heart movement pattern caused by intravenous injections of Ca2+ or Nitroprusside. Radiopaque markers have been surgically implanted in the walls and in the mitral valve of ovine hearts and 3D coordinates for each marker have been constantly measured during the cardiac cycle. By using MatLab, the volume and pressure of the left ventricle and several parameters related to the opening kinematics of the mitral valve have been analyzed. The results show, among others, that both Ca2+ and Nitroprusside reduce the volume and pressure of the left ventricle and that both substances decrease the size of the mitral annular ring. It was also shown that Ca2+ delays the opening of the mitral valve.


During a cardiac cycle action potential in the cardiac walls cause the muscle fibres in the myocardium to contract, the space surrounded by the contracting wall decreases and blood is pushed through a valve into the next chamber. Leaflets in the valves open and close in response to pressure changes in order to let the blood through.

 Aims of this Master Thesis

The purpose of this thesis work is to, by the use of surgically implanted radiopaque markers, study the effect that Ca2+ and Sodium Nitroprusside (NIP) have on the opening kinematics of the mitral valve in an ovine heart. Parameters such as left ventricular pressure and volume, end-systolic-pressure-volume relationship, the curvature of the leaflets and different angles during opening will be analyzed and compared with negative controls.

Anatomy and Physiology


The heart has four chambers, two atria and two ventricles (fig. 2.1). The right atrium receives blood from three veins, the superior vena cava, the inferior vena cava and the coronary sinus, all bringing deoxygenated blood back from the tissues. Blood passes from the right atrium through the tricuspid (=three leaflets) valve into the right ventricle and further through the pulmonary valve into the pulmonary trunk. Via the pulmonary trunk the blood reaches the lungs where it is reoxygenated before it returns to the left atrium via four pulmonary veins. From the left atrium the oxygenated blood passes through the mitral valve (also called the bicuspid (=two leaflets) valve) into the left ventricle and further through the aortic valve into the aorta. The aorta divides into smaller arteries which carry the blood to all different tissues in the body. The valves connecting atria and ventricles are called atrioventricular, AV, valves whereas the valves connecting the ventricles with aorta (left) or the pulmonary trunk (right) are called semilunar, SL, valves.

The thickness of the myocardium of the four chambers varies according to the function of each chamber. The walls of the ventricles are thicker than the walls of the atria because the ventricles pump the blood a greater distance. Also, since more force is required to pump blood to all other parts of the body than is required to pump blood to the lungs, the myocardium of the left ventricle is thicker than that of the right ventricle. The valves of the heart are composed of dense connective tissue covered by endocardium. The cusps of the bi- and tri-cuspid valves are connected to tendon-like cords, called chordae tendineae, which, in turn, are connected to the top of cone-shaped trabeculae carneae, called papillary muscles.


The Cardiac Conduction System

The electrical activity in the heart is due to specialized cardiac muscle fibres that excite themselves, called autorythmic fibres. These fibres repeatedly generate action potentials that propagate through the conduction system and trigger heart contractions. The propagation sequence starts with cells in the sinoatrial (SA) node, located in the right atrial wall, depolarizing spontaneously to the threshold value. The depolarization triggers an action potential which propagates through both atria via gap junctions in the intercalated discs of atrial muscle fibres and causes the atria to contract.