Appendix 1: Physical Quantities for Selected Arteries
6.1 Overview of Cardiac Structure and Function .1 Cardiac Anatomy and the Cardiac Cycle
activity of the heart produces currentflow in the torso, which can be registered as the electrocardiogram (ECG).
The electrical activation of each cardiac cell admits a small amount of Ca2+, which triggers release of additional Ca2+ from intracellular stores. The resulting increase in intracellular Ca2+concentration engages contractile proteins in the cell, producing mechanical force.
Cardiac cells are arranged so that contraction of the tissue acts to increase the pressure in each chamber of the heart in turn, leading to opening of the valves and the pulsatile flow of blood around the circulation. The rate and strength of con- tractions is regulated so as to balance the delivery of oxygen and removal of CO2, notably during exercise. When this regulation is disturbed then the heart may not be able to meet metabolic demands, resulting in heart failure.
6.1 Overview of Cardiac Structure and Function
Ventricular contraction follows atrial contraction, and the deoxygenated blood is then pumped through the pulmonary valve and into the pulmonary arteries and pulmonary circulation. Oxygenated blood then returns from the pulmonary circu- lation through the pulmonary veins and into the left atrium (LA). As the atria contract, this blood is pumped into the left ventricle (LV) through the mitral valve.
Contraction of the LV then ejects the oxygenated blood through the aortic valve and into the systemic circulation.
Each heartbeat is therefore reliant on a sequence of events that include mechanical contraction, as well as the opening and closing of the valves in the correct order. The outcome is an increase of pressure in the aorta, which acts to produceflow of blood around the systemic circulation. Figure6.2illustrates typical pressures and volume in the left side of the human heart during each beat. Atrial systole (contraction) produces a rise in LA pressure,filling the LV through the open mitral valve. The onset of ventricular systole results in pressure rise within the LV.
Once LV pressure exceeds LA pressure, the mitral valve shuts, and when LV pressure exceeds pressure in the aorta the aortic valve opens. Blood is then ejected through the aortic valve, producing a pressure rise in the aorta. When LV pressure falls below aortic pressure the aortic valve closes, and when LV pressure falls below LA pressure the mitral valve opens.
LV volume Aortic pressure
LA pressure LV pressure Ejection
Isovolumic contraction
Isovolumic relaxation
Atrial systole
Ventricular diastole Ventricular
systole
Mitral valve closes
Aortic valve opens
Aortic valve closes
Mitral valve opens
0 90 13 0
LV volume (ml)Pressure (mm Hg) 0 40 80 12 0
Time (s)
0.5 1.0 1.5
Fig. 6.2 Cardiac cycle, showing changes in pressure and volume in different parts of the heart during two heart beats
6.1.2 Cardiac Cells and Tissue
The myocardium is a composite material, composed primarily of myocytes, fibroblasts and the extracellular matrix. Myocytes generate mechanical tension when stimulated electrically. Fibroblasts are connective tissue cells that act to regulate the extracellular matrix that supports the structures of the heart including the valves.
Cardiac myocytes are rod-shaped cells, 50–150 μm in length and 10–20μm in diameter. When stimulated electrically, a myocyte generates tension in the direction of its long axis, and individual myocytes are connected end to end into fibres (Fig.6.3a). The interface between adjacent cells has a characteristic stepped appearance and is called the intercalated disc. The intercalated discs contain gap junctions, which provide an electrical connection from one cell to its neighbour.
Cardiac myocytes may have more than one nucleus, and may also branch, so that an individual cell may have more than two neighbours.
In the ventricles, there is evidence that thesefibres are also arranged into sheets, and this orthotropic structure contributes to the passive and active mechanical properties of the tissue (Nielsen et al. 1991). Figure6.3a illustrates the typical arrangement of myocytes in tissue.
~20 μm Intercalated
disks Nucleus
Z-disk M-line Sarcomere T tubules Sarcoplasmic
reticulum Myocyte
Thick (myosin) filaments
Thin (actin) filaments
M-line Z-disk
Elastin (titin) filaments
~2 μm Myofibril
(a)
(c) (b)
Fig. 6.3 Structure of cardiac tissue and myocytes. a Arrangement of cardiac myocytes and connections between them.bInternal structure of myocyte.cDiagram showing the contractile apparatus within a myofibril
Myocytes are also composed of striated myofibrils (Fig.6.3b). Each myofibril consists of chains of sarcomeres, each about 2μm long, which are terminated at each end by a Z-disc. These Z discs provide an anchor for the thinfilaments, which engage with thick filaments to generate tension (Fig.6.3c). The mechanism of tension generation is described in more detail in Sect.6.3.
A valve plane separates the electrically excitable atria and ventricles. It is composed of connective tissue and provides a mechanical anchor for the valves.
The connective tissue is electrically inexcitable, and is penetrated only by the atrioventricular node (see below).
6.1.3 Myocardial Perfusion and Metabolism
The heart itself requires a supply of oxygenated blood in order for its metabolic needs to be met, and has its own system of arteries and veins. A branching network of coronary arteries is perfused from left and right branches, which connect to the aorta very close to the aortic valve. The main branches of the coronary arteries remain on the epicardial surface, and smaller vessels penetrate the myocardium. If a coronary artery develops a significant stenosis, then the region of myocardium perfused by that artery may become ischaemic. Ischaemia describes the changes in cell metabolism resulting from a reduction or interruption of the supply of oxy- genated blood. These changes include altered electrical excitability, and reduced contractility. Prolonged or severe ischaemia resulting from complete blockage of a coronary artery will result in a myocardial infarction. Unless bloodflow is restored quickly, the ischaemic region of myocardium will undergo irreversible cell death.
Ultimately the region will become scar tissue, with impaired mechanical function.
Venous blood collects in the coronary sinus, which is located around the pos- terior of the heart, close to the valve plane. The coronary sinus drains into the right atrium.