2.2 Clinical Features
A 58-year-old German woman had undergone surgery in 1974 to fix a mitral stenosis.1 She later developed a restenosis, which caused the mitral valve to leak. She underwent surgery in November 1982 to replace her natural mitral valve with a Björk-Shiley convexo-concave mitral prosthesis.2
In July 1992, she suffered sudden and severe difficulty breathing and was admitted to the hospital in her hometown in Germany. She had fluid in her lungs, and the diagnosis was that she had a serious hemodynamic disturbance due to inadequate heart function (cardiogenic shock). The physician listened for heart sounds but did not hear the normal "click" associated with a prosthetic valve. The patient's heart rate was 150 bpm, her systolic blood pressure was 50 mmHg, and her arterial oxygen saturation was 78 percent. Echocardiography3 was performed, and no valve disk was seen inside the valve ring. An x-ray (see Fig. 2.1) appeared to show the valve disk in the abdominal aorta and the outflow strut in the pulmonary vein. Emergency surgery was performed, the disk and outflow strut were removed, and a new Medtronic-Hall mitral valve prosthesis was implanted into the woman. She eventually recovered.
1Narrowing or stricture.
2Artificial body part.
3Graphically recording the position and motion of the heart walls and internal structures.
The cardiovascular system can be further divided into three subsystems. The systemic circulation, the pulmonary circulation, and the coronary circulation are the subsystems that, along with the heart and lungs, make up the cardiovascular system. See Fig. 2.2.
The three systems can be divided functionally based on the tissue to which they supply oxygenated blood. The systemic circulation is the subsystem supplied by the aorta that feeds the systemic capillaries. The pulmonary circulation is the subsystem supplied by the pulmonary artery that feeds the pulmonary capillaries. The coronary circulation is the specialized blood supply that perfuses cardiac muscle. (Perfuse means to push or pour a substance or fluid through a body part or tissue.)
The cardiovascular system has four basic functions:
1. It supplies oxygen to body tissues.
2. It supplies nutrients to those same tissues.
Figure 2.2 Pulmonary circulation and systemic circulation.
Figure 2.2 Pulmonary circulation and systemic circulation.
3. It removes carbon dioxide and other wastes from the body.
The path of blood flowing through the circulatory system and the pressures of the blood at various points along the path tell us much about how tissue is perfused with oxygen. The left heart supplies oxygenated blood to the aorta at a relatively high pressure.
Blood continues to flow along the path through the circulatory system, and its path may be described as follows: Blood flows into smaller arteries and finally into systemic capillaries where oxygen is supplied to the surrounding tissues. At the same time, it picks up waste carbon dioxide from that same tissue and continues flowing into the veins. Eventually, the blood returns to the vena cava. From the vena cava, deoxygenated blood flows into the right heart. From the right heart, the still deoxygenated blood flows into the pulmonary artery. The pulmonary artery supplies blood to the lungs where carbon dioxide is exchanged with oxygen. The blood, which has been enriched with oxygen, flows from the lungs through the pulmonary veins and back to the left heart.
It is interesting to note that blood flowing through the pulmonary artery is deoxygenated and blood flowing through the pulmonary vein is oxygenated. Although systemic arteries carry oxygenated blood, it is a mistake to think of arteries only as vessels that carry oxygenated blood. A more appropriate distinction between arteries and veins is that arteries carry blood at a relatively higher pressure than the pressure within the corresponding veins.
The heart is a four-chambered pump and supplies the force that drives blood through the circulatory system. The four chambers can be broken down into two upper chambers, known as atria, and two lower chambers, known as ventricles. Check valves between the chambers ensure that the blood moves in only one direction and enables the pressure in the aorta, for example, to be much higher than the pressure in the lungs, restricting blood from flowing backward from the aorta toward the lungs.
The four chambers of the heart, namely, the right atrium, right ventricle, left atrium, and left ventricle, are shown in Fig. 2.3. Blood enters the right atrium from the vena cava. From the right atrium, blood is pumped into the right ventricle. From the right ventricle, blood is pumped downstream through the pulmonary artery to the lungs where it is enriched with oxygen and gives up carbon dioxide.
On the left side of the heart, oxygen-enriched blood enters the left atrium from the pulmonary vein. When the left atrium contracts, it
pumps blood into the left ventricle. When the left ventricle contracts, it pumps blood to a relatively high pressure, ejecting it from the left ventricle into the aorta.
The myocardium, or muscle tissue of the heart, is composed of millions of elongated, striated, multinucleated cardiac muscle cells. These cells are approximately 15 microns by 15 microns by 150 microns long and can be depolarized and repolarized like skeletal muscle cells. The meaning of the terms "depolarized" and "repolarized" will be explained in the next section. Figure 2.4 shows a typical group of myocardial muscle cells. Individual cardiac muscle cells are interconnected by dense structures known as intercalated disks. The cells form a latticework of muscular tissue known as a syncytium.
A multinucleated mass of cardiac muscle cells form a functional syncytium (pronounced sin—sish' e-um). The heart has two separate muscle
syncytia. The first is the muscle mass that makes up the two atria, and the second is the muscle mass that makes up the two ventricles. The two syncytia are separated by fibrous rings that surround the valves between atria and ventricles. When one muscle mass is stimulated, the action potential spreads over the entire syncytium. As a result, under normal circumstances, both atria contract simultaneously and both ventricles contract simultaneously.
Contraction in myocardium takes 10 to 15 times longer than it takes in average skeletal muscle. Myocardium contracts more slowly because sodium/calcium channels in myocardium are much slower than the sodium channel in skeletal muscle, during repolarization. In addition, immediately after the onset of the action potential, the permeability of cardiac muscle membrane for potassium ions decreases about fivefold. This effect does not happen in skeletal muscle. This decrease in permeability prevents a quick return of the action potential to its resting level.
Heart muscles operate due to electrical voltages which build up and diminish in the individual muscle cells. The cellular membranes of myocardial cells are electrically polarized in the resting state like any other cells in the body. The resting, transmural electrical potential difference, is approximately —90 mV in ventricular cells. The inside
of the cell is negative with respect to the outside. This transmembrane potential exists because the cell membrane is selectively permeable to charged particles. Figure 2.5 shows the transmembrane resting potential in a cardiac cell.
The principal electrolyte ions inside myocardial cells, which are responsible for the transmembrane potential, are sodium, potassium, and chloride. Negative ions, or anions, associated with proteins and other large molecules are also very important for the membrane potential. They attract the positive potassium ion that can go inside the cell.
The permeability of the membrane to sodium ions is very low at rest, and the ions cannot easily pass through the membrane. On the other hand, permeability of the membrane with respect to both potassium and chloride ions is much higher, and those ions can pass relatively easily through the membrane. Since sodium ions cannot get inside the cell and the concentration of positively charged sodium ions is higher outside the cell, a net negative electrical potential results across the cell membrane.
The net negative charge inside the cell also causes potassium to concentrate inside the cell to counterbalance the transmembrane potential difference. However, the osmotic pressure caused by the high concentration of potassium prevents a total balancing of the electrical potential across the membrane.
Since some sodium continually leaks into the cell, maintaining a steady-state balance requires continual active transport. An active sodium-potassium pump in the cell membrane uses energy to pump sodium out of the cell and potassium into the cell.
Excitability is the ability of a cell to respond to an external excitation. When the cell becomes excited, the membrane permeability changes,
allowing sodium to freely flow into the cell. In order to maintain equilibrium, potassium, which is at a higher concentration inside the cell, flows to the outside. In Fig. 2.6, a cardiac muscle cell is shown depolarizing.
In order to obtain a regulated depolarization, it is crucial that the increases in sodium and potassium permeabilities are offset in time. The sodium permeability must increase at the beginning of depolarization, and the potassium channel permeability increases during repolarization. It is also important that the potassium channels that open during an action potential are different from the leak channels that allow potassium to pass through the membrane at rest. In cardiac muscle, the action potential, or biopotential that results in muscle movement, is carried mainly by calcium from the extracellular space rather than by sodium. This calcium is then used to trigger the release of intracellular calcium to initiate contraction.
The ability of a cell to respond to excitation depends on the elapsed time since the last contraction of that cell. The heart will not respond to a new stimulation until it has recovered from the previous stimulation. That is, if you apply stimulation below the threshold before the non-responsive or refractory period has passed, the cell will not give a response. In Fig. 2.7, the effective refractory period (ERP) for a myocardial cell is shown to be approximately 200 ms. After the relative refractory period (RRP), the cell is able to respond to stimulation if the stimulation is large enough. The time for the relative refractory period in the myocardium is approximately another 50 ms.
During a short period following the refractory period, a period of super-normality (SNP) occurs. During the period of supernormality, the cell's transmembrane potential is slightly higher than its resting potential.
The refractory period in heart muscle is much longer than in skeletal muscle, because repolarization is much slower. Ventricular muscle in dogs has a refractory period of 250 to 300 ms at normal heart rates. The refractory period for mammalian skeletal muscle is 2 to 4 ms and 0.05 ms for mammalian nerve fiber.
Action +20 potential
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