7- Functional anatomy and mechanical properties of heart

7- Functional anatomy and mechanical properties of heart
Heart chambers:
The heart acts as two separate pumps, right and left sides. There are four valves in the heart. Two are called atrioventricular valves (mitral and tricuspid valves). These valves open during ventricular diastole to allow blood to fill the ventricles and close during ventricular systole. Other two valves are called semilunar valves (aortic and pulmonary valves). These valves open during systole to allow eject blood from the ventricles into the aorta or pulmonary artery and close during diastole.
Papillary muscles that attach to the vanes of the A-V valves by the chordae tendinae. The papillary muscles contract when the ventricular walls contract. They pull of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction. If chordae tendinea becomes ruptured or paralyzed the valve bulges far backward. See figure 20.
Figure (20): Structure of the heart (Fox 2006).
Both ventricles pump the same volume of blood to systemic and pulmonary circulation. The right ventricle pumps blood to pulmonary circulation at low pressure. The left ventricle pumps blood through the systemic circulation at high pressure. The left ventricle has a thicker wall than the right ventricle because of the higher pressure in the systemic circulation.
Blood normally flow continually from great veins into atria: about 75% of the blood flows directly through the atria into the ventricles even before the atria contract. Then, atrial contraction usually causes an additional 25% filling the ventricles that increase the ventricular pumping effectiveness as
much as 25%. The heart can continue to operate even without this extra blood in resting.
Blood supply of the heart:
The heart is supplied by two coronary arteries (right and left ) distal to the aortic valve. The venous system mainly follows the coronary arteries. And drains into the coronary sinus then to the right atrium.
Nerve supply of the heart:
The heart is innervated by both sympathetic and parasympathetic fibers.
The sympathetic fibers innervate the SA node and AV node and muscle fibers in the in the atriums and ventricles. Sympathetic stimulation increase heart rate (positive chronotropic effect) by release norepinephrine attached to B1 receptor to stimulate guanosine (Gs) protein which stimulate formation of cyclic adenosine mono-phosphate (cAMP) that open Na channels. It increases the force of contractility (positive inotropic effect) of muscle fibers in the in the atriums and ventricles
Parasympathetic fibers reach the heart through vagus nerve. Cholinergic nerves enervates SA node and left vagus enervates AV node. Its stimulation causes lowering the heart rate through M2 receptors (negative chronotropic effect) by decrease cAMP which slows the opening of Ca channels but it has little effect on contractility of heart.
See figure 21.
Figure (21): Nerve supply of heart (Fox 2006)
Effect of changes in the ionic composition of blood on heart:
Effect of potassium ions: The normal concentration of potassium (K+) in extracellular fluid is 3.5 – 5.5 meq/L. Excess potassium causes the heart to become flaccid and dilated, and slows the heart rate. Large quantities can block conduction of the cardiac impulse from the atria to the ventricles through AV bundle. Elevation of the plasma K level (Hyperkalemia) produce sever cardiac abnormalities, and abnormal rhythm that this can cause death. This level decreases resting membrane potential in the cardiac muscle fibers. Chronic hyperkalaemia can arise
during renal failure, acidosis, potassium overloading or during RBC haemolysis. Conversely a decrease in the plasma K levels cause ECG changes in precordial leads. Hypokalemia is serious condition but it is not as rapidly fatal as hyperkalemia.
Effect of sodium ions: Fall in the plasma level of Na may be associated with low voltage in ECG.
Effect of calcium ions: Increase in extracellular Ca2+ concentration enhance myocardial contractility. Conversely, deficiency of calcium ions causes cardiac flaccidity, similar to high potassium. Fortunately, calcium ion level in the blood normally are regulated within a very narrow range. Therefore, cardiac effect of abnormality calcium concentrations are seldom of clinical concern.
Properties of cardiac muscle:
Figure 22 shows a typical histological picture of cardiac muscle. The cardiac muscle fibers are striated in the same manner as typical skeletal muscle, branching and interdigitating, contain large number of elongated mitochondria. Cardiac muscle fibers are approximately 15?m in diameter and 100 ?m in length. It contains intercalated disks that separate individual cardiac muscle cells from one another. The heart is composed of three major types of cardiac muscle cells; Atrial, ventricular and specialized excitatory and conductive muscle fibers
Cardiac muscle contains two kinds of junctions:
1- Desmosomes junction which provides strong union between fibers.
2- Gap junction which provides low resistance bridge for the spread of excitation from one fiber to another that allow free diffusion of ions. So that action potentials travel from cardiac cell to the next. The heart is composed of two syncytiums: the atrial syncytium. And the ventricular syncytium. This allow the atria to contract a short time before of ventricular contraction, which is important for effectiveness of heart pumping.
The atrium is separated from the ventricle by fibrous tissue except the atria-ventricular opening which is called AV node to prevent spread of excitation,
Figure (22): Structure of cardiac muscle (Guyton & Hall 2006).
Spread of cardiac excitation:
Figure 23 shows the structures of conducting system are:
1-The sino-atrial node (SA node).
2- The internodes atrial pathway.
3- The atrio-ventricular node (AV node).
3-The bundle of His and its branches.
4-Purkinje fibers.
The SA node is the normal cardiac pace maker. Impulses generated in the SA no de pass through atrial pathway to AV node, through this node to the bundle of His. The bundle divides to right and left branches that lies beneath the endocardium on the two sides of the ventricular septum. Each branch spread downward toward the apex of the ventricle then turn around each ventricular chamber and back toward the base of the heart (purkinje fibers) to supply the ventricular muscle. Atrial depolarization is complete in about 0.1 second. The conduction in AV node is slow about 0.1s, due to small size of muscle fibers and diminished numbers of gap junctions. This delay is shortened by stimulation of sympathetic nerves to heart and lengthened by stimulation of vague nerve. The velocity of conduction of action potential through 1,2,3,4 of conducting system is about o.5 m/s and
in purkinjie fibers is about 4 m/s.
Figure (23): The structures of conducting system. (Guyton & Hall, 2006).
Correlation between muscle fiber length and tension:
The relation between initial fiber length and total tension in cardiac muscle is similar to that in skeletal muscle. The initial length of the fibers is determined by the degree of diastolic filling of the heart, and the pressure developed in the ventricle. It is proportional to the volume of the ventricle at end of the filling phase (Starling law of the heart). The force of contraction of cardiac muscle can be also increased by catecholamine and this increase occurs without a change in muscle length. This positive inotropic effect of catecholamine is mediated via innervated ?1-adrenergic receptors.
Excitation-contraction coupling:
It refers to mechanism by which the action potential causes the myofibrils of muscle to contract. As in skeletal muscle, the action potential spread to the interior of the cardiac muscle fiber along the membrane of cell, act on the longitudinal sarcoplasmic tubules through T tubules to cause release of calcium from sarcoplasmic reticulum. These calcium ions diffuse into the myofibrils and catalyze the chemical reaction that promotes sliding of the actin and myosin in filaments along one another; this produces the muscle contraction.
The mechanism of excitation-contraction coupling is the same as that for skeletal muscle, but there is a second effect that is quite different. In addition to the sarcoplasmic reticulum a large quantity of extra calcium ions diffuse into the sarcoplasm through the T tubule which has a volume 25 times as great in skeletal muscle and store of calcium ions, keeping of
these for diffusion to the interior of the cardiac fibers when the action potential occurs. The wall T tubule contains dihydropyridine (DHP) receptors, during rest they close calcium channel. Once these channels are opened, calcium ions enter ICF. The strength of contraction is hardly affected by change in extracellular fluid calcium concentration. At the end of the cardiac action potential, the influx of calcium ions to the interior of the muscle fiber is suddenly cut off, and the calcium ions in the sarcoplasm are rapidly pumped back out of the muscle fibers, both into sarcoplasmic reticulum and into the T tubes. As a result, the contraction then ceases until a new action potential occurs.
The basic unit of contraction is the sarcomere (2 ?m in length which giving a striated appearance due to the Z lines. During contraction, the shorting of the sarcomere results from the interdigitation of the actin and myosin molecules. Adenosine triphosphate (ATP) provides the energy for contraction.
Mechanical properties of the heart
Most important function of the heart is to push blood to different parts of the body by its contraction, this contraction follow the action potential of cardiac cells. In single muscle fiber contraction start just after depolarization and last until about 50 ms after repolarization is completed. Atrial systole starts after the P wave of ECG. Ventricular systole starts near the end of the R wave and ends just after the T wave. The mechanical properties of the heart studied in 1895 by two physiologists; Otto Frank (German, on isolated frog heart) and Ernest Starling (English, dog isolated heart-lung), both have reached the same results, they created the Frank-Starling law. Energy of contraction is proportional to the initial length of the cardiac muscle. This law is considered one of the most important factor that regulate cardiac output. So the heart muscle stretches more, the force of contraction increases. Volume of ventricle ejected in systole was determined by the end-diastolic volume, it turn depends on the volume returned to the heart, or the venous return. Cardiac output equals venous return. As venous return increases, end-diastolic volume increases and, because of the length-tension relationship, stroke volume increases.