Download 1- Functional anatomy and mechanical properties of heart

1- Functional anatomy and mechanical
properties of heart
Objectives:
1. Explain the functions of the heart.
2. Describe the flow of blood through the heart.
3. Explain the functions of the heart valves.
Heart chambers and function of valves:
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. See figure 1.
Figure (1): The heart valves.
Papillary muscles that attach to the vanes of the A-V valves by the chordae
tendinae, contract when the ventricular walls contract. They pull 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 2.
Figure (2): 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. While 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. The atrial contraction 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. Coronary veins drain into a single large vein, then coronary sinus, which
drain into 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, AV node and muscle fibers in the
atria and ventricles. Sympathetic stimulations increase heart rate (positive
chronotropic effect) by release norepinephrine attached to B1 receptor to stimulate
guanosine (Gs) protein which stimulates formation of cyclic adenosine monophosphate (cAMP) that open Na channels. It increases the force of contractility
(positive inotropic effect) of muscle fibers in the atriums and ventricles
Parasympathetic fibers innervate the heart through vagus nerve. The right vagus
nerve enervates SA node while left vagus nerve enervates AV node. Its stimulation
causes lowering the heart rate through M2 receptors (negative chronotropic effect)
by decrease cAMP.
See figure3.
Figure (3): 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. chronic hyperkalaemia which arise during renal failure, acidosis,
potassium overloading or during RBC haemolysis produce sever cardiac abnormal
rhythm that can cause death. This level decreases resting membrane potential in the
cardiac muscle fibers. Conversely a decrease in the plasma K levels
(Hypokalemia).is serious condition but it is not as rapidly fatal as hyperkalemia.
Effect of sodium ions: Fall in the plasma level of Na ions 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 4 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 15µm in diameter and 100 µm in length. They
contain intercalated disks that separate individual cardiac muscle cells from one
another. The heart is composed of three major types of cardiac muscle cells;
specialized excitatory, contractive and conductive muscle fibers
Cardiac muscle junctions:
1- Desmosomes junction which provides strong union between muscle 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 atriaventricular opening which is called AV node to prevent spread of excitation,
Figure (4): Structure of cardiac muscle (Guyton & Hall
2006).
Spread of cardiac excitation:
Figure 4 shows the structures of conducting system, they are:
1-The sino-atrial node (SA node).
2- The internodes atrial pathway.
3- The atrio-ventricular node (AV node).
4-The bundle of His and its branches.
5-Purkinje fibers.
The SA node is the normal cardiac pace maker. Impulses generated in the SA
node pass through atrial pathway to AV node, through this node to the bundle of
His. The bundle divides to right and left branches. Each branch ends with purkinje
fibers which spread downward toward the apex of the ventricle then turn around
each ventricular chamber and back toward the base of the heart to supply the
ventricular muscle fibers. The atrial depolarization is completed in about 0.1
second. The conduction in AV node is slow about 0.1 second 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. See
figure 5.
Figure (5): 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 β1-adrenergic receptors.
Excitation-contraction coupling:
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 stores 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 calcium channels are closed. 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 into sarcoplasmic reticulum and 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 µm 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 complete repolarization. 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 was 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 FrankStarling law Energy of contraction is proportional to the initial length of the
cardiac muscle. This law described the length-tension relationship in muscles; it
stated that the force of contraction of the ventricles depends on the initial length of
ventricular muscle fibers. In such a way, that the force of myocardial contraction is
directly proportional to the initial length of the cardiac muscle fibers. This means
that the greater stretching of the myocardium, greater force of contraction. In other
words, Frank-Starling law reflects the relationship between ventricular enddiastolic volume (EDV) and stroke volume. The blood returns to the heart during
the filling phase, will distend the ventricles so the ventricles will produce more
powerful contraction to pump the increased volume of the blood.
This law is considered one of the most important factor that regulate cardiac
output. When the heart muscle stretches more, the force of contraction increases.
The volume of blood in ventricle which ejected in systole was determined by the
end-diastolic volume. It turn depends on the volume of venous returned to the
heart. As venous return increases, end-diastolic volume increases and stroke
volume increases.