The synchronized contraction of the heart is intrinsically regulated by the sino-atrial node (SA node), located in the right atrium, near the superior vena cava. This specialized region of cells, also known as the pacemaker of the heart, has an inherent rate of about 100 beats per minute. Intrinsic regulation means that the heart can beat on it’s own without any input from the central nervous system. However, this rate is affected through the autonomic nervous system, which can either decrease (through the parasympathetic NS) or increase (through the sympathetic NS) this rate.
When the SA node depolarizes, the electrical signal quickly travels through the atria causing depolarization and contraction of these myocardial cells. The signal then reaches the atrio-ventricular node (AV node), located at the bottom of the right atrium. The signal is quickly conducted through the Bundle of His (a specialized bundle of the Purkinje fibers located in the interventricular septum), and then throughout the Purkinje fiber network via the right and left bundle branches. This leads to a quick depolarization and contraction of the right and left ventricles.
The process of the depolarization and quick transmission of the electrical signal to all cardiac myocytes account for a synchronized contraction of the heart muscle. If the SA node is not working (due to previous heart damage, for example), then the AV node can take over the regulation of the heart rate. The inherent rate of the AV node however, is slower, beating at a rate of 40-60 bpm. The AV node also receives input from the sympathetic and parasympathetic nervous systems. If neither of the node is firing or transmission along the network is blocked (this can happen during a heart attack, for example), then fibers within the Purkinje network, either in the atria or the ventricular can take over the regulation of the heart’s inherent rhythm. Fibers within the Bundle of His have an inherent rate same as the AV node (40-60bpm) and within the rest of the Purkinje Network of 20-40 bpm. When these “aberrant fibers” take over the regulation of the heart’s electrical conduction, then the smooth transmission of the electrical signal along the proper network can be lost and the muscle fibers may not contract synchronously. This can lead to a loss of the proper contractility of the heart and a reduction in the cardiac output to the circulatory system.
The electrical conduction of the heart can be viewed on an electrocardiogram (ECG) by placing recording electrodes on the surface of the chest wall. You will learn more about ECG interpretation later in this course. The basic form of the ECG is described here.
Figure 4. The conducting system of the heart and the typical ECG waveform observed in healthy adults.
The P-wave of the ECG tracing represents the depolarization of the atria; this is followed by:
The P-R interval represents the time it takes for the depolarization to travel from the atria to the SA node and ventricles. The depolarization of the ventricles represented by the QRS complex. The T-wave reflects repolarization of the ventricles. The S-T segment is the isoelectric line between the end of the QRS complex and the T-wave. Both the S-T segment and the T-wave are sensitive indicators of the oxygen supply-demand status of the myocardium. Changes in both of these regions can represent myocardial ischemia and/or infarction. Repolarization of the atria occurs during ventricular depolarization, but is masked by the large QRS complex, therefore is not identified as a deflection on the ECG. Atrial contraction occurs following the P-wave, while the ventricles are depolarizing. The atrial contraction fills more blood into the ventricles. As the ventricles depolarize, the muscle fibers begin to contract in a synchronized fashion. This builds pressure in the ventricles which causes the atrioventricular valves to close shut and the semilunar valves (aortic and pulmonic) to open. As the pressure peaks from contraction, blood is ejected from the right ventricle into the lungs (through the pulmonic valve, via the pulmonary artery) and left ventricle into the systemic circulation (through the aortic valve, via the aorta). The phase of ventricular contraction is called “systole”. Following contraction and during repolarization, the ventricular muscle relaxes and this phase is termed “diastole”.
Stroke volume (SV) is a term used to describe the volume of blood ejected from the heart with each systolic contraction or each beat of the heart. The average resting stroke volume is about 71 ml/beat.
Cardiac output is the most important indicator of the heart’s functional capacity. It is the product of stroke volume and heart rate. Cardiac output (Q) is expresses using the following equation:
In a typical, healthy individual, cardiac output is ~ 5 L/min (70 beats/min x 71 ml/beat). The autonomic nervous system plays a role in regulating both the heart rate (as described previously) and stroke volume. Increased output from the sympathetic nervous system increases the contractility of the myocardial cells to increase the stroke volume. On the other hand, the parasympathetic nervous reduces myocardial contractility.
Cardiovascular Conducting System
The arterial system is made up of a network of large arteries (such as the aorta), arterioles and capillaries. Artery walls have layers of smooth muscle, elastin and connective tissue. The largest artery, the aorta, is highly elastic so that it can withstand the high pressures of the blood being pushed through by the left ventricle. The aorta branches into smaller arteries and arterioles. Arterioles are the major regulator of blood flow – it has layers of smooth muscle that constrict or relax in response to stimuli to regulate blood flow to the target organs. Arterioles are particularly important for regulating blood flow during exercise.
Arterioles branch into beds of thin-walled capillaries. The diameter of capillaries is only 7-10μm, and they consist of only a single endothelial cell layer. This allows for gases, nutrients and metabolic products to rapidly transfer across the thin, porous walls of the capillaries. The pre-capillary sphincter, a thin layer of smooth muscle at the origin of the capillary, regulates capillary blood flow. Capillaries form a very large network of microscopic blood vessels and the total surface area of the capillaries is 4,500 cm2 – this allows for a large area over which diffusion can occur.
The venous system collects deoxygenated blood and returns it to the heart. It also acts as a reservoir for blood volume and in resting conditions, holds about 65% of the total blood volume. Veins are therefore known as capacitance vessels. Capillary beds carry deoxygenated blood from the tissues to small veins or venules. The lower body veins empty into the inferior vena cava and the upper body veins into the superior vena cava. Veins are thin-walled (only a thin smooth muscle layer) and carry blood at low pressures. In order to maintain venous return, the thin walled veins have one-way valves that keep blood moving towards the heart and prevent back flow. In addition, skeletal muscle surrounding the veins can contract and assist with venous return and smooth muscles within the venous walls can also contract.
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