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.Part 1
The heart is mainly made up of cardiac muscles. There are two categories of cardiac muscle, the working cardiac muscle (atrium and ventricle) and the specific conduction system of heart (sinoatrial node, A-V junction and His-Purkinje system).
ELECTRICAL ACTIVITY OF THE HEART
ELECTRICAL BEHAVIOR OF CARDIAC MUSCLE CELLS
The resting membrane potential of working cardiac myocytes as well as the maximal diastolic potential (MDP) of Purkinje fibres is around -80mV to -90mV, close to Ek. In contrast, the MDP of sinoatrial nodal cell is around -60mV, a value between the equilibrium potential of potassium and sodium.
The action potential (AP) of working cardiac muscle and Purkinje fibres belongs to the fast response type. Their depolarization (phase 0) is induced by the inflow of INa into the cell. The repolarization of these cells is composed of three phases, phase 1 is due to the outflow of Ito, phase 2 is the result from inflow of ICa-L, and the outflow of IK and IK1 accomplishes the final repolarization, phase 3.
The AP of sinoatrial nodal cells belongs to the slow response type. Since their cell membrane is deficiency of IK1, Ito and INa channel, so the inflow of ICa-L induces depolarization and the outflow of IK repolarizes their membrane.
ELECTROPHYSIOLOGICAL PROPERTIES OF CARDIAC MUSCLE
EXCITABILITY: The cardiac muscle has a long refractory period which lasts until the relaxation phase of contraction. Thus cardiac muscle has no complete tetanus and after a ventricular premature systole, there is always a compensatory pause.
CONDUCTIVITY: The conduction velocity varies within the heart. It is very slow in the region of A-V junction (A-V delay). The A-V delay permits optimal ventricular filling during atrial contraction. The conduction velocity is very fast in His-Purkinje system to ensue the synchronous contraction of ventricles.
AUTORHYTHMICITY: The sinoatrial node is the dominant pacemaker of the heart to control the rhythmic heartbeat. It suppresses the automaticity of latent pacemaker by a capture and overdrive suppression mechanism.
If current is the main pacemaker current of Purkinje fibre, and the decay of Ik and the increase of ICa-T and If makes up the automaticity of SAN.
THE ELECTROCARDIOGRAM(ECG)
A normal ECG is composed of P wave, QRS complex, and T wave. The P wave represents the depolarization process of right and left atriums. The QRS complex is caused by the depolarization of both ventricles and the T wave is generated by the repolarization process of the ventricle. The P-R interval is a measure of the time from the onset of atrial excitation to the onset of ventricular activation. The prolongation of P-R interval always indicates the disturbance in A-V conduction.
THE CARDIAC PUMP
MECHANICAL EVENTS OF THE CARDIAC CYCLE
The cardiac events that occur from the beginning of one heartbeat to the beginning of next are called the cardiac cycle. When the heart rate is 75 beats/min, the cardiac cycle lasts 0.8 S. In a cardiac cycle, the atrium acts as the primer pump and the ventricle is the cardiac pump. The diastole of ventricle occupies 0.5s and systole lasts 0.3s. During diastole, after the isovolumic relaxation phase, it is filled rapidly at first and then more slowly until atrial systole. The ventricular systole undergoes an isovolumic contraction phase and ejection phase (rapid and reduced) to pump a certain amount of blood out. The A-V valves and semilunar valves open and close passively to prevent the backflow of blood.
EVALUATION OF HEART PUMP FUNCTION
CARDIAC OUTPUT
Stroke volume is the volume of blood ejected by ventricle every beat.
Minute volume is the volume of blood ejected by left ventricle per minute, it equals to the stroke volume multiplies heart rate per minute.
CARDIAC WORK
The stroke work of the heart is the amount of energy that the heart converts to work each heartbeat while pumping blood into the arteries.
The minute work is the total amount of energy converted to work in 1 minute. It is equal to the stroke work times the heart rate per minute.
CARDIAC EFFICIENCY
During cardiac muscle contraction, most of the chemical energy is converted into heat and only a small portion into work output. The maximum efficiency of the normal heart is between 20% and 25%. In heart failure, this may decrease to as low as 5% to 10%.
CARDIAC RESERVE
The reserve of stroke volume is determined by the reserve of diastole (around 15ml) and the reserve of systole (about 35ml to 40ml). The reserve of heart rate is related to the resting heart rate. A healthy adult，the cardiac output increases with the heart rate up to about 160-180 beats/min.
REGULATION OF CARDIAC OUTPUT
PRELOAD
The initial length before the contraction of ventricular muscle is determined by the end diastolic volume of the ventricle. The energy of contraction of cardiac muscle is proportional to the initial length of the muscle. It can be expressed by the ventricular function curve (heterometric autoregulation).
AFTERLOAD
The afterload of left ventricular ejection is the blood pressure in the aorta. The cardiac output does not change when the aortic blood pressure varies within 80 to 170 mmHg in normal heart.
CONTRACTILITY
Contractility is defined as a change in developed tension at a giving cardiac myocyte length. Homeometric autoregulation means the change of cardiac contractile strength due to the alteration of contractility.
HEART SOUNDS
Closure of the AV valves at the start of ventricular systole generates the first heart sound. The second heart sound is generated when the semilunar valves close. It indicates the beginning of ventricular diastole.
Part 2
The circulatory system consists of two subdivisions: the cardiovascular system and the lymphatic system. The cardiovascular system consists of the heart and blood vessels, and the lymphatic system consists of lymphatic vessels and lymphoid tissues within the spleen, thymus, tonsils, and lymph nodes.
Blood vessels form a tubular network that permits blood to flow from the heart to all the living cells of the body and then back to the heart. Arteries carry blood away from the heart whereas veins return blood to the heart. Arteries branch extensively to form a "tree" of progressively smaller vessels. The smallest of the arteries are called arterioles. Blood passes from the arterial to the venous system in microscopic capillaries, which are the thinnest and most numerous of the blood vessels. All exchanges of fluid, nutrients, and wastes between the blood and tissues occur across the walls of capillaries. Blood flows through capillaries into microscopic veins called venules, which deliver blood into progressively larger veins that eventually return the blood to the heart.
The walls of arteries and veins are composed of three coats: tunica externa, tunica media and tunica interna, which consist of endothelium and a subendothelial layer. The endothelial cells not only provide a smooth surface for blood flow but also synthesize several substances which, when released, can affect the degree of relaxation or contraction of the arterial wall. The most important of these is a vasodilator substance called nitric oxide (NO). Once formed in the endothelium, NO rapidly diffuses into the vascular smooth muscle, which it causes to relax. The endothelium also releases prostacyclin (a vasodilator) and endothelin (a vasoconstrictor).
The blood flow that passes through a given blood vessel depends directly upon the hydrostatic pressure difference between the two ends of the blood vessel, and indirectly upon the resistance that is offered to the movement of blood. The rate of blood flow to an organ can be calculated according to Poiseuille's law. Blood flow can change from laminar flow to turbulent flow when Reynolds number exceeds 2000.
The pressure of the arterial blood is regulated by the blood volume, total peripheral resistance.
Part 3
Cardiac innervation: Impulses in the noradrenergic sympathetic nerves to the heart increase the cardiac rate (positive chronotropic effect) and the force of cardiac contraction (positive inotropic effect). Impulses in the cholinergic vagal cardiac fibres decrease heart rate. There is a good deal of tonic discharge in the cardiac sympathetic and vagal nerves at rest. When the vagi are cut in experimental animals or after the administration of parasympatholytic drugs such as atropine, the cardiac rate in humans increases from its normal resting value of 70 to 150~180 beats per minute. In humans in whom both noradrenergic and cholinergic systems are blocked, the heart rate is approximately 100 beats/min.
Innervation of the Blood vessels: Noradrenergic fibres end on vessels in all parts of the body, but the fibres from the sympathetic ganglia to the cerebral vessels are of little functional importance. The noradrenergic fibres are vasoconstrictor in function. In addition to their vasoconstrictor innervation, the resistance vessels of the skeletal muscles are innervated by vasodilator fibres that, although they travel with the sympathetic nerves, are cholinergic (the sympathetic vasodilator system).
There is no tonic discharge in the vasodilator fibres, but the vasoconstrictor fibres to most vascular beds have some tonic activity. When the sympathetic nerves are cut (sympathectomy), the blood vessels dilate. In most tissues, vasodilatation is produced by decreasing the rate of tonic discharge in the vasoconstrictor nerve, although in skeletal muscles it can also be produced by activating the sympathetic vasodilator system.
Nerves containing peptides are also found in many blood vessels. The peptides released from these peptidergic nerves include VIP, which produces vasodilation.
Afferent impulses in sensory nerves from the skin are relayed antidromically down branches of the sensory nerves, which innervate blood vessels and these impulses produce vasodilation. This local neural mechanism is called the axon reflex.
Cardiovascular regulatory mechanism
Nervous control
Cardiovascular centre: Cardiovascular centre means a certain region of the central nervous system that possesses the function to regulate a cardiovascular activity.
1.Medullary cardiovascular centre:
Recent evidence strongly supports the view that the ventrolateral medullary (VLM) area functions to maintain vasomotor tone and mediate the cardiovascular reflexes.
The VLM area includes the rostral ventrolateral medulla (rVLM) area. This area corresponds with the so-called vasoconstrictor centre or C1 area where brain stem adrenaline containing neurones are located. The electrical or chemical stimulation of rVLM area elicits to an increase in arterial blood pressure (BP) and heart rate (HR). The VLM area includes the caudal ventrolateral medulla (cVLM). This area corresponds with the so-called vasodilator area or A1 area where brain stem noradrenaline containing neurones are located. The decrease in BP an HR of the cVLM stimulation may be mediated by activation of the GABA receptors in the rVLM.
In addition, the nucleus ambiguous and the dorsal motor nucleus of vagus in the medulla are areas sometimes called the cardioinhibitory centre
2.Higher cardiovascular centres
Above the medulla, a large number of areas throughout the reticular formation of the pons, mesencephalon and diencephalon can either excite or inhibit the medullary cardiovascular centre Among these areas, the hypothalamus plays an important role in the control of cardiovascular activity. Besides, many parts of the cerebral cortex can also be of influence; they are involved in regulating cardiovascular adjustments to exercise and emotion.
Cardiovascular reflexes
1.Sino-aortic baroreceptor reflex: A rise in arterial pressure stimulates the baroreceptors and causes them to transmit signals to the central nervous system. They are involved in the following pathway
N.IX.X-(EAA)NTS-(EAA)cVLM-(GABA)rVLM-(EAA)IML-(ACh)cardiac sympathetic nerve; (2)NTS -(EAA) N.Ambiguus -(ACh)cardiac vagus nerve; (3)NTS-LC or cVLM-(Norepinephrine NE)SON.PVN-(Vasopressin. VP) the posterior pituitary or rVLM resulting in a decrease of sympathetic vasomotor tone and increase of vagal cardioinhibitory center tone. These cause a reduction of the arterial pressure toward the normal level and a decrease of HR. This homeostatic mechanism acts to maintain the constancy of arterial blood pressure.
2. Arterial chemoreceptor reflex: The afferent nerve fibres from the carotid and aortic bodies pass with the baroreceptor afferents through the carotid sinus nerves and vagus nerves respectively. The chemoreceptor discharge increases rapidly when arterial PO2 falls or when there are increases in arterial PCO2 and hydrogen ion concentration. The main function of the chemoreceptors is to regulate ventilation.
3.Cardiopulmonary receptor reflex: Experiments have shown that stretching atria or pulmonary arteries causes a reflex inhibition of the sympathetic nerve activity, a reduction of the release of vasopressin from the pituitary and an increased release of atrial natriuretic peptide from the atrial myocardium. All the above mentioned reflex effects of the cardiopulmonary receptors tend to return the blood volume back to normal.
In addition to the above mentioned cardiovascular reflexes, stimulation of somatic or visceral nerves may also cause some other reflexes affecting the cardiovascular activity.
Humoral control
1.Noradrenaline and adrenaline: Noradrenaline (NA) causes vasoconstriction almost in every vascular bed by binding with a-adrenoceptors in the vascular smooth muscle. On the other hand, adrenaline (Adr) binds with both a-and b-adrenoceptors, leading to vasoconstriction and vasodilation respectively.
2.Angiotensin: AngiotensinⅡis one of the most potent vasoconstrictor agents and so has pressor effects.
3.Vasopressin(VP): Vasopressin is a nonapeptide hormone synthesized in the neurones of the paraventricular (PVN) and supraoptic nuclei (SON) in the hypothalamus. The principal physiological effect of VP is the retention of water by increasing the permeability of the collecting ducts of the kidney and very potent vasoconstrictor and pressor effects. The baroreceptor reflex may be facilitated by the VP. In addition, the effect of VP on CNS, it also acts on the rVLM area in the brain to increase sympathetic vasomotor tone and arterial blood pressure.
Recent studies indicate that the effects of endothelium-relaxing factor (EDRF), bradykinin, prostaglandins (PG), b-endorphin and histamine are vasodilatation.
Local control of basal vascular tone
This myogenic activity results in a basal vascular tone which keeps these vessels in a state of partial constriction. When the arterial blood pressure in a tissue vascular bed is suddenly raised, the transmural pressure increases, especially in the section of precapillary resistance vessels, thus giving rise to a mechanical stretch of smooth muscle and distension of the vessels. ???? This causes a constriction of the smooth muscle.
Coronary Blood Flow
In humans the resting coronary blood flow averages 225ml/min, which is 4 to 5 percent of the total cardiac output. The blood flow in the left ventricle falls to a low value during systole, because of strong compression of intramuscular vessels by the myocardial contraction. During diastole, however, the cardiac muscle relaxes and no longer obstructs the blood flow through the left ventricular blood vessels. Coronary blood flow increases rapidly during diastole. The force of contraction of right ventricle is much less than that of the left ventricle. The phasic changes in blood flow are relatively small compared with those in the left ventricle.
Oxygen demand or consumption is a major factor in regulation of coronary blood flow, while the neural control is of secondary importance. Among metabolites known, adenosine is thought to be the most important. It plays a role in the regulation of coronary blood flow.
Pulmonary circulation
The function of the pulmonary circulation is to oxygenate the mixed venous blood which comes from the right ventricle and remove its excess of CO2 by exchange between the capillaries and the air in the alveoli.
The blood volume of the lungs is approximately 450ml. Since blood volume in the pulmonary circulation is large and its volume variation is also large, the pulmonary vascular bed serves as a blood reservoir in the body. On the other hand, the pulmonary interstitial hydrostatic pressure is very low and even subatmospheric at times. This low pressure helps to pull fluid from the alveoli into the interstitial space and into the capillaries, keeping the alveoli dry. When alveolar oxygen concentration becomes low, the adjacent blood vessels slowly constrict in a few minutes, leading to an increase in the vascular resistance. This response may cause most of the blood to flow through other areas of the lungs which are better ventilated.
Stimulation of the sympathetic fibres, NA, Adr and AngⅡ cause vasoconstriction of the pulmonary circulation.
Cerebral Blood flow
Cerebral blood flow is autoregulated extremely well between the pressure range of 60 and 160mmHg in the arterial pressure. The mechanism of this autoregulation is probably due to a combination of myogenic and metabolic factors. An increase in CO2 or H+ concentration in the arterial blood perfusing the brain greatly increases cerebral blood flow. Stimulation of the sympathetic nerves causes mild vasoconstriction, while stimulation of the parasympathetic nerves causes mild vasodilatation.
Blood-Brain and Blood cerebrospinal fluid (CSF) Barriers
The morphological basis of the blood brain barrier is the endothelial cells, the basement membrane of the capillaries and the foot processes of astroglial cells (the perivascular end foot). This property of the blood-brain barrier helps to conserve the constancy of the local environment of the neurones, preventing fluctuation in plasma composition from being transmitted to the CSF.
The blood-CSF barriers also exist. Evidently, many large molecular substances hardly pass from the blood into the CSF.
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