The Heart & the Blood Vessels

The Heart & the Blood Vessels

The Heart

The heart is the motor of the circulation it pumps blood to maintain a steady blood flow throughout the body. The heart is composed of four chambers, left atrium and ventricle and right atrium and ventricle. The atria and ventricles are separated by the atrioventricular (AV) valves, mitral on the left and tricuspid on the right. Deoxygenated blood returns from the body via the great veins (superior and inferior vena cava) to the right atrium and then passes through the tricuspid valve into the right ventricle. From here, blood is pumped through the pulmonary valve into the pulmonary artery (the only artery which carries deoxygenated blood in an adult) and on through the pulmonary capillaries in the lungs where it is oxygenated (and carbon dioxide removed). Blood returns to the left side of the heart via the pulmonary veins (the only veins to carry oxygenated blood in the adult) into the left atrium, then through the mitral valve into the left ventricle. From the left ventricle blood is pumped through the aortic valve into the aorta and then via the systemic vascular tree to the body's organs.


Passage of Blood Through the Heart Systemic-Circulation

The Vascular System

The vascular system are comprised of arteries, arterioles, capillaries, venules and veins, conventionally described in progressive order leaving from the left side of the heart and returning to the right. The arterial side of the circulation carries oxygenated blood. Both arteries and arterioles have thick, muscular walls as they carry blood under relatively high pressure. The average adult has a circulating volume of approximately 5000ml blood. In the normal resting state only about 15% (750ml) of the circulating volume is within the arterial system. As blood traverses capillary beds the pressure falls and the blood gives up oxygen and other nutrients to the tissues, while at the same time collecting carbon dioxide and other waste products of metabolism. The blood, now relatively deoxygenated starts its return journey to the heart in the venules and veins (thin-walled because of the low pressure), finally entering the venacavae. The venous system contains approximately 60% (3000ml) of the blood volume and is often referred to as a capacitance system, the volume of which can be varied significantly by the sympathetic nervous system. The remaining 25% (1250ml) of the blood volume is in the pulmonary circulation and heart.

The Heart Wall and Muscle

The heart wall consists of three layers; the outer double-walled sac called the pericardium, the myocardium, by far the thickest layer, is composed of cardiac muscle and performs the work of the heart. The endocardium forms the smooth inner lining of the chambers and valves and is continuous with the endothelium of the blood vessels.

The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized excitatory and conductive muscle fibers or pace maker. The atrial and ventricular types of muscle contract in much the same way as skeletal muscle, except that the duration of contraction is much longer. Conversely, the specialized excitatory and conductive fibers contract only feebly because they contain few contractile fibrils; providing an excitatory system that controls the rhythmical beating of the heart. Electrical activity readily spreads from one atrium to another and from one ventricle to another via this specialized conduction pathways. The normal absence of direct connections between the atria and ventricles except through the atrioventricular (AV) node delays conduction and enables atrial contraction to prime the ventricle.

The Cardiac Cycle

Refers to the serious of electrical and mechanical events that occur during the contraction (systole) and relaxation (diastole) of the ventricular muscle.


The cardiac activity is initiated by the cardiac action potential that originates in the sino-atrial (SA) node, spreads through the atrial muscle, crosses the atrio ventricular (AV) node, reaches the ventricles via the bundle of His and supplies the Purkinje fibres which innervate the ventricles. The sum of these action potentials is recorded as the ECG;
Myocardial contraction results from a change in voltage across the cell membrane (depolarization), which leads to an action potential. Although contraction may happen spontaneously, it is normally in response to an electrical impulse.
P wave - atrial depolarization PR interval - spread of excitation through the atria, AV node and bundle of His QRS complex - spread of excitation through the ventricles T wave - ventricular repolarisation

Systole is the period of ventricular contraction. As contraction starts in both ventricles, the AV valves close to prevent back flow of blood into the atria. The amount of blood ejected in one cycle is referred to as the stroke volume (SV) and this is around 70ml in an average adult at rest. However, the ventricles do not completely empty, only sixty to eighty percent of the blood present in the ventricle is ejected (the ejection fraction). As the ventricles empty, the pressure within them starts to fall. When the pressure drops below that in the aorta and pulmonary artery, the aortic and pulmonary valves respectively close, signaling the end of systole.

Diastole is the period of ventricular relaxation. As the atria fill with blood returning to the heart the pressure rises, when it exceeds that in the ventricles the AV valves open and as a period of passive filling occurs the volume of blood in the ventricles starts to increase. This passive filling is initially rapid, but slows as the pressure gradient across the AV valves decreases. Ventricular filling is completed by contraction of the atria, contributing twenty to thirty percent of ventricular volume, and signaling the end of diastole. The volume of blood in the ventricle at this point is often referred to as the end-diastolic volume (EDV) and is normally around 120ml.

Under normal resting conditions, heart rate is approximately 70 beats/min and each cardiac cycle therefore takes approximately 0.85 sec. Systole lasts 0.3 sec and diastole lasts 0.55 sec, most of the time being taken up by ventricular filling. Now consider what happens when the heart rate is 180 beats/min; each cycle takes up 0.3 sec, with diastole and systole both lasting 0.15 sec. Diastole has been reduced more than systole (0.4sec compared to 0.15sec), reducing the time for ventricular filling. Systole cannot be reduced any more without affecting the stroke volume. An increase in heart rate beyond this rate reduces diastole further resulting in insufficient time for ventricular filling and a reduction in the volume of blood pumped out with each beat. Therefore for most adults, the maximum heart rate is around 180beats/min. In addition, perfusion of the muscles of the ventricles (via the coronary arteries) occurs predominantly during diastole. Due to this, at very high heart rates, the duration of coronary blood flow is reduced. This is the very time when the heart is working maximally and so has a high oxygen demand risking myocardial ischemia (inadequate oxygen supply to cardiac muscle).

The Coronary Circulation

Myocardial blood supply is from the right and left coronary arteries, which run over the surface of the heart giving branches to the endocardium (the inner layer of the myocardium). Venous drainage is mostly via the coronary sinus into the right atrium, but a small proportion of blood flows directly into the ventricles through the Thebesian veins, delivering unoxygenated blood to the systemic circulation. Oxygen extraction by the tissues is dependent on consumption and delivery. Myocardial oxygen consumption is higher than in skeletal muscle (65% of arterial oxygen is extracted as compared to 25%).Therefore any increased myocardial metabolic demand must be matched by increased coronary blood flow. This is a local response, mediated by changes in coronary arterial tone, with only a small input from the autonomic nervous system.

Coronary blood flow occurs mostly during diastole, because during systole the blood vessels within the myocardium are compressed. Increased heart rates, which reduce the time for diastolic filling, can reduce myocardial blood supply and cause ischemia. In heart failure, the ventricle is less able to empty and therefore the intraventricular volume and pressure is higher than normal. During diastole, this pressure is transmitted to the ventricular wall and opposes and reduces coronary flow, especially in the endocardial vessels.

Cardiac Output (CO)

Is defined as the volume of blood ejected by each ventricle per minute and is the product of the stroke volume and heart rate it is expressed in litres/min. Clearly the output of both ventricles has to be the same; otherwise all the blood would end up in either the systemic or pulmonary circulation

Cardiac Output = Stroke Volume x Heart Rate

Under normal resting conditions this is approximately 70ml x 70beats/min = 4900ml/min (around 5l/min). Different sized patients will have different cardiac outputs; to allow meaningful comparisons to be made the cardiac index (CI) is often used. This relates CO to body surface area and is expressed in litres/min/m2. It is calculated by dividing CO by body surface area.

Cardiac Index = Cardiac Output/Body surface area

Cardiac output varies widely with the level of activity of the body, the basic level of body metabolism, whether the person is exercising, the person's age, and size of the body.

Factors affecting stroke volume are the degree of filling of the ventricle, or "preload", the contractility of the myocardium and the resistance against which the ventricle has to work, or "after load".

Venous Return

Is the quantity of blood flowing from the veins into the right atrium each minute. The venous return and the cardiac output must equal each other except for a few heartbeats at a time when blood is temporarily stored in or removed from the heart and lungs. Preload is end-diastolic volume, which is generally dependent on ventricular filling, which in turn depends mainly by venous return. The afterload of the ventricle is the pressure in the artery leading from the ventricle. Afterload for the intact heart is commonly equated with either ventricular wall tension during systole or arterial impedance to ejection.

  • The heart rate and contractility can be increased or decreased by the activity of the autonomic nervous system through a number of nerve reflexes which detect and respond rapidly to changes in arterial blood pressure. The heart rate is controlled predominantly by a change in sympathetic or vagal tone

The heart has an intrinsic pacemaker, the sino-atrial node, which in the absence of any other influence discharges at around 100 beats/min. Changes in heart rate are brought about by the autonomic nervous system, either directly or via effects on the adrenal glands. Generally speaking, sympathetic stimulation will increase the heart rate via adrenergic receptors (a positive chronotropic effect) and parasympathetic stimulation, via the vagus nerve, will decrease the heart rate (a negative chronotropic effect). Under normal circumstances, resting heart rate is below100 beats/min, and therefore there is dominance of vagal (parasympathetic) activity. Providing stroke volume is unchanged, an increase in heart rate will cause a rise in cardiac output and vice versa (CO=SV x HR). This is true in normal healthy individuals as the stroke volume is relatively unaffected between heart rates of 50-150/min.

Adrenergic Receptors and Their Actions

These receptors respond to stimulation by the sympathetic nervous system and catecholamines from the adrenal gland. Their primary function is to prepare the body for the primitive "fight or flight" response; ventilation increases along with bronchodilation, cardiac output is increased through an increase in rate and contractility and blood is diverted from non-vital organs (e.g. the gut) to vital organs (e.g. heart, kidneys and muscle). There are two main types of adrenergic receptors alpha (α) and beta (β), each of which is divided into two subtypes, α- 1, α-2, and β-1, β-2.


Adrenergic Receptors and Their Effects

Receptor Type Location Effects
Alpha-1 Blood vessels Vasoconstriction
Alpha-2 Blood vessels Vasoconstriction
Beta- 1 Heart Increases heart rate
Increase force of contraction
Beta- 2 Blood vessels Lung Vasodilation
Bronchodilation
The Efferent and Afferent Reflex Limbs That Control Blood Pressure and CVS
The Efferent Limb

These reflexes involve autonomic nerves regulated by centers in the medulla: The vasomotor centre and the cardio-inhibitory centre.

  • The Vasomotor centre is a collection of cells in the medulla, which have a sympathetic vasoconstrictor effect on the blood vessels and also an inotropic and chronotropic effect on the heart. A positive inotropic effect results in an increase in the force of contraction of the heart. A positive chronotropic effect results in an increase in the rate of the heart.
  • The cardio inhibitory centre is located immediately lateral to the vasomotor centre (in the medulla) is the dorsal nucleus of the vagus which has a cardio-inhibitory effect (i.e. on stimulation of these fibres there is a bradycardia and a decrease in the force of contraction via the vagus nerve). The heart rate is hence controlled predominantly by a change in sympathetic or vagal tone.

The Afferent Limbs

These reflexes involve a number of cardiovascular receptors and reflexes: baroreceptors, chemoreceptors and low pressure volume receptors.

  • Baroreceptors are specialized cells called "pressor receptors". They are sensitive to stretch which accompanies changes in pressure in the vessels or in the cardiac chamber where these receptors are situated. They are found in the carotid sinus and the aortic arch. The carotid sinus is the dilated part of the internal carotid artery at its commencement. An impulse passes upwards from these receptors. In the carotid sinus the nerve conveying the afferent impulses to the cardiac centers is the ninth or glosso-pharyngeal nerve. The vagus or the tenth cranial nerve carries these impulses from the aortic arch. As the pressure (and hence the stretch) in the carotid sinus and the aortic arch rises there is a decrease in the blood pressure. If the pressure in the aortic arch and carotid sinus falls there is a rise in the heart rate and an increase in the blood pressure, within the vessel or cardiac chamber where these receptors are situated. Atrial baroreceptors have been found which react in the same way to changes in pressure and help control blood volume.
  • Chemoreceptors: These are of primary importance in the control of respiration. The chemoreceptors are situated in the carotid body at the point at which the common carotid artery divides into the external and internal carotid artery. They are also situated in the aortic arch.
  • Their locations are close to but not identical with those of the baroreceptors. When the chemoreceptors are stimulated by a rise in arterial carbon dioxide or a fall in arterial oxygen, then, although the predominant effect is on the respiratory centre, there is also a reflex tachycardia and rise in blood pressure due to impulses conveyed via the 9th and 10th cranial nerves to the vasomotor centre.
  • Low-pressure volume receptors These are also stretch receptors found in the walls of the large veins, atria and the pulmonary trunk and are particularly sensitive to changes in the circulating blood volume. An increase in blood volume causes an increase in venous return and raises the cardiac output and arterial blood pressure. This stimulates the low-pressure volume receptors which can reduce blood pressure by reduction of vasoconstrictor sympathetic activity thereby reducing peripheral resistance and inhibition of antidiuretic hormone (ADH).

Other Mechanisms Involved in Control of HR and BP

Hormones

A number of hormones are involved in the regulation of blood pressure. Some act rapidly and others have a delayed action.

  • Catecholamines (adrenaline and noradrenaline) are released from the adrenal medulla as a result of sympathetic activity via the vasomotor centre. These hormones act within minutes causing vasoconstriction and heart rate and contractility.
  • Antidiuretic hormone/ADH/: This hormone from the pituitary gland causes direct vasoconstriction but has a more important if less rapid effect by stimulating water reabsorption in the kidney and increasing blood volume.
  • Renin/angiotensin/aldosterone This system is stimulated by a reduction in renal blood flow. Angiotensin acts as a vasoconstrictor, increasing peripheral resistance but also stimulates aldosterone secretion from the adrenal cortex. This promotes sodium and water reabsorption in the kidney increasing blood volume and blood pressure.

Emotions

Emotions, e.g. anxiety or excitement may increase the heart rate. Shock, another emotion, may decrease it. These impulses are transmitted to the vasomotor centre from the cerebral cortex and hypothalamus.

Respiration

In most adults, during quiet respiration, there is no change in the heart rate. However, in children during quiet breathing or in some adults during very deep breathing, the heart rate tends to vary. The heart rate in these cases, increases during inspiration and slows during expiration. This is termed "sinus arrhythmia". It is believed to be caused by impulses from the inspiratory (RC) centre, transmitted to the cardiac centre.

Peripheral Resistance

The peripheral resistance is the resistance to blood flow at the level of the peripheral arterioles and depends on:

  • The size or diameter of the arterioles which depends on sympathetic tone. The sympathetic outflow from the vasomotor centre (VMC) leaves via the thoracolumbar outflow to the peripheral vessels. When the venules constrict the blood is squeezed out of them and returned to the heart.
  • The viscosity of the blood which imposes a resistance to flow. Viscosity is increased if the RBCs are increased. This raises peripheral resistance. Viscosity falls in anaemia and haemorrhage and this decreases resistance.


Last modified: Wednesday, 16 November 2016, 9:14 AM