Lancashire & South Cumbria Cardiac Network
ANATOMY & PHYSIOLOGY MANUAL
Cardiac Physiologist Training Manual
ANATOMY OF THE HEART
Surface Anatomy and Position
The Anterior surface or sternocostal surface of the heart is formed mainly by the right ventricle. To the left is a small section of the left ventricle separated from the right by the anterior interventricular groove that carries the anterior descending branch of the left coronary artery. A small right atrial portion is found on the right. This anterior surface lies directly behind the sternum from which it is separated by the pericardium. The pleura and thin anterior parts of the lungs also partly cover it except for a small triangular area, the cardiac incisure in the left lung.
The superior border is formed by the upper margins of the atria, mainly the left. It is largely hidden by the ascending aorta and pulmonary trunk. The superior border extends from the upper part of the left 2nd intercostal space to the lower part of the same space on the right. This line also marks the line of the pulmonary arteries which lie along this border of the heart. The SVC enters the right atrium at the right.
The right border extends from the right end of the superior border to the right 6th costal cartilage, 1-2cm from the sternum. This convex border is formed by the right atrium and is vertical, the SVC and IVC entering in a vertical line at the top and bottom respectively.
The left border is marked by a convex line joining left ends of the superior and inferior borders. It is formed by the left ventricle except for a small part of the left atrium and its appendage at the top.
The inferior border extends from the lowest part of the right border to the apex of the heart. The apex is at the 5th intercostal space slightly median to the mid-clavicular line and is formed from the left ventricle. The position of this border varies slightly in the standing and supine position as well as respiratory movements. The lower border is formed mainly from the right ventricle but the larger part of the lower surface which is immediately above the diaphragm is formed by the left ventricle. It carries the posterior interventricular groove, which carries the posterior descending artery.
The posterior surface, vertebral surface or base is formed mainly by the left atrium and to a small extent by the posterior part of the right atrium. It is separated from the thoracic vertebrae 5th-9th by the pericardium, right pulmonary veins, oesophagus and aorta. At its junction with the diaphragmatic surface is the posterior part of the coronary sulcus containing the coronary sinus. LJR.A.001.01 Z:\Manuals\A & P manual.doc 2 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 INTERNAL STRUCTURE OF THE HEART The Atria
RIGHT ATRIUM
A quadrangular shaped chamber, which forms the right border of the heart. The SVC enters at the upper posterior part. Anterior and lateral to it is the right lung. Posterior to it is the intra-atrial septum. Medial to it is the ascending aorta and pulmonary artery.
It’s interior consists of 2 parts:
(1) Sinus Venosus (venarium)
Has a smooth thin wall and is formed from the foetal sinus venosus, which is absorbed into the right atrium. The great veins enter this part. The SVC at the upper posterior part, opening downwards and forwards. The IVC enters the lower posterior part just above the diaphragm. At its entrance is a rudimentary valve, the eustacian valve which in the embryo directs the blood from the IVC to the left atrium.
The coronary sinus, the main vein of the heart, enters between the IVC and AV opening, close to and immediately posterior to the AV orifice. At its entrance is a rudimentary valve, the thesbian valve. The IVC lies to it’s right.
(2) Atrium Proper
Lies anterior to the sinus venosus. It is derived from the primitive atrium and is continuous with the auricle. The crista terminalis is a vertical ridge of muscle, which separates the sinus venosus and atrium. It starts in the upper septum and passes anterior to the orifice of the SVC and then to the right of the orifice of the IVC, where it is continuous with the IVC valve.
The sulcus terminalis is an outer surface groove on the lateral wall, between the orifices of the SVC and IVC. Corresponding to the crista terminalis.
The crista terminalis, the valves of the IVC and the coronary sinus, represent the remains of the two venous valves which guard the opening of the sinus venosus into the right atrium in the embryo before the two merge to form the adult right atrium.
The auricle or atrial appendage is a small triangular muscular pouch which projects towards the left atrium and overlaps the root of the aorta.
Z:\Manuals\A & P manual.doc 3 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 Pectinate muscles are roughly parallel ridges of muscle which extend from the crista terminalis and extend into the atrial appendage.
The fossa ovalis is an oval depression in the lower part of the intra atrial septum above and to the left of the IVC. It is the remnants of the foramen ovale in the foetus which allows IVC blood to pass into the left atrium. The limbus fossa ovalis is a ridge derived from the free edge of the septum secundum which surrounds the fossa ovalis depression.
The IVC opening is directed towards the fossa ovalis and the IVC valve directs blood towards the fossa. The opening of the SVC lies in a more anterior plane and faces the right AV orifice. The intervenous tubercle is a small projection on the posterior wall just below the SVC which directs blood from the SVC to the tricuspid valve in the foetus. This provides separation of the IVC and SVC streams of blood in the foetus.
The anterior cardiac vein orifice opens into the right atrium on its anterior wall. This drains much of right coronary blood.
Foramen venarium minimum are the orifices of fine veins which return small amounts of blood from the heart muscle, are irregularly scattered and difficult to identify.
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Is smaller than the right atrium with slightly thicker walls. It is cuboidal in shape and lies posterior to the right atrium. Anterior and to the left are the aorta and concealed pulmonary trunk.
The cavity is largely smooth walled and is formed from the primitive pulmonary vein which is incorporate during its development. Initially a single common pulmonary vein opens into the primitive left atrium, but as the atrium expands parts of the vein are incorporated into the wall. The only part derived from the primitive atrium is the auricle.
Two pulmonary veins enter each side, often the two left ones have a common opening.
The auricle or appendage is a small conical pouch which projects forward from its upper left corner overlapping the pulmonary trunk. It is longer and narrower than the right one with margins, which are more deeply indented, with a constriction at its opening with the left atrium.
Pectinate muscles are fewer than the right atrium and are confined to the inner surface of the auricle.
The atrial septum has an oval impression bounded by a crescentic ring. This corresponds to the fossa ovalis of the right atrium.
Foramina venarium minima are minute venous openings which return blood from the heart muscle.
LJR.ISH.001.01 Z:\Manuals\A & P manual.doc 5 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 STRUCTURE OF THE HEART The Right Ventricle
Anterior is the pericardium and sternum. Inferior is the diaphragm. To the left and posterior the ventricular septum bulges into the right ventricle. It is crescent shaped in cross section and consists of two parts, the inflow and outflow portions. The inflow portion has rough walls with irregular muscle ridges, the trabeculae carnae. The outflow portion is the anetrosuperior smooth walled infundibulum (funnel) leading to the pulmonary valve. Separating the tricuspid and pulmonary orifices is a thick muscular ridge, the supraventricular crest. The infundibulum represents a persistent part of the bulbous cordis of the foetus which has been incorporated into the right ventricle. It provides support for the pulmonary valve during diastole.
The trabeculae carnae are rounded or irregular muscle columns projecting from the whole surface of the RV except the infundibulum.
They are of three kinds:
1. ridges 2. fixed at their ends and free in the centre 3. continuous at the base with the ventricular wall, apices projecting into the cavity.
The third type are the papillary muscles to which are attached the cordae tendinae, which fan out towards the tricuspid valve. The trabeculated inflow wall may help to slow inflow of blood during diastole and to increase contraction efficiency while the smooth walls of the outflow tract may help to increase velocity of ejecting blood.
The Tricuspid Valve
Three thin, roughly triangular shaped cusps, the anterior, posterior and septal make up the tricuspid valve. The cusps are not completely separated, the commisures not reaching the annulus. The valve leaflets are considered as a continuous curtain arising from or near the annulus with three grades of indentation dividing it into definable parts. The deepest indentations are the three commisures separating the main leaflets. Short fan shaped chordae attach at the margins of each commisure. Small clefts or indentations, also having fan shaped chordae divide the posterior leaflet into three scallops, while a single small notch exists on the margins of the septal and anterior leaflets.
Z:\Manuals\A & P manual.doc 6 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The anterior leaflet is the largest and is attached to the AV junction on the posterior aspect of the supraventricular crest but extends along its septal limb to the membranous septum ending at the anteroseptal commisure.
The septal leaflet is the smallest. It is attached to the posterior ventricular wall across the membranous septum to the anteroseptal commisure.
The posterior leaflet is attached to the ventricular wall.
The leaflets are formed from a continuation of the endothelial lining of the ventricle over layers of fibrous tissue, the lamina fibrosa.
The leaflets consist of three regions:
1. The rough zone is relatively thick, opaque and uneven on both faces, particularly the ventricular where most chordae are attached. Its atrial, inflowing face makes contact with another laeflet when the valve is closed i.e. the leaflets overlap to give an efficient closure. 2. The clear zone is smooth and translucent recieving few chordae and with a thinner layer of fibrous tissue. 3. The basal zone, 2-3mm from the valve attachment is thicker, with thicker connective tissue, blood vessels and some atrial muscle fibres.
The bases of the valve leaflets are attached to the AV fibrous ring and are joined to each other to form an incomplete fibrous annulus. The annulus does not correspond in every part to the valve leaflets, for some of the collagenous tissue of the leaflet may run for some distance in the ventricular wall before anchoring to the annulus. Their atrial surface is smooth and is not well demarcated from the atrium. Their ventricular surfaces are more irregular. The edges of the cusps are thin delicate and irregular in appearance and are attached to a number of thin delicate chordae tendinae.
Chordae tendinae are tough white collagenous cords continuous with the fibrous tissue of the valves. They arise from the tips or margins of the apical third of the papillary muscles and sometimes from the papillary bases or from the ventricular wall. They are attached to all zones of the valve leaflets, their commisures and clefts.
The papillary muscles of the right ventricle consist of two principle ones, the anterior and posterior and a smaller variable septal muscle. The anterior papillary muscle is the largest and is attached via chordae tendinae to the anterior and posterior cusps. The septal papillary muscle is attached to the anterior and septal cusps. It may be absent , the chordae tendinae originating directly from the septum. The posterior papillary muscle passes directly to the posterior and septal cusps. It may consist of two or three parts. A muscular band, the septomarginal trabeculae frequently extends from the ventricular septum to the base of the anterior papillary muscle and carries part of the conduction system. It has been thought to help prevent overdistention of the ventricle and to stabilise its contraction and is called the moderator band. Z:\Manuals\A & P manual.doc 7 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The Pulmonary Valve
Consists of three semilunar cusps which are attached at their convex margins to the wall of the pulmonary trunk at its junction with the ventricle. They are attached to an annulus of fibrous tissue in the vessel wall at its junction with the ventricle. Two cusps are situated anteriorly, the right and left. The third is posterior.
They consist of fibrous tissue covered by endocardium. Their free ends are strengthened by tendinous fibres and at the middle of the free margin there is a thickened nodule, the nodulus. From this, fibres radiate through the cusp to its attached margin and are continuous with the annulus. They are absent from two narrow crescentic portions, the lunules on either side of the nodule. Opposite the semilunar cusps, the pulmonary trunk has three slight dilations or sinuses.
LJR.RV.001.01 Z:\Manuals\A & P manual.doc 8 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 INTERNAL STRUCTURE OF THE HEART The left Ventricle
The left ventricle is larger and more conicle shaped than the right. It is oval or circular in cross section and has walls three times thicker (about 12mm) than the right ventricle. It forms the main parts of the diaphragmatic and left surfaces of the heart. It also forms the apex.
The AV orifice is below, behind and to the left of the aortic orifice. The mitral orifice is smaller than the tricuspid orifice. It is surrounded by an incomplete dense fibrous ring supporting the mitral valve. The aortic orifice is in front and to the right of the mitral orifice. It is circular with a diameter of about 2.5cm. The section immediately below the aortic valve is known as the aortic vestibule and has largely fibrous rather than muscular walls. The mitral and aortic valves are very close to each other and are only separated by a thin subaortic curtain of fibrous tissue. This is a sheet of fibrous tissue which descends from the adjacent halves of the left posterior and right posterior regions of the aortic annulus. The lower part of the subaortic curtain or intervalvular septum is the anterior cusp of the mitral valve. Thus the inflow and outflow tracts are separated only by the thin subaortic curtain forming a very acute angle between them.
The Mitral Valve
It consists of two triangular leaflets formed from endocardium over fibrous tissue with a few muscular fibres. As with the tricuspid valve it is attached to an incomplete fibrous annulus (one with different densities of fibrous tissue). This variation is thought to allow variations in the shape of the annulus at different stages in the cardiac cycle, ensuring optimal efficiency of the valve. The leaflets are larger, thicker and stronger than those of the tricuspid valve.As with the right valve they are not completely separate and a continuopus curtain of tissue is ergognised around the mitral orifice.
The anterior leaflet (aortic, septal or anteromedial) is the larger and is semicircular or triangular with few or no marginal indentations. It has a deep crescentic rough zone receiving various kinds of cordae tendinae and it touches the other leaflet when the valve is closed. From the rough zone to the valve annulus is the clear zone without chordae attached but with extensions of the rough zone chordae passing through its lamina fibrosa. The anterior leaflet has no basal zone and its fibrous tissue is continuous with that of the subaortic curtain.
The posterior leaflet (ventricular,mural,posterolateral), usually has two minor indentations or clefts which divide the valve into a relatively large middle scallop and smaller anterolateral commissural and posteromedial commissural scallop. Each scallop has a crescentic, opaque rough zone receiving chordal attachments on its finely serrated margins and ventricular aspects. These areas touch oter parts of the valve when the valve is closed. There is also a clear zone without chordae and a narrow basal zone which does receive chordae.
Z:\Manuals\A & P manual.doc 9 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 There are two large papillary muscles. The anterior one arises from the sternocostal surface and the posterior muscle from the diaphragmatic wall. Chordae tendinae from each papillary muscle are attached to both leaflets of the mitral valve. Opening and closure of the mitral valve;
At the beginning of diastole the valve is opened because the atrial pressure is greater than the ventricular pressure. The leaflets are parted and project into the ventricle. The leaflets begin to float passively together as filling continues. Atrial systole now occurs and the blood jet causes transient valve opening again. As maximal filling is reached the leaflets again float together. Ventricular systole starts. The co-ordinated contraction of papillary muscles raises tension in the cordae tendinae. As ventricular pressure rises rapidly, the leaflets balloon into the atrium and the atrial aspects of the rough zones come into contact. Precise papillary contraction and increasing tension in the cordae maintains valvular competence. When the ventricular pressure falls at the end of systole the process is repeated. The tricuspid valve operates in a similar manner. Both valves and orifices change their position, form and area during the cardiac cycle. The mitral valve reduces its area by as much as 40 % in systole. It also circular to crescentic at the height of systole.
The Aortic Valve
The aortic valve is similar to the pulmonary valve. The aortic annulus consists of three almost semicircular collagenous scallops, the whole encircling the vestibulo- aortic junction like a three pronged coronet. Parts of the annulus are continuous with the fibrous tissue of the subaortic curtain and the fibrous part of the IV septum. The three cusps are similar but thicker and stronger than those of the pulmonary valve. They consist of folds of endocardium with a central lamina fibrosa. With the valve half open each cusp equals slightly more than a quarter of a sphere. Each cusp has a thick basal attached border deeply concave on its aortic aspect and a horizontal free margin which is slightly thickened except at its midpoint where there is an aggregation of fibrous tissue, the valvular noduli of aranti. Fine collagenous fibres radiate from this to the attached border where the basal fibres blend with the annulus. At the apices of the commisures a few transverse collagen fibres pass between the adjacent cusps.
The cusps have a number of names;
1. anterior or right coronary cusp
2. left posterior or left coronary cusp
3. right posterior or non-coronary cusp
Z:\Manuals\A & P manual.doc 10 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The aortic sinuses of valsalva are more prominent than those of the pulmonary valve. The upper limit of each sinus reaches well above the limit of the free cuspal border and forms a well defined supraventricular ridge. Coronary arteries open near this ridge, the left often being a little lower. The walls of the sinus are collagenous close to their fibrous annulus, but become more elastic further up. At sinus mid level its wall is about half the thickness of the supravalvular aortic wall. At this level the mean diameter of the aortic root is about twice that of its origin. During diastole, the closed aortic valve supports a column of blood at high pressure. The cusps are tightly closed and opposed on their ventricular aspects. As ventricular pressure rises during systole the valve is opened. The sinus wall nearest the aortic vestibule is almost inextensible, but in the upper parts of the sinuses it is very elastic and the radius here is increased by 16 % in systole. Hence the commisures move apart and the orifice becomes triangular, with the cusps becoming straight lines between the commisures. However they do not flatten against the sinus walls even at maximum systolic pressure which is probably an important factor in subsequent closure. During ejection some blood enters the sinuses forming vortices which help to maintain the triangular mid position of the cusps during systole and probably initiates their coming together as systole end.
Thus the sinuses help to prevent regurgitation;
With sinuses – 4 % regurgitation Without sinuses – 23 % regurgitation
Normal sinuses may also promote non-turbulent flow through the coronary arteries.
LJR.LV.001.01 Z:\Manuals\A & P manual.doc 11 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 INTERNAL STRUCTURE OF THE HEART
The Interventricular septum and Pericardium
The Interventricular septum The IV septum is mostly thick, muscular and is curved with it’s convex surface towards the right ventricle. At its upper part, just below the junction of the anterior and right cusp of the aortic valve, there is a thin fibrous area, the membranous part of the septum. This section is small and oval in outline. On its right side it is crossed by the upper part of the septal cusp of the tricuspid valve dividing it into anterior and posterior sections. The anterior separates the two ventricles, while the posterior separates the aortic vestibule of the left ventricle and the right atrium near the fossa ovalis. The fibrous septum is partly continuous with the fibrous supports of the anterior and right posterior aortic cusps.
The Pericardium
The pericardium encloses the heart and the roots of the great vessels. It lies in the mediastinum, behind the sternum and the costal cartilage from 5-8. It consists of two layers of serous membranes with a film of fluid between them allowing freedom of movement for the heart.
It consists of an outer sac, the fibrous pericardium consisting of fibrous tissue and an inner double layered sac, the serous pericardium. This is a delicate membrane, which lines the sac and covers the heart.
The fibrous pericardium is cone shaped, the apex being continuous with the walls of the great vessels. Its base is attached to the central tendon and to a small part of the diaphragm. It is also attached to the posterior surface of the sternum by the sternopericardial ligaments at its upper and lower ends. It is thus anchored within the thoracic cavity and maintains the hearts position in the chest and also prevents overdistention. Anteriorly it is largely separated from the sternum by lung contact (the lower left part of the sternum and the sternal ends of the 4th and 5th ribs on the left-hand side). Posterior to it are the principle bronchi, oesophagus, the descending aorta and the medial posterior section of the lungs. To the sides are the phrenic nerves passing between the pericardium and the pleura.
Z:\Manuals\A & P manual.doc 12 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The vessels that receive parts of pericardium are the aorta, SVC, right and left pulmonary arteries and four pulmonary veins. The IVC enters the pericardium through the central tendon of the diaphragm; thus it is not directly covered by fibrous pericardium.
The serous pericardium is a closed sac lining the fibrous pericardium and covering the heart. The visceral portion or epicardium covers the heart and the great vessels and from the vessels is reflected to form the parietal layer which lines the fibrous pericardium. The part covering the vessels is formed into two tubes. The aorta and pulmonary artery are enclosed within one tube, the vena cavae and pulmonary veins are enclosed within the second tube.
The fibrous layer is made of dense collagenous tissue. The serous layer consists of a single layer of simple squamous epithelia resting on a layer of areolar tissue that lies directly over the myocardium. This areolar layer contains fat that is greatest in amount along the ventricular border of the AV sulcus.
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ANATOMY OF THE ELECTRICAL CONDUCTING SYSTEM
MYOCYTE CONTRACTION AND DEPOLARIZATION
Myocyte contraction occurs as a result of cellular depolarization brought about by ion movement across the cell membrane. The cellular structure of cardiac muscle cells allows these electrical changes to be propagated from cell to cell, so that a wave of depolarization will spread through the muscle tissue and result in a wave of contraction.
ELECTRICAL CONDUCTING TISSUE
Coordinated depolarization of cardiac muscle is essential for the heart to act as a pump. Specialized conducting tissue exists in the heart to ensure that the action potential is propagated effectively through the muscle tissue.
PACEMAKER CELLS
The intrinsic rate of depolarization of the myocytes is determined by a specialized group of cells called pacemaker cells, which are located at the Sino-Atrial Node. These cells depolarize more rapidly than other myocytes, and therefore initiate each wave of contraction/conduction of the heart muscle. These cells basically determine heart rate.
CELLS OF THE CONDUCTING SYSTEM
The cells of the SA node and conducting tissue are modified muscle cells, and still retain some of their internal features. The cells making up the conducting fibres vary in diameter at different points of the conducting pathway; this affects the rate of transmission of the action potential. The purkinje cells which form the branching network of fibres throughout the ventricles have the largest diameter and therefore conduct action potentials most rapidly.
Z:\Manuals\A & P manual.doc 14 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 DEPOLARIZATION OF THE ATRIA
The SA Node is located just below the epicardium, close to where the superior vena cava opens into the Right Atrium (RA) and it is supplied with blood by the sino- atrial artery. The wave of depolarization begins here spreading across the atria; impulses may be transmitted through the RA to the AV Node through intra–atrial tracts. These tracts are thought to be bundles of muscle fibres or myocardial muscle ridges which aid propagation of depolarization. These tracts are known as the Bachman, Thorel and Wenkebach tract. The evidence to suggest that these tracts are electrical ie. Specialized conducting tissue is controversial.
THE ATRIO-VENTRICULAR NODE
The AV Node is located on the septal surface of the RA, below the endocardial layer, in a region known as the triangle of KOCH. This region is bounded by the tendon of Todaro, the opening of the coronary sinus, and the attachment point of the septal cusp of the tricuspid valve. The tendon of Todaro is formed by the junction of the valves covering the openings of the inferior vena cava and coronary sinus, and extends to the central fibrous body. The electrical impulse which reaches this node pass into specialized conducting fibres which carry the impulse through to the ventricles. These fibres allow the action potential to be propagated across the barrier formed by the by the hearts non-conducting fibrous skeleton between the atria and ventricles.
DEPOLARIZATION OF THE VENTRICLES (1)
The transmission of the action potential from the atria to ventricles is delayed by its passage through the transitional myocytes of the AV Node. The wave of depolarization is slowed dramatically before it moves into the rapidly transmitting cells of the Bundle of His and the bundle branches. Finally it reaches the purkinje fibres which propagate it to the ventricles. This delay at the AV Node ensures atrial contraction precedes ventricular contraction, so all the blood is expelled from the atria into the ventricles before ventricular contraction takes place.
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VENTRICULAR CONDUCTING TISSUE
The cells of the conduction system leaving the AV Node are gathered into a tract called the Bundle of His (BOH), which passes into the interventricular septum (IVS) below and behind the membranous septum and then divides to form the left and right bundle branches. These branches travel along the interventricular septum and then branch to form a network of purkinje fibres beneath the endocardial tissue, which transmit the impulse across the whole ventricular surface.
DEPOLARIZATION OF THE VENTRICLES (2)
An insulating layer of fibrous tissue surrounds the bundle branches as they travel down the IVS. This prevents the action potential from reaching the surrounding myocytes. The bundle branches lose their insulating sheath as they near the apex of the heart, allowing the action potential to spread throughout the purkinje system to the adjacent myocytes. The wave of ventricular contraction therefore spreads from the apex of the heart towards the base forcing blood in the ventricles up and out through the aortic and pulmonary valves.
Z:\Manuals\A & P manual.doc 16 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 THE CONDUCTION SYSTEM
The Conducting system – overview
The heart beats because of the spread of electrical impulses to the heart muscle, causing it to contract. The cardiac conducting system, is a network of specialised tissue in the heart.
The Sino-Atrial Node
In the normal heart, the impulses are emitted by the hearts own natural pacemaker, the sinus node (Sino Atrial Node). This specialised group of neuromyocardial (conducting) cells, approximately 5 x 20mm are located epicardially, in the upper right atrial wall close to the SVC, right atrial appendage and the lateral wall of the right atrium.
From there the impulse spreads across the atrial myocardium. The myocardial cell membrane, like membranes of other muscles in the body, has the ability to conduct a propagated action potential or depolarisation wave. Likewise as in skeletal muscle, depolarisation of the myocardial cell membrane, a propagated action potential results in myocardial contraction.
The impulse spreads across the atrial muscle causing it to contract, and passes down to the atrio-ventricular node in the floor of the right atrium. Electrical depolarisation of the atrial myocardium is represented on the ECG as a ‘P’ wave.
Throughout the atria there may be pathways thought to be present due to muscular bands or tracts present in the atrial myocardial wall. These pathways are called: - The Bachman Tract, the Wenckebach tract and the Thorel tract. It is not proven however that these tracts actually exist, but that the presence of muscular ridges may propagate the atrial wave of depolarisation across the atria.
Each part of the conducting system has the ability to produce its own rate and rhythm. If an electrical signal is not received from its preceding neighbour, each component will discharge naturally. This is termed the intrinsic discharge rate, (IDR). The IDR for the SA node is approximately 80 beats per minute.
The SA Node has a rich nerve supply from the Sympathetic and Parasympathetic autonomic nervous systems. The heart rate responds briskly to stimulation from either – sympathetic stimulation causing increased heart rate, parasympathetic stimulation causing a decrease.
Z:\Manuals\A & P manual.doc 17 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The blood supply to the SA Node is conveyed by either the Right Coronary artery, the circumflex branch of the left coronary artery with equal frequency or very occasionally from both vessels.
The atrio-ventricular node
The spread of depolarisation reaches the Atrio-Ventricular node. The AV node is tadpole shaped, 2 x 5mm and sits endocardially in the septum at the junction between right atrium and right ventricle –the AV junction. Here the electrical impulses are delayed by approximately 0.15 seconds. This delay gives the atria time to expel their blood into the ventricles, allowing adequate time for ventricular filling and also provides protection to the ventricles from any fast atrial arrhythmias. This is represented on the ECG as the PR interval.
The intrinsic discharge rate of the AV Node is 60 bpm.
There is also autonomic nervous control of the AV Node but the effects are not so pronounced as for the SA Node. Sympathetic stimulation not only increases the rate of discharge, but also shortens the AV nodal conduction time and the duration of the refractory period. Parasympathetic stimulation has the opposite effect, decreasing the discharge rate, lengthening the AV conduction from the refractory period.
Blood supply to the AV Node is from the right coronary artery in approximately 95% of the population, from the circumflex artery in approximately 5 % and occasionally from both vessels.
The Bundle of His
The bundle of His is directly continuous with the AV Node. It is approximately 20mm long and is located in the endocardial surface of the interventricular septum. The AV Node and the bundle of His is normally the only pathway across the fibrous ring, which separates the atria from the ventricles.
The cardiac impulse spreads to the ventricular septum via the Bundle of His (a discreet tract of specialised conducting cells), which crosses the fibrous ring at the atrioventricular junction and runs along the walls of the ventricular septum.
The intrinsic discharge rate of the bundle of His is 50 bpm. Nervous stimulation of the Bundle of His has a minor effect only. There is no dedicated vessel for blood supply, but the most important artery is the left anterior descending artery.
Z:\Manuals\A & P manual.doc 18 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The Bundle Branches
The Bundle of His separates into two main branches, the left and right Bundle Branches, which rapidly conduct the electrical impulses to the ventricles. The left branch divides further into the Antero-Superior division and the Postero-Inferior division. The intrinsic discharge rate of the bundle Branches is approximately 40 bpm.
The purkinje fibres
The bundle branches split further into smaller fibres, which fan out from the endocardial surface to the epicardial surface, the purkinje fibres. In this manner the entire musculature of the ventricles is induced to contract almost simultaneously, guaranteeing powerful pumping performance. Bundle Branch and purkinje fibre activation constitutes ventricular depolarisation which is represented on the ECG as the QRS.
The intrinsic discharge rate is 20 bpm. Nervous stimulation of the purkinje fibres has a minor effect only. There is no dedicated blood supply, this is obtained from the arteries supplying the adjacent myocardium.
Left Bundle Branch Antero-superior Division LBB
SA Node Division Left Bundle Branch Postero-Inferior Division
Purkinje
AV Node Fibres purkinje
BundleBundle Of ofHis His
RightRight Bundle Bundle Branch Br anch
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When the body is at rest, the sinus node emits electrical impulses, which stimulate the heart about 70 times a minute. The ability of the heart to increase its rate of contraction in conjunction with mental or physical exertion, or to reduce that rate after exertion is due to the emission of both exitory (sympathetic) and inhibitory (para- sympathetic) nerve impulses causing the sinus node to work more rapidly or more slowly.
All the parts which are responsible for the hearts electrical activity jointly constitute the hearts conduction system.
The autonomic nervous system (sympathetic and parasympathetic) have only a modulating influence on impulse formation and conduction within the heart.
Fibres of the vagus nerve (parasympathetic) innervate the atria, including the sinus node and atrioventricular node, but there is only a small input to the ventricles. The sympathetic fibres form a dense network in both the atria and ventricular muscle.
LJR.TCS.OO1.01 Z:\Manuals\A & P manual.doc 20 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 CORONARY CIRCULATION
The right and left coronary arteries arise from the coronary ostia or sinuses of valsalva behind the cusps of the aortic valves. They lie on the epicardial surface of the heart and penetrate the myocardium before terminating on the endocardial surface of the heart.
The left coronary artery divides after about one centimetre into the left circumflex and the left anterior branches.
The anterior descending artery appears on the anterior surface of the heart between the uppermost part of the infundibulum of the right ventricle and the left atrial appendage. The anterior descending artery supplies the free walls of the left and right ventricles and the greater part of the IVS.
The circumflex artery arises at an acute angle from the stem of the left coronary artery. It passes forward under the left atrial appendage and then sweeps around the left surface of the lying in the fatty connective tissue of the atrio-ventricular groove or sulcus. Alongside the artery lies the great cardiac vein. It gives off branches that supply the postero-lateral and inferior part of the left ventricle, including the apex. The left atrium is supplied by the circumflex artery.
The 1st branch of the right coronary artery is the conus artery. The right coronary artery first runs forward and to the right and emerges on the anterior surface of the heart between the right atrial appendage and the root of the pulmonary trunk. It then passes round the right atrio-ventricular sulcus where it gives rise to the interventricular posterior descending artery. The right coronary artery supplies most of the right ventricle, the posterior base of the left ventricle, part of the inferior surface of the left ventricle, the posterior part of the IVS and the right atrium.
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The SA Node is usually supplied by:
The right coronary – 70 %
The left coronary – 25 %
Both – 5 %
The AV Node is usually supplied by:
The right coronary – 80 %
The left coronary – 10 %
Both – 10 %
The same artery that supplies the AV Node supplies the Bundle of His and the first few millimetres of the two bundle branches. For the remainder of their course the bundles lie on either side of the muscular part of the IVS and are normally supplied by septal branches of the LAD. The posterior descending branch of the right coronary artery also supplies the posterior fascicle of the left bundle branch as well as the LAD.
The origin of the posterior descending artery arises from:
The right coronary – 50 % (right dominance)
The left coronary – 20 % (left dominance)
Both – 30 %
Capillaries – Small vessels arise from the epicardial vessels to penetrate the myocardium. In the newborn there is a ratio of 1 capillary to 4-6 muscle fibres. This ratio is reduced with age until it is 1:1 in the adult. In hypertrophy the ratio is the same, therefore each capillary supplies a large volume of muscle.
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Venous Drainage
70 –80 % of coronary flow drains into the right atrium via the coronary sinus. This lies in the AV groove at the lowest part of the posterior surface of the heart. It is a wide venous channel about 3 cm long and it opens into the lower medial part of the sinus venarium between the opening of the IVC and the attachment of the septal cusp of the tricuspid valve. The coronary sinus orifice is guarded by the thesbian valve, which shows marked variation in size.
The drainage of blood into the coronary sinus includes mostly left ventricular blood drainage. The veins that drain into the coronary sinus are the great cardiac vein, the middle cardiac vein and the small cardiac vein.
The anterior cardiac veins drain most of the right ventricular blood opening directly into the right atrium just above the tricuspid valve. Tiny microscopic vessels (thesbian veins) drain directly into the RA and RV chambers, carrying a small amount of de- oxygenated blood into the right side of the heart.
Coronary Flow
Collateral vessels may develop in response to gradual narrowing of coronary arteries. They develop between branches of occluded and non-occluded arteries probably originating from pre-existing small vessels that undergo changes in the endothelium and smooth muscle in response to wall stress and chemicals produced by the ischaemic tissue.
Factors affecting coronary flow
A much greater percentage of oxygen (75 %) is extracted than in other tissue, therefore to increase supply (e.g. during exercise) there is great dependence on increased flow.
Aortic pressure
Flow is the result of aortic pressure, therefore changes in aortic pressure result in alterations of flow. However if the aortic pressure is increased, the heart must perform more work to eject against the increased pressure, it’s oxygen demand increases and chemical autoregulation will mostly influence control. If perfusion pressure is increased experimentally without increasing the pressure against which the heart must pump the blood, autoregulation gradually brings flow back towards the level before perfusion pressure was increased. Therefore chemical control is the important factor controlling flow. Z:\Manuals\A & P manual.doc 23 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004
Extravascular compression
When the heart contracts the smaller vessels are squeezed by the contracting muscle. Therefore flow is greatest during diastole (about 2/3rd diastole, 1/3rd systole). Left ventricular myocardial pressure is greatest near the endocardium and lowest near the epicardium. In a normal healthy heart, the flow to subendocardial and subepicardial areas is the same, indicating a difference in the resistance of the vessels. In diseased hearts with coronary occlusion, the endocardial region is affected more than the epicardium and is therefore more likely to be damaged following coronary occlusion.
Rate Changes
When heart rate increases, the length of diastole is reduced and this emphasises the problem of supply. Increased metabolic activity however increases vasodilation.
Aortic Stenosis
Aortic stenosis requires an increased differential pressure and an increased compression during systole. Therefore patients with aortic stenosis are more prone to ischaemia.
Phase Changes
Left Ventricle – early in systole the intramural pressure is greatest, flow drops to a minimum and may reverse. At the beginning of the ejection phase flow increases and coronary pressure follows aortic pressure. It gradually falls as the pressure gradient decreases. Peak flow occurs early in diastole and gradually falls as aortic pressure falls. Right Ventricle – phasic changes are not so marked in the right ventricle. Intramural pressure is not so great and may not cause cessation of flow. Reversal does not occur.
Venous blood is massaged out of the wall by ventricular contraction and venous flow speeds up during systole.
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Neural and Chemical control
Direct automatic innervation of the coronary vessels is relatively unimportant. In the sympathetic system both alpha and beta receptors are present. On balance, sympathetic stimulation probably causes slight vasodilation. Effects of vagal stimulation directly on the vessels are not well understood. The main factor increasing coronary flow in response to autonomic influences is local chemical autoregulation. When the sympathetic system is active, cardiac work and oxygen consumption is increased and metabolites build up. The metabolite acting on coronary vessels to cause dilation is adenosine. Parasympathetic activity results in vasoconstriction because of the reduction in cardiac work and the fall in adenosine levels. At the same time sympathetic activity is reduced.
LJR.CC.001.01 ACTION POTENTIALS
Basic Principles
Electrocardiography is a method of assessing the electrical activity within the heart. The basic principle of depolarisation involves the action potential and ionic change at cellular level.
Most cells within the body are ‘polarised’ i.e. there is a difference of electrical potential between the inside and outside of the cell. This difference is attributable to differences in concentration of ions.
Certain tissues have specialised functions dependant on their electrical polarisation. There are nervous and muscular tissues which have the properties of conductivity i.e. an electrical impulse initiated at one point is able to spread along a cell and from one cell to another. Muscle tissue also has the property of contractility i.e. the mechanical property to shorten (contract) and so perform work.
In normal circumstances every contraction of a muscle is preceded by a change in electrical state of the lining membrane of the cell known as ‘Depolarisation’.
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Action Potential of non-pacing cardiac cells
• Cardiac cells are surrounded by a membrane which is permeable to certain ions, sodium, potassium and chloride. In the resting state the inside of the cells has a high concentration of potassium ions and the inter-cellular potential is negative at about 90mv.
• There is a concentration of sodium ions on the outside of the cell and this area is positive relative to its environment. The concentrations of sodium ions on the outside of the cell and this area is positive relative to its environment.
• The concentrations of potassium inside and sodium outside the cell are maintained by the sodium/potassium exchange pump, which transports sodium out of the cell and potassium into the cell.
• This resting state is known as polarisation. The normal polarisation state of a cardiac cell membrane is dependant upon the maintenance of the normal ionic balance across the membrane. Any disturbance of this balance will cause ECG changes.
• When a stimulus is applied to the cell membrane its permeability changes. The fast sodium channels open allowing sodium to move into the cell and at the same time potassium leaves the cell. As a result the intercellular potential changes from –90mv to +20mv.
• This rapid phase of change is known as depolarisation.
In all excitable cells, the action potential starts with a rapid initial depolarisation (phase 0). Cardiac cells differ in that they exhibit a slow delayed repolarisation in three phases:
Phase 1 – early rapid repolarisation
Phase 2 – slow repolarisation known as the plateau
Phase 3 – terminal phase of relatively rapid repolarisation
During phases 0, 1 and 2, the inside of the cell is temporarily positive relative to the outside, which is negative. This is termed overshoot or reversal.
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Refractory period
The membrane becomes refractory once phase 0 of the action potential ascends to approximately –50mv. It remains absolutely refractory until phase 3 descends to approximately –55mv. From that point the membrane is relatively refractory.
Absolute refractory period (ARP) The cell will not depolarise again, no matter how strong the stimulus
Relative refractory period (RRP) If the stimulus is strong enough, further depolarisation can occur. This is a vulnerable and excitable period of the action potential.
+20 1 2 0
3
0 Threshold Potential -60
4 4 -90
Absolute RP Relative RP
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Cell Membrane Depolarisation
(a)Cardiac muscle in the resting state
The cell is polarised (-90mv inside the cell compared to the outside)
+ + + + + + + + + + + ------+ + - - + + ------+ + + + + + + + + + + + +
(b)Stimulus
- - - + + + + + + + - ++ + ------+ - + - + - + + ------+ - + - - - + + + + + + +
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(c)The impulse spreads down the cell
------+ + - ++ + + + + + + - - + - + - + - + + + + + + + - - + - + ------+ +
(d)The entire muscle cell is depolarised (+25mv inside the cell)
------++ + + + + + + + + - - + + - - + + + + + + + + + ------
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After contraction, the chemical and electrical status quo must be restored by a process called ‘Repolarisation’.
This sequence of myocardial depolarisation and repolarisation gives rise to the electrocardiogram.
In ordinary muscle the cells lie parallel, each being independent of the others, a depolarisation in one has no effect on its neighbours. Simultaneous depolarisation so as to produce synchronised forceful contraction is provided by virtue of the fact that the controlling nerve splits up and has a fibre terminating on each individual cell. So any nerve impulse stimulates all the nerve cells simultaneously.
Each myocardial cell is connected to its neighbour, so if one cardiac cell depolarises, adjacent cells will be depolarised in the same way and therefore the wave of depolarisation will spread across the whole muscle providing effective contraction. Depolarisation conducted in this way is much slower than in nerve fibres, but it means that co-ordinated contractions can be produced in heart muscle without dependence on outside nervous system.
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Action Potential of a pace-making cell
The action potential of a pacing cell differs in that the velocity of the upstroke of phase 0 is slower. Reversal is small or absent. The peak is rounded. Phase 2 has a steeper decline and therefore there is not normally a plateau. Depth of a resting potential is less than that of a non – pacing cell. The most characteristic feature is the slow spontaneous depolarisation during phase 4 or diastolic depolarisation. The resting potential exhibits a gradual and continuous upward slope, phase 4, starting immediately after phase 3 resulting in a gradual loss of resting potential (it becomes less negative). When it reaches its critical threshold, there is a smooth but rapid transition to the upstroke of phase 0. The effect of diastolic depolarisation is that of the resting potential regularly and automatically reaching its threshold level, resulting in regular, spontaneous automatic discharge, thus diastolic depolarisation reflects the pacemaker property of ‘Automaticity, or ‘Rhythmicity’.
1
0 R
-40 Threshold 4 Potential Resting Potential
R = The repolarisation phase is difficult to divide into phases 2,3 and 4.
LJR.AP.001.01 Z:\Manuals\A & P manual.doc 31 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The Action Potential And Drugs
The action potential process is composed of 5 phases (0-4). The ECG records the product of the action potentials of the muscle cells in the atria and ventricles as P- QRS-T waveforms. Action potential reflects the passage across the cell membrane of different currents carried mainly by sodium(Na), potassium(K) and calcium (Ca).
It is important to understand the action potential process in order to understand how ECG waveforms are generated. Knowledge of this process also helps to explain how drugs (particularly antiarrhythmics), electrolyte disorders and other conditions may alter components of the ECG.
VAUGHAN WILLIAMS CLASSIFICATION
+20 1 mv 2
0 3
4 4
-90mv
Intracellular
Cell membrane
Extracellullar Na+ Ca2+ K+ Na+ Na+/K+ ATPase
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Depolarisation – Rapid influx of Na through specific voltage gated ion channels. Triggered when specific Na+ channels have been opened to allow the cell to reach its threshold potential. When the intracellular potential is +ve, the Na+ channels close. Repolarisation is initiated by opening of specific K+ ion channels. Temporarily interrupted by Ca2+ which maintains depolarised state. Na/K+ transmembrane concentration gradients are restored by Na/K+ ATPase.
PHASE 4: ACTION POTENTIAL OF A MUSCLE CELL AT REST
At rest each muscle cell is charged (polarized). The outside of the muscle cell is positively charged and the inside is negatively charged. The action potential is directly related to the difference between the outside and inside charges. Cations (positively charged ions) generate the action potential. At rest, the cations Sodium and Calcium are outside the cell, Potassium is inside the cell. Sodium and Calcium are unable to cross into the cell at rest, but Potassium leaks out of the cell slowly. The slow loss of positive Potassium ions causes the inside of the cell to become more negatively charged, compared with the outside of the cell which is more positively charged.
PHASE 0: DEPOLARIZATION
When a muscle cell at rest is stimulated (activated) the inside of the cell suddenly becomes positively charged and the outside negatively charged. This is due to rapid inward rush of Sodium cations from outside to inside the cell. Sodium enters the cell through pathways called fast channels. Calcium cations also enter the cell but more slowly through the slow channels. The influx of Sodium and Calcium into the cell causes the inside of the cell to become positively charged.
The fast Sodium current is present in all normal atrial and ventricular myocardial cells, and exhibits an all or none conduction rate but is absent in the SA node and AV node cells which depolarize due to a much slower calcium current. This slow depolarisation is the reason for the physiological delay in conduction which occurs in the AV node.
The rapid change of polarity on the inside and outside of the cell during phase 0 is known as depolarization, through which the cell is immediately activated to contract. Depolarization is the electrical process that is recorded on the ECG. In the atrial muscle cells during phase 0 (depolarisation) their activity correlates with the P wave on the ECG. Likewise, in the ventricular muscle cells during phase 0 their activity correlates with the QRS complex on the ECG.
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PHASE 1,2 & 3: REPOLARIZATION
Immediately after depolarisation, repolarisation occurs when the muscle cell returns to its previous resting state. This is also recorded on the ECG. The polarity of the muscle cell is restored so that the outside of the cell is again positively charged and the inside negatively charged. The 3 phases are;
Phase 1: The fast sodium channels suddenly close, but the slow calcium channels remain open
Phase 2: Plateau phase. The continued flow of calcium into the cell is balanced by the flow of potassium to the outside of the cell. Phase 2 correlates with the ST segment of the ECG.
Phase 3: The calcium channels close, but potassium continues to leak to the outside. Phase 3 correlates with the T wave on the ECG.
CLINICAL IMPORTANCE OF ACTION POTENTIAL
Pacemaker cells are described as slow cells as their depolarisation is dependent on calcium entry into the cells through slow channels. Muscle cells are described as fast cells because their depolarisation is dependent on sodium entry into the cells through fast channels. Many drugs used to treat arrhythmias alter certain phases of the action potential. Their specific mechanism of an action may slow or retard the usual process of depolarisation and depolarisation to prevent or treat arrhythmias.
Calcium channel blockers (class 4) inhibit the slow channels in pacemaker cells resulting in a decrease in heart rate in patients taking these drugs.
Class I antiarrhythmics inhibit the fast sodium channels in muscle cells which effectively inhibits phase 0, depolarisation of the muscle cells to suppress ectopic impulses.
Class III drugs alter several phases of the action potential but their exact mechanism is unknown.
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Antiarrhythmic Drugs Classified by mechanism of action
Class I Block Sodium (Na) channels
Class II Beta blockers
Class III Block Multiple phases of the action potential
Class IV Calcium channel blockers
CARDIAC DRUGS
Class Drug
I Block Sodium channels Disopyramide, Flecanide, Phenytoin, Procainamide Quinidine, Lignocaine
II Beta Blockers Atenolol, Metroprolol, Propranolol, Sotalol, Timolol, Esmolol
III Block multiple phases Amiodarone, Bretylium
IV Calcium channel blockers Diltiazem, Nifedipine, Verapamil
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CLASS 1
These drugs slow the rate of rise of phase 0 by inhibiting fast Na+ channels – known as membrane stabilisers. The class is subdivided according to the effects of the drug on the duration of the action potential.
CLASS 1A
Increase the duration of the action potential. Moderate – marked Na channel blockade. Refractoriness of the cell is prolonged due to multiple K+ channel blockade.
+20
-90
DRUGS: Quinidine Disopyramide Procainamide
Quinidine: Absorbed in the gut. Peak level 1-3 hours after single oral dose and persists for 6-8 hours.
Side Effects: GI disturbances, -ve inotropic effect can also cause VF or AV block
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CLASS 1B
Reduce the duration of the action potential. Mild-Moderate Na+ channel blockade produced but has little effect on refactoriness since no blackade of K+ channels.
+20
-90
Drugs: Lignociane Metilitene Phenytoin
Lignociane: Cannot be given orally due to it being potentially toxic. Patients are given a bolus and then an IV infusion so as to get levels up quickly and maintained.
Side effects: CNS toxicity Convulsions -ve inotropic bradycardia
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These have no effect on the duration of the action potential. Marked Na channel blockade is produced and refractoriness is increased to specific blockade of K channels responsible for repolarisation.
+20
-90
Drugs: Flecanide Encainide Propafenone
Flecanide: Orally absorbed. Half life only <20 hours.
Side effects: CNS toxicity -ve inotropic
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CLASS II
B-adrenoceptor antagonist which reduces the rate of spontaneous depolarisation of sinus and AV nodal tissue and some ectopic foci in phase 4 by indirect blockade of Ca2+ channels, reversing the effects of catecholamines.
+20
-90
Drugs: Atenolol Propanolol Esmolol
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Prolonged duration of action potential, thus increasing the absolute refactory period. Result of this a reduction in K+ influx
+20
-90
Drugs: Amiodarone Bretylium Sotalol
Amiodarone: This drug also has Class 1A properties as it blocks Na channels during phases 2 + 3. Absorption is by the gut but is variable. Peak plasma levels at 6-8 hours after oral dose. Half life is 30-110 days. Therapeutic effect occurs after 10-15 days of oral therapy, but may take 3-6 weeks. This drug continues to work for up to 50 days after is has been stopped.
Side effects: GI disturbances Corneal micro deposits Hypothyroidism Photosensitive skin rashes Drug interactions – warfarin and digoxin Does not have –ve inotropic effects
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Certain slow Ca 2+ channel antagonists have specific actions on SA and AV nodes, stabilising phase 4 of the action potential.
+20
-90
Verapamil: Well absorbed orally. Only 10-20% of the drug actually enters the systemic circulation. With IV, the entire drug enters the systemic circulation therefore a smaller dose must be given. Half life is 3-4 hours.
Side effects: Reduced cardiac contractility Bradycardia/Heart block Constipation
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In addition to the drugs listed above there are 3 other arrhythmia drugs which are not in the Vaughan Williams Classification. These are:
Digoxin Adenosine Atropine
Digoxin: The receptor for digoxin is Na+/K+ATPase
Na+/K+ pump maintains Na+ and K+ gradients across the cell producing low intracellular Na+ and high extracellular K+.
Partial inhibition of the pump by Digoxin increases intracellular Na+ and reduces concentration gradient for Na+ across cell membrane.
Thus, the reduction in passive Na+/Ca+ exchange and increase in intracellular Ca+ = Enhanced contraction.
Digoxin also produces central stimulation of the vagus nerve and enhances cardiac sensitivity to acetylcholine. These actions increase the refactory period of the AV Node.
Adenosine: Potent effects on SA Node allows slowing impulse conduction through the AV Node.
Atropine: Increases conduction through the AV Node via blockade of Muscurinic M2 receptors.
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SUMMARY
Antiarrhythmic drugs have the potential to precipitate arrhythmia, particularly VT or VF.
SVT : Atrial fibrillation or Atrial flutter – Digoxin, Slows down the ventricular rate.
Class II, III or IV alternatives to Digoxin
Class 1A or 1C can be used for AF, but they can be dangerous for atrial flutter as by slowing the atrial rate you are increasing the conduction rate through the AV Node.
Atrial Tachycardia – Use verapamil or Adenosine
Class III – Very good for resistant arrhythmias
Ventricular arrhythmia: Lignocaine or Amiodarone
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CARDIOVASCULAR DRUGS
B-BLOCKERS
Actions: Antagonise effects of catecholamines, therefore reducing heart rate, myocardial contractility and systemic blood pressure. The overall effect is to reduce myocardial work and oxygen consumption. Two types of beta-receptors; cardiac (beta 1) and bronchial (beta 2). Drugs are divided into which beta-receptor they have a particular affinity for.
Indications: Used in hypertension and post MI to reduce the rate of re-infarction.
Noncardioselective: Propanolol, soataolo, Nadolol, Oxyprenolol, Pindolol and Timolol.
Cardioselective: Atenolol, Metropolol, Acebutolol, Bisoprolol
Alpha & Beta-blocker: Labetalol
Side effects: Bradycardia, Heart failure, bronchospasm, nightmares, insomnia, depression and peripheral coldness
CALCIUM ANTAGONISTS
Actions: Prevents uptake of calcium by cells so reducing sensitivity of cardiac muscle to stimulation, reducing myocardial work (myocardial oxygen consumption), reducing heart rate and causing vasodilation of coronary and peripheral blood vessels so as reducing blood pressure. Some are more effective in angina than hypertension and some have no antiarrhythmic potency depending on their specific mode of action.
Phenylalkylmines: Verapamil – a class I and Class IV antidysrhythmic particularly used for supraventricular tachycardias as an IV dose. Orally used for angina and hypertension.
Dihydropyridines: Nifedipine, Nicorandil, Amlodipine – class II. Reduces peripheral and coronary vascular resistance, used for angina and hypertension.
Benzothiazepines: Diltiazem – Class III. A vasodilator, so used in angina. Slow release preparations used for hypertension.
Side Effects: verapamil and diltiazem can cause varying degrees of heart block and asystole. Vasodilator effects (flushing, headaches and dizziness) can occur at the start of therapy and oedema is sometimes a problem. Constipation common with verapamil.
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NITRATES
Sublingual Glyceral Trinitrate (GTN), GTN spray, Buccal, Transdermal GTN, Isosorbide Dinitrate, Isosorbide Mononitrate, slow release Isosorbide mononitrate.
Actions: Relax vascular smooth muscle, mainly in venous system to increase capacitance and thus reduce preload to the heart. Arteriolar relaxation also occurs with a fall in peripheral resistance (afterload).
Indications: Used for the treatment and prophylaxis of angina. Given sublingually (GTN) used at onset of angina or prior to exercise. Can be repeated at 5 minute intervals. Orally taken as Isosorbide Dinitrate, works at 30 minutes. Suscard Buccal allows slow diffusion across the buccal membrane. Transdermal nitrates give theraputic levels after 1 hour and last for up to 24 hours. Intravenous nitrates are used in the management of unstable angina, prolonged infarction pain and LVF.
Side effects: Hypotension, headaches and tachycardia.
ANGIOTENSIN – CONVERTING ENZYME INHIBITORS
Captopril, Enalapril, Lisinopril
Actions: Inhibits the angiotensin- converting enzyme thus preventing the production of angiotensin II. This causes:- • Arterial dilation and venodilation lowering blood pressure and the work of the ventricles. • A reduction in aldosterone levels and so favours excretion of sodium and so reduces water retention
Other actions are:- • Degradation of bradykinins is reduced (bradykinins are potent vasoldilators) • Increases levels of prostaglandin E, which has vasodilator properties.
Indications: Hypertension and cardiac failure
Side effects: headache, cough, fatigue, taste dysfunction. First dose can cause a large and rapid fall in BP so first dose given is small and patient is closely monitored.
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DIURETICS
Actions – Increase urine formation. Actions vary depending on site of action. Loop diuretics – Frusemide, Bumetanide Most powerful and fastest acting. Can remove up to 1/3 of all urine filtered in glomerulus when given in high doses. Inhibits sodium and chloride reabsorption and also enhances exretion of potassium. Effects occur within 1 hour of oral intake. Thiazide Diuretics – Bendrofluazide, Hydrochlorothiazide and Metolazone Reduces sodium reabsorption and increases potassium excretion. This inhibits the enzymes concerned with sodium reabsorption so increasing urinary sodium and so urine output Potassium sparing diuretics – Amiloride, Triamterene, Spirolactone Cause retention of potassium and excretion of sodium. Spirolactone works by preventing the action of aldosterone.
Indications – Hypertension, cardiac failure, pulmonary oedema, hepatic and renal disease.
Side effects – Alteration in fluid and electrolyte balance (hypokalaemia). Can also cause hypotensive episodes, Gout, hyperglycaemia and GI disturbances.
CARDIAC GLYCOSIDES
Digoxin Actions – Increases force of contraction, slows conduction at the AV node and increases vagal activity so slowing heart rate. Indications – cardiac failure and atrial arrhythmias (AF, atrial tachycardia) Side effects – anorexia, nausea and vomiting (usually first sign of digoxin overdose), visual disturbances. Arrhythmic effects increased if serum potassium low (digoxin is often in conjunction with diuretics)
VASODILATORS
Nitroprusside, Hydralazine, Prazosin
Actions – Act directly on vascular smooth muscle Indications – Anti-hypertensive used in an emergency, for controlled hypotension in certain surgical operations and to increase myocardial work in cardiac failure. Side effects – nausea and vomiting, headache, tachycardia, fluid retention, occasional thyroid dysfunction, Prazosin – postural hypotension, dizziness, weakness
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ANTIARRHYTHMICS
Actions – Vaughan Williams classification
Class I – Drugs that block voltage sensitive sodium channels, thus reducing the excitability of the non-nodal regions of the heart where the inward sodium current is important for the propagation of the action potential. Class II – Drugs that reduce the action of the sympathetic nervous system Class III – Drugs that prolong the refractory of the myocardium, thus tending to suppress re-entrant rhythms Class IV – Drugs that block voltage sensitive calcium channels, thus impairing impulse propagation in nodal areas and in damaged areas of the myocardium.
Class IA – Quinidine, Procainamide, Disopyramide Indications – Atrial arrhythmias Side effects – Nausea and vomiting, fever, skin rashes. Disopyramide can also cause hypotension and anticholinergic effects which are dry mouth and urinary retention.
Class IB – Lignocaine, Metiletine Indications – Ventricular arrhythmias Side effects – drowsiness, disorientation. Metiletine can also cause hypotension and bradycardia
Class IC – Flecanide, Propafenone Indications – Flecanide: Ventricular and supraventricular arrhythmias. Propafenone: Ventricular arrhythmias Side effects – Dizziness and blurred vision
Class II – see B-blockers
Class III – Amiodarone, Bretylium, Sotalol Indications – Supraventricular and ventricular arrhythmias Side effects – Amiodarone – Corneal micro deposits (reversible on withdrawl), skin sensitivity to sun, thyroid dysfunction.
Class IV – Verapamil (see Ca Antagonists) Adenosine Indications – Supraventricular arrhythmias (given IV) Side effects – Transient facial flush, dyspnoea, choking sensation and severe bradycardia
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Streptokinase (SK), Anistreplase (APSAC), Alteplase(TPA)
Actions – Activiate plasminogen to form plasmin which degrades fibrin and so breaks up the thrombi. SK and APSAC act on both circulating and clot bound plasminogen Indications – Any patient with acute MI in whom benefits outweigh the risks Side effects – nausea and vomiting, bleeding, possible allergic reactions. No repetition of Streptokinase within 1 year.
ANTIPLATELET DRUGS
Asprin
Actions – Decrease platelet aggregation and so reduce thrombus formation on arterial side Indications – Unstable angina reducing risk of death by half and post MI by reducing death by 20% Side effects – upper GI effects
ANTICOAGULANTS
Warfarin, Heparin
Actions – Warfarin antagonises the effects of vitamin K, its anticoagulant effect takes 36-48 hours to develop. Heparin inhibits action of thrombin by combining with thrombin III. Indications – deep vein thrombosis, prevention of thrombi due to AF or prosthetic valves Side effects – heamorrhage
LIPID LOWERING DRUGS
Cholestyramine, Clofibrate, Bezafibrate, Gemfibrozil, Simvastatin
Actions – Cholestyramine binds bile acids preventing their reabsorption, so promoting hepatic conversion of cholesterol into bile acids. Decreases serum triglycerides Indications – Hyperlipidaemia Side effects – nausea, vomiting, constipation and diarrhoea
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THE CARDIAC CYCLE
1. Contraction signals are discharged by the sinus node. The heart is relaxed and the ventricles have been filled with blood from the atria.
On the ECG
2. Signals from the sinus node spread along the atrial myocardium to the AV node. The chambers receive supplementary filling as the atria contract.
On the ECG
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3. The atrial musculature relaxes. Closure of the AV valves occurs.
On the ECG
4. The electrical signals from the AV node spread rapidly to the ventricular musculature which contracts and pumps blood into the aorta and pulmonary artery.
On the ECG
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5. The ventricles relax and a new cardiac cycle begins.
On the ECG
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Initially, the ventricles fill with blood passively. The sinus node discharges and the electrical impulse passes through the atria causing atrial depolarisation or atrial systole. This is followed by atrial contraction and the remainder of atrial blood is pushed through the tricuspid and mitral valves which are open. This extra passage of blood from atria to ventricles is called the atrial contribution or atrial transport. As the ventricles fill, the pressure rises which forces the mitral and tricuspid valves to shut.
The electrical signal then passes through to the ventricles causing ventricular depolarisation or ventricular systole. This is followed by the mechanical action of ventricular contraction. The pressure in the ventricular chamber rises and for a short time, the pressure within the ventricles increases whilst the volume of blood within the ventricular chamber remains unchanged. At this stage all the valves are shut. This is called the iso-volumetric contraction period. Once the pressure within the ventricles exceeds that in the aorta, the aortic and pulmonary valves are forced open and the pressure is the same in the ventricles as the aorta and pulmonary artery. It continues to rise until the peak of ventricular systole.
Following electrical repolarisation, the ventricles start to relax. As the pressure falls, the aorta has its own elasticity which maintains the pressure and prevents it dropping right down to zero. At some point, the ventricular pressure drops below that in the aorta and this forces the aortic and pulmonary valves shut. The pressure in the ventricles continues to fall and this is known as the iso-volumetric relaxation period. As the pressure continues to fall it will eventually drop below the pressure in the atrium and causes the mitral and tricuspid valves to open once again.
Z:\Manuals\A & P manual.doc 52 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 The normal cardiac cycle consists of one complete heart beat and recovery. Each component of the ECG corresponds to contraction or relaxation of atrial or ventricular chambers. The electrical activity precedes the mechanical activity.
Isovolumetric Isovolumetric contraction relaxation
Aortic Pressure
Ventricular Pressure
Left atrial Pressure
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A. DEVELOPMENT OF THE HEART. B. DEVELOPMENT OF THE ARTERIAL AND VENOUS SYSTEM. C. ANOMALIES.
DEVELOPMENT OF THE HEART
INTRODUCTION
The embryonic heart develops early because blood is the foetus’s only supply of oxygen. In order for it to grow, it is essential that each part of the heart is filled with oxygenated circulating blood.
As it develops and septation takes place, the atria must not be completely divided, because the lungs in the foetus are not functional, and it is the veins that carry the oxygenated blood from the placenta and these enter the atria at the right side of the heart. A right to left atrial shunt must therefore remain throughout the development of the heart and foetal life, and must close immediately after birth when oxygenated blood will be entering the heart via the left side.
The heart develops from the cardiogenic area present in the 2-3wk embryo.
3rd week – develop two endocardial tubes which quickly fuse, and by the 4th week this sinks into the pericardial cavity within a space. It is fixed at either end so that as the heart rapidly grows it begins to buckle and twist and eventually the atria are above the ventricles. [ Unlike the sequence in the heart tube.]
At the same time septation occurs and divides the heart into a double tube.
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Incomplete atrial septation develops in such a way that it ultimately results in a thin flexible flap covering a gap through which blood passes one way down a pressure gradient – from right to left.
5th week – the first septum [ the septum primum] which is thin and flexible, grows down towards the narrowing atrioventricular junction leaving a narrow ostium [ostium primum] permitting the right to left shunt.
This eventually closes, but another part of the septum primum breaks down and leaves a new opening the ostium or foramen secundum.
8th week a thick muscular septum – the septum secundum, grows to the right of the septum primum. When it is fully formed, this covers the ostium secundum, but as long as the pressure in the RA exceeds that of the LA the septum primum will be pushed aside as blood enters the LA. through the foramen ovale.
At birth the sudden influx of large quantities of blood from the lungs into the LA raises the pressure in the LA and the flexible septum primum is pressed against the rigid septum secundum to close the foramen ovale. With time they fuse together.
REMAINING DEVELOPMENTS
At 7mm the four chambers of the heart are distinct. The atria communicate via the ostium secundum, and the ventricles via the interventricular foramen. After filling all four chambers the oxygenated blood then leaves the heart by the truncus which is already beginning to divide into the aortic and pulmonary channels.
Around the 7th week sideways fusion of the endocardial cushions occurs from which the AV valves are formed.
Early in the heart’s devt. The specialised SA node was formed with its own intrinsic rhythm which spread to the rest of the heart. Myofibrils develop in the cells and contractions begin by day 22. Much later after devt of the AV node and the rest of the conducting system, the continuity between the atrial and ventricular myocardium is elsewhere lost [apart from the Bundle of His], due to formation of the fibrous skeleton.
The early heart is sufficiently thin walled to not need any special blood supply. But as the walls thicken a capillary plexus spreads over their surface from the aorta, and from this the coronary arteries are derived.
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INTRODUCTION
Cardiovascular development before birth provides a system which is adequate for prenatal needs, and yet capable of undergoing changes at birth for post natal needs.
The foetus’s lungs are not functional and the oxygen is supplied from the placenta.
Fairly well oxygenated blood returns from the placenta via the umbilical veins and joins with the IVC via the ductus venosus, to enter the RA. Most of this passes to the LA and then via the aortic arch feeds the heart, head, neck and upper limbs.
The ductus arteriosus bringing venous blood from the pulmonary trunk to the aorta enters just beyond the arch and feeds the abdomen and lower limbs and then returns to the placenta via the umbilical arteries.
The lower part of the body receives poorly oxygenated blood throughout foetal life.
FOETUS
The oxygenated blood from the placenta traverses the ductus venosus and is joined by blood from the IVC and hepatic veins,
It is then divided into right and left atrial streams. –
The left stream consists of 75% of the blood, and passes through the foramen ovale into the LA where it joins with blood from the pulmonary veins. This well oxygenated mixture passes into the LV and then some goes to the heart, head, neck and arms, whilst the rest joins blood from the ductus arteriosus.
The right stream [25%], joins the SVC and coronary sinus blood in the RA.After the RV some passes to the lungs whilst the rest bypasses the lungs and joins the descending aorta via the ductus arteriosus, and goes to the lower body and back to the placenta.
Both ventricles work in parallel and at birth the walls are similar thickness. The placenta is a low resistance circuit with a greater volume of blood low than the systemic tissues. The unexpanded foetal lungs are a relatively high resistance circuit, with a smaller volume of blood than the systemic tissues.
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1) During delivery the oxygen sats fall in the umbilical arteries to <30%. This stimulates respiration reflexly by the effect of anoxia on chemoreceptors.
With the onset of respiration, intrathoracic pressure falls and the lungs are inflated. Pulmonary vascular resistance falls rapidly and pulmonary blood flow increases tenfold in as many minutes.
As this flow increases, the PA pressure falls and LA pressure rises. Also when venous return from the placenta ceases, the IVC pressure falls. These relative pressures produce functional closure of the foramen ovale
All blood entering the RA from the SVC and IVC now passes to the RV and this blood is now entirely venous because the arterial stream from the placenta is cut off when the umbilical cord is tied. The arterial and venous sides of the heart are now quite separate.
Some days after birth there may be some intermittent flow, but as the LA pressure continues to rise the shunt ceases, and fusion occurs.
Over the next few months connective tissue increases in area and structural closure occurs forming the fossa ovalis.
2) Within a few minutes of birth, the muscular wall of the ductus arteriosus contracts due to a reflex of pressure receptors in the LA wall as it distends with the large volume of blood from the expanded lungs.
The reduced right to left shunt continues for about an hour, but then the increases in systemic arterial pressure and the decrease in pulmonary arterial pressure combine to reverse the shunt. – this may produce a characteristic murmur.
A few days after birth, [longer in premature babies], the ductus arteriosus shuts down completely. It is occluded by overgrowth of the intima and later undergoes fibrosis and contraction to form the ligamentum arteriosum.
3) The first month after birth the RV atrophies, and the LV hypertrophies. The degree of LV preponderance characteristic of later life is reached by 6 months.
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The heart has to develop and at the same time remain in full functional activity throughout prenatal life. Developmental defects are relatively common. Most are septal in origin.
PATENT FORAMEN OVALE. [PFO]
If the foramen ovale remains open, arterial blood passes from the LA to the RA where the pressure is lower. This extra blood causes RVH and PA hypertrophy. It may take 50 years before compensation breakdown.
ENDOCARDIAL CUSHION DEFECTS
Persistent ostium primum – septum primum may be underdeveloped or fail to fuse with the atrioventricular cushions.
Persistent common atrioventricular canal – the atrioventricular cushions may fail to fuse with each other,
Membraneous ventricular septum defect – the atrioventricular cushions may fail to fuse with the ventricular septum.
Note all three cushion defects may be combined.
VALVE DEFECTS
The semilunar valves may be bicuspid.
Any valve may be site of stenosis or atresia.
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The spiral ridges may unequally separate the aorta the pulmonary trunk, so that the pulmonary trunk is poorly developed. The aorta is over developed so that it cannot now be connected to the interventricular foramen and it comes to override the interventricular septum and receives blood from both ventricles.
The two ventricles are in open communication so that the pressure in the RV is as high as that in the LV, and the wall of the RV is hypertrophied.
This following combination is Fallot’s Tetralogy :-
P.S. [narrowed pulmonary trunk.] RVH VSD Overriding aorta.
The venous blood entering the aorta causes cyanosis. [Blue baby]. Can surgically form an artificial ductus arteriosus and so increase the pulmonary circulation, increase the pressure in the LV and reduce the amount of blood entering the aorta.
COARCTATION OF THE AORTA
Constriction of the systemic arch.
In the foetus the LV blood in the aortic arch goes to the heart, head, neck and arms; whilst the descending aorta gets its own supply through the ductus arteriosus. The blood flow between the subclavian artery and the ductus is minimal. After birth this section may narrow causing coarctation.
The seriousness depends on the degree of constriction.
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If the ductus arteriosusfails to close at birth, it allows blood to pass between the systemic and pulmonary circulations. Since aortic pressure > PA pressure - the shunt is from arterial to venous side. Large volumes of blood pass through a relatively narrow ductus causing a loud murmur.
The increased pressure in the PA causes RVH, and may eventually cause compensation breakdown.
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Although the basic principles of cardiac conduction and depolarisation are the same as for adults, age related changes in the anatomy and physiology of infants and children produce differing normal ranges.
Standard adult electrode positions are used with the addition of either lead V3R or V4R to detect right ventricular or atrial hypertrophy.
How the heart develops during infancy and childhood determines the normal age related changes in paediatric traces.
1) T WAVES.
At birth the RV is larger than the LV. RAD and large precordial R waves, and upright T waves are normal.
Changes in systemic vascular resistance result in the LV increasing in size until it is larger than the RV by age one month. By 6 months the ratio of RV to LV is similar to that of an adult.
The Twave in lead V1 inverts by 7 days and remains so until at least age 7 years.
Upright T waves in right precordial leads, [V1 to V3], between ages 7 days and 7 years are a potentially important abnormality and usually indicate RVH.
2) QRS.
At birth the mean QRS axis lies between +60 and +160 degrees. R waves are prominent in the right precordium, and S waves in the left.
By one year the axis changes gradually to lie between +10 and +100
Z:\Manuals\A & P manual.doc 61 Created by ButlerL, BouncirG, Burnett G, Created on 16/01/2004, Edited on 19/07/2004 THE FOETAL ELECTRCARDIOGRAM. [FECG].
The FECG is a useful monitor for foetal well being, hypoxia, and acidosis.
The FECG is the same as an adult ECG with respect to the electrical depolarisation.
It is easily obtainable in labour using foetal scalp clips.
It is a valuable physiological parameter reflecting hypoxia and acidosis and the foetal response to them.
During hypoxia the myocardium and the brain are both spared, by autonomic control diverting the blood to the heart and brain. This results in these two organs experiencing the same metabolic environment. The monitored effect of hypoxia on myocardial function can therefore closely reflect brain function.
Research has shown that monitored ST and T wave changes with hypoxia and acidosis could predict required delivery for foetal distress.
THE FOETAL ECHOCARDIOGRAPH
Almost all women in the UK have a detailed scan during pregnancy, usually at 20 weeks, and the detection rate of renal and skeletal problems is high, whereas the diagnosis of cardiac defects varies enormously throughout the UK with rates ranging from 0% to 70%.
At 20 weeks gestation major problems such as absent valves or chambers or large septal defects can be detected. [ Earlier scans are less reliable even though the heart is fully septated by 7 weeks.]
There is evidence of improved survival and quality of life with antenatal diagnosis, especially in a foetus with a circulation that depends on patency of the arterial duct, e.g. transposition of the great arteries. These babies require a caesarian section in a hospital with paediatric surgery close at hand, whereas other defects such as atrioventricular septal defects can be delivered in local hospitals and seen in outpatient clinics within the first days or weeks of life. Also it has been shown that forewarned parents approach the perinatal period and cardiac intensive care better.
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