352 E Satellite Town Gujranwala
National Academy of Family Medicine
Pakistan Society of Family Physicians
Tel nos:0431/ 240026,217067,234836,221035,254216
Why Basics?
Editorial board has decided to initiate a series on CVS,as was done on Hepatology and Diabetes.This will obviously a review of subject.Objective is to highlight and to lay the stress on the areas where we,the family physicians,are deffecient.As more than five persons are involved in the editorial policy decisions so it is hoped that this series will reflect the specific needs of all family physicians.What are our need anyway?
First of all after listening to the patient and breif examination we should be able to suspect that main complaints of the patient lie in the CVS.We should be able to further direct our probe of questioning,our examination of patient towards this fruitful direction.
Is there any family physician who can afford not to prescribe for hypertension?Can he bypass prescribing and monitoring treatment of CCF and IHD? If answer is no then believe me you have to know your basics.We are including the bare minimum, a family physician must know if he has to survive in Pakistan.Do not suppose you know most of the things already.Writers and editors of this issue were under this illusion before taking up the subject.It is only after going through the recent literature,we got rid of this misconception.Revolution is waiting for you.
While dealing with cardiovascular system we tend to focus on heart.We do not include the effects of drugs on peripheral part.Cardiac output depends mainly upon extracardiac factors if there is no problem with the heart itself.
Mean Cardiovascular Pressure is the name given to so many factors we have been hearing in vague terms before.This is the main determinant of cardiac output.Role of Atria has been been emphysized in regard with breaking the inertia of blood flow to heart.70 % of blood is stored in venous bed and only 15 % is circulating in arterial circulation.Where is the remaining 15 %?Are these veins so important?These and many more strictly defined statements are waiting for you in this issue.You have full one month to finish it .It is not even 1 page per day.Invest this time to refine your practice tools.You will earn many more patients by satisfying the ones who enter your consulting room.
Where are You Sir?
Please participate in our planning,write for the journal,become our editor and decide what and how much should be written, or simply advise us how we can improve our journal.
Give us a ring.We will do the rest!!!
Chapter One
Applied Anatomy
Of
Heart
Dr Arshad Javaid Sh & Dr Saleem Akhtar Rana
Since ancient times many many descriptions are available.Most popular is to describe it as a conical structure.Tip of the Cone or apex is obviously towards the diaphragm and base is facing the neck.It is not exactly in midline.Two thirds of it are on left and one third is on right side of midline.Then it is not vertical but oblique ,base tilted towards right side and apex towards left.Even horizontal plane is not even.Apex is more towards anterior side and base on more posterior plane.
Pericardium
It is a conical fibro-serous sac, in which the heart and the roots of the great vessels are contained.It has an outer fibrous sac,lined with an inner serous sac.The heart and roots of great vessels invaginate this sac from behind.The visceral layer of serous pericardium is known as Epicardium.
Diagram to be scanned
The fibrous pericardium forms a flask-shaped bag, the neck of which is closed by its fusion with the external coats of the great vessels, while its base (not the base of heart,which is in opposite direction) is attached to the central tendon and to the muscular fibers of the left side of the diaphragm. Above, the fibrous pericardium not only blends with the external coats of the great vessels, but is continuous with the pretracheal layer of the deep cervical fascia. By means of these upper and lower connections it is securely anchored within the thoracic cavity. It is also attached to the posterior surface of the sternum by the superior and inferior sternopericardiac ligaments; the upper passing to the manubrium, and the lower to the xiphoid process.
Serous pericardium consists of a visceral and a parietal portion. The visceral portion, or epicardium, covers the heart and the great vessels, and from the latter is continuous with the parietal layer which lines the fibrous pericardium. The portion which covers the vessels is arranged in the form of two tubes. The aorta and pulmonary artery are enclosed in one tube, the arterial mesocardium. The superior and inferior venæ cavæ and the four pulmonary veins are enclosed in a second tube, the venous mesocardium.
Heart
To discuss the rest of the structure of heart it is necessary that we start thinking in the beginning that it is basically made up of a fibrous skeleton.This fibrous skeleton is divided in four chambers.Nature of fibrous tissues keeps on modifying at different places as the requirements of that place change.Where you need septum between chambers it becomes septum.When you need septa between atria and ventricles it becomes that.It becomes specialized to support different valves.Then most specialized form are endocardium and the structures contributing to SA and AV Nodes and conduction tissue to purkinji fibres.
The base (of the triangle or cones) is formed mainly by the left atrium, and, to a small extent, by the back part of the right atrium. The four pulmonary veins, two on either side, open into the left atrium, while the superior vena cava opens into the upper, and the inferior vena cava into the lower part of the right atrium.
The Apex lies behind the fifth left intercostal space, 8 to 9 cm. from the mid-sternal line, or about 4 cm. below and 2 cm. to the medial side of the left mammary papilla.
The right margin of the heart is
longer than the left one.It is formed by the right atrium above and
the right ventricle below. The atrial portion is rounded and almost
vertical; The ventricular portion, thin and sharp, is named the
acute margin; it is nearly horizontal, and extends from the
sternal end of the sixth right costal cartilage to the apex of the
heart.
The left or obtuse margin is shorter, full, and rounded: it is formed mainly by the left ventricle, but to a slight extent, above, by the left atrium.
The diaphragmatic surface is formed by the ventricles, and rests upon the central tendon and a small part of the left muscular portion of the diaphragm.
Right Atrium is larger than the left, but its walls are somewhat thinner, measuring about 2 mm.; its cavity is capable of containing about 57 c.c. It consists of two parts:
Sinus Venarum (sinus venosus).— principal cavity, situated posteriorly.The sinus venarum is the large quadrangular cavity placed between the two venæ cavæ. Its walls, which are extremely thin, are connected below with the right ventricle, and medially with the left atrium, but are free in the rest of their extent.
Auricula (auricula dextra; right auricular appendix).—The auricula is a small conical muscular pouch.It projects from the upper and front part of the sinus forward and toward the left side, overlapping the root of the aorta.
Right Ventricle Posterior wall is formed by the ventricular septum, which bulges into the right ventricle, so that a transverse section of the cavity presents a semilunar outline.The wall of the right ventricle is thinner than that of the left, the proportion between them being as 1 to 3; it is thickest at the base, and gradually becomes thinner toward the apex. The cavity equals in size that of the left ventricle, and is capable of containing about 85 c.c.
Left Atrium —The left atrium is rather smaller than the right, but its walls are thicker, measuring about 3 mm.; it consists, like the right, of two parts, a principal cavity and an auricula.The principal cavity is cuboidal in form, and concealed, in front, by the pulmonary artery and aorta; in front and to the right it is separated from the right atrium by the atrial septum; opening into it on either side are the two pulmonary veins.Auricula is directed forward and toward the right and overlaps the root of the pulmonary artery.
The pulmonary veins, four in number, open into the upper part of the posterior surface of the left atrium—two on either side of its middle line: they are not provided with valves. The two left veins frequently end by a common opening.
Left Ventricle —The left ventricle is longer and more conical in shape than the right.It forms a small part of the sternocostal surface and a considerable part of the diaphragmatic surface of the heart; it also forms the apex of the heart.
Ventricular Septum. The greater portion of it is thick and muscular and constitutes the muscular ventricular septum, but its upper and posterior part, which separates the aortic vestibule from the lower part of the right atrium and upper part of the right ventricle, is thin and fibrous, and is termed the membranous ventricular septum. An abnormal communication may exist between the ventricles at this part owing to defective development of the membranous septum.
The heart consists of muscular fibers, and of fibrous rings which serve for their attachment. It is covered by the visceral layer of the serous pericardium (epicardium), and lined by the endocardium. Between these two membranes is the muscular wall or myocardium
The endocardium is a thin, smooth membrane which lines and gives the glistening appearance to the inner surface of the heart; it assists in forming the valves by its reduplications, and is continuous with the lining membrane of the large bloodvessels. It consists of connective tissue and elastic fibers, and is attached to the muscular structure by loose elastic tissue which contains bloodvessels and nerves; its free surface is covered by endothelial cells.
The fibrous rings surround the atrioventricular and arterial orifices, and are stronger upon the left than on the right side of the heart. The atrioventricular rings serve for the attachment of the muscular fibers of the atria and ventricles, and for the attachment of the bicuspid and tricuspid valves. The left atrioventricular ring is closely connected, by its right margin, with the aortic arterial ring.
The nerves are derived from the cardiac plexus, which are formed partly from the vagi, and partly from the sympathetic trunks.
Valves: They are formed by duplicatures of the lining membrane of the heart, strengthened by intervening layers of fibrous tissue: their central parts are thick and strong, their marginal portions are thin and translucent.
Atrioventricual Valves. Their bases are attached to a fibrous ring surrounding the atrioventricular orifice and are also joined to each other so as to form a continuous annular membrane, while their apices project into the ventricular cavity. Their atrial surfaces, directed toward the blood current from the atrium, are smooth; their ventricular surfaces, directed toward the wall of the ventricle, are rough and irregular (prone for thrombus and vegetation formation), and, together with the apices and margins of the cusps, give attachment to a number of delicate tendinous cords, the chordæ tendineæ.
The right atrioventricular orifice is the large oval aperture of communication between the right atrium and ventricle. Situated at the base of the ventricle, it measures about 4 cm. in diameter and is surrounded by a fibrous ring, covered by the lining membrane of the heart; it is considerably larger than the corresponding aperture on the left side, being sufficient to admit the ends of four fingers. It is guarded by the tricuspid valve. The tricuspid valve consists of three somewhat triangular cusps or segments.
The tricuspid valve.The largest cusp is interposed between the atrioventricular orifice and the origin of Pulmonary Artery and is termed the anterior or infundibular cusp. A second, the posterior or marginal cusp, is in relation to the right margin of the ventricle, and a third, the medial or septal cusp, to the ventricular septum.
The left atrioventricular opening (mitral orifice) is placed below and to the left of the aortic orifice. It is a little smaller than the corresponding aperture of the opposite side, admitting only two fingers. It is surrounded by a dense fibrous ring, covered by the lining membrane of the heart, and is guarded by the bicuspid or mitral valve.
Mitral Valves
The cusps are of unequal size, and are larger, thicker, and stronger than those of the tricuspid valve. The larger cusp is placed in front and to the right between the atrioventricular and aortic orifices, and is known as the anterior or aortic cusp; the smaller or posterior cusp is placed behind and to the left of the opening. The cusps of the bicuspid valve are furnished with chordæ tendineæ, which are attached in a manner similar to those on the right side; they are, however, thicker, stronger, and less numerous.
Diagram to be scanned
Valves
between Aorta and left ventricle /Pulmonary Trunk and right
ventricle are structured on different lines.These are like three
small pockets (made of fibrous septa) attached at the root of these
vessels.These open upwards towards the vessels and not towards
ventrilces.When pressure in ventricles is high and pushing blood
through these valves,these cusps open in the lumen of the vessels
and almost touch the walls at the edges of valves.So valve becomes a
thoroughfare.But when pressure in the ventricles drops and pressure
in the vessels gets higher up blood bounces back.These flaps move
towards ventricles and get filled up with blood and balloon up and
meet in the centre of orifice,push against each other and fail to
move any further due to nature of their attachments at the base and
lack of space due to balooning up.
The pulmonary semilunar valves are three in number, two in front and one behind, formed by duplicatures of the lining membrane, strengthened by fibrous tissue. They are attached, by their convex margins, to the wall of the artery, at its junction with the ventricle, their free borders being directed upward into the lumen of the vessel.. Between the semilunar valves and the wall of the pulmonary artery are three pouches or sinuses.
The aortic opening is a circular aperture, in front and to the right of the atrioventricular, from which it is separated by the anterior cusp of the bicuspid valve. Its orifice is guarded by the aortic semilunar valves. The portion of the ventricle immediately below the aortic orifice is termed the aortic vestibule, and possesses fibrous instead of muscular walls.
The aortic semilunar valves are three in number, and surround the orifice of the aorta; two are anterior (right and left) and one posterior. They are similar in structure, and in their mode of attachment, to the pulmonary semilunar valves, but are larger, thicker, and stronger; Opposite the valves the aorta presents slight dilatations, the aortic sinuses which are larger than those at the origin of the pulmonary artery.
Chapter Two
Coronary Circulation
Dr Arshad Javaid Sh & Dr Saleem Akhtar Rana
We know,It is through two main coronary arteries ,right and left.These arise from the sinuses behind the two of the cups of Aortic valves at the root of aorta,opening in the aortic lumen.These openings are covered by aortic valves but are never occuled by these.Blood flow (Eddie;s Currents) is responsible to keep these open throughout cardiac cycle.So supply continues throughout systole and diastole.
Followings constitute blood supply of heart.
Coronary Arteries.
Right Coronary Artery
Right Ventricular Marginal Branch.
Post descending Artery, PDA
Lateral left ventricular branch.
Large right marginal branch
Left Coronary Artery
Anterior interventricular branch.
Left circumflex coronary artery.(LCA)
Left Anterior Descending Coronary Artery.(LAD)
Cardiac Veins
Collateral Circulation.
Right Coronary Artery
RCA leaves aorta to travel in the atrioventricular groove between right atrium and right ventricle.It gives off small branches ,Right Ventricular Marginal branches, which course over the surface of Rt ventricle.As RCA travels further it arrives at the crux of the heart.Here it gives off Posterior Descending Coronary Artery (PDA).
PDA travels along the inferior surface of the heart to the apex and supplies the inferior surface (Diaphragmatic) of the left ventricle.
Lateral Left Ventricular Branch:This is a small branch of RCA.It starts after the origin of PDA and runs in the atrioventricular groove.This supplies two areas of left ventricle;Low lateral wall and post wall of the left Ventricle.
Large right ventricular branch: This travels along the inferior margin of right ventricle and supplies this area.
Fig 5.1
Fig 5.2
Left Coronary Artery
Left Circumflex Cornory Artery.LCA
This is anologous to right coronary artery traveling around in left atrioventricular groove and may potentially connect to the PDA of RCA.It gives of brances which supply lateral left ventricular wall.Hence the ischaemia of lateral wall will be ascribed to blockage of this branch.
Left Anterior Descending Coronary Artery.(LAD)
LAD travels down the anterior interventricular groove,giving off two important branches.
Septal Perforator Branch which supplies most of the septal musculature.
Diagnoal branch of LAD travels over the left ventricular surface and supplies much of the anterior wall.
LAD itself continues down the interventricular groove,supplying the apex of left ventricle.Ischaemia of septal & lateral walls and apex will be due to relevant branch of LAD.
The right coronary artery has the greater flow in 50 % of individuals,left one has greater flow in another 20 % and flow is equal in rest of the 30 %.Most of the venous blood returns to the heart through the coronary sinus and anterior cardiac veins,which drain into the right atrium.There are other veins which open directly into heart chambers,thebesian veins.Anastomosis between coronary arteries in humans only pass relatively larger sized particles (40 microns) but there is evidence that these channels enlarge and increase in number in patients with coronary artery disease.
When myocardium contracts it constricts coronary arteries.The pressure in left ventricle is slightly higher than in left coronary artery during systole.Consequently flow through endocardium of left ventricle is almost nil during systole.So this is the most frequent site of myocardial infarction.
Clinicaly It is important to know which area is supplied by these arteries.When we are interpretting ECG findings even mild changes if found in the same area then these assume importance.Different ECG leads represent different walls.We are used to say this is anterior wall or posterior or lateral wall or inferior wall infarctions.We know relative prognosis of these areas.We know where septal involvement can cause additional problmes.Inferior wall infarction produces a distinct clinical picture.
So followings are the important areas invoved in IHD alongwith the relevant blood supplying brances.
Septum = Septal branches
Posterior Wall = PDA of RCA
Lateral Wall = LCA of LCA
Anterior Wall = Descending branches of LAD & LCA.
Inferior Wall = PDA of RCA
Following points should be clearly understood.
During systole arteries in the cardiac muscles are compressed.So supply to myocardium is mainly during diastole.When heart rate increases diastole becomes smaller and smaller with the increase in heart rate.So blood supply becomes less and less when need is actually increasing due to increased heart rate.Enodocardium suffers most and myocardium near the outer surface suffers least.
Even at rest myocardium extracts 70-80 % of Oxygen from the blood delivered to it.(Skeletal muscles extract only 25 % ) So Oxygen supply can be increased only by increasing the blood flow.That is what happens under the influence of metabolic products and neural factors.There is considerable autoregulation.
In Aortic stenosis left ventricle has to develop much higher pressure to push the blood through these vavles.So arteries are much more compressed during systole than in normal persons.Oxygen requirement also goes up due to increase in work load.These patients are much more at risk of developing ischaemia and infarction than normal persons.
Coronary flow is also decreased when aortic diastolic pressure is low,as in aortic incompetence.
In CCF when venous pressure is higher, coronary effective perfusion pressure is reduced.
Factors responsible for Autoregulations:
Chemical Factors: Oxygen deficiency,increased CO2,H+,K+,Lactate,Prostaglandins,adenosine nucleotides, and adenosine.Asphyxia,hypoxia etc increase the coronary blood flow upto 200-300 % under experimental conditions.
Neural Factors: Walls of coronary arterioles contain both Alpha adrenergic and Beta adrenergic receptors.Noradrenaline stimulation is basically a chronotropic and ionotropic factor.Dute to these effects metabolites produced in the myocardium dilatate coronary dilatation.But these effects are blocked then noradrenaline stimulation causes vasoconstriction.Alpha adrenergic stimuation produces vasoconstriction while beta adrenergic stimulation leads to vasodilatation.During fall of blood pressure noradrenergic activity increases but metabolites in the myocardium produces due to resultant ischaemia preserve the coronary circulation under these conditions.Vagal stimulation produces vasodilatation.
Coronary Arteries and Disease: Angina is experienced when 75 % of the lumen of coronary artery is occluded and P factor accumulates..At this level of occlusion extra blood required during activity can not be met by affacted coronary artery.At 85 % of lumen occlusion symptoms appear even at rest.
Atherosclerosis of Coronary Arteries.
Atherosclerosis of other arteries
High Cholesterol
Lipoprotein(a)
& Homocysteine levels are positively correlated with incidence of Coronary atherosclerosis.
Lipoprotien (a) interferes with fibrinolysis by down regulation of plasmin generation.
Homocystein damages endothelial cells.It is converted to nontoxic methionine in the presence of folate and B12.Clinical trials are underway to see whether administeration of folate and B12 can reduce the incidence of coronary atherosclerosis.
Inflammation and Atherosclerosis: Presence of inflammatory cells in plaques leads to the possibility of correlation of inflammation and causation of atherosclerosis.There is an interesting correlation between this condition and antibodies to Chlamydia Pneumoniae.This micro organism has an amino acid sequence in its plasma membrane that resembles a sequence in heart Alpha myosisn heavy chain.Injection of this subject causes inflammation and fibrosis of coronary artery walls in mice.This is an example of molocular mimicry.
Thrombosis: This is precipitated usually by spasm of artery,transient aggregation of platelets in severely sclerotic vessel,and rupture of haemorrhage in a atherosclerotic plaque.
Nitrates and Angina: Nitrates produce NO in the vessel walls.Normal vessels are dilated by NO.But how atherosclerotic vessels respond is not clear.Main actions is believed to be through dilatation of capacitance vessels ( Veins).This traps more blood in venous blood,reducing the venous return to heart and so reducing end diastolic volume.This reduces the O2 requirements.
Lysis of Intravascular Clots: Streptokinase and t-PA produce plasmin from plasminogen in the clot.This produces fibrinolysis in the clot and elsewhere in the body.If a lytic agent is injected withen few hours of pain coronary perfusion can be improved and maintained with the antiplatelet agents.
BMJ 2001;322:811-812 ( 7 April )
The anaemia of chronic disease
Remains hard to distinguish from iron deficiency anaemia in some cases
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Recent developments have made the anaemia of chronic disease somewhat easier to diagnose, but it remains a puzzling condition.All agree on the "big three" clinical causes: infection, inflammation (including connective tissue disorders), and neoplasia, which account for 75% of cases.Occult disease must be considered in every case of unexplained anaemia.Anaemia of chronic disease typically occurs despite adequate reticuloendothelial iron stores and is characterised by reduced concentrations of
Serum iron,
Transferrin,
Total iron binding capacity;
Normal or raised ferritin;
And high erythrocyte sedimentation rate.
It can mimic or coexist with other types of anaemia. The red cells are often normochromic normocytic but may show hypochromic microcytic indices similar to the effects of iron deficiency. This latter effect is seen most often with rheumatoid arthritis and Crohn's disease and raises an everyday problem of how best to differentiate between the microcytosis of the anaemia of chronic disease and that due to iron deficiency.
Measuring serum ferritin is essential in investigating unexplained anaemia.
Reduced serum ferritin provides unequivocal evidence of diminished iron stores and occurs in no other condition.
Unfortunately ferritin and iron concentrations both show acute phase responses to inflammation, so iron may fall and ferritin rise independent of the reticuloendothelial iron store. Thus, in the presence of inflammation, ferritin concentrations may remain normal even when reticuloendothelial iron stores are absent.Values of both soluble transferrin receptor and the soluble transferrin receptor-ferritin index are raised in iron deficiency anaemia, even in the presence of chronic disease, but are normal or only slightly raised in anaemia of chronic disease.Treatment of the anaemia of chronic disease generally means treating the underlying disorder, whereupon haemoglobin concentrations should rise.
Chapter Three
Origin of Impulse
Its Conduction
And Ultimate Contraction Of Myocardium.
Dr Ehsan Assad
Ehsan Hospital Noshehra Road
Cardiac Conduction System
SA (Sinu-Atrial) Node is located at the junctional point between Superior Vena Cava and Right Atrium.AV Node is situated in the posterior portion of lower right half of interatrial septum.
The AV node is normaly the only conducting pathways between atria and ventricles.It is continous with the Bundle of His.This further gives off first a branch on left side,
,Left Bundle Branch, at top of interventricular septum.Then this continues as Right Bundle Branch.The left bundle branch divides into left anterior and left posterior fascicles.These branches and then fascicles run underneath endocardium on each side of interventricular septum.Near the apex these come in contact with Purkinjie system whose fibres spread to all parts of the ventricular myocardium.
Fig 1.8
Conduction system is composed of modified cardiac muscles fibres with few striations and indistinct bounderies.The SA node and to a lesser extent AV node also contain small round cells with few organelles,which are connected by gap junctions.These are probably the actual cells where all electrical activity begins in the beginning of origin of impulse.These are called as P (Pace maker) Cells.
Cunduction Speed of Impulse in Cardiac Tissues.
Tissue |
Conduction Rate:m/s
|
|
SA Node |
0.05 |
|
Atrial Pathways |
1 |
|
AV Node |
0.05 |
|
Bundle of His |
1 |
|
Purkinje System |
4 |
|
Ventricular Muscle |
1 |
Atria and Ventricles are separated from each other with thich fibrous ring and normally the only conducting tissue between them is Bundle of His.
Nerve Supply: Vagus nerves supply parasympathetic fibres.Vagal fibres are endocardial.Sympathetic fibres travel along superficial vessel and are mostly epicardial.These come from Stellate Ganglion.SA node develops from right sided structures in the embryo and AV node from left sided ones.Right vagal nerve supplies mainly SA Node while left vagal nerve supplies mainly AV Node.Same is the case with sympathetic supply.Right sided maily to SA node and vice versa.However connections exist to inhibit each other’s influence. They are freely distributed both on the surface and in the substance of the heart, the separate nerve filaments being furnished with small ganglia.
Acetylcholine (from vagal nerves) acts presynaptically to reduce noradrenaline release from sympathetic nerves and conversely neuropeptide Y is released from noradrenergic endings to inhibit the release of acetylecholine.
Disease can cause Pathology (infarction,ischaemia,drugs etc) of SA node,AV node,Bundle of His and further pathways.An infarct of SA node or an infarct in the way of normal passage can cause the change of route of impulse,leading to innocent changes or changes of significant functional importance.These may change origin or route of impulse in such a way that all four chambers do not contract in an orderly manner and these may lead to functional insufficiency.
Basic Considerations
Electrophysiologic Principles
Membrane Potential/Resting Potential and Action Potential: All cells have different electrical charge on both sides of cell membrane.Inside of cells is negatively charged and outer surface of cell membrane is postitively charged as compared to inside of the cell.This charge is maintained and changed by the movement of ions across this membrane.This charge is conventionally mentioned and discussed in terms of intracellular charge i.e negative voltage.It is –10 to 90 mv.This is known as membrane potential or resting potential.We know concentration of Na + is much higher in the extracellular fluid.K+ concentration is higher in intracellular fluid.Both these ions are constantly trying to equalize this concentration gradient.Cells use energy to maintain resting potential.
Many of the cellular activities are regulated by change of this resting potenial.This is changed in opposite direction to allow certain functions inside as well as outside the cell membrane.This reversed charge is known as Action potential.This can travel to adjacent cells causing similar changes there.This is conduction of impulse.
Pacemaker Tissues: The heart continues to beat after all nerves to it are sectioned;Indeed if the heart is cut into pieces the pieces continue to beat.This is because of the presence of pacemaker tissue that can initiate repetitive action potentials.The pacemaker tissue makes up the conduction system that normally spreads impulses throughout the heart.
The pacemaker tissue is characterized by an unstable membrane potential.Instead of having a steady value in between any external impulses,the membrane potential declines steadily after each action potential until the firing level is reached and another action potential is triggered.This slow depolarization between action potentials is called a pacemaker potential (prepotential).The rate of automatic firing is different in different components of conduction system of heart.SA node has the highest rate of firing so it overlaps all other pacemaker tissues in the heart.
The Pacemakers Of The Heart: These are situated in SA node,AV node ( Described as P Cells in section on applied anatomy),The Bundle of His,Purkinje fibres and myocardial muscle fibres in atria and ventricles.
Rate of generation of impulses