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Physiology of cardiovascular system

For medical students especially for pc-1 students.
Md heart physiology by Mr.Gashaw

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Physiology of cardiovascular system

  1. 1. Physiology of the Cardiovascular System By: 1
  2. 2. Outlines  Introduction to CVS  The heart Anatomy of the heart Chambers of the heart Pathway of blood through the heart and lungs Cardiac muscle and the cardiac conduction system Innervations of the heart Cardiac cycle Heart sounds Cardiac output  Vascular Physiology 2
  3. 3. Introduction • The term cardiovascular system – refers to the passages through which the blood flows Components of the CVS 1. The heart: Driving force(Pump) for CVS 2. Blood Vessels: Passage ways  Arteries: Distribution channels to the organs  Capillaries: Exchange region  Veins: Blood reservoirs and streets for return of blood to the heart. 3. Blood: is the transport medium. 3
  4. 4. General functions of the CVS 1. Transport of O2, nutrients, water, hormones, electrolytes, and drugs. 2. Rapid washout of metabolic wastes. 4. Regulation of temperature and blood flow. 6. Contribution to defense mechanisms 4
  5. 5. Physiology of the heart 5
  6. 6. Anatomy of the heart Location: – The heart is located in the thoracic cavity in the mediastinum, the area between the lungs – Superior surface of diaphragm – Anterior to the vertebral column, posterior to the sternum Size: The heart has • The size of a clenched fist. 6
  7. 7. Gross Anatomy of Heart: Frontal Section 7
  8. 8. The Heart • The muscular pump that forces the blood through vessels made of arteries, veins and capillaries. • It is a dual pump that drives blood in two consecutive circuits, – the systemic and – pulmonary circulations • Receives blood from the rest of the body through the vena cava. 8
  9. 9. Outer Surfaces Layers: The Pericardium • The heart is enclosed in a double-walled sac called the pericardium. • Clear pericardial fluid inside pericardium(30-50ml) Function Barrier to infection Provides lubrication Prevents sudden over distention of chamber of heart 9
  10. 10. The Layers of the Heart Wall Epicardium • The outermost layer of the wall of the heart is called the epicardium. Myocardium • The second layer under the epicardium. • This makes up the bulk of the heart. • Responsible for pumping action of the heart Endocardium • Innermost layer of the wall of the heart. • It is formed by a single layer of endothelial cells • Endocardium continues as endothelium of the blood vessels. 10
  11. 11. Chambers of the Heart The heart has four chambers “two atria and two ventricles” The Atria: • Two thin-walled muscular sheaths, • Blood returning to the heart is received by two superior chambers, the right and left atria. • Blood enters right atria from – superior and inferior vena cavae and – coronary sinus • Blood enters left atria from pulmonary veins. The Ventricles: • Thicker-walled portion of the heart • The right and left ventricles are the pumps that eject blood into the arteries. 11
  12. 12. Cont,d • The right side of the heart comprises the right atrium and the right ventricle. • The left side of the heart comprises the left atrium and the left ventricle. • The right atrium receives venous blood from the systemic circulation • The right ventricle pumps it into the pulmonary circulation • The left atrium:  Receives blood from lungs by pulmonary veins. • The left ventricle  ejects the blood into the aorta, which then distributes the blood to all the organs via the arterial system. 12
  13. 13. The Pathway of Blood flow 13
  14. 14. Pathway of Blood Through the Heart and Lungs • Right atrium  tricuspid valve  right ventricle • Right ventricle  pulmonary valve  pulmonary arteries  lungs • Lungs  pulmonary veins  Left atrium  bicuspid valve  Left ventricle  aortic semilunar valve  aorta  systemic circulation 14
  15. 15. Pathway of Blood Through the Heart and Lungs cont’d 15
  16. 16. Heart Valves • Valves of the heart permit the flow of blood through heart in only one direction. • To pump blood effectively, the heart needs valves that ensure a predominantly one-way flow. • There are four valves in human heart. Two atrioventricular valves: found between atria and the ventricles  Two semilunar valves: placed at the opening of blood vessels arising from ventricles, namely systemic aorta and pulmonary artery. 16
  17. 17. Types of valves 1. Atrio-ventricular-AV valves a. Mitral (bicuspid) valve lies b/n left atrium and left ventricle.  They are responsible for preventing the back flow of blood from the LV to the LA. b. Tricuspid (three cusps) valve lies b/n Rt atrium and Rt ventricle.  They are responsible for preventing the back flow of blood from the RV to RA 17
  18. 18. 2. The semilunar valves: • Constitute the aortic and pulmonary valves located at the exits of the right and left ventricles. a. Aortic valve – allows blood to flow into the aortic tree and to the left and right main coronary arteries. – They prevent the back flow of blood from the aorta to the LV. b. Pulmonary valve allows blood to flow into the pulmonary artery. They also prevent the back flow of blood from PA to the RV. 18
  19. 19. 19
  20. 20. 20
  21. 21. Clinical conditions: 21
  22. 22. Cardiac Muscle and the Cardiac Conduction System 22
  23. 23. Structure of Cardiac Muscle • The heart is composed of three major types of cardiac muscle: Atrial muscle, Ventricular muscle, and Specialized excitatory and conductive muscle fibers. • The atrial and ventricular types of muscle – contract in much the same way as skeletal muscle, except that the duration of contraction is much longer. • Cardiac muscle is striated like skeletal muscle but – it differs from Sk.m in many structural and physiological ways. 23
  24. 24. Cont’d Cardiac myocytes (muscle cells), or cardiocytes, are relatively – short, thick, branched cells. – They usually have only one, centrally placed nucleus. – The T tubules are much larger than in skeletal muscle and – admit supplemental calcium ions from the ECF into the cell during excitation. – They are joined end to end by thick connections called intercalated discs (cell membranes that separate individual cardiac muscle cells) 24
  25. 25. 25
  26. 26. • Intercalated discs contain two types of specialized junctions: (a) Desmosomes which act like fastens and hold the cells tightly together (b) Gap junctions which permit action potentials to easily spread from one cardiac muscle cell to adjacent cells 26
  27. 27. Cont’d • Intercalated discs : offer no obstacle to conduction of excitation. • Atria and ventricle behave functionally as a – Syncytium: Excitation anywhere in atria or ventricles spread allover unexcited fibers. • This two functional syncytiums allows the atria to contract a short time ahead of ventricular contraction. • Potentials are conducted from the atrial syncytium into the ventricular syncytium through the A-V bundle. 27
  28. 28. 28
  29. 29. In cardiac muscle, there are two types of cells: Contractile cells & Autorhythmic (or automatic) cells. • Contractile cells: 99% of the cardiac muscle cells Do not contract unless stimulated electrically by pacemaker tissue. Do the mechanical work of pumping. • Autorhythmic cells: – self-stimulating – do not contract but specialized for initiating and conducting the action potentials responsible for contraction of the working cells. – Located in the conducting systems of the heart 29
  30. 30. The cardiac conducting system 30
  31. 31. Cont’d • Sinoatrial node (SA node) – Normal pacemaker – is located near the superior vena cava. – Excitation spreads over working myocardium of atria • Atrioventricular node (AV node): – Located near the right AV valve. – Only pathway for conduction to ventricles, rest of atrioventricular boundary consist of unexcitable connective tissue. 31
  32. 32. Cont’d – Propagation briefly delayed at AV node = Important for ventricular filling (this allows atria to empty before ventricular contraction begins) • Potential pacemaker (if SA node fails) • Bundle of His.  The atrioventricular (AV) bundle (bundle of His), a pathway by which signals leave the AV node.  The right and left bundle branches, divisions of the AV bundle that enter the interventricular septum and descend toward the apex. 32
  33. 33. Purkinje fibers • Nerve like processes that arise from the bundle branches and then – turn upward and – spread throughout the ventricular myocardium. • They distribute the electrical excitation to the myocytes of the ventricles. • They form a more elaborate network in the left ventricle than in the right 33
  34. 34. 34
  35. 35. Spread of cardiac excitation • Begins at the SA node & quickly spreads through both atria. • Also travels through the heart's conducting system (AV node --> AV bundle --> bundle branches --> Purkinje fibers) through the ventricles 35
  36. 36. Inter nodal pathways and transmission of the Cardiac Impulse through the Atria • The ends of the sinus nodal fibers connect directly with surrounding atrial muscle fibers. • Therefore, action potentials originating in the sinus node – travel outward into these atrial muscle fibers. • In this way, the action potential spreads through the entire atrial muscle mass and, – finally, to the A-V node. 36
  37. 37. Delay of Impulse Conduction from the Atria to the Ventricles • The cardiac impulse does not travel from the atria into the ventricles too rapidly. • This delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins. • It is primarily the A-V node and adjacent conductive fibers that delay this transmission into the ventricles. 37
  38. 38. Cont’d • The impulse, after traveling through the internodal pathways, – reaches the A-V node about 0.03 second after its origin in the sinus node. • Then there is a delay of another 0.09 second in the A-V node itself before the impulse enters A-V bundle, where it passes into the ventricles. • A final delay of another 0.04 second occurs mainly in this penetrating A-V bundle. 38
  39. 39. Cont’d • This makes a total delay of 0.16 second before the excitatory signal finally reaches the contracting muscle of the ventricles. • Cause of the Slow Conduction – is mainly by reduced numbers of gap junctions between successive cells. 39
  40. 40. Rapid Transmission in the Ventricular Purkinje System • Purkinje fibers – Largest fibers in conduction system – Conduct impulse from the A-V bundle into the ventricles. – They transmit action potentials at a fastest velocity of 4 to 6 m/sec. • The rapid transmission of action potentials is caused by – a very high level of gap junctions b/n successive cells. 40
  41. 41. Cont’d • Once the impulse reaches the ends of the Purkinje fibers, – it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves. 41
  42. 42. 42
  43. 43. Conduction velocity 43
  44. 44. 44  In the presence of parasympathetic tone
  45. 45. Cont’d • SA node has the highest or fastest rhythm &, therefore, – sets the pace or rate of contraction for the entire heart. • As a result, the SA node is referred to as the pacemaker. • Any region of spontaneous firing other than the SA node is called an abnormal Pacemakers—“Ectopic” Pacemaker. • If the SA node is damaged, – an ectopic Pacemaker may take over the governance of the heart rhythm. – The most common ectopic Pacemaker is the AV node, which produces a slower heartbeat. 45
  46. 46. Action potential on the Two Types of cells • The action potentials that occur in these two types of cells are a bit different: 46 Action potential of an autorhythmic cell Action potential of a contractile cell
  47. 47. Action potential of autorhythmic Cells • The cardiac autorhythmic cells do not have a resting potential. Instead, they display pacemaker activity. • Pacemaker potential is the unstable resting membrane potential in SA node. • RMP in SA node is –55 to –60 mV. But in other cardiac muscle fibers –85 to –95 mV. • Pacemaker potential is a gradual depolarization for the SA node. 47
  48. 48. Ionic Basis of Electrical Activity in Pacemaker 48
  49. 49. Ionic Basis of Electrical Activity in Pacemaker cont’d Pacemaker potential is due to: • The initial part is due to slow influx of sodium ions and the later part is due to the slow influx of calcium ions. Depolarization: • When the pacemaker potential reaches a threshold of - 40 mV, – voltage-gated fast calcium channels open and Ca+2 flows in from the ECF. – This produces the rising (depolarizing) phase of the action potential, which peaks slightly above 0 mV. 49
  50. 50. Cont’d 50
  51. 51. Repolarization • It is due to the efflux of potassium ions from pacemaker fibers. • When repolarization is complete, The K channels close and The pacemaker potential starts over, on its way to producing the next heartbeat. • Each depolarization of the SA node sets off one heartbeat. • When the SA node fires, It excites the other components in the conduction system; At rest, it fires every 0.8 second or so, creating a heart rate of about 75 b/min. 51
  52. 52. Action potential In Contractile cells: • Action potential in a single cardiac muscle fiber occurs in the following phases: 1. Initial depolarization 2. Initial repolarization 3. A plateau or final depolarization 4. Final repolarization. 52
  53. 53. Ionic bases of AP Has 5- phases. Phase-0: Depolarization caused by rapid Na-influx(Fast Na channels open) Phase-1: Initial repolarization due to closure of fast Na channels and efflux of a small quantity of K ions Phase-2: The plateau caused by Ca2+ influx Phase-3: Repolarization caused by K+ efflux due to calcium channels close and slow potassium channels open. Phase-4: Resting membrane potential (−90 mv) RMP re-established by Na-K-ATPase 53
  54. 54. 54
  55. 55. Two types of calcium channels • L-type calcium channels (long lasting calcium current) – Predominant type – Once open, inactivated slowly, thus provide long lasting calcium current – Activated during upstroke (-20mV) – Blocked by verapamil, amlodipine, diltiazen • T-type(transient) calcium channels – Less abundant – Activated at more negative (-70 mV) – Inactivate more quickly than L-type 55
  56. 56. Excitation-Contraction Coupling • The mechanism that couples – Excitation—an action potential in the plasma membrane of the cardiac muscle cell—and – Contraction an increase in the cell’s cytosolic calcium concentration. • As is true for skeletal muscle, – the increase in cytosolic Ca concentration in cardiac muscle is due mainly to release of Ca from the SR • But there is a difference between skeletal and cardiac muscle – in the sequence of events by which the action potential leads to increased release of Ca from the SR. 56
  57. 57. Cont’d Systole(electrical): • Spread of excitation from cell-to cell via gap junctions • Also spread to interior via T-tubules • During plateau phase, Ca++ permeability increases • This Ca++ triggers release of Ca++ from SR • Ca++ level increases in cytosol • Ca++ binds to Troponin C • Ca++ -Troponin complex interacts with tropomyosin (to unlock active site between actin and myosin) • Cross bridge cycling = contraction (systole) 57
  58. 58. 58
  59. 59. 59
  60. 60. Excitation-contraction coupling in cardiac muscle Cont’d 60
  61. 61. Cont’d • Hormonal (catecholamines): – (Phosphorylation of Ca++ channels) – Increase Ca++ into cells by phosphorylation of Ca++ channels by cAMP dependent protein kinase (cAMP-PK). 61
  62. 62. Relaxation(diastole) – As result of Ca++ removal • Ca++ removed By: – Uptake by SR – Extrusion by Na+ -Ca++ exchange – Ca++ pump (to limited extent) • Hormonal: catecholamines – Inhibition of Troponin-C-Ca++ bondage by Troponin-I and phosphorylation of phospholamban by catecholamine 62
  63. 63. Cont’d  Calcium resequestered into SR by ATP-dependent calcium pump  Sarco-endoplasmic reticulum calcium ATPase (SERCA) , that is inhibited by phospholamban.  Inhibition action on SERCA by phospholamban (protein) is relieved by phosphorylation  Calcium pump remove calcium from cell 63
  64. 64. Cardiac glycosides – Inhibit Na+/K+-ATPase – Increase more Na+ in and less Na+ outside of the cell – leads to increase in intracellular Ca++ – through the inhibiting Na+/Ca++ exchange pump (by decreasing the availability of sodium to pump calcium out. – leads to enhanced contractility 64
  65. 65. 65
  66. 66. Nature of muscle contraction • Skeletal muscle : - Tetanic contraction possible - Short refractory period - Recruitment of motor units - Summation of twitches • Cardiac muscle : - no tetanic contraction - prevented by long refractory period - no summation • Importance: Cardiac muscle must relax b/n contractions so that the ventricles fill with blood. 66
  67. 67. 67
  68. 68. 68
  69. 69. Cardiac innervation • Sympathetic  all parts of heart • Parasympathetic (from vagus) – • Mainly : SA node, Atria and AV node • No Ventricular innervations of parasympathetic • Strong stimulation of vagus, has no effect on ventricles (Vagal escape or Ventricular escape) 69
  70. 70. 70
  71. 71. 71
  72. 72. Sympathetic and Parasympathetic effects • Sympathetic stimulation ↑ HR (+ve chronotropic) ↑ force of contraction (+ve Inotropic) Increase slope of pacemaker potential • Parasympathetic stimulation Ach opens K+ channels Reduce slope of pacemaker potential →↓ HR Also hyperpolarize pacemaker potential and reduce HR 72
  73. 73. 73
  74. 74. 74
  75. 75. Actions of the heart • Chronotropic state: is the frequency of heartbeat or HR • Inotropic state: Force of contraction of heart • Bathmotropic state: refers to the excitability of cardiac muscle • Dromotropic state: Conduction velocity of the cardiac conduction system NB: SNS has positive tropic effects PNS has negative tropic effects 75
  76. 76. Effects of non-physiologic environment 1. Body temperature: Rise (eg. Fever): increases the heart rate  Decrease: decrease contractility 2. pH: • Acidosis: - ve Inotropic effect, due to depression of affinity of troponin C to Ca++ severe acidosis stops heart in diastole • Alkalosis: +inotropic effect due to increase affinity of troponinin C to Ca++ severe alkalosis stops heart in systole 76
  77. 77. 3.Inorganic ions: a.Na+ Hypernatremia • -ve inotropic effect • Stimulate Na+ -Ca++ exchanger to take Na+ in, drive Ca++ out of cardiac myocyte, cytosolic Ca++ level decreases Hyponatremia: opposite effect b. Ca++ hypercalcemia: • Increase cytosolic Ca++ level, stronger systole & incomplete diastole. • If level very high, heart stop in systole (Calcium Rigor) 77
  78. 78. Cont’d • Hypocalcemia: • decrease myocardial contractility, but no serious effect C. Potassium • Hyperkalemia: • Negative inotropic effect • Marked hyperkalemia - heart stop in diastole • Hypokalemia: weak +inotropic effect 78
  79. 79. Coronary Circulation • Heart muscle is supplied by two coronary arteries, namely right and left coronary arteries, which are the first branches of aorta. • Heart depends strongly on aerobic metabolism • Brief period of low oxygen: damage to myocardium. 79
  80. 80. Cont’d Right Coronary Artery (RCA) supplies: . RA and RV Left Coronary Artery divides into: I. Circumflex Artery (CA) supplying . LA and . Posterior part of LV II. Anterior interventricular artery supplying . Anterior walls of both ventricles 80
  81. 81. Cont’d • Interruption of the blood supply to any part of the myocardium can cause myocardial ischemia. • If a large part of myocardium is involved or if the occlusion is severe involving larger blood vessels, it leads to necrosis. • The coronary circulation has a defense against such an occurrence—points called anastomoses. • where two arteries come together and combine their blood flow to points farther downstream. • Thus, if one artery becomes obstructed, some blood continues to reach myocardial tissue through the alternative route. 81
  82. 82. Venous Drainage from the heart • After flowing through capillaries of the myocardium, • Venous drainage from heart muscle is by: Coronary sinus • Drains blood from left side of the heart and opens into RA (draining 75%) Anterior coronary veins • Drain blood from right side of the heart and open directly into RA 82
  83. 83. Cont’d Thebesian veins • Drain deoxygenated blood from myocardium, directly into the concerned chamber of the heart. • Physiological shunt 83
  84. 84. Coronary Flow in Relation to the Cardiac Cycle • Most organs receive more arterial blood flow when – the ventricles contract than when they relax, but – the opposite is true in the coronary arteries. • The reason for this is that, – contraction of the myocardium compresses the arteries and obstructs blood flow. 84
  85. 85. 85
  86. 86. 86
  87. 87. Factors affecting coronary blood flow Need for oxygen  Metabolic factors (K, H,Adenosine,CO2) Nervous factors. 87
  88. 88. Clinical conditions Coronary Artery Disease • It is one of the most common and serious effects of aging. • Fatty deposits build up in blood vessel walls and – narrow the passageway for the movement of blood. • The resulting condition, called atherosclerosis – often leads to eventual blockage of the coronary arteries and a “heart attack”. 88
  89. 89. 89
  90. 90. Myocardial Infarction • A myocardial infarction (MI) or heart attack—is the sudden death of a patch of myocardium resulting from ischemia , the loss of blood flow. Causes: A) Vascular Spasm  Spastic contraction of the vessels b)Atherosclerosis  Deposition of cholesterol on the vessel wall (plague) Atheroma: Tumors of smooth muscle cells c)Thromboembolism Blood clot breaks off, stops and impedes blood flow 90
  91. 91. 91
  92. 92. 92
  93. 93. Electrocardiography Electrocardiography • Is the technique by which electrical activities of the heart are studied. Electrocardiograph is the instrument (machine) by which electrical activities of the heart are recorded. Electrocardiogram (ECG or EKG) is the recorded tracing (recorded copy made by the machine) 93
  94. 94. Cont’d • As the heart undergoes depolarization and repolarization, – the electrical currents that are generated spread not only within the heart, but also throughout the body (body fluid good conductor of current) • A small portion of the current spreads all the way to the surface of the body. • If electrodes are placed on the skin on opposite sides of the heart, electrical potentials can be recorded. 94
  95. 95. 95
  96. 96. Difference b/n AP and ECG Action potential • AP is one electrical event in a single cell • Recorded using intracellular electrode Electrocardiogram • Is summated electrical activity of all muscle • Recorded using electrodes placed on surface of body 96
  97. 97. 97
  98. 98. Information obtained from ECG • Anatomical orientation of the heart • Relative size of chambers • Origin of excitation, rhythm and conduction disturbance • Extent, location and progress of ischemic damage • Electrolyte disturbance • Influence of drugs such as glycosides • HR = 1/cycle length or (1 divided by RR duration) Therefore, provide indirect information about heart function. 98
  99. 99. • A "typical" ECG tracing is shown to the right. • The different waves that comprise the ECG represent the sequence of – Depolarization of the atria and – Depolarization and repolarization of the ventricles. • Electrocardiogram (ECG) of the heart is recorded from specific sites of the body in graphic form relating – voltage (vertical axis) with – time (horizontal axis). 99
  100. 100. ECG Conventions • ECG paper has horizontal and vertical lines at regular intervals of 1 mm. • Every 5th line (5 mm) is thickened. • Duration of the waves on X-axis. 1 mm = 0.04 sec.,5 mm = 0.20 sec. Paper speed =25mm/sec. • Amplitude of the waves on Y-axis. (1 mm = 0.1 mV ,5 mm = 0.5 mV, 10mm deflection → 1mV • Recording points = wrist, ankle, skin on chest Right leg = ground(earth). 100
  101. 101. 101A normal electrocardiogram
  102. 102. A) Waves of normal ECG The normal electrocardiogram is composed of • P wave, • QRS complex, and • T wave. 102Waves, Intervals and Segments of the a normal ECG
  103. 103. ‘P’ wave • ‘P’ wave is positive and the first wave in ECG. • It is produced due to the depolarization of both atria. • Atrial repolarization is not recorded as a separate wave in ECG because it is obscured by the QRS complex. • Normal duration is 0.1-0.3 second. • Normal amplitude is 0.1 to 0.12 mV. 103
  104. 104. ‘QRS’ complex • Is due to depolarization of ventricles. . • ‘Q’ wave is a small negative wave. • It is continued as the tall ‘R’ wave, which is a positive wave. • ‘R’ wave is followed by a small negative wave, the ‘S’ wave. 104
  105. 105. Cont’d • ‘Q’ wave is due to the depolarization of basal portion of interventricular septum. • ‘R’ wave is due to the depolarization of apical portion of interventricular septum and apical portion of ventricule • ‘S’ wave is due to the depolarization of basal portion of ventricular muscle. • Normal duration of ‘QRS’ complex = 0.08 - 0.10 second. • Amplitude of ‘Q’ wave = 0.1 - 0.2 mV. • Amplitude of ‘R’ wave = 1 mV. • Amplitude of ‘S’ wave = 0.4 mV. 105
  106. 106. ‘T’ wave • ‘T’ wave is due to the repolarization of ventricles. • Normal duration of ‘T’ wave is 0.2 second. • Normal amplitude of ‘T’ wave is 0.3 mV. 106
  107. 107. U’ wave • Small rounded, upright wave, following T wave. • ‘U’ wave is not always seen. • Mostly seen in slow heart rate. • It is also an insignificant wave in ECG. • represents repolarization of papillary muscles. 107
  108. 108. B. Segments – lines b/n two waves 1. P-R (P-Q) segment  Represents the delay in the AV node  Duration 0.04-0.13 sec 108
  109. 109. 2) “S-T” segment • Is the time interval between the end of ‘S’ wave and the onset of ‘T’ wave. • Represents the complete depolarization of ventricles. • It is an isoelectric period. • Normal duration is 0.08 second 109
  110. 110. 3) T-P segment • From end of T wave to the beginning of P wave • Duration 0.25 sec • The heart muscle is completely repolarized and at rest and ventricular filling is taking place, 110
  111. 111. Intervals 1) P-Q or P-R Interval. • The time between the beginning of the P wave and the beginning of the QRS complex. • Is the interval between the beginning of electrical excitation of the atria and the beginning of excitation of the ventricles. • The average P-Q interval is about 0.16 second. 111
  112. 112. 2) Q-T Interval. • Is the time interval between the onset of ‘QRS’ complex and the end of ‘T’ wave. • indicates the ventricular depolarization and repolarization. • It signifies the electrical activity in ventricles. • Is about 0.35 second. 112
  113. 113. 3) R-R interval • Is the time interval between two consecutive ‘R’ waves. • Signifies the duration of one cardiac cycle. • Normal duration is 0.83 second. Determining heart rate from the ECG • HR = 1/ RR interval E.g; If the ‘R-R’ interval is 1 second, the heart rate is 60 bpm. • The normal RR interval in the adult person is about 0.83 second. • HR= 60/0.83 times per minute=72 bpm. 113
  114. 114. ECG cont’d • Firing of the autorhythmic cells, do not generate enough electricity to reach body surface • There fore no wave is recorded for such cells 114
  115. 115. Types of Electrocardiogram Recording leads 1) Bipolar 2) Unipolar: Chest leads Augmented limb 1. Bipolar/standard limb leads: • Record voltage b/n two electrodes (leads) placed on the wrists and legs. These leads include: Lead I= LA with RA, measures electric potential difference b/n LA& RA. Lead II =LL with RA, Lead III = LL with LA. 115
  116. 116. Einthoven Triangle • Is defined as an equilateral triangle that is used as a model of standard limb leads used to record electrocardiogram. • Heart is presumed to lie in the center of Einthoven triangle. • Electrical potential generated from the heart appears simultaneously on the roots of the three limbs, ( left arm, right arm and the left leg). 116
  117. 117. Einthoven Law • If electrical potentials of any two of the three leads are given, the 3rd one can be determined. • Amplitude (electrical potential) of QRS complex in one lead can be mathematically calculated, by summing up or subtracting the amplitude in other two leads • Example: Amplitude of QRS in lead II = I + III The amplitude of QRS in lead III = II – I. 117
  118. 118. 118
  119. 119. Normal electrocardiograms recorded from the three standard bipolar limb leads. 119
  120. 120. 2. Unipolar leads: A) Precordial (Chest Leads) • ECG are recorded with one electrode placed on the anterior surface of the chest – directly over the heart • They are labeled as leads V1, V2, V3, V4, V5, and V6 • Electrodes are placed on the chest as shown. • Heart surfaces are close to the chest wall and – each chest lead records mainly the electrical potential of the cardiac muscle immediately beneath the electrode. 120
  121. 121. 121 Standard Chest Leads
  122. 122. Cont,d • QRS in V1, V2, are negative because – the chest electrodes are nearer the base of the heart (direction of electro negativity). • V3 is in b/n. • QRS of leads v4-v6 are positive because – they are nearer the apex (direction of electro positivity). Fig. Normal electrocardiograms recorded from the six standard chest leads 122
  123. 123. B. Augmented Unipolar Limb Leads • A modified unipolar limb lead • The three standard leads are: I. aVF lead: an augmented unipolar limb lead in which the positive electrode is on the left leg. II. aVL lead: an augmented unipolar limb lead in which the positive electrode is on the left arm. III.aVR lead: an augmented unipolar limb lead in which the positive electrode is on the right arm. 123
  124. 124. Normal recordings of the augmented unipolar limb leads • They are all similar to the standard limb lead recordings, except that the recording from the aVR lead is inverted. 124
  125. 125. Placement of Electrocardiograph Leads 125
  126. 126. Interpretation of an ECG General questions asked: 1. What is the heart rate? Normal rate=60-100bpm Faster than normal =tachycardia Lower than normal =bradycardia 2. Is the rhythm of the heart regular? 3. Are all normal waves present in recognizable form? 4. Does a QRS complex follow each P wave? 126
  127. 127. Relationship of the ECG to Electrical Activity of the Myocardium  Red: indicates depolarized myocardium, and  Green: indicates repolarized myocardium. • Arrows: indicate the direction in which a wave of depolarization or repolarization is traveling. 127
  128. 128. Some examples of abnormal rhythm(arrythmias) Arrythmia is irregular heartbeat or disturbance in rhythm of the heart. Abnormal cardiac rhythm can be caused by: Shift of pacemaker from SA node to other part of the heart Abnormal rhythmicity of the pacemaker Blockage at different points (interference with conduction). Abnormal pathways of transmission through the heart. 128
  129. 129. Sinus arrhythmia • Sinus arrhythmia is a normal rhythmical increase and decrease in heart rate, in relation to respiration. • It is also called respiratory sinus arrhythmia (RSA). • During inspiration: HR increases RR interval is shortened • During expiration: HR decreases RR interval is prolonged 129
  130. 130. 130
  131. 131. Cont’d 131
  132. 132. 132
  133. 133. Principles of Vectorial Analysis • Cardiac vector (cardiac axis) is the direction at which electrical potential generated in the heart travels at an instant. • Vector is represented by an arrow. • Arrow head shows the direction • Length of the arrow represents the amplitude (magnitude or voltage) of electrical potential. 133 Instantaneous mean vector when current flows through interventricular septum of the heart
  134. 134. Direction of a Vector is Denoted in Terms of Degrees • When a vector is exactly horizontal & from right side towards left side of the heart, the degree of vector is zero. • From this zero reference point, the scale of vectors rotates clockwise. • From left to right of the heart = +1800 • From above and straight downward= +90o . • Straight upward= -900 (+2700 ) 134
  135. 135. Axis for Each Standard Bipolar Lead and Each Unipolar Limb Lead • The direction from negative electrode to positive electrode is called the "axis" of the lead. • In Lead I:  Because the electrodes lie exactly in the horizontal direction, with the positive electrode to the left, the axis of lead I is 0 degrees. • In recording lead II: Electrodes are placed on the right arm and left leg. Vector is from above downwards and slightly towards left, i.e. its axis is 60°. 135
  136. 136. Cont’d • In lead III, vector is from above downwards and slightly towards right ,its axis is 120°. • aVR, Vector is from below towards upper part of the heart and slightly towards right at +210 degrees; • aVF, Vector is from above downwards at +90 degrees; and • aVL ,the vector is from below, towards upper part of the heart and slightly towards left at –30°. 136
  137. 137. 137 Axes of the three bipolar and three unipolar leads
  138. 138. Polarity Convention 138
  139. 139. 139
  140. 140. Electrical vectors of atrial muscle 140
  141. 141. Mean Electrical Axis of the ventricles • Is sum total of all electrical currents generated by ventricles during depolarization. • Current flows from base of ventricles(-ve) toward apex (+ve). • The mean electrical axis of the normal ventricles is 59° • It varies between -20° and 100°. • Electrical axis is determined from standard limb leads (fig..below). 141
  142. 142. 142
  143. 143. Calculation of mean QRS vector 143 An equilateral triangle is drawn on a plain paper. From the midpoint of each side, perpendicular line is drawn towards the center. On each side of triangle, the amplitude of QRS complex is plotted From the positive end of each projected vector another perpendicular line is drawn towards interior of the triangle Now an arrow is drawn between the two meeting points.
  144. 144. Cont’d 144 Changes in mean electrical axis •Left axis deviation  More horizontal heart  Short obese individual  LV hypertrophy Left bundle-branch block •Right axis deviation  More vertical heart  Tall thin persons  RV hypertrophy Right bundle branch block Mean electrical axis and axis deviations
  145. 145. Axis deviation Cont’d 145 Right bundle-branch block Left bundle-branch block
  146. 146. Cardiac Cycle and Heart Sounds 146
  147. 147. The Cardiac Cycle • The sequence of cardiac events that occurs during each beat are called the cardiac cycle. • The cardiac cycle consists of – a period of relaxation called diastole, during which the heart fills with blood, followed by a period of contraction called systole. • It is consists of one complete contraction and relaxation of all four heart chambers. • Duration of one cardiac cycle= 0.8 sec. 147
  148. 148. Cont’d • Each Cardiac Cycle is initiated by spontaneous generation of an action potential in the sinus node. • The atria pumping blood into the ventricles before the strong ventricular contraction begins. • Thus, the atria act as primer pumps for the ventricles. • The ventricles in turn provide the major source of power for moving blood through the body’s vascular system. 148
  149. 149. Mechanical Events during Cardiac Cycle Events of cardiac cycle are classified into two: A. Atrial events: Atrial systole Atrial diastole B. Ventricular events. Ventricular systole: Isometric contraction Ejection period Ventricular diastole: Isometric relaxation Filling (Rapid, Slow & last rapid ) 149
  150. 150. 150Atrial and ventricular events of cardiac cycle
  151. 151. 151
  152. 152. A) Atrial events 1) Atrial Contraction (Atrial systole)  Is also known as last rapid filling phase  Considered as the last phase of ventricular diastole During atrial contraction: – Intra-atrial pressure increases by about 5 mm Hg. – This helps for the atria eject blood into the ventricles (Atria contribute about 20% to ventricular filling) – The ventricular volume and pressure increase slightly due to the atrial ejection of blood. – Atrial contraction not essential for ventricular filling. • Duration = 0.11sec. 152
  153. 153. 2) Atrial diastole This is the period during which atrial filling takes place. Simultaneously, ventricular systole also starts. RA receives deoxygenated blood through vena cava and LA receives oxygenated blood through pulmonary veins. • It lasts for about 0.7 sec. • NB. The heart relaxes as a whole for 0.4 sec. 153
  154. 154. B) Ventricular events I) Ventricular systole 1) Isometric Contraction (Isovolumetric Contraction) • Begins shortly after the beginning of QRS. • All valves are closed. At this point – the volume of the blood remains constant while the pressure in the ventricles rises rapidly. – The tension increases, however the A-V valves are closed no blood flows into the atria. • Duration = 0.05sec. 154
  155. 155. 2) Rapid Ejection: • As soon as the pressure in the ventricles exceeds the pressure in the arteries, – The semilunar valves open and – Blood flows rapidly from the ventricle into the arteries. – This corresponds with a sharp decrease in ventricular volume. • At the end of maximal ejection, – the onset of the T wave occurs signalizing the beginning of ventricular repolarization. • Duration = 0.09 sec. 155
  156. 156. 3) Slow Ejection: • The blood is ejected slowly. • The ventricular volumes and pressure in the arteries start to decrease. • At this point muscle fibers have reached a shorter length and can no longer contract forcefully. • Duration = 0.13sec. End systolic volume: Is the amount of blood remaining in each ventricle at the end of ejection period. About 40 to 50ml per ventricles. 156
  157. 157. II) Ventricular diastole 1)Isometric (Isovolumetric) Relaxation: • Characterized by decrease in tension. • Intraventricular pressure decreases during this period. • All valves are closed. • The amount of blood cannot change – because the valves at both ends of the ventricles are closed. • Duration = 0.08sec. 157
  158. 158. 2) Rapid Ventricular Filling: • As soon as ventricular pressure falls below atrial pressure – the A-V valves open and – There is a sudden rush of blood (which is accumulated in atria during atrial diastole) During this period: – the flow of blood from the aorta to the peripheral arteries continues and – the aortic pressure falls slowly. • Duration = 0.11 sec. 158
  159. 159. 3) Slow filling phase • After the sudden rush of blood, the ventricular filling becomes slow. • It is also called diastasis. • About 20% of filling occurs in this phase. • Duration of slow filling phase is 0.19 second. 4) Last rapid filling phase  Occurs because of atrial systole.  Flow of additional amount of blood into ventricles due to atrial systole is called atrial kick. 159
  160. 160. End-Diastolic Volume • Is the amount of blood remaining in each ventricle at the end of diastole. • It is about 110 to 120 mL per ventricle. 160
  161. 161. 161
  162. 162. 162
  163. 163. 163
  164. 164. Cont’d 164
  165. 165. 165
  166. 166. 166
  167. 167. With in a cardiac cycle, it is possible to observe the association action of the following:  Summated ECG voltage changes,  Myocardial contraction and relaxation,  Opening and closing of cardiac valves,  Pressure and volume changes,  Heart sounds 167
  168. 168. 168
  169. 169. 169
  170. 170. 170
  171. 171. The pressure Changes in the Atria • In the atrial pressure curve, three minor pressure elevations, called the a, c, and v atrial pressure waves, are noted. • The a wave – is caused by atrial contraction. – Ordinarily, the right atrial pressure increases 4 to 6 mm Hg during atrial contraction, and – the left atrial pressure increases about 7 to 8 mm Hg. 171
  172. 172. The c wave – Occurs when the ventricles begin to contract; – it is caused mainly by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles. The v wave – It results from slow flow of blood into the atria from the veins while the A-V valves are closed during ventricular contraction. – Occurs toward the end of ventricular contraction. 172
  173. 173. 173
  174. 174. Pressure changes during cardiac cycle 174
  175. 175. Heart Sounds Four separate heart sounds (S1, S2, S3 and S4) identified by:  Stethoscope mediated auscultation  Phonocardiographic recording S1: Slightly prolonged “lub” sound – Occurs at the Isometric contraction of ventricles. – Caused by sudden closure of AV-valves. S2: Shorter, high pitched “ dub” sound – Occurs at isometric relaxation of ventricles – Caused by sudden closure of semilunar valve – Both S1 & S2 is detected by Stethoscope 175
  176. 176. • S3 (sometimes): due to rapid ventricular filling • S4 (occasionally): during atrial contraction • Third and fourth sounds occur normally in children (abnormal in adult) Chest areas from which sound is best heard 176
  177. 177. Murmurs (bruits) • Abnormal sounds heard in various parts of the vascular system. • May be caused by turbulent blood flow that is speeding up when an artery or a heart valve is narrowed. Causes of murmur 177
  178. 178. Cardiac Output (CO) – is defined as the volume of blood ejected from the heart per minute. – is a product of heart rate and stroke volume. CO = HR x SV • The usual resting values of CO – for young, healthy men, resting cardiac output averages about 5.6 L/min. – for women, this value is about 4.9 L/min • At typical resting values, – CO = 75 beats/minx70 mL/beat =5,250 mL/min. 178
  179. 179. • Cardiac output is not constant. • Vigorous exercise – increases CO to as much as 21 L/min and – up to 35 L/min in world-class athletes. • The difference between the maximum and resting cardiac output is called cardiac reserve.  Cardiac Reserve = C.O during maximal exercise - C.O at rest E.g. 35L-5 L =30L  Cardiac Index = Cardiac output÷ Body surface area 3.8 L/m/m2(male), 7-10% less in female 179
  180. 180. Ejection fraction(EF) EF=Measurement of ventricular performance  is fraction of EDV ejected from ventricles per beat EF (%)= SV/EDV X 100 A healthy man has EF of 50% or more Is primary clinical index of contractility 180
  181. 181. 181
  182. 182. Factors Affecting Cardiac Output 1. Venous return 2. Force of contraction Directly proportional to CO 3. Heart rate 4. Peripheral resistance → Inversely proportional to CO Venous Return • Is the amount of blood which is returned to heart from different parts of the body. It is influenced by right atrial pressure. 182
  183. 183. Factors affecting venous return(VR) 1. Right Atrial Pressure(RAP) • Mean pressure in the right atrium accounts 2 mmHg • ↑RAP→↓VR 2. Resistance to venous return (RVR) • Occurs mainly at arterioles • The more the resistance in the arterioles lesser the VR. 3. Sympathetic stimulation:  ↑VR by inducing venoconstriction 4. Blood volume:  ↑Blood volume → ↑VR 183
  184. 184. 5.Respiratory movements • VR increases with inspiration and decreases with expiration 6. Arteriolar dilatation →↓Resistance to VR and ↑VR 7. Skeletal muscle contraction Squeezes veins b/n muscles → ↑VR 8. Gravity • Standing motionless for some time →Pooling of blood in lower extremities → ↓VR → ↓C.O →hypotension →brain ischemia → fainting episode. 184
  185. 185. Heart Rate • Heart rate and cardiac output have a direct relationship with certain limits. • As a general rule, – a patient with a heart rate that is too fast –(>150/minute – not enough filling time) or – too slow (< 50/minute - not enough rate) –requires urgent assessment for signs and symptoms of shock. • Both extreme rates can be associated with inadequate cardiac output. 185
  186. 186. Cont,d • This graph illustrates the relationship between – heart rate and cardiac output. • As heart rate increases, so does cardiac output - to a certain limit. • Cardiac output tends to fall when – heart rate exceeds 150/minute due to inadequate filling time. – Low cardiac output states also occur with low heart rates (<50/minute). 186
  187. 187. Force of contraction of the heart A. Preload • Preload is the volume or pressure in the ventricle at the end of diastole. • Increases the force of contraction and cardiac output. • Preload is connected to stroke volume and cardiac output via the Frank-Starling law. Frank-Starling phenomenon • Frank and then Starling demonstrated that – The more the stretch of the heart’s chambers, the more forceful the contraction (and indeed the greater the stroke volume). 187
  188. 188. 188
  189. 189. B. Afterload • The resistance to the ejection of blood from the ventricle is called after load. • The higher the afterload, the more difficult a job it is for the left ventricle to eject sufficient stroke volumes. • As the afterload increases, – CO and SV decreases • The left ventricle is 3 times the thickness of the walls of the right ventricle due to afterload. 189
  190. 190. Summary, Parameters that Affect Cardiac Output, 190
  191. 191. Regulation of cardiac output 1) Neural regulation 1.1. High centre areas: • Pre-motor cortex, frontal lobe, part of temporal lobe, on stimulation→↑rate and force of contraction of the Heart and increase CO. 1.2. Cardiovascular centers In Medulla Oblongata: • Cardioinhibitory centre: – ↓HR→ ↓cardiac contractility and decrease CO. • Cardioacceleratory centre: – ↑cardiac contractility → ↑ CO. 191
  192. 192. Cont’d • Autonomic innervations to the heart Sympathetic nervous system: ↑CO Parasympathetic nervous system:↓CO 192
  193. 193. 2 Hormonal and Chemical Regulation  Inotropic agents with positive effect on the heart (Those which increases force of contraction) –Glucagon, –T3/T4, –Cathecolamines –Hypercalcaemia  Inotropic agents with negative effect on the heart –Hyperkalemia, –hypocalcemia, –acidosis, –toxins 193
  194. 194. 194
  195. 195. Changes in stroke volume(SV) SV is determined by: – Pre load→ leads to a change in EDV – After load – Contractility → Leads to a change in ESV 195
  196. 196. 196
  197. 197. Cardiac function curves Cardiac function curves are of two types: 1. Cardiac output curves 2. Venous return curves. Cardiac output curves • Show the relationship between cardiac output and right atrial pressure. • Increase RA pressure increase CO (only up to a certain point) • In steady state, vol. of blood left ventricle ejects as CO = venous return. 197
  198. 198. When RA pressure = ∼4mmHg., CO can on longer keep up with venous return, thus levels off. 198
  199. 199. Venous return curve: • As RA pressure increases, pressure gradient decreases and venous return decreases. • When RA pressure negative, veins collapse, blood flow to veins impeded (although pressure gradient has increased) • Therefore, venous return levels off because veins have collapsed. 199
  200. 200. 200
  201. 201. Coupling of cardiac and vascular functions • Cardiac output →Cardiac function and • Venous return→ Vascular function • When venous return is normal (5 L/minute), the cardiac output as well as the right atrial pressure are normal. 201
  202. 202. 202
  203. 203. 203
  204. 204. Hypertrophy of the heart 1. Physiological hypertrophy Physical exercise: Heart wt. = 500gm. (350 gm. In sedentary) Length and thickness of myocardial cells increased Therefore, large vol. of blood is ejected per beat Stroke vol. is larger & HR is slower. 204
  205. 205. 2) Pathological hypertrophy e.g. Aortic stenosis-unilateral hypertrophy (LV) Degree of compensation limited Thus myocardial fiber diameter increases, Distance between capillaries and cell interior increases (diffusion distance increases), Thus inadequate O2, nutrition. Result = heart failure (myocardial insufficiency) 205
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  208. 208. 208
  209. 209. 209 THANK YOU!!!

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For medical students especially for pc-1 students. Md heart physiology by Mr.Gashaw


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