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Ppt cvs phsiology a small review for anaesthetist


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cardiac physiology for anaesthetist

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Ppt cvs phsiology a small review for anaesthetist

  1. 1. Dr.Riyas A MD anaesthesia
  3. 3.  Transport and distribute essential substances to the tissues.  Remove metabolic byproducts.  Adjustment of oxygen and nutrient supply in different physiologic states.  Regulation of body temperature.  Humoral communication.
  6. 6. The intrinsic conduction system of the heart Sinoatrial (SA) node - impulse spreads through atria -100 b.min-1 Atrioventricular (AV) node - impulse delayed for 0.1sec internodal pathway Ventricular contraction - time course approx 0.22 secs *Contraction of the atria* Bundle of His - branches - Purkinje fibers • A wringing effect starts at the apex following the same pathway as wave of excitation atria ejecting some blood superiorly
  7. 7. Normal pacemaker of the heart Self excitatory nature • less negative Er • leaky membrane to Na+/Ca++ • only slow Ca++/Na+ channels operational • spontaneously depolarizes at fastest rate  Overdrive suppression • contracts feebly
  8. 8. Delays the wave of depolarization from entering the ventricle • Allows the atria to contract slightly ahead of the ventricles (.1 sec. delay) Slow conduction velocity due to small diameter fibers In absence of SA node, AV node may act as pacemaker but at a slower rate
  9. 9.  Sympathetic nerves (release noradrenaline):  Left nerves supply atrial and ventricular muscle  Right nerves supply pacemaker and conduction system Effects:  Positive inotropic effect - increase contractility of muscle  Positive chronotropic effect – increase in rate of rise of pacemaker potential  Shorten conduction delay in AV node and increase rate of relaxation
  10. 10.  Parasympathetic innervation to the heart is carried by the vagal nerves  These have their effects by releasing acetylcholine (ACh)  Vagal stimulation produces bradycardia via 2 effects: • 1. Rate of upward drift of the pacemaker potential is slowed • 2. Initial pacemaker potential becomes more negative (hyperpolarised)
  11. 11.  Blood flow left ventricle = 80/ml/min/100g right ventricle = 40 ml/min/100g atria = 20 ml/min/100g *Flow can increase 4-fold  Capillary density - all capillaries open  Very high O2 extraction: (A-V)02 = 14 ml 02/dl  VO2 = 12 ml/min/100g ----> very high
  12. 12.  to cardiac work • influenced by  a) systolic pressure  b) heart rate  c) stroke volume • increases achieved primarily by hyperemia • 40% due to oxidation of carbohydrates, 60% fatty acids
  13. 13.  contraction (systole) leads to compression of intramural vessels and reduction in flow  pressure inside left ventricle can exceed aortic pressure during systole  vessel compression greatest in endocardium, decreases toward epicardium  O2 demand and flow/g is greatest in endocardium  LV coronary flow decreases as HR increases since diastole shorter
  14. 14. 12 010 0 80 150 100 50 0 150 100 50 0 Systole Diastole Arterial Blood Pressure Left Coronary Blood Flow Zone flow Right Coronary Blood Flow Zero Flow IntramyocardialPressure (mmHg) LeftVentricularPressure(mmHg)
  15. 15. Tachycardia: HR time in systole metabolic activity vessel compression vasodilation Bradycardia: HR time in systole vessel compression metabolic activity vasoconstriction
  16. 16. Tissue oxygenation is major regulator of vascular tone (adenosine, tiss pO2) Essentially all capillaries are open to flow (O2 diffusion distance) Flow regulation occurs at arterioles VO2 limited by blood flow (max O2 extraction)
  17. 17.  AUTOREGULATION OF CBF - extremely good over wide pressure range (50-150 mm Hg)  REACTIVE HYPEREMIA - peak flow reached after only 15 second occlusion  FUNCTIONAL HYPEREMIA - very tight coupling between 02 demand (V02) and 02 delivery (blood flow)  HYPOXEMIC HYPEREMIA - very sensitive to changes in arterial oxygen saturation  METABOLIC MECHANISMS ( eg, adenosine) account for above IntrinsicVasoregulation-CoronaryCirculation
  18. 18. in coronary arteries, -adrenergic receptors mediate vasoconstriction while -adrenergic mediate vasodilation sympathetic stimulation elicits vasodilation because increases in contractility and HR elevate VO2 metabolic vasodilation parasympathetic stimulation elicits small increment in CBF
  19. 19.  Continuous capillaries - all perfused; large surface area for exchange Most exchange occurs during diastole (when blood flow is greatest)  Tissue pressure = 15 mm Hg during diastole Tissue pressure rises with ventricular pressure during systole; greatest increase is in endocardium
  20. 20. Syncytium = many acting as one Due to presence of intercalated discs • low resistance pathways connecting cardiac cells end to end • presence of gap junctions
  22. 22. STRUCTURE OF A MYOCARDIAL CELL Mitochondria Sarcolemma T-tubule SR Fibrils
  23. 23.  In response to action potentials, the levels of calcium within cardiac muscle rises  Some Ca2+ binds to troponin C, which exists on the thin actin filaments  This exposes binding sites on the actin filaments  The thick myosin filaments have heads that can flip  These heads (powered by ATP) attach to the actin binding sites  Myosin heads flip, and the myosin and actin filaments slide over one another = contraction
  24. 24. Link between electrical excitation and muscle contraction is calcium ions AP causes sarcoplasmic [Ca2+] to rise from 0.1 M to 2 M in 10msec Some Ca2+ binds to troponin C to activate contraction proteins Intact cell level of free Ca2+ during excitation is 1-10 M Typical concn of 2 M only gives partial activation If [Ca2+] increased (e.g. by adrenaline), get more activation, and more contraction
  25. 25.  Under normal conditions, not all of the contractile cross-bridges are activated  Can activate more by: • (a) the length-tension relationship or • (b) chemically-induced rises in Ca2+ (e.g. noradrenaline from sympathetic nerves, or circulating adrenaline)
  26. 26.  Inotropic = strengthening  Catecholamines increase the amount of Ca2+ stored in the SR (a rise in the Ca2+ current during the plateau of the AP)  Uptake back into the SR is also upregulated, meaning the muscle relaxes faster, and preserves the diastolic filling period  Three mechanisms regulate contractile force: • The size of the Ca2+ current • Affinity of contractile proteins for Ca2+ (depends on stretch) • Degree of actin-myosin overlap (also depends on stretch)
  27. 27. A small population of heart cells have the ability to spontaneously depolarize – autorhythmic. The most important group of such cells makes up the sinoatrial node (SA node). • SA functions as our pacemaker..
  28. 28.  The cells of the SA node do not maintain a “normal” resting potential because Ca++ is constantly leaking into the cell through slow calcium channels = pacemaker potential.  The potential starts at ~ -60 mV and gradually depolarizes to ~ -40 mV, which triggers the opening of fast calcium channels and maybe voltage-gated Na+ channels.  The membrane potential rapidly shoots up to ~ +20 mV = depolarization..
  29. 29. +5 0 0 -50 m V 25 0 nA nA 0 -50 slope IK If (the Na+ current) ICa
  30. 30.  Repolarization begins when K+ voltage-gated gates open and K+ rushes out of the cell.  A new pacemaker potential begins when the potential reaches ~ -60 mV.  Adjacent myocardial cells begin depolarizing because of the influx of cations (probably Ca++) through the gap junctions.  At threshold, Na+ gates open and Na+ rushes into the cell.  The membrane is depolarized to ~ +15 mV.
  31. 31. Unlike noncardiac cells, repolarization does not begin immediately. Instead the potential difference is maintained for ~ 200 – 300 ms by the slow diffusion of Ca++ into the cell which balances the outward diffusion of K+. This is the plateau phase. Once the cell has slowly repolarized to threshold, K+ gates open and the cell is quickly repolarized to resting potential of ~ -90 mV..
  32. 32.  This wave of depolarization spreads throughout the atrial myocardium but cannot reach the ventricular myocardium because of the fibrous skeleton.  The only electrical connection between the myocardia is in the AV node to AV bundle to bundle of His to Purkinje fibers.  The specialized cells in the AV bundle conduct the impulse very slowly.  This time delay allows the atria to complete systole before the ventricles begin systole..
  33. 33. The electrical activity occurring in the heart can be monitored with the ECG (EKG). Each cardiac cycle produces three distinct waves; P, QRS, and T. The waves represent changes in potential between two different regions of the surface of the heart. The waves do not represent APs in individual cardiac cells nor do they represent the flow of blood through the heart..
  34. 34. The impulse then travels to the AV bundle, located in the superior interventricular septum. The AV bundle then splits into left and right bundle branches, which continue as Purkinje fibers. Conduction System Animation..
  35. 35. -90 0 0 1 2 3 4 TIME PHASE 0 = Rapid Depolarization (inward Na+ current) 1 = Overshoot 2 = Plateau (inward Ca++ current) 3 = Repolarization (outward K+ current) 4 = Resting Potential Mechanical Response
  36. 36. MEMBRANEPOTENTIAL(mV) 0 0 -50 -50 -100 -100 SANVENTRICULULAR CELL ACTION POTENTIALS 0 1 2 3 4 4 0 3
  37. 37. SINGLE VENTRICULAR ACTION POTENTIAL ECG P Q S T R 1 mV Repolarization of ventricles Depolarization of ventricles Depolarization of atria ENDOCARDIAL FIBER EPICARDIAL FIBER ATRIAL FIBER
  38. 38. SINGLE VENTRICULAR ACTION POTENTIAL ECG P Q S T R 1 mV Repolarization of ventricles Depolarization of ventricles Depolarization of atria ENDOCARDIAL FIBER EPICARDIAL FIBER ATRIAL FIBER
  39. 39. relax
  40. 40.  Cardiac Cycle  All events which occur between two consecutive heartbeats.  Systole: simultaneous contraction of the two ventricles creating pressure to pump blood to the lungs and body.  Diastole: resting phase immediately after systole and lasts about 0.5s assuming one complete cycle takes 0.8s.
  42. 42. AtrialSystole Mitral Closes Isovolumiccontract. Aortic opens S1 RapidEjection ReducedEjection IsovolumicRelax. Aortic closes RapidVentricular Filling Mitral opens S2 ReducedVentricular Filling AtrialSystole :>O :>D
  43. 43.  Volume of blood pumped/min. by each ventricle. • Pumping ability of the heart is a function of the beats/ min. and the volume of blood ejected per beat.  CO = SV x HR • Total blood volume averages about 5.5 liters.  Each ventricle pumps the equivalent of the total blood volume each min. (resting conditions).
  44. 44.  The total amount of blood pumped by the left ventricle in one minute (Q) Q = SV x HR  Average cardiac output at rest is 5-6 litres, during exercise it can exceed 30 litres in a trained endurance athlete.
  45. 45.  Without neuronal influences, the heart beats according to the rhythm set by SA node.  Regulation of HR (chronotropic effect): • May be + or – effect.  Autonomic control: • Sympathetic and parasympathetic nerve fibers to the heart modify the rate of spontaneous depolarization. • Innervate the SA node.  NE and Epi stimulate opening of Na+/Ca2+ channel.  ACH promotes opening of K+ channel.  Major means by which cardiac rate is regulated.  Cardiac control center (medulla): • Coordinates activity of autonomic innervation.
  46. 46.  Blood ejected from left ventricle - not all blood is ejected, the amount of blood remaining is called end-systolic volume.  Stroke Volume = end- diastolic volume - end-systolic volume
  47. 47. Stroke volume is regulated by 3 variables: • EDV:  Volume of blood in the ventricles at the end of diastole. • Total peripheral resistance (TPR):  Frictional resistance or impedance to blood flow in the arteries. • Contractility:  Strength of ventricular contraction.
  48. 48.  Workload on the heart prior to contraction (preload). • SV directly proportional to preload.  Increase in EDV results in an increase in SV. • SV directly proportional to contractility.  Strength of contraction varies directly with EDV.  Ejection fraction: • SV/ EDV.  Normally is 60%.  Clinical diagnostic tool.
  49. 49.  Total Peripheral Resistance: • Impedance to the ejection of blood from ventricle. • Afterload.  In order to eject blood, pressure generated in the ventricle must be greater than pressure in the arteries. • Pressure in arteries before ventricle contracts is a function of TPR.  SV inversely proportional to TPR. • Greater the TPR, the lower the SV.
  50. 50.  Relationship between EDV, contraction strength, and SV.  Intrinsic mechanism: • Varying degree of stretching of myocardium by EDV. • As EDV increases:  Myocardium is increasingly stretched.  Contracts more forcefully.
  51. 51.  As the ventricles fill, the myocardium stretches; This increases the number of interaction between actin and myosin.  Allows more force to develop.  Explains how the heart can adjust to rise in TPR.
  52. 52.  Contractility: • Strength of contraction at any given fiber length.  Depends upon sympathoadrenal system: • NE and Epi produce an increase in contractile strength.  + inotropic effect:  More Ca2+ available to sarcomeres.
  53. 53.  Parasympathetic stimulation:  - chronotropic effect.  Does not directly influence contraction strength.  CO affected 2 ways: • + inotropic effect on contractility. • + chronotropic effect on HR.
  54. 54.  Return of blood to the heart via veins.  Venous pressure is driving force for return of blood to the heart.  Veins have thinner walls, thus higher compliance. • Capacitance vessels.  2/3 blood volume is in veins.  EDV, SV, and CO are controlled by factors which affect venous return.
  55. 55. PRESSURE DIASTOLIC PRESSURE CURVE SYSTOLIC PRESSURE CURVE HEART End Diastolic VolumeEnd Systolic Volume Isovolumetric Phase Isotonic (Ejection) Phase Stroke Volume Pre-load After-load
  56. 56. PRESSURE DIASTOLIC PRESSURE CURVE SYSTOLIC PRESSURE CURVE HEART End Diastolic VolumeEnd Systolic Volume Isovolumetric Phase Isotonic (Ejection) Phase Stroke Volume Pre-load After-load
  57. 57. PRESSURE DIASTOLIC PRESSURE CURVE SYSTOLIC PRESSURE CURVE HEART End Diastolic VolumeEnd Systolic Volume Isovolumetric Phase Isotonic (Ejection) Phase Stroke Volume Pre-load After-load
  58. 58. PRESSURE DIASTOLIC PRESSURE CURVE SYSTOLIC PRESSURE CURVE HEART End Diastolic VolumeEnd Systolic Volume Isovolumetric Phase Isotonic (Ejection) Phase Stroke Volume Pre-load After-load
  59. 59. BODY O2 CONSUMPTION 250mlO2/min PaO2 0.15mlO2/ml blood PvO2 0.20mlO2/ml blood PULMONARY ARTERY PULMONARY VEIN CARDIAC OUTPUT= O2 CONSUMPTION (ml/min) PvO2 - PaO2 Pulmonary capillaries Lungs
  60. 60. MEASUREMENT OF CARDIAC OUTPUT THE FICK METHOD: VO2 = ([O2]a - [O2]v) x Flow Flow = VO2 [O2]a - [O2]v Spirometry (250 ml/min) Arterial Blood (20 ml%) Pulmonary Artery Blood (15 ml%) CARDIAC OUTPUT PERIPHERAL BLOOD FLOW VENOUS RETURN PULMONARY BLOOD FLOW
  61. 61. CARDIAC OUTPUT (Q) = VO2 [O2]a - [O2]v 250 ml/min 20 ml% - 15 ml% = = 5 L/min . Q = HR x SV . SV = Q HR . = 5 L/min 70 beats/min = 0.0714 L or 71.4 ml CARDIAC INDEX = Q m2 body surface area . 5 L/min 1.6 m2= = 3.1 L/min/m2
  62. 62.  The pressure exerted by the blood on the vessel walls  Expressed by two numbers - systolic and diastolic  Systolic= highest pressure & corresponds to ventricle contraction  Diastolic= lowest pressure & represents the ventricle relaxing
  63. 63.  Mean arterial pressure = the average pressure exerted by the blood as it travels through the arteries:  MAP = 1/3 pulse pressure + diastolic pressure  Generalised constriction of blood vessels increases blood pressure whereas dilation decreases blood pressure  Hypertension is a chronic elevation of blood pressure above normal healthy values
  64. 64. Elevated body temperature • HR increases about 10 beats for every degree F elevation in body temperature • Contractile strength will increase temporarily but prolonged fever can decrease contractile strength due to exhaustion of metabolic systems Decreased body temperature • decreased HR and strength
  65. 65. Pressure inside is 35 to 15 mmHg 5% of the blood is in capillaries exchange of gases, nutrients, and wastes flow is slow and continuous
  66. 66. Metarteriole Arteriole Precapillary Sphincters Capillaries Venule ?
  67. 67. VASOMOTION = Intermittent flow due to constriction- relaxation cycles of precapillary shpincters or arteriolar smooth muscle (5 - 10/min) AUTOREGULATION OF VASOMOTION: 1. Oxygen Demand Theory (Nutrient Demand Theory) O2 is needed to support contraction (closure) 2. Vasodilator Theory Vasodilator substances produced (via O2) e.g. Adenosine Heart CO2 Brain Lactate, H+, K+ Skeletal Muscle 3. Myogenic Activity
  68. 68. 3 central priorities of CVS: 1. adequate blood supply to brain & heart 2. “ “ “ to other organs after brain & heart supply assured 3. control capillary pressure to maintain tissue volume & composition of interstitial fluid within reasonable ranges
  69. 69.  Baroreceptors monitor BP – info from baroreceptors + info from chemoreceptors (monitoring CO2 & O2 concentrations & pH of blood) is transmitted to brain – other sensory receptors are involved in reflex effects on the CVS including mechanoreceptors (respond to mechanical distortion & pressure) & thermoreceptors (responsive to temperature changes) = all this info is integrated in a collection of brain neurons called medullary CV center (at the level of medulla/pons)
  70. 70.  Medullary CV center receives info also from medullary respiratory center, hypothalamus, amygdala nucleus & cortex – output from medullary CV center feeds into sym & para autonomic motor neurons that innervated heart & smooth muscle of arterioles & veins  Stim. of sympathetic nerves = increases rate & force of heart contraction & causes vasoconstriction = marked increase in arterial BP & CO; in general, the reverse happens when stim para nerves ending in reduction of BP & CO
  71. 71.  2 functional regions with opposing effects on BP: 1. stimulation of pressor center results in sympathetic activation & rise in BP 2. stimulation of depressor center = in parasym. activity & drop in BP fig 12-42 p. 513 Role played by baroceptors which are widely distributed in arterial system show increased rates of firing with increase in BP …
  72. 72.  unmyelinated barorecptors (mammals, amphibians & reptiles) respond only to pressures above normal initiating reflexes that reduce arterial BP  myelinated baroreceptors (only mammals) respond only to pressures below normal initiating reflexes that raise BP - many baroreceptors are located in carotid sinus & in mammals, carotid sinus is a dilation of internal carotid artery at its origin = buried in the thin walls are finely branched nerve endings function as baroreceptors ( inc. in BP stretches wall of carotid sinus causing an increase in discharge frequency)
  73. 73.  arterial chemoreceptors located in carotid & aortic bodies NB in ventilation (later) but also have some effect on CVS = when blood perfusing carotid & aortic bodies has high levels of CO2 or low O2 & pH, arterial chemoreceptors respond with increase in discharge frequency which results in peripheral vasoconstriction & slowing of HR if animal is not breathing (e.g. submersion)  CO is reduced while birds & mammals are diving
  74. 74. 1. atrial receptors (esp. mechanoreceptors in atrial walls) & 2. ventricular receptors (nerve endings of both myelinated {mechanoreceptive & chemoreceptive} & unmyelinated sensory afferent fibers imbedded in ventricles) = together monitor venous pressure & HR to ensure activity of heart is correlated with blood inflow from venous system & blood outflow into arterial system
  75. 75. Chronotropic (+ increases) (- decreases) • Anything that affects heart rate Dromotropic • Anything that affects conduction velocity Inotropic • Anything that affects strength of contraction  eg. Caffeine would be a + chronotropic agent (increases heart rate)