Downloaded 858 times
![C =
Starling’s equation for fluid movement
across capillaries
Jv = Kf [(Pe – Pi) – (πe – πi)]
Where:
Jv - fluid movement (ml/min)
Kf - hydraulic conductance (ml/min . mm Hg)
Pe - capillary hydrostatic pressure (mm Hg)
Pi - interstitial hydrostatic pressure (mm Hg)
πe - capillary oncotic pressure (mm Hg)
πi - interstitial oncotic pressure (mm Hg)](https://image.slidesharecdn.com/cvs-opthal-150218021542-conversion-gate02/85/cardiovascular-physiology-based-on-Ganong-s-92-320.jpg)
![C =
Starling’s equation for fluid movement
across capillaries
Jv = Kf [(Pe – Pi) – (πe – πi)]
Where:
Jv - fluid movement (ml/min)
Kf - hydraulic conductance (ml/min . mm Hg)
Pe - capillary hydrostatic pressure (mm Hg)
Pi - interstitial hydrostatic pressure (mm Hg)
πe - capillary oncotic pressure (mm Hg)
πi - interstitial oncotic pressure (mm Hg)](https://image.slidesharecdn.com/cvs-opthal-150218021542-conversion-gate02/75/cardiovascular-physiology-based-on-Ganong-s-92-2048.jpg)
Uploaded bydinesh
cardiovascular physiology based on Ganong's
The document provides a detailed overview of the cardiac cycle, including its seven phases, the roles of various cardiac structures, and the physiology of blood flow through the vascular system. It discusses the mechanics of blood circulation, resistance in blood vessels, and factors influencing cardiac output such as preload, afterload, and the Frank-Starling relationship. Additionally, it covers regulatory mechanisms affecting blood pressure and flow, including neural, hormonal, and local factors impacting vascular resistance and heart function.
More Related Content
Similar to cardiovascular physiology based on Ganong's
cardiovascular physiology based on Ganong's
- 2. Cardiac Cycle • Notethe 7 phases separated by vertical lines. • The ECG is used in general as an event marker
- 5. Cardiac Cycle 1. Atrialsystole • Is preceded by the P wave (electrical activation of atria) • Contributes to ventricle filling • Produce the a wave of the JVP 2. Isovolumetric contraction • Begins after the onset of the QRS of the ECG • When ventricle pressure exceeds that of the atria, AV valves close producing the 1st heart sound • Ventricular pressure increases isovolumetrically while all four valves are closed • c wave of the JVP occurs due to high ventricular pressure
- 6. Cardiac Cycle 3. Rapidventricular ejection • When ventricle pressure exceeds aortic pressure, aortic valve open • Rapid ejection of blood to aorta occurs • Most of the stroke volume is ejected during this phase • Same time, atrial filling begins. • T wave of the ECG occurs and the ventricles start repolarising 4. Reduced ventricular ejection • Blood continues to be ejected slowly • Both ventricular and aortic pressure starts dropping • Atrial filling continues
- 7. Cardiac Cycle 5. Isovolumetricventricular relaxation • Repolarisation of ventricle is now complete • Semilunar valves close and the 2nd heart sound occur • All 4 valves are closed while the ventricle relaxes – causing a rapid drop in pressure • Dicrotic notch in the aortic pressure occur • When ventricle pressure becomes lower than the atrial pressure mitral valve opens • v wave of the JVP occur at the end due to atrial filling 6. Rapid ventricular filling • Mitral valve open and ventricle fill from the atria rapidly
- 8. Cardiac Cycle 7. Reducedventricular filling (diastasis) • Longest phase of the cardiac cycle • Ventricle fill at a slower rate • The time for this varies with the heart rate
- 9. Jugular venous pulse 3pulsation – Pressure changes in Right atria a - Atrial systole. c - onset of ventricular sys. – cusp bulging. v - the end of ventricular systole
- 10.
- 11. •Humans have Parallelvascular arrangement which is important. •Flow in different capillary beds can be selectively altered •Flow to vital organs can maintained at expense of other organs •Constriction of a significant fraction of capillary bed can Increase total peripheral resistance •This is not possible if the pumps are in series
- 12. Arteries • Thick walled,extensive elastic tissue & smooth muscle • Under high pressure • The blood volume contained in them are called the stressed volume Arterioles • Smallest branches of the arteries • Site of highest resistance in the cardiovascular system • Have smooth muscle walls which have extensive autonomic innervation • 1 adrenergic - in the skin and splanchnic arterioles • Β2 adrenergic – in the skeletal muscle arterioles Components of the vasculature
- 13. Capillaries • Have thelargest cross sectional surface area • Consist of a single layer of cells – thin walled • Are the site of exchange of nutrients, water & gases Venules • Are formed from merged capillaries Components of the vasculature
- 14. Veins • Progressively formslarger and larger veins • Are thin walled • Are under low pressure • Contains the highest proportion of the blood in the cardiovascular system • Blood volume in the veins is called the unstressed volume • Are innervated by autonomic fibres Components of the vasculature
- 15. Cross sectional profileof the vessels Cross sectional area is greatest in capillaries Arteries – Pressure varies bet. Sys. and diastole Largest –pressure drop recorded at - arteriolesSite where flow can be regulated
- 17. Velocity of bloodflow • Can be expressed by: V = Q / A v = velocity (cm/sec) Q = blood flow (ml/min) A = cross sectional area (cm2) • Therefore, velocity is higher in the aorta (smaller cross sectional area) is lower in all the capillaries – Why ?
- 18. Mean velocity ofblood flow – lowest on the capillaries To maximize the exchange of substances
- 19. Blood flow • Canbe expressed by: Q = ∆P / R Q = blood flow (ml/min) ∆P = pressure gradient (mmHg) R = resistance ΔP = Mean arterial pressure MAP and Right atrial pressure –CVP Cardiac Mean arterial Right atrial output = pressure - pressure Total peripheral resistance
- 20. Cardiac Output • Isthe volume of blood ejected from each ventricle per minute • Expressed by the following: CO = SV x HR • Cardiac output of a 70 kg man is about 5L
- 21. Stroke volume • Isthe volume of blood ejected from each ventricle on each beat • Expressed by the following: Stroke volume = EDV – ESV • Normally is about 70 ml (as EDV = 140 ml & ESV = 70 ml) • SV = (~2 x pulse pressure)
- 22. Cardiac Index •Expressed bythe following: cardiac index = CO / body surface area •Gives a correct estimation of the cardiac output depending on the size of the person
- 23. Ejection fraction • Isthe fraction of end-diastolic volume ejected in each stroke volume • Is normally 0.55 or 55% • Is expressed by the following equation: Ejection fraction = SV End-diastolic volume
- 24. Stroke work • Isthe work the heart performs on each beat • Is expressed by; Stroke work = Aortic pressure x Stroke volume • Fatty acids are the primary energy source for stroke work
- 25. Myocardial oxygen consumption •Is directly related to the amount of tension developed by the ventricles • It is increased by: 1.increased afterload (aortic pressure) 2.Increased size of the heart (Laplace’s law) 3.Increased contractility 4.Increased heart rate
- 26. Control of cardiacoutput Cardiac output Heart Rate Pre Load Myocardial contraction After load 4 factors determine cardiac output
- 27. Staring law ofthe heart “ The energy of cardiac contraction is depended on the resting length of the cardiac muscle fibre” “ When stretch more contract more” Explains how heart matches input ( VR) to output (C.O) Also how Cardiac output of Right and Left Ht are equalized to prevent congestion This is an intrinsic function of the heart But alsoThis leads to increase or decrease cardiac function at constant diastolic volumes
- 28. Frank-Starling relationship • describesthe increase in stroke volume that occurs in response to an increase in venous return (or end- diastolic volume) Length-tension relationship in the ventricles Force of contract ion Left Ventricular End diastolic Volume
- 30. 1. Preload • isequivalent to end-diastolic volume • It is related to the right atrial pressure • Increase will increase the force of contraction (Frank-Starling relationship) 2. Afterload • For the left ventricle = aortic pressure • For the right ventricle = pulmonary arterial pressure • Increase of these pressures will increase the afterload Length-tension relationship in the ventricles
- 31. Venous return: •ΔP =flow x Resistance Rise of the venous Pressure leads to more Venous Return Right Atrial pressure Veins
- 32.
- 33. • MSFP isincreased by – increased blood volume or decreased venous compliance • MSFP is decreased by – decreased blood volume or increased venous compliance Cardiac & vascular function curves • Mean systemic filling pressure (MSFP) is at the point where venous return curve intersects the x axis (normally ~7 mmHg)
- 34. Control of cardiacoutput 2 relationships 1. Between Venous Return and Rt atrial pressure 2. Between cardiac output and preload (Starling's law)
- 35. Cardiac & vascularfunction curves • Its a simultaneous plot of cardiac output and venous return as a function of right atrial pressure or end diastolic volume
- 36. • The pointat which the two curves intersect is the equilibrium point or steady state point • Cardiac output can be changed by altering • The cardiac output curve • The venous return curve • Or both curves simultaneously Combining cardiac output & venous return curves
- 37. There can bedifferent equilibrium conditions • With increase contractility cardiac output is raised but CVP is lower: • With decreased contractility cardiac output is reduced but CVP is raised eg- C.C.F
- 38. 1. Inotropic agentschanges the cardiac output curve intersection point shifts to a higher cardiac output corresponding to a lower right atrial pressure Combining cardiac output & venous return curves
- 39. 2. Changes inblood volume or venous compliance change In this case both cardiac output and right atrial pressure will increase or decrease
- 40. 3. Changes inTPR changes both the cardiac output and venous return Increased TPR – decrease both CO and VR Decrease in TPR – increases both CO and VR
- 42. Pressures in thevasculature & heart
- 43. Velocity of bloodflow • Can be expressed by: v = Q / A where v = velocity (cm/sec) Q = blood flow (ml/min) A = cross sectional area (cm2) • Therefore, velocity is higher in the aorta (smaller cross sectional area) is lower in all the capillaries
- 45. Blood flow • Canbe expressed by: Q = ∆P / R where Q = blood flow (ml/min) ∆P = pressure gradient (mmHg) R = resistance • Or Cardiac Mean arterial Right atrial output = pressure - pressure Total peripheral resistance
- 46. Resistance • According toPoiseuille’s equation: R = 8 η l π r4 where R = resistance η = viscosity of blood l = length of blood vessel r = 4th power of the radius of blood vessel
- 47. Resistance • Resistance couldbe in parallel or series • Parallel resistance: Illustrated by the systemic circulation Each organ is supplied by an artery that branches off the aorta the resistance of this arrangement is given by 1 = 1 + 1 + 1 ....... 1 R total R1 R2 R3 R n • The total resistance is less than the resistance of any of the individual arteries
- 48. Resistance • Series resistance: Illustratedby the arrangement of blood vessels within a given organ Since an organ is supplied by a large artery, small arteries, arterioles, capillaries arranged in series R total = R artery + R arterioles + R capillaries The largest proportion of resistance is contributed to by arterioles
- 49. Blood flow –laminar vs turbulent • Laminar flow is in a straight line and turbulent flow is not. • Reynold’s number predicts whether blood flow is turbulent or laminar. • When Reynold’s number is increased, there will be turbulence and audible vibrations (bruits) ` • Reynold’s number is increased by: reduced viscosity (low haematocrit, anaemia) increased velocity (narrowing of a vessel)
- 50. C = Capacitance (compliance) •Describes the distensibility of blood vessels • Is inversely related to elastance • Capacitance is given by: C = V / P where C = capacitance (ml/mmHg) V = volume (ml) P = pressure (mmHg) • Describes how volume changes in response to changes in pressure
- 51. C = • Capacitanceis much greater for veins than for arteries • Changes in venous capacitance changes the venous blood volume • Eg: decrease in venous capacitance decreases the unstressed volume (venous volume) and increases the stressed volume (arterial volume) • Capacitance of arteries decreases with age. Arteries become stiffer and less distensible
- 52. Pressure profile invessels • As the blood flow through the systemic circulation, pressure decreases because of the resistance
- 53. C = • Pressureis highest in the aorta and lowest in the venae cavae • The largest decrease in pressure occurs across the arterioles (site of highest resistance) • Mean pressures: aorta - 100 mmHg end of arterioles - 30 mmHg vena cava - 4 mmHg Pressure profile in vessels
- 55. • Is pulsatile •Varies during the cardiac cycle • Systolic pressure • Diastolic pressure Arterial pressure
- 56. C = Pulse Pressure •SBP – DBP difference • The most important determinant is stroke volume • Decrease in capacitance due to aging can cause an increase of pulse pressure • Generally ~ 40 mmHg Mean Arterial Pressure • It is actually the average arterial pressure with respect to time • Is equal to DBP + 1/3 pulse pressure
- 57. C = Venous pressure •Is very low • Has a high capacitance • Able to hold a large volume without an increase in pressure
- 58. Atrial pressure • Evenlower than venous pressure • Right atrial pressure – generally similar to CVP • Left atrial pressure is estimated by pulmonary capillary wedge pressure • Catheter inserted into the smallest pulmonary artery branch, very close to pulmonary capillaries. • Pulmonary capillary pressure is only a little higher than the left atrial pressure
- 59. C = Venous pressure •Is very low • Has a high capacitance • Able to hold a large volume without an increase in pressure
- 60. Atrial pressure • Evenlower than venous pressure • Right atrial pressure – generally similar to CVP • Left atrial pressure is estimated by pulmonary capillary wedge pressure • Catheter inserted into the smallest pulmonary artery branch, very close to pulmonary capillaries. • Pulmonary capillary pressure is only a little higher than the left atrial pressure
- 61. •Most important mechanismsare: •the fast neurally mediated baroreceptor mechanism •the slower hormonally mediated renal mechanisms •Other mechanisms include; Atrial stretch receptors local vasoconstrictors and dilators Regulation of arterial blood pressure
- 62. •Most of thevasculature is innervated by sympathetics •Sympathetic noradrenergic fibres terminate on resistant vessels – mediates vasoconstriction •Exceptions: - Skeletal muscle vessels undergo vasodilatation via β2 due to circulating adrenaline - parasympathetic innervation is seen in some erectile tissue of reproductive organs, uterine vessels some facial vessels blood vessels in the salivary glands •Sympathetic innervation of veins cause a reduction in capacitance and an increase in venous return Innervation of blood vessels
- 63. •There are pressurereceptors located in the cardiovascular system •Those that monitor arterial pressure: In the carotid sinus & aortic arch •Low-pressure receptors (cardiopulmonary receptors) In walls of right atria at vena caval entrance wall of left atria pulmonary circulation •Baroreceptors Located within the walls of the carotid sinus near the bifurcation of the common carotid artery and aortic arch Baroreceptor reflex
- 64.
- 65.
- 66. •Increased baroreceptor discharge -inhibits the tonic discharge of sympathetic nerves and - excites the vagal innervation of the heart. •These neural changes produce vasodilation, venodilation, hypotension, bradycardia and a decrease in cardiac output. Baroreceptor reflex
- 67. •There are twotypes of stretch receptors in the atria Those discharging in atrial systole & In late diastole during atrial filling •Effect of increase discharge from the include; vasodilatation & a fall in BP But, an increase in heart rate Cardiopulmonary receptors
- 68. • Peripheral chemoreceptorsfound in the; Aortic & carotid bodies • Have a very high blood flow • Activated by: low PaO2, PCO2 and pH • Stimulated by hypoxic hypoxia • Main effects are on respiration, but also leads to vasoconstriction • Direct effect of chemoreceptor activation is hypoxia, increased catecholamines from medulla which increases HR and BP Peripheral chemoreceptor reflex
- 69. • When intracranialpressure increases, The pressure on the VMC and the local hypoxia and hypercapnia, increases its discharge. • Results in the rise of systemic blood pressure • Accompanied by reflex reduction in heart rate (through baroreceptor reflex) • Therefore, Increased ICP – Hypertension and bradycardia Central chemoreceptors
- 70. •The capacity oftissues to regulate their own blood flow is referred to as autoregulation. •Most vascular beds have an intrinsic capacity to compensate for moderate changes in perfusion pressure by changes in vascular resistance, so that blood flow remains relatively constant. •Seen in mainly kidney. Also in mesentery, skeletal muscle, brain, liver, myocardium. •Two theories for this: Myogenic autoregulation Metabolic theory of autoregulation Autoregulation
- 71. •Local Factors Factors affectingblood vessel calibre Vasoconstriction Vasodilatation Decreased temperature Increased CO2 & decreased O2 Autoregulation Increased K+, adenosine, lactate Decreased local pH increased temperature
- 72. •Endothelial products Factors affectingblood vessel calibre Vasoconstriction Vasodilatation Endothelin - 1 Nitric oxide Locally released platelet serotonin Kinins Thromboxane A2 Prostacyclin
- 73. •Circulating neurohormonal agents Factorsaffecting blood vessel calibre Vasoconstriction Vasodilatation Epinephrine (except in skeletal muscle and liver) In skeletal muscle & liver Norepinephrine Calcitonin-G related protein ADH (vesopressin) Substance P Angiotensin II Histamine Endogenous digitalis like substances Atrial natriuretic peptide Neuropeptide Y Vasoactive intestinal polypeptide
- 74. Stimulators Inhibitors Angiotensin IINitric oxide Catecholamines ANP Growth factors PGE2 Hypoxia Prostacyclin Insulin Oxidized LDL HDL Shear stress Thrombin Regulation of Endothelin-I secretion
- 75. • Many circulatingsubstances affect the vascular system • The vasodilator regulators include kinins VIP & ANP • Circulating vasoconstrictor hormones include vasopressin norepinephrine epinephrine & angiotensin II Systemic regulation by neurohormonal agents
- 76. C = Neurohormonal mechanismsof regulating blood pressure • Associated with volume regulation • Volume regulation is closely related to Na+ regulation • The main controller are: – Renin – angiotensin – aldosterone system – ANP and natriuretic substances
- 78. C = Renin –angiotensin – aldosterone system Renin • Referred to as an enzyme / hormone • Synthesised as prorenin • Secreted from the JG cells of the kidney as • renin or prorenin • The active form is renin and only kidney can produce this • Only known function is to cleave angiotensinogen and form angiotensin-I Angiotensinogen • Alpha-2 globulin • blood level increase by - glucocorticoids, thyroid hormones, estrogens, several cytokines and angiotensin II.
- 79. C = Angiotensin ConvertingEnzyme & Angiotensin II • ACE is formed by endothelial cells and happens in many parts of the body • Conversion of Angiotensin I happens mainly when blood passes through the lungs • Same ACE inactivates bradykinin • Angiotensin-II has a very short half life of 1-2 min • The active substance is Angiotensin-II
- 80. C =Actions ofAngiotensin II 1. Potent vasoconstrictor. Acts on AT1 receptors. Constricts arterioles and elevate SBP & DBP 2. Directly acts on adrenal cortex to increase aldosterone secretion 3. Facilitation of release of NE from sympathetic postganglionic neurones 4. Contraction of mesangial cells with a decrease in GFR 5. A direct effect on the renal tubules to increase Na+ reabsorption. 6. Acts on the brain to reduce the sensitivity of baroreflex 7. Increase thirst 8. Increase ADH and ACTH secretion
- 81. C =Juxtaglomerular apparatus •Comprise of JG cells, Lacis cells and macula densa • Renin is produced by JG cells – located in the media of afferent arterioles • Renin is also found in lacis cells that are located in the junction between the afferent & efferent arterioles – functional importance of this renin? • Macula densa – modified efferent arteriolar cells in close proximity to JG cells
- 82. C =Regulation ofrenin secretion Occur due to the balance of many factors 1. Intrarenal baroreceptor mechanism that decrease renin when pressure in the JG cells increase 2. Increased Na+ and Cl- amount delivered to the macula densa cells decrease renin secretion 3. Angiotensin-II has a direct feedback inhibition on JG cells 4. ADH also has an inhibitory effect on renin secretion
- 83. C =Regulation ofrenin secretion 5. Increased sympathetic activity Increase renin secretion by - increased circulating catecholamines acting on β1 receptors on the JG cells - stimulation of renal sympathetic nerves 6. Reduced renal artery pressure (due to renal artery constriction or aorta) produce increased renal sympathetic nerve stimulation and that increase renin secretion
- 85. Navar L Get al. Physiology 1998;13:170-176 ©1998 by American Physiological Society
- 86. Navar L Get al. Physiology 1998;13:170-176 ©1998 by American Physiological Society
- 88. Hormones of theheart & other natriuretic factors • Secreted from the muscle cells in the atria and, to a much lesser extent in the ventricles • Contain secretory granules •The granules increase in number when ECF expands due to increased Na+ in the body •The other hormones • BNP – Brain and heart • CNP - brain, pituitary, kidneys, and vascular endothelial cells (acts in a paracrine fashion) • Causes natriuresis ANP
- 89. Hormones of theheart & other natriuretic factors Actions: • Increase GFR by dilating afferent arteriole & relaxing mesangial cells •Acts on the renal tubule to inhibit Na+ reabsorption •An increase in capillary permeability, leading to extravasation of fluid and a decline in blood pressure. •Relax vascular smooth muscle in arterioles and venules. CNP has a greater dilator effect on veins • Inhibit renin secretion and • Counteract the pressor effects of catecholamines ANP
- 90. Microcirculation Blood flow throughthe tissues is regulated by contraction and relaxation of the arterioles and pre-capillary sphincters
- 91. C = Microcirculation Passage ofsubstances across capillary walls 1. Lipid soluble substances – by simple diffusion 2. Small water soluble substances – across water filled clefts between endothelial cells. Brain – clefts exceptionally tight (BBB) Liver & intestine – clefts are very wide, allow passage of proteins too. 3. Large water soluble substances – by pinocytosis
- 92. C = Starling’s equationfor fluid movement across capillaries Jv = Kf [(Pe – Pi) – (πe – πi)] Where: Jv - fluid movement (ml/min) Kf - hydraulic conductance (ml/min . mm Hg) Pe - capillary hydrostatic pressure (mm Hg) Pi - interstitial hydrostatic pressure (mm Hg) πe - capillary oncotic pressure (mm Hg) πi - interstitial oncotic pressure (mm Hg)
- 93. Control of bloodflow a. Autoregulation b. Active hyperaemia c. Reactive hyperaemia • Local control of blood flow Mechanisms of local control of blood flow a. Myogenic theory b. Metabolic theory • Extrinsic control of blood flow a. Sympathetic innervation b. Other vasoactive hormones
- 94. Other vasoactive hormones Histamine •Causes arteriolar dilatation & venous constriction • Resulting in local oedema due to increased Pe • Released in response to tissue trauma Bradykinin • Exactly like histamine Serotonin • Causes arteriolar constriction • released in response to vessel damage to prevent blood loss
- 95. Other vasoactive hormones Prostaglandins •Prostacyclin is a vasodilator in several vascular beds • E-series prostaglandins are vasodilators • F-series prostaglandins are vasoconstrictors • Thromboxane A2 is a vasoconstrictor
- 96. Special circulations Coronary Circulation •Is controlled almost entirely by local metabolic factors – most important factors are hypoxia & adenosine • Exhibits autoregulation • Exhibits active and reactive hyperaemia • Active hyperaemia: contractility increase will create an increase demand for oxygen. To meet this demand, vasodilatation of coronaries occur increasing oxygen delivery • Reactive hyperaemia: during systole, mechanical compression of coronaries, cause increase of flow after systole • Sympathetic nerves play a minor role
- 97. Special circulations Cerebral Circulation •Is controlled almost entirely by local metabolic factors – most important local vasodilator is CO2 • Exhibits autoregulation • Exhibits active and reactive hyperaemia • Sympathetic nerves play a minor role • Vasoactive substances in the systemic circulation has little or no effect as they cannot cross the BBB
- 98. Special circulations Skeletal muscle •Is controlled by sympathetic nerves of blood vessels & by local metabolic factors • Sympathetic innervation: • Primary regulator of flow at rest • There are both 1 and β2 receptors in vessels • 1 – cause vasoconstriction • β2 – cause vasodilatation • Vasoconstriction of skeletal muscle vessels is the major contributor to TPR at rest
- 99. Special circulations Skeletal muscle •Local metabolic control: • Exhibits autoregulation, active and reactive hyperaemia • Local vasodilatory substances are lactate, adenosine and K+ • Mechnical occlusion during exercise can occlude arteries temporarily and cause an oxygen debt producing a reactive hyperaemia later
- 100. Special circulations Skin • Sympatheticnerves play a Major role • Temperature regulation is the principal function of cutaneous sympathetics • trauma produce the triple response with a red line, flare and a wheal
- 101. CVS changes ina haemorrhage Arterial Baroreceptors Cardiopulmonary receptors Chemoreceptors Central nervous system cardiovascular centres Hypovolaemia Sympathetic output increasedParasympathetics output reduced Reduced CVPReduced CO Reduced MAP HR increased Heart contractility increased Arterial constrictionVenous constriction increased Fluid absorption increased Capillary hydrostatic Pressure reduced raised CO raised TPR Blood pressure restored
- 103.
- 104. • Are constructedby combining systolic and diastolic pressure curves. • It is a cycle of contraction, ejection, relaxation and refilling Ventricular pressure-volume loops
- 105. 1. Change inPreload • Refers to a change in end diastolic volume • Relates to the width of the pressure-volume loop Changes in the ventricular pressure-volume loops
- 106. 2. Change inAfterload • Refers to an increase in aortic pressure • Ventricle must eject blood against a higher pressure, resulting in a smaller stroke volume • Therefore, the end systolic volume would be more
- 107. 3. Increased Contractility •Ventricle develops greater tension than usual and contracts more forcefully • Stroke volume increases • End systolic volume decreases
- 109. Atria, ventricles andPurkinje system • Resting membrane potential is determined by the conductance to K+ • Close to the K+ equilibrium potential. Around -90 mV Cardiac action potentials Phase 1, Initial repolarization K+ efflux and the reduction of Na+ conductance Phase 4, Resting membrane potential. Approaches the K+ equilibrium potential
- 110. Sinoatrial (SA) node •Does not have a constant resting membrane potential • Exhibits phase 4 depolarization or automaticity • Phases 1 & 2 are absent in the SA node action potential Cardiac action potentials
- 112. Conduction velocity • Fastestin the Purkinje system • Slowest in the AV node • Absolute refractory period (ARP) – No action potential could be initiated • Relative refractory period (RRP) – more than the usual inward current is required to initiate an action potential Cardiac action potentials Refractory period
- 113. Autonomic effects onthe heart & vessels • Innate rate of the SA node is about 100/min • Both sympathetics and parasympathetics have effects on the rate • If parasympathetics are blocked, the rate rises to 150-180 /min • Chronotropic effect – producing changes in the heart rate • Dromotropic effect – producing changes in conduction velocity mainly in the AV node • Inotropic effect – produce an effect on the contractility of the heart
- 114. Parasympathetic effect onheart • SA node, atria and AV node has parasympathetic innervation • Neurotransmitter is Ach. Acting on muscarinic receptors • Effects are: • Decreasing heart rate (threshold potential is reached slowly) • Decrease conduction velocity through the AV node • Increase the PR interval (decreased inward Ca++ current)
- 115. Sympathetic effect onheart • Neurotransmitter is Norepinephrine. Acting on β1 receptors • Effects are: • Positive chronotropic effect (threshold potential is reached faster • Increase conduction velocity through the AV node • Decrease the PR interval (increase inward Ca++ current) • Positive inotropic effect
- 117. Cardiac muscle fibres •Large number of mitochondria – for supply of constant energy
- 118. •Cells contain myosin,actin, troponin and tropomyosin •Gap junctions are present at the intercalated disks Entire heart behaves as an electrical syncytium •Mitochondria are more numerous in cardiac muscles than in skeletal muscles •T tubules – invaginations in the cell membrane. Carry action potentials into the cell interior •Sarcoplasmic reticulum – sites of storage of Ca++ needed for excitation-contraction coupling Myocardial cell structure
- 119. 1. Action potentialspreads from the cell membrane through the T tubules 2. During the plateau phase of the AP, Ca++ enter the cell from the ECF 3. This Ca++ entry trigger the release of more Ca++ from the SR (Ca++ induced Ca++ release) – amount released depends on the amount stored and the size of the inward current 4. Intracellular Ca++ increase – actin and myosin interaction and contraction occurs 5. The magnitude of tension developed depends on the amount of Intracellular Ca++ 6. Relaxation occurs when Ca++ is pumped back into SR by Ca++ -ATPase pump Steps in excitation-contraction coupling
- 123. P wave • Representsatrial depolarization PR interval • Is the interval between the beginning of P wave to beginning of Q wave • Increases with problems in conduction velocity (heart blocks) • Varies with heart rate. QRS complex • Represents ventricular depolarization Electrocardiogram (ECG)
- 124. QT interval • Frombeginning of QRS to end of T wave • Represents entire ventricular depolarization and repolarisation ST segment • Is the segment from the end of S wave to the beginning of T wave • Is isoelectric • Represents the period when the ventricle is depolarized T wave • Represents ventricular repolarisation Electrocardiogram (ECG)
- 125. Atria, ventricles andPurkinje system • Resting membrane potential is determined by the conductance to K+ • Close to the K+ equilibrium potential. Around -90 mV Cardiac action potentials Phase 1, Initial repolarization K+ efflux and the reduction of Na+ conductance Phase 4, Resting membrane potential. Approaches the K+ equilibrium potential
- 126. 1. Explain thephysiological determinants of ejection fraction. (40 % marks 1. Importance of Ca++ in cardiac muscle contraction. (30% marks) 2. Explain the physiological basis of the following : 4.2. Tachycardia in shock. (25 marks) 4.3. Low urine output in a patient who has lost IL of blood. (25 marks) 3. 3.1. Explain how variations in arteriolar resistance affect the arterial blood flow. (50 marks) 1. Outline the factors that determine the blood flow to an organ (15 marks) 2. Explain the autoregulation of cerebral blood flow. (35 marks) 3. Describe the baroreceptor reflex regulation of blood pressure. (50 marks) 4. Give the physiological mechanisms that facilitate the venous return from 5. the extremities to the heart.
- 127. 1. Explain thephysiological basis of the following , 1.1 A drop in systolic blood pressure when standing from supine position (30 marks) 1.2 Low urine output following a haemorrhage (40 marks) 1.1. What biophysical factors determine the blood pressure? 1.2. Explain with examples how blood pressure is increased when these factors are altered by diseases.
Editor's Notes
- #86 Renin-angiotensin system. A: mechanisms mediating renin release and formation of angiotensin (ANG) I and ANG II. B: multiplicity of systemic actions of ANG II. ADH, antidiuretic hormone; CNS, central nervous system; ECF, extracellular fluid; RBF, renal blood flow.
- #87 Renin-angiotensin system. A: mechanisms mediating renin release and formation of angiotensin (ANG) I and ANG II. B: multiplicity of systemic actions of ANG II. ADH, antidiuretic hormone; CNS, central nervous system; ECF, extracellular fluid; RBF, renal blood flow.