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CVS Physiology Dr. Lapale Moipolai Head of Clinical Unit Dept. Anaesthesiology SBAH 03 June 2013 1.

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Presentation on theme: "CVS Physiology Dr. Lapale Moipolai Head of Clinical Unit Dept. Anaesthesiology SBAH 03 June 2013 1."— Presentation transcript:

1 CVS Physiology Dr. Lapale Moipolai Head of Clinical Unit Dept. Anaesthesiology SBAH 03 June 2013 1

2 Main Points Functional anatomy of the heart Functional anatomy of the heart Basics of heart physiology and the origin of heart beat Basics of heart physiology and the origin of heart beat Changes that occur during cardiac cycle Changes that occur during cardiac cycle Cardiac output and factors affecting it Cardiac output and factors affecting it Haemodynamics Haemodynamics Physiological abnormalities causing disease Physiological abnormalities causing disease 2

3 embryology CVS is one of the first systems to develop CVS is one of the first systems to develop First three weeks from the mesodermally derived endothelial cells First three weeks from the mesodermally derived endothelial cells 4 weeks bilateral cardiogenic cords 4 weeks bilateral cardiogenic cords Initial contraction at 21 to 22 days Initial contraction at 21 to 22 days Unidirectional blood flow in week 4 and further differentiation throughout to week 7 into four chambers Unidirectional blood flow in week 4 and further differentiation throughout to week 7 into four chambers 3

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5 Pump Function Heart is a pump that generates stroke volume SV X HR = CO SV X HR = CO Peripheral circulation is logistic conduit that regulates perfusion pressure and regional blood flow Peripheral circulation is logistic conduit that regulates perfusion pressure and regional blood flow Flow = Pressure / Resistance Flow = Pressure / Resistance Pressure = Flow x Resistance Pressure = Flow x Resistance BP = CO X SVR BP = CO X SVR 5

6 Excitation-Contraction coupling Purkinje fibre action potential results in coordinated contraction of a cardiac myocyte Purkinje fibre action potential results in coordinated contraction of a cardiac myocyte Five phases of the action potential involving changes in sodium, potassium and calcium conductances Five phases of the action potential involving changes in sodium, potassium and calcium conductances Calcium ions diffuse across the sarcolemma through the calcium release channels, ryanodine receptor channel Calcium ions diffuse across the sarcolemma through the calcium release channels, ryanodine receptor channel 6

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9 Exc-Con cont’d Sarcoplasmic Reticulum is responsible for efficient cycling of calcium (ryanodine receptor channel, SERCA-2 and the regulatory protein, phospholambin) Sarcoplasmic Reticulum is responsible for efficient cycling of calcium (ryanodine receptor channel, SERCA-2 and the regulatory protein, phospholambin) Calcium binds to troponin and results in a conformational change involving tropomyosin Calcium binds to troponin and results in a conformational change involving tropomyosin Actin and myosin interact and the sarcomere shortens Actin and myosin interact and the sarcomere shortens ATP depended process ATP depended process Calcium – troponin affinity is a central pathophysiologic substrate Calcium – troponin affinity is a central pathophysiologic substrate 9

10 Heart Rate SA node pacemaker SA node pacemaker Membrane potential is small and unstable enabling impulse firing readily Membrane potential is small and unstable enabling impulse firing readily Slow fibres only in the SA and AV nodes. Resting membrane potential of -50 to -60 mV. Slow fibres only in the SA and AV nodes. Resting membrane potential of -50 to -60 mV. The action potential results in opening of the slow sodium and calcium channels The action potential results in opening of the slow sodium and calcium channels Fast fibers in ordinary atrial and ventricular muscle fibres and components of specialized conducting tissues. RMP -80 to -90 mV Fast fibers in ordinary atrial and ventricular muscle fibres and components of specialized conducting tissues. RMP -80 to -90 mV Cardiac cycle of 60 to 90 beats per minute Cardiac cycle of 60 to 90 beats per minute 10

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12 Definition of terms Preload Preload Load on the muscle that stretches it before onset of contraction. Defines the end diastolic fibre length Surrogate measures: end diastolic volume end diastolic pressure end diastolic pressure Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction- Starling 12

13 cont’d Preload is affected by Blood volume Blood volume Venous tone and venous return Venous tone and venous return Left ventricular compliance Left ventricular compliance 13

14 Afterload Load on the muscle at peak contraction The load against which the left ventricle contracts The load against which the left ventricle contracts Increased afterload will increase peak tension during contraction but decrease external work. Increased afterload will increase peak tension during contraction but decrease external work. Surrogate measure: systemic vascular resistance (SVR) Surrogate measure: systemic vascular resistance (SVR) 14

15 Contractility Inotropic state of the heart by which the force of myocardial contraction is altered without a change in preload or afterload. Measures of contractility Measures of contractility Vmax the maximum velocity of contraction at zero load Vmax the maximum velocity of contraction at zero load LV dP/dt max LV dP/dt max Surrogate: Ventricular Function or Starling Curves Surrogate: Ventricular Function or Starling Curves Pressure-Volume Loops Pressure-Volume Loops 15

16 Relaxation Lusitropy Affects preload Affects preload Mediated by beta adrenergic activity Mediated by beta adrenergic activity Ischaemia impairs relaxation Ischaemia impairs relaxation 16

17 Peripheral Circulation Smooth Muscle Tone Smooth Muscle Tone Autoregulation Autoregulation Baroreceptors Baroreceptors RAS RAS ADH ADH ANP ANP 17

18 Anaesthesia and the Heart Anaesthetic agents in general affect the heart, the peripheral vessels, the baroreceptors and the autonomic nervous system to a varying degree. 1.Preload: reduction in venous tone, more with propofol. Halogenated agents do not affect preload. 2.Cardiac muscle: decrease myocardial contractility by reduction of calcium fluxes across the cardiac cell membrane, SR. Decreased sensitization may also play a role. 18

19 Cont’d 3. SVR 4. Cardiac output 5. ANS 6. Baroreceptors 7. Diastolic function 8. Coronary circulation 19

20 Conclusion References Guyton Guyton Ganong Ganong Studentconsult.com Studentconsult.com Cardiac Anesthesia 5 th Edition 2013; Glenn Gravlee Cardiac Anesthesia 5 th Edition 2013; Glenn Gravlee 20


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