CVS Physiology

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

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

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

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

6. Excitation-Contraction coupling • 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 • Calcium ions diffuse across the sarcolemma through the calcium release channels, ryanodine receptor channel

9. Exc-Con cont’d • 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 • Actin and myosin interact and the sarcomere shortens • ATP depended process • Calcium – troponin affinity is a central pathophysiologic substrate

10. Heart Rate • SA node pacemaker • 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. • 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 • Cardiac cycle of 60 to 90 beats per minute

12. Definition of terms • 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 Within physiologic limits, the larger the volume of the heart, the greater the energy of its contraction- Starling

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

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

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 • Vmax the maximum velocity of contraction at zero load • LV dP/dtmax • Surrogate: Ventricular Function or Starling Curves • Pressure-Volume Loops

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

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

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. • Preload: reduction in venous tone, more with propofol. Halogenated agents do not affect preload. • Cardiac muscle: decrease myocardial contractility by reduction of calcium fluxes across the cardiac cell membrane, SR. Decreased sensitization may also play a role.

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

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