1

CVS PhysiologyDr. Lapale Moipolai

Head of Clinical UnitDept. Anaesthesiology

SBAH03 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

4

5

Pump FunctionHeart 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

7

8

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

11

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’dPreload is affected by

• Blood volume• Venous tone and venous return• Left ventricular compliance

14

AfterloadLoad 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

ContractilityInotropic 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.

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.

19

Cont’d3. SVR

4. Cardiac output

5. ANS

6. Baroreceptors

7. Diastolic function

8. Coronary circulation

20

ConclusionReferences

• Guyton• Ganong • Studentconsult.com• Cardiac Anesthesia 5th Edition 2013;

Glenn Gravlee