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CVS PhysiologyDr. Lapale Moipolai

Head of Clinical UnitDept. Anaesthesiology

SBAH03 June 2013

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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

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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

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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

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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

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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

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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

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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

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cont’dPreload is affected by

• Blood volume

• Venous tone and venous return

• Left ventricular compliance

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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)

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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

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Relaxation Lusitropy

• Affects preload

• Mediated by beta adrenergic activity

• Ischaemia impairs relaxation

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Peripheral Circulation

• Smooth Muscle Tone

• Autoregulation

• Baroreceptors

• RAS

• ADH

• ANP

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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.

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Cont’d3. SVR

4. Cardiac output

5. ANS

6. Baroreceptors

7. Diastolic function

8. Coronary circulation

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ConclusionReferences

• Guyton

• Ganong

• Studentconsult.com

• Cardiac Anesthesia 5th Edition 2013; Glenn Gravlee