Download CVS Physiology

CVS Physiology
Dr. Lapale Moipolai
Head of Clinical Unit
Dept. Anaesthesiology
SBAH
03 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 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
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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’d
Preload is affected by
• Blood volume
• Venous tone and venous return
• Left ventricular compliance
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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)
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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
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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’d
3. SVR
4. Cardiac output
5. ANS
6. Baroreceptors
7. Diastolic function
8. Coronary circulation
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Conclusion
References
• Guyton
• Ganong
• Studentconsult.com
• Cardiac Anesthesia 5th Edition 2013; Glenn Gravlee
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