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Medicine Cardiovascular System Clinical Science Summary
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CVS BlockClinical Science
Summary
Chaandanee Bhayroo
1420214
GEMP 1
,The heart and its response to demand
Functions of the CVS:
1) Delivers O2 to working muscles
2) Oxygenates blood by returning it to the lungs
3) Transports heat from the core to the skin (by product of activity)
4) Delivers nutrients and fuel to active tissues
5) Transports hormones
Flow = Pressure/Resistance
Cardiac muscle energy is derived mainly from the metabolism of fatty acids, lactate, and glucose.
Energy is obtained using the oxidative cycle. Therefore, the rate of O2 consumption is a good
indicator of the energy liberated during contraction.
Regulatory mechanisms of the heart:
1) Neurological control (ANS system)
2) Hormonal control (RAAS system)
3) Molecular and cellular regulation
Regulatory mechanisms of the blood vessels:
1) Neurological control (ANS system)
2) Hormonal control (RAAS system)
3) Endothelial factors
a. Dilation – NO, bradykinin, adenosine, low pH, CO2, high temperature, Ach
b. Constriction – endothelin, angiotensin II, catecholamines, high pH, low temp
Heart Rate
Under the control of the ANS.
• Sympathetic activation
▪ Parasympathetic signals are greatly decreased.
▪ Increased HR and cardiac contractility.
▪ Arterioles in cardiac muscles vasodilate, while arterioles in the rest of the body
vasoconstrict.
▪ Decrease in venous pooling = increased venous return
Stroke Volume
= volume of blood ejected from the ventricle per beat
LV and RV SV should be similar unless there is a shunt, valve regurgitation or stenosis.
Determined by:
• Preload: volume of venous blood returned to the heart (Frank-Starling effect)
• End-diastolic volume (ventricular distensibility)
• Ventricular contractility (neural stimulation)
• Afterload: aortic/ pulmonary pressure, impedance, wall stress
There is a maximum at which the SV remains constant despite increasing the other factors.
, Frank-Starling Effect
The energy of the contraction is proportional to the
initial length of the muscle fibre i.e. the preload,
which is proportional to the end diastolic volume
Cardiac Output
= the amount of blood pumped out by the heart per
minute
CO = HR x SV
Can increase during intense exercise. Increases in O2
demand will require increase in coronary blood flow.
There is a maximum at which the CO remains constant despite increasing the other factors.
Coronary blood flow
• Vasodilatation is mediated via α-adrenergic receptors
• Vasoconstriction is mediated by β-adrenergic receptors
La Place’s Law
Tension = Pressure x Radius/ 2 x wall thickness
E.g. during stenosis the wall thickness hypertrophies to overcome the tension of the stenosis i.e.
indirectly proportional
Blood Pressure
SBP increase in direct proportion to increase in exercise intensity. DBP does not change significantly.
Therefore, there is little change in the MAP.
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