BIOM1060 Lecture Notes - Lecture 22: Oncotic Pressure, Capillary, Baroreceptor
BIOM1060 27/03/18
CARDIOVASCULAR PHYSIOLOGY (Part 2)
Frank-Starling principle
- Automatic variability in cardiac output (beat to beat)
oDetermined by volume of blood in ventricle at end of diastole
oHeart operates on upstroke of length-tension relationship (increased filling =
increased output) - nerve/receptor independent
- Influenced by: autonomic nervous system (sympathetic/parasympathetic), circulating
hormones, physiological hypertrophy (increase in myocardial fibre length)
Determinants of cardiac output
- Preload: initial filling/stretch (end diastolic volume)
- Afterload: pressure load during contraction (arterial BP)
- Heart rate: stroke volume x heart rate = cardiac output
- Inotropic state (contractility): changes stroke volume at constant preload and afterload
Exercise
- Increased flow to skeletal muscle, decreased flow to kidney and gastrointestinal tract
- Local metabolic changes in tissue control arteriolar diameter (allow increased blood flow)
find more resources at oneclass.com
find more resources at oneclass.com
BIOM1060 27/03/18
Venous return
- Volume of blood returning to heart each minute
oIncreases end diastolic volume
oStretches heart muscle = increases strength of next contraction
- Controlled by:
oCardiac suction:
Contraction of ventricles: atrioventricular valves close, increased atrial
volume = decreased atrial pressure (sucks blood from veins into atria)
Relaxation of ventricles: increased ventricular volume = decreased
ventricular pressure (sucks blood from veins and atria into ventricles)
oSkeletal muscle pump: muscle action compresses veins to push blood
through veins (valves prevent backflow)
oVenous valves
oSympathetic nervous system
Fainting
- Decreased venous return, cardiac output and blood to brain
- Fall over = gravity overcome (venous return and cardiac output return to normal)
Capillaries
- Site of exchange between blood and tissue (gases, nutrients and wastes)
- Primarily by diffusion
oSmall diffusion distance: thin walls, small diameter, large network
oLarge surface area available
oSlow blood flow
- Arranged into capillary beds (blood supply controlled/regulated by precapillary sphincters)
- Blood flows through metarteriole (bypasses capillary beds - shunts straight into veins)
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Automatic variability in cardiac output (beat to beat) o o. Determined by volume of blood in ventricle at end of diastole. Heart operates on upstroke of length-tension relationship (increased filling = increased output) - nerve/receptor independent. Influenced by: autonomic nervous system (sympathetic/parasympathetic), circulating hormones, physiological hypertrophy (increase in myocardial fibre length) Afterload: pressure load during contraction (arterial bp) Heart rate: stroke volume x heart rate = cardiac output. Inotropic state (contractility): changes stroke volume at constant preload and afterload. Increased flow to skeletal muscle, decreased flow to kidney and gastrointestinal tract. Local metabolic changes in tissue control arteriolar diameter (allow increased blood flow) Volume of blood returning to heart each minute o o. Stretches heart muscle = increases strength of next contraction. Contraction of ventricles: atrioventricular valves close, increased atrial volume = decreased atrial pressure (sucks blood from veins into atria) Relaxation of ventricles: increased ventricular volume = decreased ventricular pressure (sucks blood from veins and atria into ventricles) o.
