CVS physiology Flashcards
Describe the stages of the cardiac cycle
late diastole - passive filling of atria and ventricles
atrial systole - contraction of atria, small ejection into ventricles, causing small increase in intra-atrial pressure.
Isometric/volumetric contraction of ventricles - closes mitral/tricuspid valves, pressure builds in ventricles but does not exceed that in aorta/pulmonary artery.
Ventricular ejection - pressure in ventricles exceeds that in arteries, pulmonary/aortic valves open, blood ejected from ventricles
Isometric relaxation of ventricles - contraction drops, pressure in arteries exceeds ventricles, pulmonary/aortic valves close.
outline shape/process of pressure volume loop
- mitral valve opens. increase in ventricular vol, slight pressure increase until 2. mitral closes. vertical increase in pressure, no vol change (isometric ventricular contraction) 3. aortic valve opens. pressure continues to increase, volume drops from 135 to 65 mls - normal SV = 70 4. aortic aortic valve closes. pressure drops from ~100 to near 0
Describe changes in velocity and pressure through the vascular tree
Velocity highest in largest vessels i.e. aorta, arteries, pressure also highest (~90 in arteries, drops to 40 in arterioles) total cross sectional diameter is lowest
capillary pressure = 40-20
Venous pressure = 20-5
List the factors effecting venous blood flow
Gravity - standing/lying
muscular pump - i.e. calves
respiratory pump - pressure in thorax decreases on inspiration, draws blood upwards
muscular tone of veins - capacitance vessel function
systemic artery pressure
Outline arterial baroreceptor reflex
Baroreceptors in carotids and aorta. Constant firing of action potentials to CV medullary centres, via the vagus nerve for the aorta and the glossopharyngeal nerve for the carotids.
Increased MAP causes increased stretch and AP firing. Input summated in CV medullary centres, sympathetic or parasympathetic response modulated.
Sympathetic response is via sympathetic spinal nerves, acts on SA node and
What are the main factors in blood clotting
Platelet aggregation and fibrin aggregation
List the anti-clotting mechanisms of capillaries
Prostacyclin secretion and NO secretion -Inhibit platelet aggregation
Thrombomodulin, Heparin - inhibit fibrinogen to fibrin conversion
TFPI (tissue factor pathway inhibitor) - inhibits thrombin production
Plasmin and plasminogen activator - plasmin digests clots.
Darcy’s law
flow = delta pressure/Resistance
Pouseilles law
resistance = (viscosity x length x 8)/(Pi x r4)
Equation for MAP
MAP - CVP = COxTPR
= > MAP = COxTPR
List the three types of intrinsic blood pressure regulation
Active hyperaemia, Pressure autoregulation, Reactive hyperaemia
Define active/metabolic hyperaemia, Pressure auto-regulation and reactive hyperaemia
active hyperaemia - metabolite buildup in tissue as result of metabolism, causes release of EDRF aka NO, which dilates capillaries, increasing blood flow to tissue ‘washes away’ increased metabolite conc., restoring balance.
Flow autoregulation - low flow to tissue results in metabolite build up. Same response as above. This is an adaption to ensure a tissue receives adequate blood supply regardless of MAP changes.
Reactive Hyperaemia - essentially an extreme form of active hyperaemia, in response to ischaemia
What tissue displays excellent active hyperaemia response
The brain - high metabolic demand
Give examples were strong pressure autoregulation is essential
In the kidneys, traumatic blood loss.
Outline extrinsic control of arteriolar resistance
Sympathetic innervation, release of noradrenaline acting on a1 adrenoreceptors causes arteriolar restriction.
However, there is action on B2 receptors in tissues containing these i.e. skeletal and cardiac muscle have high numbers. This causes dilation.
Adrenaline also elicits these effects
The parasympthetic system has little effect.