CVS physiology Flashcards
(28 cards)
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.
What occurs in the sympathetic response to the arterial baroreceptor reflex
Sympathetic response - release of noradrenaline from sympathetic fibres, release of adrenaline from adrenal medula
Acts on B1 receptors in atria, ventricles and veins/venioles.
Results in increased HR and contractile force, dilation of veins causing increased venous return.
Acts on B2 receptors in skeletal muscle and cardiac arteries, causing arteriolar dilation
Outline cardiac response to exercise
Increased O2/nutrient demand by tissues causes dilation of arterioles to these tissues, requires greater cardiac output to meet demand.
Dilated arterioles cause MAP drop. Artery Baroreceptor response acts sympathetically to increase HR, contractility and B2 activation to maintain MAP and supply tissues.
Describe the cardiac response to standing up from lying down.
Increased pooling of blood in veins in legs as a result of gravity causes drop in venous return, preload/EDV, SV and MAP. Arterial baroreceptor response to increase MAP: reduced vagal tone, increased sympathetic tone.
Describe the effects of the Valsalva manoeuvre on the CVS
- Initial forced expiration causes increased pressure on aorta, increasing MAP for a few seconds.
- However this pressure compresses the VC, redugin venous return, therefore preload, SV and CO, causing MAP to fall.
- Arterial baroreceptor response begins to raise MAP, may reach almost normal pressure.
- Cessation of forced expiration causes sudden drop in intra-thoracic pressure, causing MAP to fall again
- Baroreceptor response returns MAP to normal.
What are the main hormones involved in long term BP control?
Renin-angiotensin-aldesterone axis
ADH/Vasopressin
BNP and ANP
What cells release renin?
Juxtaglomerular cells of kidney
What three inputs stimulate renin release?
Decreased afferent nephron arteriolar distension
Decreased Na/Cl concentration at Macula densa cells in ascending loop of Henle.
Sympathetic stimulation from CVS medullary centres in response to decreased MAP.
Outline the cascade effects of renin
renin acts on angiotensinogen, converting it to angiotensin I
Angiotensin one is converted by ubiquitous ACE to angiotensin II. Angiotensin II:
- Acts on pituitary gland, causing AADH release
- Stimulates the adrenal cortex to produce aldesterone
- Acts as a vasoconstrictor.
What are the effects of ADH?
Increases collecting duct permeability, therefore reducing diuresis
Stimulates thirst
Increases TPR (vasopressin)
