Week 1 - Haemodynamics and Vascular Control Flashcards
Define cardiac output + what regulates it
CO = The flow of blood from the heart into the circulation (vol. of blood pumped from ventricle per beat)
Regulated By:
- heart size
- ventricular contractility*
- duration of ventricular contraction*
- preload
- afterload*
- Modulated by the autonomic nervous system
Sympathetic nerves increase force and rate of contraction
Parasympathetic nerves reduce rate only
What is the relationship between heart rate (HR), stroke volume (SV) and cardiac output (CO)
SV = vol. of blood pumped form left ventricle during each systolic contraction
CO = HR x SV
- SV ↑ in response to ↑ in vol. of blood in ventricles
- As preload + cardiac myocyte stretch more the CO increases
- Sympathetic stimulation ↑ contractility (↑ myocyte stretch / right atrial pressure) = greater ↑ in CO due to ↑ HR
- Stimulating parasympathetic nervous system causes ↓ in CO due to reduced HR
List the heart valves and their roles
ROLE: keep blood flowing in one direction / prevent back flow of blood
LEFT SIDE:
Bicuspid valve (AV) - controls blood flow from atrium into ventricles
- diastolic filling = blood entering ventricles + ventricular pressure ↑
- end- diastolic volume = when ventricles are full / ↑ pressure = valves shut
Aortic valve (SL) - controls blood flow from ventricle into aorta
- 80 mmHg is when the aortic valve opens, allowing blood to be pumped out into aorta
- vol. of blood in ventricle ↓ BUT pressure ↑ due to contraction
- ↓ in vol. eventually leads to ↓ in pressure = SL valve shuts
RIGHT SIDE:
Tricuspid valve (AV) -
Pulmonary Valve (SL)
isovolumetric contraction - when both valves are shut = no change in vol. as blood isn’t escaping aorta or atrium
What is preload + afterload, what factors affect them and how do they affect cardiac function
Preload - how stretched ventricles are before contracting
- more stretched the ventricle, the more energy (+ O2) the myocytes consume per contraction
- during diastole, atrial pressure reaches its highest point
- this drives blood into ventricles, which stretch to accommodate blood
= the degree of stretch is the preload
Afterload - pressure the heart has too work against to pump blood
(force heart pumps against tot eject blood)
- the greater the pressure is the more energy (+O2) myocytes will consume
- during systole pressure in left ventricle exceeds that in aorta
- this drives blood from ventricle into systemic circulation
- the greater the difference in pressure between ventricle + aorta = the greater the flow.
The higher the aortic pressure, the more it resists flow (cardiac output) from the ventricle
Describe the anatomy of the circulation
- Blood flows away from heart through arteries then arterioles (smaller) to capillaries
- Blood returns through venules then veins (bigger)
Systemic Circulation - arteries carry oxygenated blood
Pulmonary Circulation - arteries carry de-oxygenated blood
Cerebral Circulation - brain circulation
Describe the structure of blood vessels (+ compare different vessels)
Arteries:
- thick muscular walls (helps withstand high pressure blood is pushed through them at)
- elastic recoil (allows them to accommodate stress of pulsatile flow)
- low compliance = hard to stretch
- smaller, more round lumen
Veins:
- thinner, less muscular walls
- less elastic recoil
(by time blood reaches veins pressure has ↓ and blood flow is smooth)
- high compliance = easy to stretch = can accommodate large vol. of blood
- majority of blood is in veins (act as reservoir for blood as veins are more complaint)
Capillaries:
(receive blood from arteries)
- narrow (RBC cells move in single file)
- walls are a monolayer of endothelial cells (= quick diffusion across)
- NO smooth muscle layer
- found at site where O2, CO2, metabolites + nutrient exchange occurs
- one-way valves (in lumen) which prevent back flow of blood (blood is usually moving against gravity
Muscular walls - made of smooth muscle cells (which wrap around vessel)
- contraction of these cells = vessels constrict
- relaxation of cells = vessels dilate
Endothelium - are endothelial cells that line interior surface of all vessels
- they form a barrier between circulating blood + the rest of artery / vein wall (forms endothelium)
Define blood vessel compliance and resistance
Compliance = how easily vessel stretches in response to internal pressure
- compliance = changing in vol. / change in pressure
- arteries have low compliance (hard to stretch)
- veins have high compliance
Resistance = the driving force to push blood through vessel is provided by pressure drop
- resistance = pressure ÷ flow (R = P ÷ F)
At a constant flow:
- ↓ in resistance causes pressure gradient to ↓
- ↑ in resistance causes pressure gradient to ↑
What is the significance of Poiseuille’s Law
Law describes the flow resistance of an individual vessel in terms of radius (r), length (L) of vessel and viscosity (n) of blood flowing through vessel
Resistance is directly proportional to blood viscosity + vessel length
- as viscosity ↑ = resistance also ↑
- shorter vessels have ↓ resistance
Resistance is inversely proportional to vessel radius
- as radius ↑ = resistance ↓ (to 4th power)
Flow is proportional to 4th power of radius
- ↓ diameter will ↓ blood flow
- ↓ diameter will ↑ pressure
What is the structure of the vascular system
Vascular smooth muscle:
- shorter than other muscle cells
- non-excitable
- stimulated to contract by agonist binding to receptor on cell surface
- contract in gradual + graded manner (depending on how much agonist present)
Vascular smooth muscle contractile proteins (actin / myosin) aren’t arranged in a regular pattern instead have dense bodies which anchor contractile proteins at various points in the plasma membrane
- fibres are pulled towards centre when cell stimulated causing cell to shorten + bulge in middle
What is the role of vascular smooth muscle tone (vasoconstriction) in controlling blood flow + pressure
Diameter of vessel depends on balance of internal pressure + wall tension
As pressure ↑ diameter will also ↑
- if pressure is too low (a.k.a critical closing pressure) = wall collapses = blood flow is prevented
- if pressure is too high = wall will start to break apart
As muscle cells contract generates tension = muscle constricts = diameter ↓
↑ muscle tone (vasoconstriction) causes ↑ in internal pressure = diameter increase is much smaller
- smaller change in diameter gives larger change in pressure
Arteries (flow autoregulation)
- surge in pressure causes muscle to contract = ↑ tone = more tension + constricted vessel
- ↑ resistance to flow tp balance ↑ pressure + maintain flow
- myogenic tone
What are the consequences of changing vascular muscle tone in arteries + veins
Smooth muscle contraction increases tone of a blood vessel + reduces its diameter
Arteries:
- will provide resistance to blood flow
- most significant in the smallest arteries (i.e. arterioles)
- if arterial muscle tone is altered it would change flow resistance + blood pressure
Veins:
- reduces blood vessel volume
- particularly important in the large veins where it increases venous pressure + cardiac filling
- if venous muscle tone is alter it would change cardiac function
How is vascular smooth muscle tone regulated
- Capillaries, veins, arterioles and venules are innervated by sympathetic nerves, very rarely have parasympathetic nerves
- Stimulation of sympathetic system causes relate of adrenaline or noradrenaline
- both work together + modulate tone
- act at adrenoreceptors BUT each has diff. effects + affinities
- response of each depends on ratio of a1 to b1 receptors in wall + binding affinities of each
α1-adrenergic receptors
- on all vascular smooth muscle
- receptors can be found in GI tract
- evokes vasoconstriction when activated by agonist = ↓ blood flow
- noradrenaline more potent than adrenaline
β1-adrenergic receptors
- evokes ↑ in heart rate + myocardial contraction = ↑ blood flow
β2-adrenergic receptors
- on smooth muscle cells of arterioles in cardiac and skeletal muscle
- evokes vasodilation when activated by agonist = ↑ blood flow
- adrenaline much more potent than noradrenaline
Resistance in Blood Flow Network / Regulation
- Total resistance and pressure drop is lower in blood vessels arranged in parallel (compared to in series)
- Changing resistance of a few vessels in large parallel network has little effect on total resistance to blood flow
- Resistance decreases by increasing the number of parallel vessels (= more paths for blood to flow)
- Total resistance falls when blood moves from large artery (aorta) to small one (capillaries) because vessels small vessels are present in large numbers
- total resistance to flow in parallel < resistance of smallest vessel
How does the body regulate blood flow and blood pressure in different areas of circulation
Arterioles ~ have a small diameter = small amount of constriction / dilation has a big effect on blood flow
Capillaries ~ DON’T have smooth muscle = can’t constrict / dilate to change flow
not always open have precapillary sphincters which can:
1. constrict = blood entry is prevented (closed)
2. open = ↓ flow resistance + ↑ blood flow
Reduced internal pressure + radius decreases blood flow
Dilating vessel by 2 fold will ↑ blood flow by 4 fold
- Pressure is ↑ in arterial system and during systole
- Pressure is ↓in venous system and diastole
- Largest drop in pressure occur across arterioles
- As vessels gets smaller, pressures is more constant because elasticity in arteries damp down pressure changes before reaches capillaries
- Oscillations in trace (from large arteries) are due to pulsatile nature of heartbeat
Define peripheral resistance + its role in regulating blood pressure
TPR (total peripheral resistance) - total resistance is systemic vasculature
TPR = (MAP - RAP) ÷ CO
- R = P ÷ F (P is total systemic pressure | F is CO)
- MAP = mean arterial pressure
- RAP = right arterial pressure
- units = PRU
MAP:
- needs to be kept in narrow range to avoid hypertension / hypotension
- modulated by changing CO, TPR or both
- MAP =CO x TPR
CO:
- depends on O2 need of the body
- e.g. CO ↑ during exercise due to sympathetic nerve activity (↑ cardiac contractility + rate)
Peripheral (a.k.a. systemic) circulation has high resistance + high pressure