The Cardiac Cycle Flashcards
Effect of sympathetic on heart rate
Increases heart rate by making pacemaker potential reach threshold sooner
- therefore next heartbeat occurs closer
- cardiac interval goes down and heart rate goes up
Mechanisms of sympathetic acting on heart rate
Releases noradrenaline (as well as circulating adrenaline from adrenal medulla) - both act on beta1-receptors on sinoatrial node
Effect of parasympathetic on heart rate
Slows down heart rate by hyper-polarising pacemaker cells - slowing down rate of depolarisation so reaches threshold later
Mechanism of parasympathetic on heart rate
Vagus nerve releases acetylcholine
- acts on muscarinic receptors on sinoatrial node
- hyperpolarises the cells
- decreasing heart rate
What is starlings law of preload?
Energy of contraction is proportional to the initial length of the cardiac muscle fibre
What is the preload?
The initial length of muscle before stimulated to contract
How is the preload increased
Put more blood into the heart —> greater end diastolic volume = greater stretch of the muscle around the ventricle
Greater end diastolic volum = greater tension = greater stretch volume
What is the afterload?
Load against which the muscle tries to contract
= the aortic pressure at the other side of the aortic valve that’s closing the valve
How is the aortic pressure affected?
By how much blood is pushed into the artery
How easy its for the blood to get away from there
As the blood flows away from the heart it reaches resistance in the arterioles = total peripheral resistance (TPR)
What is the total peripheral resistance (TPR)
Measure of how constricted or dilated the arterioles are
- if constricted will have higher arterial pressure
- therefore heart needs to work harder to build up enough pressure to open aortic valve and push blood out
- therefore less energy left to able to eject the blood (stroke volume will decrease)
Impact of sympathetic nervous system on end diastolic volume and stroke volume
Increases contractility
Shortens systolic phase leaving more time for diastole
Mechanism works on top of preload effect
End diastolic volume increases
Stroke volume increases
Impact of parasympathetic nervous system on end diastolic volume and stroke volume
Little effect - the vagus nerve doesnt innervate the ventricular muscle (therefore acetylcholine not released here so doesnt impact strength of contraction)
What is the preload
How full the ventricle is before it starts contracting (end diastolic volume)
Affected by the state of contractions of venules/veins
What is contractility?
How strong a contraction is produced for any given preload or afterload
Affected by the sympathetic system
What is afterload?
How difficult it is for the heart to pump out the blood (the total peripheral resistance)
Affected by the state of contraction of arterioles
Formula for cardiac output
Heart rate x stroke volume
What happens to stroke volume and cardiac output if heart rate is increased?
Increase in cardiac output
Decrease in stroke volume:
- shortened cardiac interval cuts into the rapid filling phase
- reduced end diastolic volume reduces the preload
What happens to cardiac output during exercise? What are the mechanisms for this?
Cardiac output increases 4-6x HR increases: decreased vagal tone increased sympathetic tone Contractility increases: increased sympathetic tone inotropic state altered and systole shortened Venous return increases: venoconstriction skeletal/respiratory pumps (maintains preload) Total peripheral resistance falls: arteriolar dilation in muscle, skin and heart reduces afterload
Define:
Systolic pressure
Diastolic pressure
Pulse pressure
Systolic pressure = peak pressure in aorta
Diastolic pressure = minimum pressure in aorta
Pulse pressure = systolic - diastolic
What is normal arterial pressure?
120/80mmHg
What affects the pressure wave (4)?
Stroke volume
Velocity of ejection
Elasticity of arteries
Total periphery resistance
What happens to aortic pressure wave as it passes through vascular tree?
Pressure falls through vascular tree
Small drop through arteries (low resistance conduits)
Large drop through arterioles (the resistance vessels)
Pressure already low when reaching capillaries (very thin walled)
Very small pressure difference pushing blood back through veins
What is the systemic filling pressure?
The pressure pushing blood back through veins to the heart (20mmHg - 5mmHd)
How does the pressure in pulmonary circulation differ to systemic?
Pressure in pulmonary = 1/5th that of systemic
What effects blood velocity? Which vessels is it fastest and slowest in?
Total cross-sectional area
Fastest in aorta and vena cava
Slowest in capillaries
What are the external influences affecting venous return (5)?
Gravity Skeletal muscle pump Respiratory pump Venomotor tone Systemic filling pressure
How does gravity affect venous return?
Causes venous distension (swelling) in legs
Decreases: EDV, preload, stroke volume, cardiac output, mean arterial pressure
How does skeletal muscle pump impact venous pressure?
Rhythmic contraction increases venous return and EDV
How does respiratory pump impact venous pressure?
Increased respiratory rate and depth increases venous return and EDV
How does Venomotor impact venous return?
Venomotor tone = state of contraction of smooth muscle surrounding venules and veins
Mobilises capacitance and increases EDV
What are the anti-clotting mechanisms of the endothelium?
Stops blood contacting the collagen - preventing platelet aggregation
Produces prostacyclin and nitrous oxide - both inhibit platelet aggregation
Produces tissue factor pathway inhibitor (TFPI) - stops thrombin production
Expresses thrombomodulin - binds thrombin and inactivates it
Expresses herapin - inactivates thrombin
Secretes tissue plasminogen activator - plasminogen —> plasmin which digests clot
How are the capillaries specialised for transport?
Thin walled Large surface area to volume ratio Continuous: - no clefts or pores (e.g. brain) - clefts only (muscle) Fenestrated (perforations): - clefts and pores (e.g. intestine and kidneys) - specialised for fluid exchange Discontinuous: - clefts and massive pores (liver)
How are the capillaries specialised for exchange?
Mostly exchange by diffusion
Determined by starling forces
Net filtration pressure = (Hydrostatic pressure in capillaries – Hydrostatic pressure in ISF) – (osmotic pressure plasma – osmotic pressure ISF)
How much fluid is lost and regained each day by capillaries? What happens to remaining fluid?
20L lost and 17L regained
Remaining 3L drains into lymphatic system
What is an oedema?
Accumulation of excess fluid
Reasons that oedemas form
Lymphatic obstruction - e.g. surgery Raised cardiovascular pressure - ventricular failure Hypoproteinaemia - e.g. nephrosis, liver failure, nutrition Increased capillary permeability - inflammation e.g. rheumatism
What is the formula for mean arterial pressure?
MAP= cardiac output x total peripheral resistance
Therefore varying the radius of resistance vessels is used to control total peripheral resistance and therefore regulate MAP
What is mean arterial pressure?
The force used to drive blood through all systemic blood vessels
What are the consequences of a low and high mean arterial pressure?
Low = brain notices and you faint (syncope) High = no immediate problems but leads to hypertension
What 2 mechanisms ensure sufficient blood flow to each vascular bed and keep mean arterial pressure in correct range?
Local (intrinsic) mechanisms - meeting needs of individual tissue
Central (extrinsic) mechanisms - ensures total peripheral resistance (therefore MAP) remains in correct range
What is hyperaemia?
Increase in blood flow
What triggers hyperaemia in local (intrinsic) control of blood flow? How does this impact resistance?
Trigger = increase in local metabolites (increased metabolic activity —> increased metabolite concentration in capillary)
Endothelium senses this producing paracrine signal
- endothelium derived relaxing factor (EDRF) - essentially nitrous oxide
- EDRF diffuses out of endothelium into smooth muscle surrounding arterioles —> smooth muscle relaxation
- leads to arteriolar dilation —> increased blood flow until metabolites are washed away
What triggers pressure auto regulation in local (intrinsic) control of blood flow? How does this impact resistance?
Trigger = decrease in perfusion pressure
MAP drop causes reduced flow
Metabolites accumulate as flow decreases but metabolite production remains same
Triggers release of EDRF —> arterioles dilate and flow returns to normal
(Ensures that tissue maintains blood supply despite changes in MAP)
What triggers reactive hyperaemia in local (intrinsic) control of blood flow? How does this impact resistance?
Trigger = occlusion of blood supply
Leads to subsequent increase in blood flow (once reason for occlusion removed e.g. BP cuff removed)
(Extreme version of pressure auto regulation - massive increase in metabolites but flow decreased)
What is the injury response? How is it triggered?
Trigger = skin scratched (not enough to break skin)
Scratching activates C-fibres evoking action potential
Triggers release of substance P —> acts on mast cells to release histamine —> arterioles dilation (skin goes red) & junctions between capillaries to open increasing permeability (allows leukocytes and white blood cells in to attack invading organisms)
Identify the neural factors affecting arteriolar tone (sympathetic and parasympathetic)
Sympathetic nerves:
- release noradrenaline which binds to alpha1 receptors —> arteriolar constriction - decreased flow —> increased total periphery resistance
Parasympathetic nerves:
- usually no effect (not innervated by parasympathetic system)
Identify the Hormonal factors impacting arteriolar tone
Adrenaline:
- released from adrenal medulla - binds to alpha1-receptor —> arteriolar constriction (decreased flow and increased total peripheral resistance)
In skeletal and cardiac muscle also activates beta2-receptors
- do exact opposite of alpha receptors and cause arteriolar dilation —> increased flow through tissue and decrease total peripheral resistance (significant in exercise)
What are the factors controlling blood flow in the coronary circulation? How does it deal with this?
Blood supply interrupted by systole (each time heart contracts it stops blood flowing through the vessel)
Still has to cope with demand (increased during oxygen)
- shows excellent active (metabolic) hyperaemia
- expresses many beta2-receptors (preventing arteriolar constriction)
What are the factors controlling blood flow in the cerebral circulation? How does it deal with this?
Needs to be kept stable always
Insufficient oxygen or glucose = fainting
Shows excellent pressure auto regulation
What are the factors controlling blood flow in the pulmonary circulation? How does it deal with this?
Decrease in O2 causes arteriolar constriction (complete OPPOSITE response to most other tissues)
Ensures blood is directed to best ventilated parts of lungs
What are the factors controlling blood flow in the renal circulation? How does it deal with this?
Main function is filtration which is pressure dependent
Shows excellent pressure regulation
