Week 3- Pressure and flows Flashcards
What is blood pressure caused by? Define systolic Blood pressure At what point is it measured? Define diastolic blood pressure At what point is it measured?
The pressure of blood exerted against the walls of the main arteries. Systolic blood pressure is the pressure of blood against the walls of the main arteries during ventricular contraction (systole). It is measured at the point where the first pulse sound is heard after occluding blood flow in the brachial artery and reducing the pressure from 180mmHg. Diastolic Blood pressure is the pressure of blood against the walls of the arteries during ventricular relaxation and refill (diastolic). It is measured at the last sound (korotkoff sound).
Define mean arterial blood pressure How would you calculate it?
The average arterial blood pressure during 1 cardiac cycle. MAP= 1/3 diastolic P + (Systolic P-diastolic P)
What is a baroreceptor? How many types are there? What are the most important receptors for one of the systems?
A baroreceptor is a receptor within the vascular tree that detects stretch in the vessel walls. There are high pressure baroreceptors in the arterial walls and low pressure baroreceptors in the venous system and right side of the heart.
Most important arterial baroreceptors are located in the carotid sinus (birfucation of external and internal carotids) in the aortic arch
What are the most important baroreceptors in the arterial system?
The most important arterial receptors are in the carotid sinus (at the bifurcation of the external and internal carotids) and in the aortic arch.
Describe how arterial baroreceptors regulate blood pressure under normal physiological conditions.
Describe how they would react to a sudden drop in MABP.
(learning outcome describe function of baroreceptors)
1) Baroreceptors respond to stretching of arterial walls with each cardiac cycle- systole stretches arterial wall. If arterial pressure suddenly rises, walls of the vessels expand and increases the firing frequency of AP’s generated by the receptors. If arterial BP suddenly falls, decreased stretch of arterial walls leads to decreased receptor firing.
2) Both the carotid sinus and aortic arch send this afferent information to the medulla. The carotid sinus sends its info via CNIX, the aortic arch via CNX.
3) The medulla then alters the outflow of sympathetic and parasympathetic innervation to the heart and blood vessels thereby altering blood pressure. (Mean arterial BP = Cardiac Output x Systemic vascular resistance).
4) Under normal physiological conditions baroreceptor firing exerts an inhibitory influence on sympathetic outflow from the medulla.
5) Most important role of the baroreceptors is responding to sudden changes in blood pressure. If blood pressure falls suddenly (hypovolaemic shock/ from sitting to standing), there will be decreased firing of the baroreceptors to the medulla. This will act to reduce the inhibition on sympathetic outflow so that it increases. Increased sympathetic outflow will act to vasoconstrict blood vessels (increasing systemic vascular resistance) and increase HR and force of contraction (increased Cardiac Output). This restores BP. At the same time there is a reduction in vagal output, also enhancing sympathethic outflow.
How would the baroreceptors respond to a sudden increase in blood pressure?
A sudden increase in blood pressure would increase the firing of arterial baroreceptors in the carotid sinus and aortic arch. This afferent information would be sent via CNX and CIX to the medulla. In the medulla this would act to increase inhibition on sympathetic outflow to the heart and blood vessels resulting in bradycardia and vasodilation- therefore decreasing BP.
What are low pressure/ venous baroreceptors?
Where are they primarily found? (4 main sites)
What do they respond to and therefore what do they primarily detect?
What are they also involved in regulating and how does this affect MABP control?
Venous baroreceptors (also known as atrial stretch receptors) are low pressure baroreceptors that primarily detect changes in blood pressure caused by changes in effective circulating blood volume. They mitigate blood pressure changes in response to volume.
Low pressure baroreceptors are located at strategic low pressure sites:
1) pulmonary artery
2) junction of atria and their veins
3) atria
4) ventricles
These low pressure baroreceptors fire in response to stretch caused by venous return to the heart and thereby monitor effective circulating volume. They are also involved in control of cardiac output when increased effective circulating volume is detected, therefore contribute to control of MABP by controlling the volume of blood and CO.
what would increase the activation of low pressure venous baroreceptors/atrial stretch receptors?
What nerve do these stretch receptors signal by? Where is this signal sent?
Once the afferent information has been received what two mechansims are used to alter blood pressure?
How would this affect blood pressure?
Increased venous return to the heart would increase the stretch of these low pressure receptors and therefore increase their firing to the medulla.
The atrial stretch receptors/ Low pressure venous baroreceptors are at the ends of afferent fibres that join the vagus nerve and signal back to the medulla. Increased firing to the medulla alters:
1) cardiac output and reduction of sympathethic outflow only to the kidney renal arteries:
Increased cardiac output (tachycardia) and vasodilation of the renal artery: increase in GFR- increased urine production and fluid loss to decrease the effective circulating volume.
Decreased atrial stretch little effect on CO but increases sympathetic outflow to the kidney (vasconstrict renal artery, reduce fluid loss).
2) Afferent fibres of atrial stretch receptors/low p venous baroreceptors also synapse with the paraventricular nuclei of the hypothalamus (contains hypothalamic neurons that synthesis ADH/vasopressin and transports it down its axon for release at the posterior pituitary). Increased firing of the low P receptors inhibits ADH release from the posterior pituitary, less water is reabsorbed by the kidney and there is a reduction in effective circulating volume.
Low pressure receptors attempt to respond to high blood pressure by altering effective circulating volume and eliminating fluid.
What other mechanism is activated when low pressure venous baroreceptors fire? (think in the periphery).
Peripheral vasodilation to accomodate a higher blood volume.
What are chemoreceptors and what do they primarily control?
How can they help control blood pressure?
Peripheral chemoreceptors are located in both the carotid and aortic bodies and the central chemoreceptors located within the medulla primarily regulate respiratory centre.
Chemoreceptors can also help regulate the cardiovascular system functioning.
Peripheral chemoreceptors still respond to hypoxia, hypercapnia and acidic pH. When stimulated they signal via afferent nerves to the medulla.
Leads to increased sympathetic outflow to the heart and peripheral vasculature, causes increased cardiac output and peripheral vasoconstriction to increase the blood pressure. In order to get oxygen to the tissues you need a higher cardiac output.
Describe and explain the pressure changes across the vascular tree
Reference 1) the mean arterial pressure and how this changes from aorta-arterial system- capillaries- venous system- vena cava
reference 2) the pulse pressure
Mean arterial blood pressure:
The aorta and arteries have the highest MABP, this does not fall very much as blood flows through the distributing arteries. At the small arteries and arterioles there is a large fall in MABP, approx 50-70% arterial BP drops here. By the time blood reaches the capillaries MABP is low ~ 25-30 mmHg. Pressure falls even lower in the venous system, pressure in vena cava is very low. Venous system can expand to accomodate blood volume. Pressure remains low after the blood reaches the right ventricle and is pumped out into the pulmonary vascualuture to prevent damage to the vessels. Remains low pressure until you get back to the left ventricle of the heart via pulmonary veins.
Arterial Pulse pressure:
Increases as blood flows from the aorta into the distributing arteries. The systolic pressure rises and the diastolic pressure falls- pulse pressure increases. This is because of reflective waves from vessel branching and from increased vessel stiffness from aorta to distributing vessels.
As blood flows into smaller vessels the arterial pulse pressure then declines due to decreased elasticity. In the venous system the pulse pressure declines even further as veins contain less elastic tissue.
Describe normal pressures seen in the left ventricle and aorta and how this allows blood flow in the right direction.
Pressure in the left ventricle tends to be around 140/20 mmHg.
Pressure in the aorta ranges from 120/ 70 mmHg.
Aortic diastolic pressure is usually around 70 mmHg. During ventricular contraction it creates a systolic pressure of aroun 140 mmHg which drives blood from the LV into the aorta. Aortic pressure rises to 120 mmHg during systole as blood is forced through the aortic valve. It will then drop to around 70 mmHg as blood enters the systemic circulation and the ventricle relaxes.
Pressure in the ventricle drops during diastole to 20 mmHg which allows ventricular filling. The force of contraction and ventricular filling raised this pressure to 140 mmHg (higher than aorta, forces blood out).
What is the average systolic and diastolic pressure seen in the brachial artery?
Matches that of standard blood pressure monitoring 120/ 80 mmHg. Brachial artery similar to pressure in aorta.
Explain normal pressures seen in the Right ventricle and pulmonary artery
Pressures seen in the right ventricle and pulmonary artery are much lower than that in the left side of the heart due to shorter distance to the lungs and preventing damage of lung capillary epithelium.
Standard pressure seen in Right ventricle: 25/5mmHg.
During right ventricular diastole pressure v low - 5mmHg, due to high elasticity and compliance of RV. This low pressure plus atrial contraction helps force blood from R atrium into R ventricle though tricuspid valve.
Right ventricular systole is usually 25 mmHg, exceeds that of the RA, causes closure of tricuspid valve and forces blood into pulmonary artery.
Standard pressures in pulmonary artery: 25/ 10 mmHg
Pressure in Pulmonary artery at diastole is 10 mmHg. During Right ventricular systole the pressure in the pulmonary artery will rise to equal the RV pressure, around 25mmHg.
This systolic PA pressure quickly dissipates by the high compliance of the pulmonary vascular bed, dropping back to 10 mmHg.
When flow through the circulation is constant (5l/min) why does it then follow that the volume of the pulmonary vascular bed is much higher than that of the systemic?
This is due to the the pressure difference between the pulmonary and systemic vascular beds. The pulmonary bed is at much lower pressure, meaning it can accomodate a much higher volume of blood.
Describe the arterial pressure waveform
1) what are its component parts?
2) how do you explain what each is?
The arterial pressure waveform has several components:
1) systolic upstroke, systolic peak pressure, systolic decline, dicrotic notch, diastolic run off, end diastolic pressure
1) systolic upstroke - corresponds to ventricular ejection of blood into aorta through aortic valve
2) systolic peak pressure - is the maximum pressure in the central arteries generated by systolic ejection. Systolic peak derives its shape from reflected waves coming back from the vascular tree. Blood in aorta has low resistance due to size of the vessel, remains similar in distributing arteries. Down to arterioles resistance increases dramatically, tends to iron out the pulse pressure and can be reflected back towards to aortic valve.
3) systolic decline - rapid decline in arterial pressure as ventricular contraction comes to an end
4) dicrotic notch - closing of the aortic valve causes slight increase in pressure as blood is forced into the peripheral circulation only.
5) diastolic run off - is the drop in pressure that occurs after the aortic valve has closed, gradual pressure drop due elastic recoil of arteries which helps maintain enough pressure to force blood into periphery.
6) end diastolic pressure- is the pressure exerted by the vasular tree back upon the aortic valve
What is pulse pressure?
Pulse pressure is the difference between the maximum aortic systolic pressure and minimum aortic diastolic pressure
How does pulse pressure change as you move from the aorta into the peripheral vascualar tree?
Pulse pressure (difference between maximum systolic pressure and minimum diastolic pressure) increases as you move from more proximal aorta to more distal vessels due to a decline in vessel elasticty and compliance (vessels become more rigid) leading to a greater pulse pressure as you move peripherally.
Aorta is a highly elastic vessel which can absorb some of the pressure from ventricular systole, therefore pulse pressure lowest here. As the next level of vessels are not as elastic they arent as able to absord the pressure from systole, and therefore the pulse pressure increases.
How can an arterioles alter their flow?
What is poiseulles equation and how does this relate?
If one arteriole in a vascular bed constricts what will happen to the resistance of the whole vascular bed?
Arterioles can alter the flow through them by altering their radius (either vasodilate or vasoconstrict). This relates to Poiseuille’s equation which states that Flow rate is proportional to the pressure gradient multiplied by the radius to the power four/ 8 x viscosity of the fluid x length of the tubing.
Small increase in radius will lead to large increase in flow rate (eg double actually becomes 16 times larger).
Each vessel in vascular bed controls its own flow but vasoconstriction in one will increase the combined resistance of the whole vascular bed.
Describe the structure of a lymphatic capillary
Lymphatic vessels arise in the interstitium as small, thin walled channels of endothelial cells that join together to form larger vessels. Initial lymphatics in tissues similar to capillaries with interendothelial junctions that behave as one way microvalves. Anchoring filaments tether lymphatic vessel to surrounding tissue.
Explain how the RAAS system can regulate blood pressure.
Renin is released from juxtaglomerular cells in the kidney in response to 1) sympathetic innervation 2) low Na+ detected at the macula densa (suggestive of low GFR and low BP) 3) decrease in renal arterial BP.
Renin travels within the circulation and causes the production of angiotensin 1 from angiotensinogen in the liver.
Angiotensin 1 is converted to angiotensin 2 by ACE in the pulmonary circulation.
Angiotensin ii acts to increase BP by a number of mechanisms:
1) Causes aldosterone release from adrenal cortex- aldosterone acts on MR receptor in principal cells, upregualtes Na/k ATPase and ENac, increase Na+ and water reabsorption- increase BP by increased volume.
2) Angiotensin ii directly causes vasoconstriction of blood vessels
3) increases sympathetic outflow by stimulating adrenalin/ noradrenalin release from adrenal gland
4) causes release of vasopressin from posterior pituitary, allows insertion of aquaporins in collecting duct and reabsorption of more water
