control of arterial blood pressure

Question 1

what is blood pressure?

Answer 1

• the outwards pressure exerted by the blood on blood vessel walls

Question 2

what is systemic systolic/diastolic arterial blood pressure?

Answer 2

• the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts/relaxes
• normally < 140mmHg
• normally < 90mmHg

Question 3

what is hypertension?

Answer 3

clinic blood pressure of 140/90 or higher and day time average of 135/85 or higher

Question 4

what is pulse pressure?

Answer 4

the difference between systolic and diastolic blood pressures eg 120-80 = 40mmHg

Question 5

how is blood pressure taken?

Answer 5

• usually blood flow cant be heard though a stethoscope
• a pressure is applied, allowing for the artery to be blocked
• if the pressure is kept between systolic and diastolic the flow will become turbulent and audible when the bp exceeds cuff pressure

Question 6

when are korotkoff sounds heard?

Answer 6

1. at peak systolic volume eg when the first sound is heard
   2-3. muffled sounds
2. last sound is heard at minimum/diastolic pressure
3. no sound is heard due to smooth laminar flow

Question 7

what drives the systemic circulation?

Answer 7

• the pressure gradient between the Aorta (AO) and the right atrium (RA)
• pressure gradient = mean arterial pressure - central venous pressure

Question 8

what is mean arterial blood pressure?

Answer 8

• the average arterial blood pressure durning a single cardiac cycle
• 70-105 mmHg
• at least 60mmHg is required

Question 9

how do you estimate the MAP?

Answer 9

(2 x diastolic) +systolic pressure/3

Question 10

why must MAP be regulated within a narrow range?

Answer 10

to ensure

• pressure is high enough to perfuse internal organs eg brain, heart, kidneys
• pressure is not too high to damage the blood vessels or plan an extra strain on the heart

Question 11

where are baroreceptors located?

Answer 11

• carotid baroreceptors
• ## aortic baroreceptors

Question 12

how does an increase in arterial blood pressure result in dilation?

Answer 12

• and increase in carotid sinus afferent nerve fibres firing
• then an increase in cardiac vagal efferent nerve fibres activity
• then a decrease in cardiac sympathetic efferent nerve fibres activity
• then a decrease in sympathetic vasoconstrictor nerve fibres activity
• dilation

Question 13

what is the baroreceptor reflex import for?

Answer 13

• moment to moment regulation of arterial blood pressure including prevention of postural changes

Question 14

how to baroreceptor reflexes prevent postural hypotension?

Answer 14

• when a normal person stands up from lying, the venous return to the heart decreases and the MAP decreases transiently
• this reduces firing rate of baroreceptors
• the vagal tone to the heart decreases and the sympa tone increases - this increases HR and SV
• sympa constrictor tone increases, this increases systemic vascular resistance - arterioles are the main site for SVR
• sympa constrictor tone to the veins increases the venous return to the hear and SV
• this results in rapid correction of the transient fall in MAP; HR increases, SV increases, SVR increases

Question 15

what is postural hypotension?

Answer 15

• results from failure of baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position
• drop in 20 mmHg in systolic BP within 3 mins
• drop in 20 mmHg in diastolic (with symptoms)

Question 16

what are the symptoms of postural hypotension?

Answer 16

• cerebral hypoperfusion
• lightheadedness
• dizziness
• blurred vision

Question 17

Baroreceptors only respond to acute changes in blood pressure? TRUE/FALSE

Answer 17

TRUE

Question 18

what is ECFV?

Answer 18

plasma volume + interstitial fluid volume

- when this is controlled, so will PV, BV and MAP

Question 19

what are the main factors which effect ECFV?

Answer 19

1. water excess of deficit
2. Na+ excess or deficit

• Hormones act as effectors to regulate the ECFV by regulating water and salt balances in our bodies
• healthy people stay in a stable water/salt balance where what input = water output

Question 20

which hormones regulate ECFV?

Answer 20

1. the renin-angiotensin-aldosterone system (RAAS)
2. natriuretic peptides (NPs)
3. andtidiuretic hormone (arginine vasopressin) - ADH

Question 21

what is the role of the RAAS system?

Answer 21

• regulates PV, SVR and MAP
• renin is released from kidneys and stimulates the formation of angiotensin 1 in the blood from angiotensionogen (produced in liver)
• angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzyme (ACE)
• angiotensin 2 stimulates the release of aldosterone from the adrenal cortex, causing systemic vasoconstriction - increasing SVR
• it also stimulates thirst and ADH release
• aldosterone acts on kidneys to increase sodium and water retention - increases PV

Question 22

how is renin secreted in the rate limiting step for RAAS?

Answer 22

• RAAS is regulated by mechanisms which stimulate renin release from the juxtaglomerular apparatus in the kidney. these include
  1. renal artery hypotension caused by systemic hypotension (decrease in BP)
  2. stimulation of renal sympa nerves
  3. decreased Na+ in renal tubular fluid - sensed by macula densa (kindey tubules)

Question 23

what is the role of NPs?

Answer 23

• they are peptide hormones synthesised by the heart
• released in response to cardiac distension or neurohormonal stimuli
• they cause excretion of salt and water in the kidneys, thereby reducing BV and BP
• decrease resin release - decrease BP
• act as vasodilators - decrease SVR and BP
• NPs provide a counter-regulatory system for the RAAS

Question 24

what is the structure of NPs?

Answer 24

• 2 types are released by the heart: artial (ANP) and brain-type (BNP)
• ANP is a 28 amino acid peptide synthesise and stored by atrial muscle clels (arital myocytes)
• BNP is a 32 amino acid peptide synthesised by: heart ventricles, brain and other organs

Question 25

how is BNP synthesised?

Answer 25

• first as prepro-BNP, which is then cleaved to pro-BNP (108 aa) and finally BNP (32 aa)
• serum BNP and the N-terminal piece of pro-BNP (NT-pro-BNP, 76 amino acids) can be measured in patients with suspected heart failure

Question 26

what is the role of ADH?

Answer 26

• peptide hormone derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary
• secretion stimulated by reduced ECFV or increased ECFosmolarity (main)
• plasma osmolarity indicated relative solute-water balance
• plasma osmolarity is monitored by osmoreceptors mainly in the brain in close proximity to hypothalamus
• ADH release is stimulated by increased plasma osmolarity
• ADH acts in the kidney tubules to increase the reabsorption of water ie concentrate urine
• this increases ECPV and CO and BP
• ADH also acts on blood vessels to cause vascontriction - increase SVR and BP, the effect is small in normal people but becomes important in hypovolameic shock eg haemorrhage