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CARDIO > Control of Arterial Blood Pressure > Flashcards

Control of Arterial Blood Pressure Flashcards

1
Q

define blood pressure

A

the outward hydrostatic pressure exerted by the blood on the vessels

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2
Q

define systolic arterial blood pressure

A

the pressure exerted on the walls of the aorta and systemic arteries during contraction
<140 mmHg

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3
Q

define diastolic arterial blood pressure

A

pressure exerted on the walls of the aorta and systemic arteries when the heart relaxes
< 90mmHg

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4
Q

define hypertension

A

a clinical blood pressure of 140/90 mmHg or higher (daytime average of 135/85 mmHg(

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5
Q

define pulse pressure

A

difference between systolic and diastolic pressure

30-50 mmHg

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6
Q

why are arteries usually silent

A

smooth laminar flow in arteries

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7
Q

why can we hear arteries when using a blood pressure cuff

A

when external pressure is between systolic and diastolic pressure (when BP exceeds cuff pressure) flow is turbulent = audible

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8
Q

at what cuff pressure can turbulent Korotkoff sounds be heard

A

120-80 as BP > cuff pressure

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9
Q

what is the 1st Korotkoff sound

A

peak systolic pressure

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10
Q

what are the second and third Kortokoff sounds

A

intermittent sounds due to turbulent spurts of Flow cyclically > cuff pressure

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11
Q

what is the 4th Kortokoff sound

A

last sound muffled/muted at diastolic pressure

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12
Q

what is the 5th and final Kortokoff sound

A

No sound as smooth laminar flow
diastolic pressure recorded when sound disappears at 5th sound
more reporducible

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13
Q

what is the blood flow driving force equal to

A

MAP

pressure gradient between aorta and right atrium but pressure in right atrium is 0

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14
Q

what is the mean arterial blood pressure

A

average arterial blood pressure in cardiac cycle

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15
Q

how much longer is systole than diastole

A

diastole portion = 2 x systole portion

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16
Q

equations to calculate MAP

A

[( 2xdiastolic pressure) + systolic pressure]/3

DBP + 1/3 pulse pressure

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17
Q

what is the usual values for MAP

A

70-105 mmHg

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18
Q

what MAP is needed to perfuse kidneys, brain and coronary arteries

A

60 mmHg

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19
Q

why must MAP be regulated

A

to ensure high enough pressure to perfuse organs but not too high to damage vessels/strain heart

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20
Q

what 2 factors can influence MAP

A

CO and SVR (MAP = CO x SVR)

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21
Q

what is CO

A

the volume of blood pumped by each ventricle per minute

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22
Q

what is SV

A

the volume of blood pumped by each ventricle per heart beat

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23
Q

what is systemic vascular resistance/total peripheral resistance

A

Sum of reistance of all vasculature in systemic circulation

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24
Q

what are the major resistance vessels

A

arterioles (greatest pressure change)

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25
where is the highest systolic pressure
in left ventricle and large arteries
26
what mechanism is responsible for the short term regulation of MAP
baroreceptor reflex
27
what is the sensor of changes in pressure
stretch receptors called baroreceptors
28
what is the control centre of the baroreceptors/changes in MAP
medulla
29
what are the effectors of the baroreceptor reflex
``` heart (HR, SV) blood vessels (SVR) ```
30
what are the 2 locations of the baroreceptors
carotid baroreceptors | aortic baroreceptors
31
what nerve supplies the carotid baroreceptors
glossopharyngeal
32
what nerve supplies the aortic baroreceptors
vagus nerve
33
how do baroreceptors respond to a fall in blood pressure
rate of firing decreases carotid sinus afferent decreases cardiac vagal efferent nerve firing decreases sympathetic fibre activity increases sympathetic vasoconstrictor nerve fibres activity increases causing vasoconstriction increasing HR
34
how do baroreceptors combat an increase in blood pressure
rate of firing increases cardiac vagal efferent nerve increases firing carotid sinus afferent nerve increases cardiac sympathetic nerve activity decreases sympathetic vasoconstrictor nerve fibre decreases causing vasodilation reducing MAP decreasing BP
35
how do baroreceptors regulate MAP in response to postural changes eg. when a healthy person stands up
venous return to heart decreases, MAP very transiently decreases. reducing rate of baroreceptor firing, vagal tone to heard decreases, sympathetic tone increases HR and SV Sympathetic constrictor tone increases SVR in arterioles and increased venous return and SV in veins so MAP returns to normal
36
when a healthy person suddenly stands up from lying down is there an increase/decrease/no effect on diastolic blood pressure
slight increase
37
when a healthy person suddenly stands up from lying down is there an increase/decrease/no effect on systolic blood pressure
no effect
38
what is postural (orthostatic hypotension)
failure of baroreceptors to respond to gravitational shifts in blood when moving from horizontal to vertical potion
39
risk factors of postural (orthostatic) hypotension
``` age medication disease reduced intravascular volume prolonged bed rest ```
40
what results would give a positive result when testing for postural hypotension
drop in 3 mins of standing from lying drop in systolic BP of at least 20 mmHg (with or without symptoms) drop in diastolic BP of at least 10 with symptoms
41
what effects can postural hypotension have on the body
cerebral hypoperfustion eg. lightheadedness, dizziness, blurred vision, faintness, falls
42
do baroreceptors respond to chronic changes in BP
no only acute
43
what happens to the rate of firing if high blood pressure persists for long period of time
baroreceptor firing decreases
44
in what event can baroreceptors re-set
they fire again only if there is an acute change in MAP above new higher steady level baroreceptors cannot supply info about prevailing steady state BP
45
how is MAP controlled long term
By controlling blood volume
46
how can MAP and blood volume be controlled
by controlling extracellular fluid volume
47
how much total body fluid is intracellular fluid
2/3
48
how much of total body fluid is extracellular fluid
1/3
49
what makes up the ECFV
plasma volume (PV) + interstitial fluid volume
50
what is interstitial fluid
fluid bathes cells acts as go between blood and body cells
51
what happens if plasma volume falls
compensatory mechanisms shift fluid from insterisital compartment to plasma compartment
52
what 2 factors control extracellular fluid volume (ECFV)
water excess/deficit | Na excess/deficit
53
what is responsible for regulating ECFV by regulating water and salt balance
hormones
54
name 3 hormones that regulate ECFV
``` renin-angiotensin-aldosterone system (RAAS) Natriuretic Hormone (NPs) Antidiuretic Hormone (Arginine Vaspressin) ADH ```
55
in RAAS what is the rate limiting step
renin,
56
what is the role of renin in the RAAS mechanism fo regulating ECFV
from kidneys, forms angiotensin I in blood from angiotensinogen (from liver) Angiotensin I -> angiotensin II by ACE (angiotensin converting enzyme from pulmonary vascular endothelium)
57
what is the role of angiotensin II in RAAS
- stimulates release of aldosterone from adrenal cortex which increases plasma volume and BP - increases thirst and ADH release increasing plasma volume and BP - causes vasoconstriction increasing SVR and BP
58
does RAAS increase or decrease ECFV therefore increasing or decreasing MAP
increases ECFV and so increases MAP
59
what is the role of aldosterone
steroid hormone acts on kidneys to increase Na and water retention which increases plasma volume
60
what is the RAAS regulated by
mechanisms that simulates rennin from juxtaglomerular apparatus in kidneys: 1. renal artery hypotension (systemic hypotension decreases BP) 2. stimulation of renal sympathetic nerves 3. decreased Na conc in renal tubular fluid sensed by macula densa in kidney tubules
61
what makes up the juxtaglomerular apparatus
* Macula densa * Extraglomerular mesangial cells * Granular cells (release renin)
62
where are Natriuretic Peptides (NPs) made
in heart
63
when are Natriuretic Peptides (NPs) released
in response to cardiac distension/neurohormonal stimuli | they are a counter regulator to RAAS
64
what effect does Natriuretic Peptides (NPs) have on MAP
decrease renin release - decreases BP | vasodilators - decrease SVR and BP
65
what are the 2 types of Natriuretic Peptides (NPs)
atrial Natriuretic Peptides (ANPs) | Brain-type Natruuitic Peptide (BNP)
66
what are atrial natriuretic peptides and when are they released
made and stored by atrial myocytes (28 amino acid peptide) | in response to atrial distension (hypervolemic states)
67
what is brain-type natriuretic peptides and when are they released
``` made in heart, ventricles and brain (32 amino acids) long peptide (prepare-BNP 108 amino acids cleaved to pro-BNP) ```
68
what is measured in patients with suspected heart failure
serum BNP and N-terminal pro-BNP (NT pro BNP 76 amino acids)
69
where is ADH made
hypothalamus
70
where is ADH stored
posterior pituitary
71
when is ADH secreted from the posterior pituitary glad
when there is reduced ECFV and/or increased ECF osmolarity (MAIN STIMULUS)
72
what effect do Natriuretic peptides have on MAP
decrease MAP
73
how is ECF osmolarity measured
by osmorecepors in Brian close to hypothalamus | more solute = higher osmolarity
74
what does plasma osmolarity indicate
salt-water balance
75
what does ADH act on
- kidney tubules to increase reabsorption of water to conserve water concentrate urine - antidiuresis - blood vessels - vasoconstriction
76
what effect does ADH have on ECFV and thus MAP
- Increases ECFV and plasma volume and CO and BP so increasing MAP - increases SVR and BP (not as significant as RAAS important in haemorrhage)

CARDIO (14 decks)

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