Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define systolic arterial blood pressure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

define diastolic arterial blood pressure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

define hypertension

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

define pulse pressure

A

difference between systolic and diastolic pressure

30-50 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why are arteries usually silent

A

smooth laminar flow in arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

at what cuff pressure can turbulent Korotkoff sounds be heard

A

120-80 as BP > cuff pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the 1st Korotkoff sound

A

peak systolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the second and third Kortokoff sounds

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the 4th Kortokoff sound

A

last sound muffled/muted at diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the mean arterial blood pressure

A

average arterial blood pressure in cardiac cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how much longer is systole than diastole

A

diastole portion = 2 x systole portion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

equations to calculate MAP

A

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

DBP + 1/3 pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the usual values for MAP

A

70-105 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

60 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what 2 factors can influence MAP

A

CO and SVR (MAP = CO x SVR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is CO

A

the volume of blood pumped by each ventricle per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is SV

A

the volume of blood pumped by each ventricle per heart beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is systemic vascular resistance/total peripheral resistance

A

Sum of reistance of all vasculature in systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the major resistance vessels

A

arterioles (greatest pressure change)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

where is the highest systolic pressure

A

in left ventricle and large arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what mechanism is responsible for the short term regulation of MAP

A

baroreceptor reflex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the sensor of changes in pressure

A

stretch receptors called baroreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the control centre of the baroreceptors/changes in MAP

A

medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the effectors of the baroreceptor reflex

A 
heart (HR, SV)
blood vessels (SVR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the 2 locations of the baroreceptors

A

carotid baroreceptors

aortic baroreceptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what nerve supplies the carotid baroreceptors

A

glossopharyngeal

32
Q

what nerve supplies the aortic baroreceptors

A

vagus nerve

33
Q

how do baroreceptors respond to a fall in blood pressure

A

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
Q

how do baroreceptors combat an increase in blood pressure

A

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
Q

how do baroreceptors regulate MAP in response to postural changes eg. when a healthy person stands up

A

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
Q

when a healthy person suddenly stands up from lying down is there an increase/decrease/no effect on diastolic blood pressure

A

slight increase

37
Q

when a healthy person suddenly stands up from lying down is there an increase/decrease/no effect on systolic blood pressure

A

no effect

38
Q

what is postural (orthostatic hypotension)

A

failure of baroreceptors to respond to gravitational shifts in blood when moving from horizontal to vertical potion

39
Q

risk factors of postural (orthostatic) hypotension

A 
age
medication
disease
reduced intravascular volume
prolonged bed rest
40
Q

what results would give a positive result when testing for postural hypotension

A

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
Q

what effects can postural hypotension have on the body

A

cerebral hypoperfustion eg. lightheadedness, dizziness, blurred vision, faintness, falls

42
Q

do baroreceptors respond to chronic changes in BP

A

no only acute

43
Q

what happens to the rate of firing if high blood pressure persists for long period of time

A

baroreceptor firing decreases

44
Q

in what event can baroreceptors re-set

A

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
Q

how is MAP controlled long term

A

By controlling blood volume

46
Q

how can MAP and blood volume be controlled

A

by controlling extracellular fluid volume

47
Q

how much total body fluid is intracellular fluid

A

2/3

48
Q

how much of total body fluid is extracellular fluid

A

1/3

49
Q

what makes up the ECFV

A

plasma volume (PV) + interstitial fluid volume

50
Q

what is interstitial fluid

A

fluid bathes cells acts as go between blood and body cells

51
Q

what happens if plasma volume falls

A

compensatory mechanisms shift fluid from insterisital compartment to plasma compartment

52
Q

what 2 factors control extracellular fluid volume (ECFV)

A

water excess/deficit

Na excess/deficit

53
Q

what is responsible for regulating ECFV by regulating water and salt balance

A

hormones

54
Q

name 3 hormones that regulate ECFV

A 
renin-angiotensin-aldosterone system (RAAS)
Natriuretic Hormone (NPs)
Antidiuretic Hormone (Arginine Vaspressin) ADH
55
Q

in RAAS what is the rate limiting step

A

renin,

56
Q

what is the role of renin in the RAAS mechanism fo regulating ECFV

A

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
Q

what is the role of angiotensin II in RAAS

A
  • 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
Q

does RAAS increase or decrease ECFV therefore increasing or decreasing MAP

A

increases ECFV and so increases MAP

59
Q

what is the role of aldosterone

A

steroid hormone acts on kidneys to increase Na and water retention which increases plasma volume

60
Q

what is the RAAS regulated by

A

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
Q

what makes up the juxtaglomerular apparatus

A
  • Macula densa
  • Extraglomerular mesangial cells
  • Granular cells (release renin)
62
Q

where are Natriuretic Peptides (NPs) made

A

in heart

63
Q

when are Natriuretic Peptides (NPs) released

A

in response to cardiac distension/neurohormonal stimuli

they are a counter regulator to RAAS

64
Q

what effect does Natriuretic Peptides (NPs) have on MAP

A

decrease renin release - decreases BP

vasodilators - decrease SVR and BP

65
Q

what are the 2 types of Natriuretic Peptides (NPs)

A

atrial Natriuretic Peptides (ANPs)

Brain-type Natruuitic Peptide (BNP)

66
Q

what are atrial natriuretic peptides and when are they released

A

made and stored by atrial myocytes (28 amino acid peptide)

in response to atrial distension (hypervolemic states)

67
Q

what is brain-type natriuretic peptides and when are they released

A 
made in heart, ventricles and brain (32 amino acids) 
long peptide (prepare-BNP 108 amino acids cleaved to pro-BNP)
68
Q

what is measured in patients with suspected heart failure

A

serum BNP and N-terminal pro-BNP (NT pro BNP 76 amino acids)

69
Q

where is ADH made

A

hypothalamus

70
Q

where is ADH stored

A

posterior pituitary

71
Q

when is ADH secreted from the posterior pituitary glad

A

when there is reduced ECFV and/or increased ECF osmolarity (MAIN STIMULUS)

72
Q

what effect do Natriuretic peptides have on MAP

A

decrease MAP

73
Q

how is ECF osmolarity measured

A

by osmorecepors in Brian close to hypothalamus

more solute = higher osmolarity

74
Q

what does plasma osmolarity indicate

A

salt-water balance

75
Q

what does ADH act on

A
  • kidney tubules to increase reabsorption of water to conserve water
    concentrate urine - antidiuresis
  • blood vessels - vasoconstriction
76
Q

what effect does ADH have on ECFV and thus MAP

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions