Control of Blood Pressure Flashcards

1
Q

why’s the bp tightly controlled:

  • Arterial blood pressure is the driving – of —
  • If blood pressure too low then tissues are not properly — – with varying degrees of severity depending on the – and —
    –> poor renal perfusion leads to – in – and — injury
    – >poor brain perfusion leads to — and —
  • If blood pressure too high — damage occurs in many tissues –– (damage to the capillaries in the eye)
    – —- (damage to the nephrons in the kidney)
    – — of the cardiovascular system (both heart and vasculature)
A

force
tissue perfusion
perfused
extent and duration
drop
filtration
acute kidnet
unconsciousness ad death
pathological
retinopathy
nerphropathy
remodelling

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2
Q
  • Systolic:
    – the — during –
  • Diastolic:
    – the — during —
  • Pulse:
    – the difference in– and—
    – PP = —
  • Mean:
    – the arterial pressure — the cycle – MAP = —
A

arterial pressure
systole
arterial pressure
diastole
systolic and diastolic
SBP - DBP
across
DBP + 1/3 PP
pls check slide 5

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3
Q
  • Blood flow is – and — , but — flow is not
  • A cuff placed around the arm and inflated — systolic pressure will occlude the – and — flow
    – like a tourniquet
  • As the cuff deflates, flow will occur as
    the cuff falls — systolic pressure
  • this turbulent flow will produce a – and indicate — (aka — )
  • Once the sounds disappear, —
    flow has been re-established , this is —
    so basically phase 1 is tapping , phase 2 and 3 sound become louder and phase 4 sounds become muffled and phase 5 the sound will disappear
A

laminar and silent
turbulent
above
artsy
stop
below
noise
systolic pressure
phase 1
laminar
diastolic pressure

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4
Q
  • Blood pressure is a — variable
  • Measurement can be via direct or indirect methods –
  • direct measurement: arterial – or implanted —
    – indirect measurement: cuff with — or –
  • But normal BP varies with age, sex, ethnicity, birth weight, over the course of a month, over the course of a day, with anxiety, after meals…
    hypertension:
  • Consistent readings with a systolic over — mmHg or a diastolic over
    – mmHg (Grade – )
    – Grade II is over — mmHg
    – if suspected “white coat hypertension”, 24 hr — pressures to be done
  • 95% of hypertension is — hypertension
    – also known as — or — of no known cause
    – 5% is — mostly due to— problems or— tumours
  • Uncontrolled hypertension is a major risk factor for— disease (atheroma/infarction/stroke),— disease
A

continuous
catheter
sensor
stethoscope or sensor
140
90
I
160/100
ambulatory
primary
essential or idiopathic
secondary
renal
endocrine
cardiovascular and renal

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5
Q
  • Blood pressure increases with—
  • Diastolic pressure increase from ~–mmHg at 20 to an average of – mmhm by 60 yo age
  • Systolic pressure increases from ~ – mmHg at 20 to an average of — mmHg by 70 years of age
    – mainly due to — stiffening
  • — does not change with age, but — tolerance does
    decrease
    – max HR drops from ~— bpm in young adults to ~—bpm in older adults
A

age
70
85
120
160
arterial
heart rate
excersise
200
160

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6
Q
  • Blood pressure is monitored and mediated via the —
  • Sensory afferents:
    – the baroreceptors (actually — ) – in the walls of the — and –
  • Central relays:
    – — in the brain stem
    – the –
  • Effector efferents:
    – innervating the – and –
A

baroreceptors
mechanoreceptors
aortic arch and carotid sinus
cardiovascular centres
medulla obligate
heart and blood vessels

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7
Q
  • Baroreceptors sense — of – in – and the — of pressure
    – rate = —
    – magnitude = —
  • As arterial pressure increases so does the baroreceptor —
  • A – FIBRES
    – – and – conducting ( — diameter, — nerves) – – threshold (– — mmHg) so activated at — pressures
  • C – FIBRES
    – more – and – conducting ( – diameter, – nerves) – – threshold (— – mm Hg) so only ~ – % activated at normal pressure – number activated increases as – rises
A

rate
rise
pressure
magnitude
dynamic sensitivity
static sensitivity
firing rate
fewer and far
large
myelinated
low
30-90
normal pressure
abundant
slow
small
unmylinated
high
70-140
25%
pressure

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8
Q
  • The— is the primary site for regulating SNS and PNS (vagal) outflow
  • The nucleus tractus solitarius (NTS) receives – from different receptors
    – e.g. – and –
  • The hypothalamus and higher centres – the activity of the — centres – e.g. —
  • When supine, venous return is –
    – effect of gravity is – and so – is ample (Starling’s Law)
  • On standing, gravity causes venous pooling and venous return – – with falling — , so — drops (Starling’s Law again)
    – as so does cardiac output (since VR = CO)
  • A falling cardiac output leads to a – in blood pressure – MAP=CO x TRP,so if CO falls so does MAP
  • Ordinarily, blood pressure does not drop on — due to the —
A

medulla
sensory input
barocreceptros and chemoreceptors
modify
medullary
fight or flight
increased
reduced
preload
falls
preload cardiac output
decreases
standing
bacrorecpetors

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9
Q

baroreceptors:
* Cardiac output – and pressure –
– decreased — of the baroreceptors in aortic arch/carotid sinus
* Less – of the nerves interpreted at the NTS – decreased – outflow and increased – outflow
* Cardiac effects:
– – heart rate (due to — SNS/ —PNS)
– — contractility (due to — SNS)
– — preload (due to SNS — )
– overall increase in —
* Vascular effects
– – vasoconstriction (due to – SNS) – overall – in total peripheral resistance
* CO and TRP increased and blood pressure normalised

A

drops
drops
stretch
firing
PNS
SNS
increased
increased
decreased
increased
increased
cardiac output
increased
increased
increased

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10
Q
  • Chemoreceptors in – can induce changes in —
    – pH/PaO2 sensors in carotid bodies, primarily involved in — control
  • Increased SNS activity so increase – and–
    – physiologically protects – perfusion when arterial blood pressure falls
    – minor role under normal circumstances, more important in severe hypotension
  • Cardiopulmonary reflexes contribute to overall —
    – diverse group of receptors located mainly on – pressure side of circulation
  • Elicit tonic (continuous) reduction in — and — – important in minimizing – changes in response to changes in — – role in humans poorly understood
A

carotid bodies
blood pressure
ventilation
CO and TRP
brain
circulatory regulation
low
heart rate and constriction
bp
blood volume

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11
Q

chronic bp control is — :
* The baroreceptor reflex will also last for — – after which it will reset with new set point
* Long term regulation involves — :
– —
– —
– — peptides
* Plasma volume impacts on — and so —- and — with it

A

fluid regulation
1-2 days
fluid regulation
renin-angiotensin system (RAS)
anti-diuretic hormone (vasopressin)
natuirtic
venous return
cardiac output
blood pressure
check slide 26

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12
Q

renin- angiotensin system:

  • Ang II is the – component of the –
  • Ang II is a — and stimulates release of —
    – also potentiates – activity and promotes direct — in the kidney
  • Aldosterone promotes – by — Na+ retention – primarily in kidney but also the gut
  • The— osmolality drives– secretion and — expansion
  • Increased volume, increased venous return, increased blood pressure
A

active
RAS
vasoconsctirotr
aldosterone
SNS
na+ retention
volume expansion
increases
increase
ADH
volume

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13
Q
  • RAS is regulated by the production of –
    – the precursor — and — are constitutively expressed
  • Renin release is increased in response to — activity particularly due to – blood pressure and/or volume
    – SNS activation via the baroreceptor reflex (β1-AR)
    – intrarenal stretch receptor (juxtaglomerular cells)
  • Like most endocrine systems, renin release is controlled via –
    feedback mechanisms
    – decreased by – arterial pressure/blood volume –
    • by Ang II
A

renin
angiotenigoen and ace
SNS
LOW
-ve
raised decreased

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14
Q

aldesterone:

  • The – , produced by of the – of the — – similar to glucocorticoid
  • Synthesis controlled by – and high [— ]
    – Ang II in turn controlled by —
  • Acts on principal and intercalated cells of the — and early — collecting duct
  • As a steroid, it upregulates — to increase — leading to — – thus — osmolality
A

mineralcoroicode
cortex
adrenal gland
ang ii and k+
sns
cortical
medullary
apparatus
na+ reabsorption
na+ retention
increased

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15
Q

plasma osmolaity and adh :
* The body defends plasma osmolality very tightly – approx — (mosmol/kg)
* Changes in plasma osmolality lead to changes in the release of —
– (ADH or vasopressin)
* ADH controls the— of – from the collecting duct
* Works alongside — in regulating — and –

A

285
anti- diuretic hormone
absorption of warer
ras
plasma osmolality and volume

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16
Q

Antidiuretic Hormone (ADH)
* ADH — permeability of cells to —
– via the insertion of — in the —
* ADH is secreted from the — in response to changes in plasma osmolality or volume
* Rising osmolality and/or falling volume:
– increased ADH secretion so more — – plasma is – and osmolality normalised
* Falling osmolality:
– decreased ADH secretion so less water reabsorption – plasma is concentrated and osmolality normalised

A

increased
water
aqauporins
collecting ducts
posteror pituitry
water reabsorption
diluted

17
Q

Natriuretic Peptides
* To date several natriuretic peptide identified – Atrial natriuretic peptide (ANP)
– Brain natriuretic peptide (BNP)
– C-type natriuretic peptide (CNP) … and others
* Primarily regulate — and oppose some of the actions of the —
– released in response to— due to fluid —
* Acts to inhibit — and so promotes — and — osmolality

A

blood volume
RAS/ADH
partial stretch
fluid pverload
na+ erabsption
na+ excretion
decreased

18
Q

summary:
* Blood pressure is maintain in a beat by beat manner by the—
– and over the longer term by regulation of —
* Changes is pressure lead to changes in — that either increase or decrease cardiac output
* It is in continual flux and changing throughout the day
* This is in response to the changing pressure, cardiac output does not change “in order to increase pressure”

A

baroreceptors
fluid volume
atomic outflows