3-Blood Pressure Regulation Flashcards
BP calculation
mean arterial pressure = cardiac output x total peripheral resistance
MAP = CO x TPR
resistance buffer
since biggest change in R @ arterioles it buffers pulse pressure so not transmitted to capillary vessels
waveform features
- systolic P = when heart contracting/ejecting
- diastolic P = when heart relaxing
- pulse P = diff b/t systolic and diastolic
- diacrotic notch/inclsura = dip, aortic valve closure
- diastolic run off curve = indicates arteriolar R
diastolic runoff curve
vascular resistance downstream of aorta
dec R = inc slope v/v
pulse pressure =
systolic P - diastolic P
rearrange so MAP = diastolic P + 1/3 PP
affected by stroke volume and vascular resistance
net amplitude of waveform pressure
how vascular compliance affects PP
stiffer vessel = lower compliance = higher pulse pressure, happens with age
stroke volume inc = higher PP
amplification from central to peripheral
as blood travels to periphery pulse pressure amplifies from wave reflection
dampening pulse pressure
compliant
if large arteries compliant then more dampening of PP so less PP @ small arteries/arterioles = healthy, functional cerebral vasculature
dampening in stiff arteries
in large arteries less dampening so takes longer and greater PP when it reaches small arteries = damaged, dysfunctional cerebral vasculature
wave propagation depends on
- velocity related to distensibility/compliance
- stroke vol
- aortic compliance
- distance to reflection points
what does wave reflection represent
index of how compliant vessels are overall
auscultatory method assessing BP
relies on listening to blood flow over brachial A
-korotkoff sounds = turbulent flow from inc velocity after dec cross section with cuff
short term regulation
mostly neural reflex arcs
baroreceptor reflex
long term regulation
hormones and control of circulating vol (changes in renal fxn)
arterial barorecptors activate
brainstem vasomotor center so affects
1. TPR
2. cardiac performance (SV, HR)
3. symp drive to kidney (SV)
4. venous compliance (SV)
inc BP = dec HR and TPR v/v
cardiopulmonary baroreceptors activate
brainstem vasomotor center so TPR, symps to kidney, venous compliance, cardiac perform
and hypothalamus so ADH affects SV
intrarenal baroreceptors activates
- renin angiotensin system
- GFR
- salt and water reabsorption
all impact SV
arterial baroreflex pathway
- sensory receptors @aortic arch and carotid sinus
- afferent signal synapse @ NTS
- signal sent to CVLM
- signal sent to RVLM
- spinal cord IML with cell bodies of presymp neurons
- presymp synpase in sympathetic chain
- efferents synapse on heart/vasculature
vagal efferent pathway
- reduce HR = baroreceptor act
- signal from NTS project to neurons in mucleus abiguus (NA)
- NA act vagal projections to heart esp SA and AV nodes to alter K permeability
low BP = ? discharge
decreases impulse discharge rate
v/v, high BP inc discharge
valsalva maneuver
- BP rises
- straining vs closed airway inc intrathoracic P + compresses great veins
- venous return impeded
- cardiac output fails
- HR inc from baroreceptor act
BP will inc and HR dec when airway opened
nerves must be intact and functional ANS
carotid massage
technique to activate baroreflex
-deforming carotid mimics effect of pressure = afference nerve activity inc + efferent activity causes bradycardia (from parasymps)
resetting set point
in disease processes like hypertension baroreflex will reset to defend higher point
chemoreflex
- stimulus (arterial pH, O2, inc CO2)
- detection by carotid body and aortic body
- integrate in NTS (>NA>DMNV>RVLM> CVLM)
- vagus and IML in spinal cord
- effector - vasoconstriction
renin-angiotensin II system pathway
- liver produces angiotensinogen
- renin cleaves into angiotensin I
- converted to II by ACE
- vasoconstriction, salt/water retention, dec baroreflex
- inc blood pressure
beta adrenergic blockade does what
inhibits renin so can’t make angiotensin I
ACE inhibitor does what
inhibits ACE so can’t cleave into angiotensin II
ANGII type 1 receptor blockade
ARB
blocks angiotensin II from acting on system so
no inc sodium reabsorption
no inc vasoconstriction
no inc aldosterone secretion
long term effects of ANGII
- altered peripheral resistance so rapid pressor resp
- altered renal function so slow pressor resp
- altered cardiovascular structure so hypertrophy and remodelling
endothelin 1
ETA receptor
VSMC cell type
will vasoconstrict
ANF/ANP
atrial natriuretic factor
GC-A/NPR1 receptor
many cell types
inc cGMP to vasodilate, inhibit renin and aldosterone, dec Na reabsorption in nephron
ADH/AVP
anti diuretic hormone, vasopressin
- V1 receptor, VSMC cell type, vasoconstrict
- V2, collecting duct epi, water reabsorption
epinephrine
- B2 adrenergic, skeletal muscle VSMC, vasodilate
- B1 adrenergic, cardiac cells, inc chronotropy, inotropy
- alpha1 adrenergic, VSMC, vasoconstrict
kidney role in long term BP
control of volume/urine loss from kidneys to maintain given pressure
P inc then urine output inc
sodium balance
inc P = glomerular capillary hydrostatic P inc = filtration
-more Na excreted followed by water so vol dec = BP drop
pressure natriuresis
salt sensitive hypertension
renal dysfunction = hypertension can’t match Na/vol output to maintain P
changes kidney mass, tubular reabsorption, reduced capillary filtration coefficient
if inc pre-glomerular resistance shifts normal curve to right, keep salt excretion/pressure relationship intact
regulators time response
- baroreceptors
- chemoreceptors
- renal volume control
