blood pressure Flashcards

1
Q

what’s blood pressure like in the heart

A

-under high pressure arteries receive blood directly from the heart
-high pressure
-compared to veins, arteries have a lower compliance/ capacitance which is the ability of blood vessels to expand and hold a larger volume of blood without a significant increase in blood pressure

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2
Q

what does tonically active mean

A

always a bit contracted due to vascular smooth muscle

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3
Q

what’s the blood pressure like in arterioles

A

-tonically active
-highest resistance to blood flow, changed in response to:
1) sympathetic nerves (fight or flight)
=alpha1 adrenergic recs such as skin/ mucous membranes/ splanchnic arterioles leads to contraction and constriction of vascular smooth muscle leading to a decrease in diameter of arteriole and an increase in resistance to blood flow (same amount of blood flow through a smaller hole
=beta2 adrenergic recs- skeletal muscle and heart muscle leading to dilate/ relax- more O2 needed to skeletal muscles during fight or flight
-balance of a1 and b2 receptor activation plays a crucial role in regulating blood flow through different organs and tissues in changing conditions
2) circulating catecholamines (hormones) e.g. adrenaline
3)other vasoactive substances which activate vascular bed such as NO

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4
Q

what is the blood pressure in capillaries like

A

-low pressure
-slow flow
-sit of exchange, but not all perfused with blood (not all full of blood at the same time)
-controlled by dilation/constriction of arterioles

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5
Q

what’s blood pressure like in venues and veins

A

-low pressure
-walls contain much less elastic tissue than arteries
-large capacitance so can increase their volume
-contain large percentage of blood in CVS ‘unstressed volume”
-smooth muscle in walks innervated by sympathetic nerve fibres
-increased activity via alpha1 adrenergic receptors- contraction to reduce capacitance- decrease in ;unstressed volume’

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6
Q

what’s the equation for velocity of blood flow

A

-v=Q/A
where v= velocity of blood in cm/s
Q =flow mL/s
A= cross-sectional cm2

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7
Q

what’s the relationship between velocity and cross-sectional area

A

-in identical flow, there is an inverse relationship

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8
Q

what’s the equation for blood flow

A

-Q=change in P/R
-where Q= blood volume per unit of time mL/s
change in P= pressure difference mmHg
-R= resistance mmHg/mL per min

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9
Q

what’s the relationship between blood flow, resistance and pressure

A

-in blood pressure regulation, vasoconstriction leads to an increase in resistance causing the BP to increase (alongside blood loss and stress) vice versa for vasodilation
-blood flow distribution is adjusted due to need
-disease states

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10
Q

what does TPR mean

A

-total peripheral resistance
-resistance of entire systemic vasculature

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11
Q

how can resistance of a single organ be calculated

A

by substitution flow

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12
Q

what’s the equation for the poiseuilles law

A

R=8nl/pie r4 *weird n
where R= resistance
n=viscosity of blood
l-length of blood vessel

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13
Q

what are the factors involved in blood vessels and their resistance

A

-blood vessel diameter
-vessel length
-series/parallel arrangement (side by side)
-blood viscosity

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14
Q

what are the different types of vessel arrangements

A

-series resistances
-parallel resistance

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15
Q

what’s series resistance in vessel arrangement

A

–within an organ
-total resistance= sum of individual resistances
-pressure decreases though each sequential component
-largest decrease in pressure in arterioles because of the largest resistance
-change in P= R*Q

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16
Q

what’s parallel resistance in vessel arrangement

A

-less than any of the individual resistances
-result= no loss in pressure e.g. aorta

17
Q

what’s the pressure in the cardiovascular system like

A

-varies throughout system
-pressure decreases with blood flow and energy is lost overcoming frictional resistance
-aorta- P high and late CO and low compliance
-arteries- P remains high with elastic recoil
-arterioles- huge decrease in P due to high resistance
-capillaries- frictional resistance to flow and filtration
-veins and venues- high capacitance and low pressure

18
Q

what’s arterial pressure (Pa) like in systemic circulation

A

-Pa oscillations reflect pulsatile heart activity
-diastolic pressure is lowest at Pa during ventricular relaxation
-systolic pressure is highest Pa following
-variation of different pressure in arterial pressure than pulmonary pressure

19
Q

what’s venous pressure (Pv) like in systemic circulation

A

-venules and veins, pressure less than 10mmHg
-result of decreased resistance at each level of vasculature

20
Q

is pulmonary pressure lower of high than systemic pressure

A

-lower due to much lower resistance

21
Q

how to work out pulse pressure

A

-systolic pressure- diastolic pressure
-reflects blood volume ejected from left ventricle (stroke volume)

22
Q

how to work out mean arterial pressure

A
  • diastolic pressure +1/3 pulse pressure
    -shows the average pressure in a complete cardiac cycle
23
Q

why does pressure change throughout the day

A

-BP and CO (volume of blood pushed out the heart) change throughout the day
-normally higher in the day than at night
-regulated to meet body needs and activity levels

24
Q

how does rapid regulation of blood pressure work

A

-baroreceptors (for pressure) in carotid band aortic sinuses
-increase in Pa leads to an increased stretch therefore an increase in afferent nerve firing- vice versa
-solitary nucleus receive input
-solitary nucleus and SNS and PNS changes via medullar CV centres

25
Q

how does parasympathetic control ave a negative effect on HR and BP

A

-PNS outflow via vagus nerve to SAN leads to decrease in HR and BP

26
Q

how does the sympathetic nervous system have a positive effect on HR and BP

A

-SNS control to regulate BP:
1. SAN increases HR
2. increase in cardiac muscle contractility so an increase in stroke volume
3. arteriole vasoconstriction leads to an increase in tar
4. veins vasoconstriction leads to a decrease in unstressed volume

27
Q

is the para(sympathetic) control of BP long term or short term

A

-short term

28
Q

what’s the long term control of BP

A

-hormonal system: renin- angiotensin-aldosterone system (RAAS) regulated blood volume, electrolyte balance and systemic vascular resistance
-in kidneys:
=Pa renal perfusion pressure detected by kidney afferent arteriole mechanoreceptors, prorenin released into blood
=angiotensinogen-> angiotensin I-> angiotensin II

29
Q

what are the angiotensin II effects

A

-increase in aldosterone leading to Na+ reabsorption increase in ECF
-stimulates an increase in Na+ reabsorption in ECF
-hypothallamus causes an increase for thirst and ADH secretion so more water is reabsorbed in collecting ducts
-vasoconstriction of arterioles causes an increase in TPR

30
Q

how do chemoreceptors regulate BP homeostasis

A

-in carotid and aortic sinuses bodies detected a low O2 level which leads to arteriole vasoconstriction
-within brain detects CO2 leading also to arteriole vasoconstriction

31
Q

how does chronic hypertension work

A

-desensitises baroreceptors
-prolonged exposure to high BP reduces stretch sensitivity
-decrease in sensitivity of NTS to baroreceptor input
-blunted response of CNS
-reduced sympathetic inhibition- therefore hypertension maintained/ not corrected

32
Q

why is hypertension bad

A

-people with high blood pressure don’t often experience the night time dip in BP
-small increase in BP causes an increase I risk or morbidity and mortality
-if the BP is too high then there is extra strain on blood vessels and other organs
-persistent high BP causes an increase risk of heart disease, heart attacks, strokes, heart failure, aortic aneurysms, peripheral arterial disease, kidney disease and vascular dementia

33
Q

how can we treat hypertension

A

-low slat intake
-more exercise
-less alcohol and stress
-more weight management
-several drug treatments
-diuretic
-angiotensin- converting enzyme (ACE) inhibitors
-angiotensin II receptor blockers (ARBs)
-renin inhibitors
-Ca2+ channel blockers- contractility and increased vessel relaxation
-beta blockers -HR and contractility