Long term control of blood pressure Flashcards

1
Q

Long Term Control of Blood Pressure

A

Keeps mean arterial blood pressure (MAP) constant over long period of time (ideally our life time)
 Tied into control of body fluid volume (i.e. extracellular fluid (ECF) volume & circulating blood volume (CBV)

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2
Q

Increased circulating blood volume assuming no change in vascular compliance

A

Increased volume in arteries & veins  Pressure in both arteries and veins will increase (Assuming no change in vascular compliance)
 IncreasedvenousreturnIncreasedpreload Increased stroke volume  Increased cardiac output  Increased blood pressure

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3
Q

increased circulating blood volume(Assuming no change in systemic vascular resistance)

A

Increased cardiac output  Increased flow through tissues  Stimulation of autoregulation response  Increased constriction of metarterioles / precapillary sphincters of all autoregulated tissues  Increases SVR  Increased blood pressure

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4
Q

Small change in cardiac output can cause a large change

A

in blood pressure

 5 to 10% increase in CO can raise MAP from 100 mmHg to 150 mmHg

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5
Q

Relationship Between CBV and MAP

A

 Increasing CBV will produce an Increase in MAP  Decreasing CBV will produce a Decrease in MAP

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6
Q

Control of CBV in terms of fluid and salt intake

A

Fluid Intake = Fluid Output = Constant CBV  Fluid Intake > Fluid Output = Increased CBV  Fluid Intake < Fluid Output = Decreased CBV
 Salt Intake = Salt Output = Constant CBV  Salt Intake > Salt Output = Increased CBV  Salt Intake < Salt Output = Decreased CBV
Under normal circumstances fluid and salt output is controlled by the kidneys

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7
Q

Fluid intake per day

A

2300 mls

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8
Q

Fluid intake Synthesized by oxidation of carbohydrates

A

200 mls

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9
Q

fluid intake ingested fluids per day

A

2100 mls

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10
Q

Fluid output per day

A

[2300 mls/day]  Insensible loss via respiratory tract and skin (not sweat)
(700 mls/day)  Sweat (100 mls/day)  Feces (100 mls/day)  Urine (1400 mls/day)

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11
Q

Renal Output of Water & Salt

A

OUTPUT = FILTRATION – REABSORPTION  Increased filtration / No change reabsorption
 Increased output of water & salt  Decreased CBV  No change filtration / Increased reabsorption
 Decreased output of water & salt  Increased CBV

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12
Q

Factors affecting renal filtration

A

MAP / Renal blood flow / Pressure in glomerular capillaries / Oncotic pressure in glomerular capillaries

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13
Q

factors affecting renal absorption

A

Concentration of angiotensin II, aldosterone, antidiuretic hormone (all increase rate of reabsorption)

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14
Q

Renal-Body Fluid System

A

Slow acting, but very powerful – able to bring blood pressure back to baseline
 Links changes in MAP to changes in renal filtration / reabsorption (i.e. renal output) which produces changes in CBV

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15
Q

MAP effect on renal body fluid system

A

IncreasedMAPIncreasedfiltration(pressurediuresis and pressure natriuresis) / Decreased reabsorption (decreased [angiotensin II, aldosterone])  Water / salt output > intake  Decreased CBV  Decreased MAP
 Decreased MAP  Decreased filtration / Increased reabsorption (increased [angiotensin II, aldosterone])  Water / salt output < intake  Increased CBV  Increased MAP

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16
Q

pressure diuresis Renal function curve (acute changes)

A

50 mmHg – 0 urine output
 90 mmHg – Normal urine output
 150 mmHg – urine output over 4 times normal

17
Q

Cannot change long term MAP without

A

changing either the renal output curve or the intake curve.

18
Q

What happens if there is a long term change in SVR???

A

Increased SVR will produce an acute change in MAP  Within few days, MAP returns to normal even
through there is no change in SVR
 Works if change in SVR did not affect renal blood flow i.e. equilibrium between intake and output not changed
If intrarenal vascular resistance is increased, this causes a shift of the renal function curve to the right which will result in a change in the baseline MAP
 Problem is change in renal vascular resistance NOT the change in overall SVR

19
Q

prorenin

A

inactive renin produced in juxtaglomerular cells walls of afferent arterioles) of kidneys,ecrease in pressure results in splitting of the prorenin into renin which is released into the lumen of the afferent arterioles – Circulates to rest of body

20
Q

Renin remains in the blood for _ and then ___

A

30- 60 minutes and cts on a plasma protein called renin substrate (angiotensinogen) to release angiotensin I

21
Q

angiotensin 1

A

Angiotensin I is mild vasoconstrictor – produces minimal changes in vascular constriction. Angiotensin I is carried to lungs where angiotensin converting enzyme (present in endothelial cells) mediates formation of angiotensin II Other blood vessels contain angiotensin converting enzyme

22
Q

angiotensin 2

A

persists for 1 to 2 minutes before being deactivated by variety of blood / tissue enzymes known as angiotensinases. Potent vasoconstrictor of arterioles / minor constriction of veins  Interacts with kidneys resulting in increased salt and water
reabsorption*
 Causes adrenal gland to secrete aldosterone which increases salt and water reabsorption

23
Q

Water versus Salt Intake

A

Easier to excrete water than it is to excrete salt  Increased salt concentration in ECF  Increased
osmolarity
 IncreasedosmolarityIncreasedstimulationofthirst center AND hypothalamus-posterior pituitary gland
 IncreasedstimulationofthirstcenterIncreasedwater intake  Increased ECF volume
 Increased stimulation of hypothalamus-posterior pituitary gland  increased release of antidiuretic hormone (vasopressin)  Increased reabsorption of salt and water  Increased ECF volume Increased salt intake has potential to create bigger changes in CBV than does increased water intake

24
Q

hypertension

A

 MAP greater than 110 mmHg  Produced when diastolic greater than 90 mmHg and systolic
greater than 135 mmHg

25
Q

Hypertension shortens lifetime by

A

Excess workload on heart  Damage to blood vessels of brain  Injury to kidneys

26
Q

causes of hypertension

A

Volume loading  Renin-Angiotensin imbalance  Combination volume loading / vasoconstriction

27
Q

Types of hypertension

A

Primary / essential

28
Q

Renin-Angiotensin Imbalance – Goldblatt Hypertension

A

Only one kidney and it has a constriction of renal artery
 Kidney senses a decrease in pressure and the renin- angiotensin system is stimulated
 Increased renin release
 Increase in systemic pressure due to increased SVR – Secondary increase in systemic pressure due to increased retention of salt and water
 Systemic pressure will continue to increase until renal blood flow is back to normal

29
Q

Two-Kidney Goldblatt

A

 Hypertension will occur even if one kidney normal, other kidney has obstruction of renal artery
 Obstructed kidney will increase reabsorption of water and salt due to lower pressure in tubular capillaries
 Obstructed kidney will release renin resulting in overall increase in [angiotensin II] and [aldosterone]
 Angiotensin II will increase SVR and MAP  Renal pressure returns toward normal for obstructed kidney  Renal pressure higher than normal for non-obstructed kidney
 Angiotensin II and aldosterone will increase salt and water reabsorption for both kidneys

30
Q

Essential Hypertension

A

 Accounts for 90 to 95% of all patients with hypertension
 Specific cause unknown
 Excess weight gain / obesity account for large percentage of risk for developing primary HTN (65 to 75%)
 Weight loss / exercise first line of treatment

31
Q

Characteristics of Essential HTN

A

ncreased cardiac output  Support extra fat tissue / Support increased metabolic
demand of major organs  SVR may be increased
 Increased sympathetic activity (kidneys)
 Hormones released from fat cells may stimulate regions of hypothalamus that provide excitatory stimulation of vasomotor center
 Increased levels of angiotensin II and aldosterone  2 to 3 times normal in obese patients  Result of increase sympathetic activity???
 Impairment of renal function  Requires higher pressure to remove normal amounts of salt
and water
 In treating, have to give drugs that improve renal function, can’t just decrease MAP

32
Q

Treatment of Essential HTN

A

Lifestyle modifications  Increased physical activity  Decrease weight
 Vasodilator drugs – primary target being renal arterioles
 Inhibition of sympathetic signals to kidneys  Block action of sympathetic neurotransmitter on renal
vasculature and renal tubules  Direct relaxation of renal vasculature smooth muscle  Block action of renin-angiotensin system
 Drugs that reduce reabsorption of salt and water  Block active transport of sodium in tubules