Physiological BP control Flashcards

1
Q

D: Blood Pressure

A

the outwards (hydrostatic) pressure exerted by the blood on blood vessel walls

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2
Q

D: Systolic Arterial Blood Pressure

A

the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts

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3
Q

D: Diastolic Arterial Blood Pressure

A

the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes

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4
Q

D: Hypertension

A

Clinic blood pressure of 140/90 mmHg or higher and day time average of 135/85 mmHg or higher

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5
Q

D: Pulse pressure

A

Is the difference between systolic and diastolic blood pressures

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6
Q

What drives systemic circulation?

A

the pressure gradient between the aorta and the right atrium

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7
Q

Pressure gradient =

A

Mean Arterial Pressure (MAP) – Central Venous (right atrial) Pressure (CVP)

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8
Q

D: Mean Arterial Blood Pressure (MAP)

A

the average arterial blood pressure during a single cardiac cycle, which involves contraction and relaxation of the heart

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9
Q

MAP =

A

[(2x diastolic pressure) + systolic pressure]/3 OR DBP + 1/3 Pulse Pressure

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10
Q

What is the MAP required to perfuse the coronary arteries, brain and kidneys?

A

at least 60 mmHg

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11
Q

normal systolic arterial blood pressure

A

shouldn’t exceed 140 mm Hg

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12
Q

normal diastolic arterial blood pressure

A

shouldn’t exceed 90 mm Hg

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13
Q

How is it possible to manually measure blood pressure with a cuff and stethoscope?

A

If there is laminar flow, blood flow can’t be heard
If blood flow is restricted by external pressure this causes turbulent flow which can be heard through a stethoscope
The 1st sound is at peak systolic pressure
The 5th (last) sound is at diastolic blood pressure measuremenr

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14
Q

What vessels cause the greatest systemic vascular resistance?

A

The arterioles

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15
Q

MAP is a product of

A

CO x SVR = HR x SV x SVR

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16
Q

What are the receptors responsible in the acute regulation of blood pressure?

A

Baroreceptors

17
Q

How do the baroreceptors aid in acute blood pressure regulation?

A

They send a signal to the medulla when blood pressure is beyond limits, the medula is the control centre and then causes the autonomic nervous system to appropriately signal the effectors and correct the MAP

18
Q

What happens when a person stands up from a lying position in relation to their blood pressure?

A
  • venous return to the heart decreases due to the effect of gravity MAP very transiently decreases
  • baroreceptors decrease vagal tone to the medulla causing a greater sympathetic output to the heart
  • increase sympathetic tone causes increased HR, SV and constrictor tone - increased SVR -The sympathetic constrictor tone to the veins increases the venous return (VR) to the heart and stroke volume
  • The result is: rapid correction of the transient fall in MAP: HR INCREASES; SV INCREASES; SVR INCREASES
19
Q

D: Postural Hypotension

A

a drop, within 3 minutes of standing from lying position:

  • in systolic blood pressure of at least 20 mmHg (with or without symptoms) or
  • a drop in diastolic blood pressure of at least 10 mm Hg (with symptoms)
20
Q

Risk factors of Postural Hypotension

A
Age related
Medications
Certain diseases
Reduced intravascular volume
Prolonged bed rest
21
Q

Symptoms of postural (orthostatic) hypotension

A
  • lightheadedness
  • dizziness
  • blurred vision
  • faintness
  • falls
22
Q

Total body fluid =

A

Intracellular fluid (2/3rds) + Extracellular fluid (1/3rd)

23
Q

ECF volume =

A

Plasma volume + interstitual fluid volume

24
Q

What happens physiologically when the plasma volume falls?

A

compensatory mechanisms move fluid from the interstitual compartment

25
Q

What are the 2 main factors influencing ECF volume?

A
  1. Water excess or deficit

2. Na+ excess or deficit

26
Q

What are the effectors for the regulation of the ECF volume (which influence water and salt balance)?

A

3 hormones

  1. The Renin-Angiotensin-Aldosterone (RAAS)
  2. Natriuretic Peptides (NPs)
  3. Antidiuretic Hormone (Arginine Vasopressin) ADH
27
Q

What is the role of the Renin-Angiotensin-Aldosterone System?

A
  • important to regulate PV & SVR and hence MAP
  • Renin is made in the kidneys and causes the formation of angiotension I in the blood from angiotensinogen
  • Angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme)
  • Angiotension II stimulates Aldosterone release from the adrenal cortex
  • Angiotension II causes systemic vasoconstriction increasing SVR & stimulates thirst
  • Aldosterone acts on the kidneys increasing sodium and water retention, increasing plasma volume
28
Q

How is the renin-angiotensin-aldosterone system regulated?

A

by the mechanisms which stimulate Renin release from the juxtaglomerular apparatus in the kidney

  1. renal artery hypotension due to systemic hypotension
  2. stimulation of renal sympathetic nerves
  3. decreased (Na+) in renal tubular fluid sensed by macula densa (specialised kidney tubules)
29
Q

What is the role of the Natriuretic Peptides?

A

to counteract the RAAS

30
Q

What are NPs?

A

peptide hormones synthesised by the heart (as well as the brain and other organs)

31
Q

What triggers natriuretic peptides?

A

cardiac distension or neurohormonal stimuli

32
Q

What is the effect of Natriuretic peptides?

A
  1. increased excretion of salt and water in the kidneys, reducing blood volume and blood pressure
  2. decrease renin release - decrease blood pressure
  3. act as vasodilators decreasing SVR and blood pressure
33
Q

What are the main 2 types of natriuretic peptides released by the heart?

A
  1. Atrial natriuretic peptide - 28 amino acid peptide synthesised and stored in atrial myocytes
    - ANP is released in response to atrial distension
  2. Brian-type Natriuretic Peptide (BNP) - 32 amino acid peptide, synthesised by ventricles
    - BNP is 1st synthesised as prepro-BNP, then cleaved to pro-BNP (108 amino acids) and finally BNP (32 amino acids)
    - serum BNP & N terminal od pro-BNP is a measure in patients with suspected heart failure
34
Q

What is vasopressin?

A

aka ADH, it is derives from a prehormone precursor synthesised by the hypothalamus and is stored in the posterior pituitary

35
Q

What stimulates the secretion of ADH/vasopressin?

A

reduces extracellular fluid volume or increased extracellular fluid osmolality

36
Q

What is plasma osmolality?

A
  • it indicates relative solute-water balance

- monitored by osmoreceptors mainly in the brain in close proximity to the hypothalamus

37
Q

What is the effect of ADH?

A
  • increases reabsorption of water in the kidney tubules , increasing extracellular and PV & hence increasing CO and blood pressure
  • also causes vasoconstriction, increasing SVR