Lecture 16: Regulation Of Mean Arterial Pressure Flashcards

0
Q

How do you calculate MAP again?

A

SP + 2xDP/3
SP= max aortic pressure during ventricular diastole
DP= min aortic pressure during arterial diastole

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1
Q

What is hypotension and hypertension

A

Hypotension: mean arterial pressure (MAP) below normal
-inadequate blood flow to tissue
Hypertension: MAP (mean arterial pressure) above normal
-stress on heart and blood vessels, tissue damage
MAP= average pressure exerted by blood on major arteries across the cardiac cycle

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2
Q

What are the determinants of mean arterial pressure?

A

MAP=HR x SV x TPR (total peripheral resistance)

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3
Q

Why does the pressure difference = about the same as MAP.

A

Pressure difference across the systemic circuit = mean arterial pressure -central venous pressure

  • CVP is very small and quite constant
  • MAP is a primary determinant if pressure difference
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4
Q

What happens when you increase cardiac out put to the MEan arterial pressure?
What happen when you increase total peripheral resistance?

A

Both causes MAP to increase

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5
Q

How do you regulate mean arterial pressure?

A

Blood pressure is mainly related by 3 visceral reflexes

  1. Arterial baroreceptor reflex (blood pressure)
  2. Volume receptor (blood volume)
  3. Chemoreceptor reflex (arterial O2, CO2)
    - also subject to descending control from cortex and hypothalamus
    - descending control acts through same efferent pathways as reflexes
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6
Q

What is the short term and long term regulation of mean arterial pressure?

A

Short term regulation of MAP:

  • over seconds to minutes
  • regulates CO and total peripheral resistance
  • mainly involves heart and blood vessels
  • mainly involves arterial baroreceptor and chemoreceptor reflexes

Long term regulation of MAP

  • over minutes to days
  • regulation of blood volume
  • mainly involves kidneys and endocrine system
  • mainly involves volume receptor reflex
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7
Q

Short term regulation of MAP. What are the three main contributors to short term MAP regulation?

A

A) the arterial baroreceptor reflex
B) chemoreceptor reflex
C) venous return

Arterial baroreceptor reflex is most important in blood pressure homeostasis
-crucial for moment to moment regulation

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8
Q

Tell me about the arterial baroreceptor reflex.

Then tell me about baroreceptors themselves

A

Change in blood pressure ➡ baroreceptors detect altered pressure (sensory nerves)➡ cardiovascular control centre in medulla (autonomic nerves) ➡ heart and blood vessels ➡ restoration of blood pressure

Baroreceptors: the sensors

  • baroreceptors are stretch-sensitive nerve endings
  • arterial (high pressure) baroreceptors are located in the carotid sinus and aortic arch
  • detect changes in arterial pressure
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9
Q

What is the response of arterial baroreceptors to pressure changes?

A

Increased arterial pressure ➡ increased AP firing in baroreceptors
-number of action potentials per heart beat is proportional

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10
Q

Tell me about the cardiovascular control centre- the integration centre

A
  • several nuclei in medulla oblongata
  • receive ascending inputs from sensors from:
  • arterial baroreceptors in aortic arch and carotid sinus
  • volume receptors in right atrium and systemic veins
  • chemoreceptors in the brain and carotid arteries

Receives descending inputs from hypothalamus and cerebral cortex

  • hypothalamus coordinates the figh-or flight response
  • cortex involved in cardiovascular response to anxiety, emotion

Sends outputs to heart and blood vessels via ANS

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11
Q

Autonomic innervation of the cardiovascular system- the controllers

A

Parasympathetic NS innervates
1) SA node

Sympathetic NS innervates

1) SA node
2) myocardial cells
3) arterioles
4) veins

Sympathetic activity amplified by adrenaline released from adrenal medulla
-sympathetic NS has more diverse actions but BOTH branches are involved

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12
Q
How do each of these respond to ANS?
SA node? 
Myocardial cells? 
Arterioles?
Veins?
A

SA node: sympathetic activity increases heart rate ➡ increased CO
-parasympathetic activity decreases heart rate ➡ decrease CO.
How?
Parasympathetic nerve firing (vagus)➡ muscarinic cholinergic receptors➡ opens K+ channels➡ k+ efflux ➡ hyperpolarizes SA node cell➡ decreases HR and CO
Sympathetic nerve firing➡ B1 adrenergic receptors➡ opens Na+ and Ca+ channels ➡ Na+ and Ca2+ influx ➡ rate of depolarisation increases➡ increases HR and CO

Myocardial cells:
-sympathetic activity increases ventricular contractility ➡ increased SV ➡ increased CO. How?
B1 adrenergic receptors➡ G protein➡ protein kinase which
-increases Ca2+ release from SR
-increase Ca2+ entry from ECF
-⬆ myosin ATPase activity (all above stronger, faster contraction)
-⬆ ca2+ re uptake to SR (faster relaxation)

Arterioles:
-sympathetic activity causes vasoconstriction ➡ increased TPR

Veins:
-sympathetic activity causes venoconstriction ➡ increased EDV ➡ increased stroke volume ➡ increased CO

Arteries and veins:

  • sympathetic NS innervates most blood vessels (except capillaries)
  • sympathetic activation➡ vascular smooth muscle contraction (except skeletal muscle, brain, coronary circulation)
  • constriction of arterioles and veins affects MAP via different mechanisms:
  • constriction of arterioles leads to increased TPR
  • veins store blood, therefore constriction leads to increased venous return, increased EDV, increased stroke volume and increased CO
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14
Q

Chemoreceptors and short-term blood pressure control

A
  • Sensors located in carotid body and medulla
  • detect partial pressures of O2/Co2
  • drop in tissues O2 supply➡ activation of cardiovascular control centre ➡ increase in MAP
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15
Q

Venous return and short term blood pressure control

A
  • the baroreceptor reflex is the primary regulatory of MAP in the short term, but other body systems have an impact on MAP.
  • other factors that increase venous return will ultimately increase MAP
  • according to starlings law, factors that increase EDV will increase stroke volume, which will increase cardiac output and therefor mean arterial pressure
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16
Q

End diastolic volume and mean atrial pressure

A
  • the more blood comes into the heart, the more blood it pumps out
  • bigger EDv➡ bigger stroke volume
  • this increasing venous return will increase cardiac output
17
Q

Blood volume and long term regulation of MAP

A
  • changes on blood volume alter venous return, stroke volumes cardiac output and therefore MAP
  • long term regulation of MAP requires blood volume regulation
  • normal variation in blood volume is minimal (well regulated)

Eg behavioural: increased fluid intake = increased blood volume = increased blood pressure
Decreased fluid loss from kidneys = increased blood volume= increased blood pressure
Note: kidneys can concave but cannot increase blood volume

18
Q

Long term
Regulation of blood volume-
Volume receptors.
Also tell me about volume receptor reflex and blood volume

A
  • in walls of atria and veins
  • detect volume of blood in each atrium
  • indirectly detect total blood volume
⬇ In Blood volume = ⬇ volume receptor activity. So then these tissues respond in following way
Heart and vessels: 
-effects similar to baroreceptor reflex (via ANS) 
Kidneys: 
-increased sodium retention 
-increased water retention 
Pituitary:
-⬆ADH secretion 
-⬇ water excretion in kidneys 
Hypothalamus: 
-more thirst 
All leading to increased blood volume
19
Q

Pathophysiology
Hypertension
With all these homeostatic mechanisms how does it happen?

A

-small changes over a long time reset the baseline for firing baroreceptors (become less sensitive)
What causes hypertension?
-primary hypertension, unknown cause, known risk factors
-secondary hypertension, renal or endocrine dysfunction

Why worry about hypertension?
Increased afterload ➡concentric hypertrophy
-increased stress on blood vessels ➡ increased risk of hemorrhage

31
Q

What is the response of arterial baroreceptors to pressure changes?

A

Increased arterial pressure ➡ increased AP firing in baroreceptors
-number of action potentials per heart beat is proportional to MAP