Lecture 16: Regulation Of Mean Arterial Pressure Flashcards
How do you calculate MAP again?
SP + 2xDP/3
SP= max aortic pressure during ventricular diastole
DP= min aortic pressure during arterial diastole
What is hypotension and hypertension
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
What are the determinants of mean arterial pressure?
MAP=HR x SV x TPR (total peripheral resistance)
Why does the pressure difference = about the same as MAP.
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
What happens when you increase cardiac out put to the MEan arterial pressure?
What happen when you increase total peripheral resistance?
Both causes MAP to increase
How do you regulate mean arterial pressure?
Blood pressure is mainly related by 3 visceral reflexes
- Arterial baroreceptor reflex (blood pressure)
- Volume receptor (blood volume)
- Chemoreceptor reflex (arterial O2, CO2)
- also subject to descending control from cortex and hypothalamus
- descending control acts through same efferent pathways as reflexes
What is the short term and long term regulation of mean arterial pressure?
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
Short term regulation of MAP. What are the three main contributors to short term MAP regulation?
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
Tell me about the arterial baroreceptor reflex.
Then tell me about baroreceptors themselves
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
What is the response of arterial baroreceptors to pressure changes?
Increased arterial pressure ➡ increased AP firing in baroreceptors
-number of action potentials per heart beat is proportional
Tell me about the cardiovascular control centre- the integration centre
- 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
Autonomic innervation of the cardiovascular system- the controllers
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
How do each of these respond to ANS? SA node? Myocardial cells? Arterioles? Veins?
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
Chemoreceptors and short-term blood pressure control
- 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
Venous return and short term blood pressure control
- 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
