Physiology - Integration of Cardiovascular Mechanisms Flashcards
What is Blood Pressure?
The outwards pressure exerted by the blood on blood vessel walls
What is Systemic Systolic Arterial Blood Pressure?
The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts
What is Systemic Diastolic Blood Pressure?
The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes
What is the upper limit for systemic systolic blood pressure?
Should not normal reach or exceed 140mmHg
What is the upper limit for systemic diastolic blood pressure?
Should not normally each or exceed 90mmHg
Physiological Basis for Sphygmomanometry
Blood flow is laminar, and inaudible
When external pressure exceeds systolic pressure, flow in the artery is blocked and so inaudible
When the external pressure is between systolic and diastolic pressure, blood flow becomes turbulent whenever blood pressure excess cuff pressure, and is audible
When is the systolic pressure recorded using sphygmomanometry?
At peak systolic pressure
1st Korotkoff Sound
When is the diastolic pressure recorded using sphygmomanometry?
The point at which sound disappears
5th Korotkoff Sound
Why is the diastolic pressure not recorded at the last sound heard using sphygmomanometry?
5th Korotkoff sound is more reproducible than 4th
What is Mean Arterial Blood Pressure?
The average arterial blood pressure during a single cardiac cycle
What are the two equations for estimating MAP?
[(2 x DBP) + SBP] / 3
DBP + 1/3 (SBP-80)
What is the normal range of MAP?
70-105 mmHg
What is the minimum MAP needed to perfuse the vital organs?
60 mmHg
Why must MAP be regulated within a narrow range?
High enough to perfuse internal organs
Not too high to damage blood vessels or place extra strain on the heart
Which two factors contribute to MAP?
MAP = Cardiac Output X Total Peripheral Resistance
Which two factors contribute to CO?
CO = Stroke Volume X Heart Rate
What is Total Peripheral Resistance?
The sum of resistance of all peripheral vasculature in the systemic circulation
What are the major resistance vessels?
The arterioles
What controls short-term regulation of MAP?
Baroreceptor Reflex
Where are the baroreceptors and how do their signals reach the Medulla?
Aortic Baroreceptors = In the aortic arch. Send signals via CNX
Carotid Baroreceptors = In the carotid sinus. Send signals via CNIX
Summary of Baroreceptor Response - Decreased MAP
Baroreceptors fire less
Vagal output decreases
Cardiac sympathetic output increases, increasing strength of cardiac muscle contraction
Sympathetic vasoconstrictor activity increases
Summary of Baroreceptor Response - Increased MAP
Baroreceptors increase firing
Vagal output increases
Cardiac sympathetic output decreases, decreasing strength of cardiac muscle contraction
Sympathetic vasoconstrictor activity decreases
How does the Baroreceptor Reflex prevent Postural Hypotension?
On standing up, venous return to the heart decreases due to gravity
MAP transiently decreases
reduces rate of baroreceptor firing
Vagal tone to the heart decreases and sympathetic tone increases, increasing HR and SV
Sympathetic constrictor tone increases, increasing TPR
Sympathetic constrictor tone to veins increases VR to the heart and SV
Result is rapid correction of the transient fall in MAP
INCREASED HR, INCREASED SV, INCREASED TPR
How does Postural Hypotension occur?
Results from a failure of baroreceptor response to gravitational shifts in blood, when moving from the horizontal to vertical position
Why can Baroreceptors only response to acute changes?
Will reset if high MAP is sustained
Will fire again only if there is an acute change in MAP above the new steady state level
Total Body Fluid =
Intracellular fluid (2/3) Extracellular fluid (1/3)
Extracellular Fluid =
Plasma volume
Interstitial fluid volume
How does extracellular fluid volume control blood volume and MAP?
If plasma volume falls, compensatory mechanisms shift fluid from the interstitial compartment to the plasma compartment
PV and steady state blood volume and MAP would be controlled if ECFV is controlled
Which two main factors affect extracellular fluid volume?
Water excess or deficit
Na+ excess or deficit
Which hormones regulate ECFV?
Renin-Angiotensin-Aldosterone-System (RAAS)
Atrial Natriuretic Peptide (ANP)
Antidiuretic Hormone, aka Arginine Vasopressin (ADH)
What is the role of the RAAS in MAP regulation?
Decrease in plasma volume and MAP
Renin release from kidneys stimulates formation of angiotensin I in the blood from angiotensinogen produced by the liver
Angiotensin I is converted to Angiotensin II by ACE produced by pulmonary vascular endothelium
Angiotensin II stimulates: aldosterone release form the adrenal cortex; causes systemic vasoconstriction; also stimulates thirst and ADH release
Aldosterone acts on the kidneys to increase Na+ and water retention, increasing plasma volume
What is the rate limiting step fro RAAS and how is this regulated?
Renin secretion
This is regulated by: renal artery hypotension; stimulation of renal sympathetic nerves; decreased [Na+] in renal tubular fluid
What is Atrial Natriuretic Peptide?
28 amino acid peptide synthesised and stored by atrial myocytes
What is the role of ANP in MAP regulation?
Released in response to hypervolaemic states
Causes excretion of salt and water in the kidneys, reducing blood volume and MAP
Acts as a vasodilator, decreasing MAP
Decreases renin release
Counter-regulatory mechanism for RAAS
What is Anti-Diuretic Hormone?
Peptide hormone synthesised by the hypothalamus and stored in the posterior pituitary
What is the role of ADH in MAP regulation?
Secretion stimulated by reduced ECFV or increased ECF osmolarity (main stimulus)
Plasma osmolarity is monitored by osmoreceptors in the brain in close proximity to the hypothalamus
Increased plasma osmolarity stimulates ADH release
ADH acts in the kidney tubules, increasing reabsorption of water
Increases ECFV and PV, increasing MAP
Also acts on blood vessels to cause vasoconstriction. This effect is small in normal people, but becomes important in hypovolaemic shock.
How is TPR controlled?
Relaxation/contraction of vascular smooth muscle
These are controlled by extrinsic and intrinsic mechanisms
Resistance to Blood Flow
Directly proportional to blood viscosity
Directly proportional to length of the blood vessel
Inversely proportional to the ladies of the blood vessel to the power 4
Extrinsic Control of Vascular Smooth Muscles
Involves nerves and hormones
Vascular smooth muscle is supplied by sympathetic nerve fibres. The neurotransmitter is noradrenaline acting on alpha receptors
What is Vasomotor Tone?
The partial constriction of vascular smooth muscle at rest. Caused by tonic discharge of sympathetic nerves
Extrinsic Control of Vascular Smooth Muscles - Nerves
Increased sympathetic discharge increases vasomotor tone
= vasoconstriction
Decreased sympathetic discharge decreases vasomotor tone
= vasodilatation
No parasympathetic innervation
Extrinsic Control of Vascular Smooth Muscles - Hormones
Adrenaline from the adrenal medulla
Acts on alpha receptors in skin, gut, kidney to cause vasoconstriction
Acts on beta receptors in cardiac and skeletal muscle to cause vasodilatation
Helps with strategic redistribution of blood during exercise etc.
Angiotensin II causes vasoconstriction
ADH causes vasoconstriction
Intrinsic Control of Vascular Smooth Muscles
Matches blood flow of different tissues to their metabolic needs
Can over-ride extrinsic control mechanisms
Includes local chemical and physical factors
Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Metabolites
Vasodilatation caused by: Decreased local PO2 Increased local PCO2 Increased local [H+] Increased extra-cellular [K+] Increased osmolarity of ECF Adenosine release from ATP
Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Humoral Agents
Vasodilatation caused by:
Histamine
Bradykinin
Nitric Oxide
Vasoconstriction caused by: Serotonin Thromboxane A2 Leukotrienes Endothelin
Intrinsic Control of Vascular Smooth Muscles - Chemical: Nitric Oxide
Continuously produced by the vascular endothelium
L-arginine -> NO, eNOS
Potent vasodilator which is important in regulation of blood flow and maintenance of vascular health
Short life = few seconds
NO formation can be stimulated by shear stress (flow dependent) or chemical stimuli (receptor stimulated)
NO diffuses from vascular endothelium into adjacent smooth muscle cells where it activates the formation of cGMP, which serves as a second messenger for signalling smooth muscle relaxation
Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Humoral Agents and Endothelium Importance
Endothelium is important in maintenance of vascular health
Endothelial damage/dysfunction can be caused by high BP, high cholesterol, diabetes, smoking…
Endothelial produced vasodilators are anti-inflammatory, anti-thrombotic, anti-oxidants
Endothelial produced vasoconstrictors are pro-inflammatory, pro-thrombotic, pro-oxidants
Intrinsic Control of Vascular Smooth Muscles - Physical: Temperature
Cold = Vasoconstriction Warmth = Vasodilatation
Intrinsic Control of Vascular Smooth Muscles - Physical: Myogenic Response to Stretch
If MAP rises, resistance vessels automatically constrict to limit flow
If MAP falls, resistance vessels automatically dilate to increase flow
Maintains level of blood flow to specific tissues (e.g. brain, kidneys) despite MAP
Intrinsic Control of Vascular Smooth Muscles - Physical: Sheer Stress
Dilation of arterioles cases sheer stress in the arteries upstream to make them dilate. Increases blood flow to metabolically active tissues
Factors Increasing Venous Return
Increased venomotor tone
Increased blood volume
Increased skeletal muscle pump
Increased respiratory pump
What is the Venomotor tone?
The level of constriction in the veins
Venous smooth muscles are supplied with sympathetic nerve fibres
Stimulation gives venous constriction and allows blood to move back towards the heart
What is the Skeletal Muscle Pump?
Large veins in limbs lie between skeletal muscles
Contraction of muscles aids venous return
Acute Responses of CVS to Exercise
Increased sympathetic nerve activity -> Increased HR, SV and CO
Sympathetic vasomotor nerves reduce flow to kidneys and gut by vasoconstriction
Vasodilatation on skeletal and cardiac muscles as metabolic hyperaemia overcomes vasomotor drive
Blood flow to skeletal and cardiac muscles increase in proportion to metabolic activity
Increased systolic BP, decreased TPR and DBP
Post exercise hypotensive response
Chronic Responses of CVS to Exercise
Reduced BP Reduction in sympathetic tone and noradrenaline levels Increased parasympathetic tone to heart Cardiac remodelling Reduction in plasma renin levels Improved endothelial function Decreased arterial stiffening
