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Cardio > Physiology - Integration of Cardiovascular Mechanisms > Flashcards

Physiology - Integration of Cardiovascular Mechanisms Flashcards

1
Q

What is Blood Pressure?

A

The outwards pressure exerted by the blood on blood vessel walls

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2
Q

What is Systemic 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

What is Systemic Diastolic 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

What is the upper limit for systemic systolic blood pressure?

A

Should not normal reach or exceed 140mmHg

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5
Q

What is the upper limit for systemic diastolic blood pressure?

A

Should not normally each or exceed 90mmHg

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6
Q

Physiological Basis for Sphygmomanometry

A

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

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7
Q

When is the systolic pressure recorded using sphygmomanometry?

A

At peak systolic pressure

1st Korotkoff Sound

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8
Q

When is the diastolic pressure recorded using sphygmomanometry?

A

The point at which sound disappears

5th Korotkoff Sound

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9
Q

Why is the diastolic pressure not recorded at the last sound heard using sphygmomanometry?

A

5th Korotkoff sound is more reproducible than 4th

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10
Q

What is Mean Arterial Blood Pressure?

A

The average arterial blood pressure during a single cardiac cycle

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11
Q

What are the two equations for estimating MAP?

A

[(2 x DBP) + SBP] / 3

DBP + 1/3 (SBP-80)

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12
Q

What is the normal range of MAP?

A

70-105 mmHg

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13
Q

What is the minimum MAP needed to perfuse the vital organs?

A

60 mmHg

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14
Q

Why must MAP be regulated within a narrow range?

A

High enough to perfuse internal organs

Not too high to damage blood vessels or place extra strain on the heart

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15
Q

Which two factors contribute to MAP?

A

MAP = Cardiac Output X Total Peripheral Resistance

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16
Q

Which two factors contribute to CO?

A

CO = Stroke Volume X Heart Rate

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17
Q

What is Total Peripheral Resistance?

A

The sum of resistance of all peripheral vasculature in the systemic circulation

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18
Q

What are the major resistance vessels?

A

The arterioles

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19
Q

What controls short-term regulation of MAP?

A

Baroreceptor Reflex

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20
Q

Where are the baroreceptors and how do their signals reach the Medulla?

A

Aortic Baroreceptors = In the aortic arch. Send signals via CNX
Carotid Baroreceptors = In the carotid sinus. Send signals via CNIX

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21
Q

Summary of Baroreceptor Response - Decreased MAP

A

Baroreceptors fire less
Vagal output decreases
Cardiac sympathetic output increases, increasing strength of cardiac muscle contraction
Sympathetic vasoconstrictor activity increases

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22
Q

Summary of Baroreceptor Response - Increased MAP

A

Baroreceptors increase firing
Vagal output increases
Cardiac sympathetic output decreases, decreasing strength of cardiac muscle contraction
Sympathetic vasoconstrictor activity decreases

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23
Q

How does the Baroreceptor Reflex prevent Postural Hypotension?

A

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

24
Q

How does Postural Hypotension occur?

A

Results from a failure of baroreceptor response to gravitational shifts in blood, when moving from the horizontal to vertical position

25
Q

Why can Baroreceptors only response to acute changes?

A

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

26
Q

Total Body Fluid =

A 
Intracellular fluid (2/3)
Extracellular fluid (1/3)
27
Q

Extracellular Fluid =

A

Plasma volume

Interstitial fluid volume

28
Q

How does extracellular fluid volume control blood volume and MAP?

A

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

29
Q

Which two main factors affect extracellular fluid volume?

A

Water excess or deficit

Na+ excess or deficit

30
Q

Which hormones regulate ECFV?

A

Renin-Angiotensin-Aldosterone-System (RAAS)
Atrial Natriuretic Peptide (ANP)
Antidiuretic Hormone, aka Arginine Vasopressin (ADH)

31
Q

What is the role of the RAAS in MAP regulation?

A

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

32
Q

What is the rate limiting step fro RAAS and how is this regulated?

A

Renin secretion
This is regulated by: renal artery hypotension; stimulation of renal sympathetic nerves; decreased [Na+] in renal tubular fluid

33
Q

What is Atrial Natriuretic Peptide?

A

28 amino acid peptide synthesised and stored by atrial myocytes

34
Q

What is the role of ANP in MAP regulation?

A

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

35
Q

What is Anti-Diuretic Hormone?

A

Peptide hormone synthesised by the hypothalamus and stored in the posterior pituitary

36
Q

What is the role of ADH in MAP regulation?

A

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.

37
Q

How is TPR controlled?

A

Relaxation/contraction of vascular smooth muscle

These are controlled by extrinsic and intrinsic mechanisms

38
Q

Resistance to Blood Flow

A

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

39
Q

Extrinsic Control of Vascular Smooth Muscles

A

Involves nerves and hormones
Vascular smooth muscle is supplied by sympathetic nerve fibres. The neurotransmitter is noradrenaline acting on alpha receptors

40
Q

What is Vasomotor Tone?

A

The partial constriction of vascular smooth muscle at rest. Caused by tonic discharge of sympathetic nerves

41
Q

Extrinsic Control of Vascular Smooth Muscles - Nerves

A

Increased sympathetic discharge increases vasomotor tone
= vasoconstriction
Decreased sympathetic discharge decreases vasomotor tone
= vasodilatation
No parasympathetic innervation

42
Q

Extrinsic Control of Vascular Smooth Muscles - Hormones

A

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

43
Q

Intrinsic Control of Vascular Smooth Muscles

A

Matches blood flow of different tissues to their metabolic needs
Can over-ride extrinsic control mechanisms
Includes local chemical and physical factors

44
Q

Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Metabolites

A 
Vasodilatation caused by:
Decreased local PO2
Increased local PCO2
Increased local [H+]
Increased extra-cellular [K+]
Increased osmolarity of ECF
Adenosine release from ATP
45
Q

Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Humoral Agents

A

Vasodilatation caused by:
Histamine
Bradykinin
Nitric Oxide

Vasoconstriction caused by:
Serotonin 
Thromboxane A2
Leukotrienes 
Endothelin
46
Q

Intrinsic Control of Vascular Smooth Muscles - Chemical: Nitric Oxide

A

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

47
Q

Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Humoral Agents and Endothelium Importance

A

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

48
Q

Intrinsic Control of Vascular Smooth Muscles - Physical: Temperature

A 
Cold = Vasoconstriction
Warmth = Vasodilatation
49
Q

Intrinsic Control of Vascular Smooth Muscles - Physical: Myogenic Response to Stretch

A

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

50
Q

Intrinsic Control of Vascular Smooth Muscles - Physical: Sheer Stress

A

Dilation of arterioles cases sheer stress in the arteries upstream to make them dilate. Increases blood flow to metabolically active tissues

51
Q

Factors Increasing Venous Return

A

Increased venomotor tone
Increased blood volume
Increased skeletal muscle pump
Increased respiratory pump

52
Q

What is the Venomotor tone?

A

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

53
Q

What is the Skeletal Muscle Pump?

A

Large veins in limbs lie between skeletal muscles

Contraction of muscles aids venous return

54
Q

Acute Responses of CVS to Exercise

A

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

55
Q

Chronic Responses of CVS to Exercise

A 
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

Cardio (19 decks)

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