Physiology - Integration of Cardiovascular Mechanisms

Question 1

What is Blood Pressure?

Answer 1

The outwards pressure exerted by the blood on blood vessel walls

Question 2

What is Systemic Systolic Arterial Blood Pressure?

Answer 2

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

Question 3

What is Systemic Diastolic Blood Pressure?

Answer 3

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

Question 4

What is the upper limit for systemic systolic blood pressure?

Answer 4

Should not normal reach or exceed 140mmHg

Question 5

What is the upper limit for systemic diastolic blood pressure?

Answer 5

Should not normally each or exceed 90mmHg

Question 6

Physiological Basis for Sphygmomanometry

Answer 6

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

Question 7

When is the systolic pressure recorded using sphygmomanometry?

Answer 7

At peak systolic pressure

1st Korotkoff Sound

Question 8

When is the diastolic pressure recorded using sphygmomanometry?

Answer 8

The point at which sound disappears

5th Korotkoff Sound

Question 9

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

Answer 9

5th Korotkoff sound is more reproducible than 4th

Question 10

What is Mean Arterial Blood Pressure?

Answer 10

The average arterial blood pressure during a single cardiac cycle

Question 11

What are the two equations for estimating MAP?

Answer 11

[(2 x DBP) + SBP] / 3

DBP + 1/3 (SBP-80)

Question 12

What is the normal range of MAP?

Answer 12

70-105 mmHg

Question 13

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

Answer 13

60 mmHg

Question 14

Why must MAP be regulated within a narrow range?

Answer 14

High enough to perfuse internal organs

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

Question 15

Which two factors contribute to MAP?

Answer 15

MAP = Cardiac Output X Total Peripheral Resistance

Question 16

Which two factors contribute to CO?

Answer 16

CO = Stroke Volume X Heart Rate

Question 17

What is Total Peripheral Resistance?

Answer 17

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

Question 18

What are the major resistance vessels?

Answer 18

The arterioles

Question 19

What controls short-term regulation of MAP?

Answer 19

Baroreceptor Reflex

Question 20

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

Answer 20

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

Question 21

Summary of Baroreceptor Response - Decreased MAP

Answer 21

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

Question 22

Summary of Baroreceptor Response - Increased MAP

Answer 22

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

Question 23

How does the Baroreceptor Reflex prevent Postural Hypotension?

Answer 23

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

Question 24

How does Postural Hypotension occur?

Answer 24

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

Question 25

Why can Baroreceptors only response to acute changes?

Answer 25

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

Question 26

Total Body Fluid =

Answer 26

``` Intracellular fluid (2/3) Extracellular fluid (1/3) ```

Question 27

Extracellular Fluid =

Answer 27

Plasma volume | Interstitial fluid volume

Question 28

How does extracellular fluid volume control blood volume and MAP?

Answer 28

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

Question 29

Which two main factors affect extracellular fluid volume?

Answer 29

Water excess or deficit | Na+ excess or deficit

Question 30

Which hormones regulate ECFV?

Answer 30

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

Question 31

What is the role of the RAAS in MAP regulation?

Answer 31

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

Question 32

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

Answer 32

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

Question 33

What is Atrial Natriuretic Peptide?

Answer 33

28 amino acid peptide synthesised and stored by atrial myocytes

Question 34

What is the role of ANP in MAP regulation?

Answer 34

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

Question 35

What is Anti-Diuretic Hormone?

Answer 35

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

Question 36

What is the role of ADH in MAP regulation?

Answer 36

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.

Question 37

How is TPR controlled?

Answer 37

Relaxation/contraction of vascular smooth muscle | These are controlled by extrinsic and intrinsic mechanisms

Question 38

Resistance to Blood Flow

Answer 38

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

Question 39

Extrinsic Control of Vascular Smooth Muscles

Answer 39

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

Question 40

What is Vasomotor Tone?

Answer 40

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

Question 41

Extrinsic Control of Vascular Smooth Muscles - Nerves

Answer 41

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

Question 42

Extrinsic Control of Vascular Smooth Muscles - Hormones

Answer 42

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

Question 43

Intrinsic Control of Vascular Smooth Muscles

Answer 43

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

Question 44

Intrinsic Control of Vascular Smooth Muscles - Chemical: Local Metabolites

Answer 44

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

Question 45

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

Answer 45

Vasodilatation caused by: Histamine Bradykinin Nitric Oxide ``` Vasoconstriction caused by: Serotonin Thromboxane A2 Leukotrienes Endothelin ```

Question 46

Intrinsic Control of Vascular Smooth Muscles - Chemical: Nitric Oxide

Answer 46

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

Question 47

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

Answer 47

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

Question 48

Intrinsic Control of Vascular Smooth Muscles - Physical: Temperature

Answer 48

``` Cold = Vasoconstriction Warmth = Vasodilatation ```

Question 49

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

Answer 49

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

Question 50

Intrinsic Control of Vascular Smooth Muscles - Physical: Sheer Stress

Answer 50

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

Question 51

Factors Increasing Venous Return

Answer 51

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

Question 52

What is the Venomotor tone?

Answer 52

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

Question 53

What is the Skeletal Muscle Pump?

Answer 53

Large veins in limbs lie between skeletal muscles | Contraction of muscles aids venous return

Question 54

Acute Responses of CVS to Exercise

Answer 54

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

Question 55

Chronic Responses of CVS to Exercise

Answer 55

``` 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 ```