Peripheral circulation Flashcards

1
Q

Capacitance and resistance:

A

Vascular capacitance is analogous to vascular resistance - but resistance refers to flow through a vessel, whereas capacitance relates to the volume that the vessel contains.

Changes in capacitance alter right ventricular filling and thus affect cardiac output.

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2
Q

The circulatory tree has multiple functions. It acts to:

A

Exchange O2 and CO2
Distribute nutrients to the cells of the body
Remove waste products of metabolism
Influence mean blood pressure and distribution of blood flow
Distribute endocrine secretions
Prevent bleeding or thrombosis
Combat infection
Regulate body temperature

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3
Q

What is the Windkessel effect

A

The arteries carry blood away from the heart and act as a hydraulic filter, ultimately converting the intermittent pulsatile ejection of blood from the heart into a steady flow with a constant pressure

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4
Q

Arterioles:

A

In arterioles, the small diameter provides a significant resistance to blood flow. This resistance ultimately determines the mean arterial blood pressure. Terminal arterioles provide the largest mean pressure drop (from 75 mmHg to 38 mmHg) of the normal circulation and provide about 70% of the vascular resistance.

Arterioles are normally in a state of partial vasoconstriction (tone) secondary to spontaneous contractile activity of the muscle wall and tonic sympathetic output. Systemic and local factors cause alterations in tone (degree of vasoconstriction), which in turn alters flow.

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5
Q

Venules:

A

Venules are post-capillary resistance vessels that regulate the capillary hydrostatic pressure.

Capillary hydrostatic pressure is one of the forces that determine the movement of water into and out of the intravascular and extracellular space. It is determined by the ratio of the resistances of the arterioles (pre-capillary resistance) and the venules (post-capillary resistance).

The smooth muscle tone of the post-capillary venules is controlled by the same systemic and local factors that control the tone of the arterioles. Though pre-capillary resistance influences the capillary hydrostatic pressure, the change in venous pressure has the greater effect.

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6
Q

Arteries and veins have the same three-layer structure:

A

Tunica intima (Fig 1a). This innermost layer is made up of a single layer of squamous endothelial cells surrounded by a thin layer of subendothelial connective tissue

Tunica media (Fig 1b). This layer contains circularly arranged elastic fibres and connective tissue and the vascular smooth muscle which controls the diameter of the vessel

Tunica adventitia (Fig 1c). This outermost layer is made up entirely of connective tissue and contains the nerves that supply the vessel and, in larger vessels, the vasa vasorum

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7
Q

What do you think is the velocity of pulsatile flow at the level of the ascending aorta?

A

At the level of the ascending aorta the velocity of pulsatile flow is about 1 m/s.

As the stroke volume enters the aorta, the aorta expands. Elastic recoil during diastole acts to smooth out the pulsatile nature of the heart’s pumping action (Windkessel effect).

As arteries divide and divide again, the total cross-sectional area increases, so the mean blood pressure and velocity fall. When the blood arrives at the capillary exchange beds, flow is smooth and slow, and pressure is low. Thus the role of the arterial system is to convert the high-velocity pulsatile flow, at the level of the ascending aorta, to the optimal low-velocity steady flow in the capillary bed (around 0.01 cm/s) that is necessary for cellular exchanges

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8
Q

Throughout the vascular tree, the endothelium has a number of functions including:

A

Regulating basal vasomotor tone (and hence, blood pressure) by the controlled release of:
-vasodilators, i.e. nitric oxide (NO) and prostaglandin I2 (PGI2, prostacyclin)
-vasoconstrictors, i.e. endothelins and platelet activating factor (PAF)

Acting as a non-thrombogenic surface, secondary to expressing heparan sulphate, protein C and protein S.

Presenting a smooth surface to encourage laminar flow

Regulating the growth of surrounding connective tissue

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9
Q

The capillary endothelium:

A

Unlike arteries and veins, capillaries (5-10 μm diameter) consist of just a single layer of endothelium and some connective tissue. These cells form a semipermeable or selectively permeable membrane which allows the diffusion of fluids, nutrients and waste products between the lumen of the capillary and the surrounding tissue. To increase permeability, the cells of the capillary endothelium are thinner than those of the arteries and veins.

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10
Q

There are three types of capillary depending on the arrangement of their endothelial cells:

A

1) Continuous - where endothelial cells form an uninterrupted (continuous) lining, e.g. in the brain, so that only water, gases and ions diffuse through the intercellular clefts or tight junctions
2) Fenestrated - where pores allow small molecules to diffuse
3) Sinusoidal - in the bone marrow and liver, where larger proteins and even white and red cells pass through

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11
Q

What is third spacing?

A

In disease states, e.g. sepsis, vascular permeability increases. This increased ‘leakiness’ is sometimes referred to as ‘third spacing’ or ‘third space losses’. It is mediated by histamine, prostaglandins and interleukins. Oedema results when this increased fluid and protein loss overwhelms the absorptive capacity of the lymphatic system.

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12
Q

Where is the permeability of a capillary greatest?

A

Along the length of an individual capillary, permeability is greatest at the venous end of the capillary

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13
Q

Poiseuille’s Equation

A

Flow (Q) = pi(P2-P1)r^4/ 8nl

P2-P1 = pressure difference
r= radius
n= viscosity
l= length

Flow of any liquid proceeds from a point of higher pressure to one of lower pressure.
The total flow is determined by:
The pressure gradient
The length of the vessel
The radius of the vessel
The viscosity of the fluid
Poiseuille described this relationship mathematically by studying the flow of a homogenous (Newtonian) fluid through rigid, uniform, non-branching glass tubes.

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14
Q

What is resistance characterised by?

A

The diameter and, to a lesser extent, the length of an individual vessel
The organization of the vascular network (in series or in parallel)
The physical characteristics of the blood itself (viscosity)
The type of flow (turbulent or laminar)
Within a single vessel, hydraulic resistance to flow is determined by vessel diameter or radius, vessel length and the viscosity of the blood.

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15
Q

Resistance equation:

A

R= 8nl/ pi x r^4

Mathematically then R varies directly with viscosity (η) and length (l) and inversely with the fourth power of the radius (r).

Vessel diameter - specifically of the arterioles, the ‘resistance’ vessels - is the single most important factor in controlling distribution of flow and determining mean blood pressure. Because flow directly affects oxygen delivery, any change in arteriolar diameter enables flow to tissues to be adjusted to match metabolic requirements.

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16
Q

What would be the difference in resistance in two tubes of the same radius, if one is twice the length of the other?

A

you can deduce that a vessel that has twice the length of another vessel (that has the same radius) has twice the resistance to flow (Fig 2).

However, under physiological conditions, vessel length does not change significantly and blood viscosity usually stays within a small range (except when haematocrit changes). Therefore, although resistance varies directly with η and l, both are relatively fixed values in the circulation, and have little effect on resistance.

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17
Q

How would a 2-fold increase in radius (r) affect resistance?

A

Resistance varies inversely with r4, so a 2-fold increase in r would decrease resistance 16-fold (Fig 3). A 4-fold in r would decrease resistance (R) 256-fold. By extension, flow would increase 16 and 256 times respectively.

In contrast to η and l, resistance is extremely sensitive to changes in r. Changing the radius of a vessel by contraction or relaxation of its smooth muscle profoundly alters the resistance to flow, and therefore, drugs or other modulating factors which dilate or constrict the vessels have a powerful effect on blood flow.

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18
Q

Resistance in series

A

If across each serial resistance (Fig 1a):

The driving pressure (ΔP) is 3 mmHg and
The flow (Q) is 1 ml/min
then:

For each resistance R = ΔP/Q or 3 mmHg/ml/min, and
The total resistance of the series is Rs = 9 mmHg/ml/min

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19
Q

Parallel resistance

A

In parallel resistances (Fig 1b), if the values are the same across each resistance,
ΔP is 3 mmHg and Q is 1 ml/min, then the total resistance is

1/Rp = 1/R1 + 1/R2 + 1/R3 or 1 mmHg/ml/min

In this example, Rp is only 1/9 of that of the same three resistances in series (i.e. the ratio of Rp/Rs = 1/9).

From this it can be deduced that for parallel resistances, it takes a ΔP of only 1 mmHg (instead of 9 mmHg for series resistances) to produce a flow of 1 ml/min.

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20
Q

Differentiate between the terms ‘velocity’ and ‘flow’:

A

Velocity (v) is the distance the blood moves with respect to time, usually expressed in cm/s
Flow is the volume of blood moving per unit of time, expressed as ml/min or cm3/min

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21
Q

How is the flow of blood in a vessel related to velocity?

A

Q = vA, where A is the cross-sectional area of the vessel.

Thus velocity is low where the area is large and high where the area is small (Fig 1).

To illustrate, the smallest cross-sectional area to receive the entire stroke volume is the aorta (~2.5 cm2) where velocity of flow is highest at 0.93 m/s. As arteries divide into smaller and smaller vessels, the total cross-sectional area increases and blood velocity falls. In the capillaries, where the total cross-sectional area is 1000 times that of the aorta, flow is 0.05 cm/s. This slowing of blood velocity enables efficient exchange of gases and metabolites across the short length of capillaries.

The relationship between flow in a tube (rather than velocity) and area is more complex and is described by Poiseuille’s Law.

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22
Q

What is laminar flow?

A

Laminar flow describes fluid where all the elements of the fluid move in streamlined layers parallel to the vessel wall. The central core of fluid has the highest velocity and each cylinder of fluid around this central column is progressively slower until the outermost layer, in contact with the vessel wall is stationary. The profile of flow velocity across the tube forms a parabola (Fig 2).

The ease with which each ‘layer’ of fluid slides over its neighbour is determined by the fluid viscosity. The higher the fluid viscosity, the less slippery the fluid is and flow is reduced for any given pressure.

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23
Q

What is turbulent flow?

A

Where the blood velocity is high, a point is reached at which flow is no longer directly proportional to pressure. This happens because flow is no longer laminar, but turbulent (Fig 3). In turbulent flow, fluid moves in discordant eddies and the frictional resistance to flow increases. In the ascending aorta (velocity 0.93 cm/s), flow is turbulent, and will only increase in proportion to the square root of pressure.

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24
Q

Describe Reynold’s number and its importance in the pressure-flow relationship:

A

Reynolds number is used to determine whether flow is likely to be laminar or turbulent by identifying the point when flow is no longer proportional to the driving pressure (Fig 1):

Laminar flow, which is characterized by smooth fluid motion, occurs at low Reynolds numbers, where viscous forces predominate
Turbulent flow occurs at high Reynolds numbers and is dominated by inertial forces, which tend to produce chaotic eddies, vortices and other flow instabilities

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25
Q

What is the equation for turbulent flow?

A

Poiseuille’s law on pressure-flow relationships in the circulation depends on conditions of laminar flow for accuracy. When flow becomes turbulent, Poiseuille’s law no longer holds, and the flow rate becomes proportional to the square root of the pressure gradient, rather than being directly proportional to pressure gradient. In turbulent flow:

Q ∝ √ΔP

Turbulence increases the energy required to drive blood flow because turbulence increases friction.

Additionally, the pressure drops seen through tubes can be predicted by plotting the wall friction factor f against Reynolds number Re. The relative roughness of the vessel thus plays a part in pressure-flow predictions.

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26
Q

Blood viscosity is affected by:

A

Haematocrit
Temperature
Vessel diameter
Flow rate

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27
Q

Haematocrit:

A

Under normal conditions, RBC concentration has the greatest effect on blood viscosity. An increase in the red cell haematocrit leads to an increase in viscosity which is non-linear. The viscosity of blood relative to water is 3.6, mainly due to the presence of red cells.

28
Q

How does temperature affect viscosity?

A

Blood gets ‘thicker’ or more viscid as it gets colder. Viscosity increases 2% for each degree centigrade decrease in temperature.

When hypothermia is induced in critical care, it leads to increased blood viscosity and changes in systemic haemodynamics and organ flow.

29
Q

How does vessel diameter affect viscosity?

A

In arterioles and capillaries, the Lindqvist effect leads to a reduction in the haematocrit relative to larger vessels. Cells tend to occupy the central axial stream, effectively reducing the haematocrit. This reduction in viscosity offsets the reduction in velocity in the small vessels. In the capillaries, blood viscosity is no greater than that of plasma.

30
Q

How does flow rate affect viscosity?

A

Low flow rates increase interactions between RBC (e.g. rouleaux formation) and between RBC and plasma proteins.

If clotting formation occurs, there is a dramatic increase in blood viscosity.

31
Q

Which factors may contribute to systolic aortic murmurs in pregnancy?

A

A. Aortic valve pathology causing turbulent flow:
Many patients may have their hearts auscultated for the first time in pregnancy. Aortic pathology may first come to light now.

B. Decreased haematocrit (reduced blood viscosity):
Reynolds number increases as viscosity decreases. Therefore, high velocities and low blood viscosity (as occurs in pregnancy, due to reduced haematocrit) are more likely to cause turbulence.

C. Increased flow

D. Increased blood volume: High velocities and low blood viscosity (as occurs in pregnancy) are more likely to cause turbulence as the Reynolds number rises.

32
Q

MAP equation:

A

Mean arterial pressure (MAP) is determined by the cardiac output (CO) or flow, systemic vascular resistance (SVR) and central venous pressure (CVP).

MAP = (CO x SVR) + CVP

This equation is useful because it demonstrates mathematically what is physiologically true:

SVR and CO are independent variables and
MAP is a dependent variable
It also shows that, if CO and SVR change individually and reciprocally, MAP does not change. So, for example, if your appendix burst and your CO doubled and SVR halved, MAP would remain constant (but you would be likely to require intensive care).

33
Q

How is MAP calculated in practice?

A

In practice, MAP is determined not by knowing the cardiac output or the vascular resistance but by direct or indirect measurement.

From a direct intra-arterial pressure trace, the shape of the trace yields a geometric mean pressure that is less than the arithmetic average of the systolic and diastolic pressures. Alternatively, the value of the MAP can be calculated by the formula:

MAP= Pd + (Ps-Pd)/3

where Pd is diastolic pressure and Ps is systolic pressure.

34
Q

How is renin release stimulated?

A

Sympathetic nerve activation (acting via β1-adrenoceptors)
Hypotension
Decreased sodium delivery to the distal tubules of the kidney

35
Q

What does angiotensin II do?

A

1)Constrict resistance vessels and increase systemic vascular resistance and arterial pressure
2)Cause the adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase sodium and fluid retention
3)Stimulate the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary, to increases fluid retention by the kidneys
4)Stimulate thirst centers within the brain
5)Enhance sympathetic adrenergic function by facilitating noradrenaline release whilst inhibiting re-uptake

36
Q

What is vessel diameter determined by?

A

Vessel diameter is determined by the degree of vascular smooth muscle constriction (tone). Tone is defined as the degree of vasoconstriction of a blood vessel relative to its maximally dilated state, and is under local and autonomic control.

37
Q

Local control of blood flow by the tissues (autoregulation) is by:

A

Metabolic control e.g.
Falling levels of oxygen
Rising levels of hydrogen and potassium ions
Rising lactic acid concentrations
Adenosine production
Prostaglandin and histamine

Myogenic control, where passive stretching of the smooth muscle wall by increased pressure or volume can result in either reflex vasoconstriction (negative feedback) or further vasodilation (positive feedback)

38
Q

Describe the role of nitric oxide and endothelins:

A

NO and endothelins are the main regulators of basal vascular tone. It is only when vascular function is disturbed that PGI2 and PAF come in to play.

Endothelial NO (Fig 1) is constituitively active but can be further induced by agonists like thrombin, ADP, bradykinin and substance P. Increased shear stress also induces NO production. NO binds to guanylyl cyclase to cause smooth muscle relaxation.

Hypoxia, ischaemia and shear stress induce production of
endothelin 1 (ET-1) by endothelial cells. ET-1 is the most potent known endogenous vasoconstrictor (Fig 2). Catecholamines and noradrenaline act in concert with ET-1, potentiating each other’s effects.

39
Q

What does adrenaline do to the vascular smooth muscle in the arterioles and veins and in the vascular beds supplying muscles?

A

Under basal conditions, arterioles and veins are partially constricted secondary to basal sympathetic autonomic output.

Arterioles and, to a lesser extent, venules are the prime target vessels in the control of vascular resistance via control of their smooth muscle tone. Both groups of vessels are richly innervated by sympathetic α1 and post junctional α2 adrenergic fibres, which cause vasoconstriction in the presence of adrenaline. Vessel beds in skeletal muscle are rich in ß2 adrenergic receptors and instead vasodilate in response to adrenaline.

40
Q

How is vasoconstriction and dilation in an individual tissue or organ controlled?

A

The balance between systemic and locally mediated factors determines the balance between vasoconstriction and dilation in an individual tissue or organ.

Systemic factors include:
Intrinsic vascular smooth muscle activity
Basal sympathetic adrenergic output
Circulating vasoactive hormones (e.g. adrenaline, vasopressin, angiotensin)

The balance between vasoconstrictor and vasodilator substances released by both tissues and the vascular endothelium mediates local vascular tone and regulates flow to an organ, and that flow directly affects oxygen delivery.

41
Q

Which of the following attributes are features of autoregulation?

A

A. Low neurogenic control of the supplying arteriole’s smooth muscle
B. Nearly constant blood flow over a wide range of mean blood pressure
C. Most evident in skeletal, cardiac and cerebral circulations
D. High degree of local control of vascular resistance

42
Q

What is bulk flow (convection)?

A

Bulk flow of fluid and electrolytes also occurs through ‘pores’ or clefts between the endothelial cells.
This mechanism of exchange is particularly important in renal glomerular capillaries; however, it occurs to some extent in nearly all tissues.

Fluid movement due to bulk flow or convection follows Starling’s Law. The exchange is altered by changes in the pressure driving forces (whether hydrostatic or osmotic) and in the size of pores or intercellular clefts (e.g. as occurs in sepsis).

Substances like histamine and bradykinin increase pore size and augment outward fluid and electrolyte movement by increasing the filtration constant.

43
Q

What is vesicular transport?

A

Vesicular transport involves the translocation of macromolecules across the capillary endothelium

44
Q

Explain Starling’s forces:

A

The aqueous solutions that form the plasma and the interstitial fluid are readily exchanged through the walls of the capillaries. The principle forces governing this exchange are hydrostatic pressure (BP within the capillary) and osmosis.

In the normal state, fluid gain and loss through the capillary wall is closely balanced so there is little or no net change in plasma and interstitial fluid (ISF) volumes. The small excess in fluid loss from plasma to ISF is normally drained back to the circulation via the lymphatic system.

Starling’s equation describes only the fluid movement due to filtration. Fluid movement due to filtration varies widely throughout the body. In the special circumstance of the glomerulus of the kidney, there is a net fluid filtration of 125 ml/min with no reabsorption. In other body capillaries there is a total net fluid filtration of 20 ml/min.

45
Q

Hydrostatic pressure:

A

The hydrostatic pressure in the capillaries decreases along its length. At the arteriolar end, the pressure is usually about 35 mmHg (due to the pressure drop caused by the resistance arterioles). At the venular end, the pressure is approximately 15 mmHg. The net effect of hydrostatic pressure alone is a net loss of fluid and solute from plasma to ISF.

46
Q

Oncotic pressure:

A

The plasma proteins within the lumen exert an osmotic pressure. Since the proteins are negatively charged they also hold cations in the lumen (Gibbs Donnan effect). The combined effect of osmotic and Gibbs Donnan forces is to draw waster out of the ISF and into the plasma. Compared to pure saline, the plasma exerts 28 mmHg oncotic pressure, whereas the ISF has only about 3 mmHg. This value remains constant along the length of most capillary beds.

The reflection coefficient is a correction factor applied to describe the ‘effective oncotic pressure’. Not all protein is effective in retaining water, so the effective capillary oncotic pressure is lower than the measured oncotic pressure. The reflection coefficient carries a value between 0 and 1. In capillaries where tight endothelial junctions predominate, there is very little leakage of protein across the capillary membrane and interstitial oncotic pressure is low. The reflection coefficient therefore approaches 1 (little difference between theoretic and measured oncotic pressures). In the hepatic capillaries, proteins cross the wall of the sinusoids relatively easily and the reflection coefficient is low. The reflection coefficient of pulmonary capillaries is intermediate at about 0.5.

47
Q

Oedema is the palpable swelling produced by expansion of interstitial fluid (ISF) and occurs secondary to one of the following:

A

Disruption of capillary haemodynamics, e.g. a rise in capillary hydrostatic pressure, a fall in capillary oncotic pressure or increase in capillary permeability
Obstruction to lymphatic flow
Retention of IV or dietary sodium and water by the kidneys

48
Q

What are some of the roles of the lymphatic system?

A

As an important part of the immune system, it transports antigen presenting cells and lymphocytes

It removes any excess fluid and proteins that have crossed from the capillaries into the interstitial fluid

It absorbs and transports fatty acids and fats (as chyle) from the digestive tract to the circulatory tree

49
Q

How does lymph form and where does it drain?

A

Lymph is a clear fluid formed from the fluid and proteins, which exit the capillaries to become interstitial fluid. While Starling Forces recover 90% of this fluid and return it to the venular end of the capillary, 10% enters the initial lymph vessels. These first vessels are blind-ended tubes, the majority of which are located just under the skin.

The hydrostatic pressure of fluid in the interstitium opens spaces between the cells of the lymph vessel walls to allow lymph to enter. Then, as the interstitial pressure drops, these spaces close.

The lymphatic capillaries join together first as a mesh surrounding organs and then as progressively larger lymph vessels located deeper within the body. These larger lymphatics eventually follow the paths of larger veins, developing smooth muscle walls and flap valves to ensure unidirectional flow. Lymph nodes act to filter lymph prior to its return to the systemic circulation by way of the thoracic duct and the superior vena cava.

50
Q

How does the circulation to the skin work? How is it controlled/ what is its purpose?

A

The blood supply to the skin serves two main purposes:

To supply modest requirements of nutrient flow, controlled by local factors
To provide potentially high flow concerned with heat loss under reflex control
Unlike the brain, heart and skeletal muscle, which exhibit autoregulation where local metabolic influences tend to override neural ones, the circulation of the skin is under powerful sympathetic control.

The skin contains arteriovenous (AV) anastomoses through which blood may be shunted to the venous plexuses, entirely bypassing the capillaries. These AV anastomoses are controlled by reflex influences from temperature receptors and centres in the anterior hypothalamus, which control heat transfer from the body to the environment via the skin.

51
Q

The structure and role of the vascular endothelium is:

A

A. The endothelium is made up of a single layer of endothelial cells and this surface layer is in direct contact with the blood or lymph.

B. The endothlium presents a smooth surface to encourage laminar flow.

C. The endothlium does act as a non-thrombogenic surface, however, this is secondary to expressing heparan sulfate, protein C and protein S.

D. The endothelium regulates basal vasomotor tone by the controlled release of vasodilators, i.e. NO and prostaglandin I2.

E. The endothelium regulates blood pressure by the controlled release of: vasoconstrictors, i.e. endothelins and PAF.

F. The endothelium regulates the growth of surrounding connective tissue.

52
Q

Which of the following factors cause alterations in vascular tone?

A

A. Oxygen. For most tissues, falling O2 concentration is the strongest stimulus for vasodilation.

B. Prostacyclin (PGI2) is formed in the endothelium from arachidonic acid and causes smooth muscle relaxation via increases in cAMAAP.

C. False. Haemoglobin concentration has no effect on the vascular tone.

D. H+, K+, H+CO2 and adenosine arise in the tissues and cause vasodilation by direct action on the vascular smooth muscle.

E. Adrenaline causes vasocontriction through its effects on alpha adrenergic receptors in the vascular smooth muscle of the digestive tract, skin and kidneys. In the skeletal muscle beds, a rich population of β2 adrenergic receptors causes adrenaline mediated vasodilation.

53
Q

High blood velocity causes flow to be directly proportional to pressure? T or F?

A

False. Where the blood velocity is high, a point is reached at which flow is no longer directly proportional to pressure.

54
Q

Blood velocity is 0.93 cm/s in the ascending aorta and flow is turbulent? T or F?

A

True. Flow is turbulent, very briefly, in the early part of the ascending aorta and will only increase in proportion to the square root of pressure.

55
Q

Turbulent flow occurs at low Reynolds numbers, which tend to produce chaotic eddies, vortices and other flow instabilities? T or F?

A

False. Turbulent flow occurs at high Reynolds numbers and is dominated by inertial forces, which tend to produce chaotic eddies, vortices and other flow instabilities. Laminar flow is characterized by smooth fluid motion, and occurs at low Reynolds numbers, where viscous forces predominate.

56
Q

When flow becomes turbulent, the flow rate becomes proportional to the square root of the pressure gradient? T or F?

A

True. When flow becomes turbulent, the flow rate becomes proportional to the square root of the pressure gradient, rather than being directly proportional to pressure gradient.

57
Q

Turbulence increases the energy required to drive blood flow? T or F?

A

True. Turbulence increases the energy required to drive blood flow because turbulence increases friction.

58
Q

The relative roughness of the vessel plays a part in pressure-flow predictions? T or F?

A

True. The relative roughness of the vessel plays a part in pressure-flow predictions.

59
Q

Total flow is determined entirely by the length of the vessel and radius of the vessel? T or F?

A

False. Total flow is determined by: the pressure gradient, the length of the vessel, the radius of the vessel and the viscosity of the fluid.

60
Q

Resistance is not affected by whether flow is turbulent or laminar? T Or F?

A

False. Resistance is determined by whether flow is turbulent or laminar.

61
Q

Mathematically, resistance varies directly with viscosity and length, and varies inversely with the fourth power of the radius? T or F?

A

True. Mathematically, resistance, R varies directly with viscosity and length, and varies inversely with the fourth power of the radius.

62
Q

Blood viscosity increases 2% for each degree centigrade decrease in temperature and leads to changes in systemic haemodynamics and organ flow? T or F?

A

True. Viscosity increases 2% for each degree centigrade decrease in temperature. When hypothermia is induced in critical care, it leads to increased blood viscosity and changes in systemic haemodynamics and organ flow.

63
Q

In arterioles and capillaries, the Lindqvist effect leads to a reduction in the haematocrit relative to larger vessels? T or F?

A

True. In arterioles and capillaries, the Lindqvist effect leads to a reduction in the haematocrit relative to larger vessels. Cells tend to occupy the central axial stream, effectively reducing the haematocrit. This reduction in viscosity offsets the reduction in velocity in the small vessels.

64
Q

In the capillaries, blood viscosity is greater than that of plasma? T or F?

A

False. In the capillaries, blood viscosity is no greater than that of plasma.

65
Q

T or F, Low flow rates increase the possibility of rouleaux formation and interactions between RBC and plasma proteins?

A

True

66
Q
A