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T1 - Phase 1 - Integrated (I) > Cardio - Physiology - Hemodynamics; Local Vascular Control; Blood Pressure Control; Cardiac Output & Venous Return > Flashcards

Cardio - Physiology - Hemodynamics; Local Vascular Control; Blood Pressure Control; Cardiac Output & Venous Return Flashcards

1
Q

What is fluid velocity?

A

The speed of a particle of fluid (cm/sec)

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2
Q

What is fluid flow?

A

The amount of fluid traveling a distance per time

Q = velocity * area

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3
Q

If the cross sectional area (A) of an artery increases, what effect does this have on flow rate?

If the cross sectional area (A) of an artery increases, what effect does this have on velocity?

A

The flow rate will remain the same BECAUSE

–>

the velocity decreases

Q = vA

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4
Q

What two factors affect flow rate in the cardiovascular system?

A

Fluid velocity and vessel cross-sectional area

Q = vA

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5
Q

What are the two types of flow found in the cardiovascular system?

A

Turbulent (rough, damaging) and laminar (smooth, protective)

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6
Q

In simple terms, describe the effects of turbulent and laminar flows on cardiovascular vessels.

A

Laminar = efficient, protective

Turbulent = damaging, chaotic

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7
Q

In laminar flow through the arteries, where does the fluid flow quickest?

A

The central layers

(the outer layers interact with the sationary walls)

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8
Q

What does a high Reynold’s number (> 2000) indicate about the flow in the blood vessels?

What does a low Reynold’s number (< 2000) indicate about the flow in the blood vessels?

A

It is turbulent and noisy;

it is laminar and smooth

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9
Q

What three factors increase the Reynold’s number as they increase?

What factor decreases the Reynold’s number as it increases?

(Note: An increasing Reynold’s number = increasing blood turbulence)

A

Blood density,

*diameter of the blood vessel,

*blood velocity;

blood viscosity

(*vessel diameter and blood velocity are the two most important factors here)

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10
Q

Assuming flow rate has to remain constant, which will have a bigger effect on blood turbulence, changes in vessel diameter or changes in blood velocity?

A

Velocity

(diameter follows a linear change;

velocity will respond in a squared change)

v = Q / (πr2)

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11
Q

Is velocity higher in a narrow or wide vessel lumen?

A

Narrow

v = Q / (πr2)

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12
Q

What term refers to the ability of a blood vessel to return to its normal, non-distended shape once an external force is removed?

What term refers to the ability of a blood vessel to deform (change shape) in response to a force?

What term refers to the ability of a blood vessel to change its volume in accordance with changes in internal pressure?

A

Elasticity;

distensibility;

compliance

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13
Q

Why are blood vessels in the elderly stiffer than those in younger populations?

A

Loss of elastin

(less elasticity)

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14
Q

Why are both blood vessel distensibility and elastance desirable?

A

The aorta (and other large vessels) distend with the increase in systolic pressure (this dampens pressures and decreases afterload).

The elastance means they (contracting) help distribute the fluid out into the capillaries continuously.

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15
Q

What controls the rate of blood flow?

I.e. what does the heart push against?

A

Peripheral resistance

Q = ΔP / R

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16
Q

Q = ΔP / R shows us that blood flow is impeded by resistance.

What equation shows us all the variables creating that resistance?

A

R = 8 * η * l / πr4

(8 * viscosity * length / πr4)

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17
Q

Changes in blood vessel diameter will have a bigger effect on which, blood velocity or the resistance to flow?

A

velocity = Q / πr2

Resistance to flow = 8ηl / πr4

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18
Q

50% narrowing of an artery will have what effect on the resistance in that artery?

A

A 16-fold increase

R = 8 * η * l / πr4

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19
Q

25% narrowing of an artery will have what effect on the resistance in that artery?

A

A 3.2-fold increase

R = 8 * η * l / πr4

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20
Q

Resistors in sequence are calculated as:

Resistors in parallel are calculated as:

A

R1 + R2 + R3 = RTotal

1/R1 + 1/R2 + 1/R3 = 1/RTotal

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21
Q

What effect does bifurcation of vessels off the aorta have on blood flow?

A

The resistance of all the vessels are now in parallel (and so, decreased);

this trades efficacy for function and reduced resistance –>

flow rates can now be different for different organs

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22
Q

Bifurcating the aorta into various blood vessels creates a system of reduced resistances (the resistance vessels are now in parallel).

What are the two major effects of this structure?

A

Differing blood flow through differing organs;

the heart pushes against less resistance

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23
Q

Increases in what two factors increase resistance to blood flow?

Increases in what single factor decrease resistance to blood flow?

A

Blood viscosity, vessel length

vessel lumen radius

R = 8 * η * l / πr4

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24
Q

An individual with diabetes can have an increased risk of a first heart attack high enough to be comparable to what other patient?

A

An individual that has already had a heart attack

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25
Q

Why would having a single vessel loop be an inefficient structure for the circulatory system?

How does the body get around this problem?

A

Resistance would be huge;

parallel vessels (reducing resistance and allowing for varying flow rates)

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26
Q

Where is resistance high and flow slowest in the cardiovascular system?

Elastic arteries

Muscular arteries

Arterioles

Capillaries

Venules

Medium veins

Large veins

A

Capillaries

(smallest radius –> R = 8 * η * l / πr4)

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27
Q

Describe how pressures decrease over time in the cardiovascular system and how they are affected by constriction points (i.e. valves).

A
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28
Q

Where is the largest drop in pressure in the cardiovascular system?

A

The arterioles

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29
Q

What vessel type has capillaries coming off it and serves as a connection piece between arterioles and venules (an arteriovenous connection)?

A

Metarterioles

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30
Q

What are the two major factors affecting fluid flow between capillaries and the interstitial space?

A

Hydrostatic pressure;

oncotic pressure

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31
Q

What are some of the methods via which particles get from the capillary lumen to the interstitial space?

A

Filtration (via channels and pores), diffusion, pinocytosis

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32
Q

On which side of the capillary bed is oncotic pressure the highest?

On which side of the capillary bed is hydrostatic pressure the highest?

A

It is relatively constant across the bed;

the arterial end

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33
Q

Given hydrostatic and oncotic pressures for both a given capillary and its surrounding interstitial fluid, how would you express the Starling law?

A

Qf = k[(Pc - Pi) - (πc - πi)] = ΔP - Δπ

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34
Q

Arteriolar vasoconstriction will have what effect on the hydrostatic pressure in the capillary beds it perfuses?

A

Decrease

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35
Q

Will arteriolar vasoconstriction or vasodilation increase hydrostatic pressure in capillary beds supplied by a particular arteriole?

A

Vasodilation

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36
Q

What is the law of LaPlace for a sphere (e.g. an alveolus)?

What is the law of LaPlace for a cylinder (e.g. a blood vessel)?

A

T = P*r / 2

wall tension = internal pressure * radius / 2

T = P*r

wall tension = internal pressure * radius

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37
Q

What structure in the cardiovascular system controls TPR?

What structure in the cardiovascular system has the slowest flow and largest cross-section?

What structure in the cardiovascular system has the lowest pressure?

A

Arterioles;

capillaries;

veins

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38
Q

True/False.

The venous system is highly compliant.

A

True.

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39
Q

Compliance = Δ__ / Δ__

A

V,

P

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40
Q

True/False.

Arterial pulsation can help compress nearby veins and push the blood back towards the heart.

A

True.

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41
Q

Where in the body are veins thickest and least compliant?

A

The lower limbs

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42
Q

True/False.

Lymphatic vessels have abundant tight junctions.

A

False.

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43
Q

What layers make up a venule?

A

Endothelium + a small layer of fibrous tissue

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44
Q

A patient has been diagnosed with a new DVT. What do you recommend to the person in terms of their immediate activity levels?

A

Immediate bedrest to decrease risk of PE

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45
Q

In a patient with DVT, is leg exercise or leg elevation more efficient in returning blood to the heart?

A

Leg elevation

(damaged valves means the blood flow will easily become retrograde)

(e.g. exercise will push the blood in both directions)

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46
Q

True/False.

If a patient is given proper bedrest and anticoagulation, their DVT will completely resolve.

A

False.

The clot may stabilize, but it can remain as a chronic condition

(it is difficult to remove clotted tissue and damaged valves from the venous lumen)

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47
Q

Describe the changes in blood flow to various organs as a percentage of total cardiac output at rest and during strenuous exercise.

A
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48
Q

What is cardiac output at resting state?

What is cardiac output during heavy exercise?

A

5 L / min

25 L / min

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49
Q

What is the main mechanism by which blood is shunted towards or away from certain organ systems?

A

Changes in metabolite levels

(e.g. adenosine, K+, O2, CO2)

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50
Q

Increases in what cyclic nucleotide(s) will result in smooth muscle relaxation.

A

cGMP and/or cAMP

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51
Q

Increases in extracellular K+ causes smooth muscle _____________.

A

Relaxation

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52
Q

Increases in ______________ __+ causes smooth muscle relaxation.

A

Extracellular K

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53
Q

What effect does sympathetic innervation of the α1 receptors have on the body’s vasculature?

A

Systemic vasoconstriction ONLY

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54
Q

α1 receptors are mostly involved in what organ system(s)?

α2 receptors are mostly involved in what organ system(s)?

β1 receptors are mostly involved in what organ system(s)?

β2 receptors are mostly involved in what organ system(s)?

β3 receptors are mostly involved in what organ system(s)?

A

Systemic vasculature (constriction)

Cerebral vasculature (constriction)

Heart tissue (increased contractility)

Lung tissue (bronchodilation) and skeletal muscle vasculature (relaxation)

Adipose (increased lypolysis)

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55
Q

α1 receptors are mostly involved in what organ system(s)?

α2 receptors are mostly involved in what organ system(s)?

What are their effects?

A

Systemic vasculature (constriction)

Cerebral vasculature (constriction)

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56
Q

β1 receptors are mostly involved in what organ system(s)?

β2 receptors are mostly involved in what organ system(s)?

β3 receptors are mostly involved in what organ system(s)?

What are their effects?

A

Heart tissue (increased contractility)

Lung tissue (bronchodilation) and skeletal muscle vasculature (relaxation)

Adipose (increased lypolysis)

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57
Q

α1 receptors are mostly involved in what organ system(s)?

β1 receptors are mostly involved in what organ system(s)?

β2 receptors are mostly involved in what organ system(s)?

What are their effects?

A

Systemic vasculature (constriction)

Heart tissue (increased contractility)

Lung tissue (bronchodilation) and skeletal muscle vasculature (relaxation)

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58
Q

Norepinephrine acts on which adrenergic receptors?

Epinephrine acts on which adrenergic receptors?

A

α1, α2, β1 (some β3)

α1, α2, β1, β2

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59
Q

Which catecholamine has a much stronger effect on β2 receptors?

A

Epinephrine

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60
Q

Do β-blockers typically block the β1 or β2 receptors?

Do β-blockers typically block the α1 or α2​ receptors?

A

Both;

neither

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61
Q

What are the five main cholinergic receptors and what organs do they affect?

A

Muscarinic

M1 - ganglia

M2 - heart

M3 - glands, smooth muscle

Nicotinic

Nm - NMJ

Nn - ganglia

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62
Q

What are the main M (muscarinic) cholinergic receptors and what organs do they affect?

A

Muscarinic

M1 - ganglia

M2 - heart

M3 - glands, smooth muscle

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63
Q

What are the main N (nicotinic) cholinergic receptors and what organs do they affect?

A

Nicotinic

Nm - NMJ

Nn - ganglia

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64
Q

What substance is an agonist for every cholinergic receptor (M1, M2, M3, Nn, Nm)?

A

Acetylcholine

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65
Q

What drug blocks muscarinic (M1, M2, M3) receptors?

What drug blocks nicotinic (Nn, Nm) receptors?

A

Atropine;

nicotine (also an agonist)

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66
Q

The __ receptor is activated by __________ and decreases heart rate and contractility.

The __ receptor is activated by __________ and increases heart rate and contractility.

A

M2, acetylcholine;

β1, catecholamines (norepi., epi., dopamine)

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67
Q

What substance is an agonist for the α1 and β1 receptors, but not the α2 or β2?

A

Dopamine (also D1)

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68
Q

What adrenergic receptors are activated by dopamine?

A

α1, β1, D1

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69
Q

What adrenergic receptor acts on the heart?

What adrenergic receptor acts (weakly) on the skeletal muscle vasculature?

What adrenergic receptor acts on the systemic arteries/arterioles?

What adrenergic receptor acts on the lungs?

What adrenergic receptor acts on the cerebral arteries/arterioles?

What adrenergic receptor acts on the adipocytes?

A

β1

β2

α1

β2

α2

β3

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70
Q

What cholinergic receptors act on ganglia?

What cholinergic receptor acts on glands and smooth muscle?

What cholinergic receptor acts on the neuromuscular junction?

What cholinergic receptor acts on the heart?

A

M1, Nn

M3

Nm

M2

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71
Q

True/False.

α1 receptors act on resistance arterioles and capacitance veins.

A

True.

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72
Q

True/False.

Although mainly responsible for systemic vasoconstriction, the sympathetic nervous system also plays a major role in vasodilation in skeletal muscle.

A

False.

This is almost entirely regulated via metabolite concentrations.

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73
Q

True/False.

Norepinephrine is generally responsible for systemic vasoconstriction.

AND

Epinephrine is generally responsible for vasodilation in the lungs, heart, and skeletal muscle.

A

True.

(Although there is much overlap in function between the two.)

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74
Q

What mechanism is responsible for most of the vasoconstriction that occurs in the skin (this being the main form of vascular regulation the skin receives)?

A

Sympathetic innervation

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75
Q

What causes vasodilation of vessels in the skin?

What causes vasoconstriction of vessels in the skin?

A

A lack of sympathetic input;

increased sympathetic input

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76
Q

What are the main adrenergic receptors activated by dopamine?

A

D<strong>1</strong> (renal tubules vasodilation and diuresis)

α1 (systemic vasoconstriction)

β1 (increased heart rate and contractility)

(Throw one dab of dopamine on that)

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77
Q

What is the overall effect of D1, α1, and β1 receptor activation by dopamine?

A

Shunting blood towards the kidneys

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78
Q

While the vast majority of vascular regulation comes from sympathetic innervation, what vasculature does receive parasympathetic input?

A

Vessels of the:

salivary gland,

some cerebral tissues,

gastrointestinal glands

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79
Q

Via what mechanism can acetylcholine cause vasodilation in some tissues?

A

Increased NO release from endothelial cells

–> increased cGMP in smooth myocytes

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80
Q

True/False.

The brain induces vasoconstriction and vasodilation to shunt blood around the body to various locations, and it is the main control center for this shunting.

A

False.

The brain mostly uses vasoconstriction (sympathetic);

the majority of shunting control comes from local metabolite concentrations

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81
Q

What hormonal effects cause vasoconstriction?

What hormonal effects cause vasodilation?

A

Renin-angiotensin system,

ADH,

epinephrine (if at α1 receptors);

ANP (potent),

VIP

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82
Q

What hormone can the brain release to say ‘I’m not being perfused enough.’

What hormone can the heart release to say ‘I’m too stretched out.’

What hormone can the GI tract release to say ‘I’m not being perfused enough.’

A

ADH (hypothalamus/neurohypophysis),

epinephrine (from adrenal medulla);

ANP;

VIP

83
Q

What system can the kidneys use to say ‘I’m not being perfused enough.’

A

Renin-angiotensin system

84
Q

What is myogenic reflex?

A

An intrinsic method of perfusion control –>

When stretched/dilated, smooth muscle around arterioles constricts.

When pressure drops, smooth muscle around arterioles relaxes.

(note: in the image, the vessel is trying to maintain a pressure of ~100 mmHg)

85
Q

When stretched/dilated by increases in pressure, arteriolar smooth muscle does what?

When confronted with decreases in pressure, arteriolar smooth muscle does what?

A

Constricts (to decrease pressure/flow to the area);

dilates (to increase pressure/flow to the area)

86
Q

Where is myogenic response especially strong/important?

A

The brain

87
Q

Myogenic reflex to pressure changes works to keep cerebral BP in what range?

A

50 - 150 mmHg

(centered around 100 mmHg)

88
Q

What are the two main extrinsic mechanisms of vascular tone regulation?

What are the two main intrinsic mechanisms of vascular tone regulation?

A

Neural innervation (mainly sympathetic –> vasoconstriction),

hormonal (renin-angiotensin, ADH, ANP, VIP, etc.);

local metabolites (mainly vasodilation),

myogenic response

89
Q

What are the main metabolites causing a decrease in vascular tone in tissues?

A

CO2

H+

K+

prostacyclin (PGI2)

adenosine

NO

90
Q

Highly metabolically active tissues will have a buildup of waste metabolites in the surrounding fluids.

What are some examples of these, and what will the effect be on vascular tone?

A
  • CO2*
  • H+*
  • K+*
  • adenosine*

decrease in tone –> smooth muscle relaxation

91
Q

Decreased pH promotes open ____ channels in vascular smooth muscle in metabolically active tissues.

A

KATP

(and resultant hyperpolarization –> relaxation)

92
Q

Decreasing pH has what effect on vascular tone?

For what purpose?

A

Decreased vascular tone;

to increase blood flow to the area –> wash away the metabolites and bring more O2

93
Q

How does exercise result in shunting of blood towards skeletal muscle?

A

Increase in metabolites (CO2, H+, K+, adenosine) cause vasodilation

94
Q

How does eating result in shunting of blood towards the GI tract?

A

Increase in metabolites (CO2, H+, K+, adenosine) cause vasodilation

95
Q

Why does hyperemia occur in cardiac tissue following an MI?

A

Ischemic conditions and an increase in metabolites (CO2, H+, K+, adenosine) cause vasodilation

96
Q

What two endothelium-dependent substances decrease vascular tone?

What endothelium-dependent substance increases vascular tone?

A

Prostacyclin (PGI2),

NO;

endothelin

97
Q

Describe the general effect of each of the following on vascular tone:

PGI2 (prostacyclin)

Endothelin

NO

A

Vasodilation

Vasoconstriction

Vasodilation

98
Q

Prostacyclin (PGI2) increases concentrations of what substance in smooth muscle?

A

cAMP

(promoting relaxation and dilatation)

99
Q

NO increases concentrations of what substance in smooth muscle?

A

cGMP

(promoting relaxation and dilatation)

100
Q

True/False.

Nitric oxide has a very, very short half-life and is great for short-term decreases in vascular tone.

A

True.

101
Q

How is PGI2 (prostacyclin) released from endothelial cells?

A

In response to increased pressures and shear stress

102
Q

Endothelin increases concentrations of what substances in smooth muscle?

A

IP3, Ca2+

(promoting vasoconstriction)

103
Q

Adenosine has what effect on vascular smooth muscle?

Where does it come from?

A

Vasodilation;

ATP –> ADP –> AMP –> Adenosine

104
Q

Prostacyclin (PGI2) increases concentrations of what notable substance(s) in smooth muscle?

Endothelin increases concentrations of what notable substance(s) in smooth muscle?

Nitric oxide increases concentrations of what notable substance(s) in smooth muscle?

A

cAMP (vasodilate)

IP3, Ca2+ (vasoconstrict)

cGMP (vasodilate)

105
Q

Where do nitric oxide and PGI2 (prostacyclin) come from?

A

Endothelial cells

106
Q

Release of what substance causes bronchoconstriction and widespread vasodilation in anaphylaxis?

A

Histamine

(from mast cells)

107
Q

True/False.

Antihistamines are ideal treatments for the bronchoconstriction and widespread vasodilation found in anaphylaxis.

A

False.

The histamine has already bound its H1 and H2 receptors; antihistamines have no effect if it has already bound.

Epinephrine is the ideal medication for this situation.

108
Q

What is the main factor that causes vasoconstriction?

What is the main factor that causes vasodilation?

A

Sympathetic input;

local metabolites (CO2, H+, K+, adenosine)

109
Q

What is another name for prostacyclin?

A

PGI2

110
Q

What is another name for PGI2?

A

Prostacyclin

111
Q

Nitric oxide has ____-atherosclerotic effects.

Endothelin has ____-atherosclerotic effects.

A

Anti;

pro

112
Q

Cardiac output (CO) =

Mean arterial pressure (MAP) =

A

CO = SV * HR

MAP = CO * TPR

113
Q

What is the intrinsic method of cardiac output control?

A

The Frank-Starling mechanism

114
Q

What is the primary method of heart rate control?

A

Autonomic balance

115
Q

At resting conditions, which has a greater effect on the heart, sympathetic or parasympathetic innervation?

A

Parasympathetic

116
Q

What are the two main effects of ADH release?

What causes its secretion?

A

Vasoconstriction (V1), water reabsorption (V2);

increased serum osmolarity, decreased BP

117
Q

Atrial natruretic peptide is released in response to:

It is a potent:

A

Atrial stretch;

vasodilator

118
Q

What nerve senses the Bainbridge atrial reflex?

What occurs?

A

Vagal afferents;

atrial stretch –> increased HR

119
Q

Atrial stretch leads to what effects?

A

Increased HR (Bainbridge reflex via vagal afferents);

ANP release (vasodilation and diuresis);

decreased ADH release

120
Q

What receptor does ADH activate in the vasculature?

What receptor does ADH activate in the renal collecting ducts?

A

V1 (vasoconstriction);

V2 (water reabsoprtion)

121
Q

What is the single most important regulator of blood pressure that helps the body maintain steady, consistent pressures?

A

Baroreceptors (e.g. carotid sinus, aortic arch)

122
Q

What causes increased firing of a baroreceptor in the carotid sinus or aortic arch?

A

Carotid or aortic stretch

123
Q

Vagal afferents from the heart, sympathetic nerves to the heart, and the baroreceptors all connect to what location?

A

The cardiovascular control center (medulla oblongata)

124
Q

Increased baroreceptor firing (due to stretch in the carotid sinus or aortic arch) causes what change in effect in the cardiovascular control center?

A

Decreased sympathetic firing / increased parasympathetic firing

125
Q

Decreased baroreceptor firing (due to relaxation in the carotid sinus or aortic arch) causes what change in effect in the cardiovascular control center?

A

Increased sympathetic firing / decreased parasympathetic firing

126
Q

Increases in atrial stretch will cause what to happen to heart rate via the Bainbridge reflex?

Increases in carotid or aortic sinus stretch will cause what to happen to heart rate via the baroreceptor reflex?

A

Increased HR;

decreased HR

127
Q

Which dominates during situations of increased central venous pressure, the Bainbridge (atrial stretch) reflex or the baroreceptor reflex?

Which dominates during situations of decreased central venous pressure, the Bainbridge (atrial stretch) reflex or the baroreceptor reflex?

A

Bainbridge reflex;

baroreceptor reflex

128
Q

The Bainbridge (atrial stretch) reflex dominates over the baroreceptor reflex during situations of __________ central venous pressure.

A

Increased

129
Q

The baroreceptor reflex dominates over the Bainbridge (atrial stretch) reflex during situations of __________ central venous pressure.

A

Decreased

130
Q

____________ in the carotid sinus and aortic arch sense changes in stretch (blood pressure).

____________ in the carotid body and aortic arch sense changes in pH, CO2, and O2.

A

Baroreceptors;

chemoreceptors

131
Q

Baroreceptors in the carotid sinus and aortic arch sense changes in _______ _______.

Chemoreceptors in the carotid body and aortic arch sense changes in __, __, and __.

A

Blood pressure;

pH, CO2, O2

132
Q

What is the primary effect of chemoreceptor activation (low pH, high PCO2, low PO2)?

What is the secondary (and overall) effect?

A

An increase in parasympathetic activity –> decrease in heart rate;

an increase in respiratory rate and a resulting inhibition of the medulla oblongata (where the cardiovascular control center is) –> increase in heart rate

133
Q

Unlike baroreceptor activity, chemoreceptor activity initially causes a(n) _________ in parasympathetic activity in response to hypotension and ischemia.

A

Increase

(Note: this results in increased respiratory rate and inhibition of the medulla oblongata as secondary effects –> increased heart rate)

134
Q

What will happen to an individual’s heart rate if they stop breathing (drowning, tracheal blockage, etc.)?

Why?

A

The heart will slow and eventually stop;

  1. Chemoreceptors sense ischemic conditions –> increase parasympathetic activity –> slowed heart rate
  2. Decreased respiratory rate –> no inhibition of medulla oblongata excitatory pathways –> medulla slows heart rate
135
Q

Under what conditions are chemoreceptors activated?

A

Hypoxia and severe hypotension

136
Q

Increased respiratory rate has what effect on the cardiovascular control center of the medulla oblongata?

(This has what effect on the heart?)

A

Inhibition of pathways that excite the medulla oblongata

(So, it stops medulla pathways that inhibit the heart –> heart rate increases)

137
Q

What is the overall effect of chemoreceptor activation (low pH, high PCO2, low PO2) on heart rate?

A

Heart rate increases

  • (increased sympathetic outflow;*
  • decreased parasympathetic outflow)*
138
Q

How does increased respiratory rate affect the medulla oblongata?

Via what mechanism?

How does this affect the heart?

A

It depresses medullary function;

hypocapnia,

lung stretch;

increased HR

139
Q

The primary effect of the chemoreceptor activation is to ____________ (activate/inactivate) the medulla.

The secondary effect of the chemoreceptor activation is to ____________ (activate/inactivate) the medulla.

A

Activate (supressing HR);

inactivate (increasing HR)

140
Q

Chemoreceptors are often activated by hypotension and hypoxic conditions. What is the purpose of chemoreceptor firing?

A

To increase respiratory rate –>

to increase HR –>

to boost BP

141
Q

What is the first (and quickest) compensatory mechanism to sense and respond to changes in blood pressure?

A

Baroreceptors

142
Q

In order, what are the three quickest mechanisms by which the body tries to adapt to large drops in blood pressure?

(Note: All 3 act within seconds.)

A
  1. Baroreceptors (increased sympathetic firing)
  2. Chemoreceptors (increased respiration and heart rate)
  3. CNS ischemia response (huge sympathetic outflow)
143
Q

If blood pressure drops, how long does it take for baroreceptors to increase sympathetic activity?

If blood pressure drops, how long does it take for the renin-angiotensin system to kick in?

If blood pressure drops, how long does it take for aldosterone to be released?

A

Seconds;

minutes;

hours

144
Q

True/False.

If blood pressure falls low enough, interstitial fluid will begin to be resorped back into the bloodstream through the switch in pressure gradient.

A

True.

(This is called capillary fluid shift.)

145
Q

At what blood pressure will baroreceptors no longer fire at all?

I.e. the firing rate will decrease until what level when it stops completely?

(Note: they try to maintain MAP at around 100 mmHg.)

A

50 mmHg

146
Q

At what blood pressure does the CNS ischemic response really kick in?

A

~40 mmHg

147
Q

Why does the CNS ischemic response (huge sympathetic last-ditch effort to save the brain) kick in when blood pressure drops ≤ 40 mmHg?

A

We are below the level at which the myogenic response is useful, and the neurons are not being perfused

148
Q

What is the CNS ischemic response?

A

A huge sympathetic outflow

(a last-ditch effort to save the brain at low BP)

149
Q

If a patient has chronic hypertension, what will happen with baroreceptor firing?

A

It will create a new ‘set point’ at a higher BP so that it isn’t aggressively firing all the time

150
Q

True/False.

The baroreceptors are virtually always firing to some degree and suppressing parasympathetic activity.

A

False.

The baroreceptors are virtually always firing to some degree (above 50 mmHg) and suppressing sympathetic activity.

151
Q

What is a fourth factor involved in cardiac output besides contractility, afterload, and preload?

A

Heart rate

152
Q

By using branching arteries (parallel resistance instead of one continuous loop), identify which of the following is affected most:

contractility

preload

afterload

A

Afterload

153
Q

How much greater is venous compliance vs. arterial complaince?

(Note: compliance = ΔV / ΔP)

A

20:1

154
Q

What effect does the fact that the venous system has 20x the compliance of the arterial system have on blood partioning?

A

Compliance = ΔV / ΔP

Therefore, the low pressure and much larger compliance of the venous system means that much more blood can be held there than in the arterial side

155
Q

Is there normally a much larger amount of fluid in the veins than in the arteries?

(The veins do have a much larger compliance {ΔV / ΔP] after all.)

A

Not necessarily, the heart pushing against the TPR of the arteries helps to boost the pressure on the arterial side and equalize the two volumes

(despite the 20x larger compliance of the venous system)

156
Q

What does a vascular function curve show?

A

How changes in cardiac output and central venous pressure affect each other

ΔCO <—> ΔCVP

157
Q

If the pressures on the arterial side and the venous side were the same (the heart has stopped beating), how much more blood would be in the venous system than the arterial?

(Remember, compliance is ΔV / ΔP.)

A

20:1

158
Q

So, if venous compliance (ΔV / ΔP) is 20:1 of that of arterial compliance, what effect would a 40 mmHg drop in arterial pressure have on venous pressure?

what effect would a 30 mmHg drop in arterial pressure have on venous pressure?

what effect would a 20 mmHg drop in arterial pressure have on venous pressure?

A

2 mmHg increase in venous pressure

1.5 mmHg increase in venous pressure

1 mmHg increase in venous pressure

159
Q

According to the 20:1 difference in compliances (ΔV / ΔP) between the venous and arterial systems, how much pressure is needed in the arterial system to flow 1 L into the venous system?

And 2 liters?

A

~27 mmHg

(20 mmHg per L added onto the baseline pressure if the heart wasn’t pumping [7 mmHg])

~47 mmHg

160
Q

Increases of __ mmHg on the arterial side lead to 1 mmHg _________ on the venous side and __ more L flow.

A

20,

decreases,

1

161
Q

True/False.

When the heart is not beating, the venous and arterial pressures will equlibrate to 0 mmHg, and there will be near equal amount of blood in both systems.

A

False.

The baseline pressure will be 7 mmHg on both sides,

and there will be 20x more blood in the venous system.

Compliance = ΔV / ΔP = 20x greater in the venous system

162
Q

True/False.

Central venous pressure determines preload.

MAP determines afterload.

A

True.

163
Q

A patient’s systolic blood pressure drops to 65 mmHg over a period of three hours following a wound to his femoral artery.

Which pressure response system is likely the most involved in maintaining his blood pressure?

A

Chemoreceptors

164
Q

A patient’s systolic blood pressure drops to 85 mmHg following childbirth. Which pressure response system is likely the most involved in maintaining her blood pressure?

A

Baroreceptors

165
Q

A patient’s systolic blood pressure drops to 38 mmHg over a period of a few minutes after the loss of a limb in a traffic accident.

Which pressure response system is likely the most involved in maintaining her blood pressure?

A

The CNS ischemic response

(huge sympathetic outflow)

166
Q

Vascular function curves map central venous pressure against cardiac output.

What is the relationship between the two?

A

Inversely correlated

167
Q

What is the purpose of a vascular function curve?

A

To identify the CVP for a given cardiac output

168
Q

What will happen to the vascular function curve (CVP plotted against CO) during a blood transfusion?

A

All pressures increase –> right shift –> CO increases

(red line)

169
Q

What will happen to the vascular function curve (CVP plotted against CO) during hemorrhage?

A

All pressures decrease –> left shift –> CO decreases

(green line)

170
Q

Describe the effects of either transfusion or hemorrhage on a vascular function curve.

A
171
Q

What is ‘static pressure’ in terms of CVP and CO?

A

Baseline pressure if the heart weren’t beating

(~7 mmHg)

172
Q

Describe the effects that vasoconstriction and vasodilation will each have on a vascular function curve.

A
173
Q

Describe the effect(s) that vasoconstriction will have on a vascular function curve.

A
174
Q

Describe the effect(s) that vasodilation will have on a vascular function curve.

A
175
Q

What effect will increasing TPR (vasoconstriction) have on cardiac output?

A

It will decrease cardiac output

176
Q

What effect will decreasing TPR (vasodilation) have on cardiac output?

A

It will increase cardiac output

177
Q

Why does a vascular function curve show a flat line at CVP = 0 mmHg, indicating no increase in cardiac output?

A

The venous system can’t go to negative pressures (this is just vessel collapse), so there is nothing left for the heart to withdraw/suck/pull from the venous side to pump to the arterial side.

178
Q

Do changes in blood volume change central venous pressure?

Do changes in arterial constriction or dilation change central venous pressure?

A

Yes, all pressures change.

No, cardiac output changes.

179
Q

What two graphs can be combined to allow us to understand how preload changes in response to changes in cardiac output?

(Ex. how would the body change central venous pressure if stroke volume increases?)

A

The cardiac function curve (Frank-Starling)

The vascular function curve

180
Q

If a previously healthy individual (intersection of the red & green lines) goes into heart failure, how will central venous pressure change to maintain cardiac output?

(The person was at point A. They shifted to B. What happens next?)

A

CVP increases to bring them to D

(back to their normal CO)

181
Q

If a previously healthy individual goes into heart failure, how will central venous pressure change to maintain cardiac output?

How does it accomplish this?

A

CVP increases

(they drop from A to B , then CVP increases and they’re back to their normal CO [D]);

blood volume increases (e.g. reduced diuresis)

182
Q
A

C. Decreased myocardial contractility

183
Q
A

C

  • (reduced volume: A –> B;*
  • reduced contractility: B –> C)*
184
Q

True/False.

Prolonged, severe hemorrhage decreases contractility.

A

True.

185
Q

What effect does exercise have on total peripheral resistance?

A

An overall decrease

(although sympathetic activation leads to vasoconstriction, the vasodilation in the skeletal muscle outweighs this systemic constriction)

186
Q

Total peripheral resistance decreases during exercise (due to vasodilation in skeletal muscle). Does this cause a drop in blood pressure?

A

No.

The baroreceptors notice the decrease in stretch and fire less, allow sympathetic tone to increase

187
Q

In what state are the veins during the anticipatory phase of exercise (preparing to begin workout)?

A

Venoconstriction begins –> increased preload

188
Q

What two main occurrences are responsible for the changes in blood flow during the anticipatory phase of exercise (preparing for exercise)?

A
  1. Increased sympathetic firing
  2. Venoconstriction
189
Q

How does cutaneous blood flow fluctuate during exercise (before and during)?

A

Beginning exercise –> cutaneous flow is reduced

Bradykinin is released –> cutaneous flow is increased

Severe exercise –> sympathetic outflow overcomes bradykinin mechanism –> cutaneous flow is reduced

190
Q

Upon ceasing exercise, what will happen to blood pressure?

What mechanism halts this process?

A

It drops;

the baroreceptor reflex

191
Q

Do any of the following decrease during exercise?

Heart rate

Stroke volume

Cardiac output

Arteriovenous O2 difference

Total peripheral resistance

O2 consumption

Arterial pressure

A

Total peripheral resistance only

192
Q

How does cerebral blood flow fluctuate during exercise?

A

It does not.

The myogenic response keeps it relatively constant

193
Q

Below what blood pressure is the baroreceptor no longer firing?

A

~60 mmHg MAP

194
Q

Chemoreceptors are the predominant blood pressure control mechanism in what blood pressure range?

A

40 - 60 mmHg MAP

195
Q

At what MAP ranges are each of the following the dominant force increasing blood pressure?

Baroreceptors

Chemoreceptors

CNS ischemic response

A

Baroreceptors > 60 mmHg

Chemoreceptors 40 - 60 mmHg

CNS ischemic response < 40 mmHg

196
Q

Does blood osmolarity change at all in response to hemorrhage?

A

Yes.

It decreases (interstitial fluid is absorbed in the capillary fluid shift, diluting the blood)

197
Q

Via what mechanism does the CNS ischemic response increase blood pressure?

At what mean arterial BP (MAP) does it become active?

A

Major sympathoadrenal outflow;

< 40 mmHg

198
Q

What do ischemic tissues release to promote coagulation and try to prevent further blood loss?

A

Thromboxane

199
Q

True/False.

Severe, prolonged hemorrhage is reversed by all the following:

Opioid release by ischemic cerebral tissues

Metabolic acidosis (lactic)

Thromboxane release by ischemic tissues

Increased thrombosis due to slowed blood flow

A

False.

All of these are decompensatory mechanisms, exacerbating tissue ischemia

200
Q

Will cardiac output respond well to fluids in cases of severe, prolonged (> 3 or 4 hours) hypovolemic shock?

A

No.

(See curve F.)

201
Q

In cases of hypovolemic shock, how long does it take (on average) for the Frank-Starling curve to decrease from A to F on this chart?

What does this mean for patient outcomes?

A

> 3 - 4 hours;

in cases of prolonged hemorrhage, decompensatory mechanisms prevent CO from responding well to fluid infusions

202
Q

Why is a patient that has been hemorrhaging for more than 3 or 4 hours very unlikely to make a recovery?

What are some examples of why this would be the case?

A

Decompensatory mechanisms

Opioid (depressing) release by ischemic cerebral tissues

Metabolic (lactic) acidosis drives down cardiac response

Increased thrombosis (thromboxane release by ischemic tissues + slowed blood flow)

203
Q

What are some examples of decompensatory mechanisms that exacerbate hemovolemic shock several hours (≥ ~4) after the compensatory have already tried to restore mean arterial pressure?

A

Opioid (depressing) release by ischemic cerebral tissues

Metabolic (lactic) acidosis drives down cardiac response

Increased thrombosis due to thromboxane release by ischemic tissues and/or slowed blood flow

204
Q

Endotoxins and cytokines that cause a systemic inflammatory response (and widespread vasodilation and inflammation) are increasing intracellular concentrations of what molecule(s)?

A

Nitric oxide (and cGMP) –> vasodilation;

free radicals –> inflammation

T1 - Phase 1 - Integrated (I) (28 decks)

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