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

Question 1

What is fluid velocity?

Answer 1

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

Question 2

What is fluid flow?

Answer 2

The amount of fluid traveling a distance per time

Q = velocity * area

Question 3

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?

Answer 3

The flow rate will remain the same BECAUSE

–>

the velocity decreases

Q = vA

Question 4

What two factors affect flow rate in the cardiovascular system?

Answer 4

Fluid velocity and vessel cross-sectional area

Q = vA

Question 5

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

Answer 5

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

Question 6

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

Answer 6

Laminar = efficient, protective

Turbulent = damaging, chaotic

Question 7

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

Answer 7

The central layers

(the outer layers interact with the sationary walls)

Question 8

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?

Answer 8

It is turbulent and noisy;

it is laminar and smooth

Question 9

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)

Answer 9

Blood density,

*diameter of the blood vessel,

*blood velocity;

blood viscosity

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

Question 10

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?

Answer 10

Velocity

(diameter follows a linear change;

velocity will respond in a squared change)

v = Q / (πr²)

Question 11

Is velocity higher in a narrow or wide vessel lumen?

Answer 11

Narrow

v = Q / (πr²)

Question 12

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?

Answer 12

Elasticity;

distensibility;

compliance

Question 13

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

Answer 13

Loss of elastin

(less elasticity)

Question 14

Why are both blood vessel distensibility and elastance desirable?

Answer 14

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.

Question 15

What controls the rate of blood flow?

I.e. what does the heart push against?

Answer 15

Peripheral resistance

Q = ΔP / R

Question 16

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

What equation shows us all the variables creating that resistance?

Answer 16

R = 8 * η * l / πr⁴

(8 * viscosity * length / πr⁴)

Question 17

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

Answer 17

velocity = Q / πr²

Resistance to flow = 8ηl / πr⁴

Question 18

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

Answer 18

A 16-fold increase

R = 8 * η * l / πr⁴

Question 19

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

Answer 19

A 3.2-fold increase

R = 8 * η * l / πr⁴

Question 20

Resistors in sequence are calculated as:

Resistors in parallel are calculated as:

Answer 20

R₁ + R₂ + R₃ = R_Total

1/R₁ + 1/R₂ + 1/R₃ = 1/R_Total

Question 21

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

Answer 21

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

Question 22

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?

Answer 22

Differing blood flow through differing organs;

the heart pushes against less resistance

Question 23

Increases in what two factors increase resistance to blood flow?

Increases in what single factor decrease resistance to blood flow?

Answer 23

Blood viscosity, vessel length

vessel lumen radius

R = 8 * η * l / πr⁴

Question 24

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

Answer 24

An individual that has already had a heart attack

Question 25

Why would having a single vessel loop be an inefficient structure for the circulatory system? How does the body get around this problem?

Answer 25

Resistance would be huge; parallel vessels (reducing resistance and allowing for varying flow rates)

Question 26

Where is resistance high and flow slowest in the cardiovascular system? Elastic arteries Muscular arteries Arterioles Capillaries Venules Medium veins Large veins

Answer 26

Capillaries (smallest radius --\> R = 8 \* η \* l / π**r⁴**)

Question 27

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

Answer 27

Question 28

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

Answer 28

The arterioles

Question 29

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

Answer 29

Metarterioles

Question 30

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

Answer 30

Hydrostatic pressure; oncotic pressure

Question 31

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

Answer 31

**Filtration** (via channels and pores), **diffusion**, **pinocytosis**

Question 32

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

Answer 32

It is relatively constant across the bed; the arterial end

Question 33

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

Answer 33

Q_f = k[(P_c - P_i) - (π_c - π_i)] = ΔP - Δπ

Question 34

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

Answer 34

Decrease

Question 35

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

Answer 35

Vasodilation

Question 36

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)?

Answer 36

**T = P\*r / 2** *wall tension = internal pressure \* radius / 2* **T = P\*r** *wall tension = internal pressure \* radius*

Question 37

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?

Answer 37

Arterioles; capillaries; veins

Question 38

**True/False.** The venous system is highly compliant.

Answer 38

True.

Question 39

Compliance = Δ\_\_ / Δ\_\_

Answer 39

V, P

Question 40

**True/False.** Arterial pulsation can help compress nearby veins and push the blood back towards the heart.

Answer 40

True.

Question 41

Where in the body are veins thickest and least compliant?

Answer 41

The lower limbs

Question 42

**True/False.** Lymphatic vessels have abundant tight junctions.

Answer 42

False.

Question 43

What layers make up a venule?

Answer 43

Endothelium + a small layer of fibrous tissue

Question 44

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

Answer 44

Immediate bedrest to decrease risk of PE

Question 45

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

Answer 45

Leg elevation (damaged valves means the blood flow will easily become retrograde) *(e.g. exercise will push the blood in both directions)*

Question 46

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

Answer 46

**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)*

Question 47

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

Answer 47

Question 48

What is cardiac output at resting state? What is cardiac output during heavy exercise?

Answer 48

5 L / min 25 L / min

Question 49

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

Answer 49

Changes in metabolite levels | (e.g. adenosine, K⁺, O₂, CO₂)

Question 50

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

Answer 50

**cGMP** and/or **cAMP**

Question 51

Increases in extracellular K⁺ causes smooth muscle \_\_\_\_\_\_\_\_\_\_\_\_\_.

Answer 51

Relaxation

Question 52

Increases in ______________ \_\_⁺ causes smooth muscle relaxation.

Answer 52

Extracellular K

Question 53

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

Answer 53

Systemic vasoconstriction ONLY

Question 54

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)?

Answer 54

**Systemic vasculature** (constriction) **Cerebral vasculature** (constriction) **Heart tissue** (increased contractility) **Lung tissue** (bronchodilation) and **skeletal muscle vasculature** (relaxation) **Adipose** (increased lypolysis)

Question 55

α₁ receptors are mostly involved in what organ system(s)? α₂ receptors are mostly involved in what organ system(s)? What are their effects?

Answer 55

**Systemic vasculature** (constriction) **Cerebral vasculature** (constriction)

Question 56

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?

Answer 56

**Heart tissue** (increased contractility) **Lung tissue** (bronchodilation) and **skeletal muscle vasculature** (relaxation) **Adipose** (increased lypolysis)

Question 57

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?

Answer 57

**Systemic vasculature** (constriction) **Heart tissue** (increased contractility) **Lung tissue** (bronchodilation) and **skeletal muscle vasculature** (relaxation)

Question 58

Norepinephrine acts on which adrenergic receptors? Epinephrine acts on which adrenergic receptors?

Answer 58

α₁, α₂, β₁ (some β₃) α₁, α₂, β₁, β₂

Question 59

Which catecholamine has a much stronger effect on β₂ receptors?

Answer 59

Epinephrine

Question 60

Do β-blockers typically block the β₁ or β₂ receptors? Do β-blockers typically block the α₁ or α₂​ receptors?

Answer 60

Both; neither

Question 61

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

Answer 61

**Muscarinic** M₁ - ganglia M₂ - heart M₃ - glands, smooth muscle **Nicotinic** N_m - NMJ N_n - ganglia

Question 62

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

Answer 62

**Muscarinic** M₁ - ganglia M₂ - heart M₃ - glands, smooth muscle

Question 63

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

Answer 63

**Nicotinic** N_m - NMJ N_n - ganglia

Question 64

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

Answer 64

Acetylcholine

Question 65

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

Answer 65

Atropine; nicotine (also an agonist)

Question 66

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

Answer 66

M₂, acetylcholine; β₁, catecholamines (norepi., epi., dopamine)

Question 67

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

Answer 67

Dopamine (also D₁)

Question 68

What adrenergic receptors are activated by dopamine?

Answer 68

α₁, β₁, D₁

Question 69

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?

Answer 69

β₁ β₂ α₁ β₂ α₂ β₃

Question 70

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?

Answer 70

M₁, N_n M₃ N_m M₂

Question 71

**True/False.** α₁ receptors act on resistance arterioles _and_ capacitance veins.

Answer 71

True.

Question 72

**True/False.** Although mainly responsible for systemic vasoconstriction, the sympathetic nervous system also plays a _major_ role in vasodilation in skeletal muscle.

Answer 72

**False.** This is almost entirely regulated via metabolite concentrations.

Question 73

**True/False.** Norepinephrine is generally responsible for systemic _vasoconstriction_. AND Epinephrine is generally responsible for _vasodilation_ in the lungs, heart, and skeletal muscle.

Answer 73

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

Question 74

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)?

Answer 74

Sympathetic innervation

Question 75

What causes vasodilation of vessels in the skin? What causes vasoconstriction of vessels in the skin?

Answer 75

A lack of sympathetic input; increased sympathetic input

Question 76

What are the main adrenergic receptors activated by dopamine?

Answer 76

**D**₁ (renal tubules vasodilation and diuresis) **α₁** (systemic vasoconstriction) **β₁** (increased heart rate and contractility) (Throw _one_ _dab_ of dopamine on that)

Question 77

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

Answer 77

Shunting blood towards the kidneys

Question 78

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

Answer 78

Vessels of the: salivary gland, some cerebral tissues, gastrointestinal glands

Question 79

Via what mechanism can acetylcholine cause vasodilation in some tissues?

Answer 79

Increased NO release from endothelial cells --\> increased cGMP in smooth myocytes

Question 80

**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.

Answer 80

**False**. The brain mostly uses vasoconstriction (sympathetic); the majority of shunting control comes from local metabolite concentrations

Question 81

What hormonal effects cause vasoconstriction? What hormonal effects cause vasodilation?

Answer 81

Renin-angiotensin system, ADH, epinephrine (if at α₁ receptors); ANP (potent), VIP

Question 82

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.'

Answer 82

ADH (hypothalamus/neurohypophysis), epinephrine (from adrenal medulla); ANP; VIP

Question 83

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

Answer 83

Renin-angiotensin system

Question 84

What is myogenic reflex?

Answer 84

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)

Question 85

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

Answer 85

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

Question 86

Where is myogenic response especially strong/important?

Answer 86

The brain

Question 87

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

Answer 87

50 - 150 mmHg ## Footnote *(centered around **100 mmHg**)*

Question 88

What are the two main _extrinsic_ mechanisms of vascular tone regulation? What are the two main _intrinsic_ mechanisms of vascular tone regulation?

Answer 88

Neural innervation (mainly sympathetic --\> vasoconstriction), hormonal (renin-angiotensin, ADH, ANP, VIP, etc.); local metabolites (mainly vasodilation), myogenic response

Question 89

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

Answer 89

CO₂ H⁺ K⁺ prostacyclin (PGI₂) adenosine NO

Question 90

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?

Answer 90

* CO₂* * H⁺* * K⁺* * adenosine* decrease in tone --\> smooth muscle relaxation

Question 91

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

Answer 91

K_ATP (and resultant hyperpolarization --\> relaxation)

Question 92

Decreasing pH has what effect on vascular tone? For what purpose?

Answer 92

Decreased vascular tone; to increase blood flow to the area --\> wash away the metabolites and bring more O₂

Question 93

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

Answer 93

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

Question 94

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

Answer 94

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

Question 95

Why does hyperemia occur in cardiac tissue following an MI?

Answer 95

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

Question 96

What two endothelium-dependent substances decrease vascular tone? What endothelium-dependent substance increases vascular tone?

Answer 96

Prostacyclin (PGI₂), NO; endothelin

Question 97

Describe the general effect of each of the following on vascular tone: PGI₂ (prostacyclin) Endothelin NO

Answer 97

Vasodilation Vasoconstriction Vasodilation

Question 98

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

Answer 98

cAMP | (promoting relaxation and dilatation)

Question 99

NO increases concentrations of what substance in smooth muscle?

Answer 99

cGMP | (promoting relaxation and dilatation)

Question 100

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

Answer 100

True.

Question 101

How is PGI₂ (prostacyclin) released from endothelial cells?

Answer 101

In response to increased pressures and **shear stress**

Question 102

Endothelin increases concentrations of what substances in smooth muscle?

Answer 102

IP₃, Ca²⁺ | (promoting vasoconstriction)

Question 103

Adenosine has what effect on vascular smooth muscle? Where does it come from?

Answer 103

Vasodilation; ATP --\> ADP --\> AMP --\> Adenosine

Question 104

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?

Answer 104

**cAMP** (vasodilate) **IP₃, Ca²⁺** (vasoconstrict) **cGMP** (vasodilate)

Question 105

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

Answer 105

Endothelial cells

Question 106

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

Answer 106

Histamine | (from mast cells)

Question 107

**True/False.** Antihistamines are ideal treatments for the bronchoconstriction and widespread vasodilation found in anaphylaxis.

Answer 107

**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.

Question 108

What is the main factor that causes vasoconstriction? What is the main factor that causes vasodilation?

Answer 108

Sympathetic input; local metabolites (CO₂, H⁺, K⁺, adenosine)

Question 109

What is another name for prostacyclin?

Answer 109

PGI₂

Question 110

What is another name for PGI₂?

Answer 110

Prostacyclin

Question 111

Nitric oxide has \_\_\_\_-atherosclerotic effects. Endothelin has \_\_\_\_-atherosclerotic effects.

Answer 111

Anti; pro

Question 112

Cardiac output (CO) = Mean arterial pressure (MAP) =

Answer 112

CO = SV \* HR MAP = CO \* TPR

Question 113

What is the intrinsic method of cardiac output control?

Answer 113

The Frank-Starling mechanism

Question 114

What is the primary method of heart rate control?

Answer 114

Autonomic balance

Question 115

At resting conditions, which has a _greater effect_ on the heart, sympathetic or parasympathetic innervation?

Answer 115

Parasympathetic

Question 116

What are the two main effects of ADH release? What causes its secretion?

Answer 116

Vasoconstriction (V₁), water reabsorption (V₂); increased serum osmolarity, decreased BP

Question 117

Atrial natruretic peptide is released in response to: It is a potent:

Answer 117

Atrial stretch; vasodilator

Question 118

What nerve senses the Bainbridge atrial reflex? What occurs?

Answer 118

Vagal afferents; atrial stretch --\> increased HR

Question 119

Atrial stretch leads to what effects?

Answer 119

Increased HR (Bainbridge reflex via vagal afferents); ANP release (vasodilation and diuresis); decreased ADH release

Question 120

What receptor does ADH activate in the vasculature? What receptor does ADH activate in the renal collecting ducts?

Answer 120

V₁ (vasoconstriction); V₂ (water reabsoprtion)

Question 121

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

Answer 121

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

Question 122

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

Answer 122

Carotid or aortic stretch

Question 123

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

Answer 123

The cardiovascular control center (medulla oblongata)

Question 124

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

Answer 124

**Decreased sympathetic** firing / **increased parasympathetic** firing

Question 125

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

Answer 125

**Increased sympathetic** firing / **decreased parasympathetic** firing

Question 126

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?

Answer 126

Increased HR; decreased HR

Question 127

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?

Answer 127

Bainbridge reflex; baroreceptor reflex

Question 128

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

Answer 128

Increased

Question 129

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

Answer 129

Decreased

Question 130

\_\_\_\_\_\_\_\_\_\_\_\_ in the carotid sinus and aortic arch sense changes in stretch (blood pressure). \_\_\_\_\_\_\_\_\_\_\_\_ in the carotid body and aortic arch sense changes in pH, CO_2, and O₂.

Answer 130

Baroreceptors; chemoreceptors

Question 131

Baroreceptors in the carotid sinus and aortic arch sense changes in _______ \_\_\_\_\_\_\_. Chemoreceptors in the carotid body and aortic arch sense changes in \_\_, \_\_, and \_\_.

Answer 131

Blood pressure; pH, CO₂, O₂

Question 132

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

Answer 132

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**

Question 133

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

Answer 133

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

Question 134

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

Answer 134

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

Question 135

Under what conditions are chemoreceptors activated?

Answer 135

Hypoxia and severe hypotension

Question 136

Increased respiratory rate has what effect on the cardiovascular control center of the medulla oblongata? (This has what effect on the heart?)

Answer 136

Inhibition of pathways that excite the medulla oblongata (So, it **stops** medulla pathways that **inhibit** the heart --\> heart rate increases)

Question 137

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

Answer 137

Heart rate increases ## Footnote * (increased sympathetic outflow;* * decreased parasympathetic outflow)*

Question 138

How does increased respiratory rate affect the medulla oblongata? Via what mechanism? How does this affect the heart?

Answer 138

It depresses medullary function; hypocapnia, lung stretch; increased HR

Question 139

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.

Answer 139

Activate (supressing HR); inactivate (increasing HR)

Question 140

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

Answer 140

To increase respiratory rate --\> to increase HR --\> to boost BP

Question 141

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

Answer 141

Baroreceptors

Question 142

In order, what are the three quickest mechanisms by which the body tries to adapt to large drops in blood pressure? ## Footnote *(Note: All 3 act within seconds.)*

Answer 142

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

Question 143

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?

Answer 143

Seconds; minutes; hours

Question 144

**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.

Answer 144

**True**. ## Footnote *(This is called capillary fluid shift.)*

Question 145

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.)

Answer 145

50 mmHg

Question 146

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

Answer 146

~40 mmHg

Question 147

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

Answer 147

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

Question 148

What is the CNS ischemic response?

Answer 148

A huge sympathetic outflow (a last-ditch effort to save the brain at low BP)

Question 149

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

Answer 149

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

Question 150

**True/False.** The baroreceptors are virtually always firing to some degree and suppressing parasympathetic activity.

Answer 150

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

Question 151

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

Answer 151

Heart rate

Question 152

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

Answer 152

Afterload

Question 153

How much greater is venous compliance vs. arterial complaince? (Note: compliance = ΔV / ΔP)

Answer 153

20:1

Question 154

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

Answer 154

*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

Question 155

Is there normally a much larger amount of fluid in the veins than in the arteries? ## Footnote *(The veins do have a much larger compliance {ΔV / ΔP] after all.)*

Answer 155

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 ## Footnote *(despite the 20x larger compliance of the venous system)*

Question 156

What does a vascular function curve show?

Answer 156

How changes in cardiac output and central venous pressure affect each other **ΔCO \<---\> ΔCVP**

Question 157

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? ## Footnote *(Remember, compliance is ΔV / ΔP.)*

Answer 157

20:1

Question 158

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?

Answer 158

2 mmHg increase in venous pressure 1.5 mmHg increase in venous pressure 1 mmHg increase in venous pressure

Question 159

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?

Answer 159

~27 mmHg (20 mmHg per L added onto the baseline pressure if the heart wasn't pumping [7 mmHg]) ~47 mmHg

Question 160

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

Answer 160

20, decreases, 1

Question 161

**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.

Answer 161

**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

Question 162

**True/False.** Central venous pressure determines preload. MAP determines afterload.

Answer 162

True.

Question 163

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?

Answer 163

Chemoreceptors

Question 164

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?

Answer 164

Baroreceptors

Question 165

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?

Answer 165

The CNS ischemic response | (huge sympathetic outflow)

Question 166

Vascular function curves map central venous pressure against cardiac output. What is the relationship between the two?

Answer 166

Inversely correlated

Question 167

What is the purpose of a vascular function curve?

Answer 167

To identify the CVP for a _given_ cardiac output

Question 168

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

Answer 168

**All pressures increase** --\> right shift --\> **CO increases** (red line)

Question 169

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

Answer 169

**All pressures decrease** --\> left shift --\> **CO decreases** (green line)

Question 170

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

Answer 170

Question 171

What is 'static pressure' in terms of CVP and CO?

Answer 171

Baseline pressure if the heart weren't beating (~7 mmHg)

Question 172

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

Answer 172

Question 173

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

Answer 173

Question 174

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

Answer 174

Question 175

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

Answer 175

It will decrease cardiac output

Question 176

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

Answer 176

It will increase cardiac output

Question 177

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

Answer 177

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.

Question 178

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

Answer 178

Yes, all pressures change. No, cardiac output changes.

Question 179

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?)

Answer 179

The **cardiac function curve** (Frank-Starling) The **vascular function curve**

Question 180

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?)*

Answer 180

CVP increases to bring them to D ## Footnote *(back to their normal CO)*

Question 181

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

Answer 181

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)

Question 182

Answer 182

C. Decreased myocardial contractility

Question 183

Answer 183

**C** * (reduced volume: A --\> B;* * reduced contractility: B --\> C)*

Question 184

**True/False.** Prolonged, severe hemorrhage decreases contractility.

Answer 184

True.

Question 185

What effect does exercise have on total peripheral resistance?

Answer 185

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

Question 186

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

Answer 186

**No.** The baroreceptors notice the decrease in stretch and fire less, allow sympathetic tone to increase

Question 187

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

Answer 187

**Venoconstriction** begins --\> increased preload

Question 188

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

Answer 188

1. Increased sympathetic firing 2. Venoconstriction

Question 189

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

Answer 189

Beginning exercise --\> cutaneous flow is reduced Bradykinin is released --\> cutaneous flow is increased Severe exercise --\> sympathetic outflow overcomes bradykinin mechanism --\> cutaneous flow is reduced

Question 190

Upon ceasing exercise, what will happen to blood pressure? What mechanism halts this process?

Answer 190

It drops; the baroreceptor reflex

Question 191

Do any of the following decrease during exercise? Heart rate Stroke volume Cardiac output Arteriovenous O₂ difference Total peripheral resistance O₂ consumption Arterial pressure

Answer 191

Total peripheral resistance _only_

Question 192

How does cerebral blood flow fluctuate during exercise?

Answer 192

It _does not_. The myogenic response keeps it relatively constant

Question 193

Below what blood pressure is the baroreceptor no longer firing?

Answer 193

~60 mmHg MAP

Question 194

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

Answer 194

40 - 60 mmHg MAP

Question 195

At what MAP ranges are each of the following the dominant force increasing blood pressure? Baroreceptors Chemoreceptors CNS ischemic response

Answer 195

Baroreceptors **\> 60 mmHg** Chemoreceptors **40 - 60 mmHg** CNS ischemic response **\< 40 mmHg**

Question 196

Does blood osmolarity change at all in response to hemorrhage?

Answer 196

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

Question 197

Via what mechanism does the CNS ischemic response increase blood pressure? At what mean arterial BP (MAP) does it become active?

Answer 197

_Major_ sympathoadrenal outflow; \< 40 mmHg

Question 198

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

Answer 198

Thromboxane

Question 199

**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

Answer 199

**False**. All of these are decompensatory mechanisms, exacerbating tissue ischemia

Question 200

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

Answer 200

No. | (See curve F.)

Question 201

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?

Answer 201

\> 3 - 4 hours; in cases of prolonged hemorrhage, decompensatory mechanisms prevent CO from responding well to fluid infusions

Question 202

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?

Answer 202

**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)

Question 203

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?

Answer 203

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

Question 204

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

Answer 204

**Nitric oxide (and cGMP)** --\> vasodilation; **free radicals** --\> inflammation