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CVPR > CVPR Week 6: Pulmonary Circulation > Flashcards

CVPR Week 6: Pulmonary Circulation Flashcards

1
Q

Objectives

A
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2
Q

In what way are the pulmonary and systemic circulations connected?

A

In series

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3
Q

How much of the cardiac output does the pulmonary circulation receive?

A

The entire cardiac output for the purpose of gas exchange

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4
Q

Explain the flow of air and blood in the cardiovascular and respiratory systems

A
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5
Q
A
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6
Q

What is this?

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7
Q

What is this?

A
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8
Q

Explain the difference

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9
Q

Explain the structure of pulmonary arteries

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10
Q

Identify

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11
Q

How are pulmonary capillaries arranged?

A
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12
Q

What is this?

A
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13
Q

Identify

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14
Q

Large pulmonic veins contain?

A

Cardiac muscle and can produce ectopic beats which can initiate atrial fibrilation

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15
Q

Pulmonary arteries structure

A

pulmonary arteries are not highly muscular

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16
Q

pulmonary capillaries are arranged in?

A

dense networks ideal for gas exchange

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17
Q

Pulmonary veins transport?

A

oxygenated blood from the lungs to the LV

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18
Q

Pulmonary veins caveat

A

larger veins have a layer of cardiac muscle and can produce ectopic beats initiating atrial fibrillation which can be ablated and completely cure the atrial fibrillation

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19
Q

Pulmonic pressure vs systemic pressures

A

pulmonary circulation has very little if any tone at all

for the most part there is very low tone

and only 10 mmHg pressure gradient driving the flow through here

changing diameter of the alveoli changing resistance

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20
Q

Alveolar and extra-alveolar vessel diameters are influenced by?

A
  • an increase in alveolar pressure causes reduced radius of the capillary if the pressure was high enough = ↓ radius and ↑ resistance to flow
  • When alveolar volume ↑ this will ↓ radius of capillary and ↑ resistance to flow
  • both of things lead to ↑ resistance to flow and can increase pulmonary arterial pressure and over the long term can decrease CO and lead to right heart failure
  • Setting ventilator right to minimize lung damage to infants
  • the extra-alveolar vessels are physically attached to the lung tissue so when lung volume increases these vessels are pulled open which actually reduces resistance to flow
    *
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21
Q

Alveolar and extra-alveolar vessel diameters are influenced by?

A

Alveolar Pressure

Alveolar volume

Lung volume

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22
Q

How does lung volume affect capillary pressure?

A

since the extra-alveolar vessels are physically attached to the lung, when the lung expands the vessels dilate.

Increase in lung volume = decrease in alveolar capillary pressure

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23
Q

Pulmonary circulation site of greatest vascular resistance

A

capillaries - 60%

Arteries 20%

Veins - 20%

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24
Q

What is the relative diameter of pulmonary capillaries?

A

a little bit smaller than a RBC’s diameter so they have to squeeze through creating more resistance and serving as the site of highest resistance in the pulmonary circulation

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25
Q

How does alveolar volume affect perfusion

A

increased alveolar volume can impede upon and squish alveolar-capillaries leasing to a reduced capillary diameter and increased alveolar-capillary pressure

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26
Q

Ventilation of infants or premies

A

a ventilator pressure that is too high may cause increased alveolar pressure leading to reduced alveolar-capillary radius and increase alveolar-capillary pressures and can damage the infants lungs

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27
Q

What is the relative pressure of the pulmonary circulation?

A

low pressure and low resistance circuit

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28
Q

How are the capillaries’ diameter affected in the lungs?

A

alveolar pressure and alveolar volume and lung volume can affect the diameter of the capillaries

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29
Q

What is the site of greatest vascular resistance in the pulmonary circulation?

A

the capillaries due to their smaller diameter than an average RBC

but the site of highest resistance can change in pulmonary hypertension

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30
Q

Passive effects of increasing pulmonary arterial pressure

A

leads to a passive reflex dropping in pulmonary vascular resistance by 2 mechanisms

  • recruitment of collapsed capillaries (parallel resistances add as reciprocals
  • distension of capillaries (this is not vasodilation which would be muscular an active process, this is a passive increase in diameter, an increased radius of vessels will decrease resistance)

These passive responses improve ventilation to perfusion matching (V/Q matching)

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31
Q

V/Q matching

A

Ventilation/perfusion

of alveoli

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32
Q

Pulmonary vascular resistance as a function of pulmonary arterial pressure

A
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33
Q

Pulmonary pressure vs time

A

resting pressure until flow is increased

get an increase in pressure

when pressure gets high enough more vessels are recruited and vessels are distended decreasing the pressure

This is important in protecting the lungs from high pressures

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34
Q

Racehorses and pulmonary pressure

A

their CO is so high that distention and additional vessel recruitment still doesn’t protect them

Pulmonary arterial pressures are so high that the pulmonary microvasculature is damaged and this is called stress failure of the pulmonary capillaries

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35
Q

pulmonary vascular resistance as a function of lung volume

A
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36
Q

Residual volume

A

volume left at the end of maximal forced expiration

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37
Q

functional residual capacity

A

residual volume + forced expiratory volume

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38
Q

Positive pressure ventilation effects

A
  • you are increasing alveolar pressure (PA)

this increases

  • ↑ PVR (pulmonary vascular resistance)

which leads to

  • ↑PAP (pulmonary arterial pressure)

which leads to

  • ↓CO (cardiac output)
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39
Q

Factors affecting PVR

A

Hematocrit (viscosity and/or dehydration)

Lung volume

Alveolar pressure

Recruitment and distention

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40
Q

Hematocrit and PVR

A
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41
Q

Effects of hypoxia on pulmonary vs systemic vascular tone

A
  • in systemic vasculature, as oxygen levels fall, causes relaxation so more blood (increased metabolic activity or other situations)
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42
Q

Effects of hypoxia on pulmonary vascular tone

A

In pulmonary, reduced O2 results in constriction for increased ventilation-perfusion matching (V/Q matching)

so the hypoxic alveoli capillaries constrict and increase the resistance. So, the blood goes to areas of lower resistance so the blood is shunted to more ventilated alveolar capillaries

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43
Q

When is Hypoxic Pulmonary Vasoconstriction

A

becomes more important in critical conditions like:

  • pneumonia
  • collapsed lung
  • chronic lung diseases (have heterogeneity in lung ventilation)
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44
Q

HPV AKA

A

Hypoxic Pulmonary Vasoconstriction

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45
Q

When is Hypoxic Pulmonary Vasoconstriction dangerous

A

with global lung hypoxia

then all vessels constrict and lead to pulmonary hypertension and can lead to right heart failure

if there is an increase in pressure then it is a result of increased resistance because in this case flow is constant

changing the composition of the air changes the vascular tone in the lung

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46
Q

What is the mechanism of Hypoxic Pulmonary Vasoconstriction?

A

autonomic mechanisms are not involved because they aren’t innervated

so this response is inherent to the vasculature in the pulmonary arterial smooth muscle cells

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47
Q

Verapamil effect on Hypoxic Pulmonary Vasoconstriction

A

Verapamil reverses Hypoxic Pulmonary Vasoconstriction because it causes vasodilation

48
Q

What is the mechanism of Verapamil

A

Voltage-gated L-type Ca2+ channel inhibitor

49
Q

Actual mechanism of Hypoxic Pulmonary Vasoconstriction

A
50
Q

Actual mechanism of Hypoxic Pulmonary Vasoconstriction

A

Hypoxia inhibits vascular smooth muscle voltage-sensitive K+ channels

so they are inhibited and this causes decreased K+ efflux as increases depolarization causing contraction

51
Q

summary of hypoxic pulmonary vasoconstriction

A
52
Q

hypoxic pulmonary vasoconstriction matches?

A

local ventilation and perfusion

53
Q

Generalized hypoxia results in?

A

pulmonary hypertension

54
Q

hypoxia effect on pulmonary arterial smooth muscle

A

Involves a direct contractile effect on pulmonary arterial smooth muscle by inhibiting voltage-sensitive K+ channels

55
Q

Classifications of pulmonary hypertension

A
56
Q

Group I WHO classification of pulmonary hypertension

A
57
Q

Group II WHO classification of pulmonary hypertension

A
58
Q

Group III WHO classification of pulmonary hypertension

A
59
Q

Group IV WHO classification of pulmonary hypertension

A
60
Q

Group V WHO classification of pulmonary hypertension

A
61
Q

Group I WHO classification of pulmonary hypertension AKA

A

Pulmonary Arterial Hypertension

62
Q

Group II WHO classification of pulmonary hypertension AKA

A

Pulmonary venous hypertension

63
Q

Group III WHO classification of pulmonary hypertension AKA

A

Hypoxemia-associated pulmonary hypertension

64
Q

Group IV WHO classification of pulmonary hypertension AKA

A

Thromboembolic disease

65
Q

Group V WHO classification of pulmonary hypertension AKA

A

Miscellaneous

66
Q

Group I WHO classification of pulmonary hypertension description

A

caused by increased resistance to flow on the arterial side

pressures can reach or even exceed systemic arterial pressures

the right heart is not adapted to deal with these types of pressures

this is unvariably fatal

67
Q

Idiopathic pulmonary hypertension AKA

A

Primary pulmonary hypertension

68
Q

Types of Group I WHO classification of pulmonary hypertension

A
  • idiopathic
  • familial
  • Persistant Pulmonary Hypertension of the newborn
69
Q

Idiopathic pulmonary hypertension most common in?

A

Women in 30-40s and invariably fatal

70
Q

The most common type of pulmonary hypertension

A

Pulmonary venous hypertension

71
Q

Pulmonary venous hypertension cause

A

Caused by left-sided heart or valvular disease

72
Q

Group II WHO classification of pulmonary hypertension description

A
  • caused by left-sided heart or valvular disease resulting in an increase in pulmonary venous pressure which is transmitted up stream leading to the microvasculature and pulmonary arteries and eventually lead to right-sided heart failure
  • most common form of pulmonary hypertension
    *
73
Q

Group IV WHO classification of pulmonary hypertension description

A

results from blood disorders that form microthrombi and they often get caught in the lung and build up and can lead to pulmonary hypertension

can also from dislodged Deep vein thrombosis if it is small enough, if it is too large it will obstruct flow from pulmonary artery and cause death very quickly

74
Q

Group IV WHO classification of pulmonary hypertension causes

6 listed

A
  • high-altitude
  • COPD
  • Sleep-disordered breathing
  • Interstitial lung disease
  • alveolar hypoventilation (obesity hypoventilation syndrome, when the mass of the chest wall impairs the ability to breath so they breath at low-lung volumes)
  • developmental abnormalities
75
Q

COPD V/Q mismatch

A

mismatch of ventilation to perfusion from obstruction of airflow due to inflammation and excessive mucus secretion (can also have some vasoconstriction)

76
Q

Emphysema V/Q mismatching

A
  • destruction of lung tissue and elastic lung tissue
  • increased compliance but reduced recoil
  • the airways also collapse as they try to exhale
77
Q

V/Q mismatching in COPD vs Emphysema

A

COPD: mismatch of ventilation to perfusion from obstruction of airflow due to inflammation and excessive mucus secretion (can also have some vasoconstriction)

Emphysema: the destruction of lung tissue and elastic lung tissue, increased compliance but reduced recoil, the airways also collapse as they try to exhale

78
Q

Sleep apnea and respiration

A
  • leads to chronic intermittent hypoxia from stopping and starting breathing all night
  • common risk factor for pulmonary hypertension, stroke, metabolic syndromes, etc.
79
Q

Types of sleep apnea

2 listed

A
  • central sleep apnea (impaired central control of breathing at night)
  • Obstructive sleep apnea (1/4 adults has some degree of sleep apnea)
80
Q

Sleep apnea exacerbating pHTN

A

if this occurs with other comorbid conditions such as COPD and these patients can develop severe pHTN

81
Q

Interstitial lung diseases

A

causes thickening of the alveolar walls due to inflammation, scarring or edema

82
Q

What is this?

A
83
Q

What is this?

A

normal alveoli

84
Q

Interstitial lung diseases are a _______ lung disease.

A

Restrictive

85
Q

Interstitial lung diseases effect on compliance

A

reduces lung compliance

86
Q

Interstitial lung diseases lung volumes

A

because of the reduced compliance these patients tend to operate on low lung volumes

87
Q

Interstitial lung diseases cause of pHTN

A

diffusion impairment

V/Q mismatch

and hypoxemia

88
Q

Interstitial lung diseases causes

A
  • idiopathic
  • pathogens
  • inhaled irritants
  • drugs
  • Autoimmune diseases
89
Q

Interstitial lung diseases and pHTN

A
90
Q

How does chronic hypoxia lead to pHTN?

6 listed

A
  • Vasoconstriction
  • hypertrophy
  • hyperplasia
  • fibrosis
  • polycythemia
  • right ventricular hypertrophy
91
Q

Arterial remodeling consists of?

A

hypertrophy and hyperplasia of the vascular smooth muscle cells that then encroaches upon the luminal radius

92
Q

Cows and high altitude

A
  • don’t respond well to high altitude because of high amounts of arterial remodeling
  • brisket disease
93
Q

Fibrosis secondary effects for pHTN

A

leads to arterial remodeling, inflammation, edema, scarring that physically restrict blood flow

these patients can also be hypoxic which would be additive

94
Q

Polycythemia Mechanism in pHTN

A

hypoxia stimulates erythropoietin from the kidneys

more blood cells = ↑ hematocrit

↑ blood density

also ↑ likelihood of forming emboli or microemboli that can contribute to pHTN

95
Q

How does the heart respond to chronic pHTN

A
  • adaptive right ventricle hypertrophy
  • thought to contribute to right heart failure with chronic lung disease
96
Q
A
97
Q

Endothelial dysfunction’s role in hypoxia-associated pulmonary hypertension

A
  • chronic and intermittent hypoxia leads to contraction of smooth muscle but also hypertrophy and hyperplasia
  • But endothelial cells increased production of vasoconstrictors and mitogenic factors such as Reactive oxygen species and endothelin-1 (ET-1)
  • Also, endothelial cells have reduced the production of vasodilators and anti-proliferative factors like Nitric Oxide and PGI 2
98
Q

Endothelin pathway

A
99
Q

Nitric oxide pathway

A
100
Q

Prostacyclin pathway

A
101
Q

Drugs to treat pHTN utilizing targets in the endothelin pathway

A

endothelin receptor antagonist

which prevent vasoconstriction and smooth muscle proliferation

102
Q

Drugs to treat pHTN utilizing targets in the nitric oxide pathway

A
  • Inhaled NO
  • PDE-5 inhibitors
  • soluble guanylyl cyclase activators
103
Q

Drugs to treat pHTN utilizing targets in the prostacyclin pathway

A
104
Q

Nitric oxide pathway agent targets

A
105
Q

Nitric oxide pathway agents

A
106
Q

Endothelin pathway agent targets

A
107
Q

Prostacyclin pathway agents

A

prostacyclin analogs

108
Q

Prostacyclin pathway agent targets

A
109
Q

Summary of response to hypoxia

A
110
Q

What factors contribute to pHTN

A

Active vasoconstriction

vascular remodeling

polycythemia

111
Q

Endothelium’s role in vasoconstriction and vascular remodeling

A

an imbalance in the production of endothelium-derived vasoactive and vasoproliferative factors

112
Q

drugs to treat hypoxemia-associated pHTN

A
  • stuff to help control symptoms but the endothelin, nitric oxide, or prostacyclin drugs are approved to treat group III pHTN
  • only therapies shown to prolong life are supplemental of oxygen and cessation of smoking
113
Q

In pulmonary hypertension what is the site of greatest resistance in the pulmonary circulation?

A

It can vary, for instance in LCHF the pulmonary veins may be of the highest pressure

114
Q

If pulmonary arterial pressure goes up what happens to resistance & flow?

A

P = R x Q

so

if ↑P

then ↓R

and

↑↑Q

115
Q

If pulmonary arterial pressure goes down what happens to resistance & flow?

A

P = R x Q

so

if ↓P

then ↑R

and

↓↓Q

CVPR (93 decks)

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