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Physiology > Lecture 20: pulmonary circulation and disease > Flashcards

Lecture 20: pulmonary circulation and disease Flashcards

1
Q

How many alveoli are in the adult lung?

A

300-600

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2
Q

What is the gas exchange surface area of the lung?

A

70 meters squared (size of tennis court)

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3
Q

What is the transit time of RBC?

A

1 second

as fast as 0.5 seconds if cardiac output is increased

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4
Q

What is the alveolar diffusion distance?

A

0.4 um

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5
Q

What does the pulmonary artery carry?

A

Deoxygenated blood to the lungs

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6
Q

What does the pulmonary vein carry?

A

Oxygenated blood back to the left atrium

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7
Q

Where does the pulmonary circulation arise from during development?

A

Embryonic mesoderm

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8
Q

How much of the cardiac output does the lung receive?

A

Entire cardiac output

Only organ to receive entire CO

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9
Q

What supplies nutritive flow to the lung?

A

Bronchial circulation

3% of CO

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10
Q

Properties of pulmonary arteries, arterioles and pre-ascinar and ascinar vessels

A

Pulmonary artery and larger (conduit) vessels are elastic

Pulmonary arterioles (resistance vessels) are highly muscular

Pre-ascinar and ascinar vessels are thin walled, non-muscular

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11
Q

What is the gas exchange surface composed of?

A

Extensive capillary network closely applied to alveolar walls

(minimal diffusion gradient)

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12
Q

What does each alveolus sit in?

A

A capillary basket

Pulmonary capillaries are numerous with multiple branches and anastomoses

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13
Q

Pressure changes through the pulmonary circuit

A

RAP = 0 mm Hg

RVP = 25/0 mm Hg

PAP (pulmonary arterial pressure) = 25/8 mm Hg

PCWP (?) = 5 mm Hg

LAP (left atrial pressure) = 5 mm Hg

See figure

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14
Q

Pulmonary vs systemic pressures

A

Absolute pressures are lower in the pulmonary system compared to the systemic system

We don’t want high pressure in the lung (could cause edema, pneumonia, etc)

See figure

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15
Q

What happens in systemic and pulmonary vascular smooth muscle during hypoxia?

A

Systemic: smooth muscle relaxes during hypoxia to increase blood flow

Pulmonary: smooth muscle contracts to preserve V/Q matching

No point in sending blood to the lung if there is no oxygen in the lung

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16
Q

Effect of bradykinin and prostacyclin on the systemic and pulmonary circulations

A

Lower SVR (systemic vascular resistance) and PVR by inducing nitric oxide

NO lowers resistance in all circuits

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17
Q

What can be used to treat pulmonary hypertension?

A

NO

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18
Q

What molecule increases resistance in all circuits?

A

ET-1 (Endothelin-1 )

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19
Q

What are the functions of pulmonary circulation?

A

Gas exchange (O2 and CO2)

Filter (Capture emboli)

Blood reservoir for LV (~900 ml, mostly within the thin-walled, distensible pulmonary veins)

Nutrient supply (Pulmonary circulation supplies alveolar duct & alveoli)

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20
Q

Are the functions of the lung and the pulmonary circulation the same?

A

Different! (Except gas exchange)

Lung is also an immune organ, filters irritants and pollutants

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21
Q

What is V?

A

V for Ventilation (naturally!)

Indicates effective minute ventilation of aerated pulmonary alveolar gas exchange surface with oxygenated gas

Need both alveolar recruitment and adequate respiratory activity

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22
Q

What is Q?

A

Q is for perfusion

Flow volume per unit time

Indicates proportion of cardiac output that perfuses pulmonary circuit

Commonly extrapolated by determining pulmonary vascular resistance

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23
Q

What are possible etiologies of a hypoxic alveolus?

A

Pneumonia

Bronchitis

Edema

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24
Q

What occurs when there is a hypoxic alveolus? Outcomes?

A

Hypoventilation

V/Q mismatch (no oxygen but continued perfusion)

Pulmonary vascular constriction

Outcomes: respiratory failure, acidosis, circulatory failure

See figure

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25
Q

What occurs in a well ventilated alveolus?

A

Oxygen tension rises

Endothelial NO synthesis

Relaxation of pulmonary vessels

= good gas exchange

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26
Q

What is normal resting respiratory rate?

A

12 breaths per minute

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27
Q

Pulmonary ventilation curve

A

TV: not all alveoli are inflated

Deep breath: recruiting more alveoli

RV: air is stuck, does not participate in gas exchange

See figure

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28
Q

Formula for minute ventilation

A

Volume (ml) breathed in and out per minute

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29
Q

Formula for pulmonary ventilation

A

TV (ml) x respiratory rate (breaths/min)

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30
Q

What is the normal respiratory rate?

A

~ 12 breaths/minute

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31
Q

What is minute ventilation?

A

volume (ml) of air breathed in and out per minute

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32
Q

What is pulmonary ventilation?

A

Tidal volume (ml) x respiratory rate (breaths/minute)

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33
Q

Pulmonary ventilation curve

A

See figure

TV: not all alveoli are inflated

Deep breath: recruiting more alveoli

RV: air is stuck does not participate in gas exchange

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34
Q

What is alveolar ventilation?

A

Volume of air exchanged between atmosphere and alveolae per minute

More important than pulmonary ventilation

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35
Q

Why is alveolar ventilation less than pulmonary ventilation?

A

Due to anatomic dead space

Volume of air in conducting airways that is not available for gas exchange (~150 ml in adults)

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36
Q

Formula for alveolar ventilation

A

alveolar ventilation = (TV - dead space) x respiratory rate

See figure

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37
Q

What is asthma? Characteristics?

A

A chronic inflammatory disorder of the airways characterized by:

Paroxysmal or persistent symptoms (dyspnea, chest tightness, wheeze and cough)

Variable and reversible airflow limitation

Airway hyperresponsiveness to a variety of stimuli

Can have an irreversible component – airway remodelling

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38
Q

Flow-volume loop in airway obstruction

A

FEV1/FVC < 70%

FEV1 decreased (airway resistance increased)

Scooping in F-V

FVC reduced in severe disease (hyperinflation due to gas trapping in COPD)

See figure

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39
Q

What can give a “false positive” for airway obstruction

A

Reduced FVC maneuver

Person is not trying hard enough, so FVC looks lower than it actually is

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40
Q

What is COPD? What does it include?

A

Chronic obstructive pulmonary disease

Inflammatory and lung destruction process

Chronic bronchitis, and/or

Emphysema -> enlargement of airspaces/alveoli

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41
Q

Degree of airway obstruction on COPD

A

May be partially reversible

42
Q

Prevalence of COPD

A

Incidence ~5%, projected as 4th leading cause of death world wide in next decade

~75% chronic bronchitis, 25% emphysema

43
Q

What is the principal cause of COPD?

A

Cigarette smoking (90%)

Chronic dust (silica & cotton) or chemical fume exposure also a risk factor

44
Q

What are the clinical manifestations of chronic bronchitis?

A

Productive cough and wheezing

Inspiratory and expiratory coarse crackles

Cardiac: tachycardia common in exacerbations

Pulmonary function tests: abnormal results

45
Q

What are the findings of pulmonary function tests in patients with COPD?

A

Reduced expiratory flows and volumes

FEV1, FVC, and the FEV1/FVC ratio all reduced

Expiratory F-V curve shows substantial flow limitation

Increase in RV and FRC

Air trapped in the lung due to airway obstruction & early airway closure at higher lung volumes

46
Q

Clinical manifestations of emphysema?

A

Dyspnea, progressive nonreversible airway obstruction, and abnormalities of gas exchange, particularly with exercise

Breath sounds are decreased in intensity

Pulmonary hypertension in end stage

47
Q

What are the findings of pulmonary function tests in patients with emphysema?

A

Increased dynamic compression of airways during expiration (premature airway collapse)

Reduced FEV1, FVC, and FEV1/FVC ratio

Flow limitation shows in expiratory F-V curve

Air trapping: increased RV, FRC and TLC

48
Q

Idiopathic pulmonary fibrosis - type of disease, cause, presentation

A

Restrictive lung disease

Presentes in 5th or 7th decade

49
Q

Pathophysiology of idiopathic pulmonary fibrosis

A

Chronic alveolar inflammation causes diffuse, progressive fibrosis, destroying lung architecture (thick membranes)

Restrictive defect: altered ventilation & increased work of breathing

Obliterative vascular injury

Impaired pulmonary perfusion and gas exchange (lung will not expand properly)

50
Q

Flow-volume loop of restrictive lung disease

A

FEV1:FVC > 80%

FVC decreased (reduced lung volume due to high lung stiffness/low compliance)

Forced flow (FEV1) not changed

See figure

51
Q

Why is pulmonary arterial pressure constant over a wide range of cardiac outputs?

A

Capillary recruitment (capillaries that were not perfused become perfused)

Vascular distension (vessels dilate to meet pressure)

52
Q

Why is pulmonary arterial pressure more flow-sensitive in the hypoxic lung?

A

Hypoxia induced vasoconstriction

53
Q

Formula for systemic vascular resistane

A

SVR = (MAP - CVP) / CO

MAP = mean arterial pressure
CVP = central venous pressure (pressure of blood returning to heart, usually minimal)

Simplified to SVR = MAP/CO

54
Q

Formula for pulmonary vascular resistance (PVR)

A

PVR - P(pulmonary) / Q(pulmonary)

or

PVR = (Ppa - Pla) / CO

Ppa: pressure pulmonary artery

Pla: pressure left atrium

55
Q

When can pulmonary vascular resistance not be accurately extrapolated from pressure?

A

If pulmonary flow is not the same as cardiac output

Qp is not = to Qs

56
Q

What are passive and active factors that increase PVR?

A

Passive: increasing LAP, increasing PAP, increased pulmonary blood volume, increased blood viscosity

Active (all cause vasoconstriction): alveolar hypoxia, acidemia, alveolar hypercarbnia, humoral substances

57
Q

In what conditions can shunting occur

A

Qp < Qs (flow to lungs does not match flow to systemic system)

Congenital cardiac anomalies with intracardiac arteriovenous mixing

Pulmonary hypertension

Acute hypoxic episodes in lung disease patients

58
Q

Shunting in fetal heart

A

Lungs are filled with fluid in fetus, so there is no oxygen exchange.

This hypoxic condition causes the pulmonary arteries to constrict, and pressure in the pulmonary arteries increases

Heart has bypass system to reduce this pressure

Right to left atrium shunting of blood through foramen ovale

Ductus arteriosus between pulmonary artery and aorta

59
Q

What are the causes of V:Q mismatch?

A

Perfused part of lung is not adequately ventilated (shunted ventilation)

A ventilated part of the lung is not adequately perfused (alveolar dead space ventilation)

See figure

60
Q

What can cause shunted ventilation?

A

Pneumonia

Pulmonary edema

Atelectasis (complete or partial collapse of lung)

61
Q

What can cause alveolar dead space ventilation?

A

Pulmonary embolism

Pulmonary hypertension

62
Q

How does PVR change during ventilation?

A

RV: alveoli are empty, lung is not inflated, so extra alveolar vessels are not being expanded (resistance is higher)

TLC: Alveoli are full of gas and squish alveolar capillaries (resistance increases). Also, lungs are expanded, so extra alveolar vessels are pulled open

PVR is lowest near FRC, highest at both high and low lung volumes

See figure

63
Q

Parts of lung and ventilation and perfusion

A

Apex: good ventilation; perfusion poor due to gravity and pressure effect of alveolar inflation

Mid lung: ventilation + perfusion well matched

Lower lung: perfusion better due to gravity

Basal lung: perfusion squashed by high interstitial pressure. Starling resistor created

64
Q

What is a starling resistor?

A

Narrowing of vessel due to pressure causes initial P to build up

P builds up high enough to open vessel and blood can flow through

Opening and closing occurs over and over

65
Q

West’s zones of the lung - zone 1

A

Zone 1: PA > Pa > Pv

Large alveoli

Vessels collapse

No blood flow

See figure

66
Q

West’s zones of the lung - zone 2

A

Pa > PA > Pv

Just above heart

Vessels partially collapsed

Decreased blood flow

PAP increased by 1 cm H2O for every 1 cm of vertical distance from the lung apex

Starling resistor

67
Q

West’s zones of the lung - zone 3

A

Pa > Pv > PA

Vessels open

Increased blood flow (no external resistance)

But alveoli are under inflated

68
Q

When is zone 1 seen in patients?

A

Not seen in healthy person (Pa > PA in all parts of the lung)

Typically seen in people ventilated with positive pressure (force alveoli to expand) or hemmorhage (low BP)

69
Q

What zone makes up the majority of a healthy lung?

A

Zone 3

No external resistance to flow

V:Q matching

70
Q

When is zone 4 seen?

A

Seen typically at low lung volumes or edema.

Compression of alveolar vessels resulting in decreased perfusion.

71
Q

Do lung zones reflect what is happening in reality?

A

No

All zones do not exist at one time

72
Q

State of alveoli at rest, perfusion

A

Most of alveoli are collapsed/unfilled

These alveoli do not need perfusion

Blood should be rerouted to more ventilated alveoli

73
Q

How is blood rerouted to ventilated alveoli?

A

Hypoxic vasoconstriction

Causes shrinking of zone 3 and expanding of zone 2

Reduces flow to areas of low O2 tension by increasing local vascular tone

Necessary for V:Q matching

74
Q

What is hypoxic pulmonary vasoconstriction mediated by?

A

Redox state of K channels

75
Q

What happens if whole lung is hypoxic?

A

Ex: at high altitude

Right ventricle can become overloaded (potential development of hypertrophy)

76
Q

Lung perfusion and ventilation in infant in supine position

A

Poor V/Q matching

Area of better ventilation does not coincide with area of better perfusion

See figure

77
Q

Lung perfusion and ventilation in infant in prone position

A

Optimal V/Q matching

Leads to improved oxygenation, less effort

See figure

78
Q

What are common instances of hypoxic pulmonary vasoconstriction

A

Normal respiration: decreasing blood flow to poorly aerated regions at the base of the lung, increasing blood flow to the apex of the lung, overcoming gravity effects

Matching postural changes

Bypassing diseased (poorly aerated) lung segments during pneumonia or asthma

79
Q

What are some implications of hypoxia for pulmonary circulation?

A

End stage complications of pulmonary diseases of chronic hypoxia (severe asthma, COPD)

Proliferation of pulmonary arterial smooth muscle, progressive muscularization of distal vessels, resistance to pulmonary flow

Right ventriclular after load causes right heart hypertrophy and eventual heart failure

80
Q

Incidence of persistent pulmonary hypertension of the newborn

A

PPHN

Incidence: 1-6 / 1000 live births

Mortality: 10-20%

Survivors may have high morbidity, in the forms of: neurodevelopmental impairment, cognitive delay, hearing loss, high rate of rehospitalization

81
Q

What are typical scenarios that might precipitate PPHN

A

Cold stress

Meconium aspiration (focal matter aspiration)

Perinatal asphyxia

Sepsis or pneumonia

Occasionally complicates respiratory distress syndrome

82
Q

Pathophysiology of PPHN

A

R to L shunt across ductus arteriosus, and across pre- capillary arterio-venous connections within the lung

Initially labile (pulsatile) pulmonary flow due to vasospasm

Pulmonary artery pressure&raquo_space; systemic arterial pressure

Post-ductal saturation falls, because of unoxygenated blood crossing ductus, and mixing into aorta

Later pre-ductal saturation also falls, as volume of red blood returning from lungs gets smaller and is mixing with increasingly bluer shunted blood

Hypoxia causes myocardial dysfunction and neurological consequences

83
Q

When and how does PPHN typically present itself?

A

First minutes to hours of life

Baby is cyanotic with saturation below 80% in right atrium

Pre ductal saturation is higher than post ductal saturation because of right to left shunting

Degree of desaturation depends on volume of shunted blood

Increased work of breathing due to precipitating factors = V/Q mismatching and respiratory failure

84
Q

What is pre-ductal saturation?

A

Saturation of the blood before it reaches the ductus arteriosus

Can be measured in right hand, because the upper extremities are supplied by blood coming from branches off the aorta before the ductus arteriosus attachment

85
Q

What is post-ductal saturation?

A

Saturation of the blood after the point of attachment of the ductus arteriosis

Measured in lower extremities because this part of body receives blood from branches of the aorta that occur after the attachment point of the ductus arteriosus

86
Q

How to treat PPHN?

A

Saturation can be increased using 100% O2

Inhaled NO

87
Q

Mechanism of endogenous NO

A

Oxygen sensor detects low oxygen

Endothelial NOS is activated and converts L-arginine to NO

NO diffuses into smooth muscle and activates guanylate cyclase

GC converts GTP to cGMP. PDE converts cGMP to GMP

cGMP causes decreased calcium in the cell

Decreased calcium leads to smooth muscle relaxation and decreased smooth muscle proliferation

See figure

88
Q

How does inhaled NO work?

A

See figure

89
Q

When are premature infants considered viable?

A

After 23 weeks gestation or > 500 g

23 weeks is a grey zone (mortality > 90%)

At 24 weeks, lungs are still in a canalicular phase of
development (few alveoli, big A/a gradient)

At 25 weeks, mortality 20-30%

By 26 weeks, lungs are alveolarizing, and mortality is below 20%

90
Q

What is the primary complication of preterm birth?

A

Respiratory distress due to surfactant deficiency

91
Q

What occurs in respiratory distress syndrome?

A

Hyaline membrane disease

Hyaline membrane coats alveoli, gas exchange cannot occur

92
Q

What is surfactant produced by?

A

Product of alveolar type II cells

Artificial surfactant may be synthetic or derived from animal lung extracts

93
Q

Function of surfactant

A

Lowers the surface tension at the gas liquid interface in the small airways and alveoli (decreases attraction between water molecules)

Decreases alveolar opening pressure, ie. the pressure at which the lung parenchyma begins to fill beyond dead space volume

Surfactant stabilizes the lung on deflation, maintaining a functional residual capacity by preventing complete collapse of previously inflated alveoli

94
Q

Hyaline membrane disease pre- and post-surfactant

A

See figure

95
Q

What causes ARDS?

A

Adult Respiratory Distress Syndrome

Results from acute systemic and pulmonary inflammation, presenting as refractory hypoxemia

Systemic inflammatory response syndrome (SIRS), cytokine cascade

96
Q

Pathophysiology of ARDS

A

Epithelial dysfunction and endothelial dysfunction

Disruption of the alveolar barrier

Low pressure pulmonary edema due to capillary leak into the alveolar space

Alveolar inflammatory fluid inactivates surfactant

Lungs become stiff and poorly compliant

Mortality 30 – 40 %

97
Q

Alveolar capillary interface

A

Very thin gas exchange layer

98
Q

What are the stages of alveolar edema?

A

Stage I: interstitial pulmonary edema (swelling in space between capillary bed and alveoli)

Stage II: Crescentic filling of alveoli

Stage III: alveolar flooding

See figure

99
Q

Formula for oxygen index

A

OI measures usage of O2 in the body

OI = (FiO2 x MAP) / PaO2

FiOs: inspired oxygen

100
Q

How Blue is blue?

A

If you are giving 100% O2, and the OI approaches 20 (and sometimes before that), most studies recommend you start looking for a plan B…

Plan B: inhaled nitric oxide (replaces function of damaged endothelium)

Plan C :surfactant (epithelialdamage,surfactant inactivation)

Need to also treat underlying cause (pneumonia, etc.)…

Physiology (19 decks)

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