N5315 Advanced Pathophysiology
Pulmonary and Shock
Core Concepts and Objectives with Advanced Organizers
Age related Difference in pulmonary anatomy and physiology
I. Describe the age-related changes which occur in the alveoli, chest wall, and gas exchange.
A. Normal alterations include
1. Loss of elastic recoil
2. Stiffening of the chest wall
a) Ribs become ossified (less flexible) and joints become stiffer
b) Respiratory muscle strength and endurance decreases by up to 20%
3. Changes in gas exchange
a) Decreased compensatory response to hypercapnia and hypoxemia, with an enhanced
perception of dyspnea
b) PaO2 decreases d/t alveolar changes and increased V/Q mismatch
c) PaO2= 100 - (0.3 x age)
4. Increase in flow resistance
B. Alveoli tend to lose alveoli wall tissue and capillaries, diminishing alveolar surface area available for
gas diffusion and decreases airway support provided by normal lung tissue
C. Vital capacity decreases and residual volume increases, while lung capacity remains the same→
Leading to decreased ventilation-perfusion ratios
D. Increased immune dysregulation, asymptomatic low-grade inflammation, and increased risk of
infection
E. Decreased exercise tolerance, greater risk for respiratory depression from medications
F. Change vary, being active and physically fit decreases functional changes
II. Explain the structure and physiologic differences of the pulmonary system in the infant and child.
A. Upper Airway
1. All conducting airways are present at 16wk gestation and change only in size
2. Children have airways that are smaller in diameter and can therefore suffer more obstruction
for a given degree of mucosal edema or secretion accumulation
3. Tonsils, adenoids, epiglottis are proportional larger and swelling can impose a significant site
of obstruction
4. Infants up to 2 to 3 months are obligate nose breathers and are unable to breath through their
mouths→ nasal congestion can be a serious threat
B. Lower Airway and Lung Parenchyma
1. In utero, fetal lung development leads to functional maturation of cells during which
specialized cell types manifest
2. Beginning in the second trimester, there is a loss of interstitial tissue in the lungs with
expansion of the future air spaces→ capillaries grow into the distal respiratory units that keep
subdividing (alveolarization) to maximize surface area for gas exchange
3. Number of alveoli continue to increase the first 5-8 years of life after which they continue to
increase in size and complexity
4. Surfactant: lipid-protein mix that is critical for maintaining alveolar expansion
a) Produced by 20-24 weeks gestation and secreted into the fetal airways by 30 weeks
b) Deficiency of surfactant is seen in premature infants and cause respiratory distress
syndrome (RDS), aka hyaline membrane disease
c) The more premature the infant, the higher the risk for RDS
C. Chest Wall Dynamics
1. Infants chest wall is easily collapsible d/t cartilaginous structures of the thoracic cage (not yet
ossified)
, 2. Paradoxic or diaphragmatic breathing: infants breath in and chest wall moves inward and
diaphragm moves downward, with exhalation chest wall moves outward and diaphragm
relaxes
3. Infant functional residual capacity (FRC) or resting lung volume is maintained by “braking
of their expiration” by epiglottic narrowing or increased activity of the inspiratory intercostal
muscles
D. Metabolic Characteristics
1. Basal metabolic rate is greater leading to increased oxygen consumption
2. Increased work of breathing with respiratory distress
3. Decreased efficiency of accessory muscles
4. Faster respiratory fluid loss in times of dehydration
E. Immunologic Incompetence: enhanced susceptibility to viral and fungal infections from depletion of
maternal IgG
F. Physiologic Control of Respiration
1. Newborn: blunted ventilatory response to hypoxia
2. Maternal smoking can have significant effects of lung development and subsequent
susceptibility to pulmonary disorders
Examine the pathologic basis of adult and pediatric disorders which affect the pulmonary system.
Pulmonary Vascular Disorders
I. Restrictive disorders refer to the inability of the person to breathe in adequate amounts of air. Typically,
these individuals have low lung volumes on pulmonary function tests.
A. Lung volumes are essentially the amount of air the lungs contain at a given time during respirations.
B. Disease examples include aspiration, pulmonary fibrosis, atelectasis, bronchiectasis, bronchiolitis, and
pulmonary edema.
II. Analyze the etiology, clinical manifestations and pathophysiology of pulmonary embolus, and pulmonary
edema and describe the implications for clinical practice.
Disease Etiology Clinical Manifestations Pathophysiology
Pulmonary Most commonly results DVT symptoms: calf Occlusion or partial occlusion of the
Embolus from embolization of a pain, tenderness, calf pulmonary artery or it branches
clot from DVT asymmetry: usually
Blood clot becomes an embolus when all
involving the lower leg asymptomatic
or part of it breaks away from the site of
Less common: tissue formation and travels in the bloodstream
fragments, lipids (fats),
Sudden onset of pleuritic Effects depend on size of affected vessel,
foreign body, air
chest pain, dyspnea, extent of obstruction, nature of embolus
bubble
tachypnea, tachycardia,
Can result in infarction of lung tissue and
unexplained anxiety
permanent lung damage, massive
Risk factors: venous Large emboli: pleural occlusion that occludes major portion of
stasis, effusion, fever, pulmonary circulation, multiple
hypercoagulability, leukocytosis pulmonary emboli (chronic or recurrent)
endothelial damage
Genetic risk factors:
As a result of lodging of thrombus,
factor V Leiden, ATIII,
inflammatory mediators and
protein S, or protein C
neurohormonal substance released
deficiency
, leading to vasoconstriction→ decreasing
pulmonary flow→ increased pulmonary
30% risk of recurrent
pressures→ R sided heart failure
venous
thromboembolism in
10 years
Pulmonary ventilation-perfusion
mismatch: increased dead-space,
decreased surfactant production→
atelectasis→ increased hypoxemia
Clot can be dissolved by the fibrinolytic
system and pulmonary function can return
to normal or in severe cases can lead to
infarction, dysrhythmias, decreased
cardiac output, shock, and death
Pulmonary Predisposing factors Dyspnea, chest pain, Excess water in the lungs
Edema include heart disease, hypoxemia, and increased
Normally kept dry by capillary
ARDS, and inhalation WOB
hydrostatic pressure, capillary oncotic
of toxic gases
Often have orthopnea or pressure, capillary permeability,
Most common cause: paroxysmal nocturnal surfactant lining
left sided heart disease dyspnea
Injury to the capillary Inspiratory crackles
Left sided heart disease: when the L
endothelium: ammonia (rales), dullness to
ventricle fails filling pressures on the left
inhalation, ARDS percussion over the lung
side increase and cause increased
bases, and evidence of
Blockage of lymphatic pulmonary capillary hydrostatic pressure,
ventricular dilation (S3
vessels: compression forcing fluid into the interstitial space
gallop and cardiomegaly)
from pulmonary (space between alveolus and capillary)→
edema, tumors, fibrotic Severe: pink, frothy when lymphatic system becomes
tissue or increased sputum overwhelmed, fluid accumulates and
systemic venous pulmonary edema develops (usually
pressure that elevates begins with PAWP or L atrial pressures
the hydrostatic pressure of 20 mmHg)
of the large pulmonary
vein where the
pulmonary lymphatic Injury to the capillary endothelium→
system drains (L sided increased capillary permeability and
heart failure) disruption of surfactant production by
alveoli→ movement of fluid and plasma
Postobstructive
proteins (oncotic pressure) from capillary
pulmonary edema
to interstitial space (alveolar septum) and
(POPE): rare life-
alveoli
threatening
complication after
relief of obstructed
airway Blockage of lymphatic vessels→ inability
Pulmonary and Shock
Core Concepts and Objectives with Advanced Organizers
Age related Difference in pulmonary anatomy and physiology
I. Describe the age-related changes which occur in the alveoli, chest wall, and gas exchange.
A. Normal alterations include
1. Loss of elastic recoil
2. Stiffening of the chest wall
a) Ribs become ossified (less flexible) and joints become stiffer
b) Respiratory muscle strength and endurance decreases by up to 20%
3. Changes in gas exchange
a) Decreased compensatory response to hypercapnia and hypoxemia, with an enhanced
perception of dyspnea
b) PaO2 decreases d/t alveolar changes and increased V/Q mismatch
c) PaO2= 100 - (0.3 x age)
4. Increase in flow resistance
B. Alveoli tend to lose alveoli wall tissue and capillaries, diminishing alveolar surface area available for
gas diffusion and decreases airway support provided by normal lung tissue
C. Vital capacity decreases and residual volume increases, while lung capacity remains the same→
Leading to decreased ventilation-perfusion ratios
D. Increased immune dysregulation, asymptomatic low-grade inflammation, and increased risk of
infection
E. Decreased exercise tolerance, greater risk for respiratory depression from medications
F. Change vary, being active and physically fit decreases functional changes
II. Explain the structure and physiologic differences of the pulmonary system in the infant and child.
A. Upper Airway
1. All conducting airways are present at 16wk gestation and change only in size
2. Children have airways that are smaller in diameter and can therefore suffer more obstruction
for a given degree of mucosal edema or secretion accumulation
3. Tonsils, adenoids, epiglottis are proportional larger and swelling can impose a significant site
of obstruction
4. Infants up to 2 to 3 months are obligate nose breathers and are unable to breath through their
mouths→ nasal congestion can be a serious threat
B. Lower Airway and Lung Parenchyma
1. In utero, fetal lung development leads to functional maturation of cells during which
specialized cell types manifest
2. Beginning in the second trimester, there is a loss of interstitial tissue in the lungs with
expansion of the future air spaces→ capillaries grow into the distal respiratory units that keep
subdividing (alveolarization) to maximize surface area for gas exchange
3. Number of alveoli continue to increase the first 5-8 years of life after which they continue to
increase in size and complexity
4. Surfactant: lipid-protein mix that is critical for maintaining alveolar expansion
a) Produced by 20-24 weeks gestation and secreted into the fetal airways by 30 weeks
b) Deficiency of surfactant is seen in premature infants and cause respiratory distress
syndrome (RDS), aka hyaline membrane disease
c) The more premature the infant, the higher the risk for RDS
C. Chest Wall Dynamics
1. Infants chest wall is easily collapsible d/t cartilaginous structures of the thoracic cage (not yet
ossified)
, 2. Paradoxic or diaphragmatic breathing: infants breath in and chest wall moves inward and
diaphragm moves downward, with exhalation chest wall moves outward and diaphragm
relaxes
3. Infant functional residual capacity (FRC) or resting lung volume is maintained by “braking
of their expiration” by epiglottic narrowing or increased activity of the inspiratory intercostal
muscles
D. Metabolic Characteristics
1. Basal metabolic rate is greater leading to increased oxygen consumption
2. Increased work of breathing with respiratory distress
3. Decreased efficiency of accessory muscles
4. Faster respiratory fluid loss in times of dehydration
E. Immunologic Incompetence: enhanced susceptibility to viral and fungal infections from depletion of
maternal IgG
F. Physiologic Control of Respiration
1. Newborn: blunted ventilatory response to hypoxia
2. Maternal smoking can have significant effects of lung development and subsequent
susceptibility to pulmonary disorders
Examine the pathologic basis of adult and pediatric disorders which affect the pulmonary system.
Pulmonary Vascular Disorders
I. Restrictive disorders refer to the inability of the person to breathe in adequate amounts of air. Typically,
these individuals have low lung volumes on pulmonary function tests.
A. Lung volumes are essentially the amount of air the lungs contain at a given time during respirations.
B. Disease examples include aspiration, pulmonary fibrosis, atelectasis, bronchiectasis, bronchiolitis, and
pulmonary edema.
II. Analyze the etiology, clinical manifestations and pathophysiology of pulmonary embolus, and pulmonary
edema and describe the implications for clinical practice.
Disease Etiology Clinical Manifestations Pathophysiology
Pulmonary Most commonly results DVT symptoms: calf Occlusion or partial occlusion of the
Embolus from embolization of a pain, tenderness, calf pulmonary artery or it branches
clot from DVT asymmetry: usually
Blood clot becomes an embolus when all
involving the lower leg asymptomatic
or part of it breaks away from the site of
Less common: tissue formation and travels in the bloodstream
fragments, lipids (fats),
Sudden onset of pleuritic Effects depend on size of affected vessel,
foreign body, air
chest pain, dyspnea, extent of obstruction, nature of embolus
bubble
tachypnea, tachycardia,
Can result in infarction of lung tissue and
unexplained anxiety
permanent lung damage, massive
Risk factors: venous Large emboli: pleural occlusion that occludes major portion of
stasis, effusion, fever, pulmonary circulation, multiple
hypercoagulability, leukocytosis pulmonary emboli (chronic or recurrent)
endothelial damage
Genetic risk factors:
As a result of lodging of thrombus,
factor V Leiden, ATIII,
inflammatory mediators and
protein S, or protein C
neurohormonal substance released
deficiency
, leading to vasoconstriction→ decreasing
pulmonary flow→ increased pulmonary
30% risk of recurrent
pressures→ R sided heart failure
venous
thromboembolism in
10 years
Pulmonary ventilation-perfusion
mismatch: increased dead-space,
decreased surfactant production→
atelectasis→ increased hypoxemia
Clot can be dissolved by the fibrinolytic
system and pulmonary function can return
to normal or in severe cases can lead to
infarction, dysrhythmias, decreased
cardiac output, shock, and death
Pulmonary Predisposing factors Dyspnea, chest pain, Excess water in the lungs
Edema include heart disease, hypoxemia, and increased
Normally kept dry by capillary
ARDS, and inhalation WOB
hydrostatic pressure, capillary oncotic
of toxic gases
Often have orthopnea or pressure, capillary permeability,
Most common cause: paroxysmal nocturnal surfactant lining
left sided heart disease dyspnea
Injury to the capillary Inspiratory crackles
Left sided heart disease: when the L
endothelium: ammonia (rales), dullness to
ventricle fails filling pressures on the left
inhalation, ARDS percussion over the lung
side increase and cause increased
bases, and evidence of
Blockage of lymphatic pulmonary capillary hydrostatic pressure,
ventricular dilation (S3
vessels: compression forcing fluid into the interstitial space
gallop and cardiomegaly)
from pulmonary (space between alveolus and capillary)→
edema, tumors, fibrotic Severe: pink, frothy when lymphatic system becomes
tissue or increased sputum overwhelmed, fluid accumulates and
systemic venous pulmonary edema develops (usually
pressure that elevates begins with PAWP or L atrial pressures
the hydrostatic pressure of 20 mmHg)
of the large pulmonary
vein where the
pulmonary lymphatic Injury to the capillary endothelium→
system drains (L sided increased capillary permeability and
heart failure) disruption of surfactant production by
alveoli→ movement of fluid and plasma
Postobstructive
proteins (oncotic pressure) from capillary
pulmonary edema
to interstitial space (alveolar septum) and
(POPE): rare life-
alveoli
threatening
complication after
relief of obstructed
airway Blockage of lymphatic vessels→ inability
