N5315 Advanced Pathophysiology
Pulmonary and Shock
Module 6
Age related Difference in pulmonary anatomy and physiology
1. Describe the age-related changes which occur in the alveoli, chest wall, and
gas exchange. (pg 1244-45)
● Alveoli: During adulthood and as age advances, the alveoli tend to lose alveoli wall
tissue and capillaries. This process diminishes alveolar surface area available for gas
diffusion and decreases airway support provided by normal lung tissues.
● Chest Wall: Mechanical changes involve elastic properties of the lungs and chest wall.
Chest wall compliance decreases with age, because the ribs become ossified (less
flexible) and joints become stiffer. As a result, the chest wall loses some of its ability to
expand. In addition, respiratory muscle strength and endurance decrease by up to 20%
by age 70. These mechanical changes in the lung and chest wall, along with structural
changes in the alveoli, reduce ventilatory capacity in older adults. Vital capacity
decreases and residual volume increases, however, total lung capacity remains
unchanged. These changes decrease ventilatory reserves and lead to decreased
ventilation-perfusion ratios. With advancing age there is also increased immune
dysregulation, asymptomatic low-grade inflammation, and increased risk of infection.
● Gas Exchange: Alterations in gas exchange are reflected by blood gas analysis. With
advancing age, pH and Paco2 do not change much, even though it has been
documented that the chemoreceptors become less sensitive to gas partial pressure with
age. Older adults have a decreased compensatory response to hypercapnia and
hypoxemia; however, the perception of dyspnea remains intact and is even enhanced.
Pao2 declines with age as a result of structural and mechanical changes, such as loss of
alveolar surface area and increased ventilation-perfusion mismatch. The maximum Pao2
in an older adult at sea level can be estimated by multiplying the person’s age by 0.3
and subtracting the product from 100. There is also a decrease in the capillary network.
The decrease in Pao2 and diminished ventilatory reserve in an older adult lead to a
decrease in exercise tolerance. Respiratory muscle strength and endurance decrease
with age. Furthermore, older adults are at greater risk for respiratory depression caused
by medications.
2. Explain the structure and physiologic differences of the pulmonary system
in the infant and child. (pg. 1290-1293)
1
, ● The airways of infants and children are narrower than those of adults, thus
making them more prone to obstruction.
● Infants and young children continue to form new alveoli for several years after
birth.
● Surfactant is a lipid protein mix that is produced by type II alveolar cells and is
critical for maintaining alveolar expansion (thus allowing normal gas exchange). It
lines alveoli and reduces surface tension, preventing alveolar collapse at the end
of each exhalation. Without surfactant the alveoli tend to stay closed, demanding
greater inspiratory force and work of breathing to re-expand on the next breath.
Deficiency of surfactant is often seen in premature infants and causes respiratory
distress syndrome (RDS), also known as hyaline disease. Surfactant production
is an important marker of developmental maturity of the fetal lung (produced by
20-24 weeks) and is secreted into the airways by 30 weeks of gestation.
● The immature chest wall is soft and compliant(easily collapsable), contributing to
inefficient mechanisms of breathing. During inspiration in the young child, air is
drawn in by the downward movement of the diaphragm, but the resulting
negative pressure causes the “soft” chest wall to be drawn inward; this produces
so-called paradoxic breathing, or diaphragmatic breathing. Paradoxic breathing is
especially seen during REM sleep of premature infants.
● Children have greater oxygen consumption than adults per unit of body weight.
This is because the basal metabolic rate of a child is greater than that of an adult.
The work of breathing increases VO2 exponentially with respiratory distress.
Children, have less muscle glycogen reserve, which limits the efficiency of
accessory muscles, such that fatigue with lactic acidosis can occur quickly.
● Immune mechanisms are not fully developed at birth, making young infants more
susceptible to infection.
● Physiologic control of breathing may be impaired during the first few weeks of
life. For up to 3 weeks of age, the newborn has a blunted ventilatory response to
hypoxia compared with older children and adults. The mechanisms for this are
not well understood but may reflect reduced activity of the peripheral
chemoreceptors (in the carotid body) and nonadaptive responses in the
respiratory center (in the brainstem)
Examine the pathologic basis of adult and pediatric disorders which affect
the pulmonary system.
2
, Pulmonary Vascular Disorders
1. Analyze the etiology, clinical manifestations and pathophysiology of
pulmonary embolus, and pulmonary edema and describe the implications for
clinical practice. (pg. 1260 & 1275)
Pulmonary Edema
Etiology:
The most common cause of Pulmonary edema is left sided heart disease. When the left
ventricle fails, filling pressures on the left side of the heart increase and cause a concomitant
increase in pulmonary capillary hydrostatic pressure. When the hydrostatic pressure exceeds
oncotic pressure, fluid moves in the interstitium, or interstitial space (the space within the
alveolar septum between alveolus and capillary). Fluid moves to the lymphatic vessels and is
then removed from the lung. When the flow of fluid out of the capillaries exceeds the lymphatic
system’s ability to remove it, pulmonary edema develops.
Another cause of p. Edema is capillary injury that increases capillary permeability. Capillary
injury causes edema in cases of adult respiratory distress syndrome (ARDS) or inhalation of
toxic gases, such as ammonia. Capillary injury causes water and plasma proteins to leak out of
the capillary and move into the interstitium. When plasma proteins move into the lung
interstitium, they increase the interstitial oncotic pressure, which is usually very low. As the
interstitial oncotic pressure begins to equal capillary oncotic pressure, water moves out of the
capillary and into the lung.
P. edema can also result from obstruction of the lymphatic system. Drainage can be blocked by
compression of lymphatic vessels caused by edema, tumors, and fibrotic tissue or by increased
systemic venous pressure that elevates the hydrostatic pressure of the large pulmonary veins
into which the pulmonary lymphatic system drains This can happen in left-sided heart failure.
(POPE) Postobstructive pulmonary edema, or negative pressure p. Edema is a rare life-
threatening complication that can occur after relief of upper airway obstruction (i.e.
postextubation laryngospasm after anesthesia, epiglottitis , laryngeal tumor, or obstructive
tonsils). Attempted inspiration against an occluded airway creates excessive intrathoracic
negative pressure, causing increased venous return and blood flow to the right side of the heart
from the increased afterload. This combination of events causes increased pulmonary blood
volume and venous pressure and leads to pulmonary edema.
Clinical Manifestations:
Dyspnea, orthopnea, hypoxemia, and increased work of breathing
Physical examination may reveal inspiratory crackles (rales), dullness to percussion over the
lung bases, and evidence of ventricular dilation (S3 gallop and cardiomegaly). In severe edema,
3
Pulmonary and Shock
Module 6
Age related Difference in pulmonary anatomy and physiology
1. Describe the age-related changes which occur in the alveoli, chest wall, and
gas exchange. (pg 1244-45)
● Alveoli: During adulthood and as age advances, the alveoli tend to lose alveoli wall
tissue and capillaries. This process diminishes alveolar surface area available for gas
diffusion and decreases airway support provided by normal lung tissues.
● Chest Wall: Mechanical changes involve elastic properties of the lungs and chest wall.
Chest wall compliance decreases with age, because the ribs become ossified (less
flexible) and joints become stiffer. As a result, the chest wall loses some of its ability to
expand. In addition, respiratory muscle strength and endurance decrease by up to 20%
by age 70. These mechanical changes in the lung and chest wall, along with structural
changes in the alveoli, reduce ventilatory capacity in older adults. Vital capacity
decreases and residual volume increases, however, total lung capacity remains
unchanged. These changes decrease ventilatory reserves and lead to decreased
ventilation-perfusion ratios. With advancing age there is also increased immune
dysregulation, asymptomatic low-grade inflammation, and increased risk of infection.
● Gas Exchange: Alterations in gas exchange are reflected by blood gas analysis. With
advancing age, pH and Paco2 do not change much, even though it has been
documented that the chemoreceptors become less sensitive to gas partial pressure with
age. Older adults have a decreased compensatory response to hypercapnia and
hypoxemia; however, the perception of dyspnea remains intact and is even enhanced.
Pao2 declines with age as a result of structural and mechanical changes, such as loss of
alveolar surface area and increased ventilation-perfusion mismatch. The maximum Pao2
in an older adult at sea level can be estimated by multiplying the person’s age by 0.3
and subtracting the product from 100. There is also a decrease in the capillary network.
The decrease in Pao2 and diminished ventilatory reserve in an older adult lead to a
decrease in exercise tolerance. Respiratory muscle strength and endurance decrease
with age. Furthermore, older adults are at greater risk for respiratory depression caused
by medications.
2. Explain the structure and physiologic differences of the pulmonary system
in the infant and child. (pg. 1290-1293)
1
, ● The airways of infants and children are narrower than those of adults, thus
making them more prone to obstruction.
● Infants and young children continue to form new alveoli for several years after
birth.
● Surfactant is a lipid protein mix that is produced by type II alveolar cells and is
critical for maintaining alveolar expansion (thus allowing normal gas exchange). It
lines alveoli and reduces surface tension, preventing alveolar collapse at the end
of each exhalation. Without surfactant the alveoli tend to stay closed, demanding
greater inspiratory force and work of breathing to re-expand on the next breath.
Deficiency of surfactant is often seen in premature infants and causes respiratory
distress syndrome (RDS), also known as hyaline disease. Surfactant production
is an important marker of developmental maturity of the fetal lung (produced by
20-24 weeks) and is secreted into the airways by 30 weeks of gestation.
● The immature chest wall is soft and compliant(easily collapsable), contributing to
inefficient mechanisms of breathing. During inspiration in the young child, air is
drawn in by the downward movement of the diaphragm, but the resulting
negative pressure causes the “soft” chest wall to be drawn inward; this produces
so-called paradoxic breathing, or diaphragmatic breathing. Paradoxic breathing is
especially seen during REM sleep of premature infants.
● Children have greater oxygen consumption than adults per unit of body weight.
This is because the basal metabolic rate of a child is greater than that of an adult.
The work of breathing increases VO2 exponentially with respiratory distress.
Children, have less muscle glycogen reserve, which limits the efficiency of
accessory muscles, such that fatigue with lactic acidosis can occur quickly.
● Immune mechanisms are not fully developed at birth, making young infants more
susceptible to infection.
● Physiologic control of breathing may be impaired during the first few weeks of
life. For up to 3 weeks of age, the newborn has a blunted ventilatory response to
hypoxia compared with older children and adults. The mechanisms for this are
not well understood but may reflect reduced activity of the peripheral
chemoreceptors (in the carotid body) and nonadaptive responses in the
respiratory center (in the brainstem)
Examine the pathologic basis of adult and pediatric disorders which affect
the pulmonary system.
2
, Pulmonary Vascular Disorders
1. Analyze the etiology, clinical manifestations and pathophysiology of
pulmonary embolus, and pulmonary edema and describe the implications for
clinical practice. (pg. 1260 & 1275)
Pulmonary Edema
Etiology:
The most common cause of Pulmonary edema is left sided heart disease. When the left
ventricle fails, filling pressures on the left side of the heart increase and cause a concomitant
increase in pulmonary capillary hydrostatic pressure. When the hydrostatic pressure exceeds
oncotic pressure, fluid moves in the interstitium, or interstitial space (the space within the
alveolar septum between alveolus and capillary). Fluid moves to the lymphatic vessels and is
then removed from the lung. When the flow of fluid out of the capillaries exceeds the lymphatic
system’s ability to remove it, pulmonary edema develops.
Another cause of p. Edema is capillary injury that increases capillary permeability. Capillary
injury causes edema in cases of adult respiratory distress syndrome (ARDS) or inhalation of
toxic gases, such as ammonia. Capillary injury causes water and plasma proteins to leak out of
the capillary and move into the interstitium. When plasma proteins move into the lung
interstitium, they increase the interstitial oncotic pressure, which is usually very low. As the
interstitial oncotic pressure begins to equal capillary oncotic pressure, water moves out of the
capillary and into the lung.
P. edema can also result from obstruction of the lymphatic system. Drainage can be blocked by
compression of lymphatic vessels caused by edema, tumors, and fibrotic tissue or by increased
systemic venous pressure that elevates the hydrostatic pressure of the large pulmonary veins
into which the pulmonary lymphatic system drains This can happen in left-sided heart failure.
(POPE) Postobstructive pulmonary edema, or negative pressure p. Edema is a rare life-
threatening complication that can occur after relief of upper airway obstruction (i.e.
postextubation laryngospasm after anesthesia, epiglottitis , laryngeal tumor, or obstructive
tonsils). Attempted inspiration against an occluded airway creates excessive intrathoracic
negative pressure, causing increased venous return and blood flow to the right side of the heart
from the increased afterload. This combination of events causes increased pulmonary blood
volume and venous pressure and leads to pulmonary edema.
Clinical Manifestations:
Dyspnea, orthopnea, hypoxemia, and increased work of breathing
Physical examination may reveal inspiratory crackles (rales), dullness to percussion over the
lung bases, and evidence of ventricular dilation (S3 gallop and cardiomegaly). In severe edema,
3
