N5315 Advanced Pathophysiology
Pulmonary and Shock
Core Concepts and Objectives with Advanced Organizers
Age related Difference in pulmonary anatomy and physiology ; pg1244-1245
1. Describe the age-related changes which occur in the alveoli, chest wall, and gas exchange.
Normal alterations include:
-loss of elastic recoil
-stiffening of the chest wall: ribs become less flexible(ossified) and joint become
striffer=stiff chest wall.
-changes in gas exchange: During childhood and as age advances, alveoli lose alveoli wall
tissue and capillaries which cause to diminish alveolar surface area available for gas
diffusion and decreases airway support. Loses ability to expand.
-increase in flow resistance-due to changes in lung& chest wall and structural changes of
alveoli=reduce ventilator capacity. Vital capacity decreases and residual volume
increases(total lung capacity remains the same). Ventilator reserves change and lead to
decreased ventilation-perfusion ratios.
**As we age, increase immune dysregulation, asymptomatic low-grade inflammation and
increase risk of infection** Pa O2 decreases wih age due to structural and mechanical changes
described above.
2. Explain the structure and physiologic differences of the pulmonary system in the infant and
child. ; 1291-1293, 1314
-Airway of infants and children are narrower than adults=more prone to obstruction.
-infants up to 2-3 months are “obligatory nose breathers.
-infants and young children continue to form new alveoli for years after birth
-chest wall compliance is high in infants due to cartilaginous structures of thoracic cage not
yet well ossified(ossification occurs through childhood)=chest wall easily collapsible.
-children have greater oxygen consumption than adults per unit of body weight.
Examine the pathologic basis of adult and pediatric disorders which affect the pulmonary system.
Pulmonary Vascular Disorders
1. Analyze the etiology, clinical manifestations and pathophysiology of pulmonary
embolus, and pulmonary edema and describe the implications for clinical practice.
Disease Etiology Clinical Pathophysiology Clinical
Manifestations Implications
Pulmona -definition: -most cases sx -effect of embolus -if PE suspected
ry occlusion or nonspecific depends on the (STAT): CXR(can
Embolus partial occlusion extent of be normal for 1st 24
-important to evaluate
; pg of the pulmonary pulmonary blood hrs until atelectasis
risk factors and
1275- artery or its flow obstruction, occurs),
predisposing factors
1276 branches by an the size of the ABG(hypoxemia
to dx (Wells
embolus. affected vessels, w/respiratory
prediction rule model
nature of embolus, alkalosis(usually
,-most commonly to help predict for pt and secondary hyperventilation)),
results due to with risk factors) effects. EKG(evidence of
embolization of a right heart failure).
-in suspect of PE, -PE can cause: 1.
clot from DVT
assess for DVT= calf Embolus with -serum D-dimer
involving the
pain, tenderness/calf infarction:embolus measures product
lower leg.
asymmetry when causing death of of thrombus
-less common documented with tape portion of lung degradation by
nonthromotic measure. tissue 2. Embolus fibronolytic system
emboli: tissue w/o infarction: and if normal
-DVT often
fragments, embolus that makes presence of
asymptomatic &
lipids(fats), a doesn’t cause PE highly unlikely.
clinical exam has low
foreign body or permanent lung
sensitivity for clot -CT
an air bubble. injury(perfucion to
presence(es. In thigh angiography(angiog
affected area is
-risk factors: and pelvis. ) ram) or MRI(rare to
maintained by
conditions and be done, no need to
-individual w/PE: bronchial
disorder that diagnose).
sudden onset of circulation). 3.
promote blood
pleuritic chest pain, Massive - elevated troponin
clotting as a
dyspnea, tachypnea, occlusion: level(risk and
result of venous
tachycardia, and embolus that severity of
stasis(immobiliza
unexplained anxiety. occludes major PE)=increases w/
tion, heart
portion of right ventricular
failure), -occasional syncope pulmonary strain or failure.
hypercoagulabilit or hemoptysis occurs. circulation(ex
y (inherited -Ideal tx of PE:
-sx of large emboli: main pulm artery
coagulation prevention of risk
pleural friction rub, embolus) 4.
disorders, factor recognition
pleural effusion, Multiple PE:
malignancy, and eliminating
fever, leukocytosis. chronic or
hormone predisposing
recurrent.
replacement, oral -recurrent PE those factors (such as
contraceptives, with hx of PE -As the thrombus immobile/bedrest
pregnancy, lodges into the pt=exercise,
endothelial injury -recurrent small pulmonary compression
to cells that line emboli may ot be circulation, there stockings, early
vessels(trauma, detected until is a release both of ambulation),
caustic progressive neurohumoral initiation of
intravenous incapacitation, substances prophylactic
infusions)..all precordial pain, (serotonin, anticoagulation w/
these 3 are anxiety, dyspnea, histamine, unfractioned or low
known as right ventricular catecholamines, molecular weight
Virchow’s triad. enlargement. angiotensin II, heparin, warfarin,
-massive occlusion= inflammatory or fondaparinaux. If
-genetic risks
shock, hypotension, mediators such as anticoag is
, include Factor V tachypnea, endothelin, contraindicated:
Leiden tachycardia, severe leukotrienes, placement of filter
mutation(activate pulmonary thromboxanes, and in the inferior vena
d protein C hypertension, chest toxic oxygen free cava can prevent
resistance), pain. radicals). Causing emboli reaching the
antithrombin II widespread lung.
deficiency, vasoconstriction
-Management of
protein C/S that impedes blood
PE: oxygen,
deficiency, flow to lung which
hemodynamic
prothrombin increases
stabilization w/fluid
20210 gene pulmonary artery
if needed, followed
mutation. pressures leading
by rapid
to right sided heart
**blood clot administration of
failure. Absent
becomes embolus anticoagulation.
blood flow to lung
when all or part
segment causes If massive life-
of it breaks away
ventilation- threatening
from site of
perfusion embolism=
formation and
mismatch fibrinolytic agent
begins to travel in
(increase in dead such as
the blood stream.
space) and streptokinase can
***
decrease in be used and may be
surfactant infused through
production. The pulmonary artery
affected lung catheter (pt may
causes require emergent
atelectasis=hypox percutaneous or
emia. If thrombus surgical
is large enough= embolectomy).
infarction of lung
tissue,
dysrhythmias,
decreased cardiac
output, shock,
death. If does not
cause infarction
then clot is
dissolved by the
fibrinolitic system.
Pulmona -definiton: excess -sx: dyspnea, -most common -tx (depends on
ry water in lung. orthopnea, cause: left sided cause)
Edema; Normal hypoxemia, increae heart disease.
-if edema is caused
Pulmonary and Shock
Core Concepts and Objectives with Advanced Organizers
Age related Difference in pulmonary anatomy and physiology ; pg1244-1245
1. Describe the age-related changes which occur in the alveoli, chest wall, and gas exchange.
Normal alterations include:
-loss of elastic recoil
-stiffening of the chest wall: ribs become less flexible(ossified) and joint become
striffer=stiff chest wall.
-changes in gas exchange: During childhood and as age advances, alveoli lose alveoli wall
tissue and capillaries which cause to diminish alveolar surface area available for gas
diffusion and decreases airway support. Loses ability to expand.
-increase in flow resistance-due to changes in lung& chest wall and structural changes of
alveoli=reduce ventilator capacity. Vital capacity decreases and residual volume
increases(total lung capacity remains the same). Ventilator reserves change and lead to
decreased ventilation-perfusion ratios.
**As we age, increase immune dysregulation, asymptomatic low-grade inflammation and
increase risk of infection** Pa O2 decreases wih age due to structural and mechanical changes
described above.
2. Explain the structure and physiologic differences of the pulmonary system in the infant and
child. ; 1291-1293, 1314
-Airway of infants and children are narrower than adults=more prone to obstruction.
-infants up to 2-3 months are “obligatory nose breathers.
-infants and young children continue to form new alveoli for years after birth
-chest wall compliance is high in infants due to cartilaginous structures of thoracic cage not
yet well ossified(ossification occurs through childhood)=chest wall easily collapsible.
-children have greater oxygen consumption than adults per unit of body weight.
Examine the pathologic basis of adult and pediatric disorders which affect the pulmonary system.
Pulmonary Vascular Disorders
1. Analyze the etiology, clinical manifestations and pathophysiology of pulmonary
embolus, and pulmonary edema and describe the implications for clinical practice.
Disease Etiology Clinical Pathophysiology Clinical
Manifestations Implications
Pulmona -definition: -most cases sx -effect of embolus -if PE suspected
ry occlusion or nonspecific depends on the (STAT): CXR(can
Embolus partial occlusion extent of be normal for 1st 24
-important to evaluate
; pg of the pulmonary pulmonary blood hrs until atelectasis
risk factors and
1275- artery or its flow obstruction, occurs),
predisposing factors
1276 branches by an the size of the ABG(hypoxemia
to dx (Wells
embolus. affected vessels, w/respiratory
prediction rule model
nature of embolus, alkalosis(usually
,-most commonly to help predict for pt and secondary hyperventilation)),
results due to with risk factors) effects. EKG(evidence of
embolization of a right heart failure).
-in suspect of PE, -PE can cause: 1.
clot from DVT
assess for DVT= calf Embolus with -serum D-dimer
involving the
pain, tenderness/calf infarction:embolus measures product
lower leg.
asymmetry when causing death of of thrombus
-less common documented with tape portion of lung degradation by
nonthromotic measure. tissue 2. Embolus fibronolytic system
emboli: tissue w/o infarction: and if normal
-DVT often
fragments, embolus that makes presence of
asymptomatic &
lipids(fats), a doesn’t cause PE highly unlikely.
clinical exam has low
foreign body or permanent lung
sensitivity for clot -CT
an air bubble. injury(perfucion to
presence(es. In thigh angiography(angiog
affected area is
-risk factors: and pelvis. ) ram) or MRI(rare to
maintained by
conditions and be done, no need to
-individual w/PE: bronchial
disorder that diagnose).
sudden onset of circulation). 3.
promote blood
pleuritic chest pain, Massive - elevated troponin
clotting as a
dyspnea, tachypnea, occlusion: level(risk and
result of venous
tachycardia, and embolus that severity of
stasis(immobiliza
unexplained anxiety. occludes major PE)=increases w/
tion, heart
portion of right ventricular
failure), -occasional syncope pulmonary strain or failure.
hypercoagulabilit or hemoptysis occurs. circulation(ex
y (inherited -Ideal tx of PE:
-sx of large emboli: main pulm artery
coagulation prevention of risk
pleural friction rub, embolus) 4.
disorders, factor recognition
pleural effusion, Multiple PE:
malignancy, and eliminating
fever, leukocytosis. chronic or
hormone predisposing
recurrent.
replacement, oral -recurrent PE those factors (such as
contraceptives, with hx of PE -As the thrombus immobile/bedrest
pregnancy, lodges into the pt=exercise,
endothelial injury -recurrent small pulmonary compression
to cells that line emboli may ot be circulation, there stockings, early
vessels(trauma, detected until is a release both of ambulation),
caustic progressive neurohumoral initiation of
intravenous incapacitation, substances prophylactic
infusions)..all precordial pain, (serotonin, anticoagulation w/
these 3 are anxiety, dyspnea, histamine, unfractioned or low
known as right ventricular catecholamines, molecular weight
Virchow’s triad. enlargement. angiotensin II, heparin, warfarin,
-massive occlusion= inflammatory or fondaparinaux. If
-genetic risks
shock, hypotension, mediators such as anticoag is
, include Factor V tachypnea, endothelin, contraindicated:
Leiden tachycardia, severe leukotrienes, placement of filter
mutation(activate pulmonary thromboxanes, and in the inferior vena
d protein C hypertension, chest toxic oxygen free cava can prevent
resistance), pain. radicals). Causing emboli reaching the
antithrombin II widespread lung.
deficiency, vasoconstriction
-Management of
protein C/S that impedes blood
PE: oxygen,
deficiency, flow to lung which
hemodynamic
prothrombin increases
stabilization w/fluid
20210 gene pulmonary artery
if needed, followed
mutation. pressures leading
by rapid
to right sided heart
**blood clot administration of
failure. Absent
becomes embolus anticoagulation.
blood flow to lung
when all or part
segment causes If massive life-
of it breaks away
ventilation- threatening
from site of
perfusion embolism=
formation and
mismatch fibrinolytic agent
begins to travel in
(increase in dead such as
the blood stream.
space) and streptokinase can
***
decrease in be used and may be
surfactant infused through
production. The pulmonary artery
affected lung catheter (pt may
causes require emergent
atelectasis=hypox percutaneous or
emia. If thrombus surgical
is large enough= embolectomy).
infarction of lung
tissue,
dysrhythmias,
decreased cardiac
output, shock,
death. If does not
cause infarction
then clot is
dissolved by the
fibrinolitic system.
Pulmona -definiton: excess -sx: dyspnea, -most common -tx (depends on
ry water in lung. orthopnea, cause: left sided cause)
Edema; Normal hypoxemia, increae heart disease.
-if edema is caused
