NURS 5315 UTA Exam 3 Skeletal Outlines + Practice
Questions (Cardiovascular, Pulmonary System, and Shock
States) With Complete Solutions
Explain the etiology, clinical manifestations, and
pathophysiology of pulmonary fibrosis
Etiology:
Excess fibrosis and connective tissue in lungs
Scar tissue after pulmonary disease (ARDS, TB, COVID)
Autoimmune (RA, sarcoidosis)
Inhalation of toxins
Idiopathic
Clinical manifestations:
Pathophysiology: Chronic inflammation - fibrosis of alveolar
epithelium - proliferation of myofibroblast - stiff alveoli -
decreased compliance- v/q mismatch - hypoxemia
Explain the defining characteristics, clinical manifestations, and
pathophysiology of hypoxemia
Defining characteristics: Reduced PaO2 with or without hypoxia
Respiratory failure </= 50 mmHg
Clinical manifestations: Tachycardia, cyanosis, confusion
Patho:
Hypoventilation
,V/Q mismatch, increased alveolocapillary membrane thickness
Ex. heart failure, PE, pulmonary edema, PNE
Explain the defining characteristics, clinical manifestations, and
pathophysiology of hypercarbia
Defining characteristics: Increased CO2 = PaCO2 over 50
mmHg and decreased serum pH </- 7.25
Clinical manifestations: =/- confusion, lethargy
Patho: Hypoventilation, decreased respiratory drive,
neuromuscular disease, airway obstruction, physiologic dead
space, chest wall deformity
How can you measure the severity of respiratory failure?
Two tests: Alveolar arterial oxygen gradient and PF ratio
Alveolar arterial oxygen gradient
Defines oxygenation disorders
PF ratio
Most helpful: ratio of partial pressure of oxygen in arterial blood
(PaO2) to the fraction of inspiratory oxygen concentration
(FiO2). This is how ARDs is classified.
What is the distinction between acute lung injury and acute
respiratory distress syndrome?
Inflammatory process in lungs that leads to alveolar epithelial
and vascular endothelial injury in the lungs, may be infective or
non-infective.
,Criteria: acute onset (<7 days), bilateral infiltrates, respiratory
distress not related to cardiac or fluid overload
Acute lung injury (ALI): PF ration </= 300
Acute respiratory distress syndrome (ARDS) PF ration </= 200
What are some common causes of ALI and ARDS?
Direct: PNE, aspiration, pulmonary contusion, fat emboli, near
drowning, inhalation injury, reperfusion, pulmonary edema, post
transplant
Indirect: Sepsis, trauma, cardiopulmonary bypass, drug
overdose, acute pancreatitis, blood transfusion
What are the clinical manifestations and pathophysiology of the
exudative (inflammatory) phase of ARDS?
Occurs in the first 72 hours
PF ratio: 201-300
Mild
Clinical manifestations: Dyspnea, hypoxemia, poor response to
oxygenation, hyperventilation, respiratory alkalosis, organ
dysfunction, metabolic acidosis, decreased tidal volume,
hypercapnia, decreased CO, hypotension
Patho:
What are the clinical manifestations and pathophysiology of the
proliferative phase of ARDS?
, One to three weeks
PF ration: 101-200
Moderate
Clinical manifestations: Dyspnea, hypoxemia, poor response to
oxygenation, hyperventilation, respiratory alkalosis, organ
dysfunction, metabolic acidosis, decreased tidal volume,
hypercapnia, decreased CO, hypotension
Patho: Early healing, pulmonary edema drain (increased
lymphatic drainage), increased pleural effusions, exudates
granulate - recovery of cap/alveolar barrier. Surfactant
production restarts.
What are the clinical manifestations and pathophysiology of the
fibrotic phase of ARDS?
14-21 days (overlaps with proliferative)
PF ration: less that 100
Severe
Clinical manifestations: Dyspnea, hypoxemia, poor response to
oxygenation, hyperventilation, respiratory alkalosis, organ
dysfunction, metabolic acidosis, decreased tidal volume,
hypercapnia, decreased CO, hypotension
Patho: Does not occur with everyone. Fibroblast proliferate in
alveoli, risk for pulmonary hypertension.
What is shock?
Questions (Cardiovascular, Pulmonary System, and Shock
States) With Complete Solutions
Explain the etiology, clinical manifestations, and
pathophysiology of pulmonary fibrosis
Etiology:
Excess fibrosis and connective tissue in lungs
Scar tissue after pulmonary disease (ARDS, TB, COVID)
Autoimmune (RA, sarcoidosis)
Inhalation of toxins
Idiopathic
Clinical manifestations:
Pathophysiology: Chronic inflammation - fibrosis of alveolar
epithelium - proliferation of myofibroblast - stiff alveoli -
decreased compliance- v/q mismatch - hypoxemia
Explain the defining characteristics, clinical manifestations, and
pathophysiology of hypoxemia
Defining characteristics: Reduced PaO2 with or without hypoxia
Respiratory failure </= 50 mmHg
Clinical manifestations: Tachycardia, cyanosis, confusion
Patho:
Hypoventilation
,V/Q mismatch, increased alveolocapillary membrane thickness
Ex. heart failure, PE, pulmonary edema, PNE
Explain the defining characteristics, clinical manifestations, and
pathophysiology of hypercarbia
Defining characteristics: Increased CO2 = PaCO2 over 50
mmHg and decreased serum pH </- 7.25
Clinical manifestations: =/- confusion, lethargy
Patho: Hypoventilation, decreased respiratory drive,
neuromuscular disease, airway obstruction, physiologic dead
space, chest wall deformity
How can you measure the severity of respiratory failure?
Two tests: Alveolar arterial oxygen gradient and PF ratio
Alveolar arterial oxygen gradient
Defines oxygenation disorders
PF ratio
Most helpful: ratio of partial pressure of oxygen in arterial blood
(PaO2) to the fraction of inspiratory oxygen concentration
(FiO2). This is how ARDs is classified.
What is the distinction between acute lung injury and acute
respiratory distress syndrome?
Inflammatory process in lungs that leads to alveolar epithelial
and vascular endothelial injury in the lungs, may be infective or
non-infective.
,Criteria: acute onset (<7 days), bilateral infiltrates, respiratory
distress not related to cardiac or fluid overload
Acute lung injury (ALI): PF ration </= 300
Acute respiratory distress syndrome (ARDS) PF ration </= 200
What are some common causes of ALI and ARDS?
Direct: PNE, aspiration, pulmonary contusion, fat emboli, near
drowning, inhalation injury, reperfusion, pulmonary edema, post
transplant
Indirect: Sepsis, trauma, cardiopulmonary bypass, drug
overdose, acute pancreatitis, blood transfusion
What are the clinical manifestations and pathophysiology of the
exudative (inflammatory) phase of ARDS?
Occurs in the first 72 hours
PF ratio: 201-300
Mild
Clinical manifestations: Dyspnea, hypoxemia, poor response to
oxygenation, hyperventilation, respiratory alkalosis, organ
dysfunction, metabolic acidosis, decreased tidal volume,
hypercapnia, decreased CO, hypotension
Patho:
What are the clinical manifestations and pathophysiology of the
proliferative phase of ARDS?
, One to three weeks
PF ration: 101-200
Moderate
Clinical manifestations: Dyspnea, hypoxemia, poor response to
oxygenation, hyperventilation, respiratory alkalosis, organ
dysfunction, metabolic acidosis, decreased tidal volume,
hypercapnia, decreased CO, hypotension
Patho: Early healing, pulmonary edema drain (increased
lymphatic drainage), increased pleural effusions, exudates
granulate - recovery of cap/alveolar barrier. Surfactant
production restarts.
What are the clinical manifestations and pathophysiology of the
fibrotic phase of ARDS?
14-21 days (overlaps with proliferative)
PF ration: less that 100
Severe
Clinical manifestations: Dyspnea, hypoxemia, poor response to
oxygenation, hyperventilation, respiratory alkalosis, organ
dysfunction, metabolic acidosis, decreased tidal volume,
hypercapnia, decreased CO, hypotension
Patho: Does not occur with everyone. Fibroblast proliferate in
alveoli, risk for pulmonary hypertension.
What is shock?
