Week 3 Study Guide
ARTERIAL BLOOD GAS
ACID pH 7.35 – 7.45 BASE
BASE PaCO2 35 – 45 ACID
ACID HCO3 22 – 26 BASE
UNCOMPENSATED PARTIALLY COMPENSATED FULLY COMPENSATED
Normal Abnormal Abnormal Normal Abnormal
Respiratory
CO2 or HCO3Acidosis pH CO2 > 45 ALL pH CO2 & HCO3
Respiratory Alkalosis PaCO2 < 35
Metabolic Acidosis HCO3 < 22
Metabolic Alkalosis HCO3 > 26
Hypoventilation: Hyperventilation:
Acidic Alkalotic
CO2 CO2
O2 O2
LAB LEVELS:
Clotting Bleeding PT 11 – 12.5
Clotting Bleeding INR 0.8 – 1.1 (Goal for Warfarin 2 – 3)
Clotting Bleeding aPTT 30 – 40 (higher in Heparin)
Bleeding Clotting Platelets 150k – 400k
- No PE + PE D-Dimer < 0.4
Inflammation Fibrinogen Level 200 - 400
Bleeding Clotting Fibrin Degradation < 10
Troponin 0.006 – 0.039
Anemia Dehydration HGB F: 12 – 16
M: 14 – 18
Anemia Dehydration HCT F: 37 – 47
M: 42 – 52
BUN 9 – 23
Creatinine F: 0.5 – 1.1
M: 0.7 – 1.3
, Week 3 Study Guide
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
WHAT IS HAPPENING?
Normal Lung Volume: 6 – 10 mL/kg
ARDS Lung Volume: 4 – 8 mL/kg
Sudden progressive form of acute respiratory failure
Mortality rate of 60%
A systemic inflammatory response injures the alveolar-
capillary membrane
o Becomes permeable to large molecules
o Lungs space gets filled with fluid
RISK FACTOR:
Lung injury resulting from:
o Sepsis (most common)
o Aspiration
o Pulmonary emboli
o Pneumonia
o Lung infections
o Near drowning
o Trauma
o Transfusion reactions
o CNS damage
o Smoke/toxic gas inhalation
o Drug ingestion/overdose
MANIFESTATIONS:
SOB Injury/Exudative Phase: occurs approx. 1-7 days after injury
Dyspnea w/ or w/o exertion o Edema
Orthopnea (difficulty breathing lying flat) o Filling of fluid
Rapid, shallow breathing o Intrapulmonary shunt develops leading to surfactant dysfunction
Cyanotic, mottled, dusky skin o Alveolar cell damage (atelectasis)
HR o Necrotic cell, protein, fibrin form
Hypotension o Refractory hypoxemia (hypoxemia regardless of O2 concentration)
Substernal or suprasternal retractions Proliferative/Reparative Phase: begins 1-2 weeks after injury
SaO2 (< 90%) o Influx of neutrophils, monocytes, & lymphocytes
Adventitious breath sounds (wheezing, rales)
o Fibroblast proliferation
Cardiac arrhythmias
Confusion o PVR
Lethargy o Pulmonary hypertension
Bilateral noncardiogenic pulmonary edema o Hypoxemia worsens
Reduced lung compliance o Phase complete when lung becomes dense & fibrous
Dense patchy bilateral pulmonary infiltrates Fibrotic/Chronic Phase: occurs approx. 2-3 weeks after injury
Classic Sign of ARDS: o Lung completely remodeled by collagenous fibrous tissue
o Severe hypoxemia despite o Decreased lung compliance
administration of 100% oxygen o Pulmonary hypertension
o Hypoxemia
LAB/DIAGNOSTIC TESTS:
ABGs
o PaO2 (hypoventilation, acidic)
o PaCO2 (hypoventilation, acidic)
o pH (acidic)
Chest X-Ray (to confirm)
o Pulmonary edema
o White lungs
ECG (to rule out cardiac involvement)
Hemodynamic monitoring (PAWP usually )
ARTERIAL BLOOD GAS
ACID pH 7.35 – 7.45 BASE
BASE PaCO2 35 – 45 ACID
ACID HCO3 22 – 26 BASE
UNCOMPENSATED PARTIALLY COMPENSATED FULLY COMPENSATED
Normal Abnormal Abnormal Normal Abnormal
Respiratory
CO2 or HCO3Acidosis pH CO2 > 45 ALL pH CO2 & HCO3
Respiratory Alkalosis PaCO2 < 35
Metabolic Acidosis HCO3 < 22
Metabolic Alkalosis HCO3 > 26
Hypoventilation: Hyperventilation:
Acidic Alkalotic
CO2 CO2
O2 O2
LAB LEVELS:
Clotting Bleeding PT 11 – 12.5
Clotting Bleeding INR 0.8 – 1.1 (Goal for Warfarin 2 – 3)
Clotting Bleeding aPTT 30 – 40 (higher in Heparin)
Bleeding Clotting Platelets 150k – 400k
- No PE + PE D-Dimer < 0.4
Inflammation Fibrinogen Level 200 - 400
Bleeding Clotting Fibrin Degradation < 10
Troponin 0.006 – 0.039
Anemia Dehydration HGB F: 12 – 16
M: 14 – 18
Anemia Dehydration HCT F: 37 – 47
M: 42 – 52
BUN 9 – 23
Creatinine F: 0.5 – 1.1
M: 0.7 – 1.3
, Week 3 Study Guide
ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)
WHAT IS HAPPENING?
Normal Lung Volume: 6 – 10 mL/kg
ARDS Lung Volume: 4 – 8 mL/kg
Sudden progressive form of acute respiratory failure
Mortality rate of 60%
A systemic inflammatory response injures the alveolar-
capillary membrane
o Becomes permeable to large molecules
o Lungs space gets filled with fluid
RISK FACTOR:
Lung injury resulting from:
o Sepsis (most common)
o Aspiration
o Pulmonary emboli
o Pneumonia
o Lung infections
o Near drowning
o Trauma
o Transfusion reactions
o CNS damage
o Smoke/toxic gas inhalation
o Drug ingestion/overdose
MANIFESTATIONS:
SOB Injury/Exudative Phase: occurs approx. 1-7 days after injury
Dyspnea w/ or w/o exertion o Edema
Orthopnea (difficulty breathing lying flat) o Filling of fluid
Rapid, shallow breathing o Intrapulmonary shunt develops leading to surfactant dysfunction
Cyanotic, mottled, dusky skin o Alveolar cell damage (atelectasis)
HR o Necrotic cell, protein, fibrin form
Hypotension o Refractory hypoxemia (hypoxemia regardless of O2 concentration)
Substernal or suprasternal retractions Proliferative/Reparative Phase: begins 1-2 weeks after injury
SaO2 (< 90%) o Influx of neutrophils, monocytes, & lymphocytes
Adventitious breath sounds (wheezing, rales)
o Fibroblast proliferation
Cardiac arrhythmias
Confusion o PVR
Lethargy o Pulmonary hypertension
Bilateral noncardiogenic pulmonary edema o Hypoxemia worsens
Reduced lung compliance o Phase complete when lung becomes dense & fibrous
Dense patchy bilateral pulmonary infiltrates Fibrotic/Chronic Phase: occurs approx. 2-3 weeks after injury
Classic Sign of ARDS: o Lung completely remodeled by collagenous fibrous tissue
o Severe hypoxemia despite o Decreased lung compliance
administration of 100% oxygen o Pulmonary hypertension
o Hypoxemia
LAB/DIAGNOSTIC TESTS:
ABGs
o PaO2 (hypoventilation, acidic)
o PaCO2 (hypoventilation, acidic)
o pH (acidic)
Chest X-Ray (to confirm)
o Pulmonary edema
o White lungs
ECG (to rule out cardiac involvement)
Hemodynamic monitoring (PAWP usually )
