Lung Transplant, Respiratory Failure, ARDS, and ABGs Flashcards
general indications for lung transplant
*pt’s lungs are damaged to the point of disability, with life expectancy < 5 years:
-FEV1 < 25% predicted and falling
-FVC < 30% predicted and falling
-DLCO < 30% predicted and falling
*pt otherwise has good function of other organs
*typical diseases: IPF, COPD, CF, NSIP, scleroderma, A1AT deficiency, PAH
indications to NOT do a lung transplant
*other organs are too damaged to withstand major surgery and rehab
*disease affecting the lungs is uncontrolled and likely to recur
*BMI is too high
*uncontrolled acid reflux (GERD)
*process not acceptable to patient or lungs are not available
after lung transplant: immune rejection
*a persistent and unending battle
*acute rejection = immediate and highly inflammatory
*chronic rejection = slow and progressive
*medications are use to reduce cell-mediated immunity (prednisone, mTOR inhibitors, mycophenolate mofetil)
*sine qua non feature of chronic rejection: progressive airflow obstruction on PFTS; aka bronchiolitis obliterans syndrome (BOS):
-biopsy demonstrates constrictive/obliterative bronchiolitis
3 types of respiratory failure
- Hypoxemic Respiratory Failure (Type 1)
- Hypercapnic Respiratory Failure (Type 2)
- Mixed (Hypoxemic & Hypercapnic) Respiratory Failure (Type 1 & 2)
arterial blood gas (ABG) reports what?
-pH
-PaCO2
-PaO2
-HCO3-
-base excess
-O2 saturation
hypoxia vs. hypoxemia
*hypoxia = low oxygen gas pressure (ex. tissue hypoxia, alveolar hypoxia)
*hypoxemia = low blood oxygen CONTENT
-usually due to low oxyhemoglobin
-most common: low oxyhemoglobin percentage (saturation)
-sometimes due to severe anemia or hemoglobinopathies
5 mechanisms of hypoxemia
- decreased inspired PO2
- hypoventilation or increased dead space
- diffusion limitation
- V/Q mismatching
- shunt
mechanisms of hypoxemia: decreased inspirated PO2
*due to decreased inspired oxygen
*examples: high altitudes (climbing to the top of Mt. Everest); low concentrations of oxygen in the inspired air
*not commonly seen in medical practice
mechanisms of hypoxemia: hypoventilation
*increased PCO2 (failure to eliminate CO2)
*can be due to diaphragm dysfunction, medications (ex. opioids or benzodiazepines), or brainstem stroke
mechanisms of hypoxemia: increased dead space
*air spaces that are ventilated but not perfused
*dead space first creates hypercapnia (increased PCO2) and consequently causes hypoxemia
*normal dead space in trachea and conducting airways
*abnormal increases in dead space: severe emphysema, pulmonary embolism, increased zone 1 physiology
mechanisms of hypoxemia: diffusion limitation
*decreased diffusion as a result of alveolar thickening or loss of area
*alveolar problems include emphysema and loss of alveolar units (COPD)
*interstitial problems include: pulmonary edema, pulmonary fibrosis
mechanisms of hypoxemia: V/Q mismatching
*things that decrease the “V” (ventilation):
-alveolar filling/airway obstruction (edema, pus, blood, atelectasis, mucus plugging)
*things that decrease the “Q” (perfusion):
-perfusion defects (pulmonary arterial hypertension, pulmonary embolism)
acute respiratory distress syndrome (ARDS) - overview
*a special case of V/Q mismatch
*constellation of findings with different underlying causes
*recognized in patients with infiltrates on both sides of the lung that are acute
acute respiratory distress syndrome (ARDS) - diagnostic criteria
*diagnosed by “Berlin criteria”:
-timing: onset less than 1 week
-imaging: bilateral opacities not fully explained by effusions, lung collapse, or nodules
-cause: not fully explained by hydrostatic edema (such as cardiac failure or other fluid overload)
acute respiratory distress syndrome (ARDS) - classification of severity
*severity is classified by PaO2/FiO2 ratio (P/F ratio), measured with > 5 cmH20 of PEEP:
-mild: between 300 and 200
-moderate: between 200 and 100
-severe: less than 100
note: normal P/F ratio is ~500
acute respiratory distress syndrome (ARDS) - pathophysiology
*increased alveolar capillary permeability and surfactant dysfunction
*non-cardiogenic pulmonary edema can result from inflammation and cytokine release in many conditions (esp. pneumonia, sepsis)
acute respiratory distress syndrome (ARDS) - causes
*pneumonia
*sepsis
*major trauma
*pancreatitis
acute respiratory distress syndrome (ARDS) - management
*LOW TIDAL VOLUME mechanical ventilation:
-maintain tidal volume at 6mL/kg of ideal body weight
-maintain mean airway pressure as low as possible
-“permissive hypercapnia”: tolerate some hypercapnia to keep the tidal volume low
*other management principles:
-conservative fluid management
-prone positioning (on stomach)
-corticosteroids
mechanisms of hypoxemia: shunt
*blood passing form right to left heart without seeing a functional alveolus (the blood has no opportunity to participate in gas exchange)
*normal shunts: bronchial circulation and thebesian veins (1-3% of CO)
*ABNORMAL:
-patent foramen ovale
-complete fill of airway (edema, blood, pus)
-atelectasis, mucus plugging, foreign body
mechanisms of hypoxemia: which one(s) correct with 100% oxygen?
all of them EXCEPT SHUNTS
i.e. decreased inspirated PO2, hypoventilation/increased dead space, diffusion limitation, and V/Q mismatching all can be corrected by placing the patient on 100% oxygen
hypercapnic respiratory failure - causes
*caused by an imbalance in the normal PaCO2 homeostasis, resulting from any of:
1. increased CO2 production (fever or poising)
2. decreased minute ventilation (CNS injury, depressants, obesity, hypoventilation syndrome)
3. increased dead space (severe COPD)
hypercapnic respiratory failure - clinical presentation
*somnolence
*lethargy
*asterixis
*the acutely ill respiratory patient that’s “tiring out”
*note - thing of CO2 narcolepsy
causes of respiratory acidosis
*common causes:
-airway obstruction (COPD)
-depression of respiratory control centers (sedatives, opiates)
*recall: primary disturbance = ELEVATED PCO2
causes of metabolic acidosis
*common causes:
-ingested toxins (ethylene glycol)
-lactic acidosis (shock, severe sepsis)
-diarrhea
*recall: primary disturbance = DECREASED [HCO3-]
