Key Clinical Questions
How should a clinician rapidly assess the severity and stability of a patient with acute respiratory distress?
How can principles of respiratory physiology be effectively applied to guide diagnosis and therapy?
What are the indications and contraindications for noninvasive positive pressure ventilation (NIPPV) and what outcomes does this intervention affect?
When does a patient require advanced airway management?
You are called to emergently assess a 53 years old with COPD who is hospitalized with acute pancreatitis. He has received substantial fluid resuscitation and parenteral morphine for severe epigastric pain. He has become increasingly confused and somnolent and his oxygen saturation has acutely decreased to 82% on 2 L per nasal cannula. On a nonrebreather face mask, his SpO2 is now 98%. He appears uncomfortable, is tachycardic, tachypneic and moderately confused. His expiratory phase is prolonged, and breath sounds are nearly absent at the lung bases. He has moderate peripheral edema and his epigastrium is moderately tender.
Acute respiratory failure is a common inpatient medical emergency that mandates rapid patient assessment and initiation of potentially lifesaving therapy, often with a paucity of diagnostic information. The clinician must enter this time-pressured, high-risk scenario with a preestablished diagnostic and therapeutic schema that facilitates an efficient and comprehensive approach, which can be broken into four key steps:
Rapidly assess the severity and instability of the presentation
Determine the likely cause or causes
Assess efficacy of treatment
PATHOPHYSIOLOGY AND DIFFERENTIAL DIAGNOSIS
Oxygen binds hemoglobin after it diffuses across a pressure and concentration gradient from the alveoli to the pulmonary capillaries, which is generated by the mean airway pressure (primarily positive end-expiratory pressure, or PEEP) and the fraction of inspired oxygen (FiO2). Carbon dioxide exits the pulmonary circulation across a reverse gradient, but needs to be continually expired from the mouth for that gradient to be maintained. Thus, CO2 elimination depends upon minute ventilation (expiratory tidal volume × respiratory rate). The key implication of this physiology is that oxygenation is entirely driven by the fraction of inspired oxygen (FiO2) and the pressure under which oxygen is delivered. Hyperventilation has no impact upon hypoxemia, but it does increase CO2 elimination.
Oxygenation is entirely driven by the fraction of inspired oxygen (FiO2) and the pressure under which oxygen is delivered. Hyperventilation has no impact upon hypoxemia, but it does increase CO2 elimination.
Understanding the pathophysiologic underpinnings of acute respiratory failure simplifies the diagnostic approach and informs therapeutic interventions that are physiologically sound. Respiratory failure can be broken into five major categories:
Shunt occurs when pulmonary blood flow does ...