Pulmonary Emergencies

Basic Anatomy and Physiology

• The trachea, bronchi, and bronchioles are the conducting airways and consist of a series of branching tubes that become narrower and shorter as they penetrate into the lungs. These airway structures have no diffusion capacity and represent about 150 ml of lung volume. Eventually the terminal bronchioles lead to the alveoli that form the actual gas-exchange interface. The alveolar surface consists of approximately 3000 ml of lung volume.
• The walls of the conducting airways contain smooth muscles which, when contracted, cause airway narrowing and increased resistance to airflow. These smooth muscles respond to both sympathetic and vagal input. Beta2-receptor stimulation causes muscle relaxation, while a-receptor and vagal stimulation result in bronchoconstriction. Constriction is also reflexive and may be initiated by irritants, temperature, and psychogenic causes.
• Contraction of the diaphragm and intercostals muscles increases the volume of the thoracic cavity creating a negative intrathoracic pressure. This bellows action draws air into the airways and alveoli by bulk flow. Expiration is a passive process that occurs as the elastic lung tissue returns to its preinspiratory volume.

Acute Respiratory Failure (ARF)

• Definition: ARF is an impairment of oxygen (O2) or carbon dioxide (CO2) gas exchange that results in immediate or impending breakdown of cell metabolism. There are two fundamental mechanisms (see Table 3A.1):
• Failure to oxygenate: Room air PaO2 <60 mm Hg.
• Failure to ventilate: PaCO2 >50 mm Hg.
• An increased work of breathing may signal impending ventilator failure prior to the development of hypercarbia or hypoxia.
• Patients who chronically retain CO2 have baseline elevation of their PaCO2 but usually have a normal pH via metabolic compensation. In these patients, ventilator failure is identified by an increase in PaCO2 above baseline and a corresponding decrease in pH.

Diagnosis

• Dyspnea is the most common symptom and is almost universal in awake patients.
• Crucial aspects of the physical evaluation include general appearance, vital signs, and pulmonary examination.
• General appearance
• Signs of increased work of breathing include diaphoresis, tripod positioning, intercostals muscle retractions, nasal flaring, and audible grunting. Patients may be unable to speak full sentences. Significant increases in work of breathing indicate acute or impending respiratory failure. Agonal respirations are slow, shallow breaths that identify impending respiratory arrest.

Common causes of acute respiratory failure

Failure to Oxygenate	Ventilation-perfusion mismatch (pneumonia, aspiration, ARDS* pulmonary embolism) Decrease in FiO2 Intra/extra pulmonary shunting Diffusion defects (emphysema, interstitial lung disease) Restrictive lung disease Ventilator failure
Failure to Ventilate	Depressed mental status (drugs, stroke, sepsis, seizures) Upper airway obstruction (croup, epiglottises, burns, cancer, trauma) Lower airway obstruction (asthma, COPD+, cancer) Chest wall disorders (flail chest, kyphosis, muscular dysfunction)

*ARDS: acute respiratory distress syndrome
+ COPD: chronic obstructive pulmonary disease

• Altered mental status (AMS) is an important indicator of ARF. Confusion, somnolence and agitation may occur secondary to hypoxia and/or hypercarbia. The presence of decreased mentation in patients with respiratory distress indicates the need for immediate intervention.
• Vital signs
• Respiratory rate (RR) is typically abnormal and may be elevated or depressed.
  Tachypnea occurs secondary to stimulation of central respiratory centers in patients with hypoxia or hypercarbia. Hypopnea results from drug ingestion, stroke, seizures, hypothyroidism, and other causes of impaired brainstem function.
• Patients with ARF usually have tachycardia as a result of underlying hypoxia and/ or an adrenergic response. However, severe hypoxia may also cause bradycardia.
• Pulse oximetry: all patients with oxygen saturation < 90% should be considered severely hypoxic (see following section for full discussion).
• Pulmonary examination
• Strider is associated with upper airway obstruction (larynx or trachea) and is audible without a stethoscope. Inspiratory Strider is classically seen with supraglottic obstruction and expiratory Strider with subglottic pathology.
• Wheezes are associated with lower airway obstruction. Bronchspasm is the most common cause but other etiologies include foreign body and pulmonary edema.
• Some patients with bronchospasm or airway obstruction may have little or no wheezing if airflow is severely reduced.
• Rhonchi occur with airflow through areas narrowed by inflammation, smooth muscle contraction, or mucous.
• Rales are suggestive of alveolar inflammation or fluid.
• Decreased or absent breath sounds may signify nonventilated lung segments, pleural effusion or pneumothorax.
• Pulse Oximetry (Pox) provides rapid, noninvasive measurement of oxygenation and correlates well with measured PaO2. A Pox reading of 90% corresponds to a PaO2 of approximately 60 mm Hg. Carbon monoxide (CO) poisoning may result in falsely elevated readings. Dark nail polish, peripheral vascular disease, hypoperfusion, and anemia may cause falsely depressed readings. Note that a normal Pox does not rule out the presence of hypercapnia.
• Arterial blood gas (ABG) may aid in the diagnosis in patients with suspected CO poisoning. It also allows the physician to assess the degree of hypoxia and hypercapnia but is not a necessary study in patients with a clinical picture consistent with ARF.
• Portable chest radiograph (CXR) is indicated in all patients with acute or impending respiratory failure. Findings are often useful for identification of the underlying cause and may have treatment implications. However, the decision to intubate or administer other airway interventions is nearly always based on clinical, rather than radiographic criteria. CXR should also be obtained after endotracheal intubation to assess tube placement.
• Laboratory results rarely affect management. However these patients are often critically ill with comorbid illness. Basic studies including complete blood count (CBC), electrolytes, blood urea nitrogen (BUN), creatinine and glucose as well as an electrocardiogram (EKG) should be obtained in most patients with ARF. Other studies may be indicated depending on the presentation.

Treatment

• Supplemental oxygen increases the delivered FiO2 with each liter of oxygen increasing FiO2 by approximately 4%. Many delivery devices are available but nasal cannulae and masks are the most commonly used.
• Nasal cannula delivers up to 44% FiO2. Oxygen administered at 1 to 6 L/min.
  Nasal cannula may be used for patients with mild hypoxia but is not appropriate in the setting of severe respiratory distress.
• Nonrebreather mask (NRB) delivers up to 98% FiO2 (almost 100%). Oxygen is generally administered at 15 L/min. NRB may be used in patients with moderate to severe hypoxia or as a bridge to more definitive therapy.
• Noninvasive Positive Pressure Ventilation (NPPV)
• NPPV provides positive pressure to airways using either a nasal or face mask. Both inspiratory pressure (IPAP) and expiratory pressure (EPAP) can be controlled. NPPV is probably most effective in disorders where treatment may be expected to result in rapid improvement of respiratory status, such as asthma, COPD, or pulmonary edema. Use of NPPV may avoid endotracheal intubation. The vast majority of patients who will fail treatment do so within the first 12 h.
• Most of the studies regarding NPPV have focused on COPD patients. The bulk of evidence is positive. Several controlled trials have shown improved gas exchange and lower intubation rates among patients treated with NPPV. Asthma and acute pulmonary edema have also been treated successfully with NPPV.
• NPPV does not provide airway protection. In order to be a candidate, a patient must have a clear sensorium, be able to initiate breaths, and be able to tolerate the mask.
• NPPV should be used in conjunction with a respiratory therapist, nurse, or physician who is skilled in its use. Once instituted, IPAP and EPAP are set independently. IPAP is adjusted to decrease the work of respiratory muscles and is titrated to the desired PaCO2. Avoid peak pressures >20 cm H2O. Oxygenation is controlled by adjusting the FiO2 and EPAP. Common initial settings are an EPAP of 3-5 cm H2O and IPAP of 10 cm H2O.
• Endotracheal intubation is the gold standard for respiratory support and airway management. Placement of an endotracheal tube (ETT) provides the maximum control of ventilation, oxygenation, and airway patency.
• Indications for intubation include:
• Severe or progressive hypoxemia
• Severe or progressive acute hypercapnia
• Severe or progressively increased work of breathing
• Airway protection
• Acute or impending airway occlusion
• Pulmonary support in the critically ill or injured patient
• Need for life-saving diagnostic studies or therapies in uncooperative patients
• Ventilator management varies depending upon the underlying mechanism. A detailed discussion of ventilatormanagement is beyond the scope of this text.
• Defect in oxygenation: adjust FiO2 and/or positive end expiratory pressure (PEEP) to achieve desired pO2.
• Defect in ventilation: adjust RR and/or tidal volume to achieve desired pCO2.
• Specific treatment: once the patient’s respiratory status is stabilized, directed therapy can begin. This might include medical therapy, surgical intervention, and/or specific ventilator strategies.

Disposition

• All patients with respiratory failure should be admitted to an intensive care unit (ICU).
• Patients with impending respiratory failure should be admitted to either an ICU or another closely monitored bed (e.g., step-down unit).
• Patients with a stable respiratory status who are at very low risk for deterioration can be admitted to a ward bed.