Respiratory Failure

Clues:

Type I Respiratory Failure is due to flooding of the alveole

Type II Respiratory Failure is due to abscence of O2 and acumulation of Co2

Type III Respiratory Failure is due to atelectasis

Type IV Respiratory Failure is due to respiratory muscles hypoperfusion in the context of a shock, in which the needs is near 40% of cardiac output

In hypotensive patients with clinical signs of a reduced CO, an assessment of intravascular and cardiac volume status is appropriate. A hypotensive patient with decreased intravascular and cardiac volume status may have a history suggesting hemorrhage or other volume losses (e.g., vomiting, diarrhea, polyuria). The jugular venous pressure (JVP) is often reduced in such a patient, while the change in pulse pressure as a function of respiration is increased. A hypotensive patient with increased intravascular volume status and cardiac dysfunction may have S₃ and/or S₄ gallops on cardiac examination, increased JVP, extremity edema, and crackles on lung auscultation. The chest x-ray may show cardiomegaly, widening of the vascular pedicle, Kerley B lines, and pulmonary edema. Chest pain and electrocardiographic changes consistent with ischemia may also be noted

Early intubation and mechanical ventilation are often required. Reasons for institution of endotracheal intubation and mechanical ventilation include acute hypoxemic respiratory failure as well as ventilatory failure, which frequently accompany shock. Acute hypoxemic respiratory failure may occur in patients with cardiogenic shock and pulmonary edema (Chap. 266) as well as in those in septic shock with pneumonia or acute respiratory distress syndrome (ARDS) (Chap. 265). Ventilatory failure often occurs as a result of an increased load on the respiratory system. This load may present in the form of acute metabolic acidosis (often lactic acidosis) or decreased compliance of the lungs ("stiff" lungs) as a result of pulmonary edema. Inadequate perfusion to respiratory muscles in the setting of shock may be another reason for early intubation and mechanical ventilation. Normally, the respiratory muscles receive a very small percentage of the CO. However, in patients who are in shock with respiratory distress for the reasons listed above, the percentage of CO dedicated to respiratory muscles may increase tenfold or more. Lactic acid production from inefficient respiratory muscle activity presents an additional ventilatory load.

Respiratory Failure

Type I, or Acute Hypoxemic, Respiratory Failure

This occurs when alveolar flooding and subsequent intrapulmonary shunt physiology occurs. Alveolar flooding may be a consequence of pulmonary edema, pneumonia, or alveolar hemorrhage. Pulmonary edema can be further categorized as occurring due to elevated intravascular pressures seen in heart failure and intravascular volume overload, or acute lung injury ("low-pressure pulmonary edema"; Chap. 266). ARDS (Chap. 262) represents an extreme degree of lung injury. This syndrome is defined by diffuse bilateral airspace edema seen by chest radiography, the absence of left atrial hypertension, and profound shunt physiology (Fig. 262-2), in a clinical setting in which this syndrome is known to occur. This includes sepsis, gastric aspiration, pneumonia, near drowning, multiple blood transfusions, and pancreatitis. The mortality rate of patients with ARDS was traditionally very high (50–70%), though recent changes in ventilator management strategy have led to reports of mortality in the low 30% range (see below)

For many years, physicians have suspected that mechanical ventilation of patients with acute lung injury and ARDS may propagate lung injury. Cyclical collapse and reopening of alveoli may be partly responsible for this. As seen in Fig. 261-3, the pressure-volume relationship of the lung in ARDS is not linear. Alveoli may collapse at very low lung volumes. Animal studies have suggested that stretching and overdistention of injured alveoli during mechanical ventilation can further injure the lung. Concern over this alveolar overdistention, termed ventilator induced "volutrauma," led to a multicenter, randomized, prospective trial to compare traditional ventilator strategies for acute lung injury and ARDS (large tidal volume—12 mL/kg ideal body weight) to a low tidal volume (6 mL/kg ideal body weight). This study showed a dramatic reduction in mortality in the low tidal volume group (large tidal volume—39.8% mortality versus low tidal volume—31% mortality) and confirmed that ventilator management could impact outcomes in these patients. In addition, a "fluid conservative" management strategy [maintaining a relatively low central venous pressure (CVP) or pulmonary capillary wedge pressure (PCWP)] is associated with the need for fewer days of mechanical ventilation when compared to a "fluid liberal" management strategy (maintaining a relatively high CVP or PCWP) in acute lung injury and ARDS

Type II Respiratory Failure

This type of respiratory failure occurs as a result of alveolar hypoventilation and results in the inability to eliminate carbon dioxide effectively. Mechanisms by which this occurs are categorized by impaired central nervous system (CNS) drive to breathe, impaired strength with failure of neuromuscular function in the respiratory system, and increased load(s) on the respiratory system. Reasons for diminished CNS drive to breathe include drug overdose, brainstem injury, sleep-disordered breathing, and hypothyroidism. Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis, phrenic nerve injury) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue).

The overall load on the respiratory system can be classified into increased resistive loads (e.g., bronchospasm), loads due to reduced lung compliance [e.g., alveolar edema, atelectasis, intrinsic positive end-expiratory pressure (autoPEEP)—see below], loads due to reduced chest wall compliance (e.g., pneumothorax, pleural effusion, abdominal distention), and loads due to increased minute ventilation requirements (e.g., pulmonary embolus with increased dead space fraction, sepsis).

The mainstays of therapy for type II respiratory failure are treatments directed at reversing the underlying cause(s) of ventilatory failure. Noninvasive positive-pressure ventilation using a mechanical ventilator with a tight-fitting face or nasal mask that avoids endotracheal intubation can often stabilize these patients. This approach has been shown to be beneficial in treating patients with exacerbations of chronic obstructive pulmonary disease. Noninvasive ventilation has been tested less extensively in other types of type II respiratory failure, but may be attempted nonetheless, in the absence of contraindications (hemodynamic instability, inability to protect airway, respiratory arrest).

Type III Respiratory Failure

This form of respiratory failure occurs as a result of lung atelectasis. Because atelectasis occurs so commonly in the perioperative period, this is also called perioperative respiratory failure. After general anesthesia, decreases in functional residual capacity lead to collapse of dependent lung units. Such atelectasis can be treated by frequent changes in position, chest physiotherapy, upright positioning, and aggressive control of incisional and/or abdominal pain. Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis.

Type IV Respiratory Failure

This form occurs due to hypoperfusion of respiratory muscles in patients in shock. Normally, respiratory muscles consume <5%>2 delivery. Patients in shock often suffer respiratory distress due to pulmonary edema (e.g., patients in cardiogenic shock), lactic acidosis, and anemia. In this setting, up to 40% of the CO may be distributed to the respiratory muscles. Intubation and mechanical ventilation can allow redistribution of the CO away from the respiratory muscles and back to vital organs while the shock is treated