Pulmonary failure reflects a gas exchange defect or defect of the ventilatory pump. Table 34-1 shows the classification of pulmonary failure by specific causes and the mechanisms involved. Some common predisposing conditions include primary cardiovascular and pulmonary conditions (e.g., chronic lung disease, overwhelming pneumonia, and myocardial infarction [MI]) and cardiovascular and pulmonary conditions that are secondary to other conditions (e.g., motor neuron diseases, spinal cord injury, stroke, and muscular dystrophy) (see Chapter 35). The oxygen and carbon dioxide tensions that have been used to define failure are variable because they depend on factors such as premorbid status, general health, age, prior blood gas profile, and the time frame for the development of failure. Arterial blood gases and pH are essential in the assessment of cardiovascular and pulmonary failure, which is usually diagnosed when the PaO₂ falls below 50 to 60 mm Hg and the PaCO₂ rises above 50 mm Hg.¹

Table 34-1

Classification of Respiratory Failure by Cause and Mechanism

Origin	Drugs	Metabolic	Neoplasms	Infections	Trauma	Other
Brain	Narcotics Barbiturates Sedatives Poisons Anesthetics	Hyponatremia Hypocalcemia Hypercapnia Alkalosis Hyperglycemia Myxedema	Primary Metastatic	Meningitis Encephalitis Abscess Bulbar polio	Direct injury Increased pressure	Central alveolar hypoventilation Obstructive sleep apnea
Nerves and muscles	Curariform drugs Arsenic Aminoglycosides	Hypophosphatemia Hypomagnesemia	Primary Metastatic	Polio Tetanus	Direct injury	Motor neuron disease Myasthenia gravis Multiple sclerosis Muscular dystrophy Guillain-Barré syndrome
Upper airway			Tonsillar adenoid hyperplasia Goiter Polyps Malignant tumors	Epiglottitis Laryngotracheitis	Vocal cord paralysis Tracheomalacia Cricoarytenoid arthritis Laryngeal edema
Chest bellows					Flail chest Burn with keloids	Scleroderma Pleural interposition (fibrosis, fluid, tumor, air) Spondylitis Scoliosis Kyphosis
Contributing factors						Massive obesity Ascites Ileus Pain Recumbency
Lower airway and parenchyma				Viral (bronchiolitis, bronchopneumonia) Bacterial (bronchitis, pneumonia, abscess, bronchiectasis) Fungal Mycoplasma	Contused lung	Bronchospasm Heart failure: congestive, restrictive, obstructive COPD Respiratory distress syndrome Interstitial lung disease Atelectasis Cystic fibrosis Pulmonary emboli

From Civettia, J.M. Taylor, R.W. & Kirby, R.R (1988). Critical care, Philadelphia: JB Lippincott.

Primary cardiac failure reflects failure of the myocardium to pump blood to the pulmonary and systemic circulations and maintain adequate tissue perfusion. Significant dysfunction of the left ventricle can lead to pulmonary vascular congestion and cardiogenic pulmonary edema (i.e., congestive heart failure). Conditions affecting the heart that can lead to failure include significant myocardial damage as a result of infarction or myopathy, valvular heart disease, and congenital defects.

Both primary pulmonary and cardiac failure can be classified into acute and chronic stages. The compensation mechanisms that occur in the two stages are distinct. With adequate physiological compensation, patients can tolerate some degree of chronic failure. Patients with a mild degree of failure can live reasonably independent lives. Moderate failure is significantly more limiting; these patients may require home ventilatory support (e.g., supplemental oxygen and nighttime ventilation). Severe failure necessitates hospitalization, mechanical ventilatory support, and supplemental oxygen support.

Obstructive Lung Disease

Pathophysiology and Medical Management

Obstructive lung disease can result in ventilatory failure and admission of the patient to the ICU, or it can complicate management if the patient is admitted for other reasons.² If conservative management fails or is unlikely to improve critically impaired oxygen transport and gas exchange and to adequately remove copious and tenacious secretions, intubation and mechanical ventilation are indicated (see Chapter 43). Complicating factors include impaired oxygen delivery, polycythemia, impaired respiratory mechanics secondary to lung damage and increased time constants impairing optimal inhalation and exhalation, flattened hemidiaphragms, rigid barrel-shaped chest wall, increased accessory muscle use and work of breathing, reduced diffusing capacity, impaired mucociliary transport, secretion accumulation, ineffective cough mechanism, increased oxygen consumption, increased work of the heart, and general debility and weakness.

The goal of intubation and mechanical ventilation is to support breathing by providing an airway and adequate alveolar ventilation and is based on arterial blood gas analysis. A tidal volume and a respiratory rate that provide satisfactory blood gas and pH values are established and maintained unless the clinical condition changes. The precise regulation of mechanical ventilation helps to restore adequate blood gases and cardiovascular and pulmonary function, reduce the work of breathing, rest fatigued ventilatory muscles, and provide an optimal fraction of inspired oxygen (FIO₂) and humidification (Figure 34-1).

Fig. 34-1 Patient receiving mechanical ventilation.

Minute ventilation can be seriously impaired with a leak in the mechanical ventilator circuitry. The tubes connecting sites are often the sites of air leakage. Complete disconnection at the endotracheal or tracheostomy connection may inadvertently occur in patients with high pulmonary resistance. Close monitoring of the exhaled tidal volume and end-tidal carbon dioxide will ensure that the patient is receiving sufficient ventilation.

Positive end-expiratory pressure (PEEP) is useful in promoting greater opportunity for gas exchange at end-expiration in mechanically ventilated patients. Venous return, myocardial perfusion, and cardiac output, however, may be impaired during positive-pressure ventilation with PEEP administration.³ Excessive stimulation to cough in these ventilated patients should be avoided because this accentuates the cardiovascular side effects of PEEP. Continuous positive airway pressure (CPAP) can maintain airway patency during spontaneous ventilation. This mode of ventilation, however, seems to be preferred in children, whereas PEEP is used more commonly in adults.

Interference with the gag reflex in the patient with an endotracheal tube increases the risk of aspiration of the oropharyngeal and gastric contents and can result in pneumonitis and pneumonia. Risk of aspiration from the oropharyngeal cavity can be reduced by suctioning through the airway with the cuff of the airway inflated, in addition to suctioning the oropharynx after suctioning via the airway.

Suctioning can be performed frequently in a patient with an artificial airway and is less traumatic. Patients should be suctioned only as indicated because this procedure can produce significant desaturation (up to 60%), particularly in the ventilated patient.⁴ Administration of 100% oxygen for 3 minutes before and after suctioning (i.e., hyperoxygenation) minimizes this desaturation effect. This can be accomplished by manual bagging before treatment (i.e., manual hyperventilation) or by presetting of the mechanical ventilator. Risk of aspiration of gastric contents is reduced by the use of a nasogastric tube.

A common cause of acute respiratory failure is advanced chronic airflow limitation.⁵ The pathophysiological deficits include significant loss of alveolar tissue, increased compliance of alveolar tissue, hyperinflated chest wall, impaired respiratory mechanics, flattened hemidiaphragms, impaired breathing efficiency, and reduced diffusing capacity. Proportional changes in lung volumes and capacities in patients with chronic airway limitation compared with healthy persons are presented in Figure 9-5. The primary abnormalities are significantly increased residual volume and inspiratory reserve volume and hence total lung capacity. Failure of oxygen transport ensues secondary to ventilation and perfusion mismatch, ventilatory muscle fatigue, reactive pulmonary hypertension, and right ventricular failure. Correcting the complications of respiratory failure, however, is often more problematic than treating the specific cause. Hypoxemia and hypercapnia are often present. Hypoxemia is usually improved with supplemental oxygen in the absence of significant diffusion defect or shunt.

Cardiovascular complications are among the most prevalent observed in ventilatory failure. Marked hypercapnia (increased arterial PCO₂) with acidemia (reduced pH) can produce extreme vasodilatation and hypotension resulting from the local action on blood vessels.² Mild hypercapnia can produce reflex vasoconstriction and hypertension. Occasionally, systemic hypertension is observed during weaning from the ventilator with the presence of a moderate degree of hypercapnia.

Right-sided heart failure (formerly called cor pulmonale) is a well-known complication of chronic lung disease and congestive heart failure. Both hypoxia and reduced pH cause pulmonary vasoconstriction and an increase in pulmonary artery pressure. Consequently, reversing bronchospasm, hypoxemia, hypercapnia, and acidemia can often reduce pulmonary vasoconstriction, lower pulmonary artery pressure, and thereby improve hemodynamics.

End-stage respiratory failure results in a progressive increase in airway resistance, work of breathing, oxygen consumption, and carbon dioxide production. In areas of bronchial obstruction, marked alveolar hypoventilation results and ventilation and perfusion are severely mismatched. Hypoxemia and respiratory acidosis produce reactive pulmonary hypertension and further ventilatory failure. Profound carbon dioxide retention, refractory hypoxemia, and respiratory acidemia may terminate in a fatal dysrhythmia.⁶

Acidemia from respiratory causes with a pH of less than 7.25 is often harmful with respect to dysrhythmia production. Conversely, hypoventilation is equally harmful, and pH elevations greater than 7.5 may cause neurological and cardiovascular complications. In acute respiratory failure with profound acidemia, intravenous bicarbonate is used to buffer the hydrogen ion concentration until the underlying disorder has been corrected. Bicarbonate infusion is guided by frequent pH measurements.

Transport of oxygen and carbon dioxide to and from the tissues depends on adequate pulmonary and systemic circulation. Frequently, blood volume has to be restored by fluids or blood replacement or both. Inotropic agents are used to maintain adequate circulation by augmenting myocardial contractility.

Of increasing interest in recent years has been the experience of illness and its contribution to disability. After their first episode of respiratory failure, patients with chronic obstructive pulmonary disease (COPD) report worse cognitive function and overall health status. After several months, however, these conditions may return to levels reported by individuals with similar disease severity who are being conservatively managed and have had no ICU admission.⁷ The Nottingham Health Profile and Mini-Mental State Examination can be useful tools for ongoing assessment of perceived health and cognition.

Principles of Physical Therapy Management

The principles of management of acute respiratory failure secondary to an exacerbation of COPD are based on interventions that will enhance oxygen transport (i.e., oxygen delivery, oxygen consumption, and oxygen extraction) and facilitate carbon dioxide removal. Thus the steps of the oxygen transport pathway that have been identified as impaired or threatened by the patient’s condition (i.e., restricted mobility, recumbency, and extrinsic and intrinsic factors in addition to the underlying pathophysiology) (see Chapter 2) are the focus of treatment.⁸ On the basis of a detailed analysis of these factors, treatments are selected, prioritized, and applied to optimize the steps in the pathway that are affected. These may include treatments to maximize the patency of the airways, increase alveolar ventilation, facilitate mucociliary transport, facilitate airway clearance, optimize the mechanical position of the diaphragm, optimize ventilation and perfusion matching, optimize pH, eliminate carbon dioxide, optimize peripheral circulation and tissue perfusion, and reduce the work of breathing and of the heart. To optimize oxygen transport, the primary goals of physical therapy management include the following:

1. Improve or maintain arterial oxygen tension (PaO₂) or prevent its deterioration

2. Improve or maintain arterial oxygen saturation (SaO₂) or prevent its deterioration

3. Improve or maintain arterial carbon dioxide levels (PaCO₂) and pH or prevent their deterioration

4. Optimize oxygen delivery and oxygen consumption relationship

The means by which these goals are fulfilled depends on each patient’s clinical presentation and the specific factors that contribute to cardiovascular and pulmonary dysfunction.

Mobilization: Special Considerations

Mobilization and ambulation are required for normal physiological functioning of the human body (i.e., to stimulate exercise stress and gravitational stress and thereby optimize oxygen transport).9,10 Although patients in the ICU are encouraged to move, exercise, sit up, stand, sit in chairs, take a few steps, and in some circumstances ambulate across the unit even if they are ventilated, therapeutic mobilization is prescribed to exploit its acute effects, long-term cumulative effects, and preventive effects (see Chapter 18). These effects are physiologically distinct and need to be prescribed specifically to address each patient’s problems. With the monitoring capability in the ICU to ensure safety, patients who are critically ill can move and be moved within safe as well as therapeutic limits.

Given that cardiovascular and pulmonary physical therapy is among those activities that are the most metabolically demanding for patients in the ICU,11–14 the patient’s capacity to meet a given increase in oxygen demand must be determined before treatment. Even though cardiovascular and pulmonary physical therapy stresses the oxygen transport system as a means of improving the function and efficiency of this system, unnecessary or excessive energy expenditure is undesirable and thus should be minimized. Interventions that can minimize oxygen demand include relaxation, judicious body positioning to facilitate oxygen transport, coordination of treatments with other interventions, scheduling of treatments at appropriate times, timing of treatments with medications so the maximal effect is achieved, pain control, and coordination of treatments with peak energy periods and around rest periods.

Mobilization and exercise are at the top of the hierarchy of physiological treatments in the management of patients in the ICU 15–17; therefore the potent and direct effects of these interventions are exploited first (see Chapter 17). Being moved to (passive) or moving into (active) the upright position promotes improved cardiovascular and pulmonary function and gas exchange. A supported chair should be available beside every ICU bed to provide greater opportunity for the patient to be upright when out of bed. The benefits of the upright sitting position are different from those of sitting propped up in bed. Stretcher chairs are particularly useful for patients who are unable to bear weight (Figure 34-2). There are also beds that are designed to position patients sitting. Even minimal ability of the patient to assist with his or her bed mobility and transferring must be exploited, even if the maneuver takes several minutes and multiple assistants. These minimal efforts must be exploited, or the patient’s oxygen transport system will decondition further, which also will reduce the patient’s tolerance for being mobilized. What justifies this time and personnel cost is the greater therapeutic outcome that can be expected compared with passive interventions. The ultimate goal is enhanced recovery, reduced discomfort, reduced morbidity and mortality, and reduced ICU and hospital stay.

Fig. 34-2 Intensive care unit patient sitting in a stretcher chair.

Significant benefit can be gained from standing the ventilated patient, provided there are no absolute contraindications to being upright in terms of cardiovascular and pulmonary function, neuromuscular and musculoskeletal status, and skin integrity. Ambulating the patient who is ventilated is the priority whenever possible.18–20 The potential risks, however, must be recognized. In a prospective study, Bailey and colleagues (2007)²¹ documented a total of 1449 “activity events” in 103 patients with respiratory failure. These activity events included 233 (16%) instances of sitting on the bed, 454 (31%) instances of sitting in a chair, and 762 (53%) instances of ambulating. In patients with an endotracheal tube, there were 593 activity events reported, of which 249 (42%) were ambulation. Fewer than 1% adverse activity-related events were reported (including fall to the knees without injury, feeding tube removal, systolic blood pressure greater than 200 mm Hg, systolic blood pressure less than 90 mm Hg, and desaturation less than 80%). No patient was extubated during an activity event. Thus activity and mobilization are feasible and safe in patients with respiratory failure. Of note, the majority of survivors (69%) were able to ambulate over 100 feet at discharge from the ICU. These findings have been corroborated by others.^22,23 Mobilization and exercise must be prescribed specifically, however, to ensure that the exercise stimulus is therapeutic (i.e., provides an adequate stressor to the oxygen transport pathway yet is not hazardous).

Standing and walking even a few steps can be extremely strenuous with respect to oxygen demand for the patient in the ICU. Such activities need to be introduced gradually and with continuous monitoring to ensure that the patient does not exceed the prescribed therapeutic intensity needed to maximize oxygen transport. Standing and walking are coordinated with other aspects of the patient’s care and should be carried out in several stages (Figure 34-3). Monitoring of the electrocardiogram (ECG) and arterial saturation of the critically ill patient while he or she performs activities such as standing or walking cannot be overemphasized. In anticipation of an increased workload, ventilatory parameters for ventilated patients may require adjusting. A greater concentration of oxygen should be delivered for at least 3 to 5 minutes before the activity and continued afterward for 10 minutes or so until the patient has recovered from the increased exertion and the heart rate and blood pressure have returned to within 5% to 10% of baseline values.