Metabolic Dysfunction

Complications associated with respiratory failure that can further impair tissue oxygenation are described in Box 36-1. The metabolic consequences of these complications and impairment of oxygen transport are life-threatening for the patient. Thus prevention of their development is a priority. Should complications develop, however, early detection and definitive management become the priorities if the patient is to survive.

A hallmark of these complications is the impairment of multiple steps in the oxygen transport pathway, which adds to the complexity of management.⁷ The three major components of oxygen transport (i.e., oxygen delivery, consumption, and extraction) can be affected individually or in combination.^8,9

In healthy individuals, the ratio of oxygen consumption to delivery is low (i.e., 23%, which ensures an oversupply of oxygen as a safety margin) (see Chapter 2). This safety margin also ensures that most patients are able to recover from insults to the oxygen transport system. If the insult is extreme, however, such as that resulting from complications of respiratory failure, surgery, acute lung injury and acute respiratory distress syndrome, shock, sepsis, and MOSF, metabolic dysfunction secondary to tissue hypoxia can result.

The relationship between oxygen consumption and delivery has elucidated our understanding of hemodynamic and metabolic changes observed in critical illness.¹⁰ The phenomenon of oxygen-delivery dependence of oxygen consumption occurs when a patient’s oxygen transport system is unable to supply sufficient oxygen to meet basal oxygen demand.¹¹ Oxygen delivery below 300 mL/min/m² limits the oxygen diffusion gradient and reduces oxygen extraction and usage at the cellular level. This is termed the critical level of oxygen delivery. When oxygen delivery exceeds 300 mL/min/m², does not depend on delivery. Thus the greater the delivery in relation to , the greater the safety margin. When oxygen transport is so severely compromised that oxygen delivery falls below the critical level, anaerobic metabolism is triggered. Anaerobic metabolism, however, may also be triggered at levels of oxygen delivery that exceed the normal critical threshold for anaerobic metabolism.¹² This so-called “pathological dependence” of oxygen consumption on oxygen delivery occurs when the cells are inadequately extracting and using oxygen even in the presence of supranormal oxygen delivery levels. This phenomenon is observed in patients with ARDS and shock (discussed later this chapter).

Given that physical therapy is one of the most metabolically demanding ICU interventions,13,14 the physical therapist needs to be able to calculate this safety margin to prescribe the type of treatment and its parameters (i.e., intensity, duration, and frequency) such that treatment is maximally beneficial and associated with the least risk to the patient.

The ultimate treatment outcome measures are markers of oxygen tissue metabolism.8,15,16 In addition, continuous assessment of oxygen delivery, consumption, and extraction provide the basis for directing management of oxygen transport deficits.

Pulmonary Dysfunction

Complications of the cardiovascular and pulmonary systems can lead to respiratory failure (see Box 36-1).^17,18 Some of these, such as ventilator-associated pneumonia, relate to being mechanically ventilated. Certain technical problems related to the cuffs used in conjunction with artificial airways may occur (e.g., overinflation, distortion, and herniation of the orifice of the tube). Mucus plugs can occlude the endotracheal tube or tracheostomy and impede ventilation. The common complications can be reduced if the tube is changed frequently and if minimal amounts of air are used for cuff inflation.

Prolonged endotracheal intubation can result in laryngeal edema, ulceration, and fibrosis. Mechanical ventilation may also rupture a bleb on the surface of the lung and produce a pneumothorax with rapid tension development. Chest tubes are inserted immediately to relieve the tension. Blebs occur when alveoli rupture, causing air to track to subpleural sites.

Mechanical ventilators can be a source of infection. The physical therapist can help minimize this risk by not directly handling the ventilator attachments that communicate with the airflow channels. Condensation from the hose should not be drained toward the ventilator or toward the patient. The physical therapist should be masked and gloved when connecting and disconnecting the patient to and from the ventilator.

Oxygen toxicity is a significant clinical complication of mechanical ventilation. Mechanical ventilators have precise oxygen controls to deliver the lowest possible inspired oxygen concentration needed to maintain arterial oxygen tensions. Because of the iatrogenic complications of high FiO₂ levels (i.e., denitrogen atelectasis and oxygen toxicity), oxygen above the patient’s needs is never indicated other than for short periods of hyperoxygenation before suctioning or in preparation for, during, and immediately after mobilization.

Acid-Base Abnormalities

Any combination of acid-base imbalance may occur either acutely or chronically during respiratory failure. Severe alkalemia associated with potassium and chloride losses may occur after mechanical ventilation and can precipitate serious cardiovascular and neurological complications (see Chapter 16). Significantly impaired oxygen delivery to peripheral tissue may contribute to increased anaerobic metabolism and metabolic acidosis.¹²

Fluid and Electrolyte Abnormalities

Fluid retention can occur with prolonged mechanical ventilation in a patient with no evidence of cardiac failure. Pulmonary edema, weight gain, decreased pulmonary compliance, and reduced oxygen transport are common signs. Fluid overload is a common cause of this fluid retention. Individuals who are mechanically ventilated are therefore usually maintained underhydrated. Because of a tendency for sodium retention and hence fluid retention, intravenous saline solution is kept to a minimum. Humidifiers attached to mechanical ventilators are responsible for adding a considerable amount of water by absorption through the lungs.

Cardiac Dysfunction

When the heart fails to the point of cardiac output being compromised, intracardiac volumes and pressures can be monitored. Flow-directed pulmonary artery catheters (i.e., Swan-Ganz catheters) are commonly used in the ICU for monitoring patients who develop such hemodynamic complications. Although inserted through the venous side of the circulation through the right atrium and ventricle to lodge in a branch of the pulmonary artery, they provide useful measures and indices of right-sided and left-sided heart function and the adequacy of fluid resuscitation and pharmacological support. These catheters are also associated with some complications (see Chapter 16). Infection may lead to bacteremia and septicemia. Judicious selection and application of any invasive procedure is warranted to minimize undue hazard. The presence of these catheters limits head and neck positions and requires mobilization be carried out cautiously within the patient’s hemodynamic tolerance.

Cardiac dysrhythmias are a common complication of respiratory failure. In addition, patients in respiratory failure tend to be older adults who as a group have a greater incidence of dysrhythmias secondary to cardiac disease. Electrocardiographic monitoring is therefore essential for all patients requiring ventilatory assistance in addition to patients with overt or suspected heart disease. Both atrial and ventricular tachydysrhythmias are seen in acute respiratory failure. Sinus tachycardia and premature ventricular contractions, however, are particularly common. Ventricular fibrillation or death may occur with rapid lowering of arterial PCO₂.

In the presence of respiratory failure and absence of cardiac disease, the management of cardiac dysrhythmias lies predominantly in the correction of blood-gas abnormalities. Effective supportive management can usually be achieved with pharmaceutical agents. Electrolyte replacement may also be required.

A thorough understanding of the clinical presentation, diagnosis, and correct management of cardiac dysrhythmias is fundamental to the optimization of physical therapy treatments in the ICU and minimization of any risk to the patient. Cardiac dysrhythmias resulting from any cause necessarily require ongoing evaluation and therapy.

The physical therapist must be able to treat the patient with any dysrhythmia optimally and safely when associated with other medical or surgical conditions. The implications of the dysrhythmia for the patient’s clinical presentation as well as treatment selection and response must be recognized by the physical therapist and considered in designing the treatment plan.

Thromboembolism

A high incidence of pulmonary thrombosis or embolism exists in patients in acute respiratory failure. Early diagnosis and management of pulmonary thromboembolism have been greatly facilitated by the use of serial ultrasound procedures and scans. Physical therapy has a key role in preventing the development of thromboemboli by promoting frequent changes in position; specific bed exercises, particularly of the lower limbs; and passive range-of-motion exercises if indicated. It is essential that movement and repositioning be performed regularly to maximize their cardiovascular and pulmonary protective benefits. Pneumatic extremity cuffs apply pressure intermittently over the lower legs to minimize venous pooling and assist venous return (see Chapter 33). Compression stockings also may be applied over the feet and legs to increase circulatory transit time in the dependent areas and reduce circulatory stasis.

Myocardial Dysfunction

As in any clinical situation, acute myocardial infarction can occur during the management of acute respiratory failure. The risks are increased because patients in respiratory failure tend to be older and more susceptible to positional hypoxemia. The probability of heart failure and associated dysrhythmias is increased and compounds the problems of the patient in respiratory failure.

Gastrointestinal Dysfunction

Stress ulceration leading to peptic ulcers is commonly associated with chronic airway obstruction. The stress of respiratory failure predisposes the patient to peptic ulceration. Profound hemorrhage may occur and blood replacement is necessitated.

Gastric dilation may occur in patients who are receiving mechanical ventilation. Gastric dilation is best managed by a nasogastric tube and intermittent suction. Care must be exercised to avoid hypokalemia and hypochloremia caused by excessive gastric suctioning. Special care is also taken to avoid fecal impaction, particularly in the patient who is paralyzed. This risk can be reduced with suitable fluid balance, mobilization, and frequent turning in conjunction with appropriate trunk and lower-limb movements.

Muscular and Neurological Dysfunction

A close correlation exists between state of consciousness and arterial PO₂ and PCO₂. In addition, alteration in blood gases causes changes in alertness, personality, memory, and orientation. Motor changes include generalized or localized weakness, tremors, twitching, myoclonic jerks, gross clonic movements, convulsions, and flaccidity. Neurological complications of respiratory failure must be differentiated from those of nonpulmonary origin. The physical therapist must be aware of the spectrum of neurological complications that can result from respiratory failure and recognize that apparent improvement of neurological signs may reflect improved cardiovascular and pulmonary status.

Critical illness neuropathy and critical illness myopathy are serious complications of critical illness and are associated with metabolic disturbance during illness, paralysis, neuromuscular blockade, recumbency, and restricted mobility.19,20 Prevention is a primary goal and includes early detection. Detection of risk factors is an important component of the physical therapy assessment. Additional risk factors include ICU stays over 7 days, sepsis and systemic inflammatory response syndrome (SIRS), multiorgan system dysfunction, a high Acute Physiology and Chronic Health Evaluation III (APACHE III) score, the use of high-dose steroids, and patients who have had organ transplantation, patients with severe neurological or muscle disease, and those with hyperglycemia.²¹

Periodic nerve electrical stimulation has been one means of establishing nerve conduction integrity during an assault of critical illness requiring neuromuscular blockade and sedation. Medical management is focused on addressing its causes and reversing them. Because rehabilitation potential is threatened in the presence of critical illness neuropathy and critical illness myopathy, physical therapy goals focus not only on reducing the possibility of neuropathy and myopathy and their functional sequelae but also on facilitating weaning and improving clinical outcomes overall including functional independence.²¹

Renal Dysfunction

Lung and kidney dysfunction are closely related.²² The development of renal failure greatly compromises the chances of the patient’s survival. Renal failure can result from gastrointestinal bleeding, sepsis associated with shock, drug-induced nephrotoxicity, and hypotension. Urinary outputs are maintained with adequate fluid and diuretics, with care not to induce pulmonary edema. Dialysis may need to be instituted if more conservative management fails.²³ If dialysis is anticipated, the physical therapist should review existing treatment goals to modify treatment accordingly.

Systemic Inflammatory Response Syndrome

Localized inflammation is a physiological protective response. Typically this response is controlled by the body at the site of injury.²⁴ Loss of local control or an overly active response results in an exaggerated systemic response that is known as systemic inflammatory response syndrome (SIRS). Compensatory mechanisms and outcome (such as resolution, or potentially multiple organ dysfunction syndrome or death) depend on the balance of SIRS and the effectiveness of the compensatory mechanisms. The effectiveness of therapies to date remains equivocal.