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.

Hypoxemia

The most common postoperative complication is hypoxemia secondary to alveolar hypoventilation, reduced functional residual capacity (FRC), airway closure, and postsurgical atelectasis.26,27 Adequate oxygenation, however, can be present despite hypoventilation when oxygen is being administered. The presence or absence of cyanosis may be an unreliable sign because peripheral cyanosis can occur despite adequate arterial PO₂. Morbidity and mortality have been reported to be reduced in patients with severe respiratory failure and system involvement when supranormal levels of oxygen delivery are achieved.^21,28

Pain

Pain, in addition to the effects of anesthesia, frequently contributes to alveolar hypoventilation and atelectasis after abdominal or thoracic surgery. Rapid, shallow, and monotonous breathing may be spontaneously adopted by the patient to avoid pain and coughing. Although minute ventilation is favored, alveolar ventilation is compromised by the increased ratio of dead space to tidal volume. Furthermore, in the absence of deep breaths, coughs, and sighs, atelectasis may develop in the underventilated portions of the lungs. The ventilation-perfusion ratio is disturbed because blood flow to underventilated lung segments is ineffective, physiological shunting occurs, and arterial PO₂ tends to drop although PCO₂ may be unchanged. An abnormally high transpulmonary pressure is then needed to reinflate these atelectatic alveoli. The physical therapist ensures good pain control before intervention, including mobilization. Patient-controlled analgesia is used if the patient is able to cooperate sufficiently, as well as conventionally administered analgesia, as required.

Pulmonary Embolism and Deep Vein Thrombosis

Pulmonary embolism is a life-threatening complication. Pulmonary embolism usually results from a thrombus forming in the veins of the lower limbs, in the pelvis, in the right atrium, or in the right ventricle. Patients may be at risk if they have varicose veins, chronic heart failure, or cancer or if they are obese, pregnant, or taking oral contraceptives.

The patient with a pulmonary thromboembolism usually has a sudden onset of tachypnea, radiating chest pain, and apparent anxiety. Occasionally, right-sided heart failure follows. Enzymes are often elevated. Right-sided heart strain may be evidenced on an echocardiogram or electrocardiogram (ECG). Right bundle branch block, peaked P waves, and inverted T waves may be seen. There may be no abnormality noted on chest radiographs.

Treatment consists of primary ventilatory and circulatory support, with adequate oxygenation of peripheral tissues. Anticoagulants, such as heparin, are infused intravenously to minimize further formation of thromboembolic substrates.

Principles of Physical Therapy Management

Impairments in lung volume, mechanics, and gas exchange uniformly occur after anesthesia and tissue dissection. The extent and duration of these changes increase with the magnitude of the operative procedure, the degree of anesthesia required, and the patient’s premorbid risk factors. These abnormalities observed in the postoperative period are characterized by gradual and progressive alveolar collapse. Total lung capacity, FRC, and residual volume are decreased in patients who develop complications. Because of the decrease in FRC (30% or more), lung compliance is decreased, and therefore the work of breathing is increased. Hypoxemia secondary to transpulmonary shunting usually becomes maximal within 72 hours after surgery and often is completely resolved with conservative management within 7 days. The FiO₂ will depend on the mode of supplemental oxygen administration. Low oxygen flows and low amounts of FiO₂ tend to be delivered via nasal cannulas. Higher flows can deliver higher amounts of FiO₂ via oxygen masks and masks with reservoir bags. The FiO₂ must always be taken into account in interpreting arterial blood gases. The FiO₂ is selected to provide adequate oxygenation with the lowest oxygen concentration possible.

On the basis of patient assessment, arterial blood gases, fluid and electrolyte balance, hemodynamic status, and radiographs, a decision is made as to which treatments on the physiological hierarchy will optimize oxygen transport and what parameters will be used for each treatment. Positioning these patients upright and mobilizing them whenever possible will maximize FRC and reduce closing volumes and hence enhance gas exchange and oxygenation. What precludes mobilizing these patients even minimally is their lack of alertness, which must be explained. If the patient is unable to respond to treatment because of narcotics, for example, this can be discussed at rounds, and other medications should be considered so that the patient is able to cooperate more. Thus even extreme body positioning will achieve more favorable results.29–31

Endotracheal intubation and mechanical ventilation may be indicated if blood gases fail to improve with conservative management. The treatment priorities for the ventilated patient before and during weaning are presented in Chapter 33. Special attention in the postoperative patient is given to the pulmonary complications associated with diminished ability to move spontaneously, surgical pain, restrictions imposed by dressings and binders, and diminished ability to cooperate and to periodically hyperventilate the lungs.

Facilitating mucociliary transport is a primary goal in these patients. Impaired mucociliary transport can be precipitated by alveolar hypoventilation, perhaps the most common cause of postoperative complications. Sufficient impairment can lead to mucus stasis, airway obstruction, atelectasis, and infection. Multiple positions, including upright positions and 360-degree axial turns, and multiple position changes facilitate mucociliary transport. In the event of accumulation of mucus and difficulty in removing pulmonary secretions, specific body positions are selected to optimize postural drainage of the affected bronchopulmonary segments and to maximize alveolar volume and ventilation. The addition of manual techniques can be detrimental in severely ill patients; thus their use needs to be considered carefully.

Suctioning may be most effective immediately before and after position changes. The appropriate oxygen transport variables are monitored to assess treatment outcome and minimally to ensure that the condition of the patient, which may be unstable, is not deteriorating. If the patient’s condition begins to deteriorate, treatment is discontinued until the condition stabilizes. Why the patient’s condition deteriorated is determined so that a decision can be made as to whether treatment can be reintroduced and, if so, what modifications are indicated.

Pain management is integral to the management of the surgical patient. Noninvasive and nonpharmacological pain control strategies need to be exploited for all surgical patients to augment or reduce the need for potent analgesics, especially narcotics. Chapter 30 describes some physical therapy pain-control strategies for surgical patients that can be applied with modification to the patient with surgical complications. Of these, use of electrotherapy modalities, such as transcutaneous electrical nerve stimulation, may be limited in the ICU because of electrical interference with monitoring devices.

Rest is prescribed as judiciously as treatment interventions to enable the patient to physiologically restore between and within treatments. This is particularly important for ICU patients who are hypermetabolic and have increased oxygen demands. Particular care must be observed in prescribing treatment threshold parameters for these patients. Suprathreshold states can be associated with an inappropriate balance between oxygen delivery and oxygen consumption such that the patient becomes compromised (e.g., patient becomes hemodynamically unstable, cardiovascular and pulmonary distress is precipitated, or both). A greater volume of a mobilization stimulus, however, may be delivered to these patients with an intermittent mobilization regimen than with a single prolonged course of mobilization. Thus the benefits that would be accrued would be correspondingly increased.

Prevention of thromboemboli is a major treatment objective and is best achieved with mobilization, body positioning, passive movements, and physical devices, such as pneumatic cuff devices and stockings, to augment low-dose anticoagulants in patients at risk. Patients who develop pulmonary emboli are treated medically, and physical therapy must be correspondingly modified to minimize oxygen consumption until the patient is in no imminent danger.

Principles of Physical Therapy Management

As in the management of other conditions, physical therapists need to address the immediate short-term needs of the patient related to maximizing oxygen transport as well as long-term functional outcomes, including aerobic capacity and general physical conditioning, that meet the needs of daily living.

With respect to the short-term goals of maximizing oxygen transport in patients with ARDS (comparable to others with severe respiratory distress), patients will be intubated and mechanically ventilated. Intubation and ventilatory support are implemented if arterial blood gases are severely affected and respiratory distress worsened. An endotracheal tube can be placed through the nose or mouth or a tracheostomy can be performed in cases in which prolonged ventilatory support is anticipated. A high level of PEEP maintains the alveoli open and thereby optimizes gas transfer at end expiration. Arterial oxygenation is usually improved with PEEP because the effect of shunting is reduced and a given FiO₂ tends to be more effective. Although the FiO₂ may be reduced, which reduces the possibility of oxygen toxicity, supranormal oxygen delivery can be beneficial in these patients. Survival may be improved and frequency of MOSF reduced.

Further monitoring of respiratory status in conjunction with arterial blood gases is essential for following the progress of the syndrome. In addition to the oxygen transport variables, the principal parameters monitored in ARDS are reduced lung compliance, tachypnea, and the concentration of inspired oxygen needed to maintain acceptable levels of the arterial blood gases.

ARDS is characterized by a major pathophysiological restrictive component; hence the principles of management of restrictive lung disease are applied. Changes in lung compliance and FiO₂ requirements provide guidelines to treatment required, treatment response, and course of the syndrome. Patients with ARDS require close monitoring and often treatments aimed at promoting optimal gas exchange because of the severity of the syndrome and high incidence of mortality associated with it.

Initially, if the patient is sedated, body positioning is exploited to maintain blood gases, and optimal range of motion and skin care are the focus of management. In severe ARDS the patient usually requires a high degree of ventilatory support with high FiO₂, and sedation. Severely affected patients may require neuromuscular blockade to reduce their oxygen demand and enable them to respond to ventilatory assistance more effectively. Handling and positioning patients on neuromuscular blockade requires particular care because these patients lack muscle tone to protect their muscles and joints. Rotating beds can be extremely beneficial for patients who are either too hemodynamically unstable or difficult to turn manually. These mechanical beds slowly rotate side to side through an arc, thus changing the patient’s body position continuously.40,41 When the effects of continuous axial rotation on a kinetic bed are compared with the effects in prone position, they have been shown to be comparable.⁴²

The prone position can have immediate benefit in remediating hypoxemia in patients with ARDS,43,44 and oxygenation can be significantly improved over supine.⁴⁵ This position and semirecumbent positions can augment the effects of mechanical ventilation.⁴⁶ The prescriptive parameters of the prone position in patients with ARDS, however, need to be based on a careful analysis of the pros and cons for each patient, and no single position will be maximally beneficial all the time. There are other physiological benefits to shifting the patient’s position rather than maintaining a single position (see Chapter 20), provided that oxygenation is not compromised. With improvement of ARDS (e.g., less ventilator support, reduced FiO₂, and satisfactory gases), the patient may be able to be mobilized with careful monitoring of vital signs, ECG, saturation, and subjective tolerance. Body positioning is initiated as soon as patients can tolerate it without significant desaturation. Special attention is given to body positioning to promote ventilation and perfusion matching and mucociliary transport and to minimize the effect of restriction of diaphragmatic and chest wall excursion. Some patients, for example, benefit from side-lying positions in which excursion of the inferior hemidiaphragm is favored. Other patients, however, seem to deteriorate from apparent restriction of the inferior lung in side-lying positions.

The underlying pathophysiology associated with ARDS is primarily related to respiratory mechanics, which could explain why improvements in oxygenation have not been associated with secretion clearance.⁴⁷ Each patient’s condition and specific areas of lung involvement must be taken into consideration when a turning regimen is prescribed. The effect of the patient’s body position on blood gases helps to establish a suitable regimen on a rational basis. Optimal positioning can result in reduced supplemental oxygen needs.⁴⁸ The sitting position optimizes lung capacity even when a patient is intubated and mechanically ventilated. The airway can dislodge, however, so caution must be observed and the artificial airway properly secured before any mobility activity. The use of a reclining chair at the bedside should be considered in the management of patients with acute lung injury. Theoretically, the potential function of all lung fields will be benefited with the lungs in a more upright position. Patients who are too unstable to tolerate upright positions and whose oxygenation is compromised in this position⁴⁹ may respond favorably to extreme body positions and the prone position.^50,51 The clinical benefits of the prone position in the management of the majority of patients with ARDS have been well documented over the past 20 years; thus physical therapists need to consider positioning these patients prone as a common practice barring contraindications.

Improvements in oxygenation in patients with acute lung injury and ARDS with the prone position, including prone abdomen free, have been well documented in adult and pediatric populations.33,52–55 The benefits can persist when the patient is returned to the supine position, and furthermore, the prone position does not adversely affect hemodynamics.⁵⁶ The use of the prone position in the management of ARDS has been reported to be independently associated with survival.⁵⁷ The literature is inconsistent, however, regarding whether patients respond differently depending on the underlying ARDS pathophysiology (pulmonary or nonpulmonary). Some investigators report no differences,⁵⁸ whereas others have reported marked differences with respect to radiographic changes, respiratory mechanics, and time course of oxygenation.⁵⁴ These differences may be explained by pathophysiological differences in the primary disease insult responsible for ARDS, stage and severity, and comorbidity.

The mechanisms for improved gas exchange in prone positions in these severely ill patients have been the subject of much interest. Hypotheses have included improved alveolar recruitment and lung volumes; homogeneous distributions of ventilation and perfusion⁵⁹; increased static lung compliance⁶⁰; and reduced compressive forces compared with the supine position.^61,62 In the posterior lung fields in the prone position, in the areas where atelectasis, shunt, and ventilation-perfusion mismatch are most prevalent, transpulmonary pressure exceeds airway opening pressure without apparently compromising anterior lung fields.⁶³ A decrease in PaCO₂ with prone positioning predicts survival.⁶⁴

Problems with positioning patients in prone have been reported to be rare. Studies have been focusing on the differences between patients who respond favorably and those who do not (i.e., responders versus nonresponders). Patients may respond better in the early stages in which pulmonary edema is present versus the later stages in the presence of pulmonary fibrosis.⁶⁵ Alveolar recruitment procedures are more effective in improving PaO₂ in the prone position, and lower PEEP levels are needed to sustain improved PaO₂ compared with the supine position.⁶⁶ In addition, positive inspiratory pressure, hence barotrauma, and FiO₂ can be reduced.⁵⁹ The effects of mechanical ventilation including PEEP,⁶⁷ airway pressure release ventilation,⁶⁸ and certain pharmacological agents (inhaled nitric oxide) may be augmented in the prone position.⁶⁹ Other studies have reported a particular beneficial effect of the prone position. One study reported that the prone position rather than PEEP improved oxygenation.⁷⁰ Another study reported that prone positioning improves oxygenation more than inhaled nitric oxide in patients with severe ARDS.⁷¹

Although considerable evidence supports the clinical effectiveness of the prone position to improve oxygenation, this position should be considered for the management of hypoxemia associated with other conditions as a means of simulating the normal effects of gravity on cardiovascular and pulmonary function. Favorable results have been reported in the management of hypoxemia associated with acute respiratory failure in acute myeloid leukemia,⁷² pulmonary hemorrhage,⁷³ and subarachnoid hemorrhage.⁷⁴

Few complications have been reported with the use of body positioning, and in particular the prone position. Normal precautions are taken to ensure that ventilator tubing and lines and leads are not compromised. Despite beneficial effects of oxygenation in patients with ARDS related to trauma,⁷⁵ complications associated with prone positioning have been reported for such patients, including facial and chest wall skin necrosis, wound dehiscence, and cardiac arrest.⁷⁶ Special precautions are necessary in this subgroup. Brachial plexopathy has also been reported when positioning patients prone in the ICU.¹⁹ In addition to frequent body position changes, the semiprone position may help to avoid the adverse effects of prone positioning in some patients.⁷⁷

Shock

Common causes of shock include hypovolemia, septicemia, heart failure, and direct insult to the central nervous system. Some of the classical features of shock are hypotension, reduced cardiac output, tachycardia, hyperventilation, diaphoresis, pallor, confusion, nausea, and incontinence. Inadequate tissue perfusion results in extracellular acidemia and loss of potassium ions from the cells. The pulmonary blood vessels constrict in response to hypoxemia, which tends to increase pulmonary artery pressures.

Failure of cellular function secondary to shock can result from a deficiency of substrate for energy production, a reduced ability to use the nutrients for energy production, or both. The pathophysiological mechanisms responsible include hypoperfusion of the tissues, hormonal and metabolic cellular changes, and the toxic effects of the metabolic changes. Collectively, these produce cellular damage. With hypoperfusion and decreased oxygen delivery and other nutrients, the production of adenosine triphosphate is reduced. The maintenance and repair of cell membranes is disrupted, resulting in swelling of the endoplasmic reticulum and eventually the mitochondria. Persisting cellular hypoxia contributes to rupture of the lysosomes, which releases enzymes that contribute to intracellular digestion and calcium deposition. Once the lysosomes have ruptured and intracellular digestion has been triggered, irreversible cell damage ensues, impairing oxygen extraction and uptake.⁹

The dependence between oxygen consumption and delivery is a marker for septic shock and thus provides justification for increasing oxygen delivery (see Chapter 2).⁷⁸ The relationship of oxygen consumption and delivery has been used to evaluate patients who are critically ill with SIRS and predict metabolic stress on this basis.⁷⁹

The pathology of shock and the effect on the respiratory membranes of the mitochondria follow a similar course regardless of cause. Swelling of the interstitial tissue disrupts the perfusion of the pulmonary capillaries. Congestive atelectasis and pulmonary edema ensue. In the advanced stages, hyaline membrane changes and pneumonitis may occur.

When shock is associated with heart failure, ventricular assist devices or an intraaortic balloon pump may be indicated. These devices reduce the degree to which the patient can be positioned and moved; therefore consultation with the team is essential in progressing such a patient.

Septic shock is a serious condition; patients manifest hypotension despite intensive medical treatment. Persistent hypotension leads to decreased blood flow to vital organs and can result in acute MOSF. Poulsen and colleagues (2009)⁸⁰ followed 174 patients in the ICU to evaluate the physical outcomes of survivors 1 year after septic shock. Survivors were interviewed about their physical function and socioeconomic status. Seventy-eight patients were invited to participate, and 70 replied. After 12 months, two thirds of the patients reported that they had not regained their preadmission physical status, and 81% attributed this to loss of muscle mass. Physical function is substantially reduced in survivors of septic shock 1 year after discharge; thus recovery of physical function warrants being identified as a long-term goal.

Sepsis and Multiorgan System Failure

Sepsis is the response to bacteremia or other byproducts of bacteria in the blood. The clinical features of sepsis include fever, tachycardia, tachypnea, and respiratory alkalemia. Metabolic abnormalities are also a common feature of sepsis. Sepsis is the most common predisposing factor contributing to MOSF, which typically involves failure of more than two organ systems.81,82 Table 36-1 shows the major organs affected and their clinical manifestations (i.e., pulmonary, gastrointestinal, hepatic, renal, cardiovascular, hematological, and central nervous systems). The cascade of pathophysiological features of MOSF is precipitated by multiple mediator systems. The release of these mediators impairs oxygen delivery and usage of oxygen by the cells. Inadequate tissue oxygenation may be a mechanism underlying MOSF. Thus, the supply of the major energy source to the cell, adenosine triphosphate, is reduced, which leads to structural and functional damage of the various organ systems. The mortality rate ranges from 60% to 80%.

Conditions that predispose a patient to MOSF include sepsis, overwhelming infection, multiple trauma and tissue injury, inflammation, and tissue perfusion deficits. Patients who are older, have chronic conditions, are immunosuppressed, or have a severe initial presentation have an increased risk of failure and mortality.

Sepsis causes damage to peripheral nerves and muscles as well as organs and is termed critical illness polyneuropathy (CIP).⁸³ Although the pathogenesis is not understood, these effects must be detected early and addressed to avoid clinical manifestations including muscle weakness, prolonged recovery, and delayed weaning. The systemic inflammatory response and MOSF have been implicated, and neuromuscular blockers and steroids can exacerbate these manifestations. The use of steroids and muscle relaxants should be minimized. Stabilizing the underlying critical condition and avoiding sepsis are of major importance in preventing CIP.

General guidelines for current medical strategies for sepsis and septic shock have been documented.⁸⁴ These include life support measures including fluid resuscitation, blood product administration, vasopressor and inotropic support, bicarbonate therapy, and hemodynamic stabilization. To control the sepsis process requires identification and management of the source of sepsis, as well as antibiotic and steroid administration. Sedation, analgesia, neuromuscular blockade, and glucose control are instituted to reduce excess metabolic demand. In the event of renal dysfunction, hemofiltration may be required, along with intermittent hemodialysis. The management of acute renal failure in patients who are hemodynamically unstable with fluid overloaded may include continuous renal replacement therapy (CRRT). CRRT is a dialysis treatment provided as a continuous 24-hour-per-day therapy. Intermittent dialysis treatments are treatments that are provided for brief intervals, usually every day or every 2 or 3 days as needed.

Preventive strategies are implemented to avoid the sequelae of recumbency and restricted mobility, which include risk of deep vein thrombosis and embolism. Like other patients who are critically ill, they are at risk of stress ulceration, thus, stress ulceration prophylaxis is a component of routine medical management.

Principles of Physical Therapy Management

The patient with sepsis and MOSF, like the patient in shock, is gravely ill and unlikely to be able to cooperate with treatment (Figure 36-2). The principles of management are comparable to those for managing the patient in shock; however, oxygen delivery is likely to be consistently compromised in these patients. If oxygen delivery is critically low, depends on oxygen delivery and the patient is in a state of metabolic acidosis (see Chapter 2). In this situation—when oxygen delivery is compromised to the point of not meeting tissue oxygen demands—the goal of treatment is to maximize oxygen delivery⁸⁵ and minimize oxygen demand so that oxygenation of vital organs is threatened to the least extent. Thus the physical therapist must estimate the oxygen reserve capacity (i.e., the balance between oxygen demand and oxygen supply) in every assessment to select optimal treatment that is associated with the least risk. Treatments are selected to improve the efficiency of oxygen transport and usage and thereby reduce the work of the heart and of breathing. Above all, treatment should not worsen the patient’s oxygen transport status. Selective body positioning, including the prone position, can augment oxygen transport and maximize the effective FiO₂.⁸⁶ Even though the patient will likely benefit more from some positions than others, frequent body position changes, preferably a 360-degree turning regimen, are still necessary to avoid the sequelae of static body positioning. Semiprone positions can substitute well for full prone positions if the patient is too hemodynamically unstable. Semiprone positions may be tolerated better by the patient and may be safer. Even though hourly position changes may not be feasible in these severely ill patients, prolonged periods in a static position (more than 2 hours) are deleterious. Thus a balance between these two concerns must be achieved.

Promoting optimal mucociliary transport remains a priority even in the absence of secretion accumulation. Frequent position changes and numerous positions ensure that pulmonary secretions are continually being redistributed to prevent accumulation and enhance removal. Should postural drainage be indicated, these positions may need to be modified. Head-down positions in particular may not be tolerated well. The relative benefits of superimposing manual techniques must be established on the basis of careful assessment because these procedures are associated with an increased metabolic demand to which the patient is not readily able to adapt. Increasing the oxygen demand of these patients may worsen their condition.

The assessment of neuromuscular function is challenging and inaccurate in patients who are severely ill. Patients may have marked weakness related to CIP and myopathy87,88 and from interventions themselves (e.g., resting of the respiratory muscles with mechanical ventilation; pharmacological agents including glucocorticoids, some antibiotics, and neuromuscular blockers) (Figure 36-3). Thus these interventions may be risk factors, and their use needs to be assessed.