Individuals with Acute Medical Conditions

Elizabeth Dean

This chapter describes the physical therapy management of individuals with primary, acute dysfunction of the cardiovascular and pulmonary systems. Such dysfunction may limit participation in life and its related activities in the short- or long-term. Further, such dysfunction can constitute life threat in the absence of limitations to life participation and quality of life (e.g., hypertension and dysrhythmias). Management principles for people with several types of common acute medical conditions are described. Although medical conditions are usually classified as either primary pulmonary disease or primary cardiovascular disease, the heart and lungs work synergistically to effect gas exchange and cardiac output and in series with the peripheral vascular circulation to effect tissue perfusion.1,2 Thus impairment of one organ system invariably has implications for the function of the other. Threat to or impairment of oxygen transport has implications for all other organ systems; thus a multisystem approach is essential for overall management (see Chapters 1 and 5). The primary, acute pulmonary conditions that are presented in this chapter include atelectasis, pneumonia, bronchitis, bronchiolitis, acute exacerbations of chronic airflow limitation, asthma, cystic fibrosis, interstitial pulmonary fibrosis, and tuberculosis. For further epidemiological and pathophysiological detail on these conditions, refer to Mason and colleagues (2010)³ and West⁴ (2007). The primary, acute cardiovascular conditions presented include hypertension, medically stable angina, and uncomplicated myocardial infarction. For further details on these conditions, refer to Sokolow and Cheitlin⁵ (2004), Fauci and colleagues⁶ (2008), and Woods and colleagues⁷ (2009).

The pathophysiology underlying the medical management of each condition extends the pathophysiology content of Chapter 5 and, in turn, provides a basis for each condition’s physical therapy management. The management principles presented are not intended to serve as treatment prescriptions for any particular patient. The treatment priorities presented are based on the underlying pathology, as well as the potential complexity of its manifestation for a patient. Without discussion of a specific patient and knowledge of other clinically relevant factors (i.e., the effects of restricted mobility, recumbency, and the effects of extrinsic and intrinsic factors on the patient’s presentation including sociocultural context; see Chapter 17); however, the specific parameters of the treatment prescription cannot be completely established. Integration of patient-specific information is essential for treatment to be specific and maximally effective. Chapter 31 extends the principles involved with the management of many of the acute medical conditions described in this chapter, detailing their subacute and chronic stages.

Cardiovascular Pathology

Hypertension

Pathophysiology and Medical Management

Essential hypertension, the “silent killer” (of unknown etiology), is the most common type of hypertension (90% of all reported cases). Although salt sensitivity has been implicated in hypertension in African Americans and increased rennin production in the Hispanic population,⁸ salt consumption is a serious health concern in the North American population. Widespread campaigns are being aimed at reducing salt consumption in the pediatric as well as adult population.⁹ Reducing consumption by one-third is estimated to reduce the prevalence of hypertension substantially.

Generally, hypertension is classified as mild, moderate, or severe. It is generally managed pharmacologically with vasodilators (i.e., afterload reducers), diuretics (i.e., volume reducers), and beta-blocking agents (i.e., inotropic agents). Despite a primarily pharmacological orientation to the management of hypertension, a high proportion of individuals with hypertension still have high blood pressure and are at increased risk for its deadly complications. Hypertension is a significant health care concern in that the condition is frequently associated with heart disease, stroke, and renal dysfunction and failure.¹⁰ Thus its consequences can be dire. As described in Chapter 1, hypertension often occurs in the presence of obesity and diabetes, which complicates the clinical picture further.

Pharmacological management may have a role in the control of hypertension, given its serious consequences and the necessity of maintaining blood pressure within acceptable limits. Like all medication, its effects must be monitored closely to ensure that the desired outcomes are being achieved. The following decisions must be made:

1. To what degree does pharmacological intervention appear warranted, given the patient’s severity of hypertension and overall clinical picture?

2. To what degree could the hypertension be managed with nonpharmacological interventions?

3. To what degree could pharmacological and nonpharmacological interventions be used concurrently? What type of schedule might be anticipated to wean the patient off medication with time or at least minimize it?

Principles of Physical Therapy Management

Physical therapists treat patients with hypertension as a primary or secondary diagnosis. If it is a secondary diagnosis, it is important that the diagnosis is not overlooked. What the physical therapist can do for the hypertension may be clinically more significant than management of the primary diagnosis for which the patient is referred. As with many other lifestyle-related conditions, antihypertensive medication may be perceived by the patient as addressing the problem, whereas in many instances, it only addresses the effect. Lifestyle changes are necessary to normalize blood pressure with the goal of eliminating the need for blood pressure medication.¹¹

Exercise therapy can be an effective intervention for the management of hypertension with the primary goal of eliminating the need for medication.¹² Secondarily, physical therapy with a focus on exercise and health education, including smoking cessation and basic nutritional counseling, is aimed at reducing the need for medication or its potency. The foundation of management in a patient with hypertension is a lifestyle review and recommendations in consultation with the patient. Recommendations include nutrition, weight control, exercise, smoking cessation, and stress management.¹³ Medical management may include beta blockers and diuretics to reduce plasma volume or other antihypertensive medication. A prescription of regular aerobic exercise may control hypertension.¹⁴ The prescription is based on a consideration of the patient’s coexistent problems and general health status. If obesity is a concurrent problem, an exercise program is prescribed to address both concerns.

More frequently, physical therapists treat patients whose hypertension is a secondary condition. Thus, whether the patient is being treated for osteoarthritis, stroke, or cardiovascular and pulmonary dysfunction, treatment is modified accordingly. An exercise prescription includes generalized aerobic exercise at an intensity that is optimally therapeutic and not associated with any excessive or untoward hemodynamic responses.

Patients with labile hypertension are the most difficult patients for whom to prescribe an exercise program because of the irregularity of their blood pressure responses. The intensity is modified at each session to accommodate these variations. Because beta blockers and other medications blunt heart rate responses to exercise, the exercise prescription parameters are defined on the basis of some other objective hemodynamic response or on subjective responses (e.g., the Borg scale of perceived exertion).

The benefits of a modified aerobic exercise prescription include elimination of medication, reduction of medication, and improved pharmacological control on the same dose of medication. In addition, the patient derives all the other multisystem health benefits of exercise. A program of aerobic exercise should be carried out in conjunction with other lifestyle changes associated with blood pressure control (e.g., nutrition, weight control, stress reduction, and smoking cessation program). Medications should be monitored by the physician during the training program. In addition to exercise having a direct effect on controlling hypertension, the effect of exercise on overall metabolism may alter the absorption and degradation of the medications, which in turn can reduce the prescriptive requirements of that medication. Those types of exercise that are associated with a disproportionate hemodynamic challenge (e.g., static movements and stabilizing postures) are not usually indicated. Rather, aerobic exercise that is rhythmic, involves the large muscles of the legs and possibly the arms, and is performed frequently is indicated. Physical therapy outcomes include reduction or elimination of antihypertensive medication with self-monitoring and optimal lifestyle management.

A patient who is being managed acutely with high blood pressure may benefit from relaxation strategies, breathing control, and stress management. Further, complementary therapies, as described in Chapter 27 may have an important role. For noninvasive physical therapy management of hypertension, see Chapter 31.

Angina

Pathophysiology and Medical Management

Angina refers to pain resulting from ischemia of the myocardium and often precedes myocardial infarction. Coronary artery disease is the primary cause of myocardial infarction and is among the leading causes of death in the Western world. Lifestyle factors, including high-fat diet, stress, and low activity levels, contribute to atherosclerosis and fat deposition within the coronary blood vessels. When these deposits narrow or totally occlude the vessel lumen, blood flow is restricted or totally obstructed. As the heart continues to demand oxygen and nutrients in order to work properly, blood supply must be increased. If one or more of the myocardial blood vessels is stenosed, insufficient blood reaches the working myocardial fibers, and ischemia and pain result. The classic description of anginal pain is retrosternal, vice-like, gripping pain radiating to the left side and down the arm and up into the neck; however, anginal pain may occur bilaterally anywhere above the umbilicus. Furthermore, patients vary considerably with respect to the degree to which the severity of the pain correlates with the degree of myocardial ischemia and infarction. Thus even apparently minimal chest pain may be associated with significant ischemia, and its clinical significance should not be minimized. Approximately 10% to 15% of individuals who have a myocardial infarction do not report chest pain. Chest pain can also be blunted in individuals with diabetes as a result of the autonomic neuropathy.

Principles of Physical Therapy Management

The management of patients with ischemic heart disease who are hemodynamically unstable and require intensive monitoring to assess and to monitor physical therapy treatment is described in Chapter 34. This section addresses management of the patient with a cardiac medical condition who is stable and uncomplicated. Physical therapists must be knowledgeable and proficient in management of the patient with cardiac conditions because these patients are referred with cardiac disease as a primary or secondary problem. With respect to heart disease being a secondary diagnosis, patients often come to the physical therapist for the management of an orthopedic complaint with a history of angina, frank myocardial infarction, or hypertension. The principles for physical therapy in management of patients with acute ischemic heart disease are presented within the principles of phase I cardiac rehabilitation (Table 29-1). Because physical therapy invariably involves physically stressing a patient either with therapeutic exercise or with the application of a therapeutic modality, the physical therapist must address the following questions when managing a patient with ischemic heart disease and its risk factors:

Table 29-1

Phase I of Cardiac and Pulmonary Rehabilitation (Inpatient, <7 to 10 days)*

Cardiac Rehabilitation	Pulmonary Rehabilitation
After anginal attack, myocardial infarction, operative procedures including bypass surgery and valve surgery	After acute exacerbation or thoracic surgery (e.g., admission lung resection)
Optimize oxygen transport by directing treatment to the underlying limitations of structure and function (impairments)	Optimize oxygen transport by directing treatment to the underlying limitations of structure and function (impairments)
Risk factors assessment	Risk factor assessment
Assessment of knowledge deficits and learning style	Assessment of knowledge deficits and learning style
Readiness to change assessment	Readiness to change assessment
Predischarge submaximal exercise test	Predischarge submaximal exercise test
Discharge lifestyle recommendations:	Discharge lifestyle recommendations:
Smoking cessation	Smoking cessation
Nutrition and weight control	Nutrition and weight control
Physical activity and exercise	Physical activity and exercise
Stress management	Stress management
Plan for follow-up	Plan for follow-up

^*Phases II, III, and IV are related to subacute and chronic care (see Chapter 31).

Modified from Piotrowicz R, Wolszakiewicz J: Cardiac rehabilitation following myocardial infarction. Cardiology Journal 15:481–487, 2008.

1. Does the patient’s cardiac status preclude treatment? Why?

2. Is additional information about the patient necessary before physical therapy assessment and treatment? What information?

3. How should treatment be modified? Why?

4. Is the patient using antianginal medication appropriately? Is the prescription current? Does the patient have the antianginal medication present at all times?

5. Are there other medications that may influence the patient’s cardiovascular and pulmonary status and response to treatment? What are they? How might the patient’s responses to treatment, particularly exercise, be affected?

6. What physiological parameters should be monitored before, during, and after treatment?

7. What is the patient’s knowledge about his or her condition? Can the patient clearly identify what triggers the angina and what makes it worse and better? What lifestyle changes have been made? What should be reinforced and what education is necessary?

A key consideration in the management of any person with cardiovascular dysfunction is minimizing myocardial strain. Thus mobilization and exercise prescription must incorporate appropriate warm-up, steady-rate, cool-down, and recovery phases, and the type of exercise should be rhythmic and involve the legs (i.e., areas of large muscle mass) and possibly the arms as well. Initially, low-intensity activity that restricts the heart rate to no more than 20 beats above resting heart rate may be indicated to minimize the work of the heart without immobilizing the patient completely. Ejection fraction is not necessarily a good indicator of exercise tolerance because these variables are not well correlated. Upper-extremity work alone is more hemodynamically demanding than lower extremity work and thus is prescribed cautiously, if at all, at least in the early stage. Exercise or physical activity involving sustained static postures and isometric muscle contraction are contraindicated. Breathing should be coordinated with activity such that breath holding and straining are avoided.

An individual with a history of angina, regardless of whether he or she is taking antianginal medications, must be hemodynamically monitored (i.e., heart rate, blood pressure, rate pressure product, and subjective responses; ECG monitoring may also be indicated).

Individuals prone to angina may exhibit symptoms in certain body positions.15,16 Usually, this reflects an increased workload and increased work of the heart. Recumbent positions increase the mechanical work of the heart by increasing central blood volume.¹⁷ These patients are not encouraged to lie flat. Instead, the head of bed is elevated 10 to 15 degrees. Side-lying positions, particularly left side-lying, increase the work of the heart by compressing the heart and impeding ventricular filling and ejection. Patients with impaired oxygen transport and without prior cardiac disease may exhibit myocardial stress and ischemia in these body positions. Thus patients with impaired or threatened oxygenation must be monitored closely, particularly during turning and activities in which oxygen demand is increased—at these times, oxygen delivery must be increased correspondingly.

The use of medication to minimize the risk for angina and ischemic heart disease warrants review. The need for statins, commonly prescribed lipid-lowering medications, can be reduced through optimal lifestyle choices in many patients. One inherent danger of such a drug, however, in addition to its well documented side effects, is that patients may become complacent, believing that the drug will offset the need to make necessary lifestyle changes. More important, lifestyle changes largely address the cause of the problem, whereas medication such as statins only address an effect. The principles of the physical therapy management of patients with stabilized angina include health education, risk factor reduction, and a long-term health program (see Chapters 24 and 31).

Uncomplicated Myocardial Infarction

Pathophysiology and Medical Management

Myocardial infarction, commonly referred to as a heart attack, refers to insufficient myocardial perfusion resulting in a macroscopic area of damage and necrosis of the heart. Infarction results most frequently from narrowing and occlusion of the coronary blood vessels secondary to atherosclerosis. Other causes include occlusion secondary to a thrombus or embolus, reduced blood pressure, or coronary vasospasm. Angina, or ischemic chest pain, often precedes or accompanies a myocardial infarction. Infarctions vary in severity from being silent (i.e., having no characteristic signs and symptoms and thus going undetected) to being fatal. Most infarctions, when detected, require some hospitalization and monitoring to ensure that the infarction is not evolving further and that the patient is medically stable and in no danger. Chapter 34 describes the management of patients with complicated myocardial dysfunction who are admitted to a coronary care unit. This section focuses on the patient with mild heart disease, the patient with cardiac dysfunction who is discharged from hospital, the patient who has a history of ischemic heart disease, and the patient who is hospitalized for a condition other than heart disease but develops and is being managed for myocardial ischemia. Judicious movement and body positioning are essential elements in the management of the patient with myocardial infarction.¹⁸ Because these interventions can place significant demands on cardiovascular and pulmonary function and oxygen transport, they must be prescribed specifically by physical therapists with considerable knowledge and expertise in the area.

Principles of Physical Therapy Management

Table 29-1 shows the primary components of care in the acute phase of management (phase I of cardiac rehabilitation). Physical therapy constitutes a prime hemodynamic stress secondary to exercise and gravitational stress secondary to mobilization/exercise and body position changes. Thus it is essential to establish the adequacy of the patient’s cardiovascular and pulmonary system to effect oxygen transport during and between treatments. The optimal treatment prescription is based on the patient’s overall signs and symptoms of coronary insufficiency and hemodynamic instability. The physical therapist must be knowledgeable in detecting inadequate myocardial tissue perfusion and in reducing and preventing myocardial tissue damage. In addition, acute or chronic impaired heart pump function leads to reduced cardiac output and systemic tissue perfusion. Clinical manifestations include reduced mentation, reduced renal function, fatigue, malaise, and moist, cool, and cyanotic skin.

Regardless of whether the patient is being treated in the hospital (in a general ward or in the physical therapy department within the hospital) or in the private physical therapy clinic, the patient must be hemodynamically monitored. Minimally, heart rate and blood pressure must be taken before, during, and after treatment, along with a subjective rating of anginal chest pain. ECG monitoring is usually continuous in the early stages of the infarction. The object of treatment is to have the patient remain below his or her anginal threshold so that anginal pain is avoided. Breathlessness or rating of perceived exertion may also be used. The rate pressure product (RPP) (i.e., the product of heart rate and systolic blood pressure) is highly correlated with myocardial oxygen uptake and work. Previous stress tests will establish the RPP at which angina occurs, and the intensity of the exercise dose should be set at 65% to 80% of this threshold. Patients on beta-blockers have a blunted hemodynamic response to exercise, particularly heart rate responses. In such cases, use of ratings of perceived exertion to define the upper and lower limits of an acceptable mobilization stimulus may be indicated.

In some cases, patients have labile angina (i.e., the onset of angina does not occur reliably at a given RPP). This patient and the patient who reports angina at rest are at higher risk, and appropriate precautions must be taken. First, the patient must be assessed to establish that treatment is not precluded (see pertinent questions to be answered before treating a patient with angina). Second, monitoring is essential and may include ECG monitoring. Third, treatments are prescribed below symptom threshold, which is usually consistent with a low exercise intensity in these patients. Comparable with any patient experiencing low functional work capacity, exercise prescribed on an interval schedule enables the patient to achieve a greater volume of work.

When selecting body positions for the patient with a myocardial infarction, the therapist selects those that will minimize the work of breathing and of the heart.¹⁹ Significant central fluid shifts are minimized by encouraging the upright position as much as possible to reduce the work of the heart²⁰ and by raising the head of the bed 10 to 15 degrees when the patient is recumbent. Patients with elevated intracardiac pressures are less susceptible to orthostatism (see Chapter 20).

Relaxation is central in the management of the cardiac patient who is prone to being anxious and apprehensive. Furthermore, such patients have a high prevalence of sleep-disordered breathing,²¹ so a sleep assessment is warranted. Relaxation interventions that can be suggested include autogenic relaxation, progressive relaxation, Benson’s relaxation response procedures, biofeedback, and meditation. Also, the patient needs to identify and minimize stress triggers and effective, individual-specific, nonpharmacological relaxants. Relaxation training with or without pharmacological support can be integrated into treatment.⁷ Patients with ischemic heart disease are often apprehensive and anxious about the intensity of physical activity they can undertake. Thus performing physical activity and exercise while monitored and under the supervision of a physical therapist is often reassuring and gives the patient confidence to perform activity when unsupervised.

The quality and quantity of the patient’s sleep and a profile of sleep-wake periods should be reviewed to ensure he or she is deriving maximal benefit. Rapid-eye-movement sleep with bursts of sympathetic activity during the early hours of the morning may constitute a period of increased risk for the patient with cardiac dysfunction.

Appropriate safety precautions must be taken in all settings where physical therapists practice, given that most physical therapy interventions physically stress patients and that coronary symptoms can occur regardless of whether the patient has a known underlying ischemic heart disease. In addition, because the overall U.S. population is aging, physical therapists are treating a growing number of older persons who are known to have a higher prevalence of cardiovascular conditions. In addition, young adults are presenting with symptoms and signs of cardiovascular conditions.

Optimal lifestyle habits and a lifelong health plan are central to maximizing recovery and improving an individual’s long-term prognosis. Good nutrition and hydration, good sleep habits, stress management, smoking cessation, and regular physical exercise are all salient to comprehensive physical therapy management (see Chapters 24 and 31). As in the management of patients with other lifestyle-related conditions, the physical therapist needs to reinforce public health policy and health promotion guidelines regarding healthy lifestyle choices, including avoidance of inactivity and regular physical activity.²²

Pulmonary Pathology

Atelectasis

Pathophysiology and Medical Management

Atelectasis refers to partial collapse of lung parenchyma. The pathophysiological mechanisms contributing to atelectasis are multiple (Table 29-2). These mechanisms include physical compression of the lung tissue (e.g., resulting from increased pleural fluid, pus, pneumothorax, compression during thoracic surgery, or adjacent areas of lung collapse) or obstruction of an airway (e.g., due to secretions or tumor) with subsequent reabsorption of oxygen from the trapped air by the pulmonary capillaries resulting in a collapse of the lung tissue distal to the obstruction (i.e., reabsorption atelectasis).

Table 29-2

Pathophysiological Mechanisms Contributing to Atelectasis

Central Mechanisms	Breathing at low lung volumes (e.g., when in pain or after certain medications) Inability to generate adequate inspiratory pressure and volume Central disruption of breathing centers controlling normal periodic and rhythmic breathing pattern
Extramural Mechanisms	Chest wall deformity Asymmetry of intrathoracic structures Respiratory muscle weakness (e.g., neuromuscular disease) Phrenic nerve inhibition (e.g., secondary to upper abdominal or cardiovascular thoracic surgery) Compression of lung parenchyma secondary to pleural fluid accumulation, blood, plasma, and pus Compression of lung parenchyma during surgery Reduced lung expansion secondary to reduced movement Compression of lung parenchyma secondary to static body positioning Compression of lung parenchyma secondary to prolonged static body positioning Mechanical ventilation Increased alveolar surface tension
Mural Mechanisms	Airway narrowing secondary to increased bronchial smooth muscle tone Calcification or altered anatomical integrity of airways Edema of the bronchial wall and epithelium
Intramural Mechanisms	Impaired mucociliary transport Increased pulmonary secretions Inspissated pulmonary secretions Altered distribution of pulmonary secretions Mucus plug
Space-Occupying Lesions	Exudative and transudative fluid in the lung parenchyma Foreign-body aspiration Inflammation
Other Factors	Increased compliance and dynamic airway compression secondary to age-related changes to the lung Increased time constants because of increased airway resistance, reduced compliance, or both Splinting or casting of chest wall restricting normal three-dimensional chest wall movement Pain and altered breathing pattern Medications including narcotics, sedatives, and relaxants Supplemental oxygen

There are two primary types of atelectasis: microatelectasis and segmental and lobar atelectasis. Microatelectasis is characterized by a diffuse area of lung units that are perfused but not ventilated, leading to a right-to-left shunt. Ill and hospitalized patients who are deprived of being regularly upright and moving have reduced lung volumes and are prone to breathing at low lung volumes, which leads to microatelectasis. Thus such patients require prophylactic measures to avoid the effects of atelectasis on oxygen transport and gas exchange. When the conditions for normal lung inflation are removed, alveolar collapse occurs instantly.

Microatelectasis is associated with reduced lung compliance because of reduced lung expansion. Patients who are mechanically ventilated are prone to microatelectasis because the normal mechanics of breathing are violated. This may be explained in part by restricted mobility, recumbency, and reduced arousal, in addition to reduced functional residual capacity (FRC). Positive end-expiratory pressure (PEEP) is routinely added to minimize these effects. High ventilator system pressure is required to counter reduced lung compliance, which indicates that atelectatic lung tissue it not readily re-expandable.

Microatelectasis is not diagnosed readily with chest x-ray but can be established in conjunction with clinical findings. Nonetheless, microatelectasis can be anticipated in every ill and hospitalized patient whose normal respiratory mechanics are disrupted, particularly in recumbent, relatively immobile patients. These effects are further exacerbated in patients who are smokers, older, overweight, sedated, have abdominal masses, spinal deformities, or chest wall asymmetry, or some combination of these factors.

Commensurate with its distribution, atelectasis presents with reduced chest wall movement and reduced breath sounds over the involved area. A chest x-ray shows increased density over the involved areas with a shift of the trachea and mediastinum toward the collapsed lung tissue. The patient may be tachypneic and cyanotic because of shunting. Segmental atelectasis results from progression of microatelectasis and obstruction of airways with reabsorption of gas in the distal lung units of a bronchopulmonary segment or lobe.

The patient who depends on a mechanical ventilator to breathe is predisposed to atelectasis because of an unnatural, monotonous breathing pattern, restricted movement, and abnormal and prolonged recumbent body positions. These factors contribute to reduced mucociliary transport, abnormal distribution of pulmonary mucus, and the accumulation of mucus in the dependent lung fields. Furthermore, production of mucus may be increased as a result of tracheostomy or the presence of an endotracheal tube. Mucociliary clearance is further compromised by reduced ciliary activity resulting from high concentrations of oxygen, medication, and loss of an effective cough due to an artificial airway.

The effect of atelectasis on oxygen transport reflects its type and distribution. Hypoxemia, right-to-left shunt, reduced lung compliance, and increased work of breathing are common clinical manifestations. An increased temperature reflects inflammation or infection and not atelectasis per se.

Principles of Physical Therapy Management

Because it can develop instantaneously when respiratory mechanics are disrupted, microatelectasis should be anticipated and prevented. Those factors that contribute to atelectasis for a given patient are countered accordingly with aggressive prophylactic management. Many of the causes of atelectasis outlined in Table 29-2 can be readily reversed. The assessment includes a detailed analysis of the underlying cause(s) and mechanism(s) so that these can be addressed directly for a given patient.

Atelectasis is always treated aggressively because it has the potential to worsen, develop into a severe clinical manifestation, and lead to pneumonia. In turn, overwhelming pneumonia can precipitate acute respiratory distress syndrome (Chapter 36), which is associated with considerably poorer outcomes. Based on long-standing physiological evidence, treatment continues to be primarily directed at reversing the underlying contributing mechanisms whenever possible. For example, atelectasis resulting from restricted mobility is remediated with mobilization. Atelectasis resulting from prolonged static positioning and monotonous tidal ventilation is managed with mobilization, manipulating body position to increase alveolar volume of the atelectatic area, manipulating body position to optimize alveolar ventilation, or some combination of these interventions. Atelectasis arising from reduced arousal is managed by minimizing the causative factors contributing to reduced arousal coupled with frequent sessions of mobilization and the upright position to stimulate arousal, promote greater tidal volumes and alveolar ventilation, increase zone 2 (area of optimal ventilation and perfusion matching), increase FRC, and minimize closing volume. Most often in a given patient, atelectasis results from a combination of these factors, thus necessitating a multipronged approach in its management.

Breathing control and coughing maneuvers augment the cardiovascular and pulmonary physiological effects of mobilization and body positioning. Coordinating these interventions distributes ventilation more uniformly rather than directing gas to already open alveoli, which overdistends these units. The distribution of ventilation has long been known to be altered primarily by body positioning rather than deep breathing.²³ Sustained maximal inspiratory efforts may augment alveolar ventilation; however, the parameters necessary for such efforts to be maximally therapeutic remain to be elucidated.

If impaired mucociliary transport or excessive secretions are obstructing airways and contributing to atelectasis, mobilization of pulmonary secretions is the goal. Mobilization and a physiological stir-up regimen ²⁴ are instituted as soon as possible for multiple reasons in patients who are acutely ill to augment oxygen transport and minimize reduction in aerobic capacity (Chapter 18). In the event of excessive secretions, mobilization may need to be more vigorous to stimulate eucapnic deep breaths and inspiratory efforts and, hence, effective coughs. Stir-up, coined 70 years ago by Dripps and Waters²⁵ aptly describes the clinical role of physiologically perturbing a patient to reduce risk and improve outcomes.