The heart and lungs work interdependently; thus failure of one organ has implications for the function of the other organ. Insufficiency or failure of the cardiovascular and pulmonary systems refers to the inability of these systems to maintain adequate oxygen and carbon dioxide homeostasis.

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

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 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).

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.

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 ICU15–17; 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.

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.

Active movements have greater therapeutic effect on oxygen transport than assisted or passive movements; thus the benefits of active movements are exploited first. Movement recruiting large muscle groups minimizes the disproportionate hemodynamic stress associated with movement of small muscle groups or movements requiring excessive dynamic stabilization. If active movements cannot be performed or excessively stress the oxygen transport system, then active assisted movements are indicated. A recent randomized controlled clinical trial reported evidence supporting that early exercise training (including use of a bedside ergometer for 20 minutes daily either passively or actively) enhanced the recovery of functional exercise capacity in patients in the ICU, their self-perceived functional status, and their muscle force at hospital discharge.²⁴

Passive movements have a role primarily when the patient is paralyzed or so hemodynamically unstable that his or her condition deteriorates with active movement. With respect to cardiovascular and pulmonary benefits, passive movement stimulates changes in ventilatory and circulatory patterns.²⁵ These can be particularly beneficial in patients who have significant mobility restriction; however, they should not substitute for active and active-assisted movements, which are associated with even greater benefit because they are higher-order activities on the physiologically based treatment hierarchy (see Chapter 17).

A study reported on the use of electrical stimulation in combination with active exercise of the limbs in patients with severe COPD who were mechanically ventilated.²⁶ Muscle strength was improved, and the number of days to transfer from bed to chair was reduced. The study’s design precludes electrical stimulation as being superior to extended active exercise and progressive mobilization to the chair and ambulation. Another recent study demonstrated that electrical stimulation is well tolerated and seems to preserve the muscle mass of critically ill patients.²⁷ The use of electrical stimulation as a preventive and rehabilitative tool in patients in the ICU with polyneuromyopathies, however, needs to be further investigated and should not replace mobilization. Deep sedation and bed rest are common in the routine medical care for many mechanically ventilated patients²⁰ and need to be reconsidered in light of rehabilitation initiatives to prevent iatrogenic effects of care and to maximize short- and long-term functional outcomes.

Status asthmaticus is a potentially life-threatening situation. The pathophysiological features include marked airway resistance secondary to bronchospasm, edema, and mucous secretion and retention. The work of breathing is markedly increased, resulting in respiratory distress. A cycle results in which the patient becomes more hypoxemic and hypercapnic secondary to alveolar hypoventilation, bronchospasm increases, and reactive pulmonary hypertension may ensue, along with a further increase in the work of breathing and anxiety.

The classic signs and symptoms of a severe asthmatic attack that may progress to status asthmaticus include tachypnea, dyspnea, labored breathing, audible wheezing, tachycardia, cyanosis, anxiety, and panic. If the patient is able to cooperate with spirometric testing, the degree of reduced vital capacity, peak flow, and forced expiratory volume provide indices of the severity of airway obstruction.

Medical management is aimed at administering drugs and fluids to reduce hypoxemia with oxygen, decrease airway inflammation and resistance, and hence reduce the work of breathing and anxiety. Intravenous sodium bicarbonate helps to reverse respiratory acidosis and possibly metabolic acidosis.⁵

Acute respiratory failure can be associated with primary restrictive lung disease (i.e., interstitial pulmonary fibrosis). This is distinct from restrictive defects secondary to neuromuscular and musculoskeletal diseases (e.g., Guillain-Barré syndrome, myasthenia gravis, and neuromuscular poisonings are common neuromuscular disorders that can precipitate respiratory failure in the absence of underlying primary lung disease) (see Chapter 35).

Restrictive lung dysfunction may complicate the management of patients admitted to the ICU for reasons other than cardiovascular and pulmonary disease. The lung parenchyma, the chest wall, or both may be involved. The underlying cause of respiratory failure may therefore reflect ventilatory pump failure, gas exchange failure, or both. The specific restrictions to cardiovascular and pulmonary function need to be identified and treated individually to optimize treatment. Obstructive and restrictive patterns of cardiovascular and pulmonary function frequently coexist; thus the contribution of both types of defects to a patient’s oxygen transport must be determined. Typically in restrictive lung disease, all lung volumes and capacities are reduced, although tidal volume can be relatively normal (see Figure 9-5). Patients with severe interstitial pulmonary fibrosis have increased pulmonary artery pressures with an associated increase in right ventricular work. These patients are at high risk of desaturating with minimal activity.

The initial priority of management in the acute phase of MI is the correction of the immediate problems including dysrhythmias, myocardial insufficiency, reduced cardiac output, hypoxemia, chest pain, and anxiety, followed by implementation of a progressive rehabilitation program ranging from the acute medically stable phase to the postdischarge rehabilitation phase.38,39 On admission to the coronary care unit or medical ICU, continuous monitoring of the heart rate and rhythm is established. An intravenous line is routinely started for the administration of medications and fluids. An arterial line may be started for serial blood sampling for blood gases and enzyme measures. Initially pain medications, coronary vasodilators, and diuretics are frequently used to minimize the work of the heart, anginal pain, and discomfort. Drugs such as morphine serve to depress the respiratory drive; thus the physical therapist must be aware of corresponding changes in vital signs. Less-potent sedatives and tranquilizers are more routinely prescribed. Increased pain and anxiety potentially worsen the patient’s cardiac status by increasing myocardial oxygen demand and altering normal breathing pattern and gas exchange.

The primary purpose of oxygen administration to the cardiac patient is to reduce hypoxemia, myocardial work, and angina. Dyspnea, however, is commonly observed in the initial phases of MI and can be effectively controlled by supplemental oxygen administered by nasal cannula or mask. Oxygen may also correct potential ventilation-perfusion mismatching and hypoxemia. Oxygen is always administered with humidity to avoid drying the airways.

Blood gas analysis is performed within an hour of initiating oxygen therapy to establish a baseline of arterial saturation. In this way the oxygen dose can be altered to regulate blood gases and acid-base balance.

A primary principle of the management of the patient after MI is to reduce myocardial oxygen demand and workload. The myocardium needs rest for optimal healing. Judicious rest of the myocardium is a priority that can often be balanced with gentle rhythmic, nonstatic movements. Box 34-1 illustrates several ways of reducing myocardial workload in patients with cardiovascular and pulmonary conditions.

Physical therapists need to work closely with the interprofessional team members in the ICU to provide safe and effective therapeutic interventions. The physical therapist should also be watchful at all times for signs of impending or silent infarction, including generalized or localized pain anywhere over the thorax, upper limbs, and neck, palpitations, dyspnea, lightheadedness, syncope, sensation of indigestion, hiccups, and nausea.

Depending on the degree of MI and damage, varying lengths of modified mobility may be recommended.³⁸ Shorter initial periods of restricted mobility are safe and promote faster functional recovery.⁴⁰ During this period the physical therapist concentrates on rhythmic breathing exercises, gentle coughing exercises or huffing, and modified positioning with the bed head elevated at least 30 degrees to facilitate the gravity-dependent mechanical action of the heart and thereby reduce myocardial oxygen demand. Intermittent exposure to orthostatic stress by imposing the upright position is recommended for patients after acute MI.⁴¹ The patient is encouraged to perform deep breathing and coughing every hour during the day. Bed exercises including rhythmic, unresisted hip, knee, foot, and ankle exercises are usually performed as frequently as possible by the patient or when the patient turns in bed. The patient is cautioned to exercise one leg at a time, sliding one heel up and down the bed and guarding against lifting the leg off the bed. These exercises, when performed correctly and coordinated with inspiration and expiration, require relatively little effort from and induce little additional physical stress on the individual with MI. Comparable with the management of the postoperative patient, these exercises are performed prophylactically to reduce the risk of venous stasis and formation of thromboemboli. In addition, they may help to regulate more coordinated breathing, encourage deep breaths and mucociliary transport, and reduce atelectasis. The patient is cautioned against performing the Valsalva maneuver and straining because these activities increase intrathoracic pressure and reduce cardiac output.

Electrocardiographic monitoring of the patient with cardiac disease is the responsibility of all members of the health care team involved in the patient’s care. The physical therapist has a special responsibility to be proficient in ECG interpretation in the coronary care unit because physical therapy is one of the most metabolically demanding interventions for patients.11,14 The physical therapist often has the responsibility of initiating new activities with the cardiac patient, which might include sitting over the edge of the bed, engaging in self-care (particularly involving the arms being maintained in a raised position), getting in and out of bed, sitting in a chair, going to the bathroom, walking around the room or in the hallways, and eventually exercising on the treadmill or ergometer. Changes in the ECG must be watched for, particularly in introducing new activities and increasing the intensity of workload in activities. Careful attention to ECG changes and serum enzyme levels will contribute to enhanced physical therapy care of the acute MI patient by optimizing the treatments prescribed and the margin of safety with which activities are performed.

Congestive heart failure may be unavoidable in cases of severe infarction or even milder infarction coupled with lung disease. Fluid intake and output and daily weight measurements promote early detection of congestive heart failure. Signs of imminent and established congestive heart failure are listed in Box 34-2. The work of the heart can be significantly reduced in the upright position.⁴²

Patients with cardiac conditions are prone to anxiety about their conditions and prognoses. The patient is given realistic guidelines at each stage of recovery with respect to the level of activity that can be safely performed, which can potentially avert deterioration and promote recovery. Involving the patient in rehabilitation planning from the outset facilitates the patient’s planning realistically for the future and may help to reduce the depression often experienced by the acute MI patient.

The initial rehabilitation program is planned with the long-range rehabilitation goals in mind. The program designed for the cardiac patient is progressive in terms of types of activities, usually beginning with activities of daily living, and with respect to the intensity, duration, and frequency of these activities.³⁹ The patient’s tolerance and changes in ECG and vital signs are used as indicators for establishing and modifying the treatment program. These physiological parameters must be observed carefully as the patient progresses to optimize the potential benefits of the therapeutic regimens as early as possible without endangering the patient.

Patient education and prevention of infarction are particularly important for the cardiac patient. As soon as the patient is alert and able to cooperate, information about his or her condition with guidelines about activity, diet, and stress management is reinforced. The more involved and informed the patient is in self-management, the greater the likelihood of receptivity and adherence to a rehabilitation regimen after discharge.

Patients scheduled for open heart surgery are considered moderately risky surgical candidates because of the nature and invasiveness of this type of surgery (Figure 34-4), regardless of their general level of health before surgery. Whenever possible, patients prepare for surgery in advance by decreasing or stopping smoking, by avoiding exposure to respiratory tract infections, by avoiding stress, by eating a balanced diet, and by getting adequate sleep. Patients can benefit from a modified, prescriptive exercise program before surgery to maximize their aerobic capacity and thereby improve their perioperative course.

Preoperative teaching coupled with a conditioning program before hospitalization has a role in reducing hospital stay and complications (see Chapters 18, 29, and 30). During the preoperative period the physical therapist may spend additional time with patients scheduled for open heart surgery to provide teaching of the basic anatomy and physiology related to the surgery to be performed; the effect of anesthesia; the role of intubation and mechanical ventilation; the incision lines to be expected over the chest, and the legs if veins are to be removed for bypass surgery; the lines, leads, chest tubes, and catheters that will be in place after surgery; interventions beginning during the postanesthesia and recovery period (breathing control and coughing maneuvers, body positioning, foot and ankle exercises, and early mobilization); and the course of recovery the patient might expect, barring complications (see Chapter 17). The emphasis on patient education in most open heart surgery units may contribute to the generally low incidence of complications and mortality.

Some special considerations in physical therapy management of the patient after open heart surgery appear in Table 34-2 and these expand on the concurrent medical course of patients in phase I cardiac rehabilitation (see Chapter 31). Patients are extubated early, and rehabilitation is commenced as soon as possible.⁴³ These guidelines are to be applied thoughtfully and cautiously with regard to each specific patient’s condition and observed recovery. Intermittent orthostatic stress and exercise stress are encouraged.⁴¹ These guidelines suggest the upper limit of intensity of physical therapy, which should be applied if all is progressing well initially and reduced if warranted by the patient’s condition. Progression from one stage to the next is based on an optimal and reliable treatment response at each level before proceeding. Different institutions may advocate different practices, depending on their facilities, the experience of the surgical and ICU team, and the incidence of postoperative complications and survival for that institution.

The physical therapist must guard against excessively intense treatment of both patients after open heart surgery and patients for whom periods of relatively restricted mobility are anticipated. In addition to the fact that these patients may be hemodynamically unstable initially, they may be susceptible to soft tissue bruising from being on a prophylactic course of anticoagulants.

Patients are monitored for complications (see Chapters 16 and 36) and to guide treatment progression and detect untoward responses to treatment. After cardiac surgery, tends to increase owing to increased cardiac output and oxygen delivery.⁴⁴ The oxygen extraction ratio may increase and decrease if cardiac function deteriorates.

Depression has been reported in patients in the ICU, particularly in those admitted for coronary care who are experiencing a physiological loss.⁴⁵ Signs and symptoms of depression warrant monitoring and reporting to the team to maximize clinical and psychosocial outcomes.

Complications do occur in high-risk ICU settings. Risk assessment is a fundamental component of the assessment (see Chapter 17). Common complications often related to premorbid status include restricted mobility, inability to wean from mechanical ventilation, deep vein thrombosis, pulmonary emboli, and stroke. Other complications are related to surgery (e.g., internal bleeding, overwhelming pneumonia, and lung collapse) or medication reaction. Complications are better managed if anticipated and detected early. Depending on the nature of the complication, physical therapy interventions may be stepped up in terms of intensity, duration, and frequency; modified; or discontinued until the patient is cleared with respect to stability.

Physical therapy follow-up should continue for several months beyond discharge, at which point the patient should be well integrated into a cardiac rehabilitation program. Continuity and continuation of physical therapy throughout the entire rehabilitation period, from the acute period to long term, cannot be overemphasized, given that achieving maximal recovery from surgery is the priority.

Summary

This chapter described the principles of cardiovascular and pulmonary physical therapy in the management of critically ill patients with primary cardiovascular and pulmonary dysfunction. Cardiovascular and pulmonary failure secondary to chronic lung disease and heart disease were described. Cardiovascular and pulmonary physical therapy management is based on the specific underlying pathophysiological mechanisms of these various disorders. These principles, however, cannot be interpreted to be guidelines for specific treatment because each patient is an individual whose condition reflects multiple factors contributing to impaired cardiovascular and pulmonary function or threatening to cause it (i.e., the effects of recumbency, restricted mobility, extrinsic factors related to the patient’s care, and intrinsic factors related to the patient in addition to the underlying pathophysiology). Special considerations with respect to body positioning and mobilizing patients with primary cardiovascular and pulmonary dysfunction are described.