Diagnosis and Assessment

A comprehensive assessment of all factors that affect or threaten oxygen transport is essential, particularly for patients who are not obviously at risk (i.e., those without overt cardiovascular and pulmonary conditions). The physical therapist must be able to “red-flag” a patient with an underlying problem for which physical therapy may be contraindicated or an untoward treatment response may be anticipated. Alternatively, treatment may have to be modified or treatment responses monitored more often.

Specific diagnosis of the factors that contribute to or threaten cardiovascular and pulmonary dysfunction is paramount to effective treatment across all physical therapy specialties. The overall capacity of the oxygen transport system should be established to ensure that it can adequately respond to changes in metabolic demand (including those imposed by physical therapy treatment—specifically, exercise) and changes in body position in patients who are acutely ill. Even if cardiovascular and pulmonary dysfunction is not a patient’s primary condition, it may be a secondary problem, which could seriously limit a patient’s response to exercise. Such assessment will establish whether treatment, specifically exercise, should be modified to avert an incident or whether it is contraindicated altogether.

Oxygen transport can be affected by dysfunction of virtually any one of the major organ systems of the body (Box 6-1). The pulmonary and pleural complications of heart disease and the cardiac complications of pulmonary disease are usually predictable and therefore are most readily detected clinically. However, the cardiovascular and pulmonary complications of conditions affecting other organ systems can be more subtle, if not more devastating.

Cardiovascular Conditions

The pulmonary complications of heart disease and the cardiac complications of pulmonary disease have been well documented for several decades.² A mechanically inefficient heart disrupts the normal forward propulsion of deoxygenated and oxygenated blood to and from the lungs. Because the right and left sides of the heart function in series, a problem on one side inevitably has some effect, which can lead to a problem, on the other side. For these reasons, the heart and lungs should be thought of as a single functioning unit. Disruption of the cardiovascular and pulmonary circuit leads to the backlogging of blood and an increased volume of blood in the capacitance vessels or the veins. Right heart failure contributes to increased central venous pressure (i.e., right atrial pressure) and, if sufficiently severe, leads to bilateral peripheral edema in the dependent body parts. Because blood is not forwarded to the lungs adequately, hypoxemia can result. In turn, hypoxic vasoconstriction of the pulmonary circulation leads to increased pulmonary vascular resistance and, hence, to increased right ventricular afterload and work.

Left heart failure can result in inadequate forward movement of blood through the left heart, resulting in backlogging in the pulmonary circulation and cardiogenic pulmonary edema. Pulmonary edema alters lung mechanics and lymphatic drainage, and in turn, these effects contribute to an increased risk for infection secondary to impaired macrophage function and bacterial growth. Excess pulmonary fluid around the alveolar capillary membrane creates a diffusion defect. If fluid accumulation is extreme, backlogging may be transmitted to the right side of the heart and to the periphery. Comparable to excess fluid in the lungs, backup of fluid in the peripheral circulation can impair tissue perfusion. Other cardiovascular conditions such as systemic hypertension increase systemic afterload; this, in turn, increases the work of the heart, thereby reducing its mechanical efficiency.

Pulmonary function can be altered in cardiac disease. Left heart failure, for example, is associated with accumulation of fluid in the pulmonary interstitium. This leads to reduced caliber of the airways and early airway closure, air trapping, and increased residual volume. The fluid can produce reflex constriction of bronchial smooth muscle, leading to the syndrome of cardiac asthma. The combination of airway collapse and bronchoconstriction decreases total lung capacity, flow rates, and forced expiratory volumes. Ventilation and perfusion abnormalities are also associated with cardiac disease. Ventilation of underperfused lung zones contributes to increased ventilatory dead space, and perfusion of underventilated lung zones leads to a right-to-left shunt. In left heart failure, reduced lung compliance may contribute to inhomogeneous ventilation and perfusion.

In left heart failure, the normal pattern of increased ventilation to the bases may be reversed (i.e., the apices of the lungs may be better ventilated).³ If pulmonary edema complicates the clinical picture, the alveoli become flooded, resulting in reduced ventilation and ventilation and perfusion mismatching. The alveolar-arterial oxygen (A-aO₂) gradient is then increased, diffusing capacity is decreased, and arterial partial pressure of oxygen (PaO₂) is decreased. Lung compliance is inversely related to pulmonary artery pressures and interstitial fluid accumulation.⁴ The net effect of these abnormalities is both obstructive and restrictive pathophysiological patterns of lung dysfunction (i.e., reduced forced expiratory volumes and vital capacity and an overall increase in the work of breathing).

Pleural effusions can result from heart disease, in particular, congestive heart failure. Changes in intravascular pressures lead to transudative pleural effusions, and cardiac injury leads to exudative effusions. Comparable to fluid balance in other parts of the circulation, fluid balance in the lung is dependent on Starling forces (i.e., hydrostatic and oncotic pressures). In healthy individuals, several liters of fluid a day are absorbed from the pleural space, so when the balance of these forces is disrupted in disease, considerable fluid can accumulate in the pleural space. Impaired alveolar expansion due to pleural effusions is of clinical concern. Small effusions displace rather than compress the lung.

Pulmonary Conditions

Lung conditions can contribute to cardiac dysfunction in several ways. They invariably threaten oxygen transport by their effects on respiratory mechanics and ventilation-perfusion matching. To compensate, the heart attempts to increase cardiac output, which produces a corresponding increase in cardiac work. Overall, ventilation and oxygen transport are less efficient. Hypoxemia secondary to inadequate ventilation-perfusion matching may predispose the patient to cardiac dysrhythmias.

Pleural complications can arise from lung disease as well as from heart disease. Both heart and lung function can be compromised by altered fluid balance in the pleurae. Fluid balance in the pleural space is comparable, in terms of its regulation, to that in the alveolar space. Both are determined by Starling forces. Specifically, hydrostatic pressure pushes fluid into the pleural space while oncotic pressure counters the effect of these forces. The net effect of these filtration and absorption forces is a minimal net filtration pressure. When the balance of these forces is disrupted, heart and lung function can be threatened. Excessive fluid floods the space, usually reflecting both excessive hydrostatic pressure and diminished oncotic pressure. The lymphatic vessels become overwhelmed and are unable to keep the pleural space dry. Pleural fluid accumulates and either displaces lung tissue (in small to moderate effusions) or restricts the opening of adjacent alveolar sacs, causing atelectasis (severe effusions),⁵ which, if sufficiently severe, may restrict cardiac filling. Pleural fluid accumulation poses a unique threat to oxygen transport as a result of its direct physical effect on the lungs, heart, or both, so it warrants special attention by physical therapists.

Pulmonary lymphatics control fluid balance within the lung parenchyma. Lymphatic vessels arise within the pleurae and not within the alveolar capillary space. They drain fluid from the interlobular septae and subpleural areas into the hilar vessels and the primary tracheobronchial lymph nodes. Problems arising within the heart or lungs can contribute to imbalances in the major lymphatic inflow and outflow channels. This contributes to fluid accumulation, stagnation, and physical compression of the myocardium and lungs.⁶

Both heart and lung disease can produce deleterious hematological changes to compensate for hypoxemia. Increases in the number of red blood cells raise the hematocrit and viscosity of the blood. This phenomenon increases the work of the heart further. In addition, viscous blood increases the probability of thromboemboli. This risk is superimposed on the existing risk for thromboemboli in hypoeffective hearts.

A thorough understanding of the interrelationship of the heart and lungs is essential for diagnosis and optimal management. In addition, the cardiovascular and pulmonary manifestations of other primary organ systems must be recognized and anticipated, particularly in patients with multisystem conditions.

Musculoskeletal Conditions

Musculoskeletal conditions impact cardiovascular and pulmonary function secondary to their effects on muscle (in particular, the diaphragm, muscles of the chest wall, oropharynx, larynx, and abdomen) and bones and joints (e.g., arthritis, ankylosing spondylitis, kyphoscoliosis, and deformities secondary to neuromuscular diseases and chronic lung diseases) (Table 6-1). Additional effects are imposed by inactivity (i.e., muscle wasting, joint rigidity, and deformity). Increased joint rigidity limits the amount of physical activity a patient may perform, which contributes to cardiovascular and pulmonary compromise, in addition to the local effect of increased chest wall rigidity and compromised bucket-handle and pump-handle motions. The normal three-dimensional movement of the chest wall and normal pulmonary circulation and lymphatic function are compromised (Chapter 23). The cardiovascular and pulmonary manifestations of musculoskeletal conditions are summarized in Table 6-1.

The cardiovascular and pulmonary deficits associated with musculoskeletal disorders of the chest wall include reduced and potentially asymmetric lung volumes consistent with pulmonary restriction, reduced flow rates, reduced inspiratory and expiratory pressures, atelectasis, dynamic airway compression, ventilation-perfusion mismatching, inefficient breathing pattern, impaired cough and gag reflexes, increased risk for aspiration, increased risk for obstruction secondary to impaired mucociliary clearance, restricted mobility, compression of mediastinal structures and heart, and impaired lymphatic drainage, which depends on normal expiratory and inspiratory cycles.⁷ Osteoporotic fractures also compromise normal chest wall configuration, hence, pulmonary function.⁸

Autoimmune conditions that have musculoskeletal manifestations can be associated with systemic conditions. Rheumatoid arthritis, for example, is associated with accelerated atherosclerosis.⁹

Connective Tissue Conditions

Connective tissue, or collagen, vascular disorders (e.g., scleroderma, systemic lupus erythematosus, and systemic sclerosis) invariably affect the cardiovascular and pulmonary systems (Box 6-2).¹⁰ Inflammation and tissue injury can affect the airway, lung parenchyma, pulmonary vasculature, pleurae, respiratory muscles, heart, and pericardium. Shrinking-lung syndrome associated with chronic connective tissue changes is a feature of advanced disease and is characterized by loss of alveolar surface area, diffusion capacity, and lung volumes. Fibrotic changes increase the elasticity of the lung parenchyma and reduce lung compliance, thereby increasing the work of breathing. These changes are comparable to those in idiopathic pulmonary fibrosis. Both the electrical conduction system of the heart and its mechanical behavior are adversely affected by systemic connective tissue changes. Furthermore, connective tissue changes in the skin can lead to chest wall restriction. Renal-pulmonary syndrome has been associated with connective tissue conditions.¹¹ The cardiovascular and pulmonary manifestations of connective tissue conditions are summarized in Box 6-2.

Neurological Conditions

Cardiovascular and pulmonary consequences of neurological conditions reflect the pathophysiological mechanisms involved.¹⁴ There are three basic patterns of pathology: dysfunction of the central nervous system (CNS), dysfunction of the peripheral nervous system, and dysfunction of the autonomic nervous system. The cardiovascular and pulmonary manifestations of neurological conditions are summarized in Table 6-2.

Gastrointestinal Conditions

The cardiovascular and pulmonary manifestations of gastrointestinal (GI) dysfunction are summarized in Table 6-3. Inflammatory bowel disease and pancreatitis are principal examples of GI dysfunction affecting cardiovascular and pulmonary function. Aspiration is a significant cause of morbidity and mortality in patients with GI dysfunction, so it should be prevented or detected early. The pathophysiology, management, and outcome depend on the nature of the aspirate. Several predisposing factors produce aspiration pneumonia, including a decreased level of consciousness, disorders of pharyngeal and esophageal motility, altered anatomy, disorders of gastric and intestinal motility, and iatrogenic factors such as surgery, nasogastric intubation, and general anesthesia.

Inflammatory bowel disease can lead to the following cardiovascular and pulmonary pathologies: vasculitis, fibrosis, granulomatous disease, and pulmonary thromboembolism. Bronchitis and bronchiectasis have also been associated with inflammatory bowel disease; however, their occurrence is not related to disease severity or therapy. Biopsy specimens have shown basement membrane thickening, thickening of the epithelium, and infiltration of the underlying connective tissue with inflammatory cells.³⁰

The pulmonary manifestations of acute pancreatitis are among the most important sequelae of this disease and often the cause of premature death. Problems include elevated hemidiaphragms, particularly on the right side; basal atelectasis; diffuse pulmonary infiltrates that appear more commonly on the right side than on the left side; pleural effusions that occur more commonly on the left side than on the right side; and pneumonitis. These findings are not specific for pancreatitis and are probably secondary to localized peritonitis, subphrenic collections, ascites, pain, and abdominal distension. In chronic pancreatitis, abdominal symptoms may be reduced and thoracic symptoms such as dyspnea, chest pain, and cough may predominate. Chronic effusions may result in pleural thickening.

Hepatic Conditions

Both acute and chronic liver conditions can predispose a patient to cardiovascular and pulmonary and cardiovascular complications (Box 6-3). Hepatic dysfunction can lead to hypoxemia secondary to intrapulmonary vascular dilation and noncardiogenic pulmonary edema. Hepatopulmonary syndrome, hallmarked by intrapulmonary vascular dilation, produces both diffusion and perfusion defects in the lungs and is the principal reason for severe hypoxemia.³¹

Such pulmonary vasodilation is associated with excess perfusion with respect to ventilation.³² Arterial oxygenation may range from an asymptomatic increase in alveolar-arterial oxygen pressure difference to extreme breathlessness secondary to severe hypoxemia. Of relevance to the physical therapist is that oxygenation in these patients is frequently worse when the patient is standing compared with lying supine (orthodeoxia). In severe cases, pulmonary edema may occur secondarily to hepatic encephalopathy and cerebral edema.³³

With respect to chronic liver conditions, cardiovascular and pulmonary manifestations have been associated with cirrhosis and hepatitis. The most common pulmonary abnormalities associated with these conditions are intrapulmonary vascular dilation with and without shunt, pulmonary hypertension, airflow obstruction, chest wall deformity, pleural effusions, panacinar emphysema, pleuritis, bronchitis, bronchiectasis, hypoxic vasoconstriction, interstitial pneumonitis, and fibrosis. Hypoxemia results from shunting, ventilation-perfusion mismatching, and diffusion abnormalities.

Pleural effusions and ascites interfere with diaphragm function and present unique problems in a patient with liver disease. Rich lymphatic connections exist between the abdominal and thoracic cavities, so ascitic fluid can flow into the pleural space. This effect is enhanced during inspiration, when the intraabdominal pressure is relatively positive and the intrapleural space is negative.

The liver is a primary organ for the production of procoagulants and anticoagulants in the blood, both of which are carefully regulated to maintain optimal balance. Liver dysfunction can disrupt the production of these complementary agents and lead to a tendency to bleed or clot. Disseminated intravascular coagulation refers to an extreme imbalance between these vasoactive agents in which bleeding and clotting problems occur simultaneously, resulting in serious consequences to the patient. With respect to central dysfunction, recently impaired myocardial contractility has been reported in patients with cirrhosis.³⁴

Renal Conditions

Cardiovascular and pulmonary complications can result from renal dysfunction and from the category of disorders referred to as renal-pulmonary syndromes (Box 6-4).^35,36 The pathophysiological characteristics of these disorders include alveolar hemorrhage, interstitial and alveolar inflammation, and dysfunction of the pulmonary vasculature. Pulmonary function testing may detect both obstructive and restrictive abnormalities as a result of bronchial complications and as a result of inflammation and hemorrhage, respectively.

In systemic illness, pathology of the lungs and kidneys often coexist. Physical therapy warrants being aggressive, given the course of the renal-pulmonary syndromes and the potential for relapses and irreversible organ damage. Notwithstanding the serious medical implications of renal dysfunction, even simple measures such as dietary salt restriction need to be advocated, even for patients on dialysis.³⁷

Hematological Conditions

Hematological disorders that can manifest cardiovascular and pulmonary symptoms include abnormalities of the fluid and cellular components of the blood, as well as coagulopathies.³⁸ Cardiovascular and pulmonary manifestations of hematological conditions are summarized in Box 6-5. The primary underlying mechanisms by which these conditions disrupt gas exchange include hemorrhage, infection, edema, anemia, fibrosis, and malignancies.

Endocrine Conditions

Endocrine and metabolic disorders can be associated with cardiovascular and pulmonary complications (Box 6-6).^6,40 Disorders of the thyroid gland, pancreas (diabetes mellitus), and adrenal glands are examples that are often seen clinically. Thyroid hormone influences surfactant synthesis and the central drive to breathe. Hypothyroidism can lead to sleep apnea, pleural effusions secondary to altered capillary permeability, and pericardial effusions. Decreases in vital capacity have also been reported secondary to muscle weakness. Individuals with hypothyroidism have exercise intolerance.⁴¹ Hyperthyroidism increases cellular oxidative metabolism (the metabolic rate), leading to an increase in oxygen consumption and CO₂ production and an overall increase in minute ventilation.⁴¹ Vital capacity, lung compliance, and diffusion capacity can be reduced. In addition, maximal inspiratory and expiratory pressures can be reduced secondary to muscle weakness. In thyroid dysfunction, cardiorespiratory function can be normal at rest, but dysfunction can be unmasked during exercise stress.

Immunological Conditions

Congenital and acquired defects in the immunological status of the lungs lead to cardiovascular and pulmonary dysfunction, including inflammation and infection. Acquired immunodeficiency syndrome (AIDS), an example of a primary disorder of cell-mediated immunity, has reached epidemic proportions over the past 20 years. This syndrome leads to lymphocyte death. The most serious pulmonary infection associated with AIDS is Pneumocystis carinii pneumonia.⁴⁴ The fact that a patient with the human immunodeficiency virus (HIV) is likely to have recurrent pneumonia suggests that the infecting organisms persist in the lung despite treatment.⁴⁵ The clinical presentation includes diffuse pulmonary infiltrates, cough, dyspnea, and hemoptysis. These patients can also have symptoms of upper airway obstruction.

Nutritional Disorders

The two most common nutritional disorders seen in Western countries are obesity and anorexia nervosa, which is akin to starvation. Two-thirds of the U.S. population is now categorized as being overweight and at risk for its sequelae. Obesity contributes in several ways to impaired oxygen transport.⁴⁶ Alveolar hypoventilation and impaired PaO₂ and gas exchange result from chest wall restriction. Systemic and pulmonary blood pressures are increased. In addition, large abdomens and abdominal contents impinge on diaphragmatic motion and can restrict diaphragmatic descent. This can lead to compression of the dependent lung fields. Obesity is associated with elevated C-reactive protein, a marker for inflammation and elevated cardiovascular health risk.⁴⁷ Recumbency can induce respiratory insufficiency (positional respiratory failure). Individuals who are obese have a higher incidence of snoring and obstructive sleep apnea secondary to weakness and increased compliance of the postpharyngeal structures. In addition, these patients often have weak, ineffectual coughs resulting from expiratory muscle weakness and the mechanical inefficiency of these muscles. The work of breathing is markedly increased. Furthermore, in chronic cases, reactive pulmonary vasoconstriction in response to chronic hypoxemia contributes to right ventricular insufficiency and increased work of the heart and cardiomegaly. Individuals who are obese tend to be less active and aerobically deconditioned, with reduced efficiency of oxygen transport overall and increased risk for thromboemboli. Hypertension is also a serious sequela of obesity.

In addition to the direct effects obesity has on oxygen transport, central obesity has been strongly linked with metabolic syndrome. Additional risk factors include increased blood pressure, dyslipidemia (raised triglycerides and lowered high-density lipoprotein cholesterol), increased fasting glucose and type 2 diabetes mellitus.⁴⁸ In any patient who is overweight, these risk factors need to be assessed, not only so that treatment can be prescribed accordingly, but to facilitate referral of the patient to other health care professionals, if necessary. Abdominal fat, although associated with aging, is more closely linked with health risk than subcutaneous fat. Conventional measures of body composition may not estimate health risk sufficiently (e.g., insulin resistance and cardiovascular disease).⁴⁹

The major cardiovascular and pulmonary manifestations of anorexia nervosa relate to generalized weakness and reduced endurance of all muscles, including the respiratory muscles. Cough effectiveness is correspondingly compromised. Oxygen transport reserve is minimal. Because of poor nutrition and fluid intake, the patient is at risk for anemia, fluid and electrolyte imbalances, and cardiac dysrhythmias.⁵⁰ Common manifestations of nutritional disorders are summarized in Box 6-7.

Summary

This chapter describes the cardiovascular and pulmonary consequences of common systemic conditions. Oxygen transport, the purpose of the cardiovascular and pulmonary system, can be significantly affected by dysfunction in virtually all organ systems of the body. The pathophysiological consequences of conditions of the following systems of oxygen transport are presented: cardiac, pulmonary, musculoskeletal, connective tissue/collagen vascular, neurological, gastrointestinal, hepatic, renal, hematological, endocrine, and immunological. In addition, the cardiovascular and pulmonary manifestations of nutritional disorders, including obesity and anorexia nervosa, are described.

Knowledge of these effects is essential to the practice of physical therapy across all specialties because of the prevalence of systemic conditions either singly or in combination. The presentation of the cardiovascular and pulmonary consequences of systemic conditions is often subtle or obscured and is associated with a poor prognosis, so early detection and appropriate management are essential.

Physical therapists must be able to diagnostically distinguish cardiovascular and pulmonary manifestations of systemic conditions in order to appropriately identify indications for physical therapy, contraindications, side effects, and unusual treatment responses. In addition, detailed assessment of the patient’s problems ensures that problems amenable to physical therapy are appropriately treated and that those that are not are referred back to a physician. These skills are particularly important given the advent of direct-access practice and the fact that a high proportion of patients being treated by physical therapists have systemic conditions as secondary, as well as primary, diagnoses. Further, cardiovascular and pulmonary manifestations of systemic diseases may not have been previously diagnosed, but may be identified on the physical therapy assessment or manifested by the patient during exercise stress.