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.