Work of Breathing.

Work of breathing (WOB) is the effort required to expand and contract the lungs. In the healthy individual breathing is quiet and accomplished with minimal effort. The amount of energy expended on breathing depends on the rate and depth of breathing, the ease in which the lungs can be expanded (compliance), and airway resistance.

Inspiration is an active process, stimulated by chemical receptors in the aorta. Expiration is a passive process that depends on the elastic recoil properties of the lungs, requiring little or no muscle work. Surfactant is a chemical produced in the lungs to maintain the surface tension of the alveoli and keep them from collapsing. Patients with advanced chronic obstructive pulmonary disease (COPD) lose the elastic recoil of the lungs and thorax. As a result, the patient’s work of breathing increases. In addition, patients with certain pulmonary diseases have decreased surfactant production and sometimes develop atelectasis. Atelectasis is a collapse of the alveoli that prevents normal exchange of oxygen and carbon dioxide.

Accessory muscles of respiration can increase lung volume during inspiration. Patients with COPD, especially emphysema, frequently use these muscles to increase lung volume. Prolonged use of the accessory muscles does not promote effective ventilation and causes fatigue. During assessment observe for elevation of the patient’s clavicles during inspiration, which can indicate ventilatory fatigue, air hunger, or decreased lung expansion.

Compliance is the ability of the lungs to distend or expand in response to increased intraalveolar pressure. Compliance decreases in diseases such as pulmonary edema, interstitial and pleural fibrosis, and congenital or traumatic structural abnormalities such as kyphosis or fractured ribs.

Airway resistance is the increase in pressure that occurs as the diameter of the airways decreases from mouth/nose to alveoli. Any further decrease in airway diameter by bronchoconstriction can increase airway resistance. Diseases causing airway obstruction such as asthma and tracheal edema increase airway resistance. When airway resistance increases, the amount of oxygen delivered to the alveoli decreases.

Decreased lung compliance, increased airway resistance, and the increased use of accessory muscles increase the WOB, resulting in increased energy expenditure. Therefore the body increases its metabolic rate and the need for more oxygen. The need for elimination of carbon dioxide also increases. This sequence is a vicious cycle for a patient with impaired ventilation, causing further deterioration of respiratory status and the ability to oxygenate adequately.

Lung Volumes.

Pulmonary Circulation.

The primary function of pulmonary circulation is to move blood to and from the alveolar capillary membrane for gas exchange. Pulmonary circulation begins at the pulmonary artery, which receives poorly oxygenated mixed venous blood from the right ventricle. Blood flow through this system depends on the pumping ability of the right ventricle. The flow continues from the pulmonary artery through the pulmonary arterioles to the pulmonary capillaries, where blood comes in contact with the alveolar capillary membrane and the exchange of respiratory gases occurs. The oxygen-rich blood then circulates through the pulmonary venules and pulmonary veins, returning to the left atrium.

Oxygen Transport.

The oxygen-transport system consists of the lungs and cardiovascular system. Delivery depends on the amount of oxygen entering the lungs (ventilation), blood flow to the lungs and tissues (perfusion), rate of diffusion, and oxygen-carrying capacity. Three things influence the capacity of the blood to carry oxygen: the amount of dissolved oxygen in the plasma, the amount of hemoglobin, and the tendency of hemoglobin to bind with oxygen. Hemoglobin, which is a carrier for oxygen and carbon dioxide, transports most oxygen (approximately 97%). The hemoglobin molecule combines with oxygen to form oxyhemoglobin. The formation of oxyhemoglobin is easily reversible, allowing hemoglobin and oxygen to dissociate (deoxyhemoglobin), which frees oxygen to enter tissues.

Carbon Dioxide Transport.

Myocardial Pump.

The pumping action of the heart is essential to oxygen delivery. There are four cardiac chambers, two atria and two ventricles. The ventricles fill with blood during diastole and empty during systole. The volume of blood ejected from the ventricles during systole is the stroke volume. Hemorrhage and dehydration cause a decrease in circulating blood volume and a decrease in stroke volume.

Myocardial fibers have contractile properties that allow them to stretch during filling. In a healthy heart this stretch is proportionally related to the strength of contraction. As the myocardium stretches, the strength of the subsequent contraction increases; this is known as the Frank-Starling (Starling’s) law of the heart. In the diseased heart (cardiomyopathy or myocardial infarction [MI]) Starling’s law does not apply because the increased stretch of the myocardium is beyond the physiological limits of the heart. The subsequent contractile response results in insufficient stroke volume, and blood begins to “back up” in the pulmonary (left heart failure) or systemic (right heart failure) circulation.

Myocardial Blood Flow.

Coronary Artery Circulation.

Systemic Circulation.

The arteries of the systemic circulation deliver nutrients and oxygen to tissues, and the veins remove waste from tissues. Oxygenated blood flows from the left ventricle through the aorta and into large systemic arteries. These arteries branch into smaller arteries; then arterioles; and finally the smallest vessels, the capillaries. The exchange of respiratory gases occurs at the capillary level, where the tissues are oxygenated. The waste products exit the capillary network through venules that join to form veins. These veins become larger and form the vena cava, which carry deoxygenated blood to the right side of the heart, where it then returns to the pulmonary circulation.

Blood Flow Regulation.

The amount of blood ejected from the left ventricle each minute is the cardiac output. The normal cardiac output is 4 to 6 L/min in the healthy adult at rest. The circulating volume of blood changes according to the oxygen and metabolic needs of the body. For example, cardiac output increases during exercise, pregnancy, and fever but decreases during sleep. The following formula represents cardiac output:

Cardiac output(CO)=Stroke volume(SV)×Heart rate(HR)

The amount of blood in the left ventricle at the end of diastole (preload), the resistance to left ventricular ejection (afterload), and myocardial contractility all affect stroke volume.

Preload is the end-diastolic volume. The ventricles stretch when filling with blood. The more stretch on the ventricular muscle, the greater the contraction and the greater the stroke volume (Starling’s law). In clinical situations, medical treatment can alter the preload and subsequent stroke volumes by changing the amount of circulating blood volume. For example, during treatment of a patient who is hemorrhaging, increased fluid therapy and replacement of blood increase circulating volume, thus increasing the preload and stroke volume, which increases cardiac output. If volume is not replaced, preload, stroke volume and the subsequent cardiac output decreases.

Afterload is the resistance to left ventricular ejection. The heart works harder to overcome the resistance so blood can be fully ejected from the left ventricle. The diastolic aortic pressure is a good clinical measure of afterload. In hypertension the afterload increases, making cardiac workload also increase.

Hypovolemia.

Conditions such as shock and severe dehydration cause extracellular fluid loss and reduced circulating blood volume, or hypovolemia. Decreased circulating blood volume results in hypoxia to body tissues. With significant fluid loss, the body tries to adapt by peripheral vasoconstriction and increasing the heart rate to increase the volume of blood returned to the heart, thus increasing the cardiac output.

Decreased Inspired Oxygen Concentration.

With the decline of the concentration of inspired oxygen, the oxygen-carrying capacity of the blood decreases. Decreases in the fraction of inspired oxygen concentration (FiO₂) are caused by upper or lower airway obstruction, which limits delivery of inspired oxygen to alveoli; decreased environmental oxygen (at high altitudes); or hypoventilation (occurs in drug overdoses).

Increased Metabolic Rate.

Increased metabolic activity increases oxygen demand. The level of oxygenation declines when body systems are unable to meet this demand. An increased metabolic rate is normal in pregnancy, wound healing, and exercise because the body is using energy or building tissue. Most people are able to meet the increased oxygen demand and do not display signs of oxygen deprivation. Fever increases the need of tissues for oxygen; as a result carbon dioxide production increases. When fever persists, the metabolic rate remains high, and the body begins to break down protein stores. This causes muscle wasting and decreased muscle mass, including respiratory muscles such as the diaphragm and intercostal muscles.

The body attempts to adapt to the increased carbon dioxide levels by increasing the rate and depth of respiration. The patient’s WOB increases, and the patient eventually displays signs and symptoms of hypoxemia. Patients with pulmonary diseases are at greater risk for hypoxemia.

Pregnancy.

As the fetus grows during pregnancy, the enlarging uterus pushes abdominal contents upward against the diaphragm. In the last trimester of pregnancy, the inspiratory capacity declines, resulting in dyspnea on exertion and increased fatigue.

Obesity.

Patients who are morbidly obese have reduced lung volumes from the heavy lower thorax and abdomen, particularly when in the recumbent and supine positions. Many morbidly obese patients suffer from obstructive sleep apnea. Morbidly obese patients have a reduction in lung and chest wall compliance as a result of encroachment of the abdomen into the chest, increased WOB, and decreased lung volumes. In some patients an obesity-hypoventilation syndrome develops in which oxygenation is decreased and carbon dioxide is retained. The obese patient is also susceptible to atelectasis or pneumonia after surgery because the lungs do not expand fully and the lower lobes retain pulmonary secretions.

Musculoskeletal Abnormalities.

Musculoskeletal impairments in the thoracic region reduce oxygenation. Such impairments result from abnormal structural configurations, trauma, muscular diseases, and diseases of the central nervous system. Abnormal structural configurations impairing oxygenation include those affecting the rib cage such as pectus excavatum and the vertebral column such as kyphosis, lordosis, or scoliosis.

Trauma.

Flail chest is a condition in which multiple rib fractures cause instability in part of the chest wall. The unstable chest wall allows the lung underlying the injured area to contract on inspiration and bulge on expiration, resulting in hypoxia. Patients with thoracic or upper abdominal surgical incisions use shallow respirations to avoid pain, which also decreases chest wall movement. Opioids used to treat pain depress the respiratory center, further decreasing respiratory rate and chest wall expansion.

Neuromuscular Diseases.

Neuromuscular diseases affect tissue oxygenation by decreasing the patient’s ability to expand and contract the chest wall. Ventilation is impaired, resulting in atelectasis, hypercapnia, and hypoxemia. Examples of conditions causing hypoventilation include myasthenia gravis, Guillain-Barré syndrome, and poliomyelitis.

Central Nervous System Alterations.

Diseases or trauma of the medulla oblongata and/or spinal cord result in impaired respiration. When the medulla oblongata is affected, neural regulation of respiration is impaired, and abnormal breathing patterns develop. Cervical trauma at C3 to C5 usually results in paralysis of the phrenic nerve. When the phrenic nerve is damaged, the diaphragm does not descend properly, thus reducing inspiratory lung volumes and causing hypoxemia. Spinal cord trauma below the C5 vertebra usually leaves the phrenic nerve intact but damages nerves that innervate the intercostal muscles, preventing anteroposterior chest expansion.

Left-Sided Heart Failure.

Left-sided heart failure is an abnormal condition characterized by decreased functioning of the left ventricle. If left ventricular failure is significant, the amount of blood ejected from the left ventricle drops greatly, resulting in decreased cardiac output. Signs and symptoms include fatigue, breathlessness, dizziness, and confusion as a result of tissue hypoxia from the diminished cardiac output. As the left ventricle continues to fail, blood begins to pool in the pulmonary circulation, causing pulmonary congestion. Clinical findings include crackles in the bases of the lungs on auscultation, hypoxia, shortness of breath on exertion, cough, and paroxysmal nocturnal dyspnea.

Right-Sided Heart Failure.

Right-sided heart failure results from impaired functioning of the right ventricle. It more commonly results from pulmonary disease or as a result of long-term left-sided failure. The primary pathological factor in right-sided failure is elevated pulmonary vascular resistance (PVR). As the PVR continues to rise, the right ventricle works harder, and the oxygen demand of the heart increases. As the failure continues, the amount of blood ejected from the right ventricle declines, and blood begins to “back up” in the systemic circulation. Clinically the patient has weight gain, distended neck veins, hepatomegaly and splenomegaly, and dependent peripheral edema.

Angina.

Myocardial Infarction.

Infants and Toddlers.

Infants and toddlers are at risk for upper respiratory tract infections as a result of frequent exposure to other children, an immature immune system, and exposure to secondhand smoke. In addition, during the teething process some infants develop nasal congestion, which encourages bacterial growth and increases the potential for respiratory tract infection. Upper respiratory tract infections are usually not dangerous, and infants or toddlers recover with little difficulty.

School-Age Children and Adolescents.

Young and Middle-Age Adults.

Older Adults.

Nutrition.

Nutrition affects cardiopulmonary function in several ways. Severe obesity decreases lung expansion, and increased body weight increases tissue oxygen demands. The malnourished patient experiences respiratory muscle wasting, resulting in decreased muscle strength and respiratory excursion. Cough efficiency is reduced secondary to respiratory muscle weakness, putting the patient at risk for retention of pulmonary secretions.

Patients who are morbidly obese and/or malnourished are at risk for anemia. Diets high in carbohydrates play a role in increasing the carbon dioxide load for patients with carbon dioxide retention. As carbohydrates are metabolized, an increased load of carbon dioxide is created and excreted via the lungs.

Exercise.

Smoking.

Substance Abuse.

Stress.