Acute orthopnea—shortness of breath within seconds of assuming the supine position—is especially suggestive of diaphragm dysfunction. From: Sleep Medicine Secrets, 2004
Orthopnea is a shortness of breath some people experience when lying down, which goes away once they return to an upright position. The definition of orthopnea comes from the Greek words for upright (ortho) and breath (pnoea). It’s often a sign of heart failure, but can be caused by other conditions, such as lung diseases, other heart conditions, and obesity. What Is Orthopnea?People who have orthopnea will begin having trouble breathing when they lie down. Once they stand or sit up, their breathing normalizes again. This makes it distinct from other breathing conditions such as:
Orthopnea is also distinct from paroxysmal nocturnal dyspnea (PND), a condition where the person experiences sudden difficulty breathing during sleep. Symptoms occur a few hours after the person has fallen asleep, and the sudden shortness of breath wakes them up. Like orthopnea, changing to an upright position improves their breathing. Since relaxing into sleep is challenging when you feel like you can’t breathe, both conditions can disrupt sleep. SymptomsIf you have orthopnea, you may feel short of breath upon lying down. The sensation may come on instantly or develop gradually. You may also feel tightness or pain in your chest or experience additional symptoms like wheezing, coughing, or heart palpitations. Once you stand or prop yourself up, your breathing improves, as do any other symptoms. The severity of orthopnea varies. Some people need just one pillow to prop themselves up and feel better, while others may need to sit fully upright or stand in order to feel relief. Some people with chronic heart failure may still exhibit symptoms of orthopnea even when sitting up, although they’ll feel better than they did when lying down. Orthopnea itself is commonly a symptom of a heart or lung condition. What Causes Orthopnea?Orthopnea occurs when there is a buildup of excess fluid that creates pressure around the lungs. When a person lies down, blood from the lower extremities is redistributed to the lungs. If their heart is healthy, it can handle this additional volume around the lungs and pump it out adequately. When the heart is weakened by heart failure or another condition, it’s not strong enough to perform this process effectively. The extra blood takes longer to get out of the heart, increasing pressure on the lungs. Fluid may leak out from blood vessels into small air sacs in the lungs, causing what’s known as pulmonary edema. These sacs assist with the exchange of oxygen and carbon dioxide in the body. When fluid builds up, it disrupts the exchange, making it harder for the lungs to distribute oxygen back into the bloodstream. It’s easier for the lungs to clear out excess fluid when they’re in an upright position, which is why orthopnea symptoms are relieved once the person stops lying down. Orthopnea can be associated with health conditions such as: DiagnosisA doctor suspects orthopnea when a person experiences shortness of breath when lying down, and they exhibit other symptoms of one of the conditions commonly associated with orthopnea, such as heart failure, COPD, obesity, anxiety, or another heart or lung disease. During your appointment, your doctor will ask you about the onset and timing of your symptoms, in order to distinguish orthopnea from another type of breathing difficulty. They will also ask you to describe the severity of your orthopnea; for example, they may ask how many pillows you need to use to feel relief. If you haven’t yet been diagnosed with a related underlying condition, your doctor may order additional tests, such as a chest X-ray, electrocardiogram, echocardiogram, pulmonary function test, or blood test, to evaluate for potential causes. TreatmentsTreatments for orthopnea are focused on minimizing symptoms and treating the underlying cause. Specific treatments for orthopnea include pillow positioning, supplemental oxygen, and medication. Depending on the severity of the underlying condition, doctors may prescribe lifestyle changes, medications, medical devices, or surgery. Propping yourself up with a pillow can help you breathe better by reducing pressure on the lungs and heart. You can also use an adjustable mattress to raise the head of the bed, or foam wedges underneath the mattress. Your doctor may prescribe supplemental oxygen, which can be provided through an at-home device or at a hospital. If you are overweight or obese, your doctor may work with you to help reduce your weight. A number of medications may be prescribed to improve orthopnea symptoms, including drugs that strengthen the heart, improve blood flow, or prevent fluid buildup or inflammation in the lungs. For example, if you have orthopnea due to heart failure, your doctor may prescribe diuretics, angiotensin-converting enzyme inhibitors, or beta-blockers. If your orthopnea is a symptom of COPD, your doctor may prescribe bronchodilators or inhaled steroids. If you regularly experience difficulty breathing, whether when lying down or doing something else, speak to your doctor. They can help determine what’s causing your breathing problems and recommend appropriate therapies, such as lifestyle changes, medication, and other treatments.
Dyspnea refers to the sensation of difficult or uncomfortable breathing. It is a subjective experience perceived and reported by an affected patient. Dyspnea on exertion (DOE) may occur normally, but is considered indicative of disease when it occurs at a level of activity that is usually well tolerated. Dyspnea should be differentiated from tachypnea, hyperventilation, and hyperpnea, which refer to respiratory variations regardless of the patients" subjective sensations. Tachypnea is an increase in the respiratory rate above normal; hyperventilation is increased minute ventilation relative to metabolic need, and hyperpnea is a disproportionate rise in minute ventilation relative to an increase in metabolic level. These conditions may not always be associated with dyspnea. Orthopnea is the sensation of breathlessness in the recumbent position, relieved by sitting or standing. Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position. Two uncommon types of breathlessness are trepopnea and platypnea. Trepopnea is dyspnea that occurs in one lateral decubitus position as opposed to the other. Platypnea refers to breathlessness that occurs in the upright position and is relieved with recumbency. A patient with dyspnea may say: "I feel short of breath," "I"m having difficulty breathing," "I can"t catch my breath," "I feel like I"m suffocating." Because it is a subjective phenomenon, the perception of dyspnea and its interpretation vary from patient to patient. Begin with a nonleading question: Do you have any difficulty breathing? If the response is affirmative and dyspnea is established as a problem, it should be characterized in detail. When did it begin? Has the onset been sudden or insidious? Inquire about the frequency and duration of attacks. The conditions in which dyspnea occurs should be ascertained. Response to activity, emotional state, and change of body position should be noted. Ask about associated symptoms: chest pain, palpitations, wheezing, or coughing. Sometimes a nonproductive cough may be present as a "dyspnea equivalent." What other significant medical problems does the patient have, and what medications has he been taking? How much has he smoked? Dyspnea on exertion is by no means always indicative of disease. Normal persons may feel dyspneic with strenuous exercise. The level of activity tolerated by any individual depends on such variables as age, sex, body weight, physical conditioning, attitude, and emotional motivation. Dyspnea on exertion would be abnormal if it occurred with activity that is normally well tolerated by the patient. It is helpful to ask if he has noticed any recent or progressive limitation in his ability to conduct specific tasks that he was able to perform without difficulty in the past (e.g., walking, climbing stairs, performing household chores). The degree of functional impairment can be assessed in this manner. Additional questions should be aimed at ascertaining whether the patient has orthopnea or paroxysmal nocturnal dyspnea. Inquire about the number of pillows he uses under his head at night and whether he has ever had to sleep sitting up. Does he develop coughing or wheezing in the recumbent position? Did he ever wake up at night with shortness of breath? How long after lying down did the episode occur, and what did he do to relieve his distress? Characteristically, the patient with left ventricular failure sits up at bedside, dangles his feet, and refrains from ambulation or other activity that is likely to worsen his symptoms. Spontaneous respiration is controlled by neural and chemical mechanisms. At rest, an average 70 kg person breathes 12 to 15 times a minute with a tidal volume of about 600 ml. A normal individual is not aware of his or her respiratory effort until ventilation is doubled, and dyspnea is not experienced until ventilation is tripled. An abnormally increased muscular effort is now needed for the process of inspiration and expiration. Because dyspnea is a subjective experience, it does not always correlate with the degree of physiologic alteration. Some patients may complain of severe breathlessness with relatively minor physiologic change; others may deny breathlessness even with marked cardio-pulmonary deterioration. There is no universal theory that explains the mechanism of dyspnea in all clinical situations. Campbell and Howell (1963) have formulated the "length–tension inappropriateness theory," which states that the basic defect in dyspnea is a mismatch between the pressure (tension) generated by respiratory muscles and the tidal volume (change of length) that results. Whenever such disparity occurs, the muscle spindles of the intercostal muscles transmit signals that bring the act of breathing to the conscious level. Additionally, juxtacapillary receptors (J-receptors), located in the alveolar interstitium and supplied by unmyelinated fibers of the vagus nerve, are stimulated by pulmonary congestion. This activates the Hering–Breuer reflex whereby inspiratory effort is terminated before full inspiration is achieved, resulting in rapid and shallow breathing. The J-receptors may be responsible for dyspnea in situations where pulmonary congestion occurs, such as with pulmonary edema. Other theories that have been proposed to explain dyspnea include acid-base imbalance, central nervous system mechanisms, decreased breathing reserve, increased work of breathing, increased transpulmonary pressure, fatigue of respiratory muscles, increased oxygen cost of breathing, dyssynergy of intercostal muscles and the diaphragm, and abnormal respiratory drive. Orthopnea is caused by pulmonary congestion during recumbency. In the horizontal position there is redistribution of blood volume from the lower extremities and splanchnic beds to the lungs. In normal individuals this has little effect, but in patients in whom the additional volume cannot be pumped out by the left ventricle because of disease, there is a significant reduction in vital capacity and pulmonary compliance with resultant shortness of breath. Additionally, in patients with congestive heart failure the pulmonary circulation may already be overloaded, and there may be reabsorption of edema fluid from previously dependent parts of the body. Pulmonary congestion decreases when the patient assumes a more erect position, and this is accompanied by an improvement in symptoms. Paroxysmal nocturnal dyspnea may be caused by mechanisms similar to those for orthopnea. The failing left ventricle is suddenly unable to match the output of a more normally functioning right ventricle; this results in pulmonary congestion. Additional mechanisms may be responsible in patients who experience paroxysmal nocturnal dyspnea only during sleep. Theories include decreased responsiveness of the respiratory center in the brain and decreased adrenergic activity in the myocardium during sleep. Dyspnea on exertion is caused by failure of the left ventricular output to rise during exercise with resultant increase in pulmonary venous pressure. In cardiac asthma, bronchospasm is associated with pulmonary congestion and is probably precipitated by the action of edema fluid in the bronchial walls on local receptors. Trepopnea may occur with asymmetric lung disease when the patient lies with the more affected lung down because of gravitational redistribution of blood flow. It has also been reported with heart disease when it is probably caused by distortion of the great vessels in one lateral decubitus position versus the other. Platypnea was originally described in chronic obstructive pulmonary disease and was attributed to an increased wasted ventilation ratio in the upright position. Platypnea in association with orthodeoxia (arterial deoxygenation in the upright position) has been reported in several forms of cyanotic congenital heart disease. It has been proposed that this is precipitated by a slight decrease in systemic blood pressure in the upright position, resulting in increased right-to-left shunting. Dyspnea may be induced in four distinct settings: (1) increased ventilatory demand such as with exertion, febrile illness, hypoxic state, severe anemia, or metabolic acidosis; (2) decreased ventilatory capacity such as with pleural effusion, pneumothorax, intrathoracic mass, rib injury, or muscle weakness; (3) increased airway resistance such as with asthma or chronic obstructive pulmonary disease; and (4) decreased pulmonary compliance such as with interstitial fibrosis or pulmonary edema. In early left ventricular failure, the cardiac output does not increase sufficiently in response to moderate exercise; tissue and cerebral acidosis occurs, and the patient experiences dyspnea on exertion. The shortness of breath may be accompanied by fatigue or a sensation of smothering or sternal compression. In the later stages of left ventricular failure, the pulmonary circulation remains congested, and dyspnea occurs with mild exertion. Moreover, the patient may develop orthopnea or paroxysmal nocturnal dyspnea. Acute pulmonary edema is the most dramatic manifestation of pulmonary venous overload and may occur in the setting of a recent myocardial infarction or in the last stage of chronic left ventricular failure. Cardiovascular causes of dyspnea include valvular diseases (particularly mitral stenosis and aortic insufficiency), paroxysmal arrhythmia (such as atrial fibrillation), pericardial effusion with tamponade, systemic or pulmonary hypertension, cardiomyopathy, and myocarditis. Unrestricted fluid intake or administration in a patient with oliguric renal failure is also likely to precipitate pulmonary congestion and dyspnea. Pulmonary disease constitutes another major category of conditions producing dyspnea and is discussed in Chapter 36. Important pulmonary causes include bronchial asthma, chronic obstructive pulmonary disease, pulmonary embolism, pneumonia, pleural effusion, pneumothorax, allergic pneumonitis, and interstitial fibrosis. In addition, dyspnea may occur in febrile and hypoxic states and in association with some psychiatric conditions such as anxiety and panic disorder. Diabetic ketoacidosis seldom causes dypsnea but commonly induces slow, deep respirations termed Kussmaul breathing. Cerebral lesions or intracranial hemorrhage may be associated with intense hyperventilation and sometimes irregularly periodic breathing called Biot's respiration. Cerebral hypoperfusion from any cause may also result in alternating periods of hyperventilation and apnea called Cheyne–Stokes respiration, although no breathing difficulty may be perceived by the patient. Diagnosis of the cause of dyspnea can be made relatively easily in the presence of other clinical signs of heart or lung disease. Difficulty is sometimes encountered in determining the precipitating cause of breathlessness in a patient with both cardiac and pulmonary conditions. An additional diagnostic problem may be the presence of anxiety or other emotional disorder. A careful history and physical examination are always helpful, and occasionally cardiac catheterization, pulmonary function studies, or other tests may be necessary. References
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