People presenting with dyspnea usually show signs of rapid and shallow breathing, use of their respiratory accessory muscles, and may have underlying conditions causing the dyspnea, such as cardiac or pulmonary diseases. Dyspnea can come in many forms, but it is commonly known as shortness of breath or having difficulty breathing. Īs a subjective symptom self-reported by people, dyspnea is difficult to characterize since its severity cannot be measured. For example, for people who enter the emergency room with shortness of breath, a diagnosis is achieved through a physical examination, electrocardiography, chest radiograph, and if necessary, a serum BNP level. The diagnostic workup will vary depending on the suspected cause. Common tests may include an echocardiography, cardiac magnetic resonance imaging (MRI), coronary artery angiogram, chest x-ray or chest CT scan, blood tests, physical exams, or a myocardial biopsy. Because it is commonly associated with heart failure, tests that may be run mainly focus on measuring the function and capability of the heart. Many tests can be done in order to evaluate the cause of paroxysmal nocturnal dyspnea. Paroxysmal nocturnal dyspnea is a serious medical symptom that can develop into worsening conditions. Theories include decreased responsiveness of the respiratory center in the brain and decreased adrenergic activity in the myocardium during sleep.

Other theories exist for why PND occurs, especially in those where PND only occurs while sleeping.

In congestive heart failure, left ventricular dysfunction will also increase pulmonary congestion, so further congestion caused by the redistribution of blood volume upon laying down will worsen any dyspnea. In people with underlying congestive heart failure, this redistribution may overload the pulmonary circulation, causing increased pulmonary congestion. Respiratory muscles and vagal afferent neural pathways relay information from the chest wall/airways to the central nervous system, facilitating the presentation of dyspnea. Receptors in the chest wall and central airways, as well receptors in the respiratory center of the central nervous system, produce an increased requirement for ventilation which is not matched by respiratory output, resulting in the conscious recognition of dyspnea. The perception of dyspnea is theorized to be a complicated connection between peripheral receptors, neural pathways, and the central nervous system. In addition to the redistribution of blood in the body, most cases of dyspnea are accompanied by an increase in the overall work of breathing, often caused by abnormal pulmonary mechanisms. Failure to accommodate this redistribution results in decreased vital capacity and pulmonary compliance, further causing the shortness of breath experienced in PND. When a person is recumbent, or is lying down, blood is redistributed from the lower extremities and abdominal cavity ( splanchnic circulation) to the lungs. PND can be explained by mechanisms similar to those of orthopnea and typical dyspnea. Risk factors for lung diseases include tobacco use, including second hand smoke, pollution, exposure to hazardous fumes, and allergens. Risk factors for cardiac diseases include high blood pressure, high cholesterol, diabetes, obesity, and a lifestyle lacking exercise and a healthy diet. Since paroxysmal nocturnal dyspnea occurs mainly because of heart or lung problems, common risk factors include those that affect the function of the heart and lungs.

Nocturnal proxies