Explain How J-Receptors Can Cause The Sensation Of Dyspnea

It results when one or both of these gas-exchanging functions are inadequate . It is not a disease but a symptom of an underlying pathology affecting lung tissue function, 02 delivery, cardiac output, or the baseline metabolic state. It is a condition that occurs because of one or more diseases involving the lungs or other body systems. Symptoms of this is hypoexia and hypercapnia.

This results in the person having repetitive periods of insufficient ventilation and jeopardized gas exchange. This occurs when the inhibitory input to the brain exceeds excitatory output; or in simpler terms the brain fails to signal the muscles to breathe.

• Decreased SOB, decreased crackles in the bases of the lungs, and possibly decreased O2

Oxygen is drawn into the lungs by a process called inhalation, (breathing in), which occurs when the diaphragm and intercostal muscles are contracted which causes the lungs to expand, giving a larger volume and therefore causing a lower pressure differential between the lungs, alveolar pressure, and the outside atmosphere. This inverse relationship between volume and pressure is called Boyle’s law. (Tortora & Derrickson, 2011)

Both rapid, shallow breathing patterns and hypoventilation effect gas exchange. Arterial blood gases will be monitored and changes discussed with provider. Alteration in PaCO2 and PaO2 levels are signs of respiratory failure. Patient’s body position will be properly aligned for optimum respiratory excursion, this promotes lung expansion and improved air exchange. Patient will be suctioned as needed to clear secretions and maintain patent airways. The expected outcome is that the patient’s airway and gas exchange will be maintained as evidence by normal arterial blood gases (Herdman,

The presence of fluid in the alveolar space could potentially cause the lung capacity to be effected as well.

The decrease in her PCO2 and pH will cause her central nervous system to slow down causing her breathing to slow down to try to give her body more carbon dioxide to level out the amount of oxygen/carbon dioxide ratio.

Cystic Fibrosis is a genetic disease that causes the body’s lungs to generate a different type of mucus than a non-infected body would. The contaminated lungs will produce mucus that is thick and adhesive which clogs the lungs and leads to an unpleasant and abhorrent lung infection. CF also interferes with the pancreas, disallowing the digestive enzymes from breaking down and absorbing food in the intestine. This can result in low nutrition, feeble growth, excessive sweat production, difficulties in breathing, and sometimes lung disease. When producing extra sweat and mucus, the body loses salt. If too much salt is lost, it can cause abnormal heart rhythms, disturbance of minerals in the blood, and perhaps, shock.

Small air sacks called alveoli are at the tips of the bronchioles. When air reaches them, the oxygen concentration is high, which causes diffusion into red blood cells travelling through pulmonary capillaries (7). The red blood cells then distribute the new oxygen to the rest of the body. When they reach the alveoli again, they exchange carbon dioxide (a form of cell waste) for new oxygen, and repeat the process. The carbon dioxide is moved through the bronchioles, bronchi, and trachea in the form of exhalation.

There are many diseases that greatly affect our respiratory physiology; one of those diseases is cystic fibrosis. Cystic fibrosis, according to the National Institute of Health (2013), is an inherited disease of the secretory glands or exocrine glands. Not only does this disease affect our respiratory system, it takes a toll on our digestive system. The respiratory system includes the gas exchange from our external atmosphere and our internal environment. This gas exchange of oxygen and carbon dioxide through our atmosphere and lungs does play a roll with cystic fibrosis. Cystic fibrosis is inherited, it affects many parts of the body mainly the respiratory system, and there are many signs and symptoms to this overwhelming disease.

Emphysema damage to the alveoli causes a significant decrease in the surface area available for adequate gas exchange ability.

Airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli. The mechanisms involved consist of direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons. The degree of airway hyperresponsiveness generally correlates with the clinical severity of

ANP plays important role in vasodilation, bronchorelaxation, pulmonary vascular permeability, and surfactant production and action in the airways. It also may have bronchoprotective effects in an asthma attack because it has been found in

The myocardium becomes ischemic, coronary sinus blood pH falls, cellular potassium is lost, lactate accumulates, ECG abnormalities appear, and ventricular function (both systolic and diastolic) deteriorates. Left ventricular (LV) diastolic pressure usually increases during angina, sometimes inducing pulmonary congestion and dyspnea. The exact mechanism by which ischemia causes discomfort is unclear but may involve nerve stimulation by hypoxic

As a result of Cystic Fibrosis, the body produces unusually sticky and thick mucus that has the following effects. It makes the lungs clog with significant exposure to lung infection which threatens life. It also causes obstruction of the pancreas and prevents natural enzymes in their role of