Explain how emphysema can result in high-compliance, low-elastance lungs with reduced alveolar surface area.

Emphysema is a lung condition that causes windedness. In individuals with emphysema, the air sacs in the lungs (alveoli) are destroyed. Over the long run, the internal walls of the air sacs debilitate and burst, leading to formation of bigger air spaces rather than numerous little ones. This diminishes the surface area of the lungs and simultaneous reduction in the measure of oxygen that reaches the bloodstream. 

At the point, when exhalation occurs, the destroyed alveoli do not work appropriately and old air gets caught, ruling out new, oxygen-rich air to enter. The vast majority with emphysema likewise have persistent bronchitis. Chronic bronchitis causes irritation of the air tubes that convey air to lungs, which prompts a relentless coughing. Together emphysema and constant bronchitis are two conditions that make up persistent obstructive respiratory sickness (COPD). 

The main reason behind emphysema is tobacco smoking and passive smoking both, air pollution, chemical pollution etc.

Symptoms include shortness of breath, chest pain, breathing problem, persistent coughing and wheezing etc.

The loss of elastic recoil concerning the wall of the little airways, because of the decrease of flexible tissue in the pulmonary parenchyma, is an obvious event primarily in emphysema. Air current during exhalation is the consequence of the harmony between the versatile force of the lungs causing flow and resistance of the aviation routes that cutoff flow. The components that lead to the block of the lumen and the expanded resistance, with the outcome of flow restriction, are the presence of discharges, the expanded tone of bronchial smooth muscle, the hypertrophy of sub-mucosal glands, and the distension towards the inside piece of the lumen of the dorsal piece of windpipe during lapse. These components are engaged with wind stream block because of the extraordinary contrast between intraluminal pressure and the pressure in the surrounding environment. The nonappearance of ligament in the mass of the little fringe airways offers further more to the loss of the flexible recoil.

Compliance is increased in COPDs like pneumonic emphysema. In emphysema, the elastic recoil is diminished and the P-V curve bend is displaced up and left. This is because of the loss of flexible tissue because of alveolar wall decimation. In persistent bronchitis without emphysema, in any case, the P-V bend might be normal since the parenchyma is negligibly influenced.

Emphysema can prompt devastation of the alveoli, the small air sacs that permit oxygen to get into the blood. Their devastation prompts the development of huge air pockets in the lung called bullae. These bullae don't trade oxygen and carbon dioxide like typical lung tissue. Additionally, the bullae can turn out to be exceptionally enormous. Typical normal lung tissue close to the bullae can't grow appropriately, diminishing lung work. Ongoing bronchitis influences the oxygen and carbon dioxide trade on the grounds that the airway expanding and mucus creation can likewise limit the airways and lessen the progression of oxygen-rich air into the lung and carbon dioxide out of the lung.