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explain using gas exchange and cardiovascular systems

2006-11-12 04:31:55 · 3 answers · asked by leothegr812 1 in Science & Mathematics Biology

3 answers

In normal breathing, air is drawn in through the bronchial passages and down into the increasingly fine network of tubing in the lungs called the alveoli, which are many thousands of tiny sacs surrounded by capillaries. These absorb the oxygen and transfer it into the blood. When toxins such as smoke are breathed into the lungs, the particles are trapped by the hairs and cannot be exhaled, leading to a localised inflammatory response. Chemicals released during the inflammatory response (trypsin, elastase, etc.) begin to break down the walls of alveoli (alveolar septum). This leads to fewer but larger alveoli, with a decreased surface area and a decreased ability to take up oxygen and lose carbon dioxide. The activity of another molecule called alpha 1-antitrypsin normally neutralizes the destructive action of one of these damaging molecules.

After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood, and the body compensates by vasoconstricting appropriate vessels. This leads to pulmonary hypertension. This leads to enlargement and increased strain on the right side of the heart, which in turn leads to peripheral edema (swelling of the peripherals) as blood gets backed up in the systemic circulation, causing fluid to leave the circulatory system and accumulate in the tissues.

Emphysema occurs in a higher proportion in patient with decreased alpha 1-antitrypsin (A1AT) levels (alpha 1-antitrypsin deficiency, A1AD). In A1AD, inflammatory enzymes (such as elastase) are able to destroy the alveolar tissue (the elastin fibre, for example). Most A1AD patients do not develop clinically significant emphysema, but smoking and severely decreased A1AT levels (10-15%) can cause emphysema at a young age. In all, A1AD causes about 2% of all emphysema. However, smokers with A1AD are in the highest risk category for emphysema.

2006-11-12 04:44:45 · answer #1 · answered by JV 3 · 0 0

Because Lungs cannot expand enough to achieve an adequate gas exchange. Lugs become rigid and air comes in but cannot go out, and they are rigid because fibrous tissue has replaced the normal lung’s interstitial spaces due chronic inflammatory process. Also certain enzymes activated during inflammation as trypsin and elastase destroy normal lining of alveoli.. After a prolonged period, hyperventilation becomes inadequate to maintain high enough oxygen levels in the blood, and the body compensates by vasoconstricting appropriate vessels. This leads to pulmonary hypertension. This leads to enlargement and increased strain on the right side of the heart, which in turn leads to peripheral edema (swelling of the peripherals) as blood gets backed up in the systemic circulation, causing fluid to leave the circulatory system and accumulate in the tissues. When you walk your muscles need a higher oxygen pressure, but because cells involved in that process in the lung are destroyed, no adequate levels are reached and the person have to stop.

2016-05-22 07:13:02 · answer #2 · answered by Rita 4 · 0 0

why did you ask this question 5 times

2006-11-12 04:40:56 · answer #3 · answered by darkpheonix262 4 · 0 0

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