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Mr Howe Case Study

2433 words - 10 pages

Mr Howe Case Study

Mr Howe, a 68 year old man, was admitted this morning to the general medical unit suffering from infective exacerbation of chronic obstructive pulmonary disease (COPD). The nurses caring for Mr Howe have escalated his treatment by calling a Medical Emergency Team (MET) call that was triggered in response to a low oxygen saturation, despite changing his oxygen delivery system from nasal prongs (4 L/min) to Hudson face mask (8 L/min). The nurses also state that his respiratory rate has progressively increased over the past 2 hours. Mr Howe is also reporting some increasing breathlessness and right sided chest pain that increases on inspiration. He is able to speak in ...view middle of the document...

During the inflammatory process there is increased mucous production which thickens the airways and the oedema causes bronchoconstriction with contributes to further decreased gas exchange and therefore hypoxaemia (Tsoumakidou & Siafakas, 2006).

Infection in itself increases metabolic demand by causing the patient to become febrile and tachycardic (O’Donnell & Laveneziana, 2007). The increased demand for oxygen drives his tachypnoea, while there is still a mismatch can cause Mr Howe to become more agitated. While the oxygen demand is increased and not met Mr Howe will continue to become more hypoxaemic.

A V/Q mismatch occurs when the ventilation doesn’t equal the perfusion to the lung areas. In exacerbations of COPD there is increased perfusion (from the tachycardia increasing the flow of blood) to less ventilated areas of the lungs (Diaz, Iglesia, Ferrer, Zalavala, Santos, Wagner, Roca & Rodriguez-Roisin, 1997). Some areas are less ventilated from narrowing and thickening of the airways decreasing gas exchange it causes an increase in physiological dead space and relative alveolar hypoventilation (Robinson, Freiberg, Regnis & Young, 2000). Therefore, there is less air available for gas exchange leading to worsening hypoxaemia and hypercapnia.

Decrease in ventilation can be caused by the hyperinflated chest becoming increasingly fatigued. For the intercostal muscles and diaphragm to contract during inspiration, they require oxygen which is already lacking in the hypoxaemic state. The hypoxaemia exhibited worsens the exacerbation in itself as it causes hypoxic vasoconstriction in the lungs themselves which also contributes to the V/Q mismatch (Parker & O’Donnell, 2008).

Question 2. Explain how his current clinical status may have led to changes in lung compliance and airway resistance. (4 marks)

COPD cause irreversible changes to lungs including emphysema. The lungs become hyperinflated and lose their elastic recoil due to alveolar wall destruction, known as dynamic hyperinflation (Parker & O’Donnell, 2008). The decreased lung compliance slows gas exchange as the air isn't as easily moved in and out of the lungs causing increased static lung volumes, contributing to worsening hypoxaemia and hypercapnia. Mr Howe has increased respiratory rate to increase his minute volume to optimise his oxygenation as he can’t increase his tidal volumes due to the stiffness in the alveolar walls. The stiffness in the walls also causes an overall increase work of breathing, therefore, increasing oxygen demands and worsening his hypoxaemia (Tsoumakidou & Siafakas, 2006).

Airway resistance would be increased due to neutrophilic inflammation of the airways (White, Gompertz & Stockley, 2003), particularly the smaller airways, and increased mucous production (Tsoumakidou & Siafakas, 2006). The inflammation also causes thickened airway walls and bronchoconstriction, making it more difficult for Mr Howe to breathe. This may contribute to...

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