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A 55-year-old man comes to the clinic complaining of fatigue and persistent shortness of breath, which becomes worse during exercise.


The patient has a history of respiratory infections and has a chronic cough that is worse in the morning. He worked for 20 years in an automobile manufacturing plant and was laid off 5 years ago. The patient has smoked cigarettes since he was a teenager. Currently he estimates smoking one pack of cigarettes a day.



PHYSICAL EXAMINATION



VS: T 37°C, P 72/min, R 25/min, BP 120/80 mm Hg, BMI 28

PE: Patient is in mild respiratory distress with an elevated respiratory rate and shallow breaths. An end-expiratory wheeze is heard on auscultation. Otherwise, his lungs appear normal to auscultation and percussion.


LABORATORY STUDIES



Pulmonary function tests: FEV1 was 70% of predicted and peak expiratory flow was 60% of predicted. Forced vital capacity was 90% of predicted.

Chest radiograph: Normal

Arterial blood gases: PO2 75, PCO2 42, pH 7.32


DIAGNOSIS


Chronic obstructive pulmonary disease



COURSE


Chronic obstructive pulmonary disease (COPD) is a combination of loss of elastic tissue (emphysema) and airway obstruction (chronic bronchitis), usually caused by smoking. Cigarette smoke contains numerous particles and chemicals, some of which damage lung tissue. Cigarette smoke also paralyzes cilia that line the airways, eliminating the normal route for expulsion of mucus that helps clear inhaled particulate matter.



PATHOPHYSIOLOGY OF KEY SYMPTOMS


Absorption of O2 and elimination of CO2 occur by diffusion across the alveolar membrane. Pulmonary blood flow ensures the delivery of oxygen-depleted/CO2-enriched (venous) blood to the lungs. Alveolar ventilation exchanges a portion of the air in the alveoli with the atmosphere during each breath. Alveolar ventilation requires (1) the development of a pressure gradient between the alveoli and the atmosphere and (2) an open airway. COPD, which is a combination of emphysema and chronic bronchitis, impairs both of those.


Emphysema results from the loss of elasticity in the respiratory bronchioles and alveoli of the lungs. Over time, alveoli become damaged and the multiple small alveoli are replaced by larger alveolar sacs, with the loss of surface area available for exchange. Eventually, the destruction of the alveoli results in a loss of elastic recoil of the lung, diminishing the effectiveness of the normally passive respiratory expiration. Both inspiration and expiration can require skeletal muscle effort.


Chronic bronchitis is an irritation of the bronchioles. The irritation results in a local inflammation and swelling, as well as increased mucus production, both of which act to narrow the bronchiole lumen. The reduced bronchiole diameter provides a high resistance to air flow, impeding the movement of air during breathing. The bronchitis results in the “obstructive” component of the COPD. Airway obstruction accounts for the diminished FEV1 and diminished peak excitatory flow findings of the spirometry test.


The final respiratory impairment is a consequence of the loss of surface area available for diffusion. Both oxygen and carbon dioxide diffuse across the barrier separating the alveolar air in the blood in the pulmonary capillaries. Carbon dioxide is fairly soluble, and, consequently, diffuses easily from the blood into the alveolar air. Oxygen, in contrast, is poorly soluble, and the loss of the surface area available for exchange can result in an impairment of the absorption of oxygen.


Arterial blood gas determination can be used to monitor the effectiveness of gas exchange across the alveoli. Impairments and perfusion can cause a drop in the arterial PO2 and an elevation in the arterial PCO2. The larger proportional impairment in the diffusion of oxygen is reflected in the more significant drop in the arterial PO2 than in elevation in the arterial PCO2.


Normally, ventilation is controlled by CO2 levels as sensed by the arterial chemoreceptors and the central nervous system chemoreceptors. The increase in ventilatory drive is a reflection in part of the elevation in PCO2. Over time, however, the respiratory acidosis is partially compensated by the renal retention of HCO-3. In addition, CO2 drive in the central nervous system is also attenuated by HCO-3 transport into the cerebrospinal fluid. These compensations blunt or completely remove the CO2 stimulation of ventilation. As the disease progresses, arterial PO2 levels fall below 60 mm Hg. Hypoxia, sensed by the arterial chemoreceptors, can become the primary ventilatory drive. In this instance, placing the patient on supplemental inspired oxygen can cause respiration to stop.

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 30

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