TRIPASS XR تري باس

 

toms may have a pneumothorax (from a ruptured bleb) or

a pulmonary embolus (PE). Although acute coronary syndrome should also be considered among patients presenting with dyspnea, chest tightness is a common complaint

among patients with relatively uncomplicated COPD or

asthma exacerbations. One helpful historical detail is to

discern whether chest tightness is a common feature of

past COPD exacerbations.

� Physical Examination

Patients with COPD exacerbations frequently present with

tachypnea, tachycardia, and hypoxia. Because the majority

of patients have an underlying respiratory infection, they

may also have a fever. Most of what the clinician needs to

make a quick assessment can be gathered from vital signs

and a quick glance at the patient on entering the room.

Patients with severe exacerbations may be sitting upright or

leaning forward in the "tripod" position with both of their

hands planted on their knees. Such patients may be confused

and diaphoretic, unable to converse comfortably, and use

accessory muscles in the neck and chest wall to help them

breathe. Cyanosis is an ominous, but uncommon finding.

Patients with less severe exacerbations speak in complete

sentences, and the chest exam reveals diffusely diminished

breath sounds with wheezing or a prolonged expiratory

phase. Patients with emphysema pathology are often thin

and frail appearing with a barrel chest. Some patients with

prolonged COPD will have evidence of right heart failure

including jugular venous distension and lower extremity

edema. Finally, although bedside spirometry in the form of

a peak expiratory flow rate (PEFR) assessment is more useful in asthma, it can be a helpful adjunct to the physical exam

of COPD patients because several patients with COPD have

a reversible component to their disease. In patients with a

known baseline, an easy comparison can be made to determine the severity of airflow obstruction. Most patients do

not recall past PEFR values, but a PEFR <200 L/min suggests

a significant component of airflow obstruction.

DIAGNOSTIC STUDIES

� Laboratory

Given that patients with COPD often have several comor ­

bidities, routine laboratory studies including a complete

blood count, electrolytes, and an assessment of renal function should be ordered in most patients. Brain natriuretic

peptide (BNP) appears to be tailor made to help differentiate patients with COPD from those with CHF. BNP levels

less than 100 pg/mL have a very high negative predictive

value for CHF, whereas most patients with CHF have levels

>400 pg/mL. However, many patients have values that

fall somewhere in between, and discordance between BNP

values and patient symptoms occurs often enough that

single measurements need to be interpreted carefully. If

available, the patient's prior records should be sought out

to compare current and past values to determine trends

and to establish a baseline. Furthermore, some patients

may have a mixture of presenting problems contributing to

their dyspnea, so an elevated BNP does not exclude a concomitant COPD exacerbation.

Cardiac markers such as troponin are frequently

ordered, but usually unnecessary. Because patients with

severe COPD exacerbations often suffer from hypoxia and

tachycardia, myocardial oxygen demand is increased, and

many patients will have small troponin elevations owing to

"demand ischemia." In these patients, serial troponin measurements should be used to help exclude an acute coro ­

nary syndrome.

D-dimer levels may also be useful in patients with a

presumed COPD exacerbation to help exclude PE. Given

their comorbidities (CHF, a low flow state), sedentary life ­

style, history of smoking, and increased risk for an underlying malignancy, many patients with COPD are at

increased risk for PE. Because d-dimer levels are also likely

to be falsely elevated in this population, it is wise to limit

d-dimer testing to those patients in whom there is a reasonable clinical suspicion of PE (abrupt onset, unilateral

leg swelling).

Finally, arterial blood gases (ABG) have long been part

of the routine evaluation of patients with severe COPD

exacerbations. ABGs provide information about oxygenation (PaOz), ventilation (PaCOz), and overall acid-base

status (pH). Blood gas readings in patients with significant

COPD exacerbations will reveal a primary respiratory acidosis, with elevated C02 levels (>40 mmHg) resulting in a

decreased pH ( <7.30).

� Imaging

The chest x-ray (OCR) primarily helps to diagnose pneumonia and to exclude alternative conditions s uch as CHF,

a pneumothorax, or significant atelectasis or lobar collapse. The classic findings are hyperinflation and bullous

changes (Figure 22-1). Vascular markings and heart size

are often decreased in patients with emphysema pathology

and increased in patients with chronic bronchitis.

� Electrocardiogram

As with the CXR, electrocardiograms are primarily useful

to exclude alternative diagnoses, such as cardiac ischemia.

In patients with pulmonary hypertension, peaked P waves

CHRONIC OBSTRUCTIVE PU LMONARY DISEASE

F

Figure 22-1 . Chest radiograph of a patient with

chronic obstructive pulmonary disease.

in lead II may be present (p puhnonale), reflecting right

atrial enlargement, whereas other patients may have signs

of right ventricular hypertrophy (large R wave in v1 and v2

with prominent S waves in v5 and v6), a right bundle

branch block, or right axis deviation. Multifocal atrial

tachycardia (MAT) is the classic arrhythmia associated

with COPD patients. MAT is an irregularly irregular

rhythm, like atrial fibrillation (AF), but there are P waves

of differing morphologies before every QRS complex, and

it tends to be slower than AF.