Chronic bronchitis

• Cyanosis  poor ventilation causes decreased 0₂ (less 0₂ available to couple with hemoglobin); increased deoxygenated hemoglobin leads to cyanosis.  
• Use of accessory muscles of respiration: Respiration requires much more effort because of bronchial constriction and the need to breath at high lung volumes.
• Distended jugular veins  with "a" wave: Reflects elevated diastolic pressure and volume secondary to pulmonary hypertension. This finding coupled with a congested liver and pitting edema supports the diagnosis of heart failure.
• Increased A-P chest diameter  hyper resonant percussion and decreased excursion of the diaphragm: Reflects hyper inflated lungs.
• Decreased breath sounds  with hyper-resonance is the most important physical finding for emphysema. Decreased diaphragmatic excursion, prolonged expiration are common to all of the chronic obstructive lung diseases.
• Wheezing  rhonchi, and crackles: Reflect narrowed bronchial lumina secondary to inflammation and mucous.
• Soft heart sounds: Interposition of fluid (pericardial effusion) or Lung (hyper inflated lungs).
• Loud S₂ (P₂ and  S₄.  Changes is S₂: Splitting is caused by delay in closure of pulmonary valve (pulmonary hypertension). P₂ is accentuated with hypertension. 
• S₄: Reflects forceful right atrial contraction/altered ventricular wall compliance -- Lower left sternal border indicates it is originating from right ventricle. Pulmonary hypertension.

• Tachypnea (28/min): Increased respiratory rate is an attempt to compensate for poor ventilation (decreased O2 , increased CO2). It is also compensation for air trapping with the patient breathing at a very high lung volume.

• Fever: Reflects an acute infection superimposed on chronic bronchitis. Early pneumonia? Cytokines affect the thermoregulatory mechanism.

• Palpable Liver: Could be either due to CHF or hyper inflated lungs pushing the diaphragm down. Liver span will help you distinguish between the two.

• Enlarged nodular prostate. Suggests prostatic hypertrophy with a consideration for malignancy.

Arterial blood gases reveal a chronic respiratory acidosis with complete compensation. There is hypoxia and hypercapnia. The hypoxia is due to poor V/Q matching due to severe COPD. 

• Compensated (pH is normal) respiratory acidosis
• CO2 is high hence respiratory
• bicarbonate is high (a renal compensatory effort)
• Hypoxia

Hypoxia could be due to

• Hypoventilation
• High altitude (Low FIO2)
• V/Q mismatch
• Diffusion barrier
• Anatomical shunt

A sputum culture would probably not be ordered routinely in COPD. The sputum culture would probably show mixed flora. A gram stain of the sputum might be a more helpful and economical first step. A sputum culture would be indicated if the first antibiotic failed to clear the infection. Probable organisms causing the respirator infection include Streptococcus pneumoniae, Hemophilus influenza, Branhamella catarrhalis.

The chest x-ray is ordered to rule out pneumonia. There is no evidence for pneumonia. The x-ray shows hyperinflation, low set diaphragm and possibly blebs. The transverse diameter of heart is increased.

Sspirometry.  

The most important evidence is that FEV₁/FVC is decreased (normal >75%) and is severe (<40%)

The Spirometry results are consistent with an obstructive pattern of pulmonary disease. The forced expiratory volume in 1 second FEV₁ measures the average flow rate during the first second of the forced vital capacity (FVC) maneuver, FEV₁ declines in direct proportion with clinical worsening of airway obstruction.  It increases with successful treatment of airway obstruction. The percent of  predicted FEV₁ for a normal patient should not slip below 80%. He has severe obstructive defect.

The electrocardiogram show a rate of 80 BPM, normal sinus rhythm and right axis of (+137^o); there is right ventricular hypertrophy with strain. The R is greater than S in lead V1 and the T wave is inverted in leads V₁-V₂. Strain suggests ischemia during diastole in a hypertrophied wall. S waves are deep in the left precordial leads. There is borderline right atrial hypertrophy by voltage, especially noted in leads II and AVF.

Right ventricular hypertrophy is consistent with this patient's clinical problem. He has chronic obstructive pulmonary disease with secondary hypertension and consequent cor pulmonale. Make sure the students understand the pathogenesis of the atrial/ventricular hypertrophy. Also, they should understand the pathogenesis of secondary versus primary pulmonary hypertension.

Chronic Bronchitis: mucous within bronchial lumina; chronic inflammation of the bronchial wall, marked increase in the size of the mucous glands (increase in Reid Index), patches of squamous metaplasia.  Acute bronchitis: mucosa/submucosal edema, inflammatory cells (also in sputum).

Emphysema: destruction of alveoli creating large air spaces scattered throughout both lungs. Scattered small pulmonary arteries showing smooth muscle hypertrophy. Hyper inflated lungs. 

Right ventricular/right atrial hypertrophy. Chronic passive congestion of the liver.

 Antibiotics  to treat  respiratory infection

Treatment of chronic bronchitis

Bronchodilators 

Congestive Heart failure/Corpulmonale 

 Pulmonary hypertension

Hypoxia

You need to have an understanding of the following statements. Administer oxygen like any medication with consideration for dose and method of delivery.

Work of breathing

Role for steroids

 Emphysema

Smoking cessation

• Advise him to stop smoking
• Nicotine patches/Gum
• Smoking cessation programs
• Support groups