1. Build a problem list based on the Hx .  What diseases have a higher probability of causing these clinical problems in this patient, especially when cough and shortness of breath are present together?  What additional problems have you identified?    

2. What is the basis for chronic bronchitis?  Do we have to consider other possibilities?   

Diagnosis of Chronic bronchitis is a consideration because he coughs and brings up sputum every winter for many years. We also need to consider Bronchiectasis. We will see whether there is any evidence for Bronchiectasis.

3. Is his occupation important? What are the risks of his occupation ?  

4. Let us evaluate his physical examination findings. Explain the pathogenesis of the following clinical findings:

 

5. Now after physical examination let us revisit our problem list.

6. Let us proceed with investigations. Take each problem we have listed and determine what type of investigation will help us resolve them.

Sputum Gram stain, Spirometry, ABG, CXR, EKG, CBC, Chemistry

7. Correlate and explain the laboratory data in the context of our problem list. 

The total white blood cell count is mildly increased, showing an early shift to the left. An acute bacterial infection superimposed on the chronic bronchitis may account for these findings.

The hemoglobin and hematocrit are increased. The erythrocytosis is secondary to the hypoxemia of chronic obstructive pulmonary disease. The patient is also a heavy smoker.

"Routine" chemistries show hypercholesterolemia. ALT is elevated, probably reflecting chronic passive congestive and mild hypoxia of the liver.

Electrolytes: Hyponatremia is most likely due to CHF and atrial natriuretic factor, leading to relative dilution of sodium with fluid overload.

8. How do you interpret his ABG. 

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. 

9. How would you explain his hypoxia?

Hypoxia could be due to

In him Hypoventilation and V/Q mismatch probably account for hypoxia. He obviously has alveolar hypoventilation as judged by arterial CO2. Since his A-a gradient is high we have to include V/Q mismatch as co factor for his hypoxia.

10. The results of the sputum culture are pending. What do you expect the results to be? What is the rationale, if any, for ordering sputum culture? 

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.

11. Interpret his CXR? Describe any abnormalities and correlate with the clinical problem.  (close the window to return) 

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.

12.  What is the nature of respiratory infection?  Does he have Pneumonia? Explain his chest pain.

13. Explain the significance, if any, of the results of spirometry.  

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.

14. Determine the rate, rhythm and axis of the patient's electrocardiogram. Describe any abnormalities and correlate with the clinical problem. (Close the window to return) 

The electrocardiogram show a rate of 80 BPM, normal sinus rhythm and right axis of (+137o); 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.

15. What is your diagnosis based upon the data given in the history and physical examination and lab data. 

Acute bacterial bronchitis
Chronic Bronchitis
Pulmonary Emphysema
Obstructive defect
Hypoxic hypercarbic respiratory failure
Pulmonary hypertension
Congestive Heart Failure/Corpulmonale
R/O Cancer prostate

The symptoms seem to reflect primarily a pulmonary problem, although there also is a cardiac component. An elderly smoker with a chronic, productive cough presents with acute and significant dyspnea. He apparently experienced similar episodes in the past.  The physical findings in an elderly smoker supports chronic pulmonary pathology with heart failure. He seems to have an infection of the respiratory tract. However he does not have pneumonia?  Physical signs point to pulmonary hypertension and right heart failure. His present episode is precipitated by acute bacterial bronchitis.

16. Describe the pathologic changes that you would expect to find in this patient. 

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.

17. Identify the treatable problems in this patient.     

18.  Which Antibiotic will you select to treat  respiratory infection?  

Common organisms Antibiotic
Hemophilus Influenza
Streptococcus Pneumoniae
Brahmella catarrhalis

 

First line Second line Penicillin allergy
Amoxacillin
Doxycycline
Trimethaprim/Sulfamethaxazole
Azithromycin
Ciproflaxin
Augmentin
 
Virus  

19. How do you treat chronic bronchitis?   

Pathophysiology Therapeutic option
Irritation of bronchi by Cigarettes Stop Smoking
Narrowing of bronchi:: 
  • Lymphocytic inflammation
  • Mucosal thickening/Glandular hyperplasia
  • Bronchospasm
 

? Steroids

Bronchodilators

Secretions: 
  • Tenacious secretions
  • Bacterial infections
 

?Mucolytic agents/Expectorants
Empiric Antibiotics

20. What bronchodilators will you use? Explain the significance, if any, of the results of spirometry 

Site of action Bronchodilators
Beta2 agonists Albuterol inhalers
Ipratropium bromide
Theophylline

 21. How will you treat his Congestive Heart failure/Corpulmonale ? 

Pathophysiology Therapeutic options
Pulmonary hypertension
  • Hypoxia
  • Loss of vascular bed
Continuous Oxygen
LV dysfunction if any Digoxin and diuretics

22. How will you correct Pulmonary hypertension?

Pathophysiology Therapeutic option
Alveolar hypoxia/Vasoconstriction Oxygen
Loss of vascular bed Lung transplant

 23. How will you correct his hypoxia?    

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

Physiological basis Therapeutic option
Optimal arterial oxygen level.. (Oxygen dissociation curve) Target PaO2 of 55-60
Concern for hypoxic drive (Respiratory centers) Titrate Oxygen to maintain pH over 7.25
Hypoxia due to V/Q mismatch is easily correctable Low FIO2: 1-4 Liters by nasal cannula
High flow and low flow  (Oxygen delivery systems) Acute phase: High flow (Venturi mask)

Stable phase: Low flow (Nasal cannula)

24.  How can you reduce his work of breathing? 

Pathological basis Therapeutic options
Increased airway resistance Bronchodilators
Airway collapse Pursed lip breathing
Inefficient Diaphragmatic position Lean forward with diaphragmatic breathing
Anxiety No sedatives for fear of respiratory depression

  25. What is the role for steroids? 

Pathophysiology/Anti-inflammatory Clinical setting
Acute bronchitis Acute Exacerbation
Chronic bronchitis ? Chronic use

26. What can you do to treat Emphysema?  

Pathpphysiology Therapeutics
Loss of alveolar septa/and elastic recoil/hyperinflation/Blebs and bullae Lung reduction Surgery
  Lung Transplant
Loss of capillary bed/Pulmonary hypertension Heart/Lung Transplant

27. What advise can you give regards his occupation?  

He probably has had Asbestos exposure.

With Smoking history he is at high risk for developing

He should be on annual surveillance program for early detection of these malignancies.

 28. What is your plan for Smoking cessation?