15 A 66-Year-Old Male With Progressive Dyspnea on Exertion


Case 15

A 66-Year-Old Male With Progressive Dyspnea on Exertion



Andrew Morado, Raj Dasgupta, Ahmet Baydur



A 66-year-old male presents for outpatient evaluation of progressive shortness of breath on exertion for the past 6 months. He becomes short of breath after ambulating two blocks and has noted a productive cough during this time. With rest, his shortness of breath resolves.



With shortness of breath, what organ systems should be considered as a potential cause?


Anytime shortness of breath or dyspnea are encountered, it is best to keep the differential broad to help organize a diagnostic approach. The three main categories are the lungs, heart, and anemia. In an older male such as this, the most likely causes are cardiac or pulmonary in nature, though you can never exclude less common causes on history alone. There is no immediate history of coronary artery disease, chest pain, or orthopnea that might suggest congestive heart failure (CHF) as a potential etiology. Additionally, a productive cough could support a primary pulmonary pathology as a cause of his symptoms, though CHF and other cardiac etiologies such as arrhythmias and a dilated left atrium can be other potential culprits. Anemia, regardless of the cause, can manifest as dyspnea on exertion because of decreased oxygen delivery to tissues.



He denies shortness of breath while recumbent, uses one pillow to sleep at night, and denies lower extremity edema. He describes his sputum as thick and moderate in consistency and yellowish in color. He denies fevers or chills. Further review of systems is negative.



What clues in the history might point toward CHF?


Heart failure can be due to a low ejection fraction (systolic dysfunction), most commonly caused by myocardial infarction, or with preserved ejection fraction (diastolic dysfunction), which is strongly associated with long-standing, poorly controlled hypertension. Regardless of the type, the common complaints typically are dyspnea with exertion, orthopnea reported as need to remain upright while sleeping, and peripheral edema. With the absence of orthopnea and lower extremity edema, CHF becomes lower on the differential while pulmonary causes remain high.



He reports well-controlled hypertension and no other past medical conditions. He had an uneventful cholecystectomy 20 years prior. He has no contributing family conditions. He reports occasional alcohol use, no illicit drug use, and smoking 40 cigarettes per day for the past 30 years. He has taken lisinopril for his hypertension for the past 10 years and denies allergies.



Step 2/3


Clinical Pearl


Pharmacology and adverse effects are commonly tested on all board exams, and it is worthwhile to know the effects of the more common drugs. Angiotensin-converting enzyme (ACE) inhibitors have several well-known side effects and can be remembered by the acronym CAPTOPRIL: cough, angioedema, palpitations, taste, orthostatic hypotension, potassium elevation, renal impairment, impotence, and leukocytosis. The dilation of the efferent arteriole at the level of the glomerulus is responsible for the decrease in glomerular filtration rate, while inhibition of ACE inhibitor results in potassium retention. Cough and angioedema occur from the effect on bradykinin. The cough itself can be confused clinically as a marker for worsening pulmonary disease when in fact it is an adverse effect. Additionally, make note of medications that can exacerbate chronic disease such as beta blockers in obstructive airway disease.



He reveals a 60 pack-year smoking history and no other pertinent findings. Given his presenting symptoms and his smoking, chronic obstructive pulmonary disease (COPD) rises to the top of the differential.



Step 2/3


Clinical Pearl


To calculate pack-years, multiply the number of cigarettes × years smoked and divide by 20. Risk of developing COPD substantially increases in those with more than 10 pack-years; however, only about 15% of all smokers will develop this disease.




What is your differential diagnosis?


This is a 66-year-old male with progressive dyspnea on exertion, productive cough, and a 60 pack-year smoking history. Physical exam demonstrates evidence of hyperinflation and obstructive airway disease. COPD remains number one on the differential. We gave consideration earlier to left heart failure as it can cause dyspnea as well as wheezing if significant pulmonary edema is present. However, the absence of other classic history and exam findings such as elevated jugular venous pressure (JVP), S3 gallop, or orthopnea makes it less likely. Other considerations are other causes of obstructive airway disease. Chronic asthmatics could present in such a way, though he denies having a history of asthma as a younger male or child. He is too old to be newly diagnosed with cystic fibrosis. Alpha-1 antitrypsin (A1AT) deficiency is a definite consideration but is still less likely than COPD as a cause of this patient’s symptoms. (A1AT deficiency typically presents at a young age, especially if patients are homozygous for the mutation. Other clues to the diagnosis are necrotizing panniculitis, a rare skin lesion, and abnormalities in liver enzymes.)



Step 2/3


Clinical Pearl


A1AT deficiency is a codominant genetic disorder resulting in increased neutrophil elastase within the lung parenchyma. The effect of elastase is a panacinar emphysema that can eventually lead to COPD. Patients can present as early as their 30s without significant smoking history but demonstrating clinical and objective signs of COPD. Computed tomography (CT) imaging usually reveals predominantly lower lobe emphysema. Serum enzyme levels confirm the diagnosis, whereas genetic testing for the mutation determines disease severity. A1AT is less commonly associated with cystic fibrosis and bronchiectasis.



Step 1


Basic Science Pearl


Emphysema or destruction of lung parenchyma can have varying patterns depending on the etiology of disease. For example, A1AT tends to present with panacinar emphysema, whereas smoking typically causes centrilobular emphysema. The difference pathologically is how the secondary pulmonary lobule is affected. In Figure 15.2, the functional unit of the lung otherwise known as the secondary pulmonary lobule is shown and typically houses 3 to 12 acini. Centrilobular emphysema involves loss of the proximal respiratory bronchiole within the acinus but sparing of distal alveolitis. This sparing of lung parenchyma produces the effect of normal- and abnormal-appearing lung that can be discerned by the naked eye and typically involves the upper lobes. In contrast, panacinar emphysema results in destruction of the entire acinus and mainly affects the lower lobes.



Jun 15, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on 15 A 66-Year-Old Male With Progressive Dyspnea on Exertion

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