Dyspnea

Mr. C is a 64-year-old man who comes to see you complaining of shortness of breath.

Over the last 2 years, Mr. C has noticed worsening dyspnea on exertion. He complains of shortness of breath with minimal exertion. He is unable to walk around his house without resting. Several years ago, Mr. C could walk several blocks without any difficulty. He notes that he is unable to sleep lying flat due to shortness of breath (orthopnea), and he has slept on a recliner for the last 6 months. Occasionally, he awakes from sleep acutely short of breath (paroxysmal nocturnal dyspnea). He complains that his feet are swollen.

Past medical history is notable for an MI 2 years ago. Vital signs are temperature, 37.0°C; RR, 24 breaths per minute; pulse, 110 bpm; BP, 120/78 mm Hg. His pulse is regular with an occasional irregularity. Cardiac exam reveals JVD to the angle of the jaw in the upright position, a grade II/VI systolic murmur at the apex, and a positive S3 gallop. Lung exam reveals crackles half of the way up from the bases bilaterally. He has 2+ pretibial edema to the knees.

A chest radiograph, HCT, and ECG are performed.

Mr. C has several features that are highly specific for HF. His history of prior MI, orthopnea, and most importantly the clinical findings of JVD and an S3 gallop are highly specific for HF.

Mr. C undergoes an ECG, chest film, CBC, and transthoracic echocardiogram. His CBC is normal and his chest film reveals cardiomegaly. His ECG demonstrates normal sinus rhythm with pathologic Q waves in leads V1–V4, and his echocardiogram reveals marked systolic dysfunction and an ejection fraction of 18%. There are regional wall motion abnormalities and the anterior wall is akinetic. There is no significant aortic stenosis or aortic regurgitation. Mitral regurgitation is mild.

An angiogram is performed. This reveals an unobstructed right coronary artery and circumflex but an occluded left anterior descending artery supplying the area of his large prior MI. The ejection fraction is 20%.

Mr. C is admitted for treatment of his HF. He starts a salt-restricted diet and is given diuretics, ACE inhibitors, beta-blockers (when his HF is controlled) and an aldosterone antagonist. The diuresis results in a 20-pound weight loss, and his dyspnea on exertion improves markedly. His orthopnea resolves. He declines discussing the possibility of coronary artery bypass surgery but agrees to an implantable cardiac defibrillator. He remains stable at follow-up 5 years later.

S: 64 y/o man with PMH of MI, complaining of SOB with minimal exertion, worsening DOE over the past 2 years, swollen feet, admits to orthopnea and PND and has been sleeping on a recliner the last 6 months, states he was able to walk several blocks without any difficulty years ago but now can’t walk around his house without resting.

O: BP 120/78 mm Hg, RR 24, P 110bpm irregular, T 37.0°C

Cardiac: JVD, grade II/VI systolic murmur at apex, positive S3 gallop

Lung: crackles half of the way up from the bases bilaterally and 2+ pretibial edema to the knees

CBC is normal. Chest film reveals cardiomegaly. ECG shows normal sinus rhythm with pathologic Q waves in leads V1–V4. Echocardiogram shows marked systolic dysfunction and an ejection fraction of 18%. No significant aortic stenosis or aortic regurgitation. Mitral regurgitation is mild. Angiogram reveals unobstructed right coronary artery and circumflex but an occluded left anterior descending artery supplying the area of his large prior MI and an ejection fraction of 20%.

A: Based on his history of prior MI, orthopnea, and the clinical findings of JVD and S3 gallop, the results are highly indicative of HF.

R/O aortic stenosis, aortic regurgitation, atrial fibrillation.

P: Reduce salt-intake, give diuretics, ACE inhibitors, beta-blockers (when his HF is controlled), and aldosterone antagonist. Follow up in 5 years.

Summary:

Patients that have chronic aortic regurgitation can also present with a complaint of progressive dyspnea on exertion. Conversely, the patient can also be asymptomatic, so the diagnosis would be suspected when the clinician detects an early diastolic murmur. Auscultation to hear this murmur is more sensitive when it comes to moderate to severe aortic regurgitation. In Mr. C’s case, the results showed a systolic murmur. Another presentation in aortic regurgitation is pulse pressure being wide due to the large stroke volume increasing the systolic BP, and the regurgitation of blood back into the LV rapidly lowering the diastolic BP. There wasn’t an issue in the blood pressure or pulse pressure for Mr. C. Aortic fibrillation was another differential diagnosis considered because this also presents with shortness of breath and dyspnea on exertion. Occasionally, atrial fibrillation is discovered when an irregularly irregular pulse is found and evaluated. ECG results for atrial fibrillation would demonstrate irregularly spaced QRS complexes and fibrillatory P waves, which was not the result of Mr. C’s ECG. Finally, the finding of mild mitral regurgitation is due to the fact that with decompensated mitral regurgitation, the systolic function may fail which will lead to increased LV end systolic volume, decreased stroke volume, and decreased ejection fraction. In addition to this, there is the finding of the S3 gallop Mr. C had, which is seen with mitral regurgitation.