Cardiovascular culprits
Dyspnea is a common symptom with cardiovascular diseases because cardiac output relates directly to tissue oxygenation. Any pathology that decreases the ability of the heart and blood vessels to transport oxygen will likely trigger discord between the central, peripheral, and neurochemical respiratory centers. Two uncommon cardiovascular etiologies of dyspnea are pericarditis and myocarditis.
Pericarditis
Pericarditis is generally a self-limited condition that responds promptly to initial treatment, although it can cause significant morbidity and mortality. One study showed that acute pericarditis accounted for 5% of patients presenting to the emergency department with non-ischemic chest pain.6 Another study found that the in-hospital mortality rate for acute pericarditis was 1.1%.7
Pericarditis causes dyspnea by restricting the heart’s ability to relax, thus decreasing preload and cardiac output. This occurs with large effusions (>20 mm in width on echocardiography) and can lead to cardiac tamponade—a medical emergency that should be suspected in patients with muffled heart sounds, hypotension, and increased jugular venous distention (Beck’s triad).
Pericarditis etiologies include:
- infectious causes (viral and bacterial entities, myocarditis),
- rheumatologic causes (gout, systemic lupus erythematosus, tumor necrosis factor receptor-associated periodic syndrome [TRAPS], familial Mediterranean fever),
- post-cardiac injury syndromes (either of the acute [2-4 days post injury] or late [Dressler syndrome] variety),
- metabolic disorders (hypothyroid disease, dialysis-related conditions), and
- malignancy.
More than 80% of pericarditis cases in developed countries are idiopathic and are assumed to have a viral source.8
Diagnosis. Acute pericarditis is diagnosed when 2 or more of the following symptoms are present:
- pleuritic chest pain radiating to the trapezius that is relieved by leaning forward
- pericardial friction rub
- electrocardiographic changes showing ST segment elevation in all leads but aVR and V1 and diffuse PR interval depression
- pericardial effusion on echocardiography.
Treatment. Treat non-severe and non-life threatening pericarditis with nonsteroidal anti-inflammatory drugs (NSAIDs). Avoid steroids because research has shown that they increase the risk for developing recurrent pericarditis.8 Hospitalize patients with large pericardial effusions and consider them for pericardiocentesis. Treat cardiac tamponade with urgent pericardiocentesis and hospitalization.
Myocarditis
Myocarditis can have a variety of etiologies (TABLE 29,10). Myocarditis causes dyspnea either by causing pericardial effusion or heart failure.
Diagnosis. Myocarditis can be difficult to diagnose. Suspect it in any patient with cardiogenic shock, acute or subacute left ventricular dysfunction, or myocardial damage from a non-coronary artery disease source. Echocardiography and cardiac serum biomarkers can help diagnose myocarditis, but the diagnostic gold standard remains myocardial biopsy.
Treatment. Treatment is focused on 2 goals: treating the specific etiology suspected and stabilizing any hemodynamic instability. Patients with mild cases can be treated and monitored in the outpatient setting.
Immunosuppressive therapy with immunoglobulin or steroids is not routinely recommended, but a trial may be considered in children, patients with severe hemodynamic compromise, or patients with giant cell arteritis, another autoimmune condition, sarcoidosis, or eosinophilic or non-viral myocarditis.
Because of the risk of sudden death from ventricular arrhythmias, any patient with cardiac symptoms such as chest pain, dyspnea, or palpitations should be admitted for cardiopulmonary monitoring. Patients with heart failure secondary to myocarditis should be treated according to the American Heart Association treatment guidelines for heart failure (available at: http://circ.ahajournals.org/content/128/16/e240.extract). Some patients may benefit from surgical interventions such as percutaneous cardiopulmonary support, extracorporeal membrane oxygenation, mechanical circulatory support, and left ventricular assistive devices. Ventricular arrhythmias may require implantable defibrillators or pacemakers.10