Cardiovascular Medicine: Item 83
Cardiovascular Medicine > Adult Congenital Heart Disease > Acyanotic Congenital Heart Disease > Ventricular Septal Defect
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A 75-year-old woman is evaluated in the emergency department for a 2-day history of intermittent long episodes of chest pain. When the patient arrives in the emergency department she still has mild chest discomfort, which is rapidly relieved by a sublingual nitroglycerin tablet. She is subsequently pain free. The initial cardiac enzymes are elevated. The electrocardiogram is shown (Figure 83). The patient is admitted to the coronary care unit for monitoring.
The patient does well overnight and has no recurrent chest pain. The next morning, however, she suddenly develops severe dyspnea and hypotension. Physical examination demonstrates a heart rate of 120/min. The blood pressure is 80/50 mm Hg. The jugular venous pressure is 12 cm H2O. Cardiac examination is difficult owing to prominent bilateral lung crackles and wheezes, but a systolic murmur is noted.
Which of the following is the most likely cause of clinical deterioration in this patient?
- Papillary muscle rupture and ventricular septal defect are recognized mechanical complications that occur early after myocardial infarction.
- Both papillary muscle rupture and ventricular septal defect present with hypotension and acute dyspnea.
This patient's clinical presentation is consistent with either a papillary muscle rupture or a ventricular septal defect, both of which are important mechanical complications after myocardial infarction. Because this patient's myocardial infarction involves the inferior wall, the decompensation is likely caused by a papillary muscle rupture. It is not possible to differentiate this from a myocardial infarction–related ventricular septal defect by physical examination alone. The cause of the patient's current symptoms must be promptly identified. A bedside echocardiogram will provide critical information concerning the cause of dyspnea and hypotension and confirm the suspected diagnosis of papillary muscle rupture.
Other causes of dyspnea and hypotension in patients presenting with myocardial infarction that should be considered include free wall rupture and right ventricular myocardial infarction. Free wall rupture is usually catastrophic, resulting in cardiac tamponade and sudden death. Right ventricular infarction may cause gradually progressive hypotension. This usually occurs in the setting of inferior wall myocardial infarction. Characteristic findings on physical examination include hypotension, elevated jugular venous pressure, and clear lung fields. Left ventricular aneurysm may occur following myocardial infarction but this is not an acute complication. It should be suspected in a patient with persistent ST-segment elevation, heart failure symptoms, and ventricular arrhythmia. Aortic dissection should always be considered in patients with hypotension, particularly in the setting of an inferior myocardial infarction as the dissection can shear off the right coronary artery. However, aortic dissection would be unlikely to present with pulmonary edema.
Pulmonary embolism is another possible cause of hypotension in hospitalized patients and should always be considered in the differential diagnosis. The clinical presentation of pulmonary embolism would include dyspnea with clear lung fields and, occasionally, a pleural friction rub. Pulmonary congestion would not be expected.
- Buda AJ. The role of echocardiography in the evaluation of mechanical complications of acute myocardial infarction. Circulation. 1991;84:I109-21. [PMID: 1884477] [PubMed]
- Smyllie JH, Sutherland GR, Geuskens R, Dawkins K, Conway N, Roelandt JR. Doppler color flow mapping in the diagnosis of ventricular septal rupture and acute mitral regurgitation after myocardial infarction. J Am Coll Cardiol. 1990;15:1449-55. [PMID: 2329247] [PubMed]
