A rapid response event was initiated by the bedside nurse for a patient who had a syncopal event, hypotension, and new tachyarrhythmia on the monitor. On prompt arrival of the rapid response team, chart review suggested that the patient was a 70-year-old female admitted for the management of myocardial infarction (MI) in the left anterior descending artery territory, requiring a percutaneous coronary intervention with a drug-eluting stent. She was four days post-procedure. She had a history of stage III chronic kidney disease, hypertension, type 2 diabetes, valvular heart disease, and coronary artery disease.
Temperature: 98.2 °F, axillary
Blood Pressure: 60/44 mmHg
Heart Rate: weak low volume pulse, at a rate of 140 beats per min (bpm)
Respiratory Rate: 26 breaths per min
Pulse Oximetry: 85% oxygen saturation on room air, up to 92% on 6 L NC.
Focused Physical Examination
The patient was an elderly female holding her chest in apparent distress. On auscultation of her chest, diffuse bilateral crackles were evident, along with prominent jugular venous distension. Central cyanosis was seen. Her abdomen was soft and non-distended. No peripheral edema was noted, and her extremities were cool to the touch.
A cardiac monitor and pads were attached immediately, with telemetry showing narrow, complex, regular tachycardia. The patient was given a fluid bolus. EKG was obtained, which showed sinus tachycardia with persistent ST elevations in anterior leads. A complete blood count (CBC), electrolytes, lactate, and troponin levels were ordered. Chest X-ray revealed a globular cardiac shadow which was not present before. Stat consult page was sent to intensivist and cardiology for evaluation, as the patient was status post-cardiac intervention. In-house intensivist performed a bedside ultrasound which revealed a large pericardial effusion with evidence of chamber compression. Emergency pericardiocentesis was performed by the cardiothoracic surgery team at the bedside, with frank hemorrhagic output. The patient was provided with fluids and inotropic support and transferred urgently to the operating room for direct closure of suspected ventricular wall defect and a prosthetic pericardial patch.
Ventricular free wall rupture post-MI.
Mechanical Complications After MI
Mechanical complications of ST-segment elevation MI carry high morbidity and mortality. Fortunately, the rate of these complications is low, owing to the recent advances in early coronary revascularization. Common mechanical complications include left ventricular free wall rupture, right ventricular infarction, ventricular septal defect, and acute mitral regurgitation. Acute MI results in the loss of functioning ventricular myocardium. As the amount of healthy myocardium decreases, there is a progressive fall in the ventricular ejection fraction. Left ventricular free wall rupture, right ventricular infarction, ventricular septal defect, and acute mitral regurgitation are often grouped together, as they have rupture or tearing of necrotic myocardium as part of their underlying pathophysiology. See Table 13.1 for more information on the risk factors and clinical findings.
|Ventricular wall rupture||Interventricular septal rupture||Papillary muscle rupture|
|Risk factors:||Risk factors:||Risk factors:|
|Clinical features/risk factors|
|Early rupture <48 h||Persistent pain (>4-6 h)|
|Acute arterial hypertension|
|Persistent ST-segment elevation (except lateral leads)|
|Delayed hospital admission|
|Late rupture >48 h||Recurrent chest pain|
|Persistent ST elevations|
|“Undue” physical exercise|