Hypotension in a Patient With Myocardial Infarction

Case Study

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.

Vital Signs

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.

Interventions

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.

Final Diagnosis

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.

Table 13.1

Associations and clinical findings of various mechanical complications of myocardial infarction (MI)

Ventricular wall rupture	Interventricular septal rupture		Papillary muscle rupture
Risk factors: • First large transmural infarction • Anterior wall MI • Age >70 years • Female sex • Extensive myocardial damage	Risk factors: • Single-vessel disease (especially left anterior descending artery) • Extensive myocardial damage • Poor collateral septal circulation		Risk factors: • Single-vessel disease (especially left anterior descending artery) • Extensive myocardial damage • Poor collateral septal circulation
Clinical manifestations: This often occurs within the first five days after MI. Complete rupture of the left ventricular free wall can present as sudden profound right heart failure and shock, often progressing rapidly to pulseless electrical activity Incomplete/sub-acute rupture of the left ventricular free wall may be manifested clinically by persistent or recurrent chest pain, particularly pericardial pain, nausea, restlessness and agitation, abrupt, transient hypotension, and/or electrocardiographic features of localized or regional pericarditis.	Clinical manifestations: The ruptured septum may present with a wide range of symptoms and signs, from mild compromise with dyspnea at exertion to severe cardiogenic shock. A new cardiac murmur is nearly always present. The new murmur is typically harsh, loud, and holosystolic and is heard best at the lower left and usually at the right sternal border.		Clinical manifestations: Significant papillary muscle rupture includes the acute onset of hypotension and severe pulmonary edema The precordium may be hyperactive on physical examination, and a systolic murmur may be present. Typically, a mid-, late-, or holosystolic murmur is present that may have widespread radiation. Although the murmur may be loud, a thrill is generally not present.
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