A rapid response event was initiated by the bedside nurse for a patient with acute onset chest pain. Upon prompt arrival of the response team, the patient was noted to be a 59-year-old male with a history of coronary artery disease (CAD) status post-percutaneous coronary intervention with stent placement five years ago, newly diagnosed type 2 diabetes, and chronic liver cirrhosis. Moreover, 15 min before the rapid response was initiated, the patient started experiencing severe, crushing central chest pain, which had gotten worse in intensity and was now associated with shortness of breath, nausea, dizziness, and diaphoresis. The patient became unresponsive as a cardiac monitor was being attached to his chest, and cardiopulmonary resuscitation (CPR) was initiated.
Blood Pressure: not assessed as CPR was initiated
Pulse: could not be palpated
Respiratory Rate: Ambu-bagged at 10-12 breaths per min
Pulse Oximetry: 79% on 100% oxygen with Ambu-bag
Vital signs prior to the arrest:
Temperature: 95.8 °F, axillary
Blood Pressure: 178/97 mmHg
Pulse: 178 beats per min (bpm)
Respiratory Rate: 32 breaths per min
Pulse Oximetry: 88% oxygen saturation on room air
Focused Physical Exam
A limited exam showed an unresponsive, pale, middle-aged male undergoing chest compressions and Ambu-bagging. No other examination was performed during CPR.
CPR was continued. The cardiac monitor showed a jagged, wavy rhythm consistent with ventricular fibrillation (VF) ( Fig. 15.1 ). The airway was secure with endotracheal intubation. Return of spontaneous circulation (ROSC) was achieved in 12 min after three defibrillation attempts at 360 J, four rounds of CPR, three doses of intravenous (IV) epinephrine, and one loading dose of 300 mg IV amiodarone. Normal sinus rhythm was restored. The exam after the achievement of ROSC showed that the patient was responding appropriately to painful stimuli. Stat point of care arterial blood gas analysis showed severe metabolic acidosis with pH 6.7, lactate 21 mmol/L, and bicarbonate level of 4 meq/L. The patient was immediately administered two ampules of 8.4% sodium bicarbonate and started on maintenance sodium bicarbonate drip. Epinephrine infusion was started for hemodynamic support. Post-ROSC electrocardiogram (EKG) was obtained, which showed ST-elevations in anterolateral leads concerning for acute myocardial infarction (MI) in the left anterior descending artery territory. Stat consultation with cardiology was obtained, and the patient was immediately transferred to the cardiac catheterization lab for revascularization.
Cardiac arrest in the setting of VF.
VF is a malignant non-perfusing cardiac arrhythmia that results from the replacement of coordinated ventricular myocardial depolarization by chaotic, disorganized excitation. This results in the loss of the ventricular myocytes’ synchronous contractility, and the heart loses its ability to pump blood. CAD and myocardial ischemia are the most common precipitants of VF. In the hospital setting, VF is commonly seen in association with recent MI and can be the first sign of a new myocardial event. See Table 15.1 for common predisposing factors for VF.
|Predisposing factors and associations|