The diagnosis and treatment of acute myocardial infarction (AMI) in the operational setting can be both difficult and challenging. The underlying principle in the General Medical Officer’s (GMO) treatment of AMI should be the rapid stabilization and earliest possible medical evacuation of the patient to a medical facility with the appropriate Intensive Care Unit/Cardiac Care Unit (ICU/CCU) and support capabilities. The maximum effort should be made to ensure, whenever possible, that the patient with AMI is electrically and hemodynamically stable and pain free before transfer. Treatment of cardiac arrest or hemodynamically significant arrhythmias should follow the advanced cardiac life support (ACLS) guidelines.

The diagnosis of AMI is primarily based on an appropriate clinical history. The clinician must maintain a high index of suspicion as patient complaints of chest discomfort may vary considerably. Usually lasting for greater than 30 minutes, the discomfort generally is described as a severe retrosternal squeezing, choking, or heavy pressure sensation. It may radiate to the shoulders, down the ulnar aspect of the left arm, into the neck or jaw. The patient will often report associated diaphoresis or shortness of breath. A history of antecedent exertional chest discomfort can often be elicited.

During the physical examination particular attention should be paid to the pulse, blood pressure, and respiratory rate, signs of heart failure to include elevated jugular venous pulse, rales on chest auscultation, the presence of an S3, or the development of a new heart murmur on cardiac examination.

Serial 12-lead electrocardiogram (ECG) monitoring is helpful in establishing the diagnosis of AMI, but the presence of an initially normal ECG does not exclude the diagnosis. Serial creatinine kinase (CK) determinations should be obtained every 6 to 8 hours. If laboratory facilities are not available, serum should be collected, spun down, if possible, and kept on ice until sent with the patient at the time of medical evacuation. Spectralä cards for qualitative measurement of Myoglobin, CKMB and Troponin may be available on some platforms. A right-sided V4r lead ECG recording is essential in all patients with suspected AMl as it will allow diagnosis of RV infarction. In the precepts of a right ventricular (RV) infarct, hypotension may be a problem when nitroglycerin is administered, and may require 35 liters of fluid in the first 24 hours.

All patients with diagnosed or suspected AMI should be placed on a continuous ECG monitor (one lead is sufficient) with a large bore intravenous line established. All patients should be placed on supplemental oxygen. Patients should chew at least 160 mg of aspirin and then be treated with 325 mg of aspirin orally each day. Blood pressure should be monitored every 5 minutes until stable and then hourly. The patient should be placed on complete bed rest. In the absence of contraindications (table 1), patients should receive B-blockers. Metoprolol can be given by intravenous push in 3 separate 5-mg doses. Then give 50mg PO every 6 hours or a dose of 1 to 3 mg of IV propranolol followed by 60 to 80 mg PO TID. If an IV preparation of atenolol is not available, begin the oral (PO) dosing. Atenolol 50 mg BID PO can alternatively be used.

A careful assessment of the patient’s condition should be made between each dose of beta-blocker and the dose held if hypotension (systolic pressure <90mmHg), severe bradycardia (HR < 50), or signs of congestive heart failure develop.

Pain relief

In the absence of severe hypotension (systolic BP < 90 mmHg) and in the presence of on-going chest pain, the patient should receive 0.4 mg of sublingual nitroglycerin every 5 minutes until chest pain is relieved or hypotension ensues, usually no more than 3 doses are needed. Additional therapy may be instituted with intravenous nitroglycerin at a dose of 10 mcg/min if a controlled infusion pump is available. The dosage of IV nitroglycerin may be increased 10 mcg/min every 5 minutes until clinical symptoms decrease or significant hypotension develops. If an infusion pump is not available 1/2 to 2 inches of nitroglycerin paste may be used. For pain refractory to nitroglycerin and beta-blocker, intravenous morphine sulfate in doses of 1-2 mg every 5-10 minutes may be used.

Experts no longer recommend lidocaine prophylaxis for suppression of premature ventricular contractions as its use is associated with an increase in asystolic deaths. In the presence of ventricular fibrillation or tachycardia, intravenous lidocaine is indicated with a bolus and infusion pump dosing per the ACLS protocol. If an infusion pump is not available lidocaine should not be given by continuous infusion unless the drip is monitored continuously. The Israeli's demonstrated that 100 mg of lidocaine IM before transport decreased VT in the ambulance. This may be particularly relevant to patients transported in helicopters. IM injections had been discouraged in the past due to the rise in CK, however the rise in CK is all MM and does not interfere with diagnosis by the isoenzymes. Symptomatic bradycardia can be treated with atropine 0.6 mg IV. The dose may be repeated if needed, every 5 minutes until a total dose of 2 mg is reached.

The following considerations should be evaluated before anticoagulation is initiated.

• Does the patient have any contraindications to systemic anticoagulation?
• Recent severe head injury.
• Coagulopathy.
• Bleeding ulcer or other inaccessible bleeding site.
• Uncontrollable hypertension.
• Severe hepatic or renal disease.
• Is an infusion pump is available?
• Is the laboratory capable of supporting the analysis of complete blood counts (CBC) and (partial thromboplastin time) PTT?

If these considerations are met, then the patient should receive an initial bolus of 5,000 units of heparin IV followed by a continuous infusion of 1,000 units/hour. The PTT should be checked 6 hours after beginning the infusion, and the drip rate adjusted to maintain a PTT at 1.5 to 2.0 times the control value. An excellent alternative is the use of Low Molecular Weight heparin, which does not require dose titration by PTT monitoring. Enoxaprin 1 mg/kg subcutaneous every 12 hours is equally effective to adjusted dose heparin in unstable angina and non-Q wave infarction (ESSENCE trial).

Multiple clinical trials have shown that thrombolytic therapy reduces mortality from myocardial infarction. The three currently available thrombolytic agents, Streptokinase (SK), rt-PA, and APSAC have been shown to be equally effective in reducing mortality. SK is the most economical drug to use but given APSAC's ease of administration (30 units IV push over 5 minutes), this drug may have a role in the operational setting. Reteplase is new to the market and preliminary data shows it to be equally effective as rt-PA in achieving an open artery. It is given as a double bolus making it more convenient for use at sea. Depending on the operational setting and the ability to medically evacuate (MEDEVAC) the patient to an appropriate facility within 6 hours, the use of thrombolytic therapy in a patient presenting with an AMI should be strongly considered.

Only give thrombolytics after assessing the indications for thrombolytic therapy (table 2). Ensure no contraindications to therapy exist (table 3). Recent evidence shows that thrombolytic therapy can be given safely in a secondary treatment facility (such as a large deck) without the need for emergent, or even subsequent transport to a tertiary care facility.

When transporting a patient, the GMO must ensure that the appropriate staff and equipment accompany the patient to provide advanced cardiac life support (ACLS) in route.

ACC/AHA Guidelines for the Management of Patients with Acute Myocardial infarction., JACC, November 1, 1996 Vol. 28, No. 5: pp 1328-1428.

The U.S. Department of Health and Human Services- Agency for Health Care Policy and Research Clinical Number 10; Unstable Angina: Diagnosis and Management, March 1994.