Management of arrhythmias during transportation in patients with acute myocardial infarction.
One of the most important goals in early care of patients with acute myocardial infarction (MI) is providing effective treatment promptly. The GISSI study shows that the reduction in mortality is as high as 50% when patients are treated within the first hour of MI, hence the "golden hour". Many serious arrhythmias develop before hospitalization, even before the patient is monitored. At least 75% of patients with MI have an arrhythmia during the peri-infarct period. Inasmuch as two-thirds of deaths after acute infarction occur before the patient reaches a hospital, therefore it is very important to initiate effective treatment as early as possible after the onset of symptoms. Early reperfusion to salvage myocardium has a beneficial effect on in-hospital and late prognosis. But, some serious arrhythmias requiring treatment are also seen commonly following successful reperfusion. As a conclusion, it seems necessary for every community to establish a strategy to reach patients with suspected MI and transfer them rapidly to the nearest health care facility. If there is a delay during transportation, the ambulance team should be ready to administer thrombolytics and treat the arrhythmia, which might occur. In this review the treatment of arrhythmia, which may occur during transportation will be discussed.
Keywords: acute myocardial infarction, arrhythmia, transportation
One of the most important goals in early care of patients with acute myocardial infarction (MI) is giving effective treatment as quickly as possible. There are three distinct periods of delay from symptom onset to receiving reperfusion therapy in MI (1). The first period of delay is time from symptom onset to the time of seeking treatment, such as calling emergency medical services (EMS). This initial period of delay is the longest of the three, representing nearly 70% of the total delay time. An analysis of the combined GUSTO trials shows the prehospital delay was 2.7 hours over several years (2). The second delay period results from patients' deciding to seek attention to arrival in hospital. This transport time is short and represents some 3-8% of total delay time. However, in some larger metropolitan areas or remote rural settings further delays can be observed. Prehospital thrombolysis has become the standard of care in some European cities where transport times are long and where mobile coronary care units (CCU) are staffed with doctors and nurses. The advantage of this strategy has been studied in several randomized trials. The GREAT trial showed a substantially lower mortality at 1 year among patients randomized to prehospital anistreplase (APSAC) at 10.4% compared with 21.6% among those treated in hospital (3). In the GISSI study, the maximum reduction of mortality was 50% in patients treated during the first hour of infarction, hence the "golden hour"(4). The third delay period is from hospital arrival to therapy. This period represents some 25-30% of delays. For patients experiencing chest pain or other ischemic symptoms, only about one-half of patients use the EMS system. However, care could be enhanced for patients with MI if the majority used this mode of transport to the hospital. The concept of the "chain of survival" early access, early cardiopulmonary resuscitation (CPR), early defibrillation, and early advanced life support- has been shown to improve survival following cardiac arrest to as high as 44% (5).
Many serious arrhythmias develop before hospitalization, even before the patient is monitored. At least 75% of patients with MI have an arrhythmia during the peri-infarct period (6). Of course, inasmuch as two-thirds of deaths after MI occur before the patient reaches a hospital, it is obvious that the CCU alone cannot decrease the total community mortality from coronary artery disease (7-9). Evidence suggests that arrhythmias are almost invariable in the early phases of acute MI and that many deaths are associated with small infarcts (10). Therefore, it is very important to initiate effective treatment as early as possible after the onset of symptoms. Early reperfusion to salvage myocardium has a beneficial effect on in-hospital and late prognosis. The accepted hypothesis for the mechanism of arrhythmias in MI is reentry. There is an evidence of increased sympathetic activity during very early phase of MI. In another group of patients, as a reflection of augmented vagal activity, bradycardia, sometimes associated with atrioventricular (AV) block and hypotension may occur (11). All forms of bradycardia and tachycardia can depress the cardiac output in patients with MI. Therefore in patient with MI, the optimal rate is usually lower, in range of 60 to 80 beats/min. The loss of atrial contribution is also important in patients with MI. Studies in patients without MI have demonstrated that loss of atrial kick decreases left ventricular output by 15 to 20 percent. However, atrial systole is of greater importance for left ventricular filling in patients with MI (11). In this section, management of arrhythmias in early phase of MI will be discussed.
Management of arrhythmias
Sinus tachycardia: About 30% of patients experience sinus tachycardia following MI, especially those with anterior location. It represents a physiologic response to left ventricular (LV) dysfunction or stimulation and overactivity of the sympathetic nervous system. Treatment includes optimizing hemodynamics and oxygenation, correction of anemia, and electrolyte and acid base abnormalities, pain control and anxiolytic agents. Beta blockers are indicated for patients without evidence of significant left ventricular dysfunction or hypovolemia (6, 7).
Atrial tachyarrhythmias: Although the reported incidence of atrial tachyarrhythmias, consisting of premature atrial complexes (PACs), atrial fibrillation (AF), atrial flutter, and paroxysmal supraventricular tachycardia is as high as 44%, they are less common during the early phase of MI (12). These arrhythmias are often transient and recurrent. In approximately one-third of patients, several types of atrial tachyarrhythmias may occur in the same patient (12).
As with PACs and atrial flutter, AF is usually transient, some times recurrent and tends to occur in patients with left ventricular failure but is also observed in patients with pericarditis and ischemic injury to the atria and right ventricular infarction (11). New AF in the peri-infarct period is associated with a higher mortality.
The principles of management are to treat the underlying ca uses, to control the ventricular rate, and to prevent further clinical deterioration. Premature atrial complexes are not considered an indication for therapy. Cardioversion is not necessary unless the patient is severely symptomatic with hypotension or chest pain. Therapy is aimed at controlling the ventricular rate with intravenous (iv.) beta-blockers such as metoprolol (2.5 to 5 mg every 2 to 5 minutes to a total of 15 mg) or atenolol after heart failure and underlying conduction disease have been excluded (13, 14). When there are absolute contraindications to beta adrenergic blockade, rate slowing may also be achieved by iv. diltiazem or verapamil. Given the availability of more effective agents, digoxin is no longer first-line therapy for management of acute AF, bu it plays a continuing role in patients with heart failure or LV dysfunction. For episodes of AF that do not respond to electrical cardioversion or that recur after a brief period of sinus rhythm iv. amiodarone may be used to slow the ventricular response. The approach to therapy for atrial flutter is similar to that for AF, except medical management and control of the ventricular rate with drugs (particularly digitalis compounds) are less easily accomplished. Atrial flutter usually responds to low-energy synchronous-mode cardioversion (10 to 25 J), but the self-limited nature of the arrhythmia limits its use. Beta-blockers and particularly verapamil are useful in controlling the ventricular rate in atrial flutter. Initial treatment of supraventricular tachycardia should be carotid sinus massage or other vagal maneuvers. If these maneuvers fail, beta-blockers may be effective (if not contraindicated) unless the hemodynamic status warrants urgent cardioversion. Intravenous adenosine may also be considered in this setting (7).
Both primary ventricular fibrillation (VF) and premature ventricular beats (PVCs), especially R-on-T beats, occur during the early phase of MI, when heterogeneity of electrical activity is present. Premature ventricular beats of various frequencies are ob served in up to 90% of patients with MI. Nonsustained ventricular tachycardia (VT) occurs in up to 40% of such patients, and sustained VT or VF each occurs in about 3% to 5%. Mortality in the immediate postinfarction period is most often due to sudden death from VF. Premature ventricular beats are usually asymptomatic, and it appears that isolated premature beats themselves in the setting of MI, regardless of frequency or multiformity, are not associated with an increased risk of sustained ventricular tachyarrhythmia. Prophylactic suppression of PVCs with antiarrhythmic drugs is not recommended unless they lead to hemodynamic compromise and there is the possibility that its use may be associated with increased risk of fatal bradycardic and asystolic events (15). There is no convincing evidence that the prophylactic use of lidocaine reduces mortality, and the prior practice of routine administration of lidocaine to all patients with known or suspected MI has been largely abandoned (15). Early VT occuring within 24 hours of MI is often transient and is not associated with long-term risk of sudden cardiac death. Treatment of sustained VT consists of cardioversion; if the rate is slow and hemodynamically tolerated, cardioversion may be attempted with drugs (amiodarone 150 mg infused over 10 minutes; repeat boluses of 150 mg may be given every 10 to 15 minutes as needed). Rapid VT (>150 beats/min) or VT associated with hemodynamic deterioration should be treated with prompt DC cardioversion. Primary VF occurs early after the onset of symptoms in patients without preexisting heart failure, hypotension, or major arrhythmias in contrast to the secondary form. In a series of 500 patients with MI who were monitored either in an ambulance or in the hospital within 1 hour after the onset of symptoms, primary VF occurred in 55 patients, with 54 of them occurred within 10 hours after the onset of symptoms (16). Treatment for VF consists of an unsynchronized electrical countershock with at least 200 to 300 joules, implemented as rapidly as possible. Failure of electrical countershock to restore an effective cardiac rhythm is almost always due to rapidly recurrent VT or VF, to electromechanical dissociation (EMD), or very rarely due to electrical asystole. Successful interruption of VF or prevention of refractory recurrent episodes can also be facilitated by administration of iv. amiodarone (300 mg or 5mg/kg, iv. bolus). Accelerated idioventricular rhythm (AIVR) is seen in up to 20% percent of patients with MI. Most episodes are of short duration. Accelerated idioventricular rhythm has been reported in 10% to 40% of cases of MI, especially (but not necessarily) with early reperfusion. The presence of AIVR during the peri-infarct period is not correlated with increased mortality or incidence of VF. Antiarrhythmic therapy is not indicated for AIVR (11).
Sinus bradycardia (SB): SB is the most common arrhythmia occuring during the early hours after MI and occurs in 16% to 25% of inferior and posterior infarctions. It is most often transient resulting from an increase in vagal tone and it may be related to atrial and sinus node ischemia (or to both). Sinus bradycardia during the early phase of MI may be protective, perhaps because it reduces myocardial oxygen demands. Severe bradycardia may predispose the patient to ventricular ectopy. This arrhythmia usually resolves spontaneously, and treatment is reserved for hemodynamically symptomatic arrhythmias and those accompanied by bradycardia-dependent ventricular arrhythmias. Atropine sulfate (0.6 to 1 mg iv.) is often successful in treating symptomatic bradycardia. Temporary pacing is rarely required (6).
Atrioventricular and intraventricular block: Ischemic injury can produce conduction block at any level of the AV or intraventricular conduction system. Heart block may develop in approximately 6% to 14% of patients with MI. Specific therapy is not required in patients with first degree and typed second degree AV block when the ventricular rate exceeds 50 beats/min and these types of blocks do not affect survival. If the patient is symptomatic, and heart rate falls below 50 beats/min, immediate treatment with atropine (0.6 mg) is indicated. Type II second degree block usually originates from a lesion in the conduction system below the bundle of His. Because of its potential for progression to complete heart block, type II second degree AV block should be treated with a temporary external or transvenous demand pacemaker (PM).When complete AV block (CAVB) develops in less than 6 hours after the onset of symptoms in patients with inferior MI, escape rhythm is usually stable without asystole and often junctional with a rate exceeding 40 beats/min. It is often transient, may be responsive to atropine. If the ventricular rate is very slow (<40 to 50 beats/min) pacing is indicated. In patients with anterior infarction, CAVB often occurs suddenly and escape rhythms with wide (IRS complexes and rates less than 40 beats/min, ventricular asystole may occur quite suddenly, there fore pacing is indicated. New bundle branch block (BBB) has been reported in about 15% of cases of MI and is associated with an increased risk of CAVB, congestive heart failure, cardiogenic shock, ventricular arrhythmias, and sudden death. Right BBB is the most common, while left BBB and alternating BBB is less. Temporary PM is advisable in some of these patients because of the high risk of developing CAVB. This includes patients with new bilateral BBB. Isolated new block in only one of the three fascicles even with P-R prolongation, and preexisting bifascicular block and normal P-R interval poses somewhat less risk: these patients should be monitored closely, with insertion of a temporary PM deferred unless higher degree AV block occurs. Especially during transportation, noninvasive external cardiac pacing may be used (11).
Ventricular asystole and electromechanical dissociation: Asystole and EMD occur in a small fraction of patients with MI and are usually associated with large infarcts. The prognosis is extremely poor even with aggressive therapy. Defibrillation should be attempted in patients with apparent asystole, because the rhythm may actually be fine VF. In the rare instance in which asystole can be documented, immediate transcutaneous pacing is indicated (6). Other resuscitative measures, including chest compressions, atropine, vasopressin, epinephrine should be administered to treat ventricular asystole.
The cellular electrophysiological mechanism for reperfusion arrhythmias appears to include washout of various ions such as lactate and potassium, and toxic metabolic substances that have accumulated in the ischemic zone. Transient sinus bradycardia occurs in many patients with inferior infarcts at the time of acute reperfusion. PVCs, AIVR, and nonsustained VT are also seen commonly following successful reperfusion (6, 7). All these arrhythmias should be treated as mentioned previously in the text.
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Clinic of Cardiology, Ataturk Education and Research Hospital, Izmir, Turkey
Address for Correspondence: Doc. Dr. Murat Yesil, Clinic of Cardiology, Ataturk Education and Research Hospital, Izmir, Turkey Phone: +90 232 243 18 71/2326 Fax: +90 232 244 91 15 E-mail: firstname.lastname@example.org
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|Publication:||The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)|
|Article Type:||Clinical report|
|Date:||Jul 1, 2007|
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