Successful resuscitation and neurologic recovery from refractory ventricular fibrillation after magnesium sulfate administration

CASE REPORT

magnesium sulfate, ventricular fibriUation

Successful Resuscitation and Neurologic Recovery From Refractory Ventricular Fibrillation After Magnesium Sulfate Administration

From the Residency in Emergency

Richard C Tobey, MD*

Medicine, Morristown Memorial

Glenn A Birnbaum, MD*

Hospital, Morristown, New Jersey;*

John R Allegra, MD, PhD**

Mountainside Hospital, Montclair, New Jersey.'.t and Santa Monica Hospital, Santa Monica, California. ~ Received for publication June 4, 1991. Accepted for publication August 14, 1991.

Michael S Horowitz, MD t John J Plosay III, MD*

A 46-year-old man suffered a witnessed cardiac arrest. Ventricular fibrillation persisted despite 62 minutes of basic and advanced cardiac life support measures in the field. On arrival in the emergency department, he received 4 g magnesium sulfate IV and was defibrillated successfully to normal sinus rhythm with the next countershock. The patient was discharged neurologically intact. We discuss the possible mechanisms of action and clinical use of IV magnesium sulfate in cardiac arrest. [Tobey RC, Birnbaum GA, Allegra JR, Horowitz MS, PIosay JJ IIh Successful resuscitation and neurologic recovery from refractory ventricular fibrillation after magnesium sulfate administration. Ann Emerg Med January 1992;21:92-96.]

INTRODUCTION Considerable clinical arid experimental research has demonstrated that cardiac conduction and rhythm are influenced by magnesium) -7 Magnesium deficiency has been associated with multifocal atrial tachycardia, 6"8 premature ventricular contractions, 6 torsade de pointes, ventrieular taehyeardia, and ventricular fibrillation. 9'1° Hypomagnesemia predisposes patients to digoxin-related arrhythmias 11'12 and interferes with digoxin control of ventricular rate in atrial fibrillation, la Magnesium metabolism is closely linked with that of potassium, 1¢'15 and combined deficiencies have been thought to contribute to the increased incidence of sudden death among patients with hypertension or congestive heart failure receiving diuretics. 16-18 The usefulness of magnesium is not limited to a~Thythmias associated with hypomagnesemia. Several reports document the use of magnesium to treat a wide range of arrhythmias in patients without hypomagnesemia. 19'2° In this setting, magnesium has been especially effective in safely converting torsade de pointes and monomorphic ventrieular tachyeardia. 21-26 There have been a number of reported eases in which ventrieular taehycardia and ventricular fibrillation recurred many times despite standard antiarrhythmic therapy but resolved dramatically after a magnesium sulfate bolus followed by infusion. 19'23'27 Magnesium

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therapy has also controlled digitalis-induced arrhythmias, 11,12,28 supraventrieular tachycardia, and multifocal atrial tachycardia. 8"23'29 Finally, several studies have shown that an infusion of magnesium can reduce the incidence of arrhythmias occurring after acute myocardial infarction. 3°-32 A search of the medical literature revealed no controlled studies of the efficacy of magnesium sulfate in the treatment of sustained ventricular fibrillation and no reported cases of sustained ventricular fibrillation responsive to magnesium sulfate. We report the case of a patient with refractory ventricular fibrillation who responded to a single parenteral dose of magnesium sulfate. Despite more than one hour of cardiac arrest, the patient was ultimately discharged from the hospital neurologically intact.

CASE REPORT A 46-year-old man collapsed after a brief period of lightheadedness and shortness of breath associated with diaphoresis and left arm pain. He had a medical history of gout and hypertension and an inferior wall myocardial infarction eight years earlier. The patient's medications were ehlorthalidone, potassium, verapamil, propranolol, and allopurinol. An emergency medical

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technician in the household witnessed the arrest, found the patient to be pulseless, and began CPR as an advanced life support unit was summoned. The unit arrived 13 minutes later. Online medical control was provided by the base station physician. Advanced life support personnel found the patient in ventricular fibrillation and performed three countershocks without response. Thereafter, the patient was continuously monitored and remained in ventricular fibrillation despite multiple medications and countershocks (Table). The patient arrived in the emergency department 57 minutes after he collapsed. On arrival, examination revealed him to be pulseless and apneic with CPR in progress. Pupils were sluggishly reactive. Breath sounds were equal bilaterally. The cardiac monitor revealed ventricular fibrillation. Sixty-two minutes after arrest, 4 g magnesium sulfate were administered as a bolus through a central IV line. Defibrillation two minutes later converted the patient to a junctional rhythm at 100 with a blood pressure of 100/80 mm Hg. The junctional rhythm converted spontaneously to a sinus bradycardia at 50. Within 40 minutes, the patient had regained consciousness, could follow commands, and was able to

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clearly indicate his dislike of the endotracheal tube. Laboratory results revealed hemoglobin of 15.4 g/dL (range, 13.5 to 17.5 g/dL); hematocrit, 48.1% (41% to 53%), WBCs, 15,600 cells/gL (4.5 to 11.0 x 1,000 cells/l.tL); sodium 139, mEq/L (136 to 146 mEq/L); potassium, 4.6 mEq/L (3.5 to 5.1 mEq/L); chloride, 101 mmol/L (98 to 106 retool/L); bicarbonate, 16.6 mmol/L (22 to 29

mmol/L); blood urea nitrogen, 21 mg/dL (7 to 18 mg/dL); creatinine, 1.7 mg/dL (0.6 to 1.2 mg/dL); and magnesium, 5.4 mEq/L (1.3 to 2.1 mEq/L) (drawn after patient received magnesium sulfate). Arterial blood gases drawn immediately after successful defibrillation showed pH 6.99 (7.35 to 7.45); Pco 2, 54 mm Hg (35 to 48 mm Hg); P%, 108 mm Hg (83 to 100 mm Hg); HCOs-, 13 mmol/L It"

Table. Sequence qf resu~cit~ztion events

Downtime (min) Events

Rhythm

Vital Signs

0:00 0:13 0:13 0:15 0:17 0:20 0:22 0:24 0:25 0:26 0:25 0:28 0:28

Cardiac arrest, CPR begun ALS arrival, defibrillated 200 J Defibrillated200 J Defibrillated300 J Intubated iV line Epinephrine1 mg IV Defibrillated200 J Defibrillated300 J Defibrillated360 J Defibrillated360 J Lidecaine100 mg iV Sodium bicarbonate 44 mEq IV

VF VF VF VF VF VF VF VF VF VF VF VF VF

Pulseless Pulseless Pulseless Pulseless Pulseless Pulseless PuIseless Pulseless Pulseless Pulseless Pulseless Pulseless

0:30 0:32 0:35 0:37

Defibrillated360 J Bretyllium580 mg iV Defibrillated360 J Sodium bicarbonate 44 mEq IV

VF VF VF VF

Pulseless Pulseless

0:38

Defibrillated360 J

VF

0:40 0:42 0:43 0:43 0:45 0:48 0:47 0:48 0:52 0:56

Bretyllium1,000 mg IV Defibrillated360 J Defibrillated360 J Defibrillated360 J Lidocaine100 mg IV Defibrillated360 J Bretyllium1,000 mg IV Defibrillated380 J Epinephrine1 mg IV Defibrillated360 J

VF VF VF VF VF VF VF VF VF VF

0:57 1:02 1:02 1:04 1:07 1:12

Arrival at hospital Central line started Magnesiumsulfate 4 g IV Defibrillated360 J Lidocaine100 mg IV and infusion

1:32 1:42 2:22

Atropine0.5 mg iV Transferredto ICD

VF VF VF Junctional Junctional Sinus at 54 Sinus at 48 Sinus at 88 Sinus at 88

Pulseless

Pulseless Pulseless Pulseless Pulseless Pulseless Pulseless Pulseless Pulseless Pulseless Pulsetess Pulseless Pulseless Pulsaless Pulseless Pulseless Pulseless Palpable pulse 100/80 mm Hg 120/50 mm H0 96/54 mm Hg 118/60 mm Hg

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(21 to 28 mmol/L); and 02 saturation, 95% (95% to 99%). The ECG showed a junctional rhythm at 50, left ventricular hypertrophy with strain pattern, and Q waves in the inferior leads. The patient had a prolonged hospital course and multiple complications including left popliteal artery embolism, acute renal failure, peritonitis secondary to peritoneal dialysis, adult respiratory distress syndrome, acute panereatitis with pseudoeyst formation, and pseudoeyst rupture. Despite his prolonged course, the patient remained alert and neurologically intact and was discharged on the 96th hospital day. The patient was alive and well three years after the arrest without sequelae except for a mild left-sided limp.

DISCUSSION

Prognosis in cases of prolonged cardiac arrest is uniformly dismal. 33 Our patient remained in ventrieular fibrillation for 62 minutes despite treatment that included lidoeaine, bretyllium, and other advanced cardiac life support (ACLS) measures (Table). The rationale for dev.iations from Advanced Cardiac Life Support guidelines is unclear. Our patient was defibrillated successfully from ventricular fibrillation after administration of 4 g magnesium sulfate IV.

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It is possible that prehospitax resuscitation was unsuccessful because the actual energy delivered by the prehospital defibrillator was inadequate. This may have occurred given the fact that this patient weighed 104 kg. On the other hand, the paramedics indicated no evidence of defibrillator malfunction, as the patient's movement suggested grossly that an adequate shock was delivered. Several studies have reported differences between selected and delivered defibrillation energies.34, 35

between the administration of magnesium sulfate and successful defibrillation. A pretreatment magnesium level was not obtained during resuscitation. The patient was receiving chronic diuretic therapy for hypertension. Thiazide and loop diuretics have been associated with potassium and magnesium deficiencies, arrhythmias, and sudden death) 8'36 Other causes of magnesium deficiency that did not affect this case include digoxin and aminoglycoside therapy, alcoholism, advanced age, diabetes, and malabsorption. 37'38

Other factors also may alter the outcome of defibrillation, such as paddle size, paddle placement, and type of conductive medium used. These factors were not known to differ significantly between prehospital and ED defibrillations. It is possible that successful resuscitation was a result of previously administered medications. However, an unsuccessful countershock was delivered 56 minutes after arrest. The successful eountershock was delivered at 19, 17, and 12 minutes after the last doses of lidoeaine, bretyllium, and epinephrine, respectively. Magnesium sulfate was administered at 62 minutes after arrest, and successful defibrillation followed at 64 minutes after arrest (Table). This sequence suggests a causal relationship

Recent development of automated methods for determination of serum magnesium levels has made this test widely available in the clinical setting. Hypomagnesemia is seen in 10% to 20% of hospitalized patients and in 30% to 50% of patients with hypokalemia or hyponatremia. 39 However, the value of sermn magnesium levels has been questioned. Empiric magnesium therapy frequently has been effective in patients with normal serum magnesium levels. 19 Cardiac, muscle, RBC, and mononuclear cell assays have demonstrated that intracellular magnesium depletion may exist in the presence of normal serum magnesium levels. 27,4°'41 Because magnesium is the second most concentrated

intraeellular cation (after potassium) and only 1% of the total body magnesium content is located in the extraeellular space, intraeellular magnesium content is a more relevant measure of magnesium homeostasis than serum magnesium level. Several mechanisms have been proposed to explain the effects of magnesium on cardiac rhythm. These center chiefly on magnesium's interactions with the sodiumpotassium pump or with cell membrane channels. Magnesium is a eoenzyme for membrane-bound sodiumpotassium adenosine triphosphatase (the sodium-potassium pump). Magnesium deficiency may inhibit pump function and cause a loss of cellular potassium, leading to a decreased intraeellnlar-toextracellular potassium ratio. This decreases the resting membrane potential and leads to increased Purkinje fiber excitability with consequent arrhythmia. 42 Similarly, digoxin inhibits the sodiumpotassium pump, and magnesium deficiency would thereby tend to promote digoxinrelated arrhythmias, n'12 The antiarrhythmie effects of magnesium may be due to blockage of slow calcium channels ¢3 or facilitation of flow through the inward rectifying potassium channel, which is responsible for maintaining the normal rest- I1~

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ing membrane potential. 44'45 On an electrophysiologie basis, magnesium has several

magnesium levels near 10 mEq/L. ¢8 One potential adverse side

actions: Magnesium prolongs atrioventrieular conduction time, action potential duration, and the effective refractory period in rabbit hearts, and magnesium increases the energy required to induce premature ventrieular contractions and ventricular fibrillation in dogs. 46

effect of magnesium administration in the cardiac arrest patient is vasodilatation. In cardiac arrest, peripheral vasoconstriction secondary to epinephrine administration has been shown to result in increased cerebral and myocardial blood flow and improved survival. 49,5° The

It is unknown whether magnesium is effective only because it repletes an intra-

significance of the vasodilating properties of magnesium at the doses used and magne-

cellular or extracellular magnesium deficiency or because of some intrinsic antiarrhyth-

sium's interactions with other drugs administered in the setting of cardiac arrest are unknown. In addition to the return of a perfusing rhythm after more than 60 minutes of cardiac arrest, it is also significant that our patient regained normal neurologic function. In a study of neurologic recovery after cardiac arrest, patients in whom CPR was begun within six minutes but had a total CPR time of more than 30 minutes had only a 3%

mie property irrespective of magnesium levels. The optimum antiarrhythmie dose of magnesium sulfate is unknown. We used a 4-g bolus based on the low incidence of side effects of this dose when used in patients with preeclampsia or eelampsia. 47 This is similar to doses used by other authors. 6'8'23-27'3° Furthermore, in a 70-kg patient, a dose of 4 g magnesium sulfate (32 mEq) would be expected to raise serum magnesium levels less than 2.5 mEq/L. This is well below the levels at which major toxicity has been reported. Deep tendon reflexes cease at magnesium levels of more than 6 mEq/L. Vasodilatation, central nervous system depression, respiratory paralysis, and abnormal cardiac conduction may be seen as

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chance of good neurologic recovery,st It is possible that administration of magnesium may have had a beneficial effect in cerebral resuscitation. However, this patient probably maintained adequate cerebral blood flow during CPR (as evidenced by pupillary responsiveness in the ED). This may have been the most important factor for our patient in regaining normal neurologie function.

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Brain injury during and after isehemia is thought to be the result of two phenomena: decreased cerebral blood flow secondary to vasospasm and release of toxic substances within the neuronal cells. 52 During isehemia, the sodiumpotassium pump fails, causing efflux of potassium and intracellular accumulation of sodium and calcium. This may cause vasospasm, uncoupling of oxidative phosphorylation, and generation of superoxide radicals and other substances toxic to brain tissue. 5a Magnesium is a physiologic calcium antagonist. 4z White et al demonstrated that magnesium administration in a dog model prevented cerebral hypoperfusion during the first 90 minutes after resuscitation. 5¢ Administration of magnesium may block calcium channels in brain tissue and prevent subsequent vasospasm and generation of toxic intracellular mediators. For our patient, the mechanism by which magnesium administered late in the resuscitation could block intracellular calcium accumulation is unclear. Of course, continued calcium leakage into the cell during reperfusion may be blocked by magnesium administration. Likewise, magnesium may interfere with calcium-mediated reactions that occur during reperfusion.

SUMMARY We report the case of a patient with ventricular fibrillation refractory to standard therapy who was resuscitated successfully after administration of magnesium sulfate. The patient recovered and was discharged from the hospital neurologically intact despite 64 minutes of cardiac arrest. Advanced Cardiac Life Support protocols for the treatment of ventrieular fibrillation recommend the use of sequential countershock, epinephrine, lidocaine, and bretyllium and the consideration of sodium bicarbonate. Magnesium sulfate is an antiarrhythmic agent that has been reported to be effective in a number of cases of serious ventrieular arrhythmias resistant to these medications. It has also been suggested that magnesium may alleviate "reperfusion injury." The use of magnesium sulfate should be considered in the treatment of refractory ventrieular fibrillation. Controlled studies of the use of magnesium in cardiac and cerebral resuscitation should be undertaken. []

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Address for reprints: Glenn A Birnbaum, MD, Morristown Memorial Hospital, 100 Madison Avenue, Morristown, New Jersey 07960.

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