groups with respect to calcium chloride administrations. They fail, however, to point out the weaknesses in statis-

tically comparing a group of 105 patients in asystole receiv- ing calcium to 24 patients not given calcium (Table 2). In fact, the authors do not mention whether tests of statistical power have been applied when comparing variables be- tween the two groups. Yet one can imply a statistically sig- nificant difference when 15% (16/105) of the calcium pa- tients had previous MIs compared to 8% (2/24) of the no-calcium group. Also, a considerably greater number of calcium patients in asystole took diuretics (14%) and digi- talis (7%) compared to 4% and 0% respectively in the no- calcium group. Are these differences considerable enough to skew the data so that the calcium patients had mor¢ severe coronary artery disease, and thus a greater mortality? Is coronary artery disease a confounding variable between the two groups?

Table 2 poses another question. Seven (29%) of the asystolic patients not given calcium are categorized under "Cardiac drugs: More than one above," yet only one patient received one of the three drags listed. Can the authors ex- plain this discrepancy?

If coronary artery disease is indeed a confounding factor, that is, the asystolic patients receiving calcium had more severe coronary artery disease than those who received no calcium, then the validity of the authors' conclusions is seriously jeopardized. Can the authors convincingly defend their conclusions?

Carlotta M Rinke, MD Emergency Department Glendale Heights Community Hospital Glendale, Illinois

To the Editor: American Heart Association guidelines for the resuscita-

tion of patients in asystole or EMD have long included cal- cium chloride. Yet little scientific evidence of its efficacy for these rhythms exists. In fact, recent evidence suggests that it may reduce the likelihood of a successful outcome. Car- diopulmonary resuscitation is often followed by coma or permanent brain damage. 1'2 This may be in part due to cere- bral vasospasm and neuronal death caused by a rapid cellu- lar influx of calcium during periods of global ischemia. 3 Cal- cium blockers may prevent this influx and in this way pro- tect the brain from anoxic insult. 4

Thus the conclusion of Stueven et al that the use of cal- cium in cardiopulmonary resuscitation is highly suspect is supported by others. However, their study does not provide valid support for this view. Successful resuscitation rates of 33% and 44%, respectively, for asystole and EMD are very high compared to rates reported by others ~ (Roth R, et al: Unpublished observations). The authors attribute this to the withholding of calcium. The assumption is made, however, that the medical command physician ordered calcium for the involved cardiac arrest victims on a random basis. This key assumption is supported by rather weak arguments and is scientifically untenable. The authors write, for example, that calcium was not used as a "last resort" because the

12:11 November 1983

time at which it was given was significantly earlier than the total length of resuscitation in either group. The fact that calcium was used relatively early does not imply that no selective process was involved. It is more likely that the decision to use calcium was based on a number of factors, including initial response to therapy other than calcium and the physician's perception of the patient's prognosis.

It is important to determine calcium's value in cardiac arrest. An adequately randomized prospective study is needed. It is through the accumulation of reliable methodo- logically sound data based on such studies that emergency medicine will continue to grow.

James Hawkins, MD, Resident University of Pittsburgh Affiliated Residency in Emergency Medicine

1. Rockswold G, Shrama B, Ruiz E, et al: Followup of 514 con- secutive patients with cardiopulmonary arrest outside the hospital. JACEP 8:216-220, 1979.

2. Myerburg RJ, Conde CA, Sung RJ, et al: Clinical electro- physiologic and hemodynamic profiles of patients resuscitated from prehospital cardiac arrest. Am J Med 68:568, 1980.

3. Gadzinski DS, White BC, Hoehner PJ, et al: Alterations in canine central cortical blood flow and vascular resistance post cardiac ar- rest. Ann Emerg Med 11:58-63, 1982.

4. White B, Gadzinski DS, Hoehner pJ, et al: Effect of flunarizine on canine cortical blood flow and vascular resistance post cardiac ar- rest. Ann Ernerg Med 11:119-126, 1982.

5. Iseri LT, Siner EJ: Prehospital cardiac arrest after arrival of the paramedic unit. JACEP 6:530-534, 1977.

To the Editor: Retrospective studies with complex variables certainly re-

quire close scrutiny. The scientific communi ty implies that a statist ically significant difference exists if a P value obtained by appropriate statistical method is less than .05. Statistical comparison of successful resuscitation rates in patients given calc ium vs no ca lc ium yield P < .002, suggesting that the likelihood that the relationship is due to chance is less than 2/1,000. The differences of each of the listed variables were compared for statistical significance and found not to be significant.

Dr Rinke is correct in noting a trend in the variables; however, for the variables:

No Calcium Calcium P value

Significant Cardiac History MI 16/105 2/24 .77

Cardiac Drugs Diuretics 15/105 1/24 .2

Digitalis 7/105 0/24 .25

Consequently, our conclusion stands and the caption for Table 2 summarizes "there is no significant difference be- tween the calcium and no-calcium groups."

The question of whether coronary artery disease is a c o n -

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