Clinical Pearl 73: Should We Pretreat with IV Calcium When giving CCBs for Stable Afib with RVR

Calcium channel blockers have long been an accepted treatment of hemodynamically stable Afib with RVR.  For those patients with borderline blood pressures or for those patients who are especially responsive to the antihypertensive effects of calcium channel blockers, there are few options available to prevent a hypotensive response. 

L Type calcium channels are present in the vascular smooth muscle, mycardium, conducting system of the heart, and in the pacemaker cells of the SA and AV nodes.  Of the calcium channel blockers available for clinical use, dihydropyridines require a much higher serum concentration to achieve electrophysiological activity than the concentration needed to achieve potent vasodilation, so their application in cases requiring negative chronotropy are limited especially with their propensity for inducing a concomitant sympathetic response via the baroreceptor reflex pathway. The non-dihydropyridines, (e.g. verapamil and diltiazem) exert their effects on the L-type channels in the pacemaker cells and conducting system of the SA and AV nodes at much lower concentrations, and are therefore useful for any supraventricular arrhythmia requiring reduced frequency of conduction through the AV node.  This is the basis of choosing these drugs for the treatment of hemodynamically stable Afib with RVR.

Of the two non-dihydropyridines, both can result in hypotension via their action on the vascular smooth muscle, but diltiazem to a much lesser degree than verapamil.  When treating a patient with RVR, there is still a recognized risk to causing hypotension, and aside from the strategies of slowing the infusion rates of calcium channel blockers, or by administering fluid boluses, one thought is to pretreat the patients with intravenous calcium.  The thought arises from the treatment of calcium channel blocker toxicity which involves among other things, giving calcium chloride or calcium gluconate to overwhelm the receptor blocking effect of the drugs.   The question we explore here is whether pretreating with intravenous calcium when giving non-dihydropyridine calcium channel blockers actually works to prevent or mitigate hypotension.

The literature available on this topic is mainly from the 1980s and 1990s and focused completely on verapamil, except for one study in 2004 which looked at pretreatment with IV calcium for diltiazem.    All studies had a small N of 50 or less participants, and ranged from case series, to retrospective, prospective, and finally a prospective, randomized, double-blind, placebo-controlled study for diltiazem.  Each study and their findings are summarized in the references below. 

The summation of data support pretreatment with calcium when using verapamil to prevent hypotension without mitigating the desired rate control effect.  In contrast, the one study on diltiazem did not show a significant difference between either treatment arm.  The paper does not support routine use of intravenous calicum as pretreatment to prevent hypotension.  Until further research is performed with diltiazem, perhaps the prudent course would be to continue using IV fluid boluses for borderline blood pressure while keeping IV calcium ready for treatment in the case of diltiazem induced hypotension.  However this guideline is not supported by good evidence.  See below for a review of the literature

References and Results

1. Weiss AT, et al. Int J Cardiol 1983; 4:275-84.

Prospective study design,     N = 13, Verapamil, Ca gluconate 1 gm;                     Result: SBP ↑ 5 mmHg

2. Roguin N, et al. Clin Cardiol 1984; 7:613-6.

Case series                             N = 2,  Verapamil, Ca gluconate(peds);                   Result: No hypotension

3. Haft JI, et al. Arch Intern Med 1986; 146:1085-9.

Sequential study of                N = 50, Verapamil, CaCl 1 gm,                                   Result: SBP ↑ 2 mm Hg

2 treatment protocols

4. Salerno DM, et al. Ann Intern Med 1987; 107:623-8.

Sequential study of                N = 5,  Verapamil, Ca gluconate 1 gm                      Result: SBP ↓ 12 mmHg

2 treatment protocols

5. Stringer KA, et al. Drug Intell ClinPharm 1988; 22:575-6.

Case report                            N = 1,  Verapamil,  CaCl 1 gm,                                  Result: No hypotension

6.  Barnett JC, et al. Chest 1990; 97:1106-9.

Prospective report of protocol        N = 19, Verapamil, Ca gluconate 1 gm or CaCl 1 gm,           Result: SBP ↑ 4 mm Hg

7. Kuhn M, et al. Am Heart J 1992; 124:231-2.

Retrospective chart review  N = 18, Verapamil, Ca gluconate 3 gm or CaCl 1 gm,           Result: No hypotension

8. Miyagawa K, et al. J Cardiovasc Pharmacol 1993; 22:273-9.

Sequential study of                N = 7,  Verapamil, Ca gluconate 3.75 mg/kg,          Result: SBP no change

2 treatment protocols

9. Kolkebeck T, et al. J Emerg Med 2004; 26(4):395-400.

Prospective, randomized,     N = 34, Diltiazem, CaCl 0.333 gm                  Result: SBP ↓ 8  vs ↓ 14mmHg

double-blind, placebo-controlled                           

Clinical Pearl 75: Prehospital Traumatic Arrests

Traumatic cardiopulmonary arrests are rare compared to nontraumatic arrests but are still the fifth leading cause of the death in the United States.

In 2007, Gonzalez et al evaluated MVC traumatic arrests looking at response, scene, and transport times.  On average, rural trauma mortalities increased when EMS spent more than 10 minutes getting to a scene, 18 minutes on scene, and 12 minutes getting to a hospital.  Similar effects were found in urban areas when EMS spent more than 6 minutes getting to a call, spent more than 10 minutes on scene, and when transport took more than 7 minutes.

In McCoy et al. 2013 study performed in Orange County California, blunt and penetrating trauma were evaluated to determine whether on scene time vs. transport time mattered more.  On scene time was more significant in traumatic deaths than transport time to hospitals.  Additionally, when on scene times were 20 minutes or more, risk of death increased.  If providers spent less than 10 minutes on scene in urban penetrating traumas, patients had a better survival rate.  They acknowledged limitations, such as being unable to account for paramedic experience in evaluating injuries, excluding patients needing extrication, and not looking at long term survival rates.

Brown et al. evaluated blunt and penetrating traumas from 2000-2013 and found the only time interval that was associated with mortality in blunt or penetrating traumas was prolonged scene time.  Extrication and intubation were the two most important contributing factors for mortality. Hypotension, penetrating trauma, and flail chests were associated with mortality but not to the extent of extrication and intubation.  Contrary to other studies, longer transport times to trauma centers vs the closest hospital were actually not predictive of mortality.  They proposed it was because the longer transport time was balanced by the wider availability of services at trauma centers. 

           

In 2013, NAEMSP and ACSCOT put out new guidelines on prehospital care of blunt and penetrating trauma. 

• Narrow complex PEA with a normal or tachycardic rhythm - Initiatiate resuscitation; if code lasts more than 10 minutes - termination of resuscitation (TOR)

• Asystole or wide complex bradycardic PEA of less than 40 – TOR

Support is still given for treating easily reversible causes of traumatic arrest with needle decompression and hemorrhage control, despite a study showing an increase in mortality for every EMS procedure performed, as the potential benefits of emergent intervention are high for the relative time spent.
In the case of direct medical oversight, suggestions are to establish a standardized protocol instead of reporting to medic control because reporting may take time away from the patient and delay prompt transport of the patient to a trauma center.

There appears to be a time and place for CPR for traumatic arrests, but it should not last longer than 10 minutes and not be initiated in those in asystole or bradycardic PEA.   One must weigh the amount of time spent on scene performing procedures, such as intubation, against the benefits of surgical intervention available at hospitals.  If a provider can stabilize the patient with a fast, easily performed procedure such as placement of a tourniquet and needle decompression, the benefits are real; but if the patient can be oxygenated and ventilated without risking a prolonged intubation, consider transporting the patient instead. 

Sources:

Brown JB1, Rosengart MR, Forsythe RM, Reynolds BR, Gestring ML, Hallinan WM, Peitzman AB, Billiar TR, Sperry JL. Not all prehospital time is equal: Influence of scene time on mortality.  J Trauma Acute Care Surg. 2016 Jul;81(1):93-100.

Gonzalez RP, Cummings GR, Phelan HA, Mulekar MS, Rodning CB. Does increased emergency medical services prehospital time affect patient mortality in rural motor vehicle crashes? A statewide analysis. Am J Surg. 2009 Jan;197(1):30-4.

McCoy CE, Menchine M, Sampson S, Anderson C, Kahn C. Emergency medical services out-of-hospital scene and transport times and their association with mortality in trauma patients presenting to an urban Level I trauma center.  Ann Emerg Med. 2013 Feb;61(2):167-74.

Merlin, M.  Destination procedures for traumatic cardiac arrest. MONOC clinical standard of practice.  2008, May.  Reviewed 2016, April.

Millin MG, Galvagno SM, Khandker SR, Malki A, Bulger EM; Standards and Clinical Practice Committee of the National Association of EMS Physicians (NAEMSP); Subcommittee on Emergency Services–Prehospital of the American College of Surgeons’ Committee on Trauma (ACSCOT).  Withholding and termination of resuscitation of adult cardiopulmonary arrest secondary to trauma: resource document to the joint NAEMSP-ACSCOT position statements.  J Trauma Acute Care Surg. 2013 Sep;75(3):459-67.