Calcium Channel Blocker Toxicity Treatment & Management

Updated: Mar 25, 2021
  • Author: B Zane Horowitz, MD, FACMT; Chief Editor: Michael A Miller, MD  more...
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Approach Considerations

Basic supportive care is the first, and possibly most important, mode of management for calcium channel blocker (CCB) toxicity: Establish and secure the airway and breathing, and focus on preserving adequate circulation (ABCs). Crystalloid fluid boluses can be given, and atropine for symptomatic bradycardia. [21] Correction of acid-base disturbances and electrolyte abnormalities is also important, to optimize cardiac function.

Because CCB blood concentrations are generally not available with any reasonable turnaround time, treatment must be instituted on the basis of signs and symptoms. Blood concentrations can be used to confirm the diagnosis if it is in doubt. [22, 23]

Activated charcoal has been demonstrated to significantly adsorb immediate-release medications within 1 hour of ingestion and extended-release medications as long as 4 hours after ingestion. [4] Before administration of activated charcoal, protect the patient's airway to prevent vomiting and aspiration.

In addition, extended-release tablets have a delayed onset of up to 12-24 hours; therefore, prematurely releasing a patient who has ingested an extended-release tablet from emergency or intensive care observation places him or her in jeopardy.

Admit all patients with CCB ingestion to ICU monitoring for 6-12 hours in cases of standard-release preparation overdose, and for 24-36 hours in cases of extended-release or once-a-day preparation overdose. In cases of intentional overdose, patients who remain asymptomatic after an adequate observation time may be referred for psychiatric evaluation.

Consult an American Association of Poison Control Centers–certified regional poison control center in all cases to assist in management, because poisonings can be quite severe and dynamic and treatment is often complicated and multimodal. For those reasons, when patients are critically ill, besides the initial discussion with the certified specialist in poison information, request to speak with the medical toxicologist on call. When calling a poison control center, be prepared to give as much information as possible during the initial call. Estimate amount and type of drug ingested, elapsed time since ingestion, and time treatment was started.

Poison control centers can also provide monitoring guidelines for asymptomatic patients, according to the potency and onset and duration of action of the ingested CCB. Generally, however, the recommended duration of clinical observation for patients with significant exposure to CCBs is as follows [2, 3] :

  • Immediate-release products: 6 hours
  • Standard-release products: 6-12 hours
  • Extended-release or once-a-day preparations: 24-36 hours

Many poison control centers make follow-up calls to offer additional management recommendations and learn patient outcomes. The physician can supply additional information at that time.


Prehospital Management

Establish that the patient has adequate ABCs, obtain intravenous (IV) access, provide oxygen, and monitor closely. Rapid transport before the patient with calcium channel blocker (CCB) toxicity deteriorates is crucial.

Atropine may be tried if hemodynamically significant bradycardia occurs; however, infranodal heart block is usually resistant to atropine in CCB toxicity.

Empiric use of glucagon (adults: 5-15 mg IV) may be warranted for patients with an unknown overdose who present with bradycardia or hypotension.

Treat hypotension with fluid boluses of normal saline if no evidence of decompensated congestive heart (CHF) exists. Administer IV calcium gluconate (up to 4 g) or IV calcium chloride (1 g) and/or glucagon (5-10 mg) if hypotension persists. [24] If profound hypotension fails to respond to fluid resuscitation and/or if a long transport time is likely, administer a norepinephrine drip, if permitted by local prehospital care protocols.

If the patient deteriorates to cardiac arrest from a CCB overdose, perform prolonged cardiopulmonary resuscitation (CPR) in the field. Patients with CCB overdose have survived neurologically intact after 1 hour of CPR. Consideration should be given for a bolus dose of intralipid emulsion.

Administer activated charcoal (AC) if the patient's airway is protected.


Emergency Department Management

Basic overdose management includes airway protection, gastric lavage, and activated charcoal. Patients who are hemodynamically stable who have taken extra doses of their own medication can be monitored in observation units, if available to the emergency department (ED). Adequate intensive care unit (ICU) capabilities must be present in the observation unit, because these patients may require intubation, pacemaker placement, or vasopressor support. Large and intentional overdoses should always be managed in an ICU.

Only asymptomatic patients should be watched in an observation unit. If manifestations of cardiac depression occur, transfer the patient to an ICU setting with the capacity for advanced cardiac life support (ACLS), including tracheal intubation and cardiac pacing.

Aggressive cardiovascular support is necessary for managing massive calcium channel blocker (CCB) overdose. Although calcium (gluconate or chloride) in high doses (4-6 g) may overcome some of the adverse effects of CCBs, it rarely restores normal cardiovascular status. According to case reports, glucagon has been used with good results in some cases. However, vasopressors are frequently necessary for adequate resuscitation and should be started early if hypotension occurs. [25] Dopamine may be used for isolated bradycardia, but hypotensive patients should preferentially have direct vasopressors such as norepinephrine.

Hyperinsulinemia euglycemia treatment (1 unit/kg bolus of regular insulin with 0.5 g/kg dextrose push followed by 0.5–1 unit/kg/hr of regular insulin with concomitant dextrose drip) may improve circulatory shock in CCB overdose patients. Early institution of this therapy may be useful, as the onset of benefit is delayed. Both glucose and potassium levels should be frequently monitored in patients receiving this treatment and potassium should be replaced if the level falls below 3 mmol/L [21, 26]


Indications for Inpatient Evaluation

Inpatient evaluation is indicated for patients who have ingested calcium blockers above a certain amount. [24] See Table 1, below. Co-ingestants must be taken into account; these amounts assume isolated unintentional ingestion of only the calcium-blocking med.ication

Table. Recommendations for In-hospital Evaluation Based on Drug and Dosage of Calcium Channel Blocker Ingested (Open Table in a new window)


Adult Dosage

Pediatric Dosage


>10 mg

>0.3 mg/kg


>120 mg immediate-release formulation; >360 mg sustained_release formulation

>1 mg/kg


>10 mg

>0.3 mg/kg


>20 mg

>0.1 mg/kg


>40 mg immediate release; >60 mg sustained-release

>1.25 mg/kg


>30 mg immediate-release; >120 mg sustained-release

Any amount


>60 mg

Any amount


>30 mg

Any amount


>120 mg immediate-release; >480 mg sustained-release

>2.5 mg/kg


Gastrointestinal Decontamination

Gastrointestinal (GI) decontamination may be considered because calcium channel blockers (CCBs) slow gastric motility and delay gastric emptying. Options include activated charcoal, gastric lavage, and whole-bowel lavage.

Activated charcoal

Activated charcoal has been demonstrated to significantly adsorb immediate-release medications within 1 hour of ingestion and extended-release medications as long as 4 hours after ingestion. [4] If the ingested dose is known, a 10:1 charcoal-to-drug weight ratio can be used to calculate the optimal dose of activated charcoal to completely bind the ingested drug. [27] Otherwise, a 1-g/kg initial dose is recommended.

The potential benefit of decreased drug absorption must be weighed against the risk of gastric distention with subsequent aspiration. Any conditions predisposing to aspiration (eg, altered mental status, nausea, seizures) are contraindications to administration of activated charcoal. In patients with severe toxicity, interventions such as antiemetics and intubation with satisfactory sedation should be performed before administration of activated charcoal via a nasogastric tube.

Gastric lavage

Gastric lavage is especially important for patients who may have taken a large dose of medication or for those who have ingested sustained-release preparations.

However, the usefulness of gastric lavage is still debated. Weigh the risk of aspiration against the probability of removing undigested medications remaining in the stomach. Placement of an endotracheal tube before performing the lavage protects the airway and reduces the risk of aspiration.

If gastric lavage is performed, use a large-bore orogastric hose. Sustained-release tablets, which are large and resistant to breakdown, may not fit through a simple Salem sump nasogastric tube.

Whole-bowel irrigation

If a patient has ingested a large number of CCB tablets, especially sustained-release tablets, the pills may aggregate to form bezoars and the drug can be continuously absorbed for long periods. In this situation, the clinician may consider whole-bowel irrigation with polyethylene glycol (PEG). In adults, administer PEG at a rate of 1-2 L/h for 4-6 hours or until rectal effluent becomes clear.

Whole-bowel irrigation is absolutely contraindicated if bowel sounds are absent. This suggests that an ileus, secondary to shock or drug toxicity, has occurred. In these circumstances, large volumes of intestinal fluid lead to massive bowel distention, risking bowel perforation.

Coadminister activated charcoal in a 1 g/kg initial dose; activated charcoal administration can be repeated every 4 hours at half the initial dose. Because gastric emptying may be delayed, activated charcoal may be considered even if the patient presents several hours after the ingestion.

In children, care must be used never to administer sorbitol-containing products, because of the potential to induce electrolyte disturbances. In the rare instance of large ingestion in a preschool-age child, whole-bowel irrigation with PEG solution (Go-Lightly) may be used.


Treatment of Hypotension

Blood pressure can be augmented with isotonic sodium chloride solution or Ringer lactate solution. Both are efficient volume expanders. Deliver fluid in 20-mL/kg boluses in children or 1-L boluses in adults. These may be repeated once, twice, or even three times if the patient remains hypotensive. Bedside ultrasound assessment of inferior vena cava size may guide adequate volume replacement. If blood pressure normalizes with fluid challenges, infuse IV fluid at 1-2 times the normal maintenance rate.

However, vasopressors are frequently necessary for adequate resuscitation and should be started early if hypotension occurs. [25]


Calcium Therapy

Calcium can be administered intravenously to patients who present with symptomatic hypotension or heart block. [5, 6, 7] High-dose calcium theoretically creates a concentration gradient large enough to partially overcome the channel blockade, driving calcium into the cells. Calcium is usually administered as calcium gluconate or calcium chloride. Calcium chloride is sclerosing to veins so should be avoided in children, and it should be used in adults only in a larger, free-flowing IV line. Calcium chloride has 4 times the calcium content as calcium gluconate.

Calcium gluconate, 30 mL of 10% solution, can be administered IV over 10-15 minutes in adults. The recommended pediatric dose of calcium gluconate is 60 mg/kg, with a maximum dose of 1 g. [8] Calcium chloride (1-4 g) is preferably given via central line, slowly. The bolus can be repeated, or a slow calcium infusion (eg 20-50 mg/kg/h) can be implemented.

Calcium gluconate boluses may be repeated every 15-20 minutes, if the response to the initial bolus begins to diminish, for a total of 3 doses. After the third bolus, the ionized calcium level should be checked. In cases of severe calcium channel blocker toxicity, serum calcium concentrations have been titrated to 1.5-2 times the upper limit of normal, leading to improved cardiac function.


Glucagon Therapy

Glucagon promotes calcium entry into cells via stimulation of a receptor that is considered to be separate from adrenergic receptors. Note that the actions of glucagon oppose those of insulin, yet both have beneficial effects in treating CCB toxicity.

Glucagon is supplied as a lyophilized powder and must be reconstituted. Some manufacturers include an ampule of propylene glycol that can be used for single injections. However, the administration of large amounts of propylene glycol (the same diluent that is used for phenytoin) causes hypotension and dysrhythmias.

For this reason, glucagon infusions and repeat doses should be reconstituted in D5W to avoid giving large amounts of propylene glycol. If a positive clinical effect is noted after an initial IV bolus dose of 5-10 mg, an infusion can be continued at 5-10 mg/h. Note that such high-dose usage of glucagon exhausts a typical hospital pharmacy's supply within a few hours.

Administer glucagon (5-10 mg IV bolus up to 15 mg, followed by an infusion) after fluid resuscitation is performed for persistent hypotension. Since glucagon dilates the lower esophageal sphincter, vomiting and aspiration may occur; therefore, this treatment should only occur in an awake patient who can protect his or her own airway if vomiting occurs. Pretreatment with an antiemetic and large-bore bedside suction should be used. If an initial bolus of 5 mg of glucagon has no effect on blood pressure, it is reasonable to double the dose. The recommended infusion rate for adults is 5-10 mg/h. The recommended pediatric dose is 50 mcg/kg IV over 5 minutes, followed by an infusion at 0.07 mg/kg/h. [28, 29, 30, 31, 32, 33, 34, 35]


Vasopressor Therapy

If volume expansion does not raise the blood pressure to the desired level, vasopressors (eg, norepinephrine, epinephrine) can stimulate myocardial contractility and cause vasoconstriction, thus supporting blood pressure and cardiac output. In the hypotensive and bradycardic patient, administer dopamine initially at medium-to-high doses early to support the heart rate. Failure to respond to the maximal dose of dopamine should prompt the addition of norepinephrine.

Various combinations of dopamine, norepinephrine, epinephrine, phenylephrine, vasopressin, and metaraminol have all been used in cases of hypotension and shock. [1, 2, 33, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45] Inamrinone, a phosphodiesterase inhibitor with inotropic activity, may be of additional benefit in profound cardiac contractile failure. [34, 42, 46] Bedside cardiac echocardiography may help distinguish cardiogenic shock form vasodilatory shock.


Insulin Therapy

High-dose insulin has become accepted as therapy in calcium channel blocker (CCB) toxicity refractory to standard vasopressor therapy. [47] Hyperglycemia may occur in CCB toxicity, as calcium channel blockade inhibits insulin release. [20, 48, 48] Although no human trial has been completed, animal models and numerous case reports and case series demonstrate that high-dose insulin increases inotropy, increases intracellular glucose transport, and improves vascular dilation in CCB toxicity. [41, 49, 6, 50, 51, 52, 53, 54, 55, 56, 57, 58]

High-dose insulin therapy is administered as follows: infuse one ampule of 50% dextrose in water (D50W), then give an insulin bolus of 1 U/kg, followed by an infusion of regular insulin at 1-10 U/kg/h. Remarkably, patients with CCB toxicity who receive this therapy rarely require more supplemental dextrose than a D5W infusion. However, their serum potassium and glucose levels should be monitored every 20-30 minutes.

High-dose insulin therapy has a delayed onset of action. Consequently, it should be started soon after the patient presents with refractory hypotension.

High-dose insulin euglycemia (HIE) guidelines


Hypodynamic shock due to calcium channel antagonist (CCB) or beta-blocker (BB) toxicity:

  • HIE is most effective when there is evidence of depressed myocardial activity
  • HIE can be considered for use alongside other pharmacological measures for CCB toxicity (intravenous fluid, calcium, glucagon, dopamine, or norepinephrine)


Only in a critical care area of the hospital (ED or ICU) owing to unstable hemodynamics associated with CCB toxicity, frequent requirements for central IV access/monitoring, and frequent glucose monitoring


Initial insulin bolus to saturate insulin receptors and assure adequate glucose availability:

  • 1 unit/kg regular human insulin IV
  • 1 amp (25 g) D50 IV: May hold if blood glucose >400 mg/dL (22.24 mmol/L)

Continuous infusion:

  • Insulin infusion: A rapid insulin infusion bag can be created by adding 500 U regular human insulin to 500 mL normal saline (1 U/mL). Ideally, a concentrated insulin infusion bag (10 U/ml) should be used to decrease fluid overload, since very large quantities of insulin may be needed. Start infusion at 0.5 U/kg/h with an infusion pump to avoid iatrogenic insulin overdose. Reassess cardiac function and blood pressure every 15-30 minutes. Increase infusion to 1-2 units/kg/h if there is no improvement after 30 minutes.
  • Dextrose infusion: 0.5 mg/kg/h dextrose IV as D5 (5 g of dextrose per 100 mL), D10 (10 g of dextrose per 100 mL), or D25 (25 g of dextrose per 100 mL). Titrate to maintain blood glucose of 100-200 mg/dL. Initial dextrose infusion requirement may vary depending on the patient's initial blood glucose level and the presence of underlying diabetes; higher concentrations of dextrose (ie, D25 and D50) must be administered via a central IV line, due to local issue irritant effects of concentrated dextrose solutions.


  • Bedside echocardiogram (ultrasound) for myocardial function: Ideally prior to HIE therapy, if possible; 30 minutes after initiation of HIE, if possible; 30 minutes after every dose increase, if possible
  • Continuous automated blood pressure monitoring
  • Foley catheter
  • Serial physical examinations, especially neurological status
  • Blood glucose finger-stick monitoring: Every 15-30 minutes until consistently 100-200 mg/dL for 4 hours, then every hour
  • Serum potassium : Every 1 hour
  • Lactic acid levels prior to Insulin then 1 hour after infusion

Therapeutic goals:

  • Normal myocardial ejection fraction (50%)
  • Blood pressure consistently higher than 90 mm Hg systolic
  • Improved mental status
  • Urine output 1-2 mL/kg/h
  • Decreased use of concomitant vasoactive drugs



  • It generally takes approximately 30 minutes to see effects from HIE.

  • No ceiling dose of insulin has been established; the usual titration range is 0.5-2 units/kg/h.

  • While cases have shown improved heart rate and conversion from heart block to sinus rhythm in temporal relationship to HIE administration, the main beneficial effect is on myocardial function (ie, ejection fraction and cardiac output), with subsequent improvement in blood pressure and perfusion.

  • Mean duration of insulin therapy is 31 hours (range, 1-96 h).


  • Most patients with CCB toxicity present with hyperglycemia and their initial glucose requirements to maintain euglycemia are minimal (due to insulin resistance); however, as organ perfusion improves, the offending drug is metabolized, and insulin resistance abates, dextrose requirements increase.

  • The mean maximum dextrose requirement is 24 g/h (range, 0.5-75 g/h).
  • Mean duration of dextrose infusion is 46 hours (range, 12-100 h)

  • Exogenous dextrose is often required even after insulin infusion is stopped

  • Intubated patients are at greatest risk of undetected hypoglycemia since they cannot demonstrate typical signs of hypoglycemia, and bedside fingerstick glucose should be checked every 15-30 minutes


  • Falling serum potassium levels during HIE represent a shift of potassium from the extracellular to intracellular compartments, not a loss; however, replacement to potassium concentration greater than 2.8-3 mEq/L should occur


Investigational Therapies

Treatments that have been used in refractory cases of calcium channel blocker (CCB) toxicity include the following:

  • Methylene blue [59, 60]
  • Lipid emulsion therapy [61, 62, 63, 64, 65]
  • 4-Aminopyridine and 3.4 diaminopyridine
  • Levosimendan

Methylene blue

Experimental use of methylene blue in distributive shock has prompted its consideration in calcium channel blocker overdose with cardiogenic shock. Case reports describe successful use in CCB overdose refractory to other therapies, at a starting dose of 1–2 mg/kg IV. [59, 60]

Lipid emulsion therapy

Lipid emulsion therapy (eg, Intralipid) has been studied in a few animal models of verapamil toxicity, demonstrating increased survival. [63, 66] Case reports have found either clinical improvement [61, 67] or significant drug sequestration. [68]

The therapeutic effect of lipid emulsion therapy is most commonly ascribed to the "lipid sink" theory, which posits that the lipid emulsion bolus sequesters lipophilic drugs from their target site, mitigating toxicity. Verapamil is quite lipophilic and thus is theoretically amenable to lipid emulsion therapy. [69] One case report demonstrated significant drug sequestration in a verapamil overdose, but uncertain clinical benefit. [68]

Lipid emulsion therapy can be considered as an antidotal therapy of last resort in calcium channel blocker overdose. Currently, the American College of Medical Toxicologists states that "in circumstances where there is serious hemodynamic, or other, instability from a xenobiotic with a high degree of lipid solubility, lipid resuscitation therapy is viewed as a reasonable consideration for therapy, even if the patient is not in cardiac arrest." [70]

For lipid emulsion therapy, a 20% lipid emulsion is administered initially as a 1.5-mL/kg bolus over 2-3 minutes, followed by an infusion of 0.25 mL/kg/min. The bolus may be repeated in patients who have recrudescent toxicity or cardiac arrest.

Lipid emulsion therapy guidelines

Lipid emulsion 20% should be given IV in the following dose regimen:

  • Lipid emulsion 20%: 1.5 mL/kg over 1 minute
  • Follow immediately with an infusion at a rate of 0.25 mL/kg/min
  • Continue chest compressions if patient is receiving cardiopulmonary resuscitation (CPR) (lipid must circulate)
  • Repeat bolus every 3-5 minutes, up to 3 mL/kg total dose, until circulation is restored
  • Continue infusion until hemodynamic stability is restored; increase the rate to 0.5 mL/kg/min if blood pressure declines
  • Maximum total dose of 8 mL/kg is recommended

4-Aminopyridine and 3.4 diaminopyridine

4-Aminopyridine and 3,4-diaminopyridine increase calcium entry into the cell. Their exact mechanism is not fully understood, but they may indirectly promote calcium entry by blocking voltage-sensitive potassium channels. Although these medications have reversed verapamil toxicity in feline, canine, and rabbit experiments, their value and safety in human calcium channel blocker toxicity has not been established. It cannot be recommended at this time for CCB toxicity.


Levosimendan (Simdax) is an investigational drug in the United States that acts intracellularly to sensitize myocytes to calcium by binding to cardiac troponin C but that does not increase intracellular calcium. [71] Therefore, it theoretically should help increase cardiac output while not altering the metabolic demands of the cell. It is thought to accomplish this by stabilizing the kinetics of actin-myosin cross-bridges. It also opens K+ channels, which leads to vasodilation, decreasing afterload to aid cardiac output in depressed myocardial states. It cannot be recommended at this time for CCB toxicity.



A transvenous pacemaker may be placed if the transthoracic cutaneous pacer fails to capture in the face of symptomatic bradycardia. Pacing may decrease the need for pressors in a patient who may not tolerate a positive cardiac inotrope because of cardiac ischemia, although this likely is not a concern for pediatric patients. Cardiac pacing is typically required for 12-48 hours.

Consider temporary placement of an intra-aortic balloon pump for hypotension that is refractory to all other medical treatments. Cardiopulmonary bypass can be a last resort to support the blood pressure long enough for the body to clear the ingested toxin. [72, 73]

Extracorporeal membrane oxygenation (ECMO) has also been attempted in patients who have hypotension refractory to all pharmacologic therapies. One case reported by Durward described a massive diltiazem ingestion (12 g Cardura CD) that resulted in prolonged cardiac standstill. [74] However, after 48 hours of ECMO and 15 days in the critical care unit, the patient made a very good recovery and was discharged home "fit and well," showing "no evidence of neurologic dysfunction."

Plasma exchange [75] and continuous renal replacement techniques with hemodiafiltration [76] have each been used in cases of severe poisoning resistant to aggressive medical treatments, such as patients failing glucagon and norepinephrine infusions. [72, 73, 75, 76] These cannot be recommended at this time for CCB toxicity.

Although CCBs are highly protein bound, some physicians believe that hemodialysis or charcoal hemoperfusion may be used as a last resort in severely toxic patients who have no other hope. In a case report of overdose with sustained-release diltiazem, however, charcoal hemoperfusion showed little efficacy. [77]


Diet and Activity

Do not allow patients with calcium channel blocker toxicity to eat after the ingestion, because they risk rapid mental status deterioration, including seizures, and may require intubation. Placement of an endotracheal tube when the patient has an empty stomach decreases the risk of aspiration. For these same reasons, do not administer ipecac syrup.

Orthostatic hypotension is a particular concern in patients who ingest calcium channel blockers. Limit the activity level of these patients to bed rest at the first clinical signs of calcium channel blocker toxicity.



Many different specialists can help the physician to care for a patient who has ingested a CCB.

Consult an American Association of Poison Control Centers (AAPCC)–certified regional poison control center, with a specific request to speak directly to a medical toxicologist, in all cases to assist in management, because several treatment options exist and each case is unique. Even if the ED personnel do not need care advice for the patient with CCB overdose, notify the hospital's regional poison control center to document the overdose characteristics and help create an accurate database for epidemiologic studies. In general, working in partnership with regional poison control centers on all ingestions is a good practice.

All hemodynamically unstable patients require prolonged care in an adult or pediatric ICU; arrange for consultation with this service soon after starting treatment in the ED. If the hospital does not have an appropriate ICU, critical care transport to a more specialized hospital should be considered sooner rather than later when severe toxicity has already developed.

Cardiologists may be necessary to manage hemodynamically unstable patients. Request consultation with a cardiologist to place a transvenous pacemaker if capture cannot be accomplished with transthoracic cutaneous pacing pads. Patients may require cardiopulmonary bypass, extracorporeal membrane oxygenation (ECMO), or an intra-aortic balloon pump to maintain peripheral perfusion, and a cardiologist or cardiovascular surgery team may be needed in severe cases.

After any patient who has attempted suicide is medically stable, request a psychiatric consultation.



Some patients may present with overwhelming bradycardia and hypotension that is unresponsive to available medical management. Patients with these complications may require cardiopulmonary bypass, extracorporeal membrane oxygenation (ECMO), or an intra-aortic balloon pump to maintain peripheral perfusion until the calcium channel blocker has cleared their system; transferring these patients to a facility offering such services may be reasonable.

Not all community hospitals offer a pediatric ICU for inpatient care of the hemodynamically unstable child. This is an indication to transfer pediatric patients.