Beta Blocker and Calcium Channel Blocker Overdose

Leslie Adrian, MD, OSU EM PGY-1 // Michael Barrie, MD OSU EM

 

You get a call from triage, a 34 year old female is in the waiting room, presenting to ED with chief complaint of intentional ingestion. You briefly examine her; she is well appearing but tearful with a HR of 70 and BP 120/79 and is alert and oriented. She admits to taking thirty of her friend’s blood pressure medication one hour ago, she does not know what it was called, but thinks it ended with an “-olol.” You put her on the monitor, order ingestion labs and then receive a call that a level 1 stroke patient has arrived and needs to be intubated.

15 minutes later, you get a frantic call from the psychiatric nurse stating that your patient’s HR is 30 her blood pressure is 70/40, and she is altered but protecting her airway. You put the patient on oxygen and start fluids immediately, but what do you do next?

Pathophysiology of Beta Blocker/Calcium Channel Blocker Overdose

 Beta blockers depress myocardial activity as well as the AV node, leading to bradycardia, conduction block and decreased inotropy. However, unlike CCB, there are not significant effects on the PVR.

Management of acute beta blocker/calcium channel blocker overdose

BB and CCB poisoning can produce vasopressor and inotrope resistant cardiogenic shock within a few hours of ingestion, and patients can present asymptomatic with normal vital signs, and within a few minutes can be in extremis. High-dose insulin therapy (while maintaining normal blood glucose levels) and inotropy, as well as adjunctive glucagon, calcium and intra-lipid infusion are the most effective therapies to reverse the depressive effects of these medications. It is important to remember that high dose insulin therapy can include continuous infusion of 1-10 U/kg/hr after initial bolus dosing. Atropine and transcutaneous pacing may be attempted, but it is generally advised not to attempt transvenous pacing secondary to the risk of cardiac dysrhythmias. If patients are asymptomatic, they should be closely monitored for 12-24 hours as sustained release formulations can produce symptoms insidiously. The algorithm below (EMCases) shows the most practical approach to the treatment of beta blocker and calcium channel blocker toxicity and resultant cardiogenic shock.

bb blocker

References:

DeWitt R, Waksman C. Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity. Toxicol Rev. 2004; 23(4):223-38.

Doepker B, Healy W, Cortez, E and Adkins, E. High-Dose Insulin and Intravenous Lipid Emulsion Therapy for Cardiogenic Shock Induced by Intentional Calcium-Channel Blocker and Beta-Blocker Overdose: A Case Series. The Journal of Emergency Medicine, Vol. 46, No. 4, pp. 486–490, 2014

Graudins A, Lee HM, Druda D. Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies. Br J Clin Pharmacol. 2016 Mar; 81(3):453-61.

Stonge M, Anseeuw K, Cantrell FL, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med. 2016.

Conference Review – Cardiac Tox

Thanks to Justin Carroll for writing this week’s conference review!

Digitalis toxicity

  • MOA by inhibiting the Na+/K+ channel resulting in change in increase in intracellular Na+ and extracellular K+. This affects the functioning of the Ca2+/Na+ exchanger resulting in an increase in intracellular Ca2+.
    • Increased inotropy
      • Side effect: Decreased refractory period, Delayed after depolarizations (lower threshold for dysrhythmias)
    • Decreased excitation of cell (increased vagal tone)
      • Decreased AV nod conduction (bradyarrhythmias)
    • Narrow therapeutic index
      • Severity of toxicity better correlated to severity of hyperK+ rather than Dig level (see below)
    • Acute toxicity
      • Usually by intentional/accidental ingestion (asymptomatic for several hours
        • p/w dizzy, h/a, n/v, confusion, coma
        • Xanthopsia (yellow-green halos)
        • Bradyarrhythmia, SV tachyarrhythmia w/ AV block
        • Hyper K+ with acute ingestion.
        • Dig level inaccurate due to slow absorbs and large Vd (falsely elevated in first hrs).
      • Chronic toxicity
        • Often elderly with near or w/in therapeutic window and 2/2 to comorbidities such as renal failure, drug-drug interactions (i.e. diuretic, clarithromycin)
        • p/w n/v, GI pain, diarrhea
        • more likely to have CNS manifestations (fatigue, weakness, confusion, delirium, coma)
        • Ventricular and SV dysrhythmias (V tach very common)
        • Normal to low K+, hypo Mg2+
      • Dx
        • Regular dose usually (125 – 250 mcg). Toxicity usually d/ 1-2 mg, with fatal doses of 10 mg (adult) and 4 mg (child)
        • Toxic Dig level usually >2.5 ng/mL (levels no reliable until >6hrs)
          • Digoxin-like immuno-reactive substances (DLIS) – falsely elevated dig level 9 neonates, 3rd trimester, SAH, renal/hepatic failure, plant based steroids
        • EKG changes are important findings (4 findings)
          • T-wave flattening/inversion
          • QT shortening
          • ST scooping
          • Increased U wave amplitude
        • Dysrhythmias most commonly seen are PVC’s. Also will see SVT w/ AV block or junctional escape rhythms.
        • Bidirectional VT (alternating QRS) – specific of Dig
        • Labs:
          • Acute: K+ level for hyperkalemia and dig level (Therapeutic 0.-2.0)
          • Chronic: Not very helpful. Normal to low K+. Mildly elevated dig level
        • Tx
          • Asymptomatic pt
            • Cardiac monitor, IV access, GI decontamination (charcoal), reeval
          • Symptomatic (life-threatening dysrhythmia)
            • Digoxin-Fab
              • Indications: K+ > 6.0, life threatening dysrhythmia
              • Give 80 mg (two vials) bolus and reassess. Repeat q30-60 min until hyperkalemia or dysrhythmia resolved. (Calculation usually over estimates amount needed.
              • Chronic – give 40 mg (1 vial) q1 until asymptomatic
                • Tx may unmask other conditions (A-fib) or reported cardiac arrest, or cause hypersensitivity rxn.
              • Correct symptoms – hypoxia, hypoglycemia, hypovolemia, electrolyte abnormalities.
              • IV Mg2+
              • Atropine and/or transvenous pacer
            • Dispo f/u
              • Monitor:
                • Asymptomatic – observe until dig levels begin to decrease
                • Symptomatic – admit (ICU for 6-12 hrs. if Fab given)

BB Toxicity

  • Acute presentation
    • Cardiac symptoms include hypotension, bradycardia, ventricular dysrhythmias, AV block and delays, decreased contractility and asystole. CNS symptoms include decreased mental status, seizures, psychosis and coma. Pulmonary findings include bronchospasm.
    • Severe toxicity – bradycardia leading to shock
  • Dx
    • Clinical diagnosis based on presentation and history.
  • Tx
    • No signs of toxicity, bradycardia or hypotension:
      • Cardiac monitor, IV access, GI decontamination (w/in 6 hrs.) and observation.
        • Observation 6-8 hrs. If sustained release 12-24 hrs. Peds – 24 hrs.
      • +Toxicity, bradycardia or hypotension:
        • Patients at high risk for CV collapse. Treat to improve contractility and HR.
        • IV, O2 monitor, GI decontamination
        • Supportive care including IVF, atropine, glucagon bolus 2-10 mg IV (Peds: 50-150 mcg/kg), insulin, calcium, bicarb (if wide QRS intervals).
          • Glucagon MOA: Bypass B-adrenergic receptor to stimulate cAMP w/in cardiac myocyte improving excitation.
        • If refractory consider pacer, hemodialysis, lipid emulsion therapy and ECMO.

 

CCB Toxicity

  • Dihydropyridines – L-type calcium channel selectivity in peripheral vasculature.
  • Non-didydropyridines (verapamil and diltiazem) – selectively block L-type Ca2+ in myocardium
  • Pathophysiology
    • Calcium channel block leads to vascular smooth muscle relaxation, decreased contractility and conduction.
  • Dx:
    • Similar presentation of myocardial depression with peripheral vasodilation
    • Hypotension, bradycardia, varying AV blocks (PVC’s most frequent) with complete heart block in severe overdose.
    • Diagnosis per clinical presentation and varying dysrhythmias on EKG.
  • Tx:
    • IV, O2 monitor, GI decontamination
    • Supportive care including IVF, atropine, CaCl 10% 10-20 mL IV (Peds: 0.2 mL/kg) or Ca gluconate 10% 30-60mL (peds 0.6 ml/kg) IV. May repeat q 10-20 min. Consider infusion 0.4 mL/kg/hr with serial Ca2+ q1-2hrs. High dose insulin therapy (CCB inhibits beta cells), consider glucagon, bicarb (if wide QRS intervals).
    • If refractory consider pacer, hemodialysis, lipid emulsion therapy and ECMO.

 

Other Antihypertensives:

  • Diuretics: excessive diuresis with tachycardia, hypotension, and electrolyte abnormalities specifically hyperkalemia.
    • Tx: IVF (volume repletion) and electrolyte correction
  • Alpha-agonist: Clonidine is most common cause. Present with bradycardia and hypotension with possible opiate syndrome (coma, miosis, and respiratory depression).
  • ACE-I/ARBs: cough and angioedema
  • Hydralazine: can present with DILE (drug induced lupus erythematosus)

April Conference Review

Thanks Dr. Sam Basu for creating these conference reviews on Acid-Base disorders, UTI/Pyelonephritis, and EMTALA!

Acid-base disorders
 
Acid-base disorders are a common finding in the typical ED workup.  There are four major categories of acid base disturbances:  metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis.
First look: Determine a pH. Are they acidotic or alkalotic?
  • If pH >7.45 then patient’s primary problem is alkalosis
  • If pH <7.35 the patient’s primary problem is acidosis
Second factor: Evaluate that blood gas. Remember that a VBG can be used to determine pH, pCO2, and bicarb.  ABG provides accurate pO2.
  • If pCO2 >45 then respiratory acidosis
  • If pCO2 <35 respiratory alkalosis
Note: pH may be normal in the presence of a mixed acid base disorder, particularly if other parameters of the ABG are abnormal.
Labs to consider early in evaluation: Diagnosis is based on clinical history as well as labs:
  • VBG/ABG
  • Lactate
  • Albumin
  • Chemistry
Next… If there is a metabolic acidosis, is there an anion gap?
Anion gap = [Na+]– [HCO3-] – [Cl-] If gap, think MUDPILES.
A couple of quick notes/tricks discussed during conference:
§  Arterial PCO2  =  Serum HCO3  +  15
§  You can approximate the arterial PCO2 with the last decimal digits of the pHà (30 mmHg when the arterial pH is 7.30)
Metabolic acidosis is divided into anion gap and non-anion gap acidosis. Note that an appropriate respiratory compensation can be assessed using the Winter’s formula: (1.5 x HCO3) + 8 + 2. If the actual pCO2 is within the range as calculated by the Winter’s formula, there is an adequate respiratory compensatory response to the metabolic acidosis.  A higher than expected pCO2 suggests inadequate ventilatory response.
 
And then… What is the delta gap?
 
A delta gap is used to determine if there is a coexisting metabolic alkalosis or non-gap acidosis:
∆gap = anion gap – 12
<0.4: Hyperchloremic normal anion gap acidosis
0.4-0.8: Consider combined high AG & normal AG acidosis BUT note that the ratio is often <1 in acidosis associated with renal failure
1.0-2.0: normal for a straightforward high AG-acidosis
>2.0: possibly a pre-existing elevated HCO3 at baseline
Then consider, is there any compensation here?
Most commonly used compensation formulas:
  • In metabolic acidosis: Winter’s formula: PaCO2 = 1.5 (HCO3) + 8 ± 2
  • In acute respiratory acidosis, the patient’s pH will drop by 0.08 for every 10mm Hg increase in pCO2.
Other calculations that may be required:
 
What is a base deficit?
Succinctly, a base deficit removes the respiratory component of acidosis so that the metabolic portion is all that remain. It is equal to the amount of base you would have to add to get to a pH of 7.4. For example, a base excess of -10 means you have a base deficit of 10.  A normal base deficit is between -2 and 2. It is helpful to understand this concept for quick evaluation of whether a person’s acidosis is secondary to a respiratory inadequate response. If a patient’s base deficit is normal but they are acidotic on their gas, this must be secondary to retained CO2, causing a respiratory acidosis. Serum HCO3 can act as a substitute to base deficit if this value is not available.
Osm Gap = Measured Osmal – (2 Na + Gluc/18 + BUN/2.8 + ETOH/3.7). You have a positive osm gap if >10 and differential includes:
  • Toxic alcohols (if Osm gap >50
  • Methanol
  • Ethylene glycol
  • Lithium
  • Mannitol
  • Isopropanol (isopropyl alcohol)
  • Propylene glycol
Fluid Management: This was a focus during my trauma rotation especially, and it is worth noting that NS is more acidotic than LR, so consider LR-based IVF for patients with low pH, as in DKA, lactic acidosis/sepsis, etc.
Lastly, know common toxidromes that cause metabolic abnormalities. We discussed salicylate poisoning during conference, which causes a mixed metabolic acidosis secondary to lactic acidosis. These patients will be tachypneic due to a compensatory respiratory response to their acidosis. Remember that if this patient’s airway becomes compromised, it is essential to maintain a high minute ventilation to compensate for their critical metabolic acidosis, otherwise you’re looking at likely rapid decompensation. This method holds true for all compensatory tachypneas (e.g. COPD).

 

UTI and Pyelonephritis

UTIs can be divided into lower and upper tract infections. Lower infections (cystitis) are characterized by localized symptoms, including dysuria, frequency, urgency, hematuria, suprapubic pain. Dysuria is caused by urethral irritation. Consider STIs as causes of dysuria in addition to a urinary tract infection. Pyelonephritis is simplistically an ascending UTI, characterized by systemic symptoms of fever, chills, nausea, vomiting, and flank pain.

The usual first step in evaluation of a suspected UTI is a urinalysis (UA).  There are 2 components to a UA: dipstick and microscopy. On the dipstick, the major indicators of infection are the leukocyte esterase reaction (LE, produced by PMNs and therefore indicative of pyuria) and a nitrite reaction (formed by coliform bacteria). LE has decent sensitivity and nominal specifity. A positive nitrite reaction on dipstick is highly specific for UTI, however has poor sensitivity (~50-60%). This is important as several urinary pathogens do not convert nitrates into nitrites (Pseudomonas, Enterococcus, Staph, Acinetobacter). Microscopy of a urine sample is performed after centrifugation. A leukocyte count is considered highly sensitive if WBC of >5/hpf, however has poor specificity. Bacteria/hematuria in addition to the actual signs and symptoms of active infection (i.e., dysuria, urgency, frequency, etc) is highly specific for UTI (~90%). The presence of squamous epithelial cells can be used to identify poorly acquired/contaminated samples (inadequate clean catch, commonly).   Some commonly used agents for treatment of simple UTI are below.

Some Empiric Antimicrobial Agents for Oral Treatment of UTI

Antimicrobial Agent Dosage
Amoxicillin-clavulanate 20–40 mg/kg per d in 3 doses
Sulfonamide
    Trimethoprim-sulfamethoxazole 6–12 mg/kg trimethoprim and 30-60 mg/kg sulfamethoxazole per d in 2 doses
    Sulfisoxazole 120–150 mg/kg per d in 4 doses
Cephalosporin
    Cefixime 8 mg/kg per d in 1 dose
    Cefpodoxime 10 mg/kg per d in 2 doses
    Cefprozil 30 mg/kg per d in 2 doses
    Cefuroxime axetil 20–30 mg/kg per d in 2 doses
    Cephalexin 50–100 mg/kg per d in 4 doses

Children are an interesting patient population when identifying UTIs, as pyelonephritis may present only as a cystitis. In addition to this, it may be difficult to attain a sample from a child that cannot void on command. Diaper and urine bag collections are often contaminated. Consider straight catheterization to obtain sample, and any child that is able to void on their own should be encouraged to provide a midstream clean catch. In pediatrics, we typically treat a simple UTI for 10-14 days. Cephalosporins are considered first-line.

When considering proper management of febrile UTIs in children:

  • Male or female, <28 days old: full sepsis workup + admission+ broad-spectrum antibiotics
  • 1-2 months old, <2 years old: admit for IV abx if at all clinically unwell (unable to tolerate PO, concern for significant dehydration, urosepsis, if immunocompromised, unable to attain appropriate (close) follow-up, unresponsive to outpatient therapy).
  •  If clinically well, consider an initial dose of rocephin with 2 weeks of oral antibiotics and close (24h follow-up).
  • In well children >2 years of age: 7 days of oral antibiotics, with the option of a standard 3 day course for females >13 years old with otherwise uncomplicated UTIs.

In addition, consider renal US for any of the following:

  • Children younger than two years of age with a first febrile UTI
  • Children of any age with recurrent febrile UTIs
  • Children of any age with a UTI who have a family history of renal or urologic disease, poor growth, or hypertension
  • Children who do not respond as expected to appropriate antimicrobial therapy

    Remember that not all UTIs are created equal, and that complicated UTIs can present to be clinically complicated and may require inpatient treatment and further evaluation. A UTI is considered complicated if recurrent, occurred after recent urogenital instrumentation, occurred in structurally/functionally abnormal anatomy, occurred in the setting of multiple comorbidities, occurred in pregnancy, or occurred in immunocompromised patients.

Below are some commonly used agent for parenteral treatment of UTI.

Empiric Antimicrobial Agents for Parenteral Treatment of UTI

Antimicrobial Agent Dosage
Ceftriaxone 75 mg/kg, every 24 h
Cefotaxime 150 mg/kg per d, divided every 6–8 h
Ceftazidime 100–150 mg/kg per d, divided every 8 h
Gentamicin 7.5 mg/kg per d, divided every 8 h
Tobramycin 5 mg/kg per d, divided every 8 h
Piperacillin 300/kg per d, divided every 6–8 h

Asymptomatic bacteriuria in pregnancy is a common finding in the ED, requiring aggressive management to prevent pregnancy complications like preterm labor and miscarriage. Remember that Group B Strep is a common offender, which is typically treated with ampicillin at time of delivery.

Treat asymptomatic bacteriuria of pregnancy with 1) macrobid, 2) cephalosporins. AVOID fluoroquinolones, bactrim, and tetracyclines. If pyelonephritis in pregnancy, admit for IV antibiotics and continued observation.

Pyelonephritis is an ascending UTI, with symptoms of flank or CVA tenderness (percussion is key!), and often systemic symptoms of fever, nausea, and emesis. Uncomplicated pyelonephritis can be treated outpatient with 14 days of antibiotics.

Complicated pyelonephritis requires admission and IV antibiotics (consider rocephin or Levaquin) with oral therapy following clinical improvement. Consider further imaging if failure to improve despite adequate, culture-based therapy. Key issues include noncompliance, resistant organisms, concomitant kidney stone, renal abscess, emphysematous pyelonephritis. Consider imaging and a deeper evaluation of risk factors that may lead to more complicated disease (immunocompromised state, recent instrumentation, structural abnormalities, etc). In addition, consider urologic evaluation either inpatient if admitted or outpatient as clinically indicated.

 

EMTALA

Per Annals of Emergency Medicine 2013 [Ann Emerg Med. 2013; 62:441-442.]

The American College of Emergency Physicians (ACEP) believes that:

  • Hospitals, medical staff, and payers share an ethical responsibility for the provision of emergency care.
  • Hospital emergency departments (EDs) require a reliable on-call system that provides for the availability of medical staff members for consultation and participation in the evaluation and treatment of emergency patients.
  • Such on-call systems are vital resources and must be maintained through the joint cooperation of the hospital governing body, administration, and medical staff. ACEP endorses the following principles:
  • Hospitals and their medical staff must be familiar with and comply with the requirements of the Emergency Medical Treatment and Active Labor Act (EMTALA).
  • Hospital bylaws or rules and regulations should clearly delineate which providers may participate in the EMTALA mandated medical screening examination of patients.1
  • All patients who come to a hospital requesting care must receive a medical screening examination and the necessary treatment to stabilize an emergency medical condition without unnecessary delay and without regard to the patient’s ability to pay.1 Under most circumstances, these services are best provided by emergency physicians.
  • A medical screening examination and any necessary stabilizing treatment may require the use of ancillary, consultative, or inpatient services within the capability of the hospital and its medical staff or their delegates (advance practice registered nurse, physician assistant, certified nurse midwife, etc).1
  • All hospitals that provide emergency services must maintain a schedule of medical and surgical specialists on call for the ED in a manner that best meets the needs of the hospital’s patients who are receiving services.1
  • To ensure institutional compliance with the provisions of EMTALA, hospital medical staff bylaws or rule and regulations must delineate the responsibilities of the on-call physician and should specify methods for monitoring and ensuring compliance.
  • On-call physician services must be available within a reasonable time to provide necessary stabilizing treatment1 and without regard to the patient’s ability to pay.
  • If a hospital lacks the medical staff resources to provide oncall coverage for a given specialty, the hospital must have a plan that specifies how such referrals should be managed.1
  • Follow-up care should be arranged by referral for all patients who require such care.
  • Physicians who choose to assume direct on-site emergency care responsibility for their patients must be physically present in the ED and must be members of the medical staff, privileged to provide such care.
  • When feasible, requests for consultative services should be made in accordance with the patient’s preferences or health plan.
  • Physician services (including medically necessary poststabilization care), when provided in response to the request for emergency care, should be recognized as emergency services for reimbursement purposes and should be compensated in a fair and equitable manner.
  • Transfer of patient care responsibilities between physicians must be orderly, clearly defined, and properly documented. The mechanism for such transfers and for resolution of disagreements between physicians should be clearly defined in medical staff rules and regulations.
  • All hospitals with specialized capabilities have a responsibility to accept transfer of patients when such transfer is necessary to stabilize an emergency medical condition.1 Hospitals should have a means to ensure medical staff responsibility for transfer acceptance and provision of specialized care.

 

Soooooo… what does that mean?

EMTALA basically requires two duties of the ED physician: an adequate medical screening of any patient that enters the ED, and completion of tasks to stabilize and transfer/accept a patient with an emergency medical condition.

EMTALA was created to prevent patient dumping, as the hospital cannot fail to provide medical screening or simply transfer or discharge patients based on the individual’s financial capabilities.

The medical screening exam constitutes not only an exam by an appropriate medical personnel (i.e. typically an ED physician), but also access to any needed ancillary services routinely available to the ED, such as surgical evaluation, in an effort to ascertain whether an emergency medical condition exists. They either have an emergency condition or they do not.

 

Is a medical screening exam equivalent to the triage process?

Nope. Triage is used to determine the order in which patients are seen based on the perceived severity of their presenting symptoms. Below is the Emergency Severity Index (ESI) scoring system used for the typical triage process.

A medical screening exam must contain at minimum:

  • Maintenance of and entry into a log, including disposition
  • Triage record
  • Ongoing vital signs
  • Physical examination
  • Testing used and results obtained
  • If on-call consultants were involved in the evaluation
  • Documentation of all such data listed

So what constitutes an emergency medical condition?

  • Severe pain
  • Serious dysfunction to organ
  • Serious impairment
  • Jeopardizes Health/Wellness
  • Having contractions without time for transfer

Ideally, at time of discharge or transfer, the patient is in stable condition, meaning that he or she is unlikely to deteriorate in transfer.

 

If the patient is unstable, then the hospital may not transfer the patient unless:

  • A physician certifies the medical benefits expected from the transfer outweigh the risks OR
  • A patient makes a transfer request in writing after being informed of the hospital’s obligations under EMTALA and the risks of transfer

If transfer is necessary

  • Receiving facility must be notified and accept the patient
  • The sending facility physician must certify that the transfer is medically necessary
  • Documentation of the patient’s medical condition and copies of the medical record, laboratory studies and radiographs should be sent with the mutually agreed upon transporting agency following appropriate instructions to the transporting personnel
  • Transporting personnel must be able to provide appropriate level of care to the patient

It is also important to note that the receiving facility cannot decline transfer if they have the appropriate resources and the sending hospital does not. Any EMTALA violation costs $50K (per violation). Typical receiving facilities will have specialized levels of care, typically like advanced surgical capability (burn, shock/trauma, ophthalmology, plastics) or NICU.

PREHOSPITAL MEDICAL CONTROL

 The role of EM docs in the prehospital medical control is ever-expanding, most importantly for expedited intervention for time-critical conditions, like MI and CVA. Prehospital medical control is a well-established responsibility for many emergency physicians.

Prehospital medical control by a physician is mandated for EMS in nearly all states.

A difficulty in prehospital medical control is to determine the mental capacity to refuse care from or transport by emergency medical services.

How to assess capacity:

  • The patient fully understand the consequences of their refusing care
  • The patient is not under the influence
  • No state of shock exists
  • No medical conditions are altering sensorium

In addition, there are frequently low acuity patients that initially call EMS then do not require transport or actually refuse transport despite calling EMS initially. So what to do when you cannot lay eyes on the patient in question and you receive that phone call from EMS? We must weigh the patient’s autonomy against the perceived likelihood of advanced medical need. You will be well-supported if the patient has an active medical condition and lacks medical decision making capacity. If ever in doubt, authorize transport to the hospital.

Liability and the obvious legal implications of performing medical control duties are frequent concerns and very little documentation regarding actual litigation exists at this time.  Think Good Samaritan immunity. This is all based on your sound medical judgment.

Different levels of emergency medical scene responders:

  • First Responder- 40h of training. Can perform CPR, BVM, O2, AED, Childbirth, C-spine stabilization, Splint, Vitals. Can help the patient administer their own epinephrine.
  • EMT-B- 130h of assessment based. Above + transport/extrication, assist w IV/monitor. First aid, CPR/AED use, spinal immobilization, airway management (BVM). In addition to first responder skills and the above, they can assist patient with administration of patient’s own nitroglycerin and inhalers.
  • EMT-advanced- 130h. EMTB + meds (dextrose, diphenhydramine, pain meds, nitroglycerin, albuterol, subcutaneous epinephrine) and IV access, if critical may monitor and defibrillate. Basic EKG interpretation, some advanced airway management (needle decompression and intubation).
  • EMT-paramedics- 1200 h. EMT-advanced +more drugs, cricothyrotomy, nasal intubation, BiPAP, ACLS.