As emergency physicians, it's our job to know our way around the code cart. In this installment of Carolinas Core Concepts, Dr. Trigonis breaks down the common meds, indications, and doses for what we can find in your standard code cart. Note, this may vary from the formulations you have available at your hospital, so make sure you check your concentrations!

Med: CALCIUM
Indication: Stabilize Cardiac Membranes (hyperK)
Dose: CaCl2:  1g in 10mL syringe = 14mEq ("Code Calcium" - don't give peripherally!)
        Calcium Gluconate:  2g = 9mEq.  *This CAN be given peripherally

Med: EPINEPHRINE
Indication: Cardiac Arrest
“Code Epi”  Dose: 1mg in 1mg/10mL syringe (1 dose per syringe)
"Push-dose Epi": 1mL Code Epi in 9mL NS flush (10mcg/mL). Push 1mL q2min PRN for hypotension or bradycardia in peri-arrest scenario
"Dirty Epi Drip": 1mg "Code Epi" in 1L NS (1mcg/mL conc.). Running wide open thru 18ga IV in AC is roughly 20mcg/min.

Med: NOREPINEPHRINE
Indication: Hypotension. (Vasopressor - primarily ⍺ agonist)
Dose: 4 – 30 mcg/min. Comes in 4mg / vial. 1 vial in 250cc D5W = 16mcg/mL.

​Med: ATROPINE
Indication: Bradycardia (Muscarinic antagonist)
Dose: 0.5 mg. Vial comes in 1mg/1mL (2 doses per syringe).
Repeat q 1-3 minutes. Max dose 3mg.

Med: DOPAMINE
Indication: Bradycardia (chronitropic, inotropic agent)
Dosing:
Low doses: < 2mcg/kg/min –dopamine receptors (vasodilate)
Mid dose: 5-10mcg/kg/min – β1 (contractility/HR)
High dose: > 10 mcg/kg/min – ⍺1 (vasoconstriction)

Med: ADENOSINE
Indication: SVT
Dose: 6-12mg FAST PUSH. Comes in 6mg/2mL vial. 1-2 vials/dose.

Med: AMIODARONE
 Indication: Arrhythmia
Dose:
Refractory Vfib/Vtach Arrest = 300mg (2 vials)
Repeat bolus 150mg (1 vial)
Tachycardia = 150mg (1 vial)
Amio gtt @ 1mg/min

Med: LIDOCAINE
Indication: Arrhythmia (Vfib/VTach Arrest, Stable VTach)
Dose: 1.5mg/kg. Comes in 100mg per syringe (1 dose per syringe)
Can repeat q5-10 minutes (0.5mg/kg)

Med: MAGNESIUM SULFATE
Indication(s): Arrhythmia, ecclamptic seizures
Dose: Torsades: 1-2g IV Push (1 – 2 vials)
          Ecclampsia: 5g IM per buttcheek or 6g IV load

Med: SODIUM BICARBONATE
Indication: Metabolic acidosis
Dose: “1 amp” = 50mEq NaHCO3 in 50cc (Recommended 1mEq/kg)
• 1 amp raises pH 0.1 à Goal pH 7.2ish
• 8.4% NaHCO3 ≅ 6% HTS
• 2 amps bicarb = 100cc 6% = 200cc 3% (can substitute for HTS in a pinch for reducint ICP in TBI)

Med: D50
Indication: Hypoglycemia
Dose: 1 amp = 25g dextrose in 50mL (1 – 2 amps slow push for hypoglycemia)

The meds below may not be in your code cart, but they can still get you out of trouble:

Med: NALOXONE
Indication: Opioid overdose
Dose: 0.4 – 2 mg (Titrate to effect) Comes in syringe 2mg/2mL. or vial 0.4mg/mL

Med: PHENYLEPHRINE (NEOSTICK) 
Indication: Hypotension (pure alpha adrenergic)
Dose: 200-300mcg q2-3 minutes. Comes in syringe: 800mcg/10mL (2-3mL q2-3min)

I. Myocardial injury

• In inferior MI, if ST elevation in lead III is greater than ST elevation in II: probable RCA occlusion
  • higher risk of bradycardia, AV block, atrial fibrillation and RV infarct (always with RCA MI)
• In inferior MI, if ST elevation in lead II is greater than ST elevation in III: probable LCX occlusion
  • higher risk of papillary muscle dysfunction, acute mitral regurgitation, pulmonary edema
• Presence of wide and deep Q waves suggests large transmural MI and no viability
  • in acute MI: probable late presentation, no viability
  • in remote MI: consider LV aneurysm
  • In acute anterior STEMI, new right bundle branch block suggests large MI and high mortality
• Acute myocarditis can present with STEMI picture in the ECG
  • clinical presentation is different (severe acute heart failure, pulmonary edema)
  • ST elevation is frequently diffuse
  • conduction abnormalities (A-V block) are frequently present

 

II. Secondary ST-segment elevation

• With wide QRS complexes (left bundle branch block, ventricular pacing, WPW)
  • QRS and ST-Ts are usually discordant: discordant ST elevation is normal
  • ST elevation that is concordant with the QRS complexes strongly suggests STEMI
• In severe LVH with narrow QRS complexes
  • QRS/ST-Ts are usually discordant: ST elevation in the anterior chest leads may be normal
  • in questionable cases, compare with old ECGs; perform serial ECGs; stat bedside echo

 

III. Terminal notching of the QRS complexes followed by hammock-shaped ST elevation

• Pericarditis
  • tachycardia
  • ST elevation is diffuse but usually spares leads aVR and V1
  • depressed PR segment in lead I; elevated PR segment in lead aVR
• Hypothermia
  • bradycardia
  • large and diffuse terminal QRS notching (Osborn waves)
  • prolonged QT
  • shivering artifact
• Benign early repolarization
  • frequently present in young African-American males
  • terminal QRS notch and hammock-shaped ST elevation usually best seen in V4
  • heart rate and QT are usually normal
  • concern about risk of ventricular arrhythmia and sudden death in certain small subgroups

 

IV. Brugada syndrome, Brugada sign

• High take-off upward convex (“coved”) ST elevation followed by negative T waves in V1 and V2
• Increased risk of sudden cardiac death
• Endemic in South-East Asia (Laos, Vietnam, Cambodia, Thailand)
• Male predominance
• Highest risk of sudden death is in patients with resuscitated sudden death, h/o unexplained syncope, spontaneous and dynamic Brugada ECG pattern, nonsustained VT during monitoring
• Most asymptomatic patients without the listed risk factors, especially those who are older at the time of diagnosis, are at minimal risk of unexplained sudden death (“Brugada sign”)

Epistaxis

• Epistaxis is classified as either anterior or posterior.
  • Anterior epistaxis usually originates in the vascular watershed area of the nasal septum known as Kiesselbach's plexus involving the ethmoidal artery, sphenopalatine artery, and facial artery.
  • Posterior epistaxis usually originates from the sphenopalatine artery but may also arise from the internal carotid artery.
• Diagnostic studies of coagulation panel, hemoglobin, and platelet count are not necessary in the typical healthy patient with epistaxis.
• 65% of cases achieve hemostasis with use of topical vasoconstrictive agent and 10 minutes of continues pressure of the septum.
• Maintain the patient in “sniffing position” during examination to obtain the best possible views of the anatomy.
• If anterior source is identified, then attempt cauterization.
• If patient remains symptomatic, pack the anterior naris.  Be sure to provide anxiolytics as this is incredibly uncomfortable for the patient.  Anterior packing of bilateral nares may be required in order to provide a counterforce to the lesion.
• There are few studies concerning the use of antibiotics in patients with nasal packing for TSS prophylaxis, but most specialists recommend initiating Augmentin.
• If patient continues to bleed, it is most likely a posterior bleed and will require posterior packing.  A Foley catheter (10-14 French) can be used for posterior packing in a pinch.
• Patients with posterior packing could theoretically undergo lethal bradydysrithmias and should be admitted to a monitored bed.

 Foreign Bodies

• Button batteries and paired disc magnets are especially harmful.
• Most nasal foreign bodies are radiolucent.
• Patients often present with unilateral mucopurulent drainage.
• Initial attempts at removal should involve positive pressure techniques.
  • Have the patient blow his or her nose while occluding the nostril opposite of the FB.
  • “Mothers Kiss” involves having the parent provide oral positive pressure to a pediatric patient while occluding the unaffected nostril.
  • You can provide 15 L/min of O2 via a soft rubber Christmas tree to the unaffected naris, if a pediatric patient refuses to open their mouth.
• If positive pressure fails, helpful tools for manual extraction include otoscope, nasal speculum, curette, forceps, suction, and/or Katz catheter.  A pediatric foley catheter (5 french) can be substituted for a Katz catheter.
• Remember to use sedation and application of local analgesic and vasoconstrictive agents prior to manual extraction.

Henoch-Schönlein purpura

• Henoch-Schönlein purpura = IgA Vasculitis (IgAV)
• Disease process is mostly seen in pediatric populations
• Tetrad

1. 1. Palpable purpura WITHOUT thrombocytopenia or coagulopathy
2. 2. Arthritis / arthralgia
3. 3. Abdominal Pain
4. 4. Renal disease

 

• Usually self limited,  but total disease course can be long (except in adults)
• There are some instances where steroids may help, but not all cases.
• Follow up is key! Need repeat urine and renal studies!

-Overall relatively uncommon in the US, but the ED population is particularly high risk
-More common in the extremes of age, the medicated, and the chronic alcohol abusers
 
Wernicke Encephalopathy
-Thiamine deficiency
-Clinical diagnosis, but frequently missed
-2 of 4 criteria
                1. Nutritional deficiency
                2. Altered mental status
                3. Ocular findings
                4. Ataxia
-Altered mental state is the most common finding
-Nystagmus is more common than opthalmoplegia
-Tx: 500 mg IV q8hr x 2d, then daily until oral tolerated
-Insufficient evidence for prophylaxis, IV not necessary and expensive!
-It’s okay to give glucose if your patient needs it before thiamine
-Always walk your patients!
 
B12 Deficiency
-B12 requires intrinsic factor for absorption
-More common in elderly, autoimmune, and those on proton pump inhibitors
-Consider in megaloblastic anemia with neurological symptoms
-Tx: IM injections
 
Vitamin D
-Required for dietary calcium and phosphorus absorption
-Majority obtained from dermal synthesis
-Low levels leads to increased PTH, which results in mobilization of Ca from the bone
-Increased prevalence of Rickets in infants due to relatively low concentration in breast milk and sunscreens
-Classically lower extremity bowing, thin bone cortex, poor growth, delayed fontanelle closure
-May progress to tetany, seizures, prolonged QT due to hypocalcemia
-If seizing or tetany, give calcium. If thinned bones, give oral vitamin D
-In the elderly – common cause of osteopenia, fragility fractures, secondary hyperparathyroidism
 
Vitamin K
-Necessary for activation of coagulation factors
-Typically in leafy greens, synthesized from gut bacteria
-Increasing in prevalence due to families refusing vaccinations
-Infants have low stores at birth, sterile gut, low concentrations in breast milk
-Classic bleeding at 2 days- 4 weeks with bleeding from mucosal surfaces
-Late presentation 3 weeks-8 months- higher percentage of ICH, blown pupil may be a sign of SDH
-Look for decreased Hct, prolonged PT
Tx: preventable with 0.5-1 mg IM at birth
There is an oral option! 2 mg orally with 1st feed, repeated at 1, 4, and 8 weeks of age
Emergency: 1 mg Vit K, 10-20 mL/kg FFP if life threatening
 
Board Review buzzwords, less likely to present as emergencies
-Night blindiness, dry eyes, keratomalacia – Vitamin A deficiency
-Idiopathic intracranial HTN – hypervitaminosis A
-Diarrhea, dermatitis, dementia (Pellegra) – Niacin deficiency (B3)
-Petechiae, perifollicular hemorrhage, bruising, corkscrew hairs (Scurvy)- Vitamin C deficiency
-Angular chelosis – Riboflavin deficiency (B2)
-Isoniazid + seizure – pyridoxine (B6)
-Spina bifida – folate deficiency

Posterolateral MI

• Acute thrombotic LCX occlusion – it is a STEMI
  
• Diagnostic criteria
  • presentation with acute chest pain
  • ST depression in the anterior chest leads which may be due to anterior ischemia, posterior STEMI or RVH with strain
  • posterior STEMI is frequently accompanied by subtle Q waves, subtle ST elevation or the “wishbone sign” in the inferior and/or lateral leads
• It is a STEMI but ST elevation may not be seen in the 12-lead ECG (“STEMI without  STE”)
• Place ECG leads to the back (V7-V8-V9)
• Any ST elevation in the posterior leads warrants immediate cath/reperfusion

 

Dressler - de Winter sign

• Acute thrombotic proximal LAD occlusion – a STEMI equivalent
  • in 98% of cases of acute LAD occlusion: there is frank electrocardiographic STEMI
  • in 2% of cases of acute LAD occlusion: Dressler - de Winter sign
• Diagnostic criteria
  • presentation with acute chest pain
  • very tall “hyperacute” T waves in the chest leads
  • usually accompanied by upsloping ST depression (ST depressed at the J point)
  • patients are frequently young males
  • chest pain to the “de Winter” ECG presentation is usually within 30-120 minutes
• Imminent risk of extensive anterior STEMI
• The de Winter sign warrants immediate cath/reperfusion

 

aVR sign

• 80% specific for tight left main coronary artery stenosis – high risk of large STEMI
• Diagnostic criteria
  • presentation with acute chest pain
  • diffuse ST-segment depression
  • ST elevation ³1 mm in aVR
• High but not necessarily imminent risk of STEMI, usually extensive, frequently lethal (“widow-maker artery”)
• Urgent cath/reperfusion is indicated (but not necessarily immediate cath)

 

Wellens sign, Wellens syndrome

• Suggestive of tight proximal LAD stenosis – high risk of subsequent anterior STEMI
• Diagnostic criteria
  • presentation with chest pain
  • biphasic (positive-negative) T waves in the anterior chest leads (type A – 25%) and/or
  • deep symmetrical negative T waves in the chest leads (type B – 75%)
  • no abnormal Q waves; normal R-wave progression in the chest leads
  • T-wave abnormalities can be present even in the pain-free state
  • no or only subtle troponin elevation
• If undetected/untreated, high risk of subsequent STEMI, usually days/weeks later
• In typical Wellens syndrome: cardiac cath without prior stress testing is indicated
  

Vaso-Occlusive Crises

1. Vaso-occlusive episodes are from tissue ischemia and infarction from intravascular sickling
   1. Bones, soft tissue, viscera, and CNS can all be affected

 

Pain Crises

1. Usually classic in location, character, and severity
2. Triggers: stress, cold, dehydration, hypoxia, anemia, infection, or no cause
3. In infants – first sign may be dactylitis (swelling of hands or feet) due to ischemia of metatarsal/metacarpal nutrient vessels
4. Treatment:
   1. IVF: D5 ½ NS @ 1.5 maintenance or fluid bolus in dehydrated or hypotensive pt
   2. Pain medications:

• Acetaminophen for mild pain
• NSAID for mild to moderate pain
  • Toradol 15mg (30mg not proven to be better)
• Opioids for moderate to severe pain, typical initial doses include:
  • Morphine 0.3mg/kg PO
  • Morphine 0.1 - 0.15mg/kg IV/IM
  • Dilaudid 0.06 - 0.08 mg/kg PO
  • Dilaudid 0.015 - 0.020 mg/kg IV/IM
    • Reassess response in 15-30min and may repeat with ¼ to ½ initial dose
• Home: hydroxyurea increases % of fetal hemoglobin
  1. Transfusion for acute drop in hemoglobin from baseline, or Hgb < 5

 

Acute Chest Syndrome – consolidation on CXR AND 1 of these: fever; >2% ↓SpO2, PaO2<60, tachypnea, increased work of breathing, CP, cough, wheezing or rales

1. Due to ischemia and infarction, usually a complication of PNA or as a result of bone marrow or fat emboli
2. Presenting symptom: pleuritic chest pain, dyspnea, fever, cough
3. Ask immunization history, esp.: pneumococcal and H. influenza type B
4. Dx:
   1. CBC, leukocyte differential, reticulocyte count (aplastic anemia vs. splenic sequestration), U/A
   2. If you think they may need an RBC transfusion, send a cross-match
   3. ABG for hypoxemia
   4. CXR - May be normal initially
   5. BCx
5. Tx:
   1. Oxygen
   2. Oral hydration preferred
      1. If IV: hypotonic fluids at rate 1.5x maintenance (overly aggressive fluids can worsen ACS)
   3. Pain meds but don’t decrease resp drive too much
   4. Abx: empiric Abx for CAP
      1. Ceftriaxone 50mg/kg and a macrolide
      2. Common concurrent infections: chlamydia, mycoplasma, viral, strep. pneumo, staph aureus, H. flu
   5. Bronchodilators: nebulized B2-adrnergic agonists
   6. Chest physiotherapy
   7. Transfusion for:
      1. Severe acute anemia
      2. PaO2 < 70 mmHg
      3. Oxygen saturation drop of 10% from baseline
6. Exchange transfusion for
   1. Severe acute chest syndrome and past history of requiring vent support: useful to prevent intubation and it can decrease duration of vent support if patient already intubated
   2. Suspected or confirmed fat or bone marrow embolism (from boney infarct)

 

Hematologic crises

• Acute Splenic Sequestration Crises
  1. Spleen traps much of the circulating blood volume
  2. Presentation:
     1. Usually occurs in kids b/c of splenic infarction that develops later in life
     2. Severe: sudden-onset LUQ pain, pallor, lethargy
     3. Minor episodes: insidious onset of abdominal pain, slowly progressive splenomegaly, and a more minor fall in Hb level
  3. Dx and Differential:
     1. CBC shows profound anemia
     2. Normal to elevated retic count
  4. Tx: transfusion with RBCs
     
• Aplastic Episodes
  1. Caused by viral infections (usually parvovirus B19), bacterial infections, folic acid deficiency, or bone-marrow suppressive drugs
  2. Presentation: gradual onset of pallor w/out pain or jaundice
  3. Low hemoglobin w/ decreased or absent reticulocytosis
  4. Tx:
     1. Transfusion for:
        1. Hb <6
        2. A drop in Hb by 3
        3. Symptomatic
           
• Hemolytic Crises
  1. Bacterial or viral infections can also precipitate increasing degree of active hemolysis
  2. Usually sudden onset
  3. Dx: Anemia with marked increase in reticulocytes
  4. Tx: treat underlying infection

 

• Infections
  1. Due to functional asplenia → deficient antibody production and impaired phagocytosis → bacterial infections, esp. encapsulated organisms, pose a serious threat
     1. Leading cause of death
  2. Dx: CBC and cultures
  3. Tx:
     1. Children receive penicillin ppx until age 5
     2. Ill appearing children < 1 year old treated empirically w/ Abx against S. pneumoniae and H. influenza → ceftriaxone 50mg/kg
     3. Well-appearing children >1 year with temp <40C, WBC 5-30, platelets >100,000 and Hgb >5, no CXR infiltrate → single dose ceftriaxone, 4 hours observation, and 24 hour follow-up
        1. If not meeting these criteria → admit for Abx and obs