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Silver Cross EMS September 2012 3 rd Trimester CME. Allergies and Anaphylaxis Presented by Silver Cross staff. System Updates!. Please remember… Region VII does not give Lidocaine for EZ-IO pain, even though your sales rep may have told you otherwise.

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Silver cross ems september 2012 3 rd trimester cme

Silver Cross EMS September 2012 3rd Trimester CME

Allergies and Anaphylaxis

Presented by Silver Cross staff

System updates
System Updates!

  • Please remember… Region VII does not give Lidocaine for EZ-IO pain, even though your sales rep may have told you otherwise.

  • The Region VII SMO Code 12 “Suspected Cardiac Patient” has added pregnancy as a contraindication to Aspirin

  • Region VII has also added a new SMO for Suspension Trauma, Code 21b.

  • As of September 1st – license and renewal fees are in place.

  • Sign up for our e-mail list for even more information!

  • Info on all these and more on the website…

Our agenda
Our agenda

  • Physiology and discussion of allergic reaction process.

  • Physiology and discussion of anaphyaxis.

  • Specific information on anaphylactic shock.

  • Treatment of allergies and anaphylaxis

  • Drug of the month – Epinephrine

  • Strip of the month – Ventricular rhythms


  • An allergy is an exaggerated immune response or reaction to substances that are generally not harmful.


  • Immediate, systemic, life-threatening allergic reaction - major changes in cardiovascular, respiratory, and cutaneous systems


  • Antigen - induces formation of antibodies

  • Enters body by injection, ingestion, inhalation, or absorption

  • Examples of common antigens associated with anaphylactic reactions:

    • Drugs (penicillin, aspirin)

    • Envenomation (wasp stings)

    • Foods (seafood, nuts)

    • Pollens


  • Protective protein substances developed by body in response to antigens

    • Bind to the antigen that produced them

    • Neutralizes antigens and removes from the body

  • Antigen-antibody reaction protects body from toxins by activating immune response

Immune Response

  • Immune responses are normally protective

  • Can become oversensitive or be directed toward harmless antigens to which we are often exposed

    • When this occurs, the response is termed “allergic”

    • Antigen causing allergic response called an “allergen”

  • Common allergens include drugs, insects, foods, and animals

Immune Response

  • Healthy body responds to antigen challenge through collective defense system – immunity.

    • Natural, present at birth

    • Acquired, resulting from exposure to a specific antigenic agent or pathogen

    • Artificially induced (immunization)

  • Immunity may be active or passive

Allergic Reaction

  • Increased physiological response to antigen after previous exposure (sensitization) to same antigen

    • When circulating antibody combines with specific foreign antigen, results in hypersensitivity reactions

    • Or to antibodies bound to mast cells or basophils (IgE)

Hypersensitivity Reactions

  • Divided into four distinct types

    • Type I (IgE-mediated allergic reactions)

    • Type II (tissue-specific reactions)

    • Type III (immune-complex-mediated reactions)

    • Type IV (cell-mediated – localized allergic reactions)

Hypersensitivity Reactions

  • Agents that may cause hypersensitivity reactions (including anaphylaxis)

    • Drugs and biological agents

    • Insect bites and stings

    • Foods

Localized Allergic Reaction

  • Localized allergic reactions (type IV) do not manifest multi-system involvement

  • Common signs and symptoms of localized allergic reaction include:

    • Conjunctivitis

    • Rhinitis

    • Angioedema

    • Urticaria

    • Contact dermatitis


  • Promote vascular permeability

    • Allows plasma to leak into interstitial space

  • Cause dilation of capillaries and venules

    • Profound vasodilation further decreases cardiac preload, compromising stroke volume/cardiac output

  • Cause contraction of nonvascular smooth muscle in GI tract and bronchial tree

    • Associated increase in gastric, nasal, and lacrimal secretions, resulting in tearing and rhinorrhea

  • Histamines

    • These physiological effects lead to:

      • Cutaneous flushing

      • Urticaria

      • Angioedema

      • Hypotension

    • Onset very rapid

      • But short lived, quickly broken down by plasma enzymes

    Other Chemical Mediators

    • Other chemical mediators (heparin, neutrophil chemotactic factor, and kinins) cause:

      • Fever

      • Chills

      • Bronchospasm

      • Pulmonary vasoconstriction

    • These chemical processes can rapidly lead to:

      • Upper airway obstruction and bronchospasm

      • Dysrhythmias and cardiac ischemia

      • Circulatory collapse and shock

    Don t be shocked
    Don’t be shocked….

    • But this discussion has a lot to do with shock!

    Anaphylactic Shock

    • The body needs oxygen carried by blood for cellular metabolism

      • Perfusion

        • Delivery of O2, other nutrients to cells

    • Shock

      • Inadequate tissue perfusion causes too little oxygen to cells

    All Kinds of Shock are caused by one of three things…

    • Causes: pump failure (heart)

      container failure (vessels)

      fluid failure (volume)

      • Failure of heart = inadequate cardiac output

      • Failure of blood vessels = significant changes in systemic vascular resistance

      • Inadequate blood volume = inadequate delivery of oxygen to cells

    Imagine a power steering pump

    • Your car’s power steering needs a functioning pump, intact lines and enough fluid to work.

      • Failure of any one will cause power steering to fail.

    • Our bodies work the same way…

      Failure of our heart (pump), our vessels (lines) or our blood flow (fluids) will cause the body to fail

    Distributive shock – a vessel failure

    • Anaphylaxis is a form of distributive shock.

      • Vessels dilate so much, blood stagnates in them and can never fill them up properly.

      • Also called “container” failure

    • It's like replacing the power steering lines in your car with lines that are twice as big.

      • They would need more fluid to fill them.

      • If not enough fluid, it will not flow properly.

    Anaphylactic shock/anaphylaxis

    • Etiology/causes

      • Dust, pollen, mold, animal dander

      • Foods: milk, eggs, nuts, shellfish, beans

      • Latex/rubber products

      • Blood components

      • Antibiotics

      • Insect venom (hymenoptera)

    • Local anesthetics

    • Vitamins

    • NSAIDS (ASA, ibuprophen), IV contrast dyes

    • Radiocontrast media

    • Aspirin

    Early (compensated) shock

    • Early (compensated) shock

      • Physical exam

        • Assess heart rate – probably elevated

        • Assess presence & volume of peripheral pulses

        • Assess blood pressure – may still be normal

      • Reversible if cause identified, corrected

      • Uncorrected progresses to next stage

    Late (decompensated) shock

    • Compensatory mechanisms fail

    • Epinephrine & norepinephrine – vasoconstriction

    • Precapillary sphincters dilate

      • blood rushes into capillary beds

    • Postcapillary sphincters constricted

      • causing stagnation of blood

    • Blood pressure falls

    • Altered mental status

    • Anaerobic metabolism occurs (acidosis)

    Anaphylactic shock/anaphylaxis

    • Findings

      • Angioedema

      • Inability to speak, tightness in throat, stridor, DIB, wheezing, hoarseness, cough

      • Retractions, accessory muscle use, ↓ breath sounds

      • Tachycardia, ↓ BP

      • Diaphoresis, urticaria/flushing, pruritis, pallor/cyanosis

      • N/V/D, abdominal pain/cramps, incontinence

      • AMS, anxiety, restlessness, feeling of impending doom

    Anaphylactic shock/anaphylaxis

    • Skin

      • Diaphoresis

      • Urticaria

      • Flushing

      • Pruitis

      • Angioedema

      • Pallor

      • Cyanosis

    Bee sting and angioedema
    Bee Sting and Angioedema

    Bee Sting and Angioedema of the Lips

    Anaphylactic shock/anaphylaxis

    • Respiratory findings

      • FBAO

      • Pulmonary embolism

      • Reactive airway disease

      • Tension pneumothorax

      • Panic attack

      • Vasovagal syncope

    Anaphylactic shock/anaphylaxis

    • Gastrointestinal & genitourinary findings

      • Nausea, vomiting and diarrhea

      • Abdominal pain

      • Cramping

      • Incontinence

    Initial Assessment

    • Airway and breathing

      • Airway assessment critical

        • Most deaths from anaphylaxis from upper airway obstruction

      • Evaluate for voice changes, stridor, barking cough

      • Tightness in neck, dyspnea suggest airway obstruction

      • Airway of unconscious patient should be evaluated, secured

    • If airflow impeded, perform endotracheal intubation.

    • If severe laryngeal/epiglottic edema, needle cricothyrotomy indicated

    • Monitor patient closely for signs of respiratory distress

  • Circulation

    • Assess pulse quality, rate, and location frequently

  • History

    • May be difficult to obtain but critical to rule out other medical emergencies

      • Question patient regarding the chief complaint and the rapidity of onset of symptoms

        • Signs and symptoms of anaphylaxis usually appear within 1 to 30 minutes of introduction of the antigen

    Significant Past Medical History

    • Previous exposure and response to the suspected antigen

      • Not always reliable

    • Method of introduction of the antigen

    • Chronic or current illness and medication use

      • Preexisting cardiac disease or bronchial asthma

      • Prescribed Epi-Pen

    Physical Examination

    • Assess and frequently reassess vital signs

    • Inspect face and neck for angioedema, hives, tearing, and rhinorrhea.

      • Note presence of erythema or urticaria on other body regions

    • Assess lung sounds frequently to evaluate effectiveness of interventions

    • Monitor ECG

    EMS Drug Therapy

    • Epinephrine

    • Fluid resuscitation for hypovolemia

    • Antihistamines to antagonize the effects of histamine

      • Benadryl (diphenhydramine)

        • 50mg IVP slowly over 2-3 minutes

        • 50mg IM if no IV

    • Beta agonists to improve alveolar ventilation

      • Albuterol nebulizer

    • Corticosteroids to prevent a delayed reaction

      • Solu-medrol (methylprednisolone)

        • 125mg IVP

        • No longer just for long transports

    Prevention and Patient Education

    • Clearly document allergic reactions

    • Always ascertain history of allergies before administering any medication

    • Medications that are highly allergenic should be given orally rather than parenterally

      • When parenteral medication is given, the patient should be observed for 20 to 30 minutes

    Prevention and Patient Education

    • Patients with known allergies should:

      • Receive information regarding medical identification tags, bracelets, or cards

      • Contact their physician for Epi-pen prescription for epinephrine if they have a history of anaphylaxis.

    Drug o the month epinephrine
    Drug O’ the Month - Epinephrine

    • Sympathetic agonist

    • Epinephrine is a naturally occurring catecholamine. It is a potent α- and β-adrenergic stimulant; however, its effect on β-receptors is more profound.

    Mechanism of action
    Mechanism of Action

    • Epinephrine acts directly on α- and β-adrenergic receptors. Its effect on β-receptors is much more profound, and includes the following:

      • Increased heart rate (Beta)

      • Increased cardiac contractile force (Beta)

      • Increased electrical activity in the myocardium (Beta)

      • Increased systemic vascular resistance (Alpha)

      • Increased blood pressure (Beta)

      • Increased automaticity (Beta)


    • Onset

      • < 2 minutes (IV/ET)

    • Peak effects

      • < 5 minutes (IV/ET)

    • Duration

      • 5-10 minutes (IV/ET)

    • Half-life

      • 5 minutes


    • Cardiac arrest

      • Asystole

      • Ventricular fibrillation

      • Pulseless ventricular tachycardia

      • PEA (pulseless electrical activity)

    • Severe anaphylaxis

    • Severe reactive airway disease


    • Should be protected from light

    • Can be deactivated by alkaline solutions such as sodium bicarbonate

    • The IV line must be adequately flushed between administrations of epinephrine and sodium bicarbonate.

    Side effects
    Side Effects

    • Palpitations

    • Anxiety

    • Tremulousness

    • Headache

    • Dizziness

    • Nausea

    • Vomiting

    • Increased myocardial oxygen demand


    • The effects of epinephrine can be intensified in patients who are taking antidepressants.


    • Cardiac arrest (adult)

      • 1 mg of 1:10,000 IV/IO every 3-5 minutes

    • Cardiac arrest/bradycardia (pediatrics)

      • 0.01 mg/kg of 1:10,000 IV (0.1 ml/kg) every 3-5 minutes.

    Dosage cont
    Dosage (cont.)

    • Severe anaphylaxis (adult)

      • 1:10,000 0.3 – 0.5 mg IV/IO

      • 1:1,000 0.3 – 0.5 mg IM (if no IV/IO)

    • Severe anaphylaxis (pediatrics)

      • 0.01 mg/kg of 1:1,000 IM

      • Repeat every 5-15 minutes

    Dosage cont1
    Dosage (cont.)

    • Severe asthma/COPD (adult)

      • 1:1,000 0.01 mg/kg up to 0.3 mg IM (with medical control approval)

    The ventricles
    The Ventricles

    • Ventricles are the heart’s least efficient pacemaker

      • Normally generate impulses at a rate of 20 to 40 beats/min

    • May assume responsibility for pacing the heart if:

      • The SA node fails to discharge

      • An impulse from the SA node is generated but blocked as it exits the SA node

      • The rate of discharge of SA node is slower than that of ventricles

      • An irritable site in either ventricle produces an early beat or rapid rhythm

    Premature ventricular complexes pvcs
    Premature Ventricular Complexes (PVCs)

    • Arise from an irritable focus within either ventricle

    • A PVC:

      • Is premature, occurring earlier than the next expected sinus beat

      • QRS is typically equal to or greater than 0.12 seconds

      • PVC depolarizes ventricles prematurely and in an abnormal manner

      • T wave is usually in the opposite direction of the QRS complex

    Pvcs patterns
    PVCs – Patterns

    • Pairs (couplets): two sequential PVCs

    • Runs or bursts: three or more sequential PVCs are called “ventricular tachycardia” (VT)

    • Bigeminal PVCs (ventricular bigeminy): every other beat is a PVC

    • Trigeminal PVCs (ventricular trigeminy): every third beat is a PVC

    • Quadrigeminal PVCs (ventricular quadrigeminy): every fourth beat is a PVC

    Uniform pvcs
    Uniform PVCs

    • Premature ventricular beats that look the same in the same lead and originate from the same anatomical site (focus)

    Multiform pvcs
    Multiform PVCs

    • PVCs that appear different from one another in the same lead

    • Often (but not always) arise from different anatomical sites

    Pvcs causes

    Normal variant


    Stress, anxiety


    Digitalis toxicity

    Acid-base imbalance

    Myocardial ischemia

    Electrolyte imbalance





    Congestive heart failure

    Increased sympathetic tone

    Acute myocardial infarction







    Cyclic antidepressants


    PVCs – Causes

    Pvcs clinical significance
    PVCs – Clinical Significance

    • PVCs may or may not produce palpable pulses

    • Patients may be asymptomatic or complain of:

      • Palpitations

      • “Racing heart”

      • Skipped beats

      • Chest or neck discomfort

    • If the PVCs are frequent, signs of decreased cardiac output may be present

    Pvcs intervention
    PVCs – Intervention

    • Treatment of PVCs is dependent on the:

      • Cause

      • Patient’s signs and symptoms

      • Clinical situation

    • Most patients experiencing PVCs do not require treatment with antidysrhythmic medications

    Idioventricular rhythm ivr
    Idioventricular Rhythm (IVR)

    • A ventricular escape or “idioventricular” rhythm (IVR) is three or more sequential ventricular escape beats occurring at a rate of 20 to 40 beats/min

    Idioventricular rhythm causes
    Idioventricular Rhythm – Causes

    • Myocardial infarction

    • Digitalis toxicity

    • Metabolic imbalances

    Idioventricular rhythm clinical significance
    Idioventricular Rhythm – Clinical Significance

    • Possible signs and symptoms due to the slow ventricular rate:

      • Severe hypotension

      • Weakness

      • Disorientation

      • Lightheadedness

      • Loss of consciousness

    Idioventricular rhythm intervention
    Idioventricular Rhythm – Intervention

    • Avoid lidocaine!

      • May abolish ventricular activity, possibly causing asystole

    • If the patient is symptomatic because of the slow rate and/or loss of atrial kick:

      • Atropine may be ordered

      • Transcutaneous pacing (TCP) may be attempted

    Ventricular tachycardia vt
    Ventricular Tachycardia (VT)

    • VT exists when three or more PVCs occur in immediate succession at a rate higher than 100 beats/min

      • Non-sustained VT

        • A short run lasting less than 30 seconds

      • Sustained VT

        • Persists for more than 30 seconds

    • VT may occur with or without pulses

    • Patient may be stable or unstable

    Ventricular tachycardia vt1
    Ventricular Tachycardia (VT)

    • VT may originate from an ectopic focus in either ventricle

      • The QRS complex is wide and bizarre

      • P waves, if visible, bear no relationship to QRS complex

      • The ventricular rhythm is usually regular but may be slightly irregular

    Ventricular tachycardia vt2
    Ventricular Tachycardia (VT)

    • Monomorphic VT

      • QRS complexes are of the same shape and amplitude

    • Polymorphic VT

      • QRS complexes vary in shape and amplitude

    Ventricular tachycardia causes
    Ventricular Tachycardia – Causes

    • Sustained monomorphic VT is often associated with underlying heart disease, particularly myocardial ischemia

      • Rarely occurs in patients without underlying structural heart disease

    Ventricular tachycardia other causes


    Cyclic antidepressant overdose

    Digitalis toxicity

    Valvular heart disease

    Mitral valve prolapse


    Myocardial contusion

    Invasive cardiac procedures

    Acid-base imbalance

    Electrolyte imbalance




    Increased production of catecholamines


    Cocaine abuse

    Ventricular Tachycardia – Other Causes

    Ventricular tachycardia clinical significance
    Ventricular Tachycardia – Clinical Significance

    • Signs and symptoms vary

    • Syncope may occur because of an abrupt onset of VT

      • The patient’s only warning symptom may be a brief period of lightheadedness

    Ventricular tachycardia clinical significance1
    Ventricular Tachycardia – Clinical Significance

    • Signs and symptoms of hemodynamic compromise related to the tachycardia may include:

      • Shock

      • Chest pain

      • Hypotension

      • Shortness of breath

      • Pulmonary congestion

      • Congestive heart failure

      • Acute myocardial infarction

      • Decreased level of consciousness

    Ventricular tachycardia intervention
    Ventricular Tachycardia – Intervention

    • Treatment is based on the patient’s presentation

    • Stable but symptomatic patients are treated with:

      • Oxygen therapy

      • IV access

      • Administration of ventricular antidysrhythmic to suppress the rhythm

    Ventricular tachycardia intervention1
    Ventricular Tachycardia – Intervention

    • Unstable patient with a pulse

      • Usually a sustained heart rate of 150 beats/min or more

    • If signs and symptoms are a result of rapid rate:

      • Administer oxygen

      • IV access

      • Sedate (if awake and time permits)

      • Electrical therapy

    • If the patient is pulseless:

      • Begin CPR until a defibrillator is available

    Ventricular tachycardia intervention2
    Ventricular Tachycardia – Intervention

    • When unclear whether a regular, wide-QRS tachycardia is VT or SVT, treat the rhythm as VT until proven otherwise.

    Torsade de pointes tdp
    Torsade de Pointes (TdP)

    • A dysrhythmia intermediary between VT and VF

    • A type of polymorphic VT associated with a prolonged QT interval

    • French for “twisting of the points”

      • QRS changes shape, amplitude, and width

      • Appears to “twist” around the isoelectric line, resembling a spindle

    Ventricular fibrillation vf
    Ventricular Fibrillation (VF)

    • VF is a chaotic rhythm that originates in the ventricles

    • No organized depolarization of the ventricles

      • Ventricular myocardium quivers

      • No effective myocardial contraction and no pulse

      • Resulting rhythm is irregularly irregular with chaotic deflections that vary in shape and amplitude

      • No normal-looking waveforms are visible

    Ventricular fibrillation
    Ventricular Fibrillation

    • Fine VF Low amplitude waves (less than 3 mm)

    • Coarse VF Waves more easily visible (greater than 3 mm)

    Ventricular fibrillation1
    Ventricular Fibrillation

    • Because artifact can mimic VF, always check the patient’s pulse before beginning treatment for VF

    • The patient in VF is unresponsive, apneic, and pulseless

    Vf causes

    Extrinsic factors

    Increased sympathetic nervous system activity

    Vagal stimulation

    Metabolic abnormalities



    Antidysrhythmics and other medications




    Environmental factors


    Intrinsic factors



    Myocardial failure

    Enhanced AV conduction

    Bypass tracts

    “Fast” AV node

    Abnormal repolarization


    VF – Causes

    Vf intervention
    VF – Intervention

    • Begin CPR until a defibrillator is available

    • On arrival of the defibrillator, deliver unsynchronized shocks

    • Perform endotracheal intubation, establish IV access

    • Administer medications per current resuscitation guidelines


    • Please type in the text box if you are watching the live presentation.

    • Otherwise feel free to give us a call at 815-300-7140 or email [email protected]

    • Thank you!