Silver Cross EMS September 2012 3rd Trimester CME

Allergies and AnaphylaxisPresented 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.

• 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…

www.silvercrossems.com

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

Allergies

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

Anaphylaxis

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

Antigens

• 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

Antibodies

• 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)

• Agents that may cause hypersensitivity reactions (including anaphylaxis)– Drugs and biological agents– Insect bites and stings– Foods

Hypersensitivity Reactions

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

Histamines• 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….

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.

Normal Circulation vs. Distributive Shock

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

Urticaria as a result of an allergic reaction.

Angioedema of the Eyes

Bee Sting and Angioedema of the LipsBee Sting and Angioedema

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 TherapyEpinephrineFluid resuscitation for hypovolemia• Antihistamines to antagonize the effects of histamine

Benadryl (diphenhydramine)50mg IVP slowly over 2-3 minutes50mg IM if no IV

• Beta agonists to improve alveolar ventilationAlbuterol nebulizer

• Corticosteroids to prevent a delayed reactionSolu-medrol (methylprednisolone)

125mg IVPNo longer just for long transports

ALS

ILS

BLS

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

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

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)

Pharmacokinetics

Onset< 2 minutes (IV/ET)

Peak effects< 5 minutes (IV/ET)

Duration5-10 minutes (IV/ET)

Half-life5 minutes

Indications

Cardiac arrest AsystoleVentricular fibrillationPulseless ventricular tachycardiaPEA (pulseless electrical activity)

Severe anaphylaxisSevere reactive airway disease

Precautions

Should be protected from lightCan be deactivated by alkaline solutions such as

sodium bicarbonateThe IV line must be adequately flushed between

administrations of epinephrine and sodium bicarbonate.

Side Effects

PalpitationsAnxietyTremulousnessHeadacheDizzinessNauseaVomitingIncreased myocardial oxygen demand

Interactions

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

Dosage

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.)

Severe anaphylaxis (adult) 1:10,000 0.3 – 0.5 mg IV/IO1:1,000 0.3 – 0.5 mg IM (if no IV/IO)

Severe anaphylaxis (pediatrics)0.01 mg/kg of 1:1,000 IMRepeat every 5-15 minutes

Dosage (cont.)

Severe asthma/COPD (adult) 1:1,000 0.01 mg/kg up to 0.3 mg IM (with medical

control approval)

Epi-pen autoinjector

Strip O’ the Month – Ventricular Rhythms

The Ventricles

Ventricles are the heart’s least efficient pacemakerNormally 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)

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

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

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

Multiform PVCs

PVCs that appear different from one another in

the same lead

Often (but not always) arise from different

anatomical sites

PVCs – CausesNormal variant

Hypoxia

Stress, anxiety

Exercise

Digitalis toxicity

Acid-base imbalance

Myocardial ischemia

Electrolyte imbalanceHypokalemia

Hypocalcemia

Hypercalcemia

Hypomagnesemia

Congestive heart failure

Increased sympathetic tone

Acute myocardial infarction

StimulantsAlcohol

Caffeine

Tobacco

MedicationsSympathomimetics

Cyclic antidepressants

Phenothiazines

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

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)

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

Myocardial infarction

Digitalis toxicity

Metabolic imbalances

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

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)

VT exists when three or more PVCs occur in immediate succession at a rate higher than 100 beats/minNon-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 (VT)

VT may originate from an ectopic focus in either

ventricleThe 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 (VT)

Monomorphic VTQRS complexes are of the same shape and amplitude

Polymorphic VTQRS complexes vary in shape and amplitude

Ventricular Tachycardia – Causes

Sustained monomorphic VT is often associated with underlying heart disease, particularly myocardial ischemiaRarely occurs in patients without underlying structural heart disease

Ventricular Tachycardia – Other Causes

Cardiomyopathy

Cyclic antidepressant overdose

Digitalis toxicity

Valvular heart disease

Mitral valve prolapse

Trauma

Myocardial contusion

Invasive cardiac procedures

Acid-base imbalance

Electrolyte imbalanceHypokalemia

Hyperkalemia

Hypomagnesemia

Increased production of catecholamines

Fright

Cocaine abuse

Ventricular Tachycardia – Clinical Significance

Signs and symptoms vary

Syncope may occur because of an abrupt onset of VTThe patient’s only warning symptom may be a brief period of

lightheadedness

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

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 – Intervention

Unstable patient with a pulseUsually 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 – Intervention

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

Monomorphic VT – ECG Characteristics

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)

VF is a chaotic rhythm that originates in the ventricles

No organized depolarization of the ventriclesVentricular 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

Fine VF Low amplitude waves (less than 3 mm)

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

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 factorsIncreased sympathetic nervous system activity

Vagal stimulation

Metabolic abnormalities

Hypokalemia

Hypomagnesemia

Antidysrhythmics and other medications

Psychotropics

Digitalis

Sympathomimetics

Environmental factors

Electrocution

Intrinsic factorsHypertrophy

Ischemia

Myocardial failure

Enhanced AV conduction

Bypass tracts

“Fast” AV node

Abnormal repolarization

Bradycardia

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

Questions!

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Otherwise feel free to give us a call at 815-300-7140 or email afinkel@silvercross.org.

Thank you!