Anaphylactic shock

Objectives:
• Perceive the differences between anaphylactic shock
and other types of shock.
• Recognize its nature, causes & characteristics.
• Specify its diagnostic features.
• Identify its standard emergency management
protocol.
• Justify the mechanism of action and method of
administration of each of the different used drugs to
limit its morbid outcomes.

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Titles
Very important
Extra information
Doctor’s notes

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 Anaphylaxis
Is a sudden, severe hypersensitivity reaction affecting the whole
body (generalized or systemic) in response to allergen.
Symptoms
Mucosal Difficulty Blood pressure
(hypotension)
Rash
swelling breathing

A N A P H Y L AC T I C S H O C K
A life-threatening allergic reaction that causes shock
(hypoperfusion) and airway swelling. “Anaphylactic shock” is
a term that specifically refers to an episode of anaphylaxis.

Generalized circulatory derangement causing

multiple organ HYPOPERFUSION [Inadequate
oxygen delivery to meet metabolic demands ] &
SHOCK strong sympathetic activation.
 If the shock is intense or sustained enough,
it will lead to irreversible derangements sets
then to permanent functional deficit or
death.

Adrenoceptors:
Alpha1:vasoconstriction.
Beta1:restore heart function(heart muscles
contraction).
Beta2:bronchodilation.

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 Types of shock
Caused by Type

Hemorrhage •
Hypovolemic
fluid loss (plasma, ECF) e.g. Excessive vomiting •
:.Inability to contract & pump. E.g Cardiogenic
myocardial infarction •
:Extra-cardiac obstruction
Pulmonary •
Obstructive
.embolism
.Cardiac Tamponade •
Decreased Peripheral* Resistance vasodilation
.hypotension
As in: septic shock, Neurogenic shock, anaphylactic Distributive
.shock

*Peripheral resistance is the resistance of the arteries to blood flow. As the arteries
constrict, the resistance increases and as they dilate, resistance decreases.
Peripheral resistance is determined by three factors:
Autonomic activity: sympathetic activity constricts peripheral arteries.
Pharmacologic agents: vasoconstrictor drugs increase resistance while vasodilator
drugs decrease it.
Blood viscosity: increased viscosity increases resistance.
• What we need for normal blood pressure :
1. Good cardiac output
2. Good vessels walls constriction
• If the patient is taking B2 blockers salbutamol won’t work so antimuscarinics like
ipratropium is the drug of choice.

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 ANAPHYLACTIC SHOCK

Immunologic Anaphylaxis Non-Immunologic Anaphylaxis

(known as ANAPHYLAXIS) (ANAPHYLACTOID) Directly act
It belongs to type I on mast cells Not IgE-mediated
hypersensitivity reaction (IgE)
Exogenous substances directly
Occurs after exposure to foreign
substances [antigen] such as food, degranulate mast cells. E.g.
insect or animal venom, drugs, blood Radiocontrast dye, Opiates
products. “analgesics”, Depolarizing
The immune system will then develop drugs, Dextrans
antibodies for this antigen and it will “antithrombotics”.
remain in the body for a while.
An anaphylactoid reaction can
After a 2nd exposure to the same
antigen in previously sensitized occur following a single, first-
persons (antigenspecific ige are time exposure to certain agents
present), IgE binds with mast in non-sensitized patients.
cell causing its degranulation. NO need for second exposure

Because anaphylactic and anaphylactoid reactions produce the same clinical manifestations and are
treated exactly the same way, we use the term anaphylaxis to refer to both conditions.

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 The degranulation of the mast cells will release histamine, Leukotrienes and other
inflammatory substances and will lead to:

Adrenaline Adrenaline Adrenaline Adrenaline

salbutamol Corticosteroids
H1antagonist(antihistamine)

3. 4.

Circulatory Hypo-perfusion
47% Collapse 1
.
88%
33%
Shortness of breath
Remember
2. characters of anaphylactic shock:
when there is
Mucous Swelling • Rapidly developing [ 5/30 min.can be hours ]. to much
Rhinitis 16% vasodilatation
• Severe, life-threatening. the body has
Angioedema 88%
Airway 56% • Multisystem involvement. to
GIT 30% compensate
• Mortality: due to respiratory (70%) or cardiovascular (25%). by causing
tachycardia as
ANAPHYLACTIC When the Call START a reflex
SHOCK diagnosis is ambulance EMERGENCY
made TREATMENT

Respiratory support Circulatory support : Lay Adrenaline IM

-Open airway down and raise legs up\ by auto injector
-O2 inhalation fluid replacement or Syringe

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 ANAPHYLACTIC SHOCK THERAPY PROTOCOL

RESCUE

1ST LINE

To compensate for vasodilation BC

vasodilation means you need more blood

2ND LINE
In skin

The doctor said we won’t be asked about doses.

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 ANAPHYLACTIC SHOCK THERAPY PROTOCOL

inhalator
Salbutamol,
Ipratropium
bronchodilator

parental Aminophyline
Adjuvant to 2nd line:

H1 blocker Phenaramine

H blocker
Cimetidine
H2 blocker
Ranitidine

glucagon For patients taking beta-blocker.

Objective of therapy:
• To support the respiratory & circulatory deficits
• To halt (to stop) the existing (the excessive) hyper-
reaction
• To prevent further hyper-reaction of immune
system (Biphasic phenomenon ): 2nd release of
mediators without re-exposure to antigen (in up to
20% ) Clinically evident 3-4h after the initial
manifestations clear

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 1st line
Adrenaline
Mechanism of A nonselective Adrenergic agonist [a1, a2, b1, b2 ]
action

As an adrenergic agonist:
• Reverses peripheral vasodilation  maintains Blood Pressure & directs blood
flow to major organs
• edema  reverse hives* ,swelling around face & lips & angioedema** in
nasopharynex & larynx
As a b-adrenergic agonist:
• b2 effect: Dilates bronchial airways + histamine & leukotriene release from mast
cells
• b1 effect:  force of myocardial contraction
• PHYSIOLOGICAL ANTAGONIST: Attenuates the severity of IgE-mediated allergic
Action reactions
• Indication: drug of choice
* allergic skin reaction causing localized redness, swelling, and itching
(see more http://medical-dictionary.thefreedictionary.com/hives)
** a localized edematous reaction of the deep dermis or subcutaneous or
submucosal tissues appearing as giant wheals (see more
http://medical-dictionary.thefreedictionary.com/angioedema)

Contraindications • Not given more than 40 years cardiac patient

• Rare in a setting of anaphylaxsis

Adverse effect Dysrrhythmias

Intamascular (IM), due to:

• Easily accessible (Auto-injectors Kits:
Disposable (use for once) , prefilled
devices  automatically administer a
Administration single dose of epinephrine in
emergency)
• Greater margin of safety, so no
dysrrhythmias as with IV
• No need to wait for IV line, if IV present
it given by physician under monitoring
Repeat every 5-10 min as needed Patients observed
for 4-6 hours. Why ? Fear of biphasic anaphylaxsis If hypotension persist  start dopamine

For patients taking b-blockers because they either:

• Refractory (not response); as it may antagonize b effects of adrenaline
Caution • Rebound hypertension: [ unopposed a effect], specially when adrenaline is
8 repeated ‫يعني بيجي األدرينالين مكان مستقبالت األلفا ويسبب ارتفاع ضغط‬
 corticosteroids H1 blockers H2 blockers Salbutamol Aminophylline glucagon

Ipratropium
Has both positive
inotropic &
chronotropic
through immediate effects on heart 

b2 -adrenergic agonist
GCs actions on increase cardiac
Mechanism of action

Membrane-bound Though (anti-ulcer

cyclic AMP  an

Anticholinergic
mast cells effect entirely
receptors  drugs, used independent of
modulating levels of have for adrenergic that is
2nd messengers  already de- epigastric why effective in
(within seconds or granulated pain) spite of b-
(e.g. adrenergic
minutes) which phenaramine)
means Non-genomic blockade.
Efficacy of acting
action on bronchi less
than in heart (no
evident
bronchodilation)

• Reverse 1- Short
hypotension and • help to acting,
bronchoconstrict counter rapid relief patients
ion, so it will act onset relax treatment with
decrease the histamine- of
releasing of mediated The bronchial
anaphylaxis
refractory
smooth hypotension
Decrease secretion
vasodilati significance

Less rapid in action

inflammatory muscle and when
mediators (anti- on & of H2 may inhaled
Action

bronchoco
chemotactic & nstriction. blockers is decrease Broncho- Drug of
mast cell • May not
stabilizing help to established
mediator dilators are choice for
release not
effects). limit (e.g. from mast severe
• Decrease biphasic effective & anaphylaxis
Ranitidine & cells and
mucosal swelling bronchospa
and skin reaction
reactions cimetidine) basophils. sm is in patients
by 2- Inhibit
• May help to limit decrease persistent taking b-
airway
biphasic reactions histamine microvascular blockers.
by decrease release
allergic mediators leakage.

• Not given more

Contraindicatio

No cimetidine
than 40 years in elderly, Given in
cardiac patient renal/hepatic hospital
ns

• Rare in a setting failure, or if setting as

of anaphylaxis on b-blockers levels of drug
should be
Therapeuticall
associated
longer duration of action

y Monitored
Adverse effect

with because it has

serious narrow
Dysrrhythmias adverse therapeutic
Inhalational

drug index
interactions
Administrati

slowly intravenously Ranitidine 1 mg IV q 5 min

Inhalational until hypotension
on

or intramuscularly 50 mg IV resolves

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 ‫‪More explanation‬‬

‫‪Non-genomic action‬‬ ‫‪Genomic action‬‬

‫‪genomic action is slow may take hours to days‬‬

‫هنا يدخل الدوا ويرتبط‬
‫هنا يدخل الدوا ويرتبط بمستقبل جوا الخلية‪،‬‬
‫بالمستقبالت اللي على الغشاء‬ ‫وبيأثر‬ ‫‪DNA‬‬
‫المستقبل بيدخل جوا‬ ‫هذا‬
‫البالزمي ويعطي تأثير سريع‬ ‫بتكوين البروتين بعدين يطلع التأثير‪ ،‬يأخذ‬
‫وقت طويل عشان يعطي تأثيره‬

‫‪contraction‬أسوي‬
‫‪ ،‬عشان‬ ‫‪contraction‬‬
‫مافيه‬ ‫بالتالي‬ ‫‪cAMP‬‬
‫عندي‬ ‫ماراح يصير‬ ‫‪b-blockers‬‬
‫لو كان المريض يأخذ‬
‫وبيصير‬ ‫‪contraction‬‬
‫تزيد‬ ‫وبالتالي‬ ‫على‪G‬مستقبالت خاصه‬
‫‪ cAMP‬فيه تحفز‬ ‫استخدم قلوكاجون اللي بيأثر‬
‫‪Glucag‬‬ ‫‪S‬‬

‫عندي‬
‫‪on‬‬

‫‪Gs‬‬

‫‪Gs‬‬ ‫‪M 2 & M3‬‬

‫‪-‬‬
‫‪Sympathomime‬‬ ‫‪Ipratropi‬‬
‫‪tics‬‬ ‫‪um‬‬

‫‪10‬‬
 SAQ
A 12-year-old boy is brought to the emergency department after being stung by a bee. He
had been well until he was stung on his right forearm, while playing in the yard. He
initially complained of localized pain and swelling. Fifteen minutes later, he began to
complain of shortness of breath. His parents observed him to be wheezing, very weak
and dizzy. His parents brought him immediately to the local emergency department. His
medical history shows that he has allergy.
Q1: what is the most likely diagnose in this case ?
Anaphylactic shock.

Q2: What is the drug of choice in this case ?

Adrenaline.

Q3: What is the best route of administration for this drug ?

Intra-muscular (IM).
although we can use IV line but should be given by physician under monitoring.

Q4: What is the mechanism of its action ?

It is Sympathomimetic drug, so it mimics the effect of Sympathetic system by working as Adrenergic agonist .
It is nonselective agonist which act on [α1, α2, β1, β2, β3 ], some of its action:
1\ In blood vessel, act as α agonist which cause vasoconstriction.
2\ In heart, act as β1 agonist which lead to increase the force of myocardial contraction.
3\ In bronchi & bronchioles, act as β2 agonist which cause bronchodilator and decrease histamine & leukotriene release from
mast cells .

- After 3-4 hours, he may develop what we called Biphasic Phenomenon.

Q5:What do we mean by Biphasic Phenomenon?
It is a second episode of anaphylaxis with 2nd release of mediators without re-exposure to antigen.

Q6: List some drugs we can use it to prevent Biphasic Phenomenon ?

2nd line anaphylaxix’s drugs. Such as 1\ Glucocorticoids : Hydrocortisone
2 \ First generation H1 blocker : Chlorophenamine

Q7: Later, we can give him some bronchodilators as Adjuvant 2 nd

line therapy, list some of them?
Salbutamol as β2 Agonist.
Ipratropium as Anti-muscarinic.
Aminophylline as Methyl-xanthine.

Zoom in to see the answers

11
 ‫‪QUIZ‬‬

‫‪Boys‬‬ ‫‪Girls‬‬
‫عبدالرحمن ذكري‬ ‫غادة المهنا‬
‫عبدالعزيز رضوان‬ ‫اللولو الصليهم‬
‫مؤيد أحمد‬ ‫روان القحطاني‬
‫فيصل العباد‬ ‫درة الحمدي‬
‫فارس النفيسة‬ ‫شروق الصومالي‬
‫خالد العيسى‬ ‫سما الحربي‬
‫عبدالرحمن العريفي‬ ‫انوار العجمي‬
‫عبدالرحمن الجريان‬ ‫وتين الحمود‬
‫محمد خوجة‬ ‫رنا باراسين‬
‫عمر التركستاني‬ ‫امل القرني‬

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