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SHOCK

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Page 1: Presentation1

SHOCK

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shockObjectives

Definition Approach to patient in shock

Types Specific treatment

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Definition Inadequate oxygen delivery to the tissue

to meet its metabolic demands Result in global tissue hypoperfusion and

metabolic acidosis Shock can occur with normal BP and

hypotension can occur without shock

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pathophysiology

Inadequate systemic O2 delivary activate autonomic nervous system

Sympathetic nervous system NE, epinephhrine,dopamine,cortisol release cause

Vasoconstriction+ HR+ cardiac contractility

Renin-angiotensin axis Water and sodium conservation blood volume

and BP

Vasoconstriction

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Cellular response ATP depletion,edema,hydrolysis of cell

membrane

Inability to meet body demands lead to :1-Lactic acidosis2- Cardiovasscular insufficiency3- Increase metabolic demands

Progression of physiologic effects as shock ensues: Cardiac depression Respiratory distress Renal failure DICResult in multiple organ failure (MODS).

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Recognizing shock

BP

Weak ,rapid or absent PULSE

cold clammy pale sweating.

Confused (drowsy or agitated)

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Approach to patient in shock

ABCs ( cardiopulmonary , pulse oximetry, O2 supply, I.V. access ….ect)

Dx: history physical exam Investigations ( lab. Ix, Imaging)

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Types Hypovolemic Septic Cardiogenic Neurogenic Others : Anaphylactic , Obstructive,

Vasovagal

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Hypovolemic shock Causes A- Hemorrhagic (GI bleeding, trauma) B- non-hemorrhagic (vomiting, diarrhea)

C/P: As above with hx of trauma/surgery/illness

Mx:1- lower the head and lift the foot (increase VR)2- High flow O23-Stop bleeding4-Replacement of volume deficit5-Sedation6-Monitoring BP,PR,RR ,UOP and gas analysis

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Septic shock Causes: serious G+ve infections e.g. peritonitis

C/P: intermittent fever and rigor Tachycardia low BP( systolic <90) mental status change Mx: monitoring of vital signs ,UOP, blood gases,

electrolytes,PH.Treatment must be prompt and aggressive, it

include:1- ABC2- Blood culture and then broad spectrum antibiotics3- Steroid , vasodilators

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Cardiogenic shock

Causes: MI, PE, arrythmia , vulvular heart disease , CHF.

C/P: hx of recent surgery/trauma chest pain dypnoea palpitations Rx: 1-High flow O2 2- Give 2.5mg morphine I.V. 3- Treat the cause e.g. MI with 0.1mg GTN, 300mg

aspirin 4- monitoring vital signs , ECG , CXR.

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Neurogenic shock

Occur after acute spinal cord injury disrupt sympathetic outflow leaving unopposed vagal tone result in hypotension and bradycardia.

+ warm and dry skin.

Mx: 1- ABCs 2- Fluid resuscitation 3- for bradycardia : use atropine or pacemaker 4- methyprednisolone in high dose within

8hrs.

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Anaphylactic shock Causes: drug allergy, blood product reaction, latex

allergy.

C/P: hx of sudden onset after drug adminstration, stridor or bronchospasm, angioedema, urticaria, pruritis, rash.

Rx: 1- Sit patient up, give O2 2- if I.V. access : give 1ml of 1:10000 adrenaline

bolus then100mg hydrocortisone bolus then 10mg chlorpheniramine I.V.

3- repeat every 5-10min if no improvement 4- if no I.V. access: give 1ml of 1:1000 adrenaline

I.M. then secure I.V. access.

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Multiple organ failure syndrome(MODS)

One of the end redults of septic shock, its clinical end stage of systemic hypermetabolic response to injury.its account for 75% of death in surgical ICU.

PHASES:1- Initial insult: caused either by H.g., sepsis,

ischemia, tissue injury or severe inflammation.2-Rrelative hemodynamic stability: during the next

24-72 hrs post-injury in which the patient is well.3- phase of hypermetabolism: last for 2-3 ws. In

which all organ of body go into hypermetabolic state which is manifestated by:

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a-low grade fever b-acute respiratory distress syndrome c- increase C.O. and O2 consumption d- hyperglycemia, increase urea and

nitrogen secretion >15 gm/day. 4- The patient then either passes to: recovery: (9-14 days) postinjury. Or persistence of hypermetabolism

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pathophysiology1- Metabolic changes: increase metabolic

rate+ O2 consumption and CO2 production.

2- Pulmonary changes:3- CVS changes: 4- Renal changes : maintained in first phase

(early days) but later fall into oliguric state.

5- GIT changes

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Treatment

There is no actual Rx.But the key management is : 1-prevention2- support to gain time ffor patient to heal

on its own .This occur by: a- source control b- Resuscitation c- Metabolic support( I.V. fluid+ nutrition)

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The End