Shock is defined as inadequate oxygen delivery to tissues due to global tissue hypoperfusion and metabolic acidosis. There are several types of shock including hypovolemic, septic, cardiogenic, neurogenic, and others. Treatment depends on the underlying cause but generally involves restoring oxygen delivery through airway management, oxygen supplementation, intravenous fluid resuscitation, antibiotics for infection, and treating the underlying cause of shock. Multiple organ failure may result if shock persists and damages vital organs over time.

2. Objectives
Definition
Approach to patient in shock
Types
Specific treatment

3.  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

4. 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

5.  Cellular response
ATP depletion,edema,hydrolysis of cell membrane
Inability to meet body demands lead to :
1-Lactic acidosis
2- Cardiovasscular insufficiency
3- Increase metabolic demands
Progression of physiologic effects as shock ensues:
 Cardiac depression
 Respiratory distress
 Renal failure
 DIC
Result in multiple organ failure (MODS).

6.  BP
 Weak ,rapid or absent PULSE
 cold clammy pale sweating.
 Confused (drowsy or agitated)

7.  ABCs ( cardiopulmonary , pulse oximetry, O2
supply, I.V. access ….ect)
 Dx: history
 physical exam
 Investigations ( lab. Ix, Imaging)

8.  Hypovolemic
 Septic
 Cardiogenic
 Neurogenic
 Others : Anaphylactic , Obstructive, Vasovagal

9.  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 O2
3-Stop bleeding
4-Replacement of volume deficit
5-Sedation
6-Monitoring BP,PR,RR ,UOP and gas analysis

10.  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- ABC
2- Blood culture and then broad spectrum antibiotics
3- Steroid , vasodilators

11.  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.

12.  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.

13.  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.

14.  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:

15. 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

16. 1- 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

17. There is no actual Rx.
But the key management is :
1-prevention
2- 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)

18. The End