Brief introduction about shock, types and general management of shock.

1. SHOCK
Student: Dr. Eliz Achhami(Intern)
Shree Birendra Hospital

2. Objectives
• Definition
• Types
• Pathophysiology
• Clinical features
• Management aspects

3. Definition
• Shock is a physiologic state characterized by
systemic reduction in tissue perfusion,
resulting in decreased tissue oxygen delivery.

4. Demand Supply  Demand  Supply
ShockNormal

5. Types of Shock
Shock
obstructive
Cardiogenic
Distributive
Hypovolemic

6. HYPOVOLAEMIC ETIOLOGY
Hemorrhagic
• Trauma
• Gastrointestinal
• Retroperitoneal
Non-Hemorrhagic(Fluid
depletion)
External fluid loss
- Dehydration
- Vomiting
- Diarrhea
• Interstitial fluid redistribution
- Thermal injury
- Trauma
- Anaphylaxis

7. • Valvular heart disease
• Myocardial infarction.
• Cardiac arrhythmias.
• Cardiomyopathy
CARDIOGENIC ETIOLOGY

8. OBSTRUCTIVE ETIOLOGY
• Cardiac Tamponade
• Constrictive pericarditis
• Pulmonary Embolism
• Tension Pneumothorax
• Air embolism

9. NEUROGENIC ETIOLOGY
• Paraplegia.
• Quadriplegia.
• Trauma to spinal cord.
• Spinal anesthesia.

10. ANAPHYLACTIC ETIOLOGY
• Injections - Penicillins.
• Anaesthetics
• Stings.
• Shelfish.

11. • Gram +
• Gram -
• Fungi / Virus
• Protozoa
SEPTIC ETIOLOGY
Bacterial

12. ENDOCRINE ETIOLOGY
• Hypo & Hyperthyroidism.
• Adrenal insufficiency.

13. Pathophysiology of Shock
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death

14. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
Neurohormonal response
Stimulated by baroreceptors
 Increased heart rate
 Increased contractility
 Vasoconstriction
(Afterload)
 Increased Preload
Hormonal: Renin-angiotension
system
Decrease renal perfusion
Releases renin--angiotension I
angiotension II ---potent
vasoconstriction & releases
aldosterone adrenal cortex
sodium & water retention (
intravascular volume )

15.  SNS - Hormonal:
Antidiuretic Hormone
 Osmoreceptors in
hypothalamus stimulated
 ADH released by
Posterior pituitary gland
 Vasopressor effect to
increase BP
 Acts on renal tubules to
retain water
SNS - Hormonal: Adrenal
Cortex
 Anterior pituitary releases
adrenocorticotropic hormone
(ACTH)
 Stimulates adrenal Cortex to
release glucorticoids
 Blood sugar increases to meet
increased metabolic needs

16. Shock – Effects on Organ
• Heart – ↓ CO / hypotension / myocardial
depressants
• Lung - ↓gas exchange / tachypnoea / pulmonary
edema
• Endocrine – ADH → ↑ reabsorption of water
• CNS – perfusion ↓ – drowsy
• Blood - Coagulation abnormalities – DIC
• Renal - ↓ GFR - ↓ urine output
• GIT – mucosal ischaemia – bleeding & hepatic - ↑
enzyme levels

17. Stages of shock
• Initial : The cells become leaky and switch to
anaerobic metabolism.
• Non-progressive:(compensated stage)
Attempt to correct the metabolic upset of
shock.
• Progressive: (decompensated stage )
Eventually the compensation will begin to fail.
• Refractory : Organs fail and the shock can no
longer be reversed.

18. Clinical features
• Features of shock depend on the degree of loss of
volume & on duration of shock.
• Types
– Mild shock.
– Moderate shock.
– Severe shock.

19. SHOCK
[ Management ]

20. Diagnosis and Evaluation
Laboratory
 Hb, WBC, platelets
 PT/PTT
 Electrolytes, arterial blood gases
 BUN, Creatinine
 Calcium , Magnesium
 Serum lactate
 ECG

21. Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF,
oximetry)

22. Goals of Resuscitation
• Overall goal:
– increase O2 delivery
– decrease demand
Treatment
O2 content Cardiac
output
Blood
pressure

23. Immediate Goals in Shock
Hemodynamic support MAP > 60mmHg
PAWP = 12 - 18 mmHg
Cardiac Index > 2.2 L/min/m2
Maintain oxygen delivery Hemoglobin > 9 g/dL
Arterial saturation > 92%
Supplemental oxygen and
mechanical ventilation
Reversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L)
Maintain urine output
` Reverse encephalopathy
Improving renal, liver function
tests

24. Principles of Resuscitation
• A: Airway
– patent upper airway
• B: Breathing
– adequate ventilation and oxygenation
• C: Circulation
– placement of adequate IV access
• cardiac function
• oxygenation

25. Fluid therapy
Crystalloids
• Lactated Ringer’s solution
• Normal saline
Colloids
• Hetastarch
• Albumin
Packed red blood cells
Infuse to physiologic endpoints

26. Hypovolemic Shock
Restore circulating volume with blood, colloid, or crystalloid
Control hemorrhage
Vasoconstrictor if BP still low after volume loading
Identify source of blood or fluid loss:
• Endoscopy/colonoscopy
• Angiography
• CT/MRI scan

27. Cardiogenic Shock
o Goal of Management :
o Treat Reversible Causes
o Protect ischemic myocardium
o Improve tissue perfusion
o Limiting/reducing myocardial damage during Myocardial
Infarction:
 Increased pumping action & decrease workload of the heart
• Inotropic agents/Vasoactive drugs
• Intra-aortic balloon pump
• Cautious administration of fluids
• Transplantation
 Consider thrombolytics, angioplasty in specific cases

28. Extra-cardiac Obstructive Shock
Pericardial tamponade
• pericardiocentesis
• surgical drainage (if needed)
Pulmonary embolism
• heparin
• ventilation/perfusion lung scan
• pulmonary angiography
• consider:
• thrombolytic therapy
• embolectomy at surgery

29. Distributive Shock
Anaphylactic Shock
– Early recognition, treat aggressively
– Airway support
– IV epinephrine (open airways)
– Antihistamines
– Corticosteroids
– Immediate withdrawal of antigen if possible
– Judicious crystalloid administration
– Vasopressors to maintain organ perfusion
– Positive inotropes

30. Management of septic shock
A. Initial Resuscitation
• For sepsis induced hypoperfusion, at least
30ml/kg of IV crstalloid fluid should be given
within the first 3 hour.
• Additional fluids be guided by frequent
reassessment hemodynamic status.
B. Diagnosis
• Appropriate routine microbiological cultures.

31. C. Antimicrobial therapy
• IV antimicrobials as soon as possible after
recognition and within one hour for sepsis and
shock.
• Empiric broad spectrum therapy to cover all
pathogens.
• Antimicrobial treatment duration of 7 to 10 days
is adequate for most of infections.

32. D. Source control
• Recommend that a specific anatomic diagnosis be identified or
excluded as rapidly as possible in patients with sepsis or septic
shock, and that any required source control intervention be
implemented as soon as medically and logistically practical after
the diagnosis is made.
E. Fluid therapy
• recommend crystalloids as the fluid of choice for initial
resuscitation and subsequent intravascular volume replacement
• Use albumin in addition to crystalloids (if require substantial
amounts of crystalloids)

33. F. Vasoactive agents
• Recommend norepinephrine as the first choice
vasopressor.
• Suggest adding either vasopressin (up to 0.03 U/min)
or epinephrine to norepinephrine with the intent of
raising MAP to target, or adding vasopressin (up to
0.03 U/min) to decrease norepinephrine dosage.
• Use dobutamine in patient who show evidence of
persistent hypo perfusion despite adequate fliud and
vasopressors.

34. End Points of Resuscitation
 Classic / Traditional
 Restoration of blood pressure
 Normalization of heart rate
and urine output
 Appropriate mental status
 Improved / Global
 All of the above plus
 Normalization of serum
lactate levels
 Resolution of base deficit
 Goal directed approach
 Urine output > 0.5 mL/kg/hr
 CVP 5 -10 cm H2o
 MAP 65 to 90 mmHg
 Central venous oxygen
concentration > 70%

35. Thank you