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Prof. U. Murali.
Shock
[Types,PP & Management]
Learning Objectives
•Definition
• Types of Shock & Aetiology
•Pathophysiology
• Clinical Features
•Stages of shock
• Effects of Shock
• Consequences of Shock
• Management of Shock
• Shock is a systemic state of low tissue
perfusion that is inadequate for
normal cellular respiration.
• It is either reduced oxygen delivery
(or) poor oxygen utilization (or)
increased oxygen consumption with
circulatory failure (collapse) and poor
perfusion.
• With insufficient delivery of oxygen
and glucose, cells switch from aerobic
to anaerobic metabolism.
• If perfusion is not restored in a timely
fashion, cell death ensues.
Definition
Type of Shock CO / CI
[Pump Function]
PCWP
[Preload]
SVR
[Afterload]
Venous O2
Saturation
[Perfusion]
Cardiogenic
Hypovolemic
Obstructive
Septic
Anaphylactic
Neurogenic
Hypo-adrenal N /
S & A C & O C H O S A N
Hemodynamics in Shock
Clinical Features
C F - Mnemonics
Effects of Shock
• During the period of systemic hypoperfusion,
cellular & humoral elements activated by
the hypoxia (complement, neutrophils,
microvascular thrombi), overwhelm the local
anti-inflammatory response, where they
cause injury to distant organs resulting in
SIRS.
• It is final common pathway in shock due to
any cause (trauma, sepsis, endotoxemia,
burns).
• It is a part of severely decompensated
reversible shock which eventually leads to
MODS (Multiorgan dysfunction syndrome), a
state of irreversible shock wherein patient is
anuric, drowsy, cold and terminally ill. SIRS
carries poor prognosis.
Consequences - SIRS
• The result of prolonged systemic
hypoperfusion, cellular & organ damage
progresses to end organ damage and multiple
organ failure.
• Multiple organ failure is defined as two or
more failed organ systems.
• It is progressively becoming irreversible injury
of all tissues like kidney, lungs, liver, GIT. Lungs
and liver are commonly involved (70% ). Next
organs to be involved are kidney and GIT.
• Management of MODS is critical care in ICU
with ventilator support, hemodialysis,
transfusions, antibiotics, proper nutrition in the
form of TPN or enteral. MODS stage has got
high mortality [60%].
Consequences – MOF / MODS
Monitoring
• CBP & Urine analysis
• Sr. Electrolytes
• RFT / LFT
• Chest X-ray & ECHO
• Arterial blood gas
• PT / PTT / INR
• Cardiac enzymes
• Trauma - X-rays, U/S, CT scan
29
Treatment
• Vasopressor (or) inotropic therapy is not
indicated as first line therapy in
hypovolemia.
• Vasopressor agents (phenylephrine,
noradrenaline) are indicated in distributive
shock states (sepsis, neurogenic shock)
where there is peripheral vasodilatation & a
low systemic vascular resistance. Resistant to
catecholamines vasopressin may be used.
• In cardiogenic shock, or where myocardial
depression has complicated a shock state
(e.g., severe septic shock with low cardiac
output), inotropic therapy may be required
to increase cardiac output and therefore
oxygen delivery. Dobutamine is the agent of
choice.
Vasopressor & Inotropic Support
• Definition & Types of Shock.
• Aetiology of Shock.
• Pathophysiology of Shock.
• Clinical features of various types of Shock.
• Different Stages of Shock.
• Effects of Shock on various organs in the body.
• Complications of Shock – SIRS & MODS.
• Monitoring of a patient in Shock | Treatment aspects of Shock.
To Summarize
References
• Define shock.
• Illustrate with flow-chart the pathophysiology of shock.
• Classify shock and list their aetiology.
• Mention the typical C/F of shock.
• How do you monitor a shock patient?
• Enumerate the complications of shock.
• Explain the stages of shock.
• Write about dynamic fluid response aspects of shock.
Question Time
One of the following is not true about
distributive shock –
◼ a) Decreased venous return.
◼ b) Decreased cardiac output.
◼ c) Decreased vascular resistance.
◼ d) High mixed venous saturation.
◼
First line of therapy in shock in the patients of
trauma is –
◼ a) Crystalloids.
◼ b) Colloids.
◼ c) Inotropes.
◼ d) Blood transfusion.
◼
A patient with spine, chest and abdominal injury in
road traffic accident developed hypotension and
bradycardia. The most likely reason is –
◼ a) Hypovolemic shock.
◼ b) Hypovolemic + neurogenic shock.
◼ c) Hypovolemic + septicemic shock.
◼ d) Neurogenic shock.
◼
There are several mechanisms of organ hypoperfusion
and shock. Which one of the following types of shock is
due to vasodilation? –
◼ a) Obstructive shock.
◼ b) Hypovolemic shock.
◼ c) Cardiogenic shock.
◼ d) Distributive shock.
◼
One of the following is not used as minimum
monitoring measures for patients in shock –
◼ a) ECG.
◼ b) Serum lactate.
◼ c) Blood pressure.
◼ d) Pulse oximetry.
◼
The two common organs involved in the
multiple organ failure following shock is –
◼ a) GIT & Lungs.
◼ b) Kidney & GIT.
◼ c) Lungs & Liver.
◼ d) Liver & Kidney.
◼
THANK YOU
THANK YOU . . .
Cardiogenic Shock Hypovolemic Shock
Anaphylactic Shock
Neurogenic Shock
Septic Shock
Pathogenesis of MODS
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT
Shock - Types, PP & MGT

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Shock - Types, PP & MGT

  • 2. Learning Objectives •Definition • Types of Shock & Aetiology •Pathophysiology • Clinical Features •Stages of shock • Effects of Shock • Consequences of Shock • Management of Shock
  • 3. • Shock is a systemic state of low tissue perfusion that is inadequate for normal cellular respiration. • It is either reduced oxygen delivery (or) poor oxygen utilization (or) increased oxygen consumption with circulatory failure (collapse) and poor perfusion. • With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism. • If perfusion is not restored in a timely fashion, cell death ensues. Definition
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  • 17. Type of Shock CO / CI [Pump Function] PCWP [Preload] SVR [Afterload] Venous O2 Saturation [Perfusion] Cardiogenic Hypovolemic Obstructive Septic Anaphylactic Neurogenic Hypo-adrenal N / S & A C & O C H O S A N Hemodynamics in Shock
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  • 23. C F - Mnemonics
  • 25. • During the period of systemic hypoperfusion, cellular & humoral elements activated by the hypoxia (complement, neutrophils, microvascular thrombi), overwhelm the local anti-inflammatory response, where they cause injury to distant organs resulting in SIRS. • It is final common pathway in shock due to any cause (trauma, sepsis, endotoxemia, burns). • It is a part of severely decompensated reversible shock which eventually leads to MODS (Multiorgan dysfunction syndrome), a state of irreversible shock wherein patient is anuric, drowsy, cold and terminally ill. SIRS carries poor prognosis. Consequences - SIRS
  • 26. • The result of prolonged systemic hypoperfusion, cellular & organ damage progresses to end organ damage and multiple organ failure. • Multiple organ failure is defined as two or more failed organ systems. • It is progressively becoming irreversible injury of all tissues like kidney, lungs, liver, GIT. Lungs and liver are commonly involved (70% ). Next organs to be involved are kidney and GIT. • Management of MODS is critical care in ICU with ventilator support, hemodialysis, transfusions, antibiotics, proper nutrition in the form of TPN or enteral. MODS stage has got high mortality [60%]. Consequences – MOF / MODS
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  • 28. Monitoring • CBP & Urine analysis • Sr. Electrolytes • RFT / LFT • Chest X-ray & ECHO • Arterial blood gas • PT / PTT / INR • Cardiac enzymes • Trauma - X-rays, U/S, CT scan
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  • 33. • Vasopressor (or) inotropic therapy is not indicated as first line therapy in hypovolemia. • Vasopressor agents (phenylephrine, noradrenaline) are indicated in distributive shock states (sepsis, neurogenic shock) where there is peripheral vasodilatation & a low systemic vascular resistance. Resistant to catecholamines vasopressin may be used. • In cardiogenic shock, or where myocardial depression has complicated a shock state (e.g., severe septic shock with low cardiac output), inotropic therapy may be required to increase cardiac output and therefore oxygen delivery. Dobutamine is the agent of choice. Vasopressor & Inotropic Support
  • 34. • Definition & Types of Shock. • Aetiology of Shock. • Pathophysiology of Shock. • Clinical features of various types of Shock. • Different Stages of Shock. • Effects of Shock on various organs in the body. • Complications of Shock – SIRS & MODS. • Monitoring of a patient in Shock | Treatment aspects of Shock. To Summarize
  • 36. • Define shock. • Illustrate with flow-chart the pathophysiology of shock. • Classify shock and list their aetiology. • Mention the typical C/F of shock. • How do you monitor a shock patient? • Enumerate the complications of shock. • Explain the stages of shock. • Write about dynamic fluid response aspects of shock. Question Time
  • 37. One of the following is not true about distributive shock – ◼ a) Decreased venous return. ◼ b) Decreased cardiac output. ◼ c) Decreased vascular resistance. ◼ d) High mixed venous saturation. ◼
  • 38. First line of therapy in shock in the patients of trauma is – ◼ a) Crystalloids. ◼ b) Colloids. ◼ c) Inotropes. ◼ d) Blood transfusion. ◼
  • 39. A patient with spine, chest and abdominal injury in road traffic accident developed hypotension and bradycardia. The most likely reason is – ◼ a) Hypovolemic shock. ◼ b) Hypovolemic + neurogenic shock. ◼ c) Hypovolemic + septicemic shock. ◼ d) Neurogenic shock. ◼
  • 40. There are several mechanisms of organ hypoperfusion and shock. Which one of the following types of shock is due to vasodilation? – ◼ a) Obstructive shock. ◼ b) Hypovolemic shock. ◼ c) Cardiogenic shock. ◼ d) Distributive shock. ◼
  • 41. One of the following is not used as minimum monitoring measures for patients in shock – ◼ a) ECG. ◼ b) Serum lactate. ◼ c) Blood pressure. ◼ d) Pulse oximetry. ◼
  • 42. The two common organs involved in the multiple organ failure following shock is – ◼ a) GIT & Lungs. ◼ b) Kidney & GIT. ◼ c) Lungs & Liver. ◼ d) Liver & Kidney. ◼
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