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Dr. Neeraj Kumar Jain
Dept. of General Surgery
In previous Lecture we discussed
 Shock is a systemic state of low tissue perfusion, which
is inadequate for normal cellular respiration.
 With insufficient delivery of oxygen and glucose, cells
switch from aerobic to anaerobic metabolism.
 If perfusion is not restored timely , it leads to cell
death .
Shock is
 Inadequate tissue perfusion to meet tissue demands.
Usually result of inadequate blood flow and/or oxygen
delivery.
Classification of shock
 ■ Hypovolaemic
 ■ Cardiogenic
 ■ Obstructive
 ■ Distributive
 ■ Endocrine
THE BLOOD
WHOLE
BLOOD
EXTERNAL
HG.
INTERNAL
HG.
PLASMA
GUT
*VOMITING
*NGT. DRAIN
*DIARRHOEA
* FISTULA
SKIN
•SWEAT
•* BURN
KIDNEY
*DM
*DI
*DIURETIC
3rd SPACE
* ASCITES
CARDIAC
CAUSESAFTERLOAD
PRELOAD
VALVES
MUSCLE POWER
RATE&
RHYTHEM
 Myocardial
 Infarction, contusion, myocarditis, cardiomyopathy,
pharmacologic, depressant factors
 Mechanical
 Valvular stenosis, regrurgitation
 Septal Defects
 Arrhythmogenic
Causes
In Todays lecture
 ■ Obstructive shock
 ■ Distributive shock
 ■ Endocrine shock
Obstructive shock
 In obstructive shock there is a reduction in preload because
of mechanical obstruction of cardiac filling.
 Common causes of obstructive shock include
 1. cardiac tamponade,
 2.tension pneumothorax,
 3.massive pulmonary embolus
 4. air embolus.
 There is reduced filling of the left and/or right sides of the
heart leading to reduced preload and a fall in cardiac
output.
 Extrinsic Vascular Compression
 tumors, fibrosis
 Increased Intrathoracic Pressure
 Tension pneumo; high autopeep in PPV
 Flow obstruction
 PE, Air embolism, tumors, Ao dissection, Ao
coarctation, acute pulmonary HTN, tamponade.
Shock -- Classification --
Obstructive
• Tension pneumothorax
• Air trapped in pleural space with 1 way valve,
air/pressure builds up
• Mediastinum shifted impeding venous return
• Chest pain, SOB, decreased breath sounds
• X ray chest and general Investigation are done
• Rx: Needle decompression, chest tube insertion
Obstructive Shock
• Cardiac tamponade
• Blood in pericardial sac prevents venous return to and
contraction of heart
• Related to trauma, pericarditis, MI
• Beck’s triad: hypotension, muffled heart sounds, JVD
• Diagnosis: large heart CXR, echo
• Rx: Pericardiocentisis
Obstructive Shock
• Pulmonary embolism
• Virscow triad: hypercoaguable, venous injury,
venostasis
• Signs: Tachypnea, tachycardia, hypoxia
• Low risk: D-dimer
• Higher risk: CT chest or VQ scan
• Rx: Heparin, consider thrombolytics
Obstructive Shock
Distributive shock
 It describes the pattern of cardiovascular responses
characterising a variety of conditions including
 A)septic shock,
 B) anaphylaxis and
 c)spinal cord injury.
 Inadequate organ perfusion is accompanied by vascular
dilatation with hypotension, low systemic vascular
resistance, inadequate afterload and a resulting
abnormally high cardiac output.
Distributive shock continue…
 In anaphylaxis, vasodilatation is caused by histamine
release, whereas in high spinal cord injury there is
failure of sympathetic outflow and adequate vascular
tone (neurogenic shock).
 The cause in sepsis is less clear but is related to the
release of bacterial products (endotoxins) and the
activation of cellular and humoral components of the
immune system.
 There is maldistribution of blood flow at a
microvascular level with arteriovenous shunting and
dysfunction of the cellular utilisation of oxygen.
 In the later phases of septic shock there is
hypovolaemia from fluid loss into the interstitial
spaces and there may be concomitant myocardial
depression, which complicates the clinical picture
Distributive shock continue…
 SIRS-related As sepsis (infectious); pancreatitis;
trauma; burns.
 Anaphylactic/anaphylactoid
 Spinal Trauma (low pulse, SVR low)
 Toxic, pharmacologic (B-blockers overdose)
Shock -- Classification --Distributive
Abnormal vessel tone
(decreased afterload)
Distributive Shock
Vasodilitation Venous Pooling
Decreased Afterload
Maldistribution of regional blood flow
Distributive Shock
 Neurogenic or Anaphylactic Shock
 Diminished or absent sympathetic tone
 Reduce peripheral vascular tone
 Peripheral pooling of blood volume
 Inadequate venous return
 Decreased perfusion, acidosis, hypotension
Distributive Shock
• Anaphylaxis – a severe systemic
hypersensitivity reaction characterized by
multisystem involvement
• IgE mediated
• Anaphylactoid reaction – clinically
indistinguishable from anaphylaxis, do not
require a sensitizing exposure
• Not IgE mediated
Anaphylactic Shock
• What are some symptoms of anaphylaxis?
Anaphylactic Shock
• First- Pruritus, flushing, urticaria appear
•Next- Throat fullness, anxiety, chest tightness,
shortness of breath and lightheadedness
•Finally- Altered mental status, respiratory
distress and circulatory collapse
• Risk factors for fatal anaphylaxis
• Poorly controlled asthma
• Previous anaphylaxis
• Reoccurrence rates
• 40-60% for insect stings
• 20-40% for radiocontrast agents
• 10-20% for penicillin
• Most common causes
• Antibiotics
• Insects
• Food
Anaphylactic Shock
• Mild, localized urticaria can progress to full anaphylaxis
• Symptoms usually begin within 60 minutes of exposure
• Faster the onset of symptoms = more severe reaction
• Biphasic phenomenon occurs in up to 20% of patients
• Symptoms return 3-4 hours after initial reaction has cleared
• A “lump in my throat” and “hoarseness” heralds life-
threatening laryngeal edema
Anaphylactic Shock
• Clinical diagnosis
• Defined by airway compromise, hypotension, or
involvement of cutaneous, respiratory, or GI
systems
• Look for exposure to drug, food, or insect
• Labs have no role
Anaphylactic Shock- Diagnosis
• Occurs after acute spinal cord injury
• Sympathetic outflow is disrupted leaving
unopposed vagal tone
• Results in hypotension and bradycardia
• Spinal shock- temporary loss of spinal reflex
activity below a total or near total spinal cord
injury (not the same as neurogenic shock, the
terms are not interchangeable)
Neurogenic Shock
• Loss of sympathetic tone results in warm and dry skin
• Shock usually lasts from 1 to 3 weeks
• Any injury above T1 can disrupt the entire sympathetic
system
• Higher injuries = worse paralysis
Neurogenic Shock
 Terminology in Sepsis
 Sepsis = SIRS as response to a known infection
 Severe sepsis = Sepsis + organ dysfunction
 Septic Shock = Sepsis + inadequate oxygen delivery
 Multiple Organ Dysfunction Syndrome (MODS) – organ
dysfunction that requires intervention
Septic Shock
 Components of Septic shock
 Decreased volume
 Decreased pump function
 Abnormal vessel tone
Septic Shock
 Therapy for Caridovascular Support
Preload Volume
Contractility Inotropes
Afterload Vasodilators
Septic Shock
Etiologies
 Inflammatory: too much, too little
 Coagulation pathway: DIC-bleeding, pro-coagulant,
microthombosis
 Multiple organ system failure
Septic Shock
 Early – warm shock – similar to neurogenic shock
 Late – Cold shock – similar to cardiogenic shock
Recognition of Septic Shock
Early vs Late Septic Shock
Early Late
End-organ: skin Dec. cap refill Very dec. cap
Refill
Brain Irritable,
restless
Lethargic,
unresponsive
Kidneys Oliguria Oliguria, anuria
Endocrine shock
 Endocrine shock may present as a combination of
hypovolaemic, cardiogenic and distributive shock.
 Causes of endocrine shock include
 1.Hypo- and Hyperthyroidism and
 2. Adrenal insufficiency.
Endocrine shock Continue…
 Hypothyroidism causes a shock state similar to that of
neurogenic shock as a result of disordered vascular and
cardiac responsiveness to circulating catecholamines.
 Cardiac output falls because of low inotropy and
bradycardia.
 There may also be an associated cardiomyopathy.
 Thyrotoxicosis may cause a high-output cardiac
failure.
Endocrine shock Continue…
 Adrenal insufficiency leads to shock as a result of
hypovolaemia and a poor response to circulating and
exogenous catecholamines.
 Adrenal insufficiency may result from pre-existing
Addison’s disease or it may be a relative insufficiency
caused by a pathological disease state such as systemic
sepsis.
Type PAOP C.O. SVR
HYPOVOLEMIC   
CARDIOGENIC   
DISTRIBUTIVE  or N varies 
OBSTRUCTIVE   
Summary
Co Cardiac output,svr-systemic venous resistance,paop=pressure
Thank you
In the next lecture we will dicuss
 Severity of shock
 Compensated shock
 Decompensation
 Mild , moderate ,severe shock
 Consequences
 Unresuscitatable shock
 Multiple organ failure
 RESUSCITATION

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Classification and Pathophysiology of Shock

  • 1. Dr. Neeraj Kumar Jain Dept. of General Surgery
  • 2. In previous Lecture we discussed  Shock is a systemic state of low tissue perfusion, which is inadequate for normal cellular respiration.  With insufficient delivery of oxygen and glucose, cells switch from aerobic to anaerobic metabolism.  If perfusion is not restored timely , it leads to cell death .
  • 3. Shock is  Inadequate tissue perfusion to meet tissue demands. Usually result of inadequate blood flow and/or oxygen delivery.
  • 4. Classification of shock  ■ Hypovolaemic  ■ Cardiogenic  ■ Obstructive  ■ Distributive  ■ Endocrine
  • 5.
  • 6. THE BLOOD WHOLE BLOOD EXTERNAL HG. INTERNAL HG. PLASMA GUT *VOMITING *NGT. DRAIN *DIARRHOEA * FISTULA SKIN •SWEAT •* BURN KIDNEY *DM *DI *DIURETIC 3rd SPACE * ASCITES
  • 7.
  • 9.  Myocardial  Infarction, contusion, myocarditis, cardiomyopathy, pharmacologic, depressant factors  Mechanical  Valvular stenosis, regrurgitation  Septal Defects  Arrhythmogenic Causes
  • 10. In Todays lecture  ■ Obstructive shock  ■ Distributive shock  ■ Endocrine shock
  • 11. Obstructive shock  In obstructive shock there is a reduction in preload because of mechanical obstruction of cardiac filling.  Common causes of obstructive shock include  1. cardiac tamponade,  2.tension pneumothorax,  3.massive pulmonary embolus  4. air embolus.  There is reduced filling of the left and/or right sides of the heart leading to reduced preload and a fall in cardiac output.
  • 12.  Extrinsic Vascular Compression  tumors, fibrosis  Increased Intrathoracic Pressure  Tension pneumo; high autopeep in PPV  Flow obstruction  PE, Air embolism, tumors, Ao dissection, Ao coarctation, acute pulmonary HTN, tamponade. Shock -- Classification -- Obstructive
  • 13. • Tension pneumothorax • Air trapped in pleural space with 1 way valve, air/pressure builds up • Mediastinum shifted impeding venous return • Chest pain, SOB, decreased breath sounds • X ray chest and general Investigation are done • Rx: Needle decompression, chest tube insertion Obstructive Shock
  • 14. • Cardiac tamponade • Blood in pericardial sac prevents venous return to and contraction of heart • Related to trauma, pericarditis, MI • Beck’s triad: hypotension, muffled heart sounds, JVD • Diagnosis: large heart CXR, echo • Rx: Pericardiocentisis Obstructive Shock
  • 15. • Pulmonary embolism • Virscow triad: hypercoaguable, venous injury, venostasis • Signs: Tachypnea, tachycardia, hypoxia • Low risk: D-dimer • Higher risk: CT chest or VQ scan • Rx: Heparin, consider thrombolytics Obstructive Shock
  • 16. Distributive shock  It describes the pattern of cardiovascular responses characterising a variety of conditions including  A)septic shock,  B) anaphylaxis and  c)spinal cord injury.  Inadequate organ perfusion is accompanied by vascular dilatation with hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output.
  • 17. Distributive shock continue…  In anaphylaxis, vasodilatation is caused by histamine release, whereas in high spinal cord injury there is failure of sympathetic outflow and adequate vascular tone (neurogenic shock).  The cause in sepsis is less clear but is related to the release of bacterial products (endotoxins) and the activation of cellular and humoral components of the immune system.
  • 18.  There is maldistribution of blood flow at a microvascular level with arteriovenous shunting and dysfunction of the cellular utilisation of oxygen.  In the later phases of septic shock there is hypovolaemia from fluid loss into the interstitial spaces and there may be concomitant myocardial depression, which complicates the clinical picture Distributive shock continue…
  • 19.  SIRS-related As sepsis (infectious); pancreatitis; trauma; burns.  Anaphylactic/anaphylactoid  Spinal Trauma (low pulse, SVR low)  Toxic, pharmacologic (B-blockers overdose) Shock -- Classification --Distributive
  • 20. Abnormal vessel tone (decreased afterload) Distributive Shock
  • 21. Vasodilitation Venous Pooling Decreased Afterload Maldistribution of regional blood flow Distributive Shock
  • 22.  Neurogenic or Anaphylactic Shock  Diminished or absent sympathetic tone  Reduce peripheral vascular tone  Peripheral pooling of blood volume  Inadequate venous return  Decreased perfusion, acidosis, hypotension Distributive Shock
  • 23. • Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement • IgE mediated • Anaphylactoid reaction – clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure • Not IgE mediated Anaphylactic Shock
  • 24. • What are some symptoms of anaphylaxis? Anaphylactic Shock • First- Pruritus, flushing, urticaria appear •Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness •Finally- Altered mental status, respiratory distress and circulatory collapse
  • 25. • Risk factors for fatal anaphylaxis • Poorly controlled asthma • Previous anaphylaxis • Reoccurrence rates • 40-60% for insect stings • 20-40% for radiocontrast agents • 10-20% for penicillin • Most common causes • Antibiotics • Insects • Food Anaphylactic Shock
  • 26. • Mild, localized urticaria can progress to full anaphylaxis • Symptoms usually begin within 60 minutes of exposure • Faster the onset of symptoms = more severe reaction • Biphasic phenomenon occurs in up to 20% of patients • Symptoms return 3-4 hours after initial reaction has cleared • A “lump in my throat” and “hoarseness” heralds life- threatening laryngeal edema Anaphylactic Shock
  • 27. • Clinical diagnosis • Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems • Look for exposure to drug, food, or insect • Labs have no role Anaphylactic Shock- Diagnosis
  • 28. • Occurs after acute spinal cord injury • Sympathetic outflow is disrupted leaving unopposed vagal tone • Results in hypotension and bradycardia • Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable) Neurogenic Shock
  • 29. • Loss of sympathetic tone results in warm and dry skin • Shock usually lasts from 1 to 3 weeks • Any injury above T1 can disrupt the entire sympathetic system • Higher injuries = worse paralysis Neurogenic Shock
  • 30.  Terminology in Sepsis  Sepsis = SIRS as response to a known infection  Severe sepsis = Sepsis + organ dysfunction  Septic Shock = Sepsis + inadequate oxygen delivery  Multiple Organ Dysfunction Syndrome (MODS) – organ dysfunction that requires intervention Septic Shock
  • 31.  Components of Septic shock  Decreased volume  Decreased pump function  Abnormal vessel tone Septic Shock
  • 32.  Therapy for Caridovascular Support Preload Volume Contractility Inotropes Afterload Vasodilators Septic Shock
  • 33. Etiologies  Inflammatory: too much, too little  Coagulation pathway: DIC-bleeding, pro-coagulant, microthombosis  Multiple organ system failure Septic Shock
  • 34.  Early – warm shock – similar to neurogenic shock  Late – Cold shock – similar to cardiogenic shock Recognition of Septic Shock
  • 35. Early vs Late Septic Shock Early Late End-organ: skin Dec. cap refill Very dec. cap Refill Brain Irritable, restless Lethargic, unresponsive Kidneys Oliguria Oliguria, anuria
  • 36. Endocrine shock  Endocrine shock may present as a combination of hypovolaemic, cardiogenic and distributive shock.  Causes of endocrine shock include  1.Hypo- and Hyperthyroidism and  2. Adrenal insufficiency.
  • 37. Endocrine shock Continue…  Hypothyroidism causes a shock state similar to that of neurogenic shock as a result of disordered vascular and cardiac responsiveness to circulating catecholamines.  Cardiac output falls because of low inotropy and bradycardia.  There may also be an associated cardiomyopathy.  Thyrotoxicosis may cause a high-output cardiac failure.
  • 38. Endocrine shock Continue…  Adrenal insufficiency leads to shock as a result of hypovolaemia and a poor response to circulating and exogenous catecholamines.  Adrenal insufficiency may result from pre-existing Addison’s disease or it may be a relative insufficiency caused by a pathological disease state such as systemic sepsis.
  • 39. Type PAOP C.O. SVR HYPOVOLEMIC    CARDIOGENIC    DISTRIBUTIVE  or N varies  OBSTRUCTIVE    Summary Co Cardiac output,svr-systemic venous resistance,paop=pressure
  • 41. In the next lecture we will dicuss  Severity of shock  Compensated shock  Decompensation  Mild , moderate ,severe shock  Consequences  Unresuscitatable shock  Multiple organ failure  RESUSCITATION