1. SHOCK
H.A MWAKYOMA, MD

2. Approach to study: Definition of shock Classification of shock
Causes of shock
Pathogenesis of cardiac, neurogenic, septic & anaphylactic shock
Stages of shock including compensatory mechanisms
Clinical features of shock (at each stage)
Morphology of various organs & tissues in shock

3. What is shock?
Shock is the clinical syndrome that results from inadequate tissue perfusion

4. Circulatory Homeostasis
Tissue perfusion is driven by blood pressure
BP = CO X PVR
CO – Cardiac Output
PVR – Peripheral Vascular resistance

5. Cardiac Output CO = SV X HR BP= SV X HR X PVR This means that
Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance

6. What affects Stroke volume?
Volume of Blood pumped by the heart during 1 cycle
What affects Stroke volume?
Rhythm Problems
Blood Volume
Stroke Volume
Heart Muscle Damage
MechanicalObstruction
Mechanical Obstruction

7. Classification of shock
Cardiogenic, due to heart failure
Hypovolemic (oligemic), due to fluid or blood loss
Distributive (hypotensive) owing to peripheral vasodilation

8. Types of Shock Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic
Redistributive shock

9. Redistributive Decreased Peripheral Vascular Resistance Septic Shock
Spinal / Neurogenic Shock
ANAPHYLACTIC shock

10. Common types of shock: Cardiogenic shock Hypovolemic shock
Septic shock

11. Less common types of shock
Neurogenic shock
Anaphylactic shock
Hypoadrenal shock

12. Common factor
Circulatory collapse resulting from a disproportion between circulating blood volume & the vascular space that it has to fill.
The ensuing tissue hypoxia or anoxia leads to multiple organ failure.

13. What happens with the perfusion deficit?
Insufficient delivery of oxygen & nutrients to cells and tissues.
Inadequate clearance of metabolites.

14. Outcomes of cellular hypoxia
Shift from aerobic to anaerobic metabolism.
This results in increased lactate production and later on, lactic acidosis.

15. Outcomes of cellular hypoxia
The metabolic & hemodynamic derangements are correctible at the outset & are associated with reversible cell injury.
Persistence or worsening of the shock state leads to irreversible injury and death of cells and possibly , death of the patient.

16. Cellular Response to Shock
use
Tissue
perfusion
Impaired cellular
metabolism
Anaerobic
metabolism
Stimulation of
clotting cascade &
inflammatory
response
Impaired
glucose
usage
ATP
synthesis
 Intracellular Na+
& water
Na+ Pump
Function
Cellular edema
 Vascular volume

17. Hypovolemic Shock Decreased intravascular volume Causes: Hemorrhage
external
internal
GI tract
hemothorax
peritoneal or retroperitoneal space
Loss of fluid into third space
burns
pancreatitis

18. Homeostatic Mechanisms in Shock
Baroreceptor reflexes and catecholamine release
maintain cerebral and cardiac perfusion
decrease perfusion to gut, skin and kidneys
Activation of renin-angiotensin system
angiotensin II constricts efferent arteriole of glomerulus to maintain GFR
aldosterone promotes sodium retention
Release of Arginine Vasopressin (ADH)
promotes renal conservation of water

19. Renin-Angiotensin-Aldosterone
Plasma
volume
Kidney
(juxtaglomerular
apparatus)
Detected by
&/Or
 [Na+]
Releases
Renin
Via ACE
(Angiotensin
Converting
Enzyme)
Angiotensin II…
Angiotensinogen
Angiotensin I…
Converts

20. Pathophysiological Response
“Flight or fight response”
Increased Catecholamine release
Activation of Renin-Angiotensin system
Increase glucocorticoid and mineralcorticoid release
Activation of Sympathetic nervous system

21. Cardiogenic Shock Myocardial pump failure Extrinsic compression
myocardial infarction
myocardial rupture
cardiac arrhythmia
Extrinsic compression
cardiac tamponade
Outflow obstruction(Obstructive heart
failure)
pulmonary embolus
valvular disease (Aortic stenosis)

22. Cardiogenic Shock Catecholamine R.A.S.  CO Release Activation  SVR
Impaired
myocardial function
 SVR
Volume/
Preload
Myocardial
O2 demand O2
supply
Peripheral
& pulmonary
edema
 Dyspnea

23. Anaphylactic Shock
Caused by a hypersensitivity reaction to an allergen in a previously sensitised patient

24. Anaphylactic Shock Massive & systemic allergic reaction
Large release of histamine
Increases membrane permeability & vasodilation

25. Common Features Angio-oedema Bronchoconstriction
Vasodilatation and hypotension
Urticareal rash

26. Common Features Angio-oedema Bronchoconstriction
Vasodilatation and hypotension
Urticareal rash

27. Septic Shock
“Circulatory failure”
Due to systemic infection

28. Septic Shock Leading cause of death in intensive care units
Most cases (70%) are caused by gram negative bacteria (LPS-lipopolysaccharide)
Also can occur with gram positive bacteria and fungal organisms

34. Effects of cytokine release

35. Effects Of Lipopolysaccharide (LPS) And Secondarily Induced Effector Molecules

36. MODS= Multiple organ dysfunction syndrome

37. Multiple Organ Dysfunction System
Progressive dysfunction of two or more organ systems
Caused by uncontrolled inflammatory response to injury or illness
Typically sepsis

38. STAGES OF SHOCK Nonprogressive stage (compensated phase)
Progressive stage (Decompensated phase)
Refractory stage (irreversible)

39. Features of compensated shock
Tachycardia
Skin pallor due to constriction of arterioles
Reduced urine production

43. Decompenstated Shock Defense mechanisms begin to fail Presentation
Hypotension
Marked increase in heart rate
Rapid, thready pulse
Agitation, restlessness, confusion

44. Features of decompenstaed but still reversible shock CONT--
Dyspnoea & tachypnoea
Pulmonary oedema slowly develops, further worsening hypoxia
Oliguria (urine volume<500ml/24hr)
Acidosis due to anaerobic glycolysis

45. Irreversible Shock Complete failure of compensatory mechanisms
Death even in presence of resuscitation

46. Features of irreversible shock
Marked hypotension with extreme tachycardia (filiform pulse)
Respiratory distress which is not responsive to oxygen therapy & assisted ventilation
Loss of consciousness progressing to coma
Gastrointestinal bleeding
Anuria with elevated BUN & creatinine
Severe acidosis
Laboratory & clinical signs of DIC (Disseminated Intravascular coagulation)

48. Symptoms of Shock Anxiety /Nervousness
General Symptoms
Specific Symptoms
Anxiety /Nervousness
Dizziness
Weakness
Nausea & Vomiting
Thirst
Confusion
Decreased Urine Output
History of Trauma / other illness
Vomiting & Diarrhoea
Chest Pain
Fevers / Rigors
Shortness of breath (stridor)

49. Signs of Shock Pallor Cold and clammy extremities Sweating Cyanosis
Tachypnoea
Tachycardia
Confusion & agitation
Stridor
Hypotension
Loss of consciousness

50. Clinical Course Hypovolemic shock Cardiogenic shock and septic shock
If patient is young and healthy, most survive if resuscitation restores perfusion
Cardiogenic shock and septic shock
Up to 75% mortality even with best care
Patients succumb with multi-organ failure
Tubular necrosis of kidneys
Ischemic enteropathy
Disseminated intravascular coagulation
Acute respiratory distress syndrome (septic shock)

51. Clinical Course Hypovolemic shock Cardiogenic shock and septic shock
If patient is young and healthy, most survive if resuscitation restores perfusion
Cardiogenic shock and septic shock
Up to 75% mortality even with best care
Patients succumb with multi-organ failure
Tubular necrosis of kidneys
Ischemic enteropathy
Disseminated intravascular coagulation
Acute respiratory distress syndrome (septic shock)

52. Morphology of Shock Hypoxic injury to multiple organs Kidneys
medulla and tubules most affected
acute tubular necrosis
Gastrointestinal tract
mucosa most sensitive to hypoxia
Brain
Heart
subendocardial necrosis of myocardium
Lungs
resistant to hypoxia but involved with septic shock

53. Kidney in shock:Coagulation necrosis of tubules

54. Renal Biopsy in DIC
Capillary loops of glomeruli occluded by fibrin thrombi.
H&E stain on left and MSB (Martius scarlet blue) for fibrin on the right

55. Myocardial necrosis(coagulation necrosis)

56. Adult respiratory syndrome (ARDS)
Synonyms:
Shock lung
Diffuse alveolar damage
Acute alveolar injury
Traumatic wet lungs
These are descriptive terms for a syndrome caused by diffuse alveolar capillary damage.

57. Clinically characterized by:
Rapid onset of severe life-threatening respiratory insufficiency
Cyanosis
Severe arterial hypoxemia that is refractory to oxygen therapy
Frequently progresses to extrapulmonary multisystem organ failure.

58. Some causes of ARDS: Shock Sepsis Extensive surface burns
Massive fractures & other trauma

59. Morphology:
In the acute edematous stage, the lungs are heavy, firm & boggy due to congestion, edema & inflammation.

60. Markedly congested & heavy lung

61. Microscopy
Alveoli are lined by waxy hyaline membranes.

62. This is followed by: Proliferation of type II pneumocytes.
However resolution does not usually occur.
More commonly, there is organization of the fibrin exudate, with resultant intra-alveolar fibrosis.
There is marked thickening of the alveolar septae.

63. Mortality rate of ARDS is high (60%).