1. Disturbance of Circulation Series -Shock
Jianzhong Sheng, MD PhD
new cases
2% hospital pts
75% ICU pts
Mortality 20-50%
Sirs 7
Sepsis 16
Severe sepsis 20
Septiv shock 46

2. Outline Definition Epidemiology Pathophysiology Classes of Shock
Clinical Presentation
Management
Controversies

3. Definition A pathophysiologic state characterized by
Inadequate tissue perfusion
Clinically manifested by
Hemodynamic disturbances
Organ dysfunction

4. Microcirculation

5. What is shock ?
Shock refers to a dangerous systemic pathological process under the effect of various drastic etiological factors, characterized by acute circulatory failure including decreased effective circulatory volume, inadequate tissue perfusion, cellular metabolism impediment and multiple organ dysfunction.

6. Etiology and classification
1. Classification according to cause
① Loss of blood or fluid: Blood loss: hemorrhagic shock; Fluid loss: dehydration shock (collapse); Burn: burn shock. (失血性休克)
② Trauma: traumatic shock. (创伤性休克)
③ Infection: infectious shock; endotoxic shock; septic shock (感染性休克)
④ Anaphylaxis: anaphylactic shock (过敏性休克)
⑤ Heart failure: cardiogenic shock
⑥ Strong stimulation on nerve system: neurogenic shock (神经性休克)

7. Etiology and classification
2. Classification according to the initial changes
① Hypovolemic shock
② Vasogenic shock (Distributive)
③ Cardiogenic shock

8. Etiology and classification
3. Classification by hemodynamic characteristics
① Hyperdynamic shock: warm shock
high cardiac output, low vascular resistance, warm skin
② Hypodynamic shock: cold shock
low cardiac output, high vascular resistance, cold skin

9. Epidemiology Mortality Septic shock – 35-40% (1 month mortality)
Cardiogenic shock – 60-90%
Hypovolemic shock – variable/mechanism

10. Pathophysiology Imbalance in oxygen supply and demand
Conversion from aerobic to anaerobic metabolism
Appropriate and inappropriate metabolic and physiologic responses

11. Pathophysiology Cellular pathophysiology
Cell membrane ion pump dysfunction
Leakage of intracellular contents into the extracellular space
Intracellular pH dysregulation
Resultant systemic pathophysiology
Cell death and end organ dysfunction
MSOF and death

12. Pathophysiology Characterized by three stages
Preshock (warm shock, compensated shock)
Shock
End organ dysfunction

13. Pathophysiology Compensated shock
Low preload shock – tachycardia, vasoconstriction, mildly decreased BP
Low afterload (distributive) shock – peripheral vasodilation, hyperdynamic state

14. Pathophysiology Shock Initial signs of end organ dysfunction
Tachycardia
Tachypnea
Metabolic acidosis
Oliguria
Cool and clammy skin

15. Pathophysiology End Organ Dysfunction
Progressive irreversible dysfunction
Oliguria or anuria
Progressive acidosis and decreased CO
Agitation, obtundation, and coma
Patient death

16.  Microcirculatory mechanisms
Pathogenesis of shock
 Microcirculatory mechanisms
Ischemic hypoxia stage
Stagnant hypoxia stage
Refractory stage
 Cellular and molecular mechanisms

17. Microcirculatory mechanisms
Ischemic hypoxia stage
(compensatory stage)
Stagnant hypoxia stage
(reversible decompensated stage)
Refractory stage
(microcirculatory failure stage)

18. Microcirculation

19. Microcirculatory mechanisms
1. Ischemic hypoxia stage (compensatory stage)
Microcirculatory changes 
Mechanism of microcirculatory changes 
Compensatory significances 
Clinical manifestations 

20. Microcirculatory changes
Normal
Ischemic hypoxia stage

21. Microcirculatory changes
Small blood vessel constriction.
Precapillary resistance↑↑ > postcapillary resistance↑
Closed capillary↑.
Blood inflows vein by straightforward pathway and A-V shunt.
Characteristics of inflow and outflow: inflow and outflow↓↓; inflow < outflow.

22. Mechanism of microcirculatory changes
Blood lose, Trauma etc.
Activation of sympathetic-adrenal system
Vasoconstrictive substance ↑ ↑
(catecholamine, angiotension Ⅱ, vasopressin, TAX2, endothelin)
Activation of α-receptors
Activation of β-receptors
Constriction of micrangium
Opening of A-V shunts

23. Compensatory significances
1. Maintain normal arterial pressure
(1) returned blood volume↑
(2) cardiac output ↑
(3) peripheral resistances↑
Auto blood transfusion
Auto fluid transfusion
Aldosterone and antidiuretic hormone (ADH)
heart rate↑
contractility ↑
returned blood volume ↑

24. Compensatory significances
2. Maintain blood supplying to heart and brain
(1) blood vessel of brain
(2) coronary artery
(3) normal arterial pressure

25. Hypovolemic Shock Results from decreased preload Etiologic classes
Hemorrhage - e.g. trauma, GI bleed, ruptured aneurysm（血管瘤）
Fluid loss - e.g. diarrhea, vomiting, burns, third spacing, iatrogenic（医源性）

26. Hypovolemic Shock Hemorrhagic Shock Parameter I II III IV
Blood loss (ml)
<750
750–1500
1500–2000
>2000
Blood loss (%)
<15%
15–30%
30–40%
>40%
Pulse rate (beats/min)
<100
>100
>120
>140
Blood pressure
Normal
Decreased
Respiratory rate (bpm)
14–20
20–30
30–40
>35
Urine output (ml/hour)
>30
5–15
Negligible
CNS symptoms
Anxious
Confused
Lethargic
Crit Care. 2004; 8(5): 373–381.

27. Cardiogenic Shock Results from pump failure Etiologic categories
Decreased systolic function
Resultant decreased cardiac output
Etiologic categories
Myopathic
Arrhythmic
Mechanical
Extracardiac (obstructive)

28. Distributive Shock Results from a severe decrease in SVR
Vasodilation reduces afterload
May be associated with increased CO
Etiologic categories
Sepsis
Neurogenic / spinal
Other (next page)
SVR: Systemic vascular resistance

29. Distributive Shock Other causes
Systemic inflammation – pancreatitis, burns
Toxic shock syndrome
Anaphylaxis and anaphylactoid reactions
Toxin reactions – drugs, transfusions
Addisonian crisis
Myxedema coma

30. Distributive Shock Septic Shock
SIRS: systemic inflammatory response syndrome

31. Clinical Presentation
Clinical presentation varies with type and cause, but there are features in common
Hypotension (SBP<90 or Delta>40)
Cool, clammy skin (exceptions – early distributive, terminal shock)
Oliguria
Change in mental status
Metabolic acidosis

32. Clinical manifestations
Sympathetico-adrenal-medullay system exitation
Catecholamines ↑
Heart rate↑
Contractility↑
Small blood vessel constriction
Sweat gland secretion ↑
Excitation of CNS
Peripheral resistances↑
Renal ischemia
Skin ischemia
BP(-)
Thread pulse
Narrowing pulse pressure
Urine↓
Pallor
Cool limbs
Sweating
Clammines
Agitate
Restless

33. Microcirculatory mechanisms
2. Stagnant hypoxia stage (reversible decompensated stage)
Microcirculatory changes 
Mechanism of microcirculatory stasis 
Effect of microcirculatory stasis 
Clinical manifestations 

34. Microcirculatory changes
Stagnant hypoxia stage
Normal

35. Microcirculatory changes
Precapillary resistance↓↓ > postcapillary resistance(-) or ↓.
Opened capillary↑.
Characteristics of inflow and outflow: inflow↑ and outflow↓; inflow > outflow.

36. Mechanism of microcirculatory stasis
Acidosis
Local accumulation of metabolic products
Alteration of hemorheology
Endotoxin
Effects of humoral factors

37. Effect of microcirculatory stasis
Effective circulating blood volume ↓ ↓
Blood flow resistance ↑ ↑
Blood pressure ↓ ↓
Blood supply for vitals ↓ ↓ and dysfunctional

38. Clinical manifestations
Microcirculation stasis
Returned blood volume ↓
Blood pressure ↓
Cardiac output ↓
Brain ischemia
Renal blood flow ↓
Stasis in kidney
Stasis in skin
Dull or coma
Oliguria or anuria
Cyanosis or maculation

39. Microcirculatory mechanisms
3. Refractory stage (microcirculatory failure stage)
Microcirculatory changes 
Mechanism of microcirculatory failure 
Effect of microcirculatory failure 
Clinical manifestations 

40. Microcirculatory changes
Normal
DIC stage
Characteristic: neither inflow or outflow; inflow = outflow

41. Cellular and molecular mechanisms
 Alteration of cellular metabolism
 Cell injury and apoptosis
 Humoral factors
Vasoactive amines
Endothelium-derived vasoactive mediators
Regulation peptides
 Inflammatory mediator and inappropriate
inflammatory response

42. Alterations of metabolism and function
Disturbance of microcirculation Inappropriate inflammatory response
Metabolic alteration
Multiple organ dysfunction
Negative
Nitrogen
balance
Anaerobic
glycolysis
kidney GI
brain
lung
liver
heart
Bleeding endotoxin
translocation
Dull
coma
Acute renal failure
ATP↓
Metabolic
acidosis
ARDS
Na+-K+-ATPase ↓
Respiratory acidosis
Cell swelling
vasodilation
Jundice
enzymes↑
Cardiac
dysfunction

43. Pathophysiologic basis of prevention and treatment
Improve microcirculation
Volume replacement
Acidosis correction
Vasoactive drugs application
Treatment of DIC
Blockage of humoral factors
Cell protection
Organ protection

44. Case presentation
A young man is brought to the emergency department by ambulance on the next day after a severe traffic accident. He is unconscious. his blood pressure is 78/48 mmHg, heart rate is 130 beats per minute. There is no evidence of head trauma. The pupils are 2 mm and reactive. He withdraws to pain. Cardiac examination reveals no murmurs, gallops, or rubs. The lungs are clear to auscultation. The abdomen is tense, with decreased bowel sounds. The patient shows cyanosis, with thready pulses.
Question:
What are the three major pathophysiologic causes of shock? Which was likely in this patient? Why?
What are the three general stages of shock according to the different changes in microcirculation? Which was likely in this patient? Why?
What pathogenetic mechanism accounts for this patient’s unresponsiveness and cyanosis?
What therapeutic measures are essential for this patient?

45. Evaluation Done in parallel with treatment!
Heart & Blood Pressure – helpful to distinguish type of shock
Full laboratory evaluation including hemoglobin and hematocrit (H&H), cardiac enzymes, arterial blood gases (ABG)
Basic studies – CxR, EKG, UA
Basic monitoring –urine output (UOP), central venous pressure (CVP)
Imaging if appropriate – FAST, CT
Echo vs. PA catheterization

46. Treatment Manage the emergency Determine the underlying cause
Definitive management or support

47. Manage the Emergency
Your patient is in extremis – tachycardic, hypotensive, obtunded
How long do you have to manage this?
Suggests that many things must be done at once
Draw in ancillary staff for support!
What must be done?

48. Manage the Emergency One person runs the code!
Control airway and breathing
Maximize oxygen delivery
Place lines, tubes, and monitors
Get and run IVF on a pressure bag
Get and run blood (if appropriate)
Get and hang pressors
Call your senior/fellow/attending

49. Determine the Cause Often obvious based on history
Trauma most often hypovolemic (hemorrhagic)
Postoperative most often hypovolemic (hemorrhagic or third spacing)
Debilitated hospitalized pts most often septic
Must evaluate all pts for risk factors for MI and consider cardiogenic
Consider distributive (spinal) shock in trauma

50. Determine the Cause What if you’re wrong?
85 y/o M 4 hours postop S/P sigmoid resection for perforated diverticulitis is hypotensive on a monitored bed at 70/40
Likely causes
Best actions for the first 5 minutes?

51. Definitive Management
Hypovolemic – Fluid resuscitate (blood or crystalloid) and control ongoing loss
Cardiogenic - Restore blood pressure (chemical and mechanical) and prevent ongoing cardiac death
Distributive – Fluid resuscitate, pressors for maintenance, immediate abx/surgical control for infection, steroids for adrenocortical insufficiency

52. Controversies IVF Resuscitation Pressors Monitoring
Limited resuscitation in penetrating trauma
Use of hypertonic saline resuscitation in trauma
Endpoints for prolonged resuscitation
Pressors
Best pressors for distributive shock
Monitoring
Most appropriate timing and use for PA catheterization or intermittent echocardiogram

53. Thanks!