1. Shock
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2. Shock
“Transition between life and death”
Failure to oxygenate & nourish the body
adequately
Mortality > 20%

3. Shock in surgical practices
Hypovolemic shock - due to decreased circulating blood
volume in relation to the total vascular capacity and
characterized by a reduction of diastolic filling pressures
Cardiogenic shock - due to cardiac pump failure related to
loss of myocardial contractility/functional myocardium or
structural/mechanical failure of the cardiac anatomy and
characterized by elevations of diastolic filling pressures and
volumes
Extra-cardiac obstructive shock - due to obstruction to flow
in the cardiovascular circuit and characterized by either
impairment of diastolic filling or excessive afterload
Distributive shock - caused by loss of vasomotor control
resulting in arteriolar/venular dilatation and characterized
(after fluid resuscitation) by increased cardiac output and
decreased SVR

4. Pathophysiology &Biochemistry

5. Pathophysiology
Shock affects mitochondria first
Without oxygen mitochondria convert fuels
to lactate → lactic acid
Failure of the krebs cycle
 Oxygen is the final electron accepter to form
water

6. Mechanisms of Cellular Injury in Shock
1) Cellular ischemia
2) Free radical reperfusion injury
3) Inflammatory mediators (local and
circulating)

7. Physiologic Oxygen Supply Dependency
Oxygen Consumption
Critical Delivery
Threshold
Oxygen Delivery
Mizock BA. Crit Care Med. 1992;20:80-93.

8. Oxygen Consumption
Pathologic Oxygen Supply Dependency
Pathologic
Physiologic
Oxygen Delivery
Mizock BA. Crit Care Med. 1992;20:80-93.

9. Lactic Acid
Early shock
 Skeletal muscle and splanchnic organs 1st
affected
 Lactic acid production
Resuscitation
 Pyruvate delivery from glycolysis can
overwhelm krebs cycle

10. Systemic Response
Decreased vascular wall tension increases
sympathetic stimulation (blocked in sepsis)
 Increased epi, norepi, corticosteroids, renin,
and glucagon
 Increased glycogenolysis and lipolysis
Increased glucose and FFA’s to TCA can
overwhelm it

11. Immune Response
Neutrophil and macrophage activation due
to hypoxia
 Enzymatic organ damage
 Capillary plugs causing microischemia
 TNF and Interleukins released

12. Cardiac Physiology
Contraction created by Ca++, ATP/CP, and
troponin C
Calcium inflow determines strength of
contraction
Inotropics increase Ca++ release in the
sarcoplasmic reticulum via β-receptors or
cAMP

13. Cardiac Physiology
ATP/CP supply almost entirely from
oxidative phosphorylation by mitochondria
Complete turnover of ATP/CP every 5-10
beats

14. Cardiac Physiology
Gregg Phenomenon
 Contractile strength decreases with
decreased coronary perfusion
Decreased coronary perfusion in shock
Decreased workload due to lower SVR
Very minimal cardiac ischemia even in
severe shock

15. Cardiac Physiology
Inflammatory actions of TNFα,
Interleukins, and NO decrease contractility
Acidosis can decrease contractility but
effect is minimal

18. Clinical Features &
Management

19. Shock
Classification
Rapid, but
detailed H&P
to direct
therapy
Flow diagram
 Figure 4-4 in
Rosen’s

20. Clinical Features
Frequently no obvious etiology
Rapid recognition
 H&P, ill appearance, diaphoresis
 HR and BP not reliable
 HR/SBP ratio better indicator
Normal is less than 0.8
 Urine output is great, but takes time
Normal >1.0 ml/kg/hr
 Lactic acid or base deficit

21. Hypovolemic Shock
Degree of volume loss response
• 10% well tolerated (tachycardia)
• 20 - 25% failure of compensatory mechanisms
(hypotension, orthostasis, decreased CO)
• > 40% loss associated with overt shock (marked
hypotension, decreased CO, lactic acidemia)

22. Hypovolemic Shock
Rate of volume loss and pre-existing
cardiac reserve response:
• Acute 1L blood loss results in mild to moderate
hypotension with decreased CVP and PWP
• Same loss over longer period may be tolerated
without hypotension due to increased fluid retention,
increased RBC 2,3 DPG, tachycardia, and increased
myocardial contractility
• Same slow loss in patient with diminished cardiac
reserve may cause hypotension or shock.

23. Clinical Data
CXR – infection, contusions
EKG – ischemia
Glucose
CBC – anemia, leukocytosis
Electrolytes – dehydration, GI
bleed, acidosis
ABG – base deficit, acidosis
UA – dehydration

24. Diagnosis and Evaluation
Invasive Monitoring
Arterial pressure catheter
CVP monitoring
Pulmonary artery catheter (+/- RVEF, oximetry)

25. Organ Blood Flow in Shock
Dependent on maintenance of blood
pressure within an acceptable range
For humans, good overall auto-regulation
of blood flow between 60 - 100 mm Hg
However, experimental data in animals
shows brain and heart have wider ranges
while skeletal muscle has a significantly
narrow auto-regulatory range.

26. Management
IV, O2, monitor
BP readings every 2-5 minutes
 Remember BP reading often underestimates
the level of shock until severe
Urine output
 >1 cc/kg/min

27. Management
IV access
 Peripheral vs. Central
Most patients OK with one large bore or two
smaller bore peripheral IV’s
CVP pressure may be required for patient with
cardiac failure or renal failure
Indwelling catheters should be used unless
hospital policy states against it in the ED

28. Therapeutic Steps
Admit to intensive care unit (ICU)
Venous access (1 or 2 wide-bore catheters)
Central venous catheter
Arterial catheter
EKG monitoring
Pulse oximetry
Hemodynamic support (MAP < 60 mmHg)
• Fluid challenge
• Vasopressors for severe shock unresponsive
to fluids

29. Volume Replacement
When is the tank full?
 Goal CVP slightly elevated of 10-15 cm H2O
 Must correlate CVP with SBP, urine output,
and lactate levels to adequately assess
perfusion

30. Ventilation
Rapid sequence intubation preferred
 Ketamine or etomidate are good choices due
to minimal cardiovascular depression
 Intubation protects aspiration, decreases
breathing workload, and initial treatment for
acidemia
 High negative pressures in bronchospasm or
ARDS can decrease LVEF and positive
pressure removes this

31. Acidosis
Acidosis is a negative inotrope
No evidence supports using bicarbonate
for treatment
Treat with improved ventilation and mild
hyperventilation
THAM (tris[hydroxymethl]-aminomethane)
may be used IV for acidosis reversal

32. Optimal Hemoglobin
Hemoglobin carries oxygen
High hematocrits increase viscosity and
cardiac workload
Optimal balance is a hemoglobin of 10-12
gm%

33. Goal-Directed Therapy
Goal directed therapy is the practice of
resuscitating to a defined physiologic endpoint
 Wedge pressures – measures left ventricular filling
pressures – controversial risk/benefit
 Lactate clearing index – decrease in arterial lactate by
50% in 1 hour and continued efforts until lactate < 2
mM
 GI tonography – permeable balloon in stomach or
rectum measuring pH to estimate perfusion
Questionable data supporting

34. Specific Causes &
Treatment

35. A Clinical Approach to Shock
Diagnosis and Management
Immediate Goals in Shock
Hemodynamic support MAP > 60mmHg
PAOP = 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
MAP = mean arterial pressure; PAOP = pulmonary artery
occlusion pressure.

36. A Clinical Approach to Shock
Diagnosis and Management
Hypovolemic Shock
Rapid replacement of blood, colloid, or
crystalloid
Identify source of blood or fluid loss:
• Endoscopy/colonoscopy
• Angiography
• CT/MRI scan
• Other

37. Hemorrhagic Shock
Rapid reduction in blood volume
Heart rate and blood pressure responses
can be variable
No firm conclusion can be made by simply
HR and BP readings

38. Hemorrhagic Shock
General Progression
Increased heart rate
Narrowed pulse pressure
Shunting from noncritical organs
Decreased cardiac filling
leading to decreased CO
Decreased SBP

39. Hemorrhagic Shock
Decreased perfusion to splanchnic organs
precedes lower BP
 Lactic acid production
 Base deficit
Normal base deficit is greater than -2 mEq/L
After 1/3 of blood volume lost hypotension
occurs
Acidemia occurs about then as patient
cannot create enough respiratory
compensation for the lactic acid

40. Hemorrhagic Shock
Organ injury in resuscitation
 Release of activated neutrophils &
inflammatory cytokines
 Distorted balance of vasodilatation vs.
vasoconstriction
 May lead to ARDS, acute tubular necrosis, &
centrilobular ischemic liver damage

41. Consensus Definition
Hemorrhagic Shock – 3 classifications
 Simple hemorrhage
Bleeding with normal vital signs and base deficit
 Hemorrhage with hypoperfusion
Bleeding with base deficit < -5 mmol or persistent HR >100
 Hemorrhagic shock
Bleeding with 4 or more of below
 Ill appearance or mental status
 HR >100
 RR >22 or PaCO2 <32
 Base deficit < -5 or lactate > 4
 Urine output < 0.5 cc/kg/hr
 Hypotension > 20 minutes

42. Hemorrhagic Shock Treatment
Several liters of crystalloids in adults
Three 20 cc/kg boluses in children
If still in shock after bolus start PRBC’s at
5-10 cc/kg
Blood substitutes possibly in future but not
currently advantageous

43. Hemorrhagic Shock Treatment
Controlling hemorrhage is still always the
cornerstone of treatment
Immediate surgery if hemorrhage cannot
be controlled
In very rare cases inotropics may be
beneficial

44. Septic Shock
Any microbe may cause, but gram
negative most common
Lipopolysaccharide is a key mediator
1/3 of cases no organism is identified
Higher causes recently of gram positive
due to
 Hospitalized patients
 Immunocompromised
 Indwelling catheters
 Increasing drug resistance

45. Septic Shock
3 major effects
 Hypovolemia
Relative due to increased venous capacitance
Absolute due to GI loss, diaphoresis, tachypnea
 Cardiovascular depression
Depression due to inflammatory mediators
 Systemic inflammation
Capillary leak causing ARDS in up to 40%

46. Consensus Definition
SIRS
 Two or more of the following
Temperature > 38 C or <36 C
Heart rate > 90
Respiratory rate > 20 resp/min or PaCO2 <32
WBC > 12,000, < 4,000, or >10% bands
Septic Shock
 Severe sepsis with hypotension unresponsive to fluid
resuscitation and perfusion abnormalities

47. Septic Shock Treatment
Ventilatory support
 Decrease respiratory workload and correct
hypoxia
Fluids
 Increase ventricular filing
 20-25 cc/kg crystalloids followed by 5-10
cc/kg colloids
Blood
 Used to keep Hct at 30-35% if needed

48. Septic Shock Treatment
Antibiotics
 If focus identified
Use clinical experience
 If no focus identified
Semisynthetic PCN with β-lactamase inhibitor with
an aminoglycoside and vancomycin
Imipenem-cilastatin good monotherapy choice
Antifungal in immunocompromised

49. Septic Shock Treatment
Vasopressors
 Dopamine
Most common first line agent and a bad idea
Remove from you armamentarium
 Norepinephrine
Start 0.5-1 µg/min and titrate to response
Excellent first choice; well studied
 Dobutamine
Start 5 µg/kg/min
Hypotension unresponsive to vasopressors and
IVF.

50. Cardiogenic Shock
Pump failure
Results when more than 40% of
myocardium damaged
Similar circulatory and metabolic changes
to hemorrhagic shock
May also be due to a PE

51. Consensus Definitions
Cardiogenic
 Cardiac failure
Evidence of impaired cardiac outflow including
dyspnea, tachycardia, rales, edema, or cyanosis
 Cardiogenic shock
Cardiac failure plus four of below criteria
 Ill appearance or mental status
 HR >100
 RR >22 or PaCO2 <32
 Base deficit < -5 or lactate > 4
 Urine output < 0.5 cc/kg/hr
 Hypotension > 20 minutes

52. Cardiogenic Shock Treatment
Ventilatory support
 Often needed in pulmonary edema or if
respiratory failure imminent
 Avoid barbiturates, morphine, propofol and
benzodiazepines
Negative inotropic effects
Fentanyl, ketamine and etomidate much better
choices

53. Cardiogenic Shock Treatment
Ionotropics/vasopressors
 Dobutamine and Milrinone are agents of
choice
 Amrinone (Replaced by Milrinone)
 Milrinone
Similar to amrinone
Load at 50 µg/kg (Consider half loading dose)
Infuse at 0.375 - 0.75 µg/kg/min
Be prepared for hypotension

54. Cardiogenic Shock Treatment
Intraaortic balloon pump
 When all pharmacologic therapy is failing
 Requires appropriate facility and ICU/CCU
 Improves cardiac output by 30%

55. Cardiogenic Shock Treatment
Myocardial infarction causing cardiogenic
shock
 Management not significantly different than
another MI accept additional management
Ventilatory support as needed
Treat dysrhythmias
Inotropic support
Aspirin
Heparin
PTCA vs. thrombolytics

56. Cardiogenic Shock Treatment
Pulmonary Embolism
 Ventilatory support
 IV fluids
 Norepinephrine
 Thrombolytics (systemic vs. intra-arterial)
 Possis catheter
 Surgical embolectomy at few centers

57. Anaphylactic Shock
IgE mediated response to an allergen
Mast cells release histamine
Histamine causes
Smooth muscle relaxation
Bronchial contraction
Capillary leak

58. Anaphylactic Shock Treatment
Epinephrine
 1 cc of 1:10,000 IV infused slowly and watch
response
 5 mg in 500 cc NS at 10 cc/hr thereafter
May titrate to response
 Use even with coronary artery disease if
hypotensive

59. Anaphylactic Shock Treatment
Corticosteroids
 Decrease immune response
 Methylprednisolone 125mg IV
 Hydrocortisone 5-10 mg/kg IV
Antihistamines
 Diphenhydramine 0.5 mg/kg IV
 Cimetidine 2-5 mg/kg IV
 Famotidine
Intubation if needed

60. Neurogenic Shock
CNS cord lesions above T1
 Heart gets unopposed vagal simulation
 Bradycardia and hypotension
Atropine
 First line therapy

61. Neurogenic Shock Treatment
Volume expansion
 Confirm by CVP and BP
Vasopressors
 Ephedrine
10 mg IV bolus good for 3-4 hours
 Phenylephrine
100-180 µg/min IV until stable

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

63. Fluid Therapy
Correct hypotension first (golden hour)
Decrease heart rate
Correct hypoperfusion abnormalities
Monitor for deterioration of oxygenation

65. Summary
Early recognition of shock and early
treatment is key
Do not rely solely on a HR and BP to
determine their status
Aggressive and goal directed therapy have
proven to decrease mortality