This is seminar on shock

1. Shock
General principle, cause
and classifications
Presenter: Egizeru Enedalew, R1
Moderator: Dr. Eyassu, General surgeon

2. outline
• Objective of the presentation
• Introduction
• Definition
• Pathophysiology
• Classification
• Principles of management

3. Objective
• To understand the pathophysiology and
management principles of the different shock types

4. Introduction
• Hipocrates and Cannon use the word ‘exemia’ to
describe shock
• Initially the word shock was used to refer to the
physical effect of wounding agent not the
physiologic respone
• Dr. George crile, vasomotor changes resulting from
nervous stimulation played an important role in the
pathophysiology of shock
• Blalock, the different classification of shock

5. Definition
• Inadequate tissue perfusion marked by decreased
delivery of required metabolic substrates and
inadequate removal of cellular waste products.
• This involves failure of oxidative metabolism that
can involve defects of oxygen (O2) delivery,
transport, and/or utilization.

6. Pathophysiology
I. Cellular
• As perfusion to the tissues is reduced, cells are
deprived of oxygen and must switch from aerobic to
anaerobic metabolism.
• The product of anaerobic respiration is not carbon
dioxide but lactic acid.
• When enough tissue is under perfused, the
accumulation of lactic acid in the blood produces
systemic metabolic acidosis.

7. Contd..
Microvascular
• As tissue ischemia progresses, changes in the local
milieu result in activation of the immune and
coagulation systems.
• Hypoxia and acidosis activate complement and prime
neutrophils, resulting in the generation of oxygen free
radicals and cytokine release.
• These mechanisms lead to injury of the capillary
endothelial cells.

8. Contd..
Systemic
Cardiovascular
• As preload and afterload decrease there is a
compensatory baroreceptor response resulting in
increased sympathetic activity and release of
catecholamines into the circulation.
• This results in tachycardia and systemic
vasoconstriction.

9. Contd..
Respiratory
• The metabolic acidosis and increased sympathetic
response result in an increased respiratory rate and
minute ventilation to increase the excretion of carbon
dioxide.
Renal
• Decreased perfusion pressure in the kidney leads to
reduced filtration at the glomerulus and a decreased
urine output.

10. Contd..
• The renin–angiotensin–aldosterone axis is stimulated
resulting in further vasoconstriction and increased
sodium and water reabsorption by the kidney.
Endocrine
• Cortisol is also released from the adrenal cortex,
contributing to the sodium and water reabsorption and
sensitizing the cells to catecholamine.

11. Phases of shock
The pathophysiologic responses vary with
time and in response to resuscitation
The compensated phase
the decompensated phase
The irreversible phase

12. Compensated phase
• Neuroendocrine response maintains for initial loss
of blood volume.

13. Decompensated phase
• Continued hypo perfusion
• Early manifestation; cellular/tissue level
Cellular injury and death
Microcirculatory dysfunction, parenchymal tissue
damage, and inflammatory cell activation
• Late manifestations: organ system level

14. Irreversible phase
• Persistent hypo perfusion resulting in further
hemodynamic derangements and cardiovascular
collapse
• At this point, extensive parenchymal and
microvascular injury has occurred
• Volume resuscitation fails to reverse the process

15. Contd..

17. Cont..

18. FORMS OF SHOCK
•

19. Hypovolemic/Hemorrhagic shock
• Cause of shock in a trauma or postoperative patient
• Potential sites of blood loss:
External loss
Internal/intracavitary loss
Ribs….each, 100 to 200ml
Pelvic…2000ml or more
Femur…800 to 1000ml
Tibia#...300 to 500ml

20. Contd..

21. Contd..

22. Contd..

23. Clinical signs of shock
Agitation
cool clammy extremities
Tachycardia, weak or absent peripheral pulses, and
hypotension.
25 to 30% of blood volume loss needed for this
manifestations

24. Shock index
• Designed to improve early detection and severity
• More sensitive in prediction of hypotension, the
need for massive transfusion
• SI = HR / Systolic BP (mmHg)
• Normal shock index is 0.5-0.7
• Has prognostic value

25. Diagnosis
• Clinical
• Laboratory
• Radiology…eFAST, CT of head chest,
abdominopelvic

26. Contd..
Tachycardia and hypotension
Young
Athletes
Elderly and those on medications like BBs
Comorbidities like atherosclerotic disease

27. Contd..

28. Hypotension of ⩽110 mmHg is Associated with Increased Mortality in
South African Patients After Trauma

29. Contd..
Hct:
• has been shown to be associated with 24 hour fluid
and transfusion requirements
• Normal hematocrit doesn't rule out significant
blood loss or ongoing bleeding

30. Treatment
• Shout for help
• ABCDE of life
• Open double large bore IV catheter
• Take 10ml of blood sample during iv line
for CBC , BG & Rh and cross match
• Shock position
• Intranasal O2
• Bladder catheterization for fluid balance
• Resuscitation with iv fluid
• Preparing blood
• Detect the cause and arrest hemorrhage

31. Initial management of
hemorrhage
• Control external bleeding
• Initiate resuscitation
IV fluids should be used only for hypotensive
patients, till blood is available
Blood products should be given in equivalent
amount
If available dynamic coagulopathy measuring
methods should guide resuscitation

32. Contd..

33. Iv fluid resuscitation
• Subject of debate
• 500ml NS bolus via 18G Iv cannula as fast as
possible
• Repeat till blood is available or BP is greater than or
equal to 90mm Hg, or MAP of 65mm Hg or more
• Hypertonic saline…needs further investigations
• Colloids, has no improved outcome, and expensive

34. Massive transfusion protocol
• Traditionally, 10 units of PRBCs or more transfused
over 24hr
• 10 units or more transfused over 6 hours
• For patients with severe ongoing hemorrhage

35. ABC score for MTP
1. Penetrating mechanism of injury
2. Positive FAST
3. SBP of 90 mmHg or less
4. Heart rate of 120 beats per minute (bpm) or
greater
• Each with score of one.
• a sore of 2 or more has 75% sens and 86% spes for
need for mssive transfusion

36. Damage control resuscitation
• DCR is a systematic approach to the management
of the trauma patient
• Starts in the ER, OR and the ICU
• DCR involves homeostatic resuscitation, permissive
hypotension (where appropriate) and DCS
• Aim is correct the ‘lethal triad’ till definitive
intervention is appropriate

37. Permissive hypotension
• Refers to restricting the amount of resuscitation
fluid and maintaining blood pressure in the lower
than normal range
• Avoid dilusional coagulopathy and acceleration of
hemorrhage,
but does carry the potential risk of tissue
hypoperfusion.

38. DCS
• Previously called abbreviated laparotomy
• It is an operative intervention to treat immediately
life threatening condition
• Short procedure done on a patient with limited
physiologic reserve

39. Phases of DCR
• Phase 0…triage and patient transport
• Phase 1
Arresting hemorrhage, limiting contamination and
maintaining optimal blood flow to vital organs
caution…operating time should be limited
• Phase 2 and 4

40. Contd..
3.Large volume of resuscitation required
4. Injury pattern identified during surgery
5. Need for staged abdominal or thoracic
reconstruction

41. Contd..

42. Contd..
Signs of normovolaemia being re-established
• Improvement in urine output, HR, BP
• Fast capillary refill
• Return of peripheral pulses
• Improving consciousness level
• Normalizing in arterial PH
• Rise In CVP

43. Adjuncts of therapy
• Tranexamic acid
• Inotropes
• Hypothermia mt
• Oxygen and ventilator support
• Positioning

44. Tranexemic acid
• Tranexamic acid is an IV antifibrinolytic drug
that may be used for the prevention and
treatment of hemorrhage.
• Preparation, 1g/10ml
• administration:
1ml per minute over 10 minutes
Repeat same dose If bleeding persists within 30min
or with in 24hr of first dose
It is effective if given with in 3hr of trauma

45. Tranexamic acid

46. Traumatic Shock
• Systemic response after trauma
• Due to combined effect of hemorrhage, soft tissue
injury and long bone fractures
• Results in ARDS and multiorgan failure

47. Pathophysiology
• Hypo perfusion
• Pro inflammatory activation
• Septic shock like pattern of response

48. Treatment
• prompt control of hemorrhage
• Adequate volume resuscitation to correct O2 debt
• Debridement of nonviable tissue
• stabilization of bony injuries
• Appropriate treatment of soft tissue injuries

49. Septic Shock (Vasodilatory Shock)
• Dysfunction of the endothelium and vasculature
• 2o to circulating inflammatory mediators or due to
persistent hypoperfusion.
• Hypotension is due to vascular smooth MUSCLE
dysfunction
• Characterized by fever, increased CO, micro blood
clot formation, sludging of blood

51. Pathophysiology
Microorganism or products of damage tissue
stimulate production of pro inflammatory cytokines
which in turn stimulate production of secondary
meditators of inflammation
Normally this mediators are regulated to limit
damage
In sepsis and extensive tissue damage this
regulation fails and results in excessive
inflammatory response which then leads to tissue
injury

52. Contd..

53. Diagnosis
SIRS: 2 or more of…
Sepsis: infection ➕ SIRS
severe sepsis: sepsis ➕ signs of organ dysfunction
Septic shock: severe sepsis which doesn't respond
to fluid resuscitation and which requires
vasopressors or inotropic agents.
SOFA score and qSOFA

54. Approach to sepsis and septic
shock mt
• ABC of life
• Antibiotics
• Source control
• Intubation and ventilation
• Fluid resuscitation, at least 30 mL/kg for
hypotensive patients
• Serum lactate determination

55. Contd..

56. Contd..
A. Stabilize the airway
Oxygen with conscious pulse oximetry monitoring
Intubation and MV, if depressed mentation or
increased work of breathing
B. Establish venous access
Peripheral or central
Start fluids, antibiotics and vasopressor

57. Contd..
C. Initial investigations
• CBC and urinalysis
• ABGs analysis
• Serum lactate
• OFT
• Targeted imaging
• Blood culture, aerobic and anaerobic from at least
two different sites
• Microbiologic culture

58. Contd..
D. Initial resuscitative therapy
• Iv fluids and the early administration of antibiotics
• Crystalloids given at a rate of 30ml/kg over 3hr
• Fluid choice?
• Monitor BP, chest condition and tissue perfusion
• Empiric antibiotics started with in 1hr

59. Contd..
Empiric antibiotic therapy (first hour)
• Identification of suspected source
• Timing
• Choosing a regimen
Previous exposure, comorbidity, immune defect,
site of infection, local resistance, hospitalization
hx….

60. Contd..
if Pseudomonas is an unlikely pathogen, we favor
combining vancomycin plus
•Cephalosporin, 3rd gnrn
(eg, ceftriaxone or cefotaxime) or 4th generation
(cefepime), or
•Beta-lactam/beta-lactamase inhibitor
(eg, piperacillin-tazobactam, ticarcillin-clavulanate),
or
•Carbapenem (eg, imipenem or meropenem)

61. Contd..
• Pseudomonas is a likely pathogen, vanco. plus
• Antipseudomonal cephalosporin, or
•Antipseudomonal carbapenem, or
•Antipseudomonal beta-lactam/beta-
lactamase inhibitor, or
•Fluoroquinolone with good anti-pseudomonal
activity, or
•Aminoglycoside, or
•Monobactam (eg, aztreonam)

62. Contd..
• Empirical antifungal therapy is not generally
warranted in neutropenic critically-ill patient

63. Monitoring response
• Clinical
• Hemodynamic and
• Laboratory parameters

64. Contd..
Clinical parameter
• MAP, urine output, heart rate, respiratory rate, skin
color, temperature, pulse oximetry, and mental status.
Hemodynamic
CVP at a target of 8 to 12 mmHg
ScvO2 ≥70 percent (≥65 percent if sample is drawn off a
PAC)
 Respiratory changes in the vena caval diameter, radial
artery pulse pressure, aortic blood flow peak velocity

65. Contd..
Laboratory
• Lactate clearance
• Lab results…

66. Source control
• IV antibiotics will be insufficient for the ff
Infected fluid collections
Infected foreign bodies
Devitalized tissue
Tx: percutaneous drainage and operative mt

67. Next step after initial therapy
• Identification and source control
• De escalation of fluids
• De escalation and duration of abs

68. Supportive therapies
• Blood product infusion
• Nutrition
• Stress ulcer prophylaxis
• Neuromuscular blocking agents
• Venous thromboembolism prophylaxis
• Intensive insulin therapy
• External cooling or antipyretics
• Mechanical ventilation, sedation

69. Failed initial therapy
• Vasopressors
• Glucocorticoids
• Inotropic therapy and
• Blood transfusion

70. Vasopressors
• If fluid resuscitation failed to maintainBP
• Norepinephrine is first line
• If not available adrenaline
• Arginine vasopressor for catecholamine resistant
septic shock
• Doubutmine for those with low cardiac output

71. Cardiogenic shock
• Circulatory pump failure leading to diminished
forward flow and subsequent tissue hypoxia,
• In the setting of adequate intravascular volume.

72. Hemodynamic criteria
• sustained hypotension
• Reduced cardiac index
• Elevated pulmonary artery wedge pressure

74. Pathophysiology

75. Diagnosis
• Exclude other causes of hypotension including
hemorrhage, sepsis, pulmonary embolism, and
aortic dissection
• Signs: hypotension, cool and mottled skin,
depressed mental status, tachycardia, and
diminished pulses.
• PE: dysrhythmia, precordial heave, or distal heart
tones

76. Contd..
• ECG
• ECHO
• Cxr
• Cbc, electrolytes, ABGs
• Cardiac markers

77. Treatments
• Ensuring adequate oxygenation and O2
delivery
• Maintaining adequate preload with judicious
volume restoration
• Minimizing sympathetic discharge through
adequate relief of pain
• Correcting electrolyte imbalance

78. Treatment…
• Intubation and MV
• Judicious fluid resuscitation
• Correct electrolyte abnormality
• Potent analgesics
• Mt of dysrhythmia
• Inotropic agents
• Intra aortic balloon pump

79. Inotropic agents
• Doubutamine
• Dopamine esp. for hypotensive patients
• Epinephrine; tachycardia and vasoconstriction
For refractory cardiogenic shock
phosphodiesterase inhibitors amrinone and
milrinone can be used

80. Treatment…
An intra-aortic balloon pump
 a bedside procedure in the ICU
Via the femoral artery through either a cut down or
using the percutaneous approach.

81. Treatment…
Percutaneous transluminal coronary angiography
• Cardiogenic shock with:
1. acute STEMI suggesting 100% occlusion of
the coronary artery
2. Left bundle branch block
Age should be less than 75yr

82. Treatment...
Coronary artery bypass grafting
for patients with multiple vessel disease or
left main coronary artery disease.

83. Other adjuncts of therapy
• Beta blockers
• Nitrites
• ACE inhibitors

84. Obstructive shock
• Due to mechanical obstruction of venous return
• Tension pneumothorax is commonest cause
•

85. Diagnosis and treatment
• Tension Pneumothorax
Dx:
Clinical; respiratory distress (in an awake patient),
hypotension, diminished breath sounds,
hyperresonance to percussion, jugular venous
distention….3 signs enough for dx
Chest X ray
deviation of mediastinal structures, depression of the
hemidiaphragm, and hypo-opacification with absent
lung markings

86. Treatment…
Tx: immediate
Pleural decompression, large bore needle
• Definitive tx: tube thoracostomy in the 4th ICS at
AAL

87. Contd..
• Cardiac tamponade
Beck’s triad consists of hypotension, muffled heart
tones, and neck vein distention
Absence doesn't exclude
Others: dyspnea, orthopnea, cough, peripheral edema,
chest pain, tachycardia
Invasive hemodynamic monitoring; pulsus-paradoxus,
elevated right atrial and ventricular pressure

88. Contd..
• ECG
• Echo
• Pericardiocentesis
• Diagnostic pericardial window, two approaches
Tx: Left thoracotomy

89. Neurogenic shock
• Diminished tissue perfusion as a result of loss of
vasomotor tone to peripheral arterial beds
• Loss of vasoconstrictor impulses results in
increased VC, decreased VR, and decreased CO
• 2o to high spinal cord segment injury
•

90. Pathophysiology
• spinal cord injury leads to multiple secondary injury
mechanisms:
vascular compromise: loss of autoregulation,
vasospasm, and thrombosis
loss of cellular membrane integrity and impaired
energy metabolism
neurotransmitter accumulation and release of free
radicals.

91. Diagnosis
• Bradycardia, hypotension, cardiac dysrhythmias,
reduced cardiac output, and decreased peripheral
vascular resistance.
• Warm extremities, motor and sensory deficits
indicative of a spinal cord injury, and radiographic
evidence of a vertebral column fracture

92. Treatment
• Secure airway
• Resuscitate with crystalloid
• Vasopressors…dopamine or phenylephrine
Note: life-threatening cardiac dysrhythmias and
hypotension may occur up to 14 days after spinal
cord injury

93. ENDPOINTS IN RESUSCITATION

94. References
1. Schwartz principles of surgery, 11th edn
2. Sabiston text book of surgery, 21st edn
3. Guyton and Hall text book of medical physiology,12th edn
4. WHO, The clinical use of blood, 2002
5. Uptodate, 2018
6. Does Tachycardia Correlate with Hypotension After Trauma?
Victorino, Gregory P MD, Battistella, Felix D MD, FACS; Wisner, David H
MD, FACS
7. Hypotension of ⩽110 mmHg is Associated with Increased
Mortality in South African Patients After Trauma D L Clarke , P
Brysiewicz , B Sartorius , J L Bruce, G L Laing
8. Tranexamic acid in bleeding trauma patients: an exploration of benefits
and harms Ian Roberts, Phil Edwards, David Prieto, Miland Joshi, Abda
Mahmood, Katharine Ker & Haleema

95. Thank you