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1. AMBOUNIVERSITY COLLEGE OF HEALTH
SCIENCES & MEDICINE DEPAR’T OF MEDICINE
CLASSIFICATION & MANAGEMENTOFSHOCK
PREPAREDBY:GELAYE MANDEFRO
07/20/16
1

2. OUTLINES
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 INTRO DUCTIO N
 DEFINATIO N
 PATHOPHSIOLOGY
 CLASSIFICATIO NO F SHO CK
 APPRO ACH TO THE PATIENT IN SHO CK
 MANAGEMENT PRINCIPLES

3. INTRODUCTION
07/20/16
3  Shock is the most common and the most
important cause of death among surgical
patients.
 Death may occur rapidly as a result of a
profound state of shock or be delayed,
resulting from:
 organ ischaemia and
 reperfusion injury.
 It is important that every physician
understands the pathophysiology and
diagnosis of shock as well as the priorities for
their management.

4. DEFINATION
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 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.
 With insufficient delivery of oxygen and
glucose, cells switch from aerobic to anaerobic
metabolism.
 If perfusion is not restored in a timely fashion,
cell death ensues.

5. Pathophysiology of Shock
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 Regardless of etiology, the initial physiologic
responses in shock are driven by tissue
hypoperfusion and the developing cellular
energy deficit.
 This imbalance between cellular supply and
demand leads to neuroendocrine and
inflammatory responses, the magnitude of
which is usually proportional to the degree
and duration of shock.
 The specific responses will differ based on the
etiology of shock, as certain physiologic
responses may be limited by the inciting
pathology.

6. Pathophysiology count’d
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 The cardiovascular response driven by the sympathetic
nervous system is markedly blunted in neurogenic or septic
shock.
 Decreased perfusion may occur as a consequence of
cellular activation and dysfunction, such as in septic shock
and to a lesser extent traumatic shock.
 Many of the organ-specific responses are aimed at
maintaining perfusion in the cerebral and coronary
circulation.

7. Pathophysiology count’d
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7
 These are regulated at multiple levels including:
-stretch receptors and baroreceptors in the heart and
vasculature
-chemoreceptors(CNS,Medulla)
-cerebral ischemia responses,
-release of endogenous vasoconstrictors,
-shifting of fluid into the intravascular space, and
-renal reabsorption and conservation of salt and water

8. fig 1.1
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9. Severity of shock
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compensated phase of shock
• body can compensate for the initial loss of blood volume
primarily through the neuroendocrine response to maintain
hemodynamics.
decompensation phase of shock
• Further loss of circulating volume overloads the body’s
compensatory mechanisms and there is progressive renal,
respiratory and cardiovascular decompensation.
• Microcirculatory dysfunction, parenchymal tissue damage, and
inflammatory cell activation can perpetuate hypoperfusion
-"vicious cycle" of shock.

10. 07/20/16
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Mild shock
•Initially there is tachycardia, tachypnoea and a mild reduction
in urine output and the patient may exhibit mild anxiety.
•Blood pressure is maintained although there is a decrease in
pulse pressure.
•The peripheries are cool and sweaty with prolonged capillary
refill times (except in septic distributive shock).
irreversible phase of shock
• Persistent hypoperfusion results in further hemodynamic
derangements and cardiovascular collapse.

11. 07/20/16
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Moderate shock
•Renal compensatory mechanisms fail, renal perfusion falls
and urine output dips below 0.5 ml kg–1h–1.
•There is further tachycardia and now the blood pressure
starts to fall.
•Patients become drowsy and mildly confused.
Severe shock
•In severe shock there is profound tachycardia and
hypotension.
•UOP falls to zero and patients are unconscious with
laboured respiration.

12. CLASSIFICATION OF SHOCK
07/20/16
12  There are numerous ways to classify shock but
the most common and clinically applicable way is
that based on the initiating mechanism
 Hypovolemic
 Cardiogenic (intracardiac vs extracardiac)
 Distributive
 Obstructive

13. Approach to the Patient in Shock
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 Diagnostic evaluation should occur at the same time as
resuscitation.
o Targeted History
o Physical Examination
o Investigations
 Goal of resuscitation- restore tissue perfusion and optimize
oxygen delivery, hemodynamics, and cardiac function rapidly
 Monitoring
-Careful and continuous assessment of the physiologic status is
necessary.
o Arterial pressure
o Pulse rate
o respiratory rate
o urine out put
o mental status
 Specific treatment

14. Empiric Criteria for Diagnosis of Shock
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4 out of 6 criteria have to be met
 Decreased LOC or looks ill
 HR > 100
 RR > 22 or PC02 < 32
 Base Deficit < -5 or lactate > 4
 Urine output < 0.5 ml/kg/hr
 Hyptoenstion > 20 min duration

15. HYPOVOLEMIC SHOCK
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15  The most common cause of shock in the surgical or trauma
patient is loss of circulating volume from hemorrhage
 Causes
◦ Hemorrhagic
trauma,
GI bleeding
 ruptured aneurysms,
 hemorrhagic pancreatitis
◦ Non-haemorrhagic
 vomiting
 diarrhea
 adrenal insufficiency
 dehydration
 third-space loss
 burns

16. Diagnosis
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 Shock in a trauma patient and postoperative patient
should be presumed to be due to hemorrhage until
proven otherwise.
 Medications and medical hx
 Physical examination
 Lab. Serum lactate and base deficit, Hct
 Apparent clinical shock results from at least 25 to 30%
loss of the blood volume.

17. Class of hemorrhage
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CLASS I CLASS II CLASS III CLASS IV
Blood loss ml Up to 750 750-1500 1500-2000 >2000
Blood loss % Up to 15% 15%-30% 30%-40% >40%
Pulse rate <100 >100 >120 >140
SBP normal normal decreased decreased
Pulse pressure normal decreased decreased decreased
Respiratory
rate
14-20 20-30 30-40 >35
Urine out put >30 20-30 5-15 negligible

18. Class of hemorrhage
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CLASS I CLASS II CLASS III CLASS IV
Mental status Slightly
anxious
Mildly anxious Anxious ,
confused
Confused ,
lethargic
Fluid (3:1 rule
)
Crystalloid crystalloid Crystalloid
and blood
Crystalloid
and blood

19. Management of Hypovolemic
Shock
07/20/16
19 A) RESUSCITATION
 Immediate resuscitation maneuvers for patients
presenting in shock are :
 secure the airway,
control the source of blood loss, and
IV volume resuscitation
 dam ag e co ntro lre suscitatio n -begins in ED,
continues into the OR, and ICU.
 Initial resuscitation is limited to keep SBP around
90 mmHg.
 This prevents renewed bleeding from recently
clotted vessels.
 In head injury, keep SBP around110 mmHg.

20. 07/20/16
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 The ideal fluid –crystalloids.
 Increased risk of death in bleeding trauma
patients treated with colloid compared to
patients treated with crystalloid.
 In patients with severe hemorrhage,restoration
of intravascular volume should be achieved
with blood products.

21. 07/20/16
21
 Not due to hemorrhages: Infusion of fluid (Normal
Saline or Ringer lactate) 20ml/kg fast; reassess the
patient for adequacy of treatment; if needed repeat the
bolus with maximum tolerated dose being 60 – 80
ml/kg with in the first 1 – 2 hr.
 If due to hemorrhage, transfusion of packed RBC or
whole blood 20ml/kg over 4 hrs, repeated as needed
until Hgb level reaches 10gm/dl and the vital signs are
corrected.

22. 07/20/16
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B)Monitoring
Minimum
 Electrocardiogram
 Pulse oximetry
 Blood pressure
 Urine output
Additional modalities
 Central venous pressure
 Invasive blood pressure
 Cardiac output
 Base deficit and serum lactate

23. CARDIOGENIC SHOCK
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 Defined clinically as circulatory pump failure leading
to diminished forward flow and subsequent tissue
hypoxia, in the setting of adequate intravascular
volume.
 Hemodynamic criteria include
 sustainedhypotension(i.e., SBP<90mmHgforat least 30’),
 reducedcardiac index(<2.2L/minpersquaremeter), and
 Elevatedpulmonaryarterywedgepressure(>15mmHg).
 Mortality rates for cardiogenic shock are 50 to 80%.

24. CARDIOGENIC SHOCK
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 Causes:
 Acute MI - the most common cause.
 cardiac dysrhythmias,
 valvular heart disease,
 blunt myocardial injury and
 cardiomyopathy

25. CARDIOGENIC SHOCK
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25 Clinical presentation
Signs of circulatory shock:
hypotension, cool and mottled skin, depressed
mental status, tachycardia, and diminished pulses.
Cardiac exam may include dysrhythmia, precordial
heave, or distal heart tones.
Investigations
Confirmation of a cardiac source for the shock
requires electrocardiogram and urgent
echocardiography.
Other useful diagnostic tests include chest
radiograph, arterial blood gases, electrolytes,
complete blood count, and cardiac enzymes.

26. Management of Cardiogenic shock
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Vasopressorand inotropic
 Dopamine, 2-20 mcg/kg/min IV diluted with 5%D/W, or NS/RL
S/Es - tachycardia, raise d blo o d pre ssure
AND/OR
 Dobutamine : 2.5-15 micrograms/kg/min IV diluted in 5%D/W .
P/C: severe hypotension complicating cardiogenic shock
OR
 Adrenaline, 1:10000, IV, 3-5 ml given slowly
PLUS
 Fluid administration: 5 – 10 ml/Kg IV over 1hr.
 Fluid administration has to be under extreme caution !!
 Early consultation with cardiology

27. ..CON’T
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27
 Other interventions
- IABP( intraaortic balloon pump) is utilized if
medical therapy is ineffective
- Fibrinolysis
- Surgery - for mechanical defects
- Glycemic control

28. Intra-Aortic Balloon Pump
07/20/1628

29. Obstructive shock
29
• Obstructive shock results from etiologies that
prevent adequate CO but are not intrinsically
cardiac in origin.
• Jugular venous pressure is often elevated in
these patients
Causes :
 Heart is working well but there is a block to the
outflow by:
◦ Cardiac tamponade
◦ Tension pneumothorax
◦ Massive pulmonary embolism
◦ Aortic dissection

30. 30
 othercauses
 IVC obstruction
 Deep venous thrombosis
 Gravid(Pregnant) uterus on IVC
 Neoplasm
 Increased intrathoracic pressure
 Excess positive end-expiratory pressure
 Neoplasm

31. CLINICAL PRESENTATION
 respiratory distress (in an awake patient),
 Hypotension
 Diminished breath sounds over one
hemithorax
 Hyperresonance to percussion,
 Jugular venous distention, and
 Shift of mediastinal structures to the
unaffected side with tracheal deviation.

32. DIAGNOSIS
32tension pneumothorax
three findings are sufficient:
 Respiratory distress or hypotension,
Decreased lung sounds, and
Hyperresonance to percussion.
Chest x-ray findings that may be visualized include:
 deviation of :
Mediastinal structures,
Depression of the hemidiaphragm, and
Hypo-opacification with absent lung markings.

33. MANAGEMENT
33
 Tension pneumo- or hemothoraces and
pericardial tamponade require mechanical
intervention.
 Hemothorax requires tube thoracostomy.
 Pericardial tamponade is treated by
needle decompression, often with catheter
placement for drainage.

34. ...CON’T
34 Alternatives include :
 systemic anticoagulation,
 thrombolysis, and
 surgical clot removal.
 Inferior vena cava (IVC) filters
are used in patients who have a
contraindication to systemic
anticoagulation.

35. Distributive shock(DS)
35
 Venodilation and leakage of fluid from the
microvasculature lead to vascular volume
and  preload
 peripheral vasodilation due to loss of vessel
tone
 It is a consequence of severely decreased
SVR.

36. Distributive shock CONT’D
36
 Dist. shock describes the pattern of
cardiovascular responses characterizing a
variety of conditions including:
Septic shock,
anaphylaxis and
spinal cord injury.

37. SEPSIS AND SEPTIC SHOCK
Sepsis: It is systemic response to infection manifested by ≥
2 of:
 Temp > 38o
C or < 36o
C
 HR > 90 bpm
 RR > 20 bpm or PaCO2 < 32 mmHg
 WBC > 12 x 109
/L, < 4 x 109
/L or >10% band form
Septic shock: sepsis with hypotension despite adequate
fluid resuscitation, with perfusion abnormalities that could
include, but are not limited to, lactic acidosis, oliguria,
and/oracutementalstatus.

38. Stages of Sepsis
Mortality
7%
16%
20%
70%
SIRS
SEPSIS
SEVERE
SEPSIS
SEPTIC
SHOCK
MODS/DEATH

39. SIRS and Sepsis
SIRS: Systemic Inflammatory Response
Syndrome
 Fever,
 leucocytosis,
 organ failure
 Recognises difficulty of identifying infection

40. Bacterial infection
Sepsis and septic shock
Excessive host response
Host factors lead to cellular damage
Organ damage
Death

41. Clinical Signs of Septic Shock
Hemodynamic Alterations:
A Hyperdynamic State (“Warm Shock”)
• Tachycardia.
• Elevated or normal cardiac output.
• Decreased systemic vascular resistance.
B Hypodynamic State (“Cold Shock”)
Low cardiac output.
• Myocardial Depression.
• Altered Vasculature.
• Altered Organ Perfusion.
• Imbalance of O2 delivery and Consumption.
• Metabolic (Lactic) Acidosis

42. Essentials of Diagnosis
 Infection
 Either high or low cardiac output
 Hypotension
 Low systemic vascular resistance
 Fever and chills
 Evidence of infection or perforation
 Warm, flushed skin
 Tachycardia
 Anxiety and confusion

43. High-output septic shock can be produced by
 Bowel perforation
 Necrotic intestine
 Abscesses
 Gangrene, and
 Soft-tissue infections
Cardiovascular findings of low-output sepsis are
identical to those of hypovolemic shock
 Diagnosis is usually clear from clinical
circumstances

44. Management of Sepsis
 Antibiotics (early administration)
 Hemodynamic support
– (fluid resuscitation)
 Restore tissue perfusion
 Normalize cellular metabolism
– Vasopressor agents
Dopamine, norepinephrine, dobutam

45. Management of Sepsis
 Source control
– Surgical debridement of infected, devitalized
tissue
– Catheter replacement
 Supplemental oxygen (treatment of acute
respiratory distress syndrome,ARDS)
 Nutritional support

46. ANAPHYLACTIC SHOCK
 Anaphylaxis is a severe, potentially fatal
systemic allergic reaction that occurs suddenly
(minutes to hours) after contact with an allergy-
causing substance
 Death can occur in minutes, usually due to
closure of airways
 Allergic reaction affects many body systems :
rash & swelling, breathing difficulties, vomiting
& diarrhoea, heart failure & low blood pressure.

47. Causes of Anaphylaxis
 Food allergy
 Medication allergy
 Insect (hymenoptera) sting allergy
 Physical eg exercise, cold,
 Latex allergy
 Allergy to vaccines, hormones, seminal fluid
 Allergic reactions to immunotherapy, skin tests
 Idiopathic

48. CLINICAL MANIFESTATIONS OF
ANAPHYLAXIS
 SKIN- urticaria, angioedema, pruritus, erythema
 RESPIRATO RY- rhinitis, conjunctivitis, cough, dyspnea,
wheeze, stridor, voice change
 GI– throat swelling or tightness, dysphagia, vomiting,
diarrhea, cramps
 CVS – hypotension, dizziness, syncope, cyanosis,
secondary myocardial infarction
 CNS –hypoxic seizures
Cause s o f De ath
Uppe r and/o r Lo we r Airway O bstructio n 7 0 %
Cardiac Dysfunctio n (24% )

49. Diag no stic crite ria
 Criterion 1: acute onset (minutes – hours) involving skin
and/or mucosa + at least one:
 Respiratory compromise
 Reduced blood pressure
Criterion 2: At least 2 of the following, minutes – hours after
exposure to a likely allergen for that patient:
 Skin/mucosal involvement
 Respiratory compromise
 Reduced blood pressure
 Gastrointestinal symptoms
. Criterion 3: Reduced blood pressure minutes – hours after
exposure to a known allergen for that patient

50. GENERALMANAGEMENT
 ABC of life
Initial Anaphylaxis Treatment
 Epinephrine (adrenaline) is first line treatment
 Epinephrine preferably given IM
 Antihistamines & bronchodilators are not first line
treatment but may be given after epinephrine.
 Transportation to hospital should not be delayed
to administer these once epinephrine has been
given.

51. Management
Bronchospasm
 Inhaled bronchodilators eg salbutamol.
 Oxygen
 Intubation and ventilation if needed
Laryngeal edema
 Racemic epinephrine via nebulizer
 Intubation or cricothyrotomy or tracheostomy

52. Management
Hypotension
Volume expansion with crystalloid
 Vasopressors eg dopamine, norepinephrine,
metaraminol, vasopressin
 Glucagon esp if on beta-blocker
 Trendelenberg position

53. Treatment
 Removal of the causing agent
 Epinephrine
 0.3 – 0.5 mg (0.01mg/kg) i.m. (vastus lateralis),
repeat 5 – 15 minutes
 i.v. – titrate the dose
 Oxygen
 Intubate, if stridor or arrest
 i. v. Fluids (cristalloids vs. colloids?)
 Steroides, antihistamines, inhaled beta agonists

54. Neurogenic shockNeurogenic shock
54
 In high spinal cord injury there is
failure of sympathetic outflow and
adequate vasculartone (neurogenic
shock).
loss of vasomotor tone to peripheral arterial
beds
from vertebral body fractures of the cervical
or high thoracic region that disrupt
sympathetic regulation of peripheral
vascular tone.

55. 55
Causes
 Spinal cord trauma
 Spinal cord neoplasm
 Spinal/epidural anesthetic

56. Management of Neurogenic Shock
56
 Afterthe airway is secured and ventilation is
adequate, fluid resuscitation and restoration of
intravascularvolume often will improve
perfusion in neurogenic shock.
 Most patients with neurogenic shock will
respond to restoration of intravascular volume
alone, with satisfactory improvement in
perfusion and resolution of hypotension.

57. 57
 Administration of vasoconstrictors
will :
 improve peripheral vascular tone
 decrease vascular capacitance
 increase venous return
 should only be considered once
hypovolemia is excluded as the cause
of the hypotension.

58. COMPLICATIONS OF SHOCK
58  The main complications of severe shock
include:
 Shock lung (ARDS)
 Acute renal failure
 Gastrointestinal ulceration
 Disseminated intravascular clotting
 Multiorgan failure
 Death

59. REFERENCES
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1. Baile y & lo ve ’s short practice of surgery 25th
e ditio n
2. Schwartz’s principle o f surg e ry 9 th
e ditio n

60. 60
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