A presentation on the various types of shock and the contemporary management

1. CURRENT CONCEPTS IN THE
MANAGEMENT OF SHOCK
BABALOLA R N
REGISTRAR, SURGERY DEPARTMENT

2. OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• CLASSIFICATION
• PATHO-PHYSIOLOGY
• CLINICAL FEATURES
• TREATMENT
• CURRENT TRENDS
• CONCLUSION

3. A “rude unhinging”
of the
machinery of life.
Samuel Gross
(1862)

4. INTRODUCTION
• Shock is the clinical manifestation of cellular dysfunction due to
inadequate tissue perfusion and consequent cellular hypoxia resulting
from a reduction in the effective circulating blood volume.
• Shock, at its most rudimentary definition and regardless of the
etiology, is the failure to meet the metabolic needs of the cell and the
consequences that ensue.

5. INTRODUCTION
• Despite advances in critical care management, patients who previously
would have died from their initial physiologic insult are surviving, only to
succumb to the late effects of shock.
• Although mortality from the shock states remains high, recent advances in
hemodynamic monitoring technology have significantly enhanced the
clinician's ability to improve patient outcome following the development of
shock.

6. HISTORY
• 1743 - The term “choc” – French for “push” or impact was first
published by LeDran
• 1882- Hartog Hamburger (Normal Saline)
• 1883- Sydney Ringer (Ringer’s lactate)
• 1899: Crile – a profound decline in blood pressure (BP) could account
for all symptoms of shock.
• 1934: Alfred Blalock - proposed four categories of shock:
hypovolemic, vasogenic, cardiogenic, and neurogenic.

7. HISTORY
• 1970: Swan and Ganz - introduced the flow-directed pulmonary
artery catheter
• 1972: A thermistor near the tip of the catheter- ability to calculate
cardiac output using the thermo-dilution technique.
• 1980s - continuous mixed venous oximetry capability was added
• Early 1990s: Catheters capable of calculating right ventricular volumes
introduced
• Early 2000s- “fourth generation” pulmonary catheters introduced for
continuous hemodynamic monitoring

8. EPIDEMIOLOGY
• Hypovolemic shock is the commonest kind of shock in clinical practice
• Up to one-third of patients admitted to the ICU could be in circulatory
shock
• In the 1,679 ICU patients in the European Sepsis Occurrence in
Acutely Ill Patients II (SOAP II) trial, septic shock was the most
frequent cause of shock, accounting for 62 % of cases, followed by
cardiogenic shock (17 %) and hypovolemia (16 %)
• Mortality from septic shock in the ICU is estimated to range between
45% and 63% though is declining with advances in management

9. CLASSIFICATION
• Hypovolemic – due to low preload from reduction in body fluid
volume
• Cardiogenic – Inadequate cardiac pump function due to impaired
electrical or muscular function
• Distributive – reduced systemic vascular resistance
• Anaphylactic
• Neurogenic
• Septic
• Obstructive shock/Compressive – reduced preload in the absence of
reduced body fluid volume

10. HYPOVOLEMIC SHOCK
• External blood loss
• Trauma
• GI bleeding
• Massive hemoptysis
• Hematuria
• Internal blood loss
• Ruptured aortic aneurysm
• Hemothorax
• Hemoperitoneum
• Retroperitoneal hemorrhage
• GI losses
• Diarrhea/Vomiting
• Renal losses
• DKA
• Hyperosmotic non-ketosis
• Diabetes insipidus
• Overzealous use of diuretics
• Transcutaneous losses
• Extensive burns
• Inadequate repletion of insensible loses
• Internal losses (“third space losses”)
• Pancreatitis
• Intestinal ischemia
• Peritonitis
• Bowel obstruction

11. CARDIOGENIC SHOCK
• Myopathic (reduced
contractility)
• Myocardial infarction
• Cardiomyopathy/Myocardial
contusion
• Advanced septic shock
• Myocarditis
• Severe acidosis
• Arrhythmogenic
• Tachyarrhythmias
• Bradyarrythmias
• Intracardiac mechanical
abnormalities
• Papillary muscle rupture resulting
in acute severe mitral
regurgitation
• Acute aortic insufficiency from an
aortic dissection
• Critical aortic stenosis
• Septal rupture

12. SEPTIC SHOCK
• Sepsis
• Pancreatitis
• Extensive burns
• Multiple traumatic injuries
• Other infective viral, bacterial or fungal conditions

13. ANAPHYLACTIC SHOCK
• Toxic ingestions
• Insect bites
• Transfusion reactions
• Heavy metal poisoning
• Narcotics
• Barbituates
• Anesthetics
• Arterial and venous vasodilators
• Radiocontrast agents

14. Neurogenic shock
• Spinal cord injury
• Spinal surgeries
• Regional anesthesia

15. OBSTRUCTIVE SHOCK
• Massive pulmonary embolism
• Tension pneumothorax
• Pericardial tamponade
• Severe pulmonary hypertension
• Severe constrictive pericarditis
• Intra-cardiac tumors
• Abdominal compartment syndrome
• Stiff abdominal wall as in deep circumferential burns
• Ruptured diaphragm with intra-thoracic displacement of abdominal viscera

16. PATHOPHYSIOLOGY: HYPOVOLEMIA
• The microcirculation , consisting of an arteriole, a venule and the
interposed capillaries, is the area of cellular and vascular exchanges of
gas, solute and fluids.
• It is thus responsible for tissue perfusion and the effects of shock.
• About 20% of blood is contained in the microcirculation, 10% in the
main arteries and 60-70% in the veins .
• The blood flow through the capillary bed depends on the
• (a) mean pressure gradient,
• (b) resistance between the arteriole and venule and
• (c) vascular tone

17. PATHOPHYSIOLOGY: HYPOVOLEMIA
EARLY STAGE – CARDIOVASCULAR RESPONSE
• About 25% drop in blood volume is needed for circulatory changes to begin
• Drop in venous return leads to a loss of inhibitory baro-receptor impulses
(carotid and aortic sinuses) on the vasomotor and cardio-inhibitory centres
• Chemoreceptors in the aorta and carotid bodies are sensitive to changes in
O2 tension, H+ ion concentration, and carbon dioxide (CO2) levels
• This results in increased sympatho-adrenal activity, cathecolamine
production with arteriolar and venular constriction and increased cardiac
chronotropic and inotropic action

18. PATHO-PHYSIOLOGY
MIDDLE AND LATE STAGES
• Activation of the renin-angiotensin-aldosterone system, ↑ADH
• Diminished renal blood flow, ↓GFR, oliguria/anuria, acidosis
• Splanchnic vasoconstriction → depression of gut mucosal barrier →
bacterial translocation → septicemia
• Macrophage activation → TNF-α and IL -1 → recruitment of more
cytokines and inflammatory cells
• Secondary inflammatory mediators – Prostaglandins, thromboxanes,
prostacyclins, PAF, histamine, kinins, complement system

19. PATHOPHYSIOLOGY
• Endothelial damage → increased vascular permeability and worsened
hypotension
• Coagulation cascade activation from widespread endothelial damage
• Hypoxia→ anaerobic glycolysis → lactic acidosis →ATP depletion
• ↓ATP
• Detachment of ribosomes from the rER- depressed protein synthesis
• Decreased cyclic AMP which may depress the action of hormones on the cell
• Reduced membrane potential with resulting influx of sodium and efflux of potassium
and cell swelling
• Damage of lysosomal membranes with release of hydrolytic enzymes-proteases. acid
phosphatase and esterases - which cause autolysis and cell death

20. CLASSIFICATION FOR HYPOVOLEMIC SHOCK

21. SEPTIC SHOCK PATHOGENESIS
• Initiators: PATHOGEN-ASSOCIATED MOLECULAR PATTERNS:
• Lipopolysaccharides on Gram-negative organism cell wall,
• Lipoteichoic acids and peptidoglycans on the Gram positive organism
membrane,
• Double standed RNA of viruses,
• Fungal cell walls,
• Products of tissue damage
• In gram-negative sepsis, free LPS binds to the CD14 receptor on
monocytes, macrophages, and neutrophils.

22. SEPTIC SHOCK
• Intracellular signaling occurs via "Toll-like receptor" protein 4 (TLR-4),
with activation of nuclear factor kappa B (NF-κB), leading to
transcription of a number of genes that trigger a pro-inflammatory
response and production of cytokines such as IL-1, IL-6, and TNF-α.
• In response to inflammation, a compensatory reaction of production
of anti-inflammatory substances such as IL-4, IL-10 antagonists, IL-1
receptor and cortisol occurs to limit the extent of inflammation. This
is called Compensatory Anti-inflammatory Response Syndrome
(CARS)

23. SEPTIC SHOCK
• Massive cytokine release in septic shock causes the release of
secondary inflammatory mediators - prostaglandins, thromboxane
A2, histamine, kinins, serotonins, leukotrienes, platelet activator
factor (PAF), products of complement activation (C3a, C5a) and free
O2 radicals – O2
.,H2O2 and OH-
• These mediators cause net vasodilatation of the microcirculation
resulting in peripheral pooling of blood and elevation of the
hydrostatic pressure.

24. SEPTIC SHOCK
• There is diminished force of cardiac contraction (TNF-α and NO)
causing coronary microvascular damage and myocyte injury, which
results in progressive hypotension, shock and hypoxia
• TNF-α also damages the vascular endothelium and with secondary
mediators enhances surface procoagulant activity with consequent
development of DIC
• Persistence of TNF-α and IL-6 in the serum predicts continuing
inflammation, the development of MODS and death

25. DEFINITIONS

26. DEFINITIONS

27. DEFINITIONS

28. Acute respiratory distress syndrome
• This is inflammation of the lungs with increased vascular permeability
characterized by bilateral infiltrates on chest X-ray, not caused by
cardiac failure.
• Typically, PaO2/FiO2 ≤ 200mmHg
• Following a range of local or systemic insults, there is embolization of
the pulmonary microcirculation by platelet, fibrin and white cell
microaggregates from traumatized or infected tissues or DIC.

29. ACUTE RESPIRATORY DISTRESS SYNDROME
• There is subsequent macrophage stimulation within the alveoli to
produce TNF which causes the release of proteases and other
vasoactive agents and oxygen radicals
• Subsequent endothelial neutrophil adherence and pulmonary tissue
destruction, with dilated capillaries and interstitial fluid accumulation
• Lung compliance and ventilation/perfusion is thus impaired.

30. SCHEMA: HYPOVOLEMIC SHOCK

31. SCHEMA: SHOCK CAUSES

32. METABOLIC EFFECTS OF SHOCK

33. ANAPHYLACTIC SHOCK
• Is a hypersensitivity reaction occurring within seconds of injection of
animal serum, insect bites or drugs
• The generalized vasodilation of peripheral vessels, increased capillary
permeability, broncho-constriction and laryngeal edema are caused
by leukotrienes C4, D4 and E4 (SRS-A), histamine, bradykinin and
prostaglandins released from mast cells in the antigen-antibody
reaction.
• Clinical features include choking sensation, wheezing, cough,
urticaria, oedema, loss of consciousness, severe hypotension and
faint pulse. There may be pruritus.

34. Stages of Shock
• Compensated
• The body’s compensatory mechanisms are able to maintain some degree of
tissue perfusion.
• Decompensated
• The body’s compensatory mechanisms fail to maintain tissue perfusion (blood
pressure falls).
• Irreversible
• Tissue and cellular damage is so massive that the organism dies even if
perfusion is restored.

35. CARDIOGENIC SHOCK
• Cardiogenic shock is defined by a cardiac index less 2.2L.min-1.m-2 and
a low SvO2 despite adequate preload and associated with signs of
hypoperfusion.
• An echocardiogram is extremely useful in making this diagnosis.
• There is inadequate cardiac pump function to maintain blood
pressure and tissue perfusion

36. CLINICAL FEATURES
• Cardiovascular System – Hypotension, tachycardia/bradycardia
• CNS: agitation, indifference, lethargy and coma
• Respiratory: Tachypnea
• Skin: cool clammy (peripheral vasoconstriction) but may be warm in early
stages of septic shock
• Kidneys: Decreased renal perfusion leads to oliguria, increased urine
osmolality, and increased BUN:creatinine ratio
• GI-gastritis, stress ulcers, mucosal erosions, adynamic ileus, bowel
infarction, pancreatic damage,hepatic injury
• Hematology: coagulopathy, DIC
• Cellular Injury: metabolic acidosis, hypoxemia

37. Septic shock
• Early stages – Shivering, malaise, has a warm, dry , flushed skin,
moderate hypotension, hyperventilation.
• Rapid, bounding pulse and fever
• Sudden circulatory collapse or restlessness, apprehension and
confusion may be the initial manifestation.
• As the condition progresses, the patient may become semi-comatose
with cold clammy skin, collapsed superficial veins, pale mucosa with a
tinge of cyanosis, rapid and feeble pulse, severe hypotension and
oliguria

38. INVESTIGATIONS
• Packed cell volume (serial)
• Full blood count (WBC elevation in sepsis, thrombocytopenia)
• E/U/Cr – renal function
• Chest Xray – Hemothorax, ARDS, pneumothorax
• Abdominal Ultrasound –Hemoperitoneum, Intra-abdominal sepsis
• ECG – Cardiac dysfunction
• Echocardiography
• Computed tomography scan
• Representative culture and sensitivity samples

39. TREATMENT
• It depends on the cause. But it aims to:
• expand vascular and interstitial fluid volumes and so improve tissue
perfusion,
• increase oxygen delivery and consumption, and
• support vital organ functions.

40. RESUSCITATION GOALS
• Promote cardiac output
• Cardiac index > 3L/min/m2
• MAP ≥ 65mmHg
• Urine output > 0.5ml/kg/hr
• CVP – 8-12mmHg
• Promote Oxygen delivery
• DO2 > 500 ml/min/m2
• Hb > 7-9 g/dL
• SaO2 > 90%

41. RESUSCITATION GOALS
• Promote aerobic metabolism
• VO2 > 100ml/min/m2
• SvO2 > 70%
• Serum lactate < 2mmol/L within 24 hrs
• Promote hemostasis
• INR<1.5
• aPTT<1.5 Χ control
• Platelet count >50 X 109/L

42. TREATMENT
• ABCDE OF RESUSCITATION
• FLUID THERAPY
• VASOPRESSORS
• ANTIBIOTICS/CONTROL OF INFECTION
• NUTRITION
• RESPIRATORY SUPPORT
• TRANSFUSIONS
• TREATMENT OF SPECIFIC TYPES

43. TREATMENT
• A patient with an obstructed airway should be managed immediately
with simple airway manoeuvres and an oro- or nasopharyngeal
airway if necessary.
• Where facilities exist, intubation and ventilation is indicated for
airway obstruction
• Oxygen therapy and mechanical ventilation may also be needed
• Double wide-bore intravenous access to give fluids

44. Hypovolemic shock
• Oxygen administration
• Control of on-going blood loss – surgical hemostasis
• Intravenous fluids
• Blood transfusions
• When normal MAP cannot be maintained by IV fluid administration
• Vasopressors
• Sodium bicarbonate? – CO2 increase!
• The choice of fluid does not seem to be important. Hartmann’s solution has
some advantages over 0.9% saline, but either is acceptable.
• Saline in excess - hyperchloraemic metabolic acidosis.

45. Crystalloids versus colloids
• Clinicians are faced with several options, including crystalloid solutions of
varying tonicity, several colloid preparations (albumin and others), and
blood products.
• Whereas colloids are retained in the plasma, crystalloids are retained in the
extracellular (plasma+interstitial) space
• Crystalloids can thus promote interstitial edema in excess
• Colloids theoretically stay in the intravascular space longer than
crystalloids, and may thus improve hydrostatic pressure though crystalloids
reduce blood viscosity and are more readily available
• Recently published meta-analyses concluded that colloids afford no
survival benefit in critically ill patients compared with crystalloids.

46. Blood substitutes
• Human albumin solution, fresh-frozen plasma
• Physiologic BUT action is usually short-lived;
• Expensive
• Risk of transfusion-transmitted infections
• Dextran 110 or 70
• Interfere with coagulation by impairing platelet adhesiveness and Factor VIII function
• Can over-expand the plasma and cause pulmonary edema
• Impairs blood grouping and cross-matching by forming roleaux of RBCs
• Synthetic gelatin colloids - Haemaccel, Gelofusine
• Hetastarch
• Interferes with coagulation

47. DAMAGE CONTROL RESUSCITATION
• This refers to measures adopted to limit blood loss and reduce
mortality in hemorrhagic shock
• HYPOTENSIVE RESUSCITATION
• Observations in combat injuries have shown that aggressive volume
replacement can exacerbate bleeding before the hemorrhage is controlled
• This has led to allowing low systolic BPs(=90mmHg or MAP = 50mmHg) in
trauma patients before hemostasis is secured
• Adequate tissue perfusion must however be ensured at low BPs

48. DAMAGE CONTROL RESUSCITATION
• HEMOSTATIC RESUSCITATION
• Severely injured patients have coagulopathy on presentation
• FFP: Packed RBC ratio (Previous 1:6; now 1: 1-2)
• Cryoprecipitate – achieve serum fibrinogen > 1g/L
• Platelets – maintain counts >50,000/µL while bleeding is ongoing and
>75,000/µL until bleeding is controlled
• AVOIDING HYPOTHERMIA
• Hypothermia causes reduced platelet and clotting factor activity
• In-line fluid warmers and warming blankets help to reduce incidence of
hypothermia

49. Septic shock
• Aim
• To improve the hemodynamic state,
• Restore tissue perfusion
• Combat the offending agent and cytokines
• Eliminate the septic focus
• Oxygen
• Intravenous fluids
• Vasopressors
• Antibiotics

50. Fluid therapy: recommendations
• Crystalloids as the initial fluid of choice in the resuscitation of severe sepsis
and septic shock
• Use of hydroxyethyl starches for fluid resuscitation of severe sepsis and
septic shock is discouraged
• Addition of albumin in the fluid resuscitation of severe sepsis and septic
shock when patients require substantial amounts of crystalloids
• Initial fluid challenge in patients with sepsis-induced tissue hypoperfusion
with suspicion of hypovolemia to achieve a minimum of 30 mL/kg of
crystalloids
• Fluid challenge technique be applied wherein fluid administration is
continued as long as there is hemodynamic improvement

51. Diagnosis
• Cultures as clinically appropriate before antimicrobial therapy if no
significant delay (> 45 mins) in the start of antimicrobial(s)
• At least 2 sets of blood cultures (both aerobic and anaerobic bottles)
be obtained before antimicrobial therapy with at least 1 drawn
percutaneously and 1 drawn through each vascular access device,
unless the device was recently (<48 hrs) inserted.
• Imaging studies performed promptly to confirm a potential source of
infection (UG).

52. Mechanical ventilation
Low tidal volume ventilation
• In ARDS, high tidal volumes and airway pressures should be avoided
due to reduced lung compliance
PEEP
• Prevents lung collapse and can improve oxygenation.
• Recent trials of high PEEP have not shown a mortality benefit, but did
improve secondary endpoints such as oxygenation, duration of
ventilation and use of rescue therapies

53. Recommendations: SSC Guidelines
• Norepinephrine as the first choice vasopressor
• Epinephrine (added to and potentially substituted for
norepinephrine) when an additional agent is needed to maintain
adequate blood pressure
• Vasopressin 0.03 units/minute can be added to norepinephrine (NE)
with intent of either raising MAP or decreasing NE dosage
• Low dose vasopressin is not recommended as the single initial
vasopressor for treatment of sepsis-induced hypotension

54. Recommendations: SSC Guidelines
• Dopamine as an alternative vasopressor agent to norepinephrine only
in highly selected patients (eg, patients with low risk of
tachyarrhythmias and absolute or relative bradycardia)
• Low-dose dopamine should not be used for renal protection
• All patients requiring vasopressors have an arterial catheter placed as
soon as practical if resources are available

56. DOBUTAMINE
• A synthetic catecholamine classified as an inodilator because of its
positive inotropic and vasodilatory effects
• Primarily a β1-agonist with a weak β2 agonist activity
• β1- Increased heart rate and stroke volume, β2-peripheral
vasodilatation
• Used to augment cardiac output in patients with decompensated
heart failure due to systolic dysfunction
• It is the preferred inotropic agent for myocardial depression in septic
shock but must be combined with a vasopressor

57. DOPAMINE
• An endogenous catecholamine, precursor for epinephrine
• At low doses (≤3µg/kg/min), stimulates the dopaminergic receptors in the
renal and splanchnic circulations, increasing renal blood flow and urinary
output
• Morderate doses (3-10µ/kg/min) stimulate β receptors to increase
myocardial contractility and heart rate(β1) and produce peripheral
vasodilation (β2).
• Higher doses (>10µg/kg/min) activates the α- receptors in the systemic and
pulmonary vasculature, with a vasopressor effect
• SE – sinus tachycardia, atrial fibrillation, tissue necrosis (extravasation)

58. EPINEPHRINE
• An endogenous catecholamine released by the adrenal medulla
• Stimulates both α and β receptors, with an increased heart rate,
stroke volume and peripheral vaso-constriction – particularly
splanchnic, renal and subcutaneous vessels
• Plays an important role in cardiac arrest resuscitation and is the drug
of choice in anaphylactic shock
• Concerns about its side-effects (unwanted cardiac stimulation,
splanchnic and renal hypoperfusion) have limited its use as a
vasopressor in septic shock

59. NOREPINEPHRINE
• An endogenous catecholamine that functions as a neurotransmitter
• Produces α-mediated peripheral vasoconstriction
• The preferred vasoconstrictor for circulatory support in septic shock
as it has lower side-effects than other vasopressors

60. VASOPRESSIN
• An osmo-regulatory hormone which also causes vasoconstriction
• Effects mediated by V1 receptors on vascular smooth muscle
• Although it does not produce increase in BP in healthy volunteers, it
increases BP in hypotension caused by peripheral vasodilation –
septic, anaphylactic and neurogenic shock
• Used as an adjunct in hypotension refractory to norepinephrine or
dopamine and reduces the amount of catecholamine needed
(catecholamine-sparing effect)

61. Anti-microbial therapy
• Administration of effective intravenous antimicrobials within the first
hour of recognition of septic shock and severe sepsis without septic
shock as the goal of therapy.
• Initial empiric anti-infective therapy of one or more drugs that have
activity against all likely pathogens (bacterial and/or fungal or viral)
and that penetrate in adequate concentrations into tissues presumed
to be the source of sepsis
• Antimicrobial regimen should be reassessed daily for potential
deescalation.

62. Anti-microbial therapy
• Empiric combination therapy should not be administered for more
than 3–5 days. De-escalation to the most appropriate single therapy
should be performed as soon as the susceptibility profile is known.
• Duration of therapy typically 7–10 days; longer courses may be
appropriate in patients who have a slow clinical response,
undrainable foci of infection, bacteremia with S. aureus; some fungal
and viral infections or immunologic deficiencies, including
neutropenia
• Antiviral therapy initiated as early as possible in patients with severe
sepsis or septic shock of viral origin

63. Source control
• A specific anatomical diagnosis of infection requiring consideration
for emergent source control be sought and diagnosed or excluded as
rapidly as possible, and intervention be undertaken for source control
within the first 12 hr after the diagnosis is made, if feasible
• When source control in a severely septic patient is required, the
effective intervention associated with the least physiologic insult
should be used (eg, percutaneous rather than surgical drainage of an
abscess).
• If intravascular access devices are a possible source of severe sepsis
or septic shock, they should be removed promptly after other
vascular access has been established

64. Steroids in sepsis
• Patients on long term steroid therapy or with known adrenocortical
insufficiency require steroid replacement during critical illness.
• Many studies have looked at treatment of septic patients with
corticosteroids and this remains controversial.
• One multicentre RCT showed an improvement in ICU mortality in patients
with vasopressor-unresponsive septic shock and relative adrenal
insufficiency, when they were given hydrocortisone 50mg 6 hourly and
fludrocortisone.
• A subsequent CORTICUS study, a large multicentre RCT comparing
hydrocortisone to placebo in septic shock, showed faster shock reversal but
no mortality benefit with steroids.

65. Recommendations: SSC Guidelines
• Not using intravenous hydrocortisone to treat adult septic shock
patients if adequate fluid resuscitation and vasopressor therapy are
able to restore hemodynamic stability
• Not using the ACTH stimulation test to identify adults with septic
shock who should receive hydrocortisone
• In treated patients hydrocortisone tapered when vasopressors are no
longer required
• Corticosteroids not be administered for the treatment of sepsis in the
absence of shock.
• When hydrocortisone is given, use continuous flow.

66. MANAGEMENT
• NSAID(Ibuprofen)-
• inhibits cyclo- oxygenase, thus blocking the synthesis of prostaglandins and
thromboxane.
• It also prevents neutrophil activation and aggregation, decreases production
of superoxide radicals from activated neutrophils. and stabilizes lysosomal
membrane and enzymes.
• Antioxidants - superoxide dismutase, allopurinol, α-tocopherol and
Vit. C have been shown to reduce tissue damage and MOD in septic
shock if given prophylactically

67. Management
• Prevention of further coagulopathy.
• Anti-thrombin III and C1- estearase inhibitor may prevent further
coagulopathy and help organ function.
• Protein C is anti-thrombotic, profibrinolytic and anti-inflammatory.
Recombinant human activated protein C (Drotrecogin alfa) 24 µg/kg/h
intravenously for 96h has been shown to reduce mortality. Other trials had
conflicting results and its role is still limited

68. SEPTIC SHOCK TREATMENT
• Inotropic agents: In the event of ventricular failure, digitalis or low
doses of dopamine or dobutamine may be administered to improve
myocardial contractility.
• Surgery – To eliminate a septic focus (gangrenous bowel, abscess –
source control)
• Monoclonal antibodies to TNF,IL- l, IL-6: Clinical trials have not
demonstrated improved survival. Neither have antithrombin III and
tissue factor pathway inhibitor.

69. Nutrition and stress ulcer prophylaxis
• Evidence based guidelines recommend that intensive care patients, who
are not expected to be taking a full oral diet within 3 days, should receive
enteral nutrition via a feeding tube.
• If available and affordable, parenteral nutrition may be considered in
patients who cannot be fed sufficiently enterally
• It is advisable that all ICUs use an enteral feeding protocol, describing
gradual introduction of feed to a predetermined goal, with regular
aspiration of gastric residual volume.
• The Surviving Sepsis Guidelines recommend stress ulcer prophylaxis with
ranitidine, but this can potentially increase the risk of ventilator associated
pneumonia and should be stopped when no longer required.

70. Blood glucose control
• Tight glucose control was widely adopted following Van Den Berghe’s
study in 2001, showing improvements in ICU mortality in patients
with blood glucose levels kept at 4.4-6.1mmol.L-1
• The recent NICE-SUGAR trial compared intensive (4.5-6.0mmol.L-1)
with conventional (<10mmol.L-1) glucose control. They found a much
lower incidence of severe hypoglycaemia and lower mortality in the
conventional control group.
• As a result most ICUs now aim for blood glucose less than 10mmol.L-1.
• Septic patients are at risk of both hypo- and hyperglycemia and strict
glucose monitoring is important

71. Management
Renal support
• The risk of renal failure can be reduced by early fluid resuscitation,
maintaining renal perfusion pressure and cardiac output (with inotropes if
necessary),and avoiding nephrotoxic drugs (e.g. NSAIDs, gentamicin).
• There is no evidence for using low dose dopamine for renal protection.
Lactic acidosis should be treated by optimising the circulation, not with
sodium bicarbonate.
• Renal replacement therapy should be given where indicated – hemodialysis
Deep vein thrombosis prophylaxis
• Unfractionated or LMWH; Graduated compression stockings

72. Septic shock bundles (2013 Guidelines)
• Surviving Sepsis Campaign is an internationally recognized guideline
for the management of septic shock
• The guidelines are organized in “bundles”, instructions that must be
followed without deviation to achieve a survival benefit
• Acute sepsis Bundle:
TO BE COMPLETED WITHIN 3 HOURS:
• Measure lactate level
• Obtain blood cultures prior to administration of antibiotics
• Administer broad spectrum antibiotics
• Administer 30 mL/kg crystalloid for hypotension or lactate 4mmol/L

73. ACUTE SEPSIS BUNDLE
TO BE COMPLETED WITHIN 6 HOURS:
• Apply vasopressors (for hypotension that does not respond to initial fluid
resuscitation) to maintain a mean arterial pressure (MAP) 65 mm Hg
• In the event of persistent arterial hypotension despite volume resuscitation
(septic shock) or initial lactate 4 mmol/L (36 mg/dL):
• Measure central venous pressure (CVP)
• Measure central venous oxygen saturation (ScvO2)
• Remeasure lactate if initial lactate was elevated
• Achieve the following goals
• CVP=8-12mmHg
• MAP ≥ 65mmHg
• Urine output ≥ 0.5ml/kg/hr
• SvO2 ≥65% or ScvO2 ≥ 70%

74. Septic shock bundles
• 2. Sepsis Management Bundle: Complete within 24 hrs of diagnosis.
• Administer low dose steroid if indicated
• Maintain blood glucose levels at 120-150 mg/dL
• Maintain plateau airway pressures at ≤ 30cmH2O in ventilator-dependent
patients
• Adherence to the instructions in these bundles has been shown to
improve survival in patients with septic shock, with the acute sepsis
bundle considered the most important

75. CARDIOGENIC SHOCK
• ABC of resuscitation
• Intubation and mechanical ventilation often are required, to decrease
work of breathing and facilitate sedation of the patient
• Analgesia – IV Morphine or fentanyl
• Drugs – Isoprenaline, Salbutamol, Digoxin.
• In cases of dysrhythmia; drug therapy, cardioversion, pacemakers
• Revascularization by percutaneous transluminal coronary angioplasty
or coronary artery bypass graft

76. ANAPHYLACTIC SHOCK
• Adequate airway must be provided and intravenous fluids administered rapidly .
• Adrenaline is most effective- 1ml of 1:1000 IM and repeated every 5 minutes if
necessary OR 0.1 ml I.V.
• Capable of blocking release of inflammatory mediators from sensitized mast cells and
basophils
• Intravenous fluids should be administered
• Antihistamine is added if response to adrenaline is not rapid.
• Hydrocortisone 100-250mg is also administered .
• Aminophylline 0.25-0.5mg in 10ml of saline is given intravenously slowly to
relieve bronchospasm.
• Where anaphylactic reactions are refractory to epinephrine in patients on β-
blockers, glucagon may be effective

77. Neurogenic shock
• Secure a patent airway
• Intravenous fluids are administered
• Vasoconstrictors to improve peripheral vascular tone

78. Obstructive shock
• Treatment is directed to the underlying cause.
• Passing a needle in the 2nd ICS,MCL and insertion of a chest tube for tension
pneumothorax will result in rapid improvement.
• Aspiration of pericardial blood in cardiac tamponade and subsequent surgical
exploration – pericardial window / sternotomy to repair cardiac injury

79. PHYSIOLOGIC MONITORING
• Perhaps more than for any other disease process in the intensive care
unit, physiologic monitoring is essential to the accurate diagnosis and
appropriate management of the patient presenting with shock.
• Such monitoring typically begins with use of common non-invasive
“vital signs”, but rapidly progresses to application of advanced and
frequently invasive monitoring devices
• Could be both non-invasive and invasive

80. NON-INVASIVE
• Heart rate
• Non-invasive blood pressure
• Temperature
• Urine output
• Pulse oximetry
• Cardiac output monitoring

81. NON-INVASIVE MONITORING
HEART RATE
• Tachycardia – hypovolemic, septic shock,
• Bradycardia – impending cardiovascular collapse, neurogenic shock
NON-INVASIVE BLOOD PRESSURE
• Hypotension
• Mean arterial pressure more reliable than serial measurements of the
systolic and diastolic BPs
• Normal MAP>65mmHg

82. NON-INVASIVE MONITORING
• TEMPERATURE
• Fever may be suggestive of sepsis/septic shock OR metabolic response to
trauma/injury
• Hypothermia – risk of arrhythmias
• Normal Temp – 36.5 - 37.20C
• URINE OUTPUT
• One of the most reliable clinical evidences of adequate tissue perfusion
• Normal – (1-2ml/kg/hr in children and 0.5-1ml/kg/hr in adults)

83. NON-INVASIVE MONITORING
PULSE OXIMETRY
• Based on the principles of spectrophotometry and plethysmography
• Uses the differential light absorption characteristics of oxy- and
deoxy-hemoglobin to calculate the percentage of hemoglobin in the
blood which is saturated with oxygen.
• Normal- 95-99%
CARDIAC OUTPUT
• Impedance plethysmography
• Trans-esophageal echo-cardiography

84. INVASIVE MONITORING
• Central venous pressure
• Pulmonary artery wedge pressure
• Arterial blood gases
• Base deficit
• Arterial lactate
• Mixed venous oxygen sampling

85. INVASIVE MONITORING
CENTRAL VENOUS PRESSURE
• The pressure of blood in the superior vena cava
• A surrogate for preload and can be used to predict the response to
fluid administration in shock
• Normal values – 8-15cmH2O
• Can be influenced by other factors than vascular volume like intr-
thoracic pressure, right atrial distensibility and venous tone

86. INVASIVE MONITORING
PULMONARY ARTERY CATHETER
• Placement of a catheter in a branch of the pulmonary artery and
occluding the artery can help to approximate left atrial pressure
• This can be further extrapolated to calculate left ventricular end-
diastolic pressure and cardiac output, thus assessing shock
resuscitation and patient’s cardiac function
• Normal – 8-12 cmH2O

88. INVASIVE MONITORING
MIXED VENOUS OXYGEN SAMPLING
• Measures the end result of oxygen consumption and delivery
• Used to assess the extent to which the body receives and extracts
oxygen from arterial blood
• Normal value – 65-70%. Lower values suggest either reduced oxygen
delivery to tissues or a more avid extraction from tissues from
increased demand

89. ARTERIAL BLOOD GAS MEASUREMENTS
• pH – 7.35-7.45
• pCO2 – 35-45 mmHg
• pO2 - > 80mmHg
• Arterial blood gas pictures can help to detect acidosis which may
occur in shock with a reduced pH, hypoxia and hypercapnia, all of
which should resolve with adequate resuscitation

90. ARTERIAL LACTATE
• Serum lactate levels thus provide the clinician with an excellent
laboratory marker of resuscitation adequacy.
• The normal lactate concentration is 0.5-1 mmol/L.
• Patients with critical illness can be considered to have normal lactate
concentrations of less than 2 mmol/L.
• Lactic acidosis- persistently increased blood lactate levels (usually >5
mmol/L) in association with metabolic acidosis.
• Lactate levels can be expected to reduce with resuscitation and have
been found to correlate well with patient outcome

91. BASE DEFICIT
• Is the amount of base, required to titrate whole blood to normal pH
at normal physiologic values of temperature, PaCO2, and PaO2.
• The normal range is +3 to -3 mmol/L
• The presence of an elevated base deficit correlates with the presence
and severity of shock.
• It predicts fluid resuscitation requirements and is a rapidly obtainable
monitor of resuscitation adequacy.
• Several authors have documented the usefulness of base deficit as a
predictor of morbidity and mortality in trauma patients.

92. Other invasive monitoring modalities
• Gastric tonometry
• Based on the assumption that the P co2 in the lumen of a hollow viscus will
equilibrate with the P co2 in the superficial mucosa of the organ. Mucosal P co2
increases in mucosal hypoperfusion
• Right Ventricular End-Diastolic Volume Index.
• Said to predict preload more accurately for cardiac index than does
pulmonary artery wedge pressure

93. CURRENT TRENDS
CRASH – 2: Clinical Randomization of Antifibrinolytic in Significant
Hemorrhage
• This randomised controlled trial was undertaken in 274 hospitals in 40
countries to assess the role of tranexamic acid in the management of
significant hemorrhage
• It was concluded that tranexamic acid safely reduced the risk of death
in bleeding trauma patients in this study and should be considered for
use in bleeding trauma patients

94. CURRENT TRENDS
Renal dose dopamine
• "Renal-dose" dopamine is widely used in clinical practice despite the
controversial benefit in the prophylaxis and treatment of acute renal
failure.
• Although low-dose dopamine has been shown to increase renal blood
flow, as well as promote diuresis and natriuresis, its role in improving
serum creatinine or creatinine clearance is not well established as
several studies have shown conflicting results

95. CURRENT TRENDS
• Flancbaum et al. studied 19 postoperative oliguric patients and did
not notice any difference in the mean creatinine or urine output in
patients who received low-dose dopamine.
• Davis et al however reported that creatinine clearance, urine output,
and the urine sodium excretion were improved in patients receiving
low-dose dopamine.
• CONCLUSION - Low-dose dopamine may facilitate urine output and
natriuresis but the overall benefit of this effect in renal protection
(prevention of a rise in the serum creatinine) is not established.

96. CURRENT TRENDS
• An international team of 12 experts in the field of shock was invited by the
European Society of Intensive Care Medicine in 2014 to form a Task Force
to evaluate new evidence and to revise the guidelines as judged
appropriate.
• These questions they were to answer were:
• What are the epidemiologic and pathophysiologic features of shock in the intensive
care unit?
• Should we monitor preload and fluid responsiveness in shock?
• How and when should we monitor stroke volume or cardiac output in shock?
• What markers of the regional and microcirculation can be monitored, and how can
cellular function be assessed in shock?
• What is the evidence for using hemodynamic monitoring to direct therapy in shock?

97. RECOMMENDATIONS
• They recommend frequent measurement of heart rate, blood pressure,
body temperature and physical examination variables in patients with a
history and with clinical findings suggestive of shock. Best practice.
• They recommend that the presence of arterial hypotension [defined as
systolic blood pressure of <90 mmHg, or mean arterial pressure (MAP) of
<65 mmHg, or a decrease of ≥40 mmHg from baseline], while commonly
present, should not be required to define shock. Recommendation. Level 1;
QoE moderate (B).

98. RECOMMENDATIONS
• They recommend measuring blood lactate levels in all cases where
shock is suspected
• They recommend efforts to identify the type of shock to better target
causal and supportive therapies
• They suggest that, when hemodynamic assessment is needed,
echocardiography is the preferred modality to initially evaluate the
type of shock as opposed to more invasive technologies.
Recommendation. Level 2; QoE (B).

99. RECOMMENDATIONS
• They recommend individualizing the target blood pressure during
shock resuscitation. Recommendation. Level 1; QoE moderate (B).
• They recommend to initially target a MAP of ≥65 mmHg.
Recommendation. Level 1; QoE low (C).
• They suggest to tolerate a lower level of blood pressure in patients
with uncontrolled bleeding (i.e. bleeding patients from a road traffic
accident) without severe head injury. Recommendation. Level 2; QoE
low (C).

100. RECOMMENDATIONS
• They suggest a higher MAP in septic patients with a history of
hypertension and in patients who improve with higher blood
pressure. Recommendation. Level 2; QoE moderate (B).
• They recommend arterial and CVC insertion in cases of shock
unresponsive to initial therapy and/or requiring vasopressor infusion.
Best practice.
• They recommend early treatment, including hemodynamic
stabilization (with fluid resuscitation and vasopressor treatment if
needed) and treatment of the shock etiology. Best practice

101. RECOMMENDATIONS
• They suggest that inotropic agents should be added when the altered
cardiac function is accompanied by a low or inadequate cardiac
output and signs of tissue hypoperfusion persist after preload
optimization. Recommendation. Level 2; QoE low (C).
• They recommend not to give inotropes for isolated impaired cardiac
function. Recommendation. Level 1; QoE moderate (B).
• They recommend not to target absolute values of oxygen delivery in
patients with shock. Recommendation. Level 1; QoE high (A).

102. Fluid Management
• Optimal fluid management does improve patient outcome;
hypovolemia and hypervolemia are harmful. Statement of fact.
• They recommend to assess volume status and volume
responsiveness. Best practice.
• They recommend that immediate fluid resuscitation should be started
in shock states associated with very low values of commonly used
preload parameters. Best practice.

103. RECOMMENDATIONS
• They recommend that commonly used preload measures (such as
CVP or PAOP or global end diastolic volume or global end diastolic
area) alone should not be used to guide fluid resuscitation.
Recommendation. Level 1; QoE moderate (B).
• They recommend not to target any ventricular filling pressure or
volume. Recommendation. Level 1; QoE moderate (B).
• They recommend that fluid resuscitation should be guided by more
than one single hemodynamic variable. Best practice.
• They recommend using dynamic over static variables to predict fluid
responsiveness, when applicable. Recommendation. Level 1; QoE
moderate (B).

104. RECOMMENDATIONS
• They do not recommend routine measurement of cardiac output for
patients with shock responding to the initial therapy.
Recommendation. Level 1; QoE low (C).
• They recommend measurements of cardiac output and stroke volume
to evaluate the response to fluids or inotropes in patients that are not
responding to initial therapy. Recommendation. Level 1; QoE low (C).

105. Cardiac function and micro-circulation
• Echocardiography can be used for the sequential evaluation of cardiac function in
shock Statement of fact.
• They do not recommend the routine use of the pulmonary artery catheter for
patients in shock. Recommendation. Level 1; QoE high (A).
• They suggest PAC in patients with refractory shock and RV dysfunction.
Recommendation. Level 2; QoE low (C).
• They suggest the use of transpulmonary thermodilution or PAC in patients with
severe shock especially in the case of associated acute respiratory distress
syndrome. Recommendation. Level 2; QoE low (C).
• They recommend that less invasive devices are used, instead of more invasive
devices, only when they have been validated in the context of patients with
shock. Best practice
• They suggest the techniques to assess regional circulation or microcirculation for
research purposes only. Recommendation. Level 2; QoE low (C).

106. CONCLUSION
• Shock is a condition which occurs across almost every field of clinical
practice and as such its management should be clear to every
clinician
• While management protocols are under constant review and
research is on-going in the developed world, shock mortality is still
unacceptable high in our environment
• Improvement in health care delivery with respect to prompt
recognition, resuscitation, hemodynamic monitoring and
participation in further research will help improve outcomes in our
setting

107. I THANK YOU ALL
FOR LISTENING

108. REFERENCES
• Shock: An Overview , By Michael L. Cheatham, MD, Ernest F.J. Block, MD,
Howard G. Smith, MD, John T. Promes, MD. Surgical Critical Care Service,
Department of Surgical Education, Orlando Regional Medical Center,
Orlando, Florida
• CURRENT CONCEPTS ON SHOCK- a presentation by Charles Adeyinka
Adisa, Associate Professor of Surgery, Abia State University, Nigeria.
• F. Charles Brunicardi, MD, FACS et al. Schwartz’s Principles of Surgery,
Tenth Edition, Chapter 5. Shock. Copyright © 2015 by McGraw-Hill
Education.
• E A Badoe et al. Principles And Practice Of Surgery Including Patholqgy In
The Tropics, Fourth Edition
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GM [Curr Opin Nephrol Hypertens. 2000 Sep;9(5):501-4.]

109. REFERENCES
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111. REFERENCES
• Renal-Dose Dopamine: Myth or Ally in the Treatment of Acute Renal
Failure? Shekar P. Kumar, MD, Vincent L. Sorrell, MD. Disclosures
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Published online 2014 Nov 13. doi: 10.1007/s00134-014-3525-z
PMCID: PMC4239778