Shock is a state of widespread tissue hypo perfusion caused by inadequate cardiac output or ineffective blood volume, leading to insufficient oxygen and nutrient supply to tissues. It can be classified into various types, including hypovolemic, cardiogenic, distributive, and obstructive shock, each with distinct causes and management strategies. The initial treatment aims at rapid re-expansion of the intravascular volume, use of oxygen inhalation, and targeted therapeutic interventions depending on the shock type.

1. Presented by: Dr. Mashfiqul HasanPresented by: Dr. Mashfiqul Hasan
EmOC (anaesthesia) traineeEmOC (anaesthesia) trainee
ICMHICMH

2. Shock is a state of wide spread tissueShock is a state of wide spread tissue
hypo perfusion caused byhypo perfusion caused by
an inadequate cardiac output oran inadequate cardiac output or
ineffective circulatory blood volume,ineffective circulatory blood volume,
leading to inadequate supply of oxygenleading to inadequate supply of oxygen
and nutrients to the tissues and removal ofand nutrients to the tissues and removal of
metabolic wastes from there to the organsmetabolic wastes from there to the organs
of excretion.of excretion.
What isWhat is shock ?shock ?What isWhat is shock ?shock ?

3. Shock caused by inadequate cardiacShock caused by inadequate cardiac
outputoutput
CO = SV x HRCO = SV x HR

4. Stroke
Volum
e
Stroke VolumeStroke Volume
Volume of Blood pumped by eachVolume of Blood pumped by each
ventricle during 1 cardiac cycle.ventricle during 1 cardiac cycle.
What affects Stroke volume?
Heart
Muscle
Damag
e
Blood
Volume
Mechanica
lObstructi
on
Mechanic
al
Rhythm
Problems

5. Heart rateHeart rate
Sever bradycardia due to any cause.Sever bradycardia due to any cause.

6. Shock due to ineffective circulatoryShock due to ineffective circulatory
blood volumeblood volume
BP = CO x SVRBP = CO x SVR

7. Stages of shockStages of shock
Non progressive stageNon progressive stage
Progressive stageProgressive stage
Irreversible stageIrreversible stage

8. Classification of shockClassification of shock
Hypovolemic shockHypovolemic shock
Cardiogenic shockCardiogenic shock
Distributive shockDistributive shock
Obstructive shockObstructive shock

9. Hypovolemic shockHypovolemic shock
 Loss of blood:Loss of blood:
 External hemorrhage: trauma(accidental, surgical), GIExternal hemorrhage: trauma(accidental, surgical), GI
bleeding, PV bleedingbleeding, PV bleeding
 Internal hemorrhage: hemothorax, hemoperitoneum,Internal hemorrhage: hemothorax, hemoperitoneum,
hematoma, haemorrhage due to pelvic bone fracture,hematoma, haemorrhage due to pelvic bone fracture,
femur fracture, etc.femur fracture, etc.
 Loss of plasma: burn, exfoliative dermatitisLoss of plasma: burn, exfoliative dermatitis
 Loss of fluid & electrolytes:Loss of fluid & electrolytes:
 External: diarrhoea, vomiting, excessive sweating,External: diarrhoea, vomiting, excessive sweating,
hyperosmolar state (DKA, HONKDC)hyperosmolar state (DKA, HONKDC)
 Internal: pancreatitis, ascites, bowel obstructionInternal: pancreatitis, ascites, bowel obstruction

10. Effect of hemorrhage on cardiacEffect of hemorrhage on cardiac
output & blood pressureoutput & blood pressure
100%100%
50%50%
00 1010 2020 3030 4040 5050
ArterialArterial pressurepressure
Cardiac outputCardiac output
Percentage of total blood removedPercentage of total blood removed

11. What prevented fall of bloodWhat prevented fall of blood
pressure?pressure?
 Reflex sympathetic compensation:Reflex sympathetic compensation:
 Arterioles constrict, increasing peripheral resistanceArterioles constrict, increasing peripheral resistance
 Vein & venous reservoirs constrict (esp. skin &Vein & venous reservoirs constrict (esp. skin &
splanchnic), thereby increasing the venous returnsplanchnic), thereby increasing the venous return
 Stimulation of the cardiac activityStimulation of the cardiac activity
 Activation of Renin-Angiotensin-AldosteroneActivation of Renin-Angiotensin-Aldosterone
systemsystem
 Formation and release of vasopressinFormation and release of vasopressin

12. Decreased cardiac outputDecreased cardiac output
Decreased arterial pressureDecreased arterial pressure
Decreased systemic blood flowDecreased systemic blood flow
Decreased nutrition of tissuesDecreased nutrition of tissues Intravascular clottingIntravascular clottingDecreased cardiac nutritionDecreased cardiac nutrition
Decreased nutritionDecreased nutrition
of vascular systemof vascular system
Decreased nutritionDecreased nutrition
of the brainof the brain
Tissue ischemiaTissue ischemia
Decreased vasomotorDecreased vasomotor
activityactivity
Vascular dilatationVascular dilatation
Venous poolingVenous pooling
Of bloodOf blood
Cardiac depressionCardiac depression Decreased venous returnDecreased venous return
IncreasedIncreased
CapillaryCapillary
permeabilitypermeability
DecreasedDecreased
blood volumeblood volume
Release ofRelease of
Toxins/lactic acidosisToxins/lactic acidosis
Progression of shockProgression of shock

13. Progressive shockProgressive shock

14. Classification of HaemorrhageClassification of Haemorrhage
 Class-I: Blood loss 15%Class-I: Blood loss 15%
 Normal pulse rate and blood pressureNormal pulse rate and blood pressure
 Tilt test +Tilt test +
 Class-II: Blood loss 20-25%Class-II: Blood loss 20-25%
 Tachycardia, TachypnoeaTachycardia, Tachypnoea
 Low systolic blood pressureLow systolic blood pressure
 Pulse pressure less than 30mmHgPulse pressure less than 30mmHg
 Delayed capillary fillingDelayed capillary filling
 Class-III: Blood loss 30-35%Class-III: Blood loss 30-35%
 Skin-cold, clammy and paleSkin-cold, clammy and pale
 Severe drop in blood pressureSevere drop in blood pressure
 Restlessness, oliguria, metabolic acidosisRestlessness, oliguria, metabolic acidosis
 Class-IV Blood loss 40-50%Class-IV Blood loss 40-50%
 Profound hypotensionProfound hypotension
 Carotid pulse may only be palpableCarotid pulse may only be palpable
 Irreversible shockIrreversible shock

15. DiagnosisDiagnosis
HistoryHistory
Physical signs of haemodynamic instabilityPhysical signs of haemodynamic instability
The diagnosis is more difficult when theThe diagnosis is more difficult when the
source of blood loss is occult, as into thesource of blood loss is occult, as into the
gastrointestinal tract, fracture of femur,gastrointestinal tract, fracture of femur,
pelvic fracture or when plasma volumepelvic fracture or when plasma volume
alone is depleted.alone is depleted.

16. MonitoringMonitoring
 Patients in shock require care in an intensivePatients in shock require care in an intensive
care unit.care unit.
 Arterial pressure through an indwelling line,Arterial pressure through an indwelling line,
pulse, and respiratory rate should be monitoredpulse, and respiratory rate should be monitored
continuously;continuously;
 A Foley catheter should be inserted to followA Foley catheter should be inserted to follow
urine flow;urine flow;
 Mental status should be assessed frequently.Mental status should be assessed frequently.
 Invasive monitoring: Pulmonary artery catheterInvasive monitoring: Pulmonary artery catheter
(PAC, Swan-Ganz catheter).(PAC, Swan-Ganz catheter).

17. Hemodynamic ParametersHemodynamic Parameters
CVP & PCWP CO SVR
Cardiogenic High Low High
Extra-cardiac
obstructive (Low) Low High
Hypovolemic Low Low High
Sepsis Variable Variable Low
Toxic Shock (Low) (High) Low
Anaphylaxis Low High Low

18. Management of hypovoloemic shockManagement of hypovoloemic shock
 Irrespective of etiology the first treatment ofIrrespective of etiology the first treatment of
shock is 100%Oshock is 100%O22 inhalation.inhalation.
 Initial resuscitation requires rapid re-expansionInitial resuscitation requires rapid re-expansion
of the circulating intravascular volume andof the circulating intravascular volume and
interventions to control ongoing losses.interventions to control ongoing losses.
 Volume resuscitation is initiated with the rapidVolume resuscitation is initiated with the rapid
infusion of a balanced salt solution such asinfusion of a balanced salt solution such as
Ringer's lactate or Normal saline through large-Ringer's lactate or Normal saline through large-
bore intravenous lines.bore intravenous lines.
 No distinct benefit from the use of colloid hasNo distinct benefit from the use of colloid has
been demonstrated & in some studies theybeen demonstrated & in some studies they
seem to be even harmful.seem to be even harmful.

19. Hypovolemic Shock - Fluid SelectionHypovolemic Shock - Fluid Selection
Distribution % Intravascular
Normal saline Extracellular space 25-30%
Lactated Ringer’s Extracellular space 25-30%
5% DA Total body water space 8-10%
Blood/ Colloids Intravascular space 100%

20. Distribution of fluidDistribution of fluid

21. Aims of therapyAims of therapy
To achieve and maintainTo achieve and maintain
MAP of 70-80 mm of HgMAP of 70-80 mm of Hg
Urine output >0.5 ml/kg/hourUrine output >0.5 ml/kg/hour
Treatment of the cause.Treatment of the cause.

22. Further managementFurther management
 Continuing blood loss, with hemoglobinContinuing blood loss, with hemoglobin
concentrations declining to 10 g/dL shouldconcentrations declining to 10 g/dL should
initiate blood transfusion, cross-matched wholeinitiate blood transfusion, cross-matched whole
blood.blood.
 In the presence of severe and/or prolongedIn the presence of severe and/or prolonged
hypotension, inotropic support with dopamine,hypotension, inotropic support with dopamine,
vasopressin, or dobutaminevasopressin, or dobutamine may bemay be required torequired to
maintain adequate ventricular performancemaintain adequate ventricular performance
afterafter blood volume has been restored.blood volume has been restored.
 Once hemorrhage is controlled and the patientOnce hemorrhage is controlled and the patient
has been stabilized, blood transfusions may nothas been stabilized, blood transfusions may not
be continued unless the hemoglobin is <~7g/dLbe continued unless the hemoglobin is <~7g/dL

23. Cardiogenic shockCardiogenic shock
Myocardial ischemia or infarction (pumpMyocardial ischemia or infarction (pump
failure)failure)
Myocarditis, cardiomyopathyMyocarditis, cardiomyopathy
ArrhythmiaArrhythmia
Acute valvular dysfunctionAcute valvular dysfunction

24. Cardiogenic Shock

25. Hemodynamic ParametersHemodynamic Parameters
CVP & PCWP CO SVR
Cardiogenic High Low High
Extra-cardiac
obstructive (Low) Low High
Hypovolemic Low Low High
Sepsis Variable Variable Low
Toxic Shock (Low) (High) Low
Anaphylaxis Low High Low

26. ManagementManagement
Adjusting volume status to a level thatAdjusting volume status to a level that
ensures optimum LV filling pressure.ensures optimum LV filling pressure.
Use of ionotropic drugs.Use of ionotropic drugs.

27. Hemodynamic effects ofHemodynamic effects of
adrenoceptor subtypesadrenoceptor subtypes
TypeType TissueTissue ActionsActions
AlphaAlpha Most vascular smoothMost vascular smooth
musclemuscle
ContractionContraction
Beta 1Beta 1 HeartHeart Increases force & rate ofIncreases force & rate of
contractioncontraction
Beta 2Beta 2 Vascular smoothVascular smooth
musclemuscle
RelaxationRelaxation
D 1D 1 Smooth muscleSmooth muscle Dilates renal blood vesselsDilates renal blood vessels
AdrenalineAdrenaline NoradrenalineNoradrenaline DobutamineDobutamine DopamineDopamine

28. Effects of Inotropic AgentsEffects of Inotropic Agents
EpinephrineEpinephrine α ,βα ,β11 = β= β22 0.02 – 0.50.02 – 0.5
NorepinephrineNorepinephrine αα11, β, β11 >>>> ββ22 0.05 – 0.50.05 – 0.5
DopamineDopamine DD, β, β22, β, β11, α, α 2 -202 -20
DobutamineDobutamine ββ11, β, β22 2 - 202 - 20
Drug Receptor CO SVR Dose Range
(µg/kg/min)
1

29. DopamineDopamine
An endogenous precursor of norepinephrine withAn endogenous precursor of norepinephrine with
multiple dose-related effectsmultiple dose-related effects
Low Dose (0.5 - 5 mcg/kg/min)Low Dose (0.5 - 5 mcg/kg/min)
ββ22 and dopaminergic (DR) effectsand dopaminergic (DR) effects
Enhanced blood flow to renal and splanchnicEnhanced blood flow to renal and splanchnic
bedsbeds
Moderate Dose (5 -10 mcg/kg/min)Moderate Dose (5 -10 mcg/kg/min)
Positive inotropic effectsPositive inotropic effects
High Dose (>10 mcg/kg/min)High Dose (>10 mcg/kg/min)
αα-actions (vasoconstriction)-actions (vasoconstriction)

31. Distributive shockDistributive shock
Septic shockSeptic shock
Anaphylactic shockAnaphylactic shock
Neurogenic shockNeurogenic shock
Vasodilator drugsVasodilator drugs
Acute adrenal insufficiencyAcute adrenal insufficiency

32. Septic shockSeptic shock
Sepsis with hypotension (arterial blood pressure <90Sepsis with hypotension (arterial blood pressure <90
mmHg systolic, or 40 mmHg less than patient's normalmmHg systolic, or 40 mmHg less than patient's normal
blood pressure) for at least 1 h despite adequate fluidblood pressure) for at least 1 h despite adequate fluid
resuscitation;resuscitation;
oror
Need for vasopressors to maintain systolic bloodNeed for vasopressors to maintain systolic blood
pressure 90 mmHgpressure 90 mmHg oror mean arterial pressure 70 mmHgmean arterial pressure 70 mmHg

35. Features of Septic Shock
High Cardiac OutputHigh Cardiac Output
Low Systemic Vascular ResistanceLow Systemic Vascular Resistance
Myocardial DysfunctionMyocardial Dysfunction
Hypovolemia as Ongoing CirculatingHypovolemia as Ongoing Circulating
Volume Lost To Interstitial SpaceVolume Lost To Interstitial Space

37. General managementGeneral management
Measure CVPMeasure CVP If CVP is <8 mm of Hg – fluid is infusedIf CVP is <8 mm of Hg – fluid is infused
to raise it to 8-12 mm of Hgto raise it to 8-12 mm of Hg
Measure MAPMeasure MAP If MAP is still <65 mm of HgIf MAP is still <65 mm of Hg
- use vasoactive agent- use vasoactive agent
Maintain MAP >65 mm of HgMaintain MAP >65 mm of Hg
Management of septic shockManagement of septic shock

38. Neurogenic ShockNeurogenic Shock
 Neurogenic shock is caused by-Neurogenic shock is caused by-
 traumatic spinal cord injury ortraumatic spinal cord injury or
 effects of an epidural or spinal anesthetic.effects of an epidural or spinal anesthetic.
 This results in loss of sympathetic tone with a reductionThis results in loss of sympathetic tone with a reduction
in systemic vascular resistance and hypotension withoutin systemic vascular resistance and hypotension without
a compensatory tachycardia.a compensatory tachycardia.
 The extremities are often warm, in contrast to the usualThe extremities are often warm, in contrast to the usual
vasoconstriction-induced coolness in hypovolemic orvasoconstriction-induced coolness in hypovolemic or
cardiogenic shock.cardiogenic shock.
 Reflex vagal parasympathetic stimulation evoked byReflex vagal parasympathetic stimulation evoked by
pain, gastric dilation, or fright may simulate neurogenicpain, gastric dilation, or fright may simulate neurogenic
shock, producing hypotension, bradycardia, andshock, producing hypotension, bradycardia, and
syncope.syncope.

39. Management of neurogenic shockManagement of neurogenic shock
 Treatment involves a simultaneous approach toTreatment involves a simultaneous approach to
the relative hypovolemia and to the loss ofthe relative hypovolemia and to the loss of
vasomotor tone.vasomotor tone.
 Excessive volumes of fluid may be required toExcessive volumes of fluid may be required to
restore normal hemodynamics if given alone.restore normal hemodynamics if given alone.
 A pure alpha-adrenergic agentA pure alpha-adrenergic agent
(Ephedrine/phenylephrine) may be necessary to(Ephedrine/phenylephrine) may be necessary to
augment vascular resistance and maintain anaugment vascular resistance and maintain an
adequate mean arterial pressure.adequate mean arterial pressure.
 In severe cases noradrenaline/adrenaline mayIn severe cases noradrenaline/adrenaline may
be used.be used.

40. Anaphylactic shockAnaphylactic shock
Anaphylaxis is a potentially life-Anaphylaxis is a potentially life-
threatening, systemic allergic reactionthreatening, systemic allergic reaction
caused by the release of histamine andcaused by the release of histamine and
other vasoactive mediators.other vasoactive mediators.
The most common allergens are foods,The most common allergens are foods,
latex, insect venom and drugs.latex, insect venom and drugs.

42. Anaphylaxis: IgE-mediatedAnaphylaxis: IgE-mediated
mast cell degranulationmast cell degranulation
 FoodsFoods
 PeanutsPeanuts
 Tree nutsTree nuts
 Fish and shellfishFish and shellfish
 MilkMilk
 EggsEggs
 Soy productsSoy products
 Insect stingsInsect stings
 Bee venomBee venom
 Wasp venomWasp venom
 Chemicals, drugs and other foreign proteinsChemicals, drugs and other foreign proteins
 Penicillin and other antibioticsPenicillin and other antibiotics
 Intravenous anaesthetic agents, e.g. suxamethonium, propofolIntravenous anaesthetic agents, e.g. suxamethonium, propofol
 LatexLatex

43. Anaphylactoid, non-IgE-mediatedAnaphylactoid, non-IgE-mediated
mast cell degranulationmast cell degranulation
 DrugsDrugs
 OpiatesOpiates
 AspirinAspirin
 Radiocontrast mediaRadiocontrast media
 PhysicalPhysical
 ExerciseExercise
 ColdCold
 IdiopathicIdiopathic
 No cause can be identified in 30% of patients withNo cause can be identified in 30% of patients with
anaphylaxisanaphylaxis

44. Management of anaphylaxisManagement of anaphylaxis
 Anaphylaxis is an acute medical emergency. TheAnaphylaxis is an acute medical emergency. The
immediate management includes:immediate management includes:
 preventing further contact with the allergen (e.g. removal of beepreventing further contact with the allergen (e.g. removal of bee
sting)sting)
 ensuring airway patencyensuring airway patency
 administration of oxygenadministration of oxygen
 restoration of blood pressure (laying the patient flat, intravenousrestoration of blood pressure (laying the patient flat, intravenous
fluids)fluids)
 prompt administration of adrenaline (epinephrine).prompt administration of adrenaline (epinephrine).
 Intravenous antihistamines (chlorphenamine 10-20 mg i.m. orIntravenous antihistamines (chlorphenamine 10-20 mg i.m. or
slow i.v. injection), which limit ongoing inflammation.slow i.v. injection), which limit ongoing inflammation.
 Corticosteroids (hydrocortisone 100-300 mg) prevent late-phaseCorticosteroids (hydrocortisone 100-300 mg) prevent late-phase
symptoms in severely affected patients.symptoms in severely affected patients.

45. Obstructive shockObstructive shock
 Tension pneumothoraxTension pneumothorax
 Pericardial disease (temponade, constrictivePericardial disease (temponade, constrictive
pericarditis)pericarditis)
 Disease of pulmonary vasculature (massiveDisease of pulmonary vasculature (massive
pulmonary emboli, pulmonary hypertension)pulmonary emboli, pulmonary hypertension)
 Cardiac tumor (atrial myxoma)Cardiac tumor (atrial myxoma)
 Left atrial mural thrombusLeft atrial mural thrombus
 Obstuctive valvular disease (aortic or mitralObstuctive valvular disease (aortic or mitral
stenosis)stenosis)
These are medical emergencies requiring prompt diagnosis & treatmentThese are medical emergencies requiring prompt diagnosis & treatment

46. THANKS TO EVERYBODYTHANKS TO EVERYBODY