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SEMINOR ON SHOCK
MODERATORDR.B.P.RANJANASST PROFFESORDEPT OF SURGERYS.M.C.H
PRESENTED BYDR.KANNAN.KPGTDEPT OF SURGERYS.M.C.H
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DEFINITION
Shock is a physiologic state characterized bysystemic reduction in tissue perfusion,resulting in decreased tissue oxygen delivery.
Hypotension is not a requirement.
Poor tissue perfusion.
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PATHOPHYSIOLOGY
Imbalance in oxygen supply and demand.
Conversion from aerobic to anaerobic
metabolism.Appropriate and inappropriate metabolic andphysiologic responses.
In 3 levels:1. Cellular level2. Microvascular level.3. Systemic level
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CELLULAR LEVEL
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MICROVASCULAR LEVELHypoxia
Cellular injury
Metabolic acidosis
Free radical generation & cytokines
Injury to cappilary endothelial cells
Leaky endothelium
Tissue edema
Further cellular hypoxia
Cell death
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SYSTEMIC LEVEL1. Cardiovascular : Hypotension
Depression of baroreceptor
Increased sympathetic activity & release of cathecholamines
HR & Systemic vasoconstriction.
2. Respiratory :Metabolic acidosis Ventilation CO2 wash out.
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SYSTEMIC LEVEL
3. Renal : Perfusion & stimulation of renin-angiotensin-aldosterone axis
urine output.
4. Hormonal :Adrenal systemRenin-angiotensin-aldosterone system * Acts on kidney & decrease
ADH urine outputCortisol * Sympathetic sensitization.
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STAGES OF SHOCK
1. Pre shock or compensated shock
2. Decompensated shock
3. Refractory shock
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STAGES OF SHOCK
Preshock aka compensated/warm shock Body is able to compensate for perfusionUp to ~10% reduction in blood volumeTachycardia to cardiac output & perfusion
Shock Compensatory mechanisms overwhelmedSee signs/symptoms of organ dysfunction
~20-25% reduction in blood volumeEnd-organ dysfunction
Leading to irreversible organ damage/death
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PRESHOCK OR COMPENSATED SHOCK
Cardiovascular and hormonal responseto reduce blood supply to non essential organs like skin ,
git & kidney.to maintain supply to brain, lung & heart.
Clinically , there will be increased heart rate,increased respiratory rate,
oliguria,cool clammy extremities,increased CRT in infants.
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DECOMPENSATED SHOCK
If underlying cause not treated.Progressive renal, respiratory & cardiovasculardecompensation.Early signs of end organ failure may appear.
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REFRACTORY OR IRREVERSIBLE SHOCK
Shock can be no longer reversed.
Multiple organ failure occur.
Two or more organ system failed.
No specific treatment .
Ultimately brain damage & death .
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CLASSIFICATION OF SHOCK
Hinshaw & Cox classification: Revised Hinshaw & Cox classification
1. Hypovolaemic
2. Cardiogenic
3. Obstructive
4. Distributive
1. Hypovolaemic
2. Cardiogenic
3. Obstructive
4. Distributive
5. Endocrine
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HYPOVOLEMIC SHOCK
Haemorrhagic
TraumaG I BleedRuptured aneurysmRetroparitoneal
Nonhaemorrhagic
Poor fluid intakeExternal fluid loss:
DehydrationVomitingDiarrheaPolyuria
Interstitial fluid replacement:
Thermal injuryTraumaAnaphylaxis
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HEMORHAGIC SHOCK
Degree of volume loss and response:
10% well tolerated (tachycardia)
20 - 25% failure of compensatory mechanisms(hypotension, decreased CO).
> 40% loss associated with overt shock (markedhypotension, decreased CO, lactic acidemia)
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CARDIOGENIC SHOCK
Results from pump failureDecreased systolic function.Resultant decreased cardiac output.Although normal intervascular volume.
Hemodynamic criteria:- sustained hypotension( SBP
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Obstructive shockReduction in preload due to mechanical obstruction of cardiac
filling.
Etiology:Impaired diastolic filling( rt ventricle)
Direct venous obstruction (vena cava)- intrathoracic obstructive tumors
Increased intrathoracic pressure- Tension pneumothorax- Mechanical ventilation .- Asthma/COPD
Decreased cardiac compliance- Constrictive pericarditis- Cardiac tamponade
Impaired filling of Lt ventricle- Pulmonary embolus (massive)- Acute pulmonary hypertension
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DISTRIBUTIVE SHOCK
Results from a severe decrease in SVR .Peripheral vasodilation & decreased after load.Cardiac output may be high.
Etiology:1. Septic shock2. Neurogenic / spinal shock3. Systemic inflammation pancreatitis, burns
4. Toxic shock syndrome5. Anaphylaxis and anaphylactoid reactions6. Toxin reactions drugs, transfusions
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SEPSIS AND SEPTIC SHOCKSEVERE SEPSIS:Sepsis with evidence of acute organ dysfunction
CV: SBP
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SEPTIC SHOCK
Common cause of death in surgical ICUs.Source of infection : Pulmonary
Blood stream
Genito urinaryIntra abdominalSkin & soft tissue.
Stages:
1. Early high output septic shock2. Late low output septic shock
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MECHANISAM OF SEPTIC SHOCK
Infection
Inflammatory cytokines
Decreased Preload Myocardial depression Peripheral vasodilation
Decreased CO( SVR ) Decreased SVR( CO)
Decreased MAP
Shock
MODS
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HIGH OUTPUT SEPTIC SHOCK Early stage of septic shock.
May be result of successful t/t of low output septic shock.
Organ blood flow disturbed at higher pressures suggesting
a primary microvascular regulatory defect.
Cerebral perfusion decreased by 33% while coronaryvascular resistance is significantly increased in septic shock- i.e., coronary and cerebral autoregulatory mechanismsare relatively intact .
Microvascular studies also show aberrant distribution of perfusion within tissues and organs.
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LOW OUTPUT SEPTIC SHOCKLate stage.Due to plasma loss from leaky endothelium.Extrinsic regulatory mechanisms dominate in most vascular
beds except brain and heart.
Blood flow to other organs decreased via sympatheticvasoconstrictive effects.
Post-resuscitation, perfusion abnormalities may persist for
days. (decreased perfusion of brain, kidneys, liver, splanchnicorgans) with potential persistent ischemia.
Extremities cool & clammy , oliguria & mental change.
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Neurogenic shock
Found in spinal injury.
Loss of sympathetic tone resulting peripheralvasodilation.
Decreased SVR & increased CO.
High output shock.
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ENDOCRINE SHOCK
Found in endocrine disturbances.Examples:
1. Hypothyroidism ( a form of cardiogenic shock):
2. Thyrotoxicosis ( cardiogenic shock)
3. Acute adrenal insufficiency ( Distributive shock)
4. Relative adrenal insufficiency ( Distributive shock).
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DIAGNOSIS AND EVALUATION
Primary diagnosis Hypotension( SBP < 90 )Tachycardia, tachypnoea, oliguria
Cool , clammy extremities .or Warm& hyperemicMental confusion.
Differential DX: JVP - hypovolemic vs. cardiogenicLeft S3, S4, new murmurs - cardiogenicRight heart failure - PE, tamponadePulsus paradoxus, Kussmauls sign tamponade
Fever, rigors, infection focus - septic
Clinical Signs: varies with type of shock
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DIAGNOSIS AND EVALUATION
All laboratory investigations :Hb, TLC, DLC , Platelet
ABG , electolytesS. creatine, BUN
PT/PTTS. lactateCulture
Imaging: CXR, Abd xray
FASTCT Abd or chestECG, echo
Pulmonary perfusion scan
Investigations
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TREATMENT
Manage the emergency
Determine the underlying cause
Definitive management or support
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MANAGE THE EMERGENCYResuscitation should not be delayed.
Ensure a patent airway & breathing .
Foot end to be elevated.
Keep the patient warm & comfortable.
Maximize oxygen delivery.
Place iv lines , tubes & monitors.
Fluid resuscitation .
Send blood sample for cross matching.
Call your senior or fellow.
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MONITORING
MINIMUM :
1. Heart rate.2. Oxygen saturation via pulse oximetry.3. Blood pressure.
4. Urine output.ADDITIONAL MODALITIES:1. Central venous pressure.2. Invasive blood pressure.
3. Cardiac output.4. Base deficit & serum lactate.
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IMMEDIATE GOALS IN SHOCK
Hemodynamic support MAP > 60mmHgPAOP = 12 - 18 mmHgCardiac Index > 2.2L/min/m 2
Maintain oxygen delivery Hemoglobin > 9 g/dLArterial saturation > 92%Supplemental oxygen and
mechanical ventilation
Reversal of oxygen dysfunction Decreasing lactate ( 1.5 times of control.
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DEFINITIVE MANAGEMENT
Cardiogenic Shock Restore blood pressure by IVF +/- Inotropic agent. LV infarctionIntra-aortic balloon pump (IABP).Cardiac angiography.
Revascularization.Angioplasty.coronary bypass.
RV infarction
Fluid and inotropes with PA catheter monitoring.
Mechanical abnormalityEchocardiography.Cardiac catheterisation.Corrective surgery.
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DEFINITIVE MANAGEMENT
Obstructive shock
Pericardial tamponade pericardiocentesis surgical drainage (if needed)Pulmonary embolism heparin ventilation/perfusion lung scan pulmonary angiography consider:
- thrombolytic therapy- embolectomy at surgery
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DEFINITIVE MANAGEMENTSeptic shock
Fluid resuscitation to continue until PWP 15 20mmHg.Blood transfusion if Hb
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PROTOCOL FOR RESUSCITATION INSEPTIC SHOCK
First infuse fast 250 500 ml crystalloid in 5 10min
MAP
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DEFINITIVE MANAGEMENT
Neurogenic shock
Fluid resuscitation: mainstay of t/t.
Vasopressor.
Steroid like Methylprednisolone.
Vertebral surgery if needed.
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FLUID THERAPY IN SHOCK
First line therapy in any type of shock.Access through wide , bore iv cannula.Types of fluid available:
1. Crystalloids Lactated Ringers solution Normal saline Hypertonic saline
2. Colloids
Hetastarch ( hydroxyethyl starch ) Albumin Gelatin ( Gelufusine)
3. Packed red blood cells
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FLUID THERAPY IN SHOCK
Controversy regarding colloid vs crystalloid .But study favours crystalloid.If ongoing blood loss present , ideal fluid is blood.
Responds :1. Correct hypotension.
2. Decrease heart rate.
3. Rise of CVP by 2
5 cm of H2O.4. Correct hypoperfusion abnormalities
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DYNAMIC FLUID RESPONSE
In hypovolemic & septic shock,give 250500 ml ( 20ml/kg) fluid in 5 to 10min.
Monitor HR, BP & CVP
Responder Transient responder Nonresponder
Need immediate intervention
ROLE OF VASOPRESSOR AND
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ROLE OF VASOPRESSOR ANDINOTROPIC AGENTS
Never use before fluid resuscitation in hypovolemic shock.
Vasopressors mainly indicated in distributive shock likeseptic shock.
Inotropic agent & inodilator indicated in cardiogenic shock.
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