Shock by Kannan

8/4/2019 Shock by Kannan

1/43

SEMINOR ON SHOCK

MODERATORDR.B.P.RANJANASST PROFFESORDEPT OF SURGERYS.M.C.H

PRESENTED BYDR.KANNAN.KPGTDEPT OF SURGERYS.M.C.H


2/43

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.


3/43

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


4/43

CELLULAR LEVEL


5/43

MICROVASCULAR LEVELHypoxia

Cellular injury

Metabolic acidosis

Free radical generation & cytokines

Injury to cappilary endothelial cells

Leaky endothelium

Tissue edema

Further cellular hypoxia

Cell death


6/43

SYSTEMIC LEVEL1. Cardiovascular : Hypotension

Depression of baroreceptor

Increased sympathetic activity & release of cathecholamines

HR & Systemic vasoconstriction.

2. Respiratory :Metabolic acidosis Ventilation CO2 wash out.


7/43

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.


8/43

STAGES OF SHOCK

1. Pre shock or compensated shock

2. Decompensated shock

3. Refractory shock


9/43

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


10/43

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.


11/43

DECOMPENSATED SHOCK

If underlying cause not treated.Progressive renal, respiratory & cardiovasculardecompensation.Early signs of end organ failure may appear.


12/43

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 .


13/43

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


14/43

HYPOVOLEMIC SHOCK

Haemorrhagic

TraumaG I BleedRuptured aneurysmRetroparitoneal

Nonhaemorrhagic

Poor fluid intakeExternal fluid loss:

DehydrationVomitingDiarrheaPolyuria

Interstitial fluid replacement:

Thermal injuryTraumaAnaphylaxis


15/43

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)


16/43

CARDIOGENIC SHOCK

Results from pump failureDecreased systolic function.Resultant decreased cardiac output.Although normal intervascular volume.

Hemodynamic criteria:- sustained hypotension( SBP


17/43

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


18/43

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


19/43

SEPSIS AND SEPTIC SHOCKSEVERE SEPSIS:Sepsis with evidence of acute organ dysfunction

CV: SBP


20/43

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


21/43

MECHANISAM OF SEPTIC SHOCK

Infection

Inflammatory cytokines

Decreased Preload Myocardial depression Peripheral vasodilation

Decreased CO( SVR ) Decreased SVR( CO)

Decreased MAP

Shock

MODS


22/43

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.


23/43

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.


24/43

Neurogenic shock

Found in spinal injury.

Loss of sympathetic tone resulting peripheralvasodilation.

Decreased SVR & increased CO.

High output shock.


25/43

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).


26/43

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


27/43

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


28/43

TREATMENT

Manage the emergency

Determine the underlying cause

Definitive management or support


29/43

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.


30/43

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.


31/43

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.


34/43

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.


35/43


Obstructive shock

Pericardial tamponade pericardiocentesis surgical drainage (if needed)Pulmonary embolism heparin ventilation/perfusion lung scan pulmonary angiography consider:

- thrombolytic therapy- embolectomy at surgery


36/43

DEFINITIVE MANAGEMENTSeptic shock

Fluid resuscitation to continue until PWP 15 20mmHg.Blood transfusion if Hb


37/43

PROTOCOL FOR RESUSCITATION INSEPTIC SHOCK

First infuse fast 250 500 ml crystalloid in 5 10min

MAP


38/43


Neurogenic shock

Fluid resuscitation: mainstay of t/t.

Vasopressor.

Steroid like Methylprednisolone.

Vertebral surgery if needed.


39/43

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


40/43

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


41/43

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


42/43

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.


43/43

Shock by Kannan

Documents

Transcript of Shock by Kannan