SEMINOR ON SHOCK

MODERATOR DR.B.P.RANJAN ASST PROFFESOR DEPT OF SURGERY S.M.C.H

PRESENTED BY DR.KANNAN.K PGT DEPT OF SURGERY S.M.C.H

DEFINITION
Shock is a physiologic state characterized by

systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery.

Hypotension is not a requirement. Poor tissue perfusion.

PATHOPHYSIOLOGY
Imbalance in oxygen supply and demand.

Conversion from aerobic to anaerobic metabolism.

Appropriate and inappropriate metabolic and

physiologic responses.

In 3 levels: 1. Cellular level

2. Microvascular level. 3. Systemic level

CELLULAR LEVEL

MICROVASCULAR LEVEL
Hypoxia Cellular injury

Metabolic acidosis
Free radical generation & cytokines Injury to cappilary endothelial cells Leaky endothelium Tissue edema

Further cellular hypoxia

Cell death

SYSTEMIC LEVEL
1.

Cardiovascular: Hypotension
Depression of baroreceptor Increased sympathetic activity & release of cathecholamines HR & Systemic vasoconstriction.

2. Respiratory :
Metabolic acidosis Ventilation CO2 wash out.

SYSTEMIC LEVEL
3. Renal : Perfusion & stimulation of renin-angiotensin-aldosterone
axis

urine output.

4. Hormonal:
Adrenal system Renin-angiotensin-aldosterone system ADH Cortisol * Acts on kidney & decrease urine output * Sympathetic sensitization.

STAGES OF SHOCK
1. Pre shock or compensated shock 2. Decompensated shock

3. Refractory shock

STAGES OF SHOCK
Preshock aka compensated/warm shock
Body is able to compensate for perfusion

Up to ~10% reduction in blood volume

Tachycardia to cardiac output & perfusion

Shock
Compensatory mechanisms overwhelmed See signs/symptoms of organ dysfunction ~20-25% reduction in blood volume

End-organ dysfunction
Leading to irreversible organ damage/death

PRESHOCK OR COMPENSATED SHOCK

Cardiovascular and hormonal response to 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.

DECOMPENSATED SHOCK
If underlying cause not treated. Progressive renal, respiratory & cardiovascular decompensation. Early signs of end organ failure may appear.

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 .

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.
5.

Distributive
Endocrine

HYPOVOLEMIC SHOCK
Haemorrhagic

Nonhaemorrhagic
Poor fluid intake External fluid loss:

Trauma G I Bleed Ruptured aneurysm Retroparitoneal

Dehydration Vomiting Diarrhea Polyuria Interstitial fluid replacement: Thermal injury Trauma Anaphylaxis

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 (marked

hypotension, decreased CO, lactic acidemia)

CARDIOGENIC SHOCK

Results from pump failure

Decreased systolic function.

Resultant decreased cardiac output.

Although normal intervascular volume.

Hemodynamic criteria: - sustained hypotension( SBP<90 for atleast 30min). - reduced cardiac index(<2.2L/min/m2). - elevated PAWP(>15mm Hg).

Obstructive shock
Reduction 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

DISTRIBUTIVE SHOCK
Results from a severe decrease in SVR . Peripheral vasodilation & decreased after load. Cardiac output may be high.

Etiology: 1. Septic shock 2. Neurogenic / spinal shock 3. Systemic inflammation pancreatitis, burns 4. Toxic shock syndrome 5. Anaphylaxis and anaphylactoid reactions 6. Toxin reactions drugs, transfusions

SEPSIS AND SEPTIC SHOCK

SEVERE SEPSIS:
Sepsis with evidence of acute organ dysfunction CV: SBP <90 mmHg or MAP <70 mmHg RENAL: urine output <0.5 ml/kg/hr RESPIRATORY: PaO2/FIO2 <250 HEMATOLOGIC: platelet count <80.000/ul METABOLIC ACIDOSIS: pH <7.30 or plasma lactate >2mmol/L

SEPTIC SHOCK:
Severe Sepsis with refractory hypotension: MAP <60 mmHg after fluid resucitation (30-50cc/Kg crystalloids)

SEPTIC SHOCK
Common cause of death in surgical ICUs. Source of infection : Pulmonary

Blood stream Genito urinary Intra abdominal Skin & soft tissue.
Stages:

Early high output septic shock 2. Late low output septic shock
1.

MECHANISAM OF SEPTIC SHOCK

Infection Inflammatory cytokines Decreased Preload Myocardial depression Peripheral vasodilation Decreased SVR( CO) Decreased MAP Shock MODS

Decreased CO( SVR )

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 coronary

vascular resistance is significantly increased in septic shock - i.e., coronary and cerebral autoregulatory mechanisms are relatively intact .
Microvascular studies also show aberrant distribution of

perfusion within tissues and organs.

LOW OUTPUT SEPTIC SHOCK

Late 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 sympathetic vasoconstrictive effects. Post-resuscitation, perfusion abnormalities may persist for days. (decreased perfusion of brain, kidneys, liver, splanchnic organs) with potential persistent ischemia. Extremities cool & clammy , oliguria & mental change.

Neurogenic shock
Found in spinal injury. Loss of sympathetic tone resulting peripheral vasodilation. Decreased SVR & increased CO.

High output shock.

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).

DIAGNOSIS AND EVALUATION

Clinical Signs: varies with type of Primary diagnosis shock
Hypotension( SBP < 90 ) Tachycardia, tachypnoea, oliguria Cool , clammy extremities . or Warm& hyperemic Mental confusion.

Differential DX:
JVP - hypovolemic vs. cardiogenic Left S3, S4, new murmurs - cardiogenic Right heart failure - PE, tamponade Pulsus paradoxus, Kussmauls sign tamponade Fever, rigors, infection focus - septic

DIAGNOSIS AND EVALUATION

All laboratory investigations :

Investigations

Hb, TLC, DLC , Platelet ABG , electolytes

S. creatine, BUN
PT/PTT S. lactate Culture

Imaging: CXR, Abd xray FAST CT Abd or chest ECG, echo Pulmonary perfusion scan

TREATMENT
Manage the emergency Determine the underlying cause Definitive management or support

MANAGE THE EMERGENCY

Resuscitation 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.

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.

IMMEDIATE GOALS IN SHOCK

Hemodynamic support

MAP > 60mmHg PAOP = 12 - 18 mmHg Cardiac Index > 2.2L/min/m2 Hemoglobin > 9 g/dL Arterial saturation > 92% Supplemental oxygen and mechanical ventilation

Maintain oxygen delivery

Reversal of oxygen dysfunction Decreasing lactate (< 2.2mM/L) Maintain urine output ` Reverse encephalopathy Improving renal, liver function tests.

DETERMINE THE CAUSE

Often obvious based on history. Trauma most often hypovolemic (hemorrhagic). Postoperative most often hypovolemic. (hemorrhagic or third spacing) Debilitated hospitalized pts most often septic. Must evaluate all pts for risk factors for MI and

consider cardiogenic. Consider distributive (spinal) shock in trauma.

DEFINITIVE MANAGEMENT
Hypovolemic shock
Fluid replacement ( Blood 0r IVF) is the mainstay of t/t.
Identify & control the source of bleeding or fluid loss.
Follow damage control resuscitation in severe haemorrhagic

shock. 1. Fluid resuscitation to maintain BP around 90mmHg. 2. Emergency ot to control haemorrhage. 3. Warm the pt & prevent coagulopathy in icu. Target Hb is 79 g/dl. Use FFP when PT or Aptt > 1.5 times of control.

DEFINITIVE MANAGEMENT
Cardiogenic Shock
Restore blood pressure by IVF +/- Inotropic agent. LV infarction

Intra-aortic balloon pump (IABP). Cardiac angiography. Revascularization. Angioplasty. coronary bypass.
RV infarction
Fluid and inotropes with PA catheter monitoring.

Mechanical abnormality
Echocardiography. Cardiac catheterisation. Corrective surgery.

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

DEFINITIVE MANAGEMENT
Septic shock
Fluid resuscitation to continue until PWP 1520mmHg. Blood transfusion if Hb<7. Consider vasopressor for maintenance. Identify the site of infection & drain if possible. Antimicrobial therapy ( key rule ). Anticoagulant like Protein C can be used. Intensive insuline therapy in critical patient. Goals:

- improving organ function. - decreasing lactate level.

PROTOCOL FOR RESUSCITATION IN SEPTIC SHOCK

First infuse fast 250 500 ml crystalloid in 510min

CVP>15 or PAWP is 15 --20 But MAP<65mmHg

MAP<65 & CVP<812mmHg or PAWP<812mmHg

Infuse another bolus

Dopamine/Dobutamine

If SVR<600 , add vasopressor

Irreversible

(nonepi/vasopressin)

Goal: MAP>65 & HR<120.

DEFINITIVE MANAGEMENT
Neurogenic shock
Fluid resuscitation: mainstay of t/t.

Vasopressor.
Steroid like Methylprednisolone. Vertebral surgery if needed.

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

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 25 cm of H2O. 4. Correct hypoperfusion abnormalities

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 INOTROPIC AGENTS

Never use before fluid resuscitation in hypovolemic shock.

Vasopressors mainly indicated in distributive shock like septic shock. Inotropic agent & inodilator indicated in cardiogenic shock.