Dr.

Ankush Gupta

Shock
Classification, Pathophysiology and Management

Dr. Ankush Gupta

MS, M.Ch.(Urology) Lecturer, Department Surgery, S. N. Medical College, Agra

Shock: Definition
A physiologic state characterized by Inadequate tissue perfusion Clinically manifested by Hemodynamic disturbances Organ dysfunction

Dr. Ankush Gupta

SHOCK
Hypovolemic Shock Low resistance Shock (distributive) Cardiogenic Shock

Dr. Ankush Gupta

Septic Anaphylactic

Extra-cardiac obstructive shock

Neurogenic

Dr. Ankush Gupta

ETIOLOGY

Dr. Ankush Gupta

HYPOVOLEMIC Shock
Hemorrhagic
Trauma Gastrointestinal Retroperitoneal

Fluid depletion (nonhemorrhagic) External fluid loss - Dehydration

- Vomiting - Diarrhea

Interstitial fluid redistribution - Thermal injury - Trauma

Dr. Ankush Gupta

CARDIOGENIC Shock
Myopathic
Myocardial infarction Myocarditis Cardiomyopathy Septic myocardial depression

Pharmacologic
Anthracycline cardiotoxicity Calcium channel blockers

Mechanical
Valvular failure (stenotic or regurgitant) Hypertropic cardiomyopathy Ventricular septal defect

Arrhythmic

Dr. Ankush Gupta

EXTRACARDIAC OBSTRUCTIVE Shock

Impaired diastolic filling ( ventricular preload)
Direct venous obstruction (vena cava): intrathoracic obstructive intrathoracic pressure: Tension pneumothorax cardiac compliance: Constrictive pericarditis, Cardiac tamponade
tumors

Impaired systolic contraction (ventricular afterload)

Right ventricle

Pulmonary embolus (massive) Aortic dissection

Left ventricle

Dr. Ankush Gupta

DISTRIBUTIVE Shock
Septic (bacterial, fungal, viral, rickettsial) Toxic shock syndrome Anaphylactic, anaphylactoid Neurogenic (spinal shock) Endocrinologic Adrenal crisis Thyroid storm Toxic (e.g., nitroprusside, bretylium)

Dr. Ankush Gupta

Pathophysiology

Dr. Ankush Gupta

Pathophysiology
Imbalance in oxygen supply and demand Conversion from aerobic to anaerobic metabolism Appropriate and inappropriate metabolic and physiologic responses

SHOCK

Dr. Ankush Gupta

Dynamic and progressive nature of shock, 3 clinical phases of shock can be identified: 1. Compensated phase 2. Uncompensated phase 3. Irreversible phase

Dr. Ankush Gupta

Hypovolemic Shock
Degree of volume loss response 10% well tolerated (tachycardia) 20 - 25% failure of compensatory mechanisms (hypotension, orthostasis, decreased CO) > 40% loss associated with overt shock (marked hypotension, decreased CO, lactic acidemia)

Dr. Ankush Gupta Dr. Ankush Gupta

Clinical Correlates of Hemorrhage

Class I ClassII Class III Class IV

Blood loss (mL) Blood loss (% total) Pulse rate Blood pressure CNS mental status

> 750 < 15% < 100 Normal Slight anxiety

750 - 1500 15 - 30% > 100 Normal Mild anxiety

1500 - 2000 30 - 40% > 120 Anxious/confused

> 2000 > 40% > 140 Confused/lethargic

Cardiogenic Shock

Dr. Ankush Gupta

Requires at least 40% loss of functional myocardium (single MI or cumulative damage)

Usually involves left main or left anterior descending obstruction

Dr. Ankush Gupta

Distributive Shock
Defining feature: loss of peripheral resistance Types:
1. Dominantly septic shock, 2. Anaphylactic and 3. Neurogenic shock less common

Clinical form of shock with greatest contribution of other shock elements - i.e., hypovolemia, cardiac failure

Dr. Ankush Gupta

Septic shock: stages

Early Stage (hyperdynamic)

Late Stage (cardiogenic or hypodynamic)

Hyperthermia Tachycardic Tachypnea Warm extremities Bounding pulse Normal capillary refill time Hypertensive / Normotensive Hypoxia Polyuria Increased cardiac output Decreased SVR Normal CNS Respiratory alkalosis Hyperglycemia Normal coagulation

Hypothermia Tachycardic Bradypnea Cold mottled extremities Weak, thready pulse Prolonged capillary refill time Hypotensive Hypoxia Oliguria / anuria Decreased cardiac output Increased SVR Obtunded, comatose Metabolic acidosis Hypoglycemia Disseminated intravascular coagulopathy

Anaphylactic vs. Anaphylactoid Shock

Dr. Ankush Gupta

Anaphylactic shock: immediate hypersensitivity reaction mediated by the interaction of IgE on mast cells and basophils with the appropriate antigen resulting in mediator cascade Anaphylactoid reactions involve similar release of mediators via non-immunologic mechanisms. Primary mediators include histamine, serotonin, eosinophil chemotactic factor, and proteolytic enzymes. Secondary mediators include PAF, bradykinin, prostaglandins, and leukotrienes.

Dr. Ankush Gupta

Anaphylactic shock
Insect envenomations Antibiotics (betalactams, vancomycin, sulfonamides) Heterologous serum (anti-toxin, anti-sera) Blood transfusion Egg-based vaccines Latex

Anaphylactoid shock
Ionic contrast media Protamine Opiates Polysaccharide volume expanders (dextran, hydroxyethyl starch) Muscle relaxants Anesthetics

Dr. Ankush Gupta

Pathophysiology: Summary

Dr. Ankush Gupta

Mechanisms of Cellular Injury in Shock

1) 2) 3) Cellular ischemia Free radical reperfusion injury Inflammatory mediators (local and circulating)

Dr. Ankush Gupta

Dr. Ankush Gupta

Dr. Ankush Gupta

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

Dr. Ankush Gupta

Evaluation
Laboratory
Hgb, WBC, platelets PT/PTT Electrolytes, arterial blood gases BUN, Cr Ca, Mg Serum lactate ECG

Invasive Monitoring
Arterial pressure catheter CVP monitoring Pulmonary artery catheter (+/- RVEF, oximetry)

Dr. Ankush Gupta

Management

Dr. Ankush Gupta

AIM

.restoration of perfusion of the tissues

Dr. Ankush Gupta

If shock is untreated, it will cause profound hypoxia leading to multiple organ failure and death.

Shock is the final common pathway to death

A Clinical Approach to Shock Diagnosis and Management

Immediate Goals in Shock
Hemodynamic support Maintain oxygen delivery MAP > 60mmHg

Dr. Ankush Gupta

Hemoglobin > 9 g/dL Arterial saturation > 92% Supplemental oxygen and mechanical ventilation Decreasing lactate Maintain urine output Reverse encephalopathy Improving renal, liver function tests

Reversal of oxygen dysfunction `

Dr. Ankush Gupta

Initial Therapeutic Steps

Admit to intensive care unit (ICU) Venous access (1 or 2 wide-bore catheters) Central venous catheter Arterial catheter EKG monitoring Pulse oximetry Hemodynamic support (MAP < 60 mmHg)
Fluid challenge Vasopressors for severe shock unresponsive to fluids

Dr. Ankush Gupta

Diagnosis Remains Undefined or Hemodynamic Status Requires Repeated Fluid Challenges of Vasopressors Pulmonary Artery Catheterization
Cardiac output Oxygen delivery Filling pressures

Echocardiography
Pericardial fluid Cardiac function Valve or shunt abnormalities

Dr. Ankush Gupta

Hypovolemic Shock
Identify

the source of bleeding and control bleeding

Direct pressure for external bleeding. Surgical intervention for internal bleeding.

Various other concepts in controlling bleeding are

Vasopressin and H2 blockers for GI bleed.

Traction in case of long bone fracture. Surgery in case of all Gync. bleeds.

If hypovolemia is severe or prolonged IONOTROPICS are to

be used to maintain ventricular performance after blood volume is restored.

As an adjunct the TREDELENBURGs position

Dr. Ankush Gupta

Dr. Ankush Gupta

Fluid Therapy
Crystalloids
Lactated Ringers solution Normal saline

Colloids
Hetastarch Albumin

Packed red blood cells Infuse to physiologic endpoints

Dr. Ankush Gupta

Fluid Therapy
Correct hypotension first (golden hour) Decrease heart rate Correct hypoperfusion abnormalities Monitor for deterioration of oxygenation

Dr. Ankush Gupta

Fluid Therapy
Crystalloid vs. colloid Optimal PWP 10 - 12 vs. 15 - 18 mm Hg 20 mL/kg fluid challenge in hypovolemic or septic shock with re-challenges of 5 - 10 mL/kg

Dr. Ankush Gupta

Cardiogenic Shock
INOTROPES

most important drugs in cardiogenic shock i.e. Dopamine, Dobutamine,

Nor epinephrine, Vasopressin.
OTHER DRUGS

Furosemide is used in the presence of pulm. Congestion

Morphine for anxiolysis

IABP Intra Aortic Baloon Pumping, is done if the patient fails to stabilise

with the above treatment. Finally surgical interventions like revascularisation should be done basing on the etiology.

Dr. Ankush Gupta

Extra-cardiac Obstructive Shock

Pericardial tamponade
pericardiocentesis surgical drainage (if needed)

Pulmonary embolism
heparin ventilation/perfusion lung scan pulmonary angiography consider: - thrombolytic therapy - embolectomy at surgery

Dr. Ankush Gupta

Distributive Shock: Sepsis

Treatment

Broad spectrum Antimicrobials Removal of source of infection Hemodynamic support - IV fluids 1-2 lit of NS over 2hrs
- Urine output maintained at >0.5 ml/kg/hr - Diuretic is used when needed. - If fluid resuscitation fails, inotropics and vasopressors are used.

Respiratory support by mechanical ventilation . If Hb < 7g/dL, packed RBC are given to maintain the oxygenation

Dr. Ankush Gupta

Distributive Shock: Neurogenic

Diagnosis
and dry extremities, hypotension, bradycardia, venous pooling etc. Treatment

Characteristic C/F is warm

Fluid resuscitation to restore normal hemodynamic

properties. Rule out hemorrhage Nor epinephrine augments vascular resistance Dopamine may be used as per requirement to augment the tone Atropine may be used to increase the HR and CO

Distributive Shock: Anaphylactic shock

rescue breathing

Dr. Ankush Gupta

Primary treatment is EPINEPHRINE 0.3 -0.5 ml of 1:1000 (SC

or IM) with repeated doses at 20 mins interval.

Tourniquet may be applied if the site of antigen inj. was on an

extremity

If intractable hypotension is present, NS and vasopressors

may be used.

Initial nasal catheter or intermittent positive pressure ventilation Antihistamines for relieving urticaria-angioedema Glucocorticoids used later to prevent recurrence

Dr. Ankush Gupta

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