Definition of shock . types of shock
Classification of shock on the basis of initiating mechanism:
Hypovolemic shock
Cardiogenic shock
Septic shock
Neurogenic shock
Anaphylactic shock
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SHOCK Dr. VINOD KUMAR C - ASSISTANT PROFESSOR Dr. SARAN KARTHIK S - SENIOR RESIDENT DEPARTMENT OF ORTHOPAEDICS, AIIMS MADURAI
DEFINITION Shock is defined as a state of S ystemic tissue hypoperfusion resulting from reduced cardiac output and / or reduced effective circulatory blood volume.
TYPES OF SHOCK Classification of shock on the basis of initiating mechanism: Hypovolemic shock Cardiogenic shock Septic shock Neurogenic shock Anaphylactic shock
H arrison manual of internal medicine
HYPOVOLEMIC SHOCK Results from low cardiac output due to low blood volume Haemorrhagic causes : Trauma Surgery Non-haemorrhagic causes: poor fluid intake (dehydration) excessive fluid loss due to vomiting, diarrhoea , burns
CARDIOGENIC SHOCK Results from low cardiac output due to myocardial pump failure Intrinsic myocardial damage - infarction, ventricular arrhythmias Valvular stenosis
OBSTRUCTIVE SHOCK Extrinsic compression – C ardiac tamponade , Tension pneumothorax Outflow obstruction – P ulmonary embolism (Massive)
SEPTIC SHOCK A Type of Distributive shock. A Subset of sepsis in which particularly profound circulatory , cellular, and metabolic abnormalities associated with greater risk of mortality than with sepsis alone
NEUROGENIC SHOCK Spinal cord injury causes loss of vascular tone and peripheral pooling of blood Acute vasodilatation leading to hypotension and tissue hypoperfusion
ANAPHYLACTIC SHOCK IgE mediated hypersensitivity reaction Severe reaction to an allergen, leading to the release of histamine that causes widespread vasodilation and hypotension. Allergy to insect stings, medicines or foods (Nuts, Berries, Sea foods)
STAGES OF SHOCK 1.An initial non progressive stage 2.A progressive stage 3.An irreversible stage
NONPROGRESSIVE STAGE Reflex compensatory mechanisms are activated and vital organ perfusion is maintained Baroreceptor reflexes ,release of catecholamines antidiuretic hormone [Fluid conservation by the kidney ] ,activation of RAS and generalized sympathetic stimulation [Wide spread vasoconstriction Vascular autoregulation]
Net effects are- 1. Tachycardia 2. Peripheral vasoconstriction [Cold clammy skin expect in septic shock where the skin is warm due to vasodilatation ] 3. Renal conservation of fluid Cardiac output and blood pressure maintained Resulting in restoration of circulation and tissue perfusion.
PROGRESSIVE STAGE If the underlying causes are not corrected, shock passes to the progressive phase , which is characterized by widespread tissue hypoxia . Persistent oxygen deficiency leads to intra cellular anaerobic glycolysis with lactic acidosis , thus reduce tissue pH and vasomotor response. Resulting reduce cardiac output and anoxic injury to endothelial cell leads to DIC.
IRREVERSIBLE STAGE When there is failure to restore circulation either by compensatory mechanism or by therapeutic intervention , shock enters the irreversible stage. Wide spread cell injury is reflected in lysosomal enzyme leakage Ischemia - heart - Myocardial contractile function worsens - bowel - Intestinal flora to enter the circulation - renal - Renal failure The downward spiral culminates in death.
PATHOPHYSIOLOGY OF SHOCK CELLULAR LEVEL ( aerobic - anaerobic respiration ) MICROVASCULAR LEVEL (peripheral vasoconstriction initially , pooling of blood later) SYSTEMIC LEVEL ( end organ damage)
Hypotension Tissue hypoperfusion Cellular hypoxia Reversible injury Irreversible injury with persistent of shock End organ dysfunction Death SEQUENTIAL EVENTS IN THE MECHANISM OF SHOCK:
MANAGEMENT
EVALUVATION OF PATIENT IN SHOCK HISTORY PHYSICAL EXAMINATION - Hypotension(SBP<90mmhg) - MAP(<65mmhg) - Tachycardia, Tachypnea , - Encephalopathy - Urine output (<0.5ml/kg/hr), - Capillary refilling time prolonged - JVP , creps - site of infection - cellulitis, abscess
SHOCK INDEX > 0.9 (HR/SBP) indication for blood transfusion qSOFA score is a rapid assessment scale qSOFA ≥2 (with a concern for infection) is associated with a significantly greater risk of death or prolonged ICU stay.
DIAGNOSTIC TESTING 1. Lactate [ indicator of mortality in hypovolemic shock, not corrected even with fluids in septic shock ] 2.Complete blood count (with differential) –infection 3.Renal function tests - end organ damage 4.Liver function tests - end organ damage 4.Blood cultures, urine cultures and sputum cultures 5. Serum electrolytes 6. Urinalysis
7. Cardiac enzymes – cardiac cause 8.PT, PTT, and INR – coagulation abnormalities 9. Arterial blood gas 10. ECG 11. CXR 12.POINT OF CARE ULTRASOUND in rapid protocolized manner views of heart ,lungs, IVC , abdominal aorta, pleural space, abdomen and pelvis, deep veins assessed
APPROACH TO PATIENT WITH SHOCK
MANAGEMENT OF HYPOVOLUMEIC SHOCK ABC(AIRWAY,BREATHING,CIRCULATION) CONTROL HEMORRHAGE OBTAIN IV ACCESS AND RESUSCITATE WITH FLUIDS AND BLOOD [CRYSTALLOIDS are the most preferred resuscitation fluids , Favoured crystalloid is ringer lactate which does not produce metabolic acidosis that occurs with normal saline
Washington manual of critical care
CLINICAL FINDINGS OF GOOD PERFUSION Mean arterial pressure (>65mmhg) Urine output >0.5ml/kg/ hr Lactate clearance >10% Normalizing pH Improving level of consciousness CVP 8 to 12mmHg Central venous oxyhemoglobin saturation > 70 percent
MANAGEMENT OF CARDIOGENIC SHOCK Oxygenation and airway protection Need to treat etiology Tension pneumothorax - treated by needle decompression /chest tube, C ardiac tamponade -by pericardial tap, P ulmonary embolus - anticoagulation(heparin), Embolectomy MI or acute coronary syndrome (ACS)- aspirin and heparin Hemodynamic support- dopamine, norepinephrine, and epinephrine are vasoconstricting drugs
MANAGEMENT OF SEPTIC SHOCK Management bundle includes five components within 1hr Measurement of serum lactate levels Collection of blood for culture before antibiotic administration, Administration of appropriate broad-spectrum antibiotics Initiation of 30 mL/kg crystalloid bolus for hypotension or lactate ≥4 mmol/L Treatment with vasopressors for persistent
MANAGEMENT OF NEUROGENIC SHOCK Maintain ABC Immobilizing neck to prevent further spinal cord damage Intravenous (IV) methylprednisolone - treatment option for an acute spinal cord injury Surgery is necessary to remove fragments of bones, herniated disk or fractured vertebrae that compressing the spine.
MANAGEMENT OF ANAPHYLACTIC SHOCK ABC IM Epinephrine 0.5 mg (adult)/ 0.3mg(Child) 1:1000 dilution to anterior or lateral thigh If unresponsive or poor response to IM , IV Epinephrine 0.1-0.2 mg 1:1000 in 10 ml of 0.9 NaCl every 1-2 mins until response or epinephrine infusion can be given H1 & H2 Antihistamines, steroids Intubation , cricothyroidectomy , cardiopulmonary resuscitation (CPR) may be needed
TYPES OF SHOCK ? 3 STAGES OF SHOCK ? CAUSES OF HYPOVOLUMEIC SHOCK? MANAGEMENT OF HYPOVOLUMEIC SHOCK ? SIGNIFICANCE OF SERUM LACTATE IN HYPOVOLUMEIC SHOCK ?
SHOCK INDEX AND qSOFA ? CAUSES OF CARDIOGENIC SHOCK ? MANAGEMENT OF SEPTIC SHOCK ? MANAGEMENT OF ANAPHYLACTIC SHOCK ?
TAKE HOME POINTS Shock possibility should be considered in patients presenting with new organ dysfunction or hypotension Early recognition can result in early treatment in reversible state of shock Determine the type of shock by history, physical examination, diagnostic tests