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SHOCK 2007 SHOCK 2007 Ariel G. Bentancur, MD Emergency Department, Sheba Medical Center, Israel “Dry” Definition of Shock A circulatory situation where inadequate tissue/end organ oxygenation and perfusion is present. End Organ? Brain Heart Kidneys Gut Expanded definition: A generalized circulatory derangement causing multiple organ hypoperfusion and strong sympathetic activation, and when intense or sustained enough ( minutes to hours) irreversible metabolic, inflammatory, and clotting disorders leading to the patient’s permanent function deficit or death. So how we recognize shock? Grossly by: Signs of strong sympathetic activation: Tachycardia Pallor Extremity coldness Sweating Tachypnea Signs of hemodynamic instability: Inappropriate low blood pressure values Signs of organ dysfunction: Altered consciousness Oliguria BUT… Depends on: CATEGORY of shock DEGREE of shock severity SHOCK CATEGORIES 1. 2. 3. 4. 5. 6. 7. HYPOVOLEMIC CARDIOGENIC NEUROGENIC SEPTIC ANAPHILACTIC OBSTRUCTIVE OVERDOSE/TOXIN RELATED HYPOVOLEMIC SHOCK The initial insult is a loss of circulatory fluid volume, by: Bleeding Burns Vomiting Diarrhea Sweating “Stomas” Third space fluid sequestration CARDIOGENIC SHOCK Severe myocardial pump failure due to: Extensive anterior wall myocardial infarction Right ventricular infarction Arrhythmia Commotio cordis CARDIOGENIC SHOCK Defined by: Systolic blood pressure <90 mmHg and Wedge pressure of >20 mmHg Or Cardiac index <1.8 L/min Or Inotropics or intra-aortic balloon couterpulsation used to achieve Systolic blood pressure >90 mmHg. CARDIOGENIC SHOCK Recognized by: History: Acute Cardiac Syndrome or chest trauma. ECG changes: arrhythmia or ST segment changes. Echocardiographic demonstration of ventricular hypokinesia. NEUROGENIC SHOCK Caused by severe injury to the CNS Mechanism: A distribution Shock loss of nervous control of the vascular tone and subsequent fall of peripheral vascular resistance. loss of vascular regulation. pooling of blood in the splanchnic bed Clinical characteristics: Despite of shock presence the skin is warm and pink. Pulse is normal or slow due to unmatched parasympathetic tone. SEPTIC SHOCK It is also a distribution shock caused by severe systemic infection. Mechanism: Increased circulatory demand. A loss of the vascular tone with a subsequent decrease of the peripheral vascular resistance. Circulatory volume unchanged but splachnic bed volume sequestration is present. SEPTIC SHOCK Recognized by: History: present or recent febrile disease. Physical examination: Hypotension Warm, dry skin. Tachycardia. ANAPHYLACTIC SHOCK Caused by exposure to allergen. Mechanism: Distribution shock IgE/Mastocyte mediated acute reaction. Histamine/bradichinine/cytokine(ILC4)/PAF/ PGD2 mediated vasodilatation and blood volume sequestration in the splanchnic bed. ANAPHYLACTIC SHOCK Recognized by: History of exposure. History of past anaphylactic reaction. Coexistence of: skin rush, angioedema, bronchospasm. OBSTRUCTIVE SHOCK A restriction to blood flow or diastolic heart filling like in: Pericardiac Tamponade Tension Pneumothorax Stacked cardiac prosthetic valve Massive Pulmonary Emboli OBSTRUCTIVE SHOCK Mechanism: Blood Volume is normal Cardiac pump function is normal Vascular tone is normal Increased resistance to blood flow or ventricular diastolic function cause a low cardiac output! OVERDOSE/TOXIN RELATED SHOCK Caused by: Medications: Drugs used for the treatment of hypertension: Ca++ channel blockers β-blockers or Digoxin Tryciclic antidepressants Toxins Digested- scombroid fish poisoning Snake bite OVERDOSE/TOXIN RELATED SHOCK May develop through mixed mechanisms: Vasodilatation and a decrease of peripheral vascular resistance. Decreased ventricular systolic function. SHOCK SEVERITY DEGREE Best understood by the severity classification of hemorrhagic shock: Degree of Hemorrhage Estimated volume of blood loss Class 1 Very Mild <15% <750 ml Class 2 Mild 15-25% 750-1500 ml Class 3 Moderate 26-39% 1500-2000 ml Class 4 Severe ≤40% >2000 ml Cardiovascular signs HR <100 Normal b.p. HR >100 Normal b.p. HR >120 Hypotension HR >140 Deep hypotension Respiratory signs Normal RR 14-20 Mild tachypnea 20-30 Moderate tachypnea 30-35 Severe tachypnea >35 CNS signs Anxious Irritable/confused/ combative Lethargic/low pain response Lethargic/coma Skin signs Warm/pink/normal capillary refill Cool extremities/ Delayed capillary fill Cool extremities/ Delayed capillary fill Cool extremities/ Delayed capillary fill Kidney/metabolic Normal urine output Normal serum PH Oliguria 20-30ml/m Normal serum PH Oliguria<15ml/m/↑ urea/Metabolic acidosis Anuria Severe acidosis signs Shock Signs Tachycardia-age Infant > 160 bpm Pre-school >140 bpm School-puberty >120 bpm Puberty-adult >100 bpm Shock Signs Tachycardia-age Influenced by: Age Pacemaker Medications SHOCK Summary: Should be early recognized. Sole reliance on SBP results in delayed recognition. Treat shock and the causes early. Hypovolemic versus cardiogenic versus distribution versus obstructive versus mixed shock. The clinical picture depends on type and severity. If treated partially or late it becomes almost irreversible resulting in MOF and death. DISCUSSION COMMON SENSE-MECHANISM YES, SHOCK PRESENT NO SHOCK PRESENT