Types of Shock

Types of Shock Types of Shock Causes Pathophysiology HYPOVOLEMIC Decrease in circulating volume Acute/rapid fluid loss does not allow compensatory mechanisms to restore adequate circulating volume resulting in cellular hypoperfusion, anaerobic metabolism, lactic acidosis and electrolyte and acid base disturbances. Hemorrhage Burns Injury/insult that causes a significant fluid shift from intravascular to interstitial Existing blood volume is shunted to vital organs (heart, lungs, brain) thus exacerbating the lack of perfusion to the remaining organs (kidney, liver and stomach) CARDIOGENIC Pump failure Loss of contractility Most commonly results from extensive left ventricular damage from MI Papillary muscle rupture Ventricular septal rupture Loss of effective ventricular contractibility (extreme form of heart failure) Assessment and Clinical Findings History (use of NSAIDS’s?) Serum Lactate ABG – presence of base deficit Hemodynamics Increase in SVR Decrease in CO, CVP, PAP and PCWP Tachycardia (weak and rapid) Hypotension Tachypnea Decreased O2 sat Skeletal muscle weakness Cool and clammy Changes in H&H Decrease in urine output Thirst Agitation Lethargy Confusion Tachycardia, thread, rapid Narrow pulse pressure JVD Dyspnea Tachypnea Inspiratory crackles Chest pain Dysrhythmias Cool, pale, moist skin Olguria Decreased mentation Treatment Identify and treat underlying cause Volume replacement with isotonic crystalloids (NS or LR) and colloids (Blood products, Albumin, synthetic volume expanders) Vasopressors for BP management Decreased CO and afterload resulting in a decrease in MAP Increased HR, preload and SVR Essential to break the vicious circle with mechanical augmentation and reversal of the underlying insult Optimize CO Measurement of LVEDP Less than 14 = Fluids More than 16 = Diuresis Narcotics and Cardiomyopath y Valvular disease Dysrrhythmias Sedatives Vasodilators to reduce SVR (Nipride, Nitroglycerin) a systolic BP of less than 90mmHg for more than30 minutes MAP less than 70 Cardiac index of less than 2.2L/min/m2 in the presence pulmonary capillary wedge pressure of greater than 18 mm Hg Mechanical Support, IABP or LVAD Mechanical ventilation Minimizing physical exertion/energy expenditure in providing care (cluster care) ABG – decrease in PaO2 Respiratory Alkalosis Elevated CK-MB, Troponin, BNP Radiography – Enlarged heart, pulmonary congestion DISTRUBUTIVE Vasodilation that results in a decrease in venous return Decrease in vascular tone or volume Hypotension Severe bradycardia Warm, dry skin Vasomotor depression Hypotension Severe bradycardia Warm, dry skin Types include Neurogenic, Septic and Anaphylactic NEUROGENIC Loss or disruption in sympathetic tone Spinal cord injury above T5 Spinal Anesthesia Loss or disruption in sympathetic tone Decreased SVR, CO Treatment of underlying cause Volume Resuscitation Vasoconstrictors SEPTIC Sepsis – systemic response to known infection Septic Shock – complex interactions among invading microorganism s and the immune system, inflammatory system and the coagulation system Sepsis with hypotension despite adequate fluid resuscitation 2 or more of the following: Temperature greater than 100.4°F (38°C) or less than 96.8°F (36°C) Heart rate greater than 90 (often full and bounding) Respiratory rate greater than 20 or arterial carbon dioxide tension PaCO2 less than 32 mm Hg White blood cell (WBC) count greater than 12,000 cells/mm3 or less than 4,000 cells/mm3 OR more than 10% immature (band) forms Severe Sepsis Lactic Acidosis Oligura Changes in mentation Septic Shock Sepsis with hypotension despite fluid resuscitation Early Increased CO due to a decrease in SVR Increased PAP and PCWP Late Decreased CO, CVP, PAP and PCWP Identify and treat underlying cause Volume Mechanical Ventilation Maintain adequate CO Nutritional support Monitor CBC ABG Lactate level ETCO2 monitoring to detect adequacy of tissue perfusion Pink, warm, flushed skin Treatment related factors – Indwelling medical devices, surgery, invasive diagnostic tests, medications ANAPHYLACTIC Allergic reaction that evokes a lifethreatening hypersensitivit y response Foods such as eggs, shellfish, nuts Medications such as antibiotics, antiinflammatory, narcotics Blood products IgE-mediated anaphylaxis occurs as a result of the immune response to a specific antigen after being exposed and forming antibodies. Non-IgE responses (anaphylactoid reactions) occur without the presence of IgE antibodies and can occur the first time the person is exposed to the antigen. WBCs secrete chemical mediators causing systemic vasodilation Hypotension Tachycardia Cough Dyspnea Pruritus Urticaria Generalized erythema Anxiety Restlessness Feeling of warmth Chest tightness Nausea and vomiting Later Signs Stridor Laryngeal edema Decreased LOC Decreased SVR and CO Early recognition and intervention Remove the offending antigen. Reverse effects of chemical mediators. Restore adequate tissue perfusion. Oxygen Subcutaneous or IV antihistamine (Benadryl) Epinephrine Corticosteroids, bronchodilators Latex Vasoconstrictors and positive inotropic agents Mechanical ventilation