Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Shock
Transcript
Shock Eric Kaiser M.D. Rosen’s Chapter 4 9-7-06 Slides by: Scott Gunderson D.O. Shock “Transition between life and death” Failure to oxygenate & nourish the body adequately Mortality > 20% Pathophysiology & Biochemistry Pathophysiology Shock affects mitochondria first Without oxygen mitochondria convert fuels to lactate → lactic acid Failure of the krebs cycle Oxygen is the final electron accepter to form water Lactic Acid Early shock Skeletal muscle and splanchnic organs 1st affected Lactic acid production Resuscitation Pyruvate delivery from glycolysis can overwhelm krebs cycle Systemic Response Decreased vascular wall tension increases sympathetic stimulation (blocked in sepsis) Increased epi, norepi, corticosteroids, renin, and glucagon Increased glycogenolysis and lipolysis Increased glucose and FFA’s to TCA can overwhelm it Immune Response Neutrophil and macrophage activation due to hypoxia Enzymatic organ damage Capillary plugs causing microischemia TNF and Interleukins released Cardiac Physiology Contraction created by Ca++, ATP/CP, and troponin C Calcium inflow determines strength of contraction Inotropics increase Ca++ release in the sarcoplasmic reticulum via β-receptors or cAMP Cardiac Physiology ATP/CP supply almost entirely from oxidative phosphorylation by mitochondria Complete turnover of ATP/CP every 5-10 beats Cardiac Physiology Gregg Phenomenon Contractile strength decreases with decreased coronary perfusion Decreased coronary perfusion in shock Decreased workload due to lower SVR Very minimal cardiac ischemia even in severe shock Cardiac Physiology Inflammatory actions of TNFα, Interleukins, and NO decrease contractility Acidosis can decrease contractility but effect is minimal Clinical Features & Management Clinical Features Frequently no obvious etiology Rapid recognition H&P, ill appearance, diaphoresis HR and BP not reliable HR/SBP ratio better indicator Normal is less than 0.8 Urine output is great, but takes time Normal >1.0 ml/kg/hr Lactic acid or base deficit Shock Classification Rapid, but detailed H&P to direct therapy Flow diagram Figure 4-4 in Rosen’s Clinical Data CXR – infection, contusions EKG – ischemia Glucose CBC – anemia, leukocytosis Electrolytes – dehydration, GI bleed, acidosis ABG – base deficit, acidosis UA – dehydration Management IV, O2, monitor BP readings every 2-5 minutes Remember BP reading often underestimates the level of shock until severe Urine output >1 cc/kg/min Management IV access Peripheral vs. Central Most patients OK with one large bore or two smaller bore peripheral IV’s CVP pressure may be required for patient with cardiac failure or renal failure Indwelling catheters should be used unless hospital policy states against it in the ED Volume Replacement When is the tank full? Goal CVP slightly elevated of 10-15 cm H2O Must correlate CVP with SBP, urine output, and lactate levels to adequately assess perfusion Ventilation Rapid sequence intubation preferred Ketamine or etomidate are good choices due to minimal cardiovascular depression Intubation protects aspiration, decreases breathing workload, and initial treatment for acidemia High negative pressures in bronchospasm or ARDS can decrease LVEF and positive pressure removes this Acidosis Acidosis is a negative inotrope No evidence supports using bicarbonate for treatment Treat with improved ventilation and mild hyperventilation THAM (tris[hydroxymethl]-aminomethane) may be used IV for acidosis reversal Optimal Hemoglobin Hemoglobin carries oxygen High hematocrits increase viscosity and cardiac workload Optimal balance is a hemoglobin of 10-12 gm% Goal-Directed Therapy Goal directed therapy is the practice of resuscitating to a defined physiologic endpoint Wedge pressures – measures left ventricular filling pressures – controversial risk/benefit Lactate clearing index – decrease in arterial lactate by 50% in 1 hour and continued efforts until lactate < 2 mM GI tonography – permeable balloon in stomach or rectum measuring pH to estimate perfusion Questionable data supporting Specific Causes & Treatment Hemorrhagic Shock Rapid reduction in blood volume Heart rate and blood pressure responses can be variable No firm conclusion can be made by simply HR and BP readings Hemorrhagic Shock General Progression Increased heart rate Narrowed pulse pressure Shunting from noncritical organs Decreased cardiac filling leading to decreased CO Decreased SBP Hemorrhagic Shock Decreased perfusion to splanchnic organs precedes lower BP Lactic acid production Base deficit Normal base deficit is greater than -2 mEq/L After 1/3 of blood volume lost hypotension occurs Acidemia occurs about then as patient cannot create enough respiratory compensation for the lactic acid Hemorrhagic Shock Organ injury in resuscitation Release of activated neutrophils & inflammatory cytokines Distorted balance of vasodilatation vs. vasoconstriction May lead to ARDS, acute tubular necrosis, & centrilobular ischemic liver damage Consensus Definition Hemorrhagic Shock – 3 classifications Simple hemorrhage Bleeding with normal vital signs and base deficit Hemorrhage with hypoperfusion Bleeding with base deficit < -5 mmol or persistent HR >100 Hemorrhagic shock Bleeding with 4 or more of below Ill appearance or mental status HR >100 RR >22 or PaCO2 <32 Base deficit < -5 or lactate > 4 Urine output < 0.5 cc/kg/hr Hypotension > 20 minutes Hemorrhagic Shock Treatment Several liters of crystalloids in adults Three 20 cc/kg boluses in children If still in shock after bolus start PRBC’s at 5-10 cc/kg Blood substitutes possibly in future but not currently advantageous Hemorrhagic Shock Treatment Controlling hemorrhage is still always the cornerstone of treatment Immediate surgery if hemorrhage cannot be controlled In very rare cases inotropics may be beneficial Septic Shock Any microbe may cause, but gram negative most common Lipopolysaccharide is a key mediator 1/3 of cases no organism is identified Higher causes recently of gram positive due to Hospitalized patients Immunocompromised Indwelling catheters Increasing drug resistance Septic Shock 3 major effects Hypovolemia Relative due to increased venous capacitance Absolute due to GI loss, diaphoresis, tachypnea Cardiovascular depression Depression due to inflammatory mediators Systemic inflammation Capillary leak causing ARDS in up to 40% Consensus Definition SIRS Two or more of the following Temperature > 38 C or <36 C Heart rate > 90 Respiratory rate > 20 resp/min or PaCO2 <32 WBC > 12,000, < 4,000, or >10% bands Septic Shock Severe sepsis with hypotension unresponsive to fluid resuscitation and perfusion abnormalities Septic Shock Treatment Ventilatory support Decrease respiratory workload and correct hypoxia Fluids Increase ventricular filing 20-25 cc/kg crystalloids followed by 5-10 cc/kg colloids Blood Used to keep Hct at 30-35% if needed Septic Shock Treatment Antibiotics If focus identified Use clinical experience If no focus identified Semisynthetic PCN with β-lactamase inhibitor with an aminoglycoside and vancomycin Imipenem-cilastatin good monotherapy choice Antifungal in immunocompromised Septic Shock Treatment Vasopressors Dopamine Most common first line agent and a bad idea Remove from you armamentarium Norepinephrine Start 0.5-1 µg/min and titrate to response Excellent first choice; well studied Dobutamine Start 5 µg/kg/min Hypotension unresponsive to vasopressors and IVF. Cardiogenic Shock Pump failure Results when more than 40% of myocardium damaged Similar circulatory and metabolic changes to hemorrhagic shock May also be due to a PE Consensus Definitions Cardiogenic Cardiac failure Evidence of impaired cardiac outflow including dyspnea, tachycardia, rales, edema, or cyanosis Cardiogenic shock Cardiac failure plus four of below criteria Ill appearance or mental status HR >100 RR >22 or PaCO2 <32 Base deficit < -5 or lactate > 4 Urine output < 0.5 cc/kg/hr Hypotension > 20 minutes Cardiogenic Shock Treatment Ventilatory support Often needed in pulmonary edema or if respiratory failure imminent Avoid barbiturates, morphine, propofol and benzodiazepines Negative inotropic effects Fentanyl, ketamine and etomidate much better choices Cardiogenic Shock Treatment Ionotropics/vasopressors Dobutamine and Milrinone are agents of choice Amrinone (Replaced by Milrinone) Milrinone Similar to amrinone Load at 50 µg/kg (Consider half loading dose) Infuse at 0.375 - 0.75 µg/kg/min Be prepared for hypotension Cardiogenic Shock Treatment Intraaortic balloon pump When all pharmacologic therapy is failing Requires appropriate facility and ICU/CCU Improves cardiac output by 30% Cardiogenic Shock Treatment Myocardial infarction causing cardiogenic shock Management not significantly different than another MI accept additional management Ventilatory support as needed Treat dysrhythmias Inotropic support Aspirin Heparin PTCA vs. thrombolytics Cardiogenic Shock Treatment Pulmonary Embolism Ventilatory support IV fluids Norepinephrine Thrombolytics (systemic vs. intra-arterial) Possis catheter Surgical embolectomy at few centers Anaphylactic Shock IgE mediated response to an allergen Mast cells release histamine Histamine causes Smooth muscle relaxation Bronchial contraction Capillary leak Anaphylactic Shock Treatment Epinephrine 1 cc of 1:10,000 IV infused slowly and watch response 5 mg in 500 cc NS at 10 cc/hr thereafter May titrate to response Use even with coronary artery disease if hypotensive Anaphylactic Shock Treatment Corticosteroids Decrease immune response Methylprednisolone 125mg IV Hydrocortisone 5-10 mg/kg IV Antihistamines Diphenhydramine 0.5 mg/kg IV Cimetidine 2-5 mg/kg IV Famotidine Intubation if needed Neurogenic Shock CNS cord lesions above T1 Heart gets unopposed vagal simulation Bradycardia and hypotension Atropine First line therapy Neurogenic Shock Treatment Volume expansion Confirm by CVP and BP Vasopressors Ephedrine 10 mg IV bolus good for 3-4 hours Phenylephrine 100-180 µg/min IV until stable Summary Early recognition of shock and early treatment is key Do not rely solely on a HR and BP to determine their status Aggressive and goal directed therapy have proven to decrease mortality References Jones, Alan E., & Kline, Jeffrey A. (2006). “Shock.” In Marx, John A., Hockberger, Robert S., & Walls, Ron M. (Eds.). Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed., Pg. 41-56. Mosby.
