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GEP - Shock

GEP - Shock Lecture Week 6 2009

Common denominator of all forms of shock Impaired oxygen utilization by cells that disrupts function
Causes of oxygen free radical production Reperfusion injury - O2-, H2O2, OH-, & O, attack memb structures, denature proteins, break cell DNA <BR> Immune Cells - esp. neutrophils recruited to injury, produce free radicals
Inflammatory Cytokines released at hypoxic sites TNF-a, IL-1 & others induce excessive production of Nitric Oxide (NO) which causes excessive vascular dilation and peroxynitrite free radical production
"Compensated" Shock mechanisms SNS activation - Epinephrine & NE increase HR and force, vasoconstriction: increased blood vol. & BP, renal water retention: increased blood vol. & BP (kidney low-flow state can lead to acute renal failure)
"Compensated" Shock Symptoms Narrow pulse pressure, tachycardia, fast & deep resp., decreased urine, increased urine specific gravity, cool & clammy skin, altered mentation, dilated pupils
"Progressive" Shock Compensatory mechanisms aren't enough, hypoxic injury starts. <BR> Lactic acidosis may occur & put burden on resp. and renal systems <BR> Vascular system starts to fail
"Progressive" Shcok Symptoms Low BP (<90mmHg), narrow pulse pressure, tachycardia, acute renal failure, decreased consciousness, increased resp. rate, metabolic and respiratory acidosis w/ hypoxemia
"Refractory" Shock When the patient becomes unresponsive to therapeutic interventions
Most important factors in determining adequate tissue oxygenation Cardiac Output, Arterial Oxygen Content, Distribution of Blood Flow
Cardiogenic Shock Severe dysfunction of the left, right, or both ventricles that results in inadequate cardiac pumping <BR> Primary Cause = MI <BR> Compensatory mechanisms make things worse for the heart
Cardiogenic Shock Treatment Goals Decrease myocardial oxygen demand <BR> Increase myocardial oxygen delivery <BR> Increase cardiac output <BR> This is hard to do b/c things that increase cardiac output tend to also increase myocardial oxygen demand
Cardiogenic Shock Pharmacotherapy <BR> Positive Inotropic Drugs - B-adrenergic receptor agonists NE - increases HR, contractility, and vasc. resistance <BR> dobutamine - increase contractility, decreases vasc. resistance <BR> Dopamine - Increases mesenteric and renal blood flow, increases contractility, HR, and vasc. resistance
Cardiogenic Shock Pharmacotherapy <BR> Positive Inotropic Drugs - Phosphodiesterase Inhibitor Milrinone <BR> Inhibit breakdown of cAMP leads to increased Ca ions in cell to increase contractility
Cardiogenic Shock Pharmacotherapy <BR> Vasodilators Nitroprusside & Nitroglycerin <BR> Used to decrease work load of the heart by decreasing afterload
Cardiogenic Shock Treatment <BR> Mechanical Assist Devices <BR> Itraaortic Balloon Counterpulsation Balloon in aorta just distal to left subclavian vein inflates on diastole and deflates in systole ... increases perfusion pressure to coronary arteries and reduces ventricular afterload
Hypovolemic Shock Definition Circulating blood vol is decreased by at least 1000mL and is inadequate to perfuse tissues <BR> May be result of external or internal loss
Categories of Hemorrhagic Shock <BR> Compensated Hemorrhage Compensated: up to 1000mL loss, CO maintained by compensation, vital signs normal
Categories of Hemorrhagic Shock <BR> Mild Hemorrhage Mild: 1000 - 1500mL lost, pt is anxious and restless, orthostatic hypotension, tachycardia, norm. resp., urine 20-30mL/hr
Categories of Hemorrhagic Shock <BR> Moderate Hemorrhage Moderate - 1500-2000mL lost, pt is anxious and confused, decreased BP w/ narrow pulse range, HR > 120bpm, resp. 30-40/min, 5-20mL/hr urine output, long capillary refill <BR>
Categories of Hemorrhagic Shock <BR> Severe Hemorrhage Severe - 2000mL or more lost, pt is lethargic, severe hypotension w/ narrow pulse pressure, HR > 140bpm, resp. really high, negligible urine output, prolonged capillary refill
Hypovolemic Shock - Treatment Control the blood loss <BR> Replace the lost fluid <BR> Use colloids to pull fluid into vasculature <BR> Crystalloids (esp. isotonic) <BR> Use blood products when there is anemia <BR> Use vasoconstrictor is BP remains low
Obstructive Shock - Definition Heart is prevented from pumping due to a mechanical obstruction to flow ... ventricle can't fill leads to reduced CO and symptoms of shock <BR> pulmonary embolism, cardiac tamponade, tension pneumothorax
Obstructive Shock - Treatments Identifying & removing obstruction <BR> Compensatory mechs. are harmful <BR>
Distributive Shock - Definition Excessive vasodilation leads to peripheral pooling of blood and hypovolemia <BR> Preload & SV not enough to perfuse brain and tissues <BR> Anaphylactic, neurogenic, and septic
Anaphylactic Shock - Definition Type 1: Antigen / IgE reaction; shock occurs when peripheral dilation is massive - blood vol. is normal, but sudden vascular enlargement causes blood to pool in periphery. Preload drops, CO decreases
Anaphylactic Shock - Treatment Airway management - tracheal intubation, ventilation, bronchodilators (epinephrine, aminophylline) <BR> circulatory support - IV fluid therapy to fill increased vasc. space, vasopressor to constrict and raise BP
Neurogenic Shock - Definition Often transitory <BR> From depression of vasomotor center or interruption of SNS <BR> Brain trauma, spinal cord trauma, high spinal anesthesia, drug OD <BR> Loss of SNS tone -> peripheral vasodilation and hypotension; body position is influencing facto
Septic Shock - Definition Microorganisms in blood stream cause shock when immunocompromised <BR> SIRS (systemic inflammatory response syndrome) - body's response is widespread inflammation <BR> Abnormal vasodilation, hypotension, tissue hypoxia due to maldistribution of bloodflo
Septic Shock - Symptoms First signs = high CO and warm extremities, diastolic BP falls due to decreased systemic vascular resistance & venous return, widened pulse pressure <BR> Later signs - decreased CO, organ ischemia, narrow pulse pressure, cool, clammy skin, acidosis
Septic Shock - Treatment Isotonic fluid administration to restore preload <BR> Inotropic treatment to increase CO <BR> Vasopressin <BR> Antibiotic therapy
Complications of Shock <BR> Acute Respiratory Distress Syndrome (ARDS) Mostly from septic shock <BR> refractory hypoxemia, decreased pulmonary compliance, pulmonary edema w/ norm. cardiac preload <BR> Inflammation makes pulmonary capillaries leaky and damages surfactant secreters which collapses alveoli
Disseminated Intravascular soagulation (DIC) Abnormal clot formation in microvasculature throughout the body leads to ischemic tissue damage and leaves pt at risk for bleeding
Created by: frolickinglizard