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GEP - Shock
GEP - Shock Lecture Week 6 2009
| Question | Answer |
|---|---|
| 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
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