GEP - Shock Lecture Week 6 2009
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| Common denominator of all forms of shock | Impaired oxygen utilization by cells that disrupts function
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| 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
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| 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
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| "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)
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| "Compensated" Shock Symptoms | Narrow pulse pressure, tachycardia, fast & deep resp., decreased urine, increased urine specific gravity, cool & clammy skin, altered mentation, dilated pupils
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| "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
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| "Progressive" Shcok Symptoms | Low BP (<90mmHg), narrow pulse pressure, tachycardia, acute renal failure, decreased consciousness, increased resp. rate, metabolic and respiratory acidosis w/ hypoxemia
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| "Refractory" Shock | When the patient becomes unresponsive to therapeutic interventions
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| Most important factors in determining adequate tissue oxygenation | Cardiac Output, Arterial Oxygen Content, Distribution of Blood Flow
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| 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
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| 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
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| 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
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| 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
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| Cardiogenic Shock Pharmacotherapy <BR> Vasodilators | Nitroprusside & Nitroglycerin <BR>
Used to decrease work load of the heart by decreasing afterload
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| 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
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| 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
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| Categories of Hemorrhagic Shock <BR> Compensated Hemorrhage | Compensated: up to 1000mL loss, CO maintained by compensation, vital signs normal
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| 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
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| 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>
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| 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
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| 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
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| 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
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| Obstructive Shock - Treatments | Identifying & removing obstruction <BR>
Compensatory mechs. are harmful <BR>
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| 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
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| 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
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| 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
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| 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
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| 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
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| 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
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| Septic Shock - Treatment | Isotonic fluid administration to restore preload <BR>
Inotropic treatment to increase CO <BR>
Vasopressin <BR>
Antibiotic therapy
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| 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
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| Disseminated Intravascular soagulation (DIC) | Abnormal clot formation in microvasculature throughout the body leads to ischemic tissue damage and leaves pt at risk for bleeding
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