Chapter 20 Shock (Summer 2020) - PDF

Chapter Shock 20 Dr. Tashea S. Hillard, Associate Professor  ▪ Imbalance between oxygen supply and oxygen requirements at the cellular level ▪ Shock represents a diverse...

Chapter Shock 20 Dr. Tashea S. Hillard, Associate Professor  ▪ Imbalance between oxygen supply and oxygen requirements at the cellular level ▪ Shock represents a diverse group of life-threatening conditions. ▪ Common factor among all types of shock is PATHOGENESIS hypoperfusion and impaired cellular oxygen utilization. OF SHOCK ▪ Inadequate cellular oxygenation may result from ▪ decreased cardiac output. ▪ maldistribution of blood flow. ▪ reduced blood oxygen content. Copyright © 2019, Elsevier Inc. All rights reserved. 2 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 2 PATHOGENESIS OF SHOCK (CONT.) ▪ Causes ▪ Cardiogenic: inadequate cardiac output despite sufficient vascular volume ▪ Obstructive: circulatory blockage, such as a large pulmonary embolus or cardiac tamponade, disrupts cardiac output ▪ Hypovolemic: loss of blood volume as a result of hemorrhage or excessive loss of extracellular fluids ▪ Distributive: greatly expanded vascular space because of inappropriate vasodilation Copyright © 2019, Elsevier Inc. All rights reserved. 3 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 3 Impaired Tissue Oxygenation ▪ Impaired oxygen utilization by cells: disrupts function and, if ongoing or severe, may lead to cell death, organ dysfunction, and stimulation of inflammatory reactions ▪ Lack of oxygen causes several outcomes ▪ Production of lactate ▪ Failure of ion pumps leads to sodium and water accumulation in the cell (hydropic swelling). ▪ Formation of oxygen radicals ▪ Induction of inflammatory cytokines PATHOGENESIS OF SHOCK (CONT.) Copyright © 2019, Elsevier Inc. All rights reserved. 4 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 4  Impaired Tissue Oxygenation ▪ Results in cellular hypoxia, which causes PATHOGENESIS ▪ anaerobic metabolism. ▪ free radical production. OF SHOCK ▪ macrophage induction. (CONT.) ▪ Reperfusion injury: ischemic cells may produce oxygen-free radicals when oxygen supplies are restored Copyright © 2019, Elsevier Inc. All rights reserved. 5 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 5 PATHOGENESIS OF SHOCK (CONT.) Impaired Tissue Oxygenation ▪ Tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) cytokines: increase in septic shock and are thought to be important mediators of vascular failure and progressive organ damage ▪ Increase activity of inducible nitric oxide (NO) synthase leading to excess NO ▪ Failure of microcirculation to autoregulate blood flow leads to activation of coagulation. ▪ Leads to oxygen debt in the tissues Copyright © 2019, Elsevier Inc. All rights reserved. 6 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 6  Compensatory Mechanisms and Stages of Shock ▪ Three clinical stages: compensated shock, progressive shock, and refractory shock PATHOGENESIS ▪ Compensatory stage: homeostatic OF SHOCK mechanisms are sufficient to maintain adequate tissue perfusion despite a (CONT.) reduction in CO ▪ SNS activation attempts to maintain blood pressure even though CO has fallen. ▪ Increased CO and vascular resistance Copyright © 2019, Elsevier Inc. All rights reserved. 7 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 7 PATHOGENESIS OF SHOCK (CONT.) Compensatory Mechanisms and Stages of Shock ▪ Progressive stage of shock is marked by hypotension and marked tissue hypoxia. ▪ Lactate production increases with anaerobic metabolism. ▪ Lack of ATP leads to cellular swelling, dysfunction, and death. ▪ Cellular and organ dysfunction result from oxygen-free radicals, release of inflammatory cytokines, and activation of the clotting cascade. Copyright © 2019, Elsevier Inc. All rights reserved. 8 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 8 9  Cardiogenic Shock Usually the result of severe TYPES OF ventricular dysfunction SHOCK associated with MI Diagnostic features: Elevated left ventricular Pulmonary Decreased CO end-diastolic S3 heart sounds edema pressure (preload) Copyright © 2019, Elsevier Inc. All rights reserved. 10 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 10 Cardiogenic Shock ▪ Low CO = reduced oxygen delivery to tissues = higher oxygen extraction = low SvO2 ▪ Therapy aimed at improving CO and myocardial oxygen delivery, decreasing workload ▪ Inotropic, preload reducing, and afterload reducing agents ▪ Intraaortic balloon counterpulsation, ventricular assist devices, heart transplantation TYPES OF SHOCK (CONT.) Copyright © 2019, Elsevier Inc. All rights reserved. 11 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 11 TYPES OF SHOCK (CONT.) Obstructive Shock ▪ Results from mechanical obstructions that prevent effective cardiac filling and stroke volume ▪ Common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. ▪ Manifests as right-sided heart failure ▪ Rapid management of underlying obstruction is required to prevent cardiovascular collapse. Copyright © 2019, Elsevier Inc. All rights reserved. 12 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 12 TYPES OF SHOCK (CONT.) Hypovolemic Shock Results from inadequate circulation blood volume precipitated by External hemorrhage: most common cause hemorrhage, burns, or leakage of fluid into interstitial spaces Low CO and intracardiac pressures (low preload) lead to SNS activation = elevated HR, vasoconstriction, increased contractility. Copyright © 2019, Elsevier Inc. All rights reserved. 13 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 13  Hypovolemic Shock ▪ Severity of symptoms correlates with amount of blood loss. ▪ Four classes: I (15% loss), II (15% to 30%), TYPES OF III (30% to 40%), IV (>40%) ▪ Therapy is aimed at fluid replacement and SHOCK controlling the source of volume loss. (CONT.) ▪ Colloids: increase serum colloid osmotic pressure ▪ Crystalloids: solutions that contain electrolytes ▪ Blood products Copyright © 2019, Elsevier Inc. All rights reserved. 14 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 14 TYPES OF SHOCK (CONT.) Distributive Shock ▪ Characterized by excessive vasodilation and peripheral pooling of blood ▪ CO inadequate because of reduced preload ▪ Types include: ▪ Anaphylactic shock ▪ Neurogenic shock ▪ Septic shock Copyright © 2019, Elsevier Inc. All rights reserved. 15 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 15  Anaphylactic Shock ▪ Result of excessive mast cell degranulation mediated by IgE antibodies in response to TYPES OF antigen ▪ Mast cells release vasodilatory mediators SHOCK resulting in severe hypotension. (CONT.) ▪ Causes: ▪ Antibiotic therapy, in particular β-lactams, peanuts and tree nuts, insect stings, and snake bites Copyright © 2019, Elsevier Inc. All rights reserved. 16 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 16 Anaphylactic Shock ▪ Clinical symptoms include: ▪ Urticaria ▪ Bronchoconstriction ▪ Stridor ▪ Angioedema ▪ Wheezing ▪ Itching ▪ Treatment includes maintenance of airway patency, use of epinephrine, bronchodilators, antihistamines, vasopressors, and IV fluids. TYPES OF SHOCK (CONT.) Copyright © 2019, Elsevier Inc. All rights reserved. 17 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 17  Neurogenic Shock ▪ Results from loss of sympathetic activation TYPES OF of arteriolar smooth muscle ▪ Causes include medullary depression (brain SHOCK injury, drug overdose) or lesions of sympathetic nerve fibers (spinal cord injury) (CONT.) ▪ Treatment includes vasopressors, fluids, elevation of the legs, slow position changes, and the use of pressure stockings on the legs. Copyright © 2019, Elsevier Inc. All rights reserved. 18 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 18 TYPES OF SHOCK (CONT.) Septic Shock ▪ Results from severe systemic inflammatory response to infection ▪ Body’s response to infection or other insults results in systemic signs and symptoms of widespread inflammation: systemic inflammatory response syndrome (SIRS) ▪ Common causes: ▪ Gram-negative and gram-positive bacteria, fungal infections ▪ Gram-negative shock: endotoxins in bacterial cell walls stimulate massive immune system activation Copyright © 2019, Elsevier Inc. All rights reserved. 19 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 19  Septic Shock ▪ Characterized by release of immune mediators resulting in widespread TYPES OF inflammation ▪ Clotting cascade, complement system, and SHOCK kinin system are activated ▪ Widespread inflammation leads to profound (CONT.) peripheral vasodilation with hypotension, maldistribution of blood flow with cellular hypoxia, and increased capillary permeability with edema formation. Copyright © 2019, Elsevier Inc. All rights reserved. 20 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 20 Septic Shock ▪ Initially characterized by high CO resulting from sympathetic activation of the heart and warm extremities ▪ Even though CO is high, cellular hypoxia is present. ▪ Reduced cellular oxygen utilization is manifested as high SvO2. ▪ Can deteriorate to a hypodynamic phase ▪ Decreased CO and organ ischemia TYPES OF SHOCK (CONT.) Copyright © 2019, Elsevier Inc. All rights reserved. 21 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 21 TYPES OF SHOCK (CONT.) Septic Shock ▪ Therapy aimed at improving the distribution of blood flow and managing infection with antibiotics ▪ Administration of fluids and drugs to improve cardiac and vascular performance to improve distribution of blood flow Copyright © 2019, Elsevier Inc. All rights reserved. 22 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 22 ▪ Helpful for assessing CO, volume status, and oxygen delivery and consumption ▪ Right atrial pressure, pulmonary artery pressure, and left atrial pressure monitored ▪ Used to guide management of cardiac preload, afterload, and contractility to optimize CO and minimize workload ASSESSMENT AND HEMODYNAMIC MONITORING Copyright © 2019, Elsevier Inc. All rights reserved. 23 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 23  Cardiac Output ASSESSMENT ▪ Preload—amount of blood in the ventricle at AND the end of diastole ▪ Afterload—aortic impedance that the left HEMODYNAMIC ventricle must overcome to eject blood MONITORING during systole (CONT.) ▪ Contractility—inherent state of activation of cardiac muscle fibers Copyright © 2019, Elsevier Inc. All rights reserved. 24 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 24 Arterial Oxygen Content Oxygen delivery (DO2) ASSESSMENT AND Oxygen consumption (VO2) HEMODYNAMIC MONITORING Normally 25% of oxygen in arterial blood (CONT.) is extracted from tissues, so mixed venous oxygen saturation is 75%. Low CO results in greater oxygen extraction and lower SVO2. Maldistribution of flow results in less oxygen extraction and higher SVO2. Copyright © 2019, Elsevier Inc. All rights reserved. 25 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 25  Hemodynamic Monitoring ▪ Pulmonary artery catheter inserted via ASSESSMENT jugular or subclavian vein allows AND measurement of intracardiac pressures, CO, and SVO2. HEMODYNAMIC ▪ Right atrial pressure is used to manage blood MONITORING volume (right preload). (CONT.) ▪ Left atrial pressure is important because it indicates left ventricular preload. Copyright © 2019, Elsevier Inc. All rights reserved. 26 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 26 HEMODYNAMI PULMONARY PULMONARY PULMONARY C PRESSURE IS ARTERY CAPILLARY MONITORING USED TO DIASTOLIC OCCLUSION DETECT PRESSURE PRESSURE IS A PULMONARY REFLECTS LEFT DIRECT COMPLICATION PRELOAD. MEASURE OF S. LEFT ATRIAL PRESSURE. ASSESSMENT AND HEMODYNAMIC MONITORING (CONT.) Copyright © 2019, Elsevier Inc. All rights reserved. 27 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 27  SHOCK STATES COMPLICATIO RESULT IN NS ARE REDUCED OR INFLAMMATOR INADEQUATE Y IN NATURE. CELLULAR OXYGEN CONSUMPTION AND MAY AFFECT ALL ORGANS AND SYSTEMS OF THE BODY. COMPLICATIONS OF SHOCK Copyright © 2019, Elsevier Inc. All rights reserved. 28 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 28 COMPLICATIONS OF SHOCK (CONT.) ▪ Inflammatory cytokines: mediate organ damage by altering metabolism, recruiting neutrophils, initiating the coagulation cascade, and altering capillary permeability Copyright © 2019, Elsevier Inc. All rights reserved. 29 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 29  Acute Respiratory Distress Syndrome (ARDS) COMPLICATIONS ▪ Most commonly associated with septic shock ▪ Development of refractory hypoxemia, OF SHOCK decreased pulmonary compliance, and (CONT.) radiographic evidence of pulmonary edema ▪ Primary cause of death in ARDS: multiple organ failure, not severe hypoxemia Copyright © 2019, Elsevier Inc. All rights reserved. 30 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 30  Acute Respiratory Distress Syndrome (ARDS) ▪ Neutrophils release proteolytic enzymes, produce oxygen-free radicals, and secrete COMPLICATIONS inflammatory chemicals that make pulmonary capillaries leaky. OF SHOCK ▪ Exudate leaks into the interstitial spaces (CONT.) and alveoli of the lung, where it interferes with pulmonary gas exchange. ▪ Inflammation may also damage type II pneumocytes, which normally produce surfactant. Copyright © 2019, Elsevier Inc. All rights reserved. 31 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 31 COMPLICATIONS OF SHOCK (CONT.) Disseminated Intravascular Coagulation ▪ Usually occurs in septic shock ▪ Immune activation of the clotting cascade ▪ Microcirculation obstructions lead to ischemic tissue damage. ▪ Widespread clot formation consumes platelets and clotting factors. ▪ Platelet count and fibrinogen levels are low, fibrin degradation products (D-dimer) are elevated. Copyright © 2019, Elsevier Inc. All rights reserved. 32 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 32 Acute Renal Failure Kidneys undergo long periods of hypoperfusion. COMPLICATIONS Vasoconstriction causes decreased glomerular blood flow—reduced OF SHOCK (CONT.) hydrostatic pressure and filtration rates. Acute tubular necrosis (ATN) associated with decreased urinary excretion of waste products (creatinine and urea) May need dialysis Copyright © 2019, Elsevier Inc. All rights reserved. 33 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 33 COMPLICATIONS OF SHOCK (CONT.) Multiple Organ Dysfunction Syndrome (MODS) ▪ When 2 or more systems are affected ▪ Most common causes of secondary MODS: sepsis and septic shock ▪ Initiated by immune mechanisms that are overactive and destructive ▪ Cytokines affect endothelium, recruit neutrophils, and activate inflammation in vascular beds leading to tissue destruction and organ dysfunction. Copyright © 2019, Elsevier Inc. All rights reserved. 34 Copyright © 2013, 2010, 2005 by Saunders, an imprint of Elsevier Inc. 34