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Shock/Hypotension Clinical Presentation and Pharmacological Treatment of Shock/Hypotension 7/17/2015 1 Introduction 7/17/2015 Review the current view on clinical presentation and management of shock with emphasis on pharmacotherapy. O. D. Polk, Jr., M.D. Assistant Professor of Medicine Pulmonary Critical Care Medicine 2 Topics of Discussion Clinical Presentation Types of Circulatory Shock Management of Shock Inotropic Agents Vasodilators 7/17/2015 3 Shock 7/17/2015 Term “choc” – French for “push” or impact was first published in 1743 by the physician LeDran Belief – symptoms arose from fear or some other form of altered cerebral function Crile in 1899 showed that replacement of blood volume decreased mortality experimentally 4 SHOCK - DEFINITION 7/17/2015 A profound and widespread reduction in the effective delivery of oxygen and other nutrients to tissues leads first to reversible and then, if prolonged, to irreversible cellular injury. 5 SHOCK-NEW CONCEPTS Shock is probably the most common and important problem in critical care medicine. Cardiogenic shock represents one of the most important complications of IHD, the number one cause of mortality in the US. Hypovolemic and/or extracardiac obstructive shock are major contributors to trauma-associated morbidity and mortality. Septic shock is the 13th most frequent cause of death in the US. Shock causes or contributes to multiple organ dysfunction syndrome (MODS), organ failure, and death. Parillo JE 1999 7/17/2015 6 MORTALITY FROM SHOCK Septic Shock Cardiogenic Shock 60 to 90% Hypovolemic Shock 7/17/2015 35 to 40% within one month Highly variable 7 STAGES OF SHOCK Preshock Shock End-organ dysfunction 7/17/2015 20 to 25 reduction of EBV Fall in CI to <2.5 Activation of mediators Urine output decline Restlessness evolves into agitation, obtundation, and coma Acidosis further decreases CO and alters cellular metabolic processes Multiple organ system failure proceeds to cause the demise of the patient 8 Determinants of Shock 7/17/2015 Inadequate tissue perfusion Sustained loss of effective circulatory blood volume Breakdown of cellular metabolism and microcirculatory homeostasis Hypoperfusion of peripheral tissue that leads to a diminutive transcapillary exchange function Disproportion between VO2 and DO2 9 Pathophysiology of Shock 7/17/2015 Shock develops with inadequate capillary perfusion by decreased Cardiac Output following heart attack (cardiogenic shock) or blood/volume loss (hypovolemic shock) 10 Mediators of Shock Toxins Oligo- and polypeptides Arachidonic acid metabolites Varia 7/17/2015 Complement Factors Opiods TNF, Interleukins Fatty Acid Derivatives Endotoxins Calcium 11 Main Classes of Shock 7/17/2015 Hypovolemic Shock Distributive Shock Cardiogenic Shock Obstructive Shock 12 Hypovolemic Shock 7/17/2015 Hemorrhagic/Traumatic Dehydrative Burn 13 Distributive Shock 7/17/2015 Septic Anaphylactic/ Anaphylactoid Neurogenic 14 Cardiogenic Shock Myopathies Arrhythmias Atrial fibrillation/flutter Ventricular fibrillation Bradyarrhythmias/Heart Block Mechanical abnormalities 7/17/2015 Infarction involving >40% of LV Dilated cardiomyopathies Myocardial depression of sepsis Valvular defects Ventricular aneurysm 15 Obstructive Shock 7/17/2015 Pulmonary Embolism Cardiac Tamponade Pneumothorax 16 Common Features of Shock Hypotension Systolic BP <90 mmHg Drop systolic BP >40 mmHg Cool, clammy skin Oliguria 7/17/2015 Objective measure of intravascular volume depletion Change in Mental Status Metabolic acidosis 17 Other Signs of Hypovolemia 7/17/2015 Tachycardia Orthostatic hypotension Poor skin turgor Absent axillary sweat Dry mucous membranes 18 Management of Shock 7/17/2015 Shock begins when DO2 (delivery of oxygen) to the cells is inadequate to meet metabolic demand The major therapeutic goals in shock therefore are sufficient tissue perfusion and oxygenation Early diagnosis remains a major problem 19 Shock Initial Diagnostic Steps History and Physical Laboratory CBC Coags ABG’s Biochemical profile Lactate 7/17/2015 EKG Chest x-ray 20 Shock Initial Management Venous access Central venous catheter Arterial catheter EKG monitoring Pulse oximetry Hemodynamic support (MAP<60 mmHg) 7/17/2015 Fluid Challenge Vasopressors for patients unresponsive to fluids 21 Complicated Shock Pulmonary Artery Catheterization done to measure Cardiac output Filling pressures Echocardiography done to look at Pericardial fluid Cardiac function (non-invasively) Valve or shunt abnormalities 7/17/2015 22 7/17/2015 23 Hemodynamic Characteristics in Different Types of Shock Type Preload CO PVR SVR Hemmorrhagic Anaphylactic / Cardiogenic Septic (Hyperdynamic) Septic (Hypodynamic) 7/17/2015 24 Inotropic Agents and Vasodilators Vasoactive drugs are an important pharmacologic defense in the treatment of shock. May be required to support BP in the early stages of shock. These agents may be needed to: 7/17/2015 Enhance CO through the use of inotropic agents Increase SVR through the use of vasopressors 25 Effects of Inotropic 1 Agents and Vasodilators Drug Epinephrine Receptor CO , b1, (b2) Norepinephrine , b1 SVR Dose Range 2-10 µg/min 0- 2-20 µg/min Dopamine b1, DR, () 1 - 30 Dobutamine b1, b2 2 - 20 Phenylphrine Vasopressin Angiotensin III Amrinone PDI 7/17/2015 0 0- 20-200µg/min 5 - 20 2 -15 (mg/kg/min) 26 Effects of Inotropic 2 Agents and Vasodilators Drug CO SVR Dose Range Nifedipine 0- 0.5 - 10 Nitroglycerin 0- 3-5 Nitroprusside 0- 0.5 - 5 Prostacyclin 10 - 40 (mg/kg/min) 7/17/2015 27 Dopamine An endogenous precursor of norepinephrine with multiple dose-related effects Low Dose (0.5 - 3 µg/kg/min) Predominantly dopaminergic (DR) effects Enhanced blood flow to renal and splanchnic beds Moderate Dose (5 -10 µg/kg/min) High Dose (>10 µg/kg/min) 7/17/2015 Positive inotropic effects (b1) -actions (vasoconstriction) 28 Indications for Selected Vasoactive Drugs 7/17/2015 DRUG Common Uses Phenylephrine Septic Shock, neurogenic shock, PAIH Norepinephrine Septic shock Epinephrine Anaphylaxis, ACLS, septic shock Dopamine Renal Insufficeny, septic shock, cardiogenic shock Dobutamine Cardiogenic shock (CS) Isoproterenol CS with bradycardia due to heartblock, effects HR Milrinone Cardiogenic shock- in those who don’t respond29 Complications: Vasopressors and Inotropic Agents Hypoperfusion Dysrhythmias Myocardial ischemia Local effects Hyperglycemia Unique drug interactions/contraindications 7/17/2015 Skin necrosis Pheochromocytoma Avoid dobutamine in the setting of IHSS Patients receiving MAO Inhibitors 30 Reference Pharmacotherapy of Shock. In: The Pharmacologic Approach to the Critically Ill Patient, 3rd ed. Williams & Wilkins,1994, pp 1104 – 1121. 7/17/2015 31