Shock/Hypotension

1. Shock/Hypotension Clinical Presentation and Pharmacological Treatment of Shock/Hypotension

2. Introduction • 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

3. Topics of Discussion • Clinical Presentation • Types of Circulatory Shock • Management of Shock • Inotropic Agents • Vasodilators

4. Shock • 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

5. SHOCK - DEFINITION • 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.

6. 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. MORTALITY FROM SHOCK • Septic Shock • 35 to 40% within one month • Cardiogenic Shock • 60 to 90% • Hypovolemic Shock • Highly variable

8. STAGES OF SHOCK • Preshock • Shock • 20 to 25 reduction of EBV • Fall in CI to <2.5 • Activation of mediators • End-organ dysfunction • 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

9. Determinants of Shock • 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

10. Pathophysiology of Shock • Shock develops with inadequate capillary perfusion by decreased Cardiac Output following heart attack (cardiogenic shock) or blood/volume loss (hypovolemic shock)

11. Mediators of Shock • Toxins • Endotoxins • Oligo- and polypeptides • Complement Factors • Opiods • TNF, Interleukins • Fatty Acid Derivatives • Arachidonic acid metabolites • Varia • Calcium

12. Main Classes of Shock • Hypovolemic Shock • Distributive Shock • Cardiogenic Shock • Obstructive Shock

13. Hypovolemic Shock • Hemorrhagic/Traumatic • Dehydrative • Burn

14. Distributive Shock • Septic • Anaphylactic/ Anaphylactoid • Neurogenic

15. Cardiogenic Shock • Myopathies • Infarction involving >40% of LV • Dilated cardiomyopathies • Myocardial depression of sepsis • Arrhythmias • Atrial fibrillation/flutter • Ventricular fibrillation • Bradyarrhythmias/Heart Block • Mechanical abnormalities • Valvular defects • Ventricular aneurysm

16. Obstructive Shock • Pulmonary Embolism • Cardiac Tamponade • Pneumothorax

17. Common Features of Shock • Hypotension • Systolic BP <90 mmHg • Drop systolic BP >40 mmHg • Cool, clammy skin • Oliguria • Objective measure of intravascular volume depletion • Change in Mental Status • Metabolic acidosis

18. Other Signs of Hypovolemia • Tachycardia • Orthostatic hypotension • Poor skin turgor • Absent axillary sweat • Dry mucous membranes

19. Management of Shock • 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

20. ShockInitial Diagnostic Steps • History and Physical • Laboratory • CBC • Coags • ABG’s • Biochemical profile • Lactate • EKG • Chest x-ray

21. ShockInitial Management • Venous access • Central venous catheter • Arterial catheter • EKG monitoring • Pulse oximetry • Hemodynamic support (MAP<60 mmHg) • Fluid Challenge • Vasopressors for patients unresponsive to fluids

22. 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

24. Hemodynamic Characteristics in Different Types of Shock /

25. 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: • Enhance CO through the use of inotropic agents • Increase SVR through the use of vasopressors

26. Effects of Inotropic Agents and Vasodilators 1 Drug Receptor CO SVR Dose Range 0 0 - (mg/kg/min)

27. Effects of Inotropic Agents and Vasodilators 2 Drug CO SVR Dose Range (mg/kg/min)

28. Dopamine An endogenous precursor of norepinephrine withmultiple 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) • Positive inotropic effects (1) • High Dose (>10 µg/kg/min) • a-actions (vasoconstriction)

29. Indications for Selected Vasoactive Drugs

30. Complications:Vasopressors and Inotropic Agents • Hypoperfusion • Dysrhythmias • Myocardial ischemia • Local effects • Skin necrosis • Hyperglycemia • Unique drug interactions/contraindications • Pheochromocytoma • Avoid dobutamine in the setting of IHSS • Patients receiving MAO Inhibitors

31. Reference Pharmacotherapy of Shock. In: The Pharmacologic Approach to the Critically Ill Patient, 3rd ed. Williams & Wilkins,1994, pp 1104 – 1121.