1 / 33

Vasoactive Drugs and Shock

Vasoactive Drugs and Shock. Philip Marcus, MD MPH. Shock. Acute, generalized, inadequate perfusion of critical organs Serious pathophysiologic consequences if continued Disturbed metabolic function at organ and cellular levels Disorder of cellular O 2 utilization Usually low-flow state

redford
Download Presentation

Vasoactive Drugs and Shock

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Vasoactive Drugs and Shock Philip Marcus, MD MPH

  2. Shock • Acute, generalized, inadequate perfusion of critical organs • Serious pathophysiologic consequences if continued • Disturbed metabolic function at organ and cellular levels • Disorder of cellular O2 utilization • Usually low-flow state • Maldistribution

  3. Shock • Clinical Manifestations • Hypotension • Oliguria • Acidosis • CNS dysfunction

  4. Physiologic Measurements • Pulmonary Capillary Wedge Pressure • Index of LV preload • Cardiac Output • Systemic Vascular Resistance • Index of LV afterload • Mixed Venous O2 saturation (SvO2) • O2 delivery = CO x caO2 • O2 consumption = CO x (caO2 – cvO2)

  5. Causes of Shock • Cardiogenic • Obstructive • Oligemic • Distributive

  6. Cardiogenic Shock • Arrhythmias • Cardiac mechanical factors • Regurgitant lesions • Obstructive lesions • LV outflow • LV inflow • Cardiomyopathies • Impaired LV contractility • Impaired LV compliance

  7. Obstructive Shock • Cardiac tamponade • Constrictive pericarditis • Pulmonary embolism

  8. Oligemic Shock • Hemorrhagic intravascular depletion • Nonhemorrhagic intravascular depletion • Vomiting • Diarrhea • Dehydration • Peritonitis • Pancreatitis • ascites

  9. Distributive Shock • Abnormal vascular volume distribution • Results from decreased regional vascular resistance • Etiologic factors • Sepsis, endotoxemia • Metabolic factors • Respiratory failure, renal failure, drug OD • Endocrinologic factors • Ketoacidosis, hyperosmolar state, hypothyroid • Neurologic factors • Anaphylaxis

  10. Low Preload Shock • Reduced PCWP • Reduced CO • Elevated SVR • Reduced svO2 • Treatment = Volume infusion Hemorrhage, solute loss

  11. Cardiac Dysfunction Shock • Elevated PCWP • Reduced CO • Elevated SVR • Reduced svO2 • Treatment • Inotropic agents • Vasodilators • Volume Systolic Failure: Ischemia, infarction Diastolic Failure: Tamponade Valve Dysfunction

  12. Low Afterload Shock • Reduced or Normal PCWP • Elevated CO • Reduced SVR • Elevated svO2 • Treatment • Volume infusion • Vasoconstrictors • ? Inotropic agents Sepsis, Anaphylaxis, Adrenal crisis, Toxic shock

  13. Combined Disorders • Normal PCWP • Reduced CO • Elevated SVR • Reduced svO2 • Treatment • Volume infusion, then • Inotropic agents Low preload & Cardiac Dysfunction

  14. Indications for Vasopressors • Decrease of > 30 mmHg from baseline systolic BP OR • Mean arterial pressure (MAP) < 60 mmHg when either condition results in end-organ dysfunction due to hypoperfusion. Hypovolemia must be corrected prior to institution of vasopressor therapy.

  15. Fundamental Concepts • One drug, many receptors • A given drug often has multiple effects because of actions upon more than one receptor • Dose-response curve • Many agents have dose-response curves • Primary adrenergic receptor subtype activated by the drug is dose-dependent • Direct vs. reflex actions

  16. Isoproterenol b1 + b2 activity • Positive Inotropic activity • Positive Chronotropic activity • Increased MVO2 • Increases CO, Decreases SVR • Increases systolic BP, decreases diastolic BP • Used in cardiac standstill and for profound bradyarrhythmias Use in hypotension limited to situations in which hypotension results from bradycardia; High affinity for β-2 receptors results in vasodilatation and a decrease in MAP

  17. Epinephrine • a1, b1 + b2 activity • Positive inotropic activity • Positive chronotropic activity • Constricts arterioles in skin, mucosa and splanchnic circulation • Increases systolic BP, decreases diastolic BP • Decreases SVR via dilatation of skeletal muscle vasculature • Enhances blood flow • Used primarily in cardiac standstill and hypotension following cardiac surgery α receptor induced vasoconstriction offset by β-2 receptor vasodilatation

  18. NorepinephrineLevarterenol • Peripheral vasoconstrictor • Arterial and venous • α adrenergic activity • Inotropic action • β-1 action • Reflex bradycardia may occur • Secondary to potent pressor activity

  19. NorepinephrineLevarterenol • Used in acute hypotensive states • Following sympathectomy • Following removal of pheochromocytoma • Spinal anesthesia • Septic shock • Extravasation • Necrosis and sloughing • Antidote…phentolamine

  20. Phenylephrine • Pure α-agonist • Elevates SVR • Causes reflex bradycardia • Equal effectiveness as norepinephrine • No chronotropic effects • No inotropic effects • Danger of extravasation

  21. Dopamine • Endogenous catecholamine • Acts directly on α and β1 receptors • Acts also on Dopamine receptors • Dose-dependent effects • Low-dose = dopaminergic effects • Medium-dose = β effects • Medium to high-dose = α and β effects • High-dose = α effects

  22. Dopamine • Dopaminergic effects • Vasodilatation of renal, mesenteric, coronary, splanchnic and cerebral vasculature • Natriuretic effects • Increases RBF and GFR • Induces redistribution of intrarenal blood flow to juxtamedullary nephrons • Direct tubular action • Increases urinary cAMP

  23. Dopamine • β1 actions • Inotropic effects • Increases CO • Less chronotropic effects than isoproterenol • Releases NE…further increases CO • α effects • Increases SVR • Increases MAP • Can reduce urine output • Dopaminergic receptors antagonized

  24. Dopamine • Rapid onset of action • 2 – 4 minutes • Rapid metabolism • t1/2 < 10 minutes • First-order kinetics • MAO + COMT

  25. Dopamine • Indications • Low cardiac output • Compromised renal function • Assure adequate filling pressures • Fluid administration • Use in conjunction with nitroprusside to inhibit vasoconstriction • Extravasation • Necrosis and sloughing • Nausea and vomiting often occur

  26. Dobutamine • Direct-acting catecholamine • Chemically related to dopamine • Principally stimulates β1 receptors within myocardium • INOTROPIC • Minimal chronotropic effects • No α or β2 effects • No dopaminergic effects

  27. Dobutamine

  28. Dobutamine • Increases contractility • Increases CO without tachycardia • No arrhythmogenic or vasodilatory effects • No vasoconstriction • Rapid onset of action • 1 – 2 minutes • Rapid metabolism • t ½ ~ 2-3 minutes • COMT

  29. Dobutamine • Useful in low cardiac output states • Acute and chronic heart failure without hypotension • Used in acute MI and following cardiac surgery • IHSS contraindication • Usual dose = 5-20 mcg/kg/min

  30. Dopexamine • Synthetic catecholamine • Used in Europe • Systemic and pulmonary vasodilator effects • Lesser agonist activity at Dopamine receptors (1/3 potency of dopamine) • Positive inotropic effect • Increases cerebral, renal and splanchnic blood flow • Augments CO in chronic LV dysfunction following CABG and acute MI with LV dysfunction

More Related