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Introduction Invasive Hemodynamic Monitoring Hemodynamic monitoring is necessary to assess and manage shock Information obtained through hemodynamic monitoring: ¾ Audis Bethea, Pharm.D. Assistant Professor Therapeutics IV January 21, 2004 Cardiovascular System ¾ ¾ ¾ Cardiovascular perfomance (right and left ventricular function) Changes in hemodynamic status and organ perfusion Pharmacologic and nonpharmacologic therapy Prognosis Hemodynamic monitoring supplements clinical judgment Determinants of Cardiovascular Function Vascular network of > 60,000 miles Cardiac output (CO) = Heart rate (HR) x Stroke volume (SV) Circulating 8 L of blood every day Volume of blood ejected from the left ventricle per unit time (L/min) Provides O2 to over 100 trillion cells ¾ ¾ Right side → unoxygenated blood to the lungs Left side → oxygenated blood systemically Vasculature ¾ ¾ ¾ Arteries carry blood away from the heart Veins carry blood to the heart Capillaries responsible for exchange of nutrients and gases ¾ ¾ HR is regulated by the sympathetic nervous system SV is the volume of blood ejected by the ventricles during systole Three factors influencing stroke volume ¾ ¾ ¾ Preload (LVEDV or LVEDP) → stretching of the LV muscle fibers after diastole Afterload (SVR) → force left ventricle has to overcome to eject blood Contractility (Inotropy) → force and velocity of muscular contraction Cardiac index (CI) → cardiac output adjusted for body surface area Determinants of Cardiovascular Function Preload ¾ Determines the strength of ventricular contraction Stroke volume ¾ Dependent upon EDV, pleural pressure, vascular compliance, and vascular resistance Contractility Hemodynamic Monitoring Non-invasive ¾ ¾ ¾ Vital signs → HR, BP, and RR Arterial oxygen saturation Transthoracic echocardiography Invasive ¾ ¾ ¾ ¾ Eliminates potential for error due to measurement technique Assessment is not inhibited in low-flow states Recommended for all ICU patients with cardiovascular instability In 50% of shock patients non-invasive methods underestimate BP by > 30 mmHg 1 Invasive Hemodynamic Monitoring Pulmonary Artery Catheter Arterial catheter ¾ ¾ ¾ Inserted into radial or brachial artery Used for hemodynamic monitoring MAP → driving pressure for peripheral blood flow Hemodynamic data ¾ MAP = [SBP + 2(DBP)] / 3 ¾ ¾ Central venous catheter ¾ Administration of IVF and medications Central Venous Pressure ¾ Assesses fluid status or volume ∆’s ¾ Volume status Ventricular function Oxygen delivery / consumption Fluid / medication administration CVP = RAP or RVEDP PA Catheter Hemodynamic Parameters Cardiac output (CO) → 4-7 L/min, Cardiac index (CI) → 2.4-4 L/min/m2 ¾ Assessment of cardiac function • Thermodilution → ∆ in temperature of blood after injection of cold H2O • Cardiac malformations / abnormalities may effect measurements Systemic vascular resistance (SVR) → 800 – 1400 dyne/sec/min-5 ¾ Vascular resistance across the entire systemic circulation Mean arterial pressure (MAP) → 80 – 100 mmHg ¾ PA Catheter Hemodynamic Parameters Pulmonary capillary wedge pressure (6 – 12 mmHg) ¾ ¾ Pulmonary artery pressure (20 – 30 mmHg) ¾ Driving pressure for peripheral blood flow Central venous pressure (CVP) → 1 - 6 mmHg ¾ Closest approximation of preload Objective method of evaluating left ventricular function • Elevated PCWP is often indicative of pulmonary edema Pressure produced by the right ventricle ejecting blood into the pulmonary artery • Elevated in patients with acute or chronic parenchymal pulmonary disease, PE, hypoxemia, acidosis, and patients receiving vasoactive drugs • ↓ pulmonary artery pressure occurs with diminished vascular volume Used to qualitatively assess fluid status or blood volume changes Systemic O2 Transport via PA Catheter Systemic O2 Transport via PA Catheter Oxygen consumption (Vo2) → 110 – 160 mL/min·m2 ¾ Estimates the oxygen demand of the body ¾ Vo2 is independent of supply except at low rates of Do2 and in critically ill patients Critically ill have an ↑ Vo2 resulting in O2 deprivation at normal rates of delivery O2 delivery (Do2) → 520 – 570 mL/min•m2 ¾ ¾ Product of CI and Cao2 Cao2 = Hemoglobin (Hgb) X arterial O2 (Sao2) Do2 = CI x 13.4 x Hgb x Sao2 Mixed venous O2 sat. (Svo2) → 70 – 75% ¾ ¾ Indicator of tissue perfusion Indicator of the body’s O2 consumption (Vo2) Vo2 = CI x 13.4 x Hb x (Sao2 – Svo2) ¾ Oxygen extraction ratio (O2ER) → 20 – 30% ¾ Calculation assesses the uptake of oxygen through the microcirculation (capillaries) O2ER = (Vo2 / Do2) x 100 2 Patient Case Complications of PA Catheters Infection Pulmonary infarction Pulmonary thrombosis Arrhythmias Intracardiac damage Pneumothorax Arterial-venous fistulas Pulmonary artery perforation 62 yo male admitted to the ICU following surgical repair of an abdominal aortic aneurysm. The patient is intubated and receiving 60% O2. He weights 78 kg and has a BSA of 1.8 m2. He has a history of HTN, (BP 140/100) for which he takes nadolol and HCTZ. His ABGs are adequate and he is receiving 150 mL/hr of LR solution intravenously. His 2-hour post-op and initial (in parentheses) hemodynamic profiles are as follows: BP 90/50 mmHg (130/78), MAP 63 mmHg (95), pulse 88 bpm (80), CO 4 L/min (5), PCWP 6 mmHg (12), SVR 1800 dyne·sec·cm-5 (1392), urine output 25 mL/hr (70), temperature 37oC (37), Hgb 8 g/dL (12). Based on the hemodynamic profile, determine the etiology of this patient’s cardiovascular failure. 1. What shock state is this patient experiencing? Hemodynamic Drugs Patient Case Answers tomorrow!! These medications are administered via continuous infusion Infusion rate (mL/min) = desired dose rate (R) = R drug concentration (C) C Therapeutic effects elicit vasoconstriction and increased CO Goal of therapy ¾ Adrenoreceptors Optimize MAP and/or CO → increasing tissue perfusion and O2 delivery Vasopressors and Inotropes: Norepinephrine Endogenous catecholamine Hemodynamic parameters ¾ ¾ ¾ ¾ Activates α and β1 receptors Dosing ¾ ¾ ¾ Cardiovascular effects ¾ ¾ Widespread vasoconstriction ↑ contractility and SV ↑ BP, HR ↑ PCWP, dose-dependent ↑ MAP, SVR, dose-dependent ↑ CO, mostly at lower doses 2 – 30 mcg/min; up to 200 mcg/min > 30 mcg/min ↑ risk of AE Severe acidosis ↓ effects Adverse effects ¾ HTN, ischemia, tachyarrhythmias 3 Vasopressors and Inotropes: Epinephrine Endogenous catecholamine Hemodynamic effects ¾ ¾ ¾ Activates α1, α2, β1, β2 receptors Dosing ¾ ¾ ¾ Cardiovascular effects ¾ ¾ Low dose: vasodilation and ↑ CO High dose: vasoconstriction and ↑ CO Low dose: ↑ HR, minor ↓BP and SVR High dose: ↑ HR, BP, PCWP, MAP, SVR ↑ CO throughout the dosing range Low dose → 0.01 – 0.05 mcg/kg/min High dose → > 0.05 mcg/kg/min Severe acidosis ↓ effects Adverse effects ¾ HTN, tissue ischemia, tachyarrhythmias Vasopressors and Inotropes: Phenylephrine Synthetic, non-catecholamine Selectively activates α1 receptors Cardiovascular effects ¾ ¾ ¾ ¾ ¾ ¾ ¾ ¾ ¾ ¾ Low dose: vasodilation Mid-dose: vasodilation, ↑ HR, contractility High dose: vasoconstriction, ↑ HR, contractility Mid-dose: ↑ HR, CO, mild ↓ MAP, SVR High dose: ↑ BP, HR, CO, PCWP, MAP, SVR Low dose → 0.5 – 3 mcg/kg/min Mid-dose → 3 – 10 mcg/kg/min High dose → 10 – 20 mcg/kg/min Moderate to severe acidosis ↓ effects Adverse effects ¾ ¾ HTN, ischemia, tachyarrhythmias Potential tachyphylaxis Vasopressors and Inotropes: Vasopressin Antidiuretic hormone (ADH) ¾ Physiologic activity ¾ ¾ ¾ ¾ ¾ ¾ Stimulates vascular V1 receptors Stimulation of renal V2 receptors ↓ HR, PCWP, CO ↑ BP, MAP, SVR Vasodilation due to acidosis Vasopressin reverses effects of acidosis Dosing Serum osmolality Vascular volume Hormones Alterations in serum Paco2 and Pao2 Cardiovascular effects Vasopressors and Inotropes: Vasopressin Hemodynamic effects ¾ Vasopressors and Inotropes: Dopamine Dosing ¾ ¾ HTN, tissue ischemia, reflex bradycardia Hemodynamic effects ¾ Cardiovascular effects 30 – 300 mcg/min Moderate acidosis ↓↓ effects Adverse effects Vasopressors and Inotropes: Dopamine Dose-dependent α1, α2, β1, β2, DA activity ↑ BP, ↑ PCWP, MAP, SVR Dosing ¾ Endogenous catecholamine Systemic vasoconstriction Hemodynamic effects ¾ ¾ ¾ 0.01 – 0.5 mcg/min > 0.04 mcg/min ↑ risk of AE Acidosis does not affect activity Adverse effects ¾ HTN, tissue ischemia, hypervolemia 4 Vasopressors and Inotropes: Dobutamine Synthetic catecholamine Hemodynamic effects ¾ ¾ β1, β2 w/ extremely weak α activity ¾ Phosphodiesterase inhibitor ↓ BP and SVR ↑ HR and CO Dosing ¾ Vasopressors and Inotropes: Milrinone Hemodynamic effects ¾ ¾ ↑ intracellular cAMP ↑ intracellular Ca++ Dosing (mcg/kg/min) ¾ ¾ 2 – 20 mcg/kg/min Severe acidosis may ↓ effects ¾ ¾ ¾ Cardiovascular effects ¾ ¾ ↑ in SV, HR β2 activity overcomes the minimal α activity resulting in vasodilation Adverse effects ¾ HTN, hypokalemia, tachyarrythmias ¾ Tachyphylaxis ¾ Cardiovascular effects ¾ ¾ ↑ intracellular Ca++, ↑ contractility ↑ cAMP promotes relaxation of smooth muscle tissue ↓ BP, PCWP, SVR ↑ HR, CO LD: 50 mcg/kg MD: 0.375 – 0.5 mcg/kg/min Adjust for renal dysfunction CrCl 30 – 50 mL/min → 0.33 – 0.43 CrCl 5 – 20 mL/min → 0.2 – 0.28 CrCl < 5 mL/min → not recommended Adverse effects ↓ BP, tachyarrhythmia, rare thrombocytopenia Preparation and Administration All admixtures are placed in 250 mL Vasopressin and milrinone are exceptions Dextrose 5% is preferred diluent Premix bags: Dopamine, dobutamine, and milrinone Central line infusion is preferred 5
