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Hemodynamic Monitoring Goal: maintain an adequate preload while keeping afterload to a minimum Heart rate Blood pressure Cardiac output Stroke volume Description If HR ↑ too much, SV may be compromised due to inadequate time for ventricle filling; myocardial O2 demand may be enhanced BP/MAP = CO x SVR = HR x SV x SVR CO = HR x SV Echo – gives EF Lactate ↑ in anaerobic Central venous catheter should show ScvO2 of 70-80% 4 factors that affect SV: 1. Diastolic filling pressure (preload) 2. Distensibility of ventricle 3. Mycoardial contractility 4. Aortic pressure (afterload) Pulse pressure parallels stroke volume Total systemic vascular resistance Pulmonary vascular resistance Mixed venous O2 saturation (SvO2) Mean arterial pressure (MAP) Central venous pressure (CVP) Pulmonary artery systolic pressure Normal Values 60-100 bpm 90-140/60-90 4-8 L/min CI: 2.5-4 L/min/m2 60-70 mL/beat 900-1200 absolute units 150-250 absolute units High (80-95%) – high O2 delivery; low O2 demand/ inability of tissues to extract O2 due to hypothermia, sepsis Low (< 60%) – low O2 delivery due to anemia, hypoV, hypoxemia, low CO; high O2 demand due to hyperthermia, shivering, sz, pain, anxiety (SBP + 2DBP)/3 Measured with arterial line that sits in radial, femoral or pedial artery Pressure in the right atrium At the end of diastole, when tricuspid valve is open (RA & RV are 1 chamber), CVP = pressure in RV good indicator of RV function ↓ - hypovolemia from fluid imbalance, hemorrhage, extreme vasodilation ↑ - hypervolemia Problems in right heart have most direct influence on CVP Pressure ↑ in pulmonary circulation (dz, embolism) will affect CVP less directly **doesn’t provide direct clues to left heart function **changes show up later than in PADP and PCWP Reflects pressure in the right ventricle Pressure in PA when RV is contracting reflects RV 60-80% > 65 mm Hg 0-5 mm Hg Positive ventilator: 8-12 20-30 mm Hg (PASP) Pulmonary artery diastolic pressure (PADP) Pulmonary capillary wedge pressure (PCWP) Right ventricular pressure Left atrial pressure Left ventricular pressure Urine output function Reflects pressure in the left ventricle at end of diastole **isn’t always most accurate indicator of left-heart function b/c pulmonary pressures & LV pressures influence it; only accurately mirrors if no significant pulmonary dz **can be used alone to monitor left heart function except if obstructive pulmonary dz, PE (↑ PADP > PCWP) Direct indicator of left ventricle pressure Most accurate indication of left-heart function 7-12 mm Hg 8-12 mm Hg 20-30 mm Hg (systolic) 0-5 mm Hg (diastolic) 2-7 mm Hg 90-140 mm Hg (syst) 2-7 mm Hg (diast) 0.5 mL/kg/hr During systole – pulmonic and aortic valves are open; tricuspid and mitral valves closed During diastole – tricuspid and mitral valves open; pulmonic and aortic valves closed Receptors α1 – smooth muscle vasoconstriction; increased cardiac contractility α2 – post-synaptic; vasodilation by NO production β1 – positive chronotrope (increases HR via increased SA nodal conduction) and inotrope (increases contractility via increased automaticity and conduction of ventricular cardiac muscle and increased AV nodal conduction) β2 – vasodilation; mild chronotropic and inotropic improvements D4 – increases CO by improving myocardial contractility and at certain doses increases HR D1/2 – kidneys; stimulate diuresis D1/2/4/5 – pulmonary; vasorelaxive effects Vasopressin – peptide hormone; antidiuretic hormone; regulates body’s retention of water; released when body is dehydrated, causing kidneys to conserve water (not salt), concentrating the urine and reducing urine volume; increases BP by inducing moderate vasoconstriction through V1 stimulation in peripheral arterioles Alpha agonists cause vascular constriction Beta agonists increase CO by increasing HR in SA node, increasing atrial cardiac muscle contractility, increasing contractility and automaticity of ventricular cardiac muscles and AV node VASST Trial Vasopression vs. NE in septic shock Only patients with previous administration of low-dosage NE demonstrated improved survival with vasopressin In general, no survival benefit with vasopressin over NE Drug Dobutamine Dopamine Epinephrine Norepinephrine Effects β1 agonist properties mainly = ↑ CO by ↑ inotrope β2 = vasodilation; systemic/pulm. vascular resistance DOC for cardiogenic shock w/ low CO and ↑ afterload Dose 1: ↑ CO by ↑ inotrope (minimal); renal and visceral vasodilation Dose 2: ↑ SVR/CO by ↑ inotrope/HR Dose 3: ↑ SVR Used as vasoconstrictor in vasodilatory shock Used as inotrope in low CO **Indicated in vasodilatory shock with bradycardia ↑ SVR at high doses (alpha > beta) ↑ CO by ↑ inotrope/HR at low doses Low dose: primarily β 1st line catecholamine in cardiopulmonary resuscitation & anaphylactic shock 2nd line vasopressor and inotrope ↑↑ SVR (arterial and vasoconstriction) from alpha Inotropic effects offset by increases in afterload ADRs CVS: ↑ HR, BP LYTE: hypoK Tachyarrhythmias, AF Ischemic gut; ischemic peripherals Monitor pulmonary fxn, HR, BP, site of infusion for blanching/extravasation CNS: Tremor, weakness HEENT: ocular irritation RESP: pulmonary edema/HTN CVS: tachyarrhythmia, MI GI: lactic acidosis ENDO: hyperglycemia (due to hypermetabolism, suppression of insulin release and glycolysis) CVS: peripheral ischemia; MI DERM: skin necrosis Increases MAP, effective circulating blood volume, venous return/preload, with minimal increase of HR or SV Phenylephrine Vasopressin Milrinone More potent than dopamine; associated with some survival benefit in septic shock vs. dopamine and epi 1st line for distributive shock ↑↑ in SVR Used temporarily to restore MAP, SVR and CVP in hypoT w/ vasodilation and adequate CO ↑↑ SVR CO and redistribute CO to hepatosplanchnic microcirculation ↑ CO by PDE5 inhibition mobilize intracellular Ca 2nd line in cardiogenic shock CNS: tremor, weakness CVS: ischemia; reflex bradycardia DERM: extravasation CVS: MI, venous thrombosis GI: mesenteric ischemia DERM: ischemic skin lesions, circumoral pallor; diaphoresis CVS: ventricular arrhythmia