Hemodynamic Monitoring Jessica Owen CCRN Objectives Verbalizes purposes

Hemodynamic Monitoring Jessica Owen CCRN

Objectives ▪ Verbalizes purposes of Hemodynamic Monitoring ▪ Verbalize indications for Hemodynamic Monitoring ▪ Identify components of a Pulmonary Artery Catheter ▪ Identify the correct pressure waveforms ▪ Identify the components of invasive hemodynamic monitoring ▪ Identify “normal” parameters for each component of monitoring ▪ Verbalize how to troubleshoot abnormal waveforms ▪ Verbalize definition of preload and afterload

Definitions and Principles • The measurement and interpretation of biological systems that describe performance of the cardiovascular system • Monitoring is NOT therapy • Clinicians must know how to interpret the data

Purpose of Hemodynamic Monitoring ▪ Evaluate the cardiovascular system ▪ Establish baseline values and evaluate trends – Single hemodynamic values are rarely significant. Look at trends!! ▪ Implement and guide interventions early to prevent problems

Hemodynamic Monitoring Components ▪ Heart Rate ▪ Blood Pressure and MAP ▪ CVP ▪ Pulmonary Artery Pressures ▪ Systemic Vascular Pressure (SVR) ▪ Pulmonary Vascular Pressure (PVR) ▪ Cardiac Output/ Cardiac Index ▪ Stroke Volume

Cardiac Output (L/min) = Heart Rate (beats/min) x Stroke Volume (ml/beat) Preload Contractility Afterload

Comparing Hemodynamics to an IV Pump • Fluid = Preload • Pump = Contractility (needs electricity) • Tubing = Afterload

Preload • Is the degree of muscle fiber stretching present in the ventricles right before systole • Is the amount of blood in a ventricle before it contracts; also known as “filling pressures” • Left ventricular preload is reflected by the PCWP • Right ventricular preload is reflected by the CVP

Cardiac Output reflects contractility if preload and afterload are optimized. Cardiac Index is the cardiac output adjusted for body surface area (BSI).

Afterload • Any resistance against which the ventricles must pump in order to eject its volume • How hard the heart [either side left or right] has to push to get the blood out • Also thought of as the “ resistance to flow” or how “clamped” the blood vessels are • SVR = Left ventricular afterload • PVR = Right ventricular afterload

Non-Invasive Hemodynamic Monitoring = Clinical Assessment and NBP Base Line Data q q q General appearance Level of consciousness Skin color/temperature Vital signs Peripheral pulses Urine output Base line data should correspond with data obtained from technology (i. e. ECG, ABP, CVP)

Limitations of Non- Invasive Blood Pressure Limitations of NBP ▪ Cuff must be placed correctly and must be appropriate size ▪ Auscultatory method is very inaccurate – Korotkoff sounds difficult to hear – Significant underestimation in low-flow (i. e. shock) states § Oscillometric measurements also commonly inaccurate (> 5 mm Hg off directly recorded pressures)

Indications for Arterial Blood Pressure • Frequent titration of vasoactive drips • Unstable blood pressures • Frequent ABGs or labs • Unable to obtain Non-invasive BP

Complications of Arterial Catheterization • • • Hemorrhage Hematoma Thrombosis Proximal or distal embolization Pseudoaneurysm Infection

Arterial Pressure Tracing

Waveform & Relationship to Cardiac Cycle

Waveform Distortion

Leveling and Zeroing • Leveling ü Before/after insertion ü After patient, bed or transducer move ü Aligns transducer with catheter tip • Zeroing ü Performed before insertion & readings • Level and zero transducer at the phlebostatic axis ü 4 th intercostal space, mid-axillary line ü Level of the atria

Dynamic Flush Dynamic flush ensures the integrity of the pressure tubing system. Notice how it ascends – forms a square pattern – and bounces below the baseline before returning to the original waveform. Check dynamic flush after zeroing any pressure system.

Central Venous Pressure • CVP is a direct measurement of right ventricular end diastolic • • • volume. Assesses § Intravascular volume status § Right ventricular function § Patients response to drugs &/or fluids Central line or pulmonary artery catheter Normal value = 2 -8 mm. Hg Low CVP = hypovolemia or ↓ venous return High CVP = over hydration, ↑ venous return, or right-sided heart failure Always read CVP at end expiration

The Pulmonary Artery Catheter

PA Insertion Waves

PA Insertion Waves

Right Ventricular Waveform • If the swan gets pulled back into the RV it is considered a swan emergency. • If you see an RV waveform (looks like VT) pull the swan immediately. • If the swan remains in the RV it may cause the patient to go into VT.

Complications of Pulmonary Artery Catheterization • General central line complications § Pneumothorax § Arterial injury § Infection § Embolization • Inability to place PAC into PA • Arrhythmias (heart block) • Pulmonary artery rupture

Components of PA Catheter (A. K. A. Swan-Ganz) • Proximal port – (Blue) used to measure central venous pressure/RAP and injection port for measurement of cardiac output • Distal port – (Yellow) used to measure pulmonary artery pressure and sample mixed venous blood • Balloon port – (Red) used to determine pulmonary wedge pressure • Thermistor lumen port near distal tip - monitors core temperature and thermodilution method of measuring CO

Normal Hemodynamic Values Mean Arterial Pressure (MAP) 60 -100 mm Hg Central Venous Pressure (CVP) 2 -8 mm Hg PAP Systolic (PAS) 20 -30 mm Hg PAP Diastolic (PAD) 5 -15 mm Hg PA Mean 15 -25 mm Hg Pulmonary Capillary Wedge Pressure (PWCP) 8 -12 mm Hg Cardiac Output Cardiac Index SVO 2 4 -8 L/min 2. 5 -4 L/min/M² 60 -75% Lactate Levels < 2. 0 Stroke Volume 50 -100 ml Systemic Vascular Resistance 900 -1300

Cardiac Output Measurement • Multiple techniques § Thermodilution – most common § Transpulmonary • Pulse contour analysis • Esophageal Doppler • Newer pulmonary artery catheters offer continuous cardiac output measurement

Thermodilution Method of Cardiac Output Measurement

CVP/PAWP Volume Expanders: Crystalloids & Colloids Low High Preload Vasopressors: Alpha Stimulators Positive Inotropics: Beta-1 Stimulators Phosphodiesterase Inhibitors Cardiac Glycosides Positive Chronotropics: Beta-1 Stimulators Atropine SVR/PVR Afterload Myocardial Contractility Heart Rate Diuretics Venodilators Arteriovasodilators: Ca+ Channel Blockers Alpha Inhibitors Vascular Relaxants Ace Inhibitors Negative Inotopics: Beta Blockers Ca+ Channel Blockers Negative Chronotropics: Beta Blockers Ca+ Channel Blockers

Vasopressors/Inotropes • • Dopamine Dobutamine Epinephrine Phenylephrine Norepinephrine Vasopressin Milrinone

Dopamine (start at 1 -5 mcg/kg/hr. max of 50) adrenergic agonist agent • Dose dependent receptor activation § Low dose - increases blood flow via dopamine receptors in renal, mesenteric, cerebral circulation § Intermediate dose - increases cardiac output via ß- receptors § High dose - progressive vasoconstriction via ą-receptors in systemic and pulmonary circulation • Tachyarrhythmias are most common complication (dose > 20 mcg/kg/hr) • Low dose dopamine has no proven renal benefit • Significant immunosuppressive effects through suppression of prolactin from hypothalamus

Dobutamine (2. 5 -20 mcg/kg/min max of 40) adrenergic agonist agent • Synthetic catecholamine generally considered the drug of choice for severe systolic heart failure • Increases cardiac output via ß 1 -receptor and causes vasodilation via ß 2 -receptor • Inotropic and chronotropic effects are highly variable in critically ill patients • Data supports use in septic shock when cardiac output remains low despite volume resuscitation and vasopressor support

Epinephrine alpha, beta agonist (1 -10 mcg/min or 0. 1 -0. 5 mcg/kg/min) • The most potent adrenergic agent available • Potency and high risk of adverse effects limit use to cardiac arrest (and specific situations after cardiac surgery) • Primarily ß-receptor effects at low doses and ą-receptor effects at high doses • Drug of choice in anaphylactic shock • Arrhythmogenic

Phenylephrine adrenergic agonist (10 -300 mcg/min) • Selective α 1 -adrenergic receptor agonist • Little effect on the beta-receptors of the heart • Contraindicated in severe arteriosclerotic cardiovascular and cerebrovascular disease • Complications include; arrhythmia (rare), decreased cardiac output, hypertension, pallor, precordial pain or discomfort, reflex bradycardia, severe peripheral and visceral vasoconstriction

Norepinephrine beta agonist (2 -12 mcg/min max 30) • More potent vasoconstrictor than dopamine; some inotropic effect § Potent ą1 stimulation § Moderate ß 1 activity § Minimal ß 2 activity • Use has changed from rescue drug in refractory septic shock to primary agent

Vasopressin (0. 01 -0. 08 units/min) • Antidiuretic hormone • Acts on vascular smooth muscle via V 1 receptors, independent of adrenergic receptors • Traditionally not titrated • Significant splanchnic vasoconstriction

Milrinone (0. 125 – 0. 75 mcg/kg/min) phosphodiesterase 3 enzyme inhibitor • Increases CI in patients with low CO • Risk of ventricular arrhythmias including non-sustained VT • Risk for excessive hypotension

Conclusion • Multiple different methods of hemodynamic monitoring • Keys to success – Know when to use which method – Technical skills for device placement – Know how to interpret the data • Remember the limitations of the technology