Understanding AdultHemodynamicsTheory, Monitoring, Waveforms and MedicationsVicki Clavir RN

PurposeThe primary purpose of invasive hemodynamic monitoring is the early detection, identification, and treatment of life-threatening conditions such as heart failure and cardiac tamponade. By using invasive hemodynamic monitoring the nurse is able to evaluate the patient's immediate response to treatment such as drugs and mechanical support. The nurse can evaluate the effectiveness of cardiovascular function such as cardiac output, and cardiac index.

Objectives Understands basic cardiac anatomy

Verbalizes determinates of Cardiac Output and their relationships to each other

List indications for hemodynamic monitoring

Demonstrates monitor system and set up

Describe pharmacologic strategies that manipulate the determinates of cardiac output

Indications for Hemodynamic Monitoring:One of the obvious indications for hemodynamic monitoring is decreased cardiac output. This could be from dehydration, hemorrhage, G. I. bleed, Burns, or surgery. All types of shock, septic, cardiogenic, neurogenic, or anaphylactic may require invasive hemodynamic monitoring. Any deficit or loss of cardiac function: such as acute MI, cardiomyopathy and congestive heart failure may require invasive hemodynamic monitoring.

Coronary ArteriesRCA-RA, RV&LV Inf,Inf SeptumSA node 65%AV node 80%PDA 80-90%CX-LA,LV (side/back)SA node 40%AV node 20%LAD LV (front/bottom)SeptumBundle branches Left Main

Cardiac Cycle Diastole Phase

Early DiastoleVentricles relax. Semilunar valves close. Atrioventricular valves open. Ventricles fill with blood.Mid DiastoleAtria and Ventricles are relaxed. Semilunar valves are closed. Atrioventricular valves are open. Ventricles continue to fill with blood.Late DiastoleSA node contracts. Atria contract. Ventricles fill with more blood. Contraction reaches AV node.

Cardiac Cycle Systole Phase

SystoleContraction passes from AV node to Purkinje fibers and ventricular cells. Ventricles contract. Atrioventricular valves close. Semilunar valves open. Blood is pumped from the ventricles to the arteries.

Cardiac Cycle

Electrical Conduction systemSA node Atrial muscleInternodal fibers AV node AV bundle right and leftbundle branchesVentricular muscle

Autonomic Nervous SystemThe autonomic nervous system stimulates the heart through a balance of sympathetic nervous system and parasympathetic nervous system innervations.The sympathetic nervous system plays a role in speeding up impulse formation, thus increasing the heart rateThe parasympathetic nervous system slows the heart rate.

The Cardiac Cycle

Coronary Arteries FillThe Cardiac Cycle

The Cardiac Cycle

The Cardiac Cycle

Normal CO 4-8 litersNormal Cardiac Index is 2.5 to 4.5 liters

Heart Rate Works with Stroke VolumeCompensatoryTachycardia BradycardiaDysrhythmias

Factors Causing Low Cardiac Output Inadequate Left Ventricular FillingTachycardia Rhythm disturbanceHypovolemiaMitral or tricuspid stenosisPulmonic stenosisConstrictive pericarditis or tamponade Restrictive cardiomyopathy Inadequate Left Ventricular EjectionCoronary artery disease causing LV ischemia or infarctionMyocarditis, cardiomyopathyHypertension Aortic stenosisMitral regurgitation Drugs that are negative inotropes Metabolic disorders

Hemodynamic termsPreload- Stretch of ventricular wall. Usually related to volume. (how full is the tank?) Frank Starlings Law

Hemodynamic termsIncreased preload seen in Increased circulating volume (too much volume)Mitral insufficiencyAortic insufficiencyHeart FailureVasoconstrictor use- (dopamine)Decreased Preload seen inDecreased circulating volume (bleeding,3rd spacing)Mitral stenosis Vasodilator use ( NTG)Asynchrony of atria and ventricles

Increased Preload

Decreased preload

Normal Value - 2-8 mm Hg

Or LVEDPPAOP = 8-12 mm Hg PAD = 10-15 mm Hg

Hemodynamic termsContractility-How well does the ventricular walls move? How good is the pump? Decreased due toDrugs certain drugs will decrease contractilityLido, Barbiturates, CCB, Beta-blockersInfarction, CardiomyopathyVagal stimulationHypoxia

Hemodynamic termsContractility- IncreasedPositive inotropic drugsDobutamine, Digoxin, EpinephrineSympathetic stimulationFear, anxietyHypercalcemia ( high calcium)

CONTRACTILITY - PRECAUTIONS

Do Not use Inotropes until volume deficiency is corrected

Correct Hypoxemia and electrolyte imbalance.

Hemodynamic termsAfterload resistance the blood in the ventricle must overcome to force the valves open and eject contents to circulation.

XY

Hemodynamic termsFactors that increase afterload areSystemic resistance or High Blood pressureAortic stenosis Myocardial Infarcts / CardiomyopathyPolycythemia Increased blood viscosity

Hemodynamic termsFactors that decrease AfterloadDecreased volumeSeptic shock- warm phaseEnd stage cirrhosisVasodilators

Normal PVR is 120 to 200 dynes

Normal SVR - 800-1200 dynes

Mean Arterial PressureMAP is considered to be the perfusion pressure seen by organs in the body.It is believed that a MAP of greater than 60 mmHg is enough to sustain the organs of the average person under most conditions.If the MAP falls significantly below this number for an appreciable time, the end organ will not get enough blood flow, and will become ischemic.Calculated MAP = 2x diastolic + systolic 3

vcla

EKG

1.PRELOAD-venous blood return to the heart Controlled by;.Blood Volume PRBCs Albumin Normal Saline Diuretics- lasix,bumex Thiazides Ace inhibitors . Venous Dilation Nitroglycerine Ca+ channel blockers clonidine (Catapress) methyldopa trimethaphan (arfonad) Dobutamine Morphine2. CONTRACTILITY-forcefulness of contractilityCa+ channel blockersDigoxinDopamine/DobutamineMilrinone/amrinone3.AFTERLOAD work required to open aortic valve and eject blood resistance to flow in arteries Dopamine (at higher doses) Ace inhibitors Nipride/lesser extent Nitro Calcium channel blockers LabetalolDrugs of Hemodynamics4. HEART RATE Beta blockersCalcium channel blockers Atropine Dopamine Dobutamine

O2 O2 O2O2O2O2O2ToBODYFrom Body

O2O2O2

Factors that make up SVO2 are Cardiac output SaO2 VO 2 (oxygen consumption) Hemoglobin

Causative FactorsClinical Conditions O2 Delivery Hb concentration- Anemia- HemorrhageOxygen saturation (SaO2)- Hypoxemia Lung disease Low FIO2 Cardiac Output- LV dysfunction (cardiac disease, drugs)- Shock cardiac/septic (late) Hypovolemia Cardiac Dysrhythmias Oxygen consumption Fever, infection Seizures, agitation Shivering Work of Breathing Suctioning, bathing, repositioning

Increased SVO2Most common cause is - Sepsis

Or

Wedged PA catheter

Functions of PA Catheter Allows for continuous bedside monitoring of the following Vascular tone, myocardial contractility, and fluid balance can be correctly assessed and managed.Measures Pulmonary Artery Pressures, CVP, and allows for hemodynamic calculated values. Measures Cardiac Output. (Thermodilution) SvO2 monitoring (Fiber optic). Transvenous pacing. Fluid administration.

PA CatheterKEEP COVEREDKEEP LOCKEDYELLOWClearBLUEREDMarkings on catheter. 1. Each thin line= 10 cm. 2. Each thick line= 50 cm.

Description of PA Catheter Ports/lumens.

CVP Proximal (pressure line - injectate port for CO)-BLUE PA Distal (Pressure line hook up)- Yellow Extra port - usually- ClearThermistor Red Cap

Continuous Cardiac Output and SVO2 monitoring

Indications for PA catheterThe pulmonary artery catheter is indicated in patients whose cardiopulmonary pressures, flows, and circulating volume require precise, intensive management.MI cardiogenic shock - CHFShock - all typesValvular dysfunctionPreoperative, Intraoperative, and Postoperative MonitoringARDS, Burns, Trauma, Renal Failure

PRESSURE TRANSDUCER SYSTEMS SET UP

500 ml Premixed Heparinized bag of NS

PHLEBOSTATIC REFERENCE POINT

Re-level the transducer with any change in the patients positionReferencing the system 1 cm above the left atrium decreases the pressure by 0.73 mm HgReferencing the system 1 cm below the left atrium increases the pressure by 0.73 mm Hg

Remove cap and keep sterileTurn stopcock towards pressure bagZero monitorReplace cap

SQUARE WAVE TEST- Determines the ability of the transducer to correctly reflect pressures.- Perform at the beginning of each shiftABC

Thermodilution Cardiac OutputsCardiac Outputs reading should be within .5 of each other for averaging purposes.

Except in patients with atrial fibrillation- just average 3 to 4 readings. (due to loss of atrial kick output changes from minute to minute)

Cardiac Outputs should be obtained at the end of respiration - at the same point each time

ARTERIAL WAVEFORM

RN magazine April, 2003 - PA catheter refresher course.

ALL PA measurements are calculated at end expiration because the lungs are at their most equal -(negative vs. positive pressures)

a, c,& v Waves and their Timing to the ECG tracing

RA WAVEFORM

RV WAVEFORM224

Ventricular

PAP DOCUMENTATIONMeasure at end expiration

Measure pressures from a graphic tracing

Measure pulmonary capillary wedge pressure at end-expiration using the mean of the a wavea wave indicates atrial contraction and falls within the P QRS interval of the corresponding ECG complex

PAW WAVEFORM WITH MECHANICAL VENTILATION

PAOP/PAWP Pressure Safety PointsWatch monitor during inflation and stop when you see PAOP waveformNever inject more than 1.5 ml of air or any fluid into PA portDont keep balloon inflated longer than 15 secondsWhen completed - Allow air to passively exit the balloon

OVERWEDGE

COMPLICATIONS OF PA CATHETER Infection Electrocution (Microshock) Ventricular Arrhythmias (Vtach.,Vfib., Cardiac Arrest) Atrial Dysrhythmias, RBBB Knotting and misplacement Hemo or Pneumothorax Cardiac valve trauma

COMPLICATIONS OF PA CATHETERCatheter thromboembolism or air embolism Dissection or Laceration of subclavian artery or veinCardiac Tamponade

Pulmonary infarction Pulmonary artery injury or rupture Balloon rupture

Hematoma

Trouble ShootingDampened Waveform Flush catheterCheck transducer system for air bubblesBlood in TubingLook for open StopcockPut 300mgHg pressure in pressure bagStuck in Wedge /PWP Very slowly and gently pull back catheter until you see PA waveform

ReferencesPulmonary Artery Catheter Education Project @ www.pacep.org sponsored by American Association of Critical Care Nurses American Association of Nurse Anesthetists American College of Chest Physicians American Society of Anesthesiologists American Thoracic Society National Heart Lung Blood Institute Society of Cardiovascular Anesthesiologists Society of Critical Care MedicineHemodynamics Made Incredibly Visual LWW publishing 2007 AACN practice alert Pulmonary Artery Pressure Monitoring - Issued 5/2004 Handbook of Hemodynamic Monitoring G Darovic 2nd ed.TCHP Education Consortium 2005 A Primer for Cardiovascular Surgery and Hemodynamic Monitoring Nursebob's MICU/CCU Survival Guide-Hemodynamics in Critical Care -Hemodynamic Monitoring Overview 12/04/00

SLIDE 2This slide schematically depicts the anatomy of the heart consisting of two atria and two ventricles separated by the septum and atrioventricular valves. The right atrium is separated from the right ventricle by the tricuspid valve while the left atrium is separated from the left ventricle by the mitral valve. The right heart (comprising the right atrium and right ventricle ) is connected to the left heart (comprising the left atrium and the left ventricle) via the pulmonary vascular system consisting of the pulmonary artery and its branches, the pulmonary capillaries and the pulmonary veins which empty directly into the left atrium. The left heart is connected to the systemic vascular system via the aorta.

Coronary arteries: The vessels that supply the heart muscle with blood rich in oxygen. They are called the coronary arteries because they encircle the heart in the manner of a crown. The word "coronary" comes from the Latin "corona" and Greek "koron" meaning crown. The coronary arteries arise from the aorta near the aortic valve and branches off into two main arteries. The RCA and the LCA.RCA -- the right coronary artery (RCA) which supplies the right atrium and right ventricle. It branches into the posterior descending artery (PDA 85%) which supplies the bottom portion of the left ventricle and back of the septum.SA nodal artery in 65% of patients AV nodal artery 80% of patientsLCA- the left main coronary artery, which branches into: CX -the circumflex artery-, which supplies blood to the left atrium, side and back of the left ventricle . 40% of the time, the SA nodal artery is supplied by the left circumflex artery and in 20% the AV nodal artery.LAD-the left anterior descending artery , which supplies the front and bottom of the left ventricle and the front of the septum and the bundle branches (L and R)

SLIDE 3The cardiac cycle consists of two phases: contraction (systole) and relaxation (diastole). During the contraction phase, blood is ejected from the ventricles. During the relaxation phase, blood fills the ventricles. This modification of Wiggers' classic diagram divides the cardiac cycle into systole and diastole. Simultaneous ECG and left sided pressure events (left atrium, left ventricle and aorta) are diagrammed. (Right-sided pressure tracings are omitted for the sake of simplicity.)

The spontaneous generation of an action potential within the SA node initiates a sequence of events known as the cardiac cycle. Each cardiac cycle lasts approximately 0.8 second and spans the interval from the end of one heart contraction to the end of the subsequent heart contraction. Ordinarily this occurs about 72 times each minute. Sympathetic - Catecholamines are chemical compounds that circulate in the bloodstream. The most abundant catecholamines are epinephrine (adrenaline), norepinephrine) and dopamine. Parasympathetic - acetylcholine (ACh) slows heart rate, increases digestionConsider sympathetic as "fight or flight" and parasympathetic as "rest and digest". SLIDE 4During relaxation, the period known as diastole, the tricuspid and mitral valves are open, blood leaves the atrium and fills the ventricles. In timing, this occurs after the ECG T wave and constitutes 2/3 of the cardiac cycle

SLIDE 5During this diastolic filling period, the pressures between the atria and the corresponding ventricle equalize, SLIDE 9During contraction, the period known as systole, the pulmonic and aortic valves are open, and blood is ejected rapidly from the left ventricle into the aorta and from the right ventricle into the pulmonary artery. During the ejection period, with the pulmonic and aortic valves open, the pressures between the ventricle and the corresponding artery equalize, as can be seen in the Wiggers diagram.

SLIDE 10During the ejection period, with the pulmonic and aortic valves open, the pressures between the ventricle and the corresponding artery equalize, as can be seen in the Wiggers diagram.

The end all be all of hemodynamic monitoring is cardiac output. Cardiac output is the amount of blood ejected from the ventricle in one minute We see that cardiac output is the product of the heart rate and the stroke volume.Cardiac Index is taking the CO and adjusting for a persons weight and size.

The heart rate and stroke volume should work like a teeter- totter when one goes up the other goes down this is the concept of compensatory heart rate.Most common change is tachycardia usually because of either low stroke volume or increased tissue needs- such as Hypovolemia, low blood pressure, anxiety fear pain fever, exercise.Also There are limitations to the compensation normal heart rates > 180 and Diseased hearts HR>120 stoke volume severely declines due to decreased filling times.Increased heart rates increase myocardial consumption Increased heart rates decrease coronary blood flow (less filling time)Bradycardia- compensates for high cardiac output or high blood pressure seen with athletes Dysrhythmias Loss of sync atria & ventricles - loss of 20-30%of CO seen in Fast rhythms- uncontrolled AFIB, Junctional Tachy, SVT, V tach, A tachySlow rhythms Junctional, 2 degree HB type II, 3 degree HB, IVR

Stroke volume is the volume of blood ejected from each ventricle with each heartbeat. The right and left ventricles eject nearly the same amount, which normally is between 50 and 100 mL per heartbeat. Stroke volume and EF are often mirrors of each other SV=EF

For example, if the heart rate is 100 beat/min and the ventricle ejects 50 mL per stroke, or each heartbeat, the cardiac output is 100 x 50 or 5000 mL/minute (or 5 L/min).

Factors Causing Low Cardiac OutputInadequate Left Ventricular FillingTachycardia Rhythm disturbanceHypovolemiaMitral or tricuspid stenosisPulmonic stenosisConstrictive pericarditis or tamponade Restrictive cardiomyopathy Inadequate Left Ventricular EjectionCoronary artery disease causing LV ischemia or infarctionMyocarditis, cardiomyopathyHypertension Aortic stenosisMitral regurgitation Drugs that are negative inotropes Metabolic disorders

The amount of blood ejected each beat, the stroke volume, in turn, is determined by the preload, afterload, and contractility of the ventricle.Preload is the amount of blood in the ventricle before it contract/ejects. Its the gas in the tank. It is also known as filling pressures. Frank-Starling LawThe relationship between the stroke volume and cardiacperformance was described in the late 1890s and early1900s by Drs. Frank and Starling.The Frank-Starling law describes the relationship betweenmyocardial muscle length and the force of contraction.Simply stated, the more you stretch the muscle fiber indiastole, or the more volume in the ventricle, the strongerthe next contraction will be in systole. This law also statesthat this phenomenon will occur until a physiological limithas been reached. Once that limit has been reached, theforce of contraction will begin to decline, regardless of theincrease in amount of fiber stretch.In the heart, it is this ability to increase the force ofcontraction that converts an increase in venous return to anincrease in stroke volume. Stroke volume must matchvenous return or the heart will fail.

Wedge pressure or pulmonary artery obstructive pressure PAWPLVEDP = Cath lab only Left ventricular end diastolic pressure is often the same as wedge.Definition - Inotropic: Affecting the force of muscle contraction. An inotropic heart drug is one that affects the force with which the heart muscle contracts.Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node.Afterload is how hard the heart (left and right side) has to push to get the blood (stroke volume) out it also refers to the resistance of the peripheral vesselsDetermined by Vascular resistance or pressure in the pipes dilatated or constricted???Aortic compliance Inability of heart muscle tissue to contract adequately Thickness/viscosity of the blood itself.Oxygen level- hypoxemia causes vasoconstriction-( Low oxygen content in the blood is referred to as hypoxemia) Afterload is inversely related to stroke volume or cardiac output. This is demonstrated in this ventricular function curve in which increases in resistance (on the X-axis) result in decreases in stroke volume (on the Y-axis).

Because of its complexity, true afterload cannot be measured at the bedside. However, a simple assessment of one of the components of afterload is the calculation of the resistance met during ejection. For the right ventricle, this is assessed by calculating the pulmonary vascular resistance (PVR).

Factors Regulating Arterial Blood PressureMean arterial pressure is regulated by changes in cardiac output and systemic vascular resistance. The following scheme summarizes the factors that regulate cardiac output and systemic vascular resistance.Inotropy - inotropy (contractility) heart muscle can change its force based on tension/stretch. Total blood volume is regulated by renal function, particularly renal handling of sodium and water. Blood volume shifts within the body (not shown in figure) as occurs when changing body posture, also change central venous pressure and preload The Vascular network (series versus parallel resistance elements). Generally, vascular structure remains relatively unchanged; however, pathological conditions (e.g., vascular thrombosis) can affect the number of perfused blood vessels. Vascular factors such as nitric oxide, endothelin, and prostacyclin have important influences on vessel diameter. Tissue Factors -Tissue factors (e.g., adenosine, potassium ion, hydrogen ion, histamine) are chemicals released by parenchymal cells surrounding blood vessels and can significantly alter vessel diameter. In general, tissue factors are more concerned with regulating organ blood flow than systemic arterial pressure; however, any change in vessel tone will affect both organ blood flow and systemic arterial pressure Neurohumoral mechanisms are regulated principally by arterial baroreceptors and to a lesser extent by chemoreceptors. Many of the therapies used for reducing arterial pressure involve inhibiting the action of neurohumoral mechanisms.

The maintenance of tissue viability and function is dependent on the adequate delivery and utilization of oxygen in accordance with its need or demand for oxygen.Arterial oxygen content (CaO2) is the total amount of oxygen within the arterial blood. Almost all the oxygen in arterial blood is determined by the hemoglobin.The greatest contributor of the three components of arterial blood oxygen content (hemoglobin, saturation of hemoglobin with oxygen and dissolved oxygen) is the patients hemoglobin level. The percentage of hemoglobin saturated with oxygen (SaO2) also contributes to the arterial blood oxygen content, but to a lesser degree. The third, and most minor, component is the amount of oxygen dissolved in blood at body temperature and varies directly with the partial pressure of oxygen (PaO2).Thus, it is important to remember that changes in the patients hemoglobin level have the greatest effects on arterial blood oxygen content. For example, an anemic patient may manifest inadequate CaO2 in the presence of a normal arterial saturation and partial pressure of oxygen (PaO2)

The two main determinants of the content of oxygen in the arterial blood are the hemoglobin level (the primary determinant) and the oxygen saturation (SaO2) of the hemoglobin.The reversible binding of oxygen to the hemoglobin molecule is important in oxygen delivery. This reversible binding allows for loading of oxygen in the lungs and unloading of oxygen to the tissues. There are two ways that oxygen is carried by the blood. The majority of oxygen is combined with hemoglobin (98%). A much smaller percentage is dissolved in the plasma (2%).

The amount of oxygen needed or demanded by the tissues is determined by the level of metabolic activity of the tissues. This varies among the organ systems.

Oxygen extraction is the percentage of the oxygen delivered that is extracted and utilized by the tissues. Normally, at rest, the body, as a whole, extracts approximately 25% of the total amount of oxygen delivered. (Certain organ beds subtract more; others less.) That means that approximately 75% of the oxygen delivered returns to the heart unused.SvO2 reflects the percentage of hemoglobin that is saturated with oxygen in the mixed venous blood. It is a global indicator of the balance between oxygen delivery and consumption. This represents the oxygen reserve the amount of oxygen that can be utilized in periods of increased. A drop in SvO2 is a warning sign of a potential threat to tissue oxygenation (that oxygen demand is exceeding oxygen consumption). SvO2 monitoring can alert the clinician to a change in patient condition sooner than traditional parameters. When a change in SvO2 occurs, it is important to examine each of the components of oxygen delivery (CO, Hb, SaO2) and oxygen consumption. Determination of the cause of the altered SvO2 will allow for prompt identification of appropriate interventions. SvO2 reflects the percentage of hemoglobin that is saturated with oxygen in the mixed venous blood. It is a global indicator of the balance between oxygen delivery and consumption. This represents the oxygen reserve the amount of oxygen that can be utilized in periods of increased demand. When oxygen demand increases, the body attempts to increase delivery, primarily through an increase in cardiac output. In this situation, the SvO2 may remain unchanged. If delivery does not increase in response to the increased demand, the tissues will extract a larger amount of oxygen from the available supply (delivered amount). This is reflected by a decrease in SvO2 . A drop in SvO2 is a warning sign of a potential threat to tissue oxygenation (that oxygen demand is exceeding oxygen consumption). Typically a decrease in SVO2 is the earliest indicators of the threat to tissue oxygenation.

This slide defines some of the clinical conditions that can contribute to a decrease in oxygen delivery. A fall in the patients hemoglobin concentration due to either existing anemia or an acute loss of blood/hemorrhage with a compromised cardiovascular system can decrease oxygen delivery to the tissues. Hypoxemia ,lung disease and a low FIO2 can decrease oxygen saturation in the arterial blood and hence cause a decrease in oxygen delivery. A fall in the patients cardiac output, due to cardiogenic shock, left ventricular dysfunction, Dysrhythmias or other causes. An increase in oxygen consumption (also known as oxygen demand) can also lead to a decrease in the (mixed) venous saturation to below 60%.Clinical conditions that can lead oxygen demand to exceed oxygen supply are those that increase muscle activity and metabolic rate including include fever, sepsis, seizures, and nursing care actions.Due to micro capillary obstruction, arterial blood is shunted past the capillaries and into the venous blood. This shunting effect may cause SvO2 levels to rise in patients with sepsis.When the PA Catheter is wedged the SvO2 can elevate. Blood in front of the catheter mixes with capillary blood causing the oxygen saturation to increase.The Swan-Ganz or pulmonary artery catheter is a flexible, balloon-tipped, flow-directed catheter containing two or more inner lumens for selected hemodynamic assessment, monitoring and therapeutic purposes. The number of lumens depends upon which parameters are to be measured . The catheter comes in sizes of 5, 6, 7, or 7.5 fr. Increments are marked at 10 cm intervals along the outer surface. The catheter has lumens and entry ports. The lumens are at the distal end of the catheter in the body, while the entry ports are outside of the body One of the obvious indications for hemodynamic monitoring is decreased cardiac output. This could be from dehydration, hemorrhage, G. I. bleed, Burns, or surgery. All types of shock, septic, cardiogenic, neurogenic, or anaphylactic may require invasive hemodynamic monitoring. Any deficit or loss of cardiac function: such as acute MI, cardiomyopathy and congestive heart failure may require invasive hemodynamic monitoring. A premixed 500ml bag of NS with Heparin is inverted and a small needle is inserted into the injection port to remove all of the air within the bag. The needle is then removed. Next the bag is spiked with the IV tubing and the flush chamber is squeezed until partially full the drip chamber is squeezed until it is partially full. Only partially fill the drip chamber because the fluid level increases when pressure is applied to the bag and it is necessary to be able to check the flow of fluid from the bag into the drip chamber. However, a large amount of air in the chamber increases the risk of large amounts of air entering the monitoring system. The roller clamp on the IV tubing is opened and flush device is squeezed or pulled to flush fluid through the IV tubing, the transducer, all stopcocks and the pressure tubing. carefulfully inspect for air bubbles. Elimination of all air bubbles is important to improve the accuracy of pressure monitoring. The flush device is held as demonstrated until fluid is freely exiting the end of the tubing. After flushing, the tubing, transducer and stopcocks are again checked carefully for air bubbles.

Flush fluid through the system until all the air is eliminated from tubing, stopcocks and transducer. This involves repeated flushing and a careful inspection for air bubbles. Elimination of all air bubbles is important to improve the accuracy of pressure monitoring. The flush device is held until fluid is freely exiting the end of the tubing. After flushing, the tubing, transducer and stopcocks are again checked carefully for air bubbles.

Next place the IV bag in a pressure band and inflate the pressure bag to 300 mm Hg. Replace all open stopcock caps with sterile closed (dead end) caps. maintaining sterility of their insertion ports.Attach the transducer cable to the monitor/amplifier. This slide demonstrates the use of a stopcock attached to a transducer mounted on a manifold as the air-reference stopcock. A level is being used to align the stopcock port with the patients mid-chest.

Figure A Expected square wave testFigure B Over damped -Sluggish, artificially rounded & blunted appearanceSBP erroneously low; DBP erroneously highCauses: large air bubbles in system, compliant tubing, loose/open connections, low fluid level in flush bag

Figure C Under damped - Over responsive, exaggerated, artificially spiked waveformSBP erroneously high; DBP erroneously low Causes: small air bubbles, too long of tubing, defective transducer

SLIDE 3The cardiac cycle consists of two phases: contraction (systole) and relaxation (diastole). During the contraction phase, blood is ejected from the ventricles. During the relaxation phase, blood fills the ventricles. This modification of Wiggers' classic diagram divides the cardiac cycle into systole and diastole. Simultaneous ECG and left sided pressure events (left atrium, left ventricle and aorta) are diagrammed. The A waveThis slide shows a closeup of the relationship of the waves of the CVP/RA waveform with the ECG events. Note the a wave peaking after the P wave, the c wave peaking after the QRS complex, and the v wave peaking after the T wave. Although filling of the ventricle from the atrium occurs during all of diastole, the final filling occurs during atrial contraction (the a wave of the CVP/RA waveform). Therefore, to measure the final ventricular filling pressure indirectly via the CVP/RA waveform, it is best to measure the mean pressure of the a wave of the CVP/RA waveform.

Although filling of the ventricle from the atrium occurs during all of diastole, the final filling occurs during atrial contraction (the a wave of the CVP/RA waveform). Therefore, to measure the final ventricular filling pressure indirectly via the CVP/RA waveform, it is best to measure the mean pressure of the a wave of the CVP/RA waveform.

Because the PAOP is a backward reflection of the LA pressure, there is a greater delay between the electrical and mechanical events than observed in the CVP/RA waveform. Thus, the a wave of the PAOP is found a bit later after the P wave, usually near the end of the QRS complex. The v wave, likewise, is found well after the T wave of the ECG.Arrhythmias- The development of brief, transient ventricular ectopy is common during passage of the catheter through the RV and usually subsides once the catheter reaches the PA. Sustained ventricular dysrhythmias can be prevented by assuring that the balloon is fully inflated during passage of the catheter from the RA to the PA and by minimizing the insertion time.Treatment of sustained ventricular tachycardia includes prompt removal of the catheter from the RV (either out to the PA or back to the RA) and administration of lidocaine, if the dysrhythmia persists. The development of ventricular fibrillation requires defibrillation.The development of right heart block may occur during manipulation of the catheter in the RV. In patients with pre-existing left bundle branch block, this results in complete heart block. Thus, in patients with left bundle branch block who require a PAC, it is prudent to insert a PAC with pacing electrodes or to have transvenous or transcutaneous pacing equipment readily available.Catheter knotting or kinking is best prevented by practicing gentle catheter manipulation technique, minimizing the insertion and manipulation time, never advancing the catheter if resistance is met, and carefully observing the waveforms to assure that the waveform changes from an RA to an RV or from an RV to a PA after advancing the catheter 15 cm. If this is not observed, it is likely that the catheter is coiling and should be withdrawn before attempting to re-advance. After insertion, the catheter should be assessed on a chest X-ray and if a knot is noted, attempts should be made to remove the knot before the catheter is removed.