Advanced Hemodynamics - Orlando Health

Advanced 

Hemodynamics 

Self-Learning Packet 

* See SWIFT for list of qualifying boards for continuing education hours

Advanced Hemodynamic Monitoring 

Table of Contents 

INTRODUCTION ............................................................................................................................................................ 3 

HEMODYNAMIC CONCEPTS ..................................................................................................................................... 3 

INDICATIONS FOR PAC MONITORING .................................................................................................................. 9 

CONTRAINDICATIONS FOR PAC ........................................................................................................................... 10 

PAC SET UP AND INSERTION .................................................................................................................................. 10 

CARE AND MAINTENANCE OF PAC ...................................................................................................................... 15 

COMPLICATIONS AND TROUBLESHOOTING.................................................................................................... 15 

REMOVAL OF PAC...................................................................................................................................................... 17 

PULMONARY ARTERY PRESSURES AND WAVEFORMS................................................................................. 17 

HEMODYNAMIC MONITORING SYSTEMS.......................................................................................................... 27 

POST TEST .................................................................................................................................................................... 40 

REFERENCES ............................................................................................................................................................... 44 

GLOSSARY .................................................................................................................................................................... 45 

QUICK REFERENCE VALUES.................................................................................................................................. 47 

Copyright 2010 Orlando Health, Education & Development 1

Purpose 


This packet was designed for nursing personnel who care for patients with pulmonary artery 

catheters in the critical care units. Prerequisites for this packet are a working knowledge of basic 

cardiovascular anatomy and physiology, cardiovascular pharmacology, and basic ECG 

interpretation skills. This packet meets the Florida State requirement for continuing education 

credit for nursing licensure. Orlando Health is an Approved Provider of continuing nursing 

education by Florida Board of Nursing (Provider No. FBN 2459) and the North Carolina Nurses 

Association, an accredited approver by the American Nurses Credentialing Center’s Commission on 

Accreditation (AP 085). 

Objectives 

After completing this packet, the learner should be able to: 

1. Define cardiac output, stroke volume, preload, afterload and contractility 

2. Describe the technical set-up of pulmonary artery catheter monitoring equipment 

3. Discuss the clinical significance of pulmonary artery catheter monitoring 

4. Describe accurate pulmonary artery pressure measurement 

5. Discuss clinical indications and contraindications for hemodynamic monitoring using 

pulmonary artery catheters 

6. Identify normal values and waveforms for the hemodynamic values that are obtained from 

pulmonary artery catheters 

7. Interpret all values obtained from the pulmonary artery catheter and relate them to various 

normal and abnormal physiologic states 

8. Calculate and evaluate the accuracy of invasive hemodynamic monitoring data using the 

square wave test and waveform analysis. 

9. Identify potential troubleshooting techniques when an inaccurate system is identified. 

10. Identify potential complications of pulmonary artery catheter monitoring. 

11. Identify conditions which may alter hemodynamic readings obtained from the pulmonary 

artery catheter 

12. Describe and troubleshoot abnormal assessment findings encountered with pulmonary artery 

catheter monitoring 

13. Describe correct removal of a pulmonary artery catheter 

Instructions 

In order to receive contact hours, you must: 

 

 

 

complete the posttest at the end of this packet 

submit the posttest to Education & Development with your payment, or to the Online Testing 

Center located on SWIFT via E-learning 

achieve an 84% on the posttest 

Be sure to complete all the information at the top of the answer sheet. You will be notified if you 

do not pass, and you will be asked to retake the posttest. 


Introduction 


Hemodynamic is the term used to describe the intravascular pressure and flow of blood that occurs 

when the heart muscle contracts and pumps blood throughout the body. It is important to remember 

that the vascular system is a closed circuit. Pressure and flow variations in the venous compartment 

could potentially affect the arterial compartment and vice versa. Therefore, a hemodynamic 

measurement is not simply a number in relation to a norm. Rather, it is the minute to minute 

pressure and flow variations that occur within and between compartments. This is especially 

important because how the blood moves through the body will determine how the tissues are 

replenished with oxygen and nutrients, and are able to excrete end products of metabolism. 

Invasive hemodynamic monitoring techniques are now routinely used in a variety of critical care 

areas to manage the more increasingly complex patient population. These can include central 

venous pressure catheters, intra-arterial monitoring catheters, and pulmonary artery catheters. The 

information derived from the various equipment, as well as a thorough nursing assessment of the 

patient, will guide clinicians in determining appropriate treatments and improving patient outcomes. 

The purpose of this packet is to discuss and review advanced methods for measuring and 

interpreting hemodynamics including the indications and contraindications for their use. Basic 

hemodynamic waveform analysis will be reviewed, in addition to an examination of normal and 

abnormal values and their implications in patient outcomes. A brief discussion of corresponding 

interventions will also be discussed. 

Hemodynamic Concepts 

Cardiac Output 

The heart’s ability to pump effectively is determined by its ability to ensure adequate supply to meet 

the metabolic demands of the tissues. In a normal physiological state the heart should be able to 

adequately compensate for reasonable demands placed upon it. 

Cardiac performance is based on four fundamental components: 

Heart rate 

Preload 

Afterload 

Contractility 

If the heart is diseased or there is an altered physiological state, one or more of these components 

can be affected or altered in an attempt to maintain adequate tissue perfusion. 

Cardiac output (CO) is defined as the amount of blood ejected from the ventricles in one minute 

(in liters/minute). Normal cardiac output is between 4-8 L/min. This is equivalent to an organ the 

size of your fist pumping out the volume of 2 to 4 two-liter soda bottles of blood every minute. Of 

course, a person’s size can play a significant role in the amount of blood needed to adequately meet 



the needs of the body. For example, an 80 pound elderly woman will need less blood than a 350 

pound young, male linebacker. To account for these differences the cardiac index can also be 

calculated. The cardiac index (CI) is the cardiac output adjusted for body surface area. The normal 

value for this is between 2.5 and 4.2 liters of blood per minute, per square meter of body surface 

area. The equation to determine cardiac output is seen below: 

Cardiac output = heart rate x stroke volume* 

*HR= beats per minute 

*Stroke volume= amount of blood ejected from the ventricles in one beat. 

Heart Rate 

Most non-diseased hearts can tolerate heart rate changes from 40-170 beats per minute. As cardiac 

function becomes increasingly compromised this range will become narrower. The heart rate and 

the stroke volume should work like a see-saw. If one goes up, the other should go down, and vice 

versa. The most common change is related to low stroke volume or increased tissue oxygen 

demands which cause the heart rate to increase to compensate for the change. This is termed 

compensatory tachycardia. 

Stroke Volume 

Stroke volume (SV) is the amount of blood ejected from the left ventricle each time the ventricle 

contracts. The stroke volume is the difference between end-diastolic volume (EDV), the amount of 

blood in the left ventricle at the end of diastole, and end-systolic volume (ESV), the blood volume 

in the left ventricle at the end of systole. Normal stroke volume is between 60 and 130 ml/beat. The 

equation for SV is seen below: 

SV= EDV-ESV 

When stroke volume is expressed as a percentage of the end-diastolic volume, it is referred to as the 

ejection fraction (EF). A normal left ventricular EF is approximately 55- 70%. 

The three main factors that influence the stroke volume are the remaining three components that 

determine cardiac performance: preload, afterload, and contractility. These three components are 

inter-related. If one is affected, so will it affect one or more of the others. 

Preload 

The term preload refers to the amount of end-diastolic stretch on the myocardial muscle fibers. This 

in turn is determined by the volume of blood filling the ventricle at the end of diastole. In essence, 

the greater the filling volume, then the greater the stretch of the myocardial muscle fibers. The more 

the myocardial muscle fibers are stretched, the greater the force of the myocardial contraction and 

potentially the greater the stroke volume to a physiological limit. Although the stretch of the 

myocardial muscle fibers is the most accurate method for determining preload, currently there is not 

a way to measure myocardial fiber length. Consequently, it has become the standard to estimate this 

value by evaluating the filling volumes using equipment such as central venous pressure monitoring 

or pulmonary artery catheter values which will be discussed later. It is clinically acceptable to 



measure the pressure required to fill the ventricles as a measure of left ventricular end-diastolic 

volume (LVEDV) or fiber length. Left ventricular preload can also be clinically assessed via the 

pulmonary artery (PA) catheter by obtaining the pulmonary artery wedge pressure (PAWP), also 

known as the pulmonary artery occlusion pressure (PAOP), more commonly referred to as the 

“wedge” pressure. Normal PAWP/PAOP can range from 6-12 mm Hg. Right ventricular preload is 

assessed by obtaining the central venous pressure (CVP). A normal CVP can be from 0-8 mm Hg. 

Generally speaking, lower values may indicate hypovolemia or extreme venodilation, and vice 

versa for higher values. 

Frank-Starling’s Law 

The Frank-Starling Law describes the relationship 

between myocardial muscle length and the force of Starling’s Curve 

contraction. The amount of stretch is directly affected by 

the amount of fluid volume in the ventricle, thus preload is 

most directly related to fluid volume. Starling’s Curve 

describes the relationship of preload to cardiac output. As 

preload (fluid volume) increases, cardiac output will also 

increase until the cardiac output levels off. If additional 

fluid is added after this point, cardiac output begins to fall. 

This reaction of the heart muscle to stretch can be likened 

to a slingshot. The farther the slingshot is stretched, the 

farther it propels a stone. If the slingshot is only slightly 

stretched, the stone will travel a very short distance. If the 

slingshot is repeatedly overstretched, however, it weakens 

and eventually loses its ability to launch the stone at all. 

The slingshot functions best when it is stretched just the 

Preload 

right amount, neither too little nor too much. The same is 

true of the heart. With too little preload the cardiac output cannot propel enough blood forward. 

With too much preload the heart will become overwhelmed, leading to failure. 

Afterload 

Afterload refers to the resistance, impedance, or pressure that the ventricle must overcome to eject 

its own volume. Afterload can also be viewed as the resistance of flow, or how clamped the blood 

vessels are, affecting how hard the heart (right or left) has to pump to push the blood out. In the 

clinical setting the most sensitive indicator of left ventricular afterload is the systemic vascular 

resistance (SVR), and for right ventricular afterload it is pulmonary vascular resistance (PVR). The 

normal value for the SVR is 800-1200 dynes/sec/cm. This value can also be corrected for body 

surface area and is termed the systemic vascular resistance index (SVRI), for which the normal 

values are 1680-2580 dynes/sec/cm5/m2. The normal values for the PVR is generally less than 250 

dynes/sec/cm5, and the PVRI approximately 255-285 dynes/sec/cm5/m2. Generally speaking, 

higher values indicate vasoconstriction and lower values indicate vasodilation. 

Contractility 

Contractility is the force and velocity with which the ventricular ejection occurs independent of the 

effects of preload and afterload. In other words, think of contractility as the cardiac “squeeze”. 

Contractility is primarily influenced by the effects of the sympathetic nervous system. Factors such 

as the release of catecholamines from fear, stress, anxiety, pain, or hypovolemia can increase 

Copyright 2010 Orlando Health, Education & Development 5 

Cardiac Output


contractility causing the heart to “squeeze” harder. The ventricular stroke work index (VSWI) is a 

useful measurement for myocardial contractility. Normal values for the left VSWI (LVSWI) are 35- 

85 gm/m2/beat. 

Compliance 

Myocardial compliance refers to the ventricle’s ability to stretch to receive a given volume of blood. 

Normally the ventricle is very compliant so large changes in volume will produce small changes in 

pressure. If compliance is low, small changes in volume will result in large changes in pressure 

within the ventricle (refer back to the illustration of Starling’s curve). If the ventricle cannot stretch, 

it will be unable to increase cardiac output with increased preload as described by the curve. 

Arterial Blood Oxygen Content 

Hemoglobin carries 97% of oxygen and 2% is dissolved in plasma. Together, oxygen bound 

to hemoglobin and oxygen dissolved in plasma, is called arterial oxygen content or CaO 2 = (Hgb x 

1.34 x SaO 2 ) + (0.003 x PaO 2 ). Hemoglobin can carry 1.34 ml of oxygen per gram of hemoglobin. 

Oxygen does not dissolve very well in plasma as evidenced by a solubility coefficient of 0.0031. 

Therefore, hemoglobin has the largest influence on CaO 2 . 

Saturation of hemoglobin indicates how much oxygen is being carried on the hemoglobin. 

Normal oxygen saturation of a healthy individual ranges from 97% to 99%. A value of 95% is still 

clinically acceptable with a normal hemoglobin. These readings have to be considered in relation to 

the oxyhemoglobin dissociation curve. 

The oxyhemoglobin dissociation curve indicates the relationship between oxygen saturation 

of hemoglobin and the partial oxygen pressure, and how it releases oxygen to the tissues or how it 

retains oxygen on the hemoglobin. 



Because of the higher partial oxygen pressure of saturated hemoglobin, oxygen can diffuse 

from the hemoglobin to the lower partial oxygen pressure in the tissues. 

Under normal circumstances a PO 2 of 50 mmHg saturates approximately 82% of the 

hemoglobin. However, there are certain conditions that cause a shift of the curve to the left, which 

allows for 82% hemoglobin saturation with a PO 2 of only 42 mmHg. This shift to the left (Bohr 

effect) increases the affinity of oxygen to the hemoglobin, but makes it more difficult to release 

oxygen to the tissues, and is caused by an increase in pH, hypothermia and low 2,3 DPGs. 2,3 DPG 

or 2,3-Disphosphoglycerate is an organophosphate that affects the affinity of oxygen to the 

hemoglobin. Low 2,3 DPG allows for more oxygen to be released to the tissue. 

A shift to the right decreases the affinity of oxygen to the hemoglobin, but makes it easier to 

release oxygen to the tissue. This is caused by high 2,3 DPG, hyperthermia, and a low pH. 

Oxygen Delivery 

Oxygen transport is the delivery of oxygen content or CaO 2 to the tissues. This greatly 

depends on the pulmonary function and the cardiac output. In order to transport oxygen content, an 

adequate cardiac output is required. Therefore, the formula for oxygen delivery is 

(CaO 2 )(CO/BSA)(10dL/L). Oxygen content is delivered by CO/BSA or CI times10dL/L, which is 

the conversion factor from L/min to ml/dL, in which DO 2 I is expressed. A normal range for DO 2 I is 

500 – 650 mlO 2 /min/m 2 . 

Components of 

Oxygenation 

Ventilation 

Tissues 

Utilization 

Diffusion 

Delivery 

Lung 

CV System, Hgb 



Oxygen Consumption 

Oxygen demand is the amount of oxygen the tissues require for metabolism. This demand is 

influenced by several factors such as metabolic rate, muscular work and temperature. As long as the 

oxygen demand does not exceed the oxygen delivery, homeostasis will be maintained. If the 

delivery does not match the demand, the body will use alternative sources besides oxygen to 

generate energy such as fat and proteins. This will result in anaerobe metabolism and lactate 

acidosis. 

Oxygen consumption (VO 2 I) can be measured by subtracting the volume of O 2 (arterial 

oxygen content) leaving the heart from the volume of O 2 (venous oxygen content) returning to the 

heart or [(CO/BSA x CaO 2 ) – (CO/BSA x CvO 2 )] x 10 dL/L = VO 2 I. 

Under normal conditions oxygen consumption is 25%. However, during stress response the tissues 

are capable of extracting 80% of oxygen. This is indicated by an increase in VO 2 I. Adequate 

delivery is paramount in order to balance oxygen supply and demand and prevent anaerobe 

metabolism. The normal range for VO 2 I is 120 – 160 ml/min/m 2 . 

Certain conditions cause an increase in oxygen consumption. The following table provides 

an overview of these conditions. 

Condition 

Percentage increase in VO 2 I 

Fever 

10% with every > 1C 

Work of breathing 40% 

Severe Infection 60% 

Shivering 50 – 100% 

Burns 100% 

Endotracheal suctioning 27% 

Chest trauma 60% 

MODS 20 - 80% 

Sepsis 50 – 100% 

Head injury, sedated 89% 

Head injury, unsedated 138% 

Bath 23% 

Position change 31% 

Agitation 18% 



Mixed Venous Oxygen Saturation 

The mixed venous oxygen saturation or SVO 2 is the end result of O 2 delivery and O 2 

consumption. It can be measured with a fiberoptic sensor at the tip of a PA-catheter. This 

measurement reflects an average of venous saturation for the whole body and not separate organ 

perfusion or oxygenation. Because it is a continuous measurement, it can be used to evaluate 

therapeutic interventions, or it can serve as an indicator for potential consequences of patient care, 

such as suctioning or turning. The normal values range between 60 – 80%. 

A low SVO 2 can indicate that either the O 2 extraction is increased or the O 2 delivery is 

decreased. This can be caused by anemia, decreased cardiac output, low arterial oxygen saturation 

or an increased VO 2 I. Treatment of low SVO 2 can consist of increasing the cardiac output by 

increasing heart rate, optimizing preload, modulating afterload, increasing SaO 2 , administering 

positive inotropes or improving the oxygen carrier capacity by means of a blood transfusion. Other 

interventions relate to improving the pulmonary function, such as pulmonary toilet, prevention of 

atelectasis and ventilator strategies. It is more difficult to decrease O 2 demand. Sedatives and 

neuromuscular blocking agents can help to decrease muscle activity and prevent shivering. 

Temperature management controls increased oxygen consumption caused by fever. Spacing care 

activities such as turning, bathing, suctioning and other nursing procedures, can also be of benefit. 

A high SVO 2 is often more difficult to interpret. It can indicate the inability of the tissues to 

extract oxygen, which can be seen in sepsis. Another cause could be a hyperdynamic circulation or 

an increased oxygen delivery. Appropriate ventilator management can control the increased oxygen 

delivery. 

Indications for PAC Monitoring 

PAC monitoring can be very useful with critically ill patients that are complex and difficult to 

diagnose. The PAC in and of itself is not an intervention but a tool that can be used to obtain 

specific data and guide therapies. The PAC can also be used to determine the type and amount of 

treatment to be used in more complex cases, as well as evaluate how well the treatment is working. 

Specifically, PAC pressure monitoring may be indicated in any of the following: 

 

 

 

 

 

 

 

To assist in making a differential diagnosis, enabling the parameters of the cardiac output to 

be appropriately treated 

To guide clinical management of several heart and lung disorders 

To monitor hemodynamic pressures during volume resuscitation or inotropic, vasopressor, 

vasodilator drug infusion therapy 

With complicated myocardial infarction or heart failure 

To monitor hemodynamic pressures in complicated surgical procedures 

With multisystem failure or shock 

With respiratory failure 



Contraindications for PAC 

Currently there are no absolute contraindications to inserting a PAC. However, its use must be 

justified in that its use is imperative to diagnostic or treatment strategies. Some of the relative 

contraindications include the following: 

 

 

 

 

 

 

Patients with severe coagulopathies 

Patients with a prosthetic right heart valve 

Patients with an endocardial pacemaker 

Patients with severe vascular disease 

Patients with pulmonary hypertension 

Patients in a location that lacks the availability of physicians trained and skilled in insertion 

and flotation and the principles of blood flow, measurement of intravascular pressures, and 

interpretation of hemodynamic data 

PAC Set Up and Insertion 

As Replicated from the Fundamentals of Hemodynamics SLP: 

Hemodynamic pressure monitoring systems detect changes in pressure within the vascular system 

and convert those changes into digital signals. The digital signals are then displayed on a monitor as 

waveforms and numeric data. 

What will you see: 

There are several types of PA catheters with various features and varying numbers of lumens. It is a 

long hollow flexible catheter that is generally yellow in color. The PAC can have varying numbers 

of pigtails with corresponding lumens and tunnels. Typically you may see a PAC with four or five 

lumens each representing the following: 

Proximal injectate port- used for monitoring right atrial pressures 

PA distal port- used for measuring PA systolic, diastolic, and mean pressures 

Balloon inflation port- used to inflate the balloon for the purposes of flotation during 

insertion and obtaining PA occlusion pressures (also known as pulmonary capillary wedge 

pressure or pulmonary artery occlusion pressure [PAOP/PAWP]. 

Thermistor wire connector- used for connecting to a cable for measuring cardiac output and 

blood temperature. 

The PA catheter will have a series of encircling black lines, which allow the clinician to estimate 

the location of the catheter tip in centimeters. Each thin black line will equal 10 cm, while the 

thicker black lines will equal 50 cm. 



Semi-rigid pressure tubing attaches the 

catheter to a transducer set-up. The tubing 

must be more rigid than standard IV tubing so 

that the pressure of the fluid within it does not 

distort the tubing. If the tubing is distorted in 

any way, the pressure readings will be 

inaccurate. The tubing must also be as short as 

reasonably possible, as longer tubing will 

cause distortion of the pressure as it travels 

over the longer distance. 

The transducer is a device that converts the 

pressure waves generated by vascular blood 

flow into electrical signals that can be 

displayed on electronic monitoring equipment. 

The transducer cable attaches the transducer 

to the monitor, which displays a pressure 

waveform and numeric readout. 

The flush system consists of a pressurized bag of normal saline (which may or may not contain 

added heparin, depending on the unit and facility where you work). The pressure must be 

maintained at 300 mm Hg to prevent blood from the arterial system from backing up into the 

pressure tubing. 

An intraflow valve is part of the transducer setup and maintains a continuous flow of flush solution 

(approximately 3-5 ml/hr) into the monitoring system to prevent clotting at the catheter tip. 

A fast flush device allows for general flushing of the system and rapid flushing following 

withdrawal of blood from the system or when performing a square wave test. 


Line Setup & Zeroing of a Transduced System 


The majority of hemodynamic monitoring systems are set up in a similar manner. The exact type of 

transducer system used varies among institutions. Review the policies and guidelines where you 

work for more specific information. 

Equipment 

Assemble all components of the system prior to set up (this may be performed by a nurse, a 

respiratory therapist or a technician). The components include: 

Pressure cuff (pressure pack) for IV bag 

One liter bag of normal saline 

Pre-assembled, disposable pressure tubing with flush device and disposable transducer and 

stopcocks 

I.V. pole with transducer mount (called a manifold) 

Carpenter’s level or other leveling device 

Patient monitor, pressure module and monitor cable 

Equipment Set-up 

1. Obtain a 1000 ml bag of 0.9% saline; invert the bag and spike it with IV tubing, then turn it 

upright and fill the drip chamber until it is completely full. 

2. The tubing comes with stopcock caps with holes in them so one does not have to remove 

the caps prior to priming the tubing. Position all stopcocks so the flush solution will flow 

through the entire system. Be sure to flush all the stopcock ports. Roll the tubing’s flow 

regulator to the OFF position. 

3. Activate the fast flush device and flush the saline through the entire setup one more time. 

Check to be sure that all air has been purged from the system. Examine the transducer and 

each stopcock carefully, as small bubbles tend to cling to these components. Air left in the 

tubing can cause inaccurate transmission of pressure to the transducer. 

4. Replace all vented (the ones with holes) port caps with closed (dead-end) caps, making 

sure to maintain the sterility of each cap’s insertion end. 

5. Place the bag of saline into the pressure bag, and adjust the pressure to at least 300 mm Hg. 

This is the pressure that is required to maintain a continuous flow of 3-5 ml/minute through 

the intraflow valve. This helps prevent clotting of the catheter and backflow of blood into 

the tubing. 

6. Before the monitor can measure pressures, the transducer must be zeroed to atmospheric 

pressure. The purpose of this procedure is to make sure the transducer reads zero when no 

pressure is against it. This procedure is like zeroing a scale before weighing something to 

assure accuracy. To zero the transducer, place the stopcock so it is open between the 

transducer and air, and press the zero button on the monitor. Zeroing can be performed 

whether or not the patient is attached to the system, so no particular patient position is 

required to complete this step. The transducer should be re-zeroed whenever the reading is 

in doubt, or anytime the monitor has been disconnected from the transducer setup. 



7. Before starting to monitor pressure, the stopcock 

nearest the transducer must be placed at the level of 

what is being measured. In most cases (other than 

intracranial pressure monitoring) this is at the level 

of the heart. Correct leveling is essential to achieve 

accurate pressures and should be checked during 

routine monitoring and troubleshooting of the 

monitoring system. To level the transducer, place the 

transducer at the level of the heart. This location is 

called the phlebostatic axis, and is located at the 4 th 

intercostal space, halfway between the anterior and 

posterior chest (mid-chest). The mid-axillary line is 

not accurate for patients with barrel chests or severe 

chest deformities. To assure that the stopcock is 

precisely leveled with this landmark, mark the position 

of the phlebostatic axis on the patient’s chest with 

permanent marker. The transducer can be taped 

directly to this location, or it may be mounted on a 

pole and leveled to the phlebostatic axis with a 

carpenter’s or laser level. Re-level the transducer 

phlebostatic axis 

anytime the patient changes position or if the reading is in doubt or outside of prescribed 

parameters. 

x 

From Techniques in Bedside Hemodynamic 

Monitoring by E.K. Daily and J.S. Schroeder, 

C.V. Mosby, 1981. Used with permission. 

Technical Aspects of Leveling and Zeroing 

A number of external factors may affect how accurately the hemodynamic monitoring system 

reflects the pressures within the patient’s vascular system. There are two important pressures that 

can affect hemodynamic readings. 

Hydrostatic pressure is the force that is exerted by the fluid within the hemodynamic monitoring 

system against the transducer. This pressure is the result of a combination of factors that include 

gravity and the height and weight of the fluid column (in other words, the position or height of the 

IV bag and length of tubing, which contains the fluid column), fluid density and positioning of the 

transducer. Leveling the transducer to the phlebostatic axis eliminates inaccuracies in pressure 

readings due to hydrostatic pressure. As long as the stopcock nearest the transducer is level with the 

phlebostatic axis, the patient can be positioned as high as 60 degrees and still have generally 

accurate pressure measurements. It is essential that pressures be measured at a consistent head-ofbed 

elevation for trends to be valid. 

Atmospheric pressure is the force that is exerted at the earth’s surface by the weight of the air that 

surrounds the earth. At sea level this pressure is 760 mm Hg, but it varies depending on altitude. 

Zeroing the monitor eliminates the effect of atmospheric pressure on the pressure readings. 

Remember, zeroing can be accomplished even before the patient is attached to the system. 


PAC Insertion 


Preparation for Catheter Insertion 

The nurse should: 

Explain the procedure to family or patient 

Ensure that all the necessary consents are signed 

Have emergency equipment available 

Gather all the equipment for line setup and PAC insertion per institutional guidelines. 

Prepare a sterile field 

Depending on the contents of the catheter insertion tray, gather additional 4 x 4 gauze, 

sterile towels, and a sterile gown 

Obtain syringes with 10 ml saline flush solution 

Flush all ports along with any attached stopcocks, using sterile technique. 

Cover the prepared tray with sterile towels 

The physician will use sterile technique to insert the PAC. This is done using either a percutaneous 

or a cutdown approach. Once inserted, the catheter is progressed and the balloon is inflated. The 

catheter then ‘floats’ with the flow of the blood from the right atrium to the right ventricle through 

the pulmonic valve in the pulmonary artery. Observation of the waveforms as the catheter advances 

identifies the location of the catheter. 

The distal tip of the PAC once completely inserted will rest in the pulmonary artery, where it will 

continuously measure the pressures from the right side of the heart (CVP) and the lungs (Pulmonar 

artery systolic and pulmonary artery diastolic). 

Post-Insertion 

Once the PAC is properly in place, the practitioner will suture it in place, and the nurse will perform 

the following activities: 

Place a sterile clear occlusive dressing over the site 



Document the level of the centimeter marking on the catheter 

Ensure that a chest x ray is ordered to confirm placement and to rule out any complications 

Obtain a baseline set of hemodynamic values such as Cardiac Output, Cardiac Index, and 

Systemic Vascular Resistance 

Continuously monitor and assess waveforms to ensure that the PAC remains in the correct 

place. 

Care and Maintenance of PAC 

Please refer to institutional policy and procedure for care and maintenance of the PAC lines and 

dressings. 

Complications and Troubleshooting 

During Insertion 

During the insertion of the PAC there are some immediate life-threatening complications that the 

nurse should look for. The two most common that can occur are pneumothorax and venous air 

embolism. Both of these can happen very quickly and, if unrecognized, can be fatal. Other 

complications that the clinician needs to watch for are dysrhythmias, dislodgement of the catheter 

wire, or excessive bleeding. 

Post - Insertion 

There are additional complications that can occur hours or days after the insertion of the PAC. 

These include dysrhythmias, catheter-related infection, catheter dislodgement or migration, 

thrombophlebitis, and pulmonary rupture. The catheter may migrate (or move further down) into a 

smaller arteriole where it can persistently wedge itself, leading to pulmonary artery ischemia and 

infarct. For this reason it is extremely important that the clinician is able to recognize the PAC 

waveforms, so that prompt recognition of continuous wedging can be identified. Other reported rare 

complications include pulmonary artery rupture from balloon inflation, intracardiac thrombus or 

embolus, endocarditis, and ruptured myocardium leading to cardiac tamponade. 

Pulmonary Artery Catheter Troubleshooting 

Primary Assessment: 

1. Is the patient stable (vital signs, hemoptysis); if not, address critical issues immediately. 

2. Start at one end (either end) and work towards the other end: 

a. check catheter position; has it changed from insertion? (note markings on catheter) 

b. checking for connections (need to be tight) 

i. use as few stopcocks as possible 

ii. check stopcocks to assure that they are in “open” position 

c. check tubing for kinks, air bubbles 

d. check balloon inflation to assure that the balloon is deflated 

e. check patency of catheter by withdrawing; do not flush if wedged 

f. level and zero the transducer 

g. assure that the appropriate scale is used for PA catheters and not other forms of pressure 

monitoring 

h. ensure that the continuous flush is maintained at 300 mmHg. 



Secondary Assessment: 

Problem/assessment Cause [reason] Intervention / action needed 

Overdamped waveform 

Air, blood, clots, in the tubing 

Tubing is too long, kinked, 

connections are loose 

Remove air, blood, clots 

Remove tubing extensions, replace 

kinked tubing, tighten connections 

New transducer 

Underdamped waveform Air bubbles Remove air bubbles from the 

system 

New transducer 

Deflated balloon becomes 

wedged—Requires urgent 

intervention 

Overwedged— 

Requires urgent intervention 

Ventricular irritability— 

Requires urgent intervention 

(premature ventricular 

contractions, ventricular 

tachycardia or fibrillation) 

 

Seen on insertion as 

well as during ongoing 

use 

Coil of catheter straightens as the 

catheter warms in body causing the 

catheter to “lengthen”, progressing 

further into the pulmonary system 

Balloon over-inflated 

Catheter stimulates the myocardium 

Catheter needs to be pulled back 

(out) until un-wedged, re-secured 

and new measurement markings 

seen on catheter for reference and 

new waveform documented 

On-going monitoring to assure that 

waveforms are indicative of 

appropriate catheter position 

Deflate balloon. Catheter should be 

repositioned if necessary (check 

waveform prior to initiation of 

occlusion procedure), then reinflate 

balloon with only enough air 

to produce PAOP waveform pattern 

on monitor 




Repositioning of catheter 

Suturing to maintain positioning 




PA balloon rupture— 

Requires urgent intervention. 

If suspected, further attempts 

should not occur in order to 

prevent further air embolism 

 

No sensation of 

resistance on 

Causes of balloon damage: 

Over-inflation of balloon 

Frequent inflations 

Using the syringe to deflate 

the balloon 

Cap balloon port after having 

removed the syringe and clearly 

labeling the port so that other 

clinicians will no longer utilize the 

port 



 

 

inflation 

Inability to “wedge” 

Blood can be 

aspirated from 

balloon port 

Pulmonary infarction, 

rupture— 

this is an EMERGENCY 

new occurrence: 

hemoptysis 

cough 

dyspnea 

chest pain 

Wedging of the catheter without 

being un-wedged, progresses to 

dissection or rupture; can also be 

thrombosis related to the presence of 

the catheter. 

With infarction, the catheter needs 

to be removed 

If pseudoaneurysm develops, 

transcatheter embolization or 

surgical resection 

Removal of PAC 

Removing a PAC is a decision that is reached when the data obtained from the catheter is no longer 

warranted. The PAC can be removed by a physician or a registered nurse depending on your 

facility’s policy and procedure. Removal is done after viewing the most recent chest x ray so that 

the catheter position can be visualized. The chest x ray is checked for any kinking or coiling of the 

PAC. After placement verification the following guidelines can be used: 

Explain the procedure to the patient 

Discontinue all fluids and turn off all stopcocks to the patient 

Ensure the balloon is deflated 

Place the patient in supine position with the head of bed flat (if able). 

Before the catheter is withdrawn the patient is instructed to exhale or hold their breath 

The catheter is then withdrawn in a smooth and gentle motion 

If there is any resistance, STOP and get a chest x ray to visualize placement 

 

Following the removal, place a sterile dressing over the site and monitor the patient for any 

complications. 

Pulmonary Artery Pressures and Waveforms 

PA Pressures 

The pressures in the lungs (right-sided pressures) are for the most part much lower than that of the 

systemic circulation (left -sided pressures). There are several reasons for this. One reason is 

because the lungs are located close to the heart, and so the right ventricle does not have to generate 

a high level of pressure to pump the blood that short distance. The left ventricle, however, has to 

generate much more pressure to pump the blood to the entire body from head to toe. Another reason 

for the discrepancy relates to gas exchange in the lungs. The lungs require a low pressure system 



for gas exchange to occur. Otherwise, if the pressure becomes too high, the intravascular fluid is 

forced into the alveoli which results in impaired gas exchange and pulmonary edema. 

Reading 

obtained 

from the 

PA- 

Catheter 

Once the PAC is inserted, the pulmonary artery pressures can be continuously measured. More 

specifically, the pulmonary artery systolic (PAS) and the pulmonary artery diastolic (PAD) will be 

displayed. The PAS pressure reflects the amount of pressure necessary to open the pulmonic valve 

and eject the blood into the pulmonary circulation. The PAD pressure reflects the amount of 

resistance in the lungs between heart beats. 

As previously mentioned, the PAS and PAD both reflect right-sided pressures. When elevated, this 

indicates a problem with the lungs. In addition, assessment of the PA pressures can also help in 

distinguishing between a primary lung problem and a lung problem caused by the heart. The 

pulmonary artery pressures will increase whenever the blood vessels in the lungs are constricted. 

This is also known as increased pulmonary vascular resistance (PVR). PVR is considered the 

afterload of the right ventricle. Conditions such as pulmonary hypertension, chronic hypoxemia, or 

pulmonary embolus can result in an increased PVR leading to elevated pulmonary artery pressures. 

As previously mentioned, once the PAC is inserted the tip rests in the pulmonary artery. An 

electronic signal is sent to the monitor which will display a waveform. This waveform may vary 

with respirations and the monitor will average this variation in its readings. This is why it is 

imperative that the clinician print out a copy of the wave form display to properly assess the value. 

The measurement should always be assessed at end expiration. In a spontaneously breathing patient 

the intrapulmonary pressures decrease slightly on inspiration, and increase on expiration. The 

opposite is true for a mechanically ventilated patient. In a patient that is mechanically ventilated the 



intrapulmonary pressures will increase on inspiration and decrease on expiration. Therefore, the 

point of end expiration will look different depending on how your patient ventilates. In the 

spontaneously breathing patient, end expiration will be the highest point on the waveform before it 

dips. Conversely, for the mechanically ventilated patient the end expiration will be the lowest point 

on the waveform before it rises. 

Keep in mind that the transducer must be properly leveled and zeroed prior to assessing any values. 

If too high, it will give a falsely low reading, and if too low, it will give a falsely high reading. 

PA waveform 

Please note that the pulmonary artery waveform has the same characteristics of the arterial 

waveforms. What you should see is a sharp upstroke that represents systolic ejection into the 

pulmonary artery. This is followed by a dicrotic notch that represents closure of the pulmonic 

valve, and subsequent gradual downslope that is representative of end diastole and opening of the 

pulmonic valve. 

PAOP (wedge) 

Normally when the PA catheter is resting in the pulmonary artery it will display the PAS and PAD. 

The PAOP/PAWP is obtained from the distal port of the PAC when the balloon is inflated. To 

inflate the balloon, inject with up to 1. 5 ml of air or until a wedge waveform is produced. The 

balloon should not be inflated for longer than fifteen seconds. It is important to document how 

much air it took to produce a PAOP waveform to assess for catheter migration. The air should then 

be allowed to passively escape into the syringe. The wedge waveform can be frozen on the monitor, 

so clinicians can assess for the values after the procedure is completed. 

DO’S AND DON’TS OF WEDGING 

Never wedge for more than 15 seconds 

Never leave the catheter in a permanent wedge position 

Always allow for passive deflation of the balloon 



 

 

 

The PAD should be used in place of wedging whenever possible 

Never inflate the balloon with more than 1.5 ml of air 

Only use the 1.5 ml syringe supplied with the catheter 

Once the catheter is in the PAOP position it can assess pressures from the left side of the heart. The 

PAOP value should be equilavent to the left atrial pressure and the left ventricular diastolic 

pressure or left ventricular preload. Knowing the PAOP is important because, since it represents 

preload, the clinician can assess how much volume the heart has to pump. Too much preload, or a 

high PAOP, can mean there is too much volume and conversely, too little preload, or a low PAOP, 

can mean that there is not enough volume. In patients with normal lungs and albumin levels, 

pulmonary congestion generally will begin with PAOP values greater than 18 mm Hg and 

pulmonary edema with levels greater than 24 mm Hg. However, in patients with chronic heart 

failure, pulmonary edema may not begin until the PAOP pressures are greater than 30 mm Hg. 

The components of the PAOP waveform are similar to that of the CVP waveform with a slight 

difference in where to look for the components (See below). The A wave of the CVP waveform is 

measured in the PR interval, while the A wave of the PAOP starts near the end of the QRS. 



This delay is due to the distance of the tip of the PA catheter to the left atrium. To measure the 

PAOP the clinician must again look for end expiration on the waveform. Just as with measuring the 

CVP, to obtain the PAOP value the average of the highest and lowest point on the A wave must be 

calculated. 

Normal ECG 

rhythm tracing 

CVP waveform 

CVP value recorded at the midpoint of the X descent. 



Components of the PAOP/PAWP waveform include: 

The A wave occurs after the QRS of the ECG complex. It reflects the increased left 

atrial pressure that occurs with left atrial contraction. Note that the A wave will be 

absent in patients who do not have a distinct atrial contraction, such as those with atrial 

fibrillation. Calculate the PAOP by averaging the pressure measured at the peak 

of the A wave and at the subsequent trough. 

The X descent reflects left atrial relaxation. 

The V wave reflects left atrial filling against a closed mitral valve. 

The Y descent reflects left atrial emptying associated with opening of the mitral valve 

(the onset of left ventricular diastole). 

Respiratory variation in PA waveform 

PAD-PAOP gradient 

Because there are no valves in the pulmonary arterial system when the PAC is wedged, it reflects an 

uninterrupted flow of blood to the left atrium. In other words, the tip of the catheter is able to see 

straight through the pulmonary circulation, because of the lack of valves, to the left atrium. So 

essentially during diastole the: 

LVEDP= left atrial pressure= pulmonary vascular pressure= PAOP. 

If that is so then the PAD pressure should closely correlate with the PAOP, with the PAD being 

slightly higher. The values should be no more than 4 mm Hg apart (PAD minus PAOP) to deem it 



correlated. This is also known as the PAD-PAOP gradient. This is why in many facilities, once 

correlated, the PAD can and should be used in place of the PAOP when possible. If, however, the 

PAD and the PAOP are greater than 4 mm Hg apart there are certain conditions that must be ruled 

out. Conditions that could cause an increase in the PAD-PAOP gradient are generally primary 

pulmonary issues such as pulmonary embolism, pulmonary vascular disease, hypoxemia, or 

acidemia. 

PAD~ 26 

PAOP ~ 10 

PAD-PAW gradient ~ 16 

Abnormal Waveforms 

In addition to assessing for abnormal values, analysis of the waveform shape can also assist the 

clinician in diagnosis. Abnormalities in the waveforms may indicate a pathological condition such 

as an arrhythmia or valvular problem. Any changes from the baseline should be reported to the 

physician or expert clinician for evaluation. 

Altered A waves 

Typically an A wave will be large if the atria have to contract against a partially closed, or stenotic 

mitral or tricuspid valve. Cannon A waves is a term often used to describe a giant A wave that 

develops as a result of atrial-ventricular dyssynchrony, as is the case with junctional or AV 

dissociative rhythms. In this case the A wave is produced by simultaneous contraction of the atria 

and ventricles causing it to be enlarged and to occur later in the cardiac cycle. Cannon A waves can 

also be caused by premature ventricular contractions (PVCs) or re-entrant ventricular tachycardia. 

To evaluate the A wave in these cases it is best to look to measure the CVP at the end of the QRS 

complex and the PAOP/PAWP one to two boxes after the QRS complex. 



Altered V waves 

Large V waves are most frequently caused by tricuspid and mitral insufficiency. Other causes 

include such conditions as ventricular ischemia/failure, decreased atrial compliance, increased 

pulmonary or systemic resistance, and ventricular septal defect. The large V wave is produced when 

there is increased blood volume entering the atria during the period of rapid atrial filling in the 

cardiac cycle. On the monitor, the V wave will be taller than the A wave. 

Obtaining an accurate PAOP/PAWP measurement in the presence of large V waves can be 

challenging. The challenge is that the large V wave can be mistaken for the systolic PA pressure 

wave. To avoid this mistake the clinician must continue to consistently look to measure the V wave 

in relation to the patient’s ECG. 

Calculated Values 


Monitoring the cardiac output (CO) may be indicated if there are concerns regarding adequate 

oxygenation of the tissues. As stated previously the normal CO is 4-8 L/min and it is directly 

influenced by the heart rate and stroke volume. Cardiac Index (CI) is the CO corrected for body 

surface area and is a more accurate parameter to monitor than CO. Normal CI is 2.5-4.0 L/min/m2. 

A low CO may be an indication of hypovolemia or heart failure, while a high CO may indicate 

hypermetabolic conditions such as sepsis, burns, trauma, or certain forms of shock. 



The Thermodilution Method 

The CO can be measured in a variety of ways. One of the more common methods used at the 

bedside is the thermodilution method. A specific quantity of a known fluid (generally 10 ml with a 

temperature lower than that of the blood) is injected into the proximal injectate port of the PAC. 

The clinican must inject in a rapid and smooth manner. The fluid is dispelled in the right atrium and 

then passes to the right ventricle and subsequently the pulmonary artery, where the temperature of 

the mixed blood is recorded by the thermistor at the distal tip of the PAC. The monitor will 

calculate the CO based on the temperature change and the time it takes the injected volume of 

solution to pass the thermistor. The temperature change is then graphically displayed on the monitor 

as a CO curve. This curve should be smooth with a rapid upstroke to a peak, and a gradual 

downslope back to baseline. Usually the clinician will obtain three good CO curves and average 

them for a value. Most monitors can automatically calculate the CI as long as the height and weight 

information has been entered. 

Cardiac Output Curves 

SVR/PVR 

Whenever a clinician has access to a PAC, a SVR and PVR should be calculated. As mentioned 

previously SVR and PVR reflect left and right ventricular afterload respectively. SVR/PVR will 

measure the amount of resistance caused by pulmonary or systemic arterial constriction or dilation. 



These values will help the clinician determine whether these vessels are constricted or dilated. 

Elevated SVR/PVR is an indication that there is an increase in the amount of vascular constriction, 

and conversely as it decreases that indicates vascular dilation. These values will not be displayed on 

the monitor because they can not be directly measured. The SVR and PVR are derived values 

obtained from the PAC and are calculated using the following formulas: 

SVR= MAP-RAP x 80 

CO 

PVR= Mean PA pressure – PAOP x 80 

CO 

Measured Hemodynamic Variables 

Systolic Blood Pressure 

Diastolic Blood Pressure 

Systolic Pulm. Art. Pressure 

Diastolic Pulm. Art. Pressure 

Pulm.Art.Occlusion Pressure 

Central Venous Pressure 

Heart Rate 


90 -140 mmHg 

60 - 90 mmHg 

15 - 30 mmHg 

4 -12 mmHg 

2 - 12 mmHg 

0 - 8 mmHg 

Varies by patient 

4 - 6 L/min 

Right Ventricular EF 0.40 - 0.60 

There are several conditions that can affect the SVR. Generally an increase in the SVR is the body’s 

attempt to increase the blood pressure. This is a compensatory reaction to a loss of volume or a 

decrease in CO as is the case with conditions such as hypovolemic or cardiogenic shock. This 

compensatory increase can maintain the blood pressure to a certain point. However, if the 

underlying cause is not treated the heart will become overwhelmed by trying to overcome such a 

high level of resistance leading to a fall in the blood pressure. Increases in the PVR will produce a 

strain on the right ventricle. Some of the reasons that the PVR is elevated include pulmonary 

hypertension, hypoxia, and pulmonary emboli. If the elevated PVR continues to go untreated, the 

right ventricle will enlarge because of the increased workload and eventually fail. Failure of the 

right ventricle will lead to a decrease in blood delivery to the lungs and a back-up of blood to the 

system. This will consequently lead to peripheral edema and eventually poor cardiac output and 

systemic hypotension. 

When the SVR is decreased as a result of vasodilation, the body will try and compensate by trying 

to increase the CO. So initially the CO may be elevated in an attempt to fill up the expanded space, 

but, much like when the SVR was too high, eventually these compensatory mechanisms will begin 



to fail if the underlying cause is not treated. This will consequently cause systemic hypotension. A 

low SVR is typically seen with distributive shock states such as septic or anaphylactic shocks. 

Calculated Hemodynamic Variables 

Mean Arterial Pressure 

Mean Pulmonary Art. Pressure 

Cardiac Index 

Stroke Volume (Index) 

Systemic Vasc. Resistance Index 

Pulmonary Vasc. Resistance Index 

Left Ventric. Stroke Work Index 

Right Ventric. Stroke Work Index 

Right Ventric. End.Diast.Vol.Index 

Body Surface Area (BSA) 

70 - 105 mmHg 

9 - 16 mmHg 

2.8 - 4.2L/min/m2 

Varies (30 - 65 ml/beat/m2) 

1600 - 2400 dyne.sec.cm-5 

250 - 340 dyne.sec.cm-5 

43 - 62 gm.m/m2 

7 - 12 gm.m/m2 

60 - 100 mL/m2 

Varies by patient (m2) 

Hemodynamic Monitoring Systems 

Types of Invasive Advanced Hemodynamic Monitoring 

The Pulmonary Artery Catheter 

Principles 

The most well known method of invasive hemodynamic monitoring devices is the pulmonary artery 

catheter (PAC), or the Swan-Ganz Catheter, referring to the inventors, Drs. Jeremy Swan and 

William Ganz at Cedars-Sinai, in California. This “flow-guided” catheter was introduced in 1970, 

and can be inserted via a large central vein such as the subclavian, internal jugular or femoral vein. 

A small balloon at the tip of the PAC is inflated once the waveform indicates the location of the 

right atrium. The physician advances the PAC following the path of the blood flow through the right 

ventricle and finally “wedging” in the pulmonary artery (PA) as evidenced by the waveform. The 

valve-less pulmonary circulation allows for obtaining left atrium pressures with the balloon inflated, 

blocking pressure readings from the pulmonary artery. This is called the pulmonary artery occlusion 

pressure (PAOP). The PAOP is measured intermittently by inflating the balloon with 1.5 ml of air 

for no longer than 10 –15 seconds to prevent pulmonary infarction. The central venous pressure 

(CVP) and the PA pressure are measured continuously. 

It is possible to measure cardiac output using the thermodilution method of the PAC. A thermistor 

at the tip of the PAC detects a temperature difference created by a 10 ml injection of room 



temperature saline via the central venous port of the PAC. The monitor then calculates a timetemperature 

curve, or thermodilution curve, which provides information based on the modified 

Stewart-Hamilton equation, about the patient’s cardiac output, stroke volume and vascular 

resistance. These parameters are measured intermittently unless a continuous thermodilution PAC 

is used. 

Continuous Cardiac Output (CCO) Monitoring 

This method is based on the same thermodilution method as the standard PAC. However, instead of 

using injectate saline, the catheter contains a thermal filament that produces a heat signal, warming 

up the blood. The temperature difference is detected at the thermistor at the tip of the PAC, and the 

computer then calculates a time-temperature curve. This allows for calculation of an average 

cardiac output every minute. The advantage of continuous cardiac output monitoring is the 

capability of capturing fluctuations in the hemodynamic status of the patient almost real time, thus 

allowing for immediate intervention if indicated. 

Additional parameters that can be measured using a CCO include Right Ejection Fraction (REF) 

and Right End-Diastolic Volume (REDV). REDV is a volume-based reflection of the preload status. 

This volumetric parameter, compared to pressure-based measurements (PAOP and CVP), reflects a 

superior estimate of intravascular volume. REF is a reflection of the contractility of the heart and 

the afterload. Where PAOP and CVP are influenced by increased intra-thoracic, intra-abdominal 

pressure and changing ventricular compliance, REF and REDV remain unaffected by these 

conditions. End-diastolic volume can be measured continuously using a special CCO catheter 

(CEDV). 

The REDVI (REDV Index = based on Body Surface Area) needs to be interpreted in conjunction 

with RVEF. Studies show that if the RVEF changes, the REDVI needs to be adjusted to maintain 

adequate cardiac output. If the RVEF is only 20%, indicating that only 20% of the preload volume 

(REDVI) is being ejected, the REDVI needs to be 200 mL/m 2 under normal circumstances, and 240 

mL/m 2 in the critically ill patients in order to maintain an adequate cardiac output. 

“Optimal” RVEDVI 

RVEF Normal Critically Ill 

.20 200 mL/m 2 240 mL/m 2 

.30 150 mL/m 2 180 mL/m 2 

.35 125 mL/m 2 150 mL/m 2 

.40 100 mL/m 2 120 mL/m 2 

.50 50 mL/m 2 60 mL/m 2 

Cheatham, et al (2001) 

For example, if the RVEF is 20%, and the REVD is 100 ml., the stroke volume (SV) will be 20 mL 

per beat. If the heart rate is 100 beats per minute, the cardiac output will be 20 mL x 100 = 2000 ml 

= 2.0 L per minute. This is unsustainable with life. By administering a fluid bolus the preload 



(RVED) can be increased, and by administering an inotropic agent the contractility (RVEF) can be 

increased. 

The CCO data can be influenced by an irregular heart rate, dysrhythmias, mitral valve disease, 

hyperthermia > 41° Celsius (105.8 º Fahrenheit) and inaccurate catheter placement. This could 

result in erroneous data or no data at all. 

Combo CCO SVO2 PA catheter 

Mixed Venous Saturation & Central Venous Oxygenation 

The standard PAC is capable of measuring mixed venous saturation (SVO 2 ) intermittently by 

aspirating blood from the PA-port for blood gas analysis. The more advanced PAC can 

continuously monitor SVO 2 , thus providing the practitioner with constant information about the 

patient’s tissue oxygenation balance. SVO 2 only provides information about the mixed venous 

saturation, which is a global indicator of the oxygen balance and non-specific to individual organs. 

Red blood cells absorb different amounts of light, based on oxygenated or deoxygenated 

hemoglobin. The fiberoptic sensor at the tip of the PAC is connected to an optical module, which 

uses reflectance spectrophotometry to differentiate between oxygenated and deoxygenated blood, 

resulting in the measurement of SVO 2 in the pulmonary artery. Based on these readings and 

hemodynamic calculations, the monitor can calculate oxygen transport (DO 2 ) and oxygen 

consumption (VO 2 ). 

Under normal circumstances the body consumes 25% of the oxygen delivery, resulting in a return 

of 75% to the right side of the heart. Therefore, normal SVO 2 values are between 60% and 80%, 

indicating a balance between DO 2 and VO 2. 

Central venous oxygenation monitoring (ScvO 2 ) can be accomplished by inserting a central venous 

catheter with a fiberoptic sensor at the tip. This will provide information regarding tissue 

oxygenation. However, ScvO 2 and SvO 2 are not equal. Studies have shown that, on average, ScvO 2 

values are 5% higher than SvO 2 , which is most likely due to the mixing of venous blood from the 

coronary circulation. 

It is most important to follow trends regardless of which venous oxygenation parameter is being 

used. A change of more then 10% from the baseline can be a clinically significant early indication 

of physiological instability or cardiopulmonary decline. A low SVO 2 can indicate a decrease in 

cardiac output (hypovolemia, myocardial infarction, increased intra-thoracic pressure), in oxygen 

saturation (pulmonary edema, ARDS, low FiO 2 ), in hemoglobin level (anemia, hemorrhage, 

dysfunctional hemoglobin), or an increase in oxygen consumption (pain, anxiety, restlessness, 

tachycardia, shivering, hyperthermia, burns). 



Pulmonary Artery Catheter Combinations 

Many PAC consist of combinations of different techniques. Some combinations include CCO/SVO 2 

and CCO/CEDV/SVO 2 monitoring capabilities. Other PAC allow for additional pacing ports with 

options for ventricular or atrio-ventricular pacing. Similar combinations are available for pediatric 

PACs. 

Complications 

The most common complications of PACs during insertion are arterial puncture, pneumothorax, 

hemothorax, air embolism, ventricular dysrhythmia, bundle branch block, complete heartblock, and 

catheter knotting or kinking. 

If possible, PAC insertion in patients with a left bundle branch block should be avoided because the 

ventricular irritation during insertion can result in a third degree heart block. If insertion of a PAC is 

unavoidable, the physician should consider inserting a PAC with pacing capabilities. 

Complications during the maintenance phase of the PAC include pulmonary artery rupture, 

pulmonary infarction, infection, ventricular dysrhythmia, and thrombus formation. 

Arterial Pulse Contour Analysis 

Principles 

This technology analyzes the arterial pressure waveform and provides an estimate of the stroke 

volume. It is not a new technology as it was described as early as the 1940s. The principle is based 

on the measurement of peak and slope of the arterial waveform, which reflects the stroke volume. 

Several different methods are currently available: cold saline calibration technique, lithium 

indicator technique, and computer algorithms. 

Lithium Indicator Dilution 

Lithium indicator dilution requires an arterial catheter for pulse contour analysis, and a peripheral 

catheter. Initial calibration is performed using a lithium injection via the peripheral catheter that is 

being detected by the lithium-sensing electrode attached to the arterial catheter. This links the 

arterial waveform to the cardiac output measured via the lithium dilution technique. The calibration 

has to be repeated every eight hours in order to maintain its accuracy. The main parameters 

measured are continuous CO, SV, and SVV. It does not provide any information about filling 

pressures or volumes. If used in combination with a central venous catheter and CVP monitoring, 

afterload (SVR) can be measured. The algorithm used does not depend on the morphology of the 

arterial waveform. 

If the patient is on lithium therapy, this technology cannot be used. Also, the lithium injection is 

contraindicated for patients weighing less than 40 kg and during the first trimester of pregnancy. 

Neuromuscular blocking agents can interfere with the lithium sensor and provide inaccurate 



information. Aortic regurgitation, arrhythmias, intra-cardiac shunts and aortic aneurysm are other 

factors that influence the accuracy of the measurements. 

If PA catheterization is not possible, this technology provides an acceptable and less invasive 

alternative. 

Computer Algorithm 

Another method for pulse contour analysis uses a computer algorithm and a mathematical model to 

determine the vascular tone based on patient gender, height, weight and BSA. This technology 

provides every 20 seconds updated information about CO, SV, and Stroke Volume Variation 

(SVV), as long as the patient is being mechanically ventilated, and without significant arrhythmias. 

Arterial pulse pressure rises during spontaneous inspiration, and falls during expiration as a result of 

changing intra-thoracic pressures. During mechanical ventilation this phenomenon is reversed and 

is called reverse pulsus paradoxus, or paradoxical pulsus, or respiratory paradox. This variation can 

be measured and is called SVV. A normal SVV is less than 10 –15% on controlled mechanical 

ventilation. SVV is not an actual indicator of preload, but more of fluid responsiveness. The 

combination of SV and SVV can be used to guide fluid management and optimize the preload. 

In combination with a central venous catheter (CVC), it can also provide SVR, and ScvO 2 , 

depending on the catheter type. 

Current literature only supports the use of SVV on patients that are on controlled mechanical 

ventilation with tidal volumes greater than 8cc/kg and on a fixed respiratory rate. Arrhythmias 

negatively affect SVV measurement. If increased levels of PEEP are used, SVV values can be 

increased. Changes in vascular tone with the use of vasodilatation therapy may also increase SVV 

values. 



SV max and SV min are measured over 30 seconds then the SV mean is calculated. The variation in 

stroke volume (SVV) = SVmax-SVmin/SVmean. 

Cold Saline Calibration 

In order to obtain measurements, a central venous catheter and an arterial pressure catheter is 

needed. An initial injection of cold saline is needed for calibration related to analysis of the arterial 

pulse contours. This transpulmonary thermodilution technique then calculates the CO, SV and SVV. 

Additional parameters that can be calculated intermittently are global end-diastolic volume 

(GEDV), intrathoracic blood volume (ITBV) and extravascular lung water (EVLW). The ITBV is 

the sum of the GEDV and the pulmonary blood volume. 

Limitations include the necessity to recalibrate after changes in patient position, therapy or 

condition, or at least every eight hours. The accuracy of this pulse contour analysis technique 

depends on the location of the arterial catheter. Axillary or femoral locations are more accurate 

compared to a radial arterial catheter. Aortic regurgitation, arrhythmias, intra-cardiac shunts and 

aortic aneurysm influence the accuracy of the measurements. This technology can only be 

accurately applied if the patient is on controlled mechanical ventilation and has a stable heart 

rhythm. 

The PiCCO monitor is currently the only device that utilizes this type of pulse contour analysis. 

RAEDV 

RVEDV 

ETV 

PBV 

LAEDV 

LVEDV 

Right Atrial End Diastolic Volume 

Right Ventricular End Diastolic Volume 

EVWL Extra Vascular Lung Water 

Pulmonary Blood Volume 

Left Atrial End Diastolic Volume 

Left Ventricular End Diastolic Volume 



Non-Invasive Advanced Hemodynamic Monitoring 

Ultrasound 

Ultrasound has a frequency that exceeds the limit of human hearing, which is approximately 20.000 

hertz. Ultrasound was introduced in medicine in the late 1950’s to mid 1970s and can be used in 

medical diagnostics, where the reflection of the organ being exposed to ultrasound, produces an 

image that can be studied and interpreted. 

2 –D echocardiography 

This study can provide information about the size, structure, valves, presence of pericardial fluid, 

motion patterns and analysis of physiological variables such as ECG, heart sounds and pulse 

tracings of the heart. It is a very useful method of assessing preload and contractility. 

There are different techniques of echocardiography that can be used. The M-mode is a method 

where the ultrasound beam is manually aimed at selected cardiac structures using trans-thoracic 

echographic (TTE) access, which provides information about the positions and movement of these 

structures. It can also identify time relationships between physiological variables. Newer methods 

use electromechanical techniques to produce two-dimensional (2-D) tomographic images of elected 

structures. These images can be recorded on a standard video tape recorder. 

The greatest limitation for echocardiography can be the lack of access to the heart. Overlaying 

anterior boney structures such as the sternum and ribs are practically impenetrable to ultrasound and 

make it difficult for the technician to find a transducer site that can provide good quality images. 

For critical care management, the lack of continuous monitoring and anatomical changes in 

critically ill patients, limit the use of this technology. 

Trans-esophageal echocardiogram (TEE) 

This technique uses a special probe with an ultrasound transducer attached to the tip, which is 

advanced into the esophagus till it reaches the site of the heart. Because the esophagus is posterior 

and close to the heart, the images produced using this method, are of superior quality compared to 

the TTE method. 



The procedure is uncomfortable for the patient and requires sedation to decrease the gag reflex and 

may require muscular blockade in order to obtain a clear image. It is contraindicated in patients with 

esophageal disease or a problematic airway. 

Esophageal Doppler 

The Esophageal Doppler technique uses a flexible probe with an ultrasound probe at the tip to 

measure continuous or intermittent blood flow velocity in the ascending aorta. The tip of the probe 

is placed at the mid-thoracic level and then rotated so that the transducer faces the aorta. Age, 

height, weight and gender of the patient is needed to calculate the aortic diameter and, more 

specifically, the cross-sectional area. A clear signal indicates the proper position of the probe. 

Technology used for TTE is applied to calculate SV and CO. 

The stroke volume is derived from the flow velocity, ejection time and aortic cross section. Other 

assessment parameters include peak flow velocity to estimate ventricular contractility, SVR and 

corrected flow time (Ftc), which is a superior estimate of preload status as compared to PAOP and 

CVP. The accurate alignment of the Doppler beam and blood flow is essential for a reliable blood 

flow velocity measurement. The technique is relatively simple to learn, but requires some training 

to achieve adequate probe positioning. Nursing procedures, patient movement and other factors can 

affect the position of the probe and result in erroneous CO results if the dislocation is not noticed. 

Compared to the thermodilution technique, which is often referred to as the “gold standard”, 

Esophageal Doppler does not correlate well. However, studies found that the changes in cardiac 

output measured were consistent with the changes measured using the thermodilution technique. 

Fick Principle and Carbon Dioxide 

Fick described the first method to estimate cardiac output in 1870, using a formula to determine 

cardiac output based on the ratio between oxygen consumption (VO 2 ) and the arteriovenous 

difference in oxygen (AVDO s ). This equation is accurate when the hemodynamic condition of the 

patient is stable enough to allow constant gas diffusion to the pulmonary circulation. 

The Fick Principle can also be applied to the gas diffusion of carbon dioxide. A carbon dioxide 

sensor, a disposable airflow sensor and a pulse oximeter are used to determine the CO. The patient 

must be on fully controlled mechanical ventilation. Exhaled CO 2 (VCO 2 ) is calculated from the 

minute ventilation and the carbon dioxide content, and arterial carbon dioxide content (CaCO 2 ) is 

estimated from the end-tidal carbon dioxide (etCO 2 ). 



Hemodynamic instability and intrapulmonary shunt are common problems in critically ill patients, 

and also pose significant limitations to this method of cardiac output determination. Current studies 

conclude that the carbon dioxide method is not yet reliable compared to the thermodilution 

technique, but could be potentially useful when utilized in the appropriate patient population. 

Bioimpedance Cardiac Output Determination 

The bioimpedance method measures changes in the body’s resistance (impedance) to small 

electrical currents. Blood and tissue impede electrical current. However, this doesn’t change during 

cardiac ejection. The blood volume in the chest changes during every ejection, which can be 

detected using eight electrical patches positioned on the neck and thorax. Based on these changes in 

impedance, a computer can calculate the cardiac output. 

This technology is currently less accurate in the critically ill patients. Presently clinical trials are in 

progress, which are using bioimpedance derived from an endotracheal tube. Current data is 

promising, but limited, and require further evaluation to determine its usefulness in the critically ill 

patient. 

Hemodynamic Pharmacology 

Once all of the data has been collected from the PAC, the clinician needs to have a thorough 

understanding of how various medications can help in treating the patient. This text will provide a 

brief description of hemodynamic pharmacology and its application for further information. Please 

refer to more in depth references or the designated clinical pharmacist. 

Parameter Value Consider Rule Out 

Preload 

Increased 

Dilators: 

(CVP, RAP, 

• Nitroglycerin 

PAOP/PAWP) 

• Nitroprusside 

(Nipride) 

• Milrinone 

Diuretics: 

• Furosemide 

• Bumetanide 

• Mannitol 

Morphine 

Adult Respiratory 

Distress Syndrome 

Heart Failure 

Pulmonary Edema 

Constrictive or 

obstructive conditions 

of the heart 



Afterload 

(SVR, PVR) 

Contractility 

(SV, LVSWI) 

Decreased 

Increased 

Decreased 

Increased 

Volume: 

• Colloids 

• Crystalloids 

• Blood 

• Hetastarch 

Dysrhythmia control: 

• Antiarrhythmics 

• Pacemaker 

• AICD 

Dilators: 

• Nitroglycerin 

• Nitroprusside 

(Nipride) 

• Milrinone 

• Alpha 

adrenergic 

blockers 

• Calcium 

Channel 

Blockers 

Intraaortic Balloon 

Pump 

• Increase 

augmentation 

Vasopressors: 

• Epinephrine 

• Norepinephrine 

• Dopamine 

• Neosynephrine 

Intraaortic Balloon 

Pump: 

• Decrease 

augmentation 

• Beta blocker 

• Calcium Channel 

Blocker 

Hypovolemia 

Septic Shock 

Hypovolemia 

Heart Failure 

Late Septic Shock 

Anaphylactic Shock 

Neurogenic Shock 

Early Septic Shock 

Early Anaphylactic 

Shock 

Early Neurogenic 

Shock 

Early Septic Shock 

Decreased 

Positive Inotropes: 

• Dobutamine 

• Dopamine 

• Milrinone 

• Digoxin 

Heart Failure 

Constrictive or 

obstructive conditions 

of the heart 



Increased 

Decreased 


Consider the factors 

that may increase CO 

such as: 

• Elevated preload 

• Decreased afterload 

• Elevated 

Contractility 

Consider the factors 

that may decrease CO 

such as: 

• Decreased preload 

• Increased or 

decreased afterload 

• Decreased 

contractility 

Hemodynamic Parameters of Common Critical Illnesses 

Heart Rate Blood Pressure CO/CI Preload 

(CVP/PAOP) 

Afterload 

(PVR/SVR) 

Hypovolemic 

Shock ▲ ▼↔ ▼ ▼ ▲ 

Cardiogenic 

Shock ▲ ▼↔ ▼ ▲ ▲ 

Early Septic 

Shock ▲ ▼↔ ▲ ▼ ▼ 

Late Septic 

Shock ▲ ▼ ▼ ▲ ▲ 

Anaphylactic 

Shock ▲ ▼↔ ▼↔ ▼ ▼ 

Neurogenic 

Shock ▼↔ ▼↔ ▼↔ ▼ ▼ 

▼= Decreased 

▲= Increased 

↔ = Normal 



Hemodynamic Applications 

These cases will provide the opportunity to see how advanced hemodynamic monitoring may 

assist in determining appropriate interventions for different situations. 

Case 1 

You are caring for a 29-year old male motor cycle crash patient with a BP of 74/30, heart rate 

of 52. What should you do about his hypotension? You can’t be sure without knowing the 

reason for it. In addition, the CVP reading is 1 mm Hg. This additional information indicates 

that the patient has a diminished blood volume returning to the right heart, but still doesn’t tell 

you what interventions should receive the highest priority. Further assessment reveals that the 

patient sustained a C 7 fracture with severe extremity weakness noted. You now correctly 

determine that the patient is in neurogenic shock, causing a loss of vasomotor tone, and that he 

is hypotensive not because he has lost blood volume, but because neurogenic shock results in 

massive vasodilation (decreased SVR), decreased blood return to the right atrium and 

bradycardia. Note the patient’s pulse pressure; it is wide, indicating arterial vasodilation. 

Oxygen delivery (DO2) and oxygen consumption (VO2) most likely will not be changed. 

Stroke Volume Variation (SVV) in this case would be high, and can be used to guide your fluid 

resuscitation. Considering the evident cause of his hypotension and bradycardia, advanced 

hemodynamic monitoring is not immediately indicated. Taking all the data into consideration 

allows you to intervene appropriately with a vasoconstrictor and IV fluids to fill the vascular 

space. 

Case 2 

You are caring for a 79-year old male patient with a BP of 84/40, temperature 104° F (40º C), 

heart rate 120 bpm, and SaO2 90% on 4 liters NC. He is admitted from a nursing home with 

pneumonia. What is causing his hypotension? Note that the pulse pressure is wide, indicating 

vasodilation and decreased left ventricular afterload. Additional information includes a CVP 

reading of 1 mm Hg. What does this tell us? Only that we have a decreased right ventricular 

end diastolic pressure/volume. Severe dehydration, blood loss, spinal shock and vasogenic 

shock can reveal the same findings. However, we suspect that this patient is in early septic 

shock considering his pneumonia and fever which also causes vasodilation (decreased SVR) 

and a decreased preload. Further assessment reveals lung sounds include bilateral rhonchi, and 

laboratory results show leucocytosis. This rules the patient in for severe sepsis. Upon 

examining peripheral pulses, we note them to be bounding and skin turgor is poor. The cardiac 

output will be high as the patient is in a hyperdynamic state. If oximetric measurements are 

available, expect the SVO2/ScVO2 to be either high because oxygenated blood is being 

shunted away and not being utilized by the tissues, or it could be low because of higher oxygen 

consumption (VO2). Oxygen delivery (DO2) is probably normal. If the patient would be on a 

ventilator and pulse contour analysis would be applied it would show a high Stroke Volume 

Variation (SVV) because of the decreased preload volume. This patient will need to be fluid 

resuscitated to improve preload and antibiotics need to be initiated. Ventilatory support and 

possible inotropic support can be indicated if the condition deteriorates. 



Case 3 

You are admitting a 63-year old female with a BP of 84/70 and HR of 110 bpm. History reveals 

that she was admitted with a diagnosis of chest pain. Your assessment reveals bilateral crackles 

in her lungs, and heart sounds reveal S3-S4. So what do we do? Should we give diuretics or 

fluids? A pulmonary artery catheter is inserted and shows a PAOP of 26 mmHg, CVP 24 mm 

Hg, Cardiac Index is 2.1 L/min and the SVRI is 2800 dyne.sec.cm-5. This indicates that both 

left and right atrial filling pressures are elevated, she is vasoconstricted and has a decreased 

cardiac output. Stroke volume will be low, Oxygen delivery (DO2) and SVO2 will be low due 

to a decreased cardiac output. Oxygen consumption (VO2) can be high because of increased 

heart rate and cardiac muscle workload. To increase the cardiac output, a vasodilator, a diuretic 

and an inotrope can be used as guided by your hemodynamic profiles. 

Case 4 

You are caring for a 31 year old male patient involved in a motor vehicle crash. His injuries 

include bilateral pulmonary contusions and a blunt abdominal trauma. He is intubated and 

being mechanically ventilated. He required multiple blood transfusions and received also an 

additional 6 liters of normal saline for a slow responding blood pressure of 91/55. The 

physician inserted a volumetric PA-catheter to guide the resuscitation. After several hours you 

noticed that the CVP increased to 28 mmHg and the PAOP to 32 mmHg. Does he need a 

diuretic because he could be in heart failure? Further hemodynamic assessment reveals a CI of 

2.3 L/min, SVRI 2900 dyne.sec.cm-5 and an EDVI of 80 ml/m² with a REF of 31%. His 

abdomen is firm and distended, and his inspiratory pressures on the ventilator have been 

increasing steadily. You also noticed that his urinary output decreased to 15 ml/hr and the 

laboratory results show a lactic acid of 6.2. Because of possible abdominal compartment 

syndrome, the physician orders intra-abdominal pressure monitoring. The first reading reveals 

an intra-abdominal pressure of 31 mmHg. The patient has an intra-abdominal compartment 

syndrome and requires abdominal decompression. The increased intra-abdominal pressure 

increases the intra-thoracic pressure, which increases the CVP and PAOP. However, these 

increased cardiac filling pressures do not accurately reflect the preload as evidenced by the low 

EDVI and REF. Therefore a diuretic would worsen his condition even more by decreasing the 

preload (EDVI). 


Post Test 


Directions: Complete this test using the bubble sheet provided. 

1. Which of the following statements is true regarding the distal port of the pulmonary artery 

catheter 

A. It is connected to a pressure transducer and a flush device 

B. It is the port used for cardiac output injectate 

C. It allows continuous measurement of the pulmonary artery occlusive pressure 

D. It serves as an infusion port for vasoactive medications 

2. During the insertion of the pulmonary artery catheter, how much air should be used to inflate 

the balloon? 

A. ½ ml 

B. 1 ml 

C. 1 ½ ml 

D. 2 ml 

3. Which port must be connected to a transducer to allow waveform analysis during insertion of 

a pulmonary artery catheter? 

A. Pulmonary artery distal 

B. Proximal injectate port 

C. Proximal infusion port 

D. Cardiac Output port 

4. Which of the following reflects normal pulmonary artery systolic and diastolic pressures? 

A. 120/80 mm Hg 

B. 20/5 mm Hg 

C. 25/15 mm Hg 

D. 45/25 mm Hg 

5. Which one of the following statements about respiratory variation is true? 

A. Pulmonary artery pressure rises during inspiration in a spontaneously breathing 

patient. 

B. Pulmonary artery pressure falls during inspiration in mechanically ventilated patients 

C. Pulmonary artery pressure should be read at peak inspiration 

D. Pulmonary artery pressure should be measured at end expiration 

6. The left ventricular preload is measured clinically with a pulmonary artery catheter by 

obtaining a 

A. Systemic vascular resistance 

B. Contractility pressure 

C. Pulmonary artery systolic pressure 

D. Pulmonary artery occlusive pressure (PAOP/PAWP) 

7. In determining the amount of air used to wedge a pulmonary artery catheter, the best 

guideline to use is? 

A. Inflate until the wedge waveform is greater than the systolic 

B. Always instill 1 ½ cc air 

C. Instill the same amount of air used with the previous wedge 


D. Inflate just until the wedge waveform appears 


8. Which of the following may be used to increase preload in a hypovolemic patient? 

A. Diuretics 

B. Volume 

C. Vasopressor 

D. Vasodilators 

9. Another name for systemic vascular resistance is 

A. Preload 

B. Afterload 

C. Contractility 

D. Pulmonary artery diastolic pressure 

10. The afterload pressure for the right ventricle would be the 

A. Pulmonary vascular resistance 

B. Systemic vascular resistance 

C. Pulmonary artery occlusive pressure 

D. Pulmonary artery pressure 

11. Mixed venous oxygen consumption allows us to measure which one of the following? 

A. Amount of oxygen in arterial blood 

B. Balance between oxygen supply and demand 

C. Balance between carbon dioxide supply and demand 

D. Amount of carbon dioxide in venous blood 

12. Normal cardiac output is 

A. 2-3 L/min 

B. 4-8 L/min 

C. 1-2 L/min 

D. 10-12 L/min 

13. Mr. Jones develops extreme dyspnea, anxiety, coughing up pink frothy sputum. His heart rate 

is 120 bpm and his breath sounds reveal crackles throughout both lung fields. The 

PAOP/PAWP is 30 mm Hg. Which of the following is the most likely diagnosis? 

A. Pulmonary embolus 

B. Pneumonia 

C. Pulmonary Edema 

D. Cardiogenic Shock 

14. The phlebostatic axis is located at the patient’s 

A. 4 th intercostal space, mid chest 

B. 3 rd intercostal space, mid axillary line 

C. 3 rd intercostal space, mid clavicular line 

D. 4 th intercostal space, mid clavicular line 

15. An abnormal physical finding that can cause an elevated PAOP/PAWP includes which of the 

following 

A. Tachycardia 

B. Hypovolemia 



C. Vasodilator therapy 

D. Hypervolemia 

16. In the absence of primary pulmonary disease, the pulmonary artery diastolic pressure 

correlates with which of the following? 

A. CVP 

B. PAOP/PAWP 

C. Systolic blood pressure 

D. SVR 

17. A pulmonary artery catheter is inserted in a patient with left ventricular failure. While 

deflating the balloon after wedging, the nurse notes blood in the balloon catheter. Which of 

the following is the most appropriate action? 

A. Change the syringe to prevent infection 

B. Check to see whether blood may be aspirated from the site 

C. Remove the syringe, close it with a dead end cap and mark “do not use” 

D. Inject 1.5 ml of air to see if the wedging is still possible 

18. The SVO2 is a reflection of 

A. Arterial oxygenation measured in the pulmonary artery. 

B. The end-result of oxygen consumption by the heart, lungs and kidneys 

C. The end-result of DO2 and VO2 

D. Oxygen consumption 

19. The largest influence on oxygen delivery (DO2) is 

A. PO2 and SPO2 

B. Oxyhemoglobin dissociation curve 

C. Hemoglobin 

D. Oxygen dissolved in plasma 

20. Factor that influence the Lithium Indicator Dilution technique include 

A. Controlled Mechanical ventilation 

B. Spontaneous respirations 

C. Continuous sedative infusion 

D. Infusion of neuro muscular blocking agents 

21. Stroke Volume Variation is an indicator of 

A. Preload volume 

B. Fluid responsiveness 

C. Afterload 

D. Contractility 

22. The measurement of peak flow velocity using esophageal Doppler technique is 

A. Used to calculate stroke volume 

B. Is not influenced by the ultrasound probe position 

C. Is the “gold standard” to measure cardiac output 

D. Used to calculate extra Vascular Lung Water 



23. A drop of 10% in the mixed venous oxygen saturation can be clinically significant. 

A. True 

B. False 

24. The parameter End Diastolic Volume measured using a Continuous Cardiac Output monitor 

is 

A. A pressure-based reflection of the preload status 

B. A volume-based reflection of the preload status 

C. Is effected by increased intra-thoracic pressures 

D. Is measured intermittently 

25. CVP and PAOP are reliable parameters to estimate preload status in a patient with increased 

intra-abdominal pressure? 

A. Only if the patient is breathing spontaneously 

B. Only if the patient is being mechanically ventilated 

C. CVP and PAOP are not indicators of preload 

D. This statement is incorrect 



References 

References 

Berton, C., & Cholley, B. (2002). Equipment review: new techniques for cardiac output 

measurement – oesophageal doppler, Fick principle using carbon dioxide, and pulse contour 

analysis. Critical Care, 6(3), 216-221. 

Cheatham, M. L. (2009, January 13). Hemodynamic calculations II. Retrieved November 30, 2009, 

from http://www.surgicalcariticalcare.net 

Cheatham, M. L. (2009, January 13). Hemodynamic Monitoring: Today’s Tools in the ICU. 

Retrieved November 30, 2009, from http://www.surgicalcriticalcare.net 

Engoren, M., & Barbee, D. (2005). Comparison of cardiac output determined by bioimpedance, 

thermodilution, and the Fick method. American Journal of Critical Care, 14, 40-45. 

Headley, J. M. (2002). Invasive hemodynamic monitoring: physiological principles and clinical 

applications. Retrieved November 30, 2009, from 

http://ht.edwards.com/resourcegallery/products/swanganz/pdfs/ 

invasivehdmphysprincbook.pdf. 

Jesurum, J. (2009). SVO2 Monitoring. Critical Care Nurse, 24(4), 73-76. 

Kisslo, J. A., Adams, D. B., & Graham, J. L. (2000, November 11). Two-dimensional 

echocardiography in the normal heart. Retrieved November 25, 2009, from Duke 

University School of Medicine Web Site: http://www.echoincontext.com/ 

Pinsky, M. R. (2003). Probing the limits of arterial pulse contour analysis to predict preload 

responsiveness. Anesthesia and Analgesia, 96, 1245-1247. 

Wallace, A. W., Salahieh, A., Lawrence, A., Spector, K., Owens, C., & Alonso, D. (2000). 

Endotracheal cardiac output monitor. Anesthesiology, 92(1), 178-189. 

Wiegang, D. J. & Carlson, K. K. (2005). AACN procedure manual for critical care. 5 th ed. Elsevier- 

Saunders: St. Louis. 



Glossary 

Body Surface Area (BSA): is calculated using the height and weight of the patient and is 

expressed in square meters (m 2 ). A normal BSA for adult male is 1.9 m 2 and for adult females 

1.6 m 2 . 

Cardiac Index (CI): is the cardiac output related to the body surface area (BSA). CO/BSA = 

CI. A normal CI ranges from 2.8 – 4.2 L/m 2. 

Cardiac Output (CO): is the amount of blood volume pumped out by the heart per minute, 

expressed in liters (L) per minute. A normal cardiac output is between 4 – 8 L/min. 

Continuous End Diastolic Volume (CEDV): is the continuous measurement of the right 

ventricular end-diastolic volume using a continuous cardiac output monitor that can measure 

continuous ejection fraction. 

Central Venous Pressure (CVP): is the measurement of the pressure of the blood in the 

thoracic vena cava or right atrium and reflects the preload of the right heart. 

Continuous Cardiac Output (CCO): is the continuous measurement of cardiac output. 

Various techniques can be used such as thermodilution and pulse contour analysis. 

DO 2 I: is the volume of oxygen pumped out by the ventricle per minute per meter square, and is 

an indicator of the amount of oxygen delivered to the tissues related to the BSA. Formula: 

(CaO 2 )(CO/BSA)(10dL/L) = 500 - 650ml O 2 min/m 2 (normal range). 

Extra Vascular Lung Water Index (ELWI): is an indicator of pulmonary edema related to the 

body surface area. It is obtained using the transpulmonary thermodilution technique. The normal 

values range between 3.0 – 7.0 m//kg. 

Global End-Diastolic Volume Index (GEDI): is an estimate of preload volume related to the 

body surface area, obtained by transpulmonary thermodilution technique using cold saline 

calibration. The normal values range between 680 – 800 ml/m 2 . 

Intrathoracic Blood Volume Index (ITBVI): is a global indicator that can be used to predict 

fluid resposiveness related to the body surface area, obtained by the transpulmonary 

thermodilution technique. The normal values range between 850 – 1000 ml/m 2 . 



Lithium indicator dilution technique: uses an injection of lithium via a peripheral catheter, 

which is being detected at the lithium sensor of an arterial catheter. It calibrates the arterial 

waveform in order to calculate the cardiac output. 

PA: Pulmonary artery. 

Positive End Expiratory Pressure (PEEP): is a ventilator mode that keeps the airway pressure 

above atmospheric pressure, thus increasing the surface area for gas exchange. 

Pulmonary Artery Catheter (PAC): Flow-guided catheter to measure pulmonary artery 

pressures and cardiac output. Developed by the physicians Swan and Ganz in the 1970s. 

Pulmonary Artery Occlusion Pressure (PAOP): is the pressure of the blood distal to the 

occlusion of the pulmonary artery measured by the PAC, and reflects the left ventricular 

preload. 

Pulmonary Vascular Resistance (PVR): is the opposition of flow in the pulmonary 

circulation. Formula: PVR = (MPAP-PAOP)(79.9)/CO. Normal range is between 150 - 250 

dynes/sec/cm 5 . 

Right Ejection Fraction (REF): is the percentage of blood pumped out by the right ventricle 

per beat. A normal ejection fraction is between 50 – 65%. 

Right End Diastolic Volume (REDV): is the volume of the right ventricle in diastole prior to 

ejection (systole) expressed in milliliters (ml). 

Stroke Volume (SV): is the amount of blood volume (in milliliters) ejected every with 

ventricular contraction. The normal range is between 60 – 100 ml/beat. 

Stroke Volume Index (SVI): is the relationship of stroke volume and body surface area. The 

normal range is between 33 – 47 ml/beat/m 2 . 

Stroke Volume Variation (SVV): is the measurement of variability of the arterial pressure 

waveform during inspiration and expiration on controlled mechanical ventilation. It can be used 

to guide fluid resuscitation. The normal values range between 10 – 15%. 

Systemic Vascular Resistance (SVR): is the opposition of flow in peripheral circulation. 

Formula: SVR = (MAP-CVP)(79.9)/CO. Normal range is between 1000 - 1300 dynes/sec/cm 5 . 



Transpulmonary thermodilution technique: or cold saline calibration, uses an injection of 

cold saline via a central venous catheter, creating a change in temperature (transpulmonary) 

which is being detected in a special arterial catheter. A computer calculates the cardiac output, 

global end-diastolic volume, and an estimation of extravascular lung water. 

VO 2 I: is the volume of oxygen consumed by the tissues each minute per m 2 . Formula: 

[(CO/BSA x CaO2)-(CO/BSA x CvO2) x 10dl/L = 120 – 160 ml/min/m 2 (normal range). 

Right Ventricular End Diastolic Volume Index (REDVI): is the REDV related to the body 

surface area (BSA), expressed in ml/m 2 . It can be calculated by REDV/BSA = REDVI. 

ScVO 2 : is the central venous oxygenation measured in the thoracic vena cava close to the right 

atrium. A central venous catheter with a fiber optic sensor at the tip is used to obtain the 

readings. The normal values are about 5% higher than the SVO 2 values, most likely due to the 

mixing of venous blood from the coronary circulation. 

SVO 2 : is the mixed venous oxygen saturation measured in the pulmonary artery using a 

pulmonary artery catheter equipped with a fiber optic sensor. SVO 2 is a global indicator of 

tissue oxygenation balance an does not reflect organ specific oxygen balance. Normal values 

range between 60% and 80%. 

Thermodilution technique: uses a PAC equipped with a thermistor at the tip placed in the 

pulmonary artery. Cold saline with a know temperature is injected into the CVP port and passes 

through the ventricle. The temperature difference measured by the thermistor and creates a 

time/temperature curve. Next, a computer calculates the cardiac output using the modified 

Stewart-Hamilton equation. 

Quick Reference Values 

Normal Hemodynamic Parameters – Adult 

Measured Hemodynamic Variables 

Systolic Blood Pressure 

Diastolic Blood Pressure 

Systolic Pulm. Art. Pressure 

Diastolic Pulm. Art. Pressure 

Pulm.Art.Occlusion Pressure 

Central Venous Pressure 

90 -140 mmHg 

60 - 90 mmHg 

15 - 30 mmHg 

4 -12 mmHg 

2 - 12 mmHg 

0 - 8 mmHg 



Heart Rate 


Varies by patient 

4 - 6 L/min 

Right Ventricular EF 0.40 - 0.60 

Calculated Hemodynamic Variables 

Mean Arterial Pressure 

Mean Pulmonary Art. Pressure 

Cardiac Index 

Stroke Volume (Index) 

Systemic Vasc. Resistance Index 

Pulmonary Vasc. Resistance Index 

Left Ventric. Stroke Work Index 

Right Ventric. Stroke Work Index 

Right Ventric. End.Diast.Vol.Index 

Body Surface Area (BSA) 

70 - 105 mmHg 

9 - 16 mmHg 

2.8 - 4.2L/min/m2 

Varies (30 - 65 ml/beat/m2) 

1600 - 2400 dyne.sec.cm-5 

250 - 340 dyne.sec.cm-5 

43 - 62 gm.m/m2 

7 - 12 gm.m/m2 

60 - 100 mL/m2 

Varies by patient (m2) 

“Optimal” RVEDVI 

RVEF Normal Critically Ill 

.20 200 mL/m 2 240 mL/m 2 

.30 150 mL/m 2 180 mL/m 2 

.35 125 mL/m 2 150 mL/m 2 

.40 100 mL/m 2 120 mL/m 2 

.50 50 mL/m 2 60 mL/m 2

Advanced Hemodynamics - Orlando Health

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