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Hemodynamic Monitoring: 8

Hemodynamic Monitoring Declaratives

Authors:

Scott R. Snyder, BS, CCEMT-P

EMT Program Manager, San Francisco Paramedic Association

Mike Clumpner, PhD(c), MBA, CHS, NREMT-P, CCEMT-P, PNCCT, EMT-T, FP-C
Faculty, Professional and Continuing Education: UMBC, Baltimore, MD

Reviewers:

Kelly Gahan, MD
Flight Physician: Med Center Air, Charlotte, NC
Assistant Medical Director: Mecklenburg EMS Agency, Charlotte, NC
Junior Faculty: Carolinas Medical Center Emergency Department, Charlotte, NC

Benjamin Lawner, DO, FAAEM, EMT-P

Clinical Instructor and Attending Physician: Department of Emergency Medicine
University of Maryland School of Medicine, Baltimore, MD
Deputy EMS Medical Director: Baltimore City (MD) Fire Department
Medical Director: CCEMTP Program: UMBC, Baltimore, MD

Stefan Zwolsky, MS, NREMT-P, FP-C

Rettungsassistent (Paramedic): Bayerisches Rotes Kreuz, Kreisverband Augsburg-
Stadt, Germany

Michael L. Wallace, MPA, EMT-P, CCEMT-P

EMS Captain: Central Jackson County Fire Protection District, Blue Springs, MO

John Mohler, RN, BSN, BS, CCRN, CFRN

Flight Nurse: Care Flight, Reno, NV
Seminar Leader, Nurse Consultant: johnmohler.com

Crista Lenk Stathers, MA, NREMT-P, CCEMT-P, PNCCT, FP-C

Director, Professional and Continuing Education: UMBC, Baltimore, MD

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©2011, University of Maryland, Baltimore County (UMBC).

All rights reserved.

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are the property of University of Maryland, Baltimore County (UMBC).
These materials may not be reproduced, transmitted, displayed, published,
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You are strictly prohibited from making copies of the materials and/or
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To request written permission to use this material outside of the CCEMTP

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Hemodynamic Monitoring Declaratives

• Purpose and goals of hemodynamic monitoring

o Purpose of hemodynamic monitoring:
 Evaluate the ability of the cardiovascular system to deliver blood flow
and oxygenation to the tissues
 Assesses the following:
• Cardiac output
• Blood volume
• Vascular tone
• Myocardial contractility
• Fluid balance
• Oxygen saturation
• Medication and treatment effects
 The most important aspect of hemodynamic monitoring information is
determination of cardiac output
o Goals of monitoring:
 Assess with the degree of pulmonary congestion (left ventricular
preload)
 Assess peripheral perfusion (forward flow)
 Determine left ventricular function based on preload and forward flow

• Clinical indications for hemodynamic monitoring

o To assess patient’s cardiovascular status and response to therapy in the
following:
 Myocardial infarction
 Cardiac tamponade
 Congestive heart failure
 Valvular dysfunction
 Pre or post-cardiovascular surgery
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o Assess hemodynamic status in shock:

 Hypovolemic
 Neurogenic
 Septic
 Cardiogenic
 Anaphylactic
o Assess pulmonary edema and acute respiratory failure:
 ARDS
 Pulmonary edema
 COPD
o Assess the effect of fluid therapy in the following situations:
 Burns
 Sepsis
 Trauma
 Renal failure
o Other indications for hemodynamic monitoring
 Pulmonary hypertension
 Monitoring fluid status
 Monitoring effects of pharmacological agents

• Pulmonary artery catheter

o Developed in 1970 by Dr. Jeremy Swan and Dr. William Ganz
o Flexible, multiple lumen, balloon-tip catheter
o Various sizes
 5, 6, 7, and 7.5 French
o Number of lumens, usually color-coded based on parameters to be measured
o Four lumen catheter
 Proximal lumen (blue)
• Opening is located 30 cm from the distal tip of catheter

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• Measures central venous pressure (CVP) which is the pressure

in the right atrium
• Also used as the injection port for measurement of cardiac
output
 Distal lumen (yellow)
• Opening is located at the distal tip of the catheter
• Connects to transducer via pressure tubing
• Must be continuously monitored
• Inject air only into the port, no fluids
• Never inject more than 1.5 ml of air into the port
• Uses:
o Monitors PA pressures
o Used to draw blood samples
o Used to draw SvO2 samples (mixed venous)
o Measures pulmonary artery and pulmonary capillary
wedge pressure (PCWP)
 Balloon inflation port (red)
• Located at the tip of the catheter
• Inflated to advance catheter during insertion and to wedge the
catheter when it is in the pulmonary artery
• Never leave in the inflated position
 Infusion port (white)
• Used for fluid infusion
• Thermistor
• Temperature sensitive wire extending through the catheter with
a sensor near the distal tip
• Ends approximately 4 cm from the distal tip
• Contains a fine, temperature sensitive wire to measure blood
temperature which in turn measures cardiac output
• Always keep the port covered with a red cap when not in use
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 Inflation port (balloon port)

• Syringe will passively deflate if balloon is intact
o Before transporting patient always ask for a current wedge
 This will ensure that the balloon is intact, and will provide information
on volume status
o If the balloon is ruptured, ensure that the port is not used
o Additional ports that can be used:
o Proximal infusion port (auxiliary port – usually white)
 Open approximately 31 cm from the distal catheter tip
 Essentially the same as the proximal injectate port
o Introducer port, side port, VIP port (yellow)
 Fluid does not go through the catheter but comes out between the
introducer sheath and the yellow catheter
 Uses:
• Infuse IV medications and fluids
• Will not accommodate high volumes
• Draw blood samples
• Usually not connected to the transducer and pressure tubing
o Right ventricular port (pacing port)
 Opens approximately 19 cm from the distal tips
 Lies in patient’s right ventricle
 Used to float a temporary pacing probe
o Right ventricular port- purple (Abbott catheters only)
 Opens into patient’s right ventricle
 Used to infuse fluids and medications
 Can be attached to the transducer
o Additional lumens that can be used:
o Intracardiac pacing lumen
 Atrial and ventricular pacing
 Opening located in right atrium or right ventricle
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o Venous oxygen saturation (SvO2)

 Fiberoptic
 Beam of light is transmitted through the catheter
 Light reflects oxygen level
o Catheter length is 100 centimeter
 Marked with black line every 10 centimeter for use of location during
insertion

• Insertion
o Prior to insertion
 Sites
• Subclavian vein
o Most common site
• Jugular vein
• Femoral vein
• Antecubital vein
o Location
 Usually placed at bedside
o Equipment needed
 Catheter
 Pressure transducer
 Transducer cable
 Pressure monitor
 Continuous flush tubing
 Three-way stopcock
 Flush solution
 Pressure bag
o Preparing equipment
 Connect flush system
 Fluid source is a 500 ml IV bag of NS
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 If patient has a history of or suspected heparin induced

thrombocytopenia (HIT) do not use heparin in the flush solution
 300 mmHg pressure bag
 IV bag must be pressurized to 300 mmHg to overcome the
resistance of the flush device in the transducer and to deliver 3 ml
per hour through the catheter
 Pressure also needed to prevent clots from forming in the line
 Remove all air from tubing and ports
 A continuous fluid filled line from the IV bag to the transducer and
from the transducer to the catheter tips is needed in order to
monitor pressures
 Tubing must be high pressure, rigid tubing that can accurately
transmit vascular pressure to the transducer
 Continuous flow of 3 – 5 ml/hr
o Transducer
 Transducer construction:
• The transducer contains a one-way valve that allows 3 ml/hour
of fluid to pass through unless the resistance is released by
pulling the tail or pushing the lever on the device which allows
the line to run wide open
• The transducer contains fine wires that move back and forth
with pressure changes and convert the pressure to an electrical
signal that is sent to the monitor
• In order for the transducer to work, it must be filled with fluid and
must be bubble free
 Zeroing the transducer:
• Purpose for zeroing the transducer:
o Zeroing tells the monitoring system that the atmospheric
pressure is “zero”

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o It removes the effect of hydrostatic pressure in the tubing

system and establishes a baseline of zero so all pressure
recorded by the system is the patient’s pressure
• Steps to zero the transducer:
o The three-way stopcock port on the transducer is open to
air and turned to closed between the patient
o Press the zero button on the monitor for 3 seconds and
zeroes should be displayed
o Close the stopcock port and turn to the open position
o Readings should appear on the monitor immediately
o Placement and leveling of the transducer
 The stopcock that was used to zero the system must be at the
phlebostatic axis for all pressure readings
 If the transducer is lower than the phlebostatic axis, it will cause
inaccurately high readings
 If the transducer is higher than the phlebostatic axis, it will cause
inaccurately low readings
o The transducer must always be level with right atrium
 IV pole
 Phlebostatic axis
 Fourth intercostal space
o When to level the transducer:
 Whenever a reading is taken
 Insertion
 Change in patient’s position
 For every 1 cm deviation from the true phlebostatic axis, pressure
changes 1.86 mmHg
• During insertion
o Sterile technique
o Method of insertion

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 Percutaneous cutdown approach

o Inflation of balloon
 Causes catheter to float through the heart to its final position in the
pulmonary artery
 Should never remain inflated
o Waveform on monitor identifies location of catheter during insertion
 Parts of waveform:
• “A” wave - produced when the atria contract
• “X” and “Y” wave- produced with atrial diastole
• “C” wave – produced with the closure of the tricuspid valve
• “V” wave- produced with right ventricle contraction
 Normal waveform changes during insertion:
• Right atrium
• Two small upright strokes represent “A” and “V” waveform
• Right ventricle
• Sharp systolic upstroke and diastolic dip
• Pulmonary artery
• Smoother systolic upstroke with dicrotic notch
• Pulmonary artery wedge pressure (PAWP)
• Two small upright strokes represent “A” and “V” waveform
• All waveforms should be read at the end of patient exhalation
o Final catheter position
 Proximal opening is located in the right atria
 Distal opening is located in the pulmonary artery

• Pressures
o Basic overview
 As the catheter approaches the right atrium, it reflects the CVP and RA
pressure

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 The balloon is inflated as it approaches the RA to float the catheter

through the chambers of the heart
 As the balloon advances, the waveform reflects the movement (or
turbulence) of the catheter tip
 The difference between the RV pressure and the PA pressure is
reflected in the diastolic pressure
 If the PA diastolic pressure drops to zero, the catheter position must be
reevaluated
o Central venous pressure (CVP) and right atrial pressure (RAP)
 CVP
• Reflects pressure in the venous system
• Single or multi-lumen catheter is advanced from a peripheral or
central vein until the tip is in the proximal SVC
• Can be measured with pressure transducer or water manometer
• Is the pressure in the large thoracic vessels
 RAP
• Is the pressure in the right atria
• Measured through the proximal port of the PA catheter
 CVP and RAP
• Reflects right ventricular end diastole pressure or preload
 CVP and RAP can be monitored continuously via the pressure
transducer (measured in mmHg) or intermittently via a water
manometer (measured in cm H2O)
• Normal values 2 – 6 mm Hg
 Causes of increased pressure:
• Right-sided heart failure
• Right ventricular infarct
• Chronic LV failure
• L-R shunts
• Pulmonary edema
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• COPD
• Tricuspid valve disorder
• Cardiac tamponade
• Pulmonary hypertension
• Constrictive pericarditis
• Volume overload
• Positive pressure ventilation (PPV)
 Causes of decreased pressure:
• Volume depletion
• Vasodilation
• Venous vasodilator
• Endogenous system vasodilator
o Right ventricular pressure (RVP)
 Pressure in the right ventricle
 Not routinely measured at bedside due to irritability of the RV
 Seen during insertion of the PA catheter
 Normal values
• Systolic 15 – 30 mmHg
• Diastolic 0 – 8 mmHg
 Causes of increased pressure:
• Mitral valve disorder
• Pulmonary disease
• Hypoxemia
• Chronic heart failure
• Right ventricular failure or infarction
• Ventricular septal defect
• Constrictive pericarditis
• Causes of decreased pressure:
• Hypovolemia

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• Vasodilation
o Pulmonary artery pressure (PAP)
 Reflects both right and left heart pressures
 Measured through the distal port of the catheter
 Pressure in the pulmonary artery with the balloon deflated
 Normal values
• Systolic 15 – 30 mmHg
• Diastolic 5 – 15 mmHg
 Causes of increased pressure:
• Hypervolemia
• Ventricular septal defect (with left-to-right shunt)
• Pulmonary hypertension
• Positive pressure ventilation
• Mitral valve defect
• Cardiac tamponade
• Left ventricular failure
 Causes of decreased pressure:
• Hypovolemia
• Vasodilation
o Pulmonary artery / capillary wedge pressure (PAWP, PCWP, PAOP, “wedge”)
 Indirectly reflects left atrial pressure and left ventricular end diastolic
pressure (LVEDP)
 Measured with the balloon inflated at the end of expiration
 Principles of obtaining a wedge pressure:
• Wedging of the catheter is only done to obtain the wedge
pressure
• The balloon is inflated with 1.5 ml of air and allowed to sail (or
wedge) into the distal branch of the pulmonary artery, where it is
too narrow for the balloon to pass

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• Results in cessation of forward blood flow into that balloon-

occluded segment of the pulmonary circulation
o During the occlusion, the catheter sensing tips “see
through” the pulmonary circulation (no valves) into the left
atrium giving an indirect reflection of the left atrial
pressure (LAP)
• Inflation of the balloon should not be longer than 15 – 30
seconds
o Lengthy wedges damage pulmonary capillaries and
compromises pulmonary oxygenation
• After wedging, the balloon is allowed to passively deflate and
return to the pulmonary artery
• Do not overinflate the balloon- stop inflating when the waveform
changes from a PA waveform to a PCW waveform
• Use air only to inflate
• Never flush the catheter in the wedge position
• Re-zero and recalibrate the transducer system after each
PCWP reading
 Normal values 4 – 12 mmHg
• Causes of increased pressure:
o Positive pressure ventilation
o Hypervolemia
o Mitral valve defect
o Constrictive pericarditis
o Left ventricular failure
o Severe aortic stenosis
Causes of decreased pressure:
o Hypovolemia
o Vasodilation
 The PCWP also gives information about what is going on in the lungs
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• It is reflective of the hydrostatic pressure within the pulmonary

capillary bed
• As the hydrostatic pressure rises, blood begins to seep into the
alveoli, impairing oxygen exchange
o 18 – 20 onset of pulmonary congestion
o 21 – 25 moderate congestion
o 26 – 30 severe congestion
o > 30 acute pulmonary edema
• In patients with cardiomyopathy, the pulmonary capillaries are
accustomed to higher pressure and can maintain oxygenation at
higher wedge pressures
o Cardiac output (CO)
 Amount of blood ejected by the ventricle each minute
 Evaluates cardiac function
 Normal range is 4 to 8 L/minute
 Measured by thermodilution
 Technique for determining cardiac output using the thermistor:
• Iced or room temperature injection is instilled rapidly through the
proximal port of the PA catheter
o Iced injectate is no longer routinely used because of the
irritability that it causes the heart
• This changes the temperature of the patient’s blood and the
thermistor picks this up on the temperature change
• The computer then determines the amount of blood passing
through and can determine the cardiac output
• For adults, use 10 ml of chilled D5W and quickly inject
• Use average of 3 or 4 sequential thermodilutions
• If using iced injectate, do not touch the barrel of the syringe
 Advantage of the using the thermistor:
• Requires only one catheter and can be inserted at bedside
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• No blood withdrawal required

• Procedure can be rapidly performed by one person
• Not affected by oxygen administration
 Disadvantages of using the thermistor:
• May be inaccurate in low flow states
• Inaccurate in shunts, pulmonary insufficiency, and tricuspid
insufficiency
• Technical factors can affect the accuracy of the cardiac output
measurements
• Volume and temperature of the injectate
• Speed of injection
• Degree of handling of the syringe
• Position of the patient
• Potential for electrical hazard if the thermistor wires are
damaged in the catheter
 Causes of increased cardiac output:
• Sympathetic nervous system
• Positive inotropes
• Hyperthyroidism
• Hypervolemia
• Anemia
• Catecholamines
• Causes of decreased cardiac output:
• Increase or decrease in heart rate
• Decrease in contractility
• Increase in afterload
o Cardiac index
 Cardiac output divided by body surface area (BSA)
 Normal is 2.5 – 4 L/m/m2

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 In cardiogenic shock, value will fall below 1.8 L/m/m2

o Mixed venous oxygen saturation (SvO2)
 The amount of hemoglobin saturated with oxygen in a pulmonary
artery blood sample
 Reflect venous oxygen reserve which is the amount of oxygen
remaining tissues have utilized what they need
 Monitors the balance between supply and demand
 Mixed venous means that the venous blood in the systemic capillary
beds comes from the SVC, IVC, and coronary sinus beds where it
mixes with the right atrium
 Uses fiberoptic sensor to obtain measurement
 Purpose for SvO2 measurement:
• Is an “early warning “ system of the relationship between
oxygen supply and oxygen demand
• Reflects how well the tissues’ demand for oxygen is met
• Principle of oxygen supply to the tissue
• Dependent up arterial oxygen content (PaO2)
• If tissues demand more oxygen, surrounding vessels will dilate
• This causes an increase in cardiac output as long as the heart
can met tissue demand
 Upsetting the balance of supply and demand
• When tissue oxygen demand exceeds the ability of the
cardiovascular system to deliver oxygen
• Causes of supply demand mismatch:
o Oxygen supply is disrupted by a decrease in cardiac
output leading to decreased oxygen supply to the tissues
o Decreased oxygen content resulting in less oxygen being
delivered to the tissues
o Decreased hemoglobin availability
o Mitochondrial poisoning
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• Critical ill patients have increased tissue oxygen demands:

o Fever
 Each degree C of temperature increases oxygen
demands by 10%
o Severe infection
 60% increase in tissue oxygen demands
o Skeletal injuries
 10 – 30% increase in tissue oxygen demands
o Work of breathing
 40% increase in tissue oxygen demands
o Burns
 100% increase in tissue oxygen demands
o Shivering
 50 – 100% increase in tissue oxygen demands
o Dressing change
 10% increase in tissue oxygen demands
o Bath
 23% increase in tissue oxygen demands
o Position changes
 31% increase in tissue oxygen demands
o Weigh in on a sling scale
 36% increase in tissue oxygen demands
o EKG
 16% increase in tissue oxygen demands
o Chest x-ray
 25% increase in tissue oxygen demands
o Agitation
 18% increase in tissue oxygen demands
o Physical exam
 20% increase in tissue oxygen demands

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o Visitor
 22% increase in tissue oxygen demands
• Compensatory responses for decreased SvO2
o First response
 Increase cardiac output
 Can increase oxygen delivery by 4 – 6 times
o Second response
 Decreased SvO2 in the tissues
 Tissues extract more oxygen than normal from the
blood
 This is a “red flag” that changes are getting ready
to occur in the patient’s clinical condition
o Third response
 Anaerobic metabolism occurs leading to the
production of lactic acid and then metabolic
acidosis
o Normal SvO2 value is 60 – 80%
 Causes of increased value:
• Increase in oxygen delivery
• Decrease in demand of delivery
• Inability of tissues to use oxygen
• Cyanide poisoning
• Carbon monoxide poisoning
 Causes of decreased value:
• Decrease in oxygen delivery
• Increase in demand of delivery
o Other relevant values:
 Left ventricular preload (LVP)
• The same as left ventricular end diastolic pressure

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• In a normal heart, the pressure of blood in the left atria (LAP) is

directly correlated to the pressure in the left ventricle at the end
of ventricular filling (LVP or LVEDP)
• In the normal heart, the LVP is indirectly measured by the
PCWP and PAD
 Right ventricular preload (RVP)
• The pressure of the blood in the right ventricle is directly
correlated to the pressure in the right ventricle at the end of
ventricular filling
• In a normal heart, this pressure is the same as the central
venous pressure (CVP) and is 2 – 6 mmHg
 Afterload
• The pressure or initial resistance that must be overcome by the
ventricles in order to open the semilunar valve (both the
pulmonic and aortic) and eject blood into the pulmonary and
systemic systems
 Factors affecting afterload:
• Outflow obstructions
• Aortic stenosis
• Pulmonic stenosis
• Vascular resistance
• Systemic vascular resistance
• Pulmonary vascular resistance
• Sympathetic tone of arterial system
• Vasconstriction
• Vasodilation
• Blood viscosity
• Aortic insufficiency
 Clinical measurement of afterload

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• Left ventricular afterload = systemic vascular resistance = 800

to 1200 dynes/sec/cm5
o Pulmonary vascular resistance (PVR)
 A calculated value based on mean pulmonary artery pressure and
pulmonary wedge pressure and is used as a clinical indicator of right
ventricular afterload
 Normal PVR = < 250 dynes/sec/cm5
o Systemic vascular resistance (SVR)
 A calculated value based on mean arterial pressure and CVP and is
used as a clinical indicator of left ventricular afterload
 Normal SVR = 800 – 1200 dynes/sec/cm5

• Overview of hemodynamic parameters

o Mean arterial pressure (MAP): 70 – 100 mmHg
o Central venous pressure (CVP): 2 – 6 mmHg
o Pulmonary artery pressure (PAP): 15 – 30 mmHg / 5 -15 mmHg
o Pulmonary artery diastolic pressure (PAD): 5 – 15 mmHg
o Pulmonary artery wedge pressure (PAWP/PCWP, Wedge): 4 – 12 mmHg
o Cardiac output (CO): 4 – 8 L/min
o Cardiac index (CI): 2.5 – 4 L/min

• Complication of hemodynamic monitoring

o During insertion:
 Dysrhythmias including PVCs, VT, heart block and bundle branch
blocks
 Caused by the right ventricular endocardium being irritated by the
catheter tip
 Pneumothorax
 Apex of the lung is punctured during the subclavian insertion
 Right ventricle perforation
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 Would present with cardiac tamponade, shock, and possibly cardiac

arrest
 Kinking or knotting of the catheter
 If the catheter has been advanced 15 cm and there is no wave form or
pressure see on the monitor, the catheter needs to be withdrawn
 Blood loss
o Post insertion:
o Catheter displacement
 Forward displacement
• Spontaneous wedging note by waveform change
• Prevention of forward displacement:
• Tape reference strip on monitor for transport
• Treatment
• Check to see if the balloon has been accidentally inflated
• Aspirate for blood return
o May be occluded rather than wedged
o If blood return is noted, flush with heparinized solution
• Have patient raise their arm nearest the catheter above their
head and then cough
o Try turning the patient on their left side
• If these techniques fail, immediately call a physician for
guidance as the catheter will need to be pulled back 3 – 4 cm
 Backward displacement
• The catheter tip recoils into the right ventricle
• Treatment
• The catheter must be repositioned as catheter whip (fling) may
cause ventricular dysrhythmias
o Notify the MD immediately and ensure the balloon is
deflated and pull it back into the right atrium

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o The catheter will need to be advanced and repositioned

by the MD
• Watch for sudden onset of ventricular arrhythmias and be
prepared to give lidocaine
o Pulmonary artery rupture
 Commonly caused by distal migration of the catheter tip
• Can also be caused by the following:
• Over-inflation of the balloon
• Eccentric inflation of the balloon
• Manual flushing of a wedged catheter
 Signs and symptoms
• Hemoptysis
• Severe respiratory distress
• Shock
 Prevention
• Wedge infrequently
• Use only minimal amount of air needed to wedge
• Always make sure the balloon is deflated before manually
flushing
 Treatment
• CPR if indicated
• Emergent notification of the MD
• Position patient with the affected side down
• Emergent surgical repair
o Pulmonary infarction
 Causes
• Thromboemboli
• Forward migration of the catheter
• Continuous, prolonged wedging

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• Over-inflation of the balloon while the catheter is in the wedged

position
o Balloon rupture
 Causes:
• Over-inflation of the balloon
• Frequent inflations
• Inflating with fluid and not air
o Infection
 Can be as high as 35% of insertions
o Air emboli
 Clotting of catheter
o Dysrhythmias
o Hemorrhage
o Pneumothorax
o Thrombosis

• Troubleshooting problem
o Inability to obtain a wedge pressure
 Rupture of balloon
 Catheter has moved backward
o Dampened waveform
 Over-dampened
• Results in erroneously low SBP and high DBP
• Causes:
o Air or blood in tubing
o Blood in transducer
o Loose or open connections
o Low fluid level in the flush bag
o Pressure bag failure
o Catheter has kinked
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o Catheter has spontaneously migrated forward

o Spontaneous wedge
• Treatment
o Attempt to pull the PAC back into the right atrium
o If waveform indicates spontaneous wedge and the
balloon is not inflated, be prepared to pull the catheter
slightly back into the pulmonary artery
 Under-dampened
• Results in erroneously high SBP and low DBP
• Causes:
o Small air bubbles
o Tubing too long
o Defective transducer
o Right ventricular waveform
 If the swan falls or gets pulled back into the right ventricle it is
considered an emergency
 The right ventricular waveform looks similar to ventricular tachycardia
(saw-toothed waveform)
 If this is observed, immediately pull the swan
 If the swan is allowed to stay in the right ventricle it may cause
ventricular tachycardia
o No waveform
 Stopcock is turned off to the patient
 Catheter tip is clotted
 Monitor or system is set up incorrectly
 Equipment not working
o Catheter fling (“whip”)
 Movement of the catheter forward during contraction of right ventricle
 Can also be caused by excessive tube length

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 Catheter fling can create falsely elevated systolic pressures and falsely
lowered diastolic pressures

• Arterial lines (see also 1.7 Peripheral and Central Access)

o Arterial lines are frequently being used for hemodynamic monitoring
o Note that some patients may have an arterial line and CVP lines requiring
dual transducers
o The use of color-coded lines can help to keep hemodynamic monitoring lines
separate

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Module Bibliography / Recommended Readings:

• Bigatello LM, George E. “Hemodynamic monitoring.” Minvera Anesthesiol.
2002:68(4):219-24
• Pinsky MR, Payen D. “Functional hemodynamic monitoring.” Critical Care
2005;9:566-572
• Darovic, G. Hemodynamic Monitoring 3rd Ed. 2002. Elsevier. St. Louis, MO.
• Pinsky, MR. “Hemodynamic evaluation and monitoring in the ICU.” Chest.
2007;132(6):2020-2029
• Mermel, et al. “Guidelines for the management of intravascular catheter related
infections.” Clin Infect Dis. 2001;32(9):1249-1272

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