2. What is a Swan?
⢠Full name: Swan-Ganz Catheter
⢠Pulmonary Artery (PA) Catheter = right heart catheter
⢠Used it to monitor a patientâs hemodynamics when we
cant answer the question using noninvasive/clinical
measures
⢠Useful to measure right atrial, pulmonary artery, right
ventricular pressures and indirectly measure left atrial
pressures, cardiac output and systemic vascular resistance
3. Why use a Swan?
⢠Differentiation between causes of shock>cardiogenic,
hypovolemic, septic
⢠Differentiation between causes of pulmonary
edema>cardiogenic versus noncardiogenic
⢠Diagnosis of pericardial tamponade
⢠Diagnosis of intracardiac shunt
⢠Evaluation/Management of pulmonary hypertension
⢠Diagnosis of lymphangitic spread of tumor and fat
embolism
⢠Management of complicated MI, HF
⢠Determine need for vasopressor/inotropic therapy
⢠Fluid Status>in GI bleed, renal failure, sepsis
⢠Ventilator management>determining the best PEEP
4. Some historyâŚ
⢠First pulm catheters were placed in 1940s
⢠1970-William Ganz and Harold Swan introduced this
catheter. Pulmonary artery Catheter that is balloon-tipped
and flow directed, placed bedside
⢠Revolutionized catheters>moved from diagnosis only to
help in management. No clinical trials were done to see if
they improved mortality. Benefit was assumed
⢠1987- nonrandomized trials:showed mortality was higher
in patients with an acute MI who had a Swan placed
⢠1990s-Ontorio Intensive Care Group attempted a RCT for
use of Swans>not done b/c many clinicians felt unethical
to withhold Swan placement because accurate
diagnosis=accurate treatment=better prognosis????
5. Is it unethical to withhold Swan Placement?
And are they better at predicting clinical outcomes?
⢠1996 observational study of RHC in first 24 hours said NO.
⢠Placement led to worse patient outcomes b/c of
complications of placement or misinterpretation of data
⢠Use of catheter might be a marker of more aggressive
care, which is associated with higher mortality
⢠Changes in therapy in response to the information might
have led to high mortality (i.e. using pressors)
⢠Study might not have adequately adjusted for
confounding factors
⢠Only looked at SGC placed in first 24 hours.
⢠Connors AF Jr, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization
in the initial care of critically ill patients. JAMA 1996;276:889-897
6. Randomized, Controlled Trial of the Use of Pulmonary-Artery
Catheters in High-Risk Surgical Patients. Sandman et al. NEJM-
Jan, 2003
⢠1994 high-risk surgical patients underwent randomization
for PA catheters (RCT)
⢠Preop placement, for elective or urgent surgery
⢠Looked at 6mo and 12 mo mortality
⢠No difference b/t PA catheter group from placebo in terms
of mortality and length of hospitalization
⢠Increased risk of PE in the catheter group and thus, PA
catheters may be associated with increased morbidity
7. Escape Trial
⢠The value of Swan-Ganz catheterization to
guide tailored therapy in heart failure
patients is an area of controversy.
⢠The randomized ESCAPE trial showed no
benefit on a primary end point of the
number of days alive and out of the hospital
at six months
JAMA. 2005;294:1625-1633.
8. To Swan or Not to
Swan?
INDIVIDUALIZE CARE
Understanding Swan Ganz Catheters=
Understanding Hemodynamics
9.
10. Basic Catheter Features
⢠Made of polyvinylchloride and has a
pliable shaft that softens at body
temperature
⢠Catheter is 110 cm and external diameter
is either 5 or 7 French (1
French=0.0335mm)
⢠Balloon is fastened 1-2mm from the tip
and when inflated it guides the catheter
(using fluid dynamic drag) from greater
intrathoracic veins through tight heart
into pulmonary artery
⢠Thermistor-4cm proximal to the tip,
measures temperature>important for
determining cardiac output
11. ⢠Typically catheters have 4
ports:
2. White port with blue wire is the
proximal port> terminates at
30cm from tip of catheter and is
used to measure right atrium
pressures
3. White port, yellow wire is the
PAD distal port
4. White port with red wire is for
balloon inflation
5. Last port has the connection to
the thermodilution cardiac
output computer> contains the
electrical leads for thermistor.
12. Insertion Techniques
⢠Average time from decision to use PA catheter
until onset of catheter based treatment is 120
minutes
⢠Goal: get the catheter to the pulmonary artery
⢠Cordis into right internal jugular vein or left
subclavian allows easiest passage
⢠Swan should be oriented ex-vivo to approximate
the course in the body
⢠Catheter goes through an introducer and into the
vein. The balloon stays closed until we reach
the right atrium.
⢠When we reach the right atrium (20cm), balloon
should be inflated to reduce possibility of injury
to the myocardium.
⢠Then the balloon should be moved quickly
through the right ventricle (30cm)> and then
pulmonary artery (40cm) and PCWP (50cm)
FROM SUBCLAVIAN/IJ APPROACH
13. How do you know you are in the Right
Atrium?>>20 cm
Normal right atrial presssure is 0-6mmHg.
Normal oxygen content 15%
Normal O2 saturation 75%
a=atrial contraction.
c=sudden motion of the AV ring toward
the right atrium
x descent=atrial relaxation
v=pressure generated by venous filling
of the right atrium
y descent=rapid emptying of the RA
into RV
14. What Elevates the Right Atrial Pressure?
⢠RV infarct
⢠Pulmonary hypertension
⢠Pulmonary stenosis
⢠Left to right shunt
⢠Tricuspid valvular disease
⢠Left heart failure
15. Prominent RA pulsations
⢠Prominent a wave:
⢠Tricuspid stenosis
⢠Cannon a wave:
⢠AV dissociation or Ventricular tachycardia
⢠Prominent v wave:
⢠Tricuspid regurgitation or VSD
16. How do you know you are in the right ventricle?
30cm
RV systolic=17-30
RV diastolic=0-6
RV O2 content=15%
RV O2 saturation 75%
18. How do you know you are in the pulmonary artery?
Normal PA pressure,
systolic 15-30
Normal PA pressure,
diastolic 5-13
O2 content 15%
O2 saturation 75%
19. What Elevates PA pressure?
⢠Volume Overload (backflow)
⢠Primary lung disease
⢠Primary pulmonary hypertension
⢠Pulmonary Embolism
⢠Left to right shunt
⢠Mitral Valve Disease
20. THE WEDGE:
What is the Pulmonary Artery Wedge Pressure?
The measurement is obtained when the inflated balloon impacts into a slightly
smaller branch of the pulmonary artery. This is where the arterial pressure exceeds
the venous pressure and the venous pressure exceeds the alveolar pressure, thereby
creating a continuous column of blood from the catheter tip to the left atrium
when the balloon is inflated. Pulmonary venous pressure is the best indicator of
left atrial pressure except when there is venoocclusive disease. AND ONLY
WHEN THE PA CATHETER IS IN ZONE 3 of the lung.
21. Inflation of the Balloon for PCWP Tracing
Pulmonary artery wedge 2-12 PCWP tracing looks like RA tracing
Pulmonary vein O2 content 20% except that the v wave is slightly higher
Pulmonary vein O2 sat 98% than the a wave (opposite of RA).
Also, b/c of the time required for LA
mechanical events, PAWP waveforms are
further delayed when recorded by EKG
25. Calculation of Cardiac
Output
Thermodilution versus Ficks method
â˘Thermodilution: Add an indicator substance (5ml of dextrose or
saline) that is cooler than blood. Indicator in injected through the
proximal port of the PA catheter and mixes with the blood in the
RV. The mixing lowers the temperature of the flowing blood which
is carried to the distal thermistor port. The thermistor records the
temperature change and electronically displays a temperature/time
curve. The area under the curve is inversely proportional to the
flow rate in the pulmonary artery which equals the cardiac output
in absence of intracardiac shunt
-sources of error with thermodilution are seen with tricuspid
regurgitation and intracardiac shunts
26. Fickâs Method
⢠General principle: the release or uptake of a substance by
an organ equals the product of the bloodflow through that
organ times the difference of arteriovenous concentrations
of that substance.
⢠CO= O2 consumption (ml/min)
---------------------------------------------------------------
arterial O2 content(PCWP)-mixed venous (PA) O2 content
⢠O2 consumption varies according to individual, by age and
sex. Usually estimated as being 250mL for a 70kg male.
Generally estimated at 130mL x BSA
⢠Blood O2 content=% saturation X Hb x 1.39 ml O2/gm Hb
⢠Errors: assumptions of O2 consumption, wont work at all
with intracardiac shunts. But works better with TR
27. Cardiac Output/Index
⢠What is cardiac output?
⢠What is normal cardiac output?
⢠What is normal cardiac index?
28. Effects of PEEP
⢠Effects of positive end-expiratory pressure â
Alveolar pressure will not return to atmospheric
pressure at end-expiration in the presence of
positive end-expiratory pressure (PEEP), a change
that can affect the measurement of intravascular
pressures.
⢠The effects of PEEP are generally felt not to be
clinically significant.
⢠PEEP does affect right sided pressures (i.e. RA or
CVP).
29. Systemic Vascular Resistance (SVR)
⢠Refers to the resistance to blood flow offered by all of the
systemic vascular resistance, excluding the pulmonary
vasculature.
⢠This is sometimes referred as total peripheral resistance
(TPR).
⢠Mechanisms that cause vasoconstriction increase SVR, and
those mechanisms that cause vasodilation decrease SVR.
⢠SVR can be calculated if cardiac output (CO), mean arterial
pressure (MAP), and central venous pressure (CVP) are
known.
⢠SVR = 80 X (MAP - CVP) á CO
⢠Normal Systemic Vascular Resistance is 800-1200
(dyne*sec)/cm5
30. Zeroing is performed by opening the system to air to establish atmospheric
pressure as zero.
Referencing (or leveling) is accomplished by placing the air-fluid
interface of the catheter (or the transducer) at a specific point to negate the
effects of the weight of the catheter tubing and fluid column
31. Not an Entirely Benign LignâŚ
â˘Insertion of an introducer to provide venous access>Pntx, bleeding,
infection
â˘Passage of the Swan through the introducer>minimized by inflating
the balloon tip after entering the right atrium
-Sustained ventricular arrythmias, occur in 0-3% pts
-RBBB develops in about 5% of catheter insertions, placing
pts with a preexisting LBBB in complete heart block. RBBB
is usually temporary.
-Knotting catheter-can occur during insertion if loops are
allowed to form in one of the cardiac chambers. When knotting
occurs, can usually remove transvenously but some require
venotomy or surgical extraction.
â˘Maintenance of the catheter>Inflating balloon when catheter has
moved distally>causing pulmonary artery perforation. Mortality
>30%, usu requires thoracotomy
32. Not Without Risks???
â˘Donât leave balloon inflated in wedge position for extended
period of time>can cause pulmonary infarction
⢠Thromboembolic events can occur with the catheter acting as a
nidus for thrombus formation. Less common with heparin
bonded catheters
â˘Misinterpretation of the data
â˘Mural thrombi can be induced by inflammation of infection of a
vessel wall, seen in 33% of patients at autopsy
â˘Sterile vegetations, seen in 90% of patients
â˘Endocarditis of the pulmonic valve
â˘Rupture of the catheter balloon and consequent air embolism
Several studies show that clinicians are poor at correlating clinic status with hemodynamic assessment. In a general ICU population, clinicians could correlate correlate PCWP and cardiac index only 30-70% of the time. And 60-85% of the time in CCUs. People then argued that more frequent and accurate diagnosis of the conditions that can be treated would improve patient outcome. So in the 1970s, with Swan-Ganz, it became the standard of care in hemodynamically unstable patients. Differentiation between causes of shock>cardiogenic, hypovolemic, septic Differentiation between causes of pulmonary edema>cardiogenic versus noncardiogenic Diagnosis of pericardial tamponade Diagnosis of intracardiac shunt Evaluation/Management of pulmonary hypertension Diagnosis of lymphangitic spread of tumor and fat embolism Management of complicated MI, HF Determine need for vasopressor/inotropic therapy Fluid Status>in GI bleed, renal failure, sepsis Ventilator management>determining the best PEEP
First pulm catheters were placed in 1940s. pUT in lab, just for dx. 1970-William Ganz and Harold Swan introduced this catheter. Pulmonary artery Catheter that is balloon-tipped and flow directed, placed bedside Revolutionized catheters>moved from diagnosis only to help in management. No clinical trials were done to see if they improved mortality. Benefit was assumed 1987- nonrandomized trials:showed mortality was higher in patients with an acute MI who had a Swan placed 1990s-Ontorio Intensive Care Group attempted a RCT for use of Swans>not done b/c felt unethical to withhold Swan placement. They felt that anything that helped with âMORE ACCURATEâ hemodynamic monitoring had to help.
In 1996, Connors et al did an observational study of PA catheters. They evaluated people who had a RHC put in within 24 hours of admission to the ICU. End point was pt survival. Pts who underwent RHC had an increased 30 day mortality compared to those who did not undergo the procedure. Subgroup analysis did not show any group who was assoc with improved outcome. WHY? Placement led to worse patient outcomes b/c of complications of placement or misinterpretation of data Use of cathether might be a marker of more aggressive care, which is associated with higher mortality Changes in therapy in response to the information might have led to hight mortality (i.e. using pressors) Study might not have adequately adjusted for confounding factors Only looked at SGC placed in first 24 hours and maybe no indication in first 24 hours, and later when all else fails, actually improves mortality.
1994 high-risk surgical patients underwent randomization for PA catheters (RCT) Preop placement, for elective or urgent surgery Looked at 6mo and 12 mo mortality No difference b/t PA catheter group from placebo in terms of mortality and length of hospitalization Increased risk of PE in the catheter group and thus, PA catheters may be associated with increased morbidity
To Swan or Not to Swan? Each patient think hardâŚlots of comlications which I will get into. Tammy Cannon With that caveat in mindâŚlets get into the nuts and bolts of swan placement.
Made of polyvinylchloride and has a pliable shaft that softens at body temperature Polyvinylchloride is thrombogenic so they are usually coded with heparin. Studies have shown that this is more effective in prevent catheter related thrombogenicity Catheter is 110 cm and external diameter is either 5 or 7 French (1 French=0.0335mm) Balloon is fastened 1-2mm from the tip and when inflated it guided the catheter (using fluid dynamic drag) from greater intrathoracic veins through tight heart into pulmonary artery. The balloon when it is fully inflated, is designed to protrude above the catheter tip. And distributes force over large area, minimizing chances for endocardial damage. Thermistor-4cm proximal to the tip, measures temperature>important for determining cardiac output
Typically catheters have 4 ports: White port with blue wire is the proximal port> terminates at 30cm from tip of catheter and is used to measure simultaneous right atrium and pulmonary artery pressure White port, yellow wire is the PAD distal port White port with red wire is for balloon inflation Thermistor-4cm proximal to the tip, measures temperature Last port has the connection to the thermodilution cardiac output computer> contains the electrical leads for thermistor. 6. Some catheters now available have a 5th lumen allowing passage temporary pacemaker
Average time from decision to use PA catheter until onset of catheter based treatment is 120 minutes Goal: get the catheter to the pulmonary artery Cordis into right internal jugular vein or left subclavian allows easiest passage Swan should be oriented ex-vivo to approximate the course in the body Catheter goes through an introducer and into the vein. The balloon stays closed until we reach the right atrium. When we reach the right atrium (20cm), balloon should be inflated to reduce possibility of injury to the myocardium. Then the balloon should be moved quickly through the right ventricle (30cm)> and then pulmonary artery (40cm) and PCWP (50cm) FROM SUBCLAVIAN/IJ APPROACH The balloon is inflated with air. But filtered CO2 should be used in any situation in which balloon rupture might cause air to get into arterial system>like if there is an intracardiac shunt or pulmary A-V fistula.
a=atrial contraction. A wave peak follows the electrical p wave by about 80msec c=sudden motion of the AV ring toward the right atrium. x descent=atrial relaxation v=pressure generated by venous filling of the right atrium. The peak of the v wave occurs at the end of ventricular systole when atrium is maximally filled. This occurs near the end of the t wave y descent=rapid emptying of the RA into RV Normal right atrial presssure is 0-6mmHg. Normal oxygen content 15% Normal O2 saturation 75%
We just said that a wave is atrial contraction. And we are looking at the right atrial sideâŚso What gives a prominent a wave?
Two pressures are measured in the RV. The peak of the RV systolic pressure and the RV end diastolic pressure, right after the a wave. The ventricular diastole is made up of early rapid filling phase (60%) and a slow phase (25%) filling and an atrial systolic phase which produces an a wave in the RV tracing.
PA waveform is characterized by a systolic peak and diastolic trough with a dictrotic notch due to closure of the pulmonic valve. PA systolic pressure occurs within T wave of EKG similar to the systemic arterial pressures.
The measurement is obtained when the inflated balloon impacts into a slightly smaller branch of the pulmonary artery. In this position, the balloon stop flows and catheter tip senses pressure transmitted backward through the static column of blood from the next pulmonary bed, the pulmonary veins. Pulmonary venous pressure is the best indicator of left atrial pressure except when there is venoocclusive disease The PCWP only indicates the LAP if the pressure in the surrounding capillaries exceeds the mean alveolar pressure. That is ZONE 3. This concept is based on the idea tha the lung can divided into 3 physiologic zones of blood flow which are based upon the relationship b/t alveolar pressure, PAP and pulm capillary pressure. In ZONE 1, the alveolar pressure is greater than the capillary pressure. In Zone 3, the most dependent portion of the lung, vascular pressures are the highest d/t gravity. So again PCWP is only accurately a measure of LAP IF PCP exceeds mean alveolar pressure. So how do you know you are in Zone 3? 60% of catheter insertion are only in the right place. You can look at the CXR and the catheter should be below the left atrium. If there is marked respiratory vairation in the PAWP tracing you are likely not in Zone 3 and if PAD> PCWP then you are likely not in zone 3.
Inflation of the balloon changes the tracing of the pulmonary artery. Goes from having a dicrotic notch to having more of a,c,v wave pattern like we saw in the right atrium. This is because we are measure left atrial pressure. Pulmonary artery wedge 2-12 PCWP tracing looks like RA tracing except that the v wave is slightly higher than the a wave (opposite of RA) B/c of the time required for LA mechanical events, PAWP waveforms are further delayed when recorded by EKG. The peak of the A wave follows the the peak of the EKG p wave by 240 ms and the peak of the v wave occurs after the EKG t wave. A wave=atrial systole C wave=reflecting closure of the mitral valve V wave=represents both ventricular systole and passive atrial filling in atrial diastole. Pulmonary artery wedge 2-12 Pulmonary vein O2 content 20% Pulmonary vein O2 sat 98% Confirmation of the PCWP position is done be withdrawing blood from the distal lumen and measureing the O2 aturation. If >95% are considered satisfactory.
Thermodilution: Add an indicator substance (5ml of dextrose or saline) that is cooler than blood. Indicator in injected through the proximal port of the PA catheter and mixes with the blood in the RV. The mixing lowers the temperature of the flowing blood which is carried to the distal thermistor port. The thermistor records the temperature change and electronically displays a temperature/time curve. The area under the curve is inversely proportional the the flow rate in the pulmonary artery=cardiac output in absence of intracardiac shunt sources of error with thermodilution are seen with tricuspid regurgitation and intracardiac shunts. In TR, there will be an attenuated peak and a prolonged washout phase of the temperature-time curve. This is d/t cold injectate refluxing back into the vena cava and so you have resultant decreased pulm artery cooling and delayed appearance of the injectate that has moved retrograde into the vena cava and then is recirculated. Result is an underestimated cardiac output. Intracardiac shunt> both r>l and l>r intracardiac shunts can produce falsely elevated CO measurements by the thermodilution technique. R>L intracardiac shunts produce shunting of the cold injectate into the left heart and thus, decreased PA cooling, lowers the peak of the temperature-time curve and overestimates CO . L>R shunt result in increases right heart volumes, dilutes the injectate and attenuates the height under the temp-time curve and falsely elevated estimate of CO .
. If the respiratory variation seen in the PAWP tracing exceeds that seen in the pulmonary artery tracing, then the PAWP may be unreliable due to non-zone 3 conditions. By definition, in zone 3, no airway pressure should be transmitted to the vasculature The intravascular pressure is the pressure ostensibly transmitted back from the left atrium. PEEP can alter intravascular pressures, but those PEEP-altered pressures are the "effective" filling pressures for the patient under those clinical circumstances. An estimate of the true transmural filling pressures can be made in the presence of PEEP by subtracting one-half of the PEEP level from the PAWP if lung compliance is normal, or one-quarter of the PEEP level if lung compliance is reduced [ 19 ]. Since 10 cmH2O pressure is approximately 7.7 mmHg, the effects of PEEP on PAWP are usually small, and rarely affect clinical management During normal spontaneous ventilation, alveolar pressure (relative to atmospheric pressure) decreases during inspiration and increases during expiration. These changes are reversed with positive pressure ventilation: alveolar pressure increases during inspiration and decreases during expiration. The changes in pleural pressure are transmitted to the cardiac structures and are reflected by changes in pulmonary artery and PAWP measurements during inspiration and expiration. At end-expiration, pleural and intrathoracic pressures are equal to atmospheric pressures, regardless of the mode of ventilation. Thus, the true transmural pressure and therefore the PAWP should be measured at this point. Most intensive care units use electronic pressure monitors that are designed to measure pressure in time intervals of four seconds and to display three different pressures: systolic (peak); diastolic (trough); and electronic mean pressure. The wedge pressure can be followed serially by selecting the systolic pressure for those breathing spontaneously, and by selecting the diastolic pressure for those on positive pressure ventilation. Use of these settings avoids false depression or elevation of intravascular pressure measurements due to superimposed fluctuations in pressure during respiration. Alternatively, many ICU monitors allow manual selection of the pulmonary artery wedge pressure via a cursor.