Beyond the Wedge: Clinical Physiology and the

Swan-Ganz Catheter

SCOTT W. SHARKEY, M.D. The Swan-Ganz catheter was introduced into general clinical medicine
Minneapolis, Minnesota in 1970 and quickly gained widespread use in the management of
critically ill patients. The device offers highly sophisticated physiologic
information; however, in many instances, only the wedge pressure and
the cardiac output are utilized when managing acutely ill patients. The
purpose of this review is to illustrate and explain the array of physiolog-
ic data available from the Swan-Ganz catheter in most circumstances.
A basic understanding of the information that can be obtained with the
Swan-Ganz catheter is quite useful in the diagnosis and management
of a variety of cardiovascular disorders. In addition, the Swan-Ganz
catheter can be a helpful tool for teaching cardiovascular pathophysiol-
OgY.

In 1970, Swan and Ganz revolutionized acute care medicine with the
introduction of the balloon-tipped cardiac catheter that now bears their
names [ 1,2]. This catheter is now routinely employed in the management
of critically ill patients to the extent that it has been suggested that the
device is overused [3]. Nonetheless, the Swan-Cam. catheter provides a
wealth of hemodynamic information that can be invaluable both diagnos-
tically and therapeutically in critically ill patients, Frequently, only two
hemodynamic parameters are emphasized-the mean wedge pressure
and the cardiac output-while the right atrial and pulmonary artery
pressures are given only a cursory glance. A critical analysis of the
components of the pressure waveforms with attention to the influences
of respiration and cardiac arrhythmias provides valuable insight into
cardiovascular pathophysiology. The purpose of this review is to discuss
and illustrate the detailed physiologic information that can be obtained
from the Swan-Ganz catheter. To accomplish this goal, this review
utilizes a variety of hemodynamic tracings that were obtained with
standard number 7 French Swan-Ganz thermodilution catheters (Ed-
wards Laboratories, Santa Ana, California) placed in patients hospitalized
in the George E. Fahr Cardiac Care Unit at Hennepin County Medical
Center between 1983 and 1986.
HEMODYNAMIC MONITORING METHODS
From the Hennepin County Medical Center and
the Division of Cardiology, Department of Medi- The catheters were introduced through a central vein in the cardiac care
cine, University of Minnesota, Minneapolis, Min- unit usually without fluoroscopy. The distal lumen of the catheter was
nesota. Requests for reprints should be ad- connected to a commercially available transducer (Bell and Howell,
dressed to Dr. Scott W. Sharkey, Cardiology
Division, Hennepin County Medical Center, 701
Pasadena, California, or Medex, Hilliard, Ohio) with a four-foot length of
Park Avenue South, Minneapolis, Minnesota pressure tubing. The proximal lumen was interfaced with the same
55415. Manuscript submitted December 19, transducer using a double-stopcock system similar to that described by
1986, and accepted March 11, 1987. Civetta [4]. With this system, a single transducer can be used

July 1987 The American Journal of Medicine Volume 83 111

SWAN-GANZ CATHETER-SHARKEY
Figure 1. A, normal wedge pressure waveform. The peak
of the A wave follows the peak of the electrocardiographic
P wave by 240 msec, whereas the peak of the V wave
occurs after the electrocardiographic T wave. B, normal
right atria/ (RA) pressure waveforni. The peak of the A wave
follows the peak of the electrocardiographic P wave by 80
msec, whereas the peak of the V wave occurs at the end of
the electrocardiographic T wave. During inspiration, the
right atria/ pressure falls and the A and V waves become
more prominent. C, right atrial pressure waveform from a
patient with first-degree atrioventricular block. The C wave
is clearly visible. The right atria/ pressure is elevated be-
cause of right ventricular infarction. D, normal pulmonary
artery (PA) pressure waveform. The peak systolic pressure
(S) occurs within the electrocardiographic T wave. The
dicrotic notch (/V) is present.
to monitor pressure waveforms. The pressure waveform
from either the proximal lumen or the distal lumen can be
rapidly selected for analysis by turning the stopcocks. The
dynamic response of the catheter system was quickly
tested at the bedside by the fast-flush method [5]. A Could
(Cleveland, Ohio) 2400 four-channel physiologic recorder
that could be activated at the bedside was used to simulta-
neously record the pressure waveform and a single-lead
electrocardiogram. A paper speed of 25 mm/second was
usually selected for analysis of the pressure waveforms.
A paper speed of IO mm/second was occasionally used
to assess the response of intracardiac pressures to respi-
ration or the hepatojugular reflux test. Calibrations of 0.5
mm Hg/mm, 1 mm Hg/mm, 2 mm Hg/mm, or 5 mm Hg/
112 July 1987 The American Journal of Medicine
mm could be selected to give an appropriate size pres-
sure tracing for analysis. Cardiac outputs were calculated
by a cardiac output computer (Edwards Laboratories
9520) that was interfaced with a strip-chart recorder
(Edwards Laboratories 98 10) to record the thermodilution
curve.
NORMAL HEMODYNAMICS
The proximal and distal lumens of the Swan-Ganz cathe-
ter allow direct access to the mechanical events that
occur in the right atrium and pulmonary artery, respective-
ly. Inflation of the balloon occludes a pulmonary artery
segment (wedges the catheter) and allows left atrial me-
chanical events to be transmitted to the distal lumen of the
catheter. Two major positive atrial pressure waves, the A
wave and the V wave, can usually be recorded from the
right atrium and the wedge position [8] (Figure 1A and B).
A third minor positive wave, the C wave, can occasionally
be identified, more commonly in the right atrial tracing [6]
(Figure IC). The A wave is due to atrial contraction and
follows the P wave on the electrocardiogram [6]. In the
right atrial pressure tracing, the peak of the mechanical A
wave generally follows the peak of the electrical P wave
by about 80 msec (Figure 1B and C). In the wedge tracing,
this delay is longer (240 msec) due to the time required for
the left atrial mechanical event to be transmitted through
the pulmonary vasculature to the distal lumen of the
catheter and then to the transducer (Figure 1A). The C
wave is due to the sudden motion of the mitral and
tricuspid valve rings toward the left and right atria at the
onset of ventricular systole [6]. The C wave follows the A
wave by a time period equal to the electrocardiographic
P-R interval. Prolongation of the P-R interval often makes
the C wave more readily visible in the atrial pressure
tracing (Figure IC). The V wave is due to venous filling of
the left and right atria during ventricular systole when the
mitral and tricuspid valves are closed [6]. The peak of the
V wave occurs at the end of ventricular systole at a time
when the two atria are maximally filled. In the right atrial
tracing, the peak of the V wave occurs near the end of the
electrocardiographic T wave, whereas in the wedge trac-
ing, the peak of the V wave occurs after the T wave has
been inscribed due to transmission delay (Figure IA and
B). Two negative deflections, the X and Y descents follow
the A and V waves respectively (Figure 1A, B, and C). The
X descent reflects atrial relaxation and the sudden down-
ward motion of the atrioventricular junction. The Y de-
scent is due to rapid atrial empyting following opening of
the mitral and tricuspid valves [6]. During inspiration, the
mean right atrial and the mean wedge pressures both
decline (due to the decrease in intrathoracic pressure),
whereas the A and the V waves as well as the X and the Y
descents frequently become more prominent (Figure 1B)
[7]. The pulmonary artery waveform is characterized by a
systolic peak and diastolic trough with a dicrotic notch due
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 SWAN-GANZ CATHETER--SI-IWEY

Figure 2. A, right atria/ (RA) pressure waveform demonstrates mechanical flutter waves (f) at 3OO/minute. B, right atria/
pressure waveform demonstrates a cannon wave, which is due to atrial systole (PJ at a time when the tricuspid valve has been
closed by a premature ventricular contraction (PVC). C, right atrial pressure waveform during paroxysmal supraventricular
tachycardia demonstrates regular cannon waves ( l). The sequence of atrial and ventricular contraction is reversed, but the
two events remain associated, which causes the cannon waves to be regular. When tachycardia ceases (large arrow), normal
A, C, and V waves appear with sinus rhythm. Note that the right atrial pressure is higher during tachycardia due to the
presence of the cannon waves.

to closure of the pulmonic valve (Figure 1D). The peak of
the pulmonary artery systolic wave occurs within the
electrocardiographic T wave (Figure 1D). When hemody-
namic waveforms obtained with the Swan-Ganz catheter
are analyzed, it is very helpful to define the aforemen-
tioned relationships between electrical and mechanical
events. The time values just given are approximations and
vary depending on the individual patient and the length of
the pressure monitoring tubing used.
ARRHYTHMIAS
Cardiac arrhythmias often cause recognizable changes in
the atrial pressure tracings that can be used both to
diagnose the arrhythmia and to understand the hemody-
namic consequences that the arrhythmia imposes on the
circulation. For example, with atrial fibrillation, atrial sys-
tole is lost and the A wave disappears. Atrial flutter with
2: 1 atrioventricular block is occasionally difficult to diag-
nose from the surface electrocardiogram. If this rhythm is
suspected in a patient who already has an indwelling
pulmonary artery catheter, the right atrial pressure wave-
form should be recorded. The presence of mechanical
flutter waves at approxmately 300/minute confirms the
diagnosis of atrial flutter (Figure 2A). Paroxysmal supra-
ventricular tachycardia is another commonly encountered
arrhythmia that usually results from reentry within the
atrioventricular junction [8]. The retrograde P wave is
often hidden within the QRS complex, which can make
the diagnosis of this arrhythmia challenging [8]. The pres-
ence of atrial mechanical activity can be judged by exam-
ining the right atrial pressure tracing for evidence of
regular cannon waves (Figure 2C). These cannon waves
are the result of atrial contraction at a time when the
atrioventricular valves are closed by ventricular systole. In
addition, the tachycardia shortens diastole and results in
the summation of the A and V waves. The hypotension
that accompanies this arrhythmia is due to the loss of
atrial contribution to ventricular filling and possibly to a
vasodepressor reflex initiated by the cannon waves
[9, lo]. Cannon A waves are also commonly encountered
during ventricular arrhythmias, as illustrated by the cannon
wave that follows a premature ventricular contraction in
Figure 2B. The presence of irregular cannon A waves in
the right atrial pressure tracing during a wide-complex
tachycardia is due to atrioventricular dissociation and
strongly suggests the presence of ventricular tachycardia,
as demonstrated in Figure 3. Similarly, single-chamber
ventricular pacemakers frequently provide examples of
the hemodynamic consequences of atrioventricular dis-
sociation since these devices do not sense atrial activity.
Patients with these pacemakers may experience sudden
fluctuations in arterial blood pressure accompanied by
intermittent cannon A waves that cause symptoms re-
ferred to as the pacemaker syndrome [I I] (Figure 4).
Once again, the hypotension is the result of the loss of the
atrial contribution to ventricular filling in combination with
a vasodepressor reflex stimulated by the cannon waves
[IO]. Occasionally, pulsus alternans, which is a marker of
severe left ventricular dysfunction, can be triggered by
premature ventricular contractions [ 121 (Figure 5).
ACUTE MITRAL INSUFFICIENCY
When the mitral valve suddenly becomes incompetent,
the left atrium is flooded with blood from the left ventricle
during ventricular systole. In this situation, the left ventri-
cle ejects blood into a normal-sized and relatively unyield-
ing left atrium, causing a giant V wave in the wedge
pressure tracing [13] (Figure 6). This large V wave ele-

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SWAN-GANZ CATHETER-SHARKEY

Figure 3. Arterial (ART) and right atria/ (/?A) pressure waveforms during ventricular tachycardia. The presence of atrioverr
tricular dissociation can be deduced from these tracings. The atria and the ventricles are dissociated and thus contracting at
different rates. Cannon waves (arrows) are present in the right atria/ tracing whenever the right atrium contracts against the
tricuspid valve that has been closed by ventricular systole. These cannon waves are accompanied by a fall in the arterialpres-
sure since there is no effective atria/ contribution to ventricular filling on these beats. At other times, atria! contraction does
not encounter a closed atrioventricular valve and appropriate ventricular filling occurs. On these beats, no cannon waves
occur, and the arterial pressure increases.

vates the mean pulmonary venous pressure and results in

Figure 4. Right atrial (RA) and arterial (ART) pressure
waveforms during demand ventricular pacing. Atrioventric-
ular dissociation is present, and the spontaneous atrial rate
Js slightly sldwer than the paced ventricular rate. As atrial
contraction begins to occur during ventricular systole, cas
non waves appear (double arrow). With the loss of apprcF
priately timed atria/ systole, the arterial pressure declines
(&g/e arrow).
pulmonary congestion. The V wave may in fact resemble
the pulmonary artery waveform, and the operator may not
notice that the catheter has gone from the pulmonary
artery position into the wedge position. This can result in
permanent wedging of the catheter, with the attendant risk
of pulmonary infarction [ 141. This problem can be avoided
by careful examination of the pressure waveform and its
relationship to the electrocardiographic QRS complex.
The giant V wave of acute mitral regurgitation is often
transmitted to the pulmonary artery tracing, which yields a
bifid pulmonary artery waveform comprised of the pulmo-
nary artery systolic wave and the V wave [ 151 (Figure 6).
As the catheter is wedged, the pulmonary artery systolic
wave disappears but the V wave remains (Figure 6). In
addition, the pulmonary artery systolic wave occurs earli-
er in relation to the QRS complex than does the V wave
(Figure 6). Acute mitral insufficiency is one instance in
which the pulmonary artery end-diastolic pressure is actu-
ally lower than the mean wedge pressure. In fact, the
transient reversal of pulmonary blood flow that accompa-
nies the giant left atrial V wave can result in highly
oxygenated blood entering the pulmonary artery and the
mistaken diagnosis of a left-to-right shunt at the ventricu-
lar level (i.e., post-infarction ventricular septal defect)
[ 161. The giant V wave can also cause premature closure
of the pulmonic valve [ 171. It is important to emphasize
that a large V wave in the wedge pressure tracing does

114 July 1987 The American Journal of Medicine Volume 83

 swAtuAt4.z CATHETER-~~~ARKEY

Flgure 5. Aortic and pulmonary artety

(PA) pressure waveforms from a patient
with severe congestive hear-f failure. A
premature ventricular contraction (PVC)
initiates pulsus aiternans, which is vi&
b/e in both the aortic and pulmonary ar-
tery tracings.

Figure 6. Arterial, pulmonary artery

(PA), and wedge pressure waveforms
from a patient with acute mitral regurgi-
tation. A prominent V wave(v) is present
in both the pulmonary artery and wedge
tracings and occurs after the electrocar-
diographic T wave has been inscribed.
The pulmonary artery waveform is bifid
due to the presence of both the pulm&
nary artery systolic wave (S) and the V
wave. inflation of the balloon (double
arrow) obliterates the S wave as the
catheter is wedged. The large V wave
can cause the wedge tracing to be mis-
taken for the pulmonary artery tracing if
the subtle difference in timing between
the S wave and the V wave is not n&
ticed. An A wave is not present due to
atria/ fibrillation.

not invariably indicate mitral insufficiency, and prominent TRICUSPID REGURGITATION

V waves may be observed when the left atrium is distend-
ed and noncompliant due to left ventricular failure from
any cause (i.e., ischemic heart disease, dilated cardiomy-
opathy) [18,19]. In addition, increased pulmonary blood
flow such as that with acute ventricular septal defect may
also cause a large V wave [20]. A large V wave should be
interpreted carefully and in the context of the patient’s
overall clinical status.
Tricuspid valve regurgitation generally occurs in the set-
ting of pulmonary hypertension and right ventricular dilata-
tion and usually presents as a chronic condition [21].
Tricuspid insufficiency causes accentuation of the right
atrial V wave with a steep Y descent and attendant
elevation of the mean right atrial pressure [21] (Fire
7A). The right atrial V wave of chronic tricuspid insuffi-

July 1987 The American Journal of Medicine Volume 83 115

SWAN-GANZ CATHETER-SHARKEY
ciency is not nearly as pronounced as the left atrial V
wave of acute mitral insufficiency. During inspiration, the
mean atrial pressure may remain unchanged or even rise
(Kussmaul’s sign [22] (Figure 76). Significant tricuspid
regurgitation often causes difficulty in placing the Swan-
Ganz catheter since the right heart is usually dilated and
the regurgitant jet does not allow the inflated balloon to
pass readily across the tricuspid valve. Under these cir-
cumstances, fluoroscopy may be necessary to position
the catheter. Tricuspid regurgitation also interferes with
the accuracy of measurement of cardiac output by ther-
modilution because, during each right ventricular systole,
some of the indicator (cold solution) is lost (warmed) as it
is ejected backward into the right atrium instead of for-
116 July 1987 The American Journal of Medicine
Figure 7. A, right atria/ (RA) waveform
from a patient with severe tricuspid t-e-
gurgitation. The regurgitation causes a
broad positive wave (CV) in the right
atrial tracing. When the tricuspid valve
opens, a steep Y descent occurs. The
arrow demonstrates the timing of the C V
wave. A small A wave due to atria/ syst*
le is present. 6, influence of inspiration
(INSP) and expiration (EXP) on right atria/
pressure in a patient with severe tricus-
pid regurgitation. During inspiration, the
positive CV wave and the negative Y
descent are both augmented. The mean
right atrial pressure does not decline dur-
ing inspiration, which is typical of tricus
pid regurgitation.
Figure 8. A, right atria/pressure wave-
form from a patient with right ventricular
infarction. The X and Y descents are
steep and nearly equivalent. B, influence
of inspiration (INSP) and expiration (EXP)
on right atrial pressure. An inspiratoty
increase in right atrial pressure is prs
sent (Kussmaul’s sign), which is typical
of right ventricular infarction.
ward across the pulmonic valve (Zadaca H, Santa Ana
CA, personal communication). With significant tricuspid
regurgitation, the Fick method [23] provides a more accu-
rate measure of forward cardiac output (see later).
RIGHT VENTRICULAR INFARCTION
When a Swan-Car-z catheter is placed in a patient with
acute inferior myocardial infarction, it is important to
search for hemodynamic evidence of right ventricular
infarction. With right ventricular infarction, the right atrial
pressure is often disproportionately increased relative to
the wedge pressure [24]. The mean right atrial pressure
may, in fact, equal or exceed the mean wedge pressure
[24]. With significant elevation of the right atrial pressure,
Volume 83

Figure 9. Pulmonary artery (PA),
wedge, and right atria/ (RA) pressure
waveforms from a patient with severe
right ventricular infarction. The polm&
nary arfery waveform has a narrow pulse
pressure due to reduced right ventricular
stroke volume. The right atria/, pulm&
nary arfery, and wedge waveforms all
resemble each other, which can make
placement of the catheter difficult with
out fluoroscopy. The right atria//wedge
pressure ratio is elevated at 0.8. Hepat@
jugular reflex (HJR) is present.
shunting can occur across a patent foramen ovale and
cause serious arterial desaturation [25]. The right atrial
waveform reveals prominent X and Y descents, and the Y
descent may exceed the X descent due to the presence of
a dilated noncompliant right ventricle that is confined by a
nondistensible pericardium [26,27] (Figure 8A). These
findings are most apparent when the right atrial pressure
is significantly elevated. In fact, subtle abnormalities of
the X and Y descents may become quite exaggerated as
the right atrial pressure rises during volume expansion
therapy for the right ventricular infarction. During inspira-
tion, the right atrial pressure usually does not decline and
may actually increase (Kussmaul’s sign) [26,28] (Figure
8B). In addition, hepatojugular reflux is commonly present
(Figure 9). With severe right ventricular infarction, the
pulmonary artery pulse pressure is narrow due to de-
creased right ventricular stroke volume [29] (Figure 9). In
this circumstance, it may be difficult to ascertain whether
the distal lumen of the catheter is in the right atrium, right
ventricle, pulmonary artery, or wedge position, and fluor-
oscopy may be needed to resolve the dilemma [29].
Tricuspid insufficiency due to papillary muscle dysfunction
and right ventricular dilatation may complicate right ven-
tricular infarction [30].
ACUTE PULMONARY EMBOLUS
Pulmonary hypertension is present in approximately 70
percent of patients with acute pulmonary embolus and
generally appears when 25 to 30 percent of a previously
normal pulmonary vascular bed becomes obstructed [3 I]
July
SWAN-GANZ CATHETER-SHARKEY
(Figure 1OA). A normal right ventricle cannot generate a
high pulmonary artery pressure quickly, and the mean
pulmonary artery pressure rarely exceeds 40 mm Hg
even with a massive acute pulmonary embolus [31].
Higher levels of pulmonary artery pressure suggest a
chronic component to the pulmonary hypertension (Fig-
ure 1OB). Elevation of the mean right atrial pressure is
directly related to the degree of pulmonary hypertension
and generally appears once the mean pulmonary artery
pressure exceeds 35 mm Hg [31]. When thromboemboli
obstruct the pulmonary arteries, the pulmonary vascular
resistance rises and the pulmonary artery end-diastolic
pressure remains significantly higher than the mean
wedge pressure [32,33] (Figure IOA and B). The A and V
waves frequently disappear from the wedge tracing be-
cause the abnormal pulmonary vasculature does not al-
low retrograde transmission of these pressure waves
from the left atrium to the distal catheter lumen [34,35]
(Figure 10A and B). The respiratory distress that accom-
panies acute pulmonary embolism can cause large
swings in the intrathoracic pressure, which are transmit-
ted to the wedge pressure tracing (Figure IOA). Wide
swings in the intrathoracic pressure with respiration re-
duce the accuracy af the mean wedge pressure as a
measure of the transmural left ventricular filling pressure
[36]. The true left ventricular filling pressure is usually
overestimated in this setting [36]. Caution is advised when
a Swan-Ganz catheter is inserted in patients with suspect-
ed pulmonary embolism because peripheral venous em-
boli can become trapped in the body of the right atrium or
1987 The American Journal of Medicine Volume 83 117
SWAN-GANZ CATHETER-SHARKEY

Figure 10. A, pulmonary artery (PA) and wedge pressure tracings from a patient with acute pulmonary embolism. The
pulmonary artery pressure is modestly increased, and a large pressure gradient is present between the pulmonary artery end-
diastolic pressure and the wedge pressure. Large respiratory swings are present in the wedge pressure because of respiratory
distress. Discrete A and V waves are not visible in the wedge tracing. B, pulmonaryarteryand wedge pressure tracings from a
patient with chronic pulmonary emboli. Severe pulmonary hypertension is present, with a wide pressure gradient between the
pUlmOnafy artery end-diastolic pressure and the wedge pressure. Discrete A and V waves are not present in the wedge
pressure waveform probably because of obstruction of the pulmonary vascular bed.

right ventricle as they travel through the heart [37]. Pas-

sage of the catheter could dislodge these clots. In our
institution, two-dimensional echocardiography is routinely
performed prior to insertion of a Swan-Ganz catheter
when pulmonary embolism is suspected so that the right,
atrium and right ventricle can be evaluated for entrapped
clots. Balloon inflation time should be limited in patients
with significant pulmonary hypertension because of the
risk of pulmonary artery rupture [38].

Figure 11. Right atrial (RA) and aortic pressure tracings
from a patient with pericardial tamponade. The aortic pres-
sure declines by 20 mm during inspiration (pulsus para-
doxus). The right atria/ pressure declines normally during
inspiration (INSP). The X descent is dominant, and no Y
descent is present.
PERICARDIAL TAMPONADE
The hemodynamic hallmarks of pericardial tamponade
are elevation and equalization of the right atrial and wedge
pressures coupled with pulsus paradoxus in a patient with
a pericardial effusion [39] (Figure 11). Close examination
of the right atrial pressure waveform reveals a dominant X
descent because the cardiac volume is least during ven-
tricular systole and the degree of tamponade lessens
somewhat [40] (Figure 11). The Y descent is attenuated
or absent [40] (Figure 11). During inspiration, the mean
right atrial pressure declines (Figure 1 l), which can ba
helpful in distinguishing pericardial tamponade from other
conditions that cause equalization of the right atrial and
wedge pressures, such as right ventricular infarction and
pericardial constriction [39]. In an occasional patient with
severe underlying left ventricular dysfunction, pericardial
tamponade can be present at a time when the right atrial
pressure is significantly lower than the left ventricular
filling pressure [41]. Pulsus paradoxus may be absent in

118 July 1987 The American Journal of Medicine Volume 83

 SWAN-GANZ CATHETER-SHARKEY

this small subset of patients [40]. Hypovolemia can also
modify the hemodynamics of pericardial tamponade, in
which case the venous pressures are only modestly ele-
vated [42].
ACUTE VENTRICULAR SEPTAL DEFECT
The Swan-Ganz catheter is helpful in distinguishing acute
ventricular septal defect from acute mitral insufficiency
following myocardial infarction. Rupture of the ventricular
septum causes acute volume overload of the right ventri-
cle with pulmonary-to-systemic blood flow ratios usually
greater than 2:l [43]. The diagnosis of an acute left-to-
right shunt can be confirmed with the Swan-Ganz catheter
by demonstrating a significant increase (10 percent or
more) in the oxygen saturation between the right atrium
and the pulmonary artery [44,45] (Table I). The right atrial
oxygen saturation must be interpreted carefully because
this chamber receives venous blood from three sources:
the inferior vena cava, the superior vena cava, and the
coronary sinus [44]. The right atrial oxygen saturation will
be misleadingly decreased if the proximal lumen of the
catheter happens to be adjacent to the coronary sinus. On
the other hand, the right atrial saturation will be mislead-
ingly increased when significant tricuspid regurgitation is
present in addition to an acute ventricular septal defect.
Arterial blood enters the right ventricle through the septal
defect and then refluxes across the tricuspid valve into the
right atrium. This combination is most likely to occur when
septal rupture complicates acute inferior myocardial in-
farction with concomitant right ventricular infarction and
tricuspid papillary muscle dysfunction. With an acute ven-
tricular septal defect, the mean right atrial, wedge, and
pulmonary artery pressures are all significantly elevated
[43,46] (Table I). As discussed earlier, a prominent V
wave may be present in the wedge tracing [ 191. In a few
patients, left ventricular contrast angiography may be
required to learn whether the hemodynamic collapse is
due to acute ventricular septal defect, acute mitral regur-
gitation, or both. With acute ventricular septal defect, the
systemic cardiac output averages only one half to one
TABLE I Hemodynamic Parameters and Oxygen
Saturations in a Patient with Acute
Ventricular Septal Defect
Right atrial pressure 18 mm Hg
Pulmonary artery pressure 54117 mm Hg
Pulmonary capillary wedge pressure 22 mm Hg
Cardiac output (thermodilution) 4.2 liters/minute
Right atrial oxygen saturation 49 percent
Pulmonary artery oxygen saturation 61 percent
fourth of the thermodilution-determined cardiac output
because the thermodilution method measures right-sided
cardiac output (pulmonary blood flow). Thus, a “normal”
thermodilution-measured cardiac output in a patient with
an acute ventricular septal defect usually reflects a severe
reduction in systemic blood flow.
CARDIAC OUTPUT
The thermodilution method is the most widely used means
of measuring cardiac output. The temperature of pulmo-
nary artery blood is instantly measured by a thermistor
located near the distal tip of the pulmonary artery cathe-
ter. The injection of cold solution into the proximal (right
atrial) lumen of the catheter allows the cardiac output to
be determined by the indicator-dilution technique [47]. As
right-sided cardiac output increases, the indicator (cold
solution) becomes more and more diluted by the warm
venous blood, and less temperature drop is detected by
the pulmonary artery thermistor. Cardiac output is usually
calculated by a computer that uses’an elaborate formula
incorporating the area under the thermodilution curve
(obtained by plotting the decline in pulmonary artery tem-
perature versus time) [48]. Representative curves from
patients with low, normal, and high cardiac outputs are
illustrated in Figures 12A, B, and C, respectively. In my
experience, most physicians accept the computer-gener-
ated digital display of cardiac output as accurate and do
not visually inspect the thermodilution curve. Under cer-
tain circumstances, however, the curve can be distorted

Figure 12. A spectrum of thermodilw

tion cardiac output curves (pulmonary
artery temperature versus time). A, low
cardiac output. 6, normal cardiac output.
C, high cardiac output. D, tricuspid re-
gurgitation. The notches on the descend-
ing portion of the curves are artifacts
generated by the cardiac output comput-
er.

July 1987 The American Journal of Medicine Volume 83 119

SWAN-GANZ CATHETER-SHARKEY
and the computer-generated cardiac output is inaccurate.
One of the most commonly encountered intrinsic reasons
for curve distortion is significant tricuspid regurgitation. In
this condition, a portion of the injected bolus of cold
solution “washes” back and forth between the right atri-
um and the right ventricle, yielding a curve that is easily
recognized by its prolonged decay time (Figure 12D). As
noted earlier, with significant tricuspid regurgitation, the
thermodilution method is not an accurate measure of
cardiac output. When a reliable thermodilution curve can-
not be obtained, an assessment of the cardiac output can
be made by measuring the arteriovenous oxygen differ-
ence: (percent oxygen saturation of arterial blood - per-
cent oxygen saturation of mixed venous blood) X hemo-
globin (g/dl) X 1.36 ml of oxygen per gram of hemoglo-
bin). The mixed venous (pulmonary artery) blood sample
is readily obtained from the distal lumen of the indwelling
Swan-Ganz catheter. The normal arteriovenous oxygen
content difference is 3.0 to 5.0 ml/d1 [49]. As cardiac
output declines, the peripheral tissues extract more oxy-
gen from hemoglobin, and the arteriovenous oxygen dif-
ference increases. The opposite occurs with an increase
in the cardiac output, and thus the arteriovenous oxygen
difference can be used to assess cardiac output [49]. In
certain conditions (septic shock, adult respiratory distress
syndrome), the arteriovenous oxygen difference does not
correlate well with cardiac output [50]. The thermodilution
measurement of cardiac output is easy to perform and
usually both accurate and reproducible [47]. The arterio-
venous oxygen content difference should be used to
assess cardiac output when a reliable thermodilution
curve cannot be obtained.
PROBLEM AREAS
High-quality pressure tracings cannot be obtained in every
patient. Significant tachycardia (ventricular rate of 150
beats/minute or more) may exceed the frequency re-
sponse characteristics of the catheter system and often
reduces the quality of the pressure recordings. In addition,
the A, C, and V waves as well as the X and Y descents
can be difficult to separate during significant sinus tachy-
cardia. In general, the right atrial pressure waveform is
superior to the wedge waveform for analyzing the A, C,
and V waves and the X and Y descents because some of
the fine details of left atrial mechanical events are lost
(damped) during transmission through the pulmonary vas-
culature to the distal lumen of the catheter. On occasion,
the proximal (right atrial) pressure port will lodge against
the wall of the right atrium and no phasic pressure waves
will be present on the right atrial tracing. In this instance,
the mean right atrial pressure will be inaccurate. It is
important to emphasize that precise interpretation of the
various waveforms requires simultaneous recording of
the electrocardiogram and the pressure tracing. A record-
120 July 1987 The American Journal of Medicine
er with at least two-channel capability is mandatory. Ven-
tilators are the bane of hemodynamic monitoring. The
difficult subject of hemodynamic monitoring during posi-
tive-pressure ventilation (both with and without positive
end-expiratory pressure) is beyond the scope of this pa-
per and is discussed elsewhere [51]. Finally, seemingly
minor details such as small air bubbles in the catheter
system and blood clots at the pressure monitoring lumens
can seriously degrade the pressure recordings. The quali-
ty of the dynamic response of the catheter system can
easily be tested at the bedside using the fast-flush method
[51.
SUMMARY
The Swan-Ganz catheter has been in general clinical use
for more than 15 years, and proper use of the device is
taught as a standard part of most internal medicine resi-
dency programs in this country. During these 15 years, it
has become clear that this device is capable of providing
a wealth of physiologic information, yet most physicians
routinely utilize only two parameters: the mean wedge
pressure and the cardiac output. Careful examination of
the right atrial and wedge pressure waveforms and their
response to alterations in the cardiac rhythm enhances
the catheter’s diagnostic utility. The response of the mean
right atrial pressure to various maneuvers such as inspira-
tion and the hepatojugular reflux test can also provide
useful diagnostic information, especially in the setting of
pericardial disease or right ventricular infarction. Analysis
of the pulmonary artery waveform often provides the first
evidence of the giant V wave of acute mitral regurgitation
or the narrow pulmonary artery pulse pressure of severe
right ventricular infarction. When possible, the thermodilu-
tion-determined cardiac output curve should be inspected
for distortion. If a reliable curve cannot be obtained, then
the arteriovenous oxygen difference should be calculated.
Measurement of the oxygen saturation in the right atrium
and pulmonary artery is helpful if an intracardiac shunt
(i.e., acute ventricular septal defect) is suspected. The
Swan-Ganz catheter is also a valuable tool both for teach-
ing and for learning circulatory physiology since it pro-
vides easily recorded details of the hemodynamic de-
rangements that accompany both mechanical and electri-
cal cardiac disorders. The Swan-Ganz catheter may or
may not be overused, but the information it can provide
should not be underutilized.
ACKNOWLEDGMENT
I am grateful to Dr. Morrison Hodges, Dr. Robert Puer-
inger, and Dr. Stanley Nasraway for their careful review of
the manuscript and for many excellent suggestions. Be-
linda Anderson and Maureen Adams are responsible for
the expert preparation of this manuscript.
Volume 83
 SWAN-GANZ CATHETER-SHARKEY

REFERENCES
Swan HJC, Ganz W, Forrester J, Marcus H, Diamond G, 23. Grossman W: Cardiac catheterization and angiography, 2nd
Chonette D: Catheterization of the heart in man with use ed. Philadelphia: Lea & Febiger, 1980; 90-98.
of a flow-directed balloon-tipped catheter. N Engl J Med 24. Lopez-Sendon J, Coma-Canella I, Gamallo C: Sensitivity and
1970; 283: 447-451. specificity of hemodynamic criteria in the diagnosis of
2. Ganz WW, Forrester JS, Chonette D, Donoso R, Swan HJC: acute right ventricular infarction. Circulation 1981; 64:
A new flow-directed catheter technique for measurement 515525.
of pulmonary artery and capillary wedge pressure without 25. Manno BV, Bemis CE, Carver J, Mintz GS: Right ventricular
fluoroscopy (abstr). Am J Cardiol 1970; 25: 96. infarction complicated by right to left shunt. J Am Coll
Robin E: The cult of the Swan-Ganz catheter. Ann Intern Med Cardiol 1983; 1: 554-557.
1985; 103: 445-449. 26. Coma-Canella I, Lopez-Sendon J: Ventricular compliance in
Civetta JM: Pulmonary artery catheter insertion. In: Sprung ischemic right ventricular dysfunction. Am J Cardiol
CL, ed. The pulmonary artery catheter. Baltimore: Univer- 1980; 45: 555-561.
sity Park Press, 1983; 37. 27. Lorell 8, Leinback RC, Pohost GM, et al: Right ventricular
Gardner RM: Direct blood measurement. Dynamic response infarction: clinical diagnosis and differentiation from car-
requirements. Anesthesiology 1981; 54: 227-236. diac tamponade and pericardial constriction. Am J Car-
Barry WA, Grossman W: Cardiac catheterization. In: diol 1979; 43: 465-471.
Braunwald E, ed. Heart disease. A textbook of cardiovas- 28. Dell’ltalia LJ, Starling MR, O’Rourke RA: Physical examina-
cular medicine, vol I. Philadelphia: WB Saunders, 1984; tion for exclusion of hemodynamically important right
287. ventricular infarction. Ann Intern Med 1983; 99: 608-
7. Shabetai R: The pericardium. New York: Grune & Stratton, 611.
1981; 81. 29. Cohn JN, Guiha NH, Broder MI, Limas CJ: Right ventricular
8. Zipes DP: Specific arrhythmias: diagnosis and treatment. In: infarction. Clinical and hemodynamic features. Am J Car-
Braunwald E, ed. Heart disease. A textbook of cardiovas- diol 1974; 33: 209-214.
cular medicine, vol I. Philadelphia: WB Saunders, 1984; 30. MacAllister RG, Friesinger GG, Sinclair-Smith BC: Tricuspid
706-708. regurgitation following inferior myocardial infarction.
9. Goldreyer BN, Kastor JA, Kershbaum KL: The hemodynamic Arch Intern Med 1976; 136: 95-99.
effects of induced supraventricular tachycardia in man. 31. McIntyre KM, Sasahara AA: The hemodynamic response to
Circulation 1976; 54: 783-789. pulmonary embolism in patients without prior cardiopul-
10. Erlebacher JA, Danner RL, Stelzer PE: Hypotension with monary disease. Am J Cardiol 1971; 28: 288-294.
ventricular pacing: an atrial vasodepressor reflex in hu- 32. Jenkins BS, Bradly RD, Branthwaite MA: Evaluation of pul-
man beings. J Am Coll Cardiol 1984; 4: 550-555. monary arterial end-diastolic pressure as an indirect esti-
11. Ausubel K, Furman S: The pacemaker syndrome. Ann Intern mate of left atrial mean pressure. Circulation 1970; 42:
Med 1985; 103: 420-429. 75-78.
12. Perloff JK: The clinical manifestations of cardiac failure in 33. National Cooperative Study: The urokinase-pulmonary em-
adults. Hosp Prac 1970; 5: 43-50. bolism trial. Circulation 1973; 47(suppl II): 51-59.
13. Grossman W: Cardiac catheterization and angiography, 2nd 34. Shaffer AB, Silber EN: Factors influencing the character of
ed. Philadelphia: Lea & Febiger, 1980; 310-311. the pulmonary arterial wedge pressure. Am Heart J 1956;
14. Foote GA, Schabel SI, Hodges M: Pulmonary complications 51: 5222532.
of the flow-directed balloon-tipped catheter. N Engl J Med 35. Ankeney JL: Further experimental evidence that pulmonary
1974; 290: 927-931. capillary pressures do not reflect cyclic changes in left
15. Levinson DC, Wilburne M, Meehan JP, Shubin H: Evidence atrial pressure (mitral lesions and pulmonary embolism).
for retrograde trans-pulmonary propogation of the V (or Circ Res 1953; 1: 58-61.
regurgitant) wave in mitral insufficiency. Am J Cardiol 36. Rice DL, Awe RJ, Gaasch WH, Alexander JK, Jenkins DE:
1958; 2: 159-169. Wedge pressure measurements in obstructive pulmonary
16. Tatooles CJ, Gault JH, Mason DT, Ross J: Reflux of oxygen- disease. Chest 1974; 66: 628-632.
ated blood into the pulmonary artery in severe mitral 37. Saner HE, Asinger RW, Daniel JA, Elsperger KJ: Two-dimen-
regurgitation. Am Heart J 1968; 75: 102-106. sional echocardiographic detection of right-sided cardiac
17. Grose R, Strain J, Cohen MV: Pulmonary arterial V waves in intracavitary thromboembolus with pulmonary embolus. J
mitral regurgitation: clinical and experimental observa- Am Coll Cardiol 1984; 4: 1294-1301.
tions. Circulation 1984; 69: 214-222. 38. Barash PG. Nardi D, Hammond G: Catheter-induced pulmo-
18. Pichard AD, Kay R, Smith H, Rentrop P, Holt J, Gorlin R: nary artery perforation-mechanisms, management, and
Large V waves in the pulmonary wedge pressure tracing modification. J Thorac Cardiovasc Surg 1981; 82: 5-12.
in the absence of mitral regurgitation. Am J Cardiol 1982; 39. Shabetai R: The pericardium. New York: Grune & Stratton,
50: 1044-1050. 1981; 224-278.
19. Fuchs RM, Heuser RR, Yin FCP, Brinker JA: Limitations of 40. Shabetai R, Fowler NO, Guntheroth WG: The hemodynamics
pulmonary wedge V waves in diagnosing mitral regurgita- of cardiac tamponade and constrictive pericarditis. Am J
tion. Am J Cardiol 1982; 49: 849-854. Cardiol 1970; 26: 480-489.
20. Bethen CF, Peter RH, Behar VS, Margolis JR, Kisslo JA, 41. Reddy PS, Curtiss El, O’Toole JD, Shaver JA: Cardiac tam-
Kong Y: The hemodynamic simulation of mitral regurgita- ponade: hemodynamic observations in man. Circulation
tion in ventricular septal defect after myocardial infarc- 1978; 58: 265-272.
tion. Cathet Cardiovasc Diagn 1976; 2: 97-104. 42. Antman EM, Cargill V, Grossman W: Low-pressure cardiac
21. Ockene IS: Tricuspid valve disease. In: Dalen JE, Alpert JS, tamponade. Ann Intern Med 1979; 91: 403-406.
eds. Valvular heart disease. Boston: Little, Brown, 1981; 43. Radford MJ, Johnson RA, Daggett WM, et al: Ventricular
281-328. septal rupture: review of clinical and physiologic features
22. Lingamneni R, Cha SD, Maranhao V, Gooch AS, Goldberg H: and an analysis of survival. Circulation 1981; 64: 545-
Tricuspid regurgitation: clinical and angiographic assess- 553.
ment. Cathet Cardiovasc Diagn 1979; 5: 7-17. 44. Grossman W: Cardiac catheterization and angiography, 2nd

July 1987 The American Journal of Medicine Volume 83 121

SWAN-GANZ CATHETER-SHARKEY

ed. Philadelphia: Lea & Febiger, 1980; 132-134. 48. Ganz W, Swan HJC: Measurement of blood flow by thermo-
45. Labovitz AJ, Miller LW, Kennedy HL: Mechanical complica- dilution. Am J Cardiol 1972; 29: 241-245.
tins of acute myocardial infarction. Cardiovasc Rev Rep 49. Grossman W: Cardiac catheterization and angiography, 2nd
1984; 5: 948-982. ed. Philadelphia: Lea & Febiger, 1980; 89, 415.
46. Campion BC, Harrison CE, Giuliani ER, Schattenberg TT, 50. Ferguson DW, Abboud FM: The recognition and manage-
Ellis FH: Ventricular septal defect after myocardial infarc- ment of shock. In: Hurst JW, ed. The heart, 6th ed. New
tion. Ann Intern Med 1969; 70: 251-261. York: McGraw-Hill, 1985; 385-386.
47. Weisel RD, Berger RL, Hechtman HB: Measurement of cardi- 51. Wiedemann HP, Matthay MA, Matthay RA: Cardiovascular
ac output by thermodilution. N Engl J Med 1975; 292: pulmonary monitoring in the intensive care unit (part I).
682-684. Chest 1984; 85: 537-549.

122 July 1987 The American Journal of Medicine Volume 83