Sudden hypoxemia after uneventful laparoscopic cholecystectomy: another form of SAM presentation
Fujita et al. BMC Anesthesiology
Sudden hypoxemia after uneventful laparoscopic cholecystectomy: another form of SAM presentation
Yoshihisa Fujita 0
Yuka Sakuta 0
Masatsugu Tsuge 0
0 Department of Anesthesiology & ICM, Kawasaki Medical School , Okayama , Japan
Background: Perioperative dynamic left ventricular outflow obstruction associated with systolic anterior motion of the mitral valve is well recognized as a cause for unexplained sudden hypotension in perioperative settings, even without underlying heart diseases such as hypertrophic obstructive cardiomyopathy. We treated a patient who experienced sudden hypoxemia without severe hypotension during emergence from anesthesia after an uneventful laparoscopic cholecystectomy. Case presentation: A 65-year-old female patient with a history of hypertension presented a sudden decrease in oxygen saturation to 80% after an uneventful cholecystectomy. Although a portable chest radiograph showed bilateral hilar pulmonary infiltrates consistent with pulmonary edema, we explored the underlying cause, i.e., systolic anterior motion of the mitral valve and left ventricular outflow tract obstruction with bedside transthoracic echocardiography. We speculate that dynamic mitral regurgitation resulted in pulmonary edema and, thereby, hypoxemia in this case without severe hypotension. Conclusions: Careful bedside examination with transthoracic echocardiography was useful in making diagnosis and in guiding appropriate therapy for this patient. Clinicians should be aware that systolic anterior motion of the mitral valve may present as unexplained sudden hypoxemia in the perioperative setting.
Pulmonary edema; Hypoxia; Systolic anterior motion; Echocardiography; MRI
Perioperative dynamic left ventricular outflow
obstruction (LVOTO) associated with systolic anterior motion
(SAM) of the mitral valve is well recognized as a cause
for unexplained sudden hypotension in perioperative
settings, even without underlying heart disease such as
hypertrophic cardiomyopathy (HOCM) or apical
ballooning syndrome [1-4]. We treated a woman who
experienced a sudden decrease in oxygen saturation (SpO2)
to 80% without severe hypotension during emergence
from anesthesia after an uneventful laparoscopic
cholecystectomy. SAM-related mitral regurgitation (MR) was
suspected to be responsible. Our case demonstrates that
SAM may present as unexplained hypoxemia in the
A 65-year-old woman with a 5-year history of
hypertension and depression was scheduled for laparoscopic
cholecystectomy under general anesthesia. Anesthesia
was induced with propofol, and the airway was secured
with a size #3 ProSeal laryngeal mask airway (PLMA).
Anesthesia was maintained with desflurane at 4% in an
oxygen–air mixture (FiO2 = 50%), and analgesia was
achieved by continuous infusion of remifentanil at a rate
of 0.16-0.24 μg · kg-1 · min-1 supplemented with fentanyl
to a total of 0.4 mg. Muscle relaxation was attained with
intermittent rocuronium. Oxygen saturation (SpO2) was
kept at 99–100%, and blood pressure was relatively stable
but fluctuated between 140/40 and 90/40 mmHg. The
patient’s heart rate (HR) was 65–80 beats per minute during
anesthesia. Surgery took 122 minutes, without measurable
blood loss. A total of 1475 ml of crystalloid solution was
infused intraoperatively. The anesthetic course was
uneventful until the end of surgery.
Several minutes after the end of surgery and having
confirmed spontaneous respiration, 200 mg of sugammadex
was administered intravenously to reverse the
neuromuscular blockade. Although spontaneous respiration
resumed under 100% oxygen, SpO2 decreased to 80%, with
an increase in arterial pressure to 180/100 mmHg. The
attending anesthesiologist, who suspected that a poorly
fitted PLMA was the cause of hypoxemia, replaced the
size #3 PLMA with a size #4 PLMA, and there was a
temporary increase in SpO2 to 92%. The PLMA was removed,
and the patient was transferred to the recovery room with
oxygen at 6 L/min via face mask.
Upon arrival at the post-anesthesia care unit, the
patient was calm but still had a low SpO2 of 88%. Her
blood pressure was 160/85 mmHg and her HR was 81
beats per minute. SpO2 increased to 92% soon with
high-flow oxygen via face mask at a concentration of
60%, but it remained in the range of 90–93% with a
smooth respiration at 18 breaths per minutes. Her
arterial blood gases were pH 7.354, pCO2 47.8 mmHg, pO2
53.5 mmHg and base excess +0.5 mmol/liter. A portable
chest radiograph showed bilateral hilar pulmonary
infiltrates consistent with pulmonary edema, a normal cardiac
silhouette, and air in the stomach (Figure 1). A nasogastric
tube was placed to deflate the distended stomach. Bedside
transthoracic echocardiography (TTE) revealed a
hypercontractile left ventricle, no right ventricular dilatation,
and no segmental wall motion abnormalities; however,
slight mosaic flow signals in the left ventricular outflow
tract (LVOT) and a posteriorly directed slight jet of mitral
regurgitation (MR) were noted on color-flow Doppler
mapping (CFD) (Figure 2). Suspecting the presence of
SAM, isosorbide dinitrate was sprayed under the
patient’s tongue at a dose of 2.5 mg to induce vasodilation.
The MR jet in the posterior direction and the
mosaicpattern LVOTO then increased significantly, while blood
pressure decreased to 78/42 mmHg (Figure 3) (Additional
file 1: Video 1 a, b). We could not measure LVOT velocity,
because parallel alignment with the continuous Doppler
signal to the blood flow in the LVOT was not possible.
Based on a diagnosis of dynamic MR and LVOTO
secondary to SAM, we intravenously administered 0.2 mg of
phenylephrine twice and initiated rapid infusion of
500 mL of hydroxylethyl starch over the course of an hour
and continuous infusion of a short-acting beta blocker.
The patient’s blood pressure returned to 152/68 mmHg,
and SpO2 increased to 97–99% with an oxygen mask at a
concentration of 40%. She was cared for overnight in the
intensive care unit uneventfully without recurrence of
hypoxemia, and transferred to the ward the next day.
The bilateral hilar infiltrate had disappeared on the
chest radiograph taken the next day. Troponin T and BNP
at the post-anesthesia care unit were slightly increased
to 0.012 ng/mL (normal <0.014 ng/mL) and 19.0 pg/mL
(normal <18.4 pg/mL), respectively, suggesting slight
myocardial injury. Cardiac magnetic resonance imaging (MRI)
(Figure 4) (Additional 2: Video 2) performed 4 days after
surgery, as well as transesophageal echocardiography
(TEE), showed chordal SAM with mild MR and LVOTO
at rest. The imaging showed some protrusion of the basal
septal wall toward the LVOT. The peak pressure gradient
through the LVOT was 20 mmHg on TEE.
Echocardiographic measurement was performed by TEE to assess the
Figure 1 Portable chest radiograph. There were bilateral hilar
pulmonary infiltrates, but the periphery of the lungs was relatively
spared. Cardiac silhouette was not enlarged. There was air in
Figure 2 Bedside transthoracic echocardiography with color-flow
Doppler mapping in the post-anesthesia care unit (left parasternal
long axis view). Slight mosaic flow signals in the left ventricular
outflow tract was noted on colorflow Doppler mapping. LA = left
atrium; LV = left ventricle; LVOT; left ventricular outflow
tract; Ao = aorta.
Figure 3 Bedside transthoracic echocardiography with color-flow
Doppler mapping in the post-anesthesia care unit after sublingular
nitrate (left parasternal long axis view). Significant mitral regurgitation
jet in the posterior direction (arrow)and mosaic pattern left ventricular
outflow (arrow head) appeared.
anatomical factors that contributed to SAM (Table 1). The
coaptation point of the mitral leaflets was 17 mm, shorter
than the threshold value (25 mm), indicating an anteriorly
displaced coaptation point, although other measurements
did not reach threshold values. The patient is now
regularly checked upon, and is taking 5 mg of oral bisoprolol
fumarate per day.
Figure 4 Cardiac MRI obtained 4 days after surgery. It revealed
systolic anterior motion (arrow). There were no abnormalities in
global shape, size, and systolic function of the left ventricle, except
for some protrusion of the basal interventricular septum towards
the left ventricular outflow tract. LA = left atrium; LV = left
ventricle; Ao = aorta.
Table 1 Echocardiographic predictors of systolic anterior motion (SAM)
Basal septal thickness at end-systole
Distance from coaptation point
to septum at onset of systole
Mitral-aortic angle at onset of systole
Echocardiographic predictors of SAM described in reference 5. Values outside
threshold limits indicate increased likelihood of SAM. Measurement was
performed on transesoephageal echocardiographic images. Coaptation point
of the mitral leaflets of the patient was shorter than the threshold value. Other
values were within threshold limits.
Midesophageal aortic valve long-axis view with color Doppler imaging showing
aortic insufficiency (arrow). LA = left atrium; LV = left ventricle; Ao = aorta.
SAM typically occurs in association with certain
underlying heart diseases, such as HOCM and apical
ballooning syndrome or in the perioperative setting of cardiac
surgeries, such as mitral valve repair and aortic valve
replacement . Recently, its occurrence was described in
critical care settings without underlying heart disease
[1,6]. Whether it occurs in the presence or absence of
underlying heart disease, unexpected severe hypotension
is the most typical manifestation and is caused by the
dynamic LVOTO secondary to SAM [2,4,6,7]. Our
patient suffered from unexplained severe hypoxemia upon
emergence from anesthesia, without accompanying
The use of LMA for laparoscopic cholecystectomy may
not be common, but it is well accepted in many centers.
Although we have used both Classic and ProSeal LMAs
more than ten years safely, the latter is now preferred for
ease of gastric tube placement and higher sealing pressure
. There is a theoretical possibility of silent aspiration of
residual gastric fluid in this case for hypoxemia with a
ProSeal LMA. However, transient nature of hypoxemia,
uneventful course in the ICU on the following night and
complete disappearance of infiltrate in the chest
roentgenogram on the next day exclude its possibility. Other
causes such as residual neuromuscular blockade,
atelectasis or acute pulmonary edema, are also unlikely to have
caused severe hypoxemia with hypotension, because of
reliable antagonistic effects to rocuronium with
sugammadex or a short duration of laparoscopic surgery in an
otherwise healthy patient.
Based on findings from the chest radiograph and TTE,
we speculate that MR secondary to SAM caused
pulmonary edema and hypoxemia in this patient. Because
SAM leads to LVOTO and a systolic coaptation defect
of the mitral valve, and because the severity varies in a
dynamic way depending upon cardiac loading,
chronotropy, and contractility [5-7], it is not surprising that
severe hypoxemia, rather than hypotension, manifested in
Cardiac MRI and TEE showed chordal SAM with MR
at rest, suggesting that the patient was predisposed to
SAM, although there were no apparent structural
abnormalities. It has been reported that there are several
structural predisposing factors for SAM, such as narrow LVOT,
anteriorly located mitral coaptation point, and small
mitral–aortic angle of <120° . We identified an
anteriorly located mitral coaptation point in this patient’s
heart. In addition to the echocardiographic predisposing
factors, we speculate that anesthesia-mediated factors,
such as anesthesia-mediated vasodilation, increased
catecholamine levels due to surgical stimulation, and
dehydration due to preoperative fasting, increased the severity
of SAM and secondary MR .
Treatment for pulmonary edema caused by SAM-induced
MR differs from treatment of other forms of cardiogenic
pulmonary edema, even though left atrial pressure is
increased in both conditions . The accepted treatments
for cardiogenic pulmonary edema, such as diuretics,
vasodilators, and inotropes, may worsen hypoxemia in patients
with pulmonary edema caused by SAM-induced MR or
even lead to cardiogenic shock or sudden death from
LVOTO, if the cause remains unrecognized. Correct
diagnosis of the underlying condition, i.e., SAM, is thus critically
important for initiating appropriate treatment. Although
the most common clinical finding in SAM or LVOTO is a
new onset of systolic murmur peaking late , it is often
difficult to obtain clear heart sounds during surgery or in
the critical care setting, because of interference from noise
induced by mechanical ventilation and other surrounding
Bedside TTE may be an important first-line diagnostic
tool for the diagnosis of SAM . It is also very helpful
for differentiating SAM-related pulmonary edema from
other forms of cardiogenic pulmonary edema.
Echocardiographic visualization of the mitral leaflet–ventricular
septum contact during systole on 2D or M mode, or
shark-tooth velocity contour in the LVOT on continuous
Doppler flow are diagnostic for SAM. In addition, mosaic
flow pattern in the LVOT and a posteriorly directed MR
jet on CFD may suggest LOVOT and MR, respectively,
secondary to SAM. In this case, the initial TTE revealed
only the mosaic pattern in the LVOT with a slight MR jet.
However, careful examination of TTE using sublingual
nitrate clearly demonstrated a posteriorly directed MR jet
and an increase in the LVOTO mosaic pattern. We could
thus establish a diagnosis of SAM and secondary MR as
the cause of hypoxemia in this patient.
TEE for the diagnosis of SAM is limited mostly to
intraoperative intubated patients, because of its
invasiveness. However, TEE could have clearly revealed systolic
contact of the anterior leaflet of the mitral valve to the
septum . It is thus advisable to use TEE in patients
for whom a bedside TTE is not sufficiently informative
to diagnose SAM, especially hemodynamically unstable
The present case underscores the fact that to make a
diagnosis of SAM, it is important to bear in mind its
possibility when unexplained hypoxemia or hypotension
occur, even in patients without apparent structural
abnormalities of the heart. Clinicians can then listen for
systolic murmur or perform bedside TTE under
vasodilation with nitrate, if necessary, and eventually perform
TEE for timely initiation of appropriate treatment.
We reported our experience with a patient who had sudden
hypoxemia with pulmonary edema at the end of anesthesia
following an uneventful laparoscopic surgery. With careful
bedside TTE, we were able to explore the underlying
cause, i.e., SAM. Clinicians should be aware that SAM
may result in unexplained hypoxemia in patients without
apparent structural abnormalities of the heart.
Written informed consent was obtained from the patient
for publication of this Case report and any
accompanying images. A copy of the written consent is available for
review by the Editor of this journal.
Additional file 1: Bedside transthoracic echocardiography (color-flow
Doppler mapping). Left parasternal long axis view in the post-anesthesia
care unit before (a) and after (b) sublingual nitrate. (a) hypercontractile left
ventricle with slight mosaic flow signals in the left ventricular outflow tract
and posteriorly directed slight jet of mitral regurgitation (MR) were noted
on color-flow Doppler mapping. (b) MR jet in the posterior direction and
mosaic pattern left ventricular outflow obstruction increased significantly.
Additional file 2: Cardiac MRI obtained 4 days after surgery
revealed chordal systolic anterior motion with mitral regurgitation.
There were no abnormalities in global shape, size, and systolic function of
the left ventricle, except for some protrusion of the basal interventricular
septum towards the left ventricular outflow tract.
Ao: Aorta; CFD: Color-flow Doppler mapping; HOCM: Hypertrophic
obstructive cardiomyopathy; HR: Heart rate; LMA: Laryngeal mask airway;
LA: Left atrium; LV: Left ventricle; LVOT: Left ventricular outflow tract;
LVOTO: Left ventricular outflow tract obstruction; MR: Mitral regurgitation;
MRI: Magnetic resonance imaging; PLMA: ProSeal® laryngeal mask airway;
SAM: Systolic anterior motion; SpO2: oxygen saturation; TEE: Transesophageal
echocardiography; TTE: Transthoracic echocardiography.
YF: Involvement of the patient care at the ICU and preparation of the
manuscript. YS and MT: Substantial contribution to draft the manuscript. NK:
Carrying out the TEE and MRI studies and substantial contribution to the
interpretation of TEE findings. All authors read and approved the final
1. Chockalingam A , Mehra A , Dorairajan S , Dellsperger KC. Acute left ventricular dysfunction in the critically ill . Chest . 2010 ; 138 : 198 - 207 .
2. Reddy S , Ueda K. Unexpected refractory intra-operative hypotension during non-cardiac surgery. Diagnosis and management guided by trans-oesophageal echocardiography . Indian J Anaesth . 2014 ; 58 : 51 - 4 .
3. Cavallaro F , Marano C , Sandroni C , Dell'anna A. Systolic anterior motion causing hemodynamic instability and pulmonary edema during bleeding . Minerva Anestesiol . 2010 ; 76 : 653 - 6 .
4. Luckner G1 , Margreiter J , Jochberger S , Mayr V , Luger T , Voelckel W , et al. Systolic anterior motion of the mitral valve with left ventricular outflow tract obstruction: three cases of acute perioperative hypotension in noncardiac surgery . Anesth Analg . 2005 ; 100 : 1594 - 8 .
5. Hymel BJ , Townsley MM . Echocardiographic assessment of systolic anterior motion of the mitral valve . Anesth Analg . 2014 ; 118 : 1197 - 201 .
6. Chockalingam A , Dorairajan S , Bhalla M , Dellsperger KC . Unexplained hypotension: the spectrum of dynamic left ventricular outflow tract obstruction in critical care settings . Crit Care Med . 2009 ; 37 : 729 - 34 .
7. Ibrahim M1 , Rao C , Ashrafian H , Chaudhry U , Darzi A , Athanasiou T. Modern management of systolic anterior motion of the mitral valve . Eur J Cardiothorac Surg . 2012 ; 41 : 1260 - 70 .
8. Lu PP , Brimacombe J , Yang C , Shyr M. ProSeal versus the Classic laryngeal mask airway for positive pressure ventilation during laparoscopic cholecystectomy . Br J Anaesth . 2002 ; 88 : 824 - 7 .