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Intra-Aortic Balloon Pump Effects on
Macrocirculation and Microcirculation in
Cardiogenic Shock Patients Supported by
Venoarterial Extracorporeal Membrane Oxygenation
Thibaut Petroni, MD1; Anatole Harrois, MD, PhD2; Julien Amour, MD, PhD3;
Guillaume Lebreton, MD4; Nicolas Brechot, MD, PhD1; Sébastien Tanaka, MD2;
Charles-Edouard Luyt, MD, PhD1; Jean-Louis Trouillet, MD1; Jean Chastre, MD1;
Pascal Leprince, MD, PhD4; Jacques Duranteau, MD, PhD2; Alain Combes, MD, PhD1

Objectives: This study was designed to assess the effects on
macrocirculation and microcirculation of adding an intra-aortic
balloon pump to peripheral venoarterial extracorporeal membrane
oxygenation in patients with severe cardiogenic shock and little/
no residual left ventricular ejection.
Design: A prospective, single-center, observational study where
macrocirculation and microcirculation were assessed with clinical-, Doppler echocardiography–, and pulmonary artery–derived
hemodynamic variables and also cerebral and thenar eminence
tissue oxygenation and side-stream dark-field imaging of sublingual microcirculation.
Setting: A 26-bed tertiary ICU in a university hospital.

Medical-Surgical Intensive Care Unit, iCAN, Institute of Cardiometabolism and Nutrition, Hôpital de la Pitié–Salpêtrière, Assistance Publique–
Hôpitaux de Paris, Université Pierre et Marie Curie, Paris, France.
Department of Anesthesiology and Critical Care Medicine, Hôpital
Bicêtre, Assistance Publique–Hôpitaux de Paris, Université Paris Sud,
Le Kremlin-Bicêtre, France.
Department of Anesthesiology and Critical Care Medicine, UMRS
INSERM 956, iCAN, Institute of Cardiometabolism and Nutrition, Hôpital
de la Pitié–Salpêtrière, Assistance Publique–Hôpitaux de Paris, Université Pierre et Marie Curie, Paris, France.
Department of Cardiac Surgery, iCAN, Institute of Cardiometabolism and
Nutrition, Hôpital de la Pitié–Salpêtrière, Assistance Publique–Hôpitaux
de Paris, Université Pierre et Marie Curie, Paris, France.
Dr. Petroni received a grant support for article research and an educational grant from Assistance Publique–Hôpitaux de Paris. Dr. Luyt served
as a board member for Bayer Healthcare and lectured for Novartis, MSD,
and ThermoFischer Brahms. His institution received grant support from
Janssen and Bayer. Dr. Combes served as board member for GAMBRO
and lectured for MAQUET. The remaining authors have disclosed that they
do not have any potential conflicts of interest.
For information regarding this article, E-mail:
Copyright © 2014 by the Society of Critical Care Medicine and Lippincott
Williams & Wilkins
DOI: 10.1097/CCM.0000000000000410

Critical Care Medicine

Patients: We evaluated 12 consecutive patients before and 30
minutes after interrupting and restarting intra-aortic balloon pump.
Interventions: Measurements were performed before, and 30
minutes after interrupting and restarting intra-aortic balloon pump.
Measurements and Main Results: Stopping intra-aortic balloon
pump was associated with higher pulmonary artery-occlusion
pressure (19 ± 10 vs 15 ± 8 mm Hg, p = 0.01), increased left
ventricular end-systolic (51 ± 13 vs 50 ± 14 mm, p = 0.05) and
end-diastolic (55 ± 13 vs 52 ± 14 mm, p = 0.003) dimensions, and
decreased pulse pressure (15 ± 13 vs 29 ± 22 mm Hg, p = 0.02).
Maximum pulmonary artery-occlusion pressure reduction when
the intra-aortic balloon pump was restarted was observed in the
seven patients whose pulmonary artery-occlusion pressure was
more than 15 mm Hg when intra-aortic balloon pump was off
(–6.6 ± 4.3 vs –0.6 ± 3.4 mm Hg, respectively). Thenar eminence
and brain tissue oxygenation and side-stream dark-field–assessed
sublingual microcirculation were unchanged by stopping and
restarting intra-aortic balloon pump.
Conclusions: Restoring pulsatility and decreasing left ventricular afterload with intra-aortic balloon pump was associated with
smaller left ventricular dimensions and lower pulmonary artery
pressures but did not affect microcirculation variables in cardiogenic shock patients with little/no residual left ventricular ejection
while on peripheral venoarterial extracorporeal membrane oxygenation. (Crit Care Med 2014; XX:00–00)
Key Words: cardiogenic shock; extracorporeal membrane
oxygenation; macrocirculation; microcirculation; pulmonary edema


enoarterial femoral–femoral extracorporeal membrane oxygenation (ECMO) can rescue patients with
refractory cardiogenic shock. It has been successfully
used as a bridge to myocardial recovery, cardiac transplantation, or the implantation of a ventricular-assist device (VAD)


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Petroni et al

in patients with overt cardiac failure of various etiologies, for
example, acute myocardial infarction (AMI) (1, 2), end-stage
dilated cardiomyopathy (3), viral or toxic myocarditis (4),
complications of cardiac surgery (5), or cardiac arrest (6).
Because the ECMO system reinjects oxygenated blood countercurrent into the descending aorta, it increases in left ventricular (LV) afterload and, in 15–20% of the patients, is associated
with severe hydrostatic pulmonary edema, one of the most feared
ECMO complications (1). The latter is even more frequent in
patients with little/no residual LV ejection on ECMO. In this
context, hydrostatic pulmonary edema is further aggravated by
mitral regurgitation induced by LV dilation and increased LV
end-diastolic pressure, resulting from poor LV unloading. The
intra-aortic balloon pump (IABP), which inflates during diastole and actively deflates during systole, increases coronary artery
blood flow and reduces LV afterload (7). Some ECMO centers
systematically combine IABP and ECMO to prevent pulmonary edema. Creating such a pseudopulsatile blood flow might
improve regional microcirculation, as recently suggested (8).
However, to date, no study has carefully evaluated IABP
impact on general and regional hemodynamics of patients with
severe cardiogenic shock on ECMO. This study was undertaken
to assess IABP effects on clinical-, Doppler echocardiography–,
and pulmonary artery–derived hemodynamic variables and
also cerebral and thenar eminence tissue oxygenation (Sto2)
and side-stream dark-field (SDF) imaging–evaluated intravital
sublingual microcirculation.

This study, conducted between November 2010 and October
2011 in our tertiary ICU, was approved by our hospital’s institutional review board. Informed consent was obtained from all
patients or their surrogates.
Before installing ECMO, every patient had the following signs
of acute refractory cardiogenic shock (1, 4): evidence of tissue
hypoxia concomitant with adequate intravascular volume, sustained hypotension, and low cardiac index (< 2.2 L/min/m2),
despite infusion of high-dose catecholamines (epinephrine > 0.2
μg/kg/min or dobutamine > 20 μg/kg/min with/without norepinephrine > 0.2 μg/kg/min). Femorofemoral venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated
because of acute refractory cardiogenic shock complicating AMI,
end-stage dilated cardiomyopathy, heart surgery for acute valvular dysfunction (aortic endocarditis and aortic mechanical valve
thrombosis), or fulminant myocarditis. IABP (CS100, Datascope,
Maquet; Getinge Group, Lübeck, Germany) was inserted in all
patients in the contralateral femoral artery. Hemodynamics was
monitored via a right arterial catheter for continuous blood pressure (BP) monitoring and a pulmonary artery catheter inserted
into the internal jugular vein. Only patients with no/very low
(i.e., velocity-time integral [VTI] < 5 cm) residual LV ejection
were included. Exclusion criteria were age less than 18 years,

intrabuccal bleeding making it impossible to acquire SDF images,
and IABP or ECMO implantation contraindicated.
ECMO Circuit Settings and Patients
Management Under ECMO
ECMO (1, 4, 9) consisted of polyvinyl chloride tubing, a membrane oxygenator (Quadrox Bioline; Jostra-Maquet, Orléans, France), a centrifugal pump (Rotaflow; Jostra-Maquet),
and either percutaneous arterial and venous femoral or central right atrial and aortic cannulae (Biomedicus Carmeda;
Medtronic, Boulogne-Billancourt, France). An oxygen-air
blender (Sechrist Industries, Anaheim, CA) ventilated the
membrane oxygenator. When percutaneous femoral ECMO
was instituted, an additional 7F cannula was inserted distally
into the femoral artery to prevent severe leg ischemia. Vasopressors were down-titrated to obtain a systolic BP (SBP) of
100–110 mm Hg or a mean arterial BP of 70–90 mm Hg.
Unfractionated-heparin anticoagulation was used to obtain
anti-factor-Xa activity of 0.2–0.4 IU/mL or activated partial
thromboplastin time of 45–65 seconds. Experienced perfusionists checked the circuit daily.
Study Protocol
IABP impact on general and regional hemodynamic variables
was assessed in three stages. IABP was set at 100% inflation and
1/1 frequency in automatic mode based on surface electrocardiogram recording. A first sequence of measurements was obtained;
IABP was interrupted for 30 minutes and another sequence was
obtained; and IABP was restarted for another 30 minutes prior
to obtaining the third sequence. During the procedure, patients
received midazolam, propofol, and fentanyl sedation and were
paralyzed with pancuronium. Catecholamine infusion, ECMO,
and mechanical ventilation (MV) settings were kept constant
during all protocol stages, with no fluid loading.
Variables Studied
The following data were recorded at ECMO onset: age, sex, indication for ECMO support, initiation under cardiopulmonary
resuscitation, Simplified Acute Physiology Score-2 (SAPS-2)
(range, 0–174) (10), the Sepsis-Related Organ Failure Assessment (SOFA) score (11), MV status, IV inotrope use, or requiring
renal replacement therapy. Hemodynamic status was assessed by
measuring SBP, diastolic BP (DBP), mean arterial BP, pulse pressure (SBP – DBP), and heart rate. The pulmonary artery catheter
provided pulmonary artery systolic pressure, pulmonary artery
diastolic pressure, mean pulmonary artery pressures, and pulmonary artery-occlusion pressure (PAOP) (12). Patients were
studied while in the supine position, zero pressure was taken as
atmospheric pressure at the midaxillary line and zone of West
assessed as previously described (13). All values were measured
at end expiration. Blood gases were analyzed in right atrium,
pulmonary artery, and peripheral artery samples.
Transthoracic echocardiography was performed with an
Acuson Sequoia (Siemens, Malvern, PA) and the following
variables were recorded: LV end-systolic dimension (LVESD),
LV end-diastolic dimension (LVEDD), LV ejection fraction
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Clinical Investigation

(LVEF), aortic VTI, cardiac output and cardiac index, transmitral early peak (E) and late (A) diastolic velocities, and spectral tissue Doppler lateral mitral annulus peak systolic (TDSa)
and early diastolic (Ea) velocities (14), with E/Ea estimating
LV-filling pressures (15, 16).
The InSpectra Tissue oxygenation monitor (model 650;
Hutchinson Technology, Hutchinson, MN) measured thenar
Sto2. The near-infrared spectroscopy (NIRS) probe, with 15 mm
between illumination and detection optical fibers, was placed on
the thenar eminence and transferred continuously read measurements to a computer. After assuring stabilized baseline Sto2,
a vascular occlusion test (VOT) was run as previously described
(17). Tissue desaturation and resaturation slopes were calculated automatically with the InSpectra Analysis Program V4.00
(Hutchinson Technology), as previously described (17, 18).
Although visible light penetrates tissue only short distances,
near infra-red spectrum (ranging from 700 to 1,100 nm) photons are capable of deeper penetration of several centimeters or
more and can also go through bones. NIRS Equanox cerebral
sensors (Equanox; Nonin Medical, Plymouth, MN), each with
two emitters (light-emitting diodes [LEDs] with three wavelengths in the 700–900 nm range) and two detectors to cancel
out surface and shallow tissue variations to improve accuracy
and repeatability of measurements, were placed on the left and
right forehead to measure left and right cerebral hemisphere
oxygen saturation (left and right So2) (19).
SDF imaging obtained microcirculation videos of the sublingual mucosa with a video microscope (Microscan; Microvision
Medical, Amsterdam, the Netherlands) containing a ring of
stroboscopic LEDs (20). The SDF-imaging device is noninvasive, can be used at bedside, and yields reproducible results,
with intra- and interobserver variabilities less than 10%. Images
were acquired and analyzed according to international recommendations (20) with dedicated software analysis (Automated
Vascular Analysis v1.0; Academic Medical Center, University of
Amsterdam, Amsterdam, the Netherlands). Microscan stability
was enhanced with a multiperforated sterile metal ring adapted
to the tip of the probe for acquisition. Every patient had video
sequences lasting more than or equal to 20 seconds obtained
on five different tongue fields, avoiding pressure artifacts, using
a portable computer and analog-digital video converter. Those
sequences were analyzed blindly and randomly. First, a semiquantitative score, the microvascular flow index (MFI) using an
ordinal scale (absent, 0; intermittent, 1; sluggish, 2; normal, 3),
quantified flow in each of the four quadrants on the screen. The
global MFI score is the sum of the four quadrant scores divided by
the number of quadrants in which the vessel type is seen (20, 21).
Second, we calculated the percentage of perfused vessels (PPV)
(20, 21). Flow was categorized as present (continuous for ≥ 20 s),
absent (no flow for ≥ 20 s), or intermittent (no flow for ≥ 50% of
the time). PPV was calculated as follows: 100 × (total number of
vessels – [no + intermittent flows])/total number of vessels. The
same software measured functional capillary density (FCD) and
determined the flow heterogeneity index. To determine heterogeneity of perfusion between different sublingual sites, we calculated the heterogeneity MFI index as the highest MFI of the five
Critical Care Medicine

sites minus the lowest MFI of the five sites divided by the mean of
the MFI of all sublingual sites. For each patient and each dataset,
values obtained from the five tongue fields were averaged.
Table 1. Main Characteristics of the
12 Patients



Age, yr

57 ± 14


Men, n (%)

9 (75)

Body mass index

26.9 ± 4.6


  Simplified Acute Physiology

79 ± 16


  Sepsis-Related Organ Failure

16 ± 5


  Days of ECMO

6.3 ± 5.9


  Days of intra-aortic balloon pump

4.7 ± 4.4


At ECMO initiation

Before inclusion

Diagnosis, n (%)
  Acute myocardial infarction

8 (67)

  Acute valvular dysfunction

2 (17)

  Dilated cardiomyopathy

1 (8)

  Fulminant myocarditis

1 (8)

ECMO under cardiopulmonary

3 (25)

During study protocol
  ECMO flow, L/min

4.3 ± 0.9

  ECMO rpm during study
protocol, /min


3,480 ± 740 2,200–4,580

7.5 ± 3.0

  Dobutamine (n = 4),


  Norepinephrine (n = 1), mg/hr

3.0 ± 4.0

  Epinephrine (n = 5), mg/hr
Patients on mechanical
ventilation, n (%)


12 (100)
5 (42)

Renal replacement therapy, n (%)
ICU length of stay, d


24.9 ± 7.5


Outcomes, n (%)

3 (25)

  Heart-Mate II

2 (17)


1 (8)


6 (50)

ECMO = extracorporeal membrane oxygenation.
Data are mean ± sd or number (%).


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Petroni et al

Statistical Analyses
Hemodynamic, Doppler echocardiography, tissue oxygenation, and SDF variable changes during the three protocol
stages were compared with the Friedman statistic using StatView v5.0 software (SAS Institute, Cary, NC). p value of less
than 0.05 was defined as significance.

Study Population
Clinical characteristics of the 12 patients (age 57 ± 14 yr, nine
male patients) evaluated are summarized in Table 1. Mean
SAPS-2 (69 ± 21, predicting death of > 62%) and SOFA
score (14 ± 5) were high, reflecting disease severity at ICU
admission. Among the 12 patients studied, only six were on
Table 2.

vasopressors and three of them were receiving low-dose epinephrine or norepinephrine (≤ 0.7 mg/hr). When the protocol was run, all were in sinus rhythm and mechanically
ventilated. They had been on ECMO for 6.3 ± 5.9 days and
had an IABP inserted for 4.7 ± 4.4 days. Mean ECMO flow
was 4.3 ± 0.9 L/min. Their in-ICU stays were prolonged.
Three recovered normal LVEF and were weaned off ECMO,
three received a long-term VAD (Heart-Mate II; Thoratec
Corporation, Pleasanton, CA; for two and CardioWest [Syn­
Cardia systems, Tucson, AZ], for one), and six died of multiple organ failure.
IABP Impact on General Hemodynamic Variables
When the IABP was interrupted (Table 2), DBP and mean
BP (MBP) increased, pulse pressure decreased, while heart

General Hemodynamic Variables

Heart rate

99 ± 21

101 ± 17

103 ± 20


103 ± 20

102 ± 20

100 ± 22


74 ± 17

88 ± 16

72 ± 16


87 ± 14

92 ± 16

84 ± 16


Pulse pressure (mm Hg)

29 ± 22

15 ± 13

29 ± 24


DBP increase (mm Hg)

134 ± 40

125 ± 26

  LV end-diastolic dimension (mm)

52 ± 14

55 ± 13

47 ± 13c


  LV end-systolic dimension (mm)

50 ± 14

51 ± 13

42 ± 13c


  Velocity-time integral (mm)

25 ± 13

25 ± 14

26 ± 15


0.79 ± 0.46

0.77 ± 0.78

0.81 ± 0.74


   Transmitral early peak (cm/s)

49 ± 19

61 ± 25

51 ± 26


   Transmitral late peak (A) (cm/s)

32 ± 13

31 ± 9

31 ± 12


Systolic BP (mm Hg)
DBP (mm Hg)
Mean BP (mm Hg)



IABP Restart



Echocardiographic data

  Cardiac output (L/min)
  Diastolic velocity

   Transmitral early/late peak

1.26 ± 0.38

1.95 ± 0.66

1.33 ± 0.36


   Lateral mitral early annular (cm/s)

6.4 ± 2.8

6.4 ± 2.5

5.8 ± 1.9


   Transmitral early peak/lateral mitral early annular

8.6 ± 4.0

9.8 ± 2.6

9.2 ± 4.3


   Systolic mitral annulus velocity (cm/s)

4.9 ± 2.5

5.0 ± 2.9

4.9 ± 2.3


  Pulmonary artery systolic pressure, mm Hg

24 ± 9

29 ± 11

23 ± 10


  Pulmonary artery diastolic pressure, mm Hg

16 ± 7

19 ± 10

16 ± 9


  Mean pulmonary artery pressures, mm Hg

19 ± 8

24 ± 10

19 ± 9


  Pulmonary artery-occlusion pressure, mm Hg

15 ± 8

19 ± 10

15 ± 8


  Central venous oxygen saturation, %

73 ± 11

73 ± 15

75 ± 12


Pulmonary artery catheter

IABP = intra-aortic balloon pump, BP = blood pressure, DBP = diastolic BP, LV = left ventricle. Dash indicates that this variable does not exist when IABP is off.
Friedman test for the comparisons of the mean ranks between the three study stages.
Mean arterial BP was calculated by the ICU bedside monitor from assisted systolic and diastolic pressures.
Data available for seven of 12 patients.
p for the comparison between IABP on and IABP off stages.
Data are mean ± sd.


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Clinical Investigation

healthy volunteers and comparable to those of septic shock or
trauma patients (17, 18, 22–24).
SDF microvascular variables
(FCD, MFI, PPV, and heterogeneity MFI index) did not differ
significantly among the three
protocol stages (Fig. 2).

The results of this pilot physiological study demonstrated that
for patients on femorofemoral
VA-ECMO for refractory cardiogenic shock and whose native
cardiac function was almost
completely abolished, IABP
Figure 1. Pulmonary artery-occlusion pressure before and 30 min after interrupting and restarting intra-aortic
addition to ECMO was associballoon pump (IABP) in the 12 patients on extracorporeal membrane oxygenation. The three squares represent
the mean ± sd.
ated with reduced LVEDD and
decreased pulmonary artery BPs,
rate and SBP were unchanged. Mean pulmonary SBP, DBP, without modifying microcirculation variables evaluated with
and MBP and PAOP were significantly higher when IABP thenar eminence and brain NIRS and sublingual SDF imaging.
was interrupted and returned to baseline values when it
IABP use has been proposed for more than four decades
was restarted (Fig. 1). For the seven patients whose PAOP
to treat patients with severe cardiac failure by increasing diawere more than 15 mm Hg with IABP off, maximum PAOP
stolic blood flow in the coronary and systemic circulations and
reduction was observed when it was restarted (–6.6 ± 4.3 vs
lowering cardiac afterload by the brief vacuum created by the
–0.6 ± 3.4 mm Hg for the others, respectively). Furthermore, rapid end-diastolic balloon deflation (7). However, its use has
with IABP off, Doppler echocardiography variables indicated a
been questioned in recent years (25–27) and a large randommodest LVEDD rise and significant mitral inflow E/A increase, ized trial showed that IABP did not significantly reduce 30-day
whereas the E/Ea ratio was not markedly modified, and TDSa
mortality in patients with cardiogenic shock complicating AMI
and Ea velocities, aortic VTI, mean Svo2, and other blood gas
for whom an early revascularization strategy was planned (28).
variables including lactate (not shown) were unaffected.
Conversely, cardiac index is not or only mildly affected (7) and
only ECMO can improve failing systemic perfusion in patients
Regional Hemodynamics Variables
with very low cardiac output (1, 6). However, the continuous
Like right and left cerebral hemisphere rSo2 values, thenar emiflow created by the centrifugal pump increases LV afterload
nence Sto2 values were within the normal range (Table 3) and
and may sharply increase left ventricular end-diastolic pressure
unchanged by IABP. Although unaffected by IABP, thenar tissue and induce severe pulmonary edema (1, 29), especially when
desaturation and resaturation slopes were lower than those of
LV ejection is null or residual, as for our patients.
Table 3.

Regional Hemodynamic Variables: Tissue Oxygenation


IABP Restart


82 ± 6

79 ± 8

82 ± 6


–0.13 ± 0.06

–0.13 ± 0.06

–0.14 ± 0.08


–0.04 to –0.23

–0.02 to –0.24

–0.03 to –0.28

1.26 ± 0.76

1.28 ± 0.70

1.28 ± 0.58

0.56 to –3.20



  Right, %

69.1 ± 5.3

69.4 ± 5.1

69.9 ± 5.3


  Left, %

67.4 ± 5.5

68.6 ± 4.0

68.9 ± 5.3


Near-Infrared Spectroscopy

  Baseline tissue oxygenation, %
  Tissue desaturation during VOT (%/s)
  Tissue resaturation after VOT (%/s)


Cerebral hemisphere rSo2

IABP = intra-aortic balloon pump, VOT = vascular occlusion test.
Data are mean ± sd.

Critical Care Medicine


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Petroni et al

Figure 2. Side-stream dark-field imaging of sublingual microcirculation:
sublingual functional capillary density (FCD, cm/cm2), microcirculatory
flow index (MFI), percentage of perfused vessels (PPV, %), and flow
heterogeneity index before and 30 min after interrupting and restarting
intra-aortic balloon pump (IABP) in the 12 patients on extracorporeal
membrane oxygenation. Box plots: horizontal line inside the box is the
median; lower and upper box limits are the 25th and 75th percentiles;
T-bars represent the 10th and 90th percentiles.

In animal models of cardiogenic shock, IABP restoration
of pulsatility improved hemodynamic variables (increased
MBP, pulse pressure, cardiac output, and interventricular
coronary artery flow) (30) and that pulsatility was converted
into surplus hemodynamic energy (31) in swine models of
profound cardiogenic shock. Combining IABP with peripherally inserted ECMO also reduced LV afterload and volume
in a sheep model of acute LV ischemia (32). Our findings
confirmed, in the context of patients with profound cardiogenic shock supported by peripheral VA-ECMO, that IABP
adjunction increases pulsatility and reduces LVEDD and
PAOP. Its effect was even more pronounced for the patient
subgroup with higher (> 15 mm Hg) baseline PAOP and,

hence, might prevent severe hydrostatic pulmonary edema
in this context.
In patients with AMI complicated by cardiogenic shock,
decreased perfused sublingual capillary density was associated
with worse outcomes (33), whereas ECMO achieved three-fold
increased tissue perfusion in a heterogeneous series of 10 patients
with severe heart failure or cardiogenic shock (34). However,
nonpulsatile continuous flow might induce microcirculatory
dysfunction (35–39), perhaps by decreasing hemodynamic
energy, thereby resulting in capillary collapse, microvascular
shunting, and activation of inflammatory mediators in patients
undergoing cardiopulmonary bypass (36). Recent observations
also suggested that restoring pulsatile flow can preserve microcirculatory perfusion during extracorporeal circulation for cardiac surgery and throughout the early postoperative period,
regardless of systemic hemodynamics as assessed by SDF imaging of the sublingual microcirculation (38, 39).
The specific IABP impact on the microcirculation has rarely
been tested. In 13 patients with severe cardiogenic shock,
microflow in vessels 10–50 μm in diameter was significantly
improved during IABP support (40), whereas IABP interruption did not impact on heterogeneity MFI index but paradoxically increased small vessels (< 20 μm) perfusion density
independently of global hemodynamic variables and oxygenderived variables in another series of 15 patients, who had
recovered from severe cardiogenic shock (41). To date, the only
described flow-index improvement in 10–50-μm vessels concerned a patient evaluated during an AMI phase complicated by
refractory ventricular fibrillation and receiving ECMO-IABP
support (8). Our findings did not confirm that observation in
12 patients whose baseline microvascular indexes (vessel density, vessel perfusion, and microvascular heterogeneity) were
already in the normal range. Possible explanations for this difference are higher ECMO blood flows in our study (unfortunately not reported for the former case) and that our patients
were evaluated after a mean of 6 days on ECMO support, which
may have achieved microcirculation improvement following
restoration of adequate blood flow. Whether more prolonged
interruption of IABP-induced pseudopulsatile flow might have
resulted in sublingual microcirculation alterations will remain
speculative. Parenthetically, although it had been hypothesized
that long-term continuous blood flow would be associated
with organ dysfunction or damage, this was not confirmed in
patients who received long-term support with the newest generation continuous flow left ventricular assist devices (34, 42).
Thenar eminence NIRS Sto2 measurement during a
dynamic VOT can detect functional alterations in the peripheral microcirculation (17, 18, 43). The Sto2 desaturation slope
and the Sto2 resaturation slope have been proposed as markers
of tissue oxygen consumption and postischemic vasodilatation and capillary recruitment, respectively (17, 18, 43). Sto2
desaturation and resaturation slopes were flatter for patients
with septic shock, trauma, and end-stage heart failure than for
healthy controls (17, 18, 22–24), and with increasing disease
severity (24, 44–46), they improved during recovery from sepsis (24) or after cardiac patients received IV inotropes (23). Sto2
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Clinical Investigation

desaturation and resaturation rates during dynamic VOT in
our patients with severe cardiogenic shock on VA-ECMO were
comparable to those of patients with septic shock and trauma
(17, 18, 22–24) and were unaffected by IABP interruption, suggesting persistently decreased thenar eminence oxygen consumption and vascular reserves, despite a mean of 6 days on
ECMO. Furthermore, their baseline thenar eminence Sto2 and
brain rSo2 were within normal ranges and unaffected by IABP,
indicating adequate global tissue oxygenation on high-flow
ECMO in a context of little/no residual heart function.
Our pilot study has limitations. First, it was monocentric
and included only 12 patients. Second, those patients had been
stabilized on ECMO-IABP for several days, and therefore, macrocirculation and microcirculation variables after ECMO initiation and the impact of adding IABP for patients on ECMO
alone were not evaluated. Third, IABP was interrupted for
only 30 minutes, and results might be different after a longer
time without it. Fourth, changes in LVEDD and LVESD during IABP on and IABP off stages were small, no interobserver
variability in measurements was performed, and due to a computer technical problem, echocardiographic measurements
of LVEDD and LVESD after IABP restart were only available
for seven of 12 patients. Finally, only half of our patients had
elevated baseline PAOP when the IABP was interrupted, indicating that not every patient with little/no residual LV function
is at risk of severe hydrostatic pulmonary edema under peripheral VA-ECMO.
In conclusion, restoring pulsatility and decreasing cardiac
afterload with IABP in patients receiving peripheral VA-ECMO
were associated with lower LVEDD and pulmonary artery pressures, without affecting microcirculation variables in cardiogenic shock patients with little/no residual LV ejection. Future
randomized studies should prospectively evaluate the impact
of early IABP adjunction to ECMO on short- and long-term
outcomes of severe cardiogenic shock patients in this context.


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