Intraaortic Balloon Pump Counterpulsation, Part I .21

Cardiovascular and Thoracic Anesthesiology
E NARRATIVE REVIEW ARTICLE
Intraaortic Balloon Pump Counterpulsation, Part

I: History, Technical Aspects, Physiologic Effects,
Contraindications, Medical Applications/Outcomes
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Laura S. González, MD,* and Mark A. Chaney, MD†

Ho4XMi0hCywCX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC1y0abggQZXdtwnfKZBYtws= on 09/13/2023
Intraaortic balloon pump counterpulsation is the most common form of mechanical circula-
tory support used in patients with myocardial ischemia and cardiogenic shock. The physiologic
principles of counterpulsation include diastolic augmentation of aortic pressure and systolic
reduction of left ventricular afterload, resulting in hemodynamic benefits through increased
coronary perfusion pressure and improved myocardial oxygen balance in patients with myocar-
dial ischemia. Major trials have failed to conclusively demonstrate improvements in morbidity
and mortality with counterpulsation therapy for patients with acute myocardial infarction (MI),
cardiogenic shock, and/or severe coronary artery disease undergoing revascularization therapy,
and the debate over its applications continues. Part I of this review focuses on the history of the
development of counterpulsation, technical considerations, and complications associated with
its use, its physiologic effects, and evidence for its use in myocardial ischemia and cardiogenic
shock. (Anesth Analg 2020;131:776–91)
GLOSSARY
AHA = American Heart Association; Ao P = aortic pressure; APACHE II = Acute Physiology and
Chronic Health Evaluation II scores; AV = aortic valve; BCIS-1 = Balloon Pump-Assisted Coronary
Intervention trial; BP = blood pressure; CABG = coronary artery bypass grafting; CAD = coronary
artery disease; CBF = coronary blood flow; CO = cardiac output; CPB = cardiopulmonary bypass;
CPP = coronary perfusion pressure; CRISP-AMI = Counterpulsation to Reduce Infarct Size Pre-PCI
Acute Myocardial Infarction trial; DA = diastolic augmentation; DBP = diastolic blood pressure;
DN = dicrotic notch; DPTI = diastolic pressure time index; ECG = electrocardiogram; GUSTO-1 =
Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries trial; IABP = intraaortic
balloon pump; LOE = level of evidence; LV = left ventricle or left ventricular; LVEF = left ventricular
ejection fraction; MACCE = major adverse cardiac and cerebrovascular events; MCS = mechanical
circulatory support; MI = myocardial infarction; NRMI 2 = National Registry of Myocardial Infarction
2; NSTEMI = non–ST-elevation myocardial infarction; PAMI II = Primary Angioplasty in Myocardial
Infarction trial; PCI = percutaneous coronary intervention; PTCA = percutaneous transluminal coro-
nary angioplasty; PVD = peripheral vascular disease; RCT = randomized controlled trial; SBP =
systolic blood pressure; SHOCK = Should We Emergently Revascularize Occluded Coronaries for
Cardiogenic Shock trial; STEMI = ST-elevation myocardial infarction; SV = stroke volume; SVR = sys-
temic vascular resistance; TACTICS = Thrombolysis And Counterpulsation To Improve Cardiogenic
shock Survival trial; TPA = tissue plasminogen activator; TTI = tension time index
I
ntraaortic balloon pump (IABP) counterpulsation, development, studies have provided conflicting evi-
introduced over 50 years ago, has been shown dence for morbidity and mortality benefits of coun-
to improve hemodynamic parameters and myo- terpulsation in patients with myocardial ischemia or
cardial oxygen delivery in patients with myocardial cardiogenic shock, and debate over proper applica-
ischemia and cardiogenic shock.1–3 However, since its tion of this technology continues.4–6 Despite a lack of
definitive proof regarding its outcome in medical and
From the *Department of Anesthesiology, Medical College of Wisconsin, surgical patients, IABP remains the most common
Milwaukee, Wisconsin; and †Department of Anesthesia and Critical Care,
University of Chicago, Chicago, Illinois. mechanical circulatory support (MCS) device used in
Accepted for publication May 4, 2020. cardiogenic shock, and an understanding of the physi-
Funding: None. ologic principles and benefits remains relevant to anes-
The authors declare no conflicts of interest. thesiologists and intensivists who manage patients
Supplemental digital content is available for this article. Direct URL citations perioperatively.7
appear in the printed text and are provided in the HTML and PDF versions of
this article on the journal’s website (www.anesthesia-analgesia.org).
Reprints will not be available from the authors. HISTORY
Address correspondence to Laura S. González, MD, Department of Anesthe- 1950s: Diastolic Augmentation
siology, Medical College of Wisconsin, 9200 West Wisconsin Ave, Milwaukee, A series of experiments performed by 2 broth-
WI 53226. Address e-mail to lagonzalez@mcw.edu.
Copyright © 2020 International Anesthesia Research Society
ers, Adrian Kantrowitz and Arthur Kantrowitz, in
DOI: 10.1213/ANE.0000000000004954 the 1950s demonstrated the principles of diastolic
776 www.anesthesia-analgesia.org September 2020 • Volume 131 • Number 3

Copyright © 2020 International Anesthesia Research Society. Unauthorized reproduction of this article is prohibited.
EE Narrative Review Article
augmentation.8,9 They theorized perfusing the coro- the aorta and initiating synchronized contraction via
nary bed with systolic blood pressure (SBP) during pacing during diastole, augmenting aortic diastolic
diastole would increase coronary blood flow, and, pressure.9
in 1953, they demonstrated in dogs that perfusing
the coronary arteries with blood redirected from the Early 1960s: The Auxiliary Ventricle
femoral artery delayed the arrival of the peak of the With recognition that augmentation is enhanced
systolic pressure wave until myocardial diastole and with devices closer to the heart,10 investigational
focus shifted to achieving diastolic augmentation via
increased coronary blood flow (Figure 1).8 Later, they

achieved augmentation of diastolic pressure by wrap- mechanical pumps. The Kantrowitz brothers devel-
ping a segment of the left hemidiaphragm around oped the first MCS device inserted in a human, the
auxiliary ventricle, which provided diastolic augmen-
tation via a pump conduit from the proximal ascend-
ing aorta to the distal aortic arch.11 Problems with this
device and philosophical differences led the broth-
ers to part ways, resulting in parallel investigational
efforts.10,12 During this time, others designed various
unique methods of achieving diastolic augmentation,
including external leg compression, external aortic
compression, and removal/addition of blood during
systole/diastole, respectively.13–19
Late 1960s: The Intraaortic Balloon

Because all early devices required invasive surgical
techniques and/or were associated with unique prob-
lems,10,13,15 focus transitioned to simpler methods. The
prototype IABP, first used in a canine model in 1962,
demonstrated that diastolic inflation/systolic defla-
tion of carbon dioxide–filled latex tubing increased
diastolic blood flow and decreased end-diastolic
blood pressure (DBP) in femoral and brachial arter-
ies.20 By 1967, Kantrowitz and colleagues21 revealed
the advantages of a nondistensible polyurethane bal-
loon filled with helium in dogs and first used this type
of counterpulsation device in a human, inserted via
femoral artery cutdown, later that year.22 A 45-year-
old woman in cardiogenic shock secondary to acute
myocardial infarction (MI) received counterpulsation
for 7 hours until shock resolved, surviving to hospital
discharge.22
1970s: IABP Counterpulsation Takes Off

By the 1970s, numerous reports established successful
Figure 1. Theorized increases in Ao P (top) and CBF (bottom) when use of counterpulsation in cardiogenic shock and in
an augmented arterial pressure wave arrives during diastole, out of patients undergoing a variety of noncardiac and car-
phase with the pressure wave of myocardial systole, proposed by diac procedures.23–30 Hemodynamic benefits included
Kantrowitz.8 The original study design used a length of rubbing tub-
ing, connected from the femoral artery to the left circumflex coronary decreased left ventricular (LV) afterload, decreased LV
artery, to delay the arrival of the peak pressure wave in the coronary end-diastolic pressure, decreased myocardial oxygen
artery. Solid lines represent baseline (normal) Ao P and phasic CBF. consumption, and/or decreased “cardiac work.”23–28
The dashed line represents predicted augmented Ao P with diastolic
augmentation of coronary arterial pressure. The large and small dot- In 1973, a multi-institutional trial demonstrated that
ted lines represent predicted increases in CBF in elastic and rigid counterpulsation in patients with cardiogenic shock
coronary arterial systems, respectively. With peak pressure occur- improved hemodynamics but did not improve sur-
ring during diastole, increases in CBF are expected, with a greater
increase expected in more elastic vessels. Ao P indicates aortic vival.31 Despite these results, IABP use continued,
pressure; CBF, coronary blood flow. Adapted and reproduced with and Dr Adrian Kantrowitz himself observed in 1990,
permission. This figure was published in Surgery, Volume 34, Issue “After 2 1/2 years of clinical experience with rather
4, Kantrowitz A. and Kantrowitz A., “Experimental Augmentation of
Coronary Flow by Retardation of the Arterial Pressure Pulse,” pages poor clinical results, it is not clear why the balloon
678–687, Copyright Elsevier (1953). pump effort just did not disappear. In retrospect,
September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 777

Intraaortic Balloon Pump Counterpulsation, Part I
even though there was low salvage of patients in car-

diogenic shock, the beneficial hemodynamic effects
of IABP had been demonstrated convincingly….”12
While some continued exploring other designs like
an ascending aortic cannula32 and a dual-chambered
intraaortic balloon,33 the single descending aortic bal-
loon became the “standard.” Development of modern
catheters and polyurethane balloons enabled pro-
longed support, and demonstration of percutaneous

catheter insertion in 1980 led to substantial expansion
of clinical use.1–3,34–36
TECHNICAL ASPECTS
The Balloon
While several manufacturers offer IABP, certain char-
acteristics are common to all.2,37 Balloons come in
various sizes, lengths, and volumes; while diastolic
augmentation is maximized with complete aortic
obstructionm the fully expanded balloon should not
exceed 90% of aortic diameter to avoid trauma to the
aortic wall.38 Inflation volume influences the volume
of displaced blood, and diastolic augmentation is
maximized when balloon volume equals stroke vol-
ume (SV). Augmentation is decreased with tachycar-
dia, increased aortic compliance, decreased systemic
vascular resistance, or extremely low or high SVs.39 Figure 2. Proper positioning of the IABP with the proximal tip of the
balloon below the left subclavian artery and the distal tip of the
The closer the balloon is to the aortic valve (AV), the balloon above the renal arteries. Inflation during diastole increases
greater the diastolic augmentation. Optimal position- coronary perfusion pressure and coronary blood flow. Deflation
ing of the balloon in the descending aorta, 1–2 cm during systole decreases left ventricular afterload. IABP indicates
intraaortic balloon pump.
below the left subclavian artery and above the renal
arteries (Figure 2), can be achieved through radiog-
raphy, fluoroscopy, and/or transesophageal echo- extremity vessels.42,43,45,46,51,52 These techniques allow
cardiography, regardless of the insertion site of the durable vascular access and balloon stabilization but
balloon (femoral versus upper extremity arteries).40 require deep sedation or general anesthesia. Newer
The balloon is mounted on a catheter that allows fluoroscopically guided percutaneous insertion tech-
monitoring of arterial blood pressure (BP) and trans- niques via the axillary,44 subclavian,44 or brachial arter-
fer of gas.41 Helium is most commonly used for its low ies49,50 allow performance under local anesthesia with
density (rapid inflation/deflation) and its metabolic minimal sedation, shorter procedure times, and repo-
inactivity and rapid dissolution in blood (decreased sitioning/removal outside the operating room.42,52
risk of embolus if leakage/rupture occurs). Retrospective studies suggest that the advantages
The most common balloon insertion sites are femo- of upper extremity insertion sites include decreased
ral and subclavian. While the femoral artery retains incidence of atherosclerosis at these sites,47,50 ability for
popularity due to ease of percutaneous insertion, ambulation,44–46,48 tolerance of long-term therapy,42,51
disadvantages include requirement for supine posi- and decreased cost.51 Typically, simpler femoral inser-
tioning (no ambulation), leg ischemia, high infection tion may be performed first to demonstrate hemo-
rate, and need for the femoral/iliac arteries to be free dynamic improvement with counterpulsation before
of substantial peripheral vascular disease (PVD)/ transitioning to an upper extremity site.48 Procedural
atherosclerosis.34,42 Subclavian artery insertion, first demands (need for cutdown and/or graft creation,
described in 1978, avoids femoral artery complica- operating room time, and personnel) increase time
tions and allows ambulation.42–44 Other upper extrem- to insertion at upper extremity sites, making upper
ity insertion sites include axillary44–48 and brachial extremity vessels unattractive emergent options. Use
arteries.44,49,50 Direct ascending aorta insertion to assist of an upper extremity artery carries a potential risk of
cardiopulmonary bypass (CPB) weaning has also been embolic cerebral stroke, and the presence of a pace-
described.47 Initial reports of upper extremity insertion maker and/or implantable cardioverter/defibrillator
described direct arterial access, while more recently, lead or dialysis catheter in the ipsilateral vein may
vascular grafts have been used as conduits in upper increase the risk of insertion and render one side less
778
www.anesthesia-analgesia.org ANESTHESIA & ANALGESIA
appropriate for use.42 With upper extremity insertion, through the arterial tree, and timing adjustment may
the balloon lies in the reverse of its usual orientation, be required to avoid late inflation/deflation.56 Internal
with the tip of the catheter in the distal descending triggering (operator mode) is an asynchronous mode
aorta. Thus, one must avoid advancing the IABP tip used when there is no blood flow, as in during cardiac
into a visceral artery, and patients should be moni- arrest or on CPB.37
tored for signs/symptoms of ischemia (abdominal Timing is best evaluated by examining the aortic
pain or elevated lactate) in case of malposition or arterial BP waveform from the central lumen of the
migration, which are more common in upper extrem- IABP.3 With optimal timing, the BP waveform reveals
ity insertion sites; some authors recommend daily augmented DBP greater than unassisted SBP, reduc-
radiography to monitor balloon position.48,51,53 The tions in assisted end-DBP and assisted SBP, and assisted
reverse orientation also places the arterial BP sensor SBP less than unassisted SBP (Figure 3A). Suboptimal
in a more distal aortic position, altering augmentation timing decreases counterpulsation efficiency. With
and potentially timing.50 early balloon inflation (Figure 3B), increased aortic
pressure before AV closure increases afterload and
The Console impairs LV ejection, thereby increasing myocardial
The balloon is attached to a console that delivers and oxygen demand.37,56,57 Late balloon inflation after the
retrieves gas through a pneumatic system allowing dicrotic notch (Figure 3C) reduces time and effective-
inflation/deflation.41 In general, the console consists ness of diastolic augmentation.37,56 Early balloon defla-
of a gas source, valve unit, monitor system, and con- tion before AV opening (Figure 3D) leads to an early
trol unit for timing/triggering of inflation/deflation decrease in augmented diastolic pressure (reducing
and operator control of augmentation ratio (1:1, 1:2, effectiveness of diastolic augmentation) and provides
1:3, or 1:4). The trigger source options, electrocardio- no afterload reduction.37,58 Late balloon deflation after
gram (ECG), and arterial BP tracings are displayed; AV opening (Figure 3E) increases end-diastolic pres-
the latter 2 are used to adjust timing and triggering. sure and afterload during early ejection; these effects
Consoles have alarms to detect circuit leaks, blood lead to increased SV at the cost of increased stroke
in gas line, loss of gas in outer lumen, and/or loss of work, which increases myocardial oxygen demand
trigger signal.37 and offsets the benefit of diastolic augmentation.37,57
Modes of operation vary depending on manufac-
Triggering/Timing turer.37 In automatic mode, the console determines
Optimal inflation occurs immediately following AV optimal trigger source and inflation/deflation times.
closure, and optimal deflation occurs immediately Modern devices use fiberoptic technology to auto-
before AV opening. The most common triggering matically calibrate inflation/deflation; with a com-
source is ECG (inflation triggered during T wave – P bination of ECG triggering and pressure sensing of
wave interval, deflation triggered during R wave – T the dicrotic notch, most can time balloon inflation to
wave interval); if patients are in atrial fibrillation, the occur within 12 milliseconds of AV closure even with
computer can analyze the QRS complex to time defla- arrhythmias.37,41 In semiautomatic mode, the clinician
tion with an R wave, whether positively or negatively selects trigger source, inflation/deflation times, and
deflected.37 When patients are 100% ventricularly augmentation ratio, while the console determines
paced, pacer triggering mode determines augmenta- optimal timing. In manual mode, the clinician must
tion based on the ventricular pacing spike37; intermit- also determine optimal timing based on heart rate
tent or atrial pacing can be compatible with standard and rhythm. Depending on their source (arrhythmias,
ECG triggering, although reports exist of inappropri- pressure monitoring malfunction, etc), timing or trig-
ate triggering with atrial and biventricular pacemak- gering errors may require changing modes of oper-
ers requiring manual adjustment.54,55 However, with ating, changing triggering source, changing pressure
poor ECG quality and/or arrhythmias, ECG trigger- monitoring sites, or initiating pacing.
ing becomes unreliable, requiring other trigger modes
be used.37 With pressure triggering, the aortic arterial Anticoagulation
waveform triggers inflation and deflation via iden- There are no standard recommendations for anticoag-
tification of the dicrotic notch and systolic upstroke, ulation for IABP therapy. Industry guidelines do not
respectively. If the aortic arterial waveform is of recommend anticoagulation, especially at 1:1 augmen-
poor quality (due to malfunction, small balloon, etc), tation, and a 2015 American Heart Association (AHA)
peripheral arterial BP waveforms (radial, brachial, or expert consensus statement reports insufficient data
axillary) may be used. However, peripheral arterial to provide recommendations regarding anticoagula-
waveforms are delayed from mechanical events at tion.37,59 However, if the IABP is left in a weaning mode
the aortic root due to changes in propagation veloc- (1:3 or 1:4) for longer periods, systemic anticoagulation
ity and vascular compliance as the waveform passes is recommended to minimize the risk of thrombosis.

Figure 3. Aortic pressure waveforms with

correct (A) and incorrect (B, C, D, E) timing
of intraaortic balloon inflation. A, Aortic pres-
sure during an unassisted and an assisted
beat with IABP assistance. Normal timing of
IABP inflation occurs at the DN, which corre-
sponds to the end of the T wave, and leads
to DA of aortic pressure. The assisted end-
diastolic pressure (D2) at the end of an
assisted beat is lower than end-diastolic pres-
sure at the end of an unassisted beat (D1).
Peak-assisted systolic pressure (S2) is lower
than unassisted peak systolic pressure (S1).
B, Early inflation of the balloon causes pres-
sure augmentation before aortic valve closure
leading to increased afterload, impaired LV
ejection, and reduced DA. C, Late inflation of
the balloon, after the DN, leads to increased
afterload and reduced DA. D, Early deflation of
the balloon provides brief DA and results in a
prolonged decrease in assisted end-diastolic
pressure, reduced DA, and no afterload reduc-
tion. E, Late deflation of the balloon provides
DA and a higher assisted end-diastolic pres-
sure, increased afterload, and subsequently
decreased assisted systolic pressure. DA
indicates diastolic augmentation; DN, dicrotic
notch; IABP, intraaortic balloon pump; LV, left
ventricle.
Benefits of anticoagulation include decreased risk of PHYSIOLOGIC EFFECTS

clot formation and embolization, while risks include The goal of diastolic augmentation–induced increased
bleeding and heparin-induced thrombocytopenia. coronary perfusion pressure (CPP) is achieved with
Typically, anticoagulation is reasonable in patients balloon inflation, while balloon deflation reduces
without contraindications who are at risk of thrombo- afterload and promotes LV ejection. Together, these
sis, when counterpulsation is planned for more than effects lead to improved oxygen delivery with
a day and/or during weaning mode for more than decreased myocardial oxygen consumption. These
30 minutes. The IABP should never be set in standby physiologic effects have been demonstrated in numer-
mode (no inflation) unless it is being removed.37 ous investigations (Table 1).60–73
780
counterpulsation.75–78 Given these findings, counter-

Table 1. Major Beneficial Physiologic Effects of
Intraaortic Balloon Pump Counterpulsation pulsation likely increases coronary blood flow only
Balloon Inflation Balloon Deflation when coronary autoregulation is exhausted (critical
Increased diastolic BP Decreased systolic BP (vacuum effect) coronary stenosis, ischemic/stunned myocardium,
Decreased systolic BP Increased stroke volume and/or mean aortic root BP below autoregulatory
(decreased SVR)
range).75
Increased mean BP Increased LVEF
Increased coronary perfusion Decreased LV end-diastolic volume
Afterload Reduction
pressure
Increased coronary blood flowa Decreased afterload When augmented beats are compared with nonaug-
Decreased LV end-diastolic Decreased LV wall tension mented beats, balloon inflation at the beginning of
pressure
Increased myocardial oxygen Decreased myocardial oxygen demand
diastole decreases systemic vascular resistance via
supply Increased LV compliance increased baroreceptor output in response to trans-
Decreased LV end-systolic volume mission of 2 arterial pressure waves (LV ejection
Shorter LV isometric phase of and diastolic augmentation with balloon inflation).79
contraction
Balloon deflation produces decreased afterload via
Abbreviations: BP, blood pressure; LV, left ventricular; LVEF, left ventricular
ejection fraction; SVR, systemic vascular resistance. decreased impedance to LV ejection, which leads to
a
Variable depending on the state of autoregulation. decreased peak systemic BP, LV systolic unloading,
shorter LV isometric contraction phase, and earlier
opening of the AV.62,74,80–85 While the physics for the
CPP and Coronary Blood Flow mechanism of decreased afterload remain a mat-
During a cardiac cycle augmented by counterpulsa- ter of debate, the leading theory is decreased arte-
tion, balloon inflation at the beginning of diastole rial impedance to LV ejection via the Windkessel
generates an increase in diastolic pressure in coro- effect (similar to a vacuum effect), rather than dis-
nary and systemic circulations.62,65 While balloon placement of blood volume or bulk flow.38,85,86 As a
inflation displaces a volume of blood, the effects on result, the pressure waveform of an augmented beat
BP are related to the generation of intraaortic pres- will demonstrate a higher peak diastolic pressure,
sure waves rather than changes in bulk flow.74,75 lower end-diastolic pressure, and lower peak sys-
Diastolic balloon inflation leads to increased CPP tolic pressure than an augmented beat (Figure 3A).74
with variable effects on coronary blood flow. LV afterload reduction is further demonstrated
Throughout the cardiac cycle, CPP is equal to the by deflation-induced reductions in the isometric
difference between aortic root pressure and LV pres- phase of LV contraction, decreased pressure rate
sure, while coronary blood flow is determined by the of increase (dp/dt), decreased LV end-diastolic
ratio of CPP to coronary vascular resistance. CPP is volume, decreased LV wall tension, increased LV
typically increased during counterpulsation by infla- compliance, decreased LV end-systolic volume, and
tion-induced increases in aortic pressure throughout increased LV SV and LV ejection fraction (LVEF).80–83
diastole and deflation-induced increases in SV lead- Cardiac output (CO) increases only slightly with
ing to decreased LV end-diastolic volume and end- initiation of counterpulsation (generally 0.5–1.0 L/
diastolic pressure. min), likely due to a combination of decreased after-
However, increased CPP does not always translate load leading to increased SV and enhanced myocar-
to increased coronary blood flow. Normally, intact dial contractility, since counterpulsation does not
autoregulation ensures coronary arteries dilate/ provide bulk flow.31
constrict in response to changing CPP, altering coro-
nary vascular resistance to maintain constant coro- Myocardial Oxygen Delivery
nary blood flow over a wide range of aortic root BP. The effect of counterpulsation on myocardial oxy-
Thus, counterpulsation-induced increased CPP may gen delivery is best studied through examination of
not increase coronary blood flow.62 Investigations the diastolic pressure time index (DPTI) and the ten-
reveal that counterpulsation with intact coronary sion time index (TTI). DPTI is a surrogate marker for
autoregulation leads to increased CPP, increased myocardial oxygen supply that can be calculated from
microvascular resistance, and no change in coronary the area between the aortic pressure and LV pressure
blood flow, whereas counterpulsation in an experi- curves during diastole, and it depends on aortic DBP,
mental model of maximum hyperemia with impaired LV diastolic pressure, and diastole duration; TTI is a
coronary autoregulation (isolated porcine heart surrogate marker for myocardial oxygen demand mea-
on extracorporeal circulation or use of adenosine) sured by the area below the LV pressure curve during
leads to increased CPP, no change in microvascular systole, and it depends on LV pressure and afterload
resistance, and increased coronary blood flow with (Figure 4).78,80,87 The ratio between DPTI/TTI is used

Figure 4. Schematic representation of coronary blood flow and aortic and left ventricular pressure waves, with and without IABP assistance.
The top panel depicts coronary blood flow changes during the cardiac cycle, with higher flow increasing during diastole when intraventricular
pressure is decreased. Balloon augmentation of diastolic aortic root pressure leads to augmented coronary blood flow. These coronary blood
flow changes would be expected in a system with impaired autoregulation secondary to ischemia, severe coronary stenosis, stunned myocar-
dium, or coronary pressure outside of autoregulatory range.75 The bottom panel depicts left ventricular and aortic pressures during the cardiac
cycle. The area under the left ventricular pressure curve during systole is the TTI and reflects myocardial oxygen demand. The area between
the aortic pressure curve and left ventricular pressure curve during diastole represents the DPTI and reflects myocardial oxygen supply. The
ratio of the DPTI and TTI areas is used in physiologic experiments to determine the balance between myocardial supply and demand, with a
ratio of 1.0 representing a normal balance and a value <0.7 representing clinically significant myocardial ischemia. Balloon inflation leads to
augmented aortic diastolic pressure, increased DPTI, and increased oxygen delivery, while balloon deflation reduces afterload and systolic aor-
tic root pressure, which leads decreased TTI and decreased oxygen demand. These changes increase the DPTI/TTI ratio, leading to improved
myocardial oxygen balance in ischemic myocardium. DPTI indicates diastolic pressure time index; TTI, tension time index.
in physiologic experiments to determine the balance CONTRAINDICATIONS/COMPLICATIONS

between myocardial supply and demand: a DPTI/TTI Relative or absolute contraindications to IABP inser-
ratio of 1.0 represents normal balance, while a value <0.7 tion include moderate-to-severe AV insufficiency,
suggests clinically important myocardial ischemia.61 aortic dissection/aneurysm, PVD, active bleeding,
During balloon inflation, DPTI and myocardial contraindications to anticoagulation if planned, severe
oxygen supply are increased with increased DBP.60,78 thrombocytopenia, and/or patient refusal.6,59 While
Balloon deflation increases myocardial oxygen sup- the incidence of complications fluctuates depending
ply via decreases in LV end-diastolic pressure and on definitions, incidence of major complications is
decreases myocardial oxygen demand through approximately 5%.5,88,89
decreases in afterload, which lead to decreased TTI;
when coupled with the inflation-induced increased Complications During IABP Insertion
DPTI, this leads to improved myocardial oxygen The most common complication during insertion of an
supply/demand.78,85 IABP is vascular injury, with a 5%–10% incidence even
782
in the modern era of percutaneous insertion.5,58,88–91 a promising new technology to treat these critically
Arterial trauma/dissection may be difficult to detect, ill patients, in whom mortality ranges from 30% to
and signs (hematoma, hemothorax, compartment syn- 50% despite advances in therapy.22,100 The majority
drome, and limb/organ ischemia) may present quickly of clinical investigations of counterpulsation have
or insidiously. Use of smaller diameter and/or “sheath- focused on patients with myocardial ischemia/infarc-
less” catheters without an introducer likely decreases tion, 10% of whom develop cardiogenic shock leading
vascular injury risk.37,90 Use of large catheters, prolonged to end-organ dysfunction.100 This literature spans 5
support, PVD, diabetes, female gender, advanced age, decades of substantial improvement in diagnosis and
and smoking history all increase risk.5,37,58,90,92 treatment of myocardial ischemia, including in revas-
cularization techniques (eg, coronary artery bypass
Complications During IABP Counterpulsation grafting [CABG], thrombolysis, balloon angioplasty,
Most complications during counterpulsation relate and balloon-expandable stents; the latter 2 techniques
to incorrect balloon sizing, positioning, and/or tim- may be referred to as percutaneous transluminal cor-
ing, resulting in limb or organ ischemia, vascular onary angioplasty [PTCA] or percutaneous coronary
injury, and/or reduced hemodynamic benefits.93,94 intervention [PCI]). The results of major trials of IABP
Proximal balloon malposition leading to obstruction use in myocardial ischemia/infarction are summa-
of subclavian, carotid, and/or left internal mam- rized in Table 2.
mary arteries is possible.3 Distal balloon malposition Several case series in the early 1970s documented
and/or patient size–balloon length mismatch can successful treatment of acute MI/cardiogenic shock
lead to visceral arterial compromise: a case series of with counterpulsation, and its use expanded to include
patients who received computed tomographic scan- treatment of low CO following cardiac surgery.2,27,28,117
ning during counterpulsation therapy revealed that While early observational studies suggested greater-
most (97%) patients have some degree of arterial than-predicted survival when counterpulsation was
compromise (celiac trunk, superior mesenteric artery, used in the setting of cardiogenic shock,118 the first
and/or renal arteries) leading to radiographic and/ prospective randomized trial of counterpulsation
or clinical evidence of bowel, renal, or hepatic isch- in acute MI did not find significant improvement in
emia.53,94 Catheter occlusion of the insertion artery hemodynamic parameters, reduction in infarct size, or
may lead to limb ischemia and/or thrombosis, par-
mortality benefit.119 During the 1980s, despite a lack of
ticularly in patients with PVD and/or prolonged sup-
physician consensus regarding utilization criteria or
port. Aortic dissection is reported at <5% (although
data from well-controlled studies to support its use,
clinically silent dissection may be as frequent as 20%
counterpulsation in acute MI remained popular, par-
per autopsy studies).3,91 Counterpulsation may also
ticularly as percutaneous IABP insertion techniques
worsen hemodynamics in patients with undiagnosed
allowed for rapid initiation in the intensive care unit
AV insufficiency or dynamic LV outflow obstruction.
and/or cardiac catheterization suite.35,36,120
Infection at the catheter site may occur, and bleeding
Studies from the 1990s onward evaluated the effect
issues may arise with anticoagulation (mild thrombo-
of counterpulsation on outcomes in patients under-
cytopenia and/or hemolysis may occur regardless of
going thrombolysis and PTCA and are used to guide
anticoagulation use).95,96 Clinically significant bleed-
current clinical practice. Observational studies sug-
ing occurs in 2%–10% of patients.58,88,89,96 Rare reports
gested improved outcomes when counterpulsation
of balloon rupture and entrapment exist.97–99
was combined with thrombolysis in patients present-
Complications Following IABP Removal ing with acute MI/cardiogenic shock, thought to be
Complications following removal include bleeding, related to counterpulsation-induced increased coro-
thrombosis, pseudoaneurysm, aneurysm, dissection, nary blood flow improving thrombolytic drug deliv-
compartment syndrome, and limb ischemia.58,67–73,88,89 ery.121,122 In a subanalysis of the Global Utilization of
Insertion site infection may also persist. Surgical Streptokinase and tissue plasminogen activator (TPA)
intervention (embolectomy, hematoma evacuation, for Occluded Coronary Arteries trial (GUSTO-1), a
amputation, and arterial bypass) is required in up to major trial of thrombolytics, the use of counterpulsa-
5% of patients following counterpulsation.89,90 tion was associated with a trend toward decreased
30-day and 1-year mortality among patients present-
MEDICAL APPLICATIONS/OUTCOMES ing with cardiogenic shock who were treated with
Myocardial Ischemia, Infarction, and Cardiogenic both counterpulsation and thrombolysis compared
Shock to thrombolysis, although IABP placement was not
The first documented clinical use of counterpulsa- randomized in this study.101,102 In the Thrombolysis
tion was in a patient with cardiogenic shock second- And Counterpulsation To Improve Cardiogenic
ary to acute MI, and IABP counterpulsation offered shock Survival trial (TACTICS), randomization to

Table 2. Summary of Major Trials of IABP Counterpulsation in Myocardial Ischemia, Infarction, and Cardiogenic Shock
Trial (Year) Study Design Patient Cohort Revascularization Findings Notable Features Conclusions
GUSTO-1 RCT – Acute MI with cardiogenic shock, Thrombolysis IABP reduced 30-d and 1-y mortality Subanalysis of data Favored IABP in MI
784
(1993)101–103 subanalysis n = 310 (62 with IABP, 248 (IABP placement not
without) randomized)
PAMI II RCT High risk with acute MI, n = 437 PTCA No difference in rate of hypotension, High risk defined as meeting No benefit to IABP in MI
(1997)104 (211 with IABP, 226 without) reinfarction, stroke, heart failure, ≥1 criterion: LVEF ≤45%,
or death with IABP age >70, vein graft
occlusion, malignant
ventricular arrhythmias,
suboptimal PTCA result
SHOCK RCT - Acute MI with cardiogenic shock, Thrombolysis, Lower mortality with IABP; lowest Subanalysis of data Favored IABP in MI with
(1999)105,106 subanalysis n = 884 (132 thrombolysis PTCA, or CABG in-hospital mortality with (IABP placement not cardiogenic shock if
only, 279 IABP only, 160 thrombolysis + IABP therapy randomized; IABP + thrombolysis used and/
thrombolysis + IABP, 285 Revascularization with PTCA or CABG thrombolysis group lower or immediate access to
neither thrombolysis nor IABP) associated with lowest mortality, risk) emergent revascularization
www.anesthesia-analgesia.org
independent of IABP use not available
NRMI 2 Observational Acute MI with cardiogenic shock, Thrombolysis, Lower in-hospital mortality with IABP Favored IABP in MI with
(2001)107,108 n = 23,180 (7268 with IABP, PTCA, or CABG + thrombolysis; higher mortality cardiogenic shock if
15,912 without) with IABP + PTCA thrombolysis used
TACTICS RCT Acute MI with hypotension, n = 57 Thrombolysis No overall mortality benefit with Trial ended early due to No benefit to IABP in MI;
(2005)109 (30 with IABP, 27 without) IABP; possible mortality benefit in failure to meet enrollment possible benefit to IABP in MI
hemodynamically unstable patients targets with cardiogenic shock
BCIS-1 RCT High-risk patients with severe CAD PCI No decrease in in-hospital MACCE High risk defined as LVEF No short-term mortality or
(2010)110,111 and LVEF ≤30%, n = 301 (revascularization, acute MI, stroke, ≤30% and extensive MACCE benefit to IABP in
(151 with IABP, 150 without). death) with IABP myocardium at risk high-risk patients undergoing
Excluded patients with acute MI Lower mortality with IABP at long-term PCI; possible long-term
or cardiogenic shock follow-up (median 51 mo) mortality benefit to IABP
CRISP-AMI RCT STEMI without cardiogenic shock, PCI No decrease in infarct size at 3–5 d, High rate (8.5%) of No benefit to routine use of IABP
(2011)112,113 n = 337 (161 with IABP, 176 no decrease in MACCE or mortality crossover to rescue IABP before PCI in STEMI without
without) rate at 6 mo with IABP Only significant benefit cardiogenic shock
Increased mortality at 6 mo with to IABP + PCI seen in
rescue IABP insertion composite outcome of
new/worsening heart
failure, shock or death
IABP-SHOCK RCT Acute MI with cardiogenic shock, PCI No change in APACHE II scores or Single-center study No benefit to IABP in MI with
(2012)72 n = 40 (19 with IABP, 20 hemodynamic parameters (CO, cardiogenic shock in patients
without) SVR, cardiac power) with IABP undergoing PCI
IABP-SHOCK II RCT Acute MI with cardiogenic shock, PCI, CABG No mortality benefit at 3, 6, or 12 mo Multicenter study No benefit to IABP in MI with
(2012)114–116 n = 598 (300 with IABP, 298 99% of patients underwent cardiogenic shock in patients
without) revascularization with undergoing PCI
PCI; no conclusions can
be made regarding IABP
in surgical patients
Abbreviations: APACHE II, Acute Physiology and Chronic Health Evaluation II scores; BCIS-1, Balloon Pump-Assisted Coronary Intervention trial; CABG, coronary artery bypass grafting; CAD, coronary artery disease; CO,
cardiac output; CRISP-AMI, Counterpulsation to Reduce Infarct Size Pre-PCI Acute Myocardial Infarction trial; GUSTO-1, Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries trial; IABP, intraaortic
balloon pump; LVEF, left ventricular ejection fraction; MACCE, major adverse cardiac and cerebrovascular events; MI, myocardial infarction; NRMI 2, National Registry of Myocardial Infarction 2; PAMI II, Primary Angioplasty
in Myocardial Infarction trial; PCI, percutaneous coronary intervention; PTCA, percutaneous transluminal coronary angioplasty; RCT, randomized controlled trial; SHOCK, Should We Emergently Revascularize Occluded
Coronaries for Cardiogenic Shock trial; STEMI, ST-segment elevation MI; SVR, systemic vascular resistance; TACTICS, Thrombolysis And Counterpulsation To Improve Cardiogenic shock Survival trial; TPA, tissue
plasminogen activator.
ANESTHESIA & ANALGESIA

counterpulsation therapy plus thrombolytic therapy Despite minimal evidence of clinical benefits in
for acute MI led to a trend toward decreased mortal- patients with myocardial ischemia and cardiogenic
ity at 6 months, although the study ended early due to shock, IABP use in patients continues, including in
an inability to recruit, limiting interpretation of these those presenting for high-risk revascularization with
results.109 However, as angioplasty and stent therapies PCI/PTCA. Early retrospective studies suggested
were developed and refined, these overtook throm- preemptive counterpulsation (rather than rescue
bolysis as the treatment of choice for acute MI, and the therapy) may decrease mortality in patients undergo-
results of these earlier studies involving thrombolysis ing angioplasty and/or stenting following acute MI
are less applicable to today’s patients. with124,125 or without126 cardiogenic shock, although
During the 1990s, several small studies found that, the results from randomized studies have not been
in patients with acute MI treated with angioplasty, as positive. While 1 small randomized study reported
counterpulsation had no beneficial effects on morbid- that counterpulsation and PCI together reduced in-
ity or mortality.104,107,123 In a subanalysis of the land- hospital and 30-day mortality rates compared with
mark Should We Emergently Revascularize Occluded PCI alone,127 another study of patients with MI with-
Coronaries for Cardiogenic Shock trial (SHOCK) trial, out cardiogenic shock found that adding counterpul-
which randomized patients presenting with acute sation to PCI did not result in improvements in LV
MI/cardiogenic shock to standard medical treatment wall motion or coronary blood flow.128 Two major
(including thrombolysis) or early revascularization trials of counterpulsation in patients without car-
(angioplasty, stent, or CABG),105 counterpulsation diogenic shock undergoing PCI also failed to dem-
was associated with lower overall mortality, although onstrate a benefit with IABP therapy. In the Balloon
revascularization with either PTCA or CABG led to Pump-Assisted Coronary Intervention trial (BCIS-
the greatest decrease in mortality, independent of 1) trial, the only major trial of counterpulsation in
IABP use.106 Two randomized studies investigating patients without acute MI, there were no differences
IABP use in cardiogenic shock subsequently found no in the incidence of major adverse cardiac and cerebro-
difference in clinical outcomes, including mortality, vascular events (MACCE) in high-risk patients who
when counterpulsation was added to revasculariza- received elective IABP insertion before PCI compared
tion therapy. In the single-center IABP-SHOCK trial, with those undergoing PCI alone.110 However, there
counterpulsation did not improve hemodynamics was a trend toward decreased 6-month mortality and
or decrease vasopressor/inotrope requirements in a reduction in all-cause mortality maintained after 6
patients with acute MI/cardiogenic shock receiving months in patients receiving elective counterpulsa-
PCI therapy,72 and the multicenter IABP-SHOCK II tion.111 The Counterpulsation to Reduce Infarct Size
trial found no differences in mortality (short-term, Pre-PCI Acute Myocardial Infarction trial (CRISP-
12-month, or 6-year) in patients with acute MI/car- AMI) randomized patients with acute ST-elevation
diogenic shock undergoing counterpulsation plus MI (STEMI) without hemodynamic instability or
revascularization compared with those who were cardiogenic shock to counterpulsation before pri-
revascularized without IABP support.114–116 While mary PCI and found no difference in LV infarct size,
these results do not support routine use of IABP in MACCE, or mortality rates at 6 months compared
patients with acute MI/cardiogenic shock undergo- with primary PCI alone.112 There was a high cross-
ing revascularization, definitive conclusions are pre- over rate to unplanned IABP insertion in the set-
vented by a lack of therapy standardization (CABG, ting of hemodynamic instability or suboptimal PCI
angioplasty, or PCI was performed at the discretion of revascularization, and a subgroup analysis of these
the attending in the IABP-SHOCK II trial, with most patients demonstrated higher rates of readmission,
patients receiving PCI). Investigators theorized that ventricular arrhythmias, cardiac arrest, and death at
early studies demonstrating benefits of counterpulsa- 6 months.112,113 Despite a lack of mortality benefit, the
tion, conducted during the thrombolytic era, involved investigators of both the BCIS-1 and CRISP-AMI tri-
patients with residual stenosis who benefitted from als advocate the use of a “standby-IABP” strategy for
diastolic augmentation, in contrast to patients whose primary PCI.111,112
stenosis was relieved by angioplasty, stent, or CABG.72 While the results of major trials do not suggest
While counterpulsation may not benefit the majority morbidity or mortality benefits to counterpulsation
of patients with acute MI/cardiogenic shock who are therapy in acute MI/cardiogenic shock, the study
revascularized, further study of patients with resid- designs may prevent the benefits of counterpulsa-
ual stenosis and/or ischemia following reperfusion tion from being fully realized and/or documented.
should be undertaken, as the coronary circulation of Patients in the BCIS-1 trial did not have significant
these patients would be expected to have impaired hemodynamic instability or impaired coronary auto-
autoregulation and benefit the most from counterpul- regulation and therefore would be expected to gain
sation-induced increases in coronary blood flow.75 less coronary blood flow and myocardial oxygen

supply from counterpulsation therapy. The delayed commonly used MCS device during support/stabi-
survival benefit with counterpulsation seen in the lization for angiography/angioplasty and treatment
BCIS-1 trial also raises the possibility that earlier tri- of patients with cardiogenic shock.7,138–141 Because the
als investigating only short-term mortality may not IABP was marketed before the passage of the 1976
have captured the full clinical benefit of counterpul- Medical Device Amendment of the Federal Food,
sation. The high rate of crossover to IABP with worse Drug, and Cosmetic Act, subsequent redesigns require
outcomes following rescue counterpulsation, as seen documentation of their “substantial equivalence” to
in CRISP-AMI, illustrates the challenge of perform- devices already on the market for US Food and Drug
ing randomized studies in these critically ill patients, Administration approval, without proof of efficacy
particularly when comparing IABP use as hemody- in patients with acute MI, heart failure, or under-
namic rescue therapy with patients receiving elec- going cardiac or noncardiac surgery.142 Guidelines
tive therapy. While physiologic studies suggest that have therefore arisen from specialty societies, and
the maximum effect of counterpulsation on coronary due to variability in clinical outcomes and advances
blood flow occurs when coronary autoregulation is in treatment of myocardial ischemia/infarction, it is
exhausted (eg, with ischemic or stunned myocardium unsurprising that guidelines also evolved over the
or BP below autoregulatory threshold in the setting of 5 decades of IABP use. The first guidelines to refer-
cardiogenic shock),75 these patients would be expected ence IABP (1990 American College of Cardiology/
to have worse outcomes related to their underlying AHA guidelines for management of acute MI) rec-
physiologic derangements. Future investigations ommended counterpulsation for multiple indica-
should evaluate predictive factors for clinical decom- tions including pharmacologically unresponsive
pensation to guide decision-making for prophylactic cardiogenic shock, right ventricular failure, refrac-
insertion to avoid the development of hemodynamic tory angina during angiography, intractable tachycar-
instability associated with worse outcome. dia with hemodynamic instability, ventricular septal
Whether counterpulsation benefits patients with rupture, acute mitral insufficiency, persistent angina,
acute MI has also been a popular topic for meta-anal- and progressive congestive heart failure symptoms.143
yses, and given the equivocal results of major trials,
Current guidelines (summarized in Supplemental
it is unsurprising that meta-analyses of counterpulsa-
Digital Content, Table 1, http://links.lww.com/AA/
tion have reached substantially varied conclusions.
D107) have significantly changed based on decreased
Counterpulsation has been found, via meta-analyses,
evidence for counterpulsation’s efficacy. The 2013
to have no effect on mortality in acute MI/STEMI
AHA guidelines for STEMI management recommend
patients with and without cardiogenic shock,129–134 to
IABP insertion in STEMI with cardiogenic shock
decrease mortality in certain acute MI patients with
unresponsive to pharmacologic therapy (Class IIa evi-
cardiogenic shock,132 to decrease mortality in acute
dence, level of evidence [LOE] B) or for stabilization
MI/STEMI patients with cardiogenic shock receiving
before surgical treatment for mechanical complica-
thrombolytics,130,132 to increase morbidity in STEMI
tions, such as ventricular rupture or mitral regurgi-
patients with/without cardiogenic shock,134 and
to increase mortality in acute MI/STEMI patients tation (ungraded),144 while 2014 AHA guidelines for
with cardiogenic shock receiving PCI therapy.130,134 management of non–ST-elevation MI (NSTEMI) rec-
Regarding prophylactic insertion in patients under- ommend counterpulsation therapy in the setting of
going high-risk coronary intervention, meta-analyses refractory cardiogenic shock.145 Finally, the 2011 AHA
have demonstrated that counterpulsation provides guidelines for percutaneous interventions state that
no short-term morbidity or mortality benefits135–137 a “hemodynamic support device” is recommended
yet may reduce long-term morbidity and mortality.136 during STEMI with cardiogenic shock (Class I, LOE
These conflicting results further highlight the chal- B), and elective insertion of such devices is “reason-
lenges of directly comparing patients receiving variable” in carefully selected high-risk patients (Class
ous interventions for ischemia (thrombolysis versus IIb, LOE C).146
PCI, the latter term itself encompassing a variety of In contrast to American guidelines, current
interventions from angioplasty to drug-eluting stent European guidelines are less supportive of IABP use,
placement) and pooling data from studies of IABP as only recommending therapy during NSTEMI with
rescue therapy with studies of counterpulsation as a hemodynamic instability due to mechanical compli-
risk-reduction intervention. cations (Class IIa, LOE C).147 Furthermore, they state
that counterpulsation “may be considered” in select
Guidelines STEMI patients with cardiogenic shock (ungraded)148
Despite a lack of definitive proof of improved major and do not recommend routine use in cardiogenic
outcomes with counterpulsation in patients with shock complicating acute MI (Class III, LOE B).147
myocardial ischemia/infarction, it remains the most They make no recommendations regarding the
786
use of counterpulsation for high-risk percutaneous cardiogenic shock in the United States. Clin Res Cardiol.
intervention.149 2018;107:287–303.
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CONCLUSIONS 1953;34:678–687.
IABP counterpulsation, entering its sixth decade of 9. Kantrowitz A, Mckinnon WM. The experimental use of
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in a relatively simple, low-risk manner. Despite the 11. Kantrowitz A, Akutsu T, Chaptal PA, Krakauer J, Kantrowitz
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14. Birtwell W, Giron F, Soroff H, Ruiz U, Collins J, Deterling
patient population. Part II of this review will focus on
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ACKNOWLEDGMENTS rial counterpulsation. Am Heart J. 1962;64:779–788.
We gratefully acknowledge the contributions of Dr 17. Lefemine AA, Low HB, Cohen ML, Lunzer S, Harken DE.
Naveen Nathan of Northwestern University to the cre- Assisted circulation. III. The effect of synchronized arterial
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ation of figures and illustrations for this article.
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DISCLOSURES Deterling RA Jr. Assisted circulation. I. An improved
Name: Laura S. González, MD. method for counterpulsation. Trans Am Soc Artif Intern
Contribution: This author helped draft the manuscript. Organs. 1962;8:35–42.
Name: Mark A. Chaney, MD. 19. Watkins DH, Callaghan PB. Postsystolic myocardial aug-
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Cardiovascular and Thoracic Anesthesiology

E NARRATIVE REVIEW ARTICLE

Intraaortic Balloon Pump Counterpulsation, Part

Laura S. González, MD,* and Mark A. Chaney, MD†

776 www.anesthesia-analgesia.org September 2020 • Volume 131 • Number 3

increased coronary blood flow (Figure 1).8 Later, they

Late 1960s: The Intraaortic Balloon

1970s: IABP Counterpulsation Takes Off

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 777

even though there was low salvage of patients in car-

longed support, and demonstration of percutaneous

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 779

Figure 3. Aortic pressure waveforms with

Benefits of anticoagulation include decreased risk of PHYSIOLOGIC EFFECTS

counterpulsation.75–78 Given these findings, counter-

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 781

in physiologic experiments to determine the balance CONTRAINDICATIONS/COMPLICATIONS

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 783

ANESTHESIA & ANALGESIA

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 785

tricular assistance. ASAIO Trans. 1987;33:39–48.

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 787

Organs. 1968;14:344–348. (Phila). 2017;12:472–478.

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 789

J Invasive Cardiol. 2007;19:339–346. migration/2094.pdf

September 2020 • Volume 131 • Number 3 www.anesthesia-analgesia.org 791

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