1. The document discusses the history, principles, anatomy, physiology, indications, and complications of intra-aortic balloon pumps (IABPs). 2. IABPs were developed in the 1950s and work by inflating during diastole to increase coronary blood flow and deflating during systole to reduce workload on the heart. 3. Proper positioning of the IABP catheter is important for effectiveness with tips typically placed just above the left main bronchus. 4. IABPs reduce myocardial oxygen demand and increase coronary blood flow by lowering systolic pressure and increasing diastolic pressure and flow.

1. INTRA-AORTIC BALLOON PUMP
Dr Chetan Bhole
SR Cardiology
IABP
Date : 28 April 2017
INTRA-AORTIC BALLOON PUMP

2. Points for discussion :
1. History
2. Principles of IABP function
3. Anatomy of device
4. Physiology and Pathophysiology of IABP
5. Indications and Contraindications
6. Evidence

3. History :
In 1952 Adrian Kantrowitz :
“coronary blood flow can be
increased by retardation of
the arterial pressure pulse in
animal models.”
In 1958, Harken :
“Removal of some of the blood
volume via the femoral artery
during systole and replacing it
rapidly in diastole, so called
diastolic augmentation as a
treatment for left ventricular (LV)
Adrian kantrowitz
(1998-2008)

4.  Four years later,
Moulopoulos and
colleagues
developed an
experimental
prototype of an
IABP whose
inflation and
deflation were timed
to the cardiac cycle.
(15 F catheter, latex
balloon & CO2)

5.  In 1968 Kantrowitz reported improved
systemic arterial pressure and urine output
with the use of an IABP in two subjects with
cardiogenic shock, one of who survived to
hospital discharge.

6.  Percutaneous IABPs in sizes 8.5-9.5 French
were introduced in 1979, and shortly after this,
Bergman and colleagues described the first
percutaneous insertion of IABP.

7. Basic Principles of
Counterpulsation:
 Counterpulsation :
pulsatile movement of arterial blood which
was "counter" to the normal pulsatile flow, a
reversal of the ordinary dynamic.
 balloon inflation in diastole and deflation in
early systole.

8. Balloon inflation causes 'volume displacement' of blood within
the aorta, both proximally and distally. increase in coronary
blood flow and improve systemic perfusion by augmentation
of the intrinsic 'Windkessel effect.

9. Structure of the IABP:

11. Balloon catheters:
 30-60 ml displacement volume
 have concentric central lumen inside the
helium channel which allows use of guide wire
to introduce catheter and also allows recording
of central arterial pressure.

12. Size of balloon :
Height BSA Ballon size
147-162cm < 1.8m2 30 cm3
162-182cm >1.8 m2 40 cm3
>182cm OR
aortic diometer
>20mm
>1.8 m2 50 cm3

13.  Balloon size > 50 cm3 is not available.
 40 cm³ balloon is most commonly used
 Paediatric balloons also available : sizes 2.5,
5.0, 12.0 and 20 cm³

14. Insertion of IABP :
 percutaneous Seldinger technique or surgical
 with or without sheath
 Pass balloon through sheath over guidewire
and insert estimated distance – measure from
sternal angle to umbilicus then to femoral
artery.
 Must be inserted to at least the level of the
manufacturer’s mark (usually double line) to
ensure that entire balloon has emerged from
sheath

15.  Balloon should be positioned so that the tip is
about 1-2 cm distal to the origin of the left
subclavian artery
 watch for loss of right radial pulse (too high)
 Remove wire — return of blood via central
lumen confirms that the tip is not sub-intimal
and has not caused a dissection

16. Confirmation of position
 arterial balloon waveform and pressures shown
on monitor
check for normal morphology and appropriate
timing of inflation and deflation in 1:2
augmentation ratio
 Chest x-ray or fluoroscopy
radiopaque tip lies in the 2nd intercostal spaces
just above the left main bronchus; lower end of
balloon should lie cephalad to the renal arteries
 TOE
direct visualisation 1-2cm distal to the left
subclavian artery

22. TEE showing guide wire in aorta

23. Passage of IABP ballloon over guide wire

24. Short axis view of descending aorta
showing origin of left subclavian artery

25. Short axis view showing position of IABP tip
too high to Left Subclavian artery orifice

26. Short axis view showing position of IABP in
left Subclavian artery

27. 27
ECG signal – most common
• Inflation
- middle of T wave
• Deflation
– peak of R wave
• Pacer (v/a)
• Arterial waveform
• An intrinsic pump rate
( CPB)
Triggering and timing of IABP :

28. 28

29. 29

30. 30

31. Efficiency affected by :
1. timing of inflation and deflation
2. assist ratio(1:2, 1:3)
3. heart rate (tachycardia > 130/min reduces
benefit of IABP)
4. gas leak from balloon
5. CI of 1.2-1.4 required for IABP to be effective

32. Physiology of IABP

33. The normal IABP blood pressure
waveform

34. The normal IABP balloon
waveform
The balloon itself has a pressure transducer, and it generates a
waveform.

35. About 40 milliseconds before the dicrotic notch, the IABP balloon inflates. This is
timed with the ECG, usually - the end of the T wave is used as a marker that systole
has finished

36. Hemodynamic effects of IABP:
1. Reduction in systolic blood pressure
2. Fall in end-diastolic aortic pressure
3. Shortening of the isovolumetric phase of
contraction
4. Reduction in left ventricular wall stress
5. Increase in left ventricular ejection fraction
6. Reduction of preload/afterload
7. Increase in DPTI/TTI ratio
8. Improvement of coronary flow

37. Expected changes with IABP support in
patients with Cardiogenic shock
1. Decrease in SBP by 20 %
2. Increase in aortic Diastolic Press. by 30 % ( raise
coronary blood flow)
3. Increase in MAP
4. Reduction of the HR by 20%
5. Decrease in the mean PCWP by 20 %
6. Elevation in the COP by 20%

38. Balloon inflation and diastolic
augmentation :

39. The “normal” augmented
waveform

40. Benefits of accurate time of
inflation:
 Increased Coronary blood flow
and pressure and hence
myocardial perfusion is
increased.
 Increased diastolic pressure
leads to increased perfusion of
kidney and brain(systemic
perfusion is increased)
 Increased coronary collateral
circulation

41. Diastolic pressure time index (DPTI)
and coronary perfusion :
 The DPTI is crudely the time spent in diastole
at certain pressure.
 It reflects the time during which the diastolic
pressure in the aorta fills the coronary arteries
 correlates with the driving pressure required
for perfusion of the subendocardium

43. Post IABP :

44. Empirical evidence for the benefit of
diastolic augmentation
mean diastolic pressure
flow in the great cardiac vein
(this implies, the better the perfusion of the left
ventricle).

45.  Small study : diastolic augmentation for a 40cc balloon resulted in an
increase in mean aortic diastolic pressure from an average of 77mmHg to
99mmHg, with a proportional increase in great cardiac vein flow (from
44ml/min to 54ml/min). Of great relevance is the fact that the patients all
had 90% proximal LAD stenosis.

46. Myocardial oxygen consumption
and IABP :
 The IABP decreases myocardial oxygen
consumption by decreasing the mean left
ventricular ejection pressure, and by
decreasing the duration of isovolumetric
contraction.

47.  To eject blood in aorta LV need to overcome
2 variables : mass of blood and aortic end
diastolic pressure
 Mass of blood(water plus hematocrit) we
cannot change

48.  Deflation of balloon causes sudden fall in
aortic volume(approx 40cc according to size of
balloon) when the aortic wall is relaxing.
 This leads to decrease in aortic pressure at the
end of diastole
 The result is a lower pressure required for
aortic valve opening

50. Benefits of accurate deflation :
 LV will generate less
pressure throughout the
systole i.e afterload is
reduced
 More effective emptying of
LV thus stroke volume is
increased
 Shortening of IVC phase
 Decreased afterload also
reduce hemodynamics of
MR and VSD

51. Relationship of LV ejection
pressure to LV oxygen
consumption :
 The myocardial oxygen consumption, is
related to left ventricular workload. And a
major determinant of left ventricular workload
is the area under the LV systolic pressure
curve
 This area, termed TTI (tension time index) is
directly related to myocardial oxygen
consumption.

52. TTI (tension time index)

53. Post IABP :

54. Reduced mean LV ejection
pressure and systolic ejection
period
Rediced TTI
Reduced myocardial oxygen
consumption

55.  However, the mean ejection pressure is
actually not the most important parameter.
 By the time the aortic valve opens, most of the
myocardial work has already been done.
 As far as myocardial oxygen consumption
goes, the chief benefit from IABP
counterpulsation is actually from reducing
the amount of time spent in isovolumetric
contraction

56. Aortic end-diastolic pressure &
isovolumetric contraction
 Isovolumetric contraction : phase After the
mitral valve closing, and prior to the aortic
valve opening
 left ventricle it contracts against a static
intraventricular volume
 90% of myocardial oxygen consumption

57.  Additionally, during this time left ventricular
walls squeezes the precious oxygenated blood
out of the subendocardium.
 Obviously, anything that causes the aortic
valve to open earlier reduces the duration of
this period and reduces myocardial oxygen
consumption

59. Effect of IABP in MR and VSD
 Reduced aortic end diastolic pressure(
reduced afterload)
 Improve LV ejection
 Reduce shunt

60. Indications for the Use of IABP:
 No choice but pump
1. Failure to come off bypass machine
2. Severe aortic stenosis, mitral regurgitation or
ventricular septal defect with hemodynamic
compromise, while waiting for repair

61.  Probably harmless, but probably not useful
1. High risk CABG patients (pre-op) (Left main
stenosis >70%, LVEF less than 40%, Unstable
angina perioperatively, Re-do of the CABG)
2. High-risk PCI patients (pre-op)
3. Cardiogenic shock while waiting for PCI
4. Pulmonary oedema in spite of maximal
medical management

62. Contraindications
 Absolute
contraindications
1. Aortic regurgitation
2. Aortic aneurysm
3. Aortic dissection
4. Severe sepsis
5. Uncontrolled
coagulopathy
 Relative
contraindications
1. Atherosclerosis and
arterial tortuosity
2. Left ventricular
outflow tract
obstruction
3. Contraindications to
anticoagulation

63. Complications of IABP :
 Common
complications
1. Mild limb ischaemia -
2.9%
2. Balloon leak - 1.0%
3. Major limb ischaemia -
0.9%
4. Haemorrhage - 0.8%
5. Leg amputation due to
ischaemia - 0.1%
 Rare complications
1. Atheromatous
cholesterol emboli
2. Aortic or arterial
dissection
3. Cerebrovascular
accident
4. Thrombocytopenia
5. Haemolysis
6. Helium embolism

64. Pathophysiology of Abnormal IABP
Arterial Waveforms

67. Early balloon inflation results in
increased afterload
•Increased LV oxygen demand, due to increased afterload
•Decreased LV oxygen supply, due to decreased diastolic perfusion
•Decreased cardiac output, due to decreased stroke volume

68. Consequences :
 Premature closure of aortic valves
 Increased LVEDP and LVEDV leading to
Increased LV wall stress
 Subendocardial ischemia due to sqeezing (LV is
still contracting when balloon is inflated)
 increase in coronary vascular resistance results in
decreased flow though the coronary circulation

69.  Reduced flow though the coronary circulation
despite higher peak of diastolic augmentation
 the aortic valve closes prematurely.
 The duration of systole is reduced, and thus
stroke volume is reduced
 decreases cardiac output.

70. Late balloon inflation
Delayed balloon inflation results in decreased diastolic augmentation.
This results in decreased coronary perfusion

71.  i.e few miliseconds after Aortic valve closure
 Lower than optimal diastolic augmentation,
slightly increased coronary perfusion

72. Early balloon deflation
 If the balloon deflates too early, (i.e before
peak of R wave on ECG) the aortic pressure
has time to equalise.
 The aortic end-diastolic pressure reverts to its
unassisted level,
 no reduction in the duration of left ventricular
isovolumetric contraction period

73.  left ventricle is not assisted in opening the
aortic valve, and so there is no afterload
reduction
 and therefore fails to decrease LV oxygen
demand

74. Early balloon deflation :

75. Late balloon deflation
i.e balloon is still inflated when aortic vale opens
and deflate few miliseconds after opening of
aortic valve.
Deflate late, so no reduction in aortic end
diastolic pressure
Increases aortic end-diastolic pressure, and thus
increases afterload and left ventricular oxygen
consumption

77. Causes of Poor diastolic
augmentation in spite of
appropriate timing
 very poor cardiac output
 decrease in the systemic vascular resistance,.
 too small balloon for the patient
 too high or too low position of balloon in aorta
 The low helium pressure (ie. the balloon is
filling incompletely)
 The balloon is not completely out of its sheath
(i.e. the "tail" of the balloon does not get a
chance to inflate)

78. Abnormal IABP Balloon Pressure Waveforms

79. Normal balloon waveforms :

80. IABP balloon Plateau pressure
 The balloon plateau is depend on pressure
inside the helium balloon and the pressure
inside the aorta, which relates to the elastic
recoil of the aortic walls (and to some extent to
the systemic vascular resistance as a whole).

81. 1. Too small size balloon for patient
2. low peripheral vascular resistance (eg. septic
shock)
3. greatly reduced stroke volume (i.e. there is
not enough blood to eject in the aorta to
displace)
4. too low position of balloon in aorta
Low IABP balloon Plateau
pressure

83. Consequences :
 decreased diastolic augmentation, as well as a
high aortic end-diastolic pressure.
 cannot move much blood around the aorta,
and the IABP is not being useful to its full
potential

84. High IABP balloon plateau
pressure
 Balloon is too big for the patient
 Sever hypertensive patient
 too high position of balloon in the aorta
 The balloon catheter is kinked

86. High IABP balloon baseline filling
pressure
 normal baseline pressure in the helium circuit
should be around 10-15mmHg.
 high pressure S/O there is likely some
mechanical fault with the circuit, which limits
the normal emptying of the balloon.
1. The balloon catheter is kinked and and balloon is not
emptying properly
2. The system is overpressurised because the IABP is
malfunctioning

88. Consequences :
 Eventually the balloon can rupture
 the increased baseline pressure is transmitted
to the aorta, which results in increased
afterload and increased myocardial oxygen
demand. Decompensation ensues.
(Most IABP consoles will begin to alarm with an irritating
siren if the baseline pressure climbs over 20mmHg)

89. Low (or suddenly decreasing) IABP
balloon filling pressure baseline
 The filling pressure is adjusted automatically; if
this is not happening, there must be either :
1. helium leak
2. Balloon rupture
3. disconnection of the helium pipe
4. failure of the automated filling mechanism

91. Trials for IABP

92.  SHOCK
 BCIS -1
 CRISP-AMI
 IABP SHOCK 2

93. SHOCK (EARLY REVASCULARIZATION IN ACUTE
MYOCARDIAL INFARCTION COMPLICATED BY CARDIOGENIC
SHOCK August 1999)
 Patients with shock due to LV failure
complicating myocardial infarction
 emergency revascularization (152patients) or
initial medical stabilization (150 patients).
 Revascularization was accomplished by either
CABG or PCI.

94.  IABP was performed in 86% in both groups.
 The primary end point was mortality from all
causes at 30 days.
 Six-month survival was a secondary end point.

95. Conclusion :
 In patients with cardiogenic shock, emergency
revascularization did not significantly reduce
overall mortality at 30 days. However, after six
months there was a significant survival benefit.
 Early revascularization should be strongly
considered for patients with acute myocardial
infarction complicated by cardiogenic shock.

96. Balloon-pump assisted
Coronary Intervention Study
(BCIS-1):
 The first randomized controlled trial of
elective Intra-Aortic Balloon Pump (IABP)
insertion prior to high-risk PCI vs. PCI with
no planned IABP use
 17 UK centres
 n=301 (150 in each arm)

97. 97
N= 301 Elective IABP(
151)
No elective
IABP(150)
P VALUE
MACE 15.2% 16% 0.85
All cause mortality
at 6 mths
4.6% 7.4% 0.32
Major procedural
complications
1.3% 10.7% <0.001
Major or minor
bleeding
19.2% 11.3% 0.06
Access site
complications
3.3% 0% 0.06
Patients (n = 301) had severe left ventricular dysfunction (ejection fraction ≤
30%) and extensive coronary disease (Jeopardy Score ≥ 8/12); those with
contraindications to or class I indications for IABP therapy were excluded
JAMA. 2010;304(8):867-874

98. Conclusions of long term results of BCIS1
trial(2012-2013)
In patients with severe ischemic cardiomyopathy treated
with PCI, all cause-mortality was 33% at 51 months
(median)
Elective IABP use during PCI was associated with an
observed 34% reduction in long-term all-cause mortality

99. CRISPAMI (Counterpulsation Reduces Infarct
Size Acute Myocardial Infarction)
 Published in 2011
 Selected patients with AWMI without
cardiogenic shock
 N = 300 (randomised multicentre US)
 IABP prior and 12 hr after PCI Vs routine
Primary PCI care
 Cardiac MRI 3-5 days post PCI

100. Conclusion :
 Among patients with acute STEMI AWMI
without cardiogenic shock us of IABP prior to
PCI as compared to standerd care PCI :
1. Does not reduce infarct size
2. All cause mortality at 6 months was not
different
 Does not support routine use of IAPB prior to
PCI without cardiogenic shock

101. SHOCK II trial(Intraaortic Balloon Support for
Myocardial Infarction with Cardiogenic Shock, October
2012)
 Patients with AMI + cardiogenic shock planned
for early revascularization (PCI / CABG)
 N = 600
 IABP(300) Vs optimal medical
stabilization(298)

102.  Primary end point : all cause mortality at 30
days
 Secondary end points :time to hemodynamic
stabilization, the length of stay in the intensive
care unit,serum lactate levels, the dose and
duration of catecholamine therapy, and renal
function

103. Results :
 At 30 days, 119 patients in the IABP group
(39.7%) and 123 patients in the control group
(41.3%) had died
 No significant difference between secondary
endpoints
 No significant difference between rate of major
bleeding in both groups

104. Conclusion :
 The use of IABP did not significantly reduce
30-day mortality in patients with cardiogenic
shock complicating acute myocardial infarction
for whom an early revascularization strategy
was planned

105. BCIS-1, CRISP-AMI, and IABP-
SHOCK II
 routine elective IABP insertion does not reduce
the risk of major adverse complications
associated with PCI in the context of acute or
chronic severe left ventricular impairment.
 However counterpulsation is broadly a safe
treatment, with acceptably low rates of device-
related complications

106. Thank you