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IABP
1. MODERATOR – DR SHARAD JAIN
SIR
PRESENTOR – DR PINKESH
PARMAR
IABP
2. INTRODUCTION
Intra-aortic balloon pump (IABP) remains the most widely used circulatory
assist device in critically ill patients with cardiac disease.
The primary goal of IABP treatment is to improve the ventricular
performance of the failing heart by facilitating an increase in myocardial
oxygen supply and a decrease in myocardial oxygen demand.
Advances in technology, including percutaneous insertion, smaller diameter
catheters, sheathless insertion techniques, and enhanced automation, have
permitted the use of counterpulsation in a variety of settings, with greater
efficacy and safety.
3. HISTORY
Kantrowitz described augmentation of coronary blood flow by
retardation of the arterial pressure pulse in animal models in 1952. In
1958,
Harken suggested the removal of some of the blood volume via the
femoral artery during systole and replacing it rapidly in diastole as a
treatment for left ventricular (LV) failure, so called diastolic
augmentation.
Four years later, Moulopoulos and colleagues developed an
experimental prototype of an IABP whose inflation and deflation were
timed to the cardiac cycle.
4. HISTORY
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.
Percutaneous IABs in sizes 8.5–9.5 French (rather than 15 French
used earlier which needed to be surgically grafted) were introduced in
1979, and shortly after this, Bergman and colleagues described the
first percutaneous insertion of IABP.
The first prefolded IAB was developed in 1986.
5. BASIC PRINCIPLE OF
COUNTERPULSATION
Counterpulsation is a term that describes balloon inflation in diastole
and deflation in early systole.
Balloon inflation causes ‘volume displacement’ of blood within the
aorta, both proximally and distally.
This leads to a potential increase in coronary blood flow and potential
improvements in systemic perfusion by augmentation of the intrinsic
‘Windkessel effect’, whereby potential energy stored in the aortic root
during systole is converted to kinetic energy with the elastic recoil of
the aortic root.
8. PHYSIOLOGICAL EFFECTS
Although these effects are predominately associated with
enhancement of LV performance, IABP may also have favourable
effects on right ventricular (RV) function by complex mechanisms
including accentuation of RV myocardial blood flow, unloading the
left ventricle causing reduction in left atrial and pulmonary vascular
pressures and RV afterload.
IABP inflates at the onset of diastole, thereby increasing diastolic
pressure and deflates just before systole, thus reducing LV afterload.
9. PHYSIOLOGICAL EFFECTS
The magnitude of these effects depends upon:
(i) Balloon volume: the amount of blood displaced is proportional to
the volume of the balloon.
(ii) Heart rate: LV and aortic diastolic filling times are inversely
proportional to heart rate; shorter diastolic time produces lesser
balloon augmentation per unit time.
(iii) Aortic compliance: as aortic compliance increases (or SVR
decreases), the magnitude of diastolic augmentation decreases.
10. PHYSIOLOGICAL EFFECTS
The IABP has the following hemodynamic effects:
Decrease in SBP by 20%
Increase in aortic diastolic pressure by 30%
Increase in MAP
Reduction of heart rate by 20%
Decrease in mean PCWP by 20%
Elevation of cardiac output by 20%
Renal blood flow can increase up to 25%, secondary to increase in
cardiac output.
11. INDICATIONS
Mechanical Complications of Acute
MI [i.e. acute MR or VSD, or papillary
muscle rupture]
Refractory Unstable Angina
Acute MI with Cardiogenic Shock
Support for diagnostic,
percutaneous revascularization, and
interventional procedures in high
risk patients – severe LVD, LMCA,
complex CAD
Ischemia related intractable
ventricular arrhythmias
Myocardial contusion
Septic Shock
Weaning from bypass
Cardiac support for non-cardiac
surgery
Prophylactic support in preparation
for cardiac surgery in high risk
Post surgical myocardial
dysfunction/low cardiac output
syndrome
Mechanical bridge to other assist
devices or transplant
Cardiac support following correction
of anatomical defects
13. TECHNIQUE
The IABP device has two major components:
(i) a double-lumen 8.0–9.5 French catheter with a 25–50 ml balloon
attached at its distal end; and
(ii) a console with a pump to drive the balloon. The balloon is made
of polyethylene and is inflated with gas driven by the pump.
Helium is often used because its low density facilitates rapid transfer
of gas from console to the balloon. It is also easily absorbed into the
blood stream in case of rupture of the balloon.
14. IABP KIT
Introducer needle
Guide wire
Vessel dilators
Sheath
IABP (34 or 40cc)
Gas tubing
60-mL syringe
Three-way stopcock
Arterial pressure tubing (not in kit)
15.
16. TECHNIQUE
The IABP catheter is inserted
percutaneously into the femoral
artery through an introducer
sheath using the modified
Seldinger technique.
Alternative routes of access
include subclavian, axillary,
brachial, or iliac arteries.
The catheter can also be inserted
surgically using a transthoracic
or translumbar approach, but
this is associated with an
increased periprocedural
mortality.
17. TECHNIQUE
Once vascular access is obtained,
the balloon catheter is inserted
and advanced, usually under
fluoroscopic guidance, into the
descending thoracic aorta, with
its tip 2 to 3 cm distal to the
origin of the left subclavian
artery (at the level of the carina).
18. On chest x-ray the tip should be
visible in the 2nd or 3rd
intercostal space
19. TECHNIQUE
The outer lumen of the catheter is used for delivery of gas to the
balloon and the inner lumen can be used for monitoring systemic
arterial pressure.
The diameter of the balloon, when fully expanded should not exceed
80–90% of the diameter of the patient’s descending thoracic aorta.
20.
21.
22. TIMING
IABP timing refers to inflation and deflation of the IAB in relation to
the cardiac cycle. The cardiac cycle is monitored by continuous
display of the arterial pressure waveform. As the balloon inflates at
the onset of diastole, a sharp and deep ‘V’ is observed at the dicrotic
notch.
The balloon is set to inflate after the aortic valve closure (which
corresponds to the dicrotic notch on the arterial waveform) and
deflate immediately before the opening of the aortic valve (which
corresponds to the point just before the upstroke on the arterial
pressure waveform).
23. TIMING
Balloon inflation causes augmentation of diastolic pressure and a
second peak is observed. This peak is referred to as diastolic
augmentation. Diastolic augmentation is ideally higher than the
patient’s systolic pressure except when reduced stroke volume
causes a relative decrease in augmentation
Depending upon the patient’s haemodynamic status, the balloon is
programmed to assist every beat (1:1) or less often (1:2, 1:4, or 1:8).
With haemodynamic improvement, the device can be ‘weaned’ to less
frequent cycling before complete removal.
24. TRIGGER
The signal that indicates to the IABP that systole is occurring or about
to occur
ECG:
Best choice, R wave signals electrical event prior to
systole
Cannot be used:
Asystole (no trigger)
PEA (CPR compressions aren’t in concert with
rhythm)
Artifact ( ie. use of bovie in OR)
25.
26. TRIGGER
Pressure
Best for Asystole, PEA, Artifact, and CPB
Times to CPR compressions if they are strong
enough to generate an arterial waveform
Artifact and CPB, patient should still has an arterial
waveform
Cannot be used
Loss of arterial line
Irregular heart rhythm: deflates too late on
premature beats
27.
28.
29. ARTERIAL PRESSURE WAVEFORM
1:2 ASSIST
PAEDP = Patient aortic end diastolic
pressure, this is the patient's
unassisted diastole
PSP = Peak systolic pressure, this is
the patient's unassisted systole
PDP/DA = Peak diastolic pressure or
diastolic augmentation, this is the
pressure generated in the aorta as
the result of inflation
BAEDP = Balloon aortic end diastolic
pressure, this is the lowest pressure
produced by deflation of the IAB
APSP = Assisted peak systolic
pressure, this systole follows
balloon deflation and should reflect
the decrease in LV work
30.
31. NORMAL BALLOON PRESSURE
WAVEFORM
Two important points about the shape of the waveform are:
The width of the waveform corresponds to the duration of balloon
inflation during the cardiac cycle
The plateau of the waveform reflects pressure within the aorta when
the balloon is inflated. The balloon pump has to overcome the
pressure within the aorta to fill the balloon with gas. Since the
balloon material is very compliant, the pressure on either side will be
approximately the same.
Therefore the plateau pressure on the BPW should be within ± 20
mmHg of the diastolic on the arterial pressure waveform
33. PATIENT MANAGEMENT
Educate patient on not being able to bend leg with IAB
Special attention to recording groin bleeding/ooze, peripheral perfusion,
colour, bilateral pulses, temperature, capillary return, movement and
sensation. This should be attended on lower extremities and circulation
observation chart every hour.
Pressure area care 2 – 4hourly as patient immobile
Hourly haemodynamic observations recorded
Patient nursed supine 30-45 degrees head up. May be nursed on side as
long as leg with IABP is kept straight
Check IAB site regularly for signs of infection and change occlusive clear
dressing
34. INVESTIGATIONS
Daily CXR to ensure correct placement of IABP and ensure that it has
not migrated.
Daily pathology for electrolytes, coagulation, urea , creatinine
Daily ECG and more frequently as indicated by patients clinical status
Careful monitoring of renal function (The balloon sits above the
bifurcation of the renal arteries - backward migration may
compromise blood flow to the kidneys).
35. CARDIAC ARREST
If counter pulsation is to be continued and synchronised to the CPR
effort, then arterial trigger should be selected.
If CPR generates sufficient blood pressure, then in most cases, the
IABP will pump and may improve perfusion to coronary and carotid
arteries. In the event that the CPR cannot generate a consistent and
reliable trigger, then trigger signal generated by the IABP is available
through the use of the INTERNAL TRIGGER mode.
Once the ECG or arterial signal has been re-established, the trigger
mode must be changed from INTERNAL to an acceptable patient
trigger.
36. DEFIBRILLATION
If patient needs to be defibrillated the IABP has protection and is
isolated from the patient and the defibrillators electrodes
Staff still need to stand clear of patient and the IABP
37. TROUBLESHOOTING
Suboptimal timing of inflation and deflation of the balloon will result
in haemodynamic instability
Examples of this include:
(i) Early inflation: inflation of the IAB before aortic valve closure
(ii) Late inflation: inflation of the IAB markedly after closure of the
aortic valve
(iii) Early deflation: premature deflation of the IAB during the diastolic
phase
(iv) Late deflation: deflation of the IAB after the onset of systole
38. EARLY INFLATION
Waveform Characteristics:
Inflation of IABP prior to dicrotic
notch.
Diastolic augmentation encroached
onto systole (may be unable to
distinguish).
Physiologic Effects:
Potential premature closure of aortic
valve.
Potential increase in left ventricular
end diastolic volume (LVEDV) and
left ventricular end diastolic
pressure (LVEDP) or PCWP.
Increased left ventricular wall stress
or afterload.
39. LATE INFLATION
Waveform Characteristics:
Inflation of the IABP after the
dicrotic notch.
Absence of sharp V.
Sub-optimal diastolic
augmentation.
Physiologic Effects:
Sub-optimal coronary artery
perfusion
40. EARLY DEFLATION
Waveform Characteristics:
Deflation of IAB is seen as a sharp
drop following diastolic
augmentation.
Sub-optimal diastolic augmentation.
Assisted aortic end diastolic
pressure may be equal to or less
than the unassisted aortic end
diastolic pressure.
Assisted systolic pressure may rise.
Physiologic Effects:
Sub-optimal coronary perfusion.
Potential for retrograde coronary
and carotid blood flow.
Angina may occur as a result of
retrograde coronary blood flow.
Sub-optimal afterload reduction.
41. LATE DEFLATION
Waveform Characteristics:
Assisted aortic end-diastolic
pressure may be equal to the
unassisted aortic end diastolic
pressure.
Rate of rise of assisted systole is
prolonged.
Diastolic augmentation may appear
widened.
Physiologic Effects:
Afterload reduction is essentially
absent.
Increased MVO2 consumption due
to the left ventricle ejecting against
a greater resistance and a prolonged
isovolumetric contraction phase.
IAB may impede left ventricular
42. CATHETER KINK
Rounded balloon pressure waveform,
loss of plateau. This may be due to
kink or obstruction of shuttle gas
kink in the catheter tubing
improper IAB catheter position
sheath not being pulled back to
allow inflation of the IAB
the IAB is too large for the aorta
the IAB is not fully unwrapped or
H2O condensation in the external
tubing
43. CATHETER KINK
Reposition patient. Keep affected leg straight.
Use rolled towel under hip to hyperextend hip.
Apply slight traction to the catheter if kinking at the insertion site or
in the artery is suspected.
The distal portion of the IAB may be in the sheath if a long introducer
sheath was used. Pull sheath back until IAB bladder has exited the
sheath.
Introducer sheath may be kinked which in turn is kinking the balloon.
Suspect this particularly if placement of the sheath was difficult. Pull
sheath back or rotate sheath a partial turn.
Check placement of the balloon; it may be too high or too low.
44. LOSS OF TRIGGER
Check
ECG trace
Replace ECG electrodes
ECG cable
Choose an alternate ECG lead
Check pressure trace
45. LOSS OF PRESSURE TRACE
Check
Pressure bag inflated to 300mmhg
Patency of arterial line by withdrawing blood then flushing
Transducer is level to phlebostatic axis
46. WEANING
Assess if:
CI > 2.2 -2.5
MAP >65mmhg
Stable heart rate and haemodynamics
Weaning is commenced by decreasing the IABP frequency from 1:1
then 1:2 then 1:3.
The augmentation of the balloon should never be decreased for
weaning due to the increased risk of thrombus
When the ratio of the balloon is decreased each time the patients
haemodynamics should be assessed before the next stage of weaning
is commenced
47. IABP REMOVAL
Discontinue heparin six hours prior, check platelets and coagulation
factors
Put IABP on STANDBY then turn off as this will allow for balloon to
deflate passively
Disconnect tubing from IAB to pump as this will also help deflate the
balloon passively
Remove the IAB, let site bleed for 2 seconds to help remove any
thrombus
Apply manual pressure above and below IABP insertion site
Remove and alternate pressure to expel any clots
Apply constant pressure to the insertion site for a minimum of 30
minutes
48. COMPLICATIONS
The following patients are at the greatest risk of developing
complications associated with IABP:
Females, diabetics, smokers, obese patients
Patients with PVD, HTN, high SVR, shock
49. COMPLICATIONS
Transient loss of peripheral pulse
Mild Limb ischaemia 2.9%
Major limb ischemia 0.9%
Thromboembolism
Compartment syndrome
Aortic dissection
Local vascular injury—false
aneurysm, haematoma, bleeding
from the wound
Infection
Balloon leak 1.0%
Balloon rupture (can cause gas
embolus)
Balloon entrapment
Haematological changes, for
example thrombocytopenia,
haemolysis
Malpositioning causing cerebral
or renal compromise
Cardiac tamponade
Principles of IABP
50. ACC/AHA 2013 PRACTICE
GUIDELINES
Class IIa/LOE - B
The use of IABP can be useful for patientswith cardiogenic shock after
STEMI who do not quickly stabilize with pharmacological therapy.
51. ESC 2014 GUIDELINES
Class IIa/LOE - C
IABP insertion should be considered in patients with hemodynamic
instability/ cardiogenic shock due to mechanical complications
Class III / LOE – A
Routine use of IABP in patients with cardiogenic shock is not
recommended
52. IABP IN UA/NSTEMI – 2007,2012
UPDATE
Class IIa / LOE – C
The placement of IABP could be useful in patients with recurrent
ischemia despite maximal medical management and in those with
hemodynamic instability until coronary angiography and
revascularization is completed.
53. SHOCK TRIAL (1999)
Early revascularization in AMI complicated by cardiogenic shock
In the SHOCK trial, which compared early revascularization
(CABG/PCI) (n=152) with a strategy of initial medical stabilization
(n=150) for patients presenting with cardiogenic shock, no significant
difference was found between the treatment arms in the occurrence
of the primary end point, 30-day mortality.
However, the mortality trend observed at 30 days did reach statistical
significance at 6 months (a prespecified time point), in favor of early
revascularization; a result that has profoundly influenced
contemporary management of cardiogenic shock.
54. SHOCK II TRIAL (2012)
Intraaortic balloon support for myocardial infarction with
cardiogenic shock.
N Engl J Med. 2012 Oct 4
This multicenter, open-labeled, randomized study enrolled 600
patients with AMI (with or without ST-segment elevation) with
cardiogenic shock, if early revascularization was planned.
55. SHOCK II TRIAL
Patients were randomized in a 1:1 ratio to intraaortic balloon
counterpulsation (IABP group) or no intra-aortic counterpulsation
(control group).
The primary study end point, 30-day all-cause mortality, occurred in
a similar proportion of the IABP and control groups (39.7% and 41.3%;
relative risk with IABP 0.96; P=0.69), by an intention-to-treat
analysis.
There were no significant differences in the multiplesecondary end
points (including serial assessments of serum lactate, creatinine, C-
reactive protein levels, or the Simplified Acute Physiology Score or in
the safety end points [including severe or life-threatening bleeding,
peripheral ischemic complications, sepsis, and stroke]).
56. BCIS – 1 (2012-2013)
Balloon pump-assisted Coronary Intervention Study (BCIS-1) was a
multicenter RCT that randomly assigned 301 patients with severe
ischemic cardiomyopathy to receive elective IABP before PCI or to
undergo PCI without planned IABP support.
There was no difference in the frequency of Major Adverse Cardiac
and Cerebrovascular Events (MACCE) at hospital discharge (capped at
28 days), although procedural complications occurred less often in
the elective IABP group and 12% of patients assigned to have PCI
without IABP support required rescue IABP insertion because of
hemodynamic instability.
57. CRISP AMI TRIAL (2011)
Counterpulsation Reduces Infarct Size Pre-PCI (CRISP) is the third of
the recent RCT addressing the use of IABP.
This trial examined the role of the IABP in anterior ST-segment
elevation- acute coronary syndrome without cardiogenic shock.
It was a multicenter randomized trial, including 337 patients, who
were randomized in a 1:1 ratio to either IABP before PCI or PCI alone.
There was no difference in the infarct size assessed by cardiac MRI 3-
5 days post MI, the primary end point of the trial. All cause mortality
at 6 months was not different.
58. CONCLUSIONS
IABPs are extremely useful in stabilizing pts with complicated cardiac
disease
Risk factors for complications with IABPs are: female sex, PVD, small
BSA, age
Troubleshooting with waveform analysis is critical, and is just as
important as knowing how to insert an IABP
59. CONCLUSIONS
Prophylactic insertion of an IABP for hemodynamic support in high risk
PCI pts may be superior to a “rescue” strategy
Controversy has arisen as to the utility of IABPs, but registry data,
randomized data, and anecdotal data can be quoted to support their
benefit.
63. CRITERIA FOR MECHANICAL SUPPORT
Failure to wean
inotropes
End-organ damage
Nausea
Decreased
mental status
Progressive renal
or hepatic failure
Worsening
arrhythmias
Cardiac Index < 2.0
L/min/m2
PCWP > 20 mmHg
SVR > 2,100
dynes/s/cm3
Urine output < 20
ml/hr
SBP < 80 mmHg
64. DESTINATION THERAPY VS. BRIDGE TO
TRANSPLANTATION
Long-term placement
Destination Therapy (DT)
• Not a heart transplant
candidate
• NYHA IV
• LVEF <25%
• Maximized medical therapy
>45 of 60 days; IABP for 7
days; OR 14 days
ionotropes
• Functional limitation with a
peak oxygen consumption
of less than or equal to 14
ml/kg/min
Bridge to Transplantation
(BTT)
• Patient is approved and
currently listed for transplant
• NYHA IV
• Failed maximized medical
therapy
65. CONTRAINDICATIONS FOR VAD SUPPORT
Major irreversible
neurologic deficits
Hepatic fibrosis or cirrhosis
Nonreversible end- organ
dysfunction
Non-correctable intra- cardiac
shunts
Active infection?
Mechanical ventilation & FIO2 >
70%
Morbid Obesity (BMI
>40)
Pregnancy
Previous Heart
Transplant
Psychosocial
dysfunction
67. IMPELLA 2.5 AND 5.0
• Utilized for LV support only; not
appropriate to use with RV failure
• Impella 2.5 (12F) can be inserted
through the femoral artery during a
standard catheterization procedure;
provides up to 2.5 L of flow
• Impella 5.0 (21F) inserted via femoral or
axillary artery cut down; provides up to
5L of flow
• Impella CP (14F) is also available now
• The catheter is advanced through the
ascending aorta into the left ventricle
• Pulls blood from an inlet near the tip of
the catheter and expels blood into the
ascending aorta
68. TANDEM HEART PVAD• Used for LV support; not
appropriate in RV failure
• Cannulas are inserted
percutaneously through the
femoral vein and advanced
across the intraatrial septum
into the left atrium
• The pump withdraws
oxygenated blood from the
left atrium and returns it to
the femoral arteries via
arterial cannulas
• Provides up to 5L/min of
flow
69. CENTRIMAG• Can be used for LV
and/or RV support
• Cannula are typically
inserted via a midline
sternotomy, drains
blood from LA and
pumps it back to aorta
• For RV support, cannula
is placed in right atrial
appendage drains blood
from RA and pumps
into MPA.
• Capable of delivering
flows up to 9.9 L/min
• Can be used for up to
30 days
70. ECMO (VA)
• Used for patients with a
combination of acute
cardiac and respiratory
failure
• A cannula takes
deoxygenated blood from
a central vein or the right
atrium, pumps it past the
oxygenator, and then
returns the oxygenated
blood, under pressure, to
the arterial side of the
circulation
77. SYNCARDIA CARDIOWEST TOTAL ARTIFICIAL HEART
First and only Artificial Heart to receive
FDA, Health Canada and CE Approval
Highest bridge-to-transplant rate* 79% of
all approved BTT devices
Highest cardiac output of all mechanical
circulatory support devices (up to
9.5L/min)
Indicated for use as a bridge-to-transplant
– complete circulatory support system for
patients with irreversible biventricular
heart failure
78. INTERMACS
An important milestone in the advance of MCS therapy has been the
development of the National, Heart, Lung and Blood Institute (NHLBI)–
sponsored national registry, the Interagency Registry for Mechanically
Assisted Circulatory Support (INTERMACS).
INTERMACS is the largest available data repository for the study of
durable MCS outcomes.
To date, data on more than 15,000 patients receiving durable MCS
therapy have been reported to INTERMACS.
The overall survival rate for all patients undergoing primary
implantation of a durable MCS device is approximately 80% at 1 year
and 70% at 2 years.
79. INTERMACS SCORE
Interagency Registry for Mechanically Assisted Circulatory
Support
Long-Term LVAD
Ideal candidates are
INTERMACS classes 3-4
Short-Term LVAD
Candidates are
INTERMACS classes 1-2
Not a LVAD Candidate
INTERMACS 1 or those with
multisystem organ failure
80. INTERMACS
INTERMACS patient profiles are associated with short-term survival
following LVAD implantation and are used to inform appropriate
timing of intervention with durable, implantable MCS devices.
Patients with significant organ dysfunction at MCS device
implantation, accompanied by a greater degree of hemodynamic
compromise, are significantly more likely to require BiVAD support
and are at higher risk for major adverse events and at significantly
higher risk for death during use of MCS devices.
81.
82. CONCLUSION
The rapid progress of MCS technology in recent years has extended
survival and improved quality of life for select patients with advanced
heart failure.
there is a meaningful option for lifelong support even in patients who
are not candidates for transplantation.
Novel pump design has improved clinical outcomes, altered the
profile of MCS candidates, and changed the structure of advanced
heart disease programs.
