Download IABP

Intra-aortic baloon pumps
what, who, why why why?
Daniel Lovric
Fellow, CVICU
Auckland City Hospital
Auckland Region ICU Study Day
30th October 2014
IABP – What is it?
Mechanical hemodynamic support device
Two principal parts
Mobile Console
Flexible catheter with baloon
How does it work?
Balloon is advanced through the femoral artery
to descending thoracic aorta
Ideal placement is 1-2cm distal of the origin of
left subclavian artery and above the origin of
renal arteries
Inflation triggered either by ECG (R wave) or
Pressure waveform
Inflation happens in diastole
Deflated during systole
Should occupy around 85-90% of cross-sectional
area
Multiple theoretical benefits
How does it work?
Theoretical benefits – Two basic principles
Increasing aortic
Decreasing end-diastolic
diastolic pressure augments
aortic pressure reduces
coronary blood flow heart’s afterload
Physiological effects
Hanlon-Pena et al, AJCC 2011
Reduction in LV workload
Reduction in LV workload
Commencement of IABP pulsation
Reduction in left ventricular
pressure
Reduction in left ventricular stroke work
Increase in left ventricular stroke
volume
Schreuder et al, Ann Thorac Surg 2005
Augmented coronary flow
Conficting evidence
Inflation of the balloon
diastolic pressure and diastolic perfusion pressure gradient (Port, JACC 1984; Williams, Circ
1982)
Animals with normal systemic blood pressure
myocardial oxigen consumption, no change in coronary flow (Kern, Am Heart J 1999)
Coronary flow measurements
pre-stenotic flow (MacDonald, Am J Cardiol 1987; Kern, Circ 1991)
post-stenotic flow (MacDonald, Am J Cardiol 1987; Gewirtz, Am J Cardiol 1982)
Angina symptoms
(Folland, Circ 1991)
“Artificial myoconservation” (Ohman, Circ 1994)
stimulation of collateral circulation (Ohman, Circ 1994; Fuchs, Circ 1983)
Augmented coronary flow
Laplace’s Law
Deflation of the balloon
end-diastolic pressure
wall stress
myocardial oxygen demand
How it begun...
1959 – Kantrowitz described the principle of
counterpulsation
1962 – Moulopoulos (Cleveland Clinic) described the
modern
intra-aortic counterpulsation device
- carbon dioxide
- R wave timing
1971 – Krakauer & Kantrowitz describe series of 30 pts in
cardiogenic shock 2° to STEMI treated with IABP
- 25 of 30 pts achieved hemodynamic stabilisation
and reversal of shock
1973 – Successful use of IABP in weaning of cardiopulmonary bypass published by two different groups
1980 – Development of percutaneous catheter introduction
Moulopoulos et al, Am Heart J 1962; Goldberg et al, NEJM 1999; Antman et al, Circulation 2008
Buckley et al, Circ 1973; Housman et al, JAMA 1973; Bergman et al, A. Th. Surg 1980; Subramanian et al, Circ 1980
... and took hold
1959 – Kantrowitz described the principle of
counterpulsation
1962 – Moulopoulos (Cleveland Clinic) described the
modern
intra-aortic counterpulsation device
- carbon dioxide
- R wave timing
1986 – 1997 overall ~20% of patients received IABP suport
for cardiogenic shock due to MI
1997 – 42% of patients
Moulopoulos et al, Am Heart J 1962; Goldberg et al, NEJM 1999; Antman et al, Circulation 2008
Buckley et al, Circ 1973; Housman et al, JAMA 1973; Bergman et al, A. Th. Surg 1980; Subramanian et al, Circ 1980
Randomized trials
IABP in STEMI
Randomized trials
IABP in STEMI
Analysis of trials
IABP in STEMI
1009 patients
No change in 30 day mortality
No change in LVEF at follow-up
Stroke rate by 2% (p=0.03)
Bleeding by 6%
(p=0.02)
Sjauw et al. EHJ 2009
Analysis of trials
IABP in STEMI with cardiogenic shock
10529 patients
Thrombolysis studies showed absolute mortality
decrease of 18% (p<0.0001)
Primary PCI studies showed absolute mortality
increase of 6% (p<0.0008)
Revascularization rate
IABP 39% vs control 9% (p<0.001)
Sjauw et al. EHJ 2009
IABP SHOCK II Trial
Designed to affirm guidelines
37 centres, 600 patients
240 primary end-points
Overall 30 day mortality of 40%
Thiele et al. NEJM 2012
In cardiac surgery
Pre-operative IABP in high risk CABG patients
110 hemodynamically stable subjects, LVEF <35%
Vent. wean
Discharge
Ranucci et al. Crit Care Med 2013
In high-risk PCI – BCIS-1
301 patients with severe LV dysfunction (EF<30%) and extensive coronary
disease
Routine IABP placement before PCI in treatment arm
Primary end-point was MACCE at discharge and 6 months
P=0.03
Long-term follow-up by tracking UK statistics databases
Perera et al. JAMA 2010, Circ 2013
Indications
What’s left?
Acute mitral regurgitation (Ic)
Ventricular septal defect as a complication of MI (Ic)
Intractable ventricular arrhythmias (IIa)
Unstable angina refractory to medical therapy (IIa)
Decompensated systolic HF as bridge to
mechanical support or transplant (IIb)
Patients following cardiac surgery with low cardiac output unresponsive
to pharmacologic therapy
Fotopoulos et al. Heart 1999; Ferguson et al, JACC 2001
Contraindications
Aortic regurgitation (more than mild)
Aortic dissection
Aneurysm or other anatomical disease of aorta
Severe PVD
Lack of experience with management
Will not work in distributive shock (sepsis)
Will not work in a setting of low CI and tachyarrhythmias
Positioning
Should be ~2 cm below the origin of left subclavian artery
3-4mm metalic density
2cm bellow the top of aortic knob
2nd – 3rd intercostal space
anteriorly
Positioning
Should be ~2 cm below the origin of left subclavian artery
2cm above carina
1-2cm above PAC
Kim et al, Anesth Analg 2007
Positioning
Should be ~2 cm below the origin of left subclavian artery
IABP Timing
Determines periods of inflation and deflation during cardiac cycle
Criticaly important for achieving beneficial hemodynamic effects
Newer systems can adjust timing completely automatically
Conventional Timing
Studied and used in practice since the beginning of IABC
Both inflation and deflation occur within diastole
Inflation
Deflation
Timed to commence immediately
prior or at the time of AV closure
(dictrotic notch)
Timed at onset of systole
Should occur before ejection
Isovolumetric contraction phase
Timing Errors
Early inflation
before AV closure
LV forced to eject against inflated balloon, premature closure of AV
Afterload
Oxygen demand
Stroke volume to 20%
Aortic regurgitation may appear
Trost et al, Am J Cardiol 2006
Timing Errors
Late inflation
after dicrotic notch – AV closure
Augmentation
Trost et al, Am J Cardiol 2006
Timing Errors
Early deflation
Before end of diastole, loss of sharp V diastolic pressure trace
Augmentation
May promote retrograde arterial flow from the coronaries and carotids
Trost et al, Am J Cardiol 2006
Timing Errors
Late deflation
After begining of systole during ejection phase
End-diastolic pressure
Afterload
Oxygen demand
LV workload
Trost et al, Am J Cardiol 2006
Real-time Timing
R wave deflation
Deflation occurs in early systole
Safe when ≥50% of IABP volume is removed before the start of
ejection
2-part potential effect
Delayed opening of AV brings prolongation of isovolumetric contraction
Length of ejection and stroke volume increased more than in conventional
Preferred method when arrhythmia is present
Hanlon-Pena et al, AJCC 2011
Complications
During insertion
Unable to pass the catheter up the aorta
Arterial dissection or rupture
Retroperitoneal bleeding or
damage to adjacent structures
Complications
During use
Distal limb ischemia
Poor supply to
LSCA/renal arteries/mesenteric arteries
Balloon rupture and gas embolism
Thromboembolism
Haemolysis & Thrombocytopenia
Complications
On removal
Inability to remove the catheter
Bleeding
Embolism
Pseudoaneurysm
AV fistula
Final thoughts
IABP was overutilised in the past
It is significantly falling out of favour recently
Physiologicaly sound principle, but difficult to implement
properly
It’s future seems grim...
Due to arrival of new mechanical assist therapies
Thank you...