Intra Aortic Balloon

Counterpulsation

Dr N. Seetaramji
Registrar,
Dept. Of Anaesthesiology,
Wockhardt Hospital.
History

 Willem Kolff, Stephen Topaz, et al

conceived this procedure at the
Cleveland Clinic in 1961
 Kantrowitz applied it to patients in 1967.
JAMA 203:135, 1968
Concepts of Counterpulsation
 The balloon is phasically pulsed in
counterpulsation to the patient’s cardiac
cycle (IABC)
 IABP has no ‘inotropic’ action; does not
directly increase contractility.
 Primarily benefits the left ventricle, although
the diastolic augmentation may improve
coronary flow to both ventricals.
 Some Basics of
Myocardial O2 Supply/Delivery
 Ischemic heart has maximally dilated arteries. Perfusion
is then directly related to perfusion pressure.
 Coronary perfusion occurs predominately during diastole
 Increasing diastolic time increases coronary blood flow
 Major resistance to (subendocardial) coronary blood flow
during diastole is LVEDP such that...
 CPP=AoDP-LVEDP
 AoDP and LVEDP are dynamic values
 Windkessel Effect
Contd.
 Overlapping the aortic pressure and LV pressure
curves gives a visual representation of the pressure
gradient.
 This gradient over the diastolic time cycle is
described as the Diastolic Pressure Time Index
(DPTI)
 Area within the DPTI is directly correlated with O2
availability to the myocardium (supply)
Some Basics of
MVO2/Demand

 HR, contractility, wall tension (50% of MVO2 at rest).

 Laplace’s law T=Pr/2h
 Intraventricular pressure is a modifiable variable.
 IVP greatest during systole (LVSP).
 LVSP is a dynamic value continually changing throughout
systole and altering wall tension as this occurs.
 Area under the LVSP tracing is represented by the Tension
Time Index (TTI) and is directly correllated to wall tension and
MVO2.
Contd.
 Increasing systole time (HR) or peak LV systolic
pressure increases the TTI and subsequently MVO2
 Conversely, lowering the AoEDP (decreased
afterload) decreases the pressure the LV must
overcome to eject blood and lowers the TTI
 The Endocardial Viability Ratio relates the
relationship between myocardial O2 supply and
demand and is defined by EVR=DPTI/TTI
(supply/demand).
Windkessel Effect
 Potential energy stored in aortic root during systole
 Converted to kinetic energy with elastic recoil of
aortic root
 Increases diastolic pressure/flow during early
diastole
 Less affect with hypovolemia or noncompliant
aortas
 Noted on the A-line tracing as the dicrotic notch
IABP- how does it work?
 IABP does not ‘pump’ blood per se in contrast to a
VAD.
 Requires a functioning, beating heart.
 IABP serves as an external source of energy to
allow the sick heart to pump more efficiently.
 Does this via afterload reduction and diastolic
augmentation.
 Net result is an increased DO2, decreased MVO2,
and an increased CO.
Indications
 Pump failure (reversible)
- AMI ; Ohman EM et al (1994), Kono T et al (1996).
(JACC Guidelines 1996 on IABP use in AMI)
- cardiogenic shock
-progressive deterioration despite pharmacologic
support
- Reversible mech. effects
-VSD, Ac. Mitral Regurgitation.
- Unstable Angina / PTCA.
Contd.
 Cardiac transplant patient
-as a bridge to transplantation
-post transplant support
 Prophylactic preoperative use
 Aide to separate from CPB
 Transport to tertiary centre.
 Post traumatic Heart Failure.
 Supporting High Risk Non-Cardiac Surgery.
Contraindications

 Thoracic or abdominal aortic aneurysm

 Aortic dissection
 Aortic insufficiency
 ? Severe pre-existing vascular disease,
presence of iliofemoral grafts.
 ? Prosthetic aortic graft
Balloon Selection
“Datascope”
Patient’s IABP IABP
Height Volume Length

(cm) (cc)
(mm)

< 152 25 174

153 – 162 34 219
163 – 183 40 263
Contd.
“Arrow”

Patient’s IABP IABP

BSA Volume Length
(cm) (cc)
(mm)

< 1.8 30 230

> 1.8 40 262
Placement.
 6.5 Fr Catheter, 8 Fr Introducer, Heparinisation, etc.
 If Pulses not felt, Ankle arm index.
 Placed percutaneously or surgically with or without a
sheath via the femoral artery; Seldinger technique.
 Advanced into aorta under flouroscopy until the tip is
about 2 cm distal to the origin of the left subclavian
artery.
 Catheter locations more proximal than this compromise
flow to the vessels of the aortic arch.
 More distal locations attenuate the hemodynamic benefits
of the IABP and can potentially compromise renal blood
flow.
Contd.

 Palpate the Left Radial artery pulse.

 Confirm position with X’ray Chest/TEE.
 Keep aPTT @ twice control.
 Check circulation to the relevent limb: Doppler
ankle pressure < 40 mmHg / ankle arm index < 0.25 indicate
circulatory impairement.
 Follow Sr Creatinine & urine output daily
 Compartment syndrome, watch for.
Determinants of IABP efficiency
 Ideal balloon volume causes maximal emptying of
LV without causing retrograde flow from the
coronary vasculature and vessels of the aortic arch.
 Balloon should occlude 75-90% of the aortic cross-
sectional area during inflation.
 CO2 vs Helium
 Efficiency if IABC is critically dependent on the
timing of both inflation and deflation.
IAPB Triggering
 IABP requires a trigger to determine systole and diastole.
 ECG or arterial waveform.
 ECG directly from the patient to the pump or the pump
can slave off the bedside monitor.
 T-wave default. Electrical index of diastole. Deflation
occurs prior to the next QRS (during PR interval).
 Timing is manually fine-tuned according to the aortic
pressure waveform (more representative of mechanical
events).
 External Pacemaker – Danger ?/Emergency use.
 Internal impulse generation from console
Early inflation: Aortic valve
still open, ↑Ventricular Workload.
Late Inflation: ↓rise in diastolic
aortic root pressure,
ineffective coronary perfusion.
Early Deflation: shortens
diastole, ↓coronary perfusion time
Late Deflation: balloon still
inflated, ↑ ventricular afterload.
IAB monitors self
 Volume & pressure in the balloon.
 Leaks in driving gas.
 Loss of ECG/Arterial signal
 Arrhythmia detection & change in Heart
rate.
 Improper deflation of the IAB.
Limitations of IABC

 Heart Rate, 130/min ?

 Arrhythmias (non-sinus rhythms)
 Hypovolemia
 Systolic pressure: 40 mmHg for pressure trigger.
 Cardiac Output: Minimum CI of 1.2 to 1.4
ltrs/min/m2.
Diastolic Augmentation
 Balloon inflation at the onset of diastole which is
correllated to aortic valve closure (mechanical event).
 Displacement of blood within the aorta to areas proximal
and distal to the balloon. Termed “compartmentilization”.
 Proximal compartment consists of branches of aortic arch
(carotids) and coronary vasculature.
 Diastolic balloon inflation augments cerebral and
coronary perfusion.
 Increased DPTI and EVR.
 ‘Exaggerated’ Windkessel Effect.
Afterload Reduction
 Optimal balloon deflation occurs just prior to the
opening of the aortic valve; during early
isovolemic contraction.
 Abruptly decreases intraaortic volume
 AoEDP is acutely decreased (afterload reduction).
 AoV opens sooner during cardiac cycle lending
more time for ventricular ejection
 Overall result is a larger SV (CO).
 A lower peak LVSP decreases the TTI which
leads to a decrease MVO2 and an icrease in the
EVR.
BP & IABP
 Normal BP has two reference points- SBP & DBP
 With a pump set at 1:2 you have 5 different reference
points.
 Net effect:
*SBP following an augmented beat will be lower than
SBP following an unassisted beat.
*AoEDP following an augmented beat will be lower than
AoEDP following an unassisted beat.
*Peak diastolic augmented pressure will be integrated into
the pressure reading on the arterial line. Overall BP as
read by A-line (number you see) should increase
BP & IABP
Weaning

 Frequency ratio weaning (1:1, 1:2, 1:3,

etc.).
 Volume weaning (more physiologic?)

 Stop Heparin 2 hrs & Platelet count

> 60,000/mm3 before IAB explantation.

Risk of IABC
 Reported complication rates vary, but in
general range about 20-30% of all IABP’s
placed.
 Factors which predispose to a higher
complication rate include age, pre-existing
vascular disease, duration of IABP, DM,
HTN, obesity, and vasopressor therapy.
Complications : During Insertion
 Failure: 6%, even with 8Fr sheath.
 Arterial dissection, perforation.
 Bleeding
 Misplacement to LV, Subclavian, Lt.
common carotid, contralateral Femoral
arteries were reported. Isner JM (1980)
Complications: Balloon in situ
 Limb Ischemia/compartment syndrome
 Infection
 Thrombocytopenia/hemolytic anemia
 Embolization of platelet aggregates
 Rupture of balloon/gas embolism
 IAB Entrapment
  complications with Size ≥ 9.5 Fr and balloon
in situ for > 48 hrs.
Complications: After Removal

 Surgical explantation in coagulopathy

 Hematoma
 False Aneurism
 Arterio-venous fistula