INTRA AORTIC BALLON PUMP

PRESENTED BY G.KIRAN MODERATED BY VIJAY KUMAR.

HISTORY The fundamentals of IAB technology

were first tested by Harken in 1958, who is credited with the first use of diastolic augmentation.

Moulopoulous (in the 1960’s) from the Cleveland Clinic developed the first successful prototype of an Intra-aortic balloon pump (IABP) which could be timed to the cardiac cycle.

The IABP device as we know it was reported by Dr Adrian Kantrowitz (1967) and his team from Grace Sinai hospital in Detroit.

The device was further developed for cardiac surgery by Dr David Bregman at New York Presbyterian Hospital in 1976.

The size of the balloons initially inserted were as large as 15 Fr.

Two operations were required for balloon usage, one to insert the balloon by cut down in a femoral artery, and a second operation to remove the balloon.

Advances in technology afforded progressively smaller IAB catheter sizes and eventually 8 and 9Fr. balloons were developed.

Current IAB catheter sizes are 7 and 7.5Fr.

Fundamentals of cardiac physiology

Preload: The ventricular wall tension at the end of diastole.  In clinical terms, it is the stretch on the ventricular fibers just prior to contraction, often approximated by the end-diastolic volume or end-diastolic pressure.

Afterload: The ventricular wall tension during contraction; the resistance that must be overcome in order for the ventricle to eject its contents.  It is often approximated by the systolic ventricular (or arterial) pressure.

lnotropic State (Contractility):     A measurement of the magnitude of contractile force at a given resting fiber length.

Stroke Volume:  Volume of blood ejected from the ventricle in systole (= end-diastolic volume - end-systolic volume).

Ejection Fraction:  The fraction of end-diastolic volume ejected from the ventricle per beat  (= stroke volume / end-diastolic volume).  Normal range = 55-75%

Cardiac Output:     Volume of blood ejected from the ventricle per minute (= stroke volume X  heart rate).

The effect of varying preload, after load, and contractility on the pressure-volume loop

Basic Principles 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

Haemodynamics of IABP

IABP decreases myocardial oxygen consumption

Myocardial oxygen supply and demand

Inflation of IAB during diastole increases the pressure difference between aorta and left ventricle, the so-called diastolic pressure time index (DPTI). The haemodynamic consequence of this is an increase in coronary blood flow and, therefore, myocardial oxygen supply. Myocardial oxygen demand is directly related to the area under the LV systolic pressure curve, termed as tension time index (TTI). Balloon deflation during systole causes a reduction in the LV afterload, thereby decreasing TTI. Thus, the ratio of oxygen supply (DPTI) to oxygen demand (TTI), known as the endocardial viability ratio (EVR), should increase if the IABP is working optimally. This can be evidenced by a decrease in coronary sinus lactate.

Indications for mechanical circulatory support

LV failure would be defined as cardiac index (CI) of less than 1.8L/min/m² with a systolic blood pressure of less than 90 mmhg (ref: Hensley Martin) despite maximized preload (mean atrial pressure > 20 mmhg), optimized heart rate (> 80) and normalized ionized calcium.

RV work is the function of the difference between the RA and PA mean pressure. As the difference between the two approaches zero, pulmonary blood flow is passive and RV failure is present. RV failure can occur with or without pulmonary hypertension.

Maximum inotropic support can be defined as any two or more (High et al., 1995) of the following combinations:

1. > 10 μg/kg/min of Dopamine2. > 10 μg/kg/min of Dobutamine3. > 0.2 μg/kg/min of Epinephrine4. > 0.75 μg/kg/min of Milrinone after

loading dose5. > 10 μg/kg/min of Nor–epinephrine

Indications for IAB insertion Large and prolonged inotrope infusion

will only tend to increase the workload of the ventricle. The IABP does the exact opposite, decreases the workload of the heart.

In cardiac surgery the IAB is indicated in:

Pre-op predictors:1. Grade 3 to 4 LV dysfunction or ejection fraction (EF) of

less than 0.30 (Dietl CA et al.,1996)2. Severe and/or multiple valvular disease with end stage

myocardial impairment not including aortic regurgitation3. Anticipated prolonged CPB time4. Coronary artery disease (CAD) only partially

correctible by grafting with concomitant LV dysfunction5. Persistent ST Changes before, during or after induction

of general anesthesia6. Coronary obstruction via clot or otherwise

Intra/post-op predictors:1. Pre/post CPB ischemia2. Incomplete repair or bypass3. Prolonged CPB time4. Large ventriculotomy or LV resection for

LV aneurysm repair.5. Particulate or air embolus in coronary

arteries.6. Persistent ST changes post CPB.

Clinical indications for the IAB1. Ventricular failure after myocardial infarction (MI) – (Barron et al.,

2001) or acute myocardial infarction (AMI). As in all other cases the IAB will would decrease afterload and increase coronary perfusion. Early insertion is recommended to ameliorate the threatening extension of MI.

2. Angina- chest pain is usually the initial stages of an MI and here again early insertion is recommended

3. Unstable angina with or without ST segment elevation4. Cardiomyopathy- In the majority of cases when cardiomyopathy

occurs the patient suffers from dilated cardiomyopathy and the IAB assist in raising mean blood pressure and reducing afterload. In a very few cases of initial stages of hypertrophic cardiomyopathy, where the ventricle tends to be a small volume ventricle (extremely thick myocardial wall), a sudden decrease in AEDP would result in insufficient volume left to fill the increased capacitance . This would actually result in a drop in MAP and systolic blood pressure, especially at an augmentation of 1:1

5. Acute mitral valve regurgitation (Abid et al.,2002) and/or stenosis with LV rupture

6. Aortic stenosis without aortic insufficiency (AI) or accompanied by mild AI

7. Congestive heart failure8. Intractable ventricular arrhythmias secondary to ischemia or

otherwise. In these cases IAB’s with fibre optic technology can be used to track rapid or irregular heart rhythms

9. Ventricular irritability10. Bridge to transplant or destination therapy11. Support in the catheterization laboratory (Stone GW et

al.,1997) for stenting or PTCA (Percutaneous Transluminal Coronary Angioplasty)

12. Myocardial ischemia or stunning of the heart- In this scenario much of the myocardium has suffered reversible damage and scarring has occurred only in a portion of the heart.

13. VSD (ventricular septal defect) - particularly post MI. This may be accompanied by papillary muscle rupture and acute mitral regurgitation

14. Support in the General OR for patients with ongoing heart disease or a history of heart disease

15. Transport (Sinclair TD & Verman HA,2009)for unstable patients16. Left main disease17. Cardiac contusion and/or trauma18. Septic shock or pre-shock syndrome19. Pulsatile flow (Onorati F et al.,2009)during CPB

Absolute contraindications for IAB insertion

1. Aortic regurgitation or insufficiency. In this physiology, raising AEDP would result in increase of regurgitant factor thereby increasing workload of the heart. In instances of mild AI a decision can be made if the benefits outweigh the risks.

2. Aortic dissection. Precludes IAB insertion. Attempting to Place an IAB in this situation may lead to placement in the false lumen or at the very least increase circulation into the false lumen.

Relative contraindications for IAB insertion

1. Severe peripheral vascular disease (PVD)2. Unresected thoracic, abdominal or thoraco-abdominal

aneurysm. An insertion of a mechanical device like the IAB and the counterpulsation of such a device against a diseased aortic wall may result in aortic dissection

3. Sepsis or infection4. Severe thrombocytopenia5. Coagulopathy or coagulopathic disorder6. End stage terminal disease7. End stage cardiomyopathy unless bridge to

transplant/destination therapy8. Severe atherosclerosis

Complications of IAB insertion

1. Loss of pedal pulses- Occurs in 15 – 25% of patients (funk M et al.,1989). Asymptomatic loss occurs transiently without resulting in limb ischemia and usually returns spontaneously or after IAB removal.

2. Limb ischemia- Occurs in 12 – 47% patients and is the most frequently reported complication (Curtis JJ et al., 1988). This may result from decreased cardiac output subsequent to heart failure, elevated SVR, low output syndrome, intimal injury or dissection, vessel catheter discrepancy, catheter occlusion or distal thrombo-embolism. Limb ischemia usually preceded by pain in the affected limb, change in pallor, cyanotic color changes, mottling, decreases in sensation, motor function loss, decrease in temperatures in extremity and loss of pedal pulses. Treatment is usually done by removal of IAB, thrombectomy, femoro-popiteal grafting and/or papaverine administration.

Pre-insertion predictors of risks associated with IAB insertion

1. Age- Increased age appears to be an increased risk. It is probably because of increased atherosclerosis associated with increased age (Goldberger 1986). There are other studies reporting inconsistent results.

2. Gender- women tend to have a greater risk of complication due to their smaller stature. This is probably due to the smaller lumen size of the femoral artery in women. The IAB catheter was expected to occupy greater lumen space in women thereby increasing the likelihood of ischemia and/or thrombus formation. Women are 1.6 to 1.8 more likely to experience limb ischemia/vascular complications than men (Skillman JJ et al, 1988).

3. Peripheral vascular disease (PVD) - These patients have higher likelihood for IAB complications due to insertion difficulties. Gottlieb suggested a three times likelihood for complications (Gottlieb SO et al.,1984), others have suggested less (Skillman JJ et al,.1988).

4. Type-II diabetes- Due to severe and diffuse atherosclerotic disease, higher incidence of hypertension and dampened resistance to bacterial contamination, diabetics tend to have a higher risk of complication post IAB. Some investigators found that diabetics (Wasfie T et al.,1988) had a 22% incidence of complications post IAB insertion as compared to 14% for non-diabetics. For insulin dependent diabetes a higher complication rate of 34% (Alderman JD et al., 1987) was suggested.

5. Duration of IAB therapy- Findings for the duration of safe use of IAB therapy remain inconclusive (Quaal 1993)

3. Thromboembolism- Percutaneous insertion/removal of IAB may result in dislodging of plaques or clots into the renal, splanchnic, hepatic or peripheral arteries. Clots can be seen while removing IAB catheters. Although Low molecular weight Dextran has been used, heparin is preferable as it can be reversed with protamine. Generally maintaining the aPTT 1.5 – 2 times normal is sufficient to prevent formation of thrombin, thereby protecting from subsequent embolism. It is also recommended to flush the IAB catheter with heparinized saline prior to insertion. The only incidence where this may not be necessary is when the patient is fully heparinized and on CPB. It is always a good practice even in this situation to flush with heparinized saline

4. Compartment syndrome- The legs and thighs of humans are made up of compartments containing bone, muscle, nerve tissue and blood vessels, surrounded by a fibrous membrane or fascia. Compartment syndrome is caused by an increased pressure within the non-distensible fascial space reducing capillary blood flow which in turn compromises enclosed fascial tissue. A fasciotomy can be performed to relieve the pressure.

5. Aortic Dissection- Is the most serious of complications from IAB insertion. Often unrecognized until removal or until IAB therapy is discontinued resulting in hemodynamic instability and death. Diagnosis is confirmed upon autopsy. Isner in 1980 found an incidence of aortic dissection in 36% of IAB patients (Isner JM et al,. 1980).With the advent of smaller French sizes in IAB catheters and better techniques and training, incidence of aortic dissection as a direct consequence of IAB insertion has drastically reduced .Symptoms of aortic dissection include severe back and/or abdominal pain, falling hematocrit and mediastinal enlargement. Aortic Dissection has to be treated aggressively and immediately by attempting to repair the dissection in the operating room.

6. Local injury- False aneurysm formation, hematoma, lymphedema, lymph fistula, wound hemorrhage, laceration of the femoral/iliac artery or the aorta are common complications and can be treated by evacuation and/or arterial repair.

7. Infective complication- Local wound infection is possible necessitating debridement, drainage, systemic antibiotics and rare cases removal. Sterility is very important while inserting the IAB whether in the peri-operative setting or otherwise. Generally the thigh is prepared by applying betadine prior to insertion and is covered by sterile dressing

after insertion and anchorage of the catheter by two sutures.

8. IAB rupture/entrapment- IAB rupture is rare but immediate removal/replacement is required. Rupture is more likely in women and patients with smaller size and usually occurs because of the constant contact between IAB membrane and atheroscleroticplaque on the femoral arterial/Aorta walls. The most common sign of IAB leak is blood in the drive line. IAB leak can cause either a helium embolus (in instants of patient hypotension where helium pressure within the IAB exceeds blood pressure in the aorta) or entrapment of the catheter. The leak can cause a clot to form within the catheter resulting in prevention of removal of the catheter at the time of IAB removal. This may necessitate a cut down removal of the IAB catheter.

9. Hematologic effects- Long term use of IAB has been associated with increased destruction of red cells and thrombocytopenia. The degree of decrease appears to be related to the duration of therapy (McCabe 1978)

10. Malposition of the IAB catheter- If positioned too high, the IAB may occlude blood flowing to the head vessels causing cerebral ischemia and or embolism. If positioned too low it may occlude the renal arteries thereby causing renal ischemia/perfusion and non-optimal coronary perfusion/afterload reduction.

Insertion techniques1. Cut down technique - used in patients

where femoral pulse is not palpable or where difficulty of insertion is anticipated as in patients suffering from PVD.

2. Percutaneous (Seldinger) technique3. Sheathless insertion reduces the length

of catheter indwelling in the tissue, thereby reducing limb ischemia.

4. Subclavian insertion-used in order to avoid an aorto-iliac stenosis

5. Brachial insertion-in patients with bilateral obstructive femoral and iliac disease and/or the patient has bilateral femoro-popliteal graft

6. Transthoracic Insertion-where the IAB insertion is precluded due to severe PVD or has been tried and failed percutaneously.

DESCRIPTION OF IABP1. The IABP has two parts:

(1) a large bore catheter with a long sausage-shaped balloon at the distal tip, and(2) a console containing a pump that inflates the balloon

2. balloon is made of a polyurethane membrane mounted on a vascular catheter

3. various catheter sizes —  usually 7.5 F with the balloon size chosen according to height (25–50 cc)

4. may be sheathed or sheathless5. some newer catheters have fibreoptics that assist pressure waveform

detection and timing6. helium is used to inflate the balloon as its low viscosity means there is

little turbulent flow so the balloon can inflate fast and deflate slowly. It is also relatively benign and eliminated quickly if there is a leak or the balloon ruptures

7. when inflated the balloon occludes 80-90% of the aorta

ANATOMY OF IABP

STEPS IN INSERTION OF IABP

1. Preparation patient positioned supine sterile technique (gowns, gloves, mask,

drapes, sterile prep solution) check for bleeding diathesis and other

complications

1. fully collapse balloon applying vacuum with 60 ml syringe; some kits require that the plunger is completely pulled out to achieve this

2. percutaneous Seldinger technique or surgical3. with or without sheath4. access femoral artery at 45 degrees with needle5. pass guidewire through needle and advance until

tip is is in thoracic aorta. Wire should pass very easily

6. pass sheath over wire in similar manner to insertion of PA catheter sheath (sheath is not always used)

7. 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

8. Balloon should be positioned so that the tip is about 1 cm distal to the origin of the left subclavian artery

9. watch for loss of right radial pulse (too high)10. Remove wire — return of blood via central lumen confirms

that the tip is not subintimal and has not caused a dissection11. Flush central lumen and connect to transducer to monitor

intra-aortic pressure (the outer lumen transmits helium gas to the balloon)

Confirmation of position

Arterial balloon waveform and pressures shown on console – check for normal morphology and appropriate timing of inflation and deflation in 1:2 augmentation ratio

Chest x-ray or fluoroscopy — confirms 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

or TOE — direct visualisation 1cm distal to the left subclavian artery

Triggering and timing

The balloon is timed to inflate and deflate in time with the cardiac cycle

Triggers include:— ECG (using the R wave to identify the onset of systole); if

in Sinus Rythem then deflation can be for a set time period, in AF the balloon deflates when R waves are sensed

— If paced then pacing spikes can be used to detect cardiac cycle events

— Arterial waveform (using the arterial upslope to designate systole)

— An internal trigger mode is available for asystolic arrested patients

Optimising performance correct position (balloon just distal to left subclavian artery, 2cm above

left main bronchus) optimal balloon volume balloon timing

– inflation at onset of diastole and deflation prior to beginning of systole (check in 1:2)

regular rhythm timing: 1:1 – inflation takes place at the dicrotic notch slope of augmented diastolic wave form is straight and parallel to the

systolic upstroke the augmented diastolic pressure should exceed non-augmented systolic

pressure the end-diastolic pressure at balloon deflation is lower than preceding

unassisted end-diastolic pressure by 15 mmHg the systolic pressure following a cycle of balloon inflation should be lower

than the previous unassisted systolic pressure by about 5 mmHg

Efficiency affected by

timing of inflation and deflation assist ratio heart rate (tachycardia > 130/min

reduces benefit of IABP) gas loss from balloon CI of 1.2-1.4 required for IABP to be

effective

timing of inflation and deflation

1. Early balloon inflation results in increased afterload

2. Late balloon inflation results in decreased diastolic augmentation

3. Early balloon deflation fails to decrease myocardial oxygen demand

4. Late balloon deflation increases afterload

5. Poor diastolic augmentation results in suboptimal coronary perfusion

EARLY INFLATION

DELAYED INFLATION

EARLY DEFLATION

LATE DEFLATION

Recent AdvancesProActive Counter Pulsation: ProActive Counter Pulsation is a new IABP system which incorporates

two new and unique technolo gies, the WAVE timing algorithm and the ability to monitor the Arterial Pressure (AP) signal from a Fibre Op tic Source (FOS) using the Fiber Optix IAB cathter. WAVE is an acronym for the Windkessel Aortic Valve Equation, which automatically sets inflation timing to occur precisely at the time of the Aortic Valve Closure (AVC).

The WAVE algorithm converts the arterial pressure (AP) waveform to understand the patient's aortic flow in the cardiac cycle. Aortic valve closure occurs at the lowest point in the flow wave, after peak flow occurs. Timing is set within each beat (intra-beat) for that specific beat, as it occurs. This results in highly accurate inflation timing, which is specific to that beat, for that patient at that moment in time.

For setting deflation timing, during an arrhythmia the IABP system automatically detects the irregular pattern and sets a conservative deflation to occur while assessing the balloon's performance in relation to the patient's cardiac cycle. The combination of the WAVE inflation timing with automatic 'R'-Wave deflation timing results in real time, beat to beat timing, which corresponds to the changes in the patient's cardiac cycle. The result is an improvement in the haemodynamic effect of IABP during periods of arrhythmia.

The Fiber Optix™ IAB catheter incorporates fibre optic sensor technology into the tip of the IAB catheter. Once zeroed prior to insertion, it does not require any further maintenance, such as re-zeroing or flush systems. It is immune to electrical interference, patient movement or activities that interfere with the quality of the arterial pressure signal, such as transport.

OTHER MECHANICAL SUPPORT DEVICES

Recent Trials IABP-SHOCK II trial (2012) showed no 30 day mortality benefit from IABP insertion for

cardiogenic shock following MI when early revascularisation was planned. A subsequent paper showed that there was no mortality benefit at 12 months either.

Ranucci et al (2013) found that in patients undergoing nonemergent coronary operations, with a stable hemodynamic profile and a left ventricular ejection fraction <35%, the preincision insertion of intra-aortic balloon pump does not result in a better outcome.

Sjauw et al (2009) systematic review found that only low quality observational studies support IABP use post-STEMI for thrombolysis, not for PCI. There was no support from randomised studies.

TACTICS trial (2005) was a small trial that showed no mortality benefit for IABP in addition to thrombolysis for STEMI, but there was a trend to improved Killip class in patients with severe heart failure/ cardiogenic shock

The Randomised IABP study group trial (1994) found that patients randomized to aortic counterpulsation following revascularisation for MI had significantly less reocclusion of the infarct-related artery during follow-up (median 5 days) compared with control patients (8% versus 21%, P < .03).

Despite the paucity of evidence for cardiogenic shock complicating MI, up until 2012, use of IABP for mechanical assistance had a class IC recommendation in the current European Society of Cardiology guidelines and a class IB recommendation in the American College of Cardiology/American Heart Association Guidelines.

Thank you