A previously healthy 58-year-old male was admitted to hospital following an OOH cardiac arrest. The initial cardiac rhythm was VF. He remained on the ‘shockable’ side of the ALS algorithm and was managed accordingly with defibrillation and intravenous adrenaline.  ROSC occurred after 28 minutes. A 12-lead ECG showed a STEMI in the antero-septal territories.

Coronary angiography showed a proximal occlusion of the left anterior descending artery through which a drug eluting stent was inserted. Despite this and adrenaline (10-20mcg) boluses, the patient remained persistently acidotic and hypotensive. A diagnosis of cardiogenic shock was made and an intra-aortic balloon pump (IABP) was inserted via the left common femoral artery with subsequent improvement in haemodynamic parameters. The patient was transferred to a cardiothoracic critical care.

Transthoracic echocardiography showed a globally hypokinetic left ventricle (LV) with an ejection fraction (EF) of approximately 20%. Within the first 6 hours, he developed runs of non-sustained VT and frequent ventricular ectopics, which interfered with IABP triggering causing worsening haemodynamic instability. Triggering was switched from ECG to arterial pressure. Electrolytes were supplemented and intravenous amiodarone was commenced to manage the dysrhythmias. Targeted temperature management to 36 degrees Celsius for 24 hours was initiated. Anticoagulation for IABP was commenced and peripheral pulses were regularly monitored.

His dysrhythmias resolved with subsequent improvement of IABP performance. On day 3, the IABP was weaned to 1:2 ratio for approximately 6 hours and removed. A tracheostomy was inserted on day 7 and the patient underwent long term respiratory wean and neurological rehabilitation.

Describe the indications, contraindications, complications and basic principles of intra-aortic balloon counterpulsation balloon pump.

Akshay Shah

What is cardiogenic shock?

Cardiogenic shock (CS) is a pathological state of end-organ hypoperfusion secondary to cardiac failure. It is characterized by a low cardiac output, hypotension unresponsive to fluid resuscitation, and elevated LV filling pressures resulting in oliguria, hyperlactaemia and altered mental status (1). MI with LV failure is the commonest cause of CS (1). Other causes include myocarditis, refractory artythmias and cardiomyopathies.

CS complicates 3-10% of all MIs (1,2). In-hospital mortality from CS has decreased from 44.6% to 33.6% over the past decade but still remains high.

Principles of IABP

Techniques of augmentation of coronary blood flow were first described in the 1950s (3) but the first percutaneous IABP insertion wasn’t until 1980 (4).

An IABP is a catheter-mounted, helium-filled polyethylene balloon that is inserted through the femoral artery into the descending aorta just below the left subclavian artery. Alternative routes include subclavian, axillary or brachial arteries. The low density of helium ensures a rapid transfer of gas from the console to the balloon and it can also easily be absorbed into the bloodstream in case of balloon rupture (5). The procedure is commonly performed in the cardiac catheterization laboratory under fluoroscopic guidance but can be inserted in the ICU for patients too unstable to transfer.

The primary aim of IABP is to improve myocardial oxygen supply (DO₂) and reduce oxygen demand (VO₂) through two mechanisms (6):

• Coronary perfusion pressure (CPP) is equal to aortic diastolic pressure (ADP) minus left ventricular end-diastolic pressure (LVEDP). Balloon inflation at the beginning of diastole augments ADP thereby increasing CPP and DO_2.
• Balloon deflation at the beginning of systole reduces afterload and can increase stroke volume by as much as 40%, decreasing VO₂.

ECG and arterial waveform are commonly used triggers for balloon inflation and deflation. The balloon inflates at the onset of diastole, corresponding to the middle of the T-wave, and deflates at the onset of LV systole, which corresponds to the peak of the R-wave. Normally inflation should be at the dichrotic notch (aortic valve closure) and should result in a diastolic augmented BP that is higher than unassisted systolic BP. Deflation is timed to allow assisted aortic EDP to be 10-15 mmHg less than unassisted diastolic pressure demonstrating a reduced afterload. Depending on the patient’s clinical status, the IABP is programmed to assist every beat (1:1) or less often (1:2, 1:3. 1:4).

 

Indications and contraindications 

Indications:

• Cardiogenic shock unresponsive to inotropic support
• Acute severe mitral regurgitation or ventricular septal defect
• Refractory unstable angina
• Ventricular arrhythmias refractory to medical treatments
• Weaning from cardiopulmonary bypass
• Bridging for ventricular assist device (VAD) or cardiac transplantation

Contra-indications:

Absolute	Relative
Aortic dissection Aortic regurgitation – diastolic augmentation will worsen regurgitant fraction No anticipated cardiac recovery	Peripheral vascular disease Abdominal aortic aneurysm Uncontrolled sepsis

Care of the patient with an IABP 

The following must be considered:

• Appropriate timing and triggering for optimal IABP functioning
• Regular evaluation of myocardial function and end-organ perfusion for consideration of weaning/removal
• Anticoagulation
• Complications

Significant arrhythmias are common post-MI, as highlighted in this case, and arterial pressure triggers may be best but all triggering modes are inefficient in such circumstances. Other indications for arterial pressure triggers include pacing-dependent patients, diathermy interferences or very low ECG signals. Aggressive management of dysrhythmias is paramount as suboptimal inflation can result in haemodynamic instability.

Balloon volume loss alarms, decreased augmentation and blood in the catheter are suggestive of balloon puncture/tear and the catheter needs to be replaced (7).

Indications for weaning/removal include clinical improvement, reduction of pharmacological support and development of fatal complications. A gradual reduction in the inflation ratio from 1:1 to 1:2 to 1:3 occurs over 3 to 6 hours. Accepted practice involves stopping heparin 2-4 hours prior to removal, correction of any coagulopathy, and removal is normally carried out by an experienced cardiologist / cardiac surgeon. Firm pressure is applied for at least 45 minutes and many institutions keep patients supine for an additional six hours.

Heparinisation is often required for IABP to avoid arterial thromboembolism. Our institution aims for an APTT of 45 – 70 seconds. IABPs should never be turned off in situ except for when the patient is anticoagulated due to the risk of thrombus formation on the balloon.

Complications

The incidence of major complications such as IABP-related mortality, sepsis, severe bleeding and critical limb ischaemia ranges from 7-20% (8). Compartment syndrome has been reported (9).

Haemolysis and thrombocytopenia are common and result from mechanical damage to red cells, platelets and/or heparin administration. Mechanical complications include balloon rupture, balloon entrapment, and malpositioning, which can result in renal or cerebral compromise.

Risk factors for developing complications include duration of IABP support, pre-existing peripheral vascular disease, diabetes mellitus and female gender. Prospective studies have shown that women with diabetes mellitus and peripheral vascular disease have an 83% chance of developing major IABP-related complications (10).

What is the evidence for IABP use?

The IABP-SHOCK II trial was a large RCT involving 600 patients comparing the use of IABP to no IABP in patients with CS complicated acute MI. The investigators found no difference in the primary outcome – 30-day mortality, and a range of secondary outcomes such as time to haemodynamic stabilization, ICU length of stay, dose and duration of catecholamine therapy and renal function, between both groups. The results of this study were included in an updated Cochrane meta-analysis, which confirmed no survival benefit at 30 days (Hazard Ratio 0.95, 95% CI 0.76 to 1.19) (11).

12 month follow-up data of survivors also revealed no survival benefit for patients in the IABP group. In addition, there was also no difference in rates of recurrent revascularization, stroke or quality of life measures at 12 months (12). The findings of this trial and updated meta-analysis endorse the downgraded recommendations of IABP use from the American Heart Association and European Society of Cardiology (ESC) from level IB and IC (should be used) to IIB and IIC (can/may be used) respectively (13, 14).

Alternative devices

If temporary mechanical support is needed, ESC guidelines also recommend the use of a left VAD or ECMO without any preference (IIa/C recommendation) (14). A meta-analysis demonstrated superior haemodynamic support with LAVD than with IABP, no difference in mortality and incidence of lower-limb ischaemia, but significantly increased bleeding with LVAD (15).

The Impella 2.5 device is a relatively new catheter-based, axial flow pump system that can be inserted percutaneously and generate a maximal flow of 2.5 l.min^-1 from the left ventricle into the ascending aorta which has been shown to be equally safe and provide superior haemodynamic support compared to IABP (16, 17). However, none of the trials so far have been powered to demonstrate an outcome benefit.

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Learning points

• Mortality from cardiogenic shock remains high.
• IABP treatment aims to increase myocardial DO₂ and reduce VO₂.
• Complication rate associated with IABP is high in patients who are female with a history of diabetes and peripheral vascular disease.
• Important considerations in patients with IABP include optimal timing of inflation and deflation, adequate anticoagulation and regular assessment for weaning/removal.
• Whilst all device therapy has been shown to improve haemodynamics, no trial so far has demonstrated an outcome benefit. Patient selection and risk stratification is therefore crucial.

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References

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2. Kolte D, Khera S, Aronow WS et al. Trends in incidence, management and outcomes of cardiogenic shock complicating ST-elevation myocardial infarction in the United States. J Am Heart Assoc 2014; 13: e000590
3. Harken DE. The surgical treatment of acquired valvular disease. Circulation 1958; 18: 1-6.
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6. Barnard M, Martin B. Oxford Handbook of Cardiac Anaesthesia. 1^st ed. OUP, Oxford.
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13. O’Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013; 127(4): e362-425.
14. Windecker S, Kolh P, Alfonso F et al. 2014 ESC/EACTS Guideline on myocardial revascularization: The Task Force on Myocardial Revascularization of the European Society of Cardiology and the European Association for Cardiothoracic Surgery. Eur Heart J 2014; 35: 2541-2619.
15. Cheng JM, den Uil CA, Hoeks SE, et al. Percutaneous left ventricular assist devices vs. intra-aortic balloon pump counterpulsation for treatment of cardiogenic shock: a meta-analysis of controlled trials. Eur Heart  J 2009; 30: 2102-2108.
16. Seyfarth M, Sibbing D, Bauer I et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol 2008; 52: 1584-8
17. O’Neill WW, Kleiman NS, Moses J et al. A Prospective Randomized Clinical Trial of Hemodynamic Support with Impella 2.5^TM versus Intra-Aortic Balloon Pump in Patients Undergoing High-Risk Percutaneous Coronary Intervention: the PROTECT II Stud. Circulation 2012; 126: 1717-27