Cardiogenic shock

Incremental Cardiac Output in Cardiogenic Shock with Percutaneous Hemodynamic Support Device

Oomer Aziem, DO, David H. Hsi, MD, and Jon C. George, MD, Department of Cardiology, Deborah Heart & Lung Center, Browns Mills, New Jersey

Oomer Aziem, DO, David H. Hsi, MD, and Jon C. George, MD, Department of Cardiology, Deborah Heart & Lung Center, Browns Mills, New Jersey

 Case report

A 61-year-old female presented with chest pain radiating to her left shoulder and arm for approximately 2 hours, associated with progressive shortness of breath. Physical examination on presentation was remarkable for tachycardia with heart rate of 96 beats per minute, hypotensive with blood pressure of 75/42 mmHg, and hypoxic with oxygen saturation of 88% on a non-rebreather mask. Electrocardiogram revealed sinus rhythm, ST-segment depressions in V3-V5 and diffuse T-wave inversions.

She was emergently intubated and brought to the cardiac catheterization laboratory in the setting of cardiogenic shock. Coronary angiography was normal (Figure 1). However, left ventriculogram demonstrated severe systolic dysfunction and wall motion abnormalities (basal hyperkinesis and apical akinesis) with estimated left ventricular ejection fraction (LVEF) of 20%, consistent with acute stress-induced cardiomyopathy (Figure 2).

An intra-aortic balloon pump (IABP) was inserted for hemodynamic support in the setting of cardiogenic shock. Despite IABP support, the patient progressed with worsening hypotension within 12 hours. A subsequent ECG revealed widening of the QRS complex and QT prolongation. Intravenous neosynephrine and dopamine infusions were initiated and titrated to maximal doses. A bedside echocardiogram revealed a LV outflow tract (LVOT) resting gradient of 24 mmHg, systolic anterior motion of the mitral valve leaflet, and severe LV systolic dysfunction. Hemodynamic data with bedside right heart catheterization showed elevated mean right atrial pressure of 20 mmHg, pulmonary arterial systolic pressure of 48 mmHg, and pulmonary capillary wedge pressure of 27 mmHg, consistent with low cardiac output.  

The patient was taken back to the catheterization laboratory to upgrade the IABP with a percutaneous left ventricular assist device (pLVAD; Impella Recover LP 2.5, Abiomed) (Figure 3) via left femoral artery access. Cardiac output was measured using the Fick equation at 3.84 L/minute at baseline (without hemodynamic support), 4.26 L/min with IABP, and 5.48 L/min with the pLVAD at maximal rate.   

The patient had significant improvement of blood pressure (systolic > 100 mmHg) with pLVAD support. However, she required transient hemodialysis due to development of acute kidney injury in the setting of prolonged cardiogenic shock and likely, renal hypoperfusion. By hospital day 14, the patient was weaned off all intravenous pressors and pLVAD support. LVEF by echocardiogram recovered to normal and she was extubated on hospital day 19 with full neurological recovery. 

Discussion

Stress-induced cardiomyopathy (Takotsubo syndrome) has been extensively reported in the United States since 2005, after the initial experience in Japan.1 Most patients are post-menopausal women, who present with severe LV dysfunction and spontaneous recovery in 3 days to 4 weeks.2 The exaggerated sympathetic stimulation is thought to be the primary pathologic mechanism. Up to 37% of patients may have hemodynamic compromise and require vasopressor agents and IABP counterpulsation.3

However, a recent clinical trial evaluating the utility of IABP in patients with acute myocardial infarction (MI) complicated by cardiogenic shock, who underwent coronary revascularization showed no statistical difference between the IABP and control arms.4 Although the reason for this lack of benefit is likely multifactorial, the authors did postulate that the smaller degree of hemodynamic benefit provided by IABP compared to newer technologies may be contributory.

The newer Mega 50 cc balloon (Maquet Cardiovascular), when compared to the traditional 40 cc IABP catheter, showed on average 58% more systolic unloading in bench testing and successful clinical results.5 Initial experiences with pLVADs such as Impella 2.5 and 5.0 have further demonstrated improved outcomes in patients with profound cardiogenic shock and acute MI.6 The investigators from the ISAR-SHOCK trial compared Impella LP 2.5 versus IABP in patients with acute MI: the cardiac index was significantly increased in the Impella LP 2.5 group compared with IABP patients, but 30-day mortality was 46% in both groups.7

Although the use of such devices in cardiogenic shock has been given a Class IB recommendation in the current guidelines8, the incremental support provided by pLVAD over IABP in a select patient has not been objectively compared. Our patient had paradoxical decrease in systolic blood pressure and cardiac output after IABP therapy, but responded favorably to pLVAD support using the Impella LP 2.5. Measured cardiac output using the Fick equation improved 11% from baseline with IABP support, and an additional 29% (cumulative 43%) with a pLVAD. The patient’s cardiac output and perfusion to vital organs was maintained for 2 weeks, until eventual normalization of LV systolic function. Our patient made a full cardiac, neurological, and renal recovery, and was off inotropic agents, mechanical ventilation and hemodialysis after prolonged pLVAD support. We believe that the use of pLVADs can play unique roles in patients with refractory cardiogenic shock after IABP use, in further augmenting cardiac output without aggressive afterload reduction in a step-wise fashion for incremental hemodynamic support. 

Disclosure: Dr. George reports he is a consultant for Abiomed. Dr. Aziem and Dr. Hsi report no conflicts of interest regarding the content herein. The authors can be contacted via Dr. Jon George at georgej@deborah.org.

References

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