Cardiogenic Shock: One Organ but Many Options for Mechanical Circulatory Support

Young May Cha, MD

On May 18, Marc Dickstein, MD, professor of anesthesiology at Columbia University Medical Center, moderated an educational and interactive symposium on “Advanced Hemodynamics of Cardiogenic Shock, Pharmacologic and Mechanical Circulatory Support” at the 2024 Annual Meeting, presented by IARS and SOCCA. Using an example patient in postcardiotomy shock, attendees were welcome to follow along in the simulator to see how the interventions of an intra-aortic balloon pump (IABP), extracorporeal membrane oxygenation (ECMO), and a left ventricular assist device (LVAD) affect the physiology of the patient in the Harvi Academy Simulator (Use code BPV-OOM-HDQ under “Teach” until 5/25/24).

Robert N. Sladen, MBChB, MRCP(UK), FRCPC, FCCM, Allen Hyman Professor Emeritus of Critical Care Anesthesiology at Columbia University Medical Center, kicked off the session with an overview of the myocardial pressures most at risk for ischemia. By inflating during diastole, an IABP can increase the diastolic pressure-time index (DPTI), which is the product of coronary perfusion pressure and diastolic time and is a measure of coronary blood supply. The balloon inflates after closure of the aortic valve to augment diastolic pressures and deflates to lower end-diastolic pressure. This process lowers systolic pressure immediately after deflation to a pressure that is lower than one without balloon deflation, demonstrating a decrease in systolic afterload.

One concern with using ECMO is that the femoral arterial ECMO flow can potentially increase the afterload to an already decompensated heart, and so IABPs can help with decreasing this systemic afterload. If the cardiac output increases by over 0.5 L/min, that is a sign of reversal of acute myocardial ischemia. Even if the CO output does not increase by that amount, there will still be benefit due to the unloading of the left ventricle. Additionally, by raising diastolic augmentation pressures to 100-110 mmHg, one can then tolerate lower diastolic blood pressures and mean arterial pressures (MAP). With placement in the subclavian artery, there is even the potential for a patient to be ambulating with an IABP. Because aortic valve closure is critical to device functioning, IABPs cannot be used with severe aortic valvular disease or aortic regurgitation.

Vivek Moitra, MD, Allen Hyman Professor of Critical Care Anesthesiology at Columbia University Medical Center, then continued with a review of ECMO physiology. VA-ECMO can solve the problem of heart and lung failure but can threaten the myocardium and is best suited for a left ventricle that has the potential for unloading itself. With centrally accessed ECMO, the femoral artery cannula provides flow back to the heart to increase the MAP. In turn, the pulse pressure narrows, and stroke volume can decrease. The increase in MAP also comes at the cost of increased afterload, which can be detrimental to a left ventricle that is already potentially enlarging and compromised. One option to help unload a large failing ventricle is to use an Impella device to remove blood from the left ventricle and inject it into the aorta to help offload the left ventricle. These physiologic changes can be seen in the simulator as initiation of ECMO lowers the end-diastolic pressure, distends the left ventricle, and lowers stroke volume.

Lauren Sutherland, MD, assistant professor of anesthesiology at Columbia University, explained how an LVAD can be used in cardiogenic shock. An LVAD unloads the left ventricle by decreasing left ventricular volume, pressure, and work. It can be used for temporary or long-term cardiac support. Increasing the pump speed will increase the flow and decrease the work done by the native left ventricle. This will also decrease pulsatility and decrease the size of the left ventricular chamber. The caution with increasing pump speed is that there can be a “suction event” if the left ventricle becomes overly decompressed. LVADs can temporarily slow during such an event to allow ventricular filling, but this pause can result in hypotension and arrhythmia. The other concern is that, though the LVAD can help support left ventricular output, it does so at the expense of the right ventricle. The LVAD shifts the interventricular septum to the left, which alters the geometry of the right ventricle and can decrease its function. The improved cardiac output with an LVAD also brings more preload back to the right ventricle and can cause right ventricular strain. Thus, it is important to optimize right ventricular geometry and ideally titrate LVAD speed under echo guidance. Other adjunctive therapies to consider are to decrease right ventricular afterload with pulmonary vasodilators, augment ventricular contractility with inotropes, or place a right-sided assistive device for biventricular support.

There are many configurations of external support devices, internal devices, and ECMO that can be combined to best optimize cardiac function and provide support for patients in postcardiotomy shock. Dr. Dickstein demonstrated how these devices can be added in the simulator so the user can visualize the physiologic effects of these strategies.