Extracorporeal life support is a treatment modality that provides prolonged blood circulation, gas exchange and can substitute functions of heart and lungs to provide urgent cardio-respiratory stabilization in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Generally, the therapy targets blood pressure, volume status, and end-organs perfusion. As there are significant differences in hemodynamic efficacy among different percutaneous circulatory support systems, it should be carefully considered when selecting the most appropriate circulatory support for specific medical conditions in individual patients. Despite severe metabolic and hemodynamic deterioration during prolonged cardiac arrest, venoarterial extracorporeal membrane oxygenation (VA ECMO) can rapidly revert otherwise fatal prognosis, thus carrying a potential for improvement in survival rate, which can be even improved by introduction of mild therapeutic hypothermia. In order to allow a rapid transfer of knowledge to clinical medicine two porcine models were developed for studying efficiency of the VA ECMO in treatments of acute cardiogenic shock and progressive chronic heart failure. These models allowed also an intensive research of adverse events accompanying a clinical use of VA ECMO and their possible compensations. The results indicated that in order to weaken the negative effects of increased afterload on the left ventricular function the optimal VA ECMO flow in cardiogenic shock should be as low as possible to allow adequate tissue perfusion. The left ventricle can be also unloaded by an ECG-synchronized pulsatile flow if using a novel pulsatile ECMO system. Thus, pulsatility of VA ECMO flow may improve coronary perfusion even under conditions of high ECMO blood flows. And last but not least, also the percutaneous balloon atrial septostomy is a very perspective method how to passively decompress overloaded left heart.
Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is widely used in the treatment of patients experiencing cardiogenic shock (CS). However, increased VA-ECMO blood flow (EBF) may significantly impair left ventricular (LV) performance. The objective of the present study was to assess the effect of VA-ECMO on LV function in acute CS with concomitant severe aortic stenosis (AS) or mitral regurgitation (MR) in a porcine model. Eight female swine (45 kg) underwent VA-ECMO implantation under general anaesthesia and mechanical ventilation. Acute CS was induced by global myocardial hypoxia. Subsequently, severe AS was simulated by obstruction of the aortic valve, while severe MR was induced by mechanical destruction of the mitral valve. Haemodynamic and LV performance variables were measured at different rates of EBF rates (ranging from 1 to 4 L/min), using arterial and venous catheters, a pulmonary artery catheter, and LV pressure-volume catheter. Data are expressed as median (interquartile range). Myocardial hypoxia resulted in declines in cardiac output to 2.7 (1.9-3.1) L/min and LV ejection fraction to 15.2% (10.5-19.3%). In severe AS, increasing EBF from 1 to 4 L/min was associated with a significant elevation in mean arterial pressure (MAP), from 33.5 (24.2-34.9) to 56.0 (51.9-73.3) mmHg (P ˂ 0.01). However, LV volumes (end-diastolic, end-systolic, stroke) remained unchanged, and LV end-diastolic pressure (LVEDP) significantly decreased from 24.9 (21.2-40.0) to 19.1 (15.2-29.0) mmHg (P ˂ 0.01). In severe MR, increasing EBF resulted in a significant elevation in MAP from 49.0 (28.0-53.4) to 72.5 (51.4-77.1) mmHg (P ˂ 0.01); LV volumes remained stable and LVEDP increased from 17.1 (13.7-19.1) to 20.8 (16.3-25.6) mmHg (P ˂ 0.01). Results of this study indicate that the presence of valvular heart disease may alleviate negative effect of VA-ECMO on LV performance in CS. Severe AS fully protected against LV overload, and partial protection was also detected with severe MR, although at the cost of increased LVEDP and, thus, higher risk for pulmonary oedema.
- MeSH
- Aortic Valve Stenosis * MeSH
- Ventricular Function, Left physiology MeSH
- Hypoxia MeSH
- Shock, Cardiogenic therapy MeSH
- Extracorporeal Membrane Oxygenation * methods MeSH
- Mitral Valve Insufficiency * therapy MeSH
- Swine MeSH
- Animals MeSH
- Check Tag
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Background: Arteriovenous fistulas (AVF) represent a low resistant circuit. It is known that their opening leads to decreased systemic vascular resistance, increased cardiac output and other hemodynamic changes. Possible competition of AVF and perfusion of other organs has been observed before, however the specific impact of AVF has not been elucidated yet. Previous animal models studied long-term changes associated with a surgically created high flow AVF. The aim of this study was to create a simple AVF model for the analysis of acute hemodynamic changes. Methods: Domestic female pigs weighing 62.6 ± 5.2 kg were used. All the experiments were held under general anesthesia. The AVF was created using high-diameter ECMO cannulas inserted into femoral artery and vein. Continuous hemodynamic monitoring was performed throughout the protocol. Near-infrared spectroscopy sensors, flow probes and flow wires were inserted to study brain and heart perfusion. Results: AVF blood flow was 2.1 ± 0.5 L/min, which represented around 23% of cardiac output. We observed increase in cardiac output (from 7.02 ± 2.35 L/min to 9.19 ± 2.99 L/min, p = 0.0001) driven dominantly by increased heart rate, increased pulmonary artery pressure, and associated right ventricular work. Coronary artery flow velocity rose. On the contrary, carotid artery flow and brain and muscle tissue oxygenation measured by NIRS decreased significantly. Conclusions: Our new non-surgical AVF model is reproducible and demonstrated an acute decrease of brain and muscle perfusion.
- Keywords
- animal model, arteriovenous fistula, cerebral oxygenation, coronary artery flow, hyperkinetic circulation, tissue perfusion,
- Publication type
- Journal Article MeSH
The main reason for the emergency implantation of venoarterial extracorporeal membrane oxygenation (VA-ECMO) is the restoration of adequate systemic perfusion, while protecting the failing heart and promoting myocardial recovery are equally important goals. Following initial haemodynamic stabilization and often the urgent revascularization of the culprit lesion, the clinical focus is then directed towards the most efficient strategy for cardioprotection. Frequent echocardiography measurements may help to estimate the degree of unwanted left ventricular (LV) overloading during VA-ECMO. Additionally, the estimation of high LV filling pressures by Doppler echocardiography or their (in-)direct measurement using a dedicated surgical left atrial pressure line and conventional pulmonary artery catheter in a wedge position or a pigtail catheter in the left ventricle can be performed. Mechanical overload of the left ventricle is the major adverse effect and an obvious mechanistic and prognostic challenge of contemporary ECMO care. Many efforts are under way to overcome this phenomenon by LV unloading, which was effectively achieved by the current combined approach using an axial decompression device, while novel technical developments and approaches are tested and urgently anticipated. The aim of this report is to introduce in depth pathophysiological background, current concepts, and future perspectives in LV unloading strategies.
- Keywords
- Cardiac arrest, Cardiogenic shock, Cardioprotection, Oxygenation, Unloading, Venoarterial ECMO,
- Publication type
- Journal Article MeSH
Extracorporeal life support (ECLS) is a treatment modality that provides prolonged blood circulation, gas exchange and can partially support or fully substitute functions of heart and lungs in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Due to high-volume bypass, the extracorporeal flow is interacting with native cardiac output. The pathophysiology of circulation and ECLS support reveals significant effects on arterial pressure waveforms, cardiac hemodynamics, and myocardial perfusion. Moreover, it is still subject of research, whether increasing stroke work caused by the extracorporeal flow is accompanied by adequate myocardial oxygen supply. The left ventricular (LV) pressure-volume mechanics are reflecting perfusion and loading conditions and these changes are dependent on the degree of the extracorporeal blood flow. By increasing the afterload, artificial circulation puts higher demands on heart work with increasing myocardial oxygen consumption. Further, this can lead to LV distention, pulmonary edema, and progression of heart failure. Multiple methods of LV decompression (atrial septostomy, active venting, intra-aortic balloon pump, pulsatility of flow) have been suggested to relieve LV overload but the main risk factors still remain unclear. In this context, it has been recommended to keep the rate of circulatory support as low as possible. Also, utilization of detailed hemodynamic monitoring has been suggested in order to avoid possible harm from excessive extracorporeal flow.
BACKGROUND: Venoarterial extracorporeal membrane oxygenation (VA ECMO) is widely used in the treatment of circulatory failure, but repeatedly, its negative effects on the left ventricle (LV) have been observed. The purpose of this study is to assess the influence of increasing extracorporeal blood flow (EBF) on LV performance during VA ECMO therapy of decompensated chronic heart failure. METHODS: A porcine model of low-output chronic heart failure was developed by long-term fast cardiac pacing. Subsequently, under total anesthesia and artificial ventilation, VA ECMO was introduced to a total of five swine with profound signs of chronic cardiac decompensation. LV performance and organ specific parameters were recorded at different levels of EBF using a pulmonary artery catheter, a pressure-volume loop catheter positioned in the LV, and arterial flow probes on systemic arteries. RESULTS: Tachycardia-induced cardiomyopathy led to decompensated chronic heart failure with mean cardiac output of 2.9 ± 0.4 L/min, severe LV dilation, and systemic hypoperfusion. By increasing the EBF from minimal flow to 5 L/min, we observed a gradual increase of LV peak pressure from 49 ± 15 to 73 ± 11 mmHg (P = 0.001) and an improvement in organ perfusion. On the other hand, cardiac performance parameters revealed higher demands put on LV function: LV end-diastolic pressure increased from 7 ± 2 to 15 ± 3 mmHg, end-diastolic volume increased from 189 ± 26 to 218 ± 30 mL, end-systolic volume increased from 139 ± 17 to 167 ± 15 mL (all P < 0.001), and stroke work increased from 1434 ± 941 to 1892 ± 1036 mmHg*mL (P < 0.05). LV ejection fraction and isovolumetric contractility index did not change significantly. CONCLUSIONS: In decompensated chronic heart failure, excessive VA ECMO flow increases demands and has negative effects on the workload of LV. To protect the myocardium from harm, VA ECMO flow should be adjusted with respect to not only systemic perfusion, but also to LV parameters.
- Keywords
- Artificial cardiac pacing, Extracorporeal membrane oxygenation, Heart failure, Heart ventricles, Hemodynamics, Swine,
- MeSH
- Ventricular Function, Left MeSH
- Hemodynamics MeSH
- Extracorporeal Membrane Oxygenation * MeSH
- Myocardium MeSH
- Swine MeSH
- Heart Failure * therapy MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
