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Department of Anesthesiology and Perioperative Medicine, University of Rochester School of Medicine & Dentistry, Rochester, NYDepartment of Cardiology, University of Rochester School of Medicine & Dentistry, Rochester, NYDepartments of Medicine, University of Rochester School of Medicine & Dentistry, Rochester, NY
LEFT VENTRICULAR assist devices (LVAD) are physiologically unique due to the emptying of the left ventricle (LV) during diastole and systole regardless of aortic valve opening. Echocardiography is, therefore, essential in the management and optimization of patients with LVAD support who are in shock states.
A well-described and common cause of low flow in LVAD patients is left ventricular suction events. This occurs when the pump flow exceeds mitral inflow, causing a reduction in the size of the LV cavity to a point that the LVAD inflow cannula comes into contact with a ventricular wall, resulting in decreased inflow, ectopy, or sustained ventricular arrhythmias.
During these episodes, hypotension, low pulsatility index (PI), and low-flow alarms on the LVAD console are common. Treatment involves temporarily lowering the LVAD speed, and other interventions that increase LV filling and relieve the suction on the LV wall.
Similarly, in the presence of an LVAD, if LV underfilling is severe enough that systolic pressure generated by the LV does not exceed left atrial (LA) pressure, there will be continuous or near-continuous flow from LA to LV during systole. As a result, a continuously open mitral valve is observed throughout the cardiac cycle. To the authors’ knowledge, this has been described only once before in the literature as a case report.
The authors present 2 additional LVAD cases during which echocardiographic evaluation revealed this unique physiologic state of systolic nonclosure of the mitral valve, resulting in its pan-cardiac cycle opening. Case 1 is a patient with LVAD thoracotomy site wound infection, resulting in septic shock in the operating room during incision and drainage, during which transesophageal echocardiography was used intraoperatively. Case 2 is a patient with combined hemorrhagic and septic shock, from tracheostomy stoma bleeding and pneumonia, in the intensive care unit,with transthoracic echocardiography used at the bedside. In both cases, echocardiography proved essential in hemodynamic management and LVAD optimization, while identifying systolic nonclosure of the mitral valve during shock states.
All images were obtained using the GE Healthcare Vivid E95 system. Phone consent was obtained from the patients or their surrogate for the patient data and echocardiogram images presented here.
A 52-year-old man with type 2 diabetes, hypertension, tobacco use, and ischemic cardiomyopathy status post-HeartMate 3 implantation 18 months prior, was admitted from a clinic for purulent drainage and wound dehiscence at his LVAD thoracotomy site. He was started on emprical intravenous vancomycin and piperacillin-tazobactam, and presented to the operating room for incision and drainage of his infected wound. His LVAD setting before the surgery was 5,600 revolutions per minute (rpm), with a flow of 4.5 L/min and a PI of 4.6. General anesthesia was induced with etomidate, lidocaine, and succinylcholine. He was intubated uneventfully and a postinduction arterial line, central line, and transesophageal echocardiography (TEE) probe were placed without complication.
The patient remained hemodynamically stable, with a mean arterial pressure >70 mmHg until incision. As the purulent pocket was opened and debrided, the patient's blood pressure started to decrease to a mean arterial pressure of 50 mmHg. The PI on the LVAD reduced to 2.8, with flow of 4.8 L/min. The patient remained in sinus rhythm. The TEE imaging at this time demonstrated the mitral leaflets to be open throughout the entire cardiac cycle, along with a dilated right ventricle with moderate dysfunction, and left ventricular end-diastolic diameter (LVEDD) of 1.7 cm (Fig 1A and 1B and Video 1, A and B). Based on these findings, the LVAD speed was decreased from 5,600 to 5,000 rpm. The patient was treated with volume resuscitation, and norepinephrine and epinephrine infusions were initiated. After hemodynamic stabilization, TEE imaging demonstrated normalization of mitral leaflet motion and restoration of systolic coaptation of the valve (Fig 1C and 1D ). The LVEDD had normalized to 4 cm. Both inflow and outflow cannulae were visualized and well-positioned. The planned procedure was completed without any further complications. At the end of the procedure, the LVAD speed was increased to 5,200 rpm, with flow of 4.3 L/min and PI of 2.5. The patient remained intubated and was transferred to the cardiac intensive care unit for ongoing treatment of septic shock. Vasopressors were weaned over the next several hours, and the patient was extubated the next day. He was transferred to the ward on postoperative day 2, and eventually discharged home on postoperative day 5. The wound cultures returned positive for staphylococcus capitis, and the patient was transitioned from intravenous antibiotics to oral cephalexin at discharge.
A 58-year-old man with chronic obstructive pulmonary disease, right ventricular dysfunction, and nonischemic cardiomyopathy who underwent HeartMate 3 LVAD implant 6 months prior, with recent admission for respiratory failure resulting in tracheostomy 2 months ago, now presented from home with worsening shortness of breath and lethargy over a few days.
On admission, he was found to have pneumonia, with hypercapnic and hypoxemic respiratory failure. The cuffless Jackson size 4 Shiley tracheostomy tube was upsized to a cuffed Jackson size 6 Shiley to enable ventilatory support, but ultimately led to bleeding from the stoma. His initial bloodwork revealed respiratory acidosis and leukocytosis. Also notable was a supratherapeutic international normalized ratio (INR) of 19, likely due to active infection, as well as continued warfarin use despite poor oral intake in the days preceding his admission. With initiation of positive-pressure ventilation, ongoing bleeding from tracheostomy site and developing septic shock, he became progressively more hypotensive. The PI declined from >3 on admission to <2, with intermittent low-flow alarms on the LVAD console. His electrocardiogram was unchanged from his baseline paced rhythm. He was resuscitated with intravenous fluids and started on a norepinephrine infusion, in the setting of suspected combined hemorrhagic and septic shock secondary to pneumonia and tracheostomy site bleeding. His INR also was corrected with 4-factor prothrombin complex concentrate and intravenous vitamin K for ongoing bleeding.
A transthoracic echocardiogram was obtained to aid clinical management of shock. The study demonstrated a dilated hypokinetic right ventricle, with septal shift to the left, a small LV cavity, and a systolic nonclosure of the mitral valve throughout the cardiac cycle (Fig 2A and 2B and Video 2, A and B). Based on these findings, the LVAD speed was reduced from a baseline of 5,800 to 5,400 rpm, additional fluid bolus was administered, and an epinephrine infusion was started for right-heart support. These interventions normalized LVEDD and the functioning of the mitral valve (Fig 2A and 2B ). The low-flow alarms resolved, and PI improved to 3.2 as well. Over the next 48 hours, his vasopressors and inotropes were weaned. The LVAD speed was increased to 5,700 rpm based on a repeat ramp echocardiography study 2 days after initial examination. The patient completed a course of piperacillin/tazobactam for pneumonia, was weaned from the ventilator, and was transferred to the ward 10 days after admission. He had a complicated hospital course requiring readmission to the intensive care unit a few days later for hypercarbic respiratory failure, and was weaned successfully from the ventilator over a course of 3 weeks. During this time, diuretics were continued and he returned to his dry weight. He ultimately was discharged home 8 weeks after initial admission.
All heart valves open and close based on the pressure differentials across them throughout the cardiac cycle. Mitral valve motion serves as a continuous differential pressure monitor between the LA and the LV. The goal of diastolic filling is to replace the stroke volume. Given that LVAD flow is continuous, diastolic filling must be sufficient not only for diastolic flow through the pump, but also allow for sufficient end-diastolic volume for a ventricular pressure increase with systolic contraction. In normal mitral valve physiology, it is this rapid pressure increase in the LV that closes the mitral valve, terminating diastole.
Therefore, one of the signs of insufficient diastolic filling in a LVAD-supported patient is mitral valve closure for less than the full duration of the ventricular systole. If ventricular filling becomes even more impaired, the LV systolic pressure will remain lower than LA pressure, thereby circumventing mitral valve leaflet closure and resulting in a mitral valve that remains open throughout systole.
Given the paucity of data on this echocardiographic finding, with only 1 prior case report in 2016 describing the pan-cardiac cycle opening of the mitral valve in hemorrhagic shock, this condition is perhaps underreported and underdiagnosed in the LVAD population.
During a suction event, the ventricle collapses, resulting in mid-ventricular flow gradients, thus leading to the inflow cannula orifice coming in direct contact with the LV wall, resulting in partial or complete inflow occlusion.
It is unknown if systolic nonclosure of the mitral valve is a precursor to, occurs with, or is a different entity from a suction event. The authors suspect that the LV cavity passes through various levels of underfilling before a frank suction event occurs. Clinicians managing patients need to be able to optimize LVAD settings during shock states, and early use of echocardiography for observation of mitral valve motion and LV dimensions might be helpful to guide optimization.
It is unknown how mitral valve opening in the presence of the LVAD inflow cannula is affected by anatomic factors—the position of the inflow cannula within the LV in relation to the mitral valve with regard to its angulation and distance. Flow within the LV cavity is complex, with counter-clockwise and clockwise vortexes that change throughout the cardiac cycle, and is affected by cardiac contractility and LVAD rpm.
It is unclear if angulation, or its distance to the mitral valve, is a predictor of whether low LV filling in shock states lead to systolic nonclosure of the mitral valve or a suction event. The authors speculate that suction events are more likely when the inflow cannula is angled toward the wall rather than the mitral valve. In both patients presented here, the inflow cannulae were noted to be directed toward the mitral valve.
Shock states resulted in low LV filling that led to the systolic nonclosure of the mitral valve seen in the 2 patients presented here and the one previously reported.
Common etiologies of low LV filling include hemorrhage, hypovolemia, septic shock, and right ventricle failure. Factors that exacerbate the reduction in venous return, such as positive-pressure ventilation, coughing and valsalva, or orthostasis with changes in patient position, can lead to LVAD low flow as well.
Septic shock results in systemic venous and arterial dilation, with higher cardiac output required to sustain blood pressure, thereby increasing the demand for ventricular volume in LVAD patients. Other etiologies include arrhythmias, tamponade, and mitral stenosis. The LVAD patients in shock states present with hypotension, and sometimes low-flow alarms and reduced PI. Both flow and PI are derived from power consumption, and not directly measured by the LVAD, making echocardiography an essential tool in ensuring appropriate LVAD function in the setting of shock.
Algorithms have been suggested previously for the management of hemodynamic instability in patients with LVAD support.
First, an electrocardiogram should be obtained to rule out arrhythmias. This is followed by echocardiography, which is essential in diagnosis and guiding management, because treatment ultimately depends on underlying etiology. Pressors are appropriate in patients presenting with persistent hypotension. Temporary reduction in LVAD speed usually is indicated when a small LVEDD is noted, as seen in the presence of systolic nonclosure of the mitral valve or suction events. In addition, resuscitation with intravenous fluids is indicated for hypovolemia or hemorrhagic shock. In patients with significant right heart dysfunction, inotropes and pulmonary vasodilators may be indicated to increase left heart filling.
Tamponade should be addressed with urgent percutaneous or surgical drainage. The LVAD thrombosis resulting in shock does not present with suction events or systolic nonclosure of the mitral valve; the reduced flow through the LVAD results in increased LV filling.
In conclusion, the authors reported 2 LVAD patients who exhibited continuous transmitral flow in the setting of shock states. Systolic nonclosure of the mitral valve is a unique pathologic finding in LVAD patients, as it indicates a left ventricular volume depletion that is severe enough such that the pressure in the LA exceeds LV pressure during systole. When encountered on echocardiographic evaluation, systolic nonclosure of the mitral valve should be treated with temporary reduction in LVAD speed, with further management dependent upon the underlying etiology of the shock state.
Video 1. (A) Midesophageal 4-chamber view on transesophageal echocardiography reveals a mitral valve that is wide open during systole. Also notable are the dilated right ventricle, with interventricular septum shifted to the left, along with the small left ventricle (LV). The LV assist device speed is set at 5,600 rpm, with an LV end-diastolic diameter of 1.7 cm. (B) With addition of color flow Doppler, flow can be seen from the left atrium to the LV through the open mitral valve during systole.
Video 2. (A) In this parasternal long-axis view on transthoracic echocardiography, the mitral valve is seen to be open during systole. Also notable are the dilated right ventricle, the interventricular septum shifted to the left, along with a decompressed left ventricle (LV) with an LV end-diastolic diameter of 2.7 cm. The LV assist device speed is 5,800 rpm. (B) With the addition of color flow Doppler, flow can be seen from the left atrium to the ventricle during systole through the open mitral valve.