RNs and NPs play collaborative and complementary roles.

MS. LISA SLOAN*, a 75-year-old woman with a history of hypertension, type 2 diabetes, severe aortic stenosis, combined systolic and diastolic heart failure, and asthma, undergoes uncomplicated transcatheter aortic valve replacement (TAVR). When she arrives in the post-anesthesia care unit, her vital signs are stable: respiratory rate (RR) 16 breaths per minute, blood pressure (BP) 115/70 mmHg, heart rate (HR) 79 beats per minute (bpm), and oxygen saturation (SpO2) 98% on 2 L of oxygen via nasal cannula. She’s alert, oriented, and reports no complaints.

Within 1 hour after the procedure, Ms. Sloan develops shortness of breath. Brian, the patient’s nurse, assesses her vital signs: RR 20 breaths per minute, BP 95/55 mmHg, HR 99 bpm, and SpO2 94%. Brian’s physical exam reveals dyspnea, restlessness, diffuse bilateral wheezing, and a murmur. He contacts the provider to report these abnormal findings.

Believing that Ms. Sloan is experiencing an asthma exacerbation, the certified RN anesthetist initiates treatment with nebulized albuterol and I.V. magnesium. As symptoms progress, she administers epinephrine. Ms. Sloan becomes increasingly tachypneic and agitated, prompting a STAT bedside chest radiograph, which reveals mild pulmonary edema.

Concerned about decompensated heart failure, the team initiates noninvasive ventilation with BiPap and I.V. diuretics. Despite these interventions, Ms. Sloan’s condition rapidly deteriorates. Her vital signs worsen: RR 30 breaths per minute, BP 70/40 mmHg, HR 120 bpm, and SpO2 85% on BiPap with 100% FiO2. She requires emergent endotracheal intubation due to respiratory distress and hemodynamic instability.

A bedside assessment by the cardiology nurse practitioner (NP), who wasn’t involved in the initial post-procedure care, reveals several critical findings: a high-pitched, 5/6 systolic murmur at the right upper sternal border, radiating to the neck; thready peripheral pulses; and minimal urine output despite prior diuresis. Recognizing the patient’s clinical instability and concerned about a structural cardiac complication, the NP advocates for a STAT transthoracic echocardiogram to evaluate valve function and rule out complications. The study reveals a small, hyperdynamic left ventricle with systolic anterior motion of the mitral valve and dynamic left ventricle outflow tract obstruction, consistent with a diagnosis of suicide left ventricle (SLV).

After aggressive I.V. fluid resuscitation, I.V. esmolol to reduce contractility and prolong diastolic filling, and phenylephrine to increase afterload and restore forward flow of blood, Ms. Sloan stabilizes.

TAVR and SLV

TAVR has revolutionized the management of aortic stenosis, quickly becoming a cornerstone of minimally invasive patient care. This procedure eliminates the need for surgical aortic valve replacement (SAVR) by replacing the aortic valve via a catheter inserted in a peripheral artery.
The Society of Thoracic Surgeons (STS) Adult Cardiac Surgery Database and the STS/American College of Cardiology Trans- catheter Valve Therapy Registry report that, in 2022, nearly 100,000 TAVR procedures occurred in the United States. This finding represents a significant increase from fewer than 5,000 in 2012. Over the same period, SAVR volume declined by 36%. (See TAVR approval story.)

As inclusion criteria continue to broaden, patient preferences shift toward less-invasive procedures. In addition, as the population ages, more RNs and nurse practitioners (NPs) will care for patients after they’ve undergone this procedure. Therefore, RNs and NPs should have awareness of potential complications, especially rare but life-threatening ones such as SLV. As frontline clinicians, nurses can identify concerning hemodynamic changes after TAVR to ensure timely action and improve outcomes.

SLV defined

To understand SLV, we must first review the structural changes that occur as a result of a stenotic aortic valve. As summarized in a recent systematic review by Barzallo and colleagues, the narrowed valve represents a fixed outflow tract obstruction; the resistance to blood flow doesn’t vary with changes in preload (the volume of blood filling the ventricle at end of diastole) or contractility. To maintain systolic function, the left ventricle must generate higher pressures to overcome this resistance, which leads to ventricle remodeling (the left ventricle wall thickens, increasing myocardial mass and reducing cavity size).

In most cases, structural adaptation, coupled with preload dependence, allows the left ventricle to maintain cardiac output. However, sudden relief of the increased afterload (the pressure the ventricle must pump against to eject blood) after TAVR can result in a paradoxical drop in cardiac output.

Placement of a new aortic valve exposes the left ventricle to a significant reduction in afterload, altering hemodynamic balance. Without counterpressure, the hyperdynamic, remodeled ventricle contracts forcefully and collapses inward. This creates a suction effect that persists into diastole, impairing ventricular filling, which can lead to systolic anterior motion (SAM) of the mitral valve and result in a dynamic left ventricular outflow tract (LVOT) obstruction and marked diastolic dysfunction.

Clinically, this manifests as symptoms of heart failure, profound hypotension, and cardiogenic shock. In severe cases, it can lead to complete cessation of forward flow of blood and cardiac arrest. The colloquial term “suicide left ventricle” describes this paradoxical scenario in which the heart seemingly self-sabotages after rescue from a diseased valve.

Risk factors

Identification of risk factors can guide appropriate pre- and postprocedure care. Patients with severe aortic stenosis, especially those who are older or have long-standing disease, will more likely have diastolic dysfunction (impaired ventricular relaxation, poor filling, and pressure buildup), predisposing them to ventricular underfilling and hemodynamic shifts after TAVR.

Severe or long-standing aortic stenosis leads to structural changes and a noncompliant left ventricle that depends heavily on the balance of preload and afterload. A patient with a small left ventricle cavity has less blood capacity at baseline, making it easier for the ventricle to collapse on itself. A hyperdynamic ventricle with supernormal ejection fraction increases the likelihood of excessive contraction after relieving the afterload. Septal hypertrophy, another structural change noted in long-standing aortic stenosis, narrows the LVOT and enables the anterior mitral leaflet to be pulled into the outflow tract, resulting in dynamic obstruction.

In patients with structural or hemodynamic features that predispose them to SLV, any cause of hypovolemia after TAVR can decrease ventricular filling and increase the risk of obstruction. Similarly, the use of medications such as vasodilators or inotropes may further contribute to ventricular collapse in this high-risk group.

Vasodilators reduce systemic vascular resistance, which can lower preload and impair ventricular filling. Inotropes increase myocardial contractility, potentially exacerbating dynamic obstruction by intensifying left ventricle contraction.

Recognizing patients with these risk factors before the procedure allows providers to implement preventive strategies and appropriate postprocedure monitoring.

Clinical presentation

Signs and symptoms of SLV include low cardiac output, such as hypotension, tachycardia, confusion, decreased urine output, thready pulses, fatigue or weakness, and new or worsening systolic murmur. Vigilant nursing assessment plays a key role in identifying early and evolving signs of hemodynamic instability, which may initially be misinterpreted.

Diagnosing SLV can prove challenging because it mimics other complications encountered after TAVR, such as pericardial tamponade, hypovolemia or bleeding, decompensated heart failure, valve migration, and coronary artery obstruction. Barzallo and colleagues highlight this diagnostic complexity, noting that delayed recognition can worsen outcomes. (See Post-TAVR nursing assessment.)

RNs and NPs should advocate for early echocardiography as a diagnostic strategy to diagnose this rare but potentially lethal cause of post-TAVR decompensation quickly and accurately. Echocardiography can quickly rule out other complications with evaluation of the pericardium, left ventricular function, and valve positioning, while also confirming SLV by revealing a small, hyperdynamic left ventricle; SAM; and dynamic LVOT obstruction. Misdiagnosis can lead to delayed or inappropriate treatment, resulting in hemodynamic collapse and death.

Prevention and management

The strategies for preventing and managing SLV focus on maintaining hemodynamic stability by optimizing preload, reducing contractility, and supporting afterload. These principles align with the 2020 ACC/American Heart Association Guideline for the Management of Patients with Valvular Heart Disease; however, case-based literature largely informs management of the recommendations specific to SLV. In two recent reports, Alonso and colleagues and Romano and colleagues described successful prevention and management strategies. When RNs have the knowledge to recognize patients at high risk for SLV, they can proactively intervene to prevent clinical deterioration. In addition, when they can quickly identify SLV, they can ensure timely, targeted treatment to stop progression.

Proactive strategies for high-risk patients

Prevention begins by optimizing volume status before and after TAVR, avoiding unnecessary diuresis, and closely monitoring the patient for bleeding or fluid loss. Aim for adequate preload to prevent LV collapse.

Avoid inotropes and vasodilators, as they can increase contractility or decrease systemic vascular resistance, triggering dynamic LVOT obstruction. Providers may order low-dose beta-blockers, such as esmolol, to reduce hypercontractility, slow the patient’s heart rate, and prolong diastolic filling.

Supporting afterload with a vasopressor that doesn’t stimulate myocardial contractility, such as phenylephrine, helps reduce the suction effect that contributes to obstruction and ventricular collapse. When the LV contracts against higher resistance, a reduction occurs in the velocity and force of the ejection. This assists with maintaining a wider cavity during contraction and reduces the suction effect that pulls the anterior mitral valve leaflet into the LVOT.

Acute management when SLV occurs

If you suspect SLV, urgently apply the same hemodynamic principles to reverse the obstruction and stabilize the patient. Initiate I.V. fluid administration to optimize preload, and administer beta-blockers as ordered to slow the heart rate and reduce contractility. In addition, support afterload with a vasopressor that won’t stimulate the heart.

These targeted interventions relieve LVOT obstruction and restore forward flow of blood. Early recognition and prompt implementation of these measures are critical to prevent progression to cardiogenic shock or cardiac arrest. (See SLV management.)

Nursing implications

Post-TAVR care requires a high level of clinical vigilance to recognize early signs of deterioration and rare but life-threatening complications like SLV. Frequently the first to detect subtle changes in patient status, RNs and NPs initiate escalation protocols and contribute to timely management in the event of suspected SLV.

Although closely collaborative, clearly defined RN and NP roles support timely, effective intervention. RNs contribute essential frontline monitoring and early detection of clinical changes. Their ability to question orders, voice concerns, and advocate for escalation is foundational to patient safety. NPs extend this vigilance with advanced diagnostic skills, bedside echocardiographic interpretation, and prescriptive authority, allowing them to initiate treatment and guide management strategies. (See RN and NP: Complementary roles.)

Ms. Sloan’s case highlights the importance of ongoing nursing assessment, vigilance for early signs of SLV, and prompt escalation of care. RNs and NPs must advocate for timely diagnostic evaluation with bedside echocardiography and collaborate across disciplines to implement hemodynamic strategies that prevent deterioration.

Empowering RNs and NPs

As the use of TAVR to manage aortic stenosis increases, RNs and NPs must have the knowledge to recognize postprocedure complications, especially potentially lethal conditions like SLV. Nurses should promptly recognize red flags such as sudden hypotension, shortness of breath, altered mental status, and a new or worsening systolic murmur and escalate the situation for immediate intervention.

Nurses frequently detect subtle changes in a patient’s condition first and play a vital role in advocating for bedside echocardiography to facilitate diagnosis. Successful management relies not only on clinical expertise, but also on interprofessional collaboration among nursing, cardiology, critical care, and cardiac sonographers to ensure rapid initiation of targeted therapy. Maintaining a high index of suspicion, remembering the warning signs, and ensuring a collaborative response are essential to improving outcomes for patients experiencing SLV. Ultimately, empowering RNs and NPs with the knowledge and tools to recognize and respond to SLV can mean the difference between deterioration and recovery.

*Names are fictitious.

Ashley Camp is a cardiology nurse practitioner at Memorial Hermann The Woodlands Medical Center in The Woodlands, Texas.

American Nurse Journal. 2026; 21(2). Doi: 10.51256/ANJ022641

References

Alonso M, Chacon D, Duarte G, et al. Suicide left ventricle after transcatheter aortic valve replacement, a dreaded complication. J Am Coll Cardiol. 2025;85(12):4480. doi:10.1016/S0735-1097(25)04964-2

Barzallo D, Torrado J, Benites-Moya CJ, et al. Acute hemodynamic compromise after transcatheter aortic valve replacement due to dynamic left ventricle obstruction: a systematic review. Am J Cardiol. 2024;214:125-35. doi:10.1016/j.amjcard.2023.12.005

Bowdish ME, Badhwar V. The future direction of post-transcatheter aortic valve replacement re-interventions: Insights from the Society of Thoracic Surgeons National Database. Ann Cardiothorac Surg. 2025;14(2):151-3. doi:10.21037/acs-2024-etavr-0136

Leon MB, Smith CR, Mack MJ, et al. Transcatheter or surgical aortic-valve replacement in intermediate-risk patients. N Engl J Med. 2016;374(17):1609-20. doi:10.1056/NEJMoa1514616

Mack MJ, Leon MB, Thourani VH, et al. Transcatheter aortic-valve replacement with a balloon-expandable valve in low-risk patients. N Engl J Med. 2019;380(18):1695-1705. doi:10.1056/NEJMoa1814052

Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA guideline for the management of patients with valvular heart disease. J Am Coll Cardiol. 2021;77(4):e25-197. doi:10.1016/j.jacc.2020.11.018

Popma JJ, Deeb GM, Yakubov SJ, et al. Transcatheter aortic-valve replacement with a self-expanding valve in low-risk patients. N Engl J Med. 2019;380(18):1706-15. doi:10.1056/NEJMoa1816885

Reardon MJ, Van Mieghem NM, Popma JJ, et al. Surgical or transcatheter aortic-valve replacement in intermediate-risk patients. N Engl J Med. 2017;376(14):1321-31. doi:10.1056/NEJMoa1700456

Romano S, D’Andrea E, Cozac DA, et al. Silent threats of the heart: a case series and narrative review on suicide left ventricle post-aortic valve replacement in patients with dynamic LVOT obstruction and aortic stenosis. J Clin Med. 2024;13(18):5555. doi:10.3390/jcm13185555

Smith CR, Leon MB, Mack MJ, et al. Transcatheter versus surgical aortic-valve replacement in high-risk patients. N Engl J Med. 2011;364(23):2187-98. doi:10.1056/NEJMoa1103510

Key words: aortic stenosis, transcatheter aortic valve replacement, suicide left ventricle, TAVR