What Is a Pansystolic Murmur? Causes and Treatment

A pansystolic murmur is an abnormal heart sound that lasts throughout the entire contraction phase of the heartbeat, starting with the first heart sound and continuing without interruption until the second. Doctors also call it a “holosystolic” murmur, and the two terms mean the same thing. It signals that blood is leaking backward through a valve or through an abnormal opening in the heart wall during every beat. The three conditions responsible for almost all pansystolic murmurs are mitral regurgitation, tricuspid regurgitation, and ventricular septal defect, and each has a distinct set of causes and treatments worth understanding.

What Makes a Pansystolic Murmur Different From Other Heart Murmurs

Not every murmur heard during the contraction phase of the heart qualifies as pansystolic. Some systolic murmurs start after the first heart sound, peak in the middle, and fade before the second heart sound. These “crescendo-decrescendo” murmurs are typically caused by blood being forced through a narrowed but forward-flowing valve, such as a stiffened aortic valve. A pansystolic murmur, by contrast, occupies the full span between the two heart sounds because the pressure difference driving the backward leak persists throughout the entire contraction. There is no gap at the beginning or the end. That continuous, plateau-shaped quality is what tells a clinician the problem is a regurgitant leak rather than a narrowed forward passage.

The pitch is usually high, and the sound is often described as blowing. Where on the chest it is loudest, whether it radiates to other areas, and how it responds to breathing or body-position changes all help narrow down which of the three main causes is responsible.

Mitral Regurgitation

Mitral regurgitation is the single most common cause of a pansystolic murmur. The mitral valve sits between the left atrium and the left ventricle, and when it fails to close properly, blood jets backward into the atrium with every contraction. The murmur is typically loudest at the apex of the heart, on the lower left side of the chest, and it often radiates toward the left armpit.

The reasons the mitral valve can start leaking fall into two broad categories. In primary mitral regurgitation, the valve itself is structurally damaged. Degenerative disease, where the valve leaflets become floppy or their supporting cords snap, is the most frequent culprit in older adults. Rheumatic heart disease, endocarditis, and congenital malformations are other structural causes. In rare cases, a prosthetic valve can damage the native mitral leaflet; one documented scenario involves a transcatheter aortic valve prosthesis perforating the anterior mitral leaflet, leading to severe regurgitation and subsequent infection of the valve.¹

In secondary (or “functional”) mitral regurgitation, the valve leaflets themselves are normal, but the left ventricle has enlarged or weakened so much that the valve can no longer close tightly. Heart failure and ischemic heart disease are the usual drivers. This distinction matters a great deal for treatment, because repairing or replacing a structurally normal valve does not fix the underlying heart-muscle problem.

A tricky feature of chronic, severe mitral regurgitation is that it can remain silent for years. The left atrium gradually stretches to accommodate the extra blood volume, and the left ventricle compensates by pumping harder. Symptoms such as breathlessness and fatigue often appear only once compensatory mechanisms are overwhelmed, at which point the disease may already be advanced. If left untreated, the condition leads to progressive left ventricular failure.

Tricuspid Regurgitation

The tricuspid valve sits on the right side of the heart, between the right atrium and right ventricle. When it leaks, the resulting pansystolic murmur is heard best along the left lower edge of the breastbone. A classic bedside test is the Carvallo sign: if the murmur gets louder when you breathe in, it likely originates from the tricuspid valve, because inspiration pulls more blood into the right side of the heart and amplifies the leak. That said, the sign is not always present. In patients with very severe tricuspid regurgitation and high right-atrial pressures, inspiration may actually fail to increase the leak because the right atrium is already so full that additional volume makes little difference.²

Like mitral regurgitation, tricuspid regurgitation can be primary or secondary. Primary causes include rheumatic disease, endocarditis (especially in people who inject drugs), and damage from devices that pass through the valve. Permanent pacemaker and defibrillator leads are an under-recognized but well-documented cause: in a surgical series of 41 patients, severe tricuspid regurgitation was traced to the device lead in every case, with mechanisms including leaflet perforation, lead entanglement in the valve, and lead impingement preventing leaflet closure.³

Secondary tricuspid regurgitation is more common and typically results from anything that raises pressure in the lungs or enlarges the right ventricle. Pulmonary hypertension is the dominant driver, with the odds of worsening regurgitation roughly doubling for every ten-point rise in pulmonary artery systolic pressure. Other independent factors include older age, female sex, right-heart enlargement, and even left-sided heart disease such as organic mitral valve disease.⁴

Ventricular Septal Defect

A ventricular septal defect is a hole in the wall separating the left and right ventricles. Because left-sided pressures are higher throughout the contraction phase, blood rushes through the hole continuously from left to right, producing a pansystolic murmur that is typically loudest at the left lower sternal border. In small defects the murmur is often surprisingly loud, sometimes reaching a very high grade on the clinical loudness scale, and may be accompanied by a palpable vibration (“thrill”) on the chest wall. There is no reliable relationship between the size of the defect and how loud the murmur is; paradoxically, tiny holes with high-velocity jets can create more noise than larger ones.⁵

Most ventricular septal defects are congenital, making them one of the most common heart defects present at birth. Small ones frequently close on their own during childhood. Larger defects that allow significant blood flow from left to right can overload the lungs and right side of the heart over time. In very rare cases, if the defect goes unrepaired and the lung pressures climb high enough, the flow can eventually reverse direction, a situation in which the classic pansystolic murmur may soften or disappear because there is no longer a large pressure gradient driving the jet.

Ventricular septal defects can also be acquired in adults, most often as a complication of a heart attack when the septum ruptures. This is a life-threatening emergency that demands urgent surgical repair.

How Doctors Pin Down the Cause

Listening with a stethoscope provides the first clues: where the murmur is loudest, where it radiates, and how it changes with specific maneuvers. Squatting, standing, performing a Valsalva maneuver (bearing down as if straining), and sustained handgrip all alter the amount of blood returning to the heart, the resistance the heart pumps against, and the size of the heart chambers. Those changes make certain murmurs louder and others quieter in predictable ways, helping the examiner distinguish between causes.⁶ For instance, handgrip increases the resistance the left ventricle has to pump against, which tends to make mitral regurgitation louder, while the Valsalva maneuver reduces blood return to the heart and shrinks the ventricle, which typically softens mitral regurgitation but may accentuate murmurs caused by certain obstructive conditions.

Echocardiography (an ultrasound of the heart) is the definitive next step. It shows the anatomy of the valves and septum, reveals the direction and severity of any leak, and measures chamber sizes and pressures. Color-flow Doppler mapping can pinpoint the origin of the abnormal jet, and additional measurements help classify the regurgitation as mild, moderate, or severe. In tricuspid regurgitation, for example, echocardiography can reveal whether the leak worsens or stays stable with inspiration, which correlates with right-atrial pressure.² In ventricular septal defects, imaging can locate the hole, estimate the volume of blood crossing it, and assess the impact on the lungs.

Treatment of Mitral Regurgitation

When the left ventricle is weakened and the mitral valve leaks because of that weakness rather than structural damage, the first-line approach is guideline-directed medical therapy for heart failure. Medications that reduce the workload on the heart, lower fluid overload, and allow the ventricle to remodel form the backbone of treatment for this functional type of mitral regurgitation.⁷ Drug classes typically include ACE inhibitors or related agents, beta-blockers, diuretics, and mineralocorticoid receptor antagonists. When heart-failure therapy adequately shrinks the ventricle, the valve can begin to close more effectively and the regurgitation may improve without any procedure on the valve itself.

For primary mitral regurgitation, where the valve is structurally abnormal, surgical repair remains the standard of care. A skilled surgeon can reshape the valve leaflets, repair torn cords, or place an annuloplasty ring to restore a tighter seal, and when repair is not feasible, the valve is replaced with a mechanical or biological prosthesis. In patients who are too frail or otherwise too high-risk for open-heart surgery, transcatheter edge-to-edge repair using the MitraClip device offers a less invasive alternative. This catheter-based approach clips the leaflets together at the point of the leak, reducing the backflow without requiring a chest incision.⁸ For patients with primary mitral regurgitation who are candidates for surgery, clinical trials are comparing MitraClip directly to surgical repair to determine when the catheter-based approach might serve as a first-choice option rather than a fallback.⁹

Treatment of Tricuspid Regurgitation and Ventricular Septal Defects

Mild tricuspid regurgitation is extremely common and usually does not require specific treatment. When it becomes moderate to severe and causes symptoms such as swelling, fatigue, or liver congestion, management depends on the underlying cause. If pulmonary hypertension is driving the leak, treating the lung pressure with targeted pulmonary vasodilators or managing the left-sided heart disease responsible for the high pressures is the priority. When the regurgitation is caused by a pacemaker or defibrillator lead, surgical intervention to remove or reposition the lead and repair the valve may be necessary.³ Transcatheter options for the tricuspid valve are a rapidly growing field, with several clip-based and replacement devices under investigation.

Small congenital ventricular septal defects that cause no significant extra blood flow to the lungs are often simply monitored. Moderate to large defects, and any acquired post-heart-attack septal rupture, generally need closure either with open-heart surgery or, in selected cases, a catheter-delivered closure device. Timing matters: the longer a large defect overloads the right heart and lungs, the harder it becomes to reverse the damage.

Using Biomarkers to Track Severity

One of the challenges with valve regurgitation is that patients can feel fine for a long time while their heart is quietly remodeling. Blood tests measuring natriuretic peptides, proteins the heart releases when its chambers are stretched or strained, can help fill the gap between feeling well and actually being well. In mitral regurgitation, rising natriuretic peptide levels can signal worsening heart-muscle damage before symptoms appear and help identify patients who may benefit from earlier surgical intervention rather than continued watchful waiting.¹⁰ These biomarkers are not a replacement for echocardiography, but they add another dimension to monitoring, especially for patients in the gray zone between “definitely needs surgery now” and “safe to keep watching.”

How Pregnancy Affects Pansystolic Murmurs

Pregnancy reshapes the heart’s workload in ways that directly influence regurgitant murmurs. Blood volume increases substantially, the heart rate rises, and the resistance in the blood vessels drops. That drop in resistance actually helps certain leaky valves: when the left ventricle has an easier time pumping blood forward into the body, less blood is driven backward through a leaking mitral or aortic valve. As a result, mitral regurgitation murmurs may soften during pregnancy, and echocardiographic measures of regurgitation severity can decrease.¹¹

This does not mean the valve has healed. The improvement is hemodynamic, driven by the body’s temporary adaptation, and it typically reverses after delivery. Pregnant individuals with known valve disease still need close monitoring, particularly around labor and the postpartum period when fluid shifts and blood-pressure changes can unmask or worsen regurgitation abruptly. Any new pansystolic murmur that appears during pregnancy warrants prompt evaluation, because while some flow murmurs are expected in pregnancy, a true pansystolic murmur is not one of them.

When a Pansystolic Murmur Needs Urgent Attention

Most pansystolic murmurs are discovered incidentally and managed over months or years. A few scenarios, though, demand immediate action:

Acute mitral regurgitation: Sudden chordal rupture or papillary muscle dysfunction during a heart attack can produce a new, loud pansystolic murmur alongside a rapid drop in blood pressure and flash pulmonary edema. Emergency surgery may be life-saving.
Post-infarction VSD: A septal rupture after a heart attack creates a new pansystolic murmur with rapid hemodynamic collapse. Mortality without intervention is extremely high.
Endocarditis: An infection on a heart valve can destroy leaflet tissue within days, turning a previously mild murmur into a severe one. Fever, new or changing murmur, and blood cultures positive for bacteria are the red flags.

In all three situations, the pansystolic murmur itself is the clue that something has changed. A murmur that was previously absent or soft and suddenly becomes louder is treated as a warning sign, not an incidental finding. Rapid echocardiography, hemodynamic stabilization, and early surgical consultation form the core response. For the vast majority of people living with a known pansystolic murmur from a stable, chronic condition, the path involves periodic echocardiographic surveillance, biomarker monitoring when appropriate, and timely referral for intervention once agreed-upon thresholds of severity or symptom burden are crossed.