What Is a Shunt in the Heart? Types, Symptoms & Treatment

A shunt in the heart is an abnormal pathway that lets blood flow between chambers or blood vessels that should not be directly connected. Instead of following its normal route through the lungs and then out to the body, blood crosses through a hole or open vessel, mixing oxygen-rich blood with oxygen-poor blood or overloading one side of the heart with extra volume. Some cardiac shunts are present at birth as part of normal fetal development and are supposed to close shortly after delivery. Others persist or develop later in life, and their effects range from completely harmless to life-threatening, depending on the size of the opening and which direction the blood flows through it.

Why Shunts Exist in the First Place

Before birth, every human heart has shunts. The fetal circulation relies on two key ones: the ductus arteriosus, which connects the pulmonary artery to the aorta and routes most of the right ventricle’s output away from the still-collapsed lungs, and the ductus venosus, which lets oxygen-rich blood from the umbilical vein bypass the liver and reach the central circulation quickly.¹ A third opening, the foramen ovale, allows blood to pass from the right atrium directly to the left atrium. All three are supposed to close after birth once the baby takes its first breaths, lung blood flow increases, and the pressures in the heart shift. When one of these pathways fails to close, or when a structural defect leaves an opening that should never have been there, the result is a cardiac shunt that can cause problems weeks, years, or even decades later.

Left-to-Right Shunts

The most common category of cardiac shunts sends blood from the left side of the heart back to the right side. Because the left side operates at higher pressure, blood naturally streams through any opening toward the lower-pressure right chambers. This means the right side of the heart and the lungs receive more blood than they should, which is the core problem. The three most frequent left-to-right shunts are atrial septal defects, ventricular septal defects, and patent ductus arteriosus.

Atrial Septal Defect

An atrial septal defect (ASD) is a hole in the wall between the two upper chambers of the heart. It is one of the most common congenital heart defects and can go undetected for years because symptoms are often subtle in childhood.² A small ASD might never cause trouble. A larger one gradually enlarges the right side of the heart as it handles extra blood volume, and over time this can lead to irregular heart rhythms, exercise intolerance, and elevated pressures in the lung arteries. Many ASDs are discovered incidentally during an echocardiogram done for an unrelated reason, sometimes not until adulthood.

Ventricular Septal Defect

A ventricular septal defect (VSD) is a hole in the wall between the two lower pumping chambers. VSDs are the single most common congenital heart defect at birth. The good news is that many close on their own during childhood. In one echocardiography-based review of infants diagnosed with VSDs, muscular defects accounted for about half of cases and perimembranous defects for nearly half; only about 4% of the muscular defects required surgery, compared with roughly 47% of the perimembranous type.³ The location and size of the hole dictate whether the shunt needs monitoring only or active repair.

Patent Ductus Arteriosus

A patent ductus arteriosus (PDA) occurs when the ductus arteriosus, the fetal vessel that diverts blood away from the lungs, fails to close after birth. The likelihood of PDA is inversely related to gestational age and weight, making it far more common in premature infants. In term babies a PDA usually reflects a structural problem, while in preemies it is largely a matter of immaturity: the normal closure mechanisms driven by rising oxygen levels and falling prostaglandins simply have not kicked in yet.⁴ Clinical signs of a significant PDA include a heart murmur, persistent rapid heart rate, bounding pulses, and symptoms of heart failure.

Atrioventricular Septal Defect

An atrioventricular septal defect (AVSD) combines a hole in the center of the heart with abnormalities of the valves that separate the upper and lower chambers. AVSDs have a well-known association with chromosomal conditions. The prevalence of congenital heart disease in infants with Down syndrome is about 40%, compared with roughly 0.3% in children with normal chromosomes, and atrioventricular and ventricular septal defects are among the most frequent defects seen in that population.⁵ A complete AVSD typically requires surgical repair in the first few months of life to prevent irreversible lung damage.

Right-to-Left Shunts

When blood crosses from the right side of the heart to the left without passing through the lungs, oxygen-poor blood enters the systemic circulation. The hallmark of a right-to-left shunt is cyanosis, the bluish discoloration of the skin and lips caused by low oxygen levels in the bloodstream. These defects tend to be more immediately dangerous than left-to-right shunts and often require intervention early in life.

Tetralogy of Fallot

Tetralogy of Fallot is the most common cyanotic heart defect. It involves four anatomical abnormalities that work together to force oxygen-poor blood from the right ventricle across a VSD and out to the body. One of the most dramatic features is the “tet spell,” a sudden episode of deep cyanosis and rapid breathing. Research into the mechanism behind these spells suggests they may result from stimulation of receptors in the right ventricle: increased contractility from catecholamine surges and decreased right ventricular volume can trigger a reflex causing hyperventilation and peripheral vasodilation, initiating the spell.⁶ Parents of affected infants learn to squat the child’s knees to the chest during a spell, which increases resistance in the body’s circulation and encourages blood to flow toward the lungs instead.

Transposition of the Great Arteries

In transposition of the great arteries (TGA), the two major vessels leaving the heart are swapped: the aorta rises from the right ventricle and the pulmonary artery from the left. This creates two parallel circuits instead of one continuous loop. Oxygen-poor blood recirculates through the body, and oxygen-rich blood recirculates through the lungs, with very little mixing between them. The severity depends on whether additional openings exist to allow some mixing. When a large VSD is present, cyanosis can be mild at rest and only become noticeable during crying or agitation, while signs of heart failure become the dominant problem.⁷ Without any mixing pathway, TGA is a medical emergency in the first hours of life.

Patent Foramen Ovale

A patent foramen ovale (PFO) is a remnant of the fetal foramen ovale that never fully sealed. It exists in roughly a quarter of the adult population and usually causes no symptoms whatsoever. The concern arises when a blood clot from elsewhere in the body, often the deep veins of the legs, passes through the PFO into the left side of the heart and travels to the brain, causing a stroke. This is called paradoxical embolism. A PFO can serve as a conduit for such clots, and other mechanisms including thrombus forming directly at the atrial septum or atrial arrhythmias promoting clot formation and passage through the PFO have also been described.⁸ PFO closure is now offered to selected younger patients who have had a stroke with no other identifiable cause.

Recognizing Symptoms

The symptoms of a cardiac shunt depend entirely on its direction, its size, and how long it has been present. Small shunts may never produce a single symptom. Larger ones announce themselves differently depending on whether they overload the lungs with blood or starve the body of oxygen.

• Left-to-right shunts: Fatigue during feeding or exercise, poor weight gain in infants, frequent respiratory infections, a heart murmur heard on exam, rapid breathing, and in advanced cases, signs of heart failure like swelling and breathlessness at rest.
• Right-to-left shunts: Blue or dusky skin color (especially the lips, fingers, and toes), episodes of deep cyanosis sometimes triggered by crying or exertion, clubbing of the fingertips in long-standing cases, and poor growth.
• PDA-specific signs: A continuous “machinery-like” murmur, bounding pulses, a visibly active chest wall in premature infants, persistent heart rate above 160 beats per minute, and chest X-ray findings showing an enlarged heart or congested lungs.⁹

Many adults with small ASDs or PFOs live for decades without knowing they carry a shunt. The defect is often found only after a stroke, an irregular heart rhythm, or a routine imaging study. This is part of what makes cardiac shunts tricky: size matters far more than the mere presence of an opening.

How Cardiac Shunts Are Diagnosed

Echocardiography is the workhorse of shunt diagnosis. A standard transthoracic echocardiogram (TTE) with color Doppler can detect the vast majority of ASDs, with reported sensitivities ranging from about 89% to 100% for common ASD subtypes. For PFOs, though, color Doppler alone performs poorly, with sensitivity as low as roughly 22%.¹⁰ That is where the “bubble study” comes in.

In a bubble study, a clinician injects agitated saline into a vein. The tiny microbubbles show up clearly on ultrasound as they pass through the right side of the heart. In a normal heart, the lungs filter out the bubbles before they reach the left side. If bubbles appear in the left atrium within a few heartbeats, it signals an intracardiac shunt such as a PFO or ASD.¹¹ If the bubbles appear slightly later, after three to six cardiac cycles, the shunt is more likely to be in the lungs rather than in the heart itself, a distinction that matters in conditions like hepatopulmonary syndrome.¹²

Cardiac catheterization remains important when more precise measurements are needed. By sampling oxygen levels in different chambers, cardiologists can calculate the ratio of pulmonary blood flow to systemic blood flow. This ratio, known as Qp/Qs, helps quantify the size of a shunt and guides decisions about whether repair is warranted. Cardiac MRI is sometimes used for the same purpose and may be more accurate in certain complex anatomies where catheterization data can underestimate blood flow.¹³

What Happens if a Shunt Goes Untreated

A significant left-to-right shunt floods the lungs with extra blood over months and years. The lung blood vessels respond by thickening and stiffening, which gradually drives up the pressure in the pulmonary arteries. This process is called pulmonary arterial hypertension (PAH). If it progresses far enough, the pressure on the right side of the heart can eventually exceed the pressure on the left, and the shunt reverses direction: blood now flows right to left, sending oxygen-poor blood out to the body. This reversal is called Eisenmenger syndrome, and it represents the most advanced and devastating form of PAH associated with congenital heart disease.^{14 15}

Even before full reversal occurs, the extra volume and pressure that a left-to-right shunt imposes on the heart can cause measurable injury. Research using highly sensitive troponin tests in children with congenital heart disease has shown that significant volume and pressure overload from a left-to-right shunt can cause myocardial injury and may eventually lead to irreversible remodeling of the heart muscle.¹⁶ This is one of the reasons cardiologists prefer to close significant shunts before permanent damage sets in, and why certain lesions have a limited time window beyond which repair may no longer be beneficial.¹⁷

Treatment Options

The approach to fixing a cardiac shunt depends on the defect’s type, size, location, and the patient’s overall condition. For many shunts, the options fall into three broad categories: watchful waiting, catheter-based closure, and open-heart surgery.

Catheter-Based Closure

For secundum ASDs, PFOs, and some PDAs, cardiologists can thread a device through a vein in the groin and deploy it across the defect to plug the hole. This avoids the need for open surgery. In one series of patients undergoing Amplatzer device closure of ASDs and PFOs for presumed paradoxical embolism, all devices were successfully deployed with no deaths. At three months, only a handful of patients had trivial residual shunting, and at twelve months only two out of twenty-eight monitored patients still showed any residual flow.¹⁸ After closure, patients typically take antiplatelet medications for a few months while tissue grows over the device. A recent study found that the average duration of dual antiplatelet therapy after PFO and ASD closure was about three months, and at one year there were no cases of device blood clots or device displacement.¹⁹

Surgical Repair

Larger defects, complex anatomy, or shunts that cannot be reached with a catheter still require open-heart surgery. The timing of surgery varies by defect. For tetralogy of Fallot, total surgical correction is the treatment of choice, though some infants need initial palliation with a modified Blalock-Taussig shunt, a small tube connecting a systemic artery to the pulmonary artery, to increase blood flow to the lungs while they grow large enough for full repair. For TGA, the arterial switch operation is the standard approach and is ideally performed within the first two weeks of life. Babies with TGA who are critically cyanotic may need a prostaglandin infusion to keep the ductus arteriosus open or a balloon atrial septostomy to create a temporary hole between the atria as a bridge to surgery.²⁰

Medications for Advanced Pulmonary Hypertension

When a shunt has already led to significant pulmonary hypertension, closing the defect abruptly can be dangerous because the stiffened lung vessels cannot handle the sudden change in blood flow. Some patients benefit from a “treat and repair” strategy, where medications are used to lower the pulmonary vascular resistance before defect closure is attempted.²¹ For patients who have already progressed to Eisenmenger syndrome, closing the defect is generally off the table. Instead, treatment focuses on targeted pulmonary vasodilator therapies. Three drug classes are available: prostanoids, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors, all of which have shown benefit in patients with PAH associated with both corrected and uncorrected congenital shunts.²²

Acquired Cardiac Shunts

Not every cardiac shunt is present from birth. A heart attack can destroy part of the muscular wall between the ventricles, creating a ventricular septal defect where one never existed before. These acquired VSDs are rare but carry an extremely high mortality rate. Medical therapy alone offers very poor long-term survival, and despite advances in surgical and catheter-based techniques, outcomes remain grim when this mechanical complication develops.²³ In the era of clot-dissolving drugs, the complication tends to appear sooner after a heart attack than it did historically, likely because reperfusion can weaken the already-damaged tissue.²⁴ Trauma and certain infections can also create shunts, though these are far less common.

Cardiac Shunts in the Animal Kingdom

Humans treat cardiac shunts as defects, but in reptiles they are a feature. The anatomy of the reptilian heart allows mixing of oxygenated and deoxygenated blood through what are effectively built-in cardiac shunts. In birds and mammals, such mixing is harmful, but in reptiles this arrangement appears to serve real physiological purposes. Some researchers view it as a derived trait favored by natural selection, while others argue it may be an ancestral condition or a retained embryonic pattern.²⁵ This is a useful reminder that a “shunt” is not inherently pathological. It is a plumbing arrangement, and whether it helps or hurts depends entirely on the circulatory system it sits in. In a diving turtle that can slow its heart rate and redirect blood flow away from the lungs during a long dive, a cardiac shunt is elegant engineering. In a human infant whose lungs need full blood flow to keep up with a growing body, the same arrangement becomes a problem that cardiologists work to fix.