Crab View - Pulmonary Veins

Crab view is the view of the pulmonary veins by colour Doppler using a low velocity to capture pulmonary venous flow, as it enters the left atrium (in normal configuration). Beware that pulmonary veins may partially or totally be draining in another structure than the left atrium (TAPVR or PAPVR). We attempt to locate the ostium. A PW Doppler should be done on every vein at its opening in the left atrium. The biphasic or triphasic pattern should be identified. Some flow reversal may occur during the atrial contraction. A prolonged atrial reversal duration may be associated with underlying LV diastolic dysfunction (poor compliance). This sign of diastolic dysfunction is often reported in the pediatric or adult literature. However, it has not been systematically reported in neonatal conditions with LV diastolic dysfunction (such as in the conditions with LV hypertrophy). 

More on pulmonary vein stenosis here.

Decreased  pulmonary venous velocities:

Reduced velocities in the pulmonary veins are typically indicative of a decrease in the volume of blood returning from the lungs to the atrium (or collector) where it/they connect(s). In healthy newborns during the first few days of life, normal pulmonary venous velocities average approximately 50 cm/s, eventually settling to a about 40 cm/s by one month of age. When pulmonary blood flow is pathologically low, such as in high pulmonary vascular resistance (pulmonary hypertension with low pulmonary blood flow; i.e.: Qp/Qs less than 1), severe pulmonary stenosis or pulmonary atresia, the Doppler waveform often loses its prominent, pulsatile "D" wave and the overall velocity profile may become blunted or more continuous. 

In the fetal circulation, where pulmonary blood flow is naturally restricted to only 8% to 10% of the combined ventricular output, the pulmonary venous flow is characterized by these inherently low velocities and a pattern that is predominantly antegrade with only minimal flow reversal during atrial contraction. A shift towards even lower absolute velocities or a more flattened Doppler signal in the neonate suggests that the effective pulmonary blood flow (Qp) is dimished. This stands in stark contrast to states of pulmonary overcirculation (high Qp​ ), such as a large patent ductus arteriosus, where diastolic flow velocities in the pulmonary vessels typically increase significantly, often exceeding 50 cm/s. To visualize this, imagine the pulmonary veins as a riverbed. When the upstream flow is high (normal or increased blood flow), the water moves quickly and surges with the tides (the cardiac cycle). When the upstream flow is restricted to a mere trickle (low pulmonary blood flow), the water in the riverbed moves slowly and loses those distinct, powerful surges, appearing much flatter and more sluggish.

In summary, reduced pulmonary venous velocities are consistent with low pulmonary blood flow and are typically characterized by globally low-amplitude, blunted Doppler waveforms rather than a single abnormal peak. In practical terms:

• Normal pulmonary venous velocities 

  • S-wave: ~30–50 cm/s 

  • D-wave: ~30–50 cm/s 

  • Ar: usually <20–25 cm/s 

• In reduced pulmonary blood flow, peak systolic (S) and diastolic (D) velocities are usually low, often in the range of ≤ 20–30 cm/s, and may be closer to 10–20 cm/s in severe reduction of pulmonary blood flow.

• The S and D waves are small and relatively flat, with reduced pulsatility.

• The S/D ratio is often preserved or mildly altered, but both components are uniformly reduced.

• The atrial reversal (Ar) wave is typically small or absent (especially because of low left atrial preload; unless there is high LV filling pressures or atrio-ventricular valve stenosis or regurgitation), reflecting reduced forward pulmonary venous return rather than elevated left atrial pressure.

• Low pulmonary venous velocities reflect reduced pulmonary blood flow, which may occur with:

• Markedly elevated pulmonary vascular resistance (e.g., severe PPHN)

• Functional pulmonary atresia or severe RVOT obstruction

• Critical reduction in RV output or severely restricted pulmonary perfusion

• Uniformly low S and D velocities (≈10–30 cm/s) with blunted waveforms are most consistent with low pulmonary blood flow rather than pulmonary venous obstruction or elevated left atrial pressure.

• Key distinction

  • This pattern differs from pulmonary venous abnormalities related to left atrial hypertension or obstruction, where velocities may be increased, the D wave may predominate, or there may be prominent atrial reversal.

  • Left atrial hypertension: Normal pulmonary venous flow is a pulsatile, phasic process typically characterized by systolic (S), diastolic (D), and atrial reversal (Ar) velocity components. As left atrial (LA) pressure increases, often as a result of advancing diastolic dysfunction or restrictive physiology, the morphology of these velocity patterns changes in a predictable continuum. In the early stages of pressure elevation, known as the "pseudonormal" pattern, the diastolic (D) wave velocity increases while the systolic (S) wave velocity begins to decrease. When left atrial hypertension becomes severe, such as in restrictive cardiomyopathy, the systolic flow becomes markedly blunted or even trivial, resulting in an S/D velocity ratio of less than 0.5. This blunting occurs because the elevated chronic pressure and distension within the left atrium act as a resistor, impeding forward flow from the veins during ventricular systole. Conversely, increased left atrial pressure significantly impacts the retrograde flow observed during atrial contraction. The velocity and duration of the pulmonary venous atrial reversal (Ar) wave increase because the atrium must contract against a higher end-diastolic pressure in the left ventricle. Clinically, an Ar wave duration that exceeds the duration of the mitral A-wave is a specific sign of pathologically elevated left-sided filling pressures. In the fetal circulation, where left atrial egress may be restricted by a small foramen ovale, increased pressure leads to an exaggerated degree of flow reversal during atrial systole. In extreme cases of fetal left atrial hypertension (ex: hypoplastic left heart syndrome with mitral atresia and restrictive foramen ovale), forward flow in early diastole may be entirely lost, leaving a Doppler profile of to-and-fro flow in the pulmonary veins with significant retrograde velocities. To help visualize this, imagine the pulmonary veins as a stream flowing into a reservoir (the left atrium). Under normal pressure, the stream flows forward with every cycle, only experiencing a tiny ripple of backflow when the reservoir's gate closes. If the reservoir becomes overfilled and pressurized, it pushes back against the stream, slowing its forward progress to a crawl and causing a violent backward surge every time the gate tries to shut against the pressure.

  • Severe mitral valve insufficiency, also referred to as mitral regurgitation (MR), fundamentally alters the flow dynamics within the left side of the heart by allowing blood to be ejected backward from the left ventricle into the left atrium during ventricular systole. Normally, pulmonary venous flow into the left atrium is pulsatile and predominantly antegrade, characterized by a systolic (S) wave, a diastolic (D) wave, and a small atrial reversal (Ar) wave during atrial contraction. In the presence of severe insufficiency, the regurgitant jet causes a sudden and significant increase in left atrial pressure and volume precisely during the systolic phase of the cardiac cycle. This systolic expansion of the left atrium acts as a powerful resistor to the incoming blood from the pulmonary veins. The primary diagnostic hallmark of severe mitral insufficiency on a pulmonary venous Doppler is the blunting or complete reversal of the systolic (S) wave. While mild mitral regurgitation may allow for a normal antegrade systolic flow pattern, the high-volume backflow in severe cases overpowers the venous return, causing the Doppler signal to show systolic flow reversal, where the S wave flips direction and becomes retrograde. This phenomenon is considered a specific echocardiographic criterion for grading the severity of the regurgitation as "severe". Furthermore, if the heart rate is high or if there is significant diastolic dysfunction, these patterns may be further distorted, but the loss of antegrade systolic flow remains the defining feature. The presence of this retrograde flow contributes directly to pulmonary venous hypertension. As the pressure is transmitted back from the distended and pressurized left atrium into the pulmonary vasculature, it can lead to secondary pulmonary arterial hypertension. Over time, the chronic volume overload from severe insufficiency leads to marked left atrial dilation and hyperdynamic motion of the interatrial septum, which may be visualized as the septum bulging toward the right atrium during the peak of the regurgitant event. To help visualize this, imagine the pulmonary veins as a stream flowing into a small pond (the left atrium). Under normal conditions, the stream flows forward comfortably. However, if a massive pump inside the pond (the regurgitant mitral valve) suddenly blasts water back toward the stream with every pulse, the stream’s forward progress will not only stop but will actually be pushed backward, creating a violent surge in the wrong direction.

Increased pulmonary venous velocities

Pulmonary venous velocities in the neonate are dynamic and reflect the physiological transition of the heart and lungs after birth. In the first few hours of life, systolic (S) and diastolic (D) velocities can normally be greater than 80 cm/s, but these values typically decrease to an average of approximately 50 cm/s in the ensuing hours and days as the circulation stabilizes. By one month of age, the mean pulmonary venous velocity settles further to approximately 40 cm/s, with the systolic peak usually becoming slightly higher than the diastolic peak in healthy term infants. Velocities are considered pathologically increased in several clinical contexts, primarily involving pulmonary overcirculation or venous obstruction. An increased pulmonary venous diastolic velocity exceeding 50 cm/s is a specific echocardiographic marker for a hemodynamically significant patent ductus arteriosus (hsPDA) in preterm infants. This elevation is caused by the large volume of blood recirculating from the aorta through the lungs and back into the left atrium, creating a volume load that increases the velocity of flow within the veins while maintaining a normal phasic pattern. This acceleration of flow is true until (and if) the pulmonary veins dilate from the flow coming back to the left atrium (if the veins dilate, there may be dempening of this increased velocities). Similarly, other large left-to-right shunts, such as ventricular or atrial septal defects, can elevate peak systolic and diastolic pulmonary venous velocities due to the sheer volume of returned blood. In the context of obstructive anomalies, such as total anomalous pulmonary venous connection (TAPVC) or pulmonary vein stenosis (PVS), velocities increase dramatically as blood is forced through a narrowed orifice. In infants with TAPVC, if the flow at the connecting site between the pulmonary venous confluence and the systemic circulation is turbulent with a velocity greater than 1.5 to 2 m/s, it is highly suggestive of an active obstruction to venous drainage. Patients with pulmonary vein stenosis demonstrate similar high-velocity, turbulent flow, which is typically accompanied by a loss of the normal phasic variation and the absence of the retrograde atrial wave during the cardiac cycle. Furthermore, the pressure gradient across a stenotic pulmonary vein is directly proportional to the rate of blood flow; consequently, an increase in cardiac output or the administration of pulmonary vasodilators can cause these velocities to rise even higher (these infants often present a "white out" picture on chest radiography from alveolar spillage due to post-capillary obstruction). Of note, pulmonary venous atresia will not showcase flow or acceleration as the osteum is atretric. Similarly, proximaly pulmonary venous occlusive disease, where there is heterogeneous obstruction of the pulmonary veins along their path may not showcase acceleration at the level of the osteum as the obstruction starts nearer to the capillary-venous junction. 

In children with exceptionally high pulmonary blood flows, the high velocity of flow across the pulmonary capillary bed can sometimes be so rapid that it prevents normal oxygen equilibration, resulting in reduced oxygen saturation levels in the pulmonary veins (especially in the context of concomittant alveolar edema due to alveolar spillage creating ventilation-perfusion mismatch and challenges for oxygen to diffuse appropriately and quickly accross the air-blood barrier). Oxygen diffusion in the lungs is the vital process where inhaled oxygen passively moves from the tiny air sacs (alveoli) across their thin walls into surrounding blood capillaries, driven by a higher oxygen concentration in the lungs than in the returning blood, allowing it to bind to red blood cells and be carried to the body. Of note, the oxygen gradient between the alveoli and capillaries may be reduced if there is pulmonary parenchymal or airway disease with atelectasis, underfilling of the alveoli, or low environmental oxygen tension (ex: high altitude). The oxygen diffusion lung barrier, or air-blood barrier, is an incredibly thin structure (~1 micron) made of alveolar lining (pneumocytes), fused basement membranes, and capillary endothelium, allowing rapid O2 diffusion from alveoli into capillaries and CO2 out, facilitated by a vast surface area and minimal thickness, but impaired by conditions like edema or fibrosis. These factors may be affected by various pathological or maturational conditions affecting newborns.

Certain anatomic configurations, such as the extrinsic compression of the left lower pulmonary vein by a left-sided descending aorta, can produce localized increases in Doppler velocity that may mimic pathologic stenosis. To visualize this, imagine water flowing through a garden hose. If you turn the tap up to full power (high flow from a shunt), the water moves through the hose much faster. If you then place your finger over the end of the hose to narrow the opening (venous obstruction), the water that manages to escape will spray out at an even higher, more turbulent velocity.

• • Increased pulmonary venous velocities S and/or D waves ≥ 50–80 cm/s In more extreme states, peaks may exceed 90–100 cm/s. Often accompanied by increased pulsatility and waveform distortion. The Iowa PDA score considers values above 30 cm/s of the D-Wave as a potential marker of increased velocities in the pulmonary venous return.

    • Pulmonary overcirculation (high pulmonary blood flow) 

      • Mechanism: Excess pulmonary flow returning to the LA 

      • Echo/Doppler pattern: Increased S and D velocities, often proportionally elevated 

      • Preserved or mildly increased Ar wave 

      • Typical settings: Large, unrestrictive left-to-right PDA; Large VSD or AVSD; Postnatal drop in PVR with high systemic-to-pulmonary shunt

    • Pulmonary venous obstruction:

      • Mechanism: Anatomic narrowing causes jet acceleration 

      • Echo/Doppler pattern: Focal, very high velocities at the affected vein (often >100 cm/s); Turbulence/aliasing and spectral broadening; Marked inter-vein asymmetry 

      • Typical settings: anomalous pulmonary venous return with obstruction; Post-surgical pulmonary vein stenosis; External compression (rare in neonates); progressive pulmonary venous osteal stenosis. 

Crab view with color Doppler and pulsed-wave Doppler interrogation of the pulmonary venous ostia

Two other examples of a crab view. 

Nyquist (velocity filter) is set at a lower value in order to visualize the venous flow entering the left atrium.

Pulmonary venous Doppler displays a biphasic systolic forward wave and an early-diastolic forward wave, often followed by a brief atrial reversal. The systolic wave is often split into S1 and S2: S1 occurs in early systole when the left atrium (LA) relaxes as the mitral valve has just closed, causing LA pressure to fall below pulmonary venous pressure and drawing blood forward into the LA. S2 follows in mid-to-late systole and is driven mainly by longitudinal left-ventricular (LV) shortening—the descent of the mitral annulus increases LA capacitance and further lowers LA pressure, augmenting forward venous inflow. After aortic valve closure and mitral opening, the D wave reflects early-diastolic conduit flow from the pulmonary veins through the LA into the LV; its size depends on LV relaxation (“suction”), LA pressure, and preload. Finally, Ar (atrial reversal) occurs during atrial contraction; if LV end-diastolic pressure or stiffness is high, part of the LA outflow is pushed back into the pulmonary veins, increasing Ar velocity and, classically, prolonging Ar duration relative to the mitral A wave. Patterns that increase S1/S2 include robust LV longitudinal systolic function (greater annular descent), good LA compliance, low intrathoracic/LA pressure (e.g., inspiration), and situations that decompress the LA in systole such as a nonrestrictive interatrial communication with left-to-right shunting; among these, S2 is the most sensitive to LV longitudinal performance. S1/S2 decrease when LA pressure rises during systole or LA compliance is poor—most notably with mitral regurgitation (a large V-wave blunts or reverses S, especially S2), with reduced LV longitudinal function, acute volume/pressure loading of the LA, or marked tachycardia that shortens systole and diastasis. The D wave increases when early-diastolic LA→LV driving pressure is strong or pulmonary venous return is high—examples include significant PDA with left-to-right shunt, brisk LV relaxation, or high preload; it decreases with impaired LV relaxation (prolonged relaxation), low preload, or when diastolic inflow is limited by a restrictive interatrial communication or pulmonary venous obstruction. In advanced diastolic dysfunction/restrictive physiology, a characteristic pattern emerges of blunted S with tall D and prominent Ar, reflecting high LA pressure, rapid early filling, and a stiff LV that forces more retrograde flow during atrial systole.

A tall pulmonary venous S-wave reflects strong reservoir-phase forward flow into the left atrium (LA) during LV systole. When the LV shortens longitudinally, the mitral annulus descends, the LA actively relaxes, and LA pressure falls relative to pulmonary venous pressure; that suction augments systolic inflow and makes S large. Anything that enhances annular descent (good LV longitudinal systolic function), improves LA compliance, or prevents a systolic LA pressure rise will boost S—e.g., normal/hyperdynamic LV function, absence of mitral regurgitation (no V-wave), effective LA relaxation, and even decompression across a nonrestrictive ASD/PFO (LA→RA during systole lowers LA pressure further, steepening the PV–LA gradient). Transiently, inspiration can also enlarge S by dropping intrathoracic/LA pressures. Conversely, conditions that raise LA pressure in systole—most notably mitral regurgitation or poor LV longitudinal function—blunt or reverse S.

A prominent D wave reflects augmented early-diastolic forward flow from the pulmonary veins into the left ventricle. At mitral valve opening, left atrial (LA) pressure briefly exceeds left ventricular (LV) pressure and, coupled with active LV relaxation (“suction”), releases blood that has accumulated in the LA/pulmonary venous reservoir during ventricular systole. The result is a rapid “conduit” emptying into the LV, recorded as a taller, sharper D wave. Situations that increase LA preload or enhance early-diastolic LV suction—such as left-to-right shunting with high pulmonary venous return (e.g., a significant PDA) or tachycardia with shortened diastasis—accentuate the D wave, whereas impaired LV relaxation or elevated LV filling pressures tend to blunt D and may increase the atrial reversal (Ar) wave.

• Fadel BM, Pibarot P, Kazzi BE, Al-Admawi M, Galzerano D, Alhumaid M, Alamro B, Mahjoub H, Echahidi N, Mohty D. Spectral Doppler Interrogation of the Pulmonary Veins for the Diagnosis of Cardiac Disorders: A Comprehensive Review. J Am Soc Echocardiogr. 2021 Mar;34(3):223-236. doi: 10.1016/j.echo.2020.09.012. Epub 2020 Oct 22. PMID: 33678222.

• NephroPOCUS - Review of pulmonary venous Doppler