Cardio-Respiratory Interactions in the Newborn

Targeted neonatal echocardiography was requested to guide the management of an extremely preterm infant with profound hypoxemia and marked differential cyanosis at 10 days of life. At the time of evaluation, preductal oxygen saturation ranged from 67% to 75%, while postductal saturation was markedly lower, around 40%. Blood pressure was within the expected range for postmenstrual age (24 weeks), measuring 58/47 mmHg (mean 51 mmHg) via an umbilical arterial catheter positioned in the postductal aorta. The infant was receiving inhaled nitric oxide at 20 ppm because of a prior diagnosis of pulmonary hypertension and inability to wean, in the setting of severe rebound hypoxemia. Respiratory support consisted of high-frequency jet ventilation with an FiO₂ of 100%, a mean airway pressure of 15 cmH₂O, and a rate of 420 breaths per minute.

Targeted neonatal echocardiography demonstrated right-to-left shunting at both the patent ductus arteriosus and the patent foramen ovale, with preserved right and left ventricular systolic function. Right-to-left ductal shunting directed deoxygenated blood from the pulmonary artery into the descending aorta, explaining the severe postductal desaturation, while interatrial shunting through the foramen ovale contributed to systemic hypoxemia and low preductal saturations. Pulse-wave Doppler interrogation of the right and left pulmonary arteries revealed very low flow velocities with characteristic mid-systolic notching, consistent with markedly elevated pulmonary vascular resistance.

The respiratory status was notable for significant hypercapnia, with a PaCO₂ of 65 mmHg, in the context of ventilation using a high mean airway pressure. Chest radiography showed marked lung hyperinflation with flattened diaphragms and a small cardiac silhouette. The key therapeutic intervention was prompt optimization of respiratory mechanics. The clinical team was advised to rapidly reduce the mean airway pressure, perform airway suctioning, and improve lung aeration. These interventions resulted in an immediate reversal of both ductal and interatrial shunting. As intra-alveolar pressure decreased and pulmonary perfusion improved, the shunt direction changed: the ductus arteriosus became fully left-to-right due to relief of extravascular vascular compression, and the foramen ovale shifted to predominantly left-to-right flow as right ventricular afterload decreased and left atrial preload improved through increased pulmonary venous return. This hemodynamic transition was accompanied by a striking bedside clinical response, with rapid normalization of oxygen saturations to 100%, resolution of the preductal–postductal gradient, and successful reduction of inspired oxygen from 100% to 45%. Over the subsequent 24 hours, the infant continued to improve, allowing complete discontinuation of inhaled nitric oxide, with FiO₂ requirements decreasing to approximately 25–30% by 48 hours off iNO.

Discussion and Physiology:

This case illustrates the profound and immediate impact of ventilatory strategy on neonatal cardiopulmonary physiology, highlighting how targeted respiratory optimization can rapidly reverse maladaptive shunt physiology and restore effective systemic oxygenation. The striking clinical improvement in this case can be explained by core principles governing the interaction between lung mechanics and pulmonary vascular physiology. The direction of flow across transitional shunts is governed by different but related mechanisms. Flow across the patent ductus arteriosus is primarily determined by the balance between pulmonary and systemic vascular resistance accross the various timepoints of the cardiac cycle, which establishes the pressure gradient between the pulmonary artery and the aorta. In contrast, shunting across the patent foramen ovale is largely determined by atrial pressure relationships, which are strongly influenced by ventricular compliance, filling and atrio-ventricular valve integrity (insufficiency and/or stenosis) rather than vascular resistance per se.

In the setting of normal atrioventricular and ventriculoarterial concordance, low pre-ductal oxygen saturation is most commonly attributable to impaired pulmonary oxygenation, typically due to ventilation–perfusion mismatch at the alveolar level, resulting in reduced oxygen content of pulmonary venous return. Pre-ductal desaturation may also arise from intracardiac mixing, particularly when a significant fraction of right atrial blood crosses into the left atrium, introducing deoxygenated blood directly into the systemic circulation at the pre-ductal level. Right to left shunting at the atrial level is dependent on the relationship in compliance between the downstream right and left ventricles, as well as integrity of corresponding atrio-ventricular valves and atrial filling. Additional sources of mixing that can further lower pre-ductal saturation include right-to-left shunting at the ventricular level in the presence of a ventricular septal defect, as well as retrograde delivery of desaturated blood into the ascending aorta via the ductus arteriosus. The latter is typically observed in conditions associated with left ventricular outflow tract obstruction or markedly reduced systemic ventricular output, whether due to functional impairment or structural disease of the systemic ventricle.

In this infant, severe hypoxia, hypercapnia, and acidosis created a potent milieu for pulmonary vasoconstriction. Elevated PaCO₂ and low pH are among the strongest stimuli for increasing pulmonary vascular resistance (PVR). In parallel, the use of a high mean airway pressure (MAP) during mechanical ventilation further exacerbated pulmonary hypertension by mechanically compressing alveolar and extra-alveolar capillaries, thereby increasing resistance to pulmonary blood flow and elevating pulmonary artery pressure. Together, these chemical and mechanical factors drove right ventricular afterload to suprasystemic levels, sustaining right-to-left shunting at the ductal level. The decreased pulmonary blood flow reduces left atrial preload, and de facto reduces left ventricular preload. This leads to increase right to left shunting at the atrial level due to underfilling of the left atrium, as well as a component of decreased right ventricular compliance. It can also further promote the right to left shunting at the ductal level due to decrease aortic filling. The therapeutic strategy directly targeted these determinants of elevated PVR. Reducing the MAP relieved mechanical compression of the pulmonary microvasculature, immediately lowering the mechanical component of PVR. This allows for more pulmonary blood flow and a decreased fraction of right to left ductal shunting, as well as increased left atrial preload and left ventricular filling, improving systemic flow. Improved left atrial filling also decreases the magnitude of right to left shunting at atrial level. The intrathoracic pressure by the increased mean airway pressure can also affect the right atrial pressure by extra-cardiac compression. Dropping the MAP can decrease the extra-cardiac pressure and the magnitude of right to left inter-atrial shunting. Concurrent airway suctioning and improved lung aeration enhanced alveolar ventilation, promoting more effective CO₂ elimination. As hypercapnia resolved and pH normalized, the powerful chemical stimulus for pulmonary vasoconstriction was rapidly removed, resulting in pulmonary vasodilation. With increased pulmonary blood flow, the fraction of dexoygenated blood shunting accross the inter-atrial shunt reduced and the left atrium was better preloaded, leading to improve aortic filling as well. This reversal of the afterload gradient led to immediate shunt reversal: the PDA transitioned to fully left-to-right flow, and atrial shunting across the PFO also became left-to-right. With elimination of right-to-left shunting, deoxygenated blood was no longer delivered to the systemic circulation. Instead, the full cardiac output traversed a now low-resistance pulmonary vascular bed, allowing efficient oxygenation and resulting in rapid, sustained normalization of systemic oxygen saturation.

This illustrative case highlights the tight coupling between respiratory mechanics and cardiovascular physiology in extremely preterm infants, in whom ventilatory management often becomes the dominant determinant of hemodynamic status. Very immature newborns are exquisitely sensitive to increases in mean airway pressure, which raise intra-alveolar and intrathoracic pressures and mechanically compress the pulmonary vasculature. This acute increase in pulmonary vascular resistance imposes a sudden afterload on the immature right ventricle, which has limited capacity to tolerate even modest elevations in afterload, leading to reduced pulmonary blood flow and impaired pulmonary venous return. In this context, reflex escalation of cardiovascular medications may worsen toxicity without addressing the primary pathophysiology. Instead, the initial and most effective intervention is reduction of excessive mean airway pressure to relieve pulmonary vascular compression, restore pulmonary blood flow, and re-establish left atrial and left ventricular filling, thereby improving cardiac output. Hypercapnia and respiratory acidosis further amplify this maladaptive physiology by acting as potent pulmonary vasoconstrictors, often in the setting of lung hyperinflation and auto-PEEP due to insufficient expiratory time. Sustained exposure to high airway pressures may lead to progressive right ventricular dilation, severe tricuspid regurgitation, elevated right atrial pressure, and right-to-left atrial shunting with systemic desaturation. In extreme cases, critically reduced right ventricular output results in severe underfilling of the pulmonary artery, creating a physiology that mimics functional pulmonary valve stenosis or atresia, with minimal or absent antegrade RV outflow and pulmonary blood flow becoming effectively ductal-dependent. This case underscores how targeted correction of lung mechanics, rather than escalation of cardiovascular support, is often the key to reversing profound cardiopulmonary instability in the most immature infants.

Key Messages:

Lung overdistension and high mean airway pressure markedly increase pulmonary vascular resistance, reduce pulmonary blood flow, and drive right-to-left shunting at both the atrial and ductal levels, resulting in hypoxemia and systemic hypoperfusion.
Reduced pulmonary blood flow leads to left atrial and left ventricular underfilling, decreased left ventricular cardiac output, while hypercapnia and acidosis further worsen pulmonary vasoconstriction and right ventricular afterload.
Targeted reduction of mean airway pressure and correction of hyperinflation can rapidly restore pulmonary blood flow, normalize shunt direction, improve oxygenation, and reestablish effective systemic cardiac output.
Cardiac disturbances in the most immature extremely premature infants may be secondary to adverse cardio-respiratory interactions. The first priority is to reassess respiratory status and ventilatory strategy, with close attention to mean airway pressure (MAP) and any degree of hyperinflation, as these infants are extremely sensitive to even modest increases in MAP. Hyperinflation can occur at MAPs as low as 8–9 cmH₂O and significantly affect both pulmonary vascular resistance and systemic venous return. Similarly, ventilatory settings that drive PaCO₂ into the normal range may exacerbate left-to-right ductal shunting, and in such cases mild permissive hypercapnia (PaCO₂ 50–60 mmHg) may be preferable. Once these cardio-respiratory contributors are addressed, it is essential to avoid polypharmacy and to target a single physiologic pathway rather than layering multiple drugs without a clear mechanistic rationale.
An Echo/TnECHO assessment can help define the predominant mechanism and guide more precise therapy to avoid multiple agents being introduced, but only once the respiratory care has been optimized. Finally, after optimizing respiratory status, if a patient is still considered to have cardiovascular instability requiring pharmacologic support, it is important to avoid piling on multiple agents. An ineffective drug should be discontinued before introducing another, rather than adding therapies without evidence of benefit.

Cardiorespiratory interactions:

The fundamental distinction between spontaneous breathing and positive pressure ventilation (PPV) lies in intrathoracic pressure: spontaneous breaths generate negative pressure that augments venous return, whereas PPV increases intrathoracic pressure and tends to impair preload.
Cardiac output depends on stroke volume and heart rate; PPV primarily influences cardiac output by altering preload and afterload, rather than heart rate or intrinsic contractility.
PPV reduces systemic venous return by increasing right atrial pressure and diminishing the pressure gradient driving venous drainage into the thorax, potentially lowering right ventricular preload and cardiac output.
PPV can improve right ventricular afterload by optimizing lung volume and restoring functional residual capacity, thereby reducing pulmonary vascular resistance—provided overdistension is avoided. If there is overdistension - it will increase pulmonary vascular resistance and right ventricular afterload which is poorly tolerated, especially by immature premature infants.

Right ventricular output determines left ventricular preload; impaired right-sided filling or output translates directly into reduced left atrial filling and systemic cardiac output.
A major benefit of PPV is left ventricular afterload reduction: increased intrathoracic pressure lowers left ventricular wall stress, functioning as a form of mechanical left ventricular assistance.
Abrupt withdrawal of PPV in patients with left ventricular dysfunction may precipitate acute cardiac failure due to sudden restoration of high afterload.
Right and left ventricular function are interdependent; excessive negative intrathoracic pressure increases right ventricular filling and septal shift, impairing left ventricular filling and output (e.g., pulsus paradoxus).
Negative pressure ventilation augments venous return and right ventricular preload but increases left ventricular afterload, making it beneficial in preload-dependent states and potentially harmful in left ventricular dysfunction.

DO₂ - Oxygen Delivery

Cardiopulmonary interactions in the NICU are easiest to understand when you start from the common goal: oxygen delivery to tissues for aerobic metabolism. Oxygen delivery (DO₂) depends on three linked components: cardiac output (the heart’s contribution), hemoglobin concentration (oxygen-carrying capacity), and arterial oxygen saturation (largely determined by the lungs). In practice, the heart and lungs are never operating in isolation. They sit in the same intrathoracic compartment, share transmitted pressures, and constantly reshape each other’s physiology across the respiratory and cardiac cycles. The clinician’s duty at the bedside is to think through oxygen delivery as a chain that begins at the ventilator or atmosphere and ends at the tissue, then identify which link is failing and which intervention will restore delivery without creating a new problem elsewhere.

Thoracic pressures

A foundational concept is that the heart and lungs share a pressure chamber. The intrathoracic cavity contains the lungs and the heart, and the pleural pressure is transmitted not only to the lung but also to the great vessels and, through the pericardial space, to the heart itself (with the important exception of pericardial disease, where pericardial pressure can become dissociated). The abdomen is a separate pressure chamber divided from the thorax by the diaphragm. That separation matters because venous return depends on pressure gradients between the abdominal venous reservoirs (especially the inferior vena cava) and the right atrium inside the thorax. Even small changes in these compartment pressures, particularly during ventilation, can meaningfully change preload, afterload, and ventricular output.

Spontaneous breathing vs PPV

To build the physiology, it helps to start with the mechanics of breathing. In spontaneous respiration, diaphragmatic contraction and accessory muscle use generate a more negative pleural pressure during inspiration (and a positive pressure is exerted in the abdomen by this contraction, which increases the IVC-RA gradient and promotes forward flow towards the right atrium increasing right ventricular preload). This negative intrathoracic pressure draws air into the lungs until alveolar and atmospheric pressures equilibrate. During expiration, the diaphragm relaxes, pleural pressure rises toward baseline, and air leaves the lungs until alveolar pressure again equals atmospheric pressure. Positive pressure ventilation is the opposite mechanical strategy. Instead of the patient generating negative intrathoracic pressure, the ventilator delivers positive pressure into the airways and alveoli, raising intrathoracic pressure during inspiration. This difference in the direction of thoracic pressure change is the reason ventilation is also a hemodynamic intervention. During positive pressure ventilation, there is also flattening of the diaphragm which increases intra-abdominal pressure

Figure by Dr Satyan Lakshminrusimha from Open-Source Article: Sehgal, A., Ruoss, J.L., Stanford, A.H. et al. Hemodynamic consequences of respiratory interventions in preterm infants. J Perinatol 42, 1153–1160 (2022). https://doi.org/10.1038/s41372-022-01422-5

From: Ngwenya, M. "Cardiopulmonary interactions." Southern African Journal of Anaesthesia and Analgesia (2023): 6-10.

Preload is the first major hemodynamic interface with ventilation. From the right-sided perspective, preload reflects systemic venous return and right atrial pressure. The IVC and abdominal venous reservoirs sit in the intraabdominal compartment while the right atrium sits in the thorax. During spontaneous inspiration, pleural pressure becomes more negative while intraabdominal pressure rises as the diaphragm descends. That enlarges the pressure gradient driving blood from the abdomen into the thorax and increases right heart filling during inspiration. With positive pressure ventilation, the right atrial pressure rises during inspiration because intrathoracic pressure rises. The gradient between the abdominal venous system and the right atrium is therefore reduced compared with spontaneous breathing, and the inspiratory augmentation of venous return is blunted. Mechanical ventilation does not necessarily abolish venous return, but it changes the pattern and magnitude of preload variation across the respiratory cycle, and the effect becomes more pronounced when mean airway pressure is high or when lung hyperinflation creates sustained elevations in intrathoracic pressure.

Systemic venous return can be expressed in a simple quantitative way: venous return is proportional to the pressure gradient between the upstream venous reservoir and the right atrium, divided by resistance to venous flow (Venous Return ≈ (Venous System Pressure − Right Atrial Pressure) / Venous Resistance). This framing is clinically useful because it forces the bedside clinician to ask which term has changed: has upstream venous pressure fallen (relative hypovolemia, venodilation), has right atrial pressure risen (high intrathoracic pressure, RV failure, tamponade physiology), or has venous resistance increased (venoconstriction, external compression, elevated intra-abdominal pressure)? It also explains why mechanical ventilation and patient positioning can have immediate hemodynamic effects: even small increases in right atrial pressure from elevated intrathoracic pressure reduce the driving gradient for venous return. Practical modifiers of venous return include posture and tone—Trendelenburg position and supine positioning can increase venous return by augmenting venous pressure and central blood volume, while skeletal muscle paralysis removes the “muscle pump” and can reduce venous return despite stable blood pressure. In parallel, changes in venous tone (e.g., catecholamine-driven venoconstriction - such as with the use of vasoactive agents - vs sedation-related venodilation) shift the effective stressed volume and alter Venous System Pressure even without any change in total circulating volume. A related but often under-emphasized limitation is that venous return has physical “choke points,” especially during large negative pressure swings. With vigorous spontaneous breathing, intrathoracic pressure may become markedly negative and increase the gradient for venous drainage toward the right atrium—up to a point. Beyond that point, the great veins can partially collapse at the thoracic inlet, limiting further increases in venous return despite progressively more negative pleural pressure. This helps explain why extreme work of breathing does not always translate into unlimited preload augmentation; instead, it can precipitate hemodynamic compromise by increasing LV transmural afterload and causing large swings in venous return that the immature myocardium cannot compensate for. Ventilatory strategy is tightly linked to the circulatory relationships, and the impact can be visualized as shifts in the intersection between the venous return curve and the cardiac function curve as PEEP (or mean airway pressure) increases. As PEEP rises (e.g., from moderate to high levels), right atrial pressure increases and the venous return curve shifts rightward, lowering the achievable venous return for any given upstream venous pressure unless the system compensates by increasing stressed volume and venous tone. Neurohumoral responses (baroreceptor-mediated sympathetic activation) can partially mitigate this by raising systemic venous pressure through venoconstriction, but that compensation is variable in sick preterm infants and may be offset by sedation, paralysis, or relative hypovolemia. The bedside implication is that hypotension or low cardiac output after increasing MAP/PEEP may not reflect “cardiac failure” but a predictable pressure–gradient problem: the ventilator has raised right atrial pressure and reduced the gradient between the Venous System Pressure and Right Atrial Pressure, decreasing venous return and RV preload.

Relationship between cardiac function and venous return curves illustrates the hemodynamic effects of positive end-expiratory pressure (PEEP). As PEEP increases lung volume, intrathoracic pressure rises to a degree determined by lung volume and the relative compliance of the lung and chest wall. This positive intrathoracic pressure is transmitted to the right atrium, increasing right atrial pressure and thereby reducing the pressure gradient for systemic venous return. Under theoretical conditions of zero PEEP, venous return would fall along the venous return curve from point A toward point D as right atrial pressure increases. In practice, however, increasing PEEP from 0 to 10 and then to 20 cm H₂O produces a rightward shift of the cardiac function curve, reflecting the effects of elevated intrathoracic pressure on cardiac filling and performance. Simultaneously, arterial baroreceptor-mediated neurosympathetic activation raises venous system pressure by decreasing venous capacitance. The combined effect of these changes is a progressive shift in the equilibrium point from A to B to C, which partially mitigates the decline in systemic venous return and cardiac output during mechanical ventilation. Although increased intrathoracic pressure elevates right atrial pressure and tends to reduce venous return, the compensatory increase in venous tone and stressed volume limits the fall in cardiac output, explaining why the hemodynamic consequences of PEEP are often less severe than would be predicted by intrathoracic pressure alone.

Modified from - Weisz, Dany E. "Cardiopulmonary Interactions in the Mechanically Ventilated Neonate." Neonatology Questions and Controversies: Neonatal Hemodynamics-E-Book (2023): 64.

VR0 = venous return at Zero PEEP; VR-P = venous return with PEEP.

Changes in right-sided preload also influence the left heart through ventricular interdependence. Because the ventricles share the interventricular septum and exist within the constraint of the pericardium, extra filling of the RV can shift the septum leftward and reduce relative LV diastolic filling. In spontaneously breathing infants, the inspiratory increase in RV preload can therefore transiently reduce LV filling and stroke volume. Under positive pressure ventilation, the inspiratory increase in RV filling is typically less pronounced, so this specific septal effect may be smaller. However, mechanical ventilation introduces its own complexities: lung hyperinflation can directly constrain the heart and impair LV filling, and elevated PVR can increase RV pressures and secondarily alter septal geometry. For bedside interpretation, the key is that LV stroke volume and output can show respiratory variability for more than one reason, and the direction of change depends on the combined effects of preload, pericardial constraint, lung volume, and RV afterload.

West's Zones

Lung units are not homogeneous, and neither is perfusion. West’s zones are a helpful way to conceptualize how regional blood flow depends on the relationship between alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure.

West Zone 1: When alveolar pressure exceeds both arterial and venous pressures, alveolar capillaries are compressed and perfusion can be absent, creating dead space ventilation; this can occur with excessive PEEP or very low pulmonary arterial pressure (for example, profound shock).
West Zone 2: When arterial pressure exceeds alveolar pressure but alveolar pressure remains higher than venous pressure, perfusion becomes intermittent and may occur primarily during systole.
West Zone 3: When both arterial and venous pressures exceed alveolar pressure, perfusion is continuous, which is the functional state that supports stable gas exchange and, in older patients, allows pulmonary capillary wedge pressure measurement because there is a continuous column of blood.
A fourth concept, sometimes described as “West zone 4,” adds the effect of elevated interstitial pressure, as in pulmonary edema, where extravascular compression and edema-related changes impair perfusion and gas exchange even if the classic zone relationships appear otherwise favorable. This can be seen in the context of acute kidney injury, hydrops, significant pulmonary overcirculation, etc.
In the NICU, these West-zone states can shift quickly as lung volume, airway pressure, blood pressure, and interstitial fluid change. Ideally, you want to achieve lung recruitment optimization to be at functional residual capacity (FRC) and various supporting pressures (mean airway pressures) may be necessary depending on pulmonary compliance to achieve this.

From: Bootsma IT, Boerma EC, de Lange F, Scheeren TWL. The contemporary pulmonary artery catheter. Part 1: placement and waveform analysis. J Clin Monit Comput. 2022 Feb;36(1):5-15. doi: 10.1007/s10877-021-00662-8. Epub 2021 Feb 10. PMID: 33564995; PMCID: PMC8894225.

By LungVolume.jpg: The original uploader was Vihsadas at English Wikipedia.derivative work: rscottweekly - LungVolume.jpg, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=15109470

Intra-Alveolar vs Extra-Alveolar Vessels

RV afterload is tightly linked to pulmonary vascular resistance, which is strongly dependent on lung volume through two vessel compartments: intra-alveolar and extra-alveolar vessels. Intra-alveolar vessels run along the alveoli and are compressed as alveoli distend; higher lung volumes can therefore increase intra-alveolar resistance. Extra-alveolar vessels course through the interstitium between alveoli and are held open by radial traction; higher lung volumes tend to decrease extra-alveolar resistance by increasing traction and opening these vessels. The net result is the classic U-shaped relationship between lung volume and total PVR, with the lowest PVR near functional residual capacity. This is why the “right” mean airway pressure is not a number in isolation. The goal is achieving an appropriate FRC for that infant’s lung mechanics and disease state, because both under-recruitment and over-recruitment can increase PVR, reduce pulmonary blood flow, and destabilize cardiopulmonary coupling.

Ventilation and effects on Left Ventricle (LV).

LV afterload is different because the LV ejects into the systemic circulation, which leaves the thorax and operates at higher pressures than the pulmonary circuit. A useful proxy for LV afterload is LV wall stress, classically described by the law of Laplace, where wall stress increases with intracavitary pressure and radius and decreases with greater wall thickness.

Law of Laplace is used to estimate left ventricular (LV) wall stress. The formula is: LV Wall Stress = (LV Pressure × Radius) / (2 × LV Wall Thickness)

This framework explains why a dilated ventricle experiences higher wall stress, while concentric hypertrophy can reduce wall stress as an adaptive response. It also clarifies how ventilation changes LV work. In a stable spontaneously breathing infant, intrathoracic pressure is relatively low, so the LV must generate enough pressure to overcome the gradient to the aorta. In deep negative breathing, as in severe work of breathing, intrathoracic pressure becomes more negative. That increases the transmural pressure the LV must overcome to eject into the aorta, effectively increasing LV afterload and myocardial work. Intubation and positive pressure ventilation raise intrathoracic pressure, which can reduce LV transmural afterload and unload the LV, even as it may reduce venous return. Positive pressure ventilation (PPV) generally decreases left ventricular (LV) preload by increasing intrathoracic pressure, which impedes venous return to the right heart, reduces right ventricular filling, and can cause septal shift towards the LV, limiting LV filling. While PPV also decreases LV afterload, reducing the work for the LV to pump, the dominant effect, especially with high pressures (like PEEP), is often a reduction in preload, leading to lower cardiac output, particularly in volume-depleted patients. When you combine preload effects, ventricular interdependence, and RV/LV afterload changes, it becomes clear why ventricular output can vary breath-to-breath and why changes in ventilation settings can produce immediate hemodynamic consequences.

At a practical level, this is why ventilator management belongs in the hemodynamic toolkit. “High MAP” is not inherently wrong; excessive MAP for a given lung compliance (with hyperinflation and/or air trapping) is the problem. The target is adequate recruitment to reach FRC without hyperinflation, because hyperinflation can simultaneously reduce venous return, increase PVR, and constrain the heart. In some clinical scenarios, clinicians may find themselves increasing MAP repeatedly to recruit the “bad” lung regions while inadvertently overdistending already open regions, pushing the infant into hyperinflation with adverse hemodynamic effects. Modes that allow stronger patient-driven synchrony and variable inspiratory effort, such as neurally adjusted ventilatory assist when appropriate, can sometimes improve oxygenation without the same tendency toward uniform overdistension, provided the infant has intact respiratory drive and diaphragmatic function. Regardless of mode, the most important safeguard is reassessment over time. A MAP that was appropriate six hours ago can become excessive after surfactant, diuresis, or recovery of compliance, and failure to wean in step with improving compliance is a common pathway to hyperinflation and cardiopulmonary compromise.

The heart and lungs share the same pressure environment, so changing one inevitably changes the other. The goal of ventilation is not achieving a particular number but achieving FRC for that infant’s disease state, because both under- and over-recruitment can worsen PVR and destabilize blood flow. Spontaneous and mechanical ventilation have opposing effects on intrathoracic pressures and therefore on venous return, ventricular filling, and LV transmural afterload. Finally, ventilation should be used deliberately as part of hemodynamic management: it can help oxygen delivery by improving recruitment and unloading the LV, or it can worsen oxygen delivery by reducing venous return, increasing PVR, and constraining the heart. Thinking through oxygen delivery from the ventilator to the mitochondria is the most reliable way to choose the next intervention and to anticipate its cardiopulmonary consequences.

Clinical Scenarios in Neonatology

RDS / Surfactant

In bedside reality, ventilation settings and lung recruitment state usually matter more than the named mode, because the same mode can be lung-protective at one set of settings and hemodynamically disruptive at another. Several common NICU disease states illustrate these principles. In RDS, surfactant replacement is primarily a respiratory therapy, but it predictably changes hemodynamics by improving compliance and recruitment toward FRC, thereby lowering PVR and improving RV performance. As pulmonary blood flow improves, left-sided return may increase, and ductal shunt volume may rise because the pressure-resistance relationships across the PDA change when PVR falls. Clinically, this means surfactant can shift both pulmonary and systemic flows, and post-surfactant physiology should be reassessed rather than assumed. Rapid shifts may be associated with excessive pulmonary blood flow that the immature capilaries cannot handle (see section on pulmonary hemorrhage).

Pulmonary overcirculation

Pulmonary overcirculation (such as secondary to a large left to right PDA leading to significantly increased pulmonary blood flow) can lead to pulmonary venous congestion in the setting of elevated pulmonary venous pressures (either due to the torential Qp:Qs overwhelming the pulmonary venous capacitance, or in the setting of adverse left ventricular / left atrial compliance leading to a rise in left atrial pressure). Preterm pulmonary vasculature is relatively fragile and poorly tolerant of the resulting congestion, so pulmonary edema and capillary leak can develop, potentially worsening gas exchange and increasing ventilatory requirements. This pulmonary consequence then feeds back to the heart by increasing PVR, altering RV loading conditions, and influencing interventricular coupling. PDA is therefore a cardiopulmonary condition in both directions: it is not only a cardiac shunt but also impacts lung mechanics, interstitial fluid, and PVR.

Pulmonary Hypertension (see full section here)

For pulmonary hypertension, a structured etiologic framework is helpful because the pulmonary circulation can be “high pressure” for fundamentally different reasons that require different therapies. One practical approach is to classify causes by whether pulmonary artery pressure is elevated primarily due to increased pulmonary blood flow (high-flow states), increased pulmonary vascular resistance (vasoconstriction, vascular remodeling, or mechanical compression from lung volume/pressure), or increased pulmonary venous pressure (elevated pulmonary capillary wedge pressure from left atrial hypertension). This can then be subdivided into more reversible (acute) drivers versus less reversible (chronic) drivers, which directly affects expectations for response to interventions like recruitment optimization, oxygenation/CO₂ correction, or pulmonary vasodilators. A complementary hemodynamic classification is to differentiate pre-capillary pulmonary hypertension (high PVR with relatively normal left atrial pressure), post-capillary pulmonary hypertension (elevated left atrial/pulmonary venous pressure with secondary pulmonary hypertension), and mixed physiology. This distinction matters at the bedside because pre-capillary physiology predominantly loads the RV (high RVSP, reduced pulmonary blood flow, impaired LV preload), whereas post-capillary physiology is often dominated by pulmonary venous congestion and reduced pulmonary compliance, where aggressive pulmonary vasodilation or excessive fluid can worsen edema and gas exchange. The right ventricle initially compensates to rising afterload through specific adaptive mechanisms, but those mechanisms have limits—especially in extremely preterm infants. Beyond the classic Frank–Starling response (heterometric adaptation via fiber stretch), the RV can transiently increase contractile force without major chamber dilation through homeometric adaptation, in which contractility rises through changes at the sarcomere level. This can maintain RV output early in the course of pulmonary hypertension even when pulmonary artery pressure rises. However, when afterload becomes excessive or sustained, these compensatory mechanisms fail: RV dilation develops, tricuspid regurgitation increases, right atrial pressure rises, and both venous return and pulmonary blood flow fall—creating a self-reinforcing spiral that favors right-to-left shunting at the PFO and PDA and progressive systemic hypoxemia (when these shunts are present).

Fluid administration

Fluid resuscitation for hypotension is another classic example of a cardiopulmonary intervention that is often treated as purely hemodynamic. The Frank-Starling relationship describes how stroke volume responds to preload, but the lung has a parallel vulnerability captured by the concept of increasing lung interstitial fluid as hydrostatic pressures rise, particularly when the heart is already on the flatter portion of the Frank-Starling curve. In infants who are preload responsive, a fluid bolus can raise stroke volume with relatively little penalty in lung water. In infants who are not preload responsive, the same bolus may produce minimal improvement in output while substantially increasing pulmonary interstitial pressure and edema, with downstream consequences for ventilation, oxygenation, PVR, and RV function. This is why fluid should be framed as a cardiorespiratory therapy, not just a blood pressure therapy.

The Frank–Starling curve describes the intrinsic myocardial property linking preload (end-diastolic volume or pressure) to stroke volume or cardiac output. As preload increases, stroke volume rises because of improved sarcomere overlap—up to a plateau, beyond which further preload produces little or no increase in output. This relationship is static, ventricular-centric, and assumes relatively stable contractility and afterload. It answers the question: “Given a certain preload, how much output can this ventricle generate?”

Marik–Phillips curve

The Marik–Phillips curve reframes fluid responsiveness from a dynamic, systemic perspective. Instead of plotting preload against stroke volume, the Marik-Phillips Curve is used to describe the relationship between increased preload (such as with fluid administration or passive leg raise) and the development of extravascular lung water (pulmonary edema). While both curves use Preload (filling pressure or volume) on the x-axis, they track two very different outcomes:

Frank-Starling Curve: Tracks Cardiac Output (the "Benefit"). It shows that as you increase preload, the heart pumps more effectively—until it reaches a plateau.
Marik-Phillips Curve: Tracks Lung Water/Edema (the "Risk"). It shows that as you increase preload, there is a point where fluid stops helping the heart and starts leaking into the lungs. This curve tends to be shifted in septic infants where for a given preload, there is a higher likelihood of alveolar spillage.

See more in the Neonatal Septic Shock and Hemodynamic Physiology section.

Legend - Teixeira-Neto FJ et al: "The Marik-Phillips curve and the Frank-Starling curve correlating changes in extra vascular lung water (EVLW) and stroke volume (SV) with preload, respectively. For individuals whose heart is operating on the ascending limb of the Frank-Starling curve, an increase in preload induced by a fluid challenge (a) does not substantially increase EVLW. If a fluid challenge is administered to individuals whose heart is operating on the flat portion of the Frank-Starling curve, the increase in preload (b) may result in a large increase in EVLW. Due to endothelial glycocalyx damage associated with sepsis, larger increases in EVLW can be expected in septic individuals (dashed curve)." From: Teixeira-Neto FJ, Valverde A. Clinical Application of the Fluid Challenge Approach in Goal-Directed Fluid Therapy: What Can We Learn From Human Studies? Front Vet Sci. 2021 Aug 3;8:701377. doi: 10.3389/fvets.2021.701377. PMID: 34414228; PMCID: PMC8368984.

Graphical Summary of Concepts

Relationship between functional residual capacity, lung inflation, mean airway pressure, and their impact on pulmonary vascular resistance and right ventricular afterload

Figure Legend. Relationship between lung volume, functional residual capacity (FRC), mean airway pressure, pulmonary vascular resistance (PVR), and right ventricular (RV) afterload. Pulmonary vascular resistance follows a U-shaped relationship with lung volume. At low lung volumes (near residual volume, RV), alveolar collapse and reduced lung inflation lead to narrowing and derecruitment of extra-alveolar vessels, resulting in elevated PVR. As lung volume increases toward FRC, recruitment and distension of extra-alveolar vessels (e.g., corner vessels) predominate, leading to a reduction in total PVR and optimal RV afterload conditions. With further lung inflation toward total lung capacity (TLC), increasing alveolar pressure compresses alveolar (septal) vessels, causing a rise in PVR despite continued extra-alveolar vessel distension. The net effect is a U-shaped total newborn PVR curve, highlighting FRC as the zone of minimal PVR and most favorable RV loading conditions. The schematic illustrates the balance between pulmonary vascular recruitment and compression across low and high lung volumes, emphasizing how excessive atelectasis or overdistension—often influenced by mean airway pressure—can increase RV afterload.

Positive pressure ventilation - Heart-Lung Interactions

RV Preload
- Reduction in Venous Return: Positive pressure ventilation increases intrathoracic pressure, which decreases the pressure gradient between the systemic veins and the right atrium. This reduction in the pressure gradient leads to decreased venous return to the heart. This results in reduced RV preload, which means less filling of the right ventricle during diastole. Hypovolemic Patients**: Patients with low blood volume are more susceptible to significant decreases in RV preload, potentially leading to reduced cardiac output and hypotension.
RV Afterload
- Increase in Pulmonary Vascular Resistance (PVR): Positive pressure ventilation can increase alveolar pressure, leading to compression of pulmonary capillaries and an increase in PVR.
- However, under-insufluation and alveolar collapse may also contribute negatively to PVR. As such, there is a inverse U-shape relationship where there is a tight zone where alveolar recruitment may optimize PVR.
- In patients with preexisting right heart failure or pulmonary hypertension, increased RV afterload can exacerbate right ventricular dysfunction and lead to worsening of heart failure symptoms.
LV Preload
- Reduction in Pulmonary Venous Return: The reduction in RV preload due to decreased venous return results in less blood being pumped into the pulmonary circulation and subsequently to the left atrium. This results in decreased LV preload, which means less filling of the left ventricle during diastole. Reduced LV preload can lead to decreased stroke volume and cardiac output. This effect is more pronounced in patients with compromised LV function.
LV Afterload
- Reduction in LV Afterload: Positive pressure ventilation increases intrathoracic pressure, which is transmitted to the aorta and other large arteries. This results in a reduction of transmural pressure (the difference between intrathoracic pressure and blood pressure within the aorta), effectively reducing LV afterload. This results in decreased resistance against which the left ventricle must pump blood, potentially improving LV ejection. For patients with LV dysfunction or heart failure, reduced afterload can enhance stroke volume and cardiac output.

Targeted Neonatal Echocardiography

Parasternal long-axis view demonstrates good aortic valve opening and closure, with no evidence of left ventricular outflow tract obstruction. There is a subjective appearance of increased myocardial thickness involving the right ventricular anterior wall, the interventricular septum, and the left ventricular posterior wall. Interpretation is limited, however, by concern for low left ventricular preload, with near-kissing ventricular walls in systole, which may exaggerate the impression of wall thickening.

Color Doppler over the pulmonary artery bifurcation demonstrates well-sized left and right pulmonary arteries with preserved antegrade flow (blue). A focal red color signal is noted within the main pulmonary artery, consistent with flow disturbance or swirling, which can be observed in the setting of increased downstream afterload.

Pulsed Wave (PW) Doppler envelope of the Right Pulmonary Artery. The waveform shows a sharp systolic peak with a Peak Systolic Velocity (PSV). The envelope has a relatively "clean" appearance with a well-defined spectral window, suggesting laminar flow without significant turbulence. The acceleration time appears brisk. There is mid-systolic notching, elevating the suspicion for increased pulmonary vascular resistance in the right pulmonary vasculature.

Pulsed Wave Doppler interrogation of the Left Pulmonary Artery. The waveform here is similar in morphology to the RPA. The acceleration time appears brisk. There is mid-systolic notching, elevating the suspicion for increased pulmonary vascular resistance in the left pulmonary vasculature.

Color Doppler over the left atrium and pulmonary venous confluence demonstrates pulmonary venous return to the left atrium. The Doppler sample volume is positioned at the ostium of the left lower pulmonary vein. In the setting of a strictly right-to-left patent foramen ovale, it is essential to confirm normal pulmonary venous drainage and to interrogate all pulmonary veins at their ostia to exclude anomalous pulmonary venous return.

PW-Doppler at the left lower pulmonary vein outlining the Systolic and Diastolic, as well as the Atrial reversal phases. Velocities are midly reduced (less than 30 m/s)

PW-Doppler at the right upper pulmonary vein.

Pulmonary venous flow velocities:

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.

PW-Doppler at the left upper pulmonary vein.

PW-Doppler at the right lower pulmonary vein.

PW Doppler interrogation of the right ventricular outflow tract from the subcostal short-axis view demonstrates antegrade systolic flow. In some Doppler envelopes, there is a suggestion of mid-systolic notching, a finding that may reflect increased downstream afterload, such as pulmonary vascular constriction or other causes of elevated pulmonary arterial impedance.

PW Doppler interrogation of the right ventricular outflow tract from the parasternal long axis view demonstrates antegrade systolic flow. In some Doppler envelopes, there is a suggestion of mid-systolic notching, a finding that may reflect increased downstream afterload, such as pulmonary vascular constriction or other causes of elevated pulmonary arterial impedance.

Apical four-chamber view. There is intracavitary flow acceleration in both ventricles, a pattern that may be observed in the presence of significant ventricular hypertrophy and/or reduced ventricular preload with increased wall apposition. In this case, right ventricular preload is reduced, with a small right atrium and only trace tricuspid regurgitation. Right ventricular systolic function is preserved, as assessed by TAPSE and fractional area change (not shown). Left ventricular preload is also reduced, consistent with diminished pulmonary blood flow.

B-mode apical four-chamber view. This view demonstrates preserved right and left ventricular systolic function. Left ventricular ejection fraction was calculated at 64%.

Pulsed-wave Doppler of right ventricular inflow (mitral valve). PW Doppler interrogation at the level of the mitral valve inflow demonstrates a biphasic diastolic filling pattern with distinct early (E) and late atrial (A) waves. The E wave is lower than the A wave, which can be seen in normal transitional physiology. However, this pattern here seems to be consistent with some degree of restrictive physiology from decreased RV preload.

Pulsed-wave Doppler of left ventricular inflow (mitral valve). PW Doppler interrogation at the level of the mitral valve inflow demonstrates a biphasic diastolic filling pattern with distinct early (E) and late atrial (A) waves. The E wave is lower than the A wave, which can be seen in normal transitional physiology. However, this pattern here seems to be consistent with some degree of restrictive physiology from decreased LV preload and/or presence of hypertrophy (if present underlying - challenging to ascertain in the context of decreased filling).

Apical sweep to the left ventricular apical five-chamber view. Anterior angulation from the apical window demonstrates the inflow–outflow tract relationship of the left ventricle. Color Doppler reveals intracavitary flow acceleration/aliasing at a Nyquist limit of 104 cm/s, consistent with left ventricular underfilling, with a possible contribution from ventricular hypertrophy (difficult to assess in the setting of reduced preload). There is normal inflow across the mitral valve without mitral regurgitation, and unobstructed systolic flow from the left ventricular cavity through the left ventricular outflow tract and aortic valve, excluding subvalvular or valvular obstruction.

Left ventricular outflow tract (LVOT) Doppler assessment. Pulsed-wave Doppler interrogation of the LVOT demonstrates a narrow, well-defined systolic envelope with preserved laminar flow. This pattern is often seen in the setting of reduced left ventricular preload rather than fixed obstruction.

Continuous-wave Doppler of left ventricular inflow. There is some capture of intra-cavitary acceleration from turbulence of flow.

Pulse-wave Doppler of left ventricular inflow. There is some capture of intra-cavitary acceleration from turbulence of flow.

Modified subcostal view. The right atrium is seen underfilled. The right ventricle has intra-cavitary acceleration and some degree of underfilling with apposition of ventricular walls during systole. There is a strict right to left inter-atrial shunt.

PW-Doppler at the level of the inter-atrial shunt (here a PFO). We can appreciate that the velocities are all negative, confirming that the inter-atrial shunt in completely right to left. In this context, one must rule out structural causes of this finding. The first one to rule-out is total anomalous pulmonary venous return. Then, one must rule out anything that would obstruct the flow from the right atrium to the right ventricle, and obstruction from the right ventricle to the pulmonary artery. Other reasons of a strict right to left inter-atrial shunt are outlined here.

Differential diagnosis of a strict right to left inter-atrial shunt:

TAPVR / TAPVD must be the first thing to rule out.
Persistent pulmonary hypertension of the newborn (PPHN) / severe pulmonary hypertension of any cause (e.g., CDH, MAS, RDS, pneumonia). Usually bidirectional but if there is significant RV failure (such as when the duct closes or become restrictive, or with antenatal PDA closure; the RV end-diastolic pressure will rise and there will be TR, leading to R-L shunt at the inter-atrial level).
Pulmonary atresia with intact ventricular septum
Pulmonary atresia with VSD (TOF with PA). Usually VSD is restrictive and the RV starts failing, or TR becomes apparent. The RV becomes poorly compliant and the ASD is right to left.
Critical pulmonary valve stenosis (usually with a restrictive VSD + high RV pressures).
Significant RV hypertrophy with poor RV compliance, increasing RA end-diastolic pressure relative to LA end-diastolic pressure
Hypoplastic right heart syndrome

Double-chambered right ventricle
Tricuspid atresia
Severe Ebstein anomaly / functional pulmonary atresia (massive TR)
Severe tricuspid valve dysplasia/stenosis or massive TR with RA hypertension
Cor triatriatum dexter / right atrial inflow obstruction.
Excessive preload to RA with poor RV compliance: AV malformation, VOGM, Hepatic AV malformation.
Acute severe RV failure/crisis (e.g., pulmonary hypertensive crisis, air-leak with high intrathoracic pressure)
Right-atrial mass/thrombus or catheter-related RA outflow obstruction
Post-Fontan fenestration (iatrogenic interatrial R→L shunt)
Severe acute right ventricular failure (pressure overload)
ASD with Eisenmenger physiology (suprasystemic pulmonary hypertension)

Subcostal view demonstrating a dilated inferior vena cava and subhepatic veins. This finding may reflect appropriate right-sided filling and adequate systemic venous return. However, it can also represent excessive transmission of intrathoracic pressure to the right atrium, resulting in elevated right atrial pressure due to extracardiac compression. In this setting, venous dilatation reflects impaired venous drainage rather than true intravascular volume loading. One may appreciate the Umbilical Venous catheter arriving at the IVC-RA junction through the ductus venosus.

Colour outlining that there is some degree of retrograde flow (red) in the subhepatic vein where the cursor is placed.

Doppler interrogation of the subhepatic veins demonstrates retrograde flow during ventricular systole, coinciding with tricuspid valve closure and a rise in right atrial pressure. The retrograde component comprises more than 50% of the venous flow pattern, consistent with elevated right atrial pressure. This finding may reflect impaired right heart compliance, potentially related to right ventricular hypertrophy and/or extracardiac compression from the adverse cardio-respiratory interactions and due to high intra-thoracic pressures by the elevated mean airway pressure.

The patent ductus arteriosus is large and unrestrictive, near completely right to left ("blue" blood coming from the MPA to the descending aorta). The PDA is larger than the left pulmonary artery in this tripod view.

The patent ductus arteriosus is visualized in the tripod view and appears similar in caliber to the right and left pulmonary arteries on B-mode imaging. This size suggests an unrestrictive ductus, allowing free transmission of flow with near–pressure equalization between the aortic and pulmonary circulations in both systole and diastole.

Dual-mode imaging with 2D and color Doppler over a right-to-left patent ductus arteriosus demonstrates laminar ductal flow without aliasing or turbulence, consistent with an unrestrictive PDA. A focal red color signal within the main pulmonary artery suggests flow swirling, likely related to elevated downstream pulmonary vascular resistance. Despite right-to-left ductal shunting and a reduced Qp:Qs, there is preserved antegrade flow into both the right and left pulmonary arteries, which are of good caliber.

PW Doppler of the PDA Pulsed-wave Doppler interrogation of the patent ductus arteriosus demonstrates predominantly right-to-left ductal flow, present throughout systole and diastole. The Doppler envelope is laminar with low velocities, consistent with an unrestrictive PDA allowing pressure transmission between the pulmonary artery and the aorta. The low-velocity nature of the signal supports near systolic and diastolic pressure equalization, in keeping with higher pulmonary vascular resistance relative to systemic vascular resistance. There is only a small blip of left to right at the end of systole (and/or early diastole).

M-mode imaging with superimposed color Doppler across the ductus arteriosus at a Nyquist of 61.6 cm/s confirms near continuous right-to-left shunting over time, visualized as a persistent blue signal aligned with the M-mode cursor. There is only a trace of red at end-systole/beginning diastole. There is no evidence of aliasing or focal turbulence within the ductal lumen, further supporting an unrestrictive ductus.

Zoom on the PDA that is right to left by colour.

Zoom on PDA by B-Mode.

Once Mean Airway Pressure Reduced Acutely

Interventions included on the TNE images to monitor effects during the evaluation.

Following reduction in mean airway pressure from 15–16 to 10–11 cmH₂O, along with suctioning and overall improvement in cardiopulmonary interactions, there is reduced alveolar hyperinflation and extravascular compression of the vascular bundle at the alveolar level. These changes lower pulmonary vascular resistance and improve pulmonary blood flow. On imaging, the ductus arteriosus remains unrestrictive on B-mode, and dual-mode imaging with color Doppler demonstrates fully left-to-right shunting, indicating reversal of the PVR–SVR relationship compared with the prior state. This transition occured within minutes of the ventilator adjustments, highlighting the dynamic and ventilator-sensitive nature of ductal and pulmonary vascular physiology.

The PDA has now clearly transitioned to fully left-to-right shunting, coinciding with a reduction in mean airway pressure and improved cardiopulmonary interactions. In this view, the Doppler cursor is carefully aligned with the direction of ductal flow to obtain a pulsed-wave (PW) Doppler signal. PW Doppler is used to measure instantaneous velocities, whereas continuous-wave (CW) Doppler is reserved for higher velocities across the ductus. Given the unrestrictive nature of the PDA and the expectation of low ductal velocities (<3 m/s), PW Doppler is typically preferred in this setting to accurately characterize the flow profile.

Pulsed-wave Doppler interrogation of the patent ductus arteriosus demonstrates near-continuous left-to-right shunting, with forward flow from the aorta into the pulmonary artery throughout systole and diastole. The Doppler envelope is low-velocity and non-turbulent, consistent with an unrestrictive ductus and near pressure equilibration between the systemic and pulmonary circulations. The continuous nature of the signal reflects persistent ductal patency and increased pulmonary blood flow in the setting of reduced pulmonary vascular resistance.

RPA PW-Doppler demonstrating some increased velocities.

LPA PW-Doppler demonstrating some increased velocities. However, there is persistence of mid-systolic notching.

Modified subcostal view outlining that the PFO is now near-fully left to right.

Pulsed-wave Doppler interrogation across the patent foramen ovale demonstrates predominantly left-to-right interatrial shunting, with low-velocity, laminar flow directed from the left atrium into the right atrium. This pattern reflects increased left atrial filling pressure secondary to improved pulmonary blood flow, combined with reduced right atrial pressure following decreased extrinsic cardiac compression. The latter is attributable to lower intrathoracic pressures after reduction in ventilatory mean airway pressure, resulting in more favorable cardiopulmonary interactions.