When the Heart Takes a Hit: Timing Determines How Blunt Chest Impact Disturbs Blood Flow

Every year, motor vehicle crashes claim hundreds of thousands of lives worldwide, and a substantial share of those deaths traces back to blunt chest trauma—injuries caused when the chest wall is struck by a steering wheel, dashboard, seatbelt, or airbag without any penetrating wound. Among the most elusive consequences of such impacts are disturbances to the heart itself, including cardiac contusion, arrhythmias, and, in rare but devastating cases, traumatic ventricular septal defects. What has remained poorly understood, however, is precisely how an external mechanical blow perturbs the delicate fluid dynamics of blood moving through the heart’s chambers and out into the aorta. A new experimental study published in the Annals of Biomedical Engineering by Dorian Sweidy of Université Gustave Eiffel and Aix-Marseille Université, together with colleagues at Concordia University in Montreal, now offers the first quantitative, phase-by-phase picture of what happens to left ventricular blood flow when the heart is struck at controlled moments in the cardiac cycle.

The research team approached a problem that has long frustrated trauma researchers. Animal models of blunt chest trauma, while physiologically realistic, are difficult to control and raise ethical concerns, and they confound mechanical effects with inflammatory and neurological responses. Computational models, meanwhile, require validation against physical measurements. The solution adopted by the team was a laboratory left-heart simulator built around a transparent silicone left ventricle submerged in a water–glycerol mixture that mimics the density and viscosity of blood. The working fluid circulated through a left atrium, into the ventricle, and onward through an aortic section, with bioprosthetic valves installed at both the mitral and aortic positions to reproduce realistic valve opening and closing behavior.

The engineering centerpiece of the setup was a pair of linear motors. One drove the cyclic contraction and relaxation of the artificial ventricle, replicating the pumping action of the cardiac cycle. The second delivered precisely timed external impacts to the simulator, emulating the kind of short, low-velocity blow the chest might experience in a vehicle collision. Crucially, the researchers could trigger that impact at five different timings within the cardiac cycle, allowing them to test a central hypothesis of the study: that the heart’s hemodynamic response to trauma depends not just on the force of the blow, but on exactly when in the heartbeat it lands.

To visualize what happened inside the beating chamber, the team turned to particle image velocimetry, or PIV, a laser-based optical technique widely used in experimental fluid mechanics. Microscopic particles seeded in the blood-analog fluid were illuminated in a thin laser sheet, and high-speed cameras recorded their motion. By cross-correlating successive image frames, the researchers reconstructed the full two-dimensional velocity field of the flow inside the ventricle and the aorta. From those velocity fields they derived quantities of direct physiological relevance: vorticity, a measure of the local swirling rotation of the fluid; kinetic energy carried by the moving blood; and viscous energy dissipation, often abbreviated VED, which quantifies how much of the blood’s mechanical energy is irreversibly lost to friction as chaotic, poorly organized flow.

These energy metrics matter because the healthy heart is a remarkably efficient pump. Decades of work in cardiac fluid dynamics, including landmark studies showing that nature optimizes the swirling vortex flow inside the left ventricle, have established that organized vortical structures during filling and ejection minimize energy loss and smooth the redirection of blood through the asymmetric geometry of the heart. Elevated viscous energy dissipation is a recognized marker of abnormal flow, measurable in patients today with four-dimensional flow MRI, and it has been linked to pathological conditions in both the ventricle and the aorta. If a chest impact pushes the intracardiac flow toward a more dissipative state, that shift provides an objective, quantifiable signature of the disturbance—something clinicians could eventually look for in trauma patients.

The results revealed a striking phase dependence. In every impact condition except one, the velocity field inside the left ventricle was measurably altered by the blow. The single exception was early systole, the brief window just after the mitral valve closes and the ventricle begins to contract. At that moment, the heart appears to be momentarily insensitive to external perturbation, perhaps because the contracting muscle and the rapidly accelerating outflow dominate the local fluid dynamics. By contrast, impacts delivered during late systole produced the most pronounced reduction in vorticity, suggesting that a blow near the end of contraction disrupts the swirling structures that normally organize the blood for ejection.

Viscous energy dissipation told a complementary story. At the instant of impact, VED increased in all tested conditions, indicating that the external blow consistently injected disorder into the flow, converting organized kinetic energy into heat through viscous friction regardless of cardiac timing. The aorta, however, responded in a more selective fashion. Flow velocity, volumetric flow rate, kinetic energy, and viscous energy dissipation in the aortic section all increased primarily when the impact arrived during systolic phases of the cycle. This makes intuitive mechanical sense: during systole the aortic valve is open, so any sudden compression or acceleration of the ventricular contents is transmitted directly down the outflow tract, momentarily boosting the momentum of blood entering the aorta and simultaneously increasing the dissipative losses associated with that disturbed, high-velocity flow.

The authors emphasize that the impacts they imposed were short and sub-physiological in the sense of being brief, controlled laboratory perturbations rather than full crash-level loading events. Yet even these modest, millisecond-scale disturbances were sufficient to induce measurable flow disturbances whose magnitude and character depended on cardiac timing. That finding carries a provocative implication for trauma science: the severity of blunt cardiac injury may not be a simple function of impact energy alone, but of the interaction between the impact waveform and the dynamic mechanical state of the heart at the moment of contact. Two collisions delivering identical external loads could, in principle, produce very different intracardiac flow disturbances depending on where they fall within the roughly one-second span of the cardiac cycle.

The study builds on the team’s earlier work, including a companion paper in the Journal of Biomechanics describing the in-vitro simulator itself, and on a growing body of crash-injury research that seeks to connect vehicle crash data to virtual injury assessment through finite element modeling of the thorax. By anchoring those computational efforts with hard experimental numbers—velocity fields, vorticity distributions, kinetic energy, and dissipation budgets measured under controlled impact conditions—the new results provide validation data that numerical models of blunt aortic and cardiac injury have lacked. The researchers have also made the MATLAB post-processing code for their fluid dynamics analyses publicly available, lowering the barrier for other groups to adopt the same analytical framework.

Clinically, the work points toward a future in which the fluid-dynamic signature of cardiac trauma could complement electrocardiographic and imaging findings in emergency departments, where diagnosing blunt cardiac injury remains notoriously difficult and where systematic reviews have questioned the accuracy of current diagnostic tests. It may also inform the design of passive safety systems: if certain phases of the cardiac cycle render the heart more vulnerable to flow disruption, that knowledge could eventually feed into injury criteria used to evaluate restraint systems and vehicle structures. For now, the study’s most immediate contribution is conceptual—a demonstration that the biomechanical response of the heart to external impact is fundamentally phase-dependent, and that the invisible world of intracardiac fluid dynamics responds to trauma in ways that can now be measured, quantified, and modeled with laboratory precision.

Subject of Research: Experimental quantification of left ventricular blood flow and energy changes during timed external chest impacts

Article Title: Left Ventricle Velocity Patterns and Energy Changes During Controlled External Impact: A Quantitative Experimental Insight

Article References: Sweidy, D., Mathyssen, A., Teimouri, K., Maraouch, G., Wei, W., Saleh, W., Kadem, L., & Evin, M. (2026). Left Ventricle Velocity Patterns and Energy Changes During Controlled External Impact: A Quantitative Experimental Insight. Annals of Biomedical Engineering. https://doi.org/10.1007/s10439-026-04405-1

Image Credits: AI Generated

DOI: 10.1007/s10439-026-04405-1

Keywords: blunt chest trauma, left ventricle, cardiac fluid dynamics, particle image velocimetry, viscous energy dissipation, aorta, vorticity, motor vehicle crashes, biomechanics, heart simulator, cardiac cycle, hemodynamics