A mechanically ventilated postcardiotomy ICU patient developed progressive hypotension and rising vasopressor requirements shortly after escalation of PEEP for worsening oxygenation. Bedside transthoracic echocardiography was technically limited by surgical dressings, subcutaneous emphysema, hyperinflated lungs, and suboptimal acoustic windows, and did not demonstrate unequivocal chamber collapse; the effusion size and distribution could not be confidently characterized. Given the temporal relationship between airway-pressure escalation and shock, transesophageal echocardiography was performed and confirmed pericardial effusion with features consistent with clinically relevant pericardial constraint under PPV (Fig. 5). Doppler findings were interpreted in the context of ventilator-phase dependence and the known blunting of traditional respiratory inflow “cut-offs” during PPV (Figs. 6,7). Following prompt surgical drainage, hemodynamics improved with reduced vasopressor requirement. This vignette illustrates why tamponade physiology under PPV may be underestimated on TTE and supports early escalation to TEE when suspicion remains moderate-to-high and TTE is nondiagnostic, particularly after cardiac surgery.

Fig. 5.

Pericardial effusion on TEE in a mechanically ventilated patient. Mid-esophageal four-chamber TEE view demonstrating a pericardial effusion with predominant distribution around the apical/peri-ventricular region (maximal separation ≈22 mm). This example illustrates how clinically relevant effusions may be incompletely characterized on TTE in ventilated/postoperative patients and supports early TEE when TTE is nondiagnostic or when regional/loculated disease is suspected. LV, left ventricle; PPV, positive-pressure ventilation .

Fig. 6.

Blunted transmitral respiratory variation under positive-pressure ventilation. Transesophageal pulsed‐wave Doppler of mitral inflow in a mechanically ventilated ICU patient with pericardial tamponade, showing fused E/A waves and minimal beat-to-beat (respiratory) variation in peak diastolic velocity under positive-pressure ventilation. Classic respirophasic transmitral cut-offs are therefore not met despite hemodynamically significant tamponade, illustrating the limited reliability of Doppler “pulsus paradoxus” criteria in patients receiving PPV. Abbreviations: E/A, early (E) and late atrial (A) diastolic inflow waves; ICU, intensive care unit.

Fig. 7.

Blunted tricuspid respiratory variation under positive-pressure ventilation. Transesophageal pulsed-wave Doppler of tricuspid inflow in the same mechanically ventilated ICU patient with pericardial tamponade, showing only minimal respiratory variation in diastolic flow velocities, illustrating how positive-pressure ventilation can blunt the classic respirophasic Doppler changes of cardiac tamponade.

We searched MEDLINE (Ovid), Embase, Web of Science, Cochrane Library, and Scopus from Jan 1, 1985, to Oct 29, 2025, without language restrictions. Search concepts combined: pericardial effusion; cardiac tamponade; mechanical ventilation/PPV/PEEP; TTE/TEE; postoperative/post-cardiac surgery; regional tamponade; diagnostic accuracy/impact; cardiopulmonary physiology (transmural pressure, venous return, ventricular interdependence, septal mechanics). Inclusion: perioperative/ICU cohorts; diagnostic-accuracy or diagnostic-impact studies; mechanistic/physiological experiments under PPV; major society guidance. Exclusion: single case reports unless mechanistically clarifying; non-data opinion pieces. Reference lists were hand-searched. The full database-specific search strings (controlled vocabulary and free-text terms) are reported in Supplementary Materials.

We structured the narrative synthesis around four prespecified aims: (a) to describe how PPV alters pericardial and transmural pressures, venous return, ventricular interdependence, and septal mechanics [2]; (b) to summarize how these changes modify echocardiographic signs of tamponade (timing of chamber collapse, Doppler behavior, venous surrogates) and what to prioritize under PPV [1]; (c) to appraise the relative contribution of transthoracic and transesophageal echocardiography in ventilated and postoperative patients [17]; and (d) to outline a pragmatic ICU pathway linking physiology, imaging, and drainage.

Study identification is detailed in the Search strategy section; we focused on ICU and perioperative cohorts with mechanically ventilated patients, comparative TTE–TEE data, and mechanistic experiments under PPV. We prioritized contemporary guidance (e.g., American Society of Echocardiography, American Society of Echocardiography/Society of Cardiovascular Anesthesiologists/Society of Thoracic Surgeons, American Heart Association), perioperative Doppler models under PPV, and postcardiotomy series with surgical confirmation; physiology reviews were used to frame mechanisms and terminology rather than as primary evidence for diagnostic performance or outcomes and we present conflicting findings in their clinical context (timing after surgery, effusion morphology) [8]. Reasoning proceeds from first principles (external constraint and venous return) to test performance (echo under PPV) and then to management decisions (TEE-first triggers, indications for drainage). Where available, we report quantitative indices of diagnostic performance and impact on decision-making, grouped by clinical context (ICU ventilated vs postcardiotomy), modality (TTE vs TEE), and reference standard.

PPV raises pleural pressure, much of which is transmitted to the pericardial space, increasing pericardial pressure (Pperi) and reducing the transmural filling pressure (Ptm ≈ intracavitary pressure − Pperi) [18]. As Pperi approaches right-sided diastolic pressures, diastolic filling becomes exquisitely preload-dependent [19]. The pericardium’s nonlinear pressure–volume relation explains the classic observation that draining a small volume from a tense sac produces a large fall in Pperi and immediate hemodynamic recovery [20] (Fig. 8). Human intraoperative measurements and experimental work demonstrate that pericardial pressure tracks right-atrial pressure and shifts ventricular diastolic mechanics upward; the same load transmitted by PPV can therefore precipitate tamponade at smaller effusion volumes than in spontaneous breathing [21,22].

Fig. 8.

Pathophysiological vicious cycle of cardiac tamponade under positive-pressure ventilation. PPV increases intrathoracic pressure and reduces venous return, leading to impaired RV filling, increased pulmonary vascular resistance and RV afterload, ventricular interdependence with reduced LV output, and a fall in stroke volume and blood pressure culminating in hypotension or shock. The circular arrows indicate the self-reinforcing sequence by which PPV and subsequent escalation of airway pressures may progressively amplify hemodynamic compromise in the setting of pericardial constraint. Further escalation of PEEP/airway pressures and fluid loading worsens pericardial constraint and congestion, producing pericardial effusion/cardiac tamponade with masked pulsus paradoxus. Abbreviations: LV, left ventricle; PEEP, positive end-expiratory pressure.

Echo consequences in patients receiving PPV include right-atrial systolic and right-ventricular diastolic collapse that still occur but can be intermittent or phase-shifted (often most apparent near end-expiration), and their extent can be attenuated when right-sided filling pressures are elevated. Precise timing of these events to the cardiac cycle—such as aligning M-mode with atrioventricular valve motion—remains essential for diagnosing tamponade under these conditions [6,9].

Since venous return (VR) is generated by the pressure gradient between mean systemic filling pressure (Pmsf) and right atrial pressure (RAP) over the resistance to venous return (Rvr), PPV and PEEP—which raise pleural pressure and increase RAP—narrow this venous return gradient; auto-PEEP and dynamic hyperinflation can further exacerbate this effect [23]. In hypovolemia (low stressed volume and low Pmsf), the gradient collapses; in tamponade, RAP rises toward Pperi, compounding the fall in VR and reducing stroke volume [24]. Bedside inspiratory/expiratory holds can estimate Pmsf and illustrate the venous return curve, which helps explain why PPV may be poorly tolerated as pericardial constraint increases [25]. An illustrative TEE example of pericardial effusion in a mechanically ventilated patient is shown in Fig. 5.

Under PPV and PEEP, a plethoric IVC mainly reflects raised RAP and becomes a nonspecific sign. Systemic venous Doppler (hepatic, portal, or renal venous flow) likewise reflects the hemodynamic consequences of elevated RAP and reduced right-sided compliance and is not, in isolation, etiologic. Its practical value in ventilated patients is as an additional, quantifiable marker of impaired right-sided filling when integrated with evidence of pericardial constraint (including regional/loculated collections), ventricular interdependence, and ventilator-phase dependence, and when tracked dynamically during airway-pressure adjustments and after pericardial drainage [5,9].

The normal hepatic venous flow pattern shows a biphasic wave followed by a reversal wave corresponding to atrial contraction.

Burstow et al. [43] showed that in cardiac tamponade the characteristic venous flow pattern consists of a marked predominance of the systolic component, a reduced increase in flow during inspiration, and inversion of the diastolic component during the first expiratory cardiac cycle.

In a study by Mercé and colleagues [44], abnormal venous flow showed a good correlation with the clinical features of cardiac tamponade, with higher sensitivity than right ventricular collapse and much higher specificity than right atrial collapse. The specificity further increases when associated with right chamber collapse [44].

Positive-pressure ventilation alters respiratory variations in hepatic venous flow as well; therefore, it reduces the reliability of Doppler signs based on respiratory changes. However, some features may retain diagnostic value, such as inversion of the hepatic diastolic flow and a markedly pulsatile pattern associated with venous congestion.

It should be emphasized that with the transesophageal technique the hepatic veins can be visualized in nearly all cases, whereas with transthoracic echocardiography they cannot be adequately assessed in approximately one third of patients [45].

The ventricles share the pericardium and the interventricular septum; changes in volume/pressure on one side alter the other—ventricular interdependence [27]. Under PPV, lung inflation increases RV outflow impedance (pulmonary vascular resistance) and reduces RV stroke volume; the trans-septal pressure gradient (left ventricular pressure – right ventricular pressure) oscillates, and the septum shifts accordingly. In tamponade, pericardial constraint accentuates these shifts: small inspiratory changes in RV pressures cause excessive septal excursion (the ‘septal bounce’ or inspiratory bulge into the LV), reducing LV diastolic compliance and magnifying respirophasic swings [27,28].

Under PPV, the phase of septal motion can invert compared with spontaneous breathing, and its magnitude can be attenuated when intrathoracic and pericardial pressures predominate. Septal kinetics should therefore be interpreted in conjunction with stroke-volume surrogates (e.g., LVOT velocity–time integral) rather than in isolation [27].

In spontaneous-breathing tamponade, inspiration increases RV filling and shifts the septum toward the LV, decreasing transmitral inflow and increasing tricuspid inflow [29]. Under PPV, inspiratory positive pleural pressure reduces systemic venous return and increases RV afterload, while impelling pulmonary venous blood toward the LA; patterns may invert, and as pericardial constraint intensifies, respiratory variation in transmitral flow becomes minimal or absent. A perioperative model quantified this: transmitral E-wave variation fell to ~16% in true tamponade during standard PPV—almost absent—explaining why classic Doppler cut-offs are unreliable in ventilated patients [1] (Fig. 6). A similar blunting can be observed on transtricuspid inflow under PPV (Fig. 7). American Society of Echocardiograpy guidance explicitly cautions that minimal mitral inflow variation is expected in PPV-tamponade [8].

PPV increases transpulmonary pressure and stretches alveolar vessels, raising pulmonary vascular resistance and RV afterload—especially at high lung volumes or with poor pulmonary compliance [27,30]. Cyclic increases in RV outflow impedance during tidal ventilation have been demonstrated in vivo with echo-Doppler [31]. Chest-wall compliance modulates how much airway pressure becomes pleural pressure; with a stiff chest wall (e.g., abdominal hypertension), a larger fraction of airway pressure transmits to pleura and pericardium, tightening the external constraint on the heart [32]. These interactions explain the hemodynamic fragility of tamponade during PPV and the heterogeneity of response to PEEP.

Under PPV, cyclic variation in RVOT VTI with phase-linked septal motion is expected; these changes reflect the respiratory swings in right ventricular afterload and filling. LVOT VTI (or, where appropriate, RVOT VTI) can be followed as a quantitative surrogate of stroke volume when titrating PEEP or driving pressure and after pericardial drainage [31] (Fig. 9).

Fig. 9.

LVOT VTI under positive-pressure ventilation in cardiac tamponade physiology. Pulsed-wave Doppler of the LVOT shows marked respiratory variation in systolic ejection, consistent with exaggerated ventricular interdependence and ventilator-phase–dependent hemodynamic fluctuation. Abbreviations: LVOT, left ventricular outflow tract; VTI, velocity–time integral.

When intravascular volume is low (low Pmsf) and PPV raises RAP/Pperi, even modest effusions can equilibrate with chamber pressures (low-pressure tamponade). Under sedation/PPV, classic bedside signs (pulsus paradoxus, jugular vein distension) may be attenuated or misleading, pushing the diagnostic burden onto physiological-congruent echocardiography (collapse timing, regional compression, venous Doppler) and output metrics [33,34]. Contemporary critical-care guidance warns that PPV is poorly tolerated and may unmask/worsen tamponade [8,35].

After cardiac surgery, posterior loculations or clot can selectively compress the left atrium, posterior LV, or pulmonary veins—often with minimal global signs on TTE. Accuracy for surgically confirmed tamponade is modest in the first 24 h (area under the curve ~0.64; positive predictive value ~58%) and improves later [36]; anatomical series show about 50% posterior effusions—precisely the pathology TTE tends to miss, and TEE depicts [4,37,38].

In intubated or postcardiotomy patients, TTE windows are frequently poor, and pathology is often posterior/loculated. Authoritative recommendations endorse a low threshold for TEE when TTE is limited or regional compression is suspected, and they caution against reliance on respiratory inflow variation under PPV. In a prospective ICU cohort of mechanically ventilated patients, TEE resolved 97% of prespecified clinical questions versus 38% for TTE and changed therapy more often (36% vs 16%), including prompting urgent surgery [39,40].

In a patient with a known pericardial effusion, new hypotension or a fall in LVOT VTI temporally linked to induction or increases in PEEP/driving pressure should increase the pretest probability of tamponade rather than be ascribed simply to “ventilator” or “anesthetic” effects [41,42]. Echocardiography should then be used to explain the hemodynamics rather than to confirm a single sign: confirm the effusion, time right-atrial systolic and right-ventricular diastolic collapse against the cardiac cycle, document septal motion in relation to the respiratory phase, interrogate systemic venous Doppler (SVC/hepatic), and quantify stroke volume with LVOT VTI before and after key interventions [1,9,16]. When transthoracic windows are poor, the patient is ventilated, or postcardiotomy anatomy suggests posterior or loculated disease, TEE should be used early to map posterior recesses, identify regional compression, and sample SVC/hepatic flow; once effusion, chamber compression, and low output coexist, drainage should be rapidly provided (percutaneous or surgical according to anatomy), airway pressures minimized while temporizing, and imaging repeated to document resolution of collapse, a rise in LVOT VTI, and the absence of residual loculations [8,39].