PiCCO-Guided hemodynamic monitoring in cardiogenic shock complicated by arrhythmias and acute pulmonary edema

Introduction

Cardiogenic shock (CS) represents the most severe form of acute circulatory failure and is characterized by the inability of the heart to maintain adequate tissue perfusion despite adequate preload. It is associated with systemic hypoperfusion, multiorgan dysfunction, and high mortality. CS complicates approximately 5–10% of cases of acute myocardial infarction (AMI) and accounts for the majority of AMI-related deaths [1, 2]. Over recent decades, the implementation of early revascularization strategies, modern pharmacological therapies, and mechanical circulatory support has improved survival in patients with CS [3-5]. The SHOCK trial demonstrated the long-term survival benefit of early revascularization, and current guidelines recommend urgent percutaneous coronary intervention as first-line therapy in appropriate patients [6-8].

The pathophysiology of CS is complex and involves impaired ventricular contractility, elevated filling pressures, and excessive neurohormonal activation. Compensatory systemic vasoconstriction and microcirculatory dysfunction further aggravate tissue hypoperfusion and contribute to multiorgan dysfunction [4]. In this context, associated complications, including rhythm and conduction disturbances, may critically influence clinical outcomes.

Cardiac arrhythmias represent important contributors to the pathophysiology of CS. Supraventricular tachyarrhythmias, particularly atrial fibrillation (AF), are common in acute heart failure and may reduce cardiac output through loss of atrial contraction and shortening of diastolic filling time [9, 10]. Ventricular tachyarrhythmias, including ventricular tachycardia (VT) and ventricular fibrillation (VF), are associated with severe hemodynamic instability and an increased risk of cardiac arrest [11, 12]. Conduction disturbances may reflect extensive ischemia of the His-Purkinje system and are often associated with a poor prognosis.

Although arrhythmias rarely represent the primary cause of CS, they frequently exacerbate pre-existing shock. AF may significantly reduce left ventricular end-diastolic volume and cardiac output. Ventricular tachyarrhythmias often occur in the context of myocardial ischemia and are promoted by the imbalance between oxygen supply and demand, myocyte necrosis, and ischemia-induced electrophysiological alterations. Reperfusion, inotropic therapy, and metabolic disturbances may further increase myocardial excitability and arrhythmic susceptibility. However, the literature provides heterogeneous data regarding the independent prognostic association of different arrhythmia types on mortality in CS. Some studies emphasize the adverse prognostic role of ventricular tachyarrhythmias, whereas others highlight the severity of ventricular dysfunction and systemic hypoperfusion as the primary determinants of outcome [13-16].

Pulmonary congestion and acute pulmonary edema (APE) are important markers of hemodynamic severity. In acute heart failure, APE is associated with hypoxemia, increased ventricular afterload, and worsening myocardial dysfunction. However, its specific prognostic impact in patients with CS and concomitant arrhythmias remains insufficiently explored [17]. Advanced hemodynamic monitoring, particularly with the PiCCO system (pulse contour cardiac output monitoring system), allows continuous assessment of cardiac output, stroke volume, and tissue perfusion. In addition, parameters such as the extravascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) may facilitate early detection and quantification of APE and help differentiate cardiogenic from permeability-related APE [18, 19]. This approach may facilitate optimization of fluid therapy, vasopressor and inotropic treatment, and individualized hemodynamic management [20].

Despite the high prevalence of arrhythmias and the increasing use of advanced hemodynamic monitoring, data regarding the interaction between cardiac rhythm disturbances, pulmonary congestion, and mortality in cardiogenic shock remain limited. A better understanding of the relationship between arrhythmias, pulmonary congestion, and hemodynamic monitoring may contribute to improved risk stratification and management of patients with cardiogenic shock.

The primary objective of this study was to evaluate the association between different types of cardiac rhythm disturbances and mortality in patients with cardiogenic shock. Secondary objectives included analyzing the association of APE with mortality and assessing the relationship between hemodynamic monitoring strategies and clinical outcomes.

Materials and methods

This retrospective observational study included 105 consecutive patients admitted with cardiogenic shock between June 2016 and August 2018 to the Intensive Care Unit of the Holy Trinity Municipal Clinical Hospital, Chișinău, Republic of Moldova. Patients were classified into two groups according to the type of hemodynamic monitoring applied during hospitalization: the PiCCO group (advanced hemodynamic monitoring, n = 52) and the standard ECHO group (n = 53). The decision to use PiCCO monitoring was based on clinician judgment and device availability and was not randomized. Cardiogenic shock was diagnosed at ICU admission according to predefined clinical and hemodynamic criteria, including persistent hypotension (systolic blood pressure <90 mmHg for ≥30 minutes or requiring vasopressor support despite adequate fluid resuscitation), signs of tissue hypoperfusion, and evidence of cardiac dysfunction. Inclusion criteria were age ≥18 years, clinical signs of tissue hypoperfusion, and systolic blood pressure <90 mmHg for ≥30 minutes or persistent hypotension despite fluid resuscitation. Exclusion criteria included pregnancy, non-cardiac causes of shock, age <18 years, death within the first 12 hours of admission, and incomplete medical records.

Hemodynamic assessment in the PiCCO group was performed using the PiCCO system, which allows continuous assessment of cardiac output, preload, and extravascular lung water, while the ECHO group was monitored using standard transthoracic echocardiography. All patients received standard clinical care according to hospital protocols, including fluid resuscitation, vasoactive drugs, and inotropic support as indicated. The variables analyzed included age, sex, type of arrhythmia, presence of APE, and in-hospital mortality. Continuous variables were expressed as mean ± standard deviation (SD) and compared using Student’s t-test, whereas categorical variables were analyzed using the χ² test or Fisher’s exact test where appropriate. Normality of data distribution was assessed using the Shapiro–Wilk test prior to comparative analysis. A p-value <0.05 was considered statistically significant. Because of the relatively limited sample size and imbalance between groups, multivariable regression analysis was considered statistically underpowered and was therefore not performed. Statistical analyses were performed using SPSS Statistics version 26.0 (IBM Corp., Armonk, NY, USA).

The study was conducted with the approval of the Bioethics and Deontology Committee of the Holy Trinity Municipal Clinical Hospital, Chișinău, Republic of Moldova (Protocol No. 1, January 12, 2026).

Results

A total of 105 patients with cardiogenic shock were included in the analysis, with 52 patients in the PiCCO group and 53 in the standard ECHO group (Table 1).

Comparative analysis demonstrated that the mean age was significantly higher in the ECHO group compared with the PiCCO group (73.6 ± 9.8 vs 64.8 ± 11.1 years; p = 0.0001). Sex distribution and place of residence (urban/rural) were similar between groups. Regarding the etiology of cardiogenic shock, acute myocardial infarction (AMI) was more frequent in the ECHO group (73.6% vs 55.8%; p = 0.0677), although this difference did not reach statistical significance. Unstable angina (UA) was more common in the PiCCO group (38.5% vs 18.9%; p = 0.0318). Comorbidity profiles differed between groups. Hypertension was more frequent in the ECHO group (83.0% vs 57.7%; p = 0.0055), while dyslipidemia, obesity, and cerebrovascular disease were more common in the PiCCO group (71.2% vs 30.2%; p = 0.0001, 40.4% vs 13.2%; p = 0.0020, and 73.1% vs 50.9%; p = 0.0269, respectively). Other comorbidities, including diabetes mellitus, pneumonia, COPD, smoking, liver disease, and peptic ulcer disease, were not significantly different between groups. Severity scores at admission (APACHE II, SOFA, MODS, and CardShock) were comparable between groups, although important differences in age and comorbidity burden were present. In-hospital mortality was lower in the PiCCO group compared with the ECHO group (36.5% vs 62.3%; p = 0.0112). However, interpretation of mortality differences should be cautious because of baseline differences in age and comorbidity profiles between groups.

Rhythm and conduction disorders were identified in 97 patients (92.4%) with a mean age of 69.2 ± 11.3 years and an overall mortality of 47.4% (Table 2). AF/AFL was the most frequent arrhythmia, followed by conduction blocks and other supraventricular arrhythmias. APE was present in 60.9% of patients and was associated with markedly increased mortality.

Table 3 presents the distribution of rhythm and conduction disorders according to the monitoring strategy (PiCCO vs ECHO). Other supraventricular arrhythmias were significantly more frequent in the PiCCO group than in the ECHO group (40.4% vs 15.1%; p = 0.007). In contrast, APE was significantly more frequent in the ECHO group (73.6% vs 48.1%; p = 0.0094). No statistically significant differences were observed for the remaining rhythm disorders.

Table 4 summarizes mortality according to arrhythmia type in patients with cardiogenic shock. Although mortality rates varied across arrhythmia categories, no statistically significant associations with mortality were identified in the univariate analysis. The highest mortality rate was observed among patients with cardiac arrest.

Table 5 summarizes mortality among patients with APE according to arrhythmia type. Significant associations with mortality were identified for AF/AFL (p = 0.003), VT/VF (p = 0.035), conduction blocks (p = 0.028), and cardiac arrest (p = 0.012). Mortality among patients with APE was particularly high in cases complicated by ventricular arrhythmias or cardiac arrest.

Table 6 presents mortality according to the type of monitoring (PiCCO vs ECHO) in relation to the presence or absence of rhythm and conduction disorders. Overall, mortality was significantly lower in the PiCCO group among patients with arrhythmias and conduction blocks compared with the ECHO group (34.7% vs 60.4%; p = 0.0148). In contrast, among patients without rhythm and conduction disorders, mortality remained high in both groups without significant differences.

Among patients with atrial fibrillation/flutter (AF/AFL), mortality tended to be lower in the PiCCO group (40.7% vs 62.5%), although the difference did not reach statistical significance (p = 0.1860). A similar non-significant trend toward lower mortality was observed among patients without AF/AFL (32.0% vs 61.9%; p = 0.0739). Patients without conduction blocks showed significantly lower mortality in the PiCCO group compared with the ECHO group (36.7% vs 64.5%; p = 0.0413). Likewise, among patients without cardiac arrest, mortality was significantly lower in the PiCCO group (29.7% vs 61.9%; p = 0.0065). Although lower mortality rates were consistently observed in the PiCCO group across most arrhythmia categories, differences for ventricular tachyarrhythmias, conduction blocks, and cardiac arrest did not reach statistical significance, likely because of the limited sample size.

Overall, these findings suggest that PiCCO-guided monitoring may be associated with improved survival in patients with cardiogenic shock, particularly in those with rhythm and conduction disorders.

The data suggest that the specific type of arrhythmia was not significantly associated with mortality. However, the coexistence of arrhythmias and APE was associated with increased mortality. Overall, patients monitored with the PiCCO system demonstrated lower mortality rates, with the most pronounced reduction observed among patients with arrhythmias and among those without cardiac arrest. The overall difference in in-hospital mortality between the two monitoring strategies is illustrated in Figure 2.

Discussion

This study analyzed the association between hemodynamic monitoring strategy and mortality in patients with CS in the context of a very high prevalence of rhythm and conduction disturbances (92.4%). The retrospective design and relatively small sample size limited the possibility of performing multivariable regression analysis. The main findings can be summarized in four key points: (1) lower overall in-hospital mortality in the PiCCO-monitored group; (2) the absence of a statistically significant association between specific arrhythmia type and mortality; (3) the adverse prognostic impact of APE; and (4) lower observed mortality associated with PiCCO monitoring in selected clinical subgroups.

Selection bias cannot be excluded, as the decision to use PiCCO monitoring was based on clinician judgment and device availability rather than random allocation. In addition, important baseline differences between groups, particularly regarding age and comorbidity profile, may have influenced outcomes. Because multivariable adjustment was not performed, independent predictors of mortality could not be established. Therefore, the results should be considered hypothesis-generating rather than definitive evidence of superiority of one monitoring strategy over another.

Hemodynamic monitoring and mortality.

A significant difference in in-hospital mortality was observed between groups (36.5% vs 62.3%), suggesting a possible association between PiCCO-guided monitoring and improved survival. Severity scores (APACHE II, SOFA, MODS, CardShock) were comparable between groups, indicating similar baseline clinical severity at admission. However, relevant differences in baseline characteristics were present: the ECHO group included older patients and had a higher prevalence of hypertension and dyslipidemia, whereas certain comorbidities (e.g., obesity and cerebrovascular disease) were more frequent in the PiCCO group. These imbalances may have influenced outcomes independently of the monitoring strategy and represent an important limitation. Accordingly, the observed difference in mortality should be interpreted as an association rather than evidence of causality, particularly in the absence of randomization and multivariable adjustment. The lower mortality in the PiCCO group should therefore be interpreted cautiously, as differences in age and comorbidity burden may have partially contributed to the observed survival advantage.

Arrhythmias in cardiogenic shock.

The very high prevalence of rhythm disturbances confirms their central role in the clinical profile of CS. AF/AFL was the most frequent arrhythmia, followed by conduction blocks and ventricular tachyarrhythmias. However, univariate analysis did not demonstrate a statistically significant association between specific arrhythmia type and mortality. This finding suggests that, in CS, global hemodynamic failure may be a stronger determinant of outcome than the individual arrhythmia subtype.      These results are consistent with previous reports indicating that the severity of circulatory collapse and the extent of myocardial dysfunction may outweigh the isolated electrophysiological effects of specific arrhythmias in determining prognosis in CS.

Role of acute pulmonary edema.

APE was associated with markedly increased mortality, particularly in patients with AF/AFL, ventricular tachyarrhythmias, conduction blocks, and cardiac arrest. Mortality rates in patients with APE were substantially higher, reaching over 70% in several subgroups. These findings suggest that the coexistence of electrical instability and pulmonary congestion reflects a more advanced stage of hemodynamic decompensation, with severe prognostic implications.

The adverse prognostic impact of APE in CS may be explained by several pathophysiological mechanisms [18]. Elevated left ventricular filling pressures lead to increased pulmonary capillary hydrostatic pressure and accumulation of extravascular lung water, resulting in impaired gas exchange and severe hypoxemia. Hypoxemia further aggravates myocardial ischemia and contributes to sympathetic nervous system activation, tachycardia, and increased myocardial oxygen demand [19]. This creates a vicious cycle of worsening ischemia, ventricular dysfunction, and pulmonary congestion. Moreover, pulmonary congestion may further impair right ventricular function and ventricular interdependence, thereby aggravating systemic hypoperfusion and multiorgan dysfunction [20]. These mechanisms may explain the markedly higher mortality observed in patients with CS complicated by APE, particularly in the presence of arrhythmias and cardiac arrest.

PiCCO monitoring in arrhythmia subgroups.

Advanced hemodynamic monitoring using the PiCCO system may provide additional clinical value in cardiogenic shock through continuous assessment of preload, cardiac output, and fluid responsiveness. Unlike conventional echocardiography, PiCCO allows repeated bedside quantification of the EVLWI, an indicator of pulmonary congestion, and the pulmonary vascular permeability index (PVPI), which may help differentiate cardiogenic pulmonary edema from permeability-related pulmonary edema. Early detection of increasing EVLWI may facilitate timely optimization of fluid therapy, vasopressor support, and diuretic treatment before severe respiratory and hemodynamic deterioration occurs [17-20].

Continuous hemodynamic monitoring may therefore enable more individualized therapeutic management and may partially explain the lower mortality observed in the PiCCO group. Stratified analysis indicated lower mortality with PiCCO monitoring in several subgroups, particularly among patients with arrhythmias and conduction blocks, and among those without cardiac arrest. These findings suggest that advanced hemodynamic monitoring may be more beneficial in earlier or potentially reversible stages of shock, before irreversible deterioration develops.

Study limitations.

This study has several limitations. First, the retrospective single-center design limits external validity and precludes causal inference. Second, the relatively small sample size reduced statistical power and limited the possibility of multivariable regression analysis. Third, allocation to PiCCO monitoring was not randomized and depended on clinician judgment and device availability, introducing potential selection bias. Finally, baseline differences between groups, particularly regarding age and comorbidities, may have influenced mortality independently of the monitoring strategy.

In addition, treatment strategies, including vasoactive support, antiarrhythmic therapy, mechanical ventilation, and timing of revascularization, were not analyzed in detail and may have influenced outcomes.

Conclusions

Rhythm and conduction disturbances are highly prevalent in patients with cardiogenic shock but are not significantly associated with mortality. Acute pulmonary edema represents a major marker of hemodynamic severity and is associated with significantly increased mortality, particularly in patients with arrhythmias and conduction blocks. Patients monitored with PiCCO demonstrate lower observed in-hospital mortality compared with standard echocardiographic monitoring; however, causal inference is limited by the retrospective, non-randomized design and baseline differences between groups. PiCCO monitoring is associated with lower observed mortality in patients with arrhythmias and in those without cardiac arrest, suggesting a potential greater utility in earlier or less advanced stages of shock.

Competing interests

None declared.

Acknowledgements and funding

No external funding

Ethics approval

Ethical approval for retrospective analysis of anonymized data was obtained prior to data analysis in 2026. The study protocol was reviewed and approved by the Bioethics and Deontology Committee of the Holy Trinity Municipal Clinical Hospital (Protocol No. 1, January 12, 2026).

Informed consent

Written informed consent for treatment and anonymized data use of clinical data was obtained at hospital admission.

Provenance and peer review

Not commissioned; externally peer-reviewed.

Author’s ORCID ID

Lucia Gîrbu - https://orcid.org/0009-0006-0847-2901

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