Circulatory trajectories after out-of-hospital cardiac arrest: a prospective cohort study.

BACKGROUND: Circulatory failure frequently occurs after out-of-hospital cardiac arrest (OHCA) and is part of post-cardiac arrest syndrome (PCAS). The aim of this study was to investigate circulatory disturbances in PCAS by assessing the circulatory trajectory during treatment in the intensive care unit (ICU). METHODS: This was a prospective single-center observational cohort study of patients after OHCA. Circulation was continuously and invasively monitored from the time of admission through the following five days. Every hour, patients were classified into one of three predefined circulatory states, yielding a longitudinal sequence of states for each patient. We used sequence analysis to describe the overall circulatory development and to identify clusters of patients with similar circulatory trajectories. We used ordered logistic regression to identify predictors for cluster membership. RESULTS: Among 71 patients admitted to the ICU after OHCA during the study period, 50 were included in the study. The overall circulatory development after OHCA was two-phased. Low cardiac output (CO) and high systemic vascular resistance (SVR) characterized the initial phase, whereas high CO and low SVR characterized the later phase. Most patients were stabilized with respect to circulatory state within 72 h after cardiac arrest. We identified four clusters of circulatory trajectories. Initial shockable cardiac rhythm was associated with a favorable circulatory trajectory, whereas low base excess at admission was associated with an unfavorable circulatory trajectory. CONCLUSION: Circulatory failure after OHCA exhibits time-dependent characteristics. We identified four distinct circulatory trajectories and their characteristics. These findings may guide clinical support for circulatory failure after OHCA. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02648061.

Characteristics of circulatory failure after out-of-hospital cardiac arrest: a prospective cohort study.

BACKGROUND: Circulatory failure after out-of-hospital cardiac arrest (OHCA) as part of the postcardiac arrest syndrome (PCAS) is believed to be caused by an initial myocardial depression that later subsides into a superimposed vasodilatation. However, the relative contribution of myocardial dysfunction and systemic inflammation has not been established. Our objective was to describe the macrocirculatory and microcirculatory failure in PCAS in more detail. METHODS: We included 42 comatose patients after OHCA where circulatory variables were invasively monitored from admission until day 5. We measured the development in cardiac power output (CPO), stroke work (SW), aortic elastance, microcirculatory metabolism, inflammatory and cardiac biomarkers and need for vasoactive medications. We used survival analysis and Cox regression to assess time to norepinephrine discontinuation and negative fluid balance, stratified by inflammatory and cardiac biomarkers. RESULTS: CPO, SW and oxygen delivery increased during the first 48 hours. Although the estimated afterload fell, the blood pressure was kept above 65 mmHg with a diminishing need for norepinephrine, indicating a gradually re-established macrocirculatory homoeostasis. Time to norepinephrine discontinuation was longer for patients with higher pro-brain natriuretic peptide concentration (HR 0.45, 95% CI 0.21 to 0.96), while inflammatory biomarkers and other cardiac biomarkers did not predict the duration of vasoactive pressure support. Markers of microcirculatory distress, such as lactate and venous-to-arterial carbon dioxide difference, were normalised within 24 hours. CONCLUSION: The circulatory failure was initially characterised by reduced CPO and SW, however, microcirculatory and macrocirculatory homoeostasis was restored within 48 hours. We found that biomarkers indicating acute heart failure, and not inflammation, predicted longer circulatory support with norepinephrine. Taken together, this indicates an early and resolving, rather than a late and emerging vasodilatation. TRIAL REGISTRATION: NCT02648061.

Quantification of aortic regurgitation using high-pulse repetition frequency three-dimensional colour Doppler.

AIMS: The aim of this study was to validate and assess the feasibility of a previously described method using multibeam high-pulse repetition frequency (HPRF) colour Doppler to quantify the vena contracta area (VCA) in aortic regurgitation (AR). METHODS: Twenty-nine patients with mild to severe AR were studied. Regurgitant volume and fraction measured by magnetic resonance imaging (MRI) were used as the standard of reference. The VCA was measured automatically by combining the Doppler power from multiple beams with a priori knowledge of the individual beam profiles, to give an absolute measurement of the VCA. The regurgitant volume was calculated as the product of the VCA and the velocity time integral, measured separately by continuous wave Doppler. RESULTS: The Spearman's rank correlation between regurgitant volume by MRI and multibeam HPRF colour Doppler was rs = 0.73 (P < 0.01), with 95% limits of agreement of -14.4 ± 29.1 mL. The mean difference between the methods in those with MRI regurgitant volume of ≥30 mL (n = 14) was -7.6 (95% confidence interval -13.9 to -1.2) mL. CONCLUSION: There was good agreement between MRI and multibeam HPRF colour Doppler in patients with moderate to severe AR, while agreement for those with mild AR was modest.

Quantification of mitral regurgitation using high pulse repetition frequency three-dimensional color Doppler.

BACKGROUND: The aim of this study was to validate a novel method of determining vena contracta area (VCA) and quantifying mitral regurgitation using multibeam high-pulse repetition frequency (HPRF) color Doppler. METHODS: The Doppler signal was isolated from the regurgitant jet, and VCA was found by summing the Doppler power from multiple beams within the vena contracta region, where calibration was done with a reference beam. In 27 patients, regurgitant volume was calculated as the product of VCA and the velocity-time integral of the regurgitant jet, measured by continuous-wave Doppler, and compared with regurgitant volume measured by magnetic resonance imaging (MRI). RESULTS: Spearman's rank correlation and the 95% limits of agreement between regurgitant volume measured by MRI and by multibeam HPRF color Doppler were r(s) = 0.82 and -3.0 +/- 26.2 mL, respectively. CONCLUSION: For moderate to severe mitral regurgitation, there was good agreement between MRI and multibeam HPRF color Doppler. Agreement was lower in mild regurgitation.

Quantification of valvular regurgitation area and geometry using HPRF 3-D Doppler.

It is important to determine the severity of valvular regurgitation accurately because surgery is indicated only in severe regurgitations. The evaluation of, for example, mitral regurgitation is complex, and the current methods have limitations. We have developed a 3-D Doppler method to estimate the cross-sectional area and the geometry of a regurgitant jet at the vena contracta just downstream from the actual orifice. The back-scattered Doppler signal from multiple beams distributed over the area of interest was measured. The received power from these beams was then calibrated using both a priori knowledge of the lateral extent of the beams and a reference beam that was completely enclosed by the vena contracta. To isolate the Doppler signal received from the core of a regurgitant jet, a high pulse repetition frequency and a steep clutter filter are required. The method has been implemented and verified by computer simulations and by in vitro experiments using a pulsatile flow phantom and prosthetic valves with a range of holes. We were able to distinguish between mild, moderate, and severe valvular regurgitation. We were also able to quantify the regurgitational area as well as show the geometry of the regurgitation.