RESUMO
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.
Assuntos
Débito Cardíaco Elevado/fisiopatologia , Baixo Débito Cardíaco/fisiopatologia , Parada Cardíaca Extra-Hospitalar/fisiopatologia , Resistência Vascular/fisiologia , Estudos de Coortes , Feminino , Humanos , Unidades de Terapia Intensiva , Masculino , Pessoa de Meia-Idade , Fatores de TempoRESUMO
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.
Assuntos
Coma/fisiopatologia , Microcirculação/fisiologia , Norepinefrina/uso terapêutico , Parada Cardíaca Extra-Hospitalar/complicações , Vasodilatação/fisiologia , Idoso , Coma/tratamento farmacológico , Coma/etiologia , Feminino , Seguimentos , Humanos , Masculino , Parada Cardíaca Extra-Hospitalar/fisiopatologia , Parada Cardíaca Extra-Hospitalar/terapia , Estudos Prospectivos , Vasoconstritores/uso terapêutico , Vasodilatação/efeitos dos fármacosRESUMO
BACKGROUND: The post cardiac arrest syndrome (PCAS) is responsible for the majority of in-hospital deaths following cardiac arrest (CA). The major elements of PCAS are anoxic brain injury and circulatory failure. OBJECTIVE: This study aimed to investigate the clinical characteristics of circulatory failure and inflammatory responses after out-of-hospital cardiac arrest (OHCA) and to identify patterns of circulatory and inflammatory responses, which may predict circulatory deterioration in PCAS. METHODS: This study is a single-center cohort study of 50 patients who receive intensive care after OHCA. The patients are followed for 5 days where detailed information from circulatory variables, including measurements by pulmonary artery catheters (PACs), is obtained in high resolution. Blood samples for inflammatory and endothelial biomarkers are taken at inclusion and thereafter daily. Every 10 min, the patients will be assessed and categorized in one of three circulatory categories. These categories are based on mean arterial pressure; heart rate; serum lactate concentrations; superior vena cava oxygen saturation; and need for fluid, vasoactive medications, and other interventions. We will analyze predictors of circulatory failure and their relation to inflammatory biomarkers. RESULTS: Patient inclusion started in January 2016. CONCLUSIONS: This study will obtain advanced hemodynamic data with high resolution during the acute phase of PCAS and will analyze the details in circulatory state transitions related to circulatory failure. We aim to identify early predictors of circulatory deterioration and favorable outcome after CA. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02648061; https://clinicaltrials.gov/ct2/show/NCT02648061 (Archived by WebCite at http://www.webcitation.org/6wVASuOla).
RESUMO
BACKGROUND: Regional strain rate in the left ventricle can be assessed by tissue Doppler velocity gradient and color mapped in real time. Regional contractility thus can be visualized and graded. To validate the method, we made a comparison with standard echocardiography. METHODS AND RESULTS: Fifteen patients with recent myocardial infarction were examined with the use of strain rate imaging (SRI). Velocity gradients were mapped by color. Gray-scale imaging was performed using the second harmonic mode. Cine loops of two-dimensional echocardiography (2-D echo) and SRI images from three standard apical planes were analyzed off line. A four-grade scale in 16 segments was used to score wall motion by 2-D echo and by SRI. Of a total of 236 segments, 235 segments were analyzable by 2-D echo and 218 segments were analyzable by SRI. Correlation of wall motion score index with ejection fraction was - 0.84 by 2-D echo and - 0.92 by SRI. One hundred fourteen segments had an equal score by the two methods: 51 segments differed by 1 degree and 14 segments differed by 2 degrees (kappa = 0.45). CONCLUSIONS: SRI agrees well with echocardiography in grading regional wall function, and the method can be seen as validated in a clinical setting for assessment of regional systolic wall function and is demonstrated to be applicable for semiquantitative wall motion assessment. SRI has theoretical advantages and may be a valuable addition to standard echocardiography, especially in the field of stress echocardiography.
RESUMO
BACKGROUND: In stress echocardiography, ischaemia is detected as wall motion abnormalities. The test can be done both with exercise (which is the more sensitive) and pharmacological stress (which is more specific). MATERIAL AND METHODS: The paper gives an overview of the method, of diagnostic and prognostic value as well as indications and contraindications, based on present literature. RESULTS AND INTERPRETATION: The sensitivity is 80-90%, specificity 75-100%, dependent on the extent and degree of disease. A negative test predicts a low cardiac event rate of about 1% per year and a low preoperative cardiac risk. The diagnostic accuracy is dependent on optimal equipment quality and on the experience of the examiner. Without specific training, sensitivity is about the same as with exercise ECG. The complication rate is low, dependent on the type of stress. Stress echocardiography is useful in patients unable to exercise, in preoperative risk assessment and in suspected false-negative exercise ECG. In addition it is a supplement to coronary angiography for evaluation of the significance of intermediate stenoses, to identify culprit lesion and for viability detection. Finally, it is useful in aortic stenosis with reduced left ventricular function for evaluation of stenosis and contractile reserve.