Background Using peripheral arteries to infer central hemodynamics is common among hemodynamic monitors. Doppler ultrasound of the common carotid artery has been used in this manner with conflicting results. We investigated the relationship between changing common carotid artery Doppler measures and stroke volume (SV), hypothesizing that more consecutively-averaged cardiac cycles would improve SV-carotid Doppler correlation. Methods: Twenty-seven healthy volunteers were recruited and studied in a physiology laboratory. Carotid artery Doppler pulse was measured with a wearable, wireless ultrasound during central hypovolemia and resuscitation induced by a stepped lower body negative pressure protocol. The change in maximum velocity time integral (VTI) and corrected flow time of the carotid artery (ccFT) were compared with changing SV using repeated measures correlation. Results: In total, 73,431 cardiac cycles were compared across 27 subjects. There was a strong linear correlation between changing SV and carotid Doppler measures during simulated hemorrhage (repeated-measures linear correlation [Rrm ]=0.91 for VTI; 0.88 for ccFT). This relationship improved with larger numbers of consecutively-averaged cardiac cycles. For ccFT, beyond four consecutively-averaged cardiac cycles the correlation coefficient remained strong (i.e., Rrm of at least 0.80). For VTI, the correlation coefficient with SV was strong for any number of averaged cardiac cycles. For both ccFT and VTI, Rrm remained stable around 25 consecutively-averaged cardiac cycles. Conclusions: There was a strong linear correlation between changing SV and carotid Doppler measures during central blood volume loss. The strength of this relationship was dependent upon the number of consecutively-averaged cardiac cycles.
Hemodynamic management of sepsis-induced circulatory failure is complex since this pathological state includes multiple cardiovascular derangements that can vary from patient to patient according to the degree of hypovolemia, of vascular tone depression, of myocardial depression and of microvascular dysfunction. The treatment of the sepsis-induced circulatory failure is thus not univocal and should be adapted on an individual basis. As physical examination is insufficient to obtain a comprehensive picture of the hemodynamic status, numerous hemodynamic variables more or less invasively collected, have been proposed to well assess the severity of each component of the circulatory failure and to monitor the response to therapy. In this article, we first describe the hemodynamic variables, which are the most relevant to be used, emphasizing on their physiological meaning, their validation and their limitations in patients with septic shock. We then proposed a general approach for managing patients with septic shock by describing the logical steps that need to be followed in order to select and deliver the most appropriate therapies. This therapeutic approach is essentially based on knowledge of physiology, of pathophysiology of sepsis, and of published data from clinical studies that addressed the issue of hemodynamic management of septic shock.
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Acute heart failure (AHF) has emerged as a major public health problem over the past 2 decades and AHF represents a period of high risk for patients, during which time the patients are more susceptible to have fatal outcomes or be re-hospitalized, compared to periods of chronic stable heart failure. The goals of AHF treatment are symptomatic relief and hemodynamic stabilization, which need accurate assessment of volume status and cardiac function of patients. Until now, there is a paucity of controlled clinical data to define optimal treatment for patients with AHF and most guidelines published by the American Heart Association or European Society of Cardiology have been generated by the consensus opinions of experts. In these guidelines, routine invasive hemodynamic monitoring of AHF patients is not recommended because there have not been any reports showing survival benefit in patients monitored with pulmonary artery catheters. At present, treatment strategies based on clinical characteristics such as pulmonary congestion and tissue hypoperfusion rather than invasive hemodynamic monitoring is widely accepted. In this article, we discuss an optimal management plan including appropriate assessment of the hemodynamic status of patients and treatment of AHF.
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