Benefits of Manometer in Non-Invasive Ventilatory Support

2017 ◽  
Vol 32 (6) ◽  
pp. 615-620 ◽  
Author(s):  
Rodrigo Silva Lacerda ◽  
Fernando Cesar Anastácio de Lima ◽  
Leonardo Pereira Bastos ◽  
Anderson Fardin Vinco ◽  
Felipe Britto Azevedo Schneider ◽  
...  
Keyword(s):  
Ventilatory Support ◽  
Peak Inspiratory Pressure ◽  
Coronary Perfusion Pressure ◽  
Thoracic Injury ◽  
Coronary Perfusion ◽  
Publication Type ◽  
Non Invasive ◽  
Pressure Manometer ◽  
Effective Ventilation ◽  
Student’S T

AbstractIntroductionEffective ventilation during cardiopulmonary resuscitation (CPR) is essential to reduce morbidity and mortality rates in cardiac arrest. Hyperventilation during CPR reduces the efficiency of compressions and coronary perfusion.ProblemHow could ventilation in CPR be optimized? The objective of this study was to evaluate non-invasive ventilator support using different devices.MethodsThe study compares the regularity and intensity of non-invasive ventilation during simulated, conventional CPR and ventilatory support using three distinct ventilation devices: a standard manual resuscitator, with and without airway pressure manometer, and an automatic transport ventilator. Student’s t-test was used to evaluate statistical differences between groups. P values <.05 were regarded as significant.ResultsPeak inspiratory pressure during ventilatory support and CPR was significantly increased in the group with manual resuscitator without manometer when compared with the manual resuscitator with manometer support (MS) group or automatic ventilator (AV) group.ConclusionThe study recommends for ventilatory support the use of a manual resuscitator equipped with MS or AVs, due to the risk of reduction in coronary perfusion pressure and iatrogenic thoracic injury during hyperventilation found using manual resuscitator without manometer.LacerdaRS, de LimaFCA, BastosLP, VincoAF, SchneiderFBA, CoelhoYL, FernandesHGC, BacalhauJMR, BermudesIMS, da SilvaCF, da SilvaLP, PezatoR. Benefits of manometer in non-invasive ventilatory support. Prehosp Disaster Med. 2017;32(6):615–620.

scholarly journals Predictive Factors of Ventilatory Support in Chest Trauma

Life ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1154
Author(s):  
Silvia Fattori ◽  
Elisa Reitano ◽  
Osvaldo Chiara ◽  
Stefania Cimbanassi
Keyword(s):  
Predictive Factors ◽  
Thoracic Trauma ◽  
Univariate Analysis ◽  
Ventilatory Support ◽  
Rib Fractures ◽  
Pulmonary Contusion ◽  
Thoracic Injury ◽  
Invasive Ventilation ◽  
Non Invasive ◽  
Non Invasive Ventilation

This study aims to define possible predictors of the need of invasive and non-invasive ventilatory support, in addition to predictors of mortality in patients with severe thoracic trauma. Data from 832 patients admitted to our trauma center were collected from 2010 to 2017 and retrospectively analyzed. Demographic data, type of respiratory assistance, chest injuries, trauma scores and outcome were considered. Univariate analysis was performed, and binary logistic regression was applied to significant data. The injury severity score (ISS) and the revised trauma score (RTS) were both found to be predictive factors for invasive ventilation. Multivariate analysis of the anatomical injuries revealed that the association of high-severity thoracic injuries with trauma in other districts is an indicator of the need for orotracheal intubation. From the analysis of physiological parameters, values of systolic blood pressure, lactate, and Glasgow coma scale (GCS) score indicate the need for invasive ventilatory support. Predictive factors for non-invasive ventilation include: RTS, ISS, number of rib fractures and presence of hemothorax. Risk factors for death were: age over 65, the presence of bilateral rib fractures, pulmonary contusion, hemothorax and associated head trauma. In conclusion, the need for invasive ventilatory support in thoracic trauma is associated to the patient’s systemic severity. Non-invasive ventilation is a supportive treatment indicated in physiologically stable patients regardless of the severity of thoracic injury.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

scholarly journals Cardiac arrest complicating cardiogenic shock: from pathophysiological insights to Impella-assisted cardiopulmonary resuscitation in a pheochromocytoma-induced Takotsubo cardiomyopathy—a case report

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Left Ventricle ◽  
Cardiogenic Shock ◽  
Takotsubo Cardiomyopathy ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Refractory Cardiac Arrest

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.

scholarly journals Esmolol during cardiopulmonary resuscitation reduces neurological injury in a porcine model of cardiac arrest

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Laura Ruggeri ◽  
Francesca Nespoli ◽  
Giuseppe Ristagno ◽  
Francesca Fumagalli ◽  
Antonio Boccardo ◽  
...  
Keyword(s):  
Cardiopulmonary Resuscitation ◽  
Porcine Model ◽  
Neuronal Degeneration ◽  
Neuron Specific Enolase ◽  
Coronary Perfusion Pressure ◽  
Neurological Injury ◽  
Saline Control ◽  
Preclinical Model ◽  
Coronary Perfusion ◽  
To Receive

AbstractPrimary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection.

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