Are chest compressions safe for the patient reconstructed with sternal plates? Evaluating the safety of cardiopulmonary resuscitation using a human cadaveric model

<p>Abstract</p> <p>Background</p> <p>Plate and screw fixation is a recent addition to the sternal wound treatment armamentarium. Patients undergoing cardiac and major vascular surgery have a higher risk of postoperative arrest than other elective patients. Those who undergo sternotomy for either cardiac or major vascular procedures are at a higher risk of postoperative arrest. Sternal plate design allows quick access to the mediastinum facilitating open cardiac massage, but chest compressions are the mainstay of re-establishing cardiac output in the event of arrest. The response of sternal plates and the chest wall to compressions when plated has not been studied. The safety of performing this maneuver is unknown. This study intends to demonstrate compressions are safe after sternal plating.</p> <p>Methods</p> <p>We investigated the effect of chest compressions on the plated sternum using a human cadaveric model. Cadavers were plated, an arrest was simulated, and an experienced physician performed a simulated resuscitation. Intrathoracic pressure was monitored throughout to ensure the plates encountered an appropriate degree of force. The hardware and viscera were evaluated for failure and trauma respectively.</p> <p>Results</p> <p>No hardware failure or obvious visceral trauma was observed. Rib fractures beyond the boundaries of the plates were noted but the incidence was comparable to control and to the fracture incidence after resuscitation previously cited in the literature.</p> <p>Conclusions</p> <p>From this work we believe chest compressions are safe for the patient with sternal plates when proper plating technique is used. We advocate the use of this life-saving maneuver as part of an ACLS resuscitation in the event of an arrest for rapidly re-establishing circulation.</p

Comparison of non-invasive to invasive oxygenation ratios for diagnosing acute respiratory distress syndrome following coronary artery bypass graft surgery: a prospective derivation-validation cohort study

Objective: To determine if non-invasive oxygenation indices, namely peripheral capillary oxygen saturation (SpO2)/ fraction of inspired oxygen (Fi O2) and partial pressure of alveolar oxygen (PAO2)/Fi O2 may be used as effective surrogates for the partial pressure of arterial oxygen (PaO2)/Fi O2. Also, to determine the SpO2/Fi O2 and PAO2/Fi O2 values that correspond to PaO2/Fi O2 thresholds for identifying acute respiratory distress syndrome (ARDS) in patients following coronary artery bypass graft (CABG) surgery. Methods: A prospective derivation-validation cohort study in the Open-Heart ICU of an academic teaching hospital. Recorded variables included patient demographics, ventilator settings, chest radiograph results, and SPO2, PaO2, PAO2, SaO2, and Fi O2. Linear regression modeling was used to quantify the relationship between indices. Receiver operating characteristic (ROC) curves were used to determine the sensitivity and specificity of the threshold values. Results: One-hundred seventy-five patients were enrolled in the derivation cohort, and 358 in the validation cohort. The SPO2/Fi O2 and PAO2/Fi O2 ratios could be predicted well from PaO2/Fi O2, described by the linear regression models SPO2/Fi O2 = 71.149 + 0.8PF and PAO2/Fi O2 = 38.098 + 2.312PF, respectively. According to the linear regression equation, a PaO2/Fi O2 ratio of 300 equaled an SPO2/Fi O2 ratio of 311 (R2 0.857, F 1035.742, < 0.0001) and a PAO2/Fi O2 ratio of 732 (R2 0.576, F 234.887, < 0.0001). The SPO2/Fi O2 threshold of 311 had 90% sensitivity, 80% specificity, LR+ 4.50, LR- 0.13, PPV 98, and NPV 42.1 for the diagnosis of mild ARDS. The PAO2/Fi O2 threshold of 732 had 86% sensitivity, 90% specificity, LR+ 8.45, LR- 0.16, PPV 98.9, and NPV 36 for the diagnosis of mild ARDS. SPO2/ Fi O2 had excellent discrimination ability for mild ARDS (AUC ± SE = 0.92 ± 0.017; 95% CI 0.889 to 0.947) as did PAO2/ Fi O2 (AUC ± SE = 0.915 ± 0.018; 95% CI 0.881 to0.942). Conclusions: PaO2 and SaO2 correlated in the diagnosis of ARDS, with a PaO2/Fi O2 of 300 correlating to an SPO2/ Fi O2 of 311 (Sensitivity 90%, Specificity 80%). The SPO2/ Fi O2 ratio may allow for early real-time rapid identification of ARDS, while decreasing the cost, phlebotomy, blood loss, pain, skin breaks, and vascular punctures associated with serial arterial blood gas measurements

Perioperative infusion of low- dose of vasopressin for prevention and management of vasodilatory vasoplegic syndrome in patients undergoing coronary artery bypass grafting-A double-blind randomized study

Preoperative medication by inhibitors of angiotensin-converting enzyme (ACE) in coronary artery patients predisposes to vasoplegic shock early after coronary artery bypass grafting. Although in the majority of the cases this shock is mild, in some of them it appears as a situation, "intractable" to high-catecholamine dose medication. In this study we examined the possible role of prophylactic infusion of low-dose vasopressin, during and for the four hours post-bypass after cardiopulmonary bypass, in an effort to prevent this syndrome. In addition, we studied the influence of infused vasopressin on the hemodynamics of the patients, as well as on the postoperative urine-output and blood-loss. In our study 50 patients undergoing coronary artery bypass grafting were included in a blind-randomized basis. Two main criteria were used for the eligibility of patients for coronary artery bypass grafting: ejection fraction between 30-40%, and patients receiving ACE inhibitors, at least for four weeks preoperatively. The patients were randomly divided in two groups, the group A who were infused with 0.03 IU/min vasopressin and the group B who were infused with normal saline intraoperativelly and for the 4 postoperative hours. Measurements of mean artery pressure (MAP), central venous pressure (CVP), systemic vascular resistance (SVR), ejection fracture (EF), heart rate (HR), mean pulmonary artery pressure (MPAP), cardiac index (CI) and pulmonary vascular resistance (PVR) were performed before, during, and after the operation. The requirements of catecholamine support, the urine-output, the blood-loss, and the requirements in blood, plasma and platelets for the first 24 hours were included in the data collected. The incidence of vasodilatory shock was significantly lower (8% vs 20%) in group A and B respectively (p = 0,042). Generally, the mortality was 12%, exclusively deriving from group B. Postoperatively, significant higher values of MAP, CVP, SVR and EF were recorded in the patients of group A, compared to those of group B. In group A norepinephrine was necessary in fewer patients (p = 0.002) and with a lower mean dose (p = 0.0001), additive infusion of epinephrine was needed in fewer patients (p = 0.001), while both were infused for a significant shorter infusion-period (p = 0.0001). Vasopressin administration (for group A) was associated with a higher 24 hour diuresis) (0.0001)

Definitions and pathophysiology of vasoplegic shock.

Vasoplegia is the syndrome of pathological low systemic vascular resistance, the dominant clinical feature of which is reduced blood pressure in the presence of a normal or raised cardiac output. The vasoplegic syndrome is encountered in many clinical scenarios, including septic shock, post-cardiac bypass and after surgery, burns and trauma, but despite this, uniform clinical definitions are lacking, which renders translational research in this area challenging. We discuss the role of vasoplegia in these contexts and the criteria that are used to describe it are discussed. Intrinsic processes which may drive vasoplegia, such as nitric oxide, prostanoids, endothelin-1, hydrogen sulphide and reactive oxygen species production, are reviewed and potential for therapeutic intervention explored. Extrinsic drivers, including those mediated by glucocorticoid, catecholamine and vasopressin responsiveness of the blood vessels, are also discussed. The optimum balance between maintaining adequate systemic vascular resistance against the potentially deleterious effects of treatment with catecholamines is as yet unclear, but development of novel vasoactive agents may facilitate greater understanding of the role of the differing pathways in the development of vasoplegia. In turn, this may provide insights into the best way to care for patients with this common, multifactorial condition

Venous gas embolism as a predictive tool for improving CNS decompression safety

A key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. In the present review, we highlight the findings from our laboratory related to the hypothesis that VGE formation is the main mechanism behind serious decompression injuries. In recent studies, we have determined the impact of VGE on endothelial function in both laboratory animals and in humans. We observed that the damage to the endothelium due to VGE was dose dependent, and that the amount of VGE can be affected both by aerobic exercise and exogenous nitric oxide (NO) intervention prior to a dive. We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached

Effectiveness of preoperative beta-blockade on intra-operative heart rate in vascular surgery cases conducted under regional or local anesthesia

BACKGROUND: Preoperative β-blockade has been posited to result in better outcomes for vascular surgery patients by attenuating acute hemodynamic changes associated with stress. However, the incremental effectiveness, if any, of β-blocker usage in blunting heart rate responsiveness for vascular surgery patients who avoid general anesthesia remains unknown. METHODS: We reviewed an existing database and identified 213 consecutive vascular surgery cases from 2005–2011 conducted without general anesthesia (i.e., under monitored anesthesia care or regional anesthesia) at a tertiary care Veterans Administration medical center and categorized patients based on presence or absence of preoperative β-blocker prescription. For this series of patients, with the primary outcome of maximum heart rate during the interval between operating room entry to surgical incision, we examined the association of maximal heart rate and preoperative β-blocker usage by performing crude and multivariate linear regression, adjusting for relevant patient factors. RESULTS: Of 213 eligible cases, 137 were prescribed preoperative β-blockers, and 76 were not. The two groups were comparable across baseline patient factors and intraoperative medication doses. The β-blocker group experienced lower maximal heart rates during the period of evaluation compared to the non-β-blocker group (85 ± 22 bpm vs. 98 ± 36 bpm, respectively; p = 0.002). Adjusted linear regression confirmed a statistically-significant association between lower maximal heart rate and the use of β-blockers (Beta = -11.5; 95% CI [-3.7, -19.3] p = 0.004). CONCLUSIONS: The addition of preoperative β-blockers, even when general anesthesia is avoided, may be beneficial in further attenuating stress-induced hemodynamic changes for vascular surgery patients