Impending Cardiovascular Collapse Research Articles

A case report of an unprovoked neonatal pulmonary embolism: management strategies and cardiopulmonary complications

Abstract Background Neonatal pulmonary embolism is a rare occurrence, especially when idiopathic, instead occurring in patients with identifiable risk factors including severe dehydration, presence or history of a central venous line, or identifiable genetic causes. Given the rarity of paediatric and neonatal pulmonary emboli, few guidelines exist to support the clinician in both the initial resuscitation and ongoing management of the critically ill patient with pulmonary emboli. Case summary We present a 5-day-old female with unprovoked massive pulmonary embolism and associated haemodynamic compromise. She presented with central cyanosis and weak respiratory effort with hypoxaemia, persistent tachycardia, and hypotension despite initial fluid resuscitation, intubation, and administration of 100% FiO2 with inhaled nitric oxide. She was ultimately diagnosed with a massive pulmonary embolism involving the right pulmonary artery by both echocardiography and computed chest tomography, initiated on inotropic support and systemic anticoagulation, after which she underwent mechanical thrombectomy. She was successfully extubated soon thereafter, with subsequent resolution of her emboli. No provoking factors were able to be identified for this patient. Discussion This case highlights the cumulative burden of pulmonary obstruction and inter-ventricular interactions that lead to haemodynamic compromise in the event of massive pulmonary embolism, with resultant considerations of key management strategies. These include the risks of fluid resuscitation and introduction of positive pressure ventilation, as well as the need for early consideration of inotropic support and an institutional pathway for anticoagulation, ultimately proposing a multidisciplinary algorithm for the clinician to deploy when faced with impending cardiovascular collapse from massive pulmonary embolism.

Transition ofResuscitative Endovascular Balloon Occlusion ofthe Aorta from Zone 3 to Zone 1 to Treat Hemodynamic Collapse during Continued Hemorrhage.

Noncompressible torso hemorrhage (NCTH) accounts for most potentially survivable deaths on the battlefield. Treatment of NCTH is challenging, especially in far-forward environments with limited capabilities. Resuscitative endovascular balloon occlusion of the aorta (REBOA) has shown promise in the care of patients with NCTH. REBOA involves introducing a balloon catheter into the descending aorta in a specific occlusion region (zones 1, 2, or 3) and acts as a hemorrhage control adjunct with resuscitative support. The balloon is placed in zone 3 in the infrarenal aorta for high junctional or pelvic injuries and in zone 1 proximal to the diaphragm for torso hemorrhage. Zone 1 REBOA provides more resuscitative support than zone 3; however, the potential for ischemia and reperfusion injuries is greater with zone 1 than with zone 3 REBOA placement. This study aims to determine the possible benefit of transitioning the REBOA balloon from zone 3 to zone 1 to rescue a patient with ongoing venous bleeding and impending cardiovascular collapse. Yorkshire male swine (70-90 kg, n = 6 per group) underwent injury to the femoral artery, which was allowed to bleed freely for 60 s, along with a simultaneous controlled venous hemorrhage. After 60 s, the arterial bleed was controlled with hemostatic gauze and zone 3 REBOA was inflated. Five hundred milliliters of Hextend was used for initial fluid resuscitation. The controlled venous bleed continued until a mean arterial pressure (MAP) of 30 mmHg was reached to create an impending cardiovascular collapse. The animals were then randomized into either continued zone 3 REBOA or transition from zone 3 to zone 1 REBOA. Following 30 min, a "hospital phase" was initiated, consisting of cessation of the venous hemorrhage, deflation of the REBOA balloon, and transfusion of one unit of whole blood administered along with saline and norepinephrine to maintain a MAP of 60 mmHg or higher. The animals then underwent a 2-h observation period. Survival, hemodynamics, and blood chemistries were compared between groups. No significant differences between groups were observed in hemodynamic or laboratory values at baseline, postinitial injury, or when MAP reached 30 mmHg. Survival was significantly longer in animals that transitioned into zone 1 REBOA (log-rank analysis, P = .012). The average time of survival was 14 ± 10 min for zone 3 animals vs. 65 ± 59 min for zone 1 animals (P = .064). No animals in the zone 3 group survived to the hospital phase. Zone 1-treated animals showed immediate hemodynamic improvement after transition, with maximum blood pressure reaching near baseline values compared to those in the zone 3 group. In this swine model of NCTH, hemodynamics and survival were improved when the REBOA balloon was transitioned from zone 3 to zone 1 during an impending cardiovascular collapse. Furthermore, these improved outcome data support the pursuit of additional research into mitigating ischemia-reperfusion insult to the abdominal viscera while still providing excellent resuscitative support, such as intermittent or partial REBOA.

SUDDEN CARDIOVASCULAR COLLAPSE DUE TO CALCIUM CHANNEL BLOCKER OVERDOSE: SUCCESSFUL MANAGEMENT WITH HIGH-DOSE INSULIN EUGLYCEMIC THERAPY

SUDDEN CARDIOVASCULAR COLLAPSE DUE TO CALCIUM CHANNEL BLOCKER OVERDOSE: SUCCESSFUL MANAGEMENT WITH HIGH-DOSE INSULIN EUGLYCEMIC THERAPY

Perspectives on Excited Delirium and Ketamine

Perspectives on Excited Delirium and Ketamine

PVCS AND PES: A CASE OF MASSIVE PULMONARY EMBOLISM AFTER ELECTIVE RADIOFREQUENCY ABLATION

SESSION TITLE: Medical Student/Resident Pulmonary Vascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Thromboembolic events are a known but rare complication of radiofrequency ablation despite the frequent use of intra-procedural anticoagulation. CASE PRESENTATION: A 46-year-old male with history of hypertension and dilated cardiomyopathy underwent elective, repeat ablation for refractory premature ventricular contractions (PVCs) localized to the right ventricular outflow tract (RVOT). The procedure was complicated by bleeding at the groin access sites requiring pressure bandages and bed rest. Prior to discharge at 24 hours, the patient suddenly developed tachypnea, tachycardia, diaphoresis, and worsening hypoxemia. He required intubation with inotropic support; bedside echocardiogram showed a dilated right ventricle (RV). CT angiogram demonstrated extensive bilateral pulmonary emboli (PE). Intravenous heparin was started; however, refractory obstructive shock developed. Despite high minute ventilation, the patient’s hypercarbia and acidemia worsened. The decision was made to initiate veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for impending cardiovascular collapse. Transesophageal echocardiogram during cannulation revealed a hypokinetic RV with clot in transit. The patient demonstrated improved hemodynamics and RV function while on ECMO with heparin anticoagulation, and was subsequently decannulated on day 7. He required tracheostomy and prolonged mechanical ventilation secondary to ventilator associated pneumonia and critical illness myopathy, but is now fully recovered and doing well at home. DISCUSSION: Incidence of deep vein thrombosis after non-atrial fibrillation (AF) ablations is as high as 2.38%(1). Periprocedural anticoagulation is recommended in AF and left sided ablations, but expert consensus recommends its use in RV procedures only when risk of thrombosis is considered high. The duration of the procedure and number of venous catheters used may increase the risk of venous thrombosis(2). RVOT ablations can be long and technically challenging, increasing both bleeding risk and endothelial disruption. Patients with bleeding complications may require bed rest and compression leading to stasis, tipping the coagulation balance towards thrombosis. To date, use of ECMO for massive PE is limited to single center case series with promising outcomes. ECMO should be considered in cases of refractory shock or inability to ventilate due to severe V/Q mismatch, especially when further thrombolysis may exacerbate pre-existing bleeding. PE with right heart thrombi in transit are at particularly high risk for deterioration(3). Fortunately, the diagnosis was made early in our patient’s course which allowed for timely initiation of VA-ECMO. CONCLUSIONS: Providers should maintain a high index of suspicion for PE even in patients with brief hospitalizations for elective procedures. Furthermore, VA-ECMO may be especially useful in patients with both massive PE and ongoing bleeding. Reference #1: Burstein B, Barbosa RS, Kalfon E, Joza J, Bernier M, Essebag V. Venous Thrombosis After Electrophysiology Procedures: A Systematic Review. Chest [Internet]. 2017;152(3):574–86. Reference #2: Cronin EM, Bogun FM, Maury P, Peichl P, Chen M, Namboodiri N, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. Hear Rhythm [Internet]. 2020;17(1):e2–154. Reference #3: Kronik G. The european cooperative study on the clinical significance of right heart thrombi. Eur Heart J. 1989;10(12):1046–59. DISCLOSURES: No relevant relationships by Timothy Fernandes, source=Web Response No relevant relationships by Abdurrahman Husain, source=Web Response No relevant relationships by Janna Raphelson, source=Web Response No relevant relationships by Alexandra Rose, source=Web Response

Salvage resection of advanced mediastinal tumors.

The surgical treatment of locally advanced mediastinal tumors invading the great vessels and other nearby structures still represent a tricky question, principally due to the technical complexity of the resective phase, the contingent need to carry out viable vascular reconstructions and, therefore, the proper management of pathophysiologic issues. Published large-number series providing oncologic outcomes of patients who have undergone extended radical surgery for invasive mediastinal masses are just a few. Furthermore, the wide variety of different histologies included in some of these studies, as well as the heterogeneity of chemo and radiation therapies employed, did not allow for the development of clear oncologic guidelines. Usually in the past, surgical resections of large masses along with the neighbouring structures were not offered to patients because of related morbidity and mortality and limited information available on the prognostic advantage for long term. However, in the last decades, advances in surgical technique and perioperative management, as well as increased oncologic experience in this field, have allowed radical exeresis in selected patients with invasive tumors requiring resections extended to the surrounding structures and complex vascular reconstructions. Such aggressive surgical treatment has been proposed in association or not with adjuvant chemo- or radiotherapy regimens, achieving encouraging oncologic results with limited morbidity and mortality in experienced institutions. Congestive heart failure or impending cardiovascular collapse due to the compression by the large mass are the most frequent immediately life-threatening problems that some of these patients can experience. In this setting, medical palliation is usually ineffective and an aggressive salvage surgical treatment may remain the only therapeutic option.

Partial Aortic Occlusion using Resuscitative Endovascular Balloon Occlusion of the Aorta (P-REBOA) in Ruptured Abdominal Aortic Aneurysm

Ruptured abdominal aortic aneurysm is often a fatal event without immediate intervention for the associated hemorrhagic shock and impending cardiovascular collapse. We report a case of a ruptured abdominal aortic aneurysm managed with partially occlusive resuscitative endovascular balloon occlusion of the aorta (P-REBOA) as a means to gain proximal control, tailor blood pressure goals, while allowing time to obtain access and repair the ruptured aneurysm.

Use of Transesophageal Echocardiography During Cesarean Section in A Parturient with Inferior Vena Cava Thrombosis:A Case Report

1. Abstract 1.1. Introduction: The use of transesophageal echocardiography in obstetric anesthesia is uncommon and rarely reported during cesarean section. To our knowledge, this is the first report of its use for intraoperative surveillance of a tumor thrombus that has invaded over 90% of the inferior vena cava and was at risk of embolizing in a patient undergoing a cesarean section. 1.2. Case Presentation: We present at 16-year-old Hispanic female at 37 weeks of pregnancy who presented to us for higher level of care due to a newly discovered large left renal mass and inferior vena cava tumor thrombus. She successfully underwent general anesthesia with the assistance of transesophageal echocardiography for her cesarean section. 1.3. Conclusion : We used transesophageal echocardiography to directly observe the inferior vena cava tumor thrombus which would allow for an early intervention and to potentially avoid impending cardiovascular collapse. After a review of the available literature, this is the first case report to utilize transesophageal echocardiography to monitor a tumor thrombus in the setting of a cesarean section and large renal mass. Given the broad differential diagnosis if sudden cardiovascular collapse should occur, the use of transesophageal echocardiography provides the anesthesiologist a reliable and accurate assessment tool for quick management. 2. Keywords: <span style=font-size:10.0pt;line-height: 107%;font-family: times= new= roman,serif=> Cesarean Section; Ewing’s Sarcoma; Inferior Vena Cava Thrombosis; Transesophageal Echocardiography

Aortic Balloon Occlusion for Exsanguinating Upper GI Bleeding

Uncommonly, patients with nonvariceal upper gastrointestinal bleeding (UGIB) present with massive blood loss and impending cardiovascular collapse. In

Heart period and blood pressure characteristics in splanchnic arterial occlusion shock-induced collapse.

The nature of hemodynamic instability typical of circulatory shock is not well understood, but an improved interpretation of its dynamic features could help in the management of critically ill patients. The objective of this work was to introduce new metrics for the analysis of arterial blood pressure (ABP) in order to characterize the risk of catastrophic outcome in splanchnic arterial occlusion (SAO) shock. Continuous ABP (fs=1kHz) was measured in rats during experimental SAO shock, which induced a fatal pressure drop (FPD) in ABP. The FPD could either be slow (SFPD) or fast (FFPD), with the latter causing cardiovascular collapse. Time series of mean arterial pressure, systolic blood pressure and heart period were derived from ABP. The sample asymmetry-based algorithm Heart Rate Characteristics was adapted to compute the Heart Period Characteristics (HPC) and the Blood Pressure Characteristics (BPC). Baroreflex sensitivity (BRS) was assessed by means of a bivariate model. The approach to FPD of the animals who collapsed (FFPD) was characterized by higher BRS in the low frequency band versus SFPD animals (0.36±0.15 vs. 0.19±0.12ms/mmHg, p value=0.0196), bradycardia as indicated by the HPC (0.76±0.57 vs. 1.94±1.27, p value=0.0179) and higher but unstable blood pressure as indicated by BPC (3.02±2.87 vs. 1.47±1.29, p value=0.0773). The HPC and BPC indices demonstrated promise as potential clinical markers of hemodynamic instability and impending cardiovascular collapse, and this animal study suggests their test in data from intensive care patients.

Decrease in Bispectral Index Prior to Cardiovascular Collapse During Caesarean Sections

We report a case of significant reduction in bispectral index (BIS) associated with suspected amniotic fluid embolism (AFE) that occurred prior to change in haemodynamic variables. The patient was a 29-year-old nulliparous, who was admitted for Caesarean section under general anaesthesia in the 33rd week of pregnancy. After the baby was born, the BIS value suddenly decreased to 0, with suppression ratio of 100. One minute later, saturation decreased abruptly to 85%, end-tidal carbon dioxide (EtCO2) decreased to 5 mmHg, peak inspiratory pressure increased to 35 cm H2O, and non-invasive blood pressure (BP) failed to obtain a reading. After administration of vasoactive drugs, the systolic BP was maintained at 100 mmHg or higher, the BIS value rose to 10-20, and the EtCO2 increased to 24-33 mmHg. In this case, the BIS monitoring may provide an earlier warning of impending cardiovascular collapse in the case of AFE.

Decrease in bispectral index prior to cardiovascular collapse during Caesarean sections

We report a case of significant reduction in bispectral index (BIS) associated with suspected amniotic fluid embolism (AFE) that occurred prior to change in haemodynamic variables. The patient was a 29-year-old nulliparous, who was admitted for Caesarean section under general anaesthesia in the 33rd week of pregnancy. After the baby was born, the BIS value suddenly decreased to 0, with suppression ratio of 100. One minute later, saturation decreased abruptly to 85%, end-tidal carbon dioxide (EtCO2) decreased to 5 mmHg, peak inspiratory pressure increased to 35 cm H2O, and non-invasive blood pressure (BP) failed to obtain a reading. After administration of vasoactive drugs, the systolic BP was maintained at 100 mmHg or higher, the BIS value rose to 10-20, and the EtCO2 increased to 24-33 mmHg. In this case, the BIS monitoring may provide an earlier warning of impending cardiovascular collapse in the case of AFE.

Lightweight noninvasive trauma monitor for early indication of central hypovolemia and tissue acidosis

Hemorrhage is a major cause of soldier death; it must be quickly identified and appropriately treated. We developed a prototype patient monitor that noninvasively and continuously determines muscle oxygen saturation (SmO₂), muscle pH (pHm), and a regional assessment of blood volume (HbT) using near-infrared spectroscopy. Previous demonstration in a model of progressive, central hypovolemia induced by lower body negative pressure (LBNP) showed that SmO₂ provided an early indication of impending hemodynamic instability in humans. In this review, we expand the number of subjects and provide an overview of the relationship between the muscle and sublingual microcirculation in this model of compensated shock. Healthy human volunteers (n = 30) underwent progressive LBNP in 5-minute intervals. Standard vital signs, along with stroke volume (SV), total peripheral resistance, functional capillary density, SmO₂, HbT, and pHm were measured continuously throughout the study. SmO₂ and SV significantly decreased during the first level of central hypovolemia (-15 mm Hg LBNP), whereas vital signs were later indicators of impending cardiovascular collapse. SmO₂ declined with SV and inversely with total peripheral resistance throughout LBNP. HbT was correlated with declining functional capillary density, suggesting vasoconstriction as a cause for decreased SmO₂ and subsequently decreased pHm. CLINICAL TRANSLATION: The monitor has been miniaturized to a 58-g solid-state sensor that is currently being evaluated on patients with dengue hemorrhagic fever. Early results demonstrate significant decreases in SmO₂ similar to those observed with progressive reductions in central blood volume. As such, this technology has the potential to (1) provide a monitoring capability for both nontraumatic and traumatic hemorrhage and (2) help combat medics triage casualties and monitor patients during lengthy transport from combat areas.

Early Vasopressor Use in Critical Injury Is Associated With Mortality Independent From Volume Status

Complications of excessive crystalloid after critical injury have increased interest in vasopressor support. However, it is hypothesized that vasopressor use in patients who are under-resuscitated is associated with death. We performed this study to determine whether volume status is associated with increased mortality in the critically injured exposed to early vasopressors. The intensive care unit database at a Level I center was queried for all adult admissions surviving for >24 hours from January 1, 2001, to December 31, 2008. Patients with spinal cord injury and severe traumatic brain injury were excluded. The vasopressor group [Vaso (+)] was exposed to dopamine, epinephrine, phenylephrine, norepinephrine, or arginine vasopressin within 24 hours of admission. Demographic and injury data were studied including intensive care unit admission central venous pressure. Hypovolemia [Hypov (+)] was considered an admission central venous pressure ≤8 mm Hg. The Vaso (+) group was analyzed to determine whether Hypov (+) was independently associated with death. Of 1,349 eligible patients, 26% (351) were Vaso (+). Mortality was 43.6% (153) in the Vaso (+) versus 4.2% (42) in the Vaso (-) group (17.60 [12.10-25.60], <0.01). Vasopressor exposure was associated with death independent of injury severity. In Vaso (+) patients, Hypov (+) was not associated with mortality, whereas Emergency Department admission Glasgow Coma Scale ≤8 and multiple vasopressor use were. Vasopressor exposure early after critical injury is independently associated with death and mortality is increased regardless of fluid status. Although it is not advisable to withhold support with impending cardiovascular collapse, use of any vasopressor during ongoing resuscitation should be approached with extreme caution regardless of volume status.

Use of Intralipid in an infant with impending cardiovascular collapse due to local anesthetic toxicity

Local anesthetic-associated cardiac toxicity following caudal epidural blockade is, fortunately, a rare event. Prompt recognition and early treatment is the key to successful resuscitation. Early use of the lipid emulsion Intralipid in bupivacaine-induced cardiac toxicity may lead to a good outcome.

Acute Valvular Regurgitation

Acute severe valvular regurgitation is a surgical emergency, but accurate and timely diagnosis can be difficult. Although cardiovascular collapse is a common presentation, examination findings to suggest acute regurgitation may be subtle, and the clinical presentation may be nonspecific. Consequently, the presentation of acute valvular regurgitation may be mistaken for other acute conditions, such as sepsis, pneumonia, or nonvalvular heart failure. Although acute regurgitation may affect any valve, acute regurgitation of the left-sided valves is more common and has greater clinical impact than acute regurgitation of right-sided valves. Data to guide appropriate management of patients with acute regurgitation are sparse; there are no randomized trials, and much of the literature describes either small series or the experiences of specific centers. Despite these limitations, the available data are sufficient to allow identification of general principles as well as development of applicable guidelines from both the American College of Cardiology/American Heart Association and European Society of Cardiology. The guidelines recommend valve surgery for symptomatic patients with aortic or mitral regurgitation, including those with acute regurgitation.1–3 The data and guidelines emphasize overarching clinical principles, including the need for a high clinical suspicion of acute regurgitation, timely use of echocardiography, and, in the majority of patients, rapid progression to surgery. Causes of acute regurgitation overlap with causes of chronic regurgitation and vary depending on the valve affected (Table 1). Endocarditis may affect either the aortic or mitral valve, whereas other causes are unique to the specific valve involved. The majority of causes of acute regurgitation present as an acute or subacute event. However, acute regurgitation can occur in patients with chronic regurgitation, when regurgitant severity is exacerbated by factors such as coronary ischemia, chordal rupture, or leaflet perforation from endocarditis. Acute regurgitation of either the aortic or mitral valve may result from procedural …

Fluid and Volume Monitoring

Fluid resuscitation is not only used to prevent acute kidney injury (AKI) but fluid management is also a cornerstone of treatment for patients with established AKI and renal failure. Ultrafiltration removes volume initially from the intravascular compartment inducing a relative degree of hypovolemia. Normal reflex mechanisms attempt to sustain blood pressure constant despite marked changes in blood volume and cardiac output. Thus, compensated shock with a normal blood pressure is a major cause of AKI or exacerbations of AKI during ultrafiltration. We undertook a systematic review of the literature using MEDLINE, Google Scholar and PubMed searches. We determined a list of key questions and convened a 2-day consensus conference to develop summary statements via a series of alternating breakout and plenary sessions. In these sessions, we identified supporting evidence and generated clinical practice recommendations and/or directions for future research. We defined three aspects of fluid monitoring: i) normal and pathophysiological cardiovascular mechanisms; ii) measures of volume responsiveness and impending cardiovascular collapse during volume removal, and; iii) measured indices of each using non-invasive and minimally invasive continuous and intermittent monitoring techniques. The evidence documents that AKI can occur in the setting of normotensive hypovolemia and that under-resuscitation represents a major cause of both AKI and mortality ion critically ill patients. Traditional measures of intravascular volume and ventricular filling do not predict volume responsiveness whereas dynamic functional hemodynamic markers, such as pulse pressure or stroke volume variation during positive pressure breathing or mean flow changes with passive leg raising are highly predictive of volume responsiveness. Numerous commercially-available devices exist that can acquire these signals. Prospective clinical trials using functional hemodynamic markers in the diagnosis and management of AKI and volume status during ultrafiltration need to be performed. More traditional measure of preload be abandoned as marked of volume responsiveness though still useful to assess overall volume status.

Oxygen saturation determined from deep muscle, not thenar tissue, is an early indicator of central hypovolemia in humans

To compare the responses of noninvasively measured tissue oxygen saturation (StO2) and calculated muscle oxygen tension (PmO2) to standard hemodynamic variables for early detection of imminent hemodynamic instability during progressive central hypovolemia in humans. Prospective study. Research laboratory. Sixteen healthy human volunteers. Progressive lower body negative pressure (LBNP) to onset of cardiovascular collapse. Noninvasive measurements of blood pressures, heart rate, and stroke volume were obtained during progressive LBNP with simultaneous assessments of StO2, PmO2, and muscle oxygen saturation (SmO2). Forearm SmO2 and PmO2 were determined with a novel near infrared spectroscopic measurement device (UMMS) and compared with thenar StO2 measured by a commercial device (HT). All values were normalized to the duration of LBNP exposure required for cardiovascular collapse in each subject (i.e., LBNP maximum). Stroke volume was significantly decreased at 25% of LBNP maximum, whereas blood pressure was a late indicator of imminent cardiovascular collapse. PmO2 (UMMS) was significantly decreased at 50% of maximum LBNP while SmO2 (UMMS) decreased at 75% of maximum LBNP. Thenar StO2 (HT) showed no statistical change throughout the entire LBNP protocol. Spectroscopic assessment of forearm muscle PO2 and SmO2 provides noninvasive and continuous measures that are early indicators of impending cardiovascular collapse resulting from progressive reductions in central blood volume.

Noninvasively determined muscle oxygen saturation is an early indicator of central hypovolemia in humans

Ten healthy human volunteers were subjected to progressive lower body negative pressure (LBNP) to the onset of cardiovascular collapse to compare the response of noninvasively determined skin and fat corrected deep muscle oxygen saturation (SmO2) and pH to standard hemodynamic parameters for early detection of imminent hemodynamic instability. Muscle SmO2 and pH were determined with a novel near infrared spectroscopic (NIRS) technique. Heart rate (HR) was measured continuously via ECG, and arterial blood pressure (BP) and stroke volume (SV) were obtained noninvasively via Finometer and impedance cardiography on a beat-to-beat basis. SmO2 and SV were significantly decreased during the first LBNP level (-15 mmHg), whereas HR and BP were late indicators of impending cardiovascular collapse. SmO2 declined in parallel with SV and inversely with total peripheral resistance, suggesting, in this model, that SmO2 is an early indicator of a reduction in oxygen delivery through vasoconstriction. Muscle pH decreased later, suggesting an imbalance between delivery and demand. Spectroscopic determination of SmO2 is noninvasive and continuous, providing an early indication of impending cardiovascular collapse resulting from progressive reduction in central blood volume.

Inspiratory resistance maintains arterial pressure during central hypovolemia: Implications for treatment of patients with severe hemorrhage

To test the hypothesis that an impedance threshold device would increase systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure and delay the onset of symptoms and cardiovascular collapse associated with severe central hypovolemia. Prospective, randomized, blinded trial design. Human physiology laboratory. Nine healthy nonsmoking normotensive subjects (five males, four females). Central hypovolemia and impending cardiovascular collapse were induced in human volunteers by applying progressive lower body negative pressure (under two experimental conditions: a) while breathing with an impedance threshold device set to open at -7 cm H2O pressure (active impedance threshold device); and b) breathing through a sham impedance threshold device (control). Systolic blood pressure (79 +/- 5 mm Hg), diastolic blood pressure (57 +/- 3 mm Hg), and mean arterial pressure (65 +/- 4 mm Hg) were lower (p < .02) when subjects (n = 9) breathed through the sham impedance threshold device than when they breathed through the active impedance threshold device at the same time of cardiovascular collapse during sham breathing (102 +/- 3, 77 +/- 3, 87 +/- 3 mm Hg, respectively). Elevated blood pressure was associated with 23% greater lower body negative pressure tolerance using an active impedance threshold device (1639 +/- 220 mm Hg-min) compared with a sham impedance threshold device (1328 +/- 144 mm Hg-min) (p = .02). Use of an impedance threshold device increased systemic blood pressure and delayed the onset of cardiovascular collapse during severe hypovolemic hypotension in spontaneously breathing human volunteers. This device may provide rapid noninvasive hemodynamic support in patients with hypovolemic hypotension once the blood loss has been controlled but before other definitive therapies are available.