The ACCF/AHA scientific statement on syncope needs rethinking.
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Biomedical subjects
Publications and source records attributed to David G Benditt.
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BACKGROUND: The intrathoracic pressure regulator (ITPR) was created to improve hemodynamics by generating continuous negative airway pressure between positive pressure ventilations to enhance cardiac preload in apnoeic animals. In normovolemic and hypovolemic pigs, we tested the hypothesis that continuous negative intrathoracic pressure set at -5 or -10mmHg, interrupted only for intermittent positive pressure ventilations, would decrease intracranial (ICP) and right atrial (RAP) pressure, and increase mean arterial pressure (MAP). METHODS: Twelve pigs were anesthetized with propofol and ventilated with a bag. The ITPR was used to vary baseline endotracheal pressures (ETPs) for 5min periods in the following sequence: 0, -5, 0, -10, 0mmHg under normovolemic conditions. Six pigs were bled 50% (32.5+/-mL/kg) of their estimated blood volume and the airway pressure sequence was repeated. Six other pigs were bled 35% (22.75+/-mL/kg) of their estimated blood volume and the same airway pressure sequence was repeated. Intracranial, aortic, right atrial pressures, arterial blood gases, end tidal CO(2) (ETCO(2)), were measured. ANOVA was used for statistical analysis. Linear regression analysis was performed for ETP and ICP. RESULTS: Mean arterial and vital organ perfusion pressures were significantly improved and RA pressure significantly decreased with the use of the ITPR; the effect was greater with the more negative ETPs and lower circulating blood volume. The change of ICP was linearly related to the ETP and blood loss: DeltaICP=[1.22-0.84(1-%blood loss/100)]xETP, r(2)=0.88 (in mmHg), p<0.001. There were no adverse device effects and there was a significant increase of ETCO(2) with the use of ITPR. CONCLUSION: The ITPR decreased RAP and ICP significantly and improved mean arterial and cerebral and coronary perfusion pressures without affecting acid base balance severely. The decrease in ICP was directly proportional to the reduction in intrathoracic pressure. The effects were more pronounced in severe hypovolemic and hypotensive states with more negative ETP pressure.
AIMS: We prospectively correlated the results of tilt testing (TT) and adenosine triphosphate test (ATP) with the findings observed during a spontaneous syncopal relapse by means of an implantable loop recorder (ILR) in patients with a clinical diagnosis of neurally mediated syncope. METHODS AND RESULTS: We included patients with three or more clinically severe syncopal episodes in the last 2 years without significant electrocardiographic and cardiac abnormalities. Patients with orthostatic hypotension and carotid sinus syncope were excluded. After ILR implantation, patients were followed until the first documented syncope. Among 392 enrolled patients, 343 underwent TT, which was positive in 164 (48%), and 180 ATP test, which was positive in 53 (29%). Syncope was documented by ILR in 106 (26%) patients after a median of 3 months. Patients with positive and negative TT had similar baseline characteristics, syncopal recurrence rate, and mechanism of syncope, but those with positive TT had more frequently no or slight rhythm variations during spontaneous syncope (45 vs. 21%, P=0.02). An asystolic pause was more frequently found during spontaneous syncope than during TT (45 vs. 21%, P=0.02), but there was a trend for those with an asystolic response during TT also to have an asystolic response during spontaneous syncope (75 vs. 37%, P=0.1). Patients with positive ATP test responses showed syncopal recurrence rates and mechanism of syncope similar to those with negative ATP tests. CONCLUSION: In patients with neurally mediated syncope, clinical characteristics, outcome, and mechanism of syncope are poorly correlated and not predicted by the results of TT and ATP test. Therefore, these tests are of little or no value in guiding specific therapy.
AIMS: This prospective multicentre observational study assessed the efficacy of specific therapy based on implantable loop recorder (ILR) diagnostic observations in patients with recurrent suspected neurally mediated syncope (NMS). METHODS AND RESULTS: Patients with three or more clinically severe syncopal episodes in the last 2 years without significant electrocardiographic and cardiac abnormalities were included. Orthostatic hypotension and carotid sinus syncope were excluded. After ILR implantation, patients were followed until the first documented syncope (Phase I). The ILR documentation of this episode determined the subsequent therapy and commenced Phase II follow-up. Among 392 patients, the 1-year recurrence rate of syncope during Phase I was 33%. One hundred and three patients had a documented episode and entered Phase II: 53 patients received specific therapy [47 a pacemaker because of asystole of a median 11.5 s duration and six anti-tachyarrhythmia therapy (catheter ablation: four, implantable defibrillator: one, anti-arrhythmic drug: one)] and the remaining 50 patients did not receive specific therapy. The 1-year recurrence rate in 53 patients assigned to a specific therapy was 10% (burden 0.07 +/- 0.2 episodes per patient/year) compared with 41% (burden 0.83 +/- 1.57 episodes per patient/year) in the patients without specific therapy (80% relative risk reduction for patients, P = 0.002, and 92% for burden, P = 0.002). The 1-year recurrence rate in patients with pacemakers was 5% (burden 0.05 +/- 0.15 episodes per patient/year). Severe trauma secondary to syncope relapse occurred in 2% and mild trauma in 4% of the patients. CONCLUSION: A strategy based on early diagnostic ILR application, with therapy delayed until documentation of syncope allows a safe, specific, and effective therapy in patients with NMS.
INTRODUCTION: Spontaneous gasping is associated with increased survival in animal models of cardiac arrest and in observational studies of humans. The potential beneficial effect of gasping on cerebral perfusion may underlie the observed survival benefit, but mechanisms remain unknown. HYPOTHESIS: We hypothesized that spontaneous gasping in a pig model of ventricular fibrillation (VF) decreases intracranial pressure (ICP) and increases cerebral perfusion pressure (CePP) during VF in a pig model. METHODS: The 13 female farm pigs, weighing between 16 and 33 kg, were anesthetized with propofol and intubated, and then had VF induced for 8 min without intervention. Intrathoracic pressure (ITP), aortic pressure (AoP), and ICP were measured continuously. CePP and ITP were recorded simultaneously during three maximal gasps and correlated with gasping by Spearman rank correlation. RESULTS: Gasping during VF occurred in 13/13 pigs and followed a crescendo-decrescendo pattern. Each gasp was associated with a biphasic AoP (initial fall, then rise) and ICP (initial rise, then fall) morphology. Time to first gasp (r(2)=0.06), time to maximal gasp (r(2)=0.02), duration of gasping (r(2)=0.11) and frequency of gasping (r(2)=0.32) did not correlate significantly with CePP during gasping while depth of gasping exhibited a weak but significant correlation with CePP (r(2)=0.35, p=0.05). Maximal gasping occurred at 202+/-34 s from onset of VF and resulted in an average decrease in ICP from 27.4+/-5.8 to 20+/-6.7 mmHg, p<0.01 along with an increase in CePP from -0.05+/-10.9 to 11.5+/-12.6 mmHg, p<0.05. CONCLUSIONS: Spontaneous gasping during cardiac arrest decreased intra-cranial pressure and increased cerebral perfusion pressure significantly. These results may help explain why gasping is associated with improved cardiac arrest survival rates. Based upon this new understanding of the physiology of gasping, we speculate that investigation of devices that can enhance the physiological effects of gasping on intracranial pressure and cerebral perfusion should be prioritized.
BACKGROUND: The inspiratory impedance threshold device (ITD) has been shown to improve hemodynamic variables and survival outcomes during cardiopulmonary resuscitation in animals and humans. We hypothesized that use of an ITD, with a resistance of -10 cm H2O, will improve hemodynamics and short-term survival rates during hypovolemic hypotension in spontaneously breathing pigs. METHODS: Female farm pigs ( approximately 26 kg) were intubated and anesthetized with propofol with the dose adjusted to permit spontaneous respirations. They were bled to 50% of calculated blood volume through an arterial catheter and then prospectively randomized to either treatment with an ITD or observation alone. Arterial and intratracheal pressures as well as arterial blood gases were measured. After 90 min the ITD was removed, normal saline was administered to all surviving animals, the anesthetic was discontinued, and animals were allowed to recover. Statistical analysis was performed with one-way repeated ANOVA and survival rates were calculated with Kaplan-Meier analysis. RESULTS: Treatment with the ITD resulted in lower intratracheal inspiratory pressure in the treatment group (-11+/-0.4 mmHg versus -4+/-0.7 mmHg, respectively, P<0.005). Mean arterial pressure after 30 min of treatment with the ITD was higher in the treatment group (61.1+/-5.5 mmHg versus 37.4+/-2.1 mmHg, respectively, P<0.005). All pigs in the control group died within 65 min of the initial bleed, whereas 7/8 (87%) treated with an ITD survived for >90 min (P<0.001). During the recovery phase, 6/8 (75%) in the ITD group survived for >3h and awoke without neurological deficit; one surviving animal in the ITD group never woke up. Arterial oxygenation was not compromised in the ITD group. CONCLUSIONS: Use of an ITD improved blood pressure and short-term survival rates in a spontaneously breathing porcine model of hypovolemic hypotension.
OBJECTIVES: A rapid, ice-cold saline flush combined with active compression-decompression (ACD) plus an inspiratory impedance threshold device (ITD) cardiopulmonary resusitation (CPR) will cool brain tissue more effectively than with standard CPR (S-CPR) during cardiac arrest (CA). BACKGROUND: Early institution of hypothermia after CPR and return of spontaneous circulation improves survival and outcomes after CA in humans. METHODS: Ventricular fibrillation (VF) was induced for 8 min in anesthetized and tracheally intubated pigs. Pigs were randomized to receive either ACD + ITD CPR (n = 8) or S-CPR (n = 8). After 2 min of CPR, 30 ml/kg ice-cold saline (3 degrees C) was infused over the next 3 min of CPR via femoral vein followed by up to three defibrillation attempts (150 J, biphasic). If VF persisted, epinephrine (40 microg/kg) and vasopressin (0.3 U/kg) were administered followed by three additional defibrillation attempts. Hemodynamic variables and temperatures were continuously recorded. RESULTS: All ACD + ITD CPR pigs (8 of 8) survived (defined as 15 min of return of spontaneous circulation [ROSC]) versus 3 of 8 pigs with S-CPR (p < 0.05). In survivors, brain temperature (degrees C) measured at 2-cm depth in brain cortex 1 min after ROSC decreased from 37.6 +/- 0.2 to 35.8 +/- 0.3 in ACD + ITD CPR versus 37.8 +/- 0.2 to 37.3 +/- 0.3 in S-CPR (p < 0.005). Immediately before defibrillation: 1) right atrial systolic/diastolic pressures (mm Hg) were lower (85 +/- 19, 4 +/- 1) in ACD + ITD CPR than S-CPR pigs (141 +/- 12, 8 +/- 3, p < 0.01); and 2) coronary perfusion pressures (mm Hg) were higher in ACD + ITD CPR (28.3 +/- 2) than S-CPR pigs (17.4 +/- 3, p < 0.01). CONCLUSIONS: A rapid ice-cold saline infusion combined with ACD + ITD CPR during cardiac arrest induces cerebral hypothermia more rapidly immediately after ROSC than with S-CPR.
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Improved cardiac resynchronization by pacemakers (CRT-P) and implantable defibrillators (CRT-D) benefits cardiac function, reduces heart failure (HF) admissions, and diminishes mortality in patients with severe left ventricular (LV) dysfunction. In terms of mortality benefit, current evidence suggests that CRT-D may be better than CRT-P alone when a broad range of HF patients is considered. However, the differential benefit may be small in certain patients. In individuals with severe and worsening HF due to systolic LV dysfunction, HF complications other than ventricular tachyarrhythmias contribute importantly to both quality-of-life (QoL) and duration of survival; these patients may be served cost-effectively by CRT-P enhancing QoL. A clinical trial evaluating CRT-D vs. CRT-P in terms of QoL and survival in such patients would assist physicians and payers to understand better the relative roles of CRT-P and CRT-D in the care of the sickest HF patients.
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The American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) have recently published, in both the Journal of the American College of Cardiology (JACC) and Circulation, a Scientific Statement on the Evaluation of Syncope ('Statement'). This Scientific Statement was commissioned to provide guidance for clinicians regarding the evaluation of patients who present with 'syncope'. The Statement was not intended to be a formal set of practice guidelines. However, in the absence of generally accepted practice guidelines in North America, the Statement's potential impact on clinical care may be more far-reaching than expected; it may erroneously be considered to be the authoritative 'de-facto' guideline document. This commentary, submitted by a multidisciplinary consortium of more than 60 physicians with expertise in the management of transient loss of consciousness (TLOC), points out that in many respects the ACCF/AHA Syncope Statement fails to address long-standing clinical errors associated with the evaluation of episodes of apparent TLOC, including syncope. If not appropriately revised, the current Statement may lead to both inadequate patient care as well as a potentially damaging legal environment for physicians undertaking evaluation of patients who present with transient loss of consciousness.
Syncope is a relatively common clinical syndrome that is a subset of a broader range of conditions that cause transient loss of consciousness (TLOC). Other TLOC conditions include seizures, concussions, and intoxications. However, despite frequent confusion in the medical literature, syncope is and should be clearly distinguished from those other causes of TLOC by virtue of its pathophysiology; specifically, syncope is the result of self-terminating inadequacy of global cerebral nutrient perfusion, while the other forms of TLOC have different etiologies. Unfortunately, the diagnostic evaluation of syncope remains for the most part poorly managed and inefficient. Careful history-taking, physical examination, and judicious use of tests can not only increase the diagnostic yield of the evaluation, but also increase patient safety and reduced overall healthcare costs.
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OBJECTIVES: This study compared cardiac resynchronization therapy's (CRT) impact on ventricular tachyarrhythmia susceptibility in patients who, due to worsening heart failure (HF) symptoms, underwent a replacement of a conventional implantable cardioverter-defibrillator (ICD) with a CRT-ICD. BACKGROUND: Cardiac resynchronization therapy is an effective addition to conventional treatment of HF in many patients with left ventricular systolic dysfunction. However, whether CRT-induced improvements in HF status also reduce susceptibility to life-threatening arrhythmias is less certain. METHODS: Clinical and ICD electrogram data were evaluated in 18 consecutive ICD patients who underwent an upgrade to CRT-ICD. Pharmacologic HF therapy was not altered during follow-up. The definition of ventricular tachycardia (VT) and ventricular fibrillation (VF) for each patient was as determined by device programming. Statistical comparisons used paired t tests. RESULTS: Findings were recorded during two time periods: 47 +/- 21 months (range 24 to 70 months) before and 14 +/- 2 months (range 9 to 18 months) after CRT upgrade. At time of upgrade, patient age was 69 +/- 11 years and ejection fraction was 21 +/- 8%. Before CRT the frequency of VT, VF, and appropriate ICD shocks was 0.31 +/- 1.23, 0.047 +/- 0.083, and 0.048 +/- 0.085 episodes/month/patient, respectively. After CRT-ICD, VT and VF arrhythmia burdens and frequency of shocks were respectively 0.13 +/- 0.56, 0.001 +/- 0.004, and 0.003 +/- 0.016 episodes/month/patient (p = 0.59, 0.03, and 0.05 vs. pre-CRT). CONCLUSIONS: Arrhythmia frequency and number of appropriate ICD treatments were reduced after upgrade to CRT-ICD for HF treatment. Thus, apart from hemodynamic benefits, CRT may also ameliorate ventricular tachyarrhythmia susceptibility in HF patients.
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BACKGROUND: A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled -10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest. METHODS AND RESULTS: In protocol 1, 20 pigs (weight, 30+/-0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of ITPR-CPR. This sequence was repeated. In protocol 3, 6 animals after 8 minutes of untreated VF were treated with ITPR-CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10, and 15 of CPR. A newer, leak-proof ITPR device was used. Aortic, right atrial, endotracheal pressure, intracranial pressure, and end-tidal CO2 values were measured (mm Hg); common carotid arterial flow also was measured (mL/min). Coronary perfusion pressure (diastolic; aortic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean intracranial pressure) were calculated. Unpaired Student t test and Friedman's repeated-measures ANOVA of ranks were used in protocols 1 and 3. A 2-tailed Wilcoxon signed-rank test was used for analysis in protocol 2. Fischer's exact test was used for survival. Significance was set at P<0.05. Vital organ perfusion pressures and end-tidal CO2 were significantly improved with ITPR-CPR in both protocols. In protocol 1, 1-hour survival was 100% with ITPR-CPR and 10% with STD-CPR (P=0.001). Arterial blood pH was significantly lower and Paco2 was significantly higher with ITPR-CPR in protocol 1. Arterial oxygen saturation was 100% throughout the study in both protocols. Paco2 and Pao2 remained stable, but metabolic acidosis progressed, as expected, throughout the 15 minutes of CPR in protocol 3. CONCLUSIONS: Compared with STD-CPR, use of ITPR-CPR improved hemodynamics and short-term survival rates after cardiac arrest.
Implantable cardioverter defibrillators have been shown to provide similar survival benefits for patients who have left ventricular dysfunction due to ischemic heart disease and for subsets of patients who have nonischemic cardiomyopathy. Findings in this study extend these observations by showing that patients who have ischemic or nonischemic heart disease and receive implantable cardioverter defibrillators not only have comparable mortality rates but also similar tachyarrhythmia frequencies during follow-up; further, mortality and tachyarrhythmia outcomes are independent of initial arrhythmia indication.
Recently, a mobile cardiac outpatient telemetry (MCOT) system has become available that monitors the electrocardiogram continuously, recognizes arrhythmias automatically, and transmits abnormal rhythms instantaneously. MCOT does not require activation by the patient. We report data from the first 100 consecutive patients monitored by this new technology.