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Biomedical subjects

Gardar Sigurdsson

Publications and source records attributed to Gardar Sigurdsson.

17 recordsLinked to original sources

Detection of transplant coronary artery disease using multidetector computed tomography with adaptative multisegment reconstruction.

OBJECTIVES: This study sought to determine whether multidetector computed tomography (MDCT) may be able to detect occlusive coronary disease in transplanted hearts. BACKGROUND: In heart transplant recipients, asymptomatic coronary disease requiring frequent surveillance commonly develops. Recent advancements in MDCT allow for noninvasive assessment of the coronary vessels. METHODS: Electrocardiogram-gated contrast-enhanced MDCT scans (16 x 0.75-mm detectors, 420 ms rotation, 100 ml contrast) with multisegment reconstruction were performed on 54 transplant recipients within 6 +/- 11 days of quantitative coronary angiography (QCA). Heart rate at the time of the scan was 90 +/- 11 beats/min. Coronary arterial segments >1.5 mm in diameter were analyzed by independent investigators. RESULTS: There was a good correlation between MDCT and QCA percent stenosis (r = 0.75, p < 0.01, SEE = 15%). Of the 791 segments identified by QCA, 754 (95%) were analyzable by MDCT. The sensitivity, specificity, and positive and negative predictive values of MDCT compared with QCA for the detection of segments with significant (>50%) stenosis were 86%, 99%, 81%, and 99%, respectively. The MDCT correctly identified 15 of the 16 (94%) transplant patients classified by QCA as having occlusive coronary artery disease and 29 of the 37 patients without significant stenosis (78%). In 1 patient who received intravenous beta-blockers, transient bradycardia requiring temporary pacing developed, but there were no other complications. CONCLUSIONS: Detection of occlusive coronary disease in heart transplant recipients with elevated resting heart rate by MDCT is feasible using multicycle reconstruction. The need for surveillance invasive coronary angiography in transplant recipients might be mitigated by use of MDCT.

Adult↗

Use of tissue Doppler imaging to guide tube current modulation in cardiac multidetector computed tomographic angiography.

In multidetector computed tomographic coronary angiography, strategies to minimize effective radiation dose (ERD) are urgently needed. Prospective tube current modulation (TCM) allows a decrease in ERD, although it may limit reconstruction options. We sought to determine if tissue Doppler imaging (TDI) by echocardiography could predict an optimal phase for multidetector computed tomography and be used to guide TCM. Echocardiographic studies were performed in 94 patients immediately before multidetector computed tomography (83% men; mean 60 +/- 11 years of age, mean body mass index 27.7+/-4.1 kg/m2) and identified the most quiescent phase of the cardiac cycle within the atrioventricular groove. In 40 patients, prospective TCM was programmed according to TDI (TCM(TDI) group); 54 patients underwent multidetector computed tomography without TCM (no-TCM). In 25 patients assigned to the TCM(TDI) group, multidetector computed tomograms were correlated with invasive quantitative coronary angiograms to ensure maintenance of diagnostic accuracy. Optimal phase determined by TDI was 71 +/- 11%, with a distinct bi-modal distribution. Compared with no-TCM, effective radiation dose was decreased by 42% in the TCM(TDI) group (6.6 +/- 1.2 vs 11.4 +/- 2.2 mSv, p < 0.0001). Only 8 segments (3%) were unevaluable due to motion artifact. In 296 segments, sensitivity, specificity, and positive and negative predictive values to detect lesions > 50% by multidetector computed tomography were 92%, 94%, 65%, and 99%, respectively. There was good correlation between quantitative coronary angiography and multidetector computed tomography for absolute degree of stenosis (r = 0.70, p < 0.0001). In conclusion, TDI is a useful tool to guide prospective TCM in multidetector computed tomography. ERD in multidetector computed tomography may be significantly decreased using this technique while maintaining excellent image quality.

Cardiac Catheterization↗

Tissue synchronization imaging and optimal left ventricular pacing site in cardiac resynchronization therapy.

The optimal pacing site in cardiac resynchronization therapy (CRT) remains controversial. Tissue synchronization imaging is a novel echocardiographic technique that color-codes for areas of maximal delay in myocardial velocities. This study aimed to identify whether the left ventricular (LV) pacing lead position in CRT should be guided by a patient's area of maximal mechanical delay. Fifty-four patients with advanced heart failure were assessed echocardiographically before and 6 months after CRT. Response was analyzed according to the relation between the LV lead position and the area of maximal delay to peak velocity by tissue synchronization imaging in the first half of the ejection phase: group 1 (n = 22) had lead placement corresponding to the segment of maximal delay; group 2 (n = 13) had lead placement 1 segment adjacent; and group 3 (n = 19) had lead placement remote from this site. Evidence of LV reverse remodeling and improved systolic function was documented in group 1 (mean percentage decrease in end-systolic volume 23%) more than in group 2 (mean decrease 15%), and more than in group 3 (mean increase 8.9%, p <0.0001 compared with groups 1 and 2). In group 1, 16 of 22 patients had reverse remodeling (>15% decrease in end-systolic volume); reverse remodeling was seen in 7 of 13 patients in group 2 and 1 of 19 in group 3. The placing of the lead position proximal to the site of maximal delay by tissue synchronization imaging was correlated with reverse remodeling (r = 0.449, p = 001). Of 7 patients with delay confined to the septum and anterior wall only, none had evidence of reverse remodeling after CRT. In conclusion, pacing at the site of maximal mechanical delay was associated with reverse remodeling. Individually tailored LV lead positioning should be considered before CRT.

Adult↗

Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation.

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.

Animals↗

Effects of an inspiratory impedance threshold device on blood pressure and short term survival in spontaneously breathing hypovolemic pigs.

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.

Animals↗

Rapid induction of cerebral hypothermia is enhanced with active compression-decompression plus inspiratory impedance threshold device cardiopulmonary resusitation in a porcine model of cardiac arrest.

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.

Animals↗

[Prehospital cardiac life support in the Reykjavík area 1999-2002].

OBJECTIVES: A physician manned ambulance has provided advanced resuscitation service in the Reykjavík area for over 20 years. Out of hospital resuscitation since 1982 has been done with average response time of 4.6-4.9 minutes, the survival rate to hospital admission has been 31-40% and survival to hospital discharge 16-17%. In the years preceding this study, several changes were done in the service; the service area was enlarged, dispatch was centralized to one emergency number, the training of EMT s and physicians was improved and a two-tier rendezvous system was adopted. Cell phone coverage reached over 90% of the population. The study was done in 1999-2002 with the objective to: 1. measure the results of attempted prehospital resuscitations for cardiac diseases in the area, 2. to monitor the effect of bystander response, 3. to estimate the effect of changes in the service prior to the study period. MATERIALS AND METHODS: A ambulance staffed with EMTs and one with a physician were dispatched to all possible cases of cardiac arrest. Resuscitation was attempted using the AHA guidelines for resuscitation. Prospective data was collected following the Utstein template recorded by the physician on call. RESULTS: A total of 319 resuscitative attempts were made during the years 1999-2002, excluding hanging, SIDS, drowning, suicide, trauma, internal bleeding and other diseases, a total of 232 arrests were considered of cardiac origin giving an incidence of 33/100,000/year. The average response time was 6,1 min. Of 232 cardiac resuscitation attempts 140 patients (60%) were in VF/VT, 53 (23%) in asystole and 39 (17%) in other rhythms. Ninety-six (41%) of all patients survived being admitted to hospital ward and 44 (19%) survived to discharge with 39 being alive at 12 months. Of patients in VF/VT, 79 (56%) survived to hospital admission and 39 (28%) to hospital discharge. Resuscitation was more successful in cases of witnessed arrest and if CPR was attempted by bystanders. CONCLUSION: Despite various changes in the EMS system, the results of resuscitative attempts are similar to previous studies in the area but an increased proportion of survivors is left with neurological damage. In 54% of the cases COR was performed by bystanders. Response time needs to be shortened and CPR training increased.

Advanced Cardiac Life Support↗

Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest.

INTRODUCTION: Recent data suggest that generation of negative intrathoracic pressure during the decompression phase of CPR improves hemodynamics, organ perfusion and survival. HYPOTHESIS: Incomplete chest wall recoil during the decompression phase of standard CPR increases intrathoracic pressure and right atrial pressure, impedes venous return, decreases compression-induced aortic pressures and results in a decrease of mean arterial pressure, coronary and cerebral perfusion pressure. METHODS: Nine pigs in ventricular fibrillation (VF) for 6 min, were treated with an automated compression/decompression device with a compression rate of 100 min(-1), a depth of 25% of the anterior-posterior diameter, and a compression to ventilation ratio of 15:2 with 100% decompression (standard CPR) for 3 min. Compression was then reduced to 75% of complete decompression for 1 min of CPR and then restored for another 1 min of CPR to 100% full decompression. Coronary perfusion pressure (CPP) was calculated as the diastolic (aortic (Ao)-right atrial (RA) pressure). Cerebral perfusion pressure (CerPP) was calculated multiple ways: (1) the positive area (in mmHg s) between aortic pressure and intracranial pressure (ICP) waveforms, (2) the coincident difference in systolic and diastolic aortic and intracranial pressures (mmHg), and (3) CerPP = MAP--ICP. ANOVA was used for statistical analysis and all values were expressed as mean +/- S.E.M. The power of the study for an alpha level of significance set at 0.05 was >0.90. RESULTS: With CPR performed with 100%-75%-100% of complete chest wall recoil, respectively, the CPP was 23.3 +/- 1.9, 15.1 +/- 1.6, 16.6 +/- 1.9, p = 0.003; CerPP was: (1) area: 313.8 +/- 104, 89.2 +/- 39, 170.5 +/- 42.9, p = 0.03, (2) systolic aortic minus intracranial pressure difference: 22.8 +/- 3.6, 16.5 +/- 4, 23.7 +/- 4.5, p = n.s., and diastolic pressure difference: 5.7 +/- 3, -2.4 +/- 2.4, 3.2 +/- 2.5, p = 0.04 and (3) mean: 14.3 +/- 3, 7 +/- 2.9, 12.4 +/- 2.9, p = 0.03, diastolic aortic pressure was 28.1 +/- 2.5, 20.7 +/- 1.9, 20.9 +/- 2.1, p = 0.0125; ICP during decompression was 22.8 +/- 1.7, 23 +/- 1.5, 19.7 +/- 1.7, p = n.s. and mean ICP was 37.1 +/- 2.3, 35.5 +/- 2.2, 35.2 +/- 2.4, p = n.s.; RA diastolic pressure 4.8 +/- 1.3, 5.6 +/- 1.2, 4.3 +/- 1.2 p = 0.1; MAP was 52 +/- 2.9, 43.3 +/- 3, 48.3 +/- 2.9, p = 0.04; decompression endotracheal pressure, -0.7 +/- 0.1, -0.3 +/- 0.1, -0.75 +/- 0.1, p = 0.045. CONCLUSIONS: Incomplete chest wall recoil during the decompression phase of CPR increases endotracheal pressure, impedes venous return and decreases mean arterial pressure, and coronary and cerebral perfusion pressures.

Animals↗

The ultimate development of mitral valve endocarditis: atrioventricular separation, atrioventricular groove abscess and hemorrhagic pericarditis.

A 52-year-old non-insulin-dependent diabetic man presented with cerebral emboli and mitral valve endocarditis with posterior leaflet vegetations and perforation. Surgical intervention demonstrated hemorrhagic pericarditis and an atrioventricular groove abscess. Extensive debridement of the pericardium, valve and abscess cavities, reconstruction of the mitral annulus with a patch of fresh autologous pericardium, and mitral valve replacement with a pericardial bioprosthesis was performed. The chest was left open. Postoperatively, the patient required dialysis and prolonged mechanical ventilation, but recovered well without recurrent endocarditis and was discharged home after 40 days.

Abscess↗

Hyperventilation-induced hypotension during cardiopulmonary resuscitation.

BACKGROUND: A clinical observational study revealed that rescuers consistently hyperventilated patients during out-of-hospital cardiopulmonary resuscitation (CPR). The objective of this study was to quantify the degree of excessive ventilation in humans and determine if comparable excessive ventilation rates during CPR in animals significantly decrease coronary perfusion pressure and survival. METHODS AND RESULTS: In humans, ventilation rate and duration during CPR was electronically recorded by professional rescuers. In 13 consecutive adults (average age, 63+/-5.8 years) receiving CPR (7 men), average ventilation rate was 30+/-3.2 per minute (range, 15 to 49). Average duration per breath was 1.0+/-0.07 per second. No patient survived. Hemodynamics were studied in 9 pigs in cardiac arrest ventilated in random order with 12, 20, or 30 breaths per minute. Survival rates were then studied in 3 groups of 7 pigs in cardiac arrest that were ventilated at 12 breaths per minute (100% O2), 30 breaths per minute (100% O2), or 30 breaths per minute (5% CO2/95% O2). In animals treated with 12, 20, and 30 breaths per minute, the mean intrathoracic pressure (mm Hg/min) and coronary perfusion pressure (mm Hg) were 7.1+/-0.7, 11.6+/-0.7, 17.5+/-1.0 (P<0.0001), and 23.4+/-1.0, 19.5+/-1.8, and 16.9+/-1.8 (P=0.03), respectively. Survival rates were 6/7, 1/7, and 1/7 with 12, 30, and 30+ CO2 breaths per minute, respectively (P=0.006). CONCLUSIONS: Professional rescuers were observed to excessively ventilate patients during out-of-hospital CPR. Subsequent animal studies demonstrated that similar excessive ventilation rates resulted in significantly increased intrathoracic pressure and markedly decreased coronary perfusion pressures and survival rates.

Adult↗

Reducing ventilation frequency combined with an inspiratory impedance device improves CPR efficiency in swine model of cardiac arrest.

BACKGROUND: The basic premise that frequent ventilations during cardiopulmonary resuscitation (CPR) are a necessity for tissue oxygenation has recently been challenged. An inspiratory impedance threshold device (ITD) recently has also been shown to increase CPR efficiency, principally by augmenting circulation with little impact on ventilation. The optimal compression to ventilation (C/V) is not known for this new device. The purpose of this study was to compare the currently recommended C/V ratio of 5:1 with a 10:1 ratio, +/- the ITD, to optimize circulation and oxygenation during CPR. METHODS: Thirty-two adult pigs weighing 26-31 kg were randomized to CPR with varying C/V ratios +/- the ITD as follows: A = 5:1, B = 5:1+ITD, C = 10:1, D = 10:1+ITD. After 6 min of untreated ventricular fibrillation (VF), closed-chest standard CPR was performed with an automatic piston device that does not impede passive chest wall recoil, at a continuous compression rate of 100 min(-1). Synchronous breaths were given every 5 or 10 compressions during the decompression phase depending on the group. CPR was performed for 6 min and physiological variables were measured throughout the experimental protocol. RESULTS: A reduction in the frequency of ventilation from 5:1 to 10:1 resulted in significantly improved arterial and coronary perfusion pressure in a pig model of cardiac arrest. Addition of an ITD resulted in further increases in arterial and coronary perfusion pressures with both 5:1 and 10:1 C/V ratios, without compromising oxygenation. CONCLUSION: CPR efficiency can be optimized by changing the compression: ventilation ratio from 5:1 to 10:1 and with concurrent use of the inspiratory threshold device.

Animals↗

Treatment of hypotension in pigs with an inspiratory impedance threshold device: a feasibility study.

OBJECTIVE: An inspiratory impedance threshold device was evaluated in spontaneously breathing animals with hypotension to determine whether it could help improve systemic arterial pressures when fluid replacement was not immediately available. DESIGN: Prospective, randomized. SETTING: Animal laboratory. SUBJECTS: Thirty-nine female farm pigs (weight, 28-33 kg). INTERVENTIONS: A total of 39 anesthetized spontaneously breathing pigs were treated with an impedance threshold device, with cracking pressures from 0 to -20 cm H2O. Four separate experimental protocols were performed: protocol A, in which the hemodynamics of seven pigs were examined during application of an impedance threshold device at various levels of inspiratory impedance (-5, -10, -15, and -20 cm H(2)O), both before and after a severe, controlled hemorrhage to a systolic blood pressure of 50 - 55 mm Hg; protocol B, in which nine pigs bled to systolic blood pressure of 50 -55 mm Hg were treated with an impedance threshold device set at -12 cm H2O and were compared with nine others treated with a sham device; protocol C, in which the effects of the impedance threshold device on mixed venous gases were measured in seven hemorrhaged pigs; and protocol D, in which the effects of the impedance threshold device on cardiac output in seven hemorrhaged pigs were measured. METHODS AND MAIN RESULTS: During initial studies with both normovolemic and hypovolemic pigs, sequential increases in inspiratory impedance resulted in a significant increase in systolic blood pressure, whereas diastolic left ventricular and right atrial pressures decreased significantly and proportionally to the level of impedance. When comparing the sham vs. active impedance threshold device (-12 cm H(2)O) in hypotensive pigs, systolic blood pressure (mean +/- sem) with active impedance threshold device treatment increased from 70 +/- 2 mm Hg to 105 +/- 4 mm Hg (p <.01). Pressures in the control group remained at 70 +/- 4 mm Hg (p <.01). Cardiac output increased by nearly 25% (p <.01) with the active impedance threshold device when calculated using the mixed gas equation and when determined by thermodilution. CONCLUSIONS: These studies demonstrate that it is feasible to use a device that creates inspiratory impedance in spontaneously breathing normotensive and hypotensive pigs to increase blood pressure and enhance cardiopulmonary circulation in the absence of immediate fluid resuscitation. Further studies are needed to evaluate the potential long-term effects and limitations of this new approach to treat hypovolemic hypotension.

Animals↗

Spontaneous breathing through an inspiratory impedance threshold device augments cardiac index and stroke volume index in a pediatric porcine model of hemorrhagic hypovolemia.

BACKGROUND: Hemorrhagic shock secondary to trauma is associated with poor survival. The impedance threshold device (ITD) has been shown to improve blood pressure and survival rates in an adult porcine model of hemorrhagic hypovolemia. Pediatric hemodynamics, anatomy, and physiology differ from adults. Evaluation of the ITD has not been previously assessed in a pediatric porcine model of hypovolemia induced by hemorrhage. OBJECTIVE: To determine whether ITD-assisted breathing, with and without positive end-expiratory pressure, will improve key hemodynamic parameters following hypovolemia induced by hemorrhage in a pediatric porcine model. METHODS: Intubated, anesthetized, hemodynamically stable, spontaneously breathing piglets were rapidly bled 40% of their calculated blood volume. Piglets' hemodynamic and intrathoracic pressures were continuously monitored during 10-min normovolemic baseline, bleed to hypotensive baseline, 10-min ITD-assisted breathing, 10 mins without ITD, 10-min ITD-assisted breathing randomized with or without positive end-expiratory pressure (3 cm H2O), 10 mins without ITD, reinfusion of shed blood, 10-min baseline following return to normovolemia. The ITD had an inspiratory cracking pressure of -7 cm H2O. Transthoracic echocardiographic parameters were measured at the end of each 10-min period. RESULTS: There was no significant difference in baseline assessments between groups. Systolic blood pressure, cardiac index, and stroke volume index were significantly greater during ITD-assisted breathing. There was a trend toward increased left ventricular end-diastolic dimension during ITD use. Heart rate, systemic vascular resistance index, left ventricular end-systolic dimension, and shortening fraction did not change significantly during ITD-assisted breathing. There was equivalent improvement in systolic blood pressure, cardiac index, and stroke volume index, when the ITD alone and ITD plus positive end-expiratory pressure were used. CONCLUSIONS: ITD-assisted breathing significantly augmented systolic blood pressure, cardiac index, and stroke volume index in this pediatric porcine model of hemorrhagic hypovolemia. These effects appear related to increased left ventricular preload and not by increased systemic vascular resistance or heart rate. These beneficial effects of ITD-assisted breathing are not changed by the addition of positive end-expiratory pressures of 3 cm H2O.

Animals↗

Cardiorespiratory interactions and blood flow generation during cardiac arrest and other states of low blood flow.

PURPOSE OF REVIEW: Recent advances in cardiopulmonary resuscitation have shed light on the importance of cardiorespiratory interactions during shock and cardiac arrest. This review focuses on recently published studies that evaluate factors that determine preload during chest compression, methods that can augment preload, and the detrimental effects of hyperventilation and interrupting chest compressions. RECENT FINDINGS: Refilling of the ventricles, so-called ventricular preload, is diminished during cardiovascular collapse and resuscitation from cardiac arrest. In light of the potential detrimental effects and challenges of large-volume fluid resuscitations, other methods have increasing importance. During cardiac arrest, active decompression of the chest and impedance of inspiratory airflow during the recoil of the chest work by increasing negative intrathoracic pressure and, hence, increase refilling of the ventricles and increase cardiac preload, with improvement in survival. Conversely, increased frequency of ventilation has detrimental effects on coronary perfusion pressure and survival rates in cardiac arrest and severe shock. Prolonged interruption of chest compressions for delivering single-rescuer ventilation or analyzing rhythm before shock delivery is associated with decreased survival rate. SUMMARY: Cardiorespiratory interactions are of profound importance in states of cardiovascular collapse in which increased negative intrathoracic pressure during decompression of the chest has a favorable effect and increased intrathoracic pressure with ventilation has a detrimental effect on survival rate.

Adult↗

An age-associated decrease in the frequency of C4B*Q0 indicates that null alleles of complement may affect health or survival.

We studied the distribution of complement C4, C3, and factor B allotypes in 423 healthy Icelandic subjects from 17 to 89 years of age. A marked decrease was observed in the carrier frequency of variant alleles of complement C4B (C4B(*)Q0) and C3 (C3(*)F). These results confirm our previous observations on Hungarian subjects and suggest a negative effect of C4B(*)Q0 on health or survival.

Adolescent↗