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Biomedical subjects

Gardar Sigurdsson

Publications and source records attributed to Gardar Sigurdsson.

9 recordsLinked to original sources
PubMed2005

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↗
PubMed2005

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↗
PubMed2004

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↗
PubMed2004

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↗
PubMed2004

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↗
PubMed2004

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↗
PubMed2003

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↗
PubMed2003

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↗