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K G Lurie

Publications and source records attributed to K G Lurie.

At least 19 recordsLinked to original sources
PubMed2005

What is the optimal chest compression-ventilation ratio?

PURPOSE OF REVIEW: Despite a more widespread knowledge of basic cardiopulmonary resuscitation maneuvers in the community, the survival rate for patients with cardiac arrest has remained essentially unchanged in the past 30 years. Over the past few decades, many different compression-ventilation ratios have been studied in terms of best coronary and cerebral oxygen delivery, restoration of spontaneous circulation, and neurologic outcome. This article summarizes the recent evidence presented at the International Consensus on Resuscitation Science in January 2005. RECENT FINDINGS: Recent data from animal and mathematical models suggest a move to a higher compression-ventilation ratio to maximize coronary and cerebral oxygen delivery during cardiac arrest and long-term neurologic outcome. Prospective randomized human data on alternative compression-ventilation ratios are missing and new evidence seems to indicate the inadequacy of both lay and professional rescuers in providing chest compression and ventilating the victim in cardiac arrest. Finally, observational and animal studies highlight the hidden danger of inadvertent hyperventilation during advanced cardiac life support as a reduction of both coronary and perfusion pressure secondary to increased intrathoracic pressure and decreased venous return. SUMMARY: The optimal compression-ventilation ratio is still unknown and the best tradeoff between oxygenation and organ perfusion during cardiopulmonary resuscitation is probably different for each patient and scenario. A discrepancy between what is recommended by the current guidelines and the 'real world' of cardiopulmonary resuscitation has resulted in a near flat survival rate from cardiac arrest in the past few years.

Cardiopulmonary Resuscitation↗
PubMed2001

Developing a vasopressor combination in a pig model of adult asphyxial cardiac arrest.

BACKGROUND: The purpose of this study was to investigate the effects of vasopressin versus epinephrine, and both drugs combined, in a porcine model of simulated adult asphyxial cardiac arrest. METHODS AND RESULTS: At approximately 7 minutes after the endotracheal tube had been clamped, cardiac arrest was present in 24 pigs and remained untreated for another 8 minutes. After 4 minutes of basic life support cardiopulmonary resuscitation, pigs were randomly assigned to receive, every 5 minutes, either epinephrine (45, 200, or 200 microgram/kg; n=6); vasopressin (0.4, 0.8, or 0.8 U/kg; n=6); or epinephrine combined with vasopressin (high-dose epinephrine/vasopressin combination, microgram/kg and U/kg: 45/0.4, 200/0.8, or 200/0.8; n=6; optimal-dose epinephrine/vasopressin combination, 45/0.4, 45/0.8, or 45/0.8; n=6). Mean+/-SEM coronary perfusion pressure was significantly (P<0.05) higher 90 seconds after high- or optimal-dose epinephrine/vasopressin combinations versus vasopressin alone and versus epinephrine alone (37+/-10 versus 25+/-7 versus 19+/-8 versus 6+/-3 mm Hg; 42+/-6 versus 40+/-5 versus 21+/-5 versus 14+/-6 mm Hg; and 39+/-6 versus 37+/-4 versus 9+/-3 versus 12+/-4 mm Hg, respectively). Six of 6 high-dose, 6 of 6 optimal-dose vasopressin/epinephrine combination, 0 of 6 vasopressin, and 1 of 6 epinephrine pigs had return of spontaneous circulation (P<0.05). CONCLUSIONS: Epinephrine combined with vasopressin, but not epinephrine or vasopressin alone, maintained elevated coronary perfusion pressure during cardiopulmonary resuscitation and resulted in significantly higher survival rates in this adult porcine asphyxial model.

Animals↗
PubMed2001

Syncope in pharmacologically unmasked Brugada syndrome: indication for an implantable defibrillator or an unresolved dilemma?

A 30-year-old Caucasian male was referred for evaluation of a 2-year history of recurrent post-exertion lightheadedness and near syncopal spells in the setting of a family history of unexplained sudden cardiac death. Cardiac evaluation demonstrated normal heart structure, but the 12-lead surface ECG was suggestive of but not diagnostic of Brugada syndrome. An exercise stress test reproduced the patient's usual symptoms during the recovery period, and was consistent with a typical vasovagal faint. The same symptoms were observed during a head-up tilt table test. However, given the family history and ECG, pharmacological testing with procainamide, isoprenaline and metoprolol, as well as programmed ventricular stimulation, were undertaken. Pharmacological provocation further supported a diagnosis of Brugada syndrome, whereas programmed ventricular stimulation was considered non-diagnostic regarding ventricular tachyarrhythmia susceptibility. Consequently, despite ECG and pharmacological findings suggestive of Brugada syndrome, there appeared to be sufficient evidence to believe that this patient's symptoms were the result of neurally mediated syncope and not due to ventricular tachyarrhythmias. The patient was treated with midodrine, and has remained symptom-free for 16 months. Thus, given the frequency with which vasovagal syncope occurs in young patients, its occurrence is not unexpected in individuals with concomitant diagnoses such as Brugada syndrome. In as much as current recommendations favour implantable defibrillators in symptomatic Brugada syndrome, the identification of other causes of syncope in such patients poses an uncomfortable, and currently unsettled dilemma.

Adult↗
PubMed2001

The effects of positive end-expiratory pressure during active compression decompression cardiopulmonary resuscitation with the inspiratory threshold valve.

UNLABELLED: The use of an inspiratory impedance threshold valve (ITV) during active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) improves perfusion pressures, and vital organ blood flow. We evaluated the effects of positive end-expiratory pressure (PEEP) on gas exchange, and coronary perfusion pressure gradients during ACD + ITV CPR in a porcine cardiac arrest model. All animals received pure oxygen intermittent positive pressure ventilation (IPPV) at a 5:1 compression-ventilation ratio during ACD + ITV CPR. After 8 min, pigs were randomized to further IPPV alone (n = 8), or IPPV with increasing levels of PEEP (n = 8) of 2.5, 5.0, 7.5, and 10 cm H(2)O for 4 consecutive min each, respectively. Mean +/- SEM arterial oxygen partial pressure decreased in the IPPV group from 150 +/- 30 at baseline after 8 min of CPR to 110 +/- 25 torr at 24 min, but increased in the PEEP group from 115 +/- 15 to 170 +/- 25 torr with increasing levels of PEEP (P <0.02 for comparisons within groups). Mean +/- SEM diastolic aortic minus diastolic left ventricular pressure gradient was significantly (P < 0.001) higher after the administration of PEEP (24 +/- 0 vs 17 +/- 1 mm Hg with 5 cm H(2)O of PEEP, and 26 +/- 0 vs 17 +/- 1 mm Hg with 10 cm H(2)O of PEEP), whereas the diastolic aortic minus right atrial pressure gradient (coronary perfusion pressure) was comparable between groups. Furthermore, systolic aortic pressures were significantly (P < 0.05) higher with 10 cm H(2)O of PEEP when compared with IPPV alone (68 +/- 0 vs 59 +/- 2 mm Hg). In conclusion, when CPR was performed with devices designed to improve venous return to the chest, increasing PEEP levels improved oxygenation. Moreover, PEEP significantly increased the diastolic aortic minus left ventricular gradient and did not affect the decompression phase aortic minus right atrial pressure gradient. These data suggest that PEEP reduces alveolar collapse during ACD + ITV CPR, thus leading to an increase in indirect myocardial compression. IMPLICATIONS: Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation improves perfusion pressures, and vital organ blood flow during cardiac arrest. Increasing levels of positive end-expiratory pressure during performance of active compression-decompression cardiopulmonary resuscitation with an inspiratory impedance valve improves oxygenation, and increases the diastolic aortic-left ventricular pressure gradient and systolic arterial blood pressure.

Air Pressure↗
PubMed2001

The effects of endogenous and exogenous vasopressin during experimental cardiopulmonary resuscitation.

Exogenous vasopressin is a promising vasopressor when blood pressure is critically threatened, but the role of endogenous vasopressin during cardiopulmonary resuscitation (CPR) is unknown. We assessed the role of endogenous versus exogenous vasopressin in a porcine open chest CPR model. Seven minutes before induction of cardiac arrest, seven pigs received 10 microg/kg of a selective vasopressin V(1)-receptor-antagonist (Blocked Vasopressin group); another 12 pigs in two groups received saline administration only. After 4 min of untreated ventricular fibrillation followed by 3 min of basic life support CPR, six animals received 0.8 U/kg vasopressin (Exogenous Vasopressin group), whereas the blocked vasopressin group (n = 7), and the remaining six animals received saline placebo only (Endogenous Vasopressin group). Defibrillation was attempted after 14 min of CPR. During basic life support CPR, left ventricular myocardial blood flow was significantly (P < 0.05) decreased in the Blocked Vasopressin group compared with the Exogenous Vasopressin group and Endogenous Vasopressin group (42 +/- 5 compared with 64 +/- 6 and 66 +/- 6 mL x min(-1) x 100g(-1)). Left ventricular myocardial blood flow was significantly decreased in the Blocked Vasopressin group versus Exogenous Vasopressin group versus Endogenous Vasopressin group 90 s and 5 min after drug administration, respectively (38 +/- 4 and 27 +/- 3 vs 145 +/- 32 and 110 +/- 12 vs 62 +/- 4 and 56 +/- 6 mL x min(-1) x 100g(-1), respectively). None of seven Blocked Vasopressin animals, six of six Exogenous Vasopressin pigs, and six of six Endogenous Vasopressin swine had return of spontaneous circulation after 14 min of cardiac arrest including 10 min of CPR (P < 0.05). In conclusion, pigs with blocked endogenous vasopressin had poor coronary perfusion pressure and left ventricular myocardial blood flow during open chest CPR, and could not be successfully resuscitated. All pigs with effective endogenous vasopressin or pigs with effective endogenous vasopressin and additional exogenous vasopressin had good left ventricular myocardial blood flow during experimental CPR, and survived the 1-h postresuscitation phase. We conclude that endogenous vasopressin is an adjunct vasopressor to epinephrine and may serve as a back-up regulator to maintain cardiocirculatory homeostasis.

Animals↗
PubMed2001

Improving standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve in a porcine model of cardiac arrest.

To improve the efficiency of standard cardiopulmonary resuscitation (CPR), we evaluated the potential value of impeding respiratory gas exchange selectively during the decompression phase of standard CPR in a porcine model of ventricular fibrillation. After 6 min of untreated cardiac arrest, anesthetized farm pigs weighing 30 kg were randomized to be treated with either standard CPR with a sham valve (n = 11) or standard CPR plus a functional inspiratory impedance threshold valve (ITV(TM)) (n = 11). Coronary perfusion pressure (CPP) (diastolic aortic minus right atrial pressure) was the primary endpoint. Vital organ blood flow was assessed with radiolabeled microspheres after 6 min of CPR, and defibrillation was attempted 11 min after starting CPR. After 2 min of CPR, mean +/- SEM CPP was 14 +/- 2 mm Hg with the sham valve versus 20 +/- 2 mm Hg in the ITV group (P < 0.006). Significantly higher CPPs were maintained throughout the study when the ITV was used. After 6 min of CPR, mean +/- SEM left ventricular and global cerebral blood flows were 0.10 +/- 0.03 and 0.19 +/- 0.03 mL. min(-1). g(-1) in the Control group versus 0.19 +/- 0.03 and 0.26 +/- 0.03 mL. min(-1). g(-1) in the ITV group, respectively (P < 0.05). Fifteen minutes after successful defibrillation, 2 of 11 animals were alive in the Control group versus 6 of 11 in the ITV group (not significant). In conclusion, use of an inspiratory impedance valve during standard CPR resulted in a marked increase in CPP and vital organ blood flow after 6 min of cardiac arrest.

Animals↗
PubMed2001

Comparison of epinephrine with vasopressin on bone marrow blood flow in an animal model of hypovolemic shock and subsequent cardiac arrest.

OBJECTIVE: The intraosseous route is an emergency alternative for the administration of drugs and fluids if vascular access cannot be established. However, in hemorrhagic shock or after vasopressors are given during resuscitation, bone marrow blood flow may be decreased, thus impairing absorption of intraosseously administered drugs. In this study, we evaluated the effects of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow blood flow. DESIGN: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. SETTING: University hospital laboratory. SUBJECTS: Fourteen pigs weighing 30 +/- 3 kg. INTERVENTIONS: Radiolabeled microspheres were injected to measure bone marrow blood flow during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of the estimated blood volume. In the second part of the study, ventricular fibrillation was induced; after 4 mins of untreated cardiac arrest and 4 mins of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 6) or 0.8 units/kg vasopressin (n = 6) was administered. Defibrillation was attempted 2.5 mins after drug administration, and blood flow was assessed again at 5 and 30 mins after successful resuscitation. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem bone marrow blood flow decreased significantly during induction of hemorrhagic shock from 14.4 +/- 4.1 to 3.7 +/- 1.8 mL.100 g-1.min-1 in the vasopressin group and from 18.2 +/- 4.0 to 5.2 +/- 1.0 mL.100 g-1.min-1 in the epinephrine group (p =.025 in both groups). Five minutes after return of spontaneous circulation, mean +/- sem bone marrow blood flow was 3.4 +/- 1.1 mL.100 g-1.min-1 after vasopressin and 0.1 +/- 0.03 mL.100 g-1.min-1 after epinephrine (p =.004 for vasopressin vs. epinephrine). At the same time, bone vascular resistance was significantly (p =.004) higher in the epinephrine group when compared with vasopressin (1455 +/- 392 vs. 43 +/- 19 mm Hg. mL-1.100 g.min, respectively). CONCLUSIONS: Bone blood flow responds actively to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscitation after hypovolemic cardiac arrest. In this regard, bone marrow blood flow after successful resuscitation was nearly absent after high-dose epinephrine but was maintained after high-dose vasopressin. These findings emphasize the need for pressurized intraosseous infusion techniques, because bone marrow blood flow may not be predictable during hemorrhagic shock and drug therapy.

Animals↗
PubMed2000

Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest.

BACKGROUND: Blood pressure is severely reduced in patients in cardiac arrest receiving standard cardiopulmonary resuscitation (CPR). Although active compression-decompression (ACD) CPR improves acute hemodynamic parameters, arterial pressures remain suboptimal with this technique. We performed ACD CPR in patients with a new inspiratory threshold valve (ITV) to determine whether lowering intrathoracic pressures during the "relaxation" phase of ACD CPR would enhance venous blood return and overall CPR efficiency. METHODS AND RESULTS: This prospective, randomized, blinded trial was performed in prehospital mobile intensive care units in Paris, France. Patients in nontraumatic cardiac arrest received ACD CPR plus the ITV or ACD CPR alone for 30 minutes during advanced cardiac life support. End tidal CO(2) (ETCO(2)), diastolic blood pressure (DAP) and coronary perfusion pressure, and time to return of spontaneous circulation (ROSC) were measured. Groups were similar with respect to age, gender, and initial rhythm. Mean maximal ETCO(2), coronary perfusion pressure, and DAP values, respectively (in mm Hg), were 13.1+/-0.9, 25.0+/-1.4, and 36.5+/-1.5 with ACD CPR alone versus 19.1+/-1.0, 43.3+/-1.6, and 56.4+/-1.7 with ACD plus valve (P<0.001 between groups). ROSC was observed in 2 of 10 patients with ACD CPR alone after 26.5+/-0.7 minutes versus 4 of 11 patients with ACD CPR plus ITV after 19.8+/-2.8 minutes (P<0.05 for time from intubation to ROSC). Conclusions-Use of an inspiratory resistance valve in patients in cardiac arrest receiving ACD CPR increases the efficiency of CPR, leading to diastolic arterial pressures of >50 mm Hg. The long-term benefits of this new CPR technology are under investigation.

Adult↗
PubMed2000

Measurement of adenylate cyclase activity in the right ventricular endomyocardial biopsy samples from patients with chronic congestive heart failure.

A highly sensitive fluorometric assay technique was adopted in order to examine the adenylate cyclase activity in the minute right ventricular endomyocardial biopsy samples from patients with chronic congestive heart failure (n = 10). Norepinephrine (10(-4) M) and adenosine (10(-3) M) were incubated for 30 min with 10 microl of membrane preparation (1-2 mg protein/mg) to analyze the extent of the receptor-coupled adenylate cyclase activity. Forskolin (10(-4) M) stimulation was used to estimate the maximum adenylate cyclase activity (pmol/mg protein/min, mean +/- SE). The new microanalytical cyclic AMP assay involves four steps: enzymatic destruction of noncyclic adenine nucleotides and phosphorylated metabolites, conversion of cyclic AMP to ATP, amplification of ATP by enzymatic cycling, and fluorometric measurement of NADPH, which is generated in proportion to initial cyclic AMP levels. Basal and forskolin-stimulated maximum adenylate cyclase activities were 75 +/- 8 and 123 +/- 15, respectively. Norepinephrine increased the adenylate cyclase activity to 107 +/- 14, while adenosine tended to decrease it to 65 +/- 7. In addition, elimination of adenosine by adenosine deaminase (10 U/ml) slightly increased the adenylate cyclase activity to 82 +/- 9. These results indicate that the adenylate cyclase activity can be measured in minute endomyocardial biopsy samples. Use of this new approach shows promise of becoming a new and potentially important way to predict the efficacy of pharmacological treatment.

Adenosine↗
PubMed2000

Left ventricular-based pacing in patients with chronic heart failure: comparison of acute hemodynamic benefits according to underlying heart disease.

BACKGROUND: Acute left ventricular-based pacing has been shown to improve hemodynamics in patients with severe heart failure and left bundle branch block (LBBB). However, it is not known whether the cause of the underlying heart disease influences the potential effect of left ventricular-based pacing. OBJECTIVES: The aim of this study was to determine whether beneficial hemodynamic effects of acute left ventricular-based pacing in severe chronic heart failure are dependent on underlying heart disease. METHODS: After coronary angiography, patients with severe heart failure and LBBB were separated into two groups: dilated (25 patients; 20 male) and ischemic cardiomyopathy (21 patients; 20 male). Hemodynamic parameters were evaluated at baseline and during left ventricular-based pacing. RESULTS: Improvement in hemodynamic parameters were similar in both groups, during acute left ventricular pacing (changes expressed in percentage): pulmonary capillary wedge pressure, -16+/-15% vs. -14+/-10%; V wave amplitude, -25+/-18% vs. -21+/-17%; and biventricular pacing, -15+/-15% vs. -11+/-11% and -23+/-18% vs. -16+/-18%, respectively. CONCLUSION: Underlying heart disease does not influence the response to acute left ventricular-based pacing in patients with severe heart failure and LBBB. This finding provides support for including all patients with enlarged heart and heart failure in future studies evaluating left ventricular-based pacing.

Aged↗
PubMed2000

Atrial fibrillation: defining potential curative ablation targets.

The concept that atrial fibrillation (or at least certain forms of the arrhythmia) may be amenable to reversal or amelioration by transcatheter ablation techniques has become increasingly accepted in recent years. As yet, however, the techniques being studied for ablation of atrial fibrillation address neither known critical anatomic elements nor well defined electrophysiologic markers. The approaches, although essentially empirical, are conceptually based on the 'multiple wavelet' or 'focal origin' hypotheses. To date, addressing 'focal origin' atrial fibrillation by transcatheter ablation has been the more encouraging. However, as technology evolves, both in terms of catheter design and possibly endocardial mapping techniques, approaches to wavelet or rotor mechanisms may become similarly effective. This communication examines concepts regarding the manner in which atrial fibrillation is initiated and maintained. The goals are to better understand the encouraging success of empirical ablation methods, and possibly derive insights which may help refine ablation targeting in the future.

Atrial Fibrillation↗
PubMed2000

Cardiopulmonary resuscitation during severe hypothermia in pigs: does epinephrine or vasopressin increase coronary perfusion pressure?

UNLABELLED: The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo. IMPLICATIONS: Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.

Animals↗