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J Tarnow

Publications and source records attributed to J Tarnow.

At least 37 records · Page 2Linked to original sources
PubMed1996

Small, oral dose of clonidine reduces the incidence of intraoperative myocardial ischemia in patients having vascular surgery.

BACKGROUND: Most new perioperative myocardial ischemic episodes occur in the absence of hypertension or tachycardia. The ability of alpha 2-adrenoceptor agonists to inhibit central sympathetic outflow may benefit patients with coronary artery disease by increasing the myocardial oxygen supply and -demand ratio. METHODS: A randomized double-blind study design was used in 297 patients scheduled to have elective vascular surgical procedures to evaluate the effects of 2 micrograms/kg-1 oral clonidine (n = 145) or placebo (n = 152) on the incidence of perioperative myocardial ischemic episodes, myocardial infarction, and cardiac death. Continuous real-time S-T segment trend analysis (lead II and V5) was performed during anesthesia and surgery and correlated with arterial blood pressure and heart rate before and during ischemic events. Dose requirements for vasoactive and antiischemic drugs to control blood pressure and heart rate as well as episodes of myocardial ischemia (i.e., catecholamines, beta-adrenoceptor antagonists, nitrates, and systemic vasodilators) and fluid volume load were recorded. RESULTS: Administration of clonidine reduced the incidence of perioperative myocardial ischemic episodes from 39% (59 of 152) to 24% (35 of 145) (P < 0.01). Hemodynamic patterns, percentage of ischemic time, and the number of ischemic episodes per patient did not differ. Nonfatal myocardial infarction developed after operation in four patients receiving placebo compared with none receiving clonidine (day 2 to 21; P = 0.07). The incidence of fatal cardiac events (1 vs. 2) was not different. Dose requirements for vasoactive and antiischemic drugs did not differ between the groups, but the amount of presurgical fluid volume was slightly greater in patients receiving clonidine (951 +/- 388 vs. 867 +/- 381 ml; P < 0.03). CONCLUSION: A small oral dose of clonidine, given prophylactically, can reduce the incidence of perioperative myocardial ischemic episodes without affecting hemodynamic stability in patients with suspected or documented coronary artery disease.

Administration, Oral↗
PubMed1996

[Family practice management of risk patients with reference to preclinical emergency medicine].

Chances of surviving myocardial infarction or cardiocirculatory arrest depend on an early and appropriate emergency call as well as on bystander CPR. This study uses a questionnaire to assess to what extent these factors guide the private practitioners caring for high-risk cardiac patients. Almost all physicians responding (44%) treat such patients. More than 70% try to include the patients' relatives in a medical briefing. Recognition of early warning signs is discussed with 80% of the patients and 70% of relatives. How to identify acute life-threatening conditions is discussed with 60% of patients and relatives. In case of sudden chest pain and dyspnoea, physicians commonly advise calling the family doctor, a hospital or a regional physician on call. Calling 112, the emergency physician/rescue service, is rarely recommended. Initiating CPR is recommended for an emergency by 30% of the physicians, whereas 20% encourage relatives of patients at risk to take a CPR course. CPR instruction is judged to be generally useful by 50% of physicians, of limited use by 40% and of no use by 10%. When asked why they do not encourage CPR, 15% of physicians said they have no time, 25% cited the inefficiency of the courses, 40% said CPR is psychologically too stressful for laypersons, and 50% felt it was physically too stressful. This study points out the necessity of additional, appropriate instruction of laymen regarding cardiac emergencies.

Cardiopulmonary Resuscitation↗
PubMed1996

Is inhibition of oxygen radical production of neutrophils by sympathomimetics mediated via beta-2 adrenoceptors?

Despite their beneficial effects on cardiovascular derangements in patients with severe sepsis, high doses of sympathomimetics might contribute to an impaired neutrophil function. This study was conducted to examine whether various sympathomimetics [(-)-epinephrine (EPI), dopamine (DA) and dobutamine (DOB)] differ in their potency to suppress the formation of oxygen radicals by neutrophils and whether this potency correlates with their affinity to or intrinsic activity for beta-2 adrenoceptors (beta-2 AR). Oxygen radical production of human neutrophils was induced by N-formyl-methionyl-leucyl-phenyl-alanine and detected by chemiluminescence measurements. Dose-response curves for the inhibition of chemiluminescence by sympathomimetics were measured in the absence and presence of 0.1 microM CGP 20,712 A (1-[2(3-carbamoyl-4-hydroxy phenoxy)-ethylamino]-3-[4-(1-methyl-4-trifluoromethyl-2-imidazolyl) phenoxy]-2-propanol methanesulfonate) and 0.1 microM ICI 118,551 (erythro-(+/-)-1-(7-methylindan-4-yloxy)-3 isopropylaminobutan-2-ol hydrochloride) to selectively antagonize beta-1 AR and beta-2 AR, respectively. Inhibition of chemiluminescence of neutrophils by EPI was approximately 100-fold more potent than that by DA and DOB. Only the inhibition curve by EPI exhibited two components, one at nanomolar and one at micromolar concentrations. The nanomolar component was sensitive against beta-2 AR blockade, whereas the micromolar one was insensitive against both beta AR antagonists. Dose-response curves for DA and DOB exhibited a simple hyperbolic shape at micromolar concentrations and were insensitive against both beta AR antagonists. Maximum inhibition by DA and DOB was equipotent to that by EPI. However, the EC50 for DA was much lower than its dissociation constants, KD, assayed in membrane preparations by radioligand binding, whereas the EC50 of DOB matched KD. This difference could not be explained by a different efficiency of signal transduction, which was determined in receptor-coupled adenylate cyclase activity and which only showed a slightly higher efficiency of DA (51%) than of DOB (34%). Therefore, sympathomimetics were also investigated in a cell-free system, in which chemiluminescence was generated by horseradish peroxidase with hydrogen peroxide as substrate. Surprisingly, all of the sympathomimetics suppressed chemiluminescence with micromolar concentrations. We conclude that sympathomimetics with high affinity and high intrinsic activity (EPI) inhibit neutrophil function via occupation of beta-2 AR, whereas sympathomimetics with low affinity (DA) or low intrinsic activity (DOB) may act by direct scavenging of oxygen radicals.

Adenylyl Cyclases↗
PubMed1995

The effects of prostacyclin on gastric intramucosal pH in patients with septic shock.

OBJECTIVE: To investigate whether infusing prostacyclin (PGI2) in patients with septic shock improves splanchnic oxygenation as assessed by gastric intramucosal pH (pHi). DESIGN: Interventional clinical study. SETTING: Surgical ICU in a university hospital. PATIENTS: 16 consecutive patients with septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine to maintain arterial blood pressure. INTERVENTIONS: All patients received PGI2 (10 ng/kg x min) after no further increase in oxygen delivery could be obtained by volume expansion, red cell transfusion and dobutamine infusion. The results were compared with those before and after conventional resuscitation. The patients received continuous PGI2 infusion for 33-32 days. MEASUREMENTS AND RESULTS: O2 uptake was measured directly in the respiratory gases, pHi was determined by tonometry. Baseline O2 delivery, O2 uptake and pHi were 466 +/- 122 ml/min.m2, 158 +/- 38 ml/min.m2, and 7.29 +/- 0.09, respectively. While O2 uptake remained unchanged, infusing PGI2 increased O2 delivery (from 610 +/- 140 to 682 +/- 155 ml/min.m2, p < 0.01) and pHi (from 7.32 +/- 0.09 to 7.38 +/- 0.08, p < 0.001) beyond the values obtained by conventional resuscitation. While 9 of 11 patients with final pHi > 7.35 survived, all patients with final pHi < 7.35 died (p < 0.01). CONCLUSIONS: Infusing PGI2 in patients with septic shock increases pHi probably by enhancing blood flow to the splanchnic bed and thereby improves splanchnic oxygenation even when conventional resuscitation goals have been achieved.

Adult↗
PubMed1995

Desflurane inhibits hypoxic pulmonary vasoconstriction in isolated rabbit lungs.

BACKGROUND: Inhalational anesthetics inhibit hypoxic pulmonary vasoconstriction (HPV) in vivo and in vitro with a half-maximum inhibiting effect (ED50) within concentrations applied for general anesthesia. Because it is unknown whether desflurane acts likewise, we studied its effect on HPV in isolated blood-perfused rabbit lungs and compared its ED50 with that of halothane. METHODS: Isolated blood-perfused rabbit lungs were randomly allocated to treatment with either desflurane (n = 6) or halothane (n = 6). HPV, defined as an increase in pulmonary arterial pressure (PAP) at constant flow, was elicited by decreasing inspiratory oxygen concentration from 20% to 3% for 4 min. This effect was determined without (control HPV) and with increasing concentrations of the anesthetics (fraction of inspired carbon dioxide kept constant at 4.8 +/- 0.2%, perfusate temperature at 37 degrees C, and blood flow at 100 ml.min-1). RESULTS: Before exposure to the anesthetics, PAP increased by 8.6 +/- 1.9 cmH2O for all lungs within 4 min of hypoxia (control PAP for all lungs 19.6 +/- 2.5 cmH2O). Desflurane decreased this effect in a concentration-dependent fashion with an ED50 of 14.5%, compared with that of halothane, with an ED50 of 1.7%. CONCLUSIONS: Assuming that 1 minimum alveolar concentration (MAC) values of desflurane and halothane for rabbits are 8.9% and 1.39%, respectively, this study yields ED50 values for the inhibition of HPV of approximately 1.6 MAC for desflurane and 1.2 MAC for halothane (P not statistically significant).

Anesthetics, Inhalation↗
PubMed1994

[Distal edema and hyperhidrosis of the arm. Symptoms of reflex sympathetic dystrophy (Sudeck's disease)].

Reflex sympathetic dystrophy is characterized clinically by the triad of autonomic sympathetic dysfunction, and motor and sensory disturbances of the affected extremity. Typical symptoms are distal generalized edema with cyanotic skin, pathologic function of eccrine sweat glands and diffuse dull pain. If reflex sympathetic dystrophy is not recognized an irreversible stage may be reached, with atrophic pale, cool, and anhidrotic skin, contractures and diffuse osteoporosis. The syndrome can be idiopathic but can also be precipitated by a variety of factors, including banal trauma, bone fracture, and traumatic nerve lesions. Pathophysiologically, a functional disturbance of sympathetic nerve fibres may result in a vicious circle of blood flow dysfunction, excitation of afferent nociceptors and maintenance of sympathetic dysfunction at the level of the spinal or central nervous system. In the patient presented in this paper, sympathetic dysregulation of reflex sympathetic dystrophy was cured by means of blockades of the stellate ganglion.

Adult↗
PubMed1994

Prostacyclin improves glucose utilization in patients with sepsis.

PURPOSE: In patients with sepsis, impaired glucose metabolism and altered microcirculatory blood flow are common findings. Prostacyclin (PGI2) improves tissue oxygenation, indicated by enhanced oxygen delivery (DO2) and oxygen uptake (VO2). The purpose of this study was to explore whether these effects are associated with improved glucose utilization. METHODS: In 7 patients with sepsis, glucose metabolism was analyzed using dideuterated and 13C-labeled glucose and isotope dilution mass spectrometry. All patients received total parenteral nutrition with glucose covering 60% to 70% of the predicted energy expenditure and needed continuous intravenous insulin (40 microU.kg-1.min-1) to keep blood glucose concentrations below 10 mmol.l-1.VO2 and carbon dioxide production (VCO2) were continuously measured directly from the respiratory gases via indirect calorimetry. After equilibration of the infused labeled glucose with body glucose pool, baseline variables of glucose metabolism were assessed: glucose oxidation rate was determined from the enrichment of 13CO2 in the expired gas during primed constant infusion of [U-13C]glucose, glucose turnover rate (Ra) from the plasma enrichment of simultaneously infused [6,6-2H2]glucose. Endogenous glucose production rate was calculated as the difference between Ra and glucose infusion rate. Then, we examined the effect of PGI2 infusion (5 to 12.5 ng.kg-1.min-1) on glucose metabolism and gaseous exchange. RESULTS: The PGI2-induced increase in DO2 (from 15.8 to 17.7 ml.kg-1.min-1; P < .05) resulted in an increase in directly measured VO2 from 5.0 to 5.3 ml.kg-1.min-1 (P < .01) whereas VCO2 remained unchanged. Although glucose turnover and production rates remained constant, glucose oxidation rate increased significantly from 1.21 to 1.38 mg.kg-1.min-1 (P < .02). CONCLUSIONS: Improving tissue perfusion and oxygenation with PGI2 may also modify the impaired glucose metabolism by increasing glucose oxidation rate in patients with sepsis, suggesting enhanced adenosine triphosphate production.

Adenosine Triphosphate↗
PubMed1994

High thoracic epidural anesthesia does not alter airway resistance and attenuates the response to an inhalational provocation test in patients with bronchial hyperreactivity.

BACKGROUND: The functional relevance of an intact pulmonary sympathetic innervation for airway resistance is unknown. We therefore evaluated whether or not pulmonary sympathetic denervation by thoracic epidural anesthesia decreases the threshold of an inhalational provocation with acetylcholine in 20 patients with documented bronchial hyperreactivity scheduled for elective upper abdominal or thoracic surgery. METHODS: Baseline inhalational provocation with acetylcholine was performed 2-4 days before surgery. The acetylcholine threshold concentration for a hyperreactivity response (i.e., for a 20% decrease in forced expiratory volume in 1 s and a 100% increase in total respiratory resistance by oscillometry) was determined. On the day of surgery a second inhalative provocation with acetylcholine was performed 45 min after the patients had received 6-8 ml epidural bupivacaine 0.75% (n = 10), intravenous bupivacaine (1.2 mg.min-1, n = 6), or 6-8 ml epidural saline (n = 4). The acetylcholine threshold concentration for a hyperreactive response was again determined. We also measured vital capacity, forced expiratory volume in 1 s as a percentage of vital capacity, spread of sensory blockade (pin prick), skin temperature on hand and foot (telethermography). RESULTS: During thoracic epidural anesthesia, C4-T8 skin temperature increased significantly on hand and foot indicating widespread sympathetic blockade including the lungs. Compared to values obtained immediately before pulmonary sympathetic blockade, forced expiratory volume in 1 s as a percentage of vital capacity, and total respiratory resistance by oscillometry remained unchanged, while vital capacity decreased. Compared to baseline the acetylcholine threshold concentration for the hyperreactive response increased threefold after epidural as well as after intravenous bupivacaine. Epidural saline evoked no directional changes in the acetylcholine threshold concentration. CONCLUSIONS: We conclude that in patients with bronchial hyperreactivity 1. blockade of pulmonary sympathetic innervation seems to be of no relevance for airway resistance and 2. both epidural and intravenous bupivacaine substantially attenuate the response to an inhalational provocation with acetylcholine.

Acetylcholine↗
PubMed1993

Use of the electrospinogram for predicting harmful spinal cord ischemia during repair of thoracic or thoracoabdominal aortic aneurysms.

BACKGROUND: To reduce the incidence of misleading assessments, and to derive criteria for critical spinal cord ischemia during thoracic or thoracoabdominal aortic aneurysm repair, the authors epidurally stimulated and recorded somatosensory evoked potentials (ESEP) below and above, respectively, the spinal segment at risk (electrospinogram). METHODS: Epidural somatosensory evoked potentials were analyzed in 100 consecutive patients undergoing resection of aortic aneurysms using two bipolar catheters (stimulation at the L2 level and recording at the T3 level) for the following criteria: 1) the time until ESEP disappeared completely after cross clamping, 2) the duration of complete ESEP loss during and after cross clamping, and 3) the time until ESEP recovered after declamping. Postoperatively, neurologic deficits were evaluated by a neurologist who was unaware of the ESEP recordings. RESULTS: Three types of patients could be identified. First, thirty-one patients neither showed ESEP loss nor neurologic deficits. Second, ESEP loss occurring later than 15 min after cross clamping was associated with a neurologic deficit in 2 of 29 patients (6.9%). And, third, 12 of 40 patients (30%) presented a neurologic deficit when ESEP loss occurred within 15 min after cross clamping. Further indicators of an impending risk were a total ESEP loss greater than 40 min (sensitivity 100%, specificity 68%, positive predictive value [PPV] 35%, and negative predictive value [NPV] 100%), and a recovery of ESEP later than 20 min after declamping (sensitivity 93%, specificity 86%, PPV 52%, and NPV 99%). CONCLUSIONS: Epidural somatosensory evoked potentials appeared to be a reasonable intraoperative predictor of postoperative neurologic outcome, and informs surgeons and anesthesiologists about the impending danger at an early state of the operation.

Adult↗
PubMed1992

Fat emulsions containing medium chain triglycerides in patients with sepsis syndrome: effects on pulmonary hemodynamics and gas exchange.

Fat emulsions containing medium chain triglycerides (MCT) have recently been introduced into clinical practice as a component of total parenteral nutrition. Since several authors reported increased pulmonary artery pressure and impaired gas exchange during intravenous (i.v.) fat use, in particular in septic patients, we studied the pulmonary hemodynamic and gas exchange effects of i.v. fat containing MCT and long chain triglycerides (LCT) in patients with sepsis syndrome. As the effects of fat emulsions have been attributed to increased formation of prostanoids, the production of thromboxane A2 and prostacyclin was investigated by the determination of urinary thromboxane B2 and 6-keto-prostaglandin F2 alpha, respectively. The i.v. fat use did not induce any alterations in pulmonary hemodynamics and gas exchange, the distribution of ventilation and perfusion nor urinary prostaglandin content. We conclude that fat emulsions containing MCT induce little alterations in pulmonary hemodynamics and gas exchange. This result is probably due to reduced prostaglandin formation because fat emulsions containing MCT provide less prostaglandin precursors than pure LCT emulsions.

Adult↗
PubMed1992

Isoflurane does not increase the incidence of intraoperative myocardial ischaemia compared with halothane during vascular surgery.

We have studied the incidence of new intraoperative myocardial ischaemia (IMI), myocardial infarction (MI) and cardiac death (CD) in 500 consecutive patients undergoing elective major non-cardiac vascular surgery. Patients were allocated randomly to receive either halothane (n = 226) or isoflurane (n = 274) as principal anaesthetic agent. Using real-time ST segment trend analysis (leads V5 and II) IMI (halothane 39%, isoflurane 38%), MI (halothane 1.3%, isoflurane 1.5%) and CD (halothane 0.4%, isoflurane 0.7%) did not differ significantly between the two groups. Twenty-three per cent of IMI episodes were related to haemodynamic disturbances, but unrelated to the type of surgery: 148 supra-aortic (IMI = 39%), 244 abdominal aortic (IMI = 41%) and 108 lower extremity revascularizations (IMI = 33%). We conclude that the choice of volatile anaesthetic agent does not influence cardiac morbidity or mortality in this type of patient.

Adult↗
PubMed1992

[Perioperative diagnosis of acute myocardial ischemia].

The prevalence of coronary artery disease substantially affects both cardiac and noncardiac surgery. Assuming that biometric data reported from North America are representative for Germany, the following incidences can be estimated: around 1 million out of 8 million patients operated upon each year will suffer from coronary artery disease, and 15,000 of these patients will have a perioperative myocardial infarction. Since a close relationship has been shown between pre-, intra-, and postoperative myocardial ischaemia and postoperative cardiac morbidity and mortality, early diagnosis and therapy of acute perioperative myocardial ischaemia is warranted. The purpose of this review is to weigh critically the various methods for diagnosis of myocardial ischaemia in view of their practicability and cost/benefit relationship in the perioperative setting. The symptoms of angina pectoris are unreliable in the perioperative period, since patients are premedicated preoperatively, without symptoms during anaesthesia, and usually receive analgesics postoperatively. Intraoperative detection of myocardial ischaemia focuses on standard electrocardiography (ECG) with on-line registration of the ST-segment in two leads (usually leads II and V5) and automatic analysis of ST-segment deviation, achieving a sensitivity of 80% in the detection of myocardial ischaemia. Measurement of regional wall motion abnormalities with trans-esophageal echocardiography (TEE) is a more sensitive method of myocardial ischaemia detection compared to ECG. However, several reasons preclude the broader application of this method in the perioperative phase: (1) it lacks validation by an accepted and independent gold standard; (2) there is a wide spectrum of false-positive findings (considerable interindividual variations in left ventricular contraction, bundle branch blocks, hypertension, hypervolemia); (3) changes in the inferior and apical segments of the left ventricle cannot be detected by single-plane TOE. Detection in these segments might be achieved with biplane echocardiography, but few data on this improved technique are presently available; (4) the method is semi-invasive and might be not applicable during periods with a high incidence of myocardial ischaemia, e.g., intubation, the end of anaesthesia, and extubation; (5) anaesthetists seldom fulfil standard guidelines in echocardiography training; and (6) the method is expensive, which also limits its broader application. Cardiokymography, a noninvasive technique, allows analog representation of anterior wall motion.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Disease↗
PubMed1991

Cardiovascular effect of low-dose epinephrine infusions in relation to the extent of preoperative beta-adrenoceptor blockade.

The relationship between the extent of preoperative beta-adrenoceptor blockade and the hemodynamic properties of epinephrine was investigated in patients scheduled for elective myocardial revascularization during the immediate preoperative period under steady-state hemodynamic and anesthetic conditions. Twenty patients had been treated with beta-adrenoceptor blocking drugs for at least 3 weeks before the study; 11 unblocked patients served as control group. The extent of clinical beta-adrenoceptor blockade was quantified using the isoproterenol sensitivity test. The dose of isoproterenol required to increase heart rate by 25 beats per min was defined as the chronotropic dose 25 (CD25), representing the degree of beta-adrenoceptor blockade. Geometric mean CD25 per 70 kg was 3.0 micrograms in the control group and 21.8 micrograms in the patients receiving beta-adrenoceptor blocking drugs. The authors found a significant inverse relationship between CD25 values and changes in cardiac index in response to three epinephrine infusion rates (0.01, 0.02, and 0.04 micrograms.kg-1.min-1), the correlation coefficients being -0.71, -0.81, and -0.86, respectively. Compared to unblocked patients, almost no change, or even a decrease, of the cardiac index was observed at greater degrees of clinical beta-adrenoceptor blockade, particularly in patients receiving nonselective blockers. Moreover, there was a significant linear correlation (r = 0.76-0.86) between CD25 values and the effects of epinephrine on systemic vascular resistance index (SVRI); i.e., SVRI significantly decreased in control patients but markedly increased in patients with high degrees of preoperative beta-adrenoceptor blockade. This unmasked vasoconstrictive response to low doses of epinephrine was observed despite the fact that the majority of our patients had received cardioselective adrenergic blocking drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS.

Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng.kg-1.min-1) for 45 min. We examined whether reducing the right ventricular (RV) outflow pressures by PGI2 infusion would increase the right ventricular ejection fraction (RVEF) measured by thermodilution. PGI2 reduced the pulmonary artery pressure (PAP) from 35.6 to 29.1 mmHg (p less than 0.01). The cardiac index (CI) increased from 4.2 to 5.81.min-1.m-2 (p less than 0.01) partly due to an increased stroke volume. The decreased PAP together with the increased CI resulted in a fall of the calculated pulmonary vascular resistance index (PVRI, from 5.1 to 2.5 mmHg.min.m2.1-1, p less than 0.01). In the patients with subnormal baseline RVEF the increased stroke volume was associated with an increased RVEF (from 47.6% to 51.8%, p less than 0.05) suggesting improved RV function. This result was underscored by a significant relationship between the changes in PVRI and RVEF (r = 0.789, delta % RVEF = 2.11.delta PVRI-1.45). Despite an increased venous admixture from 27.8% to 36.9% (p less than 0.05) the arterial PO2 remained constant resulting in an increased oxygen delivery from 657 to 894 ml.min-1.m-2 (p less than 0.01). We conclude that short term infusions of PGI2 increased CI concomitant to improved RV function parameters when baseline RVEF was depressed. Since improved oxygen availability should be a major goal in the management of patients with ARDS PGI2 may be useful to lower pulmonary artery pressure in ARDS.

Adult↗
PubMed1990

Prostacyclin for the treatment of pulmonary hypertension in the adult respiratory distress syndrome: effects on pulmonary capillary pressure and ventilation-perfusion distributions.

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.

Adult↗
PubMed1990

[Preoperative treatment with beta-receptor blockers and isoflurane anesthesia. Hemodynamic interactions in patients with coronary disease].

Although many patients undergoing general anesthesia and surgery are pretreated with beta-adrenoceptor blocking drugs, hemodynamic interactions of beta-blockers and volatile anesthetics have so far only been studied in animals. We therefore designed a clinical study to evaluate the relationship between the extent of preoperative beta-adrenoceptor blockade and the hemodynamic effects of isoflurane anesthesia. Sixty-one patients with coronary artery disease (CAD) and normal global left ventricular function scheduled for elective myocardial revascularization were studied immediately prior to surgery. One group of patients (n = 39) had been treated with beta-adrenoceptor blocking agents for at least 3 weeks up to and including the day of surgery. The degree of clinical beta-adrenoceptor blockade was quantified using the isoproterenol sensitivity test. The dose of isoproterenol required to increase heart rate by 25 beats/min was defined as the chronotropic dose 25 (CD25), representing the degree of beta-adrenoceptor blockade. Hemodynamic data were collected before and during isoflurane anesthesia (0.5%-0.6% end-tidal) plus 50% nitrous oxide. Twenty-two patients without preoperative beta-blocker therapy served as a control group. Preanesthetic values of cardiac index (CI), heart rate (HR) and mean arterial pressure (MAP) were lower in patients pretreated with beta-blocking drugs, but statistically these differences were not significant when compared to data obtained in unblocked patients. Isoflurane anesthesia caused significant reductions of CI and arterial blood pressure. However, there were no significant differences in the absolute values or the percentage changes compared to baseline data obtained in awake patients between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗