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Biomedical subjects

K H Lindner

Publications and source records attributed to K H Lindner.

At least 145 records · Page 8Linked to original sources
PubMed1992

Hemodynamic and metabolic effects of epinephrine during cardiopulmonary resuscitation in a pig model.

BACKGROUND AND METHODS: This study was designed to assess the effect of epinephrine during cardiopulmonary resuscitation (CPR) on left ventricular myocardial blood flow, systemic oxygen delivery and consumption, and on plasma glucose and lactate concentrations. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45 micrograms/kg epinephrine (n = 7) after 5 mins of ventricular fibrillation, and 3 mins of open-chest CPR. Left ventricular myocardial blood flow was measured with radiolabeled microspheres. Plasma catecholamine concentrations were measured by high-pressure liquid chromatography. RESULTS: During open-chest CPR, mean (+/- SD) values of left ventricular myocardial blood flow before, 90 secs, and 5 mins following drug administration were 49 +/- 10, 46 +/- 12, 43 +/- 15 mL/min/100 g, respectively, in the control group, and 52 +/- 12, 118 +/- 21, 84 +/- 28 mL/min/100 g, respectively, in the epinephrine group (p less than .05 at 90 secs and 5 mins). At the same time points, mean (+/- SD) oxygen delivery indices were 7.7 +/- 3.0, 6.0 +/- 2.1, 6.5 +/- 2.7 mL/min/kg in the control group and 7.6 +/- 2.5, 5.3 +/- 2.1, 5.5 +/- 1.9 mL/min/kg in the epinephrine group (nonsignificant). Mean oxygen consumption indices were 5.8 +/- 2.4, 4.6 +/- 1.6, 5.2 +/- 2.6 mL/min/kg in the control group and 5.4 +/- 1.6, 4.2 +/- 1.6, 4.4 +/- 1.4 mL/min/kg in the epinephrine group (nonsignificant). During CPR and before epinephrine administration, arterial plasma epinephrine concentrations increased from prearrest values of 0.77 +/- 0.70 to 62.1 +/- 48.7 micrograms/L, and plasma norepinephrine concentrations increased from 0.28 +/- 0.32 to 104.3 +/- 57.1 micrograms/L. After administered epinephrine, there was an additional increase to 271 +/- 83 micrograms/L at 90 secs in arterial plasma epinephrine, but no important alteration in the plasma norepinephrine concentration. At no time point could we find a clinically important difference in plasma glucose or lactate concentrations between the two groups. CONCLUSIONS: At a dose of 45 micrograms/kg, epinephrine caused an increase in left ventricular myocardial blood flow after a total of 8 mins of cardiac arrest, including 3 mins of CPR, while not altering systemic oxygen delivery and consumption, plasma glucose, or lactate concentrations.

Animals↗
PubMed1992

Adrenaline: relationship between infusion rate, plasma concentration, metabolic and haemodynamic effects in volunteers.

The present study investigated the relationship between supraphysiological plasma concentrations of adrenaline and the resulting haemodynamic and metabolic effects. Adrenaline was administered at five infusion rates (0.01-0.2 micrograms kg-1 min-1) in an escalating sequence to eight volunteers. The arterial plasma concentration of adrenaline increased from 53 +/- 44 to 4349 +/- 818 ng litre-1 during the highest infusion rate. Typical haemodynamic responses, such as increase in blood pressure and heart rate, were seen. The plasma concentrations of glucose and lactate increased from 5.2 +/- 0.4 to 13.7 +/- 1.3 mmol litre-1 and from 0.9 +/- 0.3 to 4.7 +/- 2.6 mmol litre-1, respectively, during the highest infusion rate without a significant increase in insulin concentration. Non-esterified fatty acids increased from 379 +/- 97 to 1114 +/- 331 mumol litre-1 during the 0.06 microgram kg-1 min-1 infusion rate. Adrenaline had no selective haemodynamic effect. If similar metabolic effects occur in patients during treatment with adrenaline or other sympathomimetics, they may further increase breakdown of energy stores in a situation of increased catabolism, and impair utilization of parenteral nutrition.

Adult↗
PubMed1992

[New aspects of mechanical cardiopulmonary resuscitation].

New results in the area of mechanical cardiopulmonary resuscitation indicate that during external cardiac massage, the blood flow is achieved both by direct cardiac compression and a generalized increase in the intrathoracic pressure. While, in accordance with the classical theory, the heart is compressed between the sternum and the vertebral column, the thoracic pump mechanism requires a consideration of all blood-carrying structures within the thorax as elastic tubes or chambers that are capable of being compressed by externally administered pressure. Only such variations of the technique presently used may be of benefit which can be achieved with simple adjuncts and which have a positive effect on both mechanisms of blood flow.

Animals↗
PubMed1991

Comparison of different doses of epinephrine on myocardial perfusion and resuscitation success during cardiopulmonary resuscitation in a pig model.

Published results of dose-response effects of adrenergic drugs (epinephrine [E]) vary so much between studies because of differences in animal models and duration of ischemia before drug administration. In this investigation the effects of different doses of E on coronary perfusion pressure (CPP), left ventricular myocardial blood flow (MBF) and resuscitation success were compared during closed-chest cardiopulmonary resuscitation (CPR) after a 4-minute period of ventricular fibrillation in 28 pigs. MBF was measured during normal sinus rhythm using tracer microspheres. After 4 minutes of ventricular fibrillation CPR was performed with the use of a pneumatic piston compressor. After 4 minutes of mechanical measures only, the animals were randomly allocated into four groups of seven, receiving 0.015, 0.030, 0.045, and 0.090 mg/kg E intravenously respectively. MBF measurements were started 45 seconds after E administration; hemodynamic measurements after 90 seconds. Four minutes after the first administration, the same E dose was given before defibrillation. The CPP of animals given 0.015, 0.030, 0.045 and 0.090 mg/kg E were as follows: 16.3 +/- 6.1, 25.6 +/- 5.8, 33.2 +/- 8.4 and 30.4 +/- 6.3 mm Hg. The left ventricular MBF values were: 14 +/- 9, 27 +/- 11, 43 +/- 6, 46 +/- 10 mL/min/100 g. The differences between the groups receiving 0.015 and 0.045 mg/kg and between the groups receiving 0.015 mg/kg and 0.090 mg/kg were statistically significant (P less than .05). Resuscitation success was 14.3%, 42.9%, 100% and 86.7% respectively. A significant difference in resuscitation success was found only between 0.015 mg/kg and 0.045 mg/kg E.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Influence of epinephrine on systemic, myocardial, and cerebral acid-base status during cardiopulmonary resuscitation.

During cardiopulmonary resuscitation (CPR), arterial pH and carbon dioxide tension (PCO2) do not reflect the marked acidosis and hypercapnia seen in venous blood samples during CPR. Epinephrine causes an increase in myocardial and cerebral blood flow during CPR, but the influence on regional venous PCO2 and pH is as yet unknown. Fourteen pigs were allocated to receive either 0.9% saline (n = 7), or 45 micrograms/kg epinephrine (n = 7) after 5 min of ventricular fibrillation and 3 min of open-chest CPR. Blood samples were obtained during CPR from the aorta, pulmonary artery, great cardiac vein, and sagittal sinus before and 90 s and 5 min after drug administration. Regional blood flow was measured with tracer microspheres. Plasma catecholamines were quantified by high-performance liquid chromatography in arterial blood. PCO2 90 s after drug administration in arterial, mixed venous, myocardial venous, and cerebral venous blood were (means +/- SD) 36 +/- 8, 67 +/- 9, 74 +/- 14, and 79 +/- 19 mmHg in the control group and 35 +/- 11, 62 +/- 12, 73 +/- 10, and 71 +/- 14 mmHg in the epinephrine group. pH values 90 s after drug administration in the same blood samples were 7.29 +/- 0.11, 7.11 +/- 0.09, 7.04 +/- 0.09, and 7.07 +/- 0.10 in the control group and 7.31 +/- 0.13, 7.17 +/- 0.07, 7.08 +/- 0.08, and 7.07 +/- 0.12 in the epinephrine group. Despite a significant increase in myocardial and cerebral blood flow after epinephrine, PCO2 and pH in all blood samples were not different from those of the control group. (ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1991

Endotracheal and endobronchial lidocaine administration: effects on plasma lidocaine concentration and blood gases.

OBJECTIVE: To compare four different methods of endotracheal lidocaine administration with respect to the site of administration. DESIGN: Randomized controlled trial. SETTING: University hospital. PATIENTS: Thirty-two female patients (43.6 +/- 11.5 years old) undergoing elective gynecologic operations with an anesthesiologic risk classification not higher than ASA II. All patients gave their written informed consent to participate in the study. INTERVENTIONS: Lidocaine at a dose of 2 mg/kg, diluted with normal saline to a total volume of 10 mL, was administered to eight patients by instilling the drug solution from a 10-mL syringe directly into the outer aperture of the endotracheal tube. All other study patients received lidocaine under bronchoscopic control through the work channel of the bronchoscope either a) deep endotracheally, b) into the right main bronchus, or c) into the right lower lobe bronchus. At 10 points in time after drug administration, blood samples were taken for measurement of lidocaine plasma concentration (using high-pressure liquid chromatography) and blood gas analysis. MAIN MEASUREMENTS AND RESULTS: Therapeutic blood concentrations (greater than or equal to 1.4 micrograms/mL) could be achieved and toxic blood concentrations (greater than or equal to 6 micrograms/mL) could be avoided with all methods of administration. No significant difference was found between the different methods with regard to peak concentration, time to peak, onset and duration of therapeutic levels, or relative bioavailability. A significant (p less than .05) decrease in PaO2 to 75% of the baseline was seen with all methods used. CONCLUSIONS: Because no route of lidocaine administration was superior to the others, the simplest method (instillation into the endotracheal tube) should be used.

Adult↗
PubMed1991

Arterial blood gases in patients with acute head injury at the accident site and upon hospital admission.

Prior to the start of supportive therapy at the site of the accident, arterial blood samples from 47 patients with acute head injury were taken for blood gas analysis. At the same time, the degree of unconsciousness was assessed using the Glasgow-Coma-Scale. After transport to the hospital, arterial blood gases and the level of unconsciousness were again determined. A very close correlation was found between the initial depth of unconsciousness and the degree of hypercapnia (R = -0.90). Patients with head injury and other multiple injuries did not differ in this report (R = -0.95) from those with isolated head injury. The correlation between PaO2 and the degree of unconsciousness was less well defined, and the results showed a greater degree of scatter (R = 0.54). The acidosis observed resulted mainly from the rise in PaCO2. The absence of any correlation between the base excess and the Glasgow-Coma-Scale levels (R = -0.27) makes a common metabolic derangement unlikely. As a result of intubation and controlled ventilation, the hypercapnia of the comatose patients had been corrected, and a correlation could no longer be found between the Glasgow-Coma-Scale level and the PaCO2. In order to avoid hypoventilation, which carries with it the danger of a rise in intracranial pressure, all patients with severe head injury should be intubated and ventilated as soon as possible after the accident.

Blood Gas Analysis↗
PubMed1991

Comparison of standard and high-dose adrenaline in the resuscitation of asystole and electromechanical dissociation.

Sixty-eight adults with cardiac arrest (asystole and electromechanical dissociation) were randomly allocated for treatment with standard (1 mg) or high-dose epinephrine (5 mg). If the first dose of adrenaline (1 or 5 mg) failed, standardized advanced life-support was applied in all cases. High-dose adrenaline was associated with higher initial resuscitation success rates (16 of 28) than standard-dose adrenaline (6 of 40), whereas hospital discharge rates were not significantly different between the groups. Blood pressure was significantly higher in the high-dose adrenaline group in comparison to the standard dose at 1 and 5 min after resuscitation. Although high-dose adrenaline appears to improve cardiac resuscitation success, the duration of global cerebral ischaemia seems to determine the ultimate outcome.

Aged↗
PubMed1990

Endobronchial drug administration: does deep endobronchial delivery have advantages in comparison with simple injection through the endotracheal tube?

Endobronchial administration of drugs is a valuable alternative to intravenous delivery when venous access cannot be established quickly enough. Some authors propose that deep endobronchial administration through a catheter or similar auxiliary device should give better absorption than simple injection through the endotracheal tube. To test this proposal in the present study two groups of each 6 patients during general anesthesia were administered 3 ml aqueous lidocaine solution at a dose of 2 mg/kg, either deep endobronchially through a catheter or simply through the endotracheal tube. The unusually low volume of administration of 3 ml was chosen because it was thought that the advantages of deep endobronchial administration would then be particularly apparent as 3 ml would lead to a more localized deposit with deep endobronchial administration thus being clearly different from simple injection. No difference in the PaO2 between the two groups could be statistically established. However, the mean lidocaine plasma concentration in the group with the deep endobronchially administered drug was in tendency lower than in the control group (P less than 0.05 at 5 min after delivery). Presumably because of the low volume of administration the mean lidocaine plasma concentrations in both groups always remained under the therapeutic level of at least 1.5 micrograms/ml. Thus, at least for small volumes and stable circulation the results after deep endobronchial administration through a catheter were somewhat worse than after simple injection through the endotracheal tube.

Adult↗
PubMed1990

What is the optimal volume of administration for endobronchial drugs?

During general anesthesia, three groups of six patients each received 2 mg/kg lidocaine as a marker substance endobronchially in either 10, 5, or 3 mL distilled water. It was found that the group receiving 10 mL initially exhibited the highest lidocaine plasma concentration with a mean of 2.01 micrograms/mL, in comparison with 1.25 micrograms/mL in the 5 mL group and 0.95 micrograms/mL in the 3 mL group. After about 10 minutes, concentration courses were almost the same in the 10 mL and the 5 mL groups. The PaO2 in the 10 mL group dropped initially by approximately 40 mm Hg on average and remained low over 60 minutes. By this time the PaO2 in the 5 mL group (initial drop 46 mm Hg) had come back to the original value (P less than .05). The 3 mL group exhibited even more favorable courses in the PaO2 (initial drop 16 mm Hg on average). However, the lidocaine plasma concentration was at the lowest at all times in this group and, moreover, under the therapeutic level of 1.5 micrograms/mL with the dosage used.

Absorption↗
PubMed1990

Effects of epinephrine and norepinephrine on cerebral oxygen delivery and consumption during open-chest CPR.

The effect of epinephrine and norepinephrine on cerebral oxygen delivery and consumption after five minutes of cardiopulmonary arrest and three minutes of open-chest cardiac massage was studied in 21 pigs. Norepinephrine, like epinephrine, has a marked alpha- and beta 1-sympathomimetic activity, but compared with epinephrine, the degree of beta 2-stimulation is weak. Epinephrine probably stimulates cerebral oxygen and glucose consumption by its beta 2-adrenergic effect. After three minutes of CPR, three groups of seven animals each blindly received either placebo (control group), 45 micrograms/kg epinephrine, or 45 micrograms/kg norepinephrine. During CPR but before drug administration, cerebral blood flow was 23 +/- 14 mL/min/100 g in the control group, 30 +/- 7 mL/min/100 g in the epinephrine group, and 30 +/- 11 mL/min/100 g in the norepinephrine group. At 90 seconds after epinephrine, cerebral blood flow increased to 54 +/- 14 mL/min/100 g and after norepinephrine, to 58 +/- 22 mL/min/100 g (P less than .05). Cerebral perfusion pressure for both drugs was significantly higher than the control group. Compared with mechanical measures alone, cerebral oxygen delivery rose from 4.3 +/- 1.2 to 7.4 +/- 1.7 mL/min/100 g after epinephrine and from 3.7 +/- 1.4 to 7.3 +/- 2.7 mL/min/100 g after norepinephrine (P less than .05). There was no increase in cerebral oxygen consumption after both catecholamines, and cerebral oxygen extraction ratio decreased. Cerebral glucose delivery increased in relation to glucose consumption, and extraction ratio did not change significantly after both catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Plasma lidocaine levels and PaO2 with endobronchial administration: dilution with normal saline or distilled water?

STUDY OBJECTIVE: To determine whether water or 0.9% saline should be used as diluent for endobronchial drug administration. PARTICIPANTS: Twelve adult patients. INTERVENTIONS: Patients were endobronchially administered 2 mg/kg lidocaine as marker substance in either 10 mL 0.9% saline or 10 mL distilled water during general anesthesia. MEASUREMENTS AND MAIN RESULTS: The differences in mean lidocaine plasma levels at five minutes (water vs saline, 2.35 vs 1.59 micrograms/mL) and ten minutes (water vs saline: 2.67 vs 1.88 micrograms/mL) were significant (P less than .05). With the initial mean PaO2 being almost (157 mm Hg; F1O2, 0.3) in the two groups, there was a mean drop of about 60 mm Hg in the saline-diluent group, but only about 40 mm Hg in the water-diluent group one minute after administration (P less than .05). CONCLUSION: The use of water resulted in better absorption of lidocaine and less impairment of the PaO2.

Adult↗
PubMed1990

Cardiopulmonary resuscitation with interposed abdominal compression after asphyxial or fibrillatory cardiac arrest in pigs.

The purpose of this study was to compare the efficacy of standard cardiopulmonary resuscitation and cardiopulmonary resuscitation with interposed abdominal compression for restoration of spontaneous circulation in an asphyxial and fibrillatory arrest model. Twenty-eight pigs weighing 19-27 kg were randomly allocated to two arrest groups. Each of these two groups was then subdivided into a treatment group and a control group resulting in four groups of seven pigs each. In the control groups standard cardiopulmonary resuscitation was performed with a pneumatically driven chest compressor at a rate of 80 beats per min. The animals' lungs were ventilated at a respiratory rate of 20 breaths per min independently of chest compression. In the treatment group, in addition to standard cardiopulmonary resuscitation, manual interposed abdominal compression was applied at the midabdomen in the second half of the relaxation phase using a blood pressure cuff to measure and standardize the compressions. Following asphyxial cardiac arrest of 3 min, none of the seven animals could be resuscitated with standard cardiopulmonary resuscitation, whereas all seven animals could be resuscitated with interposed abdominal compression and standard cardiopulmonary resuscitation after 240 +/- 84 s. Following fibrillatory cardiac arrest of 4 min, none of the seven animals that received standard cardiopulmonary resuscitation and countershocks could be resuscitated. In the group that received standard cardiopulmonary resuscitation and interposed abdominal compression spontaneous circulation was achieved in all animals in 244 +/- 117 s. End-diastolic arteriovenous pressure difference, which correlates with coronary blood flow, was significantly higher with interposed abdominal compression during resuscitation from both forms of cardiac arrest. The results of our study indicate that cardiopulmonary resuscitation with interposed abdominal compression in the second half of the relaxation phase improves diastolic arteriovenous pressure difference and resuscitation success in comparison with that following standard cardiopulmonary resuscitation. The use of interposed abdominal compression during basic cardiac life support should be investigated further in patients.

Abdomen↗
PubMed1990

Epinephrine and norepinephrine in cardiopulmonary resuscitation. Effects on myocardial oxygen delivery and consumption.

Norepinephrine, an alpha 1,2-beta 1,2-adrenergic agonist, seems to be an alternative to epinephrine, an alpha 1,2-beta 1,2-agonist, for restoration of spontaneous circulation in VF. We therefore studied the effect of epinephrine and norepinephrine on MDO2 and MVO2 using OCCM after five minutes of cardiopulmonary arrest in 21 pigs. After OCCM of three minutes, seven animals each received placebo (controls) or epinephrine (45 micrograms/kg) or norepinephrine (45 micrograms/kg). All drugs were given blindly. At 90 seconds after epinephrine or norepinephrine, mean arterial blood pressure was significantly higher than in the control group. Prior to cardiac arrest, MBF, measured with radioactive microspheres, was 193 +/- 30 ml/min/100 g. During CPR but before drug administration, MBF was 51 +/- 23 in the control group, 71 +/- 10 in the group with epinephrine, and 74 +/- 11 ml/min/100 g in the group with norepinephrine. At 90 seconds after epinephrine, MBF increased to 126 +/- 18 and after norepinephrine to 107 +/- 30 ml/min/100 g (p less than 0.05). Compared to OCCM alone, MDO2 increased from 9.6 +/- 1.7 to 17.1 +/- 3.2 ml/min/100 g after epinephrine and from 9.4 +/- 1.8 to 13.6 +/- 4.2 ml/min/100 g after norepinephrine (p less than 0.05). There was an increase in MVO2 from 4.0 +/- 1.5 to 9.4 +/- 3.0 ml/min/100 g after epinephrine (p less than 0.05), whereas MVO2 increased only from 4.2 +/- 0.8 to 5.1 +/- 2.0 ml/min/100 g after norepinephrine. Because epinephrine led to a greater increase in MVO2 than norepinephrine, the myocardial oxygen ER remained unchanged. The oxygen requirements of the fibrillating heart seemed to be increased via beta 2-adrenergic stimulation. In both the control and epinephrine-treated groups, only three of the seven animals could be successfully resuscitated, whereas all of the animals in the group with norepinephrine survived the 15-minute period of observation. In this model, norepinephrine, in contrast to epinephrine, improves the balance between MDO2 and MVO2 and eases restoration of spontaneous circulation.

Animals↗
PubMed1990

[The modification of the potassium concentration in blood by catecholamines. A literature review].

After intravenous administration of epinephrine, serum potassium level shows a typically biphasic course. The initial rise is followed by a persistent fall to a lower level than the starting-concentration. The initially observed hyperkalemia is supposed to be caused by a potassium release from hepatocytes, mediated by an alpha 1-adrenoreceptor stimulation. The subsequent hypokalemia seems to be caused by the beta 2-mimetic component of epinephrine effecting the uptake of this ion into striated muscle cells. There are numerous clinical reports of marked hypokalemia as a consequence of beta 2-mimetic therapy. The additive effect of elevated endogenous catecholamines with the therapeutically applied epinephrine during cardiopulmonary resuscitation may be the cause of the elevated potassium levels often observed under these conditions. On the other hand, low serum potassium levels were measured in patients after successful resuscitation, as well as in patients with multiple trauma and with severe head injury. Moreover, hypokalemia seems to be a frequent event in the acute phase of myocardial infarction. A catecholamine-induced potassium shift into the cell is considered to be the cause of this decrease. The question whether in the case of myocardial infarction the hypokalemia is in itself arrhythmogenic as yet is not resolved. Because of the present knowledge about the influence of catecholamines on potassium metabolism it seems advisable to monitor potassium levels regularly during the above situations.

Epinephrine↗
PubMed1989

[Endocardial dual-chamber stimulation in an anomalous persistent left superior vena cava].

A persistent left superior vena cava was noted in a 63-year-old woman during pacemaker implantation because of sinus bradycardia and AV dissociation. During atrial test stimulation a 2 degree AV block occurred at a rate of only 110/min and dual-chamber provision was thus necessary. Both catheters were introduced into the right heart via the coronary sinus, but placement of the right-ventricular lead was made more difficult than usual because of looping. One year later pacemaker function (DDI mode) was unchanged and the patient symptom-free.

Cardiac Catheterization↗