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K H Lindner

Publications and source records attributed to K H Lindner.

At least 163 records · Page 9Linked to original sources
PubMed1989

Comparison of epinephrine and dopamine during cardiopulmonary resuscitation.

The effectiveness of epinephrine and dopamine for restoring spontaneous circulation after asphyxial or fibrillatory cardiac arrest was compared using a porcine model. Asphyxial arrest: 7 animals received 45 micrograms/kg epinephrine, 7 animals 2.5 mg/kg dopamine, the remaining 7 animals received no drug treatment. All 7 animals given epinephrine could be resuscitated after 174 +/- 53 s, spontaneous circulation could be restored in only 3 of 7 animals given dopamine after 487 +/- 63 s and in none of the control animals could spontaneous circulation be established. Ventricular fibrillation: 7 animals were defibrillated without either mechanical measures or drug therapy. The following doses were given before defibrillation and after starting mechanical measures to separate groups of 7 animals each: 45 micrograms/kg epinephrine, 2.5 mg/kg dopamine, or no drug therapy. In the absence of either drug or mechanical measures and with mechanical measures only, spontaneous circulation could not be established in any of the cases. After administration of epinephrine, defibrillation and restoration of spontaneous circulation was achieved in 6 of 7 animals in 667 +/- 216 s, with dopamine, all the animals could be successfully resuscitated in the shorter time of 174 +/- 85 s. Epinephrine was found to be superior to dopamine in the treatment of asphyxial arrest whereas dopamine was found to be better in the management of ventricular fibrillation, probably by improving the balance between myocardial oxygen supply and demand.

Animals↗
PubMed1989

Endobronchial administration of emergency drugs.

Endobronchial emergency drug therapy is reviewed. Although intravenous drug administration is always preferable endobronchial application is a comparatively safe alternative when venous access is not available because an endotracheal tube is usually inserted during CPR. The optimal procedure remains to be clarified, however. Drugs and dosages currently being recommended for endobronchial use are described. With the reservations mentioned above the following recommendations can be made for the endobronchial administration of drugs to adult emergency patients: (1) Endobronchial administration of drugs is indicated in cases of cardiac arrest when an initial examination after the start of mechanical measures suggests that intravenous application will be difficult. This is also the case for emergency patients without cardiac arrest who are already intubated, and for whom the immediate administration of emergency drugs, such as lidocaine or atropine, is urgent and for whom venous injection cannot be carried out or cannot be carried out sufficiently quickly. We cannot at present share the view that the primary endobronchial administration of epinephrine is to be regarded as the treatment of first choice in every case of asystolic cardiac arrest (J. Schüttler et al., Anästh. Intensiwther. Notfallmed., 22 (1987) 63), as in most cases peripheral venous access can readily be established, thus avoiding the possible disadvantages of endobronchial administration (prolonged tachycardia, hypertension, arrhythmia from the depot effect, and also additional impairment of the pulmonary gas exchange). However, the washing-in of the administered drug is important after peripheral venous administration. (2) For adults, the present recommendation for the i.v. administration of epinephrine during resuscitation is 0.5-1 mg (7.5-15 micrograms/kg). Animal experiments show that under stable circulatory conditions ten times as much epinephrine must be administered endobronchially as intravenously in order to produce comparable pharmacodynamic effects or plasma levels. During resuscitation the corresponding value is approximately five times. Nevertheless, because of the dangers from the depot effect, an endobronchial dosage of 2-3 mg should not at present be exceeded. The best method probably consists of a combination of an initial restricted endobronchial dose with, if necessary, a further dose through a venous site which has been established in the interim. This recommendation seems to be reasonable because, as described, there are no exact data on the optimal dosage for epinephrine, even for i.v. administration (3) In the presence of a stable circulation the endobronchial dosag

Animals↗
PubMed1989

Comparison of epinephrine and norepinephrine in the treatment of asphyxial or fibrillatory cardiac arrest in a porcine model.

Many animal experiments have shown that alpha-receptor stimulation is a prerequisite for the improvement of myocardial perfusion during CPR. As there are no recent reports on the effectiveness of norepinephrine in the treatment of cardiac arrest, we investigated the effectiveness of epinephrine and norepinephrine after asphyxial or ventricular fibrillation cardiac arrest using a porcine model. After 3 min of asphyxial cardiac arrest, seven animals each received either 45 micrograms/kg epinephrine, 45 micrograms/kg norepinephrine, or placebo (controls). All drugs were given blind. All seven animals given epinephrine could be resuscitated after 174 +/- 53 sec, whereas six of seven given norepinephrine could be resuscitated after 473 +/- 116 sec. None of the seven given the placebo could be resuscitated. After 4 min of ventricular fibrillation cardiac arrest, none of the seven animals that received defibrillating countershocks at 4 min without either mechanical measures or drug therapy, and none of the seven that received CPR and countershocks but no drugs, could be resuscitated. In the group that received CPR plus 45 micrograms/kg epinephrine, defibrillation and restoration of spontaneous circulation were achieved in six of seven animals in 667 +/- 216 sec. In the group that received CPR plus 45 micrograms/kg norepinephrine, defibrillation and restoration of spontaneous circulation were achieved in all seven animals in the significantly shorter time of 86 +/- 18 sec. In this porcine model, norepinephrine appeared superior to the same dose of epinephrine in the treatment of ventricular fibrillation, with respect to resuscitation time.

Animals↗
PubMed1989

[Lidocaine levels in the plasma following peripheral or central venous administration during cardiopulmonary resuscitation. Results of an experimental animal study].

A review of the literature indicates that the intravenous bolus dose of lidocaine should be reduced in all conditions where cardiac output is diminished. During external cardiac compression the cardiac output is only approximately 20-40% of the normal resting value. Various routes of drug administration are currently used during CPR. The routine use of a central venous line is not recommended as a first-line procedure for resuscitation. This route of administration is favored by some authors, however, because it is presumed to result in a more rapid onset of drug action and higher peak concentrations of the drugs used. The aim of this study was to determine the aortic plasma concentration of lidocaine after central venous as compared to peripheral venous administration under the conditions of external cardiac compression. Twelve pigs were allocated to two groups of 6 animals each using random numbers. Ventricular fibrillation was induced by applying an alternating current via two needle electrodes placed subcutaneously. Cardiac arrest was allowed to continue for a period of 1 min before mechanical measures were applied. Cardiac massage was carried out using a pneumatic piston device set to a compression rate of 80/min. Sixty seconds after mechanical CPR had been initiated, a bolus of 1.5 mg/kg lidocaine was given to 6 animals via a central venous line. The remaining 6 animals were treated with the same dose given into a vein of the earlobe. The 2% lidocaine solution was diluted to 20 ml with physiological saline in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[An infusion of THAM (trishydroxymethylaminomethane) as therapy to lower increased intracranial pressure in acute craniocerebral injuries].

Despite of the use of all the current intensive care measures, some patients develop dangerously high intracranial pressures (ICP) after head injury. We have studied the use of THAM for the rapid control of dangerously high ICP in these patients. PATIENT AND METHODS. After all conventional methods of lowering ICP had been applied without sufficient effect, 1 mmol/kg body wt. THAM was given i.v. over a period of 10 min to ten patients with head injury. All patients were hyperventilated, sedated with thiopental (3-6 g/day), and the upper body was elevated to 30 degrees. The intracranial pressure and mean arterial pressure were monitored, arterial blood gas levels measured, and cerebral perfusion pressure (CPP) calculated. RESULTS. Our patients had a mean ICP of 37.4 Torr, which fell to 27.2 Torr within 10 min after the administration of THAM. The CPP rose from 46.5 to 56.3 Torr, no rebound was observed. There was no change in arterial blood gas values. DISCUSSION. Our study indicates that THAM not only decreases an elevated ICP, but also improves CPP. These results are of note because only patients with otherwise unresponsive increases in ICP were included.

Adult↗
PubMed1989

[The effect of adrenaline and noradrenaline on the oxygen supply of the myocardium during cardiopulmonary resuscitation].

The effect of epinephrine and norepinephrine on myocardial oxygen delivery and consumption during cardiopulmonary resuscitation using open cardiac massage after a 5-min period of electrically induced ventricular fibrillation was studied in 21 pigs with a mean body weight of 21 kg. Norepinephrine, like epinephrine, is a sympathomimetic agent with marked alpha- and beta-1-sympathomimetic activity, but the degree of beta-2-stimulation is less marked than that obtained with epinephrine. After mechanical measurements over 3 min (compression rate = 60/min), 7 animals received 10 ml physiological saline, 7 further animals, 45 micrograms/kg epinephrine, and the remaining 7 animals, 45 micrograms/kg norepinephrine. At 90 s and again at 5 min after the administration of epinephrine or norepinephrine, the mean arterial blood pressure was significantly higher than in the control group, while mean pulmonary artery pressure, central venous pressure and cardiac index were not significantly different. Total myocardial blood flow was only measured before the induction of cardiac arrest in the control group, where it was found be 193 +/- 30 ml/min/100 g. During the open cardiac massage but before the injection of catecholamines we found a myocardial blood flow of 51 +/- 23 in the control group, 71 +/- 10 in the epinephrine group, and 74 +/- 11 ml/min/100 g in the norepinephrine group. At 90 s after the injection, blood flow increased by 78% to 126 +/- 18, with epinephrine and by 45%, to 107 +/- 30 ml/min/100 g tissue with norepinephrine. At 5 min after administration of these catecholamines significant differences from the control group were present.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

The effect of epinephrine on hemodynamics, acid-base status and potassium during spontaneous circulation and cardiopulmonary resuscitation.

The effect of a bolus dose of epinephrine on hemodynamics, acid-base status and potassium during spontaneous circulation and cardiopulmonary resuscitation (CPR) was investigated in 24 pigs weighing 20-25 kg over a period of 10 min. In a study of 12 pigs in a stable hemodynamic condition, at the 1- and 2-min point after injection of epinephrine or saline the mean serum potassium concentration was significantly higher in the six animals given epinephrine (6.9 +/- 0.7 and 5.4 +/- 0.6 mmol/l, respectively) than in the six control animals (3.8 +/- 0.6 and 3.9 +/- 0.4 mmol/l, respectively). At the later points of observation (3, 4, 5 and 10 min after injection of either epinephrine or saline) no significant difference was found between the groups. Following 1 min of ventricular fibrillation 12 pigs were resuscitated by closed-chest CPR. Six of these animals received 45 micrograms/kg epinephrine (epinephrine group), the other six animals were given physiological saline (control group). Mean aortic diastolic pressure during the relaxation phase was significantly higher in the epinephrine group than in the control group. There was no difference in cardiac index or acid-base status between the groups. In the epinephrine group mean arterial serum potassium concentrations reached a peak value of 6.7 +/- 1.1 mmol/l at 3 min after injection, when they were significantly (P less than 0.05) higher than in the control group (4.4 +/- 0.5 mmol/l). At 5 and 10 min, the potassium levels sank to 5.9 +/- 0.9 and 5.6 +/- 0.8 mmol/l, respectively, in the epinephrine group, and were no longer significantly different from the control group.

Acid-Base Equilibrium↗
PubMed1988

[Arteriovenous pH- and carbon dioxide gradients during cardiopulmonary resuscitation].

During external cardiac massage and after restoration of spontaneous circulation, the arterial and central venous blood gas status of ten patients was determined. During cardiopulmonary resuscitation the median arterial pH value was 7.29 and the median central-venous pH value was 7.16. The low central-venous pH during resuscitation was probably caused by the high partial pressure of carbon dioxide, because no significant difference between arterial and central-venous base deficit was found. The arteriovenous pH and carbon dioxide gradients were significantly lower after spontaneous circulation had been restored. The arterial pH does not parallel the marked fall in central venous pH, and therefore only partly indicates acid-base changes during resuscitation. On the other hand, a central-venous blood gas status not only indicates the degree of metabolic acidosis present, but also the "respiratory" acidosis that in turn is a measure of the severity of intracellular acidosis.

Adult↗
PubMed1987

Continuous positive airway pressure effect on functional residual capacity, vital capacity and its subdivisions.

Thirty-four otherwise healthy patients having to undergo elective upper abdominal surgery were randomly assigned to two equal groups. In the treatment group, constant positive airway pressure (CPAP) with an expiratory pressure of 12 cm H2O was applied at one hour following extubation, and at daily intervals for the first five days following surgery for a continuous period of three hours. The control group received no CPAP treatment. All patients were given postoperative physiotherapy. In patients who received postoperative CPAP with an end-expiratory pressure of 12 cm H2O, marked normalization of pulmonary function was noted.

Abdomen↗
PubMed1987

[Mechanical measures for cardiopulmonary resuscitation].

Recent investigations concerning different techniques in respiratory and circulatory assistance during CPR lead to the following conclusions: Ventilation should start with two slow insufflations. To minimize ventilation pressure, insufflation should be performed in a pause between compressions for 1-1 1/2 seconds in two rescuer CPR. Due to the high arterio-venous gradient in pH and pCO2 during CPR, arterial blood gas analysis is only useful for evaluation for ventilatory efficiency and oxygenation. Acid-base dysregulation can better be determined in mixed and central venous blood. Blood flow during resuscitation seems to be generated by direct ventricular compression and thoracic pump mechanisms. Which mechanism is dominant seems to be interindividually different. Therefore a compression time of 50% of the compression cycle should be maintained.

Animals↗
PubMed1985

[Sodium bicarbonate administration in cardiopulmonary resuscitation. Results of an animal experimental study].

One minute following electrically induced ventricular fibrillation, 12 anaesthetized pigs (hybrids between German and Belgian pedigree swine of 29 kg average body weight) were resuscitated for 30 min with a mechanical thorax compressor and ventilator. Six animals were given 1 mval sodium bicarbonate per kilogram body weight via a central venous line during the first ten minutes of resuscitation, and then 0.5 mval/kg body weight during both of the remaining ten minute intervals. The remaining 6 animals served as control group. In the control group constant volume ventilation led to a fall in the arterial partial pressure of CO2 because perfusion was diminished in relation to ventilation and despite the slowly developing metabolic acidosis this initially led to an increase in pH. At the end of the period of observation an arterial base deficit of 10 mmol/l was measured. Infusion of sodium bicarbonate led to a metabolic alkalosis and to an arterial base excess which at 10 min reached a maximum value of 13.8 mmol/l. In the bicarbonate group serum osmolality rose as a result of the sodium application from 293-334 mosm/l. In contrast, the osmolality of the control group only rose to 309 mosm/l.

Animals↗
PubMed1985

[Changes in acid-base status, potassium ions and glucose concentrations in blood during cardiopulmonary resuscitation. Study of the significance of animal experiment results in emergency medicine case examples].

Results obtained during animal investigations cannot be directly applied to patients because of the anatomical and physiological differences present. Experience has shown that cases of sudden cardiac arrest can only be effectively helped if cardiac massage and artificial ventilation are carried out as soon as possible, and that no sodium bicarbonate need be given when resuscitation measures are begun immediately, or very soon after arrest. In this situation it is better to use adrenaline only, in order to improve organ perfusion. The examples presented show that giving bicarbonate can alter potassium kinetics. Very low serum potassium concentrations are often measured during and following successful resuscitation, and giving too large an amount of buffer solution can worsen this hypokalaemia and lead to a further arrest. The infusion of sodium bicarbonate and the rapid increase in blood sugar levels during resuscitation can lead to a marked rise in serum osmolality which in turn can jeopardize the return of cerebral function. Because in the presence of reduced cerebral perfusion, high blood glucose levels increase the degree of cerebral lactacidosis blood glucose levels should be measured and corrected as necessary.

Acid-Base Equilibrium↗