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PERIPHERAL VERSUS CENTRAL INTRAVENOUS LINES IN EMERGENCY CARDIAC CARE
573 PERIPHERAL VERSUS CENTRAL INTRAVENOUS LINES IN EMERGENCY CARDIAC CARE
SiR,—The success of a medical response to cardiac arrest is very dependent on the speed of the response to the emergency. Intracardiac injections have been discarded because of complications,’ and the endotracheal route for drug administration is not satisfactory because infusions cannot be given in this way.2 Experimentally, a central intravenous line has proved more efficient than a peripheral line for the administration of drugs,3 particularly adrenaline.’ a
We are studying the choice of intravenous route for adults having cardiac arrest out of hospital. 233 patients met our criteria for
attempted resuscitation-namely, they were managed by ventilation, external chest compression, and intravenous adrenaline. 175 patients were given adrenaline through a peripheral intravenous line (75-1%) and in the other 58 patients the drug was given through a central line. The choice was dictated by the recommendations of the American Heart Association’ that most anaesthetists followed and also by the fact that some cardiac arrest patients were first seen by junior doctors who cannot easily set up central intravenous lines. The two subgroups (peripheral and central lines) were in other respects similar, there being no significant differences in, for example, age, sex, duration of cardiac arrest and cardiopulmonary resuscitation, and cause of the arrest. In the group with a peripheral intravenous line 89 (50-9 %) had at least a temporary cardiac resuscitation (more than 1 min) while in the group with central lines, 22 (37-9%) attained the same temporary resuscitation. This difference in resuscitation was not significant. Of the 13 patients who survived more than 21 days 12 had had an initial peripheral line and only 1 a central line. On average, doses of adrenaline injected through the peripheral line were half those injected through the central lines. Thus the injection of adrenaline through a peripheral intravenous line is clinically at least as effective as central intravenous adrenaline. This is probably because a peripheral line can be set up more quickly in a case of cardiac arrest. The establishment of a peripheral line does not require the same skill as a central line and there are fewer risks. For these reasons a peripheral intravenous line in the superior vena cava territory should be the first-choice route in any cardiac arrest outside hospital.’
Medical Emergency Service, Department of Anaesthesia/Resuscitation VII, Hôpital E. Herriot, 69437 Lyon, France
P. Y. GUEUGNIAUD O. THEUREY T. VAUDELIN M. ROCHETTE P. PETIT
1. American Heart Association/American Academy of Pediatncs Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care
(ECC) JAMA 1986, 255: 2937. JC, Hartmarin JF, Beaufils F. Traitement médicamenteux de l’arrêt cardiaque In. Réanimation et médecine d’urgence. Paris: Expansion Scientifique Française, 1986: 315-36. Kuhn GJ, White BC, Swetnam RE, et al. Peripheral vs central circulation times during CPR a pilot study Ann Emerg Med 1981; 10: 417-19. Gueugniaud PY, Theurey O, Vaudelin T, Durand F, Petit P. Choix des voies d’abord veineuses voie veineuse périphérique versus voie veineuse centrale dans l’arrêt circulatoire. Paper read at 1st International Congress on Emergency Medical Assistance (Lyon, January, 1987).
2 Mercier
3
4
MYOCARDIAL ISCHAEMIA TRIGGERS FORMATION OF THROMBOXANE
important prostanoids in the cardiovascular system are thromboxane A2 (TxA2)and prostacyclin (PGI2). TxA is formed in activated platelets and promotes platelet aggregation SiR,—The
most
and vasoconstriction. PG 12 is formed in the vascular wall, particularly in the endothelium, and inhibits platelet aggregation and relaxes vascular smooth muscle. The role of these compounds is’ under debate. Non-invasive measurements of TxA2 and PGI2 metabolites in urine have been introduced as a means to avoid artefactual formation of eicosanoids during blood-sampling, and has yielded results indicating a role of these compounds in patients with unstable angina and acute myocardial infarction.1,2 In contrast,
patients with stable angina subjected to moderate physical exercise, there was no evidence of increased formation of either TxA2 or PGI2.l We hypothesised that heavier exercise might in
activate cardiovascular formation of eicosanoids in patients with stable angina. We report increased urinary levels of2,3-dinor- TxB2 (Tx-M, metabolite of TxA2) after leg exercise to angina pectoris of
substantial magnitude. We studied, with ethical committee approval, 8 male patients (aged 51-72) with severe but stable, effort-triggered angina pectoris. No patient was on any medication at the time of study. The patients did a supine leg-bicycle exercise, starting at a load of 30 W and increasing at 10 W/min. All patients ceased the exercise because of severe chest pain, rated 7-9 on a subjective scale graded 0-9. The mean maximum load was 130 (SD 15) W, corresponding to a mean exercise duration of 10 (2) min. Urine was sampled before exercise and within 10 min after its end. Urinary levels of Tx-M and 2,3-dinor-6-keto-PGF (PGI-M, metabolite of PGI2) were
analysed by gas chromatography/mass spectroscopy.3
Urinary excretion of metabolites to thromboxane A2 (Tx-M) and prostacyclin (PGI-M) at rest and immediately after exercise test that elicited severe angina pectoris in patients with ischaemic heart disease. Mean and SD.
Continuous computerised electrocardiogram monitoring revealed ST segment depression, typical of ischaemic heart disease, in all patients during the exercise (mean ST 60 in lead V5 - 2 2[03]mm). The resting urinary levels of Tx-M and PGI-M were in the range reported for this patient group. In urine sampled after exercise Tx-M excretion was significantly increased (p <0’02), whereas the excretion of PGI-M was unaltered (figure). The data indicate that exercise which provokes myocardial ischaemia may induce activation of platelets without a simultaneous increase in vascular PGI2 biosynthesis. Such a selective increase in TxA2 formation, if it occurred in the coronary vessels, might lead to a vicious cycle (platelet activation, TxA2 biosynthesis, and ischaemia) that promotes thrombotic events and myocardial infarction. The possible beneficial effect of inhibitors of TxA2 biosynthesis such as aspirin should be investigated in patients with stable, effort-induced angina pectoris. Department of Clinical Physiology, Karolinska Institute, 141/86 Huddinge, Stockholm, Sweden
A. EDLUND P. HENRIKSSON
University of Göteborg, Sweden
1. 2.
3.
Å. WENNMALM
Fitzgerald DJ, Roy L, Catella F, FitzGerald GA. Platelet activation in unstable coronary disease. N Engl J Med 1986; 315: 983-89. Henriksson P, Wennmalm Å, Edhag O, Vesterqvist O, Green K. In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction. Br Heart J 1986; 55: 543-48. Falardeau P, Oates JA, Brash AR. Quantitative analysis of two dinor urinary metabolites of prostaglandin I2. Analyst Biochem 1981; 115: 359-67.
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SiR,—The success of a medical response to cardiac arrest is very dependent on the speed of the response to the emergency. Intracardiac injections have been discarded because of complications,’ and the endotracheal route for drug administration is not satisfactory because infusions cannot be given in this way.2 Experimentally, a central intravenous line has proved more efficient than a peripheral line for the administration of drugs,3 particularly adrenaline.’ a
We are studying the choice of intravenous route for adults having cardiac arrest out of hospital. 233 patients met our criteria for
attempted resuscitation-namely, they were managed by ventilation, external chest compression, and intravenous adrenaline. 175 patients were given adrenaline through a peripheral intravenous line (75-1%) and in the other 58 patients the drug was given through a central line. The choice was dictated by the recommendations of the American Heart Association’ that most anaesthetists followed and also by the fact that some cardiac arrest patients were first seen by junior doctors who cannot easily set up central intravenous lines. The two subgroups (peripheral and central lines) were in other respects similar, there being no significant differences in, for example, age, sex, duration of cardiac arrest and cardiopulmonary resuscitation, and cause of the arrest. In the group with a peripheral intravenous line 89 (50-9 %) had at least a temporary cardiac resuscitation (more than 1 min) while in the group with central lines, 22 (37-9%) attained the same temporary resuscitation. This difference in resuscitation was not significant. Of the 13 patients who survived more than 21 days 12 had had an initial peripheral line and only 1 a central line. On average, doses of adrenaline injected through the peripheral line were half those injected through the central lines. Thus the injection of adrenaline through a peripheral intravenous line is clinically at least as effective as central intravenous adrenaline. This is probably because a peripheral line can be set up more quickly in a case of cardiac arrest. The establishment of a peripheral line does not require the same skill as a central line and there are fewer risks. For these reasons a peripheral intravenous line in the superior vena cava territory should be the first-choice route in any cardiac arrest outside hospital.’
Medical Emergency Service, Department of Anaesthesia/Resuscitation VII, Hôpital E. Herriot, 69437 Lyon, France
P. Y. GUEUGNIAUD O. THEUREY T. VAUDELIN M. ROCHETTE P. PETIT
1. American Heart Association/American Academy of Pediatncs Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care
(ECC) JAMA 1986, 255: 2937. JC, Hartmarin JF, Beaufils F. Traitement médicamenteux de l’arrêt cardiaque In. Réanimation et médecine d’urgence. Paris: Expansion Scientifique Française, 1986: 315-36. Kuhn GJ, White BC, Swetnam RE, et al. Peripheral vs central circulation times during CPR a pilot study Ann Emerg Med 1981; 10: 417-19. Gueugniaud PY, Theurey O, Vaudelin T, Durand F, Petit P. Choix des voies d’abord veineuses voie veineuse périphérique versus voie veineuse centrale dans l’arrêt circulatoire. Paper read at 1st International Congress on Emergency Medical Assistance (Lyon, January, 1987).
2 Mercier
3
4
MYOCARDIAL ISCHAEMIA TRIGGERS FORMATION OF THROMBOXANE
important prostanoids in the cardiovascular system are thromboxane A2 (TxA2)and prostacyclin (PGI2). TxA is formed in activated platelets and promotes platelet aggregation SiR,—The
most
and vasoconstriction. PG 12 is formed in the vascular wall, particularly in the endothelium, and inhibits platelet aggregation and relaxes vascular smooth muscle. The role of these compounds is’ under debate. Non-invasive measurements of TxA2 and PGI2 metabolites in urine have been introduced as a means to avoid artefactual formation of eicosanoids during blood-sampling, and has yielded results indicating a role of these compounds in patients with unstable angina and acute myocardial infarction.1,2 In contrast,
patients with stable angina subjected to moderate physical exercise, there was no evidence of increased formation of either TxA2 or PGI2.l We hypothesised that heavier exercise might in
activate cardiovascular formation of eicosanoids in patients with stable angina. We report increased urinary levels of2,3-dinor- TxB2 (Tx-M, metabolite of TxA2) after leg exercise to angina pectoris of
substantial magnitude. We studied, with ethical committee approval, 8 male patients (aged 51-72) with severe but stable, effort-triggered angina pectoris. No patient was on any medication at the time of study. The patients did a supine leg-bicycle exercise, starting at a load of 30 W and increasing at 10 W/min. All patients ceased the exercise because of severe chest pain, rated 7-9 on a subjective scale graded 0-9. The mean maximum load was 130 (SD 15) W, corresponding to a mean exercise duration of 10 (2) min. Urine was sampled before exercise and within 10 min after its end. Urinary levels of Tx-M and 2,3-dinor-6-keto-PGF (PGI-M, metabolite of PGI2) were
analysed by gas chromatography/mass spectroscopy.3
Urinary excretion of metabolites to thromboxane A2 (Tx-M) and prostacyclin (PGI-M) at rest and immediately after exercise test that elicited severe angina pectoris in patients with ischaemic heart disease. Mean and SD.
Continuous computerised electrocardiogram monitoring revealed ST segment depression, typical of ischaemic heart disease, in all patients during the exercise (mean ST 60 in lead V5 - 2 2[03]mm). The resting urinary levels of Tx-M and PGI-M were in the range reported for this patient group. In urine sampled after exercise Tx-M excretion was significantly increased (p <0’02), whereas the excretion of PGI-M was unaltered (figure). The data indicate that exercise which provokes myocardial ischaemia may induce activation of platelets without a simultaneous increase in vascular PGI2 biosynthesis. Such a selective increase in TxA2 formation, if it occurred in the coronary vessels, might lead to a vicious cycle (platelet activation, TxA2 biosynthesis, and ischaemia) that promotes thrombotic events and myocardial infarction. The possible beneficial effect of inhibitors of TxA2 biosynthesis such as aspirin should be investigated in patients with stable, effort-induced angina pectoris. Department of Clinical Physiology, Karolinska Institute, 141/86 Huddinge, Stockholm, Sweden
A. EDLUND P. HENRIKSSON
University of Göteborg, Sweden
1. 2.
3.
Å. WENNMALM
Fitzgerald DJ, Roy L, Catella F, FitzGerald GA. Platelet activation in unstable coronary disease. N Engl J Med 1986; 315: 983-89. Henriksson P, Wennmalm Å, Edhag O, Vesterqvist O, Green K. In vivo production of prostacyclin and thromboxane in patients with acute myocardial infarction. Br Heart J 1986; 55: 543-48. Falardeau P, Oates JA, Brash AR. Quantitative analysis of two dinor urinary metabolites of prostaglandin I2. Analyst Biochem 1981; 115: 359-67.
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