Prähospitale Thrombolyse während der kardiopulmonalen Reanimation

Zusammenfassung

Trotz einer jährlichen Inzidenz von 40–90/100 000 Einwohnern mangelt es noch an therapeutischen Optionen, um die sehr ungünstige Prognose der vom prähospitalen Kreislaufstillstand betroffenen Patienten zu verbessern. Etwa 50–70% aller Kreislaufstillstände werden durch einen akuten Myokardinfarkt (AMI) oder eine fulminante Lungenembolie (LE) verursacht. Die Thrombolyse ist eine etablierte, effektive und kausale Therapie für Patienten mit AMI oder LE, die keinen Kreislaufstillstand erleiden. Hingegen sind die Erfahrungen mit der Anwendung der Thrombolyse während eines Kreislaufstillstands bisher begrenzt. Experimentelle Untersuchungen weisen darauf hin, dass die thrombolytische Therapie während der Reanimation einerseits Thromben oder Emboli, die einen AMI oder eine LE verursachen, kausal behandeln, andererseits zu einer Verbesserung der Mikrozirkulation während der Reperfusionsphase beitragen. Die intra-und prähospital durchgeführten Fallserien und Studien zur Thrombolyse während CPR legen nahe, dass diese Therapie zu einer Wiederherstellung eines Spontankreislaufs und zum Überleben von Patienten führen kann, die mit konventionellen Maßnahmen vergeblich reanimiert worden waren. Darüber hinaus gibt es Hinweise auf ein verbessertes neurologisches outcome von Patienten, die eine thrombolytische Therapie während CPR erhielten. Ob diese neue Therapieoption die Prognose von Patienten mit Kreislaufstillstand ganz allgemein verbessern kann, wird eine große randomisierte, doppelblinde Multicenterstudie zeigen.

Summary

Although prehospital cardiac arrest has an incidence of 40–90/100 000 inhabitants per year, there has been a lack of therapeutic options to improve the outcome of these patients. Of all cardiac arrests, 50–70% are caused by acute myocardial infarction (AMI) or massive pulmonary embolism (PE). Thrombolysis has been shown to be a causal and effective therapy in patients with AMI or PE who do not suffer cardiac arrest. In contrast, experience with the use of thrombolysis during cardiac arrest has been limited. Thrombolysis during cardiopulmonary resuscitation (CPR) acts directly on thrombi or emboli causing AMI or PE. In addition, experimental studies suggest that thrombolysis causes an improvement in microcirculatory reperfusion after cardiac arrest. In-hospital and prehospital case series and clinical studies suggest that thrombolysis during CPR may cause a restoration of spontaneous circulation and survival even in patients that have been resuscitated conventionally without success. In addition, there is evidence for an improved neurological outcome in patients receiving a thrombolytic therapy during during CPR. A large randomized, double-blind multicenter trial that has started recently is expected to show if this new therapeutic option can generally improve the prognosis of patients with cardiac arrest.

Schlüsselwörter

Herzinfarkt - Kreislaufstillstand - Lungenembolie - Thrombolyse - Reanimation

Keywords

Cardiac arrest - cardiopulmonary resuscitation - myocardial infarction - pulmonary embolism - thrombolysis

• Literatur

• 1 Abu-Laban RB, Christenson JM, Innes GD. et al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med 2002; 346: 1522-8.
• 2 American College of Cardiology/American Heart Association Task Force On Practice Guidelines. ACC/AHA guidelines for the management of patients with acute myocardial infarction. J Am Coll Cardiol 1996; 28: 1328-428.
• 3 Antman EM, Anbe DT, Armstrong PW. et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction - executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation 2004; 110: 588-636.
• 4 Ballew KA, Philbrick JT, Caven DE. et al. Predictors of survival following in-hospital cardiopulmonary resuscitation. A moving target. Arch Intern Med 1994; 154: 2426-32.
• 5 Bedell SE, Delbanco TL, Cook EF. et al. Survival after cardiopulmonary resuscitation in the hospital. N Engl J Med 1983; 309: 569-76.
• 6 Böttiger BW, Bode C, Kern S. et al. Efficacy and safety of thrombolytic therapy after initially unsuccessful cardiopulmonary resuscitation: a prospective clinical trial. Lancet 2001; 357 (9268): 1583-5.
• 7 Böttiger BW, Grabner C, Bauer H. et al. Long term outcome after out-of-hospital cardiac arrest with physician staffed emergency medical services: the Utstein style applied to a midsized urban/suburban area. Heart 1999; 82: 674-9.
• 8 Böttiger BW, Motsch J, Böhrer H. et al. Activation of blood coagulation after cardiac arrest is not balanced adequately by activation of endogenous fibrinolysis. Circulation 1995; 92: 2572-8.
• 9 Böttiger BW, Padosch SA, Wenzel V. et al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med 2002; 347: 1281-2.
• 10 Crowell J, Sharpe G, Lambright R. et al. The mechanism of death after resuscitation following acute circulatory failure. Surgery 1955; 38: 696-702.
• 11 Fatovich DM, Dobb GJ, Clugston RA. A pilot randomised trial of thrombolysis in cardiac arrest (The TICA trial). Resuscitation 2004; 61: 309-13.
• 12 Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Lancet 1994; 343: 311-22.
• 13 Fischer M, Böttiger BW, Popov-Cenic S. et al. Thrombolysis using plasminogen activator and heparin reduces cerebral no-reflow after resuscitation from cardiac arrest: an experimental study in the cat. Intensive Care Med 1996; 22: 1214-23.
• 14 Gramann J, Lange-Braun P, Bodemann T. et al. Der Einsatz von Thrombolytika in der Reanimation als Ultima ratio zur Überwindung des Herztodes. Intensiv- und Notfallbehandlung 1991; 16: 134-7.
• 15 Group HaCAS. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346: 549-56.
• 16 Klefisch F, Gareis R, Störk T. et al. Präklinische ultima-ratio Thrombolyse bei therapierefraktärer kardiopulmonaler Reanimation. Intensivmedizin 1995; 32: 155-162.
• 17 Kleiner DM, Ferguson KL, King K. et al. Empiric tenecteplase use in cardiac arrest refractory to standard advanced cardiac life support interventions. Circulation 2003; 108 (Suppl IV): 318-9.
• 18 Köhle W, Pindur G, Stauch M. et al. Hochdosierte Streptokinasetherapie bei fulminanter Lungenarterienembolie. Anaesthesist 1984; 33: 469.
• 19 Krischer JP, Fine EG, Davis JH. et al. Complications of cardiac resuscitation. Chest 1987; 92: 287-91.
• 20 Kürkciyan I, Sterz F, Meron G. et al. Thrombolysis and pulmonary embolism presenting with cardiac arrest. Arch Intern Med 2000; 160: 3496-7.
• 21 Lederer W, Lichtenberger C, Pechlaner C. et al. Recombinant tissue plasminogen activator during cardiopulmonary resuscitation in 108 patients with out-of-hospital cardiac arrest. Resuscitation 2001; 50: 71-6.
• 22 Lin SR, O’Connor MJ, Fischer HW. et al. The effect of combined dextran and streptokinase on cerebral function and blood flow after cardiac arrest: and experimental study on the dog. Invest Radiol 1978; 13: 490-8.
• 23 Newman DH, Greenwald I, Callaway CW. Cardiac arrest and the role of thrombolytic agents. Ann Emerg Med 2000; 35: 472-80.
• 24 Padosch SA, Motsch J, Böttiger BW. Thrombolysis during cardiopulmonary resuscitation. Anaesthesist 2002; 51: 516-32.
• 25 Powner DJ, Holcombe PA, Mello LA. Cardiopulmonary resuscitation-related injuries. Crit Care Med 1984; 12: 54-5.
• 26 Renkes-Hegendörfer U, Herrmann K. Successful treatment of a case of fulminant massive pulmonary embolism with streptokinase. Anaesthesist 1974; 23: 500-1.
• 27 Safar P, Stezoski W, Nemoto EM. Amelioration of brain damage after 12 minutes’ cardiac arrest in dogs. Arch Neurol 1976; 33: 91-5.
• 28 Scholz KH, Hilmer T, Schuster S. et al. Thrombolysis in resuscitated patients with pulmonary embolism. Dtsch Med Wochenschr 1990; 115: 930-5.
• 29 Scholz KH, Tebbe U, Herrmann C. et al. Frequency of complications of cardiopulmonary resuscitation after thrombolysis during acute myocardial infarction. Am J Cardiol 1992; 69: 724-8.
• 30 Silfvast T. Cause of death in unsuccessful prehospital resuscitation. J Intern Med 1991; 229: 331-5.
• 31 Spaulding CM, Joly LM, Rosenberg A. et al. Immediate coronary angiography in survivors of out of-hospital cardiac arrest. N Engl J Med 1997; 336: 1629-33.
• 32 Spöhr F, Böttiger BW. Safety of thrombolysis during cardiopulmonary resuscitation. Drug Saf 2003; 26: 367-79.
• 33 Van de Werf F, Ardissino D, Betriu A. et al. Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J 2003; 24: 28-66.