James E. Manning Christopher W. Barton Laurence M. Katz
Alternative., Methods,, .o.f..C.!o.se.d.-C,h.e.s.t...C..P.R High-Impulse, CPR
InterposedAbdominal., Compression., C.P,RJ.IAC...,CP„R)
Active. „Comp„rs.ssi2n.-fiec.o.mE^es.sio.n,.„CER.„(AC„P., .CPR)
Phased ..ChesLand., Abdominal ..Compression-Decompression
Pharmacologic, .Interventions Adrenergic., Therapy
Non.adrener.flic . . Vasoconstriction
Routes., .foL.Me.dic.ation.., Delivery
Capnometry or. End-Tidal. Carbon.. Dioxide Ventricular.. Fibrillation. Waveform.. Analysis Invasive, .Hemodynamic., Pressure...Monltoring Central .Venous .Qxyge.n..Saturation ..Monitoring
Invasive Perfusion Techniques Direct. Mechanicalyentricular. .Assistance
Cardiopulmonary .Bypass Hemopump
Aortic., Catheter., Perfusion, Techniques
Minimally..Inyasiye, DirecLCardia.c., .Massage
Despite advances in the science of cardiopulmonary-cerebral resuscitation, the prospects for long-term survival with good neurologic recovery remain exceedingly poor. A major limitation of present therapy is the marginal blood flow generated by closed-chest cardiopulmonary resuscitation (CPR). Cardiac output has been reported to be 25 to 33 percent of normal at best and decreases with time delays to initiation of CPR. With increasing duration of arrest and progressive loss of peripheral arterial resistance, even optimally performed closed-chest CPR is unlikely to result in return of spontaneous circulation (ROSC).
Successful resuscitation of the patient in cardiac arrest requires at least some minimal amount of blood flow to the heart. Myocardial perfusion during closed-chest CPR has been shown to be directly related to the pressure gradient across the coronary vasculature. This gradient is equal to the aortic pressure minus the right atrial pressure and is termed the coronary perfusion pressure (CPp). Aortic pressure largely determines the CPP gradient and is dependent upon the level of residual peripheral arterial vasomotor tone. Research has shown that the CPP gradient is greatest during the relaxation phase of CPR chest compressions (CPR diastole). Both laboratory and clinical data indicate that a CPP of at least 15 mmHg is almost always required to achieve ROSC. Yet human studies indicate that CPP gradients attained with standard CPR are usually in the ineffective range of 1 to 8 mmHg.
Much of the research into cardiopulmonary resuscitation has focused on methods to improve artificial perfusion during cardiac arrest. In addition to the originally described "conventional" CPR technique, several alternative methods of performing closed-chest CPR have been investigated ( IaMe.,2—1). Vasoconstrictor agents have long been used as the pharmacologic adjunct to improve vital organ perfusion by increasing aortic pressure and coronary perfusion pressure. Adrenergic-mediated vasoconstriction remains the major pharmacologic intervention in all forms of cardiac arrest. Although epinephrine has been the principal drug used, other adrenergic agents have been studied and, more recently, nonadrenergic vasoconstrictors as well.
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Noninvasive and invasive monitoring techniques have been examined in an effort to identify clinically useful and reliable parameters to guide resuscitative efforts
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TABLE 20-2 Monitoring Techniques for Assessing CPR Effectiveness
Invasive perfusion techniques capable of providing near-normal artificial vital organ perfusion have also been described ( I§ble 20-3). Direct mechanical ventricular assistance (or actuation) and cardiopulmonary bypass have been reported in laboratory models and a few clinical reports. Methods of artificial perfusion using aortic balloon catheters have recently been described in laboratory investigations. These newer invasive techniques have attempted to address the issue of clinical feasibility during sudden cardiac death.
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TABLE 20-3 Invasive Perfusion Techniques
Reperfusion-induced injury is a major focus of research in many fields of medicine and for numerous ischemic diseases states, including cardiac arrest, and is discussed in detail elsewhere (see Chap, 19). Cerebral resuscitation with favorable neurologic outcome after prolonged global ischemia will be the ultimate obstacle to overcome in cardiac arrest therapy. Brain-oriented therapies, such as hypothermia, may substantially improve postresuscitation neuronal survival and functional neurologic recovery. Pharmacologic agents capable of limiting ischemia-induced cellular damage and reperfusion-induced injury from reactive oxygen species will likely be an important form of therapy for cardiac arrest patients in the resuscitation and postresuscitation phases.
This chapter briefly discusses some of the alternative methods of closed-chest CPR, pharmacologic agents, monitoring methods, and invasive perfusion techniques that are presently undergoing investigation and hold promise for the future clinical management of cardiac arrest.
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