Ebook Cardiac arrest - The science and practice of resuscitation medicine (2nd edition): Part 2

(BQ) Part 2 book Cardiac arrest - The science and practice of resuscitation medicine presents the following contents: Postresuscitation disease and its care, special resuscitation circumstances, special resuscitation circumstances, special issues in resuscitation.

Part V Postresuscitation disease and its care 47 Postresuscitation syndrome Erga L Cerchiari Department of Anaesthesia and Critical Care, Ospedale Maggiore, and Area of Anaesthesia and Critical Care, Surgical Department, Provincial Health Care Structure, Bologna, Italy The postresuscitation syndrome (PRS) has been defined as a condition of an organism resuscitated following prolonged cardiac arrest, caused by a combination of whole body ischemia and reperfusion, and characterized by multiple organ dysfunction, including neurologic impairment.1 Background Following resuscitation from cardiac arrest, patients either recover consciousness or remain unconscious, depending on the duration of cardiac arrest and the effectiveness of any CPR, but also on prearrest conditions such as age and comorbidities.2 Shortening no-flow times by timely interventions that can maintain some perfusion and promote the restoration of spontaneous circulation (e.g., bystander CPR, early defibrillation, and other means) improves the possibility of a successful outcome with the patient recovering consciousness.3 The wider availability of resuscitation techniques to reverse clinical death, however, has led to increasingly frequent observations of a pathological condition occurring in patients who remain unconscious, involving multiple organ injury or failure following reperfusion after prolonged cardiac arrest The concept of postresuscitation disease as a unique and new nosological entity was introduced by Negovsky in 1972;4,5 the most interesting aspect of this innov- ative concept was the recognition that the etiology depended on a combination of severe circulatory hypoxia with the unintended sequelae of measures used for resuscitation On the basis of the wide variety of ischemic/hypoxic mechanisms that can trigger its development, the disease was redefined by Safar as a syndrome in which pathogenetic processes triggered by cardiac arrest were exacerbated by reperfusion, causing damage to the brain and other organs, the complex interactions of which combine to determine overall outcome (see early experimental findings summary).6,7 The evidence of features common to the postresuscitation syndrome and multiple organ dysfunction syndrome led to the hypothesis that a systemic inflammatory response of the entire organism was triggered by ischemia and reperfusion, adding to the damage directly induced by ischemia during cardiac arrest.8 Two landmark studies, showing that mild therapeutic hypothermia started after reperfusion can improve recovery after cardiac arrest, confirm that outcome is determined not only by events occurring during arrest and CPR but also by pathogenetic processes continuing after reperfusion.9,10 Recent reports confirm the occurrence of a “sepsis-like syndrome” after resuscitation from cardiac arrest,11,12 although the mechanistic relationship to the direct damage induced by ischemia during cardiac arrest has yet to be clarified Cardiac Arrest: The Science and Practice of Resuscitation Medicine 2nd edn., ed Norman Paradis, Henry Halperin, Karl Kern, Volker Wenzel, Douglas Chamberlain Published by Cambridge University Press © Cambridge University Press, 2007 817 818 Erga L Cerchiari Early Experimental Findings Negovsky4,5 and his group of Russian investigators pioneered the concept of postresuscitation disease as a unique nosological entity, caused by the combination of severe hypoxia and resuscitation, on the basis of hundreds of experimental observations that fall into three groups: Phasic Pattern of Postresuscitation Recovery Independent of the type of insult, alterations in cerebral and extracerebral organs occur starting with reperfusion and developing over time From insult to to hours postinsult: rapid changes in cerebral and systemic hemodynamics, metabolism, and rheology (clotting disturbances, increased viscosity), increase levels of biologically active substances and prostaglandin derivatives; alterations of the immune system (increased bactericidal activity, depressed reticuloendothelial system, and hyperreactivity of B- and T-lymphocytes), and toxic factors in the blood (peptide fraction 800 to 2000 Daltons and endotoxin secondary to gram-negative bacteremia) From 10 to 24 hours postinsult: normalization of cardiovascular variables and progression of metabolic derangements ensue During this time, 50% of deaths occur as a result of recurrent cardiac arrest From to days postinsult: stable cardiovascular variables and improvement in cerebral function associated with increased intestinal permeability leading to bacteremia The stabilization phase (more than days postinsult): characterized by the prevalence of localized or generalized infection that represents the major cause of delayed deaths The degree of cerebral and extracerebral organ derangements is reported to be more severe and prolonged the longer the duration of the hypoxic–ischemic insult Interactions between Cerebral and Extracerebral Postischemic Damage on Outcome The severity of systemic and hemodynamic derangements after 20 minutes of isolated brain ischemia is comparable to that recorded after only 12–15 minutes of total circulatory arrest with ventricular fibrillation, suggesting that cerebral postischemic damage plays a role in development of extracerebral dysfunction, probably by inducing changes in neurohumoral regulation Cerebral function recovers better after bloodless global brain ischemia than after the same duration of circulatory arrest from ventricular fibrillation, leading to the conclusion that extracerebral factors account for about half of the pathological findings in the brain induced by cardiac arrest Benefical Effect of Trials with Detoxification Techniques A series of trials aimed at removing toxins and normalizing homeostasis by various detoxification techniques showed that all the techniques can improve neurological recovery and survival compared with concurrent controls; cross-circulation was the most effective, in which circulation in the body of the resuscitated dog was maintained for 30 minutes post-ROSC by the heart of a healthy donor dog, aided by an extracorporeal circulation system Safar and his group in Pittsburgh, in parallel with – but subsequent to – the Russian experimental work, confirmed that extracerebral organ dysfunction may hamper cerebral recovery following resuscitation from cardiac arrest, based on the observations that (a) cerebral function after isolated global brain ischemia recovers better than after comparable durations of total body ischemia13,14 and (b) the use of cardiopulmonary bypass for resuscitation and for short-term postresuscitation assistance improves myocardial performance after weaning, and significantly increases neurological outcome and survival.15 Extracerebral organ dysfunction following resuscitation from cardiac arrest of increasing durations was studied in animal experimental models:1,6,7,14–19 • cardiac output and arterial oxygen transport, after a transient increase, showed a prolonged and profound decrease associated with increased peripheral resistance; this starts sooner and is more severe and prolonged after longer durations of VF, resolving by 12 to 24 hours postresuscitation • pulmonary gas exchange, with assisted ventilation for to 24 hours postresuscitation, is well maintained even after extubation (normoxia, normocarbia, and rapid pH normalization) • coagulation disturbances with hypocoagulability start during resuscitation, with prolonged clotting times and decreased platelets and fibrinogen, and normalize at 24 hours after resuscitation; elevated fibrin-degradation products and decreased platelet counts were observed to 72 hours postresuscitation Postresuscitation syndrome • erythrocyte count decreases significantly • renal function (blood urea nitrogen, serum creatinine, osmolarity, sodium, potassium, and calcium) remain normal after a transient reduction in urine output with positive fluid balance, normalizing at to hours • hepatic function is altered transiently; plasma ammonia and branched chain and aromatic amino acids increase, with higher levels in the animals with poor outcome, suggesting an alteration of liver-detoxifying function • bacteremia is a constant feature after cardiac arrest, with transient leukocytosis but without hyperthermia (90% were constituents of the intestinal flora, suggesting postischemic bacterial translocation) In summary, following resuscitation from cardiac arrest, multiorgan dysfunction occurs, but the abnormalities have different time patterns (Fig 47.1) ine tok Cy 100 in tox o nd E 80 ry to ma lam nse po res Inf 60 Cardiovascular 40 Clotting/Fibrinolysis 20 Neurologic Clotting/Fibrinolysis 72 h 60 h 48 h 36 h Neurologic 24 h 12 h ROSC Cardiovascular Fig 47.1 Time pattern of organ dysfunction after resuscitation from cardiac arrest from the early experimental work.1,4–7 Incidence and prevalence The incidence of out-of-hospital cardiac arrest is estimated to be 49.5–66 per 100 000 cases per year:2 in these, return of spontaneous circulation can be achieved in 17% to 33%, depending on the efficiency of the emergency response system.20 The incidence of in-hospital cardiac arrest has been estimated as 1.4/100 admissions/year:21 in these cases, restoration of spontaneous circulation occurs in 40%–44%.22 Of the patients resuscitated from cardiac arrest, a small proportion (variable as a function of timeliness and effectiveness of response) achieve early recovery, with restoration of spontaneous respiration and consciousness Identification and treatment of the cause of arrest is the main or only therapeutic challenge for this group of subjects But most survivors of cardiac arrest (80%) are comatose postresuscitation, and are admitted to the ICU where they represent the population of patients with postresuscita- tion syndrome (PRS), amounting to about 15%–20% of all cardiac arrest victims (Fig 47.2) Among the PRS patients, mortality has been reported to be very high, reaching 80% by months postresuscitation:23–25 approximately one-third of the deaths are due to cardiac causes (early deaths usually Ͻ 24 hours), one-third to malfunction of extracerebral organs, and one-third to neurologic causes (late deaths) The prevalence of the postresuscitation syndrome can only be inferred, because of the bias of data resulting from decisions to limit treatment, including instructions for “do not attempt resuscitation,” in cases of recurrent cardiac arrest.22–26 Etiology Following resuscitation from cardiac arrest of less than minutes, recovery is rapid and complete After prolonged arrest, ROSC is impossible or only transient 819 820 Erga L Cerchiari Cardiac arrest Postresuscitation syndrome Optimal recovery No ROSC Cardiac P ROSC Neurological Death causes R S Other No resuscitation attempt Alive Fig 47.2 Estimated fate for cardiac arrest patients Therefore, the postresuscitation syndrome only develops following resuscitation given during an intermediate duration of ischemia (the limits of which are affected by prearrest conditions) and depending on the circumstances of resuscitation, leading to the “reperfusion paradox.” The insult induced by cardiac arrest and CPR is multifaceted, encompassing several contributing factors occurring during cardiac arrest, during CPR, and following restoration of spontaneous circulation:1,6,7 • ischemia – anoxia occurring during the cardiac arrest with no-flow • hypoperfusion – hypoxia during the low-flow of external cardiac compressions (inducing at best a cardiac output of 25% baseline) • reperfusion, which, although potentially permitting survival, adds to the ischemic-hypoxic–hypoperfusion insult, inducing a variety of mechanisms that continue to evolve subsequently, including reperfusion failure and injury, altered coagulation, and activation of a systemic inflammatory response Pathogenesis Two major pathways have been identified a direct insult to the brain, which is particularly sensitive to ischemia; and to the heart, which may suffer postresuscitation myocardial stunning leading in turn to a secondary insult from postreperfusion impairment of cardiac output and hypoperfusion postreperfusion activation of the systemic inflammatory response syndrome, with hypoperfusion and/or altered perfusion as one pathological mechanism;12 in this pathway, the PRS shares many features with severe sepsis, including elevation of plasma cytokines with dysregulated cytokine production, endothelial injury, complement activation, coagulation and fibrinolysis abnormalities, endotoxemia, disturbed modulation of the immune response, and adrenal dysfunction Organ function postresuscitation The postresuscitation syndrome occurs in patients resuscitated after cardiac arrest of more than minutes’ duration and is characterized by different components: neurologic functional impairment, cardiovascular functional impairment – both well characterized – and the extracerebral extracardiac functional impairment comprising a complex picture of determinants and interactions The three major components variously contribute to the complex clinical picture of the patient resuscitated from cardiac arrest and admitted to ICU Rapidly occurring early post-resuscitation changes create an acute phase of instability during which specific and aggressive treatments may favorably affect outcome After the first Postresuscitation syndrome 24 hours the clinical picture stabilizes and treatment becomes less specific, and is not different from that of a comatose ICU patient For purposes of clarity, the three components are described separately, with analysis of the relative contribution of the two pathogenetic pathways, functional derangement interactions, and contributions to outcome and specific early treatments Neurologic function postresuscitation The best defined component of the postresuscitation syndrome is neurologic functional impairment With the increased application of resuscitation interventions, postcardiac arrest unconsciousness has become the third most common cause of coma Almost 80% of patients who initially survive cardiac arrest remain comatose for variable lengths of time, approximately 40% enter a persistent vegetative state, while 10% to 30% of survivors achieve a meaningful recovery.27 Cardiac arrest causes a global ischemic insult to the brain The extent of cerebral damage is a function of the duration of interrrupted blood flow Accordingly, minimizing both the arrest (no-flow) time and the cardiopulmonary resuscitation (low-flow) time, is critical Even in selected patients with a witnessed cardiac arrest after ventricular fibrillation and an estimated arrest to ALS intervention interval no longer than 15 minutes, mortality at months was 55% and of the survivors, 61% had an unfavorable neurological outcome.9 With reperfusion, extracerebral factors may hamper neurological recovery, requiring interventions aimed at mitigating secondary postischemic anoxic encephalopathy.7 Pathophysiology The mechanisms of cerebral damage following ischemia and reperfusion have been studied in detail (for detailed reviews see refs 7,27) Changes induced by ischemia set the stage for reoxygenation-induced, free radical-triggered injury cascades, exacerbated by reduced cardiac output and local circulatory impairment that starts during cardiac arrest with altered blood–brain barrier permeability and systemic changes such as activation of complement, coagulation, platelet aggregation, and adhesion of white blood cells.28 The pattern of prolonged global and multifocal cerebral hypoperfusion is associated with variations of regional cerebral blood flow both in the cortex and in the basal ganglia29 with regional anoxic cerebral anaerobic metabolism Posthypoxic encephalopathy has been shown to be associated with a marked decrease of cerebral metabolic activity and of glucose uptake, even 24 hours after resuscitation.30 A significant activation of inflammatory mediators (Interleukin 8, soluble elastin, and polymorphonuclear elastase) immediately postinsult and lasting about 12 hours has recently been reported following both cardiac arrest and isolated brain trauma, suggesting an inflammatory response as a common pathogenetic pathway activated by cerebral damage.31 Clinical features and prognostic evaluation A variety of methods have been proposed to monitor the evolution of the depth of coma and its prognosis, including neurological examination, electrophysiologic techniques, and biochemical tests A recent meta-analysis, including nearly 2000 patients, assessed the reliability of neurological examination, including Glasgow Coma Scale (GCS) and brainstem reflexes, reviewed at different time intervals after resuscitation; it concluded that patients who lack pupillary and corneal reflexes at 24 hours and have no motor response to pain at 72 hours have an extremely small chance of meaningful recovery The most reliable signs of prognosis occur at 24 hours after cardiac arrest: earlier assessment should not be based on clinical evidence alone.32 A systematic review of 18 studies analyzed the predictive ability of somatosensory evoked potentials (SSEP) acquired early after the onset of coma (1–3 days) in 1136 adult patients with hypoxic-ischemic encephalopathy: the results showed that patients with absent cortical SSEP responses have a less than 1% chance of regaining consciousness.33 A recent study tested the value of serial measurement of serum neuron-specific enolase (NSE) at admission and daily postinsult, in combination with GCS and SSEP measurements, to predict neurological prognosis in unconscious patients admitted to the ICU after resuscitation from cardiac arrest High serum NSE levels at 24 and 48 hours after resuscitation predict a poor neurological outcome Addition of NSE to GCS and SSEP increases predictability.34 By 48–72 hours postresuscitation, predictability of unfavorable long-term neurologic outcome may guide decisions to curtail treatment, because only patients with lighter levels of coma or who have regained consciousness by this time have any realistic prospect of long-term survival.32 Treatment Research into cardiopulmonary cerebral resuscitation has attempted to mitigate the postischemic–anoxic encephalopathy but, until recently, experimental results had never been replicated in patients.7 821 822 Erga L Cerchiari Mild therapeutic hypothermia induced following reperfusion in patients who have been successfully resuscitated from ventricular fibrillation cardiac arrest is the only postresuscitation intervention that has proved effective in increasing the rate of favorable neurologic outcome in two different randomized studies conducted in Europe and Australia9,10 and in reducing mortality in one of them.9 Clinical and experimental results show a multifactorial neuroprotective effect of hypothermia during and after ischemic situations by influencing several damaging pathways.27 Thrombolytics, administered during arrest or early after reperfusion, have been shown in animal experiments to improve the microcirculation in the brain and may, by this mechanism, contribute to the favorable neurological outcome of patients as described in many case reports and small case series with predominantly positive results.35 The first properly designed, large, randomized, double-blind multicenter study of thrombolytics was stopped before completion of recruitment because the data safety monitoring board judged it unlikely that, in the population in study, tenecteplase would demonstrate superiority over placebo These results, presented at a 2006 conference, should be considered preliminary until a detailed analysis is performed and published.36 Cardiovascular function postresuscitation Following successful resuscitation from prolonged cardiac arrest, a typical component of the postresuscitation syndrome is prolonged myocardial contractile failure, associated with life-threatening ventricular arrhythmias and hemodynamic instability.37,38 Cardiac complications are stated to occur in 50% of resuscitated patients, ranging from transient – but sometimes severe – impairment of myocardial function (occurring early and normalizing several days later) to permanent malfunction and fatal rearrest The severe impairment of myocardial function in the early hours following resuscitation accounts for 25% to 45% of early postresuscitation deaths.23–25 The global nature of ischemic myocardial dysfunction38 and also its occurrence following resuscitation from respiratory arrest39 or electroconvulsive treatment40 strongly support its role during cardiac arrest and cardiopulmonary resuscitation as the primary etiological determinant, as opposed to the role of the primary cause of arrest which is cardiac in 55%–65% of cases.41 The severity and duration of postresuscitation myocardial impairment is a function of both duration of cardiac arrest and subsequent resuscitation efforts,16–42 with a contribution from adrenaline (epinephrine) used during CPR,43,44 and the energy and waveform required for defibrillation.45,46 In humans, the dose of adrenaline used during CPR has been reported to be the only variable independently associated with postresuscitation myocardial dysfunction.44 Pathophysiology The mechanisms responsible for myocardial stunning after global myocardial ischemia remain unclear, but several hypothesis have been proposed Among these are the postreperfusion long-lasting depletion of the total adenine nucleotide pool, the generation of oxygen-derived free radicals, calcium overload, and uncoupling of excitation-contraction due to sarcoplasmic reticulum dysfunction.37,38 Recently, a correlation has been established between levels of proinflammatory cytokines, synthesized and released in response to the stress of global ischemia, and the depression of myocardial function in the early postresuscitation period.47 Clinical features In animal studies, postresuscitation myocardial dysfunction is characterized by increased filling pressures, impaired contractile function, decreased cardiac index, decrease in both systolic and diastolic right ventricular function,16,38 starting at 2–6 hours and returning to normal at 24 hours postresuscitation These findings were confirmed initially by anedoctal observations of prolonged reversible myocardial dysfunction in human cardiac arrest survivors50,51 and, later, were better defined in systematic studies in patients.44,52 The global nature of postresuscitation dysfunction has been demonstrated with echocardiography and ventriculography, which show a decrease in ejection fraction and in fractional shortening Myocardial dysfunction in patients may improve at 24–48 hours postresuscitation with return to normal values; persistently low cardiac index at 24 hours postresuscitation is associated with early death by multiple organ failure.44 In the same study, despite the significant improvement of cardiac index at 24 hours, persisting vasodilatation was described, delaying the discontinuation of vasoactive drugs In parallel with the failure of the heart to sustain normal circulation, a condition of altered peripheral oxygen utilization has been described.44 These two mechanisms together account for the persistent anaerobic metabolism characteristic of the early postresuscitation phase Relationship to neurological recovery and outcome The cardiovascular impairment in the early postresuscitation hours has been reported to correlate with impaired Postresuscitation syndrome cerebral recovery from the ischemic insult of cardiac arrest.16 Indirect evidence of the role of impaired perfusion on cerebral recovery comes from the beneficial effect of cardiopulmonary bypass in augmenting flow after cardiac arrest.15 In cardiac arrest survivors, good functional neurological recovery has been independently and positively associated with arterial blood pressure during the first hours postresuscitation, whereas hypotensive episodes correlate with poor cerebral outcome.52 The latter finding could be explained by the loss or impairment of cerebral autoregulation in comatose patients resuscitated from cardiac arrest, causing a reduction in cerebral blood flow if blood pressure is low.54,55 The finding of a correlation between low cardiac index and neurologic outcome, however, has not been confirmed in a recent study in humans.44 Treatment Successful treatment of myocardial dysfunction could reduce or prevent the cardiac causes of death that are the major determinants of early postresuscitation deaths Treatment with dobutamine has proved effective in supporting output and pressure during the postresuscitation phase prior to return to baseline function.56 A dobutamine dose of mcg/kg has been shown to be better than a dose of or 7.5 mcg/kg min, and better than placebo or aortic counterpulsation in sustaining cardiovascular performance for hours postresuscitation.56–58 The similarities in cardiovascular status between septic and postresuscitation patients have suggested that in addition to the inotropic support with dobutamine the ‘early goal-directed therapy’ that has proved effective in severe sepsis should be included59 – namely normalization of intravascular volume, of blood pressure by vasoactive drugs, and of oxygen transport by red cell transfusion during the first hours postresuscitation.11,12 Data on its effectiveness in cardiac arrest patients are not yet available Extracerebral extracardiac function postresuscitation The extracerebral extracardiac function derangements, accounting for one-third of deaths,23–25 represent the less specific component of the postresuscitation syndrome.11,12 In patients surviving the early postresuscitation phase, cardiovascular function improves, neurologic function may show gradual improvement or remain severely compromised, but conditions facilitating the development of sepsis are created, leading ultimately to multiorgan dysfunction Systemic findings and pathogenesis The direct effect of cardiac arrest, besides its role in neuronal injury and myocardial dysfunction, is also involved in the genesis of coagulation disturbances,60 endothelial injury,60,61 and in triggering the cascades of inflammatory responses.7,63 A variety of changes and findings, which still need to be clearly classified and systematized, have been described following resuscitation from cardiac arrest: • a considerable increase in various acute phase response proteins64 • a sharp rise in plasma cytokines and soluble receptors within the blood compartment as early as hours postarrest31,46,65–69 • endothelial injury and release of intracellular adhesion molecules • marked activation of complement, polymorphonuclear (PMN) leukocytes, and an increased PMN-endothelial interaction61–64 • marked activation of blood coagulation and fibrinolysis60 • leukocyte dysregulation11,12 • evidence of the presence of endotoxin in plasma The complex interaction of endothelial injury, inflammatory and procoagulant host responses, intravascular fibrin formation, and microvascular thrombosis contribute to reperfusion defects,7,60,64 which augment systemic hypoperfusion induced by cardiovascular dysfunction to trigger a secondary insult of persisting anerobic metabolism The altered systemic oxygen utilization, together with circulating endotoxin and immune hyporeactivity, may facilitate development of infection.11,12 Extracerebral and extracardiac organs, however, can tolerate periods of ischemia much longer than those generally occurring in cardiac arrest and resuscitation: thus, the impairment of function in these organs appears to be the combined result of the mechanisms triggered by ischemia but compounded by reperfusion Derangements of organ function Clotting and fibrinolytic function Starting during cardiopulmonary resuscitation, marked activation of coagulation has been demonstrated, without adequate concomitant activation of endogenous fibrinolysis,60,70 suggesting that intravascular fibrin formation and microvascular thrombosis after cardiac arrest may contribute to organ dysfunction, including neurological impairment With restoration of spontaneous circulation and reperfusion, coagulation activity (thrombin-antithrombin complex) increases, anticoagulation (antithrombin, protein C, and protein S) decreases, and 823 824 Erga L Cerchiari fibrinolysis (plasmin–antiplasmin complex) is activated or in some cases inhibited (increased plasminogen activator inhibitor-1 with a peak on day 1) These abnormalities are more severe in patients dying within days and most severe in patients dying from early refractory shock Protein C and S levels are low compared with those in healthy volunteers and discriminated OHCA survivors from non-survivors.66 Marked activation of complement, polymorphonuclear leukocytes, and an increased PMN-endothelieal interaction have been clearly demonstrated during cardiopulmonary resuscitation and early reperfusion after cardiac arrest in humans.62 Adrenal function Serum cortisol levels have been reported consistently to be high in all patients resuscitated from cardiac arrest for up to 36 hours postresuscitation,74–76 with lower levels in nonsurvivors,74 particularly in those who died of early refractory shock.76 Relative adrenal insufficiency as assessed by corticotropin tests was observed in 42% of patients but showed no association with arrest duration variables or with outcome.76 Renal function Renal dysfunction,77 was recently confirmed in patients presenting with hemodynamic instability and was characterized by significant increases in plasma creatinine and by a decrease in the International Normalized Ratio.44 Intestinal function Following cardiac arrest and reperfusion, severe intestinal ischemia occurs, showing a pattern of metabolic extracellular changes similar to those recorded in the brain.78 It is associated with early intestinal dysfunction and/or endoscopic lesions identified in 60% of patients.79 A role for ischemia-reperfusion-mediated increase in intestinal permeability has been proposed as predisposing the patient to the sepsis syndrome Endotoxin and infection The finding of plasma endotoxin detected in 46% of patients 1–2 days after resuscitation (although with no relation to outcome), and of endotoxin-dependent hyporeactivity of patients’ leukocytes, with high levels of circulating cytokines and dysregulated production of plasma cytokines, delineates an immunological pattern similar to the profile characterizing patients with sepsis Half of endotoxin-positive patients have been found to develop secondarily acquired bacterial infection 3–4 days postresuscitation (mostly pulmonary, occasionally bacteremia).11,12 The finding of bacteremia, generally associated with pathogens of intestinal origin, occurring in 39% of patients within the first 24 hours of admission postresuscitation associated with increased mortality,80 was not confirmed in a subsequent study in which bacteremia was encountered only sporadically.12 The incidence of pneumonia in patients admitted to the ICU following cardiac arrest has been reported to vary from 24% to 45% of patients.9,81 In a systematic study,82 newly acquired infection developed in 46% of patients resuscitated from cardiac arrest and admitted to the ICU, the most common being pneumonia (65% of infections) Compared with cardiac arrest survivors without infection, patients with infection had longer mechanical ventilation and ICU length of stay, but mortality was similar A possible role for procalcitonin has been proposed for the early identification of post-resuscitation patients with an acute phase response and bacterial complications: it was the only marker higher in patients with ventilatoracquired pneumonia.83 Hyperthermia not associated with positive blood cultures has been reported frequently during the first 24 hours following CPR, suggesting that mechanisms other than infection may contribute to the development of fever in cardiac arrest survivors.82,84 Correlation with outcome The peak level and the time of occurrence of many of the above-mentioned mediators of the inflammatory response have been reported to correlate with outcome (differently defined as: early death, early death from cardiac causes, death at month, and others) in different case series from single centers and without precise standardization of resuscitation procedures and postresuscitation treatments.61–72 The data now available suggest the opportunity for a reassessment and systematic analysis of the interactions involving various cascades and of their role in determining outcome in a well-designed multicenter study adopting a standardized treatment and evaluation protocol The better characterization of PRS in its early phase is confirmed by the high predictive value of cerebral impairment, the severity of which can be quantified, allowing a reliable prognostication of outcome.47,52 In the later phase of PRS, when secondary multiple organ derangement syndrome (MODS) becomes apparent, the existing limitations of prognostic evaluation based on severity scoring systems85 inherent to MODS are further 1324 Index oxygenated perfluorocarbon, cold 858 oxygenation ventilation effects on status 510–11 see also membrane oxygenation/oxygenator oxygen-powered breathing devices 534 oxytocin, sublingual 627 P waves, pulseless electrical activity 436 p67 glycoprotein 254–5 pacemakers, implantable 475, 798–9 pacing electrical 15 long QT syndrome 926 non-fibrillatory cardiac arrest 739 postshock asystole 492 pulseless electrical activity 441 transthoracic/transvenous 739 see also implantable cardioverter-defibrillators paddles (defibrillator) see electrodes pain response to 890 see also analgesia palpation of pulse 699–700 pancreas, blood flow in CPR 309 pancreas ischemia–reperfusion 305 damage from cardiac arrest 311 pancreatic enzyme production in hemorrhagic shock 1003 pancreatic polypeptide (PP) 139 panic in anaphylaxis 1110 compared to without anaphylaxis 1104 Pantridge, Frank 18 paramedics 19–21 resuscitation decision-making 1204–5 witness of cardiac arrest 39 parasites, anaphylactic reactions 1106 paraspinal vein ligation 390 parasympathetic system in hemorrhage 997 parathyroid glands 134 critical illness response 145 parathyroid hormone 134 critical illness response 145 paroptosis 56 partial liquid ventilation with cold perfluorocarbon 858 pathophysiology of cardiac arrest, 667–9 patient records, electronic 29–30 Patient Self-Determination Act (1990) 1230 patient waiver exception to informed consent 1233–4 pediatric patients see adolescents and young adults; children; infants; neonates Pediatric Perioperative Cardiac Arrest (POCA) Registry 1047 pediatric self-inflatable bag 526 pediatric studies, community definition 223 penicillin allergy 1106, 1107 pentazocine 839–40 peptide YY 139 percutaneous cardiopulmonary bypass see cardiopulmonary bypass, percutaneous percutaneous coronary intervention (PCI) 764–71 after resuscitation 766–7 during resuscitation 768–70 perfluorocarbon, cold 858 perfusion, organ cerebral 902–3 coronary/myocardial induced hypothermia effects 867 vital organs in profound accidental hypothermia 1020–21 see also blood flow; hypoperfusion; reperfusion; ventilation/perfusion ratio perfusion pressures cardiopulmonary bypass animal models 600 chest compression 574, 575 load distributing band and CPR 593, 594 monitoring 700–1, 812 resuscitability 679–81 sodium bicarbonate 685 vasopressin animal models 649–50 see also cerebral perfusion pressure; coronary perfusion pressure pericardial pressure rise after cardiac arrest 359 spontaneous gasping 364 volume unloading 360 pericardiocentesis 731 pericardium, constraint 357–9, 360, 361 peripheral circulatory effects of local anesthetics 1057 peripheral perfusion measurement 319–20 peripheral resistance cardiac output 341 chest compression 337–8 fall in hemorrhage 995 peripheral venous drug administration 615–18 peritoneal lavage, cooling via 858 peritoneal resuscitation in hemorrhagic shock 1001 PERK 254 activation 255, 256 unfolded protein response 255 permeability transition pore, myocardial 833–4 peroxynitrite 246 persistent vegetative state 1205, 1230, 1237–8, 1240 personhood 1226 personnel see healthcare professionals; human factors; teams Perth study, cardiopulmonary resuscitation before or after defibrillation 466, 467 P-glycoprotein 404–5 pH intracellular during CPR 241 pulseless electrical activity 434–5 intra-ischemic 239–40 paradox 53 see also acid–base status Index pharmaceutical agents see drug(s)/drug therapy pharmacodynamics 398, 402–3 pharmacogetics/pharmacogenomics 398, 403–5 pharmacokinetics 398–402 induced hypothermia 869 pharmacology cardiac arrest 395, 405–11 processes 397–405 pharmacotherapy see drug(s)/drug therapy phenylephrine 640, 641 coronary perfusion pressure 383 pulseless electrical activity 735 phenytoin 905 Philips automated external defibrillators 487 phosphates high-energy in defibrillation 471 levels in induced hypothermia 867, 868 phosphocreatine 238 intestinal ischemia 299–300 phosphodiesterase inhibitors postresuscitation syndrome 841 type in high-altitude illness 1131 phospholipase A2 247 brain levels 238 intestinal ischemia–reperfusion 301 kidney ischemia–reperfusion 306 phosphoprotein phosphatases 93 phosphotyrosine-containing proteins 263 pH-stat 868 physical examination, non-fibrillatory cardiac arrest 728 physical exercise see athletes/sports participants; exercise/exertion piston chest compression (pneumatic) 585–6 compared with external compressions 578 pituitary gland anterior lobe 129–32, 139–42 neuroendocrine response 129–33 to critical illness 139–43 neurohypophysis 132–3, 142–3 PKB/Akt activation 95, 97 plant allergens and anaphylaxis 1105, 1106 plasma proteomics 83–4 plasminogen activators see streptokinase; tissue plasminogen activator; urokinase platelet activating factor (PAF) anaphylaxis 1109–10 liver ischemia–reperfusion 304 L-selectin shedding 169 plausibility checks 212 plethysmograph in pulse oximetry 705 pleural drainage see thoracostomy pneumatic devices for chest compression see piston chest compression; vest CPR pneumonia drowning victim 1096 postresuscitation 824 pneumoperitoneum, iatrogenic 802 pneumotach transducers 203 pneumothorax drowning victim 1097 status asthmaticus 981 see also tension pneumothorax poisoning 985–6, 1028–42 anesthetics in out-of-operating room procedures 1060 presenting symptoms and possible antidotes 1029 special considerations in treatment of arrest 1028 see also substance abuse police/law officers automated external defibrillators 485 cardiocerebral resuscitation 749 pollens, anaphylaxis 1105–6 poly(A)ϩ mRNA transport 250–1 polymorphonuclear leukocytes 168 endothelial activation 168–9 intestinal ischemia–reperfusion 301, 302 kidney ischemia–reperfusion 306 liver ischemia–reperfusion 304 sequestered in reperfusion-related myonecrosis 292 poly(ADP-ribose) polymerase (PARP) 246 polyunsaturated fatty acids (PUFA) 32, 247 pooled analyses 210 positive end-expiratory pressure see continuous positive airway pressure positive pressure ventilation (positive airway pressure) hemodynamic effects 361–2 adverse 515–16 low-flow conditions 516–17 trauma and associated hemorrhagic shock 994 unprotected airway 523–7 see also continuous positive airway pressure positron emission tomography in neurologic outcome prediction 892 postresuscitation care 902–18 brain-oriented 902–18 buffer therapy 688, 904–5 in-hospital 787–9 monitoring 717–18 cardiac output 708 goals 717, 718 laboratory tests 703–4 on-site 775–6 pediatric 947, 954–6 postresuscitation death, causes 829 postresuscitation disease/syndrome 52, 55, 139, 815–918 background/general information 817–19 definition and concept of 817 early experimental findings 817–19 etiology 819–20 pathogenesis 820 prevalence 819 1325 1326 Index postresuscitation injury 51–2 postresuscitation non-fibrillatory cardiac arrest 740 postresuscitation recovery, phasic pattern 818 post-translational modifications proteins 81, 82–3 proteomics 80 post-traumatic stress disorder 1251–2 potassium, abnormal blood levels see hyperkalemia; hypokalemia potassium current, delayed rectifier 104 potassium ion(s) brain concentration 238 current 113 extracellular in ischemia 107–8 reperfusion arrhythmias 289 translation effects 255 potassium ion channels 108 ATP-sensitive activators 839 commotio cordis 1181 hemorrhagic shock 998 mutations long QT syndrome 923, 1172 short QT syndrome 1174 voltage-dependent 111–12 power of attorney 1202 power spectral density (PSD) function 419, 420 estimation 421–2 precedent 1226, 1227 precordial thump 475 complications 792–3, 813 pre-excitations of Wolff–Parkinson–White syndrome 930, 1175 pregnancy 1076–87 arrest/sudden death risk 1076–87 amniotic fluid embolism 984, 1108 obstetric anesthesia-associated risk 1048 electrocution 1137 inferior vena cava compression 1077, 1079 physiological changes 1076–8 resuscitation 1078–85 prehospital resuscitation see on-site (field/out-ofhospital/prehospital) resuscitation preload excessive assisted ventilation impairing 515–16 myocardial contraction 431 pulseless electrical activity 439–40, 441 preservative hypothermia 849 definition 849 future of 872–4 submersion victim 1090 trauma 995–6 pressure gradient, cardiac arrest 348 pressure support ventilation, adjunctive CPAP 528 pressure transducers, extravascular/intravascular 193–4, 195 Prevost, Jean Louis 15 Priestley, Joseph 7–8 principlism 1227 privacy 1226 implied fundamental rights 1231 right to 1231–2 probability of successful defibrillation (PROSC) 716 procainamide 670 process issues with in-hospital cardiac arrest 784–5 procoagulant administration 1001 programmed cell death 55 progressive cardiac conduction defect (PCCD) 74–5 progressive familial heart block (PFHB) locus 75 prolactin 131 critical illness response 140–1 pro-opiomelanocortin complex 129 propranolol 640 metabolism 402 ProSeal laryngeal mask airway 556 prostaglandin(s) cerebral ischemia 247 kidney ischemia–reperfusion 306–7 reperfusion during resuscitation 55 prostaglandin I2 (prostacyclin) analog in high-altitude illness 1131 induced hypothermia effects 864 proteases in apoptosis 861 brain 861 myocardium 833 protein dephosphorylation, reversible 90–1 protein kinase(s) cascade 91 pro-survival 96 protein kinase C␦ (PKC␦) 93–4 protein phosphorylation, reversible 90–1 protein separation techniques 80, 81 protein synthesis cerebral ischemia 248–56 downregulation of rate 252 energy requirement 249 reperfusion 248–56 suppression in reperfused brain 248–9, 251 mechanisms 255–6 proteins, phenotype function 83 proteomics 70, 71 heart tissue 82–3 membrane channels 83 plasma 83–4 serum studies 83–4 strategies 79–80, 81, 82 sudden cardiac death 79–80, 81, 82–4, 85, 86 protons antiporters 240 source in ischemia 239 see also hydrogen ion; sarcolemmal Naϩ–Hϩ exchange proto-oncogenes, brain 259–60 P-selectin 168, 169 Index P-selectin glycoprotein ligand (PSGL-1) 169 pseudo-pulseless electrical activity 438–9, 725–6 psychological care, cardiac arrest survivors 1251 psychological effects of survival 1249 psychotropic drugs, Brugada-like ECG patterns induced by 928 public access defibrillation (PAD) 477, 483, 484, 496–505, 774–5, 810 clinical perspectives 498–9 cost-effectiveness 490 economics 1213, 1215, 1216–18, 1223 Europe 499–503 four levels of responders 497 historical perspectives 496–7 trial 483, 499 USA 496–8 see also lay public public access defibrillators 1213, 1215, 1216–18 public disclosure 217 levels 222–3 standardization 219 template 220–3 public guardians 1236 pulmonary artery hypertension at high-altitude 1120 chronic unrelated to altitude 1131 young adults/children 1124 pressure changes in CPR 354–5 unilateral absence in adolescents at high altitude 1123 pulmonary artery catheter monitoring 319 pulmonary embolism 983–4 amniotic fluid 984, 1108 anesthesia 1051 pulseless electrical activity 440 thromboembolism 732–3, 982–3 high-altitude 1126 thrombolytics 858–9 pulmonary non-vascular tissue see lung(s) pulmonary system intestinal ischemia–reperfusion 303 liver ischemia–reperfusion 305 see also edema, pulmonary pulmonary vasculature hypoxic vasoconstriction 507 resistance 517–20 pulse palpation 699–700 pregnancy 1077 pulse oximetry 705, 812 pulseless cardiac arrest 947–8 pulseless electrical activity (PEA) 395, 426–42, 445, 669 age of patients 427 animal models 433–4 aortic pressure 437, 439 ATP 435 autonomic nervous system 435 calcium role 434 cardiac pacing 441 causes 439–40, 726–7 reversible 727, 729–33 classification 426, 437 clinical spectrum 427 coronary perfusion pressure 436 drug-induced 436 ECG characteristics 426, 436–8 end-tidal CO2 monitoring 707 epinephrine effects 438, 441 feedback loop 432–3 hospital discharge rates 445 hypothermia 435–6 hypoxia 435 incidence 426–7, 725 intracellular pH 434–5 ischemia 434 mechanical causes 440 metabolic derangements 434–8 correction 440–1 normotensive 439 pathophysiology 434–8 postdefibrillation 426, 440, 727 pseudo 438–9, 725–6 subsets 727 successful resuscitation rates 427 survival chance 445 therapy 440–1 true 438–9, 725–6 pulselessness, asphyxia progressing to 974–5 pump, cardiopulmonary bypass 604–5 pump, chest compression 327–9 abdominal pressure 333–4 aortic dimensions 329 cardiac dimensions 329–30 determination 329–30, 331, 332–3, 341 mitral valve motion 330, 331, 332 modifiers 333–4, 335, 336 optimizing 339, 340 pupillary (light) reflex testing 888–9, 891 Purkinje network, arrhythmia initiation 109 pyrexia see fever pyroptosis 56 QR duration 437 QRS duration averaged 116 pulseless electrical activity 437 QRS interval Brugada syndrome 930 pulseless electrical activity 436, 438–9, 726, 727, 728 QT interval hypertrophic cardiomyopathy 1159 pulseless electrical activity 436 1327 1328 Index QT interval (cont.) shortened 926, 1171, 1174–5 torsades de pointes 403, 404 see also long QT syndrome; short QT syndrome quality assurance model 1273 quality of life after cardiac arrest 1251 postresuscitation care to restore 775–6 quality-adjusted life year (QALY) 1214–15 cost per 1217, 1218, 1219, 1223 quinidine Brugada syndrome 1173 short QT syndrome 1175 racial factors 34 survival of cardiac arrest 38 radiofrequency ablation Brugada syndrome 1173 right ventricular outflow tract tachycardia 1176 radiograph, chest in pulmonary edema 1121 radiology see imaging; specific modalities random errors 182, 185–6 randomization 209–10 randomized controlled trials (RCTs) 209–10 patient inclusion criteria 210–11 rapid response systems, prearrest 782–4 rate of cardiac arrest 33 reactive oxygen species (ROS) see free radicals receiver operating characteristics (ROC) analysis 420, 422 recovery of spontaneous circulation (ROSC) 397 coronary perfusion pressure 356–7, 380 coronary perfusion pressure predictive value 377 defibrillation outcome prediction Plate 21.4 level of consciousness assessment 1203 number of chest compressions/minute 380 probability 423, Plate 21.5 reperfusion 52 recovery position 531 red blood cells blood gas transport 510 S-nitrothiols 999, 1005 redox status of mitochondria 714 redox-mediated intracellular stress responses 52–4 Reece, Richard 14 re-entry mechanisms 112 reperfusion arrhythmias 289 reflexes, brainstem/cranial nerve bedside testing 888–90 brain death determination 897–8 regional and local anesthesia, arrest 1048–9, 1057–8 allergy to anesthetic 1051 outside operating room 1060 pregnant women 1082 treatment 1063 registries 29 clinical studies 208–9 regulation 21 CFR 50.24 217, 219 relative error 182 remote areas anesthesia-associated risk of arrest 1060 high-altitude illness treatment 1129–31 trekking 1125–6 renal hemodialysis 318 renal tract see kidney renin 136, 138 aldosterone dissociation 147 critical illness response 147, 149 renin–angiotensin–aldosterone system 136–7 critical illness response 146–7 reperfusion 52 ACTH dysregulation 140 arrhythmias associated with 831 cellular regulatory systems 259–60 cerebral circulation 242–3 eIFs 252–3 energy metabolism 239 extravascular resistance 397 free fatty acid production 247 GH levels 141 invasive techniques 600–13 lipid peroxidation 247–8 membrane damage 246–8 myocardial infarction 33 neuronal calcium ion homeostasis 244 pathophysiology 139 pH restoration 397 protein synthesis 248–56 translation 255–6 see also cerebral reperfusion reperfusion arrhythmias 288–91 animal models 288 clinical relevance 291 comorbid conditions 290 drug administration 290–1 early after depolarizations 289, 290 humans 288 mechanisms 289–90 re-entry 289 reperfusion injury 282–93, 820, 821, 860 cerebral 757–8, 863 clinical settings 282–3 cytokines 163–7 myocardial stunning 283–8 myonecrosis 291–2 prevention 283 reduced blood flow 310 reperfusion arrhythmias 288–91 sodium ions 397 Index treatment 283 triggers of sequelae 172 see also myocardial stunning repolarization, dispersion 113 rescue, drowning victim 1091–2 rescue breathing 523–9, 531–3 for children 532–3, 948 by lay public/bystander 520–3 risk of doing harm 752–3 rescue teams, in-hospital 785–6 rescuer/responder drowning victims 1091 performance 39 shock to 475, 799–800, 813 see also first responder research clinical methodology 206–15 consent 216–25 educational 1268–9 ethics 220–1 exceptions for consent 217, 218 laboratory methodology 179–204 non-approved drugs/devices 220 number of studies 219 on recently dead 1205–6 risk stratification 220–1, 222, 223 resonant frequency 184–5 respiration accidental hypothermia effects 1015 anesthesia-associated events causing arrest 1050 drowning victim care/monitoring 1095 high-altitude adaptation 1119–20 inspiratory and expiratory phase in rescuer ventilation 521 see also breathing; rescue breathing; ventilation respiratory acidosis, cardiac effects 680 respiratory arrest, lightning strike 1139 respiratory chain, postresuscitation myocardial dysfunction 833, 834 respiratory failure, asphyxia in 978–9 respiratory impedance threshold device see impedance threshold device respiratory infection see pneumonia respiratory insufficiency, pulseless electrical activity 439 respiratory system circulatory system interactions 515 pregnant women 1077–8 responder see first responder; rescuer/responder ResQPUMPR[O] 738 resting membrane potential, depolarized ischemic cells 109 resuscitation abandoning attempt 1204–5 acid–base changes 675–7 algorithms 1283, 1284, 1285, 1286 asphyxial cardiac arrest 976 cerebral 907 clinical research methodology 206–15 consensus development 1278–85, 1286 consent for research 216–25 consultation 1201–2 coronary perfusion pressure 679–81 myocardial acidosis and resuscitability 679–81 outcome correlation 377–8 decision-making 1203, 1204–5 ethical 1201 electrical shock 1142–5 emergency in trauma 995–6 ethics 1201–2 evidence-based medicine 1281–2 family presence 1205–6 futility 1202–3 guideline development 1278–85, 1286 high-altitude illness 1129–31 informing of decision 1204 laboratory research methodology 179–204 myocardial acidosis and resuscitability 679–81 neurological status prognosis 1203 outcome correlation with coronary perfusion pressure 377–8 performance quality 1284 pregnant women 1078–85 prehospital 17–19 research on recently dead 1207–8 successful 118, 1201 in PEA 427 sinoatrial activity 436–7 witnessing of cardiac arrest 37 thoracic compression 187–94 three phases 466 training 1258–73 on recently dead 1207 withdrawal of treatment 1205, 1240 withholding 1202–4 see also cardiopulmonary resuscitation; drowning; fluid management/resuscitation; hypothermia (induced/therapeutic), postresuscitation; in-hospital resuscitation/care; monitoring; on-site (field/out-ofhospital/prehospital) resuscitation; percutaneous coronary intervention; postresuscitation entries; safety considerations; thrombolysis reticular endothelium system 304–5 rewarming from accidental hypothermia 732, 1020, 1021–23 decision-making 1019 drowning victim 1019, 1096 from induced hypothermia 859, 866 rib fractures active compression–decompression 794 gender/age factors and location 795 open-chest CPR 794 ribonucleoprotein complexes (mRNPs) 250 1329 1330 Index right atrial pressure measurement 373 rise after cardiac arrest 359 spontaneous gasping 364 ventricular volumes 361, 362 right ventricle, constraint 357–9, 360, 361 right ventricular dysplasia, arrhythmogenic 451 right ventricular end diastolic pressure (RVEDP) 357 right ventricular volume 361, 362 risk factors for cardiac arrest 31–6 genetic 32 social/socioeconomic 32, 37 risk stratification research 220–1, 222, 223 sudden cardiac death Brugada syndrome 927–8 catecholaminergic polymorphic ventricular tachycardia 930 ECG in hypertrophic cardiomyopathy 1159 long QT syndrome 925 tools 452–5 Romano–Ward syndrome 922, 1172 Rose, Leonard 20–1 rubber latex allergy 1106 ryanodine receptor 77 type mutations 1161 arrhythmogenic right ventricular cardiomyopathy 1161 catecholaminergic polymorphic ventricular tachycardia 929–30, 1174, 1176 S-100/S-100B protein 871, 895 drowning victim 1098 induced hypothermia 895 Safar, Peter 9–10, 11–12, 848 safety considerations anesthesia 1046, 1063, 1064 minimal safety standards 1062 induced hypothermia 865–72 lay responders 1262 resuscitation 792–808, 813–14 chest compressions 576, 577, 792–6 thrombolytics 760–1 see also defibrillation, safety considerations saline diluent in endotracheal drug administration 622–3 hypertonic 684 salmeterol in high-altitude illness 1131 sample size for clinical studies 211 sample variance 185 sampling schemes, clinical research 208 SAPK kinase kinases, activation 93 SAPK kinases, activation 93 SAPK1 91–2 cascade 93 SAPK2 91, 92 cascade 92, 93 SAPK3 91, 92 SAPK4 91, 92 SAPK5 92 sarcolemmal Naϩ–Hϩ exchange 837–8 sarcomeres 427, 428, 429 sarcomeric proteins in hypertrophic cardiomyopathy 1154, 1157 sarcoplasmic reticulum 428 Scheele, Carl SCN5A sodium channel gene 115 mutation Brugada syndrome 927, 1173 long QT syndrome 923, 925, 1172 scorpion stings 1104 screening of athletes 1183–5, 1188 Italy 1152, 1183–4, 1185 Seattle study, cardiopulmonary resuscitation before or after defibrillation 465, 467 sedation and sedatives 905 arrest risk 1055–6, 1061 seizures see epileptic activity/seizures/convulsions selectins 168, 169 self-adhesive defibrillator pads 796 spark prevention 801 self-autonomy 1226 self-determination, right to 1231 sensor–subject interaction 181 sepsis, postresuscitation 823 sepsis syndrome 52 septic shock BNP levels 148 catecholamines 145–6 erythropoietin levels 149 ET-1 147 leptin plasma concentration 143 vasopressin levels 142–3 serum markers in neurologic outcome prediction 797, 821, 870–1, 895, 896 serum studies depletion 84, 85 protein dynamic range 84 proteomics 83–4 sex see gender Sharpey-Schafer, Edward shaving of chest hair before defibrillation 472, 797 shivering in induced hypothermia 869 shock, accidental electrical see electrical shock shock, circulatory 698 definition 698 excessive adverse ventilation during 516 postresuscitation cardiogenic 910 difference from primary cardiogenic shock 909 see also anaphylaxis/anaphylactic shock; hemorrhagic shock; septic shock shock, defibrillator 117 number and risk of myocardial damage 836 Index repeated 473 to rescuer/responder 475, 799–800, 813 short QT syndrome 75, 926, 1171, 1174–5 genetic basis 76 Sialyl Lewisx moiety 169 sick sinus syndrome 75–6, 1177 genetic defects 76 sickle cell trait and high-altitude pulmonary edema 1123 SIDS see sudden infant death syndrome signal averaged electrocardiogram (SEACG) 116 sildenafil in high-altitude illness 1131 Silvester, Henry simulation training 1264, 1265, 1266–7 debriefing 1266–7, 1268 feedback 1266–7 single nucleotide polymorphisms (SNPs) 78–9, 398 proteomics 80 single-use devices see disposable/single-use devices sinoatrial activity, successful resuscitation 436–7 sinoatrial node, proteomics 82–3 sinus node disease, genetic loci 75 sinus node failure 233 skeletal injury with chest compression 792 detection methods 795 manual compression 793 mechanical compression 794 skeletal muscle damage in defibrillation 797 skiing 1125 skills frequency of use 1261–2 retention 1261–2 in-hospital personnel 785 skin burns risk with defibrillators 796–7 transcutaneous capnometry (PtcCO2) 711, 712 small heat shock proteins hsp25/27 92 smoking in coronary disease prevention 456 Snow, John 1043 social risk factors 32 survival 37 societal attitudes to aging 959–60 socioeconomic impact of cardiovascular screening of athletes 1185 socioeconomic risk factors 32 survival 37 sodium bicarbonate see bicarbonate; Carbicarb sodium ion(s) blood level 685 brain concentration 238, 240 calcium transport 432 myocardial stunning 286 neuronal influx 243 reperfusion arrhythmias 289 reperfusion injury 397 transport 432 sodium ion channel(s) ventricular fibrillation 103–4 see also SCN5A sodium channel gene sodium ion channel blockers 118 class I antiarrhythmics 667 poisoning 1031–2 sodium ion–hydrogen ion exchange, sarcolemmal 837–8 soft tissue injury in manual chest compression 793 obstruction of airway in coma 975 see also organ(s) sojourners at high-altitude, child/young adults 1123–4 somatosensory evoked potentials 821, 871–2, 892, 893, 896–7 sparks from defibrillators 476, 800 prevention 801 spinal anesthesia see neuraxial anesthesia spinal cord ligation 390 spine see cervical spine spiral wave re-entry 102 splanchnic circulation 298 vasoconstrictor agents 300 visceral organ ischemia 318 splicing alternative 250 cerebral ischemia 249–50 spores, anaphylaxis 1105–6 sporting activity see athletes/sports participants; exercise/exertion spreading depression-like depolarizations 865 SQT mutations and short QT syndrome 1173 ST depression in myocardial bridging 1165 ST elevation Brugada syndrome 926, 927, 1173 commotio cordis 1179, 1180, 1181 ST elevation myocardial infarction coronary angiography following resuscitation 765 current management strategies 764 percutaneous coronary intervention following resuscitation 765–6 standard deviation of sample 185 standard error of estimation of the mean 186 standard operating procedures (SOPs) and anesthesia-associated arrest prevention 1065–6 stare decisis 1227 Starling’s law of the heart 431 statins 35 status asthmaticus 972, 980–1 status epilepticus 977 myoclonus prognostic value 895–6 non-convulsive and induced hypothermia 865 stellate ganglion resection 116 stenting, coronary in myocardial bridging 1166 sterilizing agents, anaphylactic reactions 1107–8 sternal approach, left to intracardiac injection 625–6 1331 1332 Index sternal compression force measurement 187 definitions 188–90 sternal compression in children, circumferential vs focal 949 sternal fracture with chest compression gender/age factors and location 795 manual chest compression 793 mechanical chest compression 794 steroids abuse of anabolic 1182 toxicity of cardioactive 1035–6 see also 21-aminosteroids; corticosteroids Sterz, Fritz 848 stimulant (CNS) overdose 1030–1 stings, allergy 1104, 1106 stomach see gastric entries streptokinase in-hospital 758–9 out-of-hospital 760 stress definition 128 emotional in cardiac arrest survival 1251 lay responder risk 1262 redox-mediated intracellular responses 52–4 stress-activated protein kinases (SAPKs) 90–3 ischemia/reperfusion effects 92 mediators of activation 92–3 myocardial death induction 93 stretch-activated channels in commotio cordis 1181 stroke, high-altitude 1126–7 stroke volume 347 spontaneous gasping 364 stunning see myocardial stunning stupor, asphyxia risk 976–7 subclavian vein, drug injection 618 subdiaphragmatic (abdominal) thrust 522–3, 976 sublingual capnometry (PslCO2) 711, 712 sublingual drug administration 626–7, 629 submersion see drowning substance abuse 33, 1030–1, 1032–3 athletes 1181–82 substance P 139, 140 subxiphoid approach to intracardiac injection 625 succinylcholine 1055 suction devices active compression–decompression 527, 587 airway clearing 534 sudden cardiac death acute causes 230 association studies 78–9 athletes 231, Plate 65.13 cardiac ion channel disease genetics 70–8 causation 229–31 children 813 devastating family impact 937, 1098–9 coronary artery fibrous plaque Plate 65.21 coronary heart disease 27–8 cost-effectiveness analysis 1213–16 definition 26–7, 449 dilated cardiomyopathy 105 early recognition out-of hospital 773–4 economics of treatment 1212–24 elderly people from myocardial infarction 959 electrical shock 1139 electrophysiology of 921–2 epidemiology 26–40, 229–31, 668 data 28–30 in home 484 incidence 28–30 survival 28–30 etiology/cause 229–33, 449–52, 668–9, 811 athletes 1150–86 children 813 rare 811 search for by EMS personnel 775–6 genetic factors 106 genomics 78–9 incidence 231 linkage studies 78 myocardial infarction 33, 105 neurological causes 229–30 pathophysiology 231–3, 668 prevention in at-risk patients 811, 921–36 proteomics 79–80, 81, 82–4, 85, 86 risk stratification Brugada syndrome 927–8 catecholaminergic polymorphic ventricular tachycardia 930 ECG in hypertrophic cardiomyopathy 1159 long QT syndrome 925 tools 452–5 speed of onset 1212 structural heart disease 104–6 subacute causes 230 survival rate 1224 survivors 1219–20 susceptibility loci 79 therapy 447–815 thrombotic occlusion Plate 65.20 trauma 230 ventricular hypertrophy 105 see also athletes/sports participants; pregnancy, arrest/sudden death risk sudden infant death syndrome (SIDS) 230–1 air travel and 1128 high-altitude residency 1124 sudden non-cardiac death, athletes 1152 sudden unexplained nocturnal death syndrome see Brugada syndrome suicide by drowning 1088 superiority trials 210 Index superoxide 53–4 ischemia effect on production 246 superoxide dismutase intestinal ischemia–reperfusion 302 myocardial stunning 286–7 supraglottic airway devices 553–9 supraventricular arrhythmias antiarrhythmics 672 defibrillation 475 surface cooling method 850, 854–5 surfactant therapy, drowning victim 1097 survival 36–7, 747–8 behavioral change 1252–3 cognitive change 1252–3 cognitive effects 1251 definition 747 elderly patients to hospital discharge 963–4 European Resuscitation Council 772 long-term emotional effects 1251–2 long-term psychological/cognitive effects 1251 memory impairment 1252–3 prehospital post-traumatic CPR 992–3 psychological care 1253 quality of life after cardiac arrest 1251 risk factors 37–9 sudden cardiac death 1219–20, 1224 see also death survival studies 747–8 chest compression 575–6 experimental studies 574 interposed abdominal compression 578–9 suspended animation 872–4 Sweden, in-hospital first responders 785 sympathetic nervous system arrhythmia generation 109 pulseless electrical activity 435 sympathetic nervous system block/inhibition hemorrhage-induced 997, 998 spinal anesthesia-induced causing bradycardic arrest 1056–8 syndrome X (metabolic syndrome) 811 systematic errors 182 systematic reviews 210 vasopressin 408 systemic disorders, postresuscitation 823 systemic inflammation, reperfusion period 139 systemic inflammatory response 163, 164 postresuscitation 820, 831–2 systemic inflammatory response syndrome 166, 171 visceral organ ischemia 313–14 systemic toxicity of local anesthetics 1057 systemic vascular resistance in pregnancy 1077 systolic dysfunction myocardial stunning 283 postresuscitation 831 T waves in long QT syndrome 923, 1171 tachycardias/tachyarrhymias hypertrophic cardiomyopathy 1157 long QT syndrome 926 see also ventricular tachycardia/tachyarrhythmia Tapai’s syndrome 803 teams emergency medical services 1203, 1204 in-hospital education in anesthesia-associated arrest prevention 1062–4 Medical Emergency Teams 783–4, 813 rescue 785–6 telephone instructions 21 temperature blood 868 core accidental hypothermia 1017–18 induced hypothermia 854, 858–9 pediatric management 954 probes in cardiopulmonary bypass 605 see also brain, temperature; hyperthermia; hypothermia temporo-parietal junction dysfunction, near-death experience 1247–8 tenecteplase 410, 759 tension pneumothorax 731–2, 982–3 anesthesia-related 1051 drowning victim 1097 non-fibrillatory arrest in 731–2 pulseless electrical activity 440 terminal illness 1237 testes, critical illness response 147 testosterone, critical illness response 147 THAM see TribonatR[O]; tromethamine theophylline poisoning 1031–2 therapeutic privilege exception to informed consent 1233–4 therapeutic window, definition 216 therapies see resuscitation; treatment; specific treatment methods and conditions thermal injury risk with defibrillators 796–7 thoracic compression see chest compression thoracic pump theory 352, 354 thoracic vest, circumferential see vest CPR thoracostomy for pleural drainage asthma 981, 982 tension pneumothorax 983 thoracotomy, resuscitative 731 thorax see chest thrombi, microscopic 864 thromboembolism see pulmonary embolism thrombolysis 757–63, 770, 812–13 clinical studies 758–60 mechanism of action 757–8 pathophysiological background to use 758 postresuscitation 822 safety 760–1 1333 1334 Index Thrombolysis in Cardiac Arrest (TROICA) trial 761 thrombolytic therapy 35, 36 pharmacology 410–11 thrombosis coronary in athletes and young adults 1165–6 occlusive Plate 65.20 risk in air travel 1124 see also pulmonary embolism thromboxane A2 induced hypothermia 864 kidney ischemia–reperfusion 306–7 thumpversion see precordial thump thyroid gland 133–4 critical illness response 144–5 thyroid-stimulating hormone (TSH) 144 thyrotropin 133 thyroxine (T4) 133 critical illness response 144 tibia, intraosseous drug administration 619 tidal volume 517–20 in upper airway obstruction 524, 525 time buying (out-of-hospital) 774 elapsed from cardiac arrest 811 defibrillation 475, 830 risk of doing harm 792 Timothy syndrome 73–4, 922, 1169, 1170 tissue plasminogen activator (tPA), recombinant in-hospital 759 drowning victim 1095 out-of-hospital 760 tissue-specific monitoring 711–14 postresuscitation 718 toddlers see infants and toddlers toluene abuse 1030, 1031 tongue, airway obstruction 523, 550 torsades de pointes (TdP) 113, 403 drug-induced 452 long QT syndrome 924, 1172 magnesium sulfate 410 QT interval 403, 404 Tossach, William toxin removal techniques, experimental studies 818–19 see also poisoning trachea Combitube placement in 557 rupture in tracheal intubation 803 tracheal drug administration 400, 621–5, 629 advantages 621 children 623, 951–2 diluent 622–3 historical review 615 intravenous comparisons 626 method of application 621–2 physiology 621 tracheal intubation 5–6, 559–63, 802–3 aids 560–1 alternative ventilation methods following successful intubation 534–5 children 813 vs bag–mask ventilation 559–60 complications/deleterious effects 554, 560, 802–3 early intubation 753–4 confirming correct tube placement 561 drowning victim in hospital 1095 prehospital 1093 pregnant women 1080–1 securing tube 562 status asthmaticus 981 tracheotomy complications 804 training see education and training transcriptional stress response 54–5 transcriptomics 71 transcutaneous procedures/route capnometry (PtcCO2) of skin 711, 712 cardiac pacing 739 drug patches and defibrillator-associated risks 476, 801 transducers, smart 184 transesophageal defibrillation 474 transesophageal echo (TEE), cardiac output measurement 202 transfemoral balloon catheter aortic occlusion 392 transferrin 247 transformer voltage 201 transforming growth factor ␤ (TGF-␤) 167 transfusion, anaphylactic reactions 1107 translation initiation complex 251–3 transmucosal drug absorption see mucosal route transport ventilators 535 transported automatic external defibrillators 484–5 transthoracic defibrillation see defibrillation transthoracic impedance 471–2, 473, 700 hairy chest 472, 797 traumatic injury asphyxia due to 977–8 brain 516, 977 with chest compression 792–6 manual 576, 579, 794 mechanical 585–6 CPR 994–5, 998–9 research on improving outcome 995–8 mountain environment 1131 sudden cardiac death 230 see also burns, electrical; electrical shock; hemorrhagic shock travelers to high-altitude, child/young adults 1123–4 treatment early access 36–7 intervals 39 rapid 36–7 successful for survival 36–7 Index see also resuscitation; specific treatment methods and conditions trekking (high-altitude) 1125–6 triage, electrical shock victims 1143 TribonatR[O] (sodium bicarbonate/THAM/phosphate/acetate mixture) 684, 687–8 tricyclic antidepressant toxicity 1033–4 buffer therapy 688–9 trigeminal (5th cranial) nerve testing 889 triglycerides, serum levels 34 tri-iodothyronine (T3) 133 critical illness response 144 triple airway maneuver 530, 974, 975 foreign body 976 Tris buffer see TribonatR[O]; tromethamine trisomy 21, high-altitude pulmonary edema 1123 trochlear (4th cranial) nerve testing 889 TROICA (Thrombolysis in Cardiac Arrest trial) 761 tromethamine (THAM; Tris buffer) 687 see also TribonatR[O] troponin 428, 430, 435 troponin I 798 tumor necrosis factor ␣ (TNF-␣) 54, 164–5 inflammatory response 171 myocardial dysfunction 166–7, 172 systemic inflammatory response syndrome 313 tumor necrosis factor receptor (TNFR) superfamily 59–60 tyrosine autophosphorylation 262, 263 tyrosine kinase activation 262, 263 U-74389G 840 ultrasound monitoring in CPR 710 see also echocardiography ultrasound Doppler flow meters 202 myocardial bridging 1166 unfolded protein response 94 PERK 255 United Kingdom (UK) ambulance services 502, 503 public access defibrillation 499, 500–3 United States (USA) athletes’ sudden death 1151 elder persons’ visits to emergency department 958 in-hospital rescue team 785 public access defibrillation 496–9 sudden cardiac arrests per year 921 United States Constitution 1231 Universal Cardiac Arrest Algorithm 1283, 1284 urine oxygen tension (PO2) 319 urokinase 759 urticaria 1108 uterus, gravid 1077 chest compression and 1079 incision for cesarean section 1080–1 Utstein-style reporting of in-hospital cardiac arrests in children 938, 939 V1 receptors 132 V2 receptors 133 vaccination, anaphylactic reactions 1107 vagal (10th cranial nerve) reflexes arrest in anesthesia relating to 1052 testing 889–90 vagal tone, pulseless electrical activity 441 validity, external/internal 206–7 Valsalva’s sinus, coronary artery origin 1063, 1163 valvular heart disease 1168–70 vascular access see cannulation vascular capacitance, total 348 vascular collapse see cardiovascular system vascular failure in anesthesia 1050 vascular injury, reperfusion-related 291–2 vascular load optimization 340–1 vascular permeability, brain 862–3 vascular resistance peripheral in hemorrhage 997 pulmonary 517–20 systemic in pregnancy 1077 vasoactive drugs, pediatric 954–5 see also vasodilator therapy; vasopressor therapy vasoactive intestinal peptide (VIP) 139, 150 vasoactive mediators and induced hypothermia 864 vasoconstriction, hypoxic pulmonary 507 vasoconstrictor agents hemorrhage-associated arrest 997 splanchnic circulation 300 vasodilatation hemorrhagic shock 998 therapeutic reversal 998–9 paradoxical to vasopressin 132 vasodilator therapy, postresuscitation 910 vasointestinal peptide (VIP) 139 vasopressin 132–3, 647–59, 671, 735–6, 811, 837 adverse effects 837 animal models 407–8 calcium channel blocker and beta-blocker overdose 1030 cardiac arrest efficacy 407–8 treatment 390–1 clinical studies 408 coronary perfusion pressure 383 CPR 649–59, 811, 837 administration during 308, 309, 310, 383, 390–1 adrenergic vasopressors compared to 642 animal studies 649–50 blood flow 308, 309 children 953 clinical studies 651–5 1335 1336 Index vasopressin (cont.) CPR (cont.) endobronchial 624 limitations 658–60 pulseless electrical activity 735–6 critical illness response 142–3 endogenous concentrations 407 hemorrhagic shock 658–9, 663, 1005 animal studies 996–7 intestinal ischemia–reperfusion 299 meta-analyses 408 osmoregulation function 407 oxygen impairment in visceral organ ischemia 316 pharmacology 406–8, 648–9 physiology 647–8 receptors 406, 648–9 serum levels 133 systematic review 408 visceral organ ischemia 318 see also epinephrine vasopressin analog, oral transmucosal 627 vasopressor agents 405–8 ROSC 397 vasopressor effects catecholamines 513–15 end-tidal CO2 536, 707 vasopressin 648–9 vasopressor therapy 639–66, 811, 837 adrenergic 639–46 adverse effects 734, 837 children 953–4 non-adrenergic 647–66 poisoning 1028 calcium channel blocker and beta-blocker overdose 1030 inhalant abuse 1033 see also named vasopressors; vasoconstrictor agents vasospasm, coronary 1168 vasovagal attacks vs anaphylaxis 1104 velocity meters 199–200 venoms see stings venous acidosis, central 685–6 venous blood gas monitoring in CPR 710 mixed 710, 910 see also central venous blood gas monitoring venous cannulation/catheterization cardiopulmonary bypass 606–7 drug administration 629 central 618–19 endotracheal route compared 626 historical review 614–15 peripheral 615–18 vasopressin animal study 649, 651 electrical injury 1144 large-volume ice-cold intravenous fluid 855–6 venous capacitance 348 venous cardiac pacing 739 venous return, continuous positive airway pressure effects 517 venous temperature probes, cardiopulmonary bypass 605 venous thrombosis risk in air travel 1124 ventilation, assisted/artificial 515–19, 802–5, 810, 904 adjunctive devices 528–9 aero-medical transport 1129 anaphylactic shock 985 anesthesia failure or deficiency causing arrest 1050 asthma severe acute crises 981 bellows method 4, 5–6 cardiocerebral resuscitation 752 children 526, 948 complications 802–5 current standards 528–9 deleterious effects of by EMS personnel 753–4 demotion as a priority intervention 810 drowning victim 1092, 1093, 1095 gasping/agonal 528, 753 hemodynamic effects 361–2 high-altitude illness 1130 high-frequency 527 history 4, 5–9, 506 hypoxia 729–30 monitoring 535–8 postresuscitation 904 pregnant women 1078 resuscitation outcome 517–18 simultaneous compression 586–7 techniques 520–9 trauma and associated hemorrhagic shock 996–7 see also hyperventilation; named modalities; positive pressure ventilation ventilation/perfusion ratio anesthesia-associated mismatch causing arrest 1050 low-flow states 508 ventricles see left ventricular entries; right ventricular entries ventricular assist devices 609 ventricular cardiomyopathy, arrhythmogenic right 1159–61 ventricular dysrhythmias Marfan syndrome 1170 theophylline-induced 1032 ventricular ejection fraction see ejection fraction ventricular fibrillation 14–15 action potential duration 103 amiodarone treatment 669–70 amplitude analysis 420–1 spectrum 422 antiarrhythmic drugs 106 arrhythmogenic right ventricular cardiomyopathy 1161 cardiac blood flow changes 350 cardiomyopathy 110–13 carotid flow 350, 353 commotio cordis 1180, 1181 Index conduction heterogeneity 103 coronary flow 350–2, 353 defibrillation Plate 21.2 success 423 diuretics 105–6 duration estimation of untreated 466–7 ECG 102, 104 electrolyte disturbance 105–6 electrophysiology 101–18 genetic factors 106 hemodynamic changes 348, 349–50 hypothermia-associated accidental 1018, 1019, 1020 induced 866–7 hypotheses 102 idiopathic 1177–8 incidence 725 initiation 102 inward rectifier potassium current 104 ion channels 103–4 ischemia 106–10 lidocaine use 670 magnesium intravenous therapy 670 maintenance 102 metabolic disturbance 105–6 mobile coronary care unit 18–19 myocardial stunning 285 myocardial substrate 106 modulation 105 neurologic injury comparison 973–4 normal heart 113–14 pathogenesis 109–10 pediatric 488–9 out-of-hospital 942–3 possible underestimated frequency 486 postshock reinitiation 114 power 422 prevention 115–16 public access defibrillation in England 501, 502 Purkinje network 109 recurrence risk 116 reperfusion-induced 107 repolarization 103 short QT syndrome 1174 spiral wave breakup 109 theophylline-induced 1032 therapy 115 three (resuscitation) phases following 466, 748 trigger identification/ablation 116 vasopressin use 651–2, 654, 655 ventilation effects 511–13 see also defibrillation; waveforms, ventricular ventricular hypertrophy, sudden cardiac death 105, 449–50 ventricular outflow tract tachycardia, right 1176 ventricular preload, excessive assisted ventilation impairing 515–16 ventricular septal myotomy–myectomy 1159 ventricular tachycardia/tachyarrhythmia 109 amiodarone 669 arrhythmogenic right ventricular cardiomyopathy 1161 athletes and medicolegal implications 1187 magnesium (intravenous) 670 pediatric 943 public access defibrillation in England 501, 502 re-entrant 233 right ventricular outflow tract origin 1176 short QT syndrome 1174 see also catecholaminergic polymorphic ventricular tachycardia (CPVT) ventricular waveforms see waveforms verbal response in Glasgow coma scale, postresuscitation patient 888 Vesalius, Andreas Vesalius technique 5–6 vest CPR 332, 336, 342, 381–2, 591–3 non-fibrillatory cardiac arrest 738–9 vestibulocochlear (8th cranial) nerve testing 889 vestibulo-ocular response 889 viral myocarditis 1178 virtual electrode polarization hypothesis 117 visceral organ ischemia–reperfusion 298–320 antioxidant therapies 314, 315 CPR 308–10 damage from cardiac arrest 310–13 extracorporeal therapy 318 free radical injury prevention 314–15 gastrointestinal intramucosal pH monitoring 319–20 gut decontamination 318 hemodilution 317–18 hormonal response alteration 318 hyperbaric oxygen therapy 317 hypothermia 317 inflammatory mediator injury prevention 314–15 intra-aortic balloon pumping 317 monitoring 319 multisystem organ dysfunction 313–14 neural–humoral response alteration 318 organ systems 298–307 oxygen delivery/consumption 315–16, 317 pulmonary artery catheter monitoring 319 systemic inflammatory response syndrome 313–14 treatment 314 volatile anesthetics in status asthmaticus 979 volatile substance abuse 1032–3 Volta, Alessandro 13 vomit aspiration by drowning victim 1092–3 water brain concentration 238 1337 1338 Index water (cont.) diluent in endotracheal drug administration 623 drowning victim aspiration of water 1090–1 rescue and basic life support 1091–2 water bath system, cardiopulmonary bypass 605 waveforms, ventricular 715–17 amplitude 420–1 analysis 417–24, 715–17 chaos theory 419 data acquisition/preprocessing 417–18 description 420, 422 structuring 419–20 defibrillation 473–5, 715–16 myocardial damage risk 836 pediatric 487 fibrillation 471, 715–17 filtering techniques 417–18 Fourier transforms 419–20 fractal dimension 419 frequency representation 419–20 frequency/spectral analysis 421–2 non-linear dynamics 419, 422–3 predictive value 417–24 scaling exponent method 423 signal amplitude behavior 419 time–frequency domain techniques 418–19 time–frequency representation 419–20 wavelet transforms 420, 421, 422 see also biphasic (truncated exponential) waveforms for defibrillation; monophasic (damped sinusoidal) waveforms for defibrillation wedges, resuscitation in pregnancy 1079, 1080 withdrawal of care 896–7 decision-making 788–9 witnessing of cardiac arrest, survival 37 Wolff–Parkinson–White syndrome 930–3, 1175 women, defibrillator electrodes 473 World Congress on Drowning (2002), Brain Resuscitation Task Force 1095, 1097 wound dressings, procoagulant-impregnated 999 wound infection and induced hypothermia 869 written directions 1202, 1229–30 xanthine oxidase 53–4 intestinal ischemia–reperfusion 300–1 kidney ischemia–reperfusion 306 liver ischemia–reperfusion 304 xanthine oxidase inhibitors in hemorrhagic shock 1003 X-ray, chest, pulmonary edema 1121 young adults see adolescents and young adults Zoll, Paul 16–17 Zoll medical systems automated external defibrillators 487 ... during cardiac resuscitation include the duration of cardiac arrest, the delivery of electrical shocks, and the use of adrenergic vasopressor agents Efforts to shorten the duration of the cardiac arrest. .. 1999; 27 : 21 37 21 41 22 Peberdy, M.A., Kaye, W., Ornato, J.P et al Cardiopulmonary resuscitation of adults in the hospital: a report of 14, 720 cardiac arrests from the National Registry of Cardiopulmonary... 24 Brain Resuscitation Clinical Trial Study Group A randomized clinical study of calcium-entry blocker in the treatment of 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 comatose survivors of