4 results
55 - Asphyxial cardiac arrest
- from Part VI - Special resuscitation circumstances
-
- By Peter Safar, University of Colorado Health Sciences Center, Norman A. Paradis, University of Colorado Health Sciences Center, Max Harry Weil, Weil Institute of Critical Care Medicine
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
-
- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 969-993
-
- Chapter
- Export citation
-
Summary
There is no malice in this burning coal;
The breath of heaven has blown his spirit out …
But with my breath I can revive it, …
William ShakespeareAlthough asphyxia literally means no pulse (in Greek), it represents an inability to breathe and therefore suffocation. Failure of gas exchange is characterized by hypoxemia and hypercarbia, as originally defined by J.B.S. Haldane. A mechanistic classification of asphyxia (Table 55.1) includes a diversity of pathophysiological processes that preclude movement of gas from the upper airway to the alveoli and ultimately to the tissues, the cells, and then to the mitochondria, thereby sustaining oxidative metabolism in vital organs.
Asphyxia is a cause of sudden death, but in contrast to primary cardiac causes, it more often presents with bradycardia and asystole rather than ventricular fibrillation (VF). In children, normothermic cardiac arrest is predominantly due to asphyxia. Asphyxia is also the predominant mechanism of cardiac arrest in neonates and in infants due to the so-called sudden infant death syndrome, Status asthmaticus is an important cause of asphyxia. The most frequent cause is failure of respiratory muscle function. Outcomes are worsewhenVF evolves during asphyxial cardiac arrest than after primary VF in adults.
Anoxia or hypoxia is defined by critical reductions in arterial oxygen saturation (SaO2) or arterial oxygen tension (PaO2). Hypercarbia is defined by increases in arterial carbon dioxide tension (PaCO2) in settings of inadequate alveolar ventilation and usually in association with hypoxia.
48 - Prevention and therapy of postresuscitation myocardial dysfunction
- from Part V - Postresuscitation disease and its care
-
- By Raúl J. Gazmuri, North Chicago VA Medical Center, IL, USA, Max Harry Weil, Rancho Springs, CA, Karl B. Kern, Tucson, AZ, Wanchun Tang, Palm Springs, CA, Iyad M. Ayoub, North Chicago, IL, Julieta Kolarova, North Chicago, IL, Jeejabai Radhakrishnan, North Chicago, IL
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
-
- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 829-847
-
- Chapter
- Export citation
-
Summary
Introduction
It is estimated that between 400 000 and 460 000 individuals suffer an episode of sudden cardiac arrest every year in the United States. Yet, the percentage of individuals who are successfully resuscitated and leave the hospital alive with intact neurological function averages less than 10% nationwide. Efforts to restore life successfully are formidably challenging. They require not only that cardiac activity be initially restored but that injury to vital organs be prevented or minimized. A closer examination of resuscitation statistics reveals that efficient Emergency Medical Services systems are able to re-establish cardiac activity in 30% to 40% of sudden cardiac arrest victims at the scene. Yet, close to 40% die before admission to a hospital presumably from recurrent cardiac arrest or complications during transport. Of those admitted to the hospital nearly 60% succumb before discharge, such that only one in four initially resuscitated victims leaves the hospital alive.
Although the causes of postresuscitation deaths have not been systematically investigated, the available information suggests that postresuscitation myocardial dysfunction, hypoxic brain damage, systemic inflammatory responses, intercurrent illnesses, or a combination thereof are the main culprits. The core pathogenic process driving such poor outcome is the intense ischemia of variable duration that organs suffer after cessation of blood flow and the subsequent reperfusion injury that accompanies the resuscitation effort. In addition, the precipitating event of cardiac arrest may also play a role in the postresuscitation phase.
46 - Bringing it all together: state-of-the-art therapy for cardiac arrest
- from Part IV - Therapy of sudden death
-
- By Max Harry Weil, Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA, Wanchun Tang, Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
-
- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 809-814
-
- Chapter
- Export citation
-
Summary
Introduction
The history of CPR is in part documented in the Old Testament, but the science of CPR is but a half century old and is still emerging from its infancy. Accordingly, it is not unexpected and certainly not shameful that as the science of resuscitation goes forward, we must sometimes retreat as often as we advance. Yet, that is indeed progress and inevitably the path that is characteristic of meaningful achievements in science and medicine.
Airway techniques and devices
One size does not fit all
The vast majority of sudden deaths in children and, indeed, in victims under the age of 40 years are attributable to failure of ventilation. Accordingly, either mechanical obstruction by foreign body, laryngospasm, or laryngeal edema, or bronchoconstriction, constrains air exchange. Neuromuscular or skeletal injury, including intrathoracic crises such as pneumothorax, may account for death, though typically not sudden death. It is in these settings that the priority is establishment and maintenance of a patent airway and external ventilation. Since a majority of the foreign bodies that are swallowed by children and adults lodge in the posterior pharynx, the rescuer is the person best prepared to remove these promptly. Hence, the traditional (A) of the ABC survives, especially for children and young adults and in settings of witnessed cardiac arrest when respiratory distress with paradoxical chest and abdominal movements and especially stridor precedes loss of consciousness.
There has been an appropriate re-examination of the role of routine endotracheal intubation during CPR, whether in the field or in the hospital.
34 - Adrenergic agonists
- from Part IV - Therapy of sudden death
-
- By Max Harry Weil, Weil Institute of Critical Care Medicine, Rancho Mirage, CA and Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA, Shijie Sun, Weil Institute of Critical Care Medicine, Rancho Mirage, CA and Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA, Wanchun Tang, Weil Institute of Critical Care Medicine, Rancho Mirage, CA and Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA
- Edited by Norman A. Paradis, University of Colorado, Denver, Henry R. Halperin, The Johns Hopkins University School of Medicine, Karl B. Kern, University of Arizona, Volker Wenzel, Douglas A. Chamberlain, Cardiff University
-
- Book:
- Cardiac Arrest
- Published online:
- 06 January 2010
- Print publication:
- 18 October 2007, pp 639-646
-
- Chapter
- Export citation
-
Summary
Introduction
Although there is persuasive evidence that the administration of adrenaline during CPR favors the success of electrical defibrillation as well as the return of pulsatile rhythm, its more ultimate benefit on survival is unproven. To the contrary, the more recent discovery of reversible myocardial dysfunction after successful resuscitation from cardiac arrest initially in experimental models and subsequently in human patients led to a re-examination of its role. Although there is only indirect evidence that impaired myocardial function accounts for early death, the high correlation between the severity of myocardial impairment and decreased survival supports this assumption. Accordingly, postresuscitation myocardial dysfunction may therefore explain, at least in part, the high fatality rate within the initial 72 hours after successful resuscitation from cardiac arrest such that fewer than 5% of victims recover to be discharged from the hospital without major impairment.
The immediate effort during CPR is to restore blood flows to sustain the functions of vital organs, and most especially, to the heart and the brain prior to successful restoration of spontaneous circulation. Blood flow to the vital organs during CPR is contingent primarily on the cardiac output generated by precordial or direct cardiac compression and by the resistance in the systemic arterial bed. Yet the cardiac output that is generated by precordial compression represents only approximately 25% to 30% of normal values. Vasopressor drugs increase arterial and arteriolar vasoconstriction, and thereby produce increases in aortic diastolic pressure.