Book contents
- Frontmatter
- Contents
- List of contributors
- Foreword
- Preface
- Part I Introduction
- Part II Basic science
- Part III The pathophysiology of global ischemia and reperfusion
- Part IV Therapy of sudden death
- 23 Prevention of sudden cardiac death
- 24 Sequence of therapies during resuscitation: application of CPR
- 25 Transthoracic defibrillation
- 26 Automated external defibrillators
- 27 Public access defibrillation
- 28 The physiology of ventilation during cardiac arrest and other low blood flow states
- 29 Airway techniques and airway devices
- 30 Manual cardiopulmonary resuscitation techniques
- 31 Mechanical devices for cardiopulmonary resuscitation
- 32 Invasive reperfusion techniques
- 33 Routes of drug administration
- 34 Adrenergic agonists
- 35 Vasopressin and other non-adrenergic vasopressors
- 36 Antiarrhythmic therapy during cardiac arrest and resuscitation
- 37 Acid–base considerations and buffer therapy
- 38 Cardiac arrest resuscitation monitoring
- 39 Special considerations in the therapy of non-fibrillatory cardiac arrest
- 40 Cardiocerebral resuscitation: a new approach to out-of-hospital cardiac arrest
- 41 Thrombolysis during resuscitation from cardiac arrest
- 42 Percutaneous coronary intervention (PCI) after successful reestablishment of spontaneous circulation and during cardiopulmonary resuscitation
- 43 Emergency medical services systems and out-of-hospital cardiac arrest
- 44 In-hospital resuscitation
- 45 Complications of CPR
- 46 Bringing it all together: state-of-the-art therapy for cardiac arrest
- Part V Postresuscitation disease and its care
- Part VI Special resuscitation circumstances
- Part VII Special issues in resuscitation
- Index
38 - Cardiac arrest resuscitation monitoring
from Part IV - Therapy of sudden death
Published online by Cambridge University Press: 06 January 2010
- Frontmatter
- Contents
- List of contributors
- Foreword
- Preface
- Part I Introduction
- Part II Basic science
- Part III The pathophysiology of global ischemia and reperfusion
- Part IV Therapy of sudden death
- 23 Prevention of sudden cardiac death
- 24 Sequence of therapies during resuscitation: application of CPR
- 25 Transthoracic defibrillation
- 26 Automated external defibrillators
- 27 Public access defibrillation
- 28 The physiology of ventilation during cardiac arrest and other low blood flow states
- 29 Airway techniques and airway devices
- 30 Manual cardiopulmonary resuscitation techniques
- 31 Mechanical devices for cardiopulmonary resuscitation
- 32 Invasive reperfusion techniques
- 33 Routes of drug administration
- 34 Adrenergic agonists
- 35 Vasopressin and other non-adrenergic vasopressors
- 36 Antiarrhythmic therapy during cardiac arrest and resuscitation
- 37 Acid–base considerations and buffer therapy
- 38 Cardiac arrest resuscitation monitoring
- 39 Special considerations in the therapy of non-fibrillatory cardiac arrest
- 40 Cardiocerebral resuscitation: a new approach to out-of-hospital cardiac arrest
- 41 Thrombolysis during resuscitation from cardiac arrest
- 42 Percutaneous coronary intervention (PCI) after successful reestablishment of spontaneous circulation and during cardiopulmonary resuscitation
- 43 Emergency medical services systems and out-of-hospital cardiac arrest
- 44 In-hospital resuscitation
- 45 Complications of CPR
- 46 Bringing it all together: state-of-the-art therapy for cardiac arrest
- Part V Postresuscitation disease and its care
- Part VI Special resuscitation circumstances
- Part VII Special issues in resuscitation
- Index
Summary
Introduction
Shock is a complex entity traditionally defined as a state in which the oxygen utilization or consumption needs of tissues are not matched by sufficient delivery of oxygen. This mismatch commonly results from states of altered tissue perfusion. From this perspective, cardiopulmonary arrest represents the most extreme of shock states.
Figure 38.1 represents the basic relationship between oxygen consumption (VO2) and oxygen delivery (DO2) that is pertinent to individual organs as well as to the whole body. VO2 can remain constant over a wide range of DO2, because most tissue beds are capable of efficiently increasing the extraction of oxygen. This will be reflected by decreasing venous oxygen saturation from each organ. When DO2 reaches a critical threshold, however, tissue extraction of oxygen cannot be further increased to meet tissue demands. At this point VO2 becomes directly dependent on DO2 (DO2crit) and cells begin to convert to anaerobic metabolism, as manifested by increases in certain metabolic products such as lactate, NADH, and reduced cytochrome oxidase. The point of DO2crit is the point of dysoxia or ischemia at which tissue DO2 cannot meet tissue oxygen demand. Oxygen debt can be defined as the amount of cumulative difference of VO2 between baseline and that spent below DO2crit. As discussed later, the level of accumulated oxygen debt in shock states is critically linked with survival.
Several unique physiologic aspects and principles of cardiac arrest and CPR exist that limit the usefulness of many monitoring modalities, some of which will be more useful in the postresuscitation period. These include the following.
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- Cardiac ArrestThe Science and Practice of Resuscitation Medicine, pp. 698 - 724Publisher: Cambridge University PressPrint publication year: 2007