Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
« Previous Article | Table of Contents | Next Article »
Circulation. 2000;102:I-105-I-111

This Article
Right arrow Extract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Related Collections
Right arrow AHA Statements and Guidelines

(Circulation. 2000;102:I-105.)
© 2000 American Heart Association, Inc.

ECC Guidelines

Part 6: Advanced Cardiovascular Life Support

Section 4: Devices to Assist Circulation


*    Alternative CPR Techniques
up arrowTop
 *Alternative CPR Techniques
down arrowAssessment of CPR
 down arrowAssessment of Hemodynamics
 down arrowAssessment of Respiratory Gases
 down arrowAssessment of Chest Compression
 down arrowReferences
 
Alternative techniques to standard manual CPR have been developed to improve perfusion during CPR. These include interposed abdominal compression (IAC) CPR, high-frequency CPR, active compression-decompression (ACD) CPR, vest CPR, mechanical (piston) CPR, simultaneous ventilation-compression (SVC) CPR, phased thoracic-abdominal compression-decompression (PTACD) CPR, and invasive CPR. Each of these approaches has been evaluated initially in animal models and then in patients. For some the data is sufficient to recommend them as alternatives to standard CPR in specific clinical settings as described below.

Compared with standard CPR, CPR adjuncts generally require additional personnel, training, or equipment. The added effort may increase forward blood flow during CPR from 20% to 100%—levels that are still significantly less than normal cardiac output. Maximum benefits are reported when adjuncts are begun early in the treatment of cardiac arrest,1 so their use is often limited to in-hospital settings. Adjunctive techniques produce little benefit when started late in a prolonged resuscitative effort or when performed as a last-ditch measure after failed ACLS.2 3 4 To date no adjunct has been shown to be universally superior to standard manual CPR for prehospital BLS.

IAC-CPR
IAC-CPR includes manual compression of the abdomen by an extra rescuer during the relaxation phase of chest compression.5 6 7 8 9 10 The abdominal compression point is located in the midline, halfway between the xiphoid process and the umbilicus (FigureDown). The recommended force of abdominal compression should be sufficient to generate approximately 100 mm Hg external pressure on the abdominal aorta and vena cava and is equivalent to that required to optimally palpate the aortic pulse when the heart is beating normally.11 12 13



View larger version (106K):
[in this window]
[in a new window]
  		Figure 1. IAC-CPR. In practice it is more convenient when chest and abdominal compressions are performed from opposite sides of the victim.

Two randomized clinical trials of IAC-CPR for in-hospital cardiac arrest have shown statistically significant improvement in outcome measures.14 Results of the first trial found improved return of spontaneous circulation (ROSC), 24-hour survival, and hospital discharge in 48 of 103 patients randomly assigned to IAC-CPR. Results of the second trial also found improved ROSC and 24-hour survival with IAC-CPR, although none of the patients with an initial rhythm of asystole or pulseless electrical activity survived to hospital discharge. Pooled data from these 2 randomized in-hospital studies shows a difference in 24-hour survival of 33% versus 13%. One smaller trial randomly assigned patients on arrival at the emergency department. If spontaneous circulation could not be successfully restored within 20 minutes, patients were assigned to the other therapy, with each patient acting as his or her own control. Mean end-tidal PCO2 was 17.1 mm Hg during IAC-CPR versus 9.6 mm Hg during standard CPR. Six of 16 patients were resuscitated before crossover with IAC-CPR versus 3 of 17 with standard CPR (P=0.19).10 One randomized trial of prehospital IAC-CPR showed no difference in outcome or complications.7 In this study, however, most patients randomly assigned to IAC-CPR received both standard CPR and IAC-CPR during at least some of the resuscitative attempt.

Analysis of all available data for both prehospital and in-hospital resuscitations shows improvement in ROSC with IAC-CPR compared with standard CPR. When only in-hospital studies are examined, the effect of IAC becomes much greater. Data from 2 studies that examined long-term, neurologically intact survival following in-hospital resuscitations shows a positive benefit of IAC-CPR compared with standard CPR. This clinical data is consistent with a series of theoretical and animal studies documenting the "abdominal pump" mechanism for hemodynamic augmentation.15 16

The safety of IAC has been reviewed.17 Increased emesis and aspiration from IAC have not been reported. In fact, there is evidence that positive abdominal pressure applied during ventilations from the beginning of an arrest reduces the rate of gastric inflation before tracheal intubation.18

In summary, randomized clinical studies have demonstrated improved outcome when IAC-CPR was compared with standard CPR for in-hospital resuscitation, but no survival benefit for out-of-hospital arrest has been shown.19 CPR-induced injuries do not appear to be more common with IAC-CPR than with standard CPR. Because of the positive hemodynamic advantages, safety record, and encouraging in-hospital results, the use of IAC-CPR for in-hospital resuscitations is recommended as an alternative intervention to standard CPR whenever sufficient personnel trained in the technique are available (Class IIb). The safety and efficacy of IAC-CPR has not been studied in patients with aortic aneurysms, pregnancy, or recent abdominal surgery.

High-Frequency ("Rapid Compression Rate") CPR
High-frequency (>100 compressions per minute) manual CPR has been advocated as a technique for improving resuscitation from cardiac arrest.20 21 22 23 Studies in some, but not all, laboratories have shown that rapid compression rates improve cardiac output, aortic and myocardial perfusion pressures, coronary blood flow, and 24-hour survival compared with standard CPR.20 21 Clinical studies on the use of high-frequency CPR are limited. There is evidence for improved hemodynamics with manual but not mechanical rapid chest compression rates in patients.22 23 24 Thus, high-frequency CPR shows some promise for improving CPR. Outcome studies in humans are needed to determine the efficacy of this technique in the management of patients in cardiac arrest (Class Indeterminate).

ACD-CPR
ACD-CPR is another technique developed to improve the efficiency of CPR.16 25 26 27 28 29 30 31 32 33 34 35 Decreasing intrathoracic pressure during the decompression phase of CPR is thought to enhance venous return and thereby "prime the pump" for the next compression. ACD-CPR is performed with a hand-held device equipped with a suction cup to actively lift the anterior chest during decompression. Early laboratory and clinical data showed that acute hemodynamic parameters such as arterial blood pressure and vital organ perfusion are superior with use of ACD-CPR compared with standard CPR.36 37 38 39 40 Clinical outcome data is less consistent and suggests that technique and training are critical. The most promising results are from Paris, France, where 1-year survival rates increased from 2% (7 of 377 patients) to 5% (17 of 373 patients) with the use of ACD-CPR.41 A number of clinical studies, however, have found no significant benefit from the use of ACD-CPR.42 43 44 45 Factors associated with clinical improvement with ACD-CPR include rigorous and repetitive training, concurrent use of low- rather than high-dose epinephrine,35 use of the force gauge, and performance of CPR for a duration sufficient to prime the pump.

There is some concern that the extra force and energy applied to the chest wall during ACD-CPR tends to induce a higher incidence of rib fractures than that which occurs during standard CPR.46 47 One case report describes massive cardiac injury in an area of myocardial infarction with pericardial tamponade.48 In women with large breasts, the presence of a deeper sternum may cause greater force to be transmitted to the lateral rims of the ACD device, enhancing the likelihood of rib fracture.49 Design improvements, such as the inclusion of cushions, may well eliminate this problem, which should not be considered fundamental. Other published concerns include difficulties with application of the technique and increased energy expenditure by rescuers.

In summary, laboratory and clinical studies to date have demonstrated that there is often measurable improvement in resuscitation hemodynamics with ACD-CPR compared with standard CPR. Clinical long-term results with ACD-CPR have been favorable (4 studies)26 28 30 50 or at least neutral (4 studies)32 51 52 53 compared with standard CPR. Complications of ACD are noteworthy but not of major concern. ACD-CPR is considered an acceptable alternative to standard CPR when rescue personnel adequately trained in use of the device are available (Class IIb).

(Note: In hearings conducted several years ago the FDA concluded that the evidence did not support the labeling information included with the device. On that basis the FDA did not approve the device for sale and distribution. This conclusion does not conflict with the International Guidelines 2000 recommendations noted above: not proved effective in the out-of-hospital setting; acceptable but weak data supports in-hospital use—Class IIb.)

Vest CPR
The CPR vest was an earlier attempt to take advantage of the thoracic pump mechanism of blood flow.24 54 55 56 57 58 59 Vest CPR uses a circumferential thoracic vest, analogous to a large blood pressure cuff, that is cyclically inflated and deflated, vest CPR produces increases in intrathoracic pressure. Vest CPR has shown improved myocardial and cerebral blood flow in animals and improved peak aortic and coronary perfusion pressures during CPR in animals and humans.60 61 A preliminary report of vest CPR did find improved 6-hour survival but not 24-hour survival.62 Large randomized trials have not been completed. One such trial was unfortunately interrupted secondary to a lack of continued funding.63

There is no evidence of increased resuscitation trauma with vest CPR. The present size and energy requirements for operation of the device continue to be substantial barriers for its widespread use. The size and weight of the device require that it be used for patients who can readily undergo vest CPR without substantial delay in either the hospital or emergency vehicle settings. Long-term survival studies of this approach are needed.

Vest CPR may be considered an alternative to standard CPR in-hospital or during ambulance transport, because vest CPR (1) shows hemodynamic improvement in animal and clinical studies, (2) does not substantially delay starting CPR, (3) presents no significant known disadvantages, (4) has been assessed for hemodynamic effect in patients in cardiac arrest, and (5) does not interfere with defibrillation efforts. Vest CPR should be used only when there are an adequate number of well-trained, in-hospital personnel to properly perform CPR (Class IIb). The manufacturer of the vest-CPR device has not yet sought and obtained FDA permission for its distribution and sale.

Mechanical (Piston) CPR
Mechanical devices that depress the sternum are not a substitute for manual external chest compression but rather an adjunct to be used by trained personnel to optimize compression and reduce rescuer fatigue in prolonged resuscitative efforts.64 The efficacy and safety of these devices have not been demonstrated in infants and children; their use should be limited to adults. A disadvantage of any mechanical chest compression device is the potential for interrupting chest compressions for extended periods while setting up and initiating compressions. Mechanical chest compressors can be manual or automatic.

Simple, manually operated mechanical chest compressors can provide effective external chest compressions. Automatic mechanical chest compressors such as the Mechanical Thumper consist of a compressed gas-powered plunger mounted on a backboard. The devices can be programmed to deliver standard CPR in a compression-ventilation ratio of 5:1, with a compression duration that is 50% of the cycle length, or other ratios. Most animal and clinical studies have shown variable hemodynamic results compared with other CPR techniques (standard, ACD, and SVC CPR).57 65 Results of the 2 most recent clinical trials both showed improved expired end-tidal CO2 compared with standard manual CPR.66 The limited clinical data has thus far shown no improvement in survival outcome when mechanical CPR was compared with standard CPR in patients with cardiac arrest.

An advantage of the mechanical devices is delivery of a consistent rate and depth of compression by eliminating such variables as operator technique and fatigue. Problems related to the use of automatic mechanical chest compressors, however, include sternal fracture, expense, size, weight, restrictions on mobility, and dislocation of the plunger in relation to the sternum. Ventilation or chest compression, or both, may be inadequate when these devices are improperly positioned or operated. In addition, the weight of the compressor on the chest may limit chest wall recoil and venous return during decompression, especially after one or more rib fractures have occurred. There is no consistent measurable improvement in hemodynamics and no observed survival outcome data showing that mechanical resuscitators similar to mechanical chest compressors are superior to standard CPR. The mechanical resuscitator is an acceptable alternative to standard manual CPR in circumstances that make manual chest compressions difficult, ie, certain transport situations or lack of adequate personnel (Class IIb).

Simultaneous Ventilation-Compression CPR
The technique of SVC-CPR was conceived to take advantage of the entire thorax as a pump in producing blood flow during cardiac arrest.24 55 57 67 68 69 70 71 72 Pressure gradients are developed between intrathoracic and extrathoracic vascular beds. Studies in experimental models showed that SVC-CPR resulted in improved peak compression ("systolic") pressures and carotid artery blood flows.67 68 69 On the basis of these studies, a mechanical CPR device that provides simultaneous ventilation and chest compression was developed and tested clinically. Laboratory studies showed improvement in short-term survival when SVC-CPR was compared with standard CPR in some laboratories55 73 but not others.57 71 Clinical studies have failed to identify any benefits of SVC-CPR. Instead the studies show standard CPR to be superior to SVC-CPR in hemodynamics24 72 and survival. SVC-CPR is not currently available for clinical use.

Phased Thoracic-Abdominal Compression-Decompression CPR
PTACD-CPR uses a hand-held device that alternates chest compression and abdominal decompression with chest decompression and abdominal compression. This innovative technique basically combines the concepts of IAC-CPR and ACD-CPR. Theoretically the combined 4-phase approach, including both compression and decompression of the chest and abdomen, could increase blood flow during cardiac arrest and CPR.16

The use of PTACD-CPR has led to hemodynamic improvement in animal and clinical studies.74 75 PTACD-CPR does not substantially delay starting CPR and presents no significant known disadvantages or harm when used correctly. No clinical outcome data is available, and the device is not yet approved by the FDA (Class Indeterminate).

Other Adjunctive CPR Devices
Several mechanical devices have been developed as adjuncts to CPR. These devices do not replace basic CPR but rather are additions to the ongoing resuscitative effort. They can be combined with a variety of CPR techniques, eg, standard CPR, IAC-CPR, ACD-CPR, vest CPR, and mechanical CPR. Such adjunctive CPR devices can be recommended only after they have been shown to improve the efficacy of CPR in patients in cardiac arrest (hemodynamic changes are equal or better) and to have no significant increase in complications compared with standard manual CPR.

Impedance Threshold Valve
The impedance threshold valve (ITV, or ResQ-Valve) is associated with lower intrathoracic pressure.76 77 When used with a compression/decompression device, the valve is inserted into a standard tracheal tube ventilation circuit and does not disrupt CPR performance. The airway must be secured with a cuffed tracheal tube. By preventing inspiration during chest decompression, the impedance threshold valve produces more negative intrathoracic pressure, enhancing blood return to the thorax.

The impedance threshold valve (ResQ-Valve) is not intended for use with standard CPR. Future clinical studies may indicate efficacy of the impedance valve during standard CPR, but no recommendation can now be made for this device as an adjunct for standard CPR (Class Indeterminate). Observations from 2 animal studies and 1 small (n=11) human trial77A showed significant improvements in hemodynamic parameters when this device was used as an adjunct to ACD-CPR. Despite better hemodynamics, no improvement in short- or long-term outcome occurred, and no complications were noted in the 11 study patients. The impedance threshold valve is acceptable as an adjunct to be used with a cardiac compression/decompression device to augment hemodynamic parameters (Class IIb).

Invasive CPR
Direct cardiac compression is a special technique that may provide near-normal perfusion of the brain and heart.3 4 78 79 80 Experimental studies have shown that direct cardiac massage used early in cardiac arrest after a short period of ineffective closed-chest CPR can improve survival from cardiac arrest.81 Limited clinical series have shown similar beneficial hemodynamic effects with open-chest massage. Experimental and clinical studies have shown that direct cardiac massage does not improve outcome when applied late (after >25 minutes of total arrest time) in the treatment of patients in cardiac arrest.3 4 One prospective, nonrandomized, historically controlled series, however, did show improved ROSC with the use of open-chest direct cardiac massage.82

In the emergency thoracotomy, open-chest cardiac massage is, by necessity, associated with some morbidity. An experienced team is needed to successfully perform this technique and optimally care for the patient afterward. We do not recommend its routine use for cardiac arrest victims. In particular, it should not be used as a last effort at the end of a lengthy resuscitation treatment sequence. Outcome studies assessing the use of open-chest direct cardiac massage early in the cardiac arrest treatment sequence are needed.

Specific indications for the use of open-chest direct cardiac compression in the clinical setting are changing. Previous recommendations included cardiac arrest from nonpenetrating, blunt trauma. Blunt abdominal trauma associated with cardiac arrest does not respond to invasive resuscitative efforts and should not be considered an indication. A thoracotomy is indicated for patients with penetrating chest trauma who develop cardiac arrest. Other clinical circumstances in which a thoracotomy could be considered include (1) cardiac arrest caused by hypothermia, pulmonary embolism, or pericardial tamponade; (2) chest deformity where closed-chest CPR is ineffective; and (3) penetrating abdominal trauma with deterioration and cardiac arrest. The use of open-chest direct cardiac massage can be considered under special circumstances but should not be done simply as a late last-ditch effort (Class IIb).

Emergency cardiopulmonary bypass has been advocated as a circulatory adjunct for treatment of patients in cardiac arrest.83 84 85 The bypass pump can be applied by using the femoral artery and vein without requiring a thoracotomy. Experimental studies have shown improved hemodynamics and survival when cardiopulmonary bypass is used after prolonged cardiac arrest.83 84 Clinical studies have shown the feasibility of cardiopulmonary bypass in the treatment of patients in cardiac arrest from specific, potentially reversible causes (such as drug overdoses and poisonings).84 No outcome studies of significance have been done to date. Further clinical studies are needed to define the role of cardiopulmonary bypass in the treatment of patients in cardiac arrest (Class Indeterminate). Its success in the special situations of drug overdoses and hypothermic arrest may be sufficient justification alone for its use in specific hospital settings.


*    Assessment of CPR
up arrowTop
 up arrowAlternative CPR Techniques
 *Assessment of CPR
down arrowAssessment of Hemodynamics
 down arrowAssessment of Respiratory Gases
 down arrowAssessment of Chest Compression
 down arrowReferences
 
At present there are no good prognostic criteria that clinicians can use to assess the efficacy of CPR. Clinical outcome—either resuscitation or death—is often the only way to judge the adequacy of CPR efforts. Assessment of ongoing CPR efforts would allow clinicians to modify resuscitative efforts and individualize treatment protocols for patients in cardiac arrest. Ideally clinicians could judge the value of specific adjuncts in individual patients. If a less-than-optimal response were documented, a new strategy could be attempted and individualized, depending on such real-time feedback during the resuscitative effort. Several adjuncts may be useful in the assessment of ongoing CPR efforts.


*    Assessment of Hemodynamics
up arrowTop
 up arrowAlternative CPR Techniques
 up arrowAssessment of CPR
 *Assessment of Hemodynamics
down arrowAssessment of Respiratory Gases
 down arrowAssessment of Chest Compression
 down arrowReferences
 
Perfusion pressures. Studies in experimental models have repeatedly shown the importance of the aortic diastolic and myocardial perfusion (aortic-to–right atrial diastolic gradient) pressures during CPR for successful resuscitation from cardiac arrest.86 87 88 89 90 91 92 The aortic diastolic and myocardial perfusion pressures have been correlated with coronary blood flow during CPR.93 Much CPR research has focused on drugs or adjuncts that improve these pressures. Although the placement of arterial and central venous lines during resuscitative efforts has been accomplished by a resuscitation research team in some settings, placement of these lines is impractical in most clinical settings.86 94 When arterial lines are available, the clinician should attempt to optimize the aortic diastolic and myocardial perfusion pressures during the resuscitative effort.

Pulses. Clinicians frequently use the presence or absence of pulses resulting from chest compressions during the resuscitative effort to assess the adequacy of artificial perfusion during CPR. The presence of pulses does not indicate any meaningful arterial blood flow during CPR. No studies have shown the clinical utility of checking pulses during ongoing CPR. A palpable pulse represents the difference between the peak pressure and nadir pressure within a vascular bed. The important factor for perfusion of the myocardium is coronary perfusion pressure (aortic minus right atrial pressure during the relaxation phase of chest compressions). The difference in peak and nadir pressures does not correlate with perfusion. It is important to remember that because there are no valves in the inferior vena cava, retrograde blood flow may occur in the femoral vein. Palpation of a pulse in the femoral area may be misleading and may indicate venous rather than arterial blood flow. In summary, the presence of carotid pulses during CPR may indicate the presence of a pulse wave and perhaps some forward blood flow, but it cannot be used to gauge the efficacy of myocardial or cerebral perfusion from ongoing CPR efforts.


*    Assessment of Respiratory Gases
up arrowTop
 up arrowAlternative CPR Techniques
 up arrowAssessment of CPR
 up arrowAssessment of Hemodynamics
 *Assessment of Respiratory Gases
down arrowAssessment of Chest Compression
 down arrowReferences
 
Some clinicians use arterial blood gases to gauge the efficacy of ongoing CPR efforts. Adequate oxygen concentration in arterial blood during low-flow states may not imply adequate oxygen delivery to the peripheral tissue beds. Physiologically, arterial blood gases do not reflect tissue pH and PCO2. Mixed venous gases often show severe hypercarbia despite normal arterial gases.95 No correlation between arterial blood gases and resuscitation success has been demonstrated in experimental models of cardiac arrest.96 Thus, arterial blood gases can be useful for evaluating oxygenation but should not be used to assess adequacy of CPR efforts.

Studies on the use of oximetry for assessing tissue perfusion during CPR have shown that transconjunctival oxygen tension falls rapidly when a patient goes into cardiac arrest and returns to baseline when spontaneous circulation is restored.97 Oximetry, however, has not been shown to be a useful prognostic guide for predicting resuscitation from cardiac arrest. Pulse oximetry is commonly used in emergency departments and critical care units. However, measurements depend on the presence of a peripheral pulse, and the technique is unreliable when used on patients in cardiac arrest.

Capnometry shows the most promise as a measurement of CPR effectiveness. Measuring expired end-tidal CO2 is a noninvasive technique for monitoring cardiac output generated during ongoing CPR.98 During cardiac arrest CO2 continues to be generated throughout the body. Once delivered to the lungs, it is excreted. The major determinant of CO2 excretion is its rate of delivery from the peripheral production sites to the lungs. If ventilation is reasonably constant, then end-tidal CO2 concentration reflects cardiac output. Capnometry measures CO2 excretion through the tracheal tube. In experimental models, end-tidal CO2 concentration during ongoing CPR correlated with cardiac output, coronary perfusion pressure, and successful resuscitation from cardiac arrest.98 99 100 101 Clinical studies have shown that patients who were successfully resuscitated from cardiac arrest had significantly higher end-tidal CO2 levels than patients who could not be resuscitated.102 103 104 105 106 Capnometry can also be used as an early indicator of ROSC.102 103 104

Despite these promising studies, other variables can cause changes in CO2 excretion. Large changes in the minute ventilations will affect the end-tidal CO2 reading. Ventilations must be held relatively constant during the resuscitative effort. Administration of bicarbonate will increase CO2 excretion for several minutes before it returns to stable conditions for measurement.104 105 High doses of pressor agents such as epinephrine will increase myocardial perfusion pressure but decrease cardiac output. CO2 excretion will decrease with decreased blood flow to the lungs.107 108 In summary, end-tidal CO2 monitoring during cardiac arrest can be useful as a noninvasive indicator of cardiac output generated during CPR (Class IIa). Research is needed to define the ability of end-tidal CO2 monitoring to predict cardiac arrest victims who could be resuscitated with more aggressive interventions or prolonged resuscitations.


*    Assessment of Chest Compression
up arrowTop
 up arrowAlternative CPR Techniques
 up arrowAssessment of CPR
 up arrowAssessment of Hemodynamics
 up arrowAssessment of Respiratory Gases
 *Assessment of Chest Compression
down arrowReferences
 
The quality of chest compressions and resuscitative effort is an important aspect of CPR. Even physicians recently trained in ACLS have difficulty meeting the recommended compression and ventilatory rates. Simple metronome guidance can correct this.109 Guaranteeing the depth of chest compressions has been even more difficult to ensure.

A device called CPR-Plus has been developed to improve the rescuer’s performance of chest compression. When this device is placed on the victim’s chest and used as a baseplate for chest compressions, the rescuer obtains feedback that includes a metronome-guided rate and force of compression performed. To date, only manikin studies using the CPR-Plus device have been reported.110 111 These studies showed that performance of chest compressions was significantly improved when rescuers used the CPR-Plus device rather than standard CPR alone. Animal and clinical studies, however, are needed to assess whether CPR-Plus improves or detracts from resuscitation hemodynamics in animal models and patients with cardiac arrest. Until such studies are available, informed commentary on this promising device is not possible. We do not recommend the use of CPR-Plus during CPR (Class Indeterminate).


*    Footnotes
 
Circulation. 2000;102(suppl I):I-105–I-111.


*    References
up arrowTop
 up arrowAlternative CPR Techniques
 up arrowAssessment of CPR
 up arrowAssessment of Hemodynamics
 up arrowAssessment of Respiratory Gases
 up arrowAssessment of Chest Compression
 *References
 
1. Walker LI, MacMath T, Chipman H, Bayne E. MAST application in the treatment of paroxysmal supraventricular tachycardia in a child. Ann Emerg Med. 1988;17:529–531.[Medline]

2. Adams CP, Martin GB, Rivers EP, Ward KR, Smithline HA, Rady MY. Hemodynamics of interposed abdominal compression during human cardiopulmonary resuscitation. Acad Emerg Med. 1994;1:498–502.[Abstract]

3. Geehr EC, Lewis FR, Auerbach PS. Failure of open-heart massage to improve survival after prehospital nontraumatic cardiac arrest. N Engl J Med. 1986;314:1189–1190. Letter.[Medline]

4. Bodai BI, Smith JP, Ward RE, O’Neill MB, Auborg R. Emergency thoracotomy in the management of trauma. JAMA. 1983;249:1891–1896.[Medline]

5. Ralston SH, Babbs CF, Niebauer MJ. Cardiopulmonary resuscitation with interposed abdominal compression in dogs. Anesth Analg. 1982;61:645–651.[Abstract]

6. Sack JB, Kesselbrenner MB, Jarrad A. Interposed abdominal compression–cardiopulmonary resuscitation and resuscitation outcome during asystole and electromechanical dissociation [see comments]. Circulation. 1992;86:1692–1700.[Abstract]

7. Mateer JR, Stueven HA, Thompson BM, Aprahamian C, Darin JC. Interposed abdominal compression CPR versus standard CPR in prehospital cardiopulmonary arrest: preliminary results. Ann Emerg Med. 1984;13:764–766.[Medline]

8. Barranco F, Lesmes A, Irles JA, Blasco J, Leal J, Rodriguez J, Leon C. Cardiopulmonary resuscitation with simultaneous chest and abdominal compression: comparative study in humans. Resuscitation. 1990;20:67–77.[Medline]

9. Berryman CR, Phillips GM. Interposed abdominal compression-CPR in human subjects. Ann Emerg Med. 1984;13:226–229.[Medline]

10. Ward KR, Sullivan RJ, Zelenak RR, Summer WR. A comparison of interposed abdominal compression CPR and standard CPR by monitoring end-tidal PCO2 [see comments]. Ann Emerg Med. 1989;18:831–837.[Medline]

11. Babbs CF, Ralston SH, Geddes LA. Theoretical advantages of abdominal counterpulsation in CPR as demonstrated in a simple electrical model of the circulation. Ann Emerg Med. 1984;13:660–671.[Medline]

12. Beyar R, Kishon Y, Kimmel E, Neufeld H, Dinnar U. Intrathoracic and abdominal pressure variations as an efficient method for cardiopulmonary resuscitation: studies in dogs compared with computer model results. Cardiovasc Res. 1985;19:335–342.[Medline]

13. Voorhees WD, Niebauer MJ, Babbs CF. Improved oxygen delivery during cardiopulmonary resuscitation with interposed abdominal compressions. Ann Emerg Med. 1983;12:128–135.[Medline]

14. Sack JB, Kesselbrenner MB, Bregman D. Survival from in-hospital cardiac arrest with interposed abdominal counterpulsation during cardiopulmonary resuscitation [see comments]. JAMA. 1992;267:379–385.[Medline]

15. Babbs CF, Sack JB, Kern KB. Interposed abdominal compression as an adjunct to cardiopulmonary resuscitation. Am Heart J. 1994;127:412–421.[Medline]

16. Babbs CF. CPR techniques that combine chest and abdominal compression and decompression: hemodynamic insights from a spreadsheet model. Circulation. 1999;100:2146–2152.[Abstract/Full Text]

17. Sack JB, Kesselbrenner MB. Hemodynamics, survival benefits, and complications of interposed abdominal compression during cardiopulmonary resuscitation. Acad Emerg Med. 1994;1:490–497.[Abstract]

18. Babbs CF, Schoenlein WE, Lowe MW. Gastric insufflation during IAC-CPR and standard CPR in a canine model. Am J Emerg Med. 1985;3:99–103.[Medline]

19. Mateer JR, Stueven HA, Thompson BM, Aprahamian C, Darin JC. Pre-hospital IAC-CPR versus standard CPR: paramedic resuscitation of cardiac arrests. Am J Emerg Med. 1985;3:143–146.[Medline]

20. Feneley MP, Maier GW, Kern KB, Gaynor JW, Gall SA Jr, Sanders AB, Raessler K, Muhlbaier LH, Rankin JS, Ewy GA. Influence of compression rate on initial success of resuscitation and 24 hour survival after prolonged manual cardiopulmonary resuscitation in dogs. Circulation. 1988;77:240–250.[Abstract]

21. Halperin HR, Tsitlik JE, Guerci AD, Mellits ED, Levin HR, Shi AY, Chandra N, Weisfeldt ML. Determinants of blood flow to vital organs during cardiopulmonary resuscitation in dogs. Circulation. 1986;73:539–550.[Abstract]

22. Kern KB, Sanders AB, Raife J, Milander MM, Otto CW, Ewy GA. A study of chest compression rates during cardiopulmonary resuscitation in humans: the importance of rate-directed chest compressions. Arch Intern Med. 1992;152:145–149.[Medline]

23. Ornato JP, Gonzalez ER, Garnett AR, Levine RL, McClung BK. Effect of cardiopulmonary resuscitation compression rate on end-tidal carbon dioxide concentration and arterial pressure in man. Crit Care Med. 1988;16:241–245.[Medline]

24. Swenson RD, Weaver WD, Niskanen RA, Martin J, Dahlberg S. Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation. Circulation. 1988;78:630–639.[Abstract]

25. Tucker KJ, Redberg RF, Schiller NB, Cohen TJ, Cardiopulmonary Resuscitation Working Group. Active compression-decompression resuscitation: analysis of transmitral flow and left ventricular volume by transesophageal echocardiography in humans. J Am Coll Cardiol. 1993;22:1485–1493.[Medline]

26. Cohen T, Goldner B, Maccaro P, et al. A comparison of active compression-decompression cardiopulmonary resuscitation with standard cardiopulmonary resuscitation for cardiac arrests occurring in the hospital. N Engl J Med. 1993;329:1918–1921.[Medline]

27. Shultz JJ, Coffeen P, Sweeney M, Detloff B, Kehler C, Pineda E, Yakshe P, Adler SW, Chang M, Lurie KG. Evaluation of standard and active compression-decompression CPR in an acute human model of ventricular fibrillation. Circulation. 1994;89:684–693.[Abstract]

28. Tucker KJ, Galli F, Savitt MA, Kahsai D, Bresnahan L, Redberg RF. Active compression-decompression resuscitation: effect on resuscitation success after in-hospital cardiac arrest. J Am Coll Cardiol. 1994;24:201–209.[Medline]

29. Orliaguet GA, Carli PA, Rozenberg A, Janniere D, Sauval P, Delpech P. End-tidal carbon dioxide during out-of-hospital cardiac arrest resuscitation: comparison of active compression-decompression and standard CPR. Ann Emerg Med. 1995;25:48–51.[Medline]

30. Plaisance P, Adnet F, Vicaut E, Hennequin B, Magne P, Prudhomme C, Lambert Y, Cantineau JP, Leopold C, Ferracci C, Gizzi M, Payen D. Benefit of active compression-decompression cardiopulmonary resuscitation as a prehospital advanced cardiac life support: a randomized multicenter study. Circulation. 1997;95:955–961.[Abstract/Full Text]

31. Malzer R, Zeiner A, Binder M, Domanovits H, Knappitsch G, Sterz F, Laggner AN. Hemodynamic effects of active compression-decompression after prolonged CPR. Resuscitation. 1996;31:243–253.[Medline]

32. Stiell IG, Hebert PC, Wells GA, Laupacis A, Vandemheen K, Dreyer JF, Eisenhauer MA, Gibson J, Higginson LA, Kirby AS, Mahon JL, Maloney JP, Weitzman BN. The Ontario trial of active compression-decompression cardiopulmonary resuscitation for in-hospital and prehospital cardiac arrest [see comments]. JAMA. 1996;275:1417–1423.[Medline]

33. Urban P, Cereda J. Glasgow coma score one hour after cardiac arrest. Lancet. 1985;2:1012–1014.

34. Lindner KH, Pfenninger EG, Lurie KG, Schurmann W, Lindner IM, Ahnefeld FW. Effects of active compression-decompression resuscitation on myocardial and cerebral blood flow in pigs. Circulation. 1993;88:1254–1263.[Abstract]

35. Gueugniaud PY, Vaudelin T, Gaussorgues P, Petit P. Out-of-hospital cardiac arrest: the teaching of experience at the SAMU of Lyon. Resuscitation. 1989;17(suppl):S79–S98; discussion S199–S206.

36. Tzivoni D, Banai S, Schuger C, et al. Treatment of torsades de pointes with magnesium sulfate. Circulation. 1988;77:392–399.[Abstract]

37. Tucker KJ, Idris A. Clinical and laboratory investigations of active compression-decompression cardiopulmonary resuscitation [editorial]. Resuscitation. 1994;28:1–7.[Medline]

38. Tresch D, Wetherbee J, Siegel R, Troup P, Keelan MJ, Olinger G, Brooks H. Long-term follow-up of survivors of prehospital sudden cardiac death treated with coronary bypass surgery. Am Heart J. 1985;110:1139–1145.[Medline]

39. Clinton J, McGill J, Irwin G, Peterson G, Lilja G, Ruiz E. Cardiac arrest under age 40: etiology and prognosis. Ann Emerg Med. 1984;13:1011–1015.[Medline]

40. Tuggle D. Meeting the emotional needs of survivors of sudden cardiac arrest. Cardiovasc Nurs. 1982;18:25–30.[Medline]

41. Plaisance P, Lurie KG, Vicaut E, Adnet F, Petit JL, Epain D, Ecollan P, Gruat R, Cavagna P, Biens J, Payen D, French Active Compression-Decompression Cardiopulmonary Resuscitation Study Group. A comparison of standard cardiopulmonary resuscitation and active compression-decompression resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 1999;341:569–575.[Medline]

42. Timerman A, Piegas L, Sousa J. Results of cardiopulmonary resuscitation in a cardiology hospital. Resuscitation. 1989;18:75–84.[Medline]

43. Tonkin A. Prevention of sudden cardiac death: the ICD, or an electrical end-point with preceding opportunities for intervention? Aust N Z J Med. 1992;22:631–635.[Medline]

44. Tomlinson T, Brody H. Futility and the ethics of resuscitation. JAMA. 1990;264:1276–1280.[Medline]

45. Thies W. Risk of infection during CPR training and rescue: supplemental guidelines. JAMA. 1989;262:2714–2715.[Medline]

46. Siscovick DS, Raghunathan TE, Psaty BM, Koepsell TD, Wicklund KG, Lin X, Cobb L, Rautaharju PM, Copass MK, Wagner EH. Diuretic therapy for hypertension and the risk of primary cardiac arrest [see comments]. N Engl J Med. 1994;330:1852–1857.[Medline]

47. Rabl W, Baubin M, Broinger G, Scheithauer R. Serious complications from active compression-decompression cardiopulmonary resuscitation. Int J Legal Med. 1996;109:84–89.[Medline]

48. Klintschar M, Darok M, Radner H. Massive injury to the heart after attempted active compression-decompression cardiopulmonary resuscitation. Int J Legal Med. 1998;111:93–96.[Medline]

49. Haid C, Rabl W, Baubin M. Active compression-decompression resuscitation: the influence of different chest geometries on the force transmission. Resuscitation. 1997;35:83–85.[Medline]

50. Lurie KG, Shultz JJ, Callaham ML, Schwab TM, Gisch T, Rector T, Frascone RJ, Long L. Evaluation of active compression-decompression CPR in victims of out-of-hospital cardiac arrest [see comments]. JAMA. 1994;271:1405–1411.[Medline]

51. Schwab T, Callaham M, Madsen C, Utecht T. A randomized clinical trial of active compression-decompression CPR vs standard CPR in out-of-hospital cardiac arrest in two cities. JAMA. 1995;273:1261–1268.[Medline]

52. Mauer D, Schneider T, Dick W, Withelm A, Elich D, Mauer M. Active compression-decompression resuscitation: a prospective, randomized study in a two-tiered EMS system with physicians in the field. Resuscitation. 1996;33:125–134.[Medline]

53. Luiz T, Ellinger K, Denz C. Active compression-decompression cardiopulmonary resuscitation does not improve survival in patients with prehospital cardiac arrest in a physician-manned emergency medical system [see comments]. J Cardiothorac Vasc Anesth. 1996;10:178–186.[Medline]

54. Babbs CF. New versus old theories of blood flow during CPR. Crit Care Med. 1980;8:191–195.[Medline]

55. Niemann JT, Rosborough JP, Niskanen RA, Alferness C, Criley JM. Mechanical "cough" cardiopulmonary resuscitation during cardiac arrest in dogs. Am J Cardiol. 1985;55:199–204.[Medline]

56. Krischer JP, Fine EG, Weisfeldt ML, Guerci AD, Nagel E, Chandra N. Comparison of prehospital conventional and simultaneous compression-ventilation cardiopulmonary resuscitation. Crit Care Med. 1989;17:1263–1269.[Medline]

57. Kern KB, Carter AB, Showen RL, Voorhees WD III, Babbs CF, Tacker WA, Ewy GA. Comparison of mechanical techniques of cardiopulmonary resuscitation: survival and neurologic outcome in dogs [published erratum appears in Am J Emerg Med. 1987;5:304]. Am J Emerg Med. 1987;5:190–195.

58. Niemann JT, Rosborough JP, Niskanen RA, Criley JM. Circulatory support during cardiac arrest using a pneumatic vest and abdominal binder with simultaneous high-pressure airway inflation. Ann Emerg Med. 1984;13:767–770.[Medline]

59. Halperin HR, Guerci AD, Chandra N, Herskowitz A, Tsitlik JE, Niskanen RA, Wurmb E, Weisfeldt ML. Vest inflation without simultaneous ventilation during cardiac arrest in dogs: improved survival from prolonged cardiopulmonary resuscitation. Circulation. 1986;74:1407–1415.[Abstract]

60. Weinstein M, Stason W. Foundations of cost-effectiveness analysis for health and medical practice. N Engl Med. 1977;296:716–721.

61. Marley CD Jr, Eitel DR, Anderson TE, Mum AJ, Patterson GA. Evaluation of a prototype esophageal detection device. Acad Emerg Med. 1995;2:503–507.[Abstract]

62. Cummins RO, Chamberlain DA. Advisory statements of the International Liaison Committee on Resuscitation. Circulation. 1997;95:2172–3217.[Full Text]

63. Chamberlain D, Bossaert L. Personal communication.

64. Taylor GJ, Rubin R, Tucker M, Greene HL, Rudikoff MT, Weisfeldt ML. External cardiac compression: a randomized comparison of mechanical and manual techniques. JAMA. 1978;240:644–646.[Medline]

65. McDonald JL. Systolic and mean arterial pressures during manual and mechanical CPR in humans. Crit Care Med. 1981;9:382–383.[Medline]

66. Ward KR, Menegazzi JJ, Zelenak RR, Sullivan RJ, McSwain NE Jr. A comparison of chest compressions between mechanical and manual CPR by monitoring end-tidal PCO2 during human cardiac arrest. Ann Emerg Med. 1993;22:669–674.[Medline]

67. Rudikoff MT, Maughan WL, Effron M, Freund P, Weisfeldt ML. Mechanisms of blood flow during cardiopulmonary resuscitation. Circulation. 1980;61:345–352.[Medline]

68. Chandra N, Snyder LD, Weisfeldt ML. Abdominal binding during cardiopulmonary resuscitation in man. JAMA. 1981;246:351–353.[Medline]

69. Chandra N, Rudikoff M, Weisfeldt ML. Simultaneous chest compression and ventilation at high airway pressure during cardiopulmonary resuscitation. Lancet. 1980;1:175–178.[Medline]

70. Niemann JT, Rosborough JP, Hausknecht M, Garner D, Criley JM. Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation. 1981;64:985–991.[Medline]

71. Sanders AB, Ewy GA, Alferness CA, Taft T, Zimmerman M. Failure of one method of simultaneous chest compression, ventilation, and abdominal binding during CPR. Crit Care Med. 1982;10:509–513.[Medline]

72. Martin GB, Carden DL, Nowak RM, Lewinter JR, Johnston W, Tomlanovich MC. Aortic and right atrial pressures during standard and simultaneous compression and ventilation CPR in human beings. Ann Emerg Med. 1986;15:125–130.[Medline]

73. Kern KB, Carter AB, Showen RL, Voorhees WD III, Babbs CF, Tacker WA, Ewy GA. Twenty-four hour survival in a canine model of cardiac arrest comparing three methods of manual cardiopulmonary resuscitation. J Am Coll Cardiol. 1986;7:859–867.[Medline]

74. Tang W, Weil MH, Schock RB, Sato Y, Lucas J, Sun S, Bisera J. Phased chest and abdominal compression-decompression: a new option for cardiopulmonary resuscitation. Circulation. 1997;95:1335–1340.[Abstract/Full Text]

75. Sterz F, Behringer W, Berzlanovich A,Wernigg H, Domanovits H, Muellner M, Schreiber W, Ohley WJ, Schoerkhuber W, Laggner AN. Active compression-decompression of thorax and abdomen (LifestickTM-CPR) in patients with cardiac arrest. Circulation. 1996;94(suppl I):I-9. Abstract.

76. Lurie KG, Mulligan KA, McKnite S, Detloff B, Lindstrom P, Lindner KH. Optimizing standard cardiopulmonary resuscitation with an inspiratory impedance threshold valve. Chest. 1998;113:1084–1090.[Abstract]

77. Tresch D, Grove J, Siegal R, Keelan M, Brooks H. Survivors of prehospitalization sudden death: characteristic clinical and angiographic features. Arch Intern Med. 1981;141:1154–1157.[Medline]

77. Plaisance P, Lurie KG, Payen D. Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation of patients in cardiac arrest. Circulation. 2000;101:989–994.[Abstract/Full Text]

78. Robertson C. The value of open chest CPR for non-traumatic cardiac arrest. Resuscitation. 1991;22:203–208.[Medline]

79. Babbs CF. Hemodynamic mechanisms in CPR: a theoretical rationale for resuscitative thoracotomy in non-traumatic cardiac arrest. Resuscitation. 1987;15:37–50.[Medline]

80. Shocket E, Rosenblum R. Successful open cardiac massage after 75 minutes of closed massage. JAMA. 1967;200:333–335.[Medline]

81. Kern KB, Sanders AB, Badylak SF, Janas W, Carter AB, Tacker WA, Ewy GA. Long-term survival with open-chest cardiac massage after ineffective closed-chest compression in a canine preparation. Circulation. 1987;75:498–503.[Abstract]

82. Takino M, Okada Y. The optimum timing of resuscitative thoracotomy for non-traumatic out-of-hospital cardiac arrest. Resuscitation. 1993;26:69–74.[Medline]

83. Cogbill TH, Moore EE, Millikan JS, Cleveland HC. Rationale for selective application of emergency department thoracotomy in trauma. J Trauma. 1983;23:453–460.[Medline]

84. Danne PD, Finelli F, Champion HR. Emergency bay thoracotomy. J Trauma. 1984;24:796–802.[Medline]

85. Roberge RJ, Ivatury RR, Stahl W, Rohman M. Emergency department thoracotomy for penetrating injuries: predictive value of patient classification. Am J Emerg Med. 1986;4:129–135.[Medline]

86. Paradis NA, Martin GB, Rivers EP, Goetting MG, Appleton TJ, Feingold M, Nowak RM. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation [see comments]. JAMA. 1990;263:1106–1113.[Medline]

87. Redding JS. Abdominal compression in cardiopulmonary resuscitation. Anesth Analg. 1971;50:668–675.[Medline]

88. Redding JS, Pearson JW. Resuscitation from ventricular fibrillation: drug therapy. JAMA. 1968;203:255–260.[Medline]

89. Sanders AB, Ewy GA, Taft TV. Prognostic and therapeutic importance of the aortic diastolic pressure in resuscitation from cardiac arrest. Crit Care Med. 1984;12:871–873.[Medline]

90. Ditchey RV, Winkler JV, Rhodes CA. Relative lack of coronary blood flow during closed-chest resuscitation in dogs. Circulation. 1982;66:297–302.[Abstract]

91. Michael JR, Guerci AD, Koehler RC, Shi AY, Tsitlik J, Chandra N, Niedermeyer E, Rogers MC, Traystman RJ, Weisfeldt ML. Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. Circulation. 1984;69:822–835.[Abstract]

92. Ralston SH, Voorhees WD, Babbs CF. Intrapulmonary epinephrine during prolonged cardiopulmonary resuscitation: improved regional blood flow and resuscitation in dogs. Ann Emerg Med. 1984;13:79–86.[Medline]

93. Sanders A, Ewy G, Taft T. Prognostic and therapeutic importance of the aortic diastolic pressure in resuscitation from cardiac arrest. Crit Care Med. 1984;12:871–873.[Medline]

94. Sanders AB, Ogle M, Ewy GA. Coronary perfusion pressure during cardiopulmonary resuscitation. Am J Emerg Med. 1985;3:11–14.[Medline]

95. Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI. Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med. 1986;315:153–156.[Medline]

96. Sanders AB, Ewy GA, Taft TV. Resuscitation and arterial blood gas abnormalities during prolonged cardiopulmonary resuscitation. Ann Emerg Med. 1984;13:676–679.[Medline]

97. Abraham E, Fink S. Conjunctival oxygen tension monitoring in emergency department patients. Am J Emerg Med. 1988;6:549–554.[Medline]

98. Weil MH, Bisera J, Trevino RP, Rackow EC. Cardiac output and end-tidal carbon dioxide. Crit Care Med. 1985;13:907–909.[Medline]

99. Sanders AB, Atlas AB, Ewy GA, Kern KB, Bragg S. Expired PCO2 as an index of coronary perfusion pressure. Am J Emerg Med. 1985;3:147–149.[Medline]

100. Sanders AB, Ewy GA, Bragg S, Atlas AB, Kern KB. Expired PCO2 as a prognostic indicator of successful resuscitation from cardiac arrest. Ann Emerg Med. 1985;14:948–952.[Medline]

101. Gudipati CV, Weil MH, Bisera J, Deshmukh HG, Rackow EC. Expired carbon dioxide: a noninvasive monitor of cardiopulmonary resuscitation. Circulation. 1988;77:234–239.[Abstract]

102. Kalenda Z. The capnogram as a guide to the efficacy of cardiac massage. Resuscitation. 1978;6:259–263.[Medline]

103. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1987;257:512–515.[Medline]

104. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318:607–611.[Medline]

105. Sanders AB, Kern KB, Otto CW, Milander MM, Ewy GA. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation: a prognostic indicator for survival [see comments]. JAMA. 1989;262:1347–1351.[Medline]

106. Callaham M, Barton C. Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration [see comments]. Crit Care Med. 1990;18:358–362.[Medline]

107. Callaham M, Barton C, Matthay M. Effect of epinephrine on the ability of end-tidal carbon dioxide readings to predict initial resuscitation from cardiac arrest. Crit Care Med. 1992;20:337–343.[Medline]

108. Martin GB, Gentile NT, Paradis NA, Moeggenberg J, Appleton TJ, Nowak RM. Effect of epinephrine on end-tidal carbon dioxide monitoring during CPR. Ann Emerg Med. 1990;19:396–398.[Medline]

109. Milander M, Hiscok P, Sanders A, Kern K, Berg R, Ewy G. Chest compression and ventilation rates during cardiopulmonary resuscitation: the effects of audible tone guidance. Acad Emerg Med. 1995;1:708–713.

110. Jones BR, Dorsey MJ. Sensitivity of a disposable end-tidal carbon dioxide detector. J Clin Monit. 1991;7:268–270.[Medline]

111. Thomas BW, Falcone RE. Confirmation of nasogastric tube placement by colorimetric indicator detection of carbon dioxide: a preliminary report. J Am Coll Nutr. 1998;17:195–197.[Medline]




This article has been cited by other articles:


Home page
 CirculationHome page
Part 7.4: Monitoring and Medications
Circulation, December 13, 2005; 112(24_suppl): IV-78 - IV-83.
[Full Text] [PDF]

This Article
Right arrow Extract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Related Collections
Right arrow AHA Statements and Guidelines

Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.