From laboratory science to six emergency medical services systems: New understanding of the physiology of cardiopulmonary resuscitation increases survival rates after cardiac arrest.
OBJECTIVE
The purpose of this study is to: 1) describe a newly mechanism of blood flow to the brain during cardiopulmonary resuscitation using the impedance threshold device in a piglet model of cardiac arrest, and 2) describe the survival benefits in humans of applying all of the highly recommended changes in the 2005 guidelines related to increasing circulation during cardiopulmonary resuscitation, including use of the impedance threshold device, from six emergency medical services systems in the United States.


METHODS
Animal studies prospective trial with each piglet serving as its own control. Historical controls were used for the human studies.


METHODS
Piglets and patients with out-of-hospital cardiac arrest.


METHODS
Piglets (10-12 kg) were treated with an active (n = 9) or sham (n = 9) impedance threshold device after 6 mins of ventricular fibrillation. Humans were treated with cardiopulmonary resuscitation per the American Heart Association 2005 guidelines and the impedance threshold device.


RESULTS



METHODS
The primary endpoint in the piglet study was carotid blood flow which increased from 59 mL/min without an impedance threshold device to 91 mL/min (p = 0.017) with impedance threshold device use. Airway pressures during the chest recoil phase decreased from -0.46 mm Hg to -2.59 mm Hg (p = 0.0006) with the active impedance threshold device. Intracranial pressure decreased more rapidly and to a greater degree during the decompression phase of cardiopulmonary resuscitation with the active impedance threshold device. Humans: Conglomerate quality assurance data were analyzed from six emergency medical services systems in the United States serving a population of approximately 3 million people. There were 920 patients treated for cardiac arrest after implementation of the 2005 American Heart Association guidelines, including impedance threshold device use, and 1750 patients in the control group during the year before implementation. Demographics were similar between the two groups. Survival to hospital discharge was 9.3% in the control group versus 13.6% in the intervention group. The odds ratio, 95% confidence interval, and p value were 1.54 (1.19-1.99) and p = 0.0008, respectively. This survival advantage was conferred to patients with a presenting cardiac arrest rhythm of ventricular fibrillation (28.5% vs. 18.0%, p = 0.0008).


CONCLUSIONS
Use of the impedance threshold device in piglets increased carotid blood flow and coronary and cerebral perfusion pressures and reduced intracranial pressure during the decompression phase of cardiopulmonary resuscitation at a faster rate than controls, resulting in a longer duration of time when intracranial pressures are at their nadir. Patients in six emergency medical services systems treated with the impedance threshold device together with the renewed emphasis on more compressions, fewer ventilations, and complete chest wall recoil had a nearly 50% increase in survival rates after out-of-hospital cardiac arrest compared with historical controls.
Aufderheide
Tom P
TP
Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee, WI, USA. taufderh@mcw.edu
Alexander
Carly
C
Lick
Charles
C
Myers
Brent
B
Romig
Laurie
L
Vartanian
Levon
L
Stothert
Joseph
J
McKnite
Scott
S
Matsuura
Tim
T
Yannopoulos
Demetris
D
Lurie
Keith
K
D000368:Aged; D000818:Animals; D001921:Brain / Q000098:blood supply*; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D002339:Carotid Arteries / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D003326:Coronary Circulation; D017097:Electric Impedance; D005260:Female; D006323:Heart Arrest / Q000401:mortality / Q000503:physiopathology / Q000628:therapy*; D017052:Hospital Mortality; D006801:Humans; D007427:Intracranial Pressure; D008297:Male; D015425:Myocardial Reperfusion; D017410:Practice Guidelines as Topic; D015996:Survival Rate; D013552:Swine; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology
Chest. 1998 Apr;113(4):1084-90
9554651
Resuscitation. 2005 Jul;66(1):13-20
15993724
J Appl Physiol (1985). 1993 Jan;74(1):147-52
8444685
Resuscitation. 2005 Mar;64(3):363-72
15733767
Circulation. 2007 Dec 18;116(25):2900-7
18071072
JAMA. 2005 Jan 19;293(3):305-10
15657323
Resuscitation. 2005 Mar;64(3):353-62
15733766
Resuscitation. 2004 Apr;61(1):75-82
15081185
Acad Emerg Med. 2005 Jan;12(1):79-80
15635142
JAMA. 2005 Jan 19;293(3):299-304
15657322
Circ Res. 1985 Jan;56(1):20-30
3967345
J Cardiovasc Electrophysiol. 1997 May;8(5):584-600
9160235
Resuscitation. 2005 Oct;67(1):103-8
16150530
JAMA. 2003 Mar 19;289(11):1389-95
12636461
Respir Care. 2005 May;50(5):628-35
15871757
Emerg Med Serv. 2005 Sep;34(9):42-5
16274172
Circulation. 2002 Jan 1;105(1):124-9
11772887
Circulation. 2004 Apr 27;109(16):1960-5
15066941
N Engl J Med. 1992 Oct 8;327(15):1075-80
1522844
Ann Emerg Med. 1991 Apr;20(4):355-61
2003661
JAMA. 1999 Apr 7;281(13):1182-8
10199427
Crit Care Med. 2005 Apr;33(4):734-40
15818098
Crit Care Med. 2006 May;34(5):1444-9
16557155
Circulation. 2005 Dec 13;112(24 Suppl):IV1-203
16314375
Curr Opin Crit Care. 2006 Jun;12(3):198-203
16672776
Neurologist. 2007 Nov;13(6):369-75
18090715
JAMA. 1960 Jul 9;173:1064-7
14411374
Emerg Med Australas. 2005 Feb;17(1):39-45
15675903
Curr Opin Crit Care. 2006 Jun;12(3):207-12
16672778
Resuscitation. 2006 Dec;71(3):341-51
17070644
Ann Emerg Med. 1990 Feb;19(2):179-86
2301797
Circulation. 1995 Mar 15;91(6):1629-32
7882467
Resuscitation. 2006 Sep;70(3):445-53
16901611