Editorials 20. Huskins WC, Huckabee CM, O’Grady NP, et al; STAR*ICU Trial Investigators: Intervention to reduce transmission of resistant bacteria in intensive care. N Engl J Med 2011; 364:1407–1418 21. Labeau SO, Van de Vyver K, Brusselaers N, et al: Prevention of ventilator-associated pneumonia with oral antiseptics: A systematic review and meta-analysis. Lancet Infect Dis 2011; 11:845–854 22. van Rijen M, Bonten M, Wenzel R, et al: Mupirocin ointment for preventing Staphylococcus aureus infections in nasal carriers. Cochrane Database Syst Rev 2008; 4:CD006216 23. Climo MW, Yokoe DS, Warren DK, et al: Effect of daily chlorhexidine bathing on hospital-acquired infection. N Engl J Med 2013; 368:533–542 24. Huang SS, Septimus E, Kleinman K, et al; CDC Prevention Epicenters Program; AHRQ DECIDE Network and HealthcareAssociated Infections Program: Targeted versus universal
decolonization to prevent ICU infection. N Engl J Med 2013; 368:2255–2265 25. Fritz SA, Hogan PG, Camins BC, et al: Mupirocin and chlorhexidine resistance in Staphylococcus aureus in patients with communityonset skin and soft tissue infections. Antimicrob Agents Chemother 2013; 57:559–568 26. Stenehjem E, Stafford C, Rimland D: Reduction of methicillin-resistant Staphylococcus aureus infection among veterans in Atlanta. Infect Control Hosp Epidemiol 2013; 34:62–68 27. Perlin JB, Hickok JD, Septimus EJ, et al: A bundled approach to reduce methicillin-resistant Staphylococcus aureus infections in a system of community hospitals. J Healthc Qual 2013; 35:57–68 28. Welsh CA, Flanagan ME, Kiess C, et al: Implementing the MRSA bundle in ICUs: One citywide collaborative’s key lessons learned. Infect Control Hosp Epidemiol 2011; 32:918–921
Intermittent Positive-Pressure Ventilation, Chest Compression Synchronized Ventilation, Bilevel Ventilation, Continuous Chest Compression, Active Compression Decompression, and Impedance Threshold Device—The Complexity of Ventilation During Cardiopulmonary Resuscitation* Nicolas Segal, MD, PhD Services des Urgences Hôpital Lariboisière University Paris Diderot Paris, France
A
s many as 300,000 out-of-hospital cardiac arrests may occur annually in the United States. Despite 50 years of research, survival rate remains low between 3% and 17% (1). To maximize the chances of survival of patients with cardiac arrest, it is necessary for the chain of survival to be as efficient as possible. Chest compression method has not significantly changed since its first description by Kouwenhoven et al (2) in 1960. The two main additions for this mechanical part of the cardiopulmonary resuscitation (CPR) are the active compression decompression (ACD) CPR (3) and the mechanical CPR techniques (4). Even taking into account those changes, the basic idea remains the same: push hard and fast on the chest and do not stop. *See also p. e89. Key Words: cardiopulmonary resuscitation; chest compression; gas exchange; hemodynamics; resuscitation; ventilation The author has disclosed that he does not have any potential conflicts of interest. Copyright © 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/01.ccm.0000435688.85468.3a
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For ventilation, the second part of CPR, things are much more complicated. There are several competing theories. The first one defended by Ewy et al (5) is in favor of performing continuous chest compressions only CPR, without ventilation, up to the first 15 minutes of CPR. The physiological explanation behind his theory is to limit interruptions of chest compressions by paramedics/firefighters. The second theory promoted by Lurie et al (3) favors the use of an impedance threshold device in combination with ACD CPR. The use of this combination, by decreasing negative intrathoracic and intracranial pressures, increases blood flow to the heart and the brain. This combination, in a prospective randomized trial, improves survival to hospital discharge with favorable neurological function 1 year after out-of-hospital cardiac arrest (6). A third theory is to optimize compression to ventilation ratios. The increase of this ratio caused a direct increase in cardiac output during CPR, related to the increased number of compressions delivered over a minute (30:2 vs 15:2 and vs 15:1) (7). Those three theories go in the same direction of limiting ventilation to control elevation of positive intrathoracic pressure and pauses during CPR, which are responsible for a decrease in venous return to the heart. The last theory promotes the use of mechanical ventilation with more “complicated” multipressure ventilation levels. In this issue of Critical Care Medicine, Kill et al (8) have studied a novel mode of ventilation called “chest compression synchronized ventilation” (CCSV). In this ventilation mode, a February 2014 • Volume 42 • Number 2
Editorials
ventilator with a modified trigger detects chest compression starting efforts by sensing a rise in airway pressure and initiates an instant inspiratory pressure. During chest compression, the CCSV mode leads to ventilations with a respiratory rate of 100 per minute synchronized with the start of each chest compression for a duration of only 205 ms and inspiration being stopped before the decompression period begins. Kill et al (8) have demonstrated that CCSV elicited the highest mean arterial pressure when compared with intermittent positive-pressure ventilation and bilevel ventilation without corrupting oxygenation and decarboxylation. Their first finding is to demonstrate that even with a small volume/high rate ventilation, a good blood oxygenation, as the most important ventilation variable, can be achieved. This was the major goal of this investigation. However, the real finding here concerns the increase of blood pressure. It is not so much the magnitude of this increase, but rather that there was any increase at all, since most other studies have shown that higher intrathoracic pressures lead to lower (not higher) perfusion pressures (9). This result can be explained in two different ways. First, the inflation of the lungs supports the external compression of the chest by an internal pressure via the airway, squeezing the lung vessels like a sponge, improving the blood flow return to the left atrium. Second, this lack of blood pressure decrease is probably the effect of the short duration of the positive-pressure ventilation during the CCSV. Each ventilation was stopped before the decompression period started, to allow an unopposed venous blood flow toward the right heart. These results must be mitigated by several limits. First, each group only had a small number of animals. Second, the reduced arterial carbon dioxide with CCSV might be disadvantageous on perfusion of vital organs (9). Finally, even if there is an increase, clinical significance of those effects cannot be certain.
Critical Care Medicine
In conclusion, this study was the first to evaluate CCSV and to demonstrate that positive effects on hemodynamics and on oxygenation are possible by reprogramming a ventilator in this way. In this ventilation mode, ventilation rate is high and tidal volume is low, but because ventilation stops before the decompression period begins, it does not impair the blood flow return to the heart.
REFERENCES
1. Nichol G, Thomas E, Callaway CW, et al; Resuscitation Outcomes Consortium Investigators: Regional variation in out-of-hospital cardiac arrest incidence and outcome. JAMA 2008; 300:1423–1431 2. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closed-chest cardiac massage. JAMA 1960; 173:1064–1067 3. Lurie KG, Lindo C, Chin J: CPR: The P stands for plumber’s helper. JAMA 1990; 264:1661 4. Halperin HR, Guerci AD, Chandra N, et al: Vest inflation without simultaneous ventilation during cardiac arrest in dogs: Improved survival from prolonged cardiopulmonary resuscitation. Circulation 1986; 74:1407–1415 5. Ewy GA: Cardiocerebral resuscitation: The new cardiopulmonary resuscitation. Circulation 2005; 111:2134–2142 6. Aufderheide TP, Frascone RJ, Wayne MA, et al: Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: A randomised trial. Lancet 2011; 377:301–311 7. Yannopoulos D, Aufderheide TP, Gabrielli A, et al: Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation. Crit Care Med 2006; 34:1444–1449 8. Kill C, Hahn O, Dietz F, et al: Mechanical Ventilation During Cardiopulmonary Resuscitation With Intermittent Positive-Pressure Ventilation, Bilevel Ventilation, or Chest Compression Synchronized Ventilation in a Pig Model. Crit Care Med 2014; 42:e89–e95 9. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al: Hyperventilationinduced hypotension during cardiopulmonary resuscitation. Circulation 2004; 109:1960–1965
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decolonization to prevent ICU infection. N Engl J Med 2013; 368:2255–2265 25. Fritz SA, Hogan PG, Camins BC, et al: Mupirocin and chlorhexidine resistance in Staphylococcus aureus in patients with communityonset skin and soft tissue infections. Antimicrob Agents Chemother 2013; 57:559–568 26. Stenehjem E, Stafford C, Rimland D: Reduction of methicillin-resistant Staphylococcus aureus infection among veterans in Atlanta. Infect Control Hosp Epidemiol 2013; 34:62–68 27. Perlin JB, Hickok JD, Septimus EJ, et al: A bundled approach to reduce methicillin-resistant Staphylococcus aureus infections in a system of community hospitals. J Healthc Qual 2013; 35:57–68 28. Welsh CA, Flanagan ME, Kiess C, et al: Implementing the MRSA bundle in ICUs: One citywide collaborative’s key lessons learned. Infect Control Hosp Epidemiol 2011; 32:918–921
Intermittent Positive-Pressure Ventilation, Chest Compression Synchronized Ventilation, Bilevel Ventilation, Continuous Chest Compression, Active Compression Decompression, and Impedance Threshold Device—The Complexity of Ventilation During Cardiopulmonary Resuscitation* Nicolas Segal, MD, PhD Services des Urgences Hôpital Lariboisière University Paris Diderot Paris, France
A
s many as 300,000 out-of-hospital cardiac arrests may occur annually in the United States. Despite 50 years of research, survival rate remains low between 3% and 17% (1). To maximize the chances of survival of patients with cardiac arrest, it is necessary for the chain of survival to be as efficient as possible. Chest compression method has not significantly changed since its first description by Kouwenhoven et al (2) in 1960. The two main additions for this mechanical part of the cardiopulmonary resuscitation (CPR) are the active compression decompression (ACD) CPR (3) and the mechanical CPR techniques (4). Even taking into account those changes, the basic idea remains the same: push hard and fast on the chest and do not stop. *See also p. e89. Key Words: cardiopulmonary resuscitation; chest compression; gas exchange; hemodynamics; resuscitation; ventilation The author has disclosed that he does not have any potential conflicts of interest. Copyright © 2013 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins DOI: 10.1097/01.ccm.0000435688.85468.3a
480
www.ccmjournal.org
For ventilation, the second part of CPR, things are much more complicated. There are several competing theories. The first one defended by Ewy et al (5) is in favor of performing continuous chest compressions only CPR, without ventilation, up to the first 15 minutes of CPR. The physiological explanation behind his theory is to limit interruptions of chest compressions by paramedics/firefighters. The second theory promoted by Lurie et al (3) favors the use of an impedance threshold device in combination with ACD CPR. The use of this combination, by decreasing negative intrathoracic and intracranial pressures, increases blood flow to the heart and the brain. This combination, in a prospective randomized trial, improves survival to hospital discharge with favorable neurological function 1 year after out-of-hospital cardiac arrest (6). A third theory is to optimize compression to ventilation ratios. The increase of this ratio caused a direct increase in cardiac output during CPR, related to the increased number of compressions delivered over a minute (30:2 vs 15:2 and vs 15:1) (7). Those three theories go in the same direction of limiting ventilation to control elevation of positive intrathoracic pressure and pauses during CPR, which are responsible for a decrease in venous return to the heart. The last theory promotes the use of mechanical ventilation with more “complicated” multipressure ventilation levels. In this issue of Critical Care Medicine, Kill et al (8) have studied a novel mode of ventilation called “chest compression synchronized ventilation” (CCSV). In this ventilation mode, a February 2014 • Volume 42 • Number 2
Editorials
ventilator with a modified trigger detects chest compression starting efforts by sensing a rise in airway pressure and initiates an instant inspiratory pressure. During chest compression, the CCSV mode leads to ventilations with a respiratory rate of 100 per minute synchronized with the start of each chest compression for a duration of only 205 ms and inspiration being stopped before the decompression period begins. Kill et al (8) have demonstrated that CCSV elicited the highest mean arterial pressure when compared with intermittent positive-pressure ventilation and bilevel ventilation without corrupting oxygenation and decarboxylation. Their first finding is to demonstrate that even with a small volume/high rate ventilation, a good blood oxygenation, as the most important ventilation variable, can be achieved. This was the major goal of this investigation. However, the real finding here concerns the increase of blood pressure. It is not so much the magnitude of this increase, but rather that there was any increase at all, since most other studies have shown that higher intrathoracic pressures lead to lower (not higher) perfusion pressures (9). This result can be explained in two different ways. First, the inflation of the lungs supports the external compression of the chest by an internal pressure via the airway, squeezing the lung vessels like a sponge, improving the blood flow return to the left atrium. Second, this lack of blood pressure decrease is probably the effect of the short duration of the positive-pressure ventilation during the CCSV. Each ventilation was stopped before the decompression period started, to allow an unopposed venous blood flow toward the right heart. These results must be mitigated by several limits. First, each group only had a small number of animals. Second, the reduced arterial carbon dioxide with CCSV might be disadvantageous on perfusion of vital organs (9). Finally, even if there is an increase, clinical significance of those effects cannot be certain.
Critical Care Medicine
In conclusion, this study was the first to evaluate CCSV and to demonstrate that positive effects on hemodynamics and on oxygenation are possible by reprogramming a ventilator in this way. In this ventilation mode, ventilation rate is high and tidal volume is low, but because ventilation stops before the decompression period begins, it does not impair the blood flow return to the heart.
REFERENCES
1. Nichol G, Thomas E, Callaway CW, et al; Resuscitation Outcomes Consortium Investigators: Regional variation in out-of-hospital cardiac arrest incidence and outcome. JAMA 2008; 300:1423–1431 2. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closed-chest cardiac massage. JAMA 1960; 173:1064–1067 3. Lurie KG, Lindo C, Chin J: CPR: The P stands for plumber’s helper. JAMA 1990; 264:1661 4. Halperin HR, Guerci AD, Chandra N, et al: Vest inflation without simultaneous ventilation during cardiac arrest in dogs: Improved survival from prolonged cardiopulmonary resuscitation. Circulation 1986; 74:1407–1415 5. Ewy GA: Cardiocerebral resuscitation: The new cardiopulmonary resuscitation. Circulation 2005; 111:2134–2142 6. Aufderheide TP, Frascone RJ, Wayne MA, et al: Standard cardiopulmonary resuscitation versus active compression-decompression cardiopulmonary resuscitation with augmentation of negative intrathoracic pressure for out-of-hospital cardiac arrest: A randomised trial. Lancet 2011; 377:301–311 7. Yannopoulos D, Aufderheide TP, Gabrielli A, et al: Clinical and hemodynamic comparison of 15:2 and 30:2 compression-to-ventilation ratios for cardiopulmonary resuscitation. Crit Care Med 2006; 34:1444–1449 8. Kill C, Hahn O, Dietz F, et al: Mechanical Ventilation During Cardiopulmonary Resuscitation With Intermittent Positive-Pressure Ventilation, Bilevel Ventilation, or Chest Compression Synchronized Ventilation in a Pig Model. Crit Care Med 2014; 42:e89–e95 9. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al: Hyperventilationinduced hypotension during cardiopulmonary resuscitation. Circulation 2004; 109:1960–1965
www.ccmjournal.org
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