16923
013
ACC0010.1177/2048872613516923European Heart Journal: Acute Cardiovascular CareChalkias and Xanthos
EUROPEAN SOCIETY OF CARDIOLOGY ®
Review
Timing positive-pressure ventilation during chest compression: the key to improving the thoracic pump?
European Heart Journal: Acute Cardiovascular Care 2015, Vol. 4(1) 24–27 © The European Society of Cardiology 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/2048872613516923 acc.sagepub.com
Athanasios Chalkias1,2 and Theodoros Xanthos1,2
Abstract Given the importance of increased coronary and cerebral perfusion pressure during cardiopulmonary resuscitation, the recommendation of limiting tidal volume and ventilation rate to 10 per minute in order not to inhibit venous return seems to be correct. However, although the resuscitation community believes that positive-pressure ventilation during cardiopulmonary resuscitation is bad for the circulation, proper timing of compression and ventilation may actually improve the circulation. Keywords Chest compressions, haemodynamics, resuscitation, ventilation Received: 19 September 2013; accepted: 25 November 2013
Introduction Apart from uninterrupted high-quality chest compressions, recent guidelines suggest that positive-pressure ventilation should be provided as soon as possible for any patient in cardiac arrest, although few studies address specific aspects of ventilation during advanced life support. Furthermore, automatic ventilators are recommended during cardiopulmonary resuscitation (CPR) as they provide a constant flow of gas to the patient during inspiration and deliver an inspiratory time-dependent volume, helping the rescuer to avoid excessive ventilation. In addition, they are associated with lower peak airway pressures than manual ventilation,1 which reduces intrathoracic pressure and facilitates improved venous return and subsequent cardiac output, which is 25–40% of pre-arrest values during optimal CPR. Therefore, given the importance of increased coronary and cerebral perfusion pressure, the recommendation of limiting tidal volume and ventilation rate to 10 per minute in order not to inhibit venous return seems to be correct, although based on very little animal data. Considering, however, the potentially negative haemodynamic effects of artificial ventilation, the question that arises is: could positive-pressure ventilation be a way to control intrathoracic pressure and enhance cardiac output during CPR? The concept of intrathoracic pressure mandates that it can be increased mainly during chest compression and when
positive-pressure ventilation is applied. As happens with most parameters of human physiology, it should be an upper limit beyond of which the beneficial effects of increased intrathoracic pressure on compression-related blood flow are superseded by its unfavourable consequences. Therefore, a major challenge for the resuscitation community would be to use the increase in intrathoracic pressure in favour of optimizing coronary and cerebral perfusion pressure.
Methods We searched for studies addressing important aspects on the potent favourable effects of intrathoracic pressure on blood flow during CPR which would have a potential impact on the resuscitation of victims. The literature search was performed using PubMed, CINAHL, and 1National
and Kapodistrian University of Athens, Medical School, MSc “Cardiopulmonary Resuscitation”, Athens, Greece. 2Hellenic Society of Cardiopulmonary Resuscitation, Athens, Greece. Corresponding author: Dr. Athanasios Chalkias, National and Kapodistrian University of Athens, Medical School, MSc “Cardiopulmonary Resuscitation”, Hospital ‘Henry Dunant’, 107 Mesogion Ave, 115 26, Athens, Greece. Email: [email protected]
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
25
Chalkias and Xanthos Scopus databases from 1980 until now. The inclusion criteria were ‘cardiac arrest’, ‘cardiopulmonary resuscitation’, ‘chest compression’, ‘intrathoracic pressure’, ‘positive-pressure ventilation’, ‘coronary perfusion pressure’, and ‘cerebral perfusion pressure’. All articles not available in English were excluded, while cross-referencing was performed using the bibliographies from the articles obtained. The authors completed the literature search and selected by consensus the studies based on inclusion criteria as judged by title, abstract, and complete manuscript, identifying 11 citations. Paediatric studies were not included.
Timing positive-pressure ventilation At the start of chest compression intrathoracic pressure rises and establishes an arteriovenous pressure gradient across the heart forcing blood to move down the gradient through the heart and to flow from the thoracic to the systemic circulation (thoracic pump theory). This requires that the atrioventricular valves be open during cardiac compression.2–4 If blood moves due to changes in intrathoracic pressure, then lateral pleural pressure and intrathoracic arterial and venous pressures are similar and nearly equal to extrathoracic arterial pressure, which is in turn significantly higher than extrathoracic venous pressure.2,5,6 Also, the direct compression of the ventricles between the sternum and vertebral column creates a pressure gradient between the left ventricle and the aorta, as well as between the right ventricle and the pulmonary artery resulting in forward blood flow out of the ventricles (cardiac pump theory). This theory requires that the atrioventricular valves be closed during cardiac compression. If blood moves due to direct vascular or cardiac compression, lateral pleural and intrathoracic arterial and venous pressures are dissimilar. Even in such instances, extrathoracic arterial pressures may be similar to intrathoracic arterial pressures, but because of venous valves and possibly venous collapse, the intrathoracic venous pressure is significantly higher than extrathoracic venous pressure.2,5 Thus, a peripheral arterial–venous pressure gradient is generated and results in the forward flow of blood. Despite advances in resuscitation and the scientific background of these theories, it remains unknown whether the ‘thoracic pump’ plays a role in promoting blood flow in the absence of positive-pressure ventilation. Rudikoff et al.2 found that systolic pressures were similar in each of the cardiac chambers and intrathoracic great vessels for each beat of the compression cycle. Interestingly, increasing intrathoracic pressure by maintaining the lungs fully inflated during compression or by abdominal binding to prevent paradoxical diaphragmatic motion led to a rise in aortic systolic pressure and an increase in carotid blood flow. In a similar study in humans, the increased intrathoracic pressure by positive-pressure ventilation synchronous
with chest compression resulted in higher blood pressure and index of carotid flow.7 Halperin et al.8 found in a canine model that, during certain situations, mitral valve closure can occur with cyclic elevation of intrathoracic pressure alone. In another model it was found that when the compressive force was 200 N, the mitral valve closed in 16% of cardiac cycles, while at 500 N, the mitral valve closed in 95% of cardiac cycles.9 Interestingly, the increased rates of mitral valve closure were associated with increased diastolic myocardial perfusion pressures, systolic cerebral pressures, and cardiac output. A logical conclusion could be that that the higher pressures (by insufflation) during chest compression improve closure of the mitral valve and therefore promote forward flow. Swenson et al.10 compared conventional vs. pneumatic vest CPR and found that simultaneous ventilation along with the vest compression caused an increase in aortic systolic pressure (from an average of 71±33 to 93±27 mmHg, p=0.008). However, simultaneous ventilation also caused an abrupt drop in the coronary perfusion gradients which was related to a significant rise in right atrial pressure (from 7±3 during conventional CPR to 13±14 mmHg) caused by high end-expiratory airway pressures attributable to incomplete exhalation between ventilations (air trapping). End-expiratory airway pressures during simultaneous ventilation averaged 19±10 mmHg and ranged from 5 to 38 mmHg. However, this finding was not present during any other CPR method and as chest compressions may be performed on a ‘volume-primed’ heart, it remains unknown whether the effect of inhibition of venous return may occur after the inspiratory phase of ventilation. Aufderheide et al.11 demonstrated that excessive ventilation rates result in a persistently increased intrathoracic pressure during the decompression phase of CPR, thereby markedly decreasing cardiac preload, cardiac output, and coronary perfusion pressure. However, in this study the flow rate of the ventilator was 160 l/min, which at higher ventilation rates will lead to persistent very high thoracic pressures. On the contrary, Gazmuri et al.12 very recently showed in pigs that increasing respiratory rate and tidal volume up to a minute-volume 10-fold higher than currently recommended had no adverse effects on coronary and cerebral flow during resuscitation, but reduced endtidal carbon dioxide (PETCO2), suggesting that ventilation at controlled rate and volume could enhance the precision with which PETCO2 reflects CPR quality, predicts restoration of spontaneous circulation, and serves to guide optimization of resuscitation interventions. In either case, the mechanism of blood flow during CPR may be dependent on the stage and momentum of compression or decompression, without forgetting that the effect of ventilation, as well as that of compression force and rate, may vary during CPR (Table 1). Research should focus on these aspects and especially in relation to
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
26
European Heart Journal: Acute Cardiovascular Care 4(1)
Table 1. Stages of cardiopulmonary resuscitation for which research should focus on the relationship between intrathoracic pressure and blood flow. Compression/decompression before insufflation Compression/decompression during simultaneous insufflation Compression/decompression immediately after the end of insufflation Compression/decompression during simultaneous exsufflation Compression/decompression immediately after the end of exsufflation
Figure 1. The effect of thoracic and cardiac pump theory on blood flow in relation to ventilation and ventilation-induced intrathoracic pressure. ITP, intrathoracic pressure.
Table 2. Proposed approaches for timing the raising intrathoracic pressure in relation to compressions. Passive leg raising during positive-pressure ventilation Pressure on the abdominal region during positive-pressure ventilation Clumping of the endotracheal tube after the inspiratory phase of ventilation (reversing the function of impedance threshold device) Use of positive end-expiratory pressure
time, because both compressions and insufflations gradually increase the intrathoracic pressure, which reaches a peak value and then gradually decreases. Of course, this depends on several factors such as the compression force and depth, the volume of the inflated air, the insufflation rate, the elasticity of the chest wall, the underlying pulmonary and/or heart disease, the amount of cardiac fat, the intra-abdominal hypertension, and the correct implementation of guidelines.13–16 In addition, although during lay CPR only the cardiac pump mechanism seems to apply, during advanced life support both theories may play a role. It is the opinion of the authors that during positive-pressure ventilation, blood flow is promoted by the ‘thoracic pump’, but by the beginning of the expiratory phase (ventilator pause) the ‘thoracic pump’ effect decreases as the ‘cardiac pump’ begins to take over, reaching a peak effect by the end of ventilator pause and just before the inspiratory phase (Figure 1). As this manuscript presents the possible physiology that could be implicated in resuscitation, further research is needed for the full clarification of the interplay between ventilation and compression as eventually, it seems to be a key point in order to optimize coronary and cerebral perfusion pressure during CPR.
Conclusion Although the resuscitation community believes that positive-pressure ventilation during CPR is bad for the circulation, proper timing of compression and ventilation may actually improve the circulation. During CPR, not only a much broader range of respiratory rates and tidal volumes can be delivered before compromising venous return and cardiac output, but, also, as increases in minute-volume influence PETCO2,12 monitoring of these parameters in relation to intrathoracic pressure could be a valuable tool towards optimal forward blood flow. Thus, it would be of major scientific interest to study the temporal relationship between compression, intrathoracic pressure differences, and pressure/flow in the carotids and aorta, to optimize intrathoracic pressure, and to evaluate intrathoracic pressure difference before and after each compression as a non-invasive parameter to reflect the thoracic pump (Table 2). Chest compression alone may be not sufficient in order for thoracic pump to work, and positive-pressure ventilation may be the key for this, potentially leading to new ventilation strategies. Conflict of interest The authors declare that there is no conflict of interest.
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
27
Chalkias and Xanthos Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Deakin CD, Nolan JP, Soar J, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support. Resuscitation 2010; 81: 1305–1352. 2. Rudikoff MT, Maughan WL, Effron M, et al. Mechanism of blood flow during cardiopulmonary resuscitation. Circulation 1980; 61: 345–352. 3. Niemann JT, Rosborough JP, Hausknecht M, et al. Pressuresynchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981; 64: 985–991. 4. Weisfeldt M and Chandra N. Physiology of cardiopulmonary resuscitation. Annu Rev Med 1981; 32: 435–442. 5. Werner JA, Greene HL, Janko CL, et al. Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Implications regarding the mechanism of blood flow. Circulation 1981; 63: 1417–1421. 6. Frenneaux MP and Steen S. Hemodynamics of cardiac arrest. In: Paradis NA, Halperin HR , Kern KB, et al., eds. Cardiac arrest. The science and practice of resuscitation medicine, 2nd ed. Cambridge: Cambridge University Press, 2007. pp 347–366. 7. Chandra N, Rudikoff M and Weisfledt M. Simultaneous chest compression and ventilation at high airway pressure during cardiopulmonary resuscitation. Lancet 1980; 1: 175–178. 8. Halperin HR, Weiss JL, Guerci AD, et al. Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs. Circulation 1988; 78: 754–760.
9. Hackl W, Simon P, Mauritz W, et al. Echocardiographic assessment of mitral valve function during mechanical cardiopulmonary resuscitation in pigs. Anesth Analg 1990; 70: 350–356. 10. Swenson RD, Weaver WD, Niskanen RA, et al. Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation. Circulation 1988; 78: 630–639. 11. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004; 109: 1960–1965. 12. Gazmuri RJ, Ayoub IM, Radhakrishnan J, et al. Clinically plausible hyperventilation does not exert adverse hemodynamic effects during CPR but markedly reduces end-tidal PCO2. Resuscitation 2012; 83: 259–264. 13. Chalkias A and Xanthos T. Potent biomechanical and molecular behaviour of cardiac adipose tissue during cardiopulmonary resuscitation and post-resuscitation period. Acta Physiol (Oxf) 2012; 205: 3–5. 14. Chalkias A and Xanthos T. Intra-abdominal hypertension: a potent silent killer of cardiac arrest survivors. Am J Emerg Med 2012; 30: 502–504. 15. Runck H, Schumann S, Tacke S, et al. Effects of intraabdominal pressure on respiratory system mechanics in mechanically ventilated rats. Respir Physiol Neurobiol 2012; 180: 204–210. 16. Maertens VL, De Smedt LE, Lemoyne S, et al. Patients with cardiac arrest are ventilated two times faster than guidelines recommend: an observational prehospital study using tracheal pressure measurement. Resuscitation 2013; 84: 921–926.
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
013
ACC0010.1177/2048872613516923European Heart Journal: Acute Cardiovascular CareChalkias and Xanthos
EUROPEAN SOCIETY OF CARDIOLOGY ®
Review
Timing positive-pressure ventilation during chest compression: the key to improving the thoracic pump?
European Heart Journal: Acute Cardiovascular Care 2015, Vol. 4(1) 24–27 © The European Society of Cardiology 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/2048872613516923 acc.sagepub.com
Athanasios Chalkias1,2 and Theodoros Xanthos1,2
Abstract Given the importance of increased coronary and cerebral perfusion pressure during cardiopulmonary resuscitation, the recommendation of limiting tidal volume and ventilation rate to 10 per minute in order not to inhibit venous return seems to be correct. However, although the resuscitation community believes that positive-pressure ventilation during cardiopulmonary resuscitation is bad for the circulation, proper timing of compression and ventilation may actually improve the circulation. Keywords Chest compressions, haemodynamics, resuscitation, ventilation Received: 19 September 2013; accepted: 25 November 2013
Introduction Apart from uninterrupted high-quality chest compressions, recent guidelines suggest that positive-pressure ventilation should be provided as soon as possible for any patient in cardiac arrest, although few studies address specific aspects of ventilation during advanced life support. Furthermore, automatic ventilators are recommended during cardiopulmonary resuscitation (CPR) as they provide a constant flow of gas to the patient during inspiration and deliver an inspiratory time-dependent volume, helping the rescuer to avoid excessive ventilation. In addition, they are associated with lower peak airway pressures than manual ventilation,1 which reduces intrathoracic pressure and facilitates improved venous return and subsequent cardiac output, which is 25–40% of pre-arrest values during optimal CPR. Therefore, given the importance of increased coronary and cerebral perfusion pressure, the recommendation of limiting tidal volume and ventilation rate to 10 per minute in order not to inhibit venous return seems to be correct, although based on very little animal data. Considering, however, the potentially negative haemodynamic effects of artificial ventilation, the question that arises is: could positive-pressure ventilation be a way to control intrathoracic pressure and enhance cardiac output during CPR? The concept of intrathoracic pressure mandates that it can be increased mainly during chest compression and when
positive-pressure ventilation is applied. As happens with most parameters of human physiology, it should be an upper limit beyond of which the beneficial effects of increased intrathoracic pressure on compression-related blood flow are superseded by its unfavourable consequences. Therefore, a major challenge for the resuscitation community would be to use the increase in intrathoracic pressure in favour of optimizing coronary and cerebral perfusion pressure.
Methods We searched for studies addressing important aspects on the potent favourable effects of intrathoracic pressure on blood flow during CPR which would have a potential impact on the resuscitation of victims. The literature search was performed using PubMed, CINAHL, and 1National
and Kapodistrian University of Athens, Medical School, MSc “Cardiopulmonary Resuscitation”, Athens, Greece. 2Hellenic Society of Cardiopulmonary Resuscitation, Athens, Greece. Corresponding author: Dr. Athanasios Chalkias, National and Kapodistrian University of Athens, Medical School, MSc “Cardiopulmonary Resuscitation”, Hospital ‘Henry Dunant’, 107 Mesogion Ave, 115 26, Athens, Greece. Email: [email protected]
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
25
Chalkias and Xanthos Scopus databases from 1980 until now. The inclusion criteria were ‘cardiac arrest’, ‘cardiopulmonary resuscitation’, ‘chest compression’, ‘intrathoracic pressure’, ‘positive-pressure ventilation’, ‘coronary perfusion pressure’, and ‘cerebral perfusion pressure’. All articles not available in English were excluded, while cross-referencing was performed using the bibliographies from the articles obtained. The authors completed the literature search and selected by consensus the studies based on inclusion criteria as judged by title, abstract, and complete manuscript, identifying 11 citations. Paediatric studies were not included.
Timing positive-pressure ventilation At the start of chest compression intrathoracic pressure rises and establishes an arteriovenous pressure gradient across the heart forcing blood to move down the gradient through the heart and to flow from the thoracic to the systemic circulation (thoracic pump theory). This requires that the atrioventricular valves be open during cardiac compression.2–4 If blood moves due to changes in intrathoracic pressure, then lateral pleural pressure and intrathoracic arterial and venous pressures are similar and nearly equal to extrathoracic arterial pressure, which is in turn significantly higher than extrathoracic venous pressure.2,5,6 Also, the direct compression of the ventricles between the sternum and vertebral column creates a pressure gradient between the left ventricle and the aorta, as well as between the right ventricle and the pulmonary artery resulting in forward blood flow out of the ventricles (cardiac pump theory). This theory requires that the atrioventricular valves be closed during cardiac compression. If blood moves due to direct vascular or cardiac compression, lateral pleural and intrathoracic arterial and venous pressures are dissimilar. Even in such instances, extrathoracic arterial pressures may be similar to intrathoracic arterial pressures, but because of venous valves and possibly venous collapse, the intrathoracic venous pressure is significantly higher than extrathoracic venous pressure.2,5 Thus, a peripheral arterial–venous pressure gradient is generated and results in the forward flow of blood. Despite advances in resuscitation and the scientific background of these theories, it remains unknown whether the ‘thoracic pump’ plays a role in promoting blood flow in the absence of positive-pressure ventilation. Rudikoff et al.2 found that systolic pressures were similar in each of the cardiac chambers and intrathoracic great vessels for each beat of the compression cycle. Interestingly, increasing intrathoracic pressure by maintaining the lungs fully inflated during compression or by abdominal binding to prevent paradoxical diaphragmatic motion led to a rise in aortic systolic pressure and an increase in carotid blood flow. In a similar study in humans, the increased intrathoracic pressure by positive-pressure ventilation synchronous
with chest compression resulted in higher blood pressure and index of carotid flow.7 Halperin et al.8 found in a canine model that, during certain situations, mitral valve closure can occur with cyclic elevation of intrathoracic pressure alone. In another model it was found that when the compressive force was 200 N, the mitral valve closed in 16% of cardiac cycles, while at 500 N, the mitral valve closed in 95% of cardiac cycles.9 Interestingly, the increased rates of mitral valve closure were associated with increased diastolic myocardial perfusion pressures, systolic cerebral pressures, and cardiac output. A logical conclusion could be that that the higher pressures (by insufflation) during chest compression improve closure of the mitral valve and therefore promote forward flow. Swenson et al.10 compared conventional vs. pneumatic vest CPR and found that simultaneous ventilation along with the vest compression caused an increase in aortic systolic pressure (from an average of 71±33 to 93±27 mmHg, p=0.008). However, simultaneous ventilation also caused an abrupt drop in the coronary perfusion gradients which was related to a significant rise in right atrial pressure (from 7±3 during conventional CPR to 13±14 mmHg) caused by high end-expiratory airway pressures attributable to incomplete exhalation between ventilations (air trapping). End-expiratory airway pressures during simultaneous ventilation averaged 19±10 mmHg and ranged from 5 to 38 mmHg. However, this finding was not present during any other CPR method and as chest compressions may be performed on a ‘volume-primed’ heart, it remains unknown whether the effect of inhibition of venous return may occur after the inspiratory phase of ventilation. Aufderheide et al.11 demonstrated that excessive ventilation rates result in a persistently increased intrathoracic pressure during the decompression phase of CPR, thereby markedly decreasing cardiac preload, cardiac output, and coronary perfusion pressure. However, in this study the flow rate of the ventilator was 160 l/min, which at higher ventilation rates will lead to persistent very high thoracic pressures. On the contrary, Gazmuri et al.12 very recently showed in pigs that increasing respiratory rate and tidal volume up to a minute-volume 10-fold higher than currently recommended had no adverse effects on coronary and cerebral flow during resuscitation, but reduced endtidal carbon dioxide (PETCO2), suggesting that ventilation at controlled rate and volume could enhance the precision with which PETCO2 reflects CPR quality, predicts restoration of spontaneous circulation, and serves to guide optimization of resuscitation interventions. In either case, the mechanism of blood flow during CPR may be dependent on the stage and momentum of compression or decompression, without forgetting that the effect of ventilation, as well as that of compression force and rate, may vary during CPR (Table 1). Research should focus on these aspects and especially in relation to
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
26
European Heart Journal: Acute Cardiovascular Care 4(1)
Table 1. Stages of cardiopulmonary resuscitation for which research should focus on the relationship between intrathoracic pressure and blood flow. Compression/decompression before insufflation Compression/decompression during simultaneous insufflation Compression/decompression immediately after the end of insufflation Compression/decompression during simultaneous exsufflation Compression/decompression immediately after the end of exsufflation
Figure 1. The effect of thoracic and cardiac pump theory on blood flow in relation to ventilation and ventilation-induced intrathoracic pressure. ITP, intrathoracic pressure.
Table 2. Proposed approaches for timing the raising intrathoracic pressure in relation to compressions. Passive leg raising during positive-pressure ventilation Pressure on the abdominal region during positive-pressure ventilation Clumping of the endotracheal tube after the inspiratory phase of ventilation (reversing the function of impedance threshold device) Use of positive end-expiratory pressure
time, because both compressions and insufflations gradually increase the intrathoracic pressure, which reaches a peak value and then gradually decreases. Of course, this depends on several factors such as the compression force and depth, the volume of the inflated air, the insufflation rate, the elasticity of the chest wall, the underlying pulmonary and/or heart disease, the amount of cardiac fat, the intra-abdominal hypertension, and the correct implementation of guidelines.13–16 In addition, although during lay CPR only the cardiac pump mechanism seems to apply, during advanced life support both theories may play a role. It is the opinion of the authors that during positive-pressure ventilation, blood flow is promoted by the ‘thoracic pump’, but by the beginning of the expiratory phase (ventilator pause) the ‘thoracic pump’ effect decreases as the ‘cardiac pump’ begins to take over, reaching a peak effect by the end of ventilator pause and just before the inspiratory phase (Figure 1). As this manuscript presents the possible physiology that could be implicated in resuscitation, further research is needed for the full clarification of the interplay between ventilation and compression as eventually, it seems to be a key point in order to optimize coronary and cerebral perfusion pressure during CPR.
Conclusion Although the resuscitation community believes that positive-pressure ventilation during CPR is bad for the circulation, proper timing of compression and ventilation may actually improve the circulation. During CPR, not only a much broader range of respiratory rates and tidal volumes can be delivered before compromising venous return and cardiac output, but, also, as increases in minute-volume influence PETCO2,12 monitoring of these parameters in relation to intrathoracic pressure could be a valuable tool towards optimal forward blood flow. Thus, it would be of major scientific interest to study the temporal relationship between compression, intrathoracic pressure differences, and pressure/flow in the carotids and aorta, to optimize intrathoracic pressure, and to evaluate intrathoracic pressure difference before and after each compression as a non-invasive parameter to reflect the thoracic pump (Table 2). Chest compression alone may be not sufficient in order for thoracic pump to work, and positive-pressure ventilation may be the key for this, potentially leading to new ventilation strategies. Conflict of interest The authors declare that there is no conflict of interest.
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
27
Chalkias and Xanthos Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Deakin CD, Nolan JP, Soar J, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 4. Adult advanced life support. Resuscitation 2010; 81: 1305–1352. 2. Rudikoff MT, Maughan WL, Effron M, et al. Mechanism of blood flow during cardiopulmonary resuscitation. Circulation 1980; 61: 345–352. 3. Niemann JT, Rosborough JP, Hausknecht M, et al. Pressuresynchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation 1981; 64: 985–991. 4. Weisfeldt M and Chandra N. Physiology of cardiopulmonary resuscitation. Annu Rev Med 1981; 32: 435–442. 5. Werner JA, Greene HL, Janko CL, et al. Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Implications regarding the mechanism of blood flow. Circulation 1981; 63: 1417–1421. 6. Frenneaux MP and Steen S. Hemodynamics of cardiac arrest. In: Paradis NA, Halperin HR , Kern KB, et al., eds. Cardiac arrest. The science and practice of resuscitation medicine, 2nd ed. Cambridge: Cambridge University Press, 2007. pp 347–366. 7. Chandra N, Rudikoff M and Weisfledt M. Simultaneous chest compression and ventilation at high airway pressure during cardiopulmonary resuscitation. Lancet 1980; 1: 175–178. 8. Halperin HR, Weiss JL, Guerci AD, et al. Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs. Circulation 1988; 78: 754–760.
9. Hackl W, Simon P, Mauritz W, et al. Echocardiographic assessment of mitral valve function during mechanical cardiopulmonary resuscitation in pigs. Anesth Analg 1990; 70: 350–356. 10. Swenson RD, Weaver WD, Niskanen RA, et al. Hemodynamics in humans during conventional and experimental methods of cardiopulmonary resuscitation. Circulation 1988; 78: 630–639. 11. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004; 109: 1960–1965. 12. Gazmuri RJ, Ayoub IM, Radhakrishnan J, et al. Clinically plausible hyperventilation does not exert adverse hemodynamic effects during CPR but markedly reduces end-tidal PCO2. Resuscitation 2012; 83: 259–264. 13. Chalkias A and Xanthos T. Potent biomechanical and molecular behaviour of cardiac adipose tissue during cardiopulmonary resuscitation and post-resuscitation period. Acta Physiol (Oxf) 2012; 205: 3–5. 14. Chalkias A and Xanthos T. Intra-abdominal hypertension: a potent silent killer of cardiac arrest survivors. Am J Emerg Med 2012; 30: 502–504. 15. Runck H, Schumann S, Tacke S, et al. Effects of intraabdominal pressure on respiratory system mechanics in mechanically ventilated rats. Respir Physiol Neurobiol 2012; 180: 204–210. 16. Maertens VL, De Smedt LE, Lemoyne S, et al. Patients with cardiac arrest are ventilated two times faster than guidelines recommend: an observational prehospital study using tracheal pressure measurement. Resuscitation 2013; 84: 921–926.
Downloaded from acc.sagepub.com at UNIV CALGARY LIBRARY on May 24, 2015
