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Computer models in bedside physiology
Zhang, Y.
Publication date
2013
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Zhang, Y. (2013). Computer models in bedside physiology.
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COMPUTER MODELS IN BEDSIDE PHYSIOLOGY
ACADEMISCH PROEFSCHRIFT
ter verkrijging van de graad van doctor
aan de Universiteit van Amsterdam
op gezag van de Rector Magnificus
prof. dr. D.C. van den Boom
ten overstaan van een door het college voor promoties ingestelde
commissie, in het openbaar te verdedigen in de Agnietenkapel
op vrijdag 20 september 2013, te 12:00 uur
door
Yanru Zhang
Promotor: Prof.dr. J.H.R. Ravesloot
Copromotor: Dr. J.M. Karemaker
Overige leden: Prof.dr. E.T. van Bavel
Prof.dr.ir. C. Ince
Dr. R.W. Koster
Prof.dr. J.J. van Lieshout
Prof.dr. R.J.G. Peters
Faculteit der Geneeskunde
This thesis has been prepared in the department of Anatomy, Embryology and Physiology
of the Academic Medical Center, Amsterdam, The Netherlands
Table of contents
Chapter 1 General Introduction; aims of the thesis ... 5
Chapter 2 Optimal Cardiopulmonary Resuscitation as Identified by Computer
Modeling ... 11
Chapter 3 Abdominal counter pressure in CPR: What about the lungs? An in
silico study ... 33
Chapter 4 Search for HRV‐parameters that detect a sympathetic shift in heart
failure patients on ß‐blocker treatment ... 51
Chapter 5 A subgroup of Brugada patients shows low orthostatic blood pressures
as a sign of decreased sympathetic outflow ... 75
Chapter 6 Dynamics of Pulse Pressure Variability and the Difficulty of Predicting
Fluid Responsiveness. ... 91
Chapter 7 Summary and general conclusions ... 121
Nederlandse samenvatting ...125
Curriculum Vitae ... 127
Acknowledgements and colophon ... 128
Chapter 1
General Introduction; aims of the thesis
I have been trained in Biomedical Engineering (BME), a field that is, broadly speaking, geared to putting engineering methods to the assistance of clinical diagnosis and therapy. Biomedical engineering methods cover a wide range – from chemical engineering (tissue engineering and biomaterials) to electrical and mechanical engineering, as in the development of medical devices (12). In this thesis I apply bioelectrical (BME‐) methods to solve several medical problems. The thesis consists of two parts: the first part is about cardiovascular modeling and simulation; the second about analysis of beat‐to‐beat heart rate and blood pressure variability.1. Modeling and simulation of the human cardiovascular system
Models of the circulation are constructed to help understand physiological problems or to simulate interventions which are difficult or impossible to perform in real life. In this thesis we have reduced a number of aspects of the human cardiovascular model to a computer program. A good model can accurately describe (some of) the behavior of a particular system; use of the computer model may reduce experiment time and cost, avoid unnecessary injuries and ethical controversies. Since the first two‐element Windkessel (arteries) model was developed in 1899 by Otto Frank (11), until the overall circulation regulation model developed in 1972 by A. C. Guyton(5), the cardiovascular models went from very simple to very complex. Today circulation models are developed simple or complex according to the research requirements. In the following two sections the medical background of our specific cardiovascular model is introduced. Modeling or simulation can never replace real experiments, but it can always make real experiments better, or smarter. a. Cardiopulmonary Resuscitation simulation Cardiopulmonary arrest (CPA, also called cardiac arrest, CA) is a condition in which the heart suddenly and unexpectedly stops beating. Data from the Sudden Cardiac Arrest Association (www.suddencardiacarrest.org) show that in the U.S.A more than 300,000 people suffer a CPA each year, only 8% of whom survive. When CPA occurs, cardiopulmonary resuscitation (CPR) is an emergency procedure to preserve brain function (and that of other vital organs) until further measures are taken to restore spontaneous circulation and breathing. No matterwhere CPA occurs: on the street or in a hospital, in‐time and proper CPR and advanced life support can dramatically improve the survival rate to 50%! The International Liaison Committee on Resuscitation (www.ilcor.org ) holds consensus meetings and publishes updated CPR guidelines every five years since the first in 2000. There are also free training courses (in hospitals, on websites, and in TV programs). In Chapter 2 the question to be answered is: which CPR technique is the best one to improve cardiac output and organ perfusion? We compared five different CPR techniques, from conventional to innovative methods, by way of a cardiovascular circulation model. In Chapter 3 the question to be answered is: if we apply all those efforts described in chapter 2 to improve cardiac output and organ perfusion, is that really the best we can do for the patient? When we pushed this CPR optimization we found that with high pressures of thorax and abdomen compression and large venous returns, we had to consider the lungs as well. With improved mechanical techniques, ‘faster and harder’ compressions are not difficult to obtain (in‐hospital that is, with bare hands it is still difficult); the question is: can the lungs take it? b. Pulse Pressure Variation simulation Cardio‐pulmonary interaction is in the spotlight again. Over the last 20 years pulse pressure variation (PPV) has proven itself as an accurate predictor of volume responsiveness (1, 2, 4, 7, 9, 10): lower PPV implies that the volume status has pushed cardiac filling to the plateau of the Frank‐Starling curve to a saturation state(9). PPV is in clinical use to steer volume infusion for instance during surgery. However PPV does not work in situations like low tidal volume or spontaneous respiration(9). The question when PPV may reliably be used as indicator of volume responsive is still in discussion. In Chapter 6 we use a cardiovascular circulation model, with respiration and ANS control to simulate how PPV changes with changes in circulating volume, whether PPV can predict volume responsiveness in different situations. We compare these results to recordings in healthy test subjects who received a large intravenous saline infusion.
2. Analysis of beat‐to‐beat heart rate and blood pressure variability
Before going into heart rate variability (HRV) and blood pressure variability (BPV), we have toIntroduction; aims of the thesis
contraction, constriction and dilatation of blood vessels, contraction and relaxation of smooth muscle in various organs, visual accommodation, pupillary size and secretions from exocrine and endocrine glands. The ANS consists of two separate divisions: the parasympathetic and sympathetic systems, distinguished on the basis of anatomical and functional differences. The sympathetic nervous system aids in the control of most of the body's internal organs. Stress—as in the flight‐or‐fight response—is thought to counteract the parasympathetic system, which generally works to promote maintenance of the body at rest. Disturbances of the autonomic nervous system can be the cause of serious health problems. Autonomic nervous system disorders can occur alone or as the result of another disease, such as Parkinson's disease, alcoholism and diabetes. Therefore evaluation of the condition of the autonomic nervous system can be of diagnostic or predictive value. a. Heart rate variability (HRV) in CHF patients Heart rate variability (HRV) has emerged as a simple, noninvasive method to evaluate ANS activity. Reduced heart rate variability (HRV) is a powerful and independent predictor of an adverse prognosis in patients with heart disease and in the general population. In Chapter 4 we test which analysis method for HRV discriminates Chronic Heart Failure (CHF) patients on beta‐blocker treatment from healthy control subjects; next we test which of these parameter(s) detects the situation where such a patient would ‘slip into’ a more sympathetic condition. b. Challenge: Active standing up in Brugada patients When we stand up blood tends to shift towards the lower part of the body, sympathetic activity will raise heart rate, peripheral resistance, cardiac performance etc. to maintain blood pressure, at the same time parasympathetic activity will withdraw. Active standing‐up from supine or sitting is clinically used to test ANS function in control of blood pressure and heart rate (3, 6, 8, 13). In Chapter 5 we compare the change of beat‐to‐beat parameters like heart rate, blood pressure from supine to upright position in healthy control subjects and Brugada patients. The Brugada syndrome (BrS) is a genetic disease that is characterized by abnormal ECG‐findings and an increased risk of sudden cardiac death. The stand test is used to test thefunction of the ANS in Brugada patients and, ultimately, to find predictors for the risk of sudden cardiac death.
3. Chapter overview
In all there are seven chapters, as follows: 1. General introduction and aims of the thesis; 2. Optimal cardiopulmonary resuscitation as tested by computer modeling; 3. Abdominal counter pressure in CPR: What about the lungs? An in silico study; 4. Search for HRV‐parameters that detect a sympathetic shift in heart failure patients on β‐blocker treatment 5. A subgroup of Brugada patients shows low orthostatic blood pressures as a sign of decreased sympathetic outflow 6. Dynamics of pulse pressure variability and the difficulty of predicting fluid responsiveness; 7. Summary and general conclusions See the flowchart in Figure 1.References
1. Bendjelid K, Suter PM, and Romand JA. The respiratory change in preejection period: a new method to predict fluid responsiveness. J Appl Physiol 96: 337‐342, 2004.Introduction; aims of the thesis
3. Den Heijer JC, Bollen WL, Reulen JP, van Dijk JG, Kramer CG, Roos RA, and Buruma OJ. Autonomic nervous function in Huntington's disease. Arch Neurol 45: 309, 1988. 4. Freitas F, Bafi A, Nascente A, Assunção M, Mazza B, Azevedo L, and Machado F. Predictive value of pulse pressure variation for fluid responsiveness in septic patients using lung‐protective ventilation strategies. Br J Anaesth 110: 402‐408, 2013. 5. Guyton AC, Coleman TG, and Granger HJ. Circulation: overall regulation. Annu Rev Physiol 34: 13‐46, 1972. 6. Hägglund H, Uusitalo A, Peltonen JE, Koponen AS, Aho J, Tiinanen S, Seppänen T, Tulppo M, and Tikkanen HO. Cardiovascular autonomic nervous system function and aerobic capacity in type 1 diabetes. Front Physiol 3, 2012. 7. Kramer A, Zygun D, Hawes H, Easton P, and Ferland A. Pulse pressure variation predicts fluid responsiveness following coronary artery bypass surgery. Chest 126: 1563‐1568, 2004. 8. Martinmäki K, Rusko H, Saalasti S, and Kettunen J. Ability of short‐time Fourier transform method to detect transient changes in vagal effects on hearts: a pharmacological blocking study. Am J Physiol‐Heart C 290: H2582‐H2589, 2006. 9. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology 103: 419‐428, 2005. 10. Michard F, Boussat S, Chemlad D, Anguel N, Mercat A, Lecarpentier Y, Richard C, Pinsky MR, and Teboul J‐L. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Resp Crit Care 162: 134‐138, 2000. 11. Sagawa K, Lie RK, and Schaefer J. Translation of Otto Frank's paper "Die Grundform des Arteriellen Pulses" Zeitschrift fur Biologie 37: 483‐526 (1899). J Mol cell cardiol 22: 253‐254, 1990. 12. Wikipedia. Biomedical engineering. Last updated :2013 31 May, [cited 2013 15 June]; Available from: http://en.wikipedia.org/wiki/Biomedical_engineering. 13. Ziemssen T and Reichmann H. Cardiovascular autonomic dysfunction in Parkinson's disease. J Neurol Sci 289: 74‐80, 2010.Chapter 2
Optimal Cardiopulmonary Resuscitation as Identified by Computer
Modeling
Yanru Zhang, Xiaoming Wu, Hengxin Yuan, Lin Xu and John M.Karemaker Most of the work in this chapter has been the subject of 2 congress papers (2009 and 2010) on one of which Ms. Zhang was co‐author; moreover a full paper was published: Xu, L, Wu, X, Zhang, Y and Yuan, H.: The Optimization Study on Time Sequence of Enhanced External Counter‐Pulsation in AEI‐CPR. J. Computers 4; 1243‐1248 (2009) In view of this publication history and the fact that chapter 3 originated from the study reported here (as a warning not to ‘overdo’ the combination of abdominal and chest compression) an extensive discussion of the findings has been deferred to chapter 3. The appendix of chapter 2 (modeling details) applies to both the chapters 2 and 3.Abstract
Objective and Design: We aimed to find the optimal mode of cardiopulmonary resuscitation (CPR) in a computer model of the circulation. At least four variants of the simple compression of the heart between sternum and spine exist. For several reasons the efficacy of these modes is difficult to compare in clinical trials. In order to identify the optimal mode we conducted in silico experiments. Setting and Interventions: A Matlab® computer model of the circulation was developed. At simulated cardiac arrest the model was subjected to the various modeled CPR‐variants. The effects on cardiac output and perfusion of critical organs were compared. Measurements and Main Results: We compared Chest Only CPR (CO‐CPR), Active Compression‐Decompression CPR (ACD‐CPR), Interposed Abdominal Compression CPR (IAC‐CPR), thoracic‐abdominal compression‐decompression CPR (Lifestick‐CPR) and chest compression assisted with Enhanced External Counterpulsation on the legs and abdomen (EECP‐CPR). They were combined with the action of an Impedance Threshold Valve (ITV) to support venous return in the chest decompression phase. The three techniques that involve abdominal compression were at least twice as effective as the two that only apply force to the chest, independent of which parameter was used to quantify the result. Compression of the abdominal veins played a more important role than arterial compression in generating cardiac output and organ perfusion. Conclusions: In this in silico study Lifestick‐CPR was the most effective of the CPR techniques tested.Optimal cardiopulmonary resuscitation
Introduction
Sudden cardiac arrest is the most critical manifestation of cardiac disease, requiring immediate action to save the patient’s life. Outside a hospital this will mostly be done by cardiopulmonary resuscitation (CPR). This aims to keep the perfusion of heart, brain and lungs going while the heart is in arrest. Since the introduction of closed‐chest CPR several improvements to the classical, or Chest Only CPR (CO‐CPR) have been proposed (5, 11, 12, 19). These have in common that they either require the availability of equipment, or the presence of a second person assisting the one that delivers CPR. Therefore, the application of improved CPR is normally limited to a medical setting such as an ambulance or emergency room. The first variant is the combination of chest compression with Interposed Abdominal Compression (IAC‐CPR) (11). This involves the application of abdominal pressure during the relaxation phase of chest compression in otherwise classical CO‐CPR. This requires the presence of a second rescuer or a dedicated machine. In a second variant, chest compression is combined with active thorax expansion by the Active Compression‐Decompression CPR (ACD‐CPR) (5). This variant uses a suction device to actively compress and decompress the chest. A third variant involves machine‐driven, phased thoracic‐abdominal compression–decompression CPR (Lifestick‐CPR) (17). Lifestick‐CPR combines IAC and ACD‐CPR by alternately compressing and decompressing the chest and the abdomen through adhesive pads. And finally, a G‐suit like device has been designed to ‘milk’ the venous blood by inflatable cuffs wrapped around legs and buttocks. This variant is knows as Enhanced External Counterpulsation (EECP‐CPR) (8, 21). An inspiratory impedance threshold valve (ITV) has been proven as a beneficial adjunct (15). The valve closes the airways while the chest is being decompressed, with the objective to improve venous return due to the enhanced subatmospheric intrathoracic pressure during the recoil phase of chest compression. In our modeling ITV is combined with the aforementioned five CPR variants (Fig. 1) mentioned. At present there is no decisive evidence which one of the alternative CPR‐techniques is superior to Chest Only CPR (10, 20). In 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations emphasizes CO‐CPR as the only accepted resuscitation method (7). Clinical evidence is lackingsince for obvious reasons, it is not feasible to compare the various CPR techniques under the same condition. We therefore turned to computer models of the circulation. Otto Frank’s computational model of cardiac function in conjunction to the Windkessel concept conceived in the late 19th century (13), paved the way for the current era. In our time, with ever increasing calculation speed, computer modeling of circulation has shaped a new avenue of research to investigate medical problems (6, 16). A computer model may avoid the major disadvantages of animal and clinical experiments such as ethical issues, high costs, complexity, influence of external factors and operator‐dependent effects. Furthermore, it overcomes time and space limitations. We argue that to conquer the difficulties inherent to finding ‘evidence‐based’ best practice in an emergency situation like CPR, computer modeling is an obvious choice. This approach can quantify and evaluate the effects of the different components of the various CPR‐techniques to help decide which ones are effective and which are of little consequence. In this paper a circulatory model has been used as an experimental platform to test the five CPR techniques. In silico experiments do not put a critically ill patient at risk, and allow comparison of the various CPR techniques under highly‐defined conditions. We extended the model developed by Charles F. Babbs (1‐3) to simulate CO‐CPR, ACD‐CPR, IAC‐CPR, Lifestick CPR and EECP‐CPR. In all experiments we assumed that an ITV was in place. We focused on their hemodynamic effects to identify the optimal CPR technique. Here we report that Lifestick‐CPR is the most effective of the five CPR techniques.
Optimal cardiopulmonary resuscitation
Methods
Model description The model we adopted for this study is largely based on the work of Babbs et al. (1‐3). The model is an electrical equivalent circuit and has sufficient details to allow simulation of the five CPR techniques except for the initial blood volumes immediately after the cardiac arrest (CA). These blood volumes were estimated by us (Table 1). The model has 14 compartments, including four heart chambers, the pulmonary circulation, the thoracic aorta feeding an upper body and an abdominal compartment (Fig. 2). The structure of each lumped artery and vein compartment is the same, including a resistance followed by a capacitance (compliance). The peripheral circulation for each compartment is a simple resistance. Each ventricle has two valves. Each vein outside the trunk has one valve to ensure unidirectional blood flow. In view of the low blood velocity in CPR, inertial effects were neglected. The initial pressure of all systemic compartments in simulated CA is set to 5 mmHg, and to 8mmHg in the pulmonary part. Finally, it was assumed that coronary perfusion stopped during the compression phase.Optimal cardiopulmonary resuscitation
Figure 2. Bottom (detail): model of the chest pump including heart and pulmonary circulation. Relevant parameter values of the model are listed in the appendix. To help understand Fig. 2 a list of symbols and subscripts is given in Table 1 Table 1. Symbols and subscripts used in Fig. 2Symbol Electrical Mechanical
C capacitor Compliance (i.e. compliant compartment)
i current (blood) flow
R resistance resistance to flow
Subscript Definition Subscript Definition
aa abdominal aorta la left atrium and central pulmonary
ao thoracic aorta lv left ventricle
c / car carotid arteries mv mitral valve
cppa central to peripheral pulm aa. pa pulmonary arteries
cppv peripheral to central pulm vv. pc pulmonary capillary
fa femoral arteries ppa peripheral pulmonary arteries
fv femoral veins ppv peripheral pulmonary veins
h head vasculature pv pulmonary valve
ht heart (coronary) ra right atrium
iv iliac veins rv right ventricle
ivc / v inferior vena cava s splanchnic
CPR description CPR chest compression theoretically has two mechanically distinct effects on the central circulation. In the thoracic pump mechanism compression of lungs and mediastinal organs, including atria and great vessels (pulmonary trunk, ‐ arteries and aorta) causes blood to flow. In the cardiac pump mechanism compression of the heart causes blood to flow. Which one of the two mechanisms prevails remains controversial (18). In our model we left the controversy alone. Like in Babb’s model (2) we defined a factor ftp (0 ≤ ftp ≤ 1) to allocate the relative contribution of both mechanisms: ftp = 0 denotes pure cardiac pump mechanism, ftp = 1 denotes pure thoracic pump mechanism. Values between 0 and 1 denote a mixture of the two mechanisms. Every CPR technique involves chest compression. In our in silico experiments chest compression is modeled as described earlier (2, 4). Briefly, the resistance of the chest to external compression is represented by a simple spring and damper system defined by spring constant k and damping µ. During chest compression the force applied, F(t), leads to downward movement of both sternum and anterior chest wall over a distance x1 (cm). The reactive force due to damping depends on the speed of movement (x´1). We can now define F(t) as follows ' 1 1
)
(
t
k
x
x
F
(1) During the decompression phase F(t) will, initially, expand the cardiac chambers by filling with blood over a distance x2 (cm). The compression effects on the organs in the thorax can be expressed by x1 and x2 directly. For example, when V is the blood volume in a particular heart chamber and A its cross sectional area, thenA
V
x
2
/
(2) The mechanical effects of chest compression are translated in equivalent electrical events and applied to our model. The equations are presented in the appendix. For example, in IAC‐CPR, Lifestick CPR when the abdomen is compressed, the pressure to the abdomen is taken as a voltage source in series with the appropriate compliances (Civc and Caa in Fig.2). InOptimal cardiopulmonary resuscitation
allows positive pressure ventilation but prevents inspiration caused by subatmospheric airway pressures. Following the 2010 International Consensus on CPR and ECC Science with Treatment Recommendations (14), the compression frequency was set to 100 times/min. As compression/decompression waveforms we adopted sine waves or rather half‐sine waves as suggested by Babbs (2005) and Noordergraaf et al. (2005) (2, 9); the pressure patterns for the various CPR‐techniques are shown in Fig. 3A‐E. The model was solved using MAT LAB/Simulink. The solver was ODE4. To make the model reach steady state in a convenient time frame, step size was set at 0.0001s; simulation time was 40 s. The model reached a steady state after 8 seconds.Figure 3 Pressure waveforms: A: CO‐CPR; chest compression only; B: ACD‐CPR; chest compression and decompression combined; C: IAC‐CPR; chest compression and abdomen compression combined (abdomen: red dashed line); D: Lifestick CPR; chest compression and decompression, combined with abdomen compression and decompression. E: EECP‐CPR; chest compression and decompression, combined with abdomen and lower body compression (green line). Peak
Optimal cardiopulmonary resuscitation
Results
Comparison of the five CPR techniques To compare the relative effects of CO‐CPR, ACD‐CPR, IAC‐CPR, Lifestick CPR and EECP‐CPR (combined with ITV), we chose to present Cardiac Output (CO), carotid artery flow (Qcar) and myocardial flow (Qheart). Qcar reflects global cerebral perfusion, while Qheart reflects coronary perfusion. The results are summarized in Fig. 4. Figure 4 Comparison of the five different CPR techniques: A: CO cardiac output (L/min). B: Qcar average carotid blood flow and Qheart average coronary blood flow (ml/s). These three parameters are considered the most important parameters for CPR. The effects of IAC‐CPR, LIFESTICK CPR and EECP‐CPR give great improvement over CO‐CPR and ACD‐CPR Compared to CO‐CPR and ACD‐CPR, the three techniques that involve abdominal and/or lower body compression (IAC‐CPR, LIFESTICK CPR and EECP‐CPR) produce at least a two times higher CO. The same holds for Qcar and Qheart which are at least doubled compared to CO‐CPR and ACD‐CPR. Of the three superior variants Lifestick CPR has the best efficacy in terms of cardiac output and cerebral perfusion. Finally, in our model, ACD‐CPR is only slightly better than CO‐CPR. The aforementioned experiments were conducted with ftp = 0.75. To test for the sensitivity of our results for ftp we repeated the in silico experiments with ftp = 0, which represents thepure cardiac pump mechanism, and ftp = 1 which represents the thoracic pump mechanism. The results are summarized in Fig. 5. Figure 5 Comparison of CO between pure cardiac pump (Ft=0) and pure thoracic pump (Ft=1. Compared to CO‐CPR, IAC‐CPR, LIFESTICK CPR and EECP‐CPR give a higher CO irrespective of ftp. Of the three superior variants Lifestick CPR again has the best efficacy in terms of cardiac output regardless of ftp. Furthermore, except for EECP‐CPR, CO is higher when a cardiac pump mechanism is operative. Another striking result is the large difference between cardiac pump mechanism CO and thoracic pump mechanism CO in CO‐CPR and ACD‐CPR but not the other three. Veins/ Arteries‐only compression in abdomen and limbs IAC‐CPR, LIFESTICK CPR and EECP‐CPR have abdominal compression during chest decompression in common. Next, we aimed to analyze which aspect of this maneuver is more important, compression of the abdominal veins or compression of the abdominal arteries. Such an analysis, of course, is only possible in computer models of the circulation. Venous compression pushes blood towards the heart, thus favoring a higher cardiac output. Arterial compression raises the resistance of the vessels and tends to trap blood in the proximal arteries. This mechanism resembles the action of a balloon pump. Arterial compression potentially limits the arterial pressure fall upon chest decompression in the phase of diastolic runoff. To address this question we first determined CO, Qcar and Qheart when both the arteries and veins were compressed (V + A)compr. Next we determined the same three parameters if only the veins are compressed (Vonly) or if only the arteries are compressed (Aonly). Finally
Optimal cardiopulmonary resuscitation
Table 2. Ratios of veins‐ or arteries‐only compression to compression of both
IAC‐CPR LIFESTICK CPR EECP‐CPR
Veins‐ Arteries‐ Veins‐ Arteries‐ Veins‐ Arteries‐
CO (%) 94 52 93 43 89 46 Qcar (%) 91 45 94 41 92 41 Qheart (%) 71 86 76 67 57 93 Regardless of the CPR technique used, CO benefits most from venous compression. 89‐94% of the CO is preserved when only the veins are compressed. In contrast, CO halves (43 – 52%) when only the arteries are compressed. Similar observations were made for Qcar. Qheart, on the other hand, benefits most from arterial compression in IAC‐CPR and EECP‐CPR but not so much in Lifestick CPR. This follows directly from the assumption of stopped coronary flow during chest compression. These results explain to why IAC‐CPR, Lifestick CPR and EECP‐CPR are superior to CO‐CPR with regard to the resulting CO. The inferior vena cava (as simple model for the abdominal venous pool) is the largest vein in the body and a large amount of blood can be stored here. Compressing this vein restores a considerable venous return, thus favoring CO.
Discussion
In this paper CO‐CPR, ACD‐CPR, IAC‐CPR, Lifestick CPR and EECP‐CPR have been assessed using a computer model of the circulation. We reasoned that this model offers a uniform and unique platform to evaluate the different CPR techniques. We observed that abdominal and lower body compression in counter phase with thorax compression lead to substantially improved hemodynamic results and is therefore recommended. We concluded that Lifestick CPR gave the best effects in cardiac output, blood flow to brain and heart, EECP‐CPR increased mainly CO and Qcar. EECP‐CPR and Lifestick CPR produced better effects, but they are mechanical CPR techniques, which require the appliance at hand and trained professionals, which limits their use. IAC‐CPR can be performed just by hand, and the effects are tightly following EECP‐CPR and Lifestick CPR. If cardiac arrest happens in a public space, IAC‐CPR presumably is the best choice. Our model is restricted to the hemodynamic effects of CPR. Ventilation effects and oxygen saturation of the blood, important for survival, are not included. Another limitation is that thecompression pressure is set to fixed values, according to the recommendations of the Guidelines or clinical empirical setting. However, it is very likely that during actual resuscitation the compression pressure vary. Finally, our model is based on a ‘standard’ 70‐kg ‘textbook’ human subject, this potentially limits generalizability of our results.
References
1. Babbs CF. CPR techniques that combine chest and abdominal compression and decompression: hemodynamic insights from a spreadsheet model. Circulation 100: 2146‐2152, 1999. 2. Babbs CF. Effects of an impedance threshold valve upon hemodynamics in Standard CPR: studies in a refined computational model. Resuscitation 66: 335‐345, 2005. 3. Babbs CF. Efficacy of interposed abdominal compression‐cardiopulmonary resuscitation (CPR), active compression and decompression‐CPR, and Lifestick CPR: Basic physiology in a spreadsheet model. Crit Care Med 28, 2000. 4. Babbs CF, Weaver JC, Ralston SH, and Geddes LA. Cardiac, thoracic, and abdominal pump mechanisms in cardiopulmonary resuscitation: studies in an electrical model of the circulation. Am J Emerg Med 2: 299‐308, 1984. 5. Cohen TJ, Tucker KJ, Lurie KG, Redberg RF, Dutton JP, Dwyer KA, Schwab TM, Chin MC, Gelb AM, Scheinman MM, and . Active compression‐decompression. A new method of cardiopulmonary resuscitation. Cardiopulmonary Resuscitation Working Group. JAMA 267: 2916‐2923, 1992. 6. Guyton AC, Coleman TG, and Granger HJ. Circulation: overall regulation. Annu Rev Physiol 34:13‐46.: 13‐46, 1972. 7. Hazinski MF, Nolan JP, Billi JE, Bottiger BW, Bossaert L, de Caen AR, Deakin CD, Drajer S, Eigel B, Hickey RW, Jacobs I, Kleinman ME, Kloeck W, Koster RW, Lim SH, Mancini ME, Montgomery WH, Morley PT, Morrison LJ, Nadkarni VM, O'Connor RE, Okada K, Perlman JM, Sayre MR, Shuster M, Soar J, Sunde K, Travers AH, Wyllie J, and Zideman D. Part 1: Executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 122: S250‐275, 2010. 8. Yuan HX, Zheng ZS, Zhong HF, Liao XX, Du ZM and Huang X. “Double Pump” Cardiopulmonary Resuscitation: The Hemodynamic Study of the Inflational VEST with External Counterpulsation (II). J of Jinan Univ (Nature Science & Medicine Edition): S1, 1997 9. Noordergraaf JG, Dijkema JT, Kortsmit WJPM., Schilders WHA, Scheffer GJ, and Noordergraaf A. Modeling in Cardiopulmonary Resuscitation: Pumping the Heart.Optimal cardiopulmonary resuscitation
11. Ralston SH, Babbs CF, and Niebauer MJ. Cardiopulmonary Resuscitation with Interposed Abdominal Compression in Dogs. Anesth Analg 61: 645‐651, 1982. 12. Safar P. Closed chest cardiac massage. Anesth Analg 40: 609‐613, 1961. 13. Sagawa K, Lie RK, and Schaefer J. Translation of Otto Frank's paper "Die Grundform des Arteriellen Pulses" Zeitschrift fur Biologie 37: 483‐526 (1899). J Mol Cell Cardiol 22: 253‐277, 1990. 14. Sayre MR, Koster RW, Botha M, Cave DM, Cudnik MT, Handley AJ, Hatanaka T, Hazinski MF, Jacobs I, Monsieurs K, Morley PT, Nolan JP, Travers AH, and Adult Basic Life Support Chapter C. Part 5: Adult basic life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 122: S298‐324, 2010. 15. Shuster M, Lim SH, Deakin CD, Kleinman ME, Koster RW, Morrison LJ, Nolan JP, Sayre MR, Techniques CPR, and Devices C. Part 7: CPR techniques and devices: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 122: S338‐344, 2010. 16. Snyder MF, Rideout VC, and Hillestad RJ. Computer modeling of the human systemic arterial tree. J Biomech 1: 341‐353, 1968. 17. Tang W, Weil MH, Schock RB, Sato Y, Lucas J, Sun S, and Bisera J. Phased chest and abdominal compression‐decompression. A new option for cardiopulmonary resuscitation. Circulation 95: 1335‐1340, 1997. 18. von Planta M and Trilló G. Closed chest compression: a review of mechanisms and alternatives. Resuscitation 27: 107‐115, 1994. 19. W.B.Kouwenhoven, R.Jude J, and Knickerbocker GG. Closed‐chest cardiac massage. JAMA 173: 1064‐1067, 1960. 20. Ward KR. Possible reasons for the variability of human responses to IAC‐CPR. Acad Emerg Med 1: 482‐489, 1994. 21. Yuan H, Zheng Z, and Jiang S. The Hemodynamic Study of The Chest Compression Assisted with Enhanced External Counterpulsation. Chinese J Emerg Med 4: 140‐144, 1995.Appendix ‐ modeling details
Table 1A Definitions and values of resistances Definition R i t f S b l H /L/ carotid arteries Rc 60 head vasculature Rh 5520 jugular veins Rj 30 tricuspid valve Rtv 5 pulmonic valve Rpv 10 path from central to peripheral pulmonary arteries Rcppa 10 path from peripheral to central pulmonary veins Rcppv 5 mitral valve Rmv 5 aortic valve Rav 10 pulmonary capillary bed Rpc 105 coronary vessels (heart) Rht 15780 aorta Ra 25 inferior vena cava Rv 25 splanchnic vasculature Rs 1800 iliac arteries Ria 360 iliac veins Riv 180 leg vasculature Rl 8520 airways to ventilation Rairway 1.2Optimal cardiopulmonary resuscitation
Table 1B Definitions and values of compliances Definition Compliance of the ….. Symbol L/mmHg Initial volume (L) Unstressed volume (L) arrested right ventricle Crv 0.01600 0.150 0.070 large pulmonary arteries Cpa 0.00420 0.109 0.076 peripheral pulmonary arteries Cppa 0.00042 0.160 0.157 peripheral pulmonary veins Cppv 0.00128 0.300 0.290 central pulmonary veins and left atrium Cla 0.01280 0.250 0.148 arrested left ventricle Clv 0.00800 0.150 0.086 carotid arteries Ccar 0.00020 0.132 0.131 jugular veins Cjug 0.01200 0.216 0.156 thoracic aorta Cao 0.00080 0.078 0.074 right atrium and intrathoracic great veins Crh 0.00950 0.367 0.320 abdominal aorta Caa 0.00040 0.114 0.112 inferior vena cava Civc 0.02340 1.930 1.813 femoral arteries Cfa 0.00020 0.078 0.078 femoral veins Cfv 0.00470 0.267 0.244 combined lung‐chest wall Clung 0.15800 ‐ ‐ Initial conditions: 5 mmHg filling pressure in the systemic, 8 mmHg in the pulmonary circulation. Valves are supposed to be ideal, driven by pressure differences with the resistances as indicated, immediately closing when reverse flow would occur. Compliances are supposed to behave as follows: For positive pressures, volumes are increasing linearly above the unstressed volume as indicated by the index of compliance; for negative pressures volumes are supposed to be zero and the unstressed volume is emptied. For more details the reader is referred to: Koeken, Y, Aelen P, Noordergraaf GJ et al. The influence of nonlinear intra‐thoracic vascular behaviour and compression characteristics on cardiac output during CPR. Resuscitation 2011; 82: 538‐544.Table 2 Miscellaneous: Abbreviations and definitions
Abbreviation Definition
ValueAl Cross section area of lung squeezed by sternal compression 100 cm2 Ara Ala Arv Alv Cross section area of cardiac chambers in front to back 20 cm2 Frequency Number of cycle per minute for chest and abdominal pressure 100/min Duty cycle Fraction of cycle time for chest compression 0.5 ftp Thoracic pump factor (0.75=adult, 0.25=child, 1.0=emphysema, 0=open chest) 0 ‐ 1.0 Pinit Initial equilibrium pressure of arrested circulation 5 mmHg Fmax_chest Maximum external force on sternum 400 N X0 Effective compression threshold 2 cm Table 3 Blood flow Abbreviations and definitions
Abbreviation Definition
ic Blood flow in both carotid arteries ih Blood flow in the head vasculature ij Blood flow in both jugular veins ii The input blood flow to thoracic io The output blood flow from thoracic iht Blood flow in coronary vessels(heart) ia Blood flow in the aorta is Blood flow in residential systemic vasculature iv Blood flow in the inferior vena cava ifa Blood flow in both femoral arteries ifv Blood flow in both femoral veins i2 Blood flow in the pulmonary veins i3 Blood flow between central and peripheral pulmonary arteries i4 Blood flow in the pulmonary capillaries i5 Blood flow in between central and peripheral pulmonary veinsOptimal cardiopulmonary resuscitation
Table 4 Volumes and pressures: Abbreviations and definitionsAbbreviation Definition
Blood volume Vaa Blood volume in the abdominal aorta Vivc Blood volume in the inferior vena cava Via Blood volume in both iliac arteries Vfa Blood volume in both femoral arteries Vfv Blood volume in both femoral veins Blood pressure Pao Blood pressure of thoracic aorta Paa Blood pressure of the abdominal aorta Pivc Blood pressure of the inferior vena cava Pfa Blood pressure of both femoral arteries Pra Blood pressure of the right atrium Pfv Blood pressure of the femoral veins Peecp Compression pressure to lower body Pabd compression pressure to the abdomenThere are 14 compartments in the model; there are 14 pairs of formulas to describe the relationship between pressure and volume. ‘P’ stands for pressure, ‘V’ stands for volume, and Subscripts indicate which compartment the formulas describe. ( ) [ ] car c h car jug ao car c h car car car V i i t P P P P t R R V P C (1) ( ) [ max(0, )] jug h j
car jug jug ra
h j jug jug jug V i i t P P P P t R R V P C (2) When the chest is compressed, the organs in the chest pump undergo different pressure weights. ‘F(t)’ is the chest compression force, ‘PM’ is the pressure to the mediastinum, ‘Plung’ is
the pressure to the lungs. ‘ftp’ is thoracic pump factor; more information in references 2, 3. 1 1 ( ) 0 F t kx x (3) 1 2 0
(
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d
(4) 1 [ lung month] lung L lung airway P P dt dP x A C R (5) 3 4 ( ) [ ] ppa pa ppa ta tv cppa pa ppa ppa lung ppa V i i t P P P P t R R V P P C (6)Optimal cardiopulmonary resuscitation
4 5 ( ) [ ] ppv ppa ppv ppv la pc cppv ppv ppv lung ppv V i i t P P P P t R R V P P C (7) 1 0 ( ) [max(0, ) ] ao o c a ht lv ao ao car ao car ao ra av c a ht pa ao lung tp pa V i i i i t P P P P P P P P t R R R R V E P P f x t C d (8) 2 3 1 0 ( ) [max(0, ) ] pa rv pa pa ppa pv cppa pa pa lung tp pa V i i t P P P P t R R V E P P f x t C d (9) 1 0(
)
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ra j v ht i jug ra ivc ra ao ra ra rv j v ht tv ra ra ra lung tp ra raV
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(10) 2 1 0 ( ) [max(0, ) max(0, )] ( ) rv i rv pa ra rv tv pv rv rv rv lung rv rv V i i t P P P P t R R V E V P P x t C d A (11) 5 6 1 0 ( ) [ max(0, )] ( ) la ppv la la lv cppv mv la la la lung tp la la V i i t P P P P t R R V E V P P f x t C d A (12)6 1 0
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lv o la lv lv ao mv av lv lv lv lung lv lvV
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(13)When the abdomen is compressed in IAC-CPR, the abdominal aorta and inferior vena cava are directly exposed to the compression pressure.
( ) [ ] aa a s ia aa fa ao aa aa ivc a s ia aa aa abd aa V i i i t P P P P P P t R R R V P P C (14)
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ivc s v fv fv ivc aa ivc ivc ra s v iv ivc ivc abd ivcV
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(15)When the lower body is compressed in EECP-CPR, it undergoes the compression pressure directly. )] , 0 max( [ ) ( 1 ] [ ) ( 1 iv ivc fv l fv fa fv l fv l fv l fv l fv fa ia fa aa fa l l ia fa l fa R P P R P P C t P t i i C P P R P P R P P C t P t i i C P P (16)
Chapter 3
Abdominal counter pressure in CPR: What about the lungs?
An in silico study
Yanru Zhang and John M. Karemaker This chapter had been published as: Zhang Y and Karemaker JM. Abdominal counter pressure in CPR: What about the lungs? An in silico study. Resuscitation 83: 1271‐1276, 2012. The appendix of chapter 2 equally applies to the model used in this chapter.Abstract
The external pumping action in CPR should generate sufficient flow and pressure, but the pump must also be ‘primed’ by ongoing venous return. Different additions to standard CPR are in use just for this purpose. Active decompression of the thorax (ACD‐CPR) to ‘suck in’ venous blood has proven successful, but, theoretically, compression of venous reservoirs in the abdomen should be even more effective. We compared different techniques for improved CPR with specific attention to the pulmonary circulation. We did our comparisons ‘in silico’ rather than ‘in vivo’ in a well‐evaluated computer model. Methods: We used an adapted version of Babb’s computer model for CPR, reprogrammed in Matlab®. 1) We compared standard chest compression‐only CPR (CO‐CPR) and ACD‐CPR to CPR with interposed abdominal compression (IAC‐CPR). 2) Since the thorax/heart configuration differs between patients, and consequently the way blood is propelled by the chest compressions, we checked the influence of the ratio thoracic/cardiac pump effectiveness. Results: 1) Only IAC‐CPR leads to physiological values for mean aortic pressure and cardiac output. 2) However, since the whole heart is in the pressure chamber of the compressed thorax, pulmonary artery pressure rises to about the same level as aortic pressure. In practice, this might lead to pulmonary edema during and after CPR, unless 3) Intra‐abdominal compression pressure is strictly limited; simulations indicate that intra‐abdominal pressure should not exceed 30‐40 mmHg. Conclusions: IAC‐CPR outperforms the other techniques in achieving good aortic pressure and cardiac output. However, abdominal pressure should be limited.CPR-optimisation and the lungs
Introduction
Mechanical adjunct devices which do more than just compressing the thorax to improve CPR have been proposed and tried in various studies (1‐6).Despite the initial high hopes of the inventors, to date these CPR techniques fail to give consistently better outcomes than standard CPR (S‐CPR) (7‐9). In 2010 the AHA published its updated guidelines (10) for how and when to perform Cardiopulmonary Resuscitation (CPR). The new guidelines devote only 1.5 out of 330 pages to the option of more complex, possibly machine‐supported, modalities of CPR in view of the lack of supporting clinical evidence (10,11).One wonders why praxis is lagging behind, since it makes perfect sense, theoretically, to improve venous return by intermittent abdominal in counter phase with thoracic compressions (IAC‐CPR). In early 2011 the Lancet published a large randomized, multicenter trial that shows improved outcome of CPR when the effect of chest compressions is supported by mechanical devices (12), these are: A hand‐held suction cup with handle placed on the thorax to support active thoracic recoil in the relaxation phase (ACD‐CPR) and an impedance‐threshold valve (ITV) to connect to a facemask or advanced airway access that would not open until intrathoracic pressure would fall below – 16 cm H2O pressure. The latter was in place to promote venous return during the supported chest recoil phase. The Lancet study thus encourages adjuncts to S‐CPR. It showed that ACD‐CPR with ITV gave the same survival rate, but better neurological function than S‐CPR (12). The only significant adverse effect where intervention‐ and S‐CPR groups differed was in the prevalence of pulmonary edema: 11% in the intervention group (94/840) compared to 8% (62/813) in the SCPR group. This inspired us further to elaborate on our earlier modeling work (13), looking more specifically into the pulmonary effects of increased venous return during CPR. For the present study, we used a computer model to simulate compression‐only (CO‐CPR) following the new (2010) guidelines, i.e. 100 compressions per minute, no breaks for chest inflation; next ACD‐CPR with and without ITV and, additionally, CPR with Interposed abdominal compression (IAC‐CPR). The aim was to explore favorable and potentially unfavorable hemodynamic changes produced by augmented CPR techniques compared to standard manual CPR, specifically looking at the effects of improved venous return. For the purpose of this theoretical study, we used a well‐known mathematical model of the circulation and the application of CPR, which has been developed and extensively published by Babbs (14‐16). A computer model allows analyzing the effects of alternative CPR techniques on many aspects of the cardiovascular and respiratory systems at the same time.In the experimental laboratory, this would require sacrificing many experimental animals and in the clinic, it would be next to impossible. In the model we checked the effects on systemic and pulmonary pressures, ventricular pressures, flow to vital organs and so on. Our working hypothesis was that the CPR techniques with supported venous return may have side effects which prevent them from reaching their full beneficial effect.
CPR-optimisation and the lungs
Methods
Model description The computer model used is essentially Babbs’ circulatory model, programmed in Matlab® as we used it in earlier studies; details are in (13,15). In short, the model simulates a 70‐kg adult, it includes four heart chambers, the pulmonary circulation, the thoracic aorta feeding an upper body compartment and an abdominal compartment, the latter feeds the lower body (legs, buttocks) compartment. CPR is modeled by the application of external forces to the various compartments. Figure1A gives a mechanical representation of the model, Figure1B its electrical analogue as used in the calculations; Table 1 in the Appendix to chapter 2 summarizes the most important model parameters; Table 1A gives the resistances in the model, Table 1B the compliances, initial volumes and unstressed volumes in all compartments. The model supposes a constant blood volume of 4.36 liters, the subject starts in the condition of cardiac arrest, where blood flow has stopped and the blood volume is distributed over the various compartments in relation to their volume compliance. The mean filling pressure in the systemic circulation was chosen to be 5 mmHg (17) that of the pulmonary circulation 8 mmHg while supine. Figure 1 A: Schematic of the circulation under CPR. ACD: Alternating Compression‐Decompression, IAC: Interposed Abdominal Compression, ITV: Impedance threshold valve, impeding inflow of air at negative intrathoracic pressures. NV: Niemann’s valve, preventing reverse venous flow from the thorax to head and neck. VV: venous valves in the legs, preventing reverse venous flow from the abdominal compartment. The (upper) arterial side is connected by lumped Starling resistors to the (lower) venous side.Figure 1 B: Electrical analogue of the circulation as used in the calculations. Top: the whole circulation; Bottom: the details inside the chest pump. Symbols as explained in Appendix: Table 1.
CPR-optimisation and the lungs
‘circulatory pumps’ to the generation of flow and blood pressure. We followed Babbs’ model in attributing 75% of the CPR effect to the ‘thoracic pump’ and ‘25% to the ‘cardiac pump’ effects (15). As this choice influences the result, we also checked various other values of this factor. Abdominal compression is supposed to lead to an immediate pressure increase within the abdomen, compressing in particular the capacity veins feeding the right heart, but also the abdominal aorta, giving the effect of an aortic balloon pump, and changing diastolic runoff. Babbs’ original model does not include abdominal wall mechanics, which in general is much less of a hindrance to externally applied pressures. Therefore, we assumed a homogeneous pressure in the abdominal cavity, following the set time pattern not bothering about how much pressure was applied to the outside to generate this inside pressure. The model does not take displacement of the diaphragm into account, neither during thoracic nor abdominal compression. Computed pressures in the aorta (minus right atrial pressure) lead to organ flow, depending on the estimated resistances of the various organs (brain in particular). To get a realistic estimate of coronary flow, we suppose that no flow passes while the heart is being compressed. CPR techniques We simulated three different CPR techniques: first chest‐compression only CPR (CO‐CPR) as applied by one rescuer and Active Compression‐Decompression CPR (ACD‐CPR) with and without an impedance–threshold valve (ITV) as in the Lancet study (12). Furthermore, we implemented one technique that combines thorax ‐ with abdomen compression in the relaxation phase to support venous return, i.e. Interposed Abdominal Compression CPR (IAC‐CPR). Two rescuers together, one administering thorax compression and the other one compressing the abdomen in counter phase, can administer this (3,18). In keeping with the new guidelines, a compression frequency of 100/min is used for all techniques; no time is devoted to ventilation. The chest is compressed by a force of 400 N, or around 40 kilo’s, which clinically relates to a depth of 5.1 cm; non‐overlapping half‐sinusoids with 50% duty cycle are used (15,19) as external pressure waveforms. A force of 150 N supports active decompression of the thorax in ACD‐CPR; abdominal compression is supposed to result in (up to) 100 mmHg intra‐abdominal pressure in IAC‐CPR. The latter two are also shaped as half‐sinusoids, with 50% duty cycle in exact counter phase to the thorax compressions.Results
Effects of various CPR techniques The successive columns of Table 1 show that with increasing complexity of the applied technique the numbers get better: higher aortic pressures, higher CO. Indeed, by using IAC‐CPR almost physiological levels for mean aortic pressure and cardiac output can be reached. Figure 2 demonstrates how this is obtained: in the phase of abdominal compression, thoracic aortic pressures rise again due to increased systemic vascular resistance during diastolic runoff. In line with the definitions for the working heart, we have defined diastolic pressures as those pressures at the start of thorax compression.Figure 2: Aortic (Pao fat –red‐ line) and peripheral pulmonary venous pressures (Pppv thin –blue‐ line)
during Interposed Abdominal Compression CPR (IAC‐CPR) at a compression rate of 100/min, abdominal compression pressure: 40mmHg, thoracic pump factor of 0.75.
CPR-optimisation and the lungs
for ventricular end‐diastolic and pulmonary artery pressures. All numbers indicate that pulmonary capillary pressures will be above normal plasma colloid osmotic pressures (around 25‐30 mmHg (20)), which may cause acute pulmonary edema. However, one may well ask to what extent these results are due to choices made in the modeling process, in particular the division between cardiac pump and thoracic pump. In the computations for Table 1 a thoracic pump factor of 0.75 was used. Table 1. Blood pressures and flows for the tested CPR‐techniques. Thoracic pump factor is 0.75Ventilation/ITV CO‐CPR‐ ACD‐CPR
No ITV ACD‐CPR With ITV IAC‐CPR No ITV IAC‐CPR No ITV IAC‐CPR No ITV AC‐CPR No ITV Chest comp/decomp (force in N) 400/‐ 400/150 400/150 400/‐ 400/‐ 400/‐ 400/‐ Abdominal compression ‐ ‐ ‐ 40 80 100 Continuo us 40 Pao (sys/dia; mean) 47/22; 30 52/27; 35 55/28; 37 61/34; 46 75/45; 62 83/52; 71 66/41; 49 Plv (sys/end‐dia) 48/7 53/8 56/10 62/26 76/44 84/53 67/27 CO (l/min) 1.3 1.5 1.7 2.0 2.8 3.2 1.4 Ppa (sys/dia; mean) 41/7; 18 41/7; 17 42/6; 18 62/27; 39 82/47; 58 92/57; 68 62/27; 39 Prv (sys/end‐dia) 42/4 41/4 43/1 63/25 83/47 93/57 62/22 Pppv (sys/dia; mean) 33/7; 16 31/7; 14 34/5; 15 53/26; 35 72/44; 53 81/53; 62 53/27; 36 Qheart (ml/s) 0.8 0.9 1.0 1.0 1.2 1.4 0.8 Qhead (ml/s) 5.3 6.0 6.6 8.5 11.8 13.6 6.1 All pressures are in mmHg. Pao: aortic pressure; Plv: left ventricular pressure; Ppa: pulmonary arterial pressure; Prv: right ventricular pressure; Pppv: peripheral pulmonary veins; sys: systolic pressure; dia: diastolic pressure; end‐dia: end‐diastolic pressure. CO: cardiac output; Qheart: coronary blood flow; Qhead: blood flow to neck and head; AC‐CPR: abdominal compression CPR (the pressure is no longer interposed, but continuous).
Cardiac vs thoracic pump The ‘cardiac pump’ theory supposes that forward blood flow is caused by direct compression of the heart under the sternum (with blood flow similar to an intact circulation); while the ‘thoracic pump’ theory supposes that blood flow is secondary to changes in intrathoracic pressure (21). The exact contribution of either pump mechanism in a specific case is unknown (21‐24),and may depend on thorax‐heart configuration: a deep thorax translating CPR‐pressure more into a thoracic pump effect, a flat (or child’s‐) thorax more into a cardiac pump effect. Therefore, we tested how the alternative attribution of ‘thoracic pump’ or ‘cardiac pump’ might influence the results. In the model a thoracic pump factor 0 implies a pure cardiac pump, 1 a pure thoracic pump. Figure 3 Top: Effects of thoracic pump factor in CO‐CPR (cardiac pump factor + thoracic pump factor = 1); a higher thoracic pump fraction leads to lower aortic pressures and higher pulmonary pressures. A thoracic pump factor = 0 is comparable to direct cardiac massage. Chest compression force: 400 N. Bottom: Effects of thoracic pump factor in IAC‐CPR; a higher thoracic pump factor has little effect on aortic pressures and leads to higher pulmonary pressures. Chest compression Force: 400 N; abdominal compression pressure: 100 mmHg.
