American Heart Journal
Volume 156, Issue 6 , Pages 1222.e1-1222.e7, December 2008

Direction of blood flow from the left ventricle during cardiopulmonary resuscitation in humans—its implications for mechanism of blood flow

  • Hyun Kim, MD

      Affiliations

    • Department of Emergency Medicine, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Sung Oh Hwang, MD

      Affiliations

    • Department of Emergency Medicine, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • Corresponding Author InformationReprint requests: Sung Oh Hwang, MD, Department of Emergency Medicine, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, 162 Ilsandong, Wonju 220-701, South Korea.
    • ,
  • Christopher C. Lee, MD

      Affiliations

    • Department of Emergency Medicine, Stony Brook University Hospital, Stony Brook, NY
    • ,
  • Kang Hyun Lee, MD

      Affiliations

    • Department of Emergency Medicine, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Jang Young Kim, MD

      Affiliations

    • Department of Cardiology, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Byung Su Yoo, MD

      Affiliations

    • Department of Cardiology, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Seung Hwan Lee, MD

      Affiliations

    • Department of Cardiology, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Jung Han Yoon, MD

      Affiliations

    • Department of Cardiology, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Kyung Hoon Choe, MD

      Affiliations

    • Department of Cardiology, Institute of Lifelong Health, Wonju College of Medicine, Yonsei University, Wonju, South Korea
    • ,
  • Adam J. Singer, MD

      Affiliations

    • Department of Emergency Medicine, Stony Brook University Hospital, Stony Brook, NY

Received 3 April 2008; accepted 8 September 2008. published online 03 November 2008.

Article Outline

Background

Common mechanisms proposed to explain forward blood flow during cardiopulmonary resuscitation (CPR) include the cardiac and thoracic pumps. However, the exact role of the left ventricle in promoting forward blood flow during standard CPR in humans is mostly unknown. The aim of this study was to explore the role of the left ventricle in generating forward blood flow during standard CPR in humans by observing the direction of blood flow during CPR.

Methods

Ten patients with non-traumatic cardiac arrest were enrolled in this study. During CPR, contrast echocardiography with agitated saline was performed in the left ventricle and the aorta, and the direction of contrast flow was assessed using transesophageal echocardiography.

Results

On injecting the contrast in the aortic root, anterograde flow from the aorta during the compression phase was observed. No aortic regurgitation was present. Retrograde blood flow from the left ventricle into the left atrium as well as anterograde blood flow from the left ventricle into the aorta during the compression phase of CPR was observed in all cases. On injecting the contrast in the aortic root, anterograde flow from the aorta during the compression phase was observed. During each cycle of chest compression, the mitral valve closed during compression and opened during relaxation, and the aortic valve opened during compression and closed during relaxation.

Conclusions

Retrograde flow to the left atrium and forward blood flow onto the aorta on left ventricular contrast echocardiography during the compression phase suggests that extrinsic compression of the left ventricle by external chest compression acts as a pump in generating blood flow during standard CPR in humans.

 

The blood flow generated during cardiac arrest by standard cardiopulmonary resuscitation (CPR) is known to be only 17% to 27% of the normal cardiac output.1, 2, 3, 4 Although more than 40 years have passed since the introduction of the current technique for CPR, controversies over the mechanism of blood flow during standard CPR continue. Although the thoracic pump5, 6, 7 and cardiac pump8, 9 theories are currently considered as the most likely mechanisms for generating blood flow by external chest compression, the phenomenon of actual blood-flow generation in the human body still remains poorly understood. However, identification of the mechanism of blood-flow generation during CPR is a prerequisite for developing improved methods of CPR to augment blood flow.

At the time external chest compression was suggested as a method of artificial circulation, the “cardiac pump mechanism” was proposed as the mechanism of blood flow.10 According to this theory, the mechanism of blood flow during external chest compression is the result of direct compression of the heart between the sternum and the vertebrae, which squeezes the blood from the heart while the cardiac valves prevent retrograde blood flow through the mitral valve. The cardiac pump theory was challenged by several investigators11, 12, 13, 14 who observed that increased intrathoracic pressure alone can generate blood flow. According to the thoracic pump theory, external chest compression during standard CPR causes an increase in the intrathoracic pressure, which generates a pressure gradient between the intrathoracic vascular compartment and the extrathoracic vascular compartment that causes blood to flow from intrathoracic arteries to extrathoracic arteries. According to this theory, the heart is presumed to be a passive conduit of blood flow during CPR.

Evidence to identify the mechanism(s) of blood flow has been gathered from animal experiments and from observations of indirect phenomena, such as the closure of the mitral valve during chest compression in the humans.7, 8, 9, 11, 12 The results obtained from animal experiments cannot be generalized to humans because the chest configurations of the animals used in these experiments were different from those of the human body. Recently, transesophageal echocardiography (TEE) was introduced to investigate the mechanism of blood flow during CPR in humans because it provides high-resolution images of the thoracic cardiovascular structures and can be performed without interrupting external chest compression. Transesophageal echocardiography studies have focused on the position of the mitral valve during chest compression. However, consistent analysis has yet to be established.

The most controversial issue concerning the mechanism of blood flow during CPR is the role of the cardiac chamber during external chest compression. If the pressure of the left ventricle during compression systole is highest (cardiac pump) among adjacent structures, the blood will flow away from the left ventricle, including anterograde flow into the aorta as well as retrograde flow into the left atrium. In contrast, if the pressure of the left ventricle during compression systole is equal to that of the surrounding intrathoracic vascular compartment (as proposed by the thoracic pump theory), the blood would flow only in the anterograde direction from the left ventricle into the aorta. To test these opposing “cardiac pump” and “thoracic pump” theories, we performed contrast echocardiography of the left ventricle to verify the direction of blood flow during standard CPR in humans in cardiac arrest.

Back to Article Outline

Methods 

Study design 

A prospective observational study design was used to determine the direction of blood flow in patients undergoing CPR during cardiac arrest. The study was approved by the institutional review board with a waiver of informed consent. Verbal instructions were given to the patients families.

Subjects 

We included nontraumatic cardiac arrest patients older than 15 years who had been admitted to the emergency department in cardiopulmonary arrest or who had developed cardiac arrest during their stay in the emergency department. We excluded patients with aortic disease, such as a dissection or an aneurysm, with cardiac arrest due to massive hemorrhage, or with a structural cardiac abnormality.

Setting 

The study was conducted at a university-based tertiary care emergency department in South Korea. Subjects were only enrolled during the daytime (8:00 am to 6:00 pm) due to the limited availability of TEE and catheterization after hours.

Interventions 

Cardiopulmonary resuscitation 

A team of 3 emergency medicine residents and 2 nurses performed CPR once a cardiac arrest patient arrived at the ED or when cardiac arrest occurred in the ED. Cardiopulmonary resuscitation was performed according to the guidelines set by the American Heart Association.15 After endotracheal intubation was performed, an end-tidal carbon dioxide detection probe (Capnostat mainstream CO2 module, GE Medical Systems, Milwaukee, WI) was attached to the endotracheal tube for continuous monitoring of carbon dioxide. Uninterrupted external chest compressions were performed by an emergency medicine resident at a rate of 100 times per minute according to the rhythm of a metronome. Artificial ventilation was performed using a self-inflating bag-valve mask with a rate of 10 to 12 per minute. An intravenous dose of 1 mg of epinephrine was administered every 3 minutes through a vein in the upper extremities or through a central vein.

Transesophageal echocardiography and catheter insertion 

After endotracheal intubation, a team of physicians that did not belong to the CPR team performed catheterization and TEE. Transesophageal echocardiography was performed by an experienced cardiologist (S.O.H.) with 500 such examinations. After insertion of the TEE transducer (5 MHz, Ultramark-9, Advanced Technology Laboratories Inc, Bothell, WA, or 5-MHz, Sequoia C256 echocardiography system, Acuson Corp, Malvern, PA) into the esophagus, structural abnormalities of the heart were excluded through a transverse 4-chamber view, and the presence of aortic dissection was determined by observing the ascending aorta and the descending thoracic aorta. The left ventricle, the left atrium, and the ascending aorta were assessed through a 135° longitudinal view. All procedures from intubation to removal of the TEE transducer were recorded on S-VHS videotape.

Immediately after a brief assessment of the heart and the aorta with TEE, catheterization was performed. After the right internal jugular vein had been punctured according to the Seldinger method, a central venous catheter was inserted into the right atrium to measure the right atrial pressure. The insertion of the right atrial catheter was guided by a right atrium-left atrium longitudinal view on TEE. An introducer sheath (6.5 F, Arrow International Inc, Reading, PA) was inserted into the left or the right femoral artery and a pigtail catheter (5 F, Cordis, A Johnson & Johnson Company, Warren, NJ) was introduced into the left ventricle using a guiding wire. The position of the pigtail catheter in the aorta was confirmed by using an aortic longitudinal view on TEE. The insertion of the catheter into the left ventricle was verified while observing the ascending aorta and the left ventricle together in a state in which the TEE transducer was rotated to 135°. Subsequent to the completion of catheter insertion, the left ventricular pressure was monitored by using a fluid-filled system (Solar 8000 Modular Patient Monitor, GE Medical Systems). After left ventricular contrast echocardiography, the aortic and right atrial pressures were measured. The coronary perfusion pressure was calculated by subtracting the right atrial pressure from the aortic pressure during compression diastole. Each measured pressure was recorded on a paper printer. Performance of TEE and introduction of the catheters did not delay any resuscitative attempts because the TEE transducer was inserted after endotracheal intubation and the right internal jugular vein was chosen to access the right atrium.

Contrast echocardiography 

A single bolus of agitated saline (10 mL) was injected into the pigtail catheter to perform contrast echocardiography with a 135° longitudinal view. After injection of the agitated saline, the left ventricle, the left atrium, and the ascending aorta were observed by using TEE until the contrast bubbles disappeared from the left ventricle. Subsequently, another bolus of the agitated saline was injected into the aorta when the pigtail catheter was pulled back in the aorta. During the contrast echocardiography, the same medical staff performed external chest compressions.

Interpretation 

Direction of blood flow 

Two cardiologists determined the direction of blood flow by analyzing the images recorded during contrast echocardiography in the left ventricle and the aorta. The presence of retrograde flow during the left ventricular contrast echocardiography was determined by observing whether an echocardiographic contrast appeared in the left atrium. The magnitude of retrograde flow was estimated according to the Sellers method,16 which is used to semiquantitatively determine mitral regurgitation during cardiac catheterization. Mild degree (grades I and II) retrograde flow were determined as being present when a narrow-to-moderate-width regurgitant jet of slight to moderate density was noted and a minimum-to-moderate opacification of the left atrium quickly cleared. Moderate-degree (grade III) retrograde flow was determined as being present when a well-defined jet was absent and left atrial opacification was intense, immediate, and lingering. Severe-degree (grade IV) retrograde flow was determined as being present when the left atrium appeared denser than the left ventricle or aorta.

Stroke volume and ejection fraction of the left ventricle 

The images recorded during CPR were analyzed using the internal cardiac measurement program of the echocardiography system. After the recorded images from the cardiac analysis system had been frozen, calibration was performed using an internal calibrator. To evaluate the change of the left ventricle, we calculated the left ventricular volumes in compression systole and compression diastole by means of a single plane area-length method in a horizontal 4-chamber view.17 The calculations of the stroke volume and the left ventricular ejection fraction were done continuously using the formulas: end diastolic volume minus end systolic volume and stroke volume divided by the end diastolic volume, respectively. The values calculated from the recorded images of 5 successive chest compressions were then averaged.

Data analysis 

Data were entered into SPSS for Windows (version 15.0, SPSS Inc, Chicago, IL) for statistical analyses. The results are expressed as mean ± SD. The relationships between the elapsed time from cardiac arrest to contrast echocardiography and the left ventricular stroke volume, the left ventricular ejection fraction, the peak aortic pressure during compression systole, the coronary perfusion pressure, and the end-tidal carbon dioxide tension were analyzed using linear regression analysis. P values <.05 were considered significant.

Back to Article Outline

Results 

Patient characteristics 

Among 10 patients with nontraumatic cardiac arrest (8 males and 2 females, mean age 54 years, 7 patients had out-of-hospital cardiac arrest and 3 patients had cardiac arrest in the emergency department. None of patients with out-of-hospital cardiac arrest had received prehospital resuscitation by bystanders or emergency medical personnel. In all cases, resuscitation attempts were initiated upon arrival to the emergency department. The estimated time from collapse to emergency department arrival ranged from 10 to 25 minutes (mean 18.7 minutes). The time from ED arrival to the left ventricular contrast echocardiography ranged from 5 to 11 minutes (mean 7.7 minutes). Four patients regained spontaneous circulation, and none survived beyond 24 hours after restoration of spontaneous circulation. The clinical characteristics of the patients are shown in Table I.

Table I. Patient characteristics
CaseSex/agePlace of CATime from collapse to ED arrival (min)Time from collapse to contrast echocardiography (min)Initial rhythmPresumed etiologyOutcome
1M/73OHCA2028AsystoleNoncardiacNo ROSC
2F/60OHCA2030AsystoleNoncardiacNo ROSC
3M/52OHCA2328VFCardiacDied in 24 h
4M/49OHCA2534AsystoleCardiacNo ROSC
5F/62ED<16AsystoleNoncardiacDied in 24 h
6M/39ED<16VFCardiacDied in 24 h
7M/71ED<18AsystoleNoncardiacDied in 24 h
8M/54OHCA1020PEANoncardiacNo ROSC
9M/17OHCA1829AsystoleNoncardiacNo ROSC
10M/53OHCA1522AsystoleNoncardiacNo ROSC

CA, Cardiac arrest; OHCA, out-of-hospital cardiac arrest; ED, emergency department; PEA, pulseless electrical activity; ROSC, restoration of spontaneous circulation; VF, ventricular fibrillation.

Direction of the blood flow from the left ventricle on contrast echocardiography 

On left ventricular contrast echocardiography, retrograde blood flow toward the left atrium and anterograde flow toward the aorta from the left ventricle during the compression phase of CPR were observed in all cases, as shown in Figure 1. In all instances, contrast bubbles entered the left atrium and the aorta during the first and subsequent chest compressions after injection of the contrast into the left ventricle. The retrograde flow from the left ventricle persisted during entire compression period. The contrast bubbles remained in the left atrium during a significant period of the chest compressions, ranging from 18 to 82 seconds (mean 27 seconds), after injection of the contrast. Mild-degree retrograde flow toward the left atrium was present in 4 cases, moderate-degree retrograde flow was present in 4 cases, and severe-degree retrograde flow was present in 2 cases. Contrast echocardiography in the aorta was performed in 4 patients. When the contrast was injected into the aortic root, the contrast bubbles were cleared along progression of chest compression. A small amount of contrast was entered to the left ventricle with interruption of compression.

  • View full-size image.
  • Figure 1. 

    Direction of blood flow on left ventricular contrast echocardiography with 135° longitudinal view. Before (A) injection of contrast, the mitral valve remains open and aortic valve is closed during compression diastole. Contrast begins to inject into the left ventricle at initiation of compression systole (B). At the end of compression systole, the image of the left ventricle is obscured due to sudden compression and opacification of the ventricular cavity by contrast, and retrograde flow (arrow) into the left atrium through the mitral valve was seen. During relaxation period, the contrast is seen in the left atrium (D and E). After 2 successive compression, the contrast remains in the left atrium, the left ventricle, and the aorta (F).

During each cycle of chest compression, the mitral valve closed during compression systole and opened during compression relaxation. In contrast, the aortic valve opened during compression systole and closed during compression diastole.

Echocardiographic and hemodynamic findings 

Peak pressure of the left ventricle, the aorta, and the right atrium during compression systole was 112 ± 37 (range 74-198), 105 ± 41 (range 62-202), and 89 ± 27 mm Hg, respectively. Pressure of the left ventricle, the aorta, and the right atrium at the end of compression diastole was 8 ± 11 (range 0-30), 33 ± 10 (range 20-50), and 8 ± 6 mm Hg, respectively. Mean coronary perfusion pressure was 25 ± 9 (range 10-35) mm Hg and end-tidal carbon dioxide tension was 10 ± 5 (range 6-23) mm Hg, respectively.

Calculated left ventricular stroke volume and ejection fraction was 25 ± 8 mL (range 12-35 mL) and 34% ± 16% (range 14%-60%), respectively.

No significant relationship was found between the elapsed time from collapse to echocardiography and the left ventricular stroke volume, the left ventricular ejection fraction, the peak aortic pressure during compression systole, the coronary perfusion pressure, or the end tidal carbon dioxide tension.

Back to Article Outline

Discussion 

The results of this study, in which left ventricular contrast echocardiography was performed during CPR, demonstrate that retrograde blood flow toward the left atrium and anterograde blood flow toward the aorta from the left ventricle occur during compression phase of standard CPR in humans. Our observation implies that the left ventricular pressure is higher than those of the left atrium and the aorta, which suggests that the left ventricle acts like a pump during external chest compression.

Controversies over the mechanism of blood-flow generation during standard CPR in humans are usually about which mechanism, the cardiac pump or the thoracic pump, plays the major role in inducing blood flow. Echocardiography has been used to study the mechanism of blood flow generated by external chest compression in humans. Systolic closure of the mitral valve on echocardiography has been considered to be evidence for the cardiac pump theory. However, contradictory observations concerning whether the mitral valve is closed or open during compression systole have been reported. Werner et al18 reported systolic opening of the mitral valve, whereas Higano et al19 found systolic closure of the mitral valve. Diverse reports that the status of the mitral valve during external chest compression was associated with the degree of left ventricular compression,20 the duration of CPR,21 or hypothermia22 followed. Halperin et al23 have reported that the mitral valve could be closed by an increase in the intrathoracic pressure without compression of the ventricle in an animal model of cardiac arrest. The determination of the closing or the opening of the mitral valve is not easy because of the limitations of 2-dimensional echocardiography. In addition, if the development of papillary muscle dysfunction during cardiac arrest is considered, mitral leaflets might not coapt completely, even when the pressure rise in the left ventricle due to external chest compression. Consequently, the echocardiographic observation of whether the mitral valve is closed or open is an inaccurate method for identifying the mechanism for blood-flow generation during CPR. Another method for determining the direction of blood flow is Doppler echocardiography. Color-flow imaging, based on pulsed-wave Doppler principles, and spectral Doppler profiles can also provide information about the direction of the blood flow. However, it is not easy to obtain high-resolution images of color-flow mapping or spectral Doppler profiles during CPR because of the motion of the heart caused by chest compressions and the artifact signals produced by external chest compression. In the present study, we found that left ventricular contrast echocardiography could clearly demonstrate the direction of the blood flow generated from the left ventricle, helping to understand the mechanism for generating blood flow during CPR.

The occurrence of retrograde and forward blood flow from the left ventricle during compression systole is evidence that the cardiac pump is the predominant mechanism for generating blood flow during CPR in humans. If the thoracic pump were the predominant mechanism for generating blood flow during CPR, only forward blood flow toward the aorta without retrograde flow into the left atrium would be observed. Maier et al24 found that the left ventricular dimensions decreased during compression systole in intact chronically instrumented dogs and suggested that direct cardiac compression appeared to be the major determinant of stroke volume during CPR. They measured the anterior-posterior and the medial-lateral dimensions of the left ventricle with ultrasonic transducers directly attached to the epicardium, which is more helpful in determining the change in the left ventricular dimensions than 2-dimensional echocardiography. Ma et al25 proposed the left ventricle pump, the thoracic pump, and the left atrium pump as 3 possible mechanisms for generating forward flow during manual CPR based on the mitral valve position, transmitral flow, and the flow in the pulmonary vein during chest compression. Interestingly, these 3 different pump models were associated with duration of downtime from collapse and were related to patient survival. If the thoracic pump or left atrium pump were the predominant mechanisms responsible for blood flow during CPR, retrograde flow from the left ventricle would not have been observed during contrast echocardiography. Unfortunately, we cannot explain the difference in observations between Ma's and our study because we did not measure Doppler profiles. The downtime of the patients or the small number of study subjects might be a cause of this difference in observations between 2 studies. Klouche et al26 in an animal model of cardiac arrest, quantified the stroke volume generated by precordial compression with TEE during CPR, and demonstrated its relationship to the coronary perfusion pressure and the success of resuscitation. They found that the decreases in the stroke volume, which is linearly correlated with the coronary perfusion pressure, resulted from reductions in the left ventricular end diastolic volume. Our study did not demonstrate a relationship between the elapsed time from cardiac arrest and parameters calculated from echocardiographic observation. The varying degrees of retrograde flow from the left ventricle observed in our study also have implications as to the mechanism of blood flow. Considering that the papillary muscles do not function during cardiac arrest, one would expect similar degrees of retrograde flow if the cardiac pump mechanism were solely responsible for blood flow during precordial compression. The variation in the degree of retrograde flow from individual to individual in our study suggests that, in addition to the cardiac pump, another mechanism, such as the thoracic pump or the left atrium pump, might supplement the blood flow, although the cardiac pump is predominant.

Development of retrograde flow from the left ventricle may have 3 consequences. First, retrograde flow will reduce the amount of systemic blood flow induced by external chest compression. The rapid drop in the left ventricular pressure due to retrograde flow might result in lower cardiac output during CPR. Second, the occurrence of retrograde flow implies that the mitral papillary muscles do not function during CPR, which is not surprising because the heart does not contract during cardiac arrest. Because of papillary muscle dysfunction, the degree of retrograde flow will be increase as the left ventricle is further compressed. Although the arterial pressure during compression systole is known to be related to the amount of force applied to the sternum,27 an increase in the force applied to the sternum to augment blood flow may also lead to an increase in the volume of retrograde flow. Third, retrograde blood flow raises the pressure in the left atrium. This can also increase the pulmonary venous pressure, which has already been raised by the thoracic pump. This additional increase in the pulmonary venous pressure can result in barotrauma to the pulmonary capillary beds.28

Limitations 

Our study has several limitations. First, most of the patients had relatively long downtimes of >20 minutes before contrast echocardiography, and only 2 of the 10 patients presented with ventricular fibrillation. This may limit the applicability of our data to populations in which resuscitation is attempted at an earlier stage of cardiac arrest or ventricular fibrillation is the predominant rhythm. Second, left ventricular contrast echocardiography was performed several minutes after initiation of CPR. The mechanism of blood flow might vary with the elapsed time from cardiac arrest because of the development of a stiff myocardium.29, 30 Third, although retrograde flow from the left ventricle was observed in all patients, irrespective of the elapsed time from cardiac arrest, the degree of retrograde flow varied from individual to individual. The patient with a small volume of retrograde flow might be experiencing a change in the process for generating blood flow by precordial compression. An instantaneous increase in the ventricular pressure might have induced retrograde flow when the echo contrast was injected into the left ventricle to conduct the left ventricular contrast echocardiography. If this possibility were true, retrograde flow from the left ventricle should not have happened during successive chest compressions. However, retrograde flow occurred during successive chest compressions in all patients.

Back to Article Outline

Conclusions 

Retrograde flow to the left atrium and forward blood flow onto the aorta on left ventricular contrast echocardiography during the compression phase suggest that extrinsic compression of the left ventricle by external chest compression acts as a pump in generating blood flow during standard CPR in humans.

Back to Article Outline

References 

  1. Barsan WG, Levy RC. Experimental design for study of cardiopulmonary resuscitation in dogs. Ann Emerg Med. 1981;10:135–137
  2. Rubertsson S, Grenvik A, Zemgulis V. Systemic perfusion pressure and blood flow before and after administration of epinephrine during experimental cardiopulmonary resuscitation. Crit Care Med. 1995;23:1984–1996
  3. Fitzgerald KR, Babbs CF, Frissora HA, et al. Cardiac output during cardiopulmonary resuscitation at various compression rates and durations. Am J Physiol. 1981;H442–H448
  4. Voorhees WD, Babbs CF, Tacker WA. Regional blood flow during cardiopulmonary resuscitation in dogs. Crit Care Med. 1980;8:134–136
  5. Beattie C, Guerci AD, Hall T, et al. Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation. J Appl Physiol. 1991;70:454–465
  6. Criley JM, Nieman JT, Rosborough JP, et al. Modifications of cardiopulmonary resuscitation based on the cough. Circulation. 1986;74(Suppl IV):IV-42–IV-50
  7. Guerci AD, Halperin HR, Beyar R, et al. Aortic diameter and pressure-flow sequence identify mechanism of blood flow during external chest compression in dogs. J Am Coll Cardiol. 1989;14:790–798
  8. Kuhn C, Juchems R, Frese W. Evidence for the ‘cardiac pump theory’ in cardiopulmonary resuscitation in man by transesophageal echocardiography. Resuscitation. 1991;22:275–282
  9. Maier GW, Newton JR, Wolfe JA, et al. The influence of manual chest compression rate on hemodynamic support during cardiac arrest: high-impulse cardiopulmonary resuscitation. Circulation. 1986;76:IV51–IV59
  10. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed chest cardiac massage. JAMA. 1960;173:1064–1067
  11. Chandra NC, Tsitlik JE, Halperin HR, et al. Observation of hemodynamics during human cardiopulmonary resuscitation. Crit Care Med. 1990;18:929–934
  12. Nieman JT, Rosborough JP, Hausknecht M, et al. Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation. Circulation. 1981;64:985–991
  13. Paradis NA, Martin GB, Goetting MG, et al. Simultaneous aortic, jugular bulb, and right atrial pressures during cardiopulmonary resuscitation in humans. Insights into mechanisms. Circulation. 1989;80:361–368
  14. 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
  15. American Heart Association . Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. International Consensus on Science. Circulation. 2000;102:I–22-59
  16. Sellers RD, Levy MJ, Amplatz K, et al. Left retrograde cardioangiography in acquired cardiac disease: technique, indications and interpretations in 700 cases. Am J Cardiol. 1964;14:437–447
  17. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989;2:358–367
  18. 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
  19. Higano ST, Oh JK, Ewy GA, et al. The mechanism of blood flow during closed chest cardiac massage in humans: transesophageal echocardiographic observation. Mayo Clin Proc. 1990;65:1432–1440
  20. Redberg RF, Tucker KJ, Cohen TJ, et al. Physiology of blood flow during cardiopulmonary resuscitation. A transesophageal echocardiographic study. Circulation. 1993;88:534–542
  21. Porter TR, Ornato JP, Guard CS, et al. Transesophageal echocardiography to assess mitral valve function and flow during cardiopulmonary resuscitation. Am J Cardiol. 1992;70:1056–1060
  22. Mair P, Kornberger E, Schwarz B, et al. Forward blood flow during cardiopulmonary resuscitation in patients with severe accidental hypothermia. An echocardiographic study. Acta Anaesthesiol Scand. 1998;42:1139–1144
  23. 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
  24. Maier GW, Tyson GS, Olsen CO, et al. The physiology of external cardiac massage: high-impulse cardiopulmonary resuscitation. Circulation. 1984;70:86–101
  25. Ma MH, Hwang JJ, Lai LP, et al. Transesophageal echocardiographic assessment of mitral valve position and pulmonary venous flow during cardiopulmonary resuscitation in humans. Circulation. 1995;92:854–861
  26. Klouche K, Weil MH, Sun S, et al. Stroke volumes generated by precordial compression during cardiac resuscitation. Crit Care Med. 2002;30:2626–2631
  27. Ornato JP, Levine RL, Young DS, et al. The effect of applied chest compression force on systemic arterial pressure and end-tidal carbon dioxide concentration during CPR in human beings. Ann Emerg Med. 1989;18:732–737
  28. Hillman K, Albin M. Pulmonary barotrauma during cardiopulmonary resuscitation. Crit Care Med. 1986;14:606–609
  29. Klouche K, Weil MH, Sun S, et al. Evolution of the stone heart after prolonged cardiac arrest. Chest. 2002;122:1006–1011
  30. Takino M, Okada Y. Firm myocardium in cardiopulmonary resuscitation. Resuscitation. 1996;33:101–106

PII: S0002-8703(08)00790-4

doi:10.1016/j.ahj.2008.09.003

American Heart Journal
Volume 156, Issue 6 , Pages 1222.e1-1222.e7, December 2008

Article Tools

* Image Usage & Resolution