16. July 2009 · Comments Off · Categories: Cryonics · Tags: , ,

CPR: A Pair of Hands Aren’t Enough: You Also Need a Heart and a Brain

“Anyone, anywhere, can now initiate cardiac resuscitation procedures. All that is needed are two hands.” [Kouwenhoven WB, Jude J, Knickerbocker G. Closed chest cardiac massage. JAMA 1960;173:1064–7.

Sudden Cardiac Arrest

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Figure 1: Mortality from sudden cardiac arrest (SCA) in 2004 as a result of myocardial infarction compared to death from other ‘high profile’ causes of mortality in the US.

Each year in the United States there are ~450,00 deaths from heart attack – myocardial infarction (MI)* with 310,000 of these deaths occurring before the patient reaches the hospital as a result of unsynchronized electrical activity in the heart, ventricular fibrillation, which stops the effective delivery of blood to the body. [2]  This mode of sudden cardiac arrest[1, 2] (SCA) is also responsible for the majority of the 190,000 in-hospital deaths from MI, which typically occur within the first 24 hours following admission.[3]   Especially tragic is that 50% of these deaths occur in persons ~60 years of age or less and thus lose at least a decade of active, productive life.[4]  An estimated additional 20,000 incidents of SCA occur as a result of asphyxiation, drowning, electrocution, and genetic or developmental predisposition to lethal arrhythmias such as Wolf-Parkinson’s White Syndrome, congenital thickening of the interventricular septum, and idiopathic arrhythmic disease and other causes not related to non-atherosclerosis. This latter category of SCA typically occurs in individuals whose mean age is less than 35.[5, 6]

At this time the principal treatments for SCA consist of initiation of manual, ‘bystander’ cardiopulmonary resuscitation, so-called Basic Cardiac Life Support (BCLS or BLS), followed by ‘definitive’ treatment of the arrhythmia beginning with defibrillation and the application of Advanced Cardiac Life Support (ACLS or ALS).[7]

ACLS consists of the application of an algorithm of manual CPR, electrical defibrillation and pharmacologic therapy aimed at restoring a perfusing cardiac rhythm and adequate blood pressure and cardiac output to sustain life until definitive treatment of the underlying cause of the cardiac arrest can be achieved (e.g., coronary revascularization, implantation of an automatic defibrillator, or life-long anti-arrhythmic therapy).

What are the Odds?

Figure 2: Probability of survival as a function of time following cardiac arrest. [8]

Figure 2: Probability of survival as a function of time following cardiac arrest. [8]

As is shown in Figure 3 below, the time to survival without neurological deficit following cardiac arrest in the absence of BCLS declines rapidly following a sigmoid curve with survival without neurological deficit being ~80-90% following 1 minute of arrest time, and less than 10% following 9 minutes of arrest.[8] Put another way, 50% of patients will experience significant morbidity or death following 4 minutes of circulatory arrest (Figure 2).

What is not shown in this graph is that the effect of immediate bystander CPR on survival is negligible in most studies [9,10] with the primary benefit being observed in patients who’s time from the initiation of BCLS to successful cardiac resuscitation was greater than 8 minutes.[11] There is evidence in the literature that morbidity is improved with prompt by-stander CPR [12] providing that EMS response is also rapid, although this remains controversial.[11,13]  A corollary of this is that the overall survival rate following SCA, with or without serious neurological morbidity, ranges between 1% (New York City, NY) [14] to 17% (Seattle, WA).[15] The mean survival (defined as survival to discharge from the hospital) in the United States as a whole is generally agreed to be at best 15%  [16] with ~70% of these patients experiencing lasting neurological morbidity (ranging from ‘mild’ cognitive impairment to total incapacitation in the Persistent Vegetative State (PVS).[17,18,19]

The primary cause of non-survival in patients experiencing SCA is failed cardiac or cerebral resuscitation. Arguably, it is failed cerebral resuscitation, since most underlying causes of refractory cardiac arrest could be treated by ‘bridging’ supportive technologies such as emergency femoral-femoral cardiopulmonary bypass (CPB) until myocardial revascularization and hemodynamic stabilization were achieved.[20] When emergency CPB is applied to patients who are candidates for good neurological outcome, the survival rate is increased.[21, 22, 23, 24] However, these technologies are not typically used on patients who are unsuccessfully resuscitated (restoration of adequate cardiac rhythm and perfusion) because of the justified perception that irreversible brain damage would have occurred during the prolonged period of cardiac arrest or CPR/ACLS.[21]  Similarly, it is for this reason that most attempts to achieve cardiopulmonary resuscitation in hospitalized patients who are not hypothermic or intoxicated with sedative drug(s) are terminated after 15 minutes.[25, 26]

Within medicine it is widely understood that ‘CPR doesn’t really work’ and that if the return of spontaneous circulation (ROSC) is not achieved within ~ 5 minutes of cardiac arrest, the chances for survival are slim, and the chances for survival absent neurological impairment are slimmer still.[8] The principal reasons that conventional CPR is not effective are that it fails to supply an adequate amount of flow at an adequate pressure. Cardiac output (CO) is typically ~1/3rd of the at-rest requirement (~1.5 versus ~4.5 liters per minute), and mean arterial pressure (MAP) is typically 25 mm Hg to 45 mm Hg; well short of the 60 mmHg required to sustain cerebral viability.[27, 28]

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Figure 3: The impact of a delay of 10 min in inducing MHT is a dog model of cardiac arrest followed by 3 min of systemic ischemia, 7 minutes of mechanical CPR and 50 minutes of advanced life support. Hypothermia to 34oC was induced beginning at 10 min post arrest in the early hypothermia group˜ and at 20 min post arrest in the delayed hypothermia group ¢. In the early hypotherrmia group group, 5 of 7 surviving dogs were functionally normal (OPC 1 or 2), 1 had OPC 3, and 1 had OPC 4 (coma) at 96 hours of recovery. Histologically, 4 of 8 dogs in this group were normal (HDS 0), 1 had HDS 16, 1 had 22, and 1 had 98. The only surviving dog in the DH group was functionally normal at 96 hours (OPC 1, NDS 0) with an HDS of score of32 (mild injury) Due to early mortality only two other dogs in the delayed hypothermia group were evaluated histologically and their HDS scores 38 and 45, respectively. Dogs in this study were scored by overall performance categories (OPC; 1=normal, 2=moderate disability, 3=severe disability but conscious, 4=coma, and 5=death) Neurological function and neurological deficit scores (NDS; 0% to 10%=normal, 100%=brain death). [72],[73] Histological damage scores were obtained by neuropathological examination of 19 distcrete brain regions for severity and extent of ischemic neuronal changes, infarcts, and edema. A total brain histological damage score (HDS) >40 represented moderate damage, and HDS >100 represented severe damag.[74] Redrawn from Nozari, A., et al., Critical time window for intra-arrest cooling with cold saline flush in a dog model of cardiopulmonary resuscitation. Circulation, 2006. 113(23): p. 2690-6.

The condition of the typical sudden cardiac arrest patient and the circumstances under which he experiences cardiac arrest are far from the ideal of a patient who is a candidate for emergency cardiopulmonary bypass in hospital. The typical SCA patient is middle aged or elderly, often suffering from one or more co-morbidities (diabetes, obesity, COPD, hypertension), and if subjected to prolonged CPR will invariably have impaired gas exchange due accumulation of fluid in both the parenchyma and the air-spaces of the lungs (pulmonary edema with alveolar flooding). This occurs because closed chest CPR quickly causes pulmonary edema.[29, 30]  As previously noted, even when the SCA patient is a ‘good’ candidate for salvage; someone who is relatively young and free of co-morbidities, CPR will likely prove futile due to cerebral ischemia-reperfusion injury and the post-resuscitation syndrome.

Over the past 25 years a vast number of therapeutic interventions have shown great promise in animal models of regional and global cerebral ischemia in the laboratory.[31, 32, 33, 34] In the last 6 years alone, over 1000 experimental papers and over 400 clinical articles on pharmacological neuroprotection have been published.[35, 36] However, with one exception, none of these interventions has been successfully applied clinically despite many attempts. [37, 38, 39, 40, 41, 42, 43, 44] The sole exception to this frustrating debacle has been the introduction of moderate therapeutic hypothermia (MTH) as the standard of care for a select (and very small) minority of SCA patients.[45, 46, 47, 48, 49, 50, 51]

The question thus arises, how good is MTH? Is it, like CPR, just another ‘ritual therapy’ that works well in the laboratory but fails to deliver under the real world conditions of the in-field and clinical environments? And, of potentially great importance to cryonicists is the question of whether techniques being developed for clinical use in SCA have relevance or even merit direct application to the cryonics patient? The answer to those questions will be reviewed here in the near future.

References

1.         American-Heart-Association, Heart Disease and Stroke Statistics – 2008 Update. . 2008, American Heart Association: Dallas, Texas.

2.         de Vreede-Swagemakers, J., et al., Out-of-hospital cardiac arrest in the 1990’s: a population-based study in the Maastricht area on incidence, characteristics and survival. . J Am Coll Cardiol, 1997. 30: p. 1500-5.

3.         American-Heart-Association-and-National-Research-Council, Standards for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). . JJ Amer Med Assoc, 1974. 227(suppl): p. 833-68.

4.         Sakai, A., Sudden deaths among male employees: a six-year epidemiological survey. J Cardiol, 1990. 20: p. 957-61.

5.         Safranek, D., Eisenberg, MS, Larsen, MP., The epidemiology of cardiac arrest in young adults. Ann Emerg Med, 1992. 21: p. 1102-6.

6.         Viskin, S., Belhassen, B., Idiopathic ventricular fibrillation. American Heart Journal, 1990. 120: p. 661 – 671.

7.         Skogvoll, E., et al., Out-of-hospital cardiopulmonary resuscitation: a population-based Norwegian study of incidence and survival. . Eur J Emerg Med, 1999. 6: p. 323-30.

8.         Weale, F., The efficacy of cardiac massage. Lancet, 1960. 1: p. 990-96.

9.         Eisenberg, M., Cardiac Arrest and Resuscitation: A tale of 29 cities. Ann of Emer Med, 1990. 19: p. 179-86.

10.       Kentsch, M., et al., Early prediction of prognosis in out-of-hospital cardiac arrest. Intensive Care Med, 1990. 16: p. 378-83.

11.       Troiano, P., et al., The effect of bystander CPR on neurologic outcome in survivors of prehospital cardiac arrests. Resuscitation, 1989. 17: p. 91-8.

12.       Bossaert, L., Van Hoeyweghen, R., Bystander cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest. The Cerebral Resuscitation Study Group. . Resuscitation, 1989. 17(Suppl): p. S55-69; discussion S199-206.

13.       Stueven, H., et al. , Bystander/first responder CPR: ten years experience in a paramedic system. Ann Emerg Med, 1986. 15: p. 707-10.

14.       Lombardi, G., Gallagher, J, Gennis, P., Outcome of out-of-hospital cardiac arrest in New York City. The Pre- Hospital Arrest Survival Evaluation (PHASE) Study [see comments]. JAMA, 1994. 271: p. 678-83.

15.       McCarthy, M., Looking after your neighbors Seattle-style. Lancet, 1998. 351: p. 732.

16.       Hayward, M., Cardiopulmonary resuscitation: are practitioners being realistic? Br J Nurs, 1999. 8: p. 810-4.

17.       Bengtsson, M., A psychiatric-psychosocial investigation of patients who had survived circulatory arrest. Acta Psychiat Scan, 1969. 45: p. 327.

18.       Roewer, N., Kloss, T, Puschel, K., Long-term result and quality of life following preclinical cardiopulmonary resuscitation. Anasth Intensivther Notfallmed, 1985. 20: p. 244-50.

19.       de Vos, R., Quality of life after cardiopulmonary resuscitation. Resuscitation, 1997. 35: p. 231-6.

20.       Phillips, S., Resuscitation for cardiogenic shock with extracorporeal membrane oxygenation systems. Semin Thorac Cardiovasc Surg, 1994. 6: p. 131-5.

21.       Younger, J., et al., Extracorporeal resuscitation of cardiac arrest [see comments]. Acad Emerg Med, 1999. 6: p. 700-7.

22.       Matsuwaka, R., et al., Emergency percutaneous cardiopulmonary support for patients with cardiac arrest or severe cardiogenic shock. Nippon Kyobu Geka Gakkai Zasshi, 1996. 44: p. 2006-10.

23.       Myerburg, R., Clinical, electrophysiologic, and hemodynamic profiles of patients resuscitated from pre-hospital cardiac arrest. . Amer J Med, 1980. 68: p. 568.

24.       Safar, P., Abramson, NS, Angelos, M, et al., Emergency cardiopulmonary bypass for resuscitation from prolonged cardiac arrest. Am J Emerg Med, 1990. 8: p. 55-67.

25.       Peterson, M., et al., Outcome after cardiopulmonary resuscitation in a medical intensive care unit. Chest, 1991. 100: p. 168-74.

26.       Gener, J., et al., Immediate and 1-year survival after cardiopulmonary resuscitation at an intensive care unit. Med Clin (Barc), 1989. 93: p. 445-8.

27.       Rubertsson, S., et al., Blood flow and perfusion pressure during open-chest versus closed-chest cardiopulmonary resuscitation in pigs. Am J Emerg Med, 1984. 23: p. 568-571.

28.       Bircher, N., Safar, P., Open-chest CPR: An old method whose time has returned. Am J Emerg Med, 1984. 2: p. 568-71.

29.       McDonald, J., Systolic and mean arterial pressures during manual and mechanical CPR in humans. Ann Emerg Med, 1982. 11: p. 292-5.

30.       Ornato, J., et al., Measurement of ventilation during cardiopulmonary resuscitation. Crit Care Med., 1983. 1: p. 79-82.

31.       Kim, H., et al., Amelioration of impaired cerebral metabolism after severe acidotic ischemia by tirilazad post-treatment in dogs. . Stroke, 1996. 27: p. 114-21.

32.       Iwatsuki, N., et al., Hyperbaric oxygen combined with nicardipine administration accelerates neurologic recovery after cerebral ischemia in a canine model. . Crit Care Med, 1994. 22: p. 858-63.

33.       Cervantes, M., Moralı´, G, Letechipı´a-Vallejo, G., Melatonin and ischemia reperfusion injury of the brain. J. Pineal Res, 2008. 45: p. 1-7.

34.       Krep, H., Bernd W, Bottiger, BW, et al., Time course of circulatory and metabolic recovery of cat brain after cardiac arrest assessed by perfusion- and diffusion-weighted imaging and MR-spectroscopy. Resuscitation, 2003. 58: p. 337-348.

35.       DeGraba, T., Pettigrew, C., Why do neroprotectivedrugs work in animals but not in humans? Neurologic Clinics, 2000. 18: p. 475-493.

36.       Ginsberg, M., Adventures in the Pathophysiology of Brain Ischemia: Penumbra, Gene Expression, Neuroprotection. The 2002 Thomas Willis Lecture. Stroke, 2003. 34: p. 214-223.

37.       Cheng, J., Al-Khoury, L, Zivin, JA., Neuroprotection for Ischemic Stroke: Two Decades of Success and Failure. NeuroRX, 2004. 1: p. 36-45.

38.       Roine, R.O., et al., Nimodipine after resuscitation from out-of-hospital ventricular fibrillation. A placebo-controlled, double-blind, randomized trial. JAMA, 1990. 264(24): p. 3171-3177.

39.       Longstreth, W.T., Jr., et al., Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest. Neurology, 2002. 59(4): p. 506-514.

40.       Landau, W.M., et al., Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest. Neurology, 2003. 60(11): p. 1868-1869.

41.       Halstrom, A., Rea, TD, et al., Manual chest compression vs use of an automated chest compression device during resuscitation following out-of-hospital cardiac arrest: a randomized trial. JAMA, 2006. 295: p. 2620-8.

42.       Lafuente-Lafuente, C., Melero-Bascones, M., Active chest compression-decompression for cardiopulmonary resuscitation. Cochrane Database Syst Rev., 2004. (2):CD002751.

43.       Aung, K., Htay, T., Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med, 2005. 10: p. 17-24.

44.       Callaham, M., Madsen, CD, Barton, CW, Saunders, CE, Pointer, J., A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest. JAMA, 1992. 268: p. 2667-72.

45.       Rincon, F., Mayer, SA., Therapeutic hypothermia for brain injury after cardiac arrest. . Semin Neurol 2006. 26: p. 387-395.

46.       Bernard, S., Gray, TW, Buist, MD, et al., Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med, 2002. 346: p. 557-563.

47.       Liu, L. and M.A. Yenari, Therapeutic hypothermia: neuroprotective mechanisms. Front Biosci, 2007. 12: p. 816-25.

48.       The-Hypothermia-after-Cardiac-Arrest-Study-Group, Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med, 2002. 346: p. 549-556.

49.       Nolan, J., Morley, PT, Vanden Hoek, TL, Hickey, RW., Therapeutic Hypothermia After Cardiac Arrest: An Advisory Statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Circulation, 2003. 108: p. 118-121.

50.       Arrich, J., Clinical application of mild therapeutic hypothermia after cardiac arrest. Crit Care Med, 2007. 35(4): p. 1041-7.

51.       Sandroni, C., et al., In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Med, 2007. 33(2): p. 237-45.


* The author rejects the conventional designation of ‘sudden cardiac death’ because it is inaccurate; death is, by definition, the irreversible loss of life. Acute cardiac arrest is not death and the nomenclature used to describe it should reflect that fact.

And the Lord God formed man of the dust of the ground, and breathed into his nostrils the breath of life; and man became a living soul. Genesis 2:7

For breath is life, and if you breathe well you will live long on earth.  – Sanskrit Proverb

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In the Beginning…

Since the beginning of modern resuscitation over 40 years ago the sequence of interventions, and to a great extent their importance, has been determined by the ABCs of cardiopulmonary resuscitation (CPR): Airway, Breathing and Circulation. [1] Without breath there is no life and the most obviously and easily detected sign that life is fleeing is the absence of breath. What’s more, in many in whom breathing has newly ceased, simply opening the airway, or giving a single rescue breath will restore spontaneous respiration. We are told that breath is life and there is great truth in this saying.

Negative Pressure Ventilation

The physiology of the vertebrate chest is a truly amazing thing and it can take very bright men years to master its implications. One of the hardest concepts for me to grasp was that under normal conditions the pressure inside the pleural space (the space around the lungs) and the mediastinal spaces (the space that surrounds the heart and the great vessels of the chest) is always negative relative to both the atmospheric pressure and the pressure in the rest of the body (more on this later). [2] In other words, there is always a slight vacuum in those parts of the chest. Mostly this is a result of the fact that we breathe using our diaphragms and the muscles of our chest wall to create a low grade vacuum inside the chest into which air rushes via the trachea to fill our lungs.  When we relax those muscles, the natural elasticity, or recoil of the chest wall and diaphragm acts to squeeze the air out [I], and the cycle is then repeated. We thus breathe by means of negative pressure ventilation.

Naturally enough, when medicine began to try to restore breathing when it had ceased, most of the attempts that were made were attempts to simulate the natural process whereby air is moved in and out of the lungs; principally by negative intrathoracic pressure. [3]

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Above: an illustration of the Silvester method of artificial respiration circa 1880. (Silvester HR., A new method of resuscitating still-born children, and of restoring the persons apparently drowned or dead. BMJ 1858;2:576-9.)

Understandably, trying to mimic the complex action of the diaphragm and accessory muscle of the chest wall in normal negative pressure ventilation were difficult, cumbersome and often ineffective.  By 1959 rescue breathing using the mouth-to-mouth technique had become the mandated medical standard. [4]

There is no question that mouth-to-mouth resuscitation is vastly more effective than the medically endorsed methods that preceded it. What’s more, the class of ventilation to which mouth-to-mouth belongs, intermittent positive pressure ventilation (IPPV), has become essentially the only modality for assisting or replacing breathing in humans.  IPPV long ago displaced negative pressure ventilation (NPV) in the form of the iron lung and the cuirass shortly after polio was vanquished in the 1950s.

Below: Polio patients suffering from respiratory paralysis in iron lungs during an epidemic in the early 1950s.

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Below: A contemporary cuirass ventilator; this new breed of machines uses a biphasic approach that employs negative pressure on inspiration and positive pressure assisted exhalation. The Hayek biphasic cuirass ventilator is capable of  delivering higher tidal volumes (negative inspiratory tidal volume and positive expiratory tidal volume),  greatly increased frequency of ‘breaths’ from 6 to 1200CPM, and allows control of the inhalation to exhalation ratio without depending upon the passive recoil of the patient’s chest. Courtesy of United Hayek Medical: http://www.unitedhayek.com/products/mrtx

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While IPPV has many advantages over NPV, it is un-physiologic in one way that turns out to be of crucial importance in the setting of CPR. IPPV dramatically reduces the return flow of blood from the body to heart. The physics and physiology of this are complex, and even the shortest and most lucid tutorials run to many pages of text; often studded with equations and difficult to interpret graphs and charts. Among the many reasons IPPV’s effects are so complex in the human with a beating heart is that the body can respond to changes in venous blood flow, ventricular volume, and so on by dynamically adapting; heart rate can be increased, vascular tone can be altered, and even the amount of fluid retained by the body can be altered. [5]

The Danger of Positive Pressure Ventilation in CPR

For the patient in cardiac arrest none of these adaptive changes is possible. That makes discussion of the problems posed by IPPV much simpler, while at the same time making the adverse consequences more serious and potentially life threatening.

To understand why IPPV is so dangerous in the setting of CPR it is necessary to understand the concept of preload. Most simply, preload can be defined as “the load to which a muscle is subjected before shortening.” If this doesn’t leap out at as a point of great significance it is because this definition needs to be understood in connection with a physiological principle named after the two great physiologists who discovered it, the Frank-Starling Law of the Heart [II]. The Frank-Starling law of the heart (also known as Starling’s law or the Frank-Starling mechanism) states that the greater the volume of blood entering the heart during diastole (the period between cardiac contractions or the end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume). This may seem pretty obvious: what you put into the heart before it contracts determines what you’ll get out of it after contraction is complete. But, as it turns out, this relationship is rather more complex than simple double entry bookkeeping would suggest.

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Above: Frank-Starling Cardiac Function Curve. Courtesy of Wikimedia Commons.

In the diagram above the Y-axis shows the cardiac output and the X-axis shows right atrial pressure. While the above diagram shows only one line, a classic Frank-Starling plot often shows three separate lines, each roughly the same shape, one atop of each other, to illustrate that shifts on the same line indicate a change in preload, while shifts from one line to another indicate a change in afterload or contractility. This allows the cardiac output to be synchronized with the venous return and with the cardiac output; without depending upon external regulation to make changes. For our purposes this diagram does the job in that it shows that the relationship between venous return from the body to the right heart has a powerful effect not only on how much the blood the heart pumps, but also on the efficiency with which it pumps that blood.

As the heart is increasingly loaded with blood it becomes better and better at pumping it out to the body (up to a point) by contracting more forcefully and emptying the cardiac chambers more completely with each heartbeat. However, as the graph also shows, there is a threshold of filling or stretching of the ventricles beyond which further filling, or preload, causes no further improvement in cardiac output and (not shown) ultimately causes a decrease in pumping efficiency with a corresponding decrease in cardiac output.

Special attention needs to be paid to the Y-axis on the graph because the huge change in cardiac output shown on X-axis happens due to a change in right atrial pressure of just 3 mm Hg, or 4.1 cm H20. [6]

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To put this change in right atrial pressure in context it is only necessary to look at the graphic above to realize that a change in pressure of 3-4 mm Hg is the maximum that occurs over the course of the whole respiratory cycle. Even more importantly, as is also illustrated above, is the seeming impossibility that the pressure inside the pleural mediastinal spaces, the latter of which which contains the heart and the great vessels, is always negative throughout the entire respiratory cycle. Put another way, the areas inside the chest that conduct blood away from and back to the heart always operate under a low vacuum: ~ -6.8 cm H2O during the height of inspiration, and ~ -2.0 cm H2O at the end of exhalation. [7] This continuous negative intrathoracic pressure serves to aid venous (and lymphatic) return from the body to the heart and thus to facilitate preload and optimize cardiac output.

By contrast, a quick glance at the graphic below, which is an actual pleural pressure tracing from a patient undergoing mechanical IPPV, shows that the thoracic viscera, including the vena cavae and right heart, are subjected to positive pressures throughout the respiratory cycle which, at their peak, are typically 30 to 40 times higher than those experienced during normal (negative) pressure breathing! In fact, the situation is even worse than it seems at first glance because not only does the intrathoracic pressure never go to zero (let alone to a negative value), it is deliberately kept positive, in this case by about 8 cm H2O. This is done because in the absence of lung expansion under the influence of the intrathoracic vacuum, the alveoli, the small air sacs of the lungs, begin to collapse and stick to each other. Collapsed alveoli are very difficult to re-open and restore ventilation to. Thus, it is necessary to keep them inflated at the end of exhalation by maintaining some positive pressure in the airways. Since this pressure is applied and maintained at the end of a breath (and between breaths) it is called positive end expiratory pressure, or PEEP, for short. [8]

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Intrapleural pressure tracing of a patient with acute respiratory distress syndrome unergoing intermittent positive pressure mechanical ventilation wih a PEEP of 8 cm H2O

The graphic below shows the effect of only 3 cm of H2O PEEP on blood flow from the head and upper body through the superior vena cava (SVC). Just 3 cm H2O of PEEP reduces superior vena cava (SVC) blood flow by 25%! [9]  A patient with a spontaneously beating heart can (and does) usually compensate for this reduction in return blood flow from the body in many ways, none of which are available to the patient in cardiac arrest.

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The effect of a 3cm H2O water change in PEEP on the flow of venous blood returning to the right heart from the upper body via the superior vena cava. [9]

During conventional closed chest CPR, or in the case of the cryonics patient cardiopulmonary support (CPS), the patient experiences truly massive increases in intrathoracic pressure that last longer and reach extremes never seen in IPPV. The largest and most deleterious source of this pressure results from the physical compression of the thoracic contents during the down-stroke of chest compressions. This raises the intrathoracic pressure to between 80 and 110 cm H2O for roughly 50% of the CPR duty cycle – in other words, the pressure inside the chest is about the same as the normal averaged (mean) blood pressure in a healthy adult for half of the time the patient is undergoing CPR/S! Added to this pressure is the additional pressure of IPPV and the PEEP (usually 5 cm H2O) required to keep the small airways open. The effects of these profoundly un-physiologic pressures on the return of venous blood to the heart and consequently on cardiac output during CPR are devastating. [10]

Overcoming Increased Intrathoracic Pressure and Preserving Cardiac Output

Following the development of active compression decompression CPR (ACD-CPR) by Cohen, et al., in 1992  [11] the critical importance of maintaining negative intrathoracic pressure during the decompression phase of the CPR duty cycle has become increasingly understood. [12, 13, 14]  There is a rapidly growing body of both animal and clinical CPR research documenting improved survival and decreased neurological morbidity when the intrathoracic pressure is kept negative during the decompression (release of chest compression) phase of CPR by the use of inspiratory impedance threshold devices, such as the ResQPod, and ACD-CPR. [15, 17, 18]  An instructive video demonstration of how the ResQPod works can be seen at: http://www.advancedcirculatory.com/

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ResQPod impedance threshold device. Courtesy of Advanced Circulatory systems, Inc. http://www.advancedcirculatory.com/

Similarly, there is accumulating evidence that the increased intrathoracic pressure that results from excessive IPPV during CPR dramatically reduces cardiac output (CO) and causes increased morbidity and mortality. [19, 20, 21].

In 2004, Yannopoulos, et al., reported the development of a device which allows for the continuous application of negative intrathoracic pressure by applying controlled suction to the airway. [22] This device combines an ITD with a vacuum source and a negative pressure regulating valve to maintain an intrathoracic vacuum of between 5 to10 mm Hg (6.8 to 13.6 cm H2O), while allowing IPPV to proceed normally. This device, called the intrathoracic pressure regulator (ITPR) allows IPPV to be delivered as needed during ACD-CPR, while maintaining negative intrathoracic pressure when PPV is not being administered. The device effectively restores the intrathoracic space to its natural state as a low negative pressure (vacuum) chamber; increasing venous return from the body and consequently increasing preload and cardiac output. The ITPR also markedly increases coronary perfusion pressure (CPP) [III] while at the same time decreasing intracranial pressure (ICP). In CPR ICP is typically elevated from the basal value of 12-16 mm Hg to 22-30 mm Hg (as the result of pressure transmission by blood in non-valved veins and by transmission of intrathoracic pressure via the cerebrospinal fluid) further compromising already inadequate cerebral perfusion. [23] Reduction of ICP during CPR has been shown to improve both survival and neurological outcome in an animal model of CPR. [24]

Prototype ITPR (Advanced Circulatory Systems, Inc.) in position in a typical bag-vale resuscitator – ET tube set-up.

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The ITPR has been shown to dramatically improve gas exchange, hemodynamics, cardiac output, vital organ perfusion, and short-term survival during ventricular fibrillation (VF) cardiac arrest in a porcine model of sudden cardiac arrest and CPR. [25] The ITPR is able to not only overcome the high intrathoracic pressures associated with CPR (45 to 55 mmHg or ~61 to 75 cmH20 [26]) but to both create and sustain negative intrathoracic pressure (determined indirectly by measuring the ET tube pressure) continuously during prolonged periods of ITPR-CPR, even in the presence of induced hypovolemia. [27]  In hemorrhaged (hypovolemic) pigs, Yannopoulos, et al., were able to sustain CPP at >15 mm Hg (the accepted threshold for successful defibrillation in human sudden cardiac arrest) and the isovolemic VF animals in the study maintained CPP at >25 mm Hg throughout the full 15 minutes of ITPR-CPR. In both groups, the ETCO2 was consistently maintained above 25 mm Hg, and the 1-hour survival was 100%, as contrasted with 10% in control animals receiving AHA standard CPR (P = 0.0001).

By comparison, after 3 minutes of conventional CPR the control animals had a mean coronary perfusion pressure of less than 15 mm Hg and all had developed pseudo-respiratory alkalosis indicative of the ventilation/perfusion mismatch of standard CPR. [28] Blood gases in VF animals were strikingly preserved during ITPR-CPR; paO2, which was 96±2 mm Hg at baseline, was 214±12.37 mm Hg after 10 min and 198±6.75 mm Hg after 15 min of ITPR-CPR. These findings would seem to suggest that ITPR-CPR may be reducing or eliminating the pulmonary edema that accompanies CPR and the high intrathoracic (and thus pulmonary arterial and venous pressures) generated during CPR.  ITPR is similarly effective at improving both hemodynamics and survival in a swine model of severe hypovolemic hypotension. [29]

The Breath of Death?

However, even with the use of the ITPR, each ventilation transiently raises intrathoracic pressure and decreases CO. In the setting of CPR/S it might be said that each breath is potentially a ‘breath of death’ in terms of its impact on perfusion.

In 2007 the author began experimenting with ways to eliminate tidal ventilation during CPR/S using simple mechanical systems to simulate the lungs and thorax. Based on this preliminary work it appears that it will be possible to eliminate tidal ventilations completely while at the same time maintaining a negative intrathoracic pressure during the non-compression portion of the CPR/S duty cycle. This is possible by the simple expedient of connecting the patient’s airway to a regulated vacuum source while at the same time delivering the desired minute volume of ventilating gas to the carina of the trachea. This scheme is illustrated in the schematic below.

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Above: Experimental implementation of continuous negative pressure ventilation in CPR/S. A conventional endotracheal tube is modified by passing a fenestrated suction catheter down the lumen to the level of the carina through a side opening in the tube through which ventilating gas is continuously delivered at the desired minute ventilation volume. Negative intrathoracic pressure and removal of waste gas is achieved by applying continuous, regulated suction to the 15 mm adapter on the end of the ET tube. Movement of gas to and from the distal airways is achieved by the action of the ACD chest compressor-de-compressor operating at 100 cycles/min on the ventral thorax.

Continuous Non-Tidal Negative Pressure Ventilation

A (negative) airway pressure regulator is attached to the 15 mm connector of a modified endotracheal tube. Continuous negative airway pressure is generated by connecting the airway pressure regulator to a vacuum/suction source. Ventilating gas of the desired composition (i.e., oxygen concentration, therapeutic additives, etc.) is continuously delivered to the patient’s lungs by a ventilation gas delivery catheter that can be advanced or withdrawn through the lumen of the ET tube. The ideal position for the ventilation gas delivery catheter is at the point where the trachea bifurcates into the main-stem bronchi; the carina. Movement of the ventilating gas to the distal airways is achieved by the dynamically varying force on the chest resulting from cardiac compressions, with or without  active decompressions. The desired minute volume is determined by the flow rate of ventilating gas delivered to the carina.

In cases where pulmonary edema is preventing adequate gas exchange and it is deemed necessary to apply positive intrathoracic pressure (at the expense of cardiac output) it is easy to do this by adjusting the pressure on the airway pressure regulator to the desired positive pressure setting; as would be done with the application of positive end expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) as is done for the treatment of pulmonary edema by a different means with the Boussignac tube. [30, 31]

breath11

The illustration above shows a possible configuration of a dual-lumen endotracheal tube that would accomplish continuous non-tidal negative pressure ventilation in conjunction with an attached airway pressure control valve.

breath12

Prototype Active Comnpression-Decompression square-wave HLR constructed to the author’s specifications by Michigan Instruments, Inc., of Grand Rapids, MI. The device incorporates a continuous ventilation gas flow meter (red arrow) which allows for delivery of air blended oxygen at the desired oxygen concentration and minute volume.

In 1996 a prototype heart–lung resuscitator capable of delivering non-tidal continuous negative pressure ventilation in conjunction with ACD-square wave-CPR was fabricated by Michigan instruments of Grand Rapids, MI (shown above). Unfortunately, this device was never evaluated in a canine or porcine model of CPR in cardiac arrest. Bench testing with a sophisticated test lung did demonstrate that the unit could deliver adequate minute ventilation while maintaining operator specified negative (or positive) intrathoracic pressure throughout the decompression phase of the CPR/S duty cycle.

If animal research confirms that this mode of ventilation (which is an extension of the ITPR) is both safe and effective it should be possible to apply it to cryonics patients without the years-long wait for regulatory approval. In the case of CPR in the clinical environment, non-tidal continuous negative pressure ventilation using this scheme will likely remain one of the many intriguing and potentially useful ideas in CPR that await another time and place, or perhaps more accurately, a different universe in order to find application.

The End of the Thumper Era?

With clinical advent of ACD-CPR, and the experimental debut of the ITPR and negative intrathoracic pressure CPR delivered via the trachea, it would seem that the days of the Michigan Instruments, Inc. (MII) Thumper CPR devices, which have been the dominant technology used in cryonics transport operations, are over. Despite the very low cost of used Thumper HLRs ($150 to $500 US) the capability of doubling or trebling cardiac output (and sometimes quadrupling cerebral blood flow during CPR) would seem to mandate the expense of either custom fabricated MII equipment, or purchase of a  LUCAS or LUCAS 2 device ($20,000 US).

However, the reality is that the ITPR offers the older generations of conventional CPR machines a new lease on life. The raison d’être for ‘suction cup’ CPR is to create negative intrathoracic pressure by forcefully pulling up on the ventral chest wall between compressions. This method of creating negative intrathoracic pressure was developed as a consequence of the case of a successful resuscitation from cardiac arrest having been carried out by a layman using a lavatory toilet plunger; not as a result of systematic academic or medical laboratory investigation. [32]

It is the principle that is important, and in this case the principle is negative intrathoracic pressure; something that can be applied by surrounding the thorax with a vacuum in a cuirass, or by using a suction cup to decompress the chest wall. Importantly, it can also be accomplished by the ITPR and without the use of complex pneumatic or electromechanical machinery to move a suction cup to and fro. [IV] The ITPR and continuous negative pressure ventilation suggest a number of novel ways that may allow for the continued use of costly first and second generation mechanical CPR equipment – perhaps with even greater efficacy than is possible with the latest generation HLRs. But, alas, that is a subject for another article.

REFERENCES

1) Eisenberg MS., Cardiac Arrest. The science and practice of resuscitation medicine. In: Paradis NA, Halperin HR, Nowak RM, editors. The quest to reverse sudden death: a history of cardiopulmonary resuscitation. Baltimore: Williams and Wilkins; 1996.

2) West, JB., Pulmonary Physiology and Pathophysiology, Lippincott Williams & Wilkins, Philadelphia, 2000.

3) Baskett, FF., The Holger Nielsen Method of Artificial Respiration Resuscitation (2007) 74, 403-405.

4) Acierno LJ, Worrell LT., Peter Safar: father of modern cardiopulmonary resuscitation. Clin Cardiol. 2007 Jan;30(1):52-4.

5) Luecke , T, Pelosi, P., Clinical review: Positive end-expiratory pressure and cardiac output. Critical Care 2005, 9:607-621 (DOI 10.1186/cc3877).

6) JE, A.D., Carlson CJ, et al., Continuous positive-pressure ventilation decreases right and left ventricular end diastolic volumes in the dog. Circ Res, 1980. 46: p. 125-132.

7) West, JB., Pulmonary Physiology and Pathophysiology, Lippincott Williams & Wilkins, Philadelphia, 2000.

8) Acosta, E, Varon, S. The Use of Positive End-Expiratory Pressure in Mechanical Ventilation. Critical Care Clinics, Volume 23, Issue 2, Pages 251-261.

9) de Waal, KA, Evans, N. Osborn, DA, Kluckow , K, Cardiorespiratory effects of changes in end expiratory pressure in ventilated newborns. Arch Dis Child Fetal Neonatal Ed 2007;92:F444–F448. doi: 10.1136/adc.2006.103929.

10) Jellinek, H., Krenn, H, Oczenski, W, et al., Influence of positive airway pressure on the pressure gradient for venous return in humans. J Appl Physiol, 2000. 88: p. 926-932.

11)  Cohen, T., Tucker, KJ, Redberg, RF, Lurie, KG, Chin, MC, Dutton, JP, Scheinman, MM., Active compression-decompression resuscitation: a novel method of cardiopulmonary resuscitation. Am Heart J, 1992. 124: p. 1145-50.

12) Jellinek, H., Krenn, H, Oczenski, W, et al., Influence of positive airway pressure on the pressure gradient for venous return in humans. J Appl Physiol, 2000. 88: p. 926-932.

13) Aufderheide, T., Sigurdsson, G, Pirrallo, RG, et al. , Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation, 2004. 109: p. 1960-1965.

14) Cheifetz, I., Craig, DM, Quick, G, et al., Increasing tidal volumes and pulmonary overdistention adversely affect pulmonary vascular mechanics and cardiac output in a pediatric swine model. Crit Care Med, 1998. 26: p. 710-716.

15) Cabrini, L., Beccaria, P, Landoni, G, Biondi-Zoccai, GG, Sheiban, I, Cristofolini, M, Fochi, O, Maj, G, Zangrillo, A., Impact of impedance threshold devices on cardiopulmonary resuscitation: a systematic review and meta-analysis of randomized controlled studies. Crit Care Med, 2008. 36: p. 1625-32.

16) Plaisance, P., Lurie, K, Payen, D., Inspiratory impedance during active compression decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest. . Circulation, 2000. 10: p. 989-994.

17) Wolcke, B., Mauer, DK, Schoefmann, MF, Teichmann, H, Provo, TA, Lindner. KH, Dick WF, Aeppli D, Lurie KG., Comparison of standard cardiopulmonary resuscitation versus the combination of active compression-decompression cardiopulmonary resuscitation and an inspiratory threshold device for out-of-hospital cardiac arrest. Circulation, 2003. 108: p. 2201-2205.

18)  Lurie, K., Voelckel, W, Plaisance, P, et al., Use of an inspiratory impedance threshold valve during cardiopulmonary resuscitation: A progress report. Resuscitation, 2000. 44: p. 219-30.

19) O’Neil, J., Deakin, CD., Do we hyperventilate cardiac arrest patients? Resuscitation, 2007. 73: p. 82-85.

20) Chandra, N.C., et al., Observations of hemodynamics during human cardiopulmonary resuscitation. Crit Care Med, 1990. 18: p. 929-34.

21) Aufderheide, T., Lurie, KG., Death by hyperventilation: A common and life-threatening problem during cardiopulmonary resuscitation. Crit Care Med, 2004. 32(No. 9 (Suppl.)): p. S345–S351.

22) Yannopoulos, D., Nadkarni, VM, McKnite, SH, Rao, A, Kruger, K, Metzger, J, Benditt, D, Lurie,KJ., Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest. Circulation, 2005. 112: p. 803-81.

23) Guerci, A., Shi, AY, Levin, H, Tsitlik, J, Weisfeldt, ML, Chandra, N., Transmission of Intrathoracic Pressure to the Intracranial Space during Cardiopulmonary Resuscitation in Dogs. Circ Res, 1985. 56: p. 20-30.

24) Srinivasana, V., Nadkarnia, VA, Yannopoulosb, D, Marinoa, BS, Sigurdssonc, G,  McKnitec, SH, Zookc, M, Bendittc, DG, Lurie, KG., Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation. Resuscitation, 2006. 69: p. 329-334

25) Yannopoulos, D., Nadkarni, VM, McKnite, SH, Rao, A, Kruger, K, Metzger, J, Benditt, D, Lurie,KJ., Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest. Circulation, 2005. 112: p. 803-81.

26) Chandra, N.C., et al., Observations of hemodynamics during human cardiopulmonary resuscitation. Crit Care Med, 1990. 18: p. 929-34.

27) Lurie, K., Zielinski, T, Voelckel, W, et al., Augmentation of ventricular preload during treatment of cardiovascular collapse and cardiac arrest. Crit Care Med 2002. 30: p. (Suppl):S162-5.

28) Weil, M., Rackow, EC, Trevino, R, Grundler, W, Falk, JL, Griffel, MI., Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med, 1986. 315: p. 153-156.

29) Sigurdsson, G., Yannopoulos, D, McKnite, S, et al., Lowering of intrathoracic pressure improves blood pressure and survival rates in a porcine model of hemorrhagic shock. Resuscitation, 2006. 68: p. 399-404.

30) Srinivasana, V., Nadkarnia, VA, Yannopoulosb, D, Marinoa, BS, Sigurdssonc, G,  McKnitec, SH, Zookc, M, Bendittc, DG, Lurie, KG., Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation. Resuscitation, 2006. 69: p. 329-334.

31) Weil, M., Rackow, EC, Trevino, R, Grundler, W, Falk, JL, Griffel, MI., Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med, 1986. 315: p. 153-156.

32) Leman P, Greene S, Whelan K, Legassick T., Simple lightweight disposable continuous positive airways pressure mask to effectively treat acute pulmonary oedema: Randomized controlled trial. Emergency Medicine Australasia, 2005. 17 p. 224 – 230.

33) Templier F, Dolveck F, Baer M, Chauvin M, Fletcher D., ‘Boussignac’ continuous positive airway pressure system: practical use in a prehospital medical care unit. Eur J Emerg Med, 2003. 10 P.87-93.

34) Malzer R, Zeiner A, Binder M, Domanovits H, Knappitsch G, Sterz F., Laggner AN. Hemodynamic effects of active compression-decompession after prolonged CPR Resuscitation, Volume 31, Issue 3, Pages 243-253


[I] While most exhalations are passive and do not require muscular  assistance, we do sigh, cough and sometimes forcibly assist air out of our lungs and these instances of assisted exhalation are important to health.

[II] The German Otto Frank and Briton Ernest Starling.

[III] In the setting of resuscitation from cardiac arrest as opposed to CPS in cryonics Transports, the  coronary perfusion pressure during CPR  is the single most important predictor of successful defibrillation and thus of successful  resuscitation.

[IV] It is important to note that this applies only in situations where the chest still possesses its basic structural integrity. In cases of rib fracture or ‘flail chest’ where the thorax has lost its rigidity, only ACD-CPR or the application of an integrated chest compressor and cuirass device would be effective in generating blood flow.

03. July 2009 · Comments Off · Categories: Cryonics · Tags: , , , ,

In 2005 the American heart association revised its standards for CPR increasing the number of compressions from 80 cpm to 100 cpm, eliminating pauses for ventilation, and urging that focus be shifted to compressions (perfusion) rather than ventilation. This latter change is more profound than it might seem at first glance. In the past, a central focus (many would argue the central focus) of early ACLS was securing the airway by endotracheal intubation. Intubation is a demanding and skill-intensive task and it tends to absorb not only most of the focus of the rescue effort, but also the attention of the most skilled and experienced personnel on the scene.

As Gordon Ewy has demonstrated, minute ventilation with chest compressions in the presence of an open airway is usually adequate to provide for sufficient gas exchange for the first 6 to 10 minutes of CPR. [1,2]  Indeed, the limiting factor is not a failure of oxygen delivery resulting from the 100 tiny breaths a minute produced by the new AHA standard chest compressions, but rather hypercarbia from progressive accumulation of CO2 due to inadequate alveolar ventilation. This change in the guidelines has meant a refocusing of paramedical attention on perfusion – on chest compressions – and on the way chest compressions are carried out. The new AHA standards call for square wave compressions and emphasize the importance of delivering compressions of adequate force, depth and frequency. [3]

Anyone who has had sustained contact with paramedics (at least in the US) will know that if there is anything paramedics are more enamored of than badges and certifications, it is gadgets. Paramedics (and rightly so) are great users of equipment that makes their work faster, more effective and safer. In a profession where every second counts, anything that can improve speed or efficiency has the potential to translate into additional lives saved. To this end, Zoll (Philips and Laerdal) has introduced the Q-CPR, the first device designed to improve the quality of CPR by providing transducer derived surrogate data which is processed and transformed into verbal instructions which the device gives the EMS personnel.

standards_1

In other words, the Q-CPR measures chest compressions and provides real time verbal feedback during cardiopulmonary resuscitation. This is accomplished using a compression sensor which is placed between the rescuer’s hands and the patient’s sternum where it measures motion and force. Compression rate and depth are presented as a waveform on the monitor and if either the depth or rate drifts outside the target range established by AHA, the Q-CPR provides audible feedback. The sensor tells the EMS personnel to “press harder” or give compressions “more frequently” through verbal commands. Data on the frequency and adequacy of ventilation are collected and analyzed using impedance technology employing sensors built into the adhesive pads placed to deliver the defibrillating shock.  Changes in thoracic impedance are interpreted and displayed as lung volume and ventilation rate on the monitor screen. The Q-CPR is pictured above. As a standalone, this device would likely not have been launched. However, it is available as a ‘value added’ option to Phillips defibrillators and, as such, it has the advantage of being part of the first device, indeed the only definitive device, currently available to restore adequate perfusion and ventilation; the defibrillator. In this case the Phillips HeartStart MRx defibrillator.

Still, this technology does not come cheaply; the Q-CPR add-on retails for $3800. The latest models of the Q-CPR have a miniature LCD screen embedded in the chest sensor enabling the rescuer to see the ‘adequacy’ of his compressions continuously and without interruption.  Preliminary studies indicate that the Q-CPR improves retention of CPR skills via the ongoing verbal feedback the device provides.  Arguably just as importantly, the Q-CPR captures an enormous amount of data about each case, including how well CPR was performed and what courses of treatment are effective. The device not only stores CPR data, but also the complete ECG record and, obviously, a record of all defibrillation attempts. These data are useful not only for post-event debriefing, but will hopefully help to guide the development of more effective treatments, as well.  The Q-CPR weighs about 200 g, adding virtually no weight to the HeartStart MRx.  The module was cleared by FDA earlier this year and is now available for purchase in the U.S.

A useful video review of the Q-CPR system can be seen at:

http://www.youtube.com/watch?v=mZDxZYBneNU&feature=related

As a grimly humorous aside; only a few of us are still alive who hail from the beginnings of ‘practical’ cryonics in the late 1960s. The first HLR used in cryonics was the Westinghouse Iron Heart.

Robert Ettinger with the Iron Heart in 1964

standards_2

The second heart-lung resuscitator used in cryonics (after the Westinghouse Iron Heart) was the Brunswick HLR-50-90 which used a strap-on piston to provide chest compressions. While there are more of us left alive from those days, few of us are still active in cryonics.

standards_3

The HLR-50-90 is shown on Youtube in action with the Q-CPR in a clip entitled ‘Vintage Ambulance Equipment – HLR with MRx.”

http://www.youtube.com/watch?v=FXaFCRr-1ss&feature=related

I should also note that the Brunswick  HLR 50-90 is still being manufactured and sold and is still much cheaper to purchase than competing HLRs. It has been updated by the manufacturer to deliver 2005 AHA compliant CPR, including ventilations: http://www.brunswick-biomedical.com/

Vintage, indeed.

REFERENCES

1. Ewy GA, Kern KB. Recent advances in cardiopulmonary resuscitation: cardiocerebral resuscitation. J Am Coll Cardiol 2009; 53: 149–57.

2. Davis, DP, Cardiocerebral resuscitation: a broader perspective. Journal of the American College of Cardiology 2009; 53: 158-59.

3.2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2005; 112: IV-12 – IV-18.

If conventional cardiopulmonary support (CPS) in cryonics is difficult to perform adequately, and impossible to sustain for more than brief periods (30-60 min) before exhausting even a 3-man standby team, this is even more the case for active compression-decompression CPS (ACD-CPS) using the ResQPump (formerly the Ambu CardioPump). Even in the conventional medical setting of comparatively brief periods of CPR before defibrillation ACD-CPR is difficult to do, let alone do well. Indeed, if ACD-CPR (in conjunction with an impedance threshold device such as the ResQPod) continues to show superior results in terms of outcome (as it is now doing in recent and ongoing clinical trials) it may be the advance that makes heart-lung resuscitators both medically acceptable and cost effective. There is some evidence that this may actually be happening; while not yet profitable, the LUCAS CPR device is gaining in popularity and continues to be the subject of consistently favourable laboratory and clinical studies.

Currently, mechanical CPS is viewed by paramedical personnel as not just dangerous (i.e., the myth of routinely broken ribs and lacerated lungs and livers) but also as ineffective and, perhaps just as importantly, as a potentially professionally demeaning or threatening piece of technology. In my 30 years of experience interfacing with EMTs and paramedics in both the US and UK regarding mechanical CPR, the most frequent remark I’ve heard is, “I can do better CPR than that machine can.” Since CPR is the most dramatic, and arguably one of the most defining practices in emergency medicine, it is perhaps understandable that many emergency medical system (EMS) personnel will equate replacement of manual CPR as equivalent to replacement of the people who perform it. Many paramedics perceive the heart-lung resuscitator (HLR) as a device that will make high quality CPR something anyone can do ‘with the push of a button.’

1

In reality, deploying and applying even the most automated and technologically sophisticated HLRs will require more skill and expertise on the part of EMS personnel, not less.

Mechanically delivered ACD-CPR is also more effective than conventional mechanical CPR, even when delivered per the new AHA standards. As an example, coronary and cerebral blood flows during LUCAS CPR are improved by 25-30% over those obtained with the Michigan Instruments Thumper HLR.

2

Steen S, Liao Q, Pierre L, Paskevicius A, Sjöberg T. “Evaluation of LUCAS, a new device for automatic mechanical chest compression and active decompression for cardiopulmonary resuscitation.” Resuscitation. 2002; 55: 289-299.

3

Rubertsson S, Karlsten R. “Increased cortical cerebral blood flow with LUCAS, a new device for mechanical chest compressions compared  to standard external compressions during experimental cardiopulmonary resuscitation.” Resuscitation 2005; 65: 357-363

But of even greater interest in the context of cryopatient Transport is the dramatic improvement in the durability of perfusion being demonstrated with ACD-CPR using the LUCAS, as opposed to what can be achieved with conventional CPR. While mean arterial pressure (MAP) and cardiac output (CO) are often adequate to maintain cerebral viability during the first minute or two of chest compressions, they rapidly fall to levels that are inconsistent with survival thereafter. Deterioration of cardiac preload, rapid and progressive loss of chest wall elasticity (and thus recoil) and possibly elevated intrathoracic pressure from ‘auto-PEEP’ (gas trapping at the end of expiration and dynamic hyperinflation of the lungs) all likely contribute to the rapid decay in mean arterial pressure (MAP) and perfusion seen in conventional CPR.

4

ACD-CPR using the LUCAS preserves MAP and perfusion, even during prolonged CPR; in one case up to 240 minutes. The representative waveforms above are from LUCAS CPR performed on 13 patients who experienced cardiac arrest during cardiac catheterization and who underwent CPR for times ranging from 45 to 245 minutes. Mean systolic and diastolic blood pressure were 81±23 and 34±21 mmHg, respectively; pressures fully compatible with preservation of brain viability and long-term survival.

Compressed Gas Bottles & the Autopulse

Aside from the problem of interrupting CPR while HLRs are applied, and the historically complex and clumsy nature of the devices, the other major barrier to the use of mechanical CPR has been the need for a bulky and heavy supply of compressed gas to power the devices. Typically, two E-cylinders containing 640 liters of oxygen or air will run an HLR for only 15 to 20 minutes. This is a major logistic hurdle in conventional emergency medicine which becomes far more serious in the setting of cryopatient Transport. Oxygen (compressed or in chemical form in ‘oxygen generators’ of the type used in commercial jetliners) cannot be transported on commercial aircraft nor shipped by common carrier because of the hazard it represents. As a result, cryonics Standby/Transport teams must find a way to acquire compressed gas immediately upon landing – something that is becoming increasingly difficult since the advent of electrically powered oxygen concentrators which have largely eliminated the need for 24/7 home delivery of oxygen in high pressure cylinders.

One solution to this problem was the development of the Autopulse (Zoll Medical Corporation) which is a battery powered HLR that delivers vest CPR. While vest CPR has been shown to be superior to conventional CPR in some studies, it lacks the ability of ACD-CPR to dramatically reduce intrathoracic pressure and to maintain MAP and CO during long duration CPR. An additional problem with the Autopulse for cryonics is that the device contains the electronics; control circuitry, motors and associated mechanical devices used to power and operate it which are located in the backboard that the patient rests upon.

5

Since cryopatients are immersed in ice water, this means that the device must be extensively re-engineered for this application. Suspended Animation, Inc., of Boynton Beach, FL has reportedly developed such a portable ice bath (PIB) compatible Autopulse which they have patented and plan to market to the cryonics community at a considerable mark-up over the Autopulse’s already high retail price of ~$20,000. Another problem facing the Autopulse is the increasing gap in the quantity and quality of both the published animal and human clinical research between the Autopulse and ACD-ITD-CPR. The strong selling point of the Autopulse has been its ability to operate on compact batteries for up to 20 minutes with the ability to rapidly and easily change out batteries without any interruption in CPR.

I Sing the LUCAS Electric!

A few months ago, LUCAS announced what has certainly been a long and desperately desired advance in HLR technology – in and out of the cryonics community. LUCAS is now marketing the LUCAS 2, which is a completely battery powered version of their pneumatically driven LUCAS 1 machine.

6

This second generation LUCAS uses the basic, the well-proven LUCAS 1 platform, with a number of potentially critical added improvements. In addition to using microprocessor controlled electronic actuators, the device contains a ventilation reminder; with plans to allow interface of the device to a sophisticated, compact ventilator in the near future. Most importantly, the LUCAS 2 operates for 45 minutes on the on the newly available lithium ion polymer (LiPo ) battery technology (with no test-cycles or reconditioning required) and may also be connected to and operated from electrical power points (wall outlets) or car outlets. The battery is neatly integrated in the hood of the HLR and it can easily and rapidly be changed out, making the LUCAS 2 a lightweight and compact device to store and carry (17 kg, complete).

7

Incredibly important to cryonics operations is the fact that the device uses a softer start during the initial adjustment to the patient’s chest, and is much quieter when in operation. This latter consideration is of critical importance in institutional settings where the noise generated by pneumatically driven HLRs has resulted in significant resistance (and even refusal to allow their use in a few cases) on the part of hospital, extended care facility, and hospice administrators. The LUCAS 2 should go a long way towards overcoming this problem since the noise level is actually less than that often encountered when conventional manual CPR is administered.

8

The LUCAS user interface remains very simple with fingertip access to all operating modes and 3-step, 3-button actuation. Delightfully, the LUCAS 2 can operate from wall current (100-240V / 50/60 Hz) or from an automobile car outlet (12-24V); if the engine is running to power the vehicle alternator, the unit can operate from the vehicle power supply indefinitely (or as long as the petrol supply lasts)!

One of the most neglected aspects of cryonics is that its procedures, and the research to support them, can have important practical applications in mainstream fields such as organ preservation and emergency medicine. Contrary to popular opinion, cryonics does not just involve an optimistic extrapolation of existing science but can set the standard for these disciplines. As a matter of fact, that is exactly what cryonics, and cryonics associated research, has been doing over the last 25 years.

The most striking example is the progress in vitrification as an alternative for conventional cryopreservation. Although the idea of eliminating ice formation at low subzero temperatures has been discussed since the beginning of cryobiology, vitrification as a serious research agenda was largely driven by the demand for ice-free preservation of the human brain. Over the last decades this research has culminated in the development of the least toxic vitrification agent to date, 21st Century Medicine’s M22.

The contributions of cryonics to mainstream science and medical practice are not confined to cryobiology. Researchers Jerry Leaf and Mike Darwin made impressive progress in the formulation of bloodless whole body organ preservation solutions to resuscitate dogs from ultraprofound hypothermic temperatures, an intervention that is increasingly being recognized as essential to stabilize trauma victims. In the mid 1990s, Mike Darwin and Steve Harris conceived and developed the idea of using liquid breathing with perfluorocarbons as a method to induce rapid hypothermia. They further validated a multi-modal medications protocol to resuscitate dogs from up to 17 minutes of normothermic cardiac arrest without neurological damage.

Although progress has slowed considerably in the non-cryobiology research areas over the last 10 years, it is encouraging to observe that some of the procedures that are routine in cryonics  stabilization protocol  are starting to catch on in mainstream emergency medicine practice as well. For example, contemporary cryonics stabilization protocol has been strongly shaped by the idea that the best strategy to limit brain injury after cardiac arrest is to combine a number of different interventions: cardiopulmonary support, induction of hypothermia, and administration of circulation-supporting and neuroprotective medications.

It is therefore very encouraging to learn that the Wake County EMS group in North Carolina has achieved impressive results in treating out-of-hospital cardiac arrest victims using a protocol that closely follows elements of current cryonics stabilization protocol. Systematic implementation of immediate induction of hypothermia, continuous compression CPR, and the use of an impedance threshold device (ResQPOD) produced an almost 400% improvement in survival and vast improvements in neurological outcome. A PowerPoint presentation about their experience and protocols are available at their website.

Such real world outcomes do not only inspire confidence in the procedures cryonics organizations can use to protect patients from brain damage after cardiac arrest, it should also serve as a wake-up call to relaunch an aggressive research agenda to push the limits of hypothermic and normothermic resuscitation. In absence of this, it will only be a matter of time before cryonics activists can no longer claim that “we did it first.”

HT Mike Darwin

An important objective during stabilization of cryonics patients is restoring circulation of blood to the brain. In ideal cases, this can be achieved by aggressive mechanical cardiopulmonary support, hemodilution ,and administration of vasoactive medications. In not-so-ideal cases, one or more of these interventions are omitted or delayed. This raises the question if low flow perfusion scenarios can be detrimental to the brain because of increased reperfusion injury.  In a previous post, a paper was reviewed that found that (very) low cerebral blood flow was better than no flow at all, allowing a wider therapeutic window for successful resuscitation. Why do the low flows generated during manual cardiopulmonary resuscitation (or cardiopulmonary support in cryonics) improve the likelihood of successful neurological recovery?

In a recent paper (2008) in Resuscitation, Rea, Cook and Hallstrom propose that the low flow state generated by manual CPR simultaneously protects against ischemic injury and limits reperfusion injury. They speculate that low flow during CPR “arrests” ischemia and induces post-ischemic conditioning, which reduces exposure to peak values of oxidative stress and increases resistance to reperfusion injury when normal flow is restored:

If full flow was restored early on after collapse, the accumulation of stress mediators would be relatively modest and so the cell could tolerate reperfusion injury without moderating the peak level of oxidative substrate or priming the cell’s protective pathways. However as the duration of no flow increases, stress mediators accumulate to a level where full or near-full flow would produce oxidative injury that would overwhelm the cell unless peak oxidative stress levels are mitigated and protective pathways are preemptively up-regulated, as might occur with graded flow.

The authors even speculate that in some scenarios manual CPR might be superior to newer devices and techniques (such as  automated vest CPR or active compression-decompression CPR) that can restore blood to physiological levels because manual closed chest CPR protects the heart and brain from peak levels of stress mediators.

As the authors note, if this hypothesis is correct, treatment of cardiac arrest would require a highly individualized approach “whereby certain physiologic states would be best served by different levels of circulation and hence distinct doses of CPR.” Such treatment modalities will require complicated monitoring and resuscitation efforts, such as automated control over perfusion pressure and ventilation during CPR.

Although this model makes sense from a theoretical level, it seems to be at odds with the discovery that low flow perfusion cannot reverse the “no-reflow” phenomenon. If blood flow cannot be restored to some parts of the brain, it is not likely that ischemic injury can be “arrested” in those areas. It also seems to be at odds with the work of other resuscitation researchers who found that increased perfusion pressures and hemodilution can increase the time that resuscitation from normothermic ischemia is possible. And because low flow perfusion limits the rate of external and internal cooling, such graded resuscitation strategies decrease cooling rates if resuscitation is complemented with induction of hypothermia. Perhaps the authors could also improve on their own model by allowing aggressive reperfusion but without oxygen (or just room air) during the early stages of reperfusion.

Because rapid induction of hypothermia is the most fundamental intervention in human cryonics preservation, the relevance of this model may be limited. However, in cryonics stabilization circulation is usually restored before any significant temperature decreases are possible.  Cryonics patients often have distinctly different pathophysiological characteristics, which makes straightforward application of such models, if practical at all, extremely challenging. As has been reiterated before, without the creation of realistic cryonics research models and serious efforts at monitoring cryonics patients during transport, it will be hard to evaluate the relevance of recent insights in resuscitation medicine and extrapolate its findings.

18. July 2008 · Comments Off · Categories: Cryonics · Tags: , , ,

It is difficult to match concerns about reperfusion injury during cardiopulmonary resuscitation (CPR) with specific proposals for alternative interventions. After all, no matter how harmful the effects of oxygenation may be, not restoring circulation in a patient in cardiac arrest is hardly a credible option. One alternative would be to restore circulation but withhold oxygen (or ventilate with room air). Another alternative would be to induce hypothermia during circulatory arrest before restoring circulation.

A recent paper in Resuscitation investigated the latter option and reports that delaying reperfusion  in mice until induction of mild hypothermia has been achieved can improve hemodynamics, survival and neurological outcome.  The time to drop the temperature from 37 degrees Celsius to 30 degrees Celsius was 90 seconds in mice. As the authors note, “this is not currently feasible in humans and it is likely that much longer resuscitation delays in the clinical setting might counteract the benefit of cooling before ROSC (return of spontaneous circulation)”.

Rapid partial cooling (as the authors suggest) may solve this problem but restoring circulation will result in moving warm blood to the very organs (such as the heart and the brain) that just had been cooled. Such an intervention will only work if some of the protective mechanisms of hypothermia, such as altered gene expression, are (partially) retained during subsequent rewarming.

One treatment modality that the authors did not research, but warrants investigation, would be to “mimic” intra-arrest hypothermia by restoring circulation and giving a cocktail of neuroprotective agents prior to restoring oxygenation. Such an approach may not eliminate all free radical injury upon restoring circulation, or eliminate other elements of reperfusion injury such as calcium overload and inflammatory responses, but it might be an interesting treatment to compare with induction of intra-arrest hypothermia and delayed CPR.

One concern about prolonged cardiopulmonary support in cryonics is that its decreasing effectiveness may not be able to meet cerebral oxygen demand, and may even become detrimental. Some investigators have  observed that severely reduced flow (cerebral blood flow less than 10% of control) to the brain may actually be more harmful than no flow at all.  Explanations of why incomplete (“trickle flow”) ischemia may be worse than complete ischemia include aggregation of slow moving blood cells,  glucose-induced excessive lactate production, and oxygen-induced free radical damage to membranes.

In contrast, a study by Steen et al. concluded that some blood flow is better than no flow at all. The authors found that dogs could sustain only 8 to 9 minutes of complete ischemia but 10 to 12 minutes of incomplete ischemia (cerebral blood flow less than 10% of control) without neurological impairment. These results are at odds with the findings of Hossmann et al. who found better electrophysiological recovery in cats and monkeys after complete ischemia, and studies by Nordstrom et al. who observed increased metabolic recovery in rats after complete ischemia.

The authors speculate that these differences may reflect the different durations of (in)complete ischemia. Hossmann et al. studied 60 minutes of ischemia and Nordstrom studied 30 minutes of ischemia. The authors note that the durations they studied (8-14 minutes) are more clinically relevant because neurological recovery with contemporary technologies is not possible after 30 or 60 minutes of cerebral ischemia. Although these findings provide support for restoration of any kind of cerebral circulation after cardiac arrest, it does not offer much guidance in evaluating the practice of prolonged cardiopulmonary support in cryonics.

The authors also draw awareness to the difficulty of correlating electrophysiological and metabolic recovery to neurological recovery. They quote a study by Salford et al. who observed some return of metabolism even though histological abnormalities had already been developed. Such studies warrant caution about using return of electrophysiological activity as an indicator of cerebral viability because it is not likely that such viability can be sustained over the long term, let alone predict functional recovery of the brain.  It is doubtful that viability in the latter, stricter, sense can be maintained during stabilization of most, if any, cryonics patients. At best, the studies that demonstrate recovery of electrophysiological and metabolic activity after prolonged cerebral ischemia offer hope that such periods of circulatory arrest do not produce acute information-theoretic death.

No metabolic or histological evidence was found to support the implication of no-reflow, lactate accumulation, and free radical damage in incomplete ischemia.  Again, the authors speculate that no-reflow may be more pronounced during longer periods of incomplete ischemia, an observation that seems to be indirectly supported by Fisher et al. who observed progressive impairment of perfusion for longer periods of ischemia.

Cryonics patients often experience shock, blood coagulation abnormalities, and decreased cerebral perfusion prior to pronouncement of legal death and cardiopulmonary support.  An additional complicating factor in cryonics is that cardiopulmonary support is often supplemented by induction of hypothermia and administration of vasopressors and neuroprotective agents. Although the paper by Steen et al. addresses a lot of issues that are important to evaluate cryonics procedures, it is clear that for real empirical guidance regarding the wisdom of prolonged cardiopulmonary support specific cryonics research models are required.

As discussed in a previous post, perfusion of the brain following long-term (>5 min) ischemia has been shown to be significantly compromised, particularly in subcortical regions. An interesting recent article by Ristagno, et. al in Resuscitation (May 2008) has added new data to the equation, using some of the most advanced technologies available for measuring cerebral microvascular blood flow.

To briefly summarize the experiment, pigs were subjected to 3 minutes of untreated ventricular fibrillation followed by 4 minutes of cardiopulmonary resuscitation and subsequent defibrillation. Blood flow in large (>20 micrometers) and small (<20 micrometers) cerebral vessels was measured during and after CPR by direct visualization using orthogonal polarization spectral imaging (OPS) together with cortical-tissue partial pressure of carbon dioxide.

Though prior studies implied a dissociation between microcirculatory flow and macrocirculation during CPR, Ristagno, et. al found “a close relationship between microvascular flows and the macrocirculation during cardiac arrest, during CPR and following return of spontaneous circulation (ROSC).” Interestingly, they also noted that cerebral blood flow was reduced, but did not stop, for more than 2 minutes after cardiac arrest, most likely due to residual compliance in the arterial circuit. After ROSC, flow progressively increased back to normal (pre-arrest) values within 3 minutes.

Importantly, the researchers also noted that cerebral cortical-tissue partial pressure of carbon dioxide (a measure of the severity of cerebral ischemia) increased progressively througout CPR, providing evidence for the fact that the pressure and flow generated during chest compressions “may minimise but do not reverse the magnitude of the brain ischaemia which preceded the start of CPR.”

Though many investigations, such as the previously reported study by Fischer & Ames reported no-reflow or hypoperfusion following ischemia, these authors observed no such phenomena, possibly because of the short duration of cardiac arrest. Indeed, they ultimately conclude that “a 3-min interval of ischaemia was therefore probably not long enough to induce alterations in blood flow during reperfusion.” Also of importance is the fact that OPS technology limits visualization of microvessels to within 1mm of the cortical surface. However, this paper still gives us better insight into the immediate effects of cardiac arrest, cardiopulmonary resuscitation, and reperfusion on microcirculatory flow in the brain.

05. March 2008 · Comments Off · Categories: Cryonics · Tags: , , , ,

Conventional CPR typically generates around one-third to one-fourth of normal cardiac output, which is not sufficient to meet cerebral energy demands. In cryonics patients, cardiac output may be further compromised because many patients are atherosclerotic and/or have gone through a prolonged period of shock / multiple organ failure prior to pronouncement of legal death. However, conventional chest compression techniques can be improved and augmented to produce higher cardiac output and cerebral blood flow.

In cryonics, chest compression techniques range from manual chest compressions to mechanical high impulse active compression-decompression cardiopulmonary support (CPS). A recent technology that has been introduced to cryonics is the use of a mechanical load-distributing band CPS device, the Autopulse. Cerebral blood flow can be further augmented by using a respiratory impedance valve (such as the ResQPOD) and administration of vasoactive medications, such as epinephrine and vasopressin.

Although these interventions can improve cerebral blood flow during CPS, it is a well documented fact that many cryonics patients do not benefit from such improvements. Administration of vasoactive medications requires intravenous access which is often difficult to obtain in the typical cryonics patient. Similarly, the use of an impedance valve requires a patent airway which requires rapid and successful intubation of the patient. Clearly, it would be beneficial to have a technology that can be rapidly applied, is non-invasive, and does not require special technical knowledge or manual skills.

Abdominal compression appears to be such a technology. An air-inflatable cuff is positioned on top of the abdomen and secured in place. In some versions of the technology, a contoured cuff follows the lower border of the rib cage to minimize the chance of interference of the cuff with lung inflation during positive pressure ventilation. Constant abdominal compression is achieved by inflating the cuff during chest compressions. Abdominal compression increases coronary and cerebral blood flow by a) increasing intrathoracic pressure, b) increasing functional arterial resistance, and c) redistributing blood volume above the diaphragm out of the abdominal compartment (in: Biomedical Engineering Fundamentals, 2006).

In a recent study by Lottes et al. (2007), sustained abdominal compression was able to raise coronary perfusion pressure as much as vasopressor drugs. Progressively better results were obtained when abdominal pressure was increased from 100 mmHg to 500 mmHg. Optimal results were obtained when abdominal compression was used in combination with vasopressor drugs. This technology has also been evaluated in humans; Chandra et al. (1981) reported increased mean arterial, systolic, and diastolic blood pressure during CPR following cardiac arrest in humans.

Advantages of sustained abdominal compression in cryonics include: low fabrication costs, light in weight, indefinite shelf life, no refrigeration requirements, no electrical power requirements, easy to apply, immediate onset of action, constant effect over time (unlike medications), and immediately reversibility of the procedure.

The disadvantages of sustained abdominal compression are not evident but warrant careful consideration: (a) Abdominal compression may exacerbate ischemia-induced abdominal hemorrhage – this disadvantage is highly speculative since rupture of the inner lining of the gastric mucosa is a biochemical, not mechanical, event. It is clear, however, that abdominal compression is contra-indicated in patients with abdominal swelling and related gastrointestinal complications. The band and cuff may also interfere with placing a gastric tube to administer an antacid (I owe this point to Stephen Van Sickle). (b) Reversal of abdominal compression may rewarm the upper part of the body as a result of warmer blood having increased access to the upper torso and brain – this, again, is speculative and depends on the question of whether abdominal compression induces selective cooling of the torso. If such a scenario is possible, this effect might be limited by not reversing compression until internal cooling is started. The question remains, however, if better perfusion of the brain will offset slower cooling of the brain as a result of decreased surface cooling. (c) The inflatable cuff may interfere with the Autopulse technology – it is not likely that the two technologies will interfere because the lower part of the Autopulse band does not come into contact with the upper part of the abdominal compression cuff.

Another concern that has been raised about using this technology in cryonics concerns the possibility that abdominal binding has the effect of shunting blood to the upper torso and brain. The resulting lack of perfusion, and subsequent collapse of the vascular bed in the lower extremities, may make raising and cannulating the femoral vessels very difficult, if not impossible. An opposite view is that abdominal compression may actually facilitate femoral cannulation because it creates a bloodless field and enhances visibility of the vein by inflating and distending it (I owe this point to Brian Wowk). It should also be noted that not all cryonics stabilization cases are followed by blood washout through the femoral vessels. Examples include remote cases without blood washout, local cases, and cases in which the patient is cryoprotected in the field (in which surgical access may be obtained through median sternotomy or the cerebral vessels).

It remains to be seen if sustained abdominal compression becomes more popular in resuscitation medicine. Provided this technology is as effective as documented in the Lottes paper, contemporary cryonics stabilization procedures may benefit from such a simple technology to increase blood flow to the brain during CPS.

Selected Bibliography

Lottes AE, Rundell AE, Geddes LA, Kemeny AE, Otlewski MP, Babbs CF.
Sustained abdominal compression during CPR raises coronary perfusion pressures as much as vasopressor drugs.
Resuscitation. 2007 Dec;75(3):515-24.

Wik L, Naess PA, Ilebekk A, Steen PA.
Simultaneous active compression-decompression and abdominal binding increase carotid blood flow additively during cardiopulmonary resuscitation (CPR) in pigs.
Resuscitation. 1994 Jul;28(1):55-64.

Babbs CF, Blevins WE.
Abdominal binding and counterpulsation in cardiopulmonary resuscitation.
Critical Care Clinics. 1986 Apr;2(2):319-32.

Koehler RC, Chandra N, Guerci AD, Tsitlik J, Traystman RJ, Rogers MC, Weisfeldt ML.
Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs.
Circulation. 1983 Feb;67(2):266-75.

Chandra N, Snyder LD, Weisfeldt ML.
Abdominal binding during cardiopulmonary resuscitation in man.
JAMA. 1981 Jul 24-31;246(4):351-3.