(Special Resuscitation Situations)

参考文献 No. 2


No. 1


Ann Emerg Med 1993 Feb;22(2 Pt 2):324-49

Published erratum appears in Ann Emerg Med 1993 Apr;22(4):759 Cerebral resuscitation after cardiac arrest: research initiatives and future directions.

Safar P

Department of Anesthesiology and Critical Care Medicine, University of Pittsburgh, Pennsylvania.

At present, fewer than 10% of cardiopulmonary resuscitation (CPR) attempts prehospital or in hospitals outside special care units result in survival without brain damage. Minimizing response times and optimizing CPR performance would improve results. A breakthrough, however, can be expected to occur only when cerebral resuscitation research has achieved consistent conscious survival after normothermic cardiac arrest (no flow) times of not only five minutes but up to ten minutes. Most cerebral neurons and cardiac myocytes tolerate normothermic ischemic anoxia of up to 20 minutes. Particularly vulnerable neurons die, in part, because of the complex secondary post-reflow derangements in vital organs (the postresuscitation syndrome) which can be mitigated. Brain-orientation of CPR led to the cardiopulmonary-cerebral resuscitation (CPCR) system of basic, advanced, and prolonged life support. In large animal models with cardiac arrest of 10 to 15 minutes, external CPR, life support of at least three days, and outcome evaluation, the numbers of conscious survivors (although not with normal brain histology) have been increased with more effective reperfusion by open-chest CPR or emergency cardiopulmonary bypass, an early hypertensive bout, early post-arrest calcium entry blocker therapy, or mild cerebral hypothermia (34 C) immediately following cardiac arrest. More than ten drug treatments evaluated have not reproducibly mitigated brain damage in such animal models. Controlled clinical trials of novel CPCR treatments reveal feasibility and side effects but, in the absence of a breakthrough effect, may not discriminate between a treatment's ability to mitigate brain damage in selected cases and the absence of any treatment effect. More intensified, coordinated, multicenter cerebral resuscitation research is justified.

Publication Types: Review, Review-academic


  1. Comment in: Ann Emerg Med 1993 Apr;22(4):759
    Cerebral resuscitation.
    Safar P
    Publication Types: Comment, Letter

No. 2


Ann Fr Anesth Reanim 1995;14(1):122-8

[Mild hypothermia and cerebral protection].

[Article in French]

Krivosic-Horber R

Departement d'Anesthesie-Reanimation Chirurgicale 1, Hopital B, CHU de Lille.

To define the part played by mild-to-moderate hypothermia in neuroprotection, it is necessary to take into account the thermoregulatory responses that occur in the normal human as the change in central temperature exceeds 0.2 degrees C. The mechanisms induced by cold are cutaneous vasoconstriction and shivering. They must be suppressed before starting controlled hypothermia. In these conditions, controlled moderate hypothermia between 32 and 35 degrees C does not seem to have deleterious side-effects, especially on coagulation. Caution is needed with the analysis of the numerous papers reporting experiments concerning the effects of moderate hypothermia in animals with induced cerebral ischaemia because of significant differences in the study designs. These differences concern mainly the time of onset of hypothermia, viz before or after ischaemia, the fact that the ischaemia is either global or focal, that it is caused by vascular occlusion posttraumatic or initiated by hypo or hyperglycemia. Some differences are also existing in the criteria used to appreciate the neuronal damage, as well as in the level of temperature and the site where it is measured. The mechanism of neuroprotection from moderate hypothermia seems to be not only a decrease in cerebral metabolism, but also involves a specific action on some intra-cellular events such as the blocking of the release of glutamate and of lipid peroxydation in brain tissue. An indirect proof of the neuroprotective effect of moderate hypothermia is the increase in the neuronal damage induced by moderate hyperthermia. It is conceivable that moderate hypothermia could exert a better neuroprotective effect than the drugs having this reputation, such as barbiturates, isoflurane and propofol.

PMID: 7677276, UI: 95407776

No. 3


Brain Res 1992 Sep 11;590(1-2):6-12

Changes of labile metabolites during anoxia in moderately hypo- and hyperthermic rats: correlation to membrane fluxes of K+.

Katsura K, Minamisawa H, Ekholm A, Folbergrova J, Siesjo BK

Laboratory for Experimental Brain Research, University Hospital of Lund, Sweden.

The objective of this study was to assess the influence of temperature on the coupling among energy failure, depolarization, and ionic fluxes during anoxia. To that end, we induced anoxia by cardiac arrest in anesthetized rats maintained at a body temperature of either 34 degrees C or 40 degrees C, measured extracellular K+ concentration (K+e), and froze the neocortex through the exposed dura for measurements of phosphocreatine (PCr), creatine (Cr), ATP, ADP, and AMP, glucose, glycogen, pyruvate and lactate content after ischemic intervals of maximally 130 s. Free ADP (ADPf) concentrations were derived from the creatine kinase equilibrium. Hypothermia reduced the initial rate of rise in K+e, and delayed the terminal depolarization; however, both hypo- and hyperthermic animals showed massive loss of ion homeostasis at a K+e of 10-15 mM. The initial rate of rise in K+e did not correlate to changes in ATP, or ATP/ADPf ratio, suggesting that temperature changes per se may control the degree of activation of K+ conductances. The results clearly showed that, in both hyper- and hypothermic subjects, energy failure preceded the sudden activation of membrane conductances for ions. The results indicate that temperature primarily influences membrane permeability to ions like K+e (and Na+), and that cerebral energy state is secondarily affected. It is proposed that the higher rate of rise of K+e at high temperatures accelerates ATP hydrolysis primarily by enhancing metabolic rate in glial cells.

PMID: 1422848, UI: 93045535

No. 4


Crit Care Med 1991 Mar;19(3):379-89

Mild hypothermic cardiopulmonary resuscitation improves outcome after prolonged cardiac arrest in dogs.

Sterz F, Safar P, Tisherman S, Radovsky A, Kuboyama K, Oku K

International Resuscitation Research Center, University of Pittsburgh, PA 15260.

BACKGROUND AND METHODS: This study was designed to explore the effect of mild cerebral and systemic hypothermia (34 degrees C) on outcome after prolonged cardiac arrest in dogs. After ventricular fibrillation with no flow of 10 min, and standard external CPR with epinephrine (low flow) from ventricular fibrillation time of 10 to 15 min, defibrillation and restoration of spontaneous normotension were between ventricular fibrillation time of 16 and 20 min. This procedure was followed by controlled ventilation to 20 hr postarrest and intensive care to 72 hr postarrest. In control group 1 (n = 10), core temperature was 37.5 degrees C; in control group 2 (n = 10), cooling was started immediately after restoration of spontaneous normotension; and in group 3 (n = 10), cooling was initiated with start of CPR. Cooling was by clinically feasible methods.

RESULTS: Best overall performance categories achieved (1 = normal; 5 = brain death) were better in group 2 (p = .012) and group 3 (p = .005) than in group 1. Best neurologic deficit scores were 36 +/- 14% in group 1, 22 +/- 15% in group 2 (p = .02), and 19 +/- 18% in group 3 (p = .01). Brain histopathologic damage scores were also lower (better) in groups 2 (p = .05) and 3 (p = .03). Myocardial damage was the same in all three groups.

CONCLUSION: Mild cerebral hypothermia started during or immediately after external CPR improves neurologic recovery.


  1. Comment in: Crit Care Med 1991 Mar;19(3):315
    Hypothermia after cardiac arrest.
    Weil MH, Gazmuri RJ
    Publication Types: Comment, Editorial

  2. Comment in: Crit Care Med 1992 Mar;20(3):441-3
    Hypothermic cardiopulmonary resuscitation.
    Gilston A
    Publication Types: Comment, Letter

No. 5


Ann Surg 1982 Apr;195(4):492-5

Management of profound accidental hypothermia with cardiorespiratory arrest.

Althaus U, Aeberhard P, Schupbach P, Nachbur BH, Muhlemann W

Complete recovery following rapid rewarming is described in three tourists who were admitted in a state of profound hypothermia with total cardiorespiratory arrest (rectal temperature ranging from 19 to 24 C). In all three patients, respiration and circulation had ceased during the rescue operation. Rapid core rewarming was achieved by thoracotomy and continuous irrigation of the pericardial cavity with warm fluids in one patient, whereas in the other two patients rewarming was accomplished with extracorporeal circulation using femoro-femoral bypass. In the first patient, the heart could not be defibrillated earlier than 90 minutes following thoracotomy; in the other patients rewarming was attained very rapidly, and within half an hour after institution of bypass, resuscitation of the heart was successful. The patients fully recovered their intellectual and physical abilities, despite the prolonged periods of circulatory arrest lasting from 2 1/2 to 4 hours. We conclude that rapid core rewarming is the adequate therapy for profound accidental hypothermia with circulatory arrest or low cardiac output. If feasible extracorporeal circulation represents the method of choice because it combines the advantage of immediate central rewarming with the benefit of efficient circulatory support, the heart is rewarmed before the shell, thus preventing the "rewarming shock" due to peripheral vasodilatation. Resuscitative efforts should be promptly initiated and vigorously pursued, even in the state of clinical death; in profound hypothermia neurologic examination is inconclusive regarding prognosis.

PMID: 7065752, UI: 82159185

No. 6


Ann Intern Med 1978 Oct;89(4):519-27

Hypothermia: pathophysiology, clinical settings, and management.

Reuler JB

Hypothermia, defined as a core temperature less than 35 degrees C, is frequently not recognized, in part because of the inadequacy of standard thermometers. This entity has multiple causes and unique pathophysiologic consequences that complicate diagnosis and treatment. Understanding of the physiology of thermoregulation is important in light of recent advances in therapy using core rewarming. Pathophysiology, etiology and management of the hypothermia syndrome are reviewed.

Publication Types: Review

PMID: 358883, UI: 79019640

No. 7


Ann Emerg Med 1984 Apr;13(4):263-73

Neardrowning and cold water immersion.

Martin TG

Though usually preventable, drowning remains a major cause of accidental death in our society. The lethal common denominator in drowning and neardrowning deaths is hypoxia. Aggressive treatment both at the scene and in the hospital is recommended even in those who initially appear lifeless. Hypothermia and the diving reflex probably explain the incredible survival stories in neardrowning. Remember the maxim in cold water immersion: "One is not dead until warm and dead!"

Publication Types: Review

PMID: 6367555, UI: 84151994

喘 息 (Asthma)

No. 1


Am Rev Respir Dis 1990 Jul;142(1):108-11

Sudden asphyxic asthma: a distinct entity?

Wasserfallen JB, Schaller MD, Feihl F, Perret CH

Department of Medicine, University Hospital, Lausanne, Switzerland.

This study analyzed the history, clinical characteristics, and acid-base data in relation to the speed of decompensation in 34 patients intubated and mechanically ventilated for severe asthma. Three patterns of decompensation were established according to the delay between the onset of symptoms and endotracheal intubation: Group I, rapid decompensation (less than 3 hours); Group II, gradual development of respiratory failure (9.2 +/- 7.7 days); Group III, acute exacerbation after unstable asthma (4.2 +/- 3.6 days). Patients who developed sudden asphyxia (Group I) showed features distinct from those with a gradual worsening. Sudden asphyxic asthma is more frequent in young men and is characterized by a severe mixed acidosis with extreme hypercapnia (mean PaCO2 = 112.8 +/- 43.9 mm Hg), a higher incidence of respiratory arrest, and silent chest upon admission. Recovery is more rapid, with a shorter duration of mechanical ventilation (33.7 +/- 25.3 h versus 91.4 +/- 64.1 h in Group II). Several arguments suggest that bronchospasm plays the primary role in the pathogenesis of sudden asphyxic asthma.

PMID: 2368957, UI: 90314070

No. 3


Chest 1992 Jun;101(6):1699-702

Sudden cardiac death in bronchial asthma, and inhaled beta-adrenergic agonists.

Robin ED, McCauley R

Tsurai Indian Health Care Clinic, Trinidad, California.

Publication Types: Review, Review-tutorial

PMID: 1350972, UI: 92289329

No. 4


Pediatrics 1992 Dec;90(6):983-6

Malignant vasovagally mediated hypotension and bradycardia: a possible cause of sudden death in young patients with asthma.

Grubb BP, Wolfe DA, Nelson LA, Hennessy JR

Division of Cardiology, Medical College of Ohio, Toledo 43699.

PMID: 1359501, UI: 93065042

No. 5


J Am Coll Cardiol 1994 Mar 1;23(3):741-6

Conduction system findings in sudden death in young adults with a history of bronchial asthma.

Bharati S, Lev M

Congenital Heart and Conduction System Center, Palos Heights, Illinois 60463.

OBJECTIVES. This study was conducted to determine whether there are any pathologic changes in the conduction system when death occurs suddenly in young adults with a history of bronchial asthma. BACKGROUND. There is a worldwide increase in sudden death, especially in young adults with a history of bronchial asthma.

METHODS. We studied the conduction system by serial section examination in six male patients (16 to 23 years old) with a history of bronchial asthma who died suddenly.

RESULTS. The sinoatrial node artery was narrowed in two patients, with chronic inflammatory cells in three; it was fibrosed in one. The atrioventricular (AV) node was within the central fibrous body in three patients and isolated by fat in one. The AV bundle was markedly fragmented in five patients and fibrosed in two. The right and left bundle branches showed fat, fibrosis and disruption in five patients. Increased fibrosis on the summit of the ventricular septum with patchy fibrosis was present in five patients, and inflammatory cells in the conduction system were found in one. CONCLUSIONS. 1) There are distinct pathologic findings in the conduction system of young adults with a history of bronchial asthma who die suddenly. 2) The significant findings appear to be a markedly fragmented bundle and changes in the sinoatrial node that are not found in normal healthy young adults. 3) The changes in the conduction system may create an arrhythmic event, and sudden death may occur in some persons during an altered physiologic state. 4) We hypothesize that bronchial asthma may be associated with an alteration in immune complexes that affects the conduction system in some patients.

PMID: 8113559, UI: 94157260

No. 6


Chest 1991 Feb;99(2):492-3

Auto-PEEP during CPR. An "occult" cause of electromechanical dissociation?

Rogers PL, Schlichtig R, Miro A, Pinsky M

Veterans Administration Medical Center, Pittsburgh.

A 64-year-old man with severe COPD developed refractory nonperfusing sinus rhythm after intubation and positive-pressure ventilation. Fifteen minutes after resuscitative efforts were halted, the patient was noted to have spontaneous respirations and blood pressure, suggesting that dynamic hyperinflation was responsible for the observed electromechanical dissociation (EMD). We recommend a brief trial of apnea for patients with COPD and EMD when conventional measures are unsuccessful.

PMID: 1989814, UI: 91114417

(註.著者名が違っています。Schlichting Rではなく Schlichtig R)

No. 7


JAMA 1993 Apr 28;269(16):2128-31

Ventilatory management of respiratory failure in asthma.

Wiener C

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Md. 21205-2196.

Publication Types: Clinical conference

PMID: 8468769, UI: 93225204

No. 8


N Engl J Med 1991 Jan 31;324(5):285-8

Respiratory arrest in near-fatal asthma.

Molfino NA, Nannini LJ, Martelli AN, Slutsky AS

Hospital Nacional Maria Ferrer, Buenos Aires, Argentina.

BACKGROUND AND METHODS. The majority of asthma-related deaths occur outside the hospital, and therefore the exact factors leading to the terminal event are difficult to ascertain. To examine the mechanisms by which patients might die during acute exacerbations of asthma, we studied 10 such patients who arrived at the hospital in respiratory arrest or in whom it developed soon (within 20 minutes) after admission.

RESULTS. The characteristics of the group were similar to those associated in the literature with a high risk of death from asthma, including a long history of the disease in young to middle-aged patients, previous life-threatening attacks or hospitalizations, delay in obtaining medical aid, and sudden onset of a rapidly progressive crisis. Extreme hypercapnia (mean [+/- SD] partial pressure of arterial carbon dioxide, 97.1 +/- 31.1 mm Hg) and acidosis (mean [+/- SD] pH, 7.01 +/- 0.11) were found before mechanical ventilation was begun, and four patients had hypokalemia on admission. Despite the severe respiratory acidosis, no patient had a serious cardiac arrhythmia during the resuscitation maneuvers or during hospitalization. We observed systemic hypertension and sinus tachycardia in eight patients, atrial fibrillation in one, and sinus bradycardia in another. In both patients with arrhythmia the heart reverted to sinus rhythm immediately after manual ventilation with 100 percent oxygen was begun. The median duration of mechanical ventilation was 12 hours, and all patients had normocapnia on discharge from the hospital.

CONCLUSIONS. We conclude that at least in this group of patients, the near-fatal nature of the exacerbations was the result of severe asphyxia rather than cardiac arrhythmias. These results suggest that undertreatment rather than overtreatment may contribute to an increase in mortality from asthma.

(註.著者名が違っています。Molfini NAではなく、Molfino NA。)


  1. Comment in: N Engl J Med 1991 Feb 7;324(6):409-11
    Fatal and near-fatal asthma.
    McFadden ER Jr
    Publication Types: Comment, Editorial

  2. Comment in: N Engl J Med 1991 Jul 18;325(3):205-6
    Molfino NA
    Respiratory arrest in near-fatal asthma.
    Publication Types: Comment, Letter

No. 1


Mayo Clin Proc 1994 May;69(5):495-6

Sudden-onset fatal asthma.

Sur S, Hunt LW, Crotty TB, Gleich GJ

Publication Types: Editorial

No. 10


Chest 1993 Jan;103(1):221-5

High serum albuterol levels and tachycardia in adult asthmatics treated with high-dose continuously aerosolized albuterol.

Lin RY, Smith AJ, Hergenroeder P

Department of Medicine, St. Vincent's Hospital and Medical Center, New York, New York 10011.

To study the feasibility of using high-dose continuously aerosolized albuterol aerosol in adults, seven adult asthmatic patients were treated eight times with 0.4 mg/kg/h albuterol delivered by continuous nebulization over 4 h. One patient withdrew at 3 h after supraventricular tachycardia developed. This subsided promptly on discontinuing albuterol therapy. Heart rate increases were observed in six of eight treatments and serum albuterol levels at the end of treatment were greater than 25.0 ng/ml in all but one treatment. A mean increase in heart rate of 16.3 percent was observed for the entire group. Of the treatments with elevated (> 25.0 ng/ml) serum albuterol levels, a significant cumulative increase in heart rate was observed with time. A significant improvement of FEV1 was observed (p = 0.0025) with a net increase of 36.8 percent. These data suggest that high-dose continuously aerosolized albuterol treatment in some adult asthmatics can result in markedly elevated serum albuterol levels and potential cardiac stimulation despite spirometric improvement.

PMID: 8417883, UI: 93114039

No. 11


Chest 1992 Sep;102(3):742-7

Effects of ipratropium bromide nebulizer solution with and without preservatives in the treatment of acute and stable asthma.

Bryant DH, Rogers P

Thoracic Unit, St. Vincent's Hospital, Sydney, Australia.

In a recent study, it was suggested that the preservatives in ipratropium bromide nebulizer solution may cause a paradoxic bronchoconstrictor response in 20 percent or more of patients with stable asthma. The frequency of this response in patients with acute asthma is unknown. The aim of this study was to examine the acute effects of the usual dose of nebulized ipratropium bromide (0.25 mg) in patients with either stable or acute asthma using formulations with and without added preservatives. Twenty-five patients with stable asthma and 25 patients with acute asthma were studied. Each subject was given preservative-containing ipratropium bromide, preservative-free ipratropium bromide, pH 7 preservative-free ipratropium bromide, and saline solution in random order using a double-blind crossover technique with at least 4 h between drug administrations. Very frequent measurements of FEV1 were made for 30 min after each drug administration and then 5 mg of albuterol was nebulized and the FEV1 was measured again after another 30 min. Changes in FEV1 were expressed as a percentage of the predicted FEV1. Paradoxic bronchoconstriction to ipratropium was detected in only one patient with acute asthma (12 percent fall in FEV1) but in none of the patients with stable asthma. A 6 percent fall in FEV1 change occurred with the saline solution in this subject suggesting that the response may have been a nonspecific one due to increased bronchial responsiveness. The mean response (+/- 1 SD) to albuterol plus either preservative-containing ipratropium, preservative-free ipratropium, or pH7 preservative-free ipratropium was significantly greater (p less than 0.05) than the response to albuterol alone both in the patients with acute asthma (25 +/- 12 percent, 27 +/- 15 percent, 26 +/- 15 percent, and 20 +/- 15 percent, respectively) and stable asthma (26 +/- 7 percent, 25 +/- 8 percent, 24 +/- 6 percent, and 22 +/- 9 percent) supporting the use of ipratropium bromide as an additional bronchodilator in patients with asthma who do not show a satisfactory response to nebulized beta-adrenergic agonist.

Publication Types: Clinical trial, Randomized controlled trial

No. 12


JAMA 1989 Sep 1;262(9):1210-3

Intravenous magnesium sulfate for the treatment of acute asthma in the emergency department.

Skobeloff EM, Spivey WH, McNamara RM, Greenspon L

Medical College of Pennsylvania, Department of Emergency Medicine, Philadelphia 19129.

Conventional nebulized beta-agonist therapy has met with disappointing results in an increasing number of moderate to severe asthmatics who may be characterized as "poor responders." Thirty-eight patients suffering from acute exacerbations of moderate to severe asthma were treated in an emergency department with an intravenous infusion of saline placebo or 1.2 g of magnesium sulfate after conventional beta-agonist therapy failed to produce significant improvement in peak expiratory flow rate. Nineteen patients were randomized into each of two groups in a placebo-controlled, double-blind clinical trial. The treatment group demonstrated an increase in peak expiratory flow rate from 225 to 297 L/min as compared with 208 to 216 L/min seen in the placebo group. In addition, the number admitted vs discharged was significantly better for the treatment group (7 vs 12) than the placebo group (15 vs 4). Intravenous magnesium sulfate may represent a beneficial adjunct therapy in patients with moderate to severe asthma who show little improvement with beta-agonists.

Publication Types: Clinical trial, Randomized controlled trial


  1. Comment in: JAMA 1990 Jan 26;263(4):516-7
    Routine simultaneous administration of childhood vaccines.
    Damon RA
    Publication Types: Comment, Letter

No. 13


Am J Emerg Med 1994 Mar;12(2):164-6

Rapid infusion of magnesium sulfate obviates need for intubation in status asthmaticus.

Schiermeyer RP, Finkelstein JA

Joint Military Medical Centers, Wilford Hall Medical Center, Brooke Army Medical Center, San Antonio, TX 78236.

Rapid infusion of intravenous magnesium sulfate (MgSO4) was given to two young adults with impending respiratory failure caused by status asthmaticus. The infusion of 2 g of MgSO4 during a 2-minute period was associated with an immediate, dramatic reversal of their severe bronchospasm. This treatment obviated the need for intubation. Continuous beta 2-agonist therapy was performed simultaneously, taking advantage of the MgSO4-induced bronchodilation to deliver the beta 2-agonist to the target tissues. Rapid infusion of intravenous MgSO4 has been documented as safe in standard obstetric literature. Previous reports of MgSO4 therapy for acute asthma have used slow infusion. This is the first report of rapid infusion of MgSO4 for the emergency department management of asthma. In both cases, this therapy obviated the need for endotracheal intubation and mechanical ventilation.

Publication Types: Review, Review of reported cases

No. 14


Mithoefer J, Rinser R, Karetzky M. The use of sodium bicarbonate in the treatment of acute bronchial asthma.

N Engl J Med. 1965;272:1200-1205.

No. 15


Am Rev Respir Dis 1984 Mar;129(3):385-7

Mechanical controlled hypoventilation in status asthmaticus.

Darioli R, Perret C

This study reports the results obtained with mechanical ventilation in severe respiratory failure secondary to status asthmaticus. Of the 159 patients with status asthmaticus admitted to the Intensive Respiratory Unit over a 5-yr period, 26 required mechanical ventilation for a total of 34 episodes of acute respiratory acidosis. At the time of intubation, 10 patients were in coma and 5 were in respiratory arrest. Controlled mechanical ventilation was maintained for a mean of 2.5 days. Complications were few and reversible. All patients survived. These favorable results are attributed to a new strategy: mechanical ventilation is used to obtain a correction of hypoxemia with hyperoxic mixtures without attempting to restore an adequate alveolar ventilation. The respirator is adjusted to avoid high airway pressures, which appear to be more dangerous than persistent hypercapnia itself. Correction of hypercapnia is obtained later when bronchial obstruction relief provides better conditions of ventilation-perfusion distribution. So the risks of barotrauma and cardiocirculatory failure, which are frequently reported as fatal complications, appear to be significantly decreased.

No. 16


Chest 1986 Jan;89(1):152-4

Enflurane and halothane in status asthmaticus.

Echeverria M, Gelb AW, Wexler HR, Ahmad D, Kenefick P

A patient with status asthmaticus deteriorated while receiving conventional therapy including mechanical ventilation. She failed to respond to the inhalation of enflurane but had a beneficial response to halothane. Her subsequent course was complicated by a prolonged metabolic encephalopathy which was associated with an elevated plasma bromide level from the metabolism of halothane.

No. 17


Crit Care Med 1986 May;14(5):514-6

Use of ketamine in asthmatic children to treat respiratory failure refractory to conventional therapy.

Rock MJ, Reyes de la Rocha S, L'Hommedieu CS, Truemper E

We treated two pediatric patients suffering respiratory failure associated with status asthmaticus. Neither patient responded to maximal bronchodilatory therapy and mechanical ventilation; however, continuous infusion of ketamine (1.0 to 2.5 mg/kg X h) immediately improved airway obstruction. Ketamine appears to increase catecholamine levels and directly relax bronchial smooth muscle. Except for increased secretions during the infusion, our patients showed no immediate or long-term sequelae from ketamine therapy. However, ketamine should only be used for asthmatics whose respiratory failure does not respond to conventional management and mechanical ventilation.

No. 18


Crit Care Med 1993 Dec;21(12):1908-14

Cardiorespiratory consequences of expiratory chest wall compression during mechanical ventilation and severe hyperinflation.

Van der Touw T, Tully A, Amis TC, Brancatisano A, Rynn M, Mudaliar Y, Engel LA

Department of Respiratory Medicine, Westmead Hospital, Australia.

OBJECTIVES: To measure and compare the effects of manual expiratory compression of either the rib cage or abdomen on cardiac output, end-expiratory lung volume, and other cardiorespiratory variables in an animal model that mimics the severe pulmonary hyperinflation and hemodynamic impairment occurring in patients with severe acute asthma during mechanical ventilation.

DESIGN: Prospective, randomized, crossover trial.

SETTING: Research laboratory. SUBJECTS: Seven cross-bred, anesthetized, supine dogs.

INTERVENTIONS: The following sequence was employed: a) spontaneous breathing without pulmonary hyperinflation; b) positive-pressure ventilation with severe pulmonary hyperinflation (produced by an external variable expiratory flow resistor); c) approximately 7 mins of manual expiratory compression of either the rib cage or abdomen during positive-pressure ventilation-hyperinflation. This sequence was then repeated, incorporating the alternative type of expiratory compression.

MEASUREMENTS AND MAIN RESULTS: Cardiac output (measured by thermodilution), aortic pressure, pleural (esophageal) pressure, and changes in end-expiratory lung volume were measured. The decrease in cardiac output due to mechanical ventilation with pulmonary hyperinflation was exacerbated by rib cage compression (p < .001; spontaneous breathing 2.9 +/- 0.2 L/min, hyperinflation 1.5 +/- 0.1 L/min, and rib cage compression 1.0 +/- 0.1 [SEM] L/min). However, the positive-pressure ventilation-hyperinflation-induced decrease in cardiac output was attenuated by abdominal compression (p < .001; spontaneous breathing 3.3 +/- 0.2 L/min, hyperinflation 1.4 +/- 0.1 L/min, and abdominal compression 2.1 +/- 0.1 L/min). Mean aortic pressure returned to prehyperinflation levels during abdominal compression (p < .001; spontaneous breathing 126 +/- 2 mm Hg, hyperinflation 75 +/- 5 mm Hg, and abdominal compression 120 +/- 3 mm Hg). Both types of compression were similarly effective (p > .75) in increasing mean expiratory pleural pressure, so that end-expiratory lung volume was similarly (p > .25) reduced (0.45 +/- 0.05 and 0.40 +/- 0.05 L for rib cage and abdominal compressions, respectively) in this non-air flow, limiting animal model.

CONCLUSIONS: The cardiorespiratory effects of manually compressing the rib cage or abdomen during expiration in this animal study suggest that these techniques should be carefully evaluated in mechanically ventilated patients with severe acute asthma.


  1. Comment in: Crit Care Med 1993 Dec;21(12):1824
    Compression-assisted expiration in asthma.
    Fisher M
    Publication Types: Comment, Editorial

Special Resuscitation Situations