参考文献 No. 2
No. 1
[PubMed]
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
Comments: No. 2
[PubMed]
[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
[PubMed]
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
[PubMed]
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.
Comments:
No. 5
[PubMed]
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
[PubMed]
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
[PubMed]
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
No. 1
[PubMed]
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
[PubMed]
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
[PubMed]
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
[PubMed]
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.
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
[PubMed]
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
[PubMed]
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
[PubMed]
Respiratory arrest in near-fatal asthma.
Molfino NA, Nannini LJ, Martelli AN, Slutsky AS
Hospital Nacional Maria Ferrer, Buenos Aires, Argentina.
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。)
Comments:
No. 1
[PubMed]
Sudden-onset fatal asthma.
Sur S, Hunt LW, Crotty TB, Gleich GJ
Publication Types: Editorial
No. 10
[PubMed]
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
[PubMed]
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
[PubMed]
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
Comments: No. 13
[PubMed]
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
[PubMed] N Engl J Med.
1965;272:1200-1205.
No. 15
[PubMed]
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
[PubMed]
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
[PubMed]
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
[PubMed]
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.
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.
Comments:
低体温(Hypothermia)/高体温(Hyperthermia)
Safar P
Publication Types: Comment, Letter
Weil MH, Gazmuri RJ
Publication Types: Comment, Editorial
Gilston A
Publication Types: Comment, Letter
喘 息 (Asthma)
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.
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.
McFadden ER Jr
Publication Types: Comment, Editorial
Respiratory arrest in near-fatal asthma.
Publication Types: Comment, Letter
Damon RA
Publication Types: Comment, Letter
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.
Fisher M
Publication Types: Comment, Editorial
(個々の状況での蘇生)