Drowning treated with intermittent positive pressure breathing

1960 ◽  
Vol 15 (5) ◽  
pp. 849-854 ◽  
Author(s):  
Joseph Redding ◽  
G. Carl Voigt ◽  
Peter Safar
Keyword(s):  
Ventricular Fibrillation ◽  
Sea Water ◽  
Venous Pressure ◽  
Arterial Hypotension ◽  
Positive Pressure ◽  
Partial Restoration ◽  
Anesthetized Dogs ◽  
Slight Rise ◽  
Intermittent Positive Pressure Breathing ◽  
Comparable Period

A standardized dog experiment was designed to simulate human victims of submersion who seem to first develop laryngospasm, followed by flooding of the lungs. The tracheal tube of lightly anesthetized dogs was clamped until the onset of apnea. The lungs were then flooded for 30 seconds with fresh water or sea water, or apnea was permitted to continue for a comparable period without flooding. Resuscitation was attempted with intermittent positive pressure breathing (IPPB), utilizing room air. All control dogs (obstructive asphyxia, without flooding) survived. Freshwater drowning caused mild arterial hypotension, severe rise in venous pressure and bradycardia, followed by sudden ventricular fibrillation in 1–4 minutes in spite of IPPB. Sea-water drowning caused severe arterial hypotension, slight rise in venous pressure and bradycardia. IPPB led to partial reoxygenation and partial restoration of circulation. When IPPB was discontinued all dogs started breathing spontaneously, but within a few minutes developed asystole with pulmonary edema. Submitted on January 25, 1960

DROWNING AND THE TREATMENT OF NON-FATAL SUBMERSION

PEDIATRICS ◽  
1966 ◽  
Vol 37 (4) ◽  
pp. 684-698
Author(s):  
Jerome Imburg ◽  
Thomas C. Hartney
Keyword(s):  
Ventricular Fibrillation ◽  
Pulmonary Function ◽  
Fresh Water ◽  
Animal Studies ◽  
Sea Water ◽  
The Body ◽  
Positive Pressure ◽  
Cardiac Massage ◽  
Central Nervous System Damage ◽  
Intermittent Positive Pressure Breathing

Animal studies have shown that fluid enters the body via the lungs in sea-water and fresh-water drowning. In fresh-water drowning in dogs, there is marked and rapid hemodilution with death due to ventricular fibrillation in about 4 minutes. In sea-water drowning in dogs, there is hemoconcentration; the blood water is lost into the sea water in the lungs with bradycardia and death due to asystole in 6 to 8 minutes. Studies of human drowning victims show similar, but less striking, changes in hemodynamics. In human non-fatal submersion the problems are usually those produced by impaired pulmonary function and central nervous system damage due to hypoxia. Hemodilution and ventricular fibrillation have not been documented in human nonfatal submersion. Therapeutic measures may be divided into those of an immediate urgent nature to be employed at the accident scene: expired air resuscitation, which should be started on reaching the unconscious victim in the water, and external cardiac massage, when indicated. Later measures to be instituted in the hospital include: cardiac resuscitation, intermittent positive-pressure breathing, hypothermia, tracheostomy and tracheal tiolet, oxygen therapy, antibiotics, steroids, and intravenous fluids to correct defects in blood elements (hemoglobin, electrolytes, pH). Later, pulmonary function should be studied for impairment due to alveolar damage and fibrosis. Permanent neurologic sequellae may develop.

Sympathetic influence on alveolar surface activity in hyperventilated dog

1978 ◽  
Vol 44 (3) ◽  
pp. 327-332 ◽  
Author(s):  
T. Kobayashi ◽  
S. Kishizuchi ◽  
S. Murakami
Keyword(s):  
Surface Activity ◽  
Stability Index ◽  
Positive Pressure ◽  
Sympathetic Block ◽  
Volume Relationship ◽  
Anesthetized Dogs ◽  
Pressure Volume Relationship ◽  
Sympathetic Influence ◽  
Intermittent Positive Pressure Breathing ◽  
Alveolar Surface

Hyperventilating IPPB, defined as intermittent positive-pressure breathing with a frequency of 32 beats/min and inspiratory pressure of 30 cmH2O, was administered for 14 h to open-chested anesthetized dogs in which nerves to one bronchus were operatively blocked. In the nerve-intact lungs, the lung stability index calculated from the pressure-volume relationship decreased with the duration of the hyperventilating IPPB (correlation coefficient r = -0.66, P less than 0.001), and atelectasis and hemorrhage appeared. In the nerve-blocked lungs, the index did not decrease during the 14 h of hyperventilating IPPB, and the appearance was almost normal. After pharmacologic sympathetic block with phenoxybenzamine, the lung stability index of both the operatively nerve-blocked lung and the nerve-intact lung was not decreased by hyperventilating IPPB. From these findings, we conclude that sympathetic block can protect pulmonary surface activity from the adverse effects of hyperventilating IPPB.

Effect of increased intra-abdominal pressure on various circulatory parameters of the anesthetized dog

1959 ◽  
Vol 14 (6) ◽  
pp. 940-942 ◽  
Author(s):  
E. T. Jach ◽  
S. F. Marotta ◽  
J. P. Marbarger
Keyword(s):  
Plasma Volume ◽  
Venous Pressure ◽  
Control Level ◽  
Urine Volume ◽  
Vena Cava ◽  
Elevated Pressure ◽  
Positive Pressure ◽  
Abdominal Pressure ◽  
Anesthetized Dogs ◽  
Marked Drop

Abdominal pressure of anesthetized dogs was elevated by the introduction of 18.5 mm Hg compressed air through a cannula tied securely into the peritoneal cavity. Significant decreases in circulating plasma volume (T-1824) were observed during the first 80 minutes of elevated pressure. Thereafter, plasma volume returned toward the control level except for a marked drop when the pressure was released. Hematocrit levels and plasma protein concentrations also indicated a loss of fluid. Mean vena cava pressure at the level of the heart did not markedly change, although the venous pressure below the diaphragm increased significantly. Arterial pressures decreased immediately upon elevation of the abdominal pressure, but returned to pre-experimental levels prior to release of elevated abdominal pressure. Concomitant with these circulatory alterations was a decrease in urine volume as well as a slight increase in serum potassium. Serum sodium remained essentially unaltered. These observations are compared to similar circulatory changes which occur during positive pressure breathing. Submitted on April 27, 1959

Treatment of sea-water aspiration

1960 ◽  
Vol 15 (6) ◽  
pp. 1113-1116 ◽  
Author(s):  
Joseph S. Redding ◽  
G. Carl Voigt ◽  
Peter Safar
Keyword(s):  
Body Weight ◽  
Pulmonary Edema ◽  
Intravenous Infusion ◽  
Spontaneous Breathing ◽  
Sea Water ◽  
Artificial Respiration ◽  
Positive Pressure ◽  
Plasma Infusion ◽  
Dog Plasma ◽  
Anesthetized Dogs

Lightly anesthetized dogs were subjected to obstructive asphyxia (simulating laryngospasm). When spontaneous breathing efforts ceased, the lungs were flooded with sea water for 30 seconds, according to a standardized experiment described previously. Five dogs were treated with intermittent positive pressure artificial respiration with 100% oxygen (IPPB/O2) for 3 hours. Five additional dogs were treated identically except for the addition of an intravenous infusion of dog plasma 50 ml/kg body weight, 10 minutes after the start of artificial respiration. All the dogs treated only with IPPB/O2 for 3 hours were more completely reoxygenated than were those ventilated with IPPB/air for 10 minutes in the earlier experiment. However, death with pulmonary edema followed the cessation of IPPB/O2 as well as IPPB/air. When the hemoconcentration and hypovolemia, caused by flooding of the lungs with sea water, were corrected by plasma infusion in addition to IPPB/O2, four of the five dogs survived. Submitted on May 19, 1960

Restoration of circulation after fresh water drowning

1961 ◽  
Vol 16 (6) ◽  
pp. 1071-1074 ◽  
Author(s):  
Joseph S. Redding ◽  
Richard A. Cozine
Keyword(s):  
Ventricular Fibrillation ◽  
Fresh Water ◽  
Hypertonic Saline ◽  
Vertebral Column ◽  
Artificial Respiration ◽  
Respiratory Arrest ◽  
Spontaneous Circulation ◽  
Positive Pressure ◽  
Artificial Circulation ◽  
Anesthetized Dogs

Lightly anesthetized dogs were subjected to obstructive asphyxia, simulating laryngospasm. After respiratory arrest the lungs were flooded with fresh water for 30 sec, according to a standardized experiment. Ten dogs were treated with intermittent positive-pressure artificial respiration with 100% oxygen. Six of the ten dogs suddenly developed ventricular fibrillation less than 2 min after artificial respiration was started. In these animals an artificial circulation was maintained for 20 min by repeated compression of the heart between the sternum and vertebral column. Then, after intravenous administration of hypertonic saline and epinephrine solutions, a 480-v shock was applied to the chest wall. In five of the six dogs there was an immediate resumption of spontaneous circulation. In an additional ten dogs ventricular fibrillation was produced by the same sequence of obstructive asphyxia and flooding of the lungs. In five, treatment was identical except that injection of hypertonic saline was omitted. Circulation was restored in four. In the remaining five, ventilation was performed with air. Restoration of circulation was successful in one. Submitted on June 12, 1961

Circulating plasma volume changes in anesthetized dogs during positive pressure breathing

1959 ◽  
Vol 14 (6) ◽  
pp. 937-939 ◽  
Author(s):  
S. Sobel ◽  
S. F. Marotta ◽  
J. P. Marbarger
Keyword(s):  
Mean Arterial Pressure ◽  
Plasma Volume ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Fluid Loss ◽  
Progressive Decrease ◽  
Volume Changes ◽  
Alkaline Urine ◽  
Anesthetized Dogs ◽  
Pressure Changes

Various circulatory functions were measured in anesthetized dogs subjected to 18.5 mm Hg positive pressure breathing. Immediately upon raising the intrapulmonary pressure there occurred a five- to sixfold increase in venous pressure as well as a decrease in mean arterial pressure. Accompanying these pressure changes was a progressive decrease in circulating plasma volume as measured by the T-1824 method. A 30% decrease in plasma volume was recorded after 160 minutes of increased intrapulmonary pressure. Hemoconcentration was also indicated by the increased hematocrits, although calculated fluid loss was only 13%. All circulatory changes returned to prepressure breathing levels upon release of pressure breathing. Other changes, such as oliguria, periods of apnea and an alkaline urine accompanied positive pressure breathing. The data suggest that the decrease in plasma volume is the result of venostasis caused by the rapid increase in venous pressure. Submitted on April 27, 1959

Intermittent Positive Pressure Breathing in Patients with Respiratory Muscle Weakness

CHEST Journal ◽  
1986 ◽  
Vol 90 (4) ◽  
pp. 546-552 ◽  
Author(s):  
F. Dennis McCool ◽  
Raymond F. Mayewski ◽  
David S. Shayne ◽  
Charles J. Gibson ◽  
Robert C. Griggs ◽  
...  
Keyword(s):  
Muscle Weakness ◽  
Respiratory Muscle ◽  
Positive Pressure ◽  
Respiratory Muscle Weakness ◽  
Intermittent Positive Pressure Breathing

Physiotherapy in chest disease

1980 ◽  
Vol 18 (8) ◽  
pp. 29-31
Keyword(s):  
Respiratory Function ◽  
Positive Pressure ◽  
Forced Expiration ◽  
Breathing Exercises ◽  
Postural Drainage ◽  
Chest Disease ◽  
General Mobility ◽  
Intermittent Positive Pressure Breathing ◽  
Do So

Physiotherapy is given to patients with chest disease in the hope of aiding the removal of secretions, improving respiratory function and increasing general mobility. Evaluating physiotherapy is difficult and until recently few attempts have been made to do so. This article considers the use of postural drainage, chest percussion and vibration, intermittent positive pressure breathing, forced expiration technique, breathing exercises and general exercises for some common chest conditions.

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