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

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.

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

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

Cardiac and Respiratory Arrest in a 12-Year-Old Girl with Acute Permethrin Toxicity: A Case Report

2021 ◽  
Author(s):  
Hesam Adin Atashi ◽  
Hamid Zaferani Arani ◽  
Seyyed Mojtaba Ghorani ◽  
Mahya Sadat Teimouri Khorasani ◽  
Masoumeh Moalem
Keyword(s):  
Case Report ◽  
Brain Damage ◽  
Respiratory Arrest ◽  
Spontaneous Circulation ◽  
Type I ◽  
Medical Problems ◽  
Present Case Report ◽  
Case Presentation ◽  
Hypoxic Brain Damage ◽  
Hypoxic Brain

Abstract Background: Permethrin (PER) is widely employed as the most frequently used type I synthetic pyrethroid insecticide. Despite its worldwide application, reports of pediatric toxicity following permethrin administration are scarce.Case presentation: The present case report involves a 12-year-old Afghan girl, with no previous medical problems, who drank an unknown insecticide covertly at home. Two hours after ingestion, she was taken to the emergency room with neither breathing signs nor a heartbeat. She was immediately transferred to the cardiopulmonary resuscitation (CPR) room, and her spontaneous circulation was returned after a few minutes of CPR. She was then intubated, volume resuscitated with intravenous normal saline, and connected to the mechanical ventilator after being transferred to the ICU ward. The patient remained comatose without spontaneous breathing, her pupils became bilateral mydriasis, and central diabetes insipidus became evident after three days due to apnea and hypoxic brain damage following insecticide ingestion. The chemical analysis of the insecticide bottle showed 10% permethrin without organophosphates, as initially expected. Unfortunately, after seven days, the patient passed away due to resistant hypotension and severe brain damage.Conclusion: Permethrin is widely used globally as an insecticide. However, there are many unmet needs in permethrin toxicity treatment, and the treatment is mainly supportive. Depending on the amount and dose of permethrin, the most common symptoms can vary from headache, dyspnea, and vomiting to metabolic acidosis and cardiac and respiratory arrest, which can lead to hypoxic brain damage and death, as was the outcome in our case.

Abstract 17847: Gasping is a Valid Predictor Of ROSC and Hospital Discharge for In-hospital Cardiac Arrest Occurring on the Ward

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Luca Marengo ◽  
Wolfgang Ummenhofer ◽  
Gerster Pascal ◽  
Falko Harm ◽  
Marc Lüthy ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Hospital Discharge ◽  
Survival Data ◽  
Neurological Outcome ◽  
Rapid Response Team ◽  
Spontaneous Circulation ◽  
University Hospital ◽  
Data Set ◽  
Hospital Cardiac Arrest

Introduction: Agonal respiration has been shown to be commonly associated with witnessed events, ventricular fibrillation, and increased survival during out-of-hospital cardiac arrest. There is little information on incidence of gasping for in-hospital cardiac arrest (IHCA). Our “Rapid Response Team” (RRT) missions were monitored between December 2010 and March 2015, and the prevalence of gasping and survival data for IHCA were investigated. Methods: A standardized extended in-hospital Utstein data set of all RRT-interventions occurring at the University Hospital Basel, Switzerland, from December 13, 2010 until March 31, 2015 was consecutively collected and recorded in Microsoft Excel (Microsoft Corp., USA). Data were analyzed using IBM SPSS Statistics 22.0 (IBM Corp., USA), and are presented as descriptive statistics. Results: The RRT was activated for 636 patients, with 459 having a life-threatening status (72%; 33 missing). 270 patients (59%) suffered IHCA. Ventricular fibrillation or pulseless ventricular tachycardia occurred in 42 patients (16% of CA) and were associated with improved return of spontaneous circulation (ROSC) (36 (97%) vs. 143 (67%; p<0.001)), hospital discharge (25 (68%) vs. 48 (23%; p<0.001)), and discharge with good neurological outcome (Cerebral Performance Categories of 1 or 2 (CPC) (21 (55%) vs. 41 (19%; p<0.001)). Gasping was seen in 128 patients (57% of CA; 46 missing) and was associated with an overall improved ROSC (99 (78%) vs. 55 (59%; p=0.003)). In CAs occurring on the ward (154, 57% of all CAs), gasping was associated with a higher proportion of shockable rhythms (11 (16%) vs. 2 (3%; p=0.019)), improved ROSC (62 (90%) vs. 34 (55%; p<0.001)), and hospital discharge (21 (32%) vs. 7 (11%; p=0.006)). Gasping was not associated with neurological outcome. Conclusions: Gasping was frequently observed accompanying IHCA. The faster in-hospital patient access is probably the reason for the higher prevalence compared to the prehospital setting. For CA on the ward without continuous monitoring, gasping correlates with increased shockable rhythms, ROSC, and hospital discharge.

Venom of the lionfish Pterois volitans

1959 ◽  
Vol 197 (2) ◽  
pp. 437-440 ◽  
Author(s):  
Paul R. Saunders ◽  
Peter B. Taylor
Keyword(s):  
Blood Pressure ◽  
Myocardial Ischemia ◽  
Intravenous Injection ◽  
Artificial Respiration ◽  
Active Material ◽  
Respiratory Arrest ◽  
Pterois Volitans ◽  
Electrocardiographic Changes ◽  
The Mean ◽  
Primary Action

Extracts prepared from the venomous dorsal spines of lionfish ( Pterois volitans) were investigated in mice and rabbits. Intravenous injection into mice produced death in from less than a minute up to about one-half hour. The primary action in rabbits was a fall in blood pressure, accompanied by increase in respiratory rate; with larger doses there was evidence of myocardial ischemia or injury. After injection of fatal doses a variety of electrocardiographic changes occurred and the blood pressure fell to zero; respiratory arrest occurred terminally, but artificial respiration did not prolong the life of the animal. The active material was nondialyzable and the extracts contained considerable amounts of protein. Extracts retained substantial activity after lyophilization or addition of glycerol when stored for over a year at –20°C. The mean ld50 following intravenous injection into mice was about 1 mg of protein/kg.

Effect of pulmonary arterial PCO2 on breathing pattern

1988 ◽  
Vol 64 (5) ◽  
pp. 1844-1850 ◽  
Author(s):  
E. R. Schertel ◽  
D. A. Schneider ◽  
L. Adams ◽  
J. F. Green
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Middle Level ◽  
Positive Pressure ◽  
Breathing Patterns ◽  
Arterial Pco2 ◽  
Anesthetized Dogs ◽  
Steady State Levels ◽  
Pulmonary Arterial

We studied breathing patterns and tidal volume (VT)-inspiratory time (TI) relationships at three steady-state levels of pulmonary arterial PCO2 (PpCO2) in 10 anesthetized dogs. To accomplish this we isolated and then separately pump perfused the pulmonary and systemic circulations, which allowed us to control blood gases in each circuit independently. To ventilate the lungs at a rate and depth determined by central drive, we used an electronically controlled positive-pressure ventilator driven by inspiratory phrenic neural activity. Expiratory time (TE) varied inversely with PpCO2 over the range of PpCO2 from approximately 20 to 80 Torr. VT and TI increased with rising PpCO2 over the range from approximately 20 to 45 Torr but did not change further as PpCO2 was raised above the middle level of approximately 45 Torr. Thus minute ventilation increased as a function of TE and VT as PpCO2 was increased over the lower range and increased solely as a function of TE as PpCO2 was increased over the upper range. The VT-TI relationship shifted leftward on the time axis as PpCO2 was lowered below the middle level but did not shift in the opposite direction as PpCO2 was raised above the middle level. In addition to its effect on breathing pattern, we found that pulmonary hypocapnia depressed inspiratory drive.

Ventricular fibrillation during uniform myocardial anoxia due to asphyxia

1960 ◽  
Vol 198 (5) ◽  
pp. 955-958 ◽  
Author(s):  
Jay D. Coffman ◽  
D. E. Gregg
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Potassium Level ◽  
Serum Potassium Level ◽  
Current Theory ◽  
The Other ◽  
Right Atrial ◽  
Serum Electrolytes ◽  
Anesthetized Dogs ◽  
A Current

Thirty-three anesthetized dogs of varying weights were subjected to complete asphyxia by tracheal occlusion to produce uniform anoxia of the heart. Eleven showed electrocardiographic evidence of ventricular fibrillation while the other twenty-two demonstrated cardiac arrest. The development of ventricular fibrillation correlated with the heavier body and heart weights and with a lower average right atrial serum potassium level as compared to the dogs not fibrillating. Other serum electrolytes, pH, body temperature and sex showed no correlation with the arrhythmia. The importance of the fact that large dogs have a greater susceptibility to develop ventricular fibrillation during uniform anoxia of the heart is discussed in relation to experimental research on dogs and to a current theory of the cause of ventricular fibrillation.

RESUSCITATION AND TREATMENT FOLLOWING SUBMERSION

PEDIATRICS ◽  
1966 ◽  
Vol 37 (4) ◽  
pp. 666-668
Author(s):  
Joseph S. Redding
Keyword(s):  
Fresh Water ◽  
Positive Pressure Ventilation ◽  
Sea Water ◽  
Intermittent Positive Pressure Ventilation ◽  
Positive Pressure ◽  
Cardiac Massage ◽  
Closed Chest ◽  
Myocardial Failure ◽  
Exhaled Air ◽  
Electrical Defibrillation

In resuscitation from drowning it must be remembered that when breathing movements are absent no time must be wasted in attempts to drain the lungs. Reoxygenation must be started immediately with exhaled air. Positive pressure ventilation with oxygen should be substituted as soon as possible. It should be continued in victims of sea water submersion until a blood specimen can be examined and any plasma deficiency corrected. In fresh water drowning intermittent positive pressure ventilation combined with closed chest cardiac massage is a preliminary to external electrical defibrillation. Prevention of delayed death depends upon the management of massive hemolysis, hypervolemia, electrolyte imbalances, aspiration pneumonitis, and myocardial failure.

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