Extreme Tachypnea Research Articles

A rare case of congenital thoracic arteriovenous fistula between the brachiocephalic truncus and the superior vena cava resulting in heart failure

Abstract We present a case of a full-term 13 days old female baby administered to the PICU with extreme tachypnea with suspicion of a huge left-to-right-shunt at vascular or cardiac level. Echocardiography revealed an open arterial duct and a huge arterio-venous fistula from the proximal right subclavian artery directly into the superior vena cava. The fistula was cross-clamped, resected and both vesselstumps were oversewn. Histopathologically the fistula presented either as an artery of the elastic type or an arterialized vein, which is a typical finding in fistulas. The patient was extubated shortly after repair and referred home five days after surgery. To the best of our knowledge, this is first report of a direct fistulous connection between the brachiocephalic trunk (proximal to the right subclavian artery) and the SVC with congestive heart failure and ASD.

Extreme Maternal Metabolic Acidosis Leading to Fetal Distress and Emergency Caesarean Section

A 31-year-old pregnant woman (32 + 3 weeks) was admitted with extreme tachypnea. She had a previous history of congenital muscular dystrophy (Ullrich's disease) and isolated glucosuria. The patient had reduced food intake during the last 24 hours prior to admission and vomited twice. Serum glucose level was normal (112 mg/dL), while urinalysis revealed glucosuria 4+ and ketonuria 4+. ABG revealed pH 7.06, PCO2 9 mm Hg, and bicarbonate 2 mmol/L. Anion gap was 28 mmol/L. Tachypnea was a compensatory mechanism for a severe nonlactic metabolic acidosis. The diagnosis of starvation ketoacidosis was established. The patient received supplemental dextrose 10% intravenously and sodium bicarbonate. As fetal heart monitoring was pathological, an emergency caesarean section was performed. Umbilical cord venous pH was 7.01, with PCO2 34 mm Hg and bicarbonate 8 mmol/L. Starvation ketoacidosis is a rare metabolic disorder that may occur mainly in the third trimester of pregnancy. Muscular dystrophy and renal glucosuria were precipitating factors.

A Teenage Girl with Extreme Tachypnea

Dyspnea and tachypnea are common presenting complaints in an emergency department. Respiratory and cardiac causes are the most common etiology. Functional respiratory disorders should be considered in patients with atypical presentation to avoid extensive investigations. We describe an adolescent who presented to our emergency department with extreme tachypnea.

Predicting deterioration in previously healthy infants hospitalized with respiratory syncytial virus infection.

To estimate the incidence of clinical deterioration leading to intensive care unit transfer in previously healthy infants with respiratory syncytial virus (RSV) infection hospitalized on a general pediatric unit and, to assess the hypothesis that history, physical examination, oximetry, and chest radiographic findings at time of presentation can accurately identify these infants. A virology database was used to identify and determine the disposition of all children </=1 year of age admitted to the Children's Hospital at Strong (CHaS) with RSV infection during the 1985 to 1994 respiratory seasons. Index patients were all previously healthy, full-term infants admitted initially to the general inpatient services at CHaS or Rochester General Hospital, a second University of Rochester teaching hospital, whose clinical deterioration led to transfer to the pediatric intensive care unit (PICU). These infants were matched retrospectively (for year and date of infection, sex, chronologic age, and race) with two hospitalized controls who did not require PICU transfer. Chest radiographic findings, respiratory rate (RR), O(2) saturation, and presence of wheezing at time of presentation to the emergency department (ED) were compared. During the study years, 542 previously healthy, full-term infants were admitted to the general pediatric unit at CHaS with proven RSV infection. Ten (1.8%; 95% confidence interval, 0.9%, 3.4%) were transferred subsequently to the PICU, primarily for close monitoring of progressive respiratory distress. Data for these patients and 7 patients transferred from Rochester General Hospital to the PICU at the CHaS were compared with those for control patients. The mean RR in the ED (63 vs 50), and O(2) saturation in the ED (88% vs 93%) were modestly abnormal in cases compared with controls. Wheezing on examination at time of presentation and chest radiographic findings did not differ between the two groups. A RR >80 and an O(2) saturation <85% at time of presentation each had a specificity >97% for predicting subsequent deterioration. Each parameter, however, had a sensitivity </=30%. Clinical deterioration requiring PICU admission is an uncommon occurrence in previously healthy infants admitted to a general pediatric inpatient unit with RSV infection. Extreme tachypnea and hypoxemia were both associated with subsequent deterioration; however, only a small proportion of patients who clinically deteriorated presented in this way. The clinical usefulness of these parameters, therefore, is limited. respiratory syncytial virus, deterioration, healthy infants, prediction.

Apneustic breathing in children with brainstem damage due to hypoxic–ischemic encephalopathy

To confirm the presence of apneusis in patients with hypoxic–ischemic encephalopathy and to clarify which factors influence their respiratory patterns, polygraphic studies were performed on two patients. Apneusis was clinically suspected in both patients who had severe brainstem damage. In one subject, inputs of vagal afferents from the gastrointestinal tract and the urinary bladder often resulted in extreme tachypnea instead of apneusis. Lung inflation facilitated expiration during inspiratory arrest. Expiration preceded a periodic inhibition of rigospastic discharge in the right biceps muscle. In the other subject, prolonged inspiratory pauses with cyanosis occurred with or without preceding epileptic seizure. Both phenytoin dose reduction and treatment with tandospirone, a serotonin‐1A agonist, were effective in improving the respiratory distress in this subject.

Respiratory patterning following cerebral ventricular administration of cocaine

Intravenous (IV) cocaine in the conscious cat causes extreme tachypnea and reduction in breath-to-breath variability. In this study, we examined respiratory patterning following administration of cocaine into the cerebral ventricles. Intraventricular cocaine elicited a tachypnea that was nearly identical to that for IV cocaine. At the high dose, peak respiratory rate increased by 380%. Breath-to-breath variability was dramatically reduced by cocaine, especially in the early stages of the intoxication; during these stages, the tachypnea was occasionally interrupted by prolonged inspiratory efforts. Procaine was administered as a control for the anestetic effects of cocaine and caused an initial tachypnea that was similar to that for cocaine. For both cocaine and procaine, the mean ratios of inspiratory to expiratory durations were unaffected, indicating that the tachypnea was accomplished by approximately equal reductions in inspiratory and expiratory durations. We conclude that the tachypnea following cocaine administration results principally from central rather than peripheral mechanism. In addition, the data suggest that anesthetic actions mediate the principal respiratory effects of cocaine.

Dynamic properties of respiratory timing following cocaine administration

We assessed the timing and amplitude characteristics of diaphragmatic muscle activity following administration of intravenous cocaine HCl (10 mg/kg) to awake, unrestrained cats. Cocaine produced a pronounced tachypnea which was interrupted by deep inspiratory efforts coincident with tonic-clonic movements over the first 10 min following cocaine administration. Following that period, diaphragmatic cycle rates slowly increased for up to 1 h and were interrupted occasionally by longer inspiratory efforts which were not associated with other overt motor activities. As respiratory rate increased, breath-to-breath variability decreased, and the incidence of deep inspiratory efforts decreased. As total cycle time decreased, the ratio of inspiratory time to expiratory time remained the same between precocaine and early, intermediate and late intoxication periods. The amplitude of diaphragmatic EMG activity increased with the extreme tachypnea. A number of neural mechanisms may mediate the changes in diaphragmatic muscle activity, including hyperthermia and alteration of rostral brain influences on brainstem timing mechanisms.

Respiratory responses to focal and generalized seizures in cats

We studied the effects on breathing of seizures induced by focal injection of penicillin G into the parietal cortex in 13 anesthetized cats. Electrocorticograms, ventilation, end-tidal PCO2, and intrapleural and arterial pressures were monitored; changes of these variables were related to the stages of motor seizure. The first respiratory responses, tachypnea and hyperpnea, usually occurred before any peripheral muscular contractions developed. Progression of the seizure was always accompanied by further tachypnea and hyperpnea. The hyperpnea associated with all stages of seizure activity resulted in hypocapnia, which was sustained even during prolonged tonic-clonic motor convulsions that caused a threefold increase of metabolic rate. The extreme tachypnea of tonic generalized convulsions led to increased end-expiratory lung volume because of dynamic hyperinflation associated with very short expiratory durations in the tonic phase. We suggest that the profound effects of seizures on respiration are by feedforward mechanisms from the cortical focus itself and from subcortical circuits, such as hypothalamus, that become involved during seizure propagation and generalization. Peripheral respiratory feedback mechanisms are not important for the genesis of seizure-induced hyperpnea.

Pulmonary disease following chronic chemical ganglionic blockade: A clinical and pathologic study

In eight non-uremic patients with malignant hypertension and moderate azotemia who were treated with ganglionic blocking agents and hydralazine, extreme tachypnea developed. On postmortem examination they were found to have fibrinous pneumonitis resembling so-called “uremic pneumonia.” Pyrexia, relative tachycardia and leukocytosis, without uremia, alkalosis or hyponatremia, characterized their terminal clinical episode. Previous control of the hypertension had been poor, with high average diastolic pressures and extreme fluctuations in systolic pressure despite large doses of ganglionic blocking agents. The microscopic pulmonary lesions were studied in twenty-seven patients with a primary anatomic diagnosis of arteriolar nephrosclerosis who had received methonium salts and in sixtyseven such patients who had not been treated. Fibrinous pneumonitis was (1) significantly more frequent in methonium-treated patients than in untreated patients, (2) qualitatively similar anatomically in these two groups of patients, and (3) rare in non-uremic patients except those treated with hexamethonium. Fibrinous pneumonitis was not pronounced in any of the thirty-nine patients with mitral stenosis who also were studied; this tends to eliminate increased pulmonary venous pressure secondary to left heart failure as an important pathogenetic factor. These data suggest that methonium salts may exert effects similar to those of the nitrogen retention products of the uremic state in the pathogenesis of fibrinous pneumonitis.

Simulated Auricular Flutter in the Electrocardiogram of the Dog

ConclusionsBaseline movements which simulated impure auricular flutter developed following intravenous epinephrine injections. These are shown to be extracardiac in nature. They are induced by extreme tachypnea and the diaphragmatic movements associated with retching and vomiting.