Respiratory inductive plethysmography (RIP) is a well-accepted noninvasive technology for monitoring breathing patterns in adults. Prior attempts to calibrate this device in babies have been fraught with technical difficulties, thereby limiting applications in this population. Recently, a new method, qualitative diagnostic calibration (QDC), has been shown to provide accurate calibration of tidal volume in adults. The QDC method is based upon principles of the isovolume maneuver and carried out during natural breathing without specialized respiratory maneuvers or postural changes. We calibrated RIP with QDC in the supine posture and compared tidal volume (VT) measured with RIP to VT by a face mask-pneumotachograph (PNT) in 21 healthy full-term newborns in supine and prone postures. Eleven of the babies were calibrated during active sleep and 10 in quiet sleep. The mean VT in the supine and prone postures were 19 and 25 ml, respectively. In the supine and prone postures, weighted mean difference between RIP (VT) and PNT (VT) and 95% confidence intervals were -0.05 ml (-0.27, 0.18) and -0.32 ml (-0.08, 0.55), respectively. There was no difference in the accuracy of RIP relative to PNT calibrated during active sleep when thoracoabdominal incoordination was present or quiet sleep when it was not in either the supine or the prone postures. Therefore, in full-term infants, RIP calibrated with QDC solely in the supine posture provides clinically acceptable measurements of VT in both supine and prone postures.

The current study was undertaken to ascertain whether shift from supine to prone posture alters the pattern of natural breathing in healthy fullterm newborns. Breathing patterns were measured in the supine and prone posture in 20 healthy fullterm infants using calibrated, noninvasive respiratory inductive plethysmography (RIP). The values for breathing pattern components in supine and prone postures expressed as means (+/- SD) were, respectively, tidal volume (VT), 14.1(+/- 3.2) and 18.9(+/- 4.9)mL; mean inspiratory flow 26.7(+/- 11.5) and 32.8(+/- 13.0)mL/s; and minute ventilation 232(+/- 75) and 288(+/- 96)mL/kg/min (P < 0.01). Less thoracoabdominal incoordination, expressed as the labored breathing index (LBI), occurred with shift from supine to prone posture in infants studied in the active behavioral stage, changing from 2.0(+/- 0.5) to 1.3(+/- 0.4) (P < 0.01). Placement of a facemask-pneumotachograph system increased VT measured with RIP by 26% in the supine, and 18% in the prone posture. Neither respiratory rate nor inspiratory time (Ti) changed with the postural shift. Therefore, change from supine to prone posture improved ventilation and increased respiratory drive as expressed by VT/Ti. Further, thoracoabdominal incoordination which took place during active sleep in the supine posture, lessened with change to the prone posture.

Measurement of breath amplitude (BA) and similarly tidal volume (VT) in newborn infants is the standard for detection of apnea and hypopneas. The purpose of our study was to compare the accuracy for BA by three frequently utilized noninvasive respiratory monitors: respiratory inductive plethysmography (RIP), mercury in silastic strain gauges (SG), and impedance pneumography (IP). Twenty healthy full-term infants were studied in both supine and prone postures. The RC and AB gain factors for RIP were obtained using qualitative diagnostic calibration (QDC) procedure. The electrical gain of IP was set equivalent to the BA signal of a pneumotachograph (PNT). The three devices were calibrated in the supine posture and measurements were repeated in the prone posture without changing their calibration factors. Compared to PNT, postural change did not significantly alter BA measured by RIP. The accuracy of breath-to-breath BA measurement in the prone posture was worse for IP and SG compared to RIP and PNT. In contrast to SG or IP, the accuracy of BA measurement maintained was by RIP after a postural change from supine to prone in fullterm newborns.

Studies of severe hypoxemic events, defined as an arterial oxygen saturation < 80% greater than 4 s in spontaneously breathing infants, have been limited. The purpose of our study was to examine the distribution of respiratory events that lead to a fall in oximetrically measured oxygen saturation by using breathing patterns, heart rate, and validated pulse oximetry analysis. A total of 161 hypoxemic events were detected in 18 of 30 premature infants studied. Using an inductive plethysmographic based monitor, a total of 460 h of cardiorespiratory monitor recordings were analyzed. Hypoxemic events were categorized as being the direct result of apnea (duration longer than 15 s) or pauses (duration 4-14 s) with either unchanged or lower end-expiratory lung volumes compared with the preevent breaths. The breaths in the preevent period were analyzed for volume, timing, and thoracoabdominal coordination indices. Forty of the 161 events (25%) were associated with apnea of which 80% (31/40) had a mixed/obstructive basis. Ninety-four of the 161 severe hypoxemic events (58%) were associated with pauses with unchanged end-expiratory lung volume. Twenty-two of the 161 events (14%) showed pauses with lower end-expiratory lung volume. There were 5/161 events (3%) with severe hypoxemia in which no pause was observed. Comparison of the preevent periods in each category showed significant differences for only percent tidal volume from initial calibration and arterial oxygen saturation. Sixty-two percent (100/161) of severe hypoxemic events were preceded by hypopneic values of percent tidal volume. Seventy-five percent (40/161) of these hypoxemic events and their etiology would have gone undetected using respiratory monitoring from impedance pneumograms and ECGs. The varied basis for these events underscores the importance of analyzing detailed respiratory wave forms along with movement-free signal of arterial oxygen saturation and ECG, to formulate appropriate intervention strategies.

Twenty two c h i l d r e n (age range :3-14 years, Sex:m:f: :12:lO) adm i t t e d t o Kings County H o s p i t a l o f Brooklyn w i t h s t a t u s asthmaticus were s t u d i e d t o determine t h e i r plasma ADH l e v e l s i n r e l a t i o n t o the s e v e r i t y o f the s t a t u s asthmaticus. Plasma ADH l e v e l s were measured b y RIA a t t h e time o f admission and again a t 1-2 weeks f o l l o w i n g recovery from s t a t u s . The r e s u l t s are shown i n t h e table.We conclude from t h e study t h a t 1. AOH r esponse increases w i t h s e v e r i t y o f s t a t u s asthmaticus 2. With h i g h sp. g r . o f u r i n e d u r i n g s t a t u s , i n add i t i o n t o dehydration increased ADH s e c r e t i o n should be k e p t i n mind and 3. I n a d d i t i o n t o o t h e r known f a c t o r s , increased ADH may p l a y a r o l e i n pulmonary edema w i t h s t a t u s asthmaticus.GROUP I GROUP I I n=14 n =8 W e s t u d i e d t h e v e n t i l a t o r y response t o hypoxia i n 7 newborn k i t t e n s (n=12), 2 t o 28 days o l d , K i t t e n s were s u r g i c a l l y instrumented t o record diaphragmatic EMG (EMGD~), eye movements (EOG), e l e c t r o c o r t i c a l a c t i v i t y (ECoG), and neck EMG, Ventilat i o n (OE) was measured with a mask and a flow-through system. K i t t e n s i n h a l e d 21% 02 f o r a c o n t r o l period of a t l e a s t 2 min, 10% 02 f o r 10 min, and 21% 02 f o r 2 min again. Measurements were made i n q u i e t s l e e p . With a decrease i n Fi02 t o lo%, t h e r e was an immediate i n c r e a s e i n OE (0,210+0.017 t o 0.30020,025 L/min/kg; p<0,005) which was n o t s u s t a i n e d , v e n t i l a t i o n decreasing t o 0,224 20,028 by 10 min of hypoxia. VT i n c r e a s e d from 3,820.2 mllkg t o 5.0'0,4 (p<0.005) and then decreased t o 3,9'0.2. Frequency in-c r e r s e d from 56'4.0 breathslmin t o 6323 (p<0.02) and then decreased t o 5525, The changes i n I E M G D~X~ followed those i n vE0 K i t t e n s s t u d i e d b e f o r e 7 days of l i f e had a more pronounced dec r e a s e i n v e n t i l a t o r y output a t 10 min of hypoxia than o l d e r k i tt e n s , Breathing p a t t e r n became i r r e g u l a r o r p e r i o d i c during hypoxia.On r e t u r n t o 21% 02 v e n t i l a t o r y output decreased a b r u p t l y due t o apnea. These r e s u l t s suggest; 1) t h e hyperventil a t o r y response t o hypoxia i n unanesthetized k i t t e n s i s not w e l l s u s t a i n e d with values a t end of hypoxia c l o s e t o c o n t r o l l e v e l s ;2) t h e b i p h a s i c response t o hypoxia i s p r i m a r i l y a f u n c t i o n of frequency; 3) younger k i t t e n s a r e l e s s a b l e t o s u s t a i n hypervent i l a t i o n than o l d e r k i t t e n s , W e s p e c u l a t e t h a t t h e l a t e f a l l i n v e n t i l a t i o n i s due t o a c e n t r a l mechanism a f f e c t i n g frequency. Arousal from q u i e t sleep (QS) i n response t o a hypoxic challenge (HC) does n o t occur i n many apnea o f infancy (AOI) p ...