Evidence Of Cardiopulmonary Disease Research Articles

Vertebral heart size and vertebral left atrial size reference ranges in healthy Miniature Schnauzers.

The inclusion of vertebral heart score (VHS) and, more recently, the inclusion of the vertebral left atrial size (VLAS) in radiographic evaluation have become important screening tools for identifying dogs with occult cardiac disease. Several recent papers have shown there are interbreed variations in the VHS reference range. Our hypothesis is that the Miniature Schnauzer would also have a higher reference range for its VHS. The electronic medical records of IDEXX Telemedicine Consultants were searched for Miniature Schnauzers undergoing thoracic radiographs between March 1, 2022, and February 28, 2023. Dogs were included if they had 3 view thoracic radiographs performed and no evidence of cardiopulmonary disease was detected. Dogs with incomplete radiographic studies or cardiac or extracardiac disease were excluded. The VHS and VLAS measurements were performed by 2 board-certified cardiologists independent of one another. A total of 1,000 radiographs were obtained of which 272 were included for the study. The overall range for the VHS in this cohort was 9.68 to 12.07 with a median of 10.9. For VLAS measurements, a range of 1.71 to 2.4 was documented with a median of 2.0. The VHS for Miniature Schnauzers without cardiac disease was confirmed to be higher than the canine reference range.

Distinct effects of type 2 diabetes and obesity on cardiopulmonary performance.

Effort intolerance is frequent in patients with overweight/obesity and/or type 2 diabetes (T2D) free from cardiac and respiratory disease. We sought to quantify the independent effects of T2D and body mass index (BMI) on cardiopulmonary capacity and gain insights on the possible pathophysiology by case-control and regression analyses. Patients at high/moderate cardiovascular risk, with or without T2D, underwent spirometry and combined echocardiography-cardiopulmonary exercise test as part of their clinical workup. Subjects with evidence of cardiopulmonary disease were excluded. The effects of T2D and obesity were estimated by multivariable models accounting for known/potential confounders and the major pathophysiological determinants of oxygen uptake at peak exercise (VO2peak ) normalized for fat-free mass (FFM). In total, 109 patients with T2D and 97 controls were included in the analysis. The two groups had similar demographic and anthropometric characteristics except for higher BMI in T2D (28.6 ± 4.6 vs. 26.3 ± 4.4 kg/m2 , p = .0003) but comparable FFM. Patients with T2D achieved lower VO2peak than controls (18.5 ± 4.4 vs. 21.7 ± 8.3 ml/min/kg, p = .0006). Subclinical cardiovascular dysfunctions were observed in T2D: concentric left ventricular remodelling, autonomic dysfunction, systolic dysfunction and reduced systolic reserve. After accounting for confounders and major determinants of VO2peakFFM , T2D still displayed reduced VO2peak by 1.0 (-1.7/-0.3) ml/min/kgFFM , p = .0089, while the effect of BMI [-0.2 (-0.3/0.1) ml/min/kgFFM , p = .06 per unit increase], was largely explained by a combination of chronotropic incompetence, reduced peripheral oxygen extraction, impaired systolic reserve and ventilatory (in)efficiency. T2D is an independent negative determinant of VO2peak whose effect is additive to other pathophysiological determinants of oxygen uptake, including BMI.

RARE LOSS-OF-FUNCTION VARIANT ANALYSIS IN LONE ATRIAL FIBRILLATION

Atrial fibrillation (AF) is a complex heritable disorder that substantially increases the risk for stroke, sudden death and all-cause mortality. Lone AF is a subset defined by early diagnosis (less than 60 years) and with no evidence of cardiopulmonary disease. Genome-wide association studies have associated loci near genes for structural integrity and function of muscles with AF susceptibility. In addition, some studies have identified rare loss-of-function (LoF) variants in dilated cardiomyopathy (DCM) genes in lone AF. The increased burden of these variants in lone AF patients may indicate a shared predisposition between AF and DCM. We performed a retrospective study on 252 adult patients and a control group of 503 healthy European subjects. Exome sequencing and microarray assays were performed at the McGill Genome Center while exome data from the controls was retrieved from 1KG Consortium. Principal component analysis was performed to define a group with common ancestry using SVS software. Variants within candidate DCM genes were filtered by minor allele frequency of ≤0.1%, a Combined Annotation Dependent Depletion (CADD) Phred score of >20 and a LoF variant type (frameshift, splice acceptor, splice donor and stop gain). These factors were retrieved from public annotation databases and applied using VarSeq software for variant analysis. All variants were confirmed with Sanger sequencing. Cascade screening was attempted on all cases positive for variants. The AF cohort, an ethnically homogenous composite of 181 lone AF cases, had 6 heterozygous LoF variants, including 4 novel variants, in 6 individuals, while the controls had 4 in 503 individuals. Half of variants in the cases were in the TTN gene (3/6). The prevalence of rare LoF variants in the lone AF cohort was 3.3% while in the control cohort 0.79%, the odds ratio of rare LoF variants found in lone AF patients compared to controls is 4.28 (95%CI: 1.19-15.33, P-value: 2.5E-02). Cascade screening in one family demonstrated co-segregation of one of the rare TTN variants and AF. Patients with lone AF carry a significant burden of heterozygous LoF variants in DCM genes. Our results are in agreement with a previous study identifying TTN variants in lone AF patients. Further, we identified novel variants in different DCM genes and confirmed the co-segregation of a TTN variant and AF in one family. Our findings may indicate a common genetic predisposition between lone AF and DCM, which may help elucidate novel pathophysiologic mechanisms, and improve diagnosis and treatment.

Evaluation of the global longitudinal strain and segmental strain of the right ventricle with two-dimensional speckle-tracking echocardiography with elevation of the legs.

Speckle-tracking echocardiography has shown its usefulness in the evaluation of the right ventricle (RV) in healthy subjects and in pulmonary hypertension. It is unknown whether this technique could be sensitive to assess healthy RV with increases in preload. Consecutive subjects were studied without evidence of cardiopulmonary disease. They underwent speckle-tracking echocardiography in General Electric Vivid 7® equipment. The "segmental longitudinal strain" (SLS) and "global longitudinal strain" (GLS) of the RV was determined at rest and with an increase in the preload through elevation the legs to 45°. We analyzed 31 subjects, 16 men and 15 women, aged 16-53 years, in which were measured SLS and GLS. Basal of the RV free wall: -29.1 ± 3.3 versus -32.7 ± 5.5%, p = 0.0002. Mid of the RV free wall: -28.6 ± 6.4 versus -31.5 ± 4.9%, p = 0.001. Apical of the free wall of the RV: -21.9 ± 6.5 versus -23.3 ± 6.1%, p = 0.118. Basal inferoseptum: -19.40 ± 3.2 versus -18.9 ± 3.0%, p = 0.204. Mid inferoseptum: -19.3 ± 3.2 versus -19 ± 3.1%, p = 0.249. Apical septum: -17.1 ± 5.1 versus -17 ± 5.4%, p = 0.457. GLS of the RV: -23.06 ± 3.4 versus -24.5 ± 2.9%, p = 0.002. ICC: 0.773, 95% CI: 0.534-0.890, p < 0.001. This method was sensitive to detect differences in the GLS and SLS basal and mid of the RV free wall.

Should we quantify the diameters of the right heart in relation to the body surface area

Background: The evaluation of the right heart cavities represents a challenge for echocardiography, given the impossibility of their approach to a geometric model. Moreover, there are no recommendations on the need to adjust right heart dimensions to body surface area. Objective: The aim of this study was to establish the relationship between right heart chamber dimensions and body surface area in a population with no evidence of cardiopulmonary disease. Methods: The study included patients attending the echocardiography laboratory for a regular health examination. Patients with cardiac disease, right or left ventricular dysfunction, significant valve diseases, known pulmonary disease or pulmonary systolic pressure ≥45 mmHg were excluded from the study. Patients’ affiliation, weight (kg), height (meters), and body surface area (m2) data were recorded. Right heart measurements were based on guideline recommendations. The population was distributed in quartiles according to body surface area (25%-50%-75%-100%). Simple regression analysis was performed between each dimension of the right heart and body surface area. Results: A prospective, consecutive, observational and descriptive cohort study was performed including 1,045 patients with the following characteristics: mean age 41±15.1 years, 53% men, mean weight 77.4±19.6 kg, height 1.69±0.09 and BSA 1.89±0.87 m². Significant differences were observed in each of the variables according to the distribution by quartiles. A positive correlation was demonstrated between all right heart dimensions and body surface area. Conclusions: Body surface area is an important determinant of right heart dimensions measured by echocardiography. We therefore suggest the use of measurements indexed by body surface area, since it could influence clinical decision making.

Loss of Small Vessel Volume Fraction as a Marker for Pulmonary Hypertension in COPD

SESSION TITLE: Pulmonary Hypertension SESSION TYPE: Original Investigation Poster PRESENTED ON: Wednesday, November 1, 2017 at 01:30 PM - 02:30 PM PURPOSE: Pulmonary hypertension develops in a subset of subjects with COPD, and when present is accompanied by increasing morbidity and mortality. Early diagnosis, prognostication and selection of subjects that may benefit from pulmonary vasodilatory therapy remains challenging. In prior work it has been shown that smokers show evidence of pulmonary vascular pruning in 3D reconstruction of the pulmonary vasculature. In this study we examine changes to the pulmonary vascular tree in patients with COPD and pre-capillary pulmonary hypertension proven by right heart catheterization (PAH). METHODS: A retrospective database query of subjects with diagnosis of COPD and PH possessing ct angiograms yielded approximately 200 subjects. From these, 21 subjects with non-elevated PCWP (<15mmHg), PH (elevated PVR and mPAP) and FEV1/FVC of less than 70% by PFT were selected. Of these, seven had 1mm cuts appropriate for reconstruction. A cohort of 15 subjects having undergone right heart catheterization, imaging and exercise testing with no evidence of cardiopulmonary disease was used as control subjects. Vascular reconstruction was performed as previously described. Small vessel volume fraction, defined as the vascular volume in small vessels (less than 5mm2 in cross-sectional area) divided by total vascular volume, was used to measure pruning. Association was tested using a two-tailed t-test, assuming unequal variances. RESULTS: Seven patients (Age 65.7±10.5) with COPD (FEV1pp 61.7±6.8%) were identified with precapillary PAH (mPAP 45±14.3mmHg; PVR 8.6±6WU; mPCWP 10.8±2.2mmHg, max 14mmHg). Fifteen subjects (Age 46 ; mPAP 15mmHg; PVR 1.1 WU; mPCWP 9mmHg) were used as controls. Subjects with PAH and COPD had significant proximal dilation and distal loss of vasculature, which was quantified by dividing the volume in small vessels (defined as those with cross sectional area of less than 5mm2 ) by the total volume of the vasculature detected. Small vessel volume fraction in the COPD group was lower (0.37 ± 0.12) as compared to control subjects (0.55 ±0.11) with a p-value of 0.006 for the comparison. CONCLUSIONS: The vascular pruning previously described in smokers is quantifiable from CT angiography in subjects with precapillary pulmonary arterial hypertension in the context of significant COPD burden. CLINICAL IMPLICATIONS: Measurement of pulmonary vascular morphology in smokers may be useful in detecting and subtyping the extent of pulmonary vascular disease in smokers. DISCLOSURE: The following authors have nothing to disclose: Farbod Rahaghi, Viviana Paz, James Ross, Raúl San José Estépar, George Washko, Franck Rahaghi Image processing techniques for reconstruction of the vasculature used are currently in exploratory stage and appropriate only for research purposes.

Case study: haemoglobin rothschild in a case presenting with cyanosis

Introduction Here we describe a case presenting with episodic cyanosis in the absence of any evidence of cardio-pulmonary disease. Case The patient was a 27-year-old female who sought medical attention for a productive cough. On examination she was cya-nosed but not in distress. Systematic examination, notably cardio-respiratory system, revealed no abnormalities. A positive family history of episodic cyanosis in one of the siblings, but not the parents, was obtained. Results The full blood count, renal and liver functions were essentially normal. A normal haptoglobin level effectively excluded haemolysis. The oxygen saturation at the time of examination was 87%. An abnormal band was noted on Hb electrophoresis confirm-ing the presence of an Hb variant. Gene sequencing revealed a cod 37 (Tryp>Arg) mutation in exon 2 of the beta-globin gene, identi-fied as Hb Rothschild. Discussion Tryptophan at β37 is recognised as an important α1β2 contact point of the haemoglobin molecule. Disruption of the β37 contact point favours a T-quaternary (low oxygen affinity) state of the haemoglobin tetramer. Premature oxygen off-loading decreases the percentage oxygen saturation and may lead to cyanosis. Causes of cyanosis include cardio-respiratory disease, meth-aemoglobinaemia, sulfhaemoglobinaemia and low oxygen affinity haemoglobin variants.

Continuous positive airway pressure administered via face mask in tranquilized dogs

To evaluate the tolerance of a continuous positive airway pressure (CPAP) mask in tranquilized dogs and compare PaO₂ in arterial blood in dogs receiving oxygen with a regular face mask or CPAP mask set to maintain a pressure of 2.5 or 5 cm H₂O. Prospective, randomized clinical study. University teaching hospital. Sixteen client-owned dogs without evidence of cardiopulmonary disease were studied. Eight animals were randomly assigned to each of 2 treatment groups: group A received 2.5 cm H₂O CPAP and group B received 5 cm H₂O CPAP after first receiving oxygen (5 L/min) by a regular face mask. Animals were tranquilized with acepromazine 0.05 mg/kg, i.v. and morphine 0.2 mg/kg, i.m.. An arterial catheter was then placed to facilitate blood sampling for pHa, PaO₂, and PaCO₂ determinations before and after treatments. Direct mean arterial pressure, heart rate, respiratory rate, and temperature were also recorded after each treatment. CPAP administration was well tolerated by all animals. The mean arterial pressure, heart rate, respiratory rate, temperature, PaCO₂, and pHa, did not differ at any time point between groups. Differences were seen in oxygenation; in group A, PaO₂ significantly increased from a mean of 288.3 ± 47.5 mm Hg with a standard mask to a mean of 390.3 ± 65.5 mm Hg with the CPAP mask and in group B, PaO₂ increased similarly from 325.0 ± 70.5 to 425.2 ± 63.4 mm Hg (P<0.05); no differences were detected between the 2 CPAP treatments. In healthy tranquilized dogs noninvasive CPAP is well tolerated and increases PaO₂ above values obtained when using a regular face mask.

Multiple coil closure of isolated aortopulmonary collateral

A 7-month-old girl was diagnosed to have large aortopulmonary collateral during evaluation for congestive heart failure. There was no other evidence of cardiopulmonary disease. The collateral was successfully closed with multiple coils delivered sequentially. We describe the issues associated during closure of the aortopulmonary collateral in this case. To the best of our knowledge, this is the first reported case of large aortopulmonary collateral presenting with heart failure in an otherwise structurally normal heart that was closed successfully with multiple coils delivered sequentially.

Identification of Multiple Oxidative Post-Translational Modifications of Plasma Albumin in Patients with Pulmonary Hypertension of Sickle Cell Anemia

Background: Pulmonary hypertension (PH) in sickle cell anemia (SCA) is characterized by decreased nitric oxide bioavailability; which may, in part, be related to increased oxidative stress. It is possible that via protein post-translational modifications, oxidants are able to affect both protein structure and function. We hypothesized that, in patients with SCA and PH, oxidative post-translational modifications (PTMs) occur on plasma proteins and are important in disease pathogenesis. We previously reported the identification of one PTM, a malondialdehyde adduct on peptide 146–159 of albumin and sought to do a more extensive evaluation of this protein to determine the presence of other abnormalities.Methods: Plasma was obtained from subjects with:SCA and PH (n=5);SCA steady-state without PH (n=4);Pulmonary Arterial Hypertension (PAH) (n=4);no evidence of cardiopulmonary disease (n=4).Platelet-poor plasma was separated into albumin-enriched and albumin-depleted fractions. The albumin-enriched fraction was subjected to proteolytic digestion by trypsin and studied by matrix-assisted-laser desorption/ionization (MALDI) mass spectrometry (MS) and liquid chromatography (LC)-MS/MS tandem mass spectrometry. Proteomic analyses were performed on all samples and post-translational modifications characterized by MS/MS.Results: We have characterized several additional peptides of albumin from patients with PH of SCA that bear lipid peroxidation and glycation adducts. Our comprehensive LC-MS/MS results have allowed us to identify 4-hydroxynonenal (HNE), hexose (HEX) and malonyl adduction at numerous, distinct cysteine, histidine, lysine, and threonine albumin residues.Conclusion: Increased oxidant burden and altered redox biology is characteristic of PH in SCA. Plasma proteins, such as albumin, are a target for oxidants and changes in their structure may play a role in disease pathogenesis.

Identification of Oxidative Post-Translational Modifications on Plasma Albumin in Patients with Pulmonary Hypertension of Sickle Cell Anemia.

Pulmonary hypertension (PH) in sickle cell anemia (SCA) is characterized by decreased nitric oxide bioavailability; which may, in part, be related to increased oxidative stress. It is possible that via protein post-translational modifications, oxidants are able to affect both protein structure and function. We hypothesized that, in patients with SCA and PH, oxidative post-translational modifications occur on plasma proteins and are important in disease pathogenesis. To examine this hypothesis, we chose to determine if oxidative post-translational modifications occur in a large-abundance protein, albumin, as a reflection of the presence of more widespread protein oxidative damage. Plasma was obtained from subjects with:SCA and PH (n=5);SCA steady-state without PH (n=4);Pulmonary Arterial Hypertension (PAH) (n=4);no evidence of cardiopulmonary disease (n=4).Platelet-poor plasma was separated into albumin-enriched and albumin-depleted fractions. The albumin-enriched fraction was subjected to proteolytic digestion by trypsin and studied by matrix assisted laser desorption ionization (MALDI) mass spectroscopy (MS) and liquid chromatography (LC)-MS/MS tandem mass spectrometry. Proteomics analyses were performed on all samples and post-translational modifications characterized by MS/MS. Results were confirmed by Western and dot-blot analysis using commercially available antibodies. In the albumin fraction, we identified peaks of differential post-translational modification on albumin peptide 146–159 only in PAH and SCA and PH samples; this PTM was identified to be a malondialdehyde adduct. The presence of a malondialdehyde adduct on albumin was confirmed by LC-MS/MS and Western analysis. We have identified a malondialdehyde adduct in plasma albumin that appears to be a common link between PH related to SCA and PAH. This finding supports the notion that oxidative stress modulates the pathogenesis of PH of SCA and suggests that this and other post-translational modifications may be important biomarkers of disease.

Intravascular ultrasound imaging of the pulmonary arteries in primary pulmonary hypertension

Intravascular ultrasound has the unique ability to provide cross-sectional images of the arterial wall. This study examined intravascular ultrasound (IVUS) images of the proximal pulmonary arteries in primary pulmonary hypertension (PPH). Study 1: Specimens from four patients who had died of PPH (in vitro PPH group) were compared with those of three patients who had died of subarachnoid haemorrhage but had no evidence of cardiopulmonary disease (in vitro control group). Three-centimetre segments of the following levels were examined by IVUS: pulmonary trunk, eight secondary branch arteries of the upper, middle, and lower lobes of both lungs, and the thoracic descending aorta. Study 2: Four patients with PPH (in vivo PPH group) and five patients without pulmonary hypertension and no evidence of cardiopulmonary disease (in vivo control group) were examined. The IVUS images of the apical segmental artery of the right upper lobe and the descending branch of the right pulmonary artery were studied. Echographic examination of formalin-fixed preparations of secondary branch sections of the pulmonary artery failed to show a clear three-layer structure in the in vitro control group (24 preparations), but a distinct three-layer structure and increased vessel wall thickness were observed in the in vitro PPH group (32 preparations). Similar findings were obtained in the in vivo study. The mean echo density of the proximal pulmonary arterial wall correlated well with the mean pulmonary arterial pressure (mPA) in the in vitro PPH, and also correlated with the mPA in the in vivo study (r = 0.960, P < 0.0001). The echo intensity of secondary branch sections of the pulmonary artery was higher in the in vitro PPH group than in the in vitro control group (180.5 +/- 27.0 vs 132.5 +/- 26.7 counts, P < 0.001); similar results were obtained in the in vivo study (144.7 +/- 23.4 vs 85.0 +/- 14.3 counts, P < 0.01). These results suggest that the histological changes detected in the pulmonary artery walls in the PPH group were responsible for the increased echo intensity.

Clinical factors that affect blood gases in non-smoking women with chronic liver disease

Chronic liver disease is often accompanied by hypoxaemia. We investigated the clinical factors that were related to the arterial oxygen tension ( PaO 2) in 40 women, all non-smokers with chronic liver disease. They were positive for hepatitis C virus (HCV) antibody and had no evidence of cardiopulmonary disease. Arterial blood was collected from patients at rest (>15 min) for analysis of blood gases. We determined the correlation between blood gas tension and the clinical variables, i.e. the presence or absence of skin manifestations such as cutaneous spider nevi and palmar erythema, the presence or absence of splenomegaly, vital capacity, forced expiratory volume in one second, V̇ 25/body height, serum alanine aminotransferase (AST), serum asparate aminotransferase (ALT), serum cholinesterase, serum γ-globulin/total protein, excretion of indocyanine green at 15 min (15-min retention rate, ICG level), blood level of ammonia, blood level of endotoxin, plasma level of glucagon and the serum level of type IV collagen-7S. The mean level of PaO 2 was 78 ± 11 (range: 43–95) torr. The mean alveolar-arterial oxygen tension gradient ( A- aDO 2) was 19 ± 13 (range: 2–60) torr. Multiple regression analysis used PaO 2 and A- aDO 2 as objective variables, and the clinical findings as explanatory variables. The explanatory variables that were significantly correlated with blood gas values were ICG level, blood level of endotoxin and presence of skin manifestations. The ICG level showed a high correlation with blood gas values; the ICG level increased, the PaO 2 decreased ( r = − 0·69), while the A- aDO 2 showed a high positive correlation ( r = + 0·78, P < 0·001). Findings suggest that a reduction in hepatic blood flow and hepatocellular function interfere with the inactivation of vasoactive substances such as endotoxin by the liver, leading to the development of skin manifestations, the dilatation of intrapulmonary capillaries and the induction of hypoxaemia.

Heart rate to work rate relation throughout peak exercise in normal subjects as a guideline for rate-adaptive pacemaker programming

We investigated the physiologic heart rate (HR) to work rate (WR) relation throughout peak exercise in normal subjects as a guideline for rate-adaptive pacemaker slope programming. The study group consisted of 41 middle-aged subjects (22 men and 19 women) without evidence of cardiopulmonary disease. Peak-exercise stress tests were performed on a calibrated treadmill by usina the symptom-limited “ramping incremental treadmill exercise” (RITE) protocol. The HR response, oxygen uptake, and treadmill workload increments were assessed simultaneously. The HR/WR slope, as determined using linear regression analysis, was 0.37 ± 0.13 beats/min/W for the entire study group, which indicates an upper range increase of 5 beats/10 W increase of external treadmill work performed, using the mean value ±1 SD. Men generated an HR/WR slope of 0.32 ± 0.09 beats/min/W, and women, 0.43 ± 0.15 beats/min/W, indicating a significant sex-related difference in the HR/WR relation (p < 0.01). Thus, to achieve an appropriate matching or HR with patient effort, rate-adaptive pacemakers should generate an average increase of approximately 5 beats per increase in 10 W of external treadmill work. The HR/WR relation can easily be determined to provide the clinician with a minimal check system to avoid a hyper- or hypochronotropic paced response to exercise.

Automated determination of the right ventricular ejection fraction by digital processing of 81mKr scintigrams.

A method is presented for the automated determination of the right ventricular ejection fraction (RVEF) by digital image processing of scintigrams obtained by intravenous infusion of Krypton 81m (81mKr) dissolved in a glucose solution. End-diastolic and end-systolic sum pictures were computed by the addition of approximately 30-40 frames selected from the time-activity curve of a preliminary, manually drawn, right ventricular region of interest. After processing these two images with an adaptive Wiener filter, the right ventricular contour was determined by a recently developed algorithm using morphological and functional criteria. The RVEF was calculated for a series of 51 patients from the counts in the detected right ventricular regions in the end-diastolic and end-systolic sum images. In 16 patients without evidence of cardiopulmonary disease, the mean RVEF was 50 +/- 6.1%. RVEF was significantly reduced in 18 patients with obstructive pulmonary disease (42 +/- 6.5%) and in 17 patients with congestive cardiomyopathy (36 +/- 7.1%). The correlation coefficient between two determinations of the RVEF was r = 0.94. Through digital image processing, the determination of the RVEF by radioventriculography with 81m Kr showed high reliability and reproducibility.

The role of chest radiography in the evaluation of the 'geriatric giants'.

Three hundred and eighty admissions to a geriatric assessment unit had a routine chest radiograph. Forty-four per cent presented atypically with one or more of Isaacs' 'geriatric giants'--falls, immobility, incontinence or deteriorating mental function. The chest radiograph was abnormal in 164 (44%), of whom 57 had no classical clinical cardiopulmonary features. The chest radiograph was especially useful in the investigation of the geriatric giants, where 22% had evidence of cardiopulmonary disease, in the absence of classical clinical features.

Intracardiac Calcification in a Child

A and lateral chest roentgenograms (Fig 1 and 2) were obtained of this 3%-year-old white boy who had symptoms of a mild upper respiratory illness. He had dered significant birth hypoxia with resultant cerebral palsy, seizure disorder, and mental retardation. At birth, large cavernous hemangiomas covered most of his thorax. Congestive heart failure appeared during the neonatal period and was thought to be secondary to high output through the hemangiomas and a patent ductus arteriosus. During the first year of life, the patent ductus closed spontaneously and the hemangiomas resolved after radiation therapy. There had been no evidence of cardiopulmonary disease since the age of one. The physical examination on this admission was entirely normal from a cardiopulmonary standpoint. Blood count, routine chemistries and electrocardiogram were all within normal limits.

The effect of d-tubocurarine upon the static elastic recoil of the thorax

IN CHILDREN, the compliance of the lung is related to height and vital capacity 1,2,a as is the total compliance of the thorax. 4 If the volume history of the lung is standardized before measurement of compliance early in anaesthesia, there is evidence from adult subjects that values for static compliance differ little from those reported in normal conscious subjects. 5 It has been shown that in normal anaesthetized children, the compliance of the total thorax, lung, and chest wall are related to height and predicted vital capacity and furthermore, that lung compliance measured early in anaesthesia has a value similar to that reported for conscious children. 6,7 This relationship allows compliance to be compared under anaesthesia in normal children and young children with cardiorespiratory disease who are difficult to study in the conscious state. The anaesthetic technique involves the use of halothane, which has no effect upon lung compliance s and d-tubocurarine, which has on occasion caused broncho-constriction ~ which may be associated with a decrease in the lung compliance, a~ In dogs, d-tubocurarine has been found both to reduce lung compliance and to decrease collateral ventilation, n In man, although this relaxant does not produce significant changes in the compliance of the total thorax 12,13 the effects on the lung have not been differentiated from those on the chest wall. An effect upon the lung could be opposed by the effect of muscle relaxation upon the chest wall and abdomen. Since any effect of curare upon the elastic recoil of the lung must influence the results of comparative studies in young children, the static elastic recoil of the total thorax, lung, and chest wall was measured before and after the intravenous administration of this agent to 10 normal children. METHODS The subjects studied were 10 children aged 7-15 years, with no evidence of cardio-pulmonary disease, who were undergoing orthopaedic operations. Anaesthesia was induced with thiopentone, 5 mg/kg, with atropine, 0.02 rag/ kg. A cuffed endotracheal tube was passed under succinylcholine paralysis and an oesophageal balloon inserted to the lower oesophagus. When spontaneous