Arterial Unsaturation Research Articles

Enfermedades cardiovasculares en el Cuzco

Se estudiaron en el Cuzco 4 casos de cardiopatía: 3 congénitos y uno de cardiopatía reumática con estenosis mitral. En los dos casos de cardiopatía congénita, que tuvieron cateterismo cardíaco se comprobó ligera hipertensión pulmonar e insaturación arterial sistemática que se pensó correspondían a lo que ocurre en el hombre aclimatado a las grandes altitudes. Las dos mujeres operadas de persistencia del conducto arterial viven en el Cuzco, a los 10 años del tratamiento quirúrgico con capacidad funcional cardíaca normal. Una de ellas tiene el ductus calcificado. Se puede aseverar que en nuestros 3 casos de Cardiopatía congénita son shunts post-tricuspídeos, nacidos y resistentes en grandes altitudes, la hipertensión arterial pulmonar fue de grado ligero, sin carácter progresivo. El caso de cardiopatía reumática con estenosis mitral, que correspondió al Grupo 4 de Harken y con severa calcificación valvular, falleció a los 10 meses de la intervención en insuficiencia cardíaca irreductible.

Pulmonary–Hepatic vascular Disorders (PHD)

⇓“The tantalizing problem of the connective link in cirrhotic patients between oxygen unsaturation and possible arteriovenous shunting in the lungs remains unsolved, and any relation between arterial unsaturation and pulmonary vasodilation remains obscure.” Fig. 1.— Working model of molecular alterations in the pulmonary microcirculation in experimental hepatopulmonary syndrome (HPS). a) In the normal microvasculature, a balance of vasoconstrictive and vasodilatory factors, including paracrine endothelin (ET)-1-mediated vasoconstriction through the ETA receptor (▪) on smooth muscle cells (SMCs) and ET-1-mediated vasodilatation mediated through the ETB receptor (□) linked to endothelial nitric oxide synthase (eNOS) in endothelial cells (ECs), maintain tone. b) During the development of HPS, a number of alterations, both directly and indirectly related to hepatic injury and portal hypertension, result in the production or release of mediators into the venous circulation, where they influence the pulmonary microcirculation. Increased expression of pulmonary endothelial ETB receptors and increased hepatic production and release of ET-1 contribute to an increase in eNOS expression and enhanced nitric oxide (NO) production in the microvascular endothelium during the initiation of HPS. Tumour necrosis factor (TNF)-α-mediated accumulation of intravascular macrophage-like cells also occurs after chronic common bile duct ligation. Haem oxygenase (HO)-1 and inducible nitric oxide synthase (iNOS) expression increase in these cells and contribute to the progression of HPS. CO: carbon monoxide. Fig. 2.— Algorithm for screening and therapeutic decisions in hepatopulmonary syndrome (HPS). OLT: orthotopic liver transplantation; P a,O2: arterial oxygen tension; P A–a,O2: alveolar–arterial oxygen tension difference; CEE: contrast-enhanced echocardiography; PFT: pulmonary function test; MAA: macroaggregated albumin. #: high-resolution thoracic computed tomographic scanning is highly recommended in order to exclude chronic respiratory comorbid conditions; ¶: high risk for post-operative OLT mortality. 1 mmHg=0.133 kPa. Fig. 3.— Plot demonstrating the relationship between cardiac output ( Q ') and transpulmonary pressure gradient (TPG; mean pulmonary arterial …

Effect of body position changes on pulmonary gas exchange in Eisenmenger's syndrome.

Preliminary studies on sleep of patients with congenital heart disease and Eisenmenger's syndrome (ES) at our institution demonstrated nocturnal worsening arterial unsaturation, which appeared to be a body position-related phenomenon. To investigate the potential effect of body position on gas exchange in ES, we carried out a prospective study of 28 patients (mean age, 34.8 +/- 11.7 yr) with established ES due to congenital heart disease. In every patient, arterial blood gases were performed during both sitting and supine positions under three different conditions: room air, while breathing 100% oxygen, and after breathing oxygen at a flow rate of 3 L/min through nasal prongs. Alveolar oxygen pressure (PaO2) for the calculation of alveolar-arterial oxygen tension differences (AaPO2) was derived from the alveolar gas equation using PaCO2 and assuming R = 1. We used paired t test, repeated-measures two-way ANOVA with Bonferroni's test, and regression analysis. From sitting to supine position on room air, there was a significant decrease in PaO2 (from 52.5 +/- 7.5 to 47.5 +/- 5.5 mm Hg; p < 0. 001) and SaO2 (from 86.7 +/- 4.6 to 83.3 +/- 4.9%; p < 0.001), both of which were corrected by nasal O2 (to 68.2 +/- 21 mm Hg and to 92 +/- 4%, respectively, p < 0.005). PaCO2 and pH remained unchanged. The magnitude of the change in PaO2 correlated with the change in AaPO2 on room air (r = 0.77; p < 0.01) but not with the change in AaPO2 on 100% oxygen. It is concluded that in adult patients with ES there is a significant decrease in PaO2 and SaO2 when they change from the sitting to the supine position. A ventilation-perfusion (V/Q) distribution abnormality and/or a diffusion limitation phenomenon rather than an increase in true shunt may be the mechanisms responsible for this finding. The response to nasal O 2 we observed warrants a trial with long-term nocturnal oxygen therapy in these patients.

High altitude pulmonary edema: hemodynamic aspects.

Over 30 years ago hemodynamic studies on patients with high altitude pulmonary edema (HAPE) excluded the prior contention that the basic cause was left ventricular failure and correctly implicated the pulmonary circulation as the culprit. Physiological studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (pre-capillary) resistance was elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury with leakage of protein and red cells into the alveoli. While hypoxic vasoconstriction appears to be the major cause of patchy vascular obstruction the occurrence of thrombi in the pulmonary vessels may also play a role in more severe and advanced cases. The above concept of the mechanism of HAPE has been further supported by animal studies showing pulmonary edema occurring when increased pressure and flow is produced in a portion of the pulmonary vascular bed. Clinical studies which have supported this concept include the susceptibility to HAPE of patients with an absent pulmonary artery, pulmonary edema occurring in pulmonary embolism, following removal of pulmonary arterial thrombi and following balloon dilatation of stenoses of branches of the pulmonary artery. In addition to those hemodynamic factors an increase in capillary permeability due to cell derived products resulting from capillary wall injury is an important aspect of edema formation.

High-altitude pulmonary edema: current concepts.

High-altitude pulmonary edema (HAPE) occurs in unacclimatized individuals who are rapidly exposed to altitudes in excess of 2450 m. It is commonly seen in climbers and skiers who ascend to high altitude without previous acclimatization. Initial symptoms of dyspnea, cough, weakness, and chest tightness appear, usually within 1-3 days after arrival. Common physical signs are tachypnea, tachycardia, rales, and cyanosis. Descent to a lower altitude, nifedipine, and oxygen administration result in rapid clinical improvement. Physiologic studies during the acute stage have revealed a normal pulmonary artery wedge pressure, marked elevation of pulmonary artery pressure, severe arterial unsaturation, and usually a low cardiac output. Pulmonary arteriolar (precapillary) resistance is elevated. A working hypothesis of the etiology of HAPE suggests that hypoxic pulmonary vasoconstriction is extensive but not uniform. The result is overperfusion of the remaining patent vessels with transmission of the high pulmonary artery pressure to capillaries. Dilatation of the capillaries and high flow results in capillary injury, with leakage of protein and red cells into the alveoli and airways. HAPE represents one of the few varieties of pulmonary edema where left ventricular filling pressure is normal.

Contribution of the Haldane effect to the rise of arterial Pco2 in hypoxic patients breathing oxygen

Arterial (PaCO2), alveolar (PACO2), mixed expired (PECO2) CO2 pressures, CO2 production (VCO2) as well as arterial O2 saturation (SaO2) were measured on 20 severely hypoxic and hypercapnic patients breathing air (A) and 100% O2 (HO). On HO, mean PaCO2 increased to 56.6 torr from 50.8 torr on A, whereas there was no significant change in PACO2 (38.3 on A, 38.6 on HO), so that the arterial-alveolar gradient (aADCO2) increased from 12.5 to 18.0 torr. PECO2 remained essentially the same. There was a statistically significant correlation between the increase in PaCO2 on HO and the arterial unsaturation (100 - SaO2) on A and also between PaCO2 on A and its increment on HO. When the rise in PaCO2 and aADCO2 were estimated which resulted from the shift in the Co2 dissociation curve due to complete oxygenation of hemoglobin on HO (Haldane effect), 78% of the observed change in PaCO2 could be accounted for. The deadspace/tidal volume ratio (VD/VT) increased from 0.59 on A to 0.64 and 87% of this difference could be attributed to the Haldane effect. The results emphasize the importance of considering this effect when interpreting alterations in PaCO2, aADCO2 and VD/VT on transition from air to hyperoxia, particularly in patients with severe hypoxemia and hypercapnia.

Pulmonary Hypertension in Sepsis: Measurement by the Pulmonary Arterial Diastolic-Pulmonary Wedge Pressure Gradient and the Influence of Passive and Active Factors

To examine the relative roles of passive factors (flow; filling pressures of left side of heart) and active factors (acidosis; arterial unsaturation) in the genesis of pulmonary hypertension when associated with sepsis, 37 patients with sepsis and 24 patients without sepsis were examined. Pulmonary hypertension was measured by the pulmonary arterial diastolic-pulmonary wedge pressure gradient (PAd-PWP gradient) and correlated reasonably with a standard formula for calculated resistance ([PA--PWP]/CI, where PA is mean pulmonary artery pressure and CI is cardiac index). In 22 of 37 patients, sepsis was associated with a significant degree of resistance to flow in the pulmonary circulation, as measured by the PAd-PWP gradient: and the higher the PAd--PWP gradient, the greater the likelihood of early death. None of the examined passive or active factors appeared to be adequate to explain pulmonary hypertension when present. By the use of previously derived formulae to estimate the compliance of the elastic pulmonary arteries, factors affecting this part of the pulmonary microcirculation could not be held accountable for apparent pulmonary hypertension. Therefore, the presence of pulmonary hypertension in sepis appears to be an active, rather than a passive, phenomenon and unrelated to arterial oxygen saturation or acid-base imbalance. Although the exact cause is unknown, pulmonary hypertension in sepis is associated with a high mortality and may be clinically followed by measurement of the PAd-PWP gradient.

Mixed venous and arterial Pco2.

The rebreathing method of measuring oxygenated mixed venous Pco(2) (Pvco(2)) was originally introduced as a bloodless way to estimate arterial Pco(2) (Paco(2)). It has become common practice to subtract 6 mm Hg from the Pvco(2) to obtain the Paco(2) but there are many circumstances in which this leads to an overestimate of the Paco(2). Measurements of Pvco(2) and Paco(2) in 19 patients have shown that a better approximation to Paco(2) under normal conditions of cardiac output and arterial O(2) saturation is Paco(2) = 0.8 Pvco(2). These studies also showed that the Pvco(2) - Paco(2) difference may be much wider, particularly in the presence of arterial unsaturation and a low cardiac output.The factors governing the venoarterial Pco(2) difference are reviewed and their magnitude is calculated to emphasize the complementary roles of measurements of Pvco(2) and Paco(2) in the assessment of patients with cardiorespiratory disease.

Use of continuous positive airway pressure breathing in the improved management of neonatal emergencies

A ventilatory system consisting of spontaneous breathing with continuous positive airway pressure has dramatically decreased mortality in newborn infants with hyaline membrane disease. 1 In the past 2 yr, we have applied this new technique in the management of noncardiac thoracic and abdominal emergencies in more than 25 small infants, most of whom were newborn. The purpose of this paper is to describe the use of continuous positive airway pressure breathing (CPAPB) in this group of babies with life-threatening conditions, which included intestinal atresia, meconium peritonitis, fecal peritonitis, gastroschisis, omphalocele, tracheoesophageal fistula, and diaphragmatic hernia (Table 1). As an adjunctive measure in the management of respiratory insufficiency associated with these conditions, we believe this new system has contributed importantly to the survival of these infants. A common denominator in this group of varied newborn emergencies was pulmonary dysfunction which was usually manifested by peripheral arterial unsaturation associated with right to left pulmonary shunting. The pulmonary abnormality was often a concomitant complication of severe metabolic acidosis, sometimes in the presence of gram-negative septicemia. Since these congenital anomalies all required urgent operative procedures, the above physiologic derangements were further distorted by anesthesia and the surgical trauma. In the past, pulmonary insufficiency, combined with severe sepsis and metabolic acidosis, was frequently lethal; but the postoperative courses in this group of infants have demonstrated improved respiratory function with the use of CPAPB. Selected cases have been chosen from this series to illistrate this experience.

Cyanosis: Pathophysiology and differential diagnosis

HE WORD CYANOSIS is derived from the Greek and in its strictest sense means dark blue. The general and basic concepts leading to our understanding of cyanosis were delineated many years ago. 1-3'57 Cyanosis to the clinician means a bluish color of the skin or mucous membranes. It is usually, but not always, general in distribution and most obvious on the lips, cheeks, nose, ears, mucous membranes, and nailbeds. This bluish discoloration is produced by the color of the blood within the capillaries of the dermal papillae, mucous membranes, and in the subpapillary venous plexus of the dermis. It is most frequently the result of cardiovascular or pulmonary defects and depends on the absolute amount of reduced hemoglobin present in the blood. Less commonly cyanosis is due to abnormal pigments within the red blood cell such as methemoglobin and sulfhemoglobin and more rarely is the result of abnormal pigments or other substances within the plasma. It was determined many years ago that the presence of about 5 g of reduced hemoglobin within the capillary blood is required before cyanosis can be detected. 1,z This also may be stated to represent an oxygen unsaturation of 6.7 cc/100 cc of blood inasmuch as 1 g of hemoglobin can combine with 1.34 cc of oxygen. Thus, as frequently pointed out in the past with profound anemia, cyanosis may not be apparent (because of an insufficient amount of reduced hemoglobin) even though marked degrees of arterial unsaturation exist. Conversely, if a patient is polycythemic, cyanosis may be readily apparent due to the increased amount of reduced hemoglobin, although the degree of arterial unsaturation may be minimal. Factors that may modify the visual awareness of cyanosis were pointed out by Lundsgaard and VanSlyke and are related to the thickness of the epidermis which can mask the color of the blood within the underlying capillary bed. ~ The amount and type of pigment within the skin, such as normally found in different ethnic groups or pigment present in abnormal conditions such as jaundice or Addison's disease, also may obscure the color of the underlying capillary and venous blood. The extent of the capillaries and venules and the presence of dilatation or constriction of these vessels also will affect the transmission of the color of the blood to the surface of the skin. It should be remembered that eyanosis is only a reflection of the amount of reduced hemoglobin within the underlying capillaries and venules and is not necessarily a reflection of the presence of reduced hemoglobin or the degree of oxygenation of the blood within the arterial system. Thus cyanosis, while frequently indicating arterial unsaturation, by no means

Adjustment of Ventilation in the Newborn

In adapting to extrauterine life, ventilation and perfusion must soon become well-matched. the time course of this process can be assessed by measurement of the urinary-alveolar nitrogen gradient (uADN2). An elevated uADN2 is an indication of the maldistribution of VA/Q, specifically the presence of areas of low VA/Q. Seventeen healthy full-term neonates were studied serially from the first day of life. Values of uADN2 within the range for normal adults were found (less than 10mm Hg). Serial studies on 3 infants with evidence of aspiration pneumonia revealed uADN2 consistently elevated above the normal. Children and adults with obstructive pulmonary disease were tested as a validation of the method and the expected elevation of uADN2 was found. Thw studies indicate that (1) ventilation is uniformly distribution in the first days of life in normal infants; (2) maldistribution of ventilation is an important cause of arterial unsaturation in aspiration pneumonia. These results will be considered in the context of other studies of extrauterine pulmonary adaptation.

Lungs in progressive systemic sclerosis

Impairment of pulmonary function in scleroderma is commoner than would be expected on clinical or radiological grounds alone. There is a poor correlation between the severity of functional derangement and the extent of pulmonary lesion detectable by clinical or radiological means. Reduced vital capacity and maximum mid-expiratory flow rate, however, are the most frequent abnormalities and would appear to be the earliest defects commonly occurring in the course of this disease. Characteristic changes in the mechanics of the lung are reduced pulmonary compliance and increased expiratory resistance. The occurrence of generalized airways obstruction of clinical significance is infrequent. The pulmonary diffusing capacity was decreased in about half of the cases in our series. Mild arterial unsaturation exists and frequently there is a tendency to alveolar hyperventilation.

Ventilation-perfusion abnormalities in the premature infant: triple gradient.

Extract: Serial studies of arterial and alveolar oxygen, carbon dioxide, and nitrogen tensions, arterial pH, and ratios of dead space: tidal volume were made in 24 nondistressed premature infants. By determining arterial-alveolar gradients, the sequence of development of ventilation/perfusion relations in the non-distressed premature infant can be determined. The presence of an arterial-alveolar carbon dioxide gradient and elevated VD/VT ratio indicate the presence of overventilated/underperfused areas. Alveolar-arterial oxygen gradients may be due to shunting, underventilation (low ventilation/perfusion ratio), or diffusion block. Although underventilation exists, as evidenced by the presence of a urinary-alveolar gradient for N2, it is not a major cause of arterial unsaturation. This evidence suggests that shunting of blood, either through intracardiac shunts or atelectatic lung, is a major cause of arterial unsaturation in the premature infant. Speculation: Further extension of this work should make possible the construction of VA/Q curves for the individual patient and thus show in even greater detail the maturation of pulmonary ventilation and perfusion.

Atrial myxoma, a continuing diagnostic challenge

Despite increased awareness of atrial myxoma, the lesion remains a diagnostic challenge, largelydue to a highly variable clinical picture. Some unusual manifestations of atrial myxoma are illustrated by 6 cases. The relatively slow growth of left atrial myxoma was demonstrated in a 15 year old boy thought to have mitral insufficiency from birth and by a 10 year period of observation in a 63 year old woman. The woman also had co-existent mitral stenosis. Coexistent congenital heart disease was found in a 73 year old man thought to have severe lung disease with arterial unsaturation. Cardiac catheterization showed a right to left shunt through an atrial septal defect due to a right atrial myxoma obstructing the tricuspid valve. Angiocardiography demonstrated the above lesions, as well as left atrial myxomas in 2 patients with clinical findings of mitral valve disease. A fatal complication occurred during transseptal catheterization in a woman believed clinically to have mitral stenosis. Occlusion of the mitral valve by a left atrial myxoma occurred when the catheter entered the left atrium above the tumor. The importance of angiography in the diagnosis of atrial myxoma is stressed, and the avoidance of transseptal catheterization in suspected cases is emphasized.

Angiographic and catheterization findings in patients with difficulties after total correction of tetralogy of Fallot.

Tetralogy of fallot is an anatomically complex intracardiac defect resulting in right-to-left or bidirectional shunts at the ventricular level and decreased pulmonary blood flow. The peripheral arterial unsaturation varies with the size of the interventricular defect and its anatomic relationship to the enlarged aortic root, as well as with the severity of the right ventricular outflow obstruction. The muscular hypertrophy of the right ventricle may be pronounced. Total repair of the anomaly achieves physiologic correction by separation of the intracardiac streams and by relief of the pulmonic stenosis. The repair may or may not result in perfect anatomic or entirely normal intracardiac pressure relationships. Of 124 patients operated upon, there were 102 long-term survivors in this series. Twelve of these were restudied by cardiac catheterization and angiocardiography performed from two months to ten years after total correction of the defects. The most common indication for re-examination was the presence of a loud systolic murmur over the pulmonary area suggesting significant residual pulmonary stenosis. Other indications were a loud diastolic murmur or parasternal systolic murmur, cardiac enlargement and failure, a bulge along the left upper cardiac border on the chest roentgenogram suggestive of right ventricular outflow tract aneurysm, and electrocardiographic evidence of increasing right ventricular hypertrophy. Table I summarizes the catheterization and angiographic findings in these patients as well as their subsequent course. Three have had repeat operations with good results. Examples of the lesions found in seven patients are described in the following brief case reports and illustrated in the accompanying figures. Case Reports Case I (N. R): The diagnosis of tetralogy of Fallot was established in this boy at three years of age. Preoperatively a bidirectional shunt was found at the ventricular level. No atrial septal defect was diagnosed. The right ventricular systolic pressure was 88 mm Hg, and there was a 76 mm Hg gradient across the pulmonary valve. One of the views from the lateral angiocardiogram is shown in Figure 1, A. At operation, a moderate amount of infundibular stenosis was encountered and resection was done. The stenosed pulmonary valve was opened by incising two of the commissures, and the ventricular septal defect was closed with a Teflon patch. After surgery, digitalization was necessary because of congestive heart failure, and systolic and diastolic murmurs persisted over the pulmonic area. The electrocardiogram revealed complete right bundle branch block. The child was recatheterized at five years of age because of the persistent murmurs and cardiac failure. At this time the systolic right ventricular pressure was 110 mm Hg in the inflow tract.

VENTILATION AND RESPIRATORY GAS TRANSFER OF INFANTS WITH INCREASED PULMONARY BLOOD FLOW

Ventilation and respiratory gas transfer was studied in 44 infants; 13 of whom had pulmonary overperfusion without pulmonary edema or transposed great arteries. In order to assess the evenness of ventilation/perfusion ratios throughout the lung, (VA/Q distribution) measurements were made of the urine-alveolar nitrogen tension difference (U-Ā)DN2 in a separate group of six normal children and seven children with pulmonary overperfusion. Infants with pulmonary overperfusion (left-to-right shunts) had normal alveolar ventilation (149.6±18.2 ml/minute/kg). Respiratory rate (38.1±10.2) was slightly increased and tidal volume (6.0±1.3 ml/kg) was diminished, possibly due to reduced lung compliance. Measurements of dead space, dead space/tidal volume ratio, and alveolar ventilation/oxygen consumption ratio were unremarkable. No significant arterial-alveolar CO2 difference was detected in either normal subjects or those with heart disease, but a significantly increased alveolar-arterial O2 tension difference (A-a)DO2 of 22.4±8.6 mm Hg was found in infants with overperfused lungs. Measurements of (A-a)DO2 during 100% oxygen breathing and measurements of (U-Ā)DN2 in the air-breathing subjects both suggested that intrapulmonary venous admixture rather than VA/Q unevenness was the principal factor causing lowered oxygen tensions in the arterial blood of infants with overperfused lungs. Lowered arterial oxygen tension was associated with only trivial arterial unsaturation (92.8±2.4%) due to the high affinity of hemoglobin for oxygen.

Diagnosis and Surgical Treatment of Infants with Critical Pulmonary Outflow Obstruction

The records of 15 infants with pulmonary atresia and 19 infants with critical pulmonic stenosis and intact ventricular septum, all under 1 year of age, have been reviewed. Symptoms started earlier and were more severe in the group with pulmonary atresia. All patients showed arterial unsaturation, and many had congestive heart failure The electrocardiogram was the most helpful tool in differentiating pulmonary atresia from pulmonic stenosis with intact ventricular septum. The presence of P pulmonale, significant right axis deviation, and right ventricular hypertrophy favors pulmonic stenosis. At cardiac catheterization, patients belonging to both groups showed right ventricular hypertension of significant degree, but this was more marked in infants with pulmonic stenosis. Results of surgery for pulmonary atresia with intact ventricular septum, by a variety of methods, have been uniformly poor up to the present. Direct attack on the pulmonary outflow tract, when possible, may offer more promise for the future. Pulmonary valvotomy is the operation of choice for pulmonic stenosis and the results are good.

Pulmonary diffusing capacity and capillary blood flow during forward acceleration

We studied possible causes of the decreased arterial oxygen saturation seen when a subject is accelerated in a centrifuge by measuring simultaneously the pulmonary diffusing capacity, DlCO, and the effective pulmonary capillary blood flow, Qc, using breath-holding techniques with carbon monoxide and acetylene. After 1 min of forward ("eyeballs in") acceleration at eight times normal gravity, 8 G, average Dl decreased 35% from an initial control of 33.7 to 21.5 ml/(min x mm Hg) in four subjects. Although this decrease was statistically significant, the values observed were not low enough to indicate that impaired diffusion was a prime cause of arterial unsaturation. Average Qc decreased 35% during acceleration from an initial control value of 12.9 to 8.2 liters/min, also a significant change. These values may have indicated that total pulmonary blood flow was reduced, but a more likely explanation is that a large portion of pulmonary flow perfused nonventilated regions. Dl and Qc returned toward initial control levels within 8 min after acceleration in most instances. lung volume during acceleration Submitted on March 1, 1965

RELATIVE HYPERMETABOLISM IN INFANTS WITH CONGENITAL HEART DISEASE AND UNDERNUTRITION

1. Twenty-one infants with various forms of congenital heart disease leading to congestive heart failure, arterial unsaturation, or a combination of both events were studied with respect to resting oxygen consumption. Comparison was made with 21 control infants considered to be of normal growth and to have normal cardiac and respiratory systems. 2. Mean oxygen consumption for infants with heart disease was 9.3±2.4 ml/min/ kg compared to 7.3±0.8 ml/mm/kg for controls. Markedly undergrown infants with heart disease (60% or less of the 50th percentile weight for age) had a mean oxygen consumption of 10.9±1.4 ml/mm/kg compared to a mean of 7.5±2.0 ml/min/kg for infants with heart disease who were greater than 60% of the 50th percentile weight for age. Relative hypermetabolism seemed to relate to the degree of undernutrition rather than to any specific clinical finding. 3. Possible mechanisms of undernutrition and of relative hypermetabolism in the infant with heart disease are discussed.

Oxyhemoglobin dissociation curve in liver disease

The in vivo oxyhemoglobin dissociation curves of patients with liver disease appear to be displaced to the right of those of normal men. Although the displacement is small it may contribute to the arterial unsaturation which sometimes occurs. hemoglobin; oxygen electrode; unsaturation Submitted on March 9, 1964