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At least 91 records · Page 5Linked to original sources
PubMed1985

Pathophysiology of chronic cyanosis in a canine model. Functional and metabolic response to global ischemia.

To investigate the pathophysiology of chronic cyanosis, we subjected 14 adult mongrel dogs to diversion of the inferior vena cava to the right inferior pulmonary vein. This produced a mean oxygen tension of 42 +/- 2 mm Hg and a calculated right-to-left shunt of 52.0% +/- 3.9%. These animals (Group C) and 15 normal dogs (Group N) were subjected to cardiopulmonary bypass with 20 minutes of normothermic global ischemia. Functional indices studied were rate of rise of left ventricular pressure and the end-systolic pressure/volume ratio. Metabolic status was assessed by obtaining transmural myocardial biopsy specimens for measurement of adenosine triphosphate content. Myocardial blood flow was measured with radiolabeled microspheres. There were no significant differences between Group C and Group N in either functional index or blood flow measurement prior to global ischemia. At 45 minutes after ischemia, Group N animals had a significantly greater rate of rise of left ventricular pressure (at a left ventricular end-diastolic pressure of 0, 5, 10, and 15 mm Hg, p less than 0.025 to 0.05) and subendocarial perfusion (endocardial/epicardial flow ratio 0.961 +/- 0.037 versus 0.815 +/- 0.021, p less than 0.01). At 90 minutes after ischemia, Group N animals exhibited a significantly higher end-systolic pressure/volume ratio (4.9 +/- 0.7 versus 3.0 +/- 0.4 mm Hg/ml, p less than 0.05), rate of rise of left ventricular pressure (at an end-diastolic pressure of 0 to 20 mm Hg, p less than 0.005 to 0.05), and endocardial/epicardial flow ratio (1.065 +/- 0.046 versus 0.829 +/- 0.059, p less than 0.01). No differences in adenosine triphosphate content were found at any sampling period. The Group C left ventricles exhibited no hypertrophy but were significantly dilated compared to Group N (38.8 +/- 0.3 versus 30.1 +/- 0.2 mm, p less than 0.05). Inferior vena cava to pulmonary vein diversion produces cyanosis with left ventricular dilatation but without hypertrophy. It is proposed that abnormal loading characteristics of the left ventricle are responsible for the functional derangements that result from global ischemia.

Adenosine Triphosphate↗
PubMed1978

Cyanosis in a patient with combined ostium primum and secundum atial septal defects and anomalous inferior vena cava with azygos continuation. Case report and surgical considerations.

A case is described of combined ostium primum and ostium secundum atrial septal defects and azygos connection of the inferior vena cava plus cyanosis. Emphasis is made to recognize the functional mechanism of cyanosis and to demonstrate the anatomic site of hepatic venous drainage so that an appropriate corrective operative procedure can be planned. A gratifying result was achieved in this case after closure of the atrial septal defects.

Adult↗
PubMed1983

[Hypoplasia of the right ventricle and cyanosis due to left-right atrial shunt within the framework of Turner's syndrome. Surgical closing of the interatrial connection after occlusion testing with balloon catheterization].

The authors describe the unusual cardiac malformation in a young girl with Turner's syndrome: right ventricular hypoplasia and atrial septal defect, resulting in central cyanosis. A trial of temporary occlusion of the atrial septal defect at cardiac catheterisation before surgical closure suppressed the right-to-left shunt and the cyanosis without significantly changing the hemodynamic parameters. The authors review the types of cardiovascular abnormalities associated with Turner's syndrome and emphasize the value of a temporary occlusion test of defects in certain cyanotic cardiac malformations with atrial right-to-left shunts; it may lead to a relatively simple surgical procedure, as in the case described.

Adult↗
PubMed1981

Left ventricular dynamic geometry and diastolic mechanics in a model of chronic cyanosis and right ventricular pressure overload.

Left ventricular (LV) mechanics and dynamic geometry were studied in eight dogs 1 to 151 days after creation of a model of cyanosis and increased right ventricular (RV) pressure. In each dog, an 8 mm conduit was interposed between the main pulmonary artery and left atrium; the pulmonary artery was then banded distal to this shunt. Ultrasonic dimension transducers were subsequently implanted for the measurement of LV equatorial minor axis and wall thickness. Catheter-tipped micromanometers were used to measure LV and pleural pressures; RV pressure was measured with a fluid-filled catheter and an external transducer. Eight control animals were similarly instrumented. At the time of study, the cyanotic dogs had significantly decreased arterial oxygen saturations (66% +/- 7% versus controls: 96% +/- 5%), significantly elevated peak RV pressures, (55 +/- 7 mm Hg versus controls: 30 +/- 5 mm Hg) and significantly elevated ratios of RV to LV mass (0.52 +/- 0.05 versus controls: 0.36 +/- 0.05). Diastolic pressure-dimension curves were generated and time constant for LV relaxation were calculated for each animal. The diastolic curves obtained from the cyanotic dogs were not significantly different from those of the control animals, and LV relaxation was not prolonged in the cyanotic dogs. In the three dogs that were cyanotic for 4 months or longer, there was a profound abnormality in the geometric pattern of LV contraction, manifested by asynchronous shortening of the anteroposterior equatorial minor axis. In two of these three dogs, inotropic reserves were assessed by means of postextrasystolic potentiation and were found to be normal. The results of this study indicate that short-term mild cyanosis and RV pressure overload do not alter diastolic compliance nor prolong relaxation of the LV. LV dynamic geometry may become abnormal after 4 months, with preservation of global LV inotropic reserves.

Animals↗
PubMed1993

An unusual cause for cyanosis.

Cyanosis is a common physical sign in clinical medicine. Cardiac or respiratory conditions are the usual causes. We report a patient with an unusual cause for cyanosis and highlight the salient clues that lead to the diagnosis.

Adult↗
PubMed1985

Cyanosis after surgical correction of pulmonary valve stenosis: an old problem revisited.

The presence of cyanosis following repair of congenital cardiac defects may result from several different mechanisms. We report two patients in whom early postoperative arterial hypoxemia manifested by cyanosis was caused by right-to-left interatrial shunting. Two-dimensional contrast echocardiography correctly identified the site and direction of shunting, leading to surgical correction of the complication.

Journal Article↗
PubMed1963

HYPOVENTILATION, CYANOSIS AND POLYCYTHEMIA IN A THIN MAN.

A lack of respiratory centrogenic drive of undetermined origin is a rare cause of cyanosis. In this condition, voluntary hyperventilation restores arterial oxygen saturation to normal. Secondary changes consist of polycythemia, somnolence, headache and right heart failure. The present report of a 43-year-old thin man with idiopathic alveolar hypoventilation is combined with a review of 12 similar patients reported by others. His resting oxygen saturation increased from 60% to 98% with hyperventilation. The pulmonary artery pressure was 68/26 mm. Hg and cardiac output 12.3 l./min. Death resulted from pulmonary infarction, and no specific abnormalities were found in the brain.

Cyanosis↗
PubMed2004

Stent implantation in right-sided patent ductus arteriosus to relieve severe cyanosis in adult patient with pulmonary atresia and ventricular septal defect.

Patients with unrepaired pulmonary atresia and ventricular septal defect may develop stenosis of collaterals or shunts to the pulmonary arteries leading to hypoperfusion of lungs and systemic hypoxemia. A 25-year-old female with pulmonary atresia and ventricular septal defect presented with progressively increasing cyanosis and exercise intolerance. A restrictive right-sided patent ductus arteriosus was identified as the main source of pulmonary blood flow. We report transcatheter implantation of a balloon-expandable stent across the stenosed duct to augment the pulmonary blood flow as a palliative management option. Patient had immediate improvement in arterial oxygen saturation from 66% to 85% with excellent clinical improvement and stable oxygen saturation on 8 months of follow-up.

Adult↗
PubMed2001

Transcatheter closure of large persistent left superior vena cava causing cyanosis in two patients post-Fontan operation utilizing the Gianturco Grifka vascular occlusion device.

We report the successful transcatheter closure of a large persistent left superior vena cava draining into the pulmonary venous circulation causing cyanosis in two patients who had previously undergone the Fontan operation utilizing the Gianturco Grifka vascular occlusion device. Cathet Cardiovasc Intervent 2001;53:398-404.

Adolescent↗
PubMed2001

Endovascular stent implantation in a coronary artery to pulmonary artery fistula in a patient with pulmonary atresia with ventricular septal defect and severe cyanosis.

A 31-year-old male with pulmonary atresia, ventricular septal defect presented with exercise intolerance and severe cyanosis. A restrictive coronary-pulmonary artery fistula was identified as the main source of pulmonary blood flow. We report transcatheter stent implantation in the fistula to augment pulmonary flow as a palliative management option in the adult patient with complex congenital heart disease.

Adult↗
PubMed2006

Endovascular stents for relief of cyanosis in single-ventricle patients with shunt or conduit-dependent pulmonary blood flow.

UNLABELLED: Hypoxemia is a significant cause of early and interstage death in patients with single ventricle (SV). Obstruction of Blalock-Taussig shunts (BTS) in patients with SV has traditionally been managed with surgical revision. PURPOSE: We report on the experience at our institution of deploying endovascular stents within BTS as well as obstructed right-ventricle (RV) to pulmonary artery (PA) conduits in patients with modified Norwood (ie Sano modification). METHODS: Medical records were reviewed for the time period between January 1, 2002 and November 30, 2005. All patients with SV who presented for intervention for BTS or RV-PA conduit stenosis were reviewed. Specific endpoints reviewed included pre- and post-intervention arterial oxygen saturation, type of intervention (stent vs. ballon dilation), need for subsequent surgical shunt/conduit revision, and interval to second stage palliation. RESULTS: Fifteen patients with SV underwent intervention for acute cyanosis. Eight patients had BTS, and the other seven patients had RV-PA conduit stenosis. Coronary stents were deployed in 14 of the 15 patients. Four patients also underwent balloon angioplasty of branch PAs. Oxygen saturations improved in all patients, with a mean increase of 13.9% (p = 0.0001). Four patients died before second stage palliation--one due to complications of the catheterization. Of the eleven remaining patients, nine have undergone second stage palliation; interval from intervention to Glenn ranged from 28-205 days (mean 163d). Two patients are awaiting cavo-pulmonary anastamosis. CONCLUSIONS: Endovascular stenting in this high-risk population is effective at improving oxygen saturation as well as obviating need to surgical shunt/conduit revision.

Angioplasty, Balloon, Coronary↗
PubMed1982

Selective cyanosis of the right arm. Isolation of right subclavian artery from aorta with bilateral ductus arteriosus and pulmonary hypertension.

A sixteen-month-old child presented with cyanosis of the right arm. Investigation revealed bilateral persistent ductus arteriosus with isolation of the right subclavian artery from the aorta. Pulmonary vascular resistance and pulmonary arterial pressure were elevated so that the right subclavian artery received desaturated blood from the right pulmonary artery via the persistent right ductus arteriosus.

Arm↗
PubMed2003

Micropulmonary arteriovenous fistula causing cyanosis.

This article presents a young girl who came to the Department of Pediatrics, AIIMS, with cyanosis and was diagnosed to be having multiple pulmonary arteriovenous fistulae. The cardiovascular evaluation was normal and so was the respiratory evaluation. The desaturation did not improve with oxygen. The chest X-ray was also normal. The echocardiogram did not reveal any abnormality but agitated saline contrast echocardiography suggested an extracardiac right to left shunt which was confirmed on pulmonary angiography.

Angiography↗
PubMedDate not supplied

Enlarged left vitelline vein remnant as a cause of cyanosis after the Fontan procedure: resolution with an Amplatzer vascular plug.

A 6-year-old girl with heterotaxy and a functional single ventricle had persistent cyanosis 4 years after a fenestrated Fontan procedure. Cardiac catheterization revealed a large venous fistula from a left-sided hepatic vein to the coronary sinus, resulting in desaturation. The anomalous vein was occluded with an Amplatzer vascular plug.

Child↗