The adaptive reactions of the cardiorespiratory system in chronic bronchitis and its premorbid forms

AIM: Investigation of pulmonary ventilation, blood flow and cardiodynamics in subjects at risk of chronic nonspecific pulmonary disease (CNPD), prebronchitis (PB) and chronic bronchitis (CB). MATERIALS AND METHODS: 118 workers exposed to toxico-chemical factors underwent zonal rheography. RESULTS: At early stages of CB marked disorders of pulmonary ventilation and blood flow in the lungs were revealed. These disorders in subjects with threatened CNPD were regional and accompanied by a moderate increase in power inputs of the cardiorespiratory system. The maintenance of adequate pulmonary exchange in patients with PB entailed functional tension of the respiratory and cardiovascular systems that contributed to decompensation of adaptive mechanisms and occasionally to development of rheographic signs of pneumosclerosis in the lung zones with damaged ventilation and low perfusion of the pulmonary vessels. CONCLUSION: Overloading and decompensation of respiratory and cardial mechanisms of gas exchange regulation in the lungs in response to external damage may lead to development of myocardiodystrophy and pneumosclerosis which appear to be the "price of adaptation".     

A clinical method to determine the effectiveness of dental handpiece sterilization

The interaction of ventilation and hemodynamics in the posttraumatic period has been studied in 131 patients with severe craniocerebral trauma. Indexes of respiratory function, central and pulmonary hemodynamics were determined over the first week and on days 10, 14, 21 and 28 after trauma. The data obtained have shown that respiratory function and circulation damages during brain trauma are predetermined by the reduction in pulmonary volume and capacity, impaired alveolar ventilation and bronchial patency, followed by development of atelectasis of the lungs and pulmonary shunt. Patients with severe brain injury more often develop bronchospasm and disorders of central and pulmonary hemodynamics, as compared to patients with moderate injury.     

Errors in diagnosis of strangulated irreducible hernias

In the paper, the errors in diagnosis of strangulated irreducible hernias are analysed. The attention of specialists is drawn to the fact that in some cases irreducible hernias may be the cause of different cardiovascular and pulmonary disorders (angina, bronchial asthma). It is recommended to treat patients with irreducible hernias irrespective of their age. This measure would obviate not only complications relative to the principle lesion but also the development of reflex vascular and pulmonary complications.     

Possible association between maternal indomethacin therapy and primary pulmonary hypertension of the newborn

Indomethacin purportedly arrests premature labor by inhibiting the production of prostaglandins. Animal experimentation has demonstrated that prostaglandins are involved in the neonatal rerouting of the circulation. Experience with two neonates with disorders circulatory adjustment at birth following prenatal exposure to indomethacin indicates that indomethacin may interfere with these adjustments in man and favor the development of the serious oxygen dependency known as primary pulmonary hypertension of the newborn.     

Pulmonary vascular disorders in portal hypertension

The wide spectrum of pulmonary vascular disorders in liver disease and portal hypertension ranges from the hepatopulmonary syndrome characterized by intrapulmonary vascular dilatations, to pulmonary hypertension (portopulmonary hypertension), in which pulmonary vascular resistance is elevated. Since hepatopulmonary syndrome and portopulmonary hypertension have been reported in patients with nonhepatic portal hypertension, the common factor that determines their development must be portal hypertension. The clinical presentations are very different, with gas exchange impairment in the hepatopulmonary syndrome and haemodynamic failure in portopulmonary hypertension. The severity of hepatopulmonary syndrome seems to parallel the severity of liver failure, whereas no simple relationship has been identified between hepatic impairment and the severity of portopulmonary hypertension. Resolution of hepatopulmonary syndrome is common after liver transplantation, which has an uncertain effect in portopulmonary hypertension. The pathophysiology of both syndromes may involve vasoactive mediators and angiogenic factors.     

Recurrent sinopulmonary disease in a young adult

In 50 patients aged 60 +/- 4 operated for colorectal carcinoma simultaneous combined radionuclide phlebography (RNP) and pulmonary perfusion scintigraphy (PPS) using 99Tcm labeled macroaggregates of the human serum albumin (MAHSA) were performed within 20 postoperative days aiming to detect deep vein thrombosis (DVT) and pulmonary thromboembolism (PTE). The aim of the study was to determine the incidence and segmental DVT localization as well as incidence, localization and clinical characteristics of developed pulmonary perfusion disorders. Deep vein thrombosis was detected in 33 (66%) patients with rather uniform distribution in vein segments. According to their scintigraphic characteristics the findings suggested recent thrombosis in almost all cases (only two of them had signs of chronic thrombosis). Of patients with detected DVT 17 (52%) had pulmonary perfusion disorders of which 10 (59%) were unilateral (7 right and 3 left) and 7 (42%) bilateral. Characteristics and extent of perfusion defects suggested very probable PTE in 11 (65%) patients and less probable in 6 (35%). It has been concluded that patients operated for colorectal carcinoma were highly exposed to DVT and PTE development which necessitates all measures contributing to their prevention.     

The impact of major congenital malformations on mortality in a neonatal intensive care unit

Neonatal mortality due to congenital malformations or genetic disorders has not decreased despite a decrease in overall neonatal deaths with recent advances in medical technology. As a consequence, an increasing percentage of neonatal deaths is attributable to congenital malformations and genetic disorders. This study retrospectively reviewed neonatal deaths associated with congenital malformations over an 11-year period in the neonatal intensive care unit (NICU) at Kosair Children's Hospital, Louisville, Kentucky. Presently, congenital malformations are responsible for approximately 45% (range 32% to 61%) of deaths in the NICU with congenital heart disease, lethal genetic disorders, and pulmonary hypoplasia being the main contributors. Other major causes of neonatal death included extreme prematurity, respiratory disorders, necrotizing enterocolitis, sepsis, asphyxia, and primary pulmonary hypertension. It is important that clinicians are aware that improved survival is expected for most diseases because of technological advances, but that further significant reductions in neonatal mortality will depend on genetic counseling and prevention of congenital malformations.     

Pulmonary manifestations in cerebrotendinous xanthomatosis

We investigated five cases with cerebrotendinous xanthomatosis (CTX) with particular reference to biochemical and pathological pulmonary disorders. To date, few reports discuss the pathophysiology of pulmonary disorders of CTX patients. This study is the first investigation of such pulmonary disorders. All 5 patients had no pulmonary symptoms and no disturbances on radiological studies and pulmonary function tests. However, in bronchoalveolar lavage (BAL) fluids, many cells with cruciform reflexes, which is characteristic of intracellular sterol accumulation, were found under phase contrast microscopy. Biochemically, cholestanol was found to be increased in the BAL fluid as well as in serum. Pathological findings of transbronchial lung biopsy (TBLB) samples disclosed foamy macrophages and small granulomas in alveolar septa. In conclusion, the lung was apparently involved in CTX, and the lesions were characterized with the accumulation of foamy and giant cells with a high concentration of cholestanol, which likely results in the formation of foreign body granulomas.     

Can preoperative lung function diagnosis detect risk of intraoperative pulmonary gas exchange insufficiency in artificial hip replacement with polymethylmethacrylate cement?

In a study of 90 patients in whom a hipjoint had been replaced for the first time using polymethylmetacrylate cement, the extent of intraoperative pulmonary gas exchange disorders was established. The effect of a preexisting disorder of lung function was determined. We checked whether an appraisal of the risk patients who are operated on can be assisted by a preoperative analysis of lung function. After preoperative diagnosis of lung function, the arterial blood gases were analysed at defined times during the operation. An intraoperative fall in the partial pressure of oxygen and an increase in carbon dioxide partial pressure in the arterial blood were found in all patients. There were pronounced interindividual differences in the extent of the disorder of pulmonary gas exchange. The degree of severity of the respective acute disorder of lung function did not show any correlation with the pre-existing disorder of pulmonary ventilation. Major hemodynamic changes were not observed. According to the present findings, a definitive statement with regard to the degree of severity of intraoperatively occurring disorders of pulmonary function cannot be expected from a preoperative analysis of pulmonary function.     

Pulmonary capillary pressure and tissue perfusion: clinical implications during resuscitation from shock

During shock resuscitation, a combination of fluids, vasopressors, vasodilators, and inotropes is administered in order to achieve a cardiac output or overall oxygen delivery as per guidelines of individual clinicians. The measurement of ventricular end-diastolic pressure allows a clinician to describe a therapeutic goal of optimum cardiac output response to changes in end-diastolic pressure. This concept has formed the backbone of resuscitative strategies in many forms of shock. Ventricular end-diastolic pressure is indirectly measured as the pulmonary artery occlusion pressure (PAOP) in critically ill patients with the use of a pulmonary artery catheter. Cytokines and other mediators may injure the pulmonary capillary endothelium which will affect the rate of leakage in the pulmonary capillaries. This may have important clinical implications in the therapy of shock in inflammatory states such as sepsis and the adult respiratory distress syndrome. Therefore, the true edema-forming pressure within the pulmonary bed is of considerable importance to the intensivist at the bedside. True pulmonary capillary pressure represents the midpoint of the capillary bed and is the hydrostatic pressure which directly drives the rate of pulmonary interstitial edema formation. During shock resuscitation in disorders in which vascular integrity may be impaired, the ability to measure pulmonary capillary pressure would be of great clinical benefit. It is impossible to directly measure pulmonary capillary hydrostatic pressure in the intact lung and, therefore, only indirect measurements are clinically possible. Numerous studies have demonstrated the lack of consistent relationship between the pulmonary capillary pressure, PAOP, pulmonary artery diastolic pressure, and the severity of acute lung injury. The assumption that PAOP, and thus left atrial pressure, is a good indirect measurement of pulmonary filtration pressure within the capillary bed is erroneous, in particular in the presence of increased resistance within the pulmonary venous bed between the capillaries and the left atrium, as may exist in disorders in which there is cytokine production. It is now clear that a significant gradient between pulmonary capillary pressure and PAOP may be present in inflammatory disorders which are not present in noninflammatory states, and that pulmonary capillary pressure may be measured at the bedside of critically ill patients. Bedside measurement of pulmonary capillary pressure may allow for added precision in our therapeutic goals in resuscitation from inflammatory shock. If further studies confirm the reliability and reproducibility of bedside measurement, pulmonary capillary pressure may become an invaluable part of the hemodynamic profile in the critically ill patient in shock.     

The prostacyclin-thromboxane system and bronchial patency in patients with pulmonary tuberculosis

The paper is concerned with a study in which a contribution was assessed of the prostacyclin-thromboxane system to the development of disturbances in bronchial patency in patients with pulmonary tuberculosis. It has been established that the prostacyclin-thromboxane system has an active part to play in the evolution and formation both the pattern of the tuberculous process and ventilatory disorders, the most important contribution being made by the proportion prostacyclin:thromboxane.     

Mechanisms of acute respiratory insufficiency in patients with hyperglycemic coma

Basic parameters of pulmonary gas exchange, central and pulmonary hemodynamics, and colloid osmotic pressure were investigated in 31 patients in diabetic hyperglycemic coma over the course of intensive care. Pulmonary gas exchange disorders were observed in all patients in the presence of increased shunting of the blood in the lungs and disorders of transcapillary liquid exchange. On the other hand, we failed to obtain data indicative of an increase in the volume of extravascular water in the lungs. However, it does not rule out the possibility of iatrogenic disorders of gas exchange during noncontrolled rehydration.     

Recognition and management of pulmonary hypertension

Pulmonary hypertension (mean pulmonary arterial pressure > 20mm Hg at rest or > 30mm Hg during exercise) occurs (i) as primary pulmonary hypertension (no known underlying cause), (ii) as persistent pulmonary hypertension of the newborn or (iii) secondary to a variety of lung and cardiovascular diseases. In the last 10 to 15 years there have been significant advances in the medical management of this debilitating and life-threatening disorder. The main drugs in current use are anticoagulants (warfarin, heparin) and vasodilators, especially oral calcium antagonists, intravenous prostacyclin (prostaglandin I2; epoprostenol) and inhaled nitric oxide. Calcium antagonists, (e.g. nifedipine, diltiazem) are used chiefly in primary pulmonary hypertension. They are effective in patients who give a pulmonary vasodilator response to an acute challenge with a short acting vasodilator (e.g. prostacyclin, nitric oxide or adenosine), and are used in doses greater than are usual in the treatment of other cardiovascular disorders. Prostacyclin, given by continuous intravenous infusion, is effective in patients even if they do not respond to an acute vasodilator challenge. The long term benefit in these patients is thought to reflect the antiproliferative effects of the drug and/or its ability to inhibit platelet aggregation. It is used either as long term therapy or as a bridge to transplantation. Inhaled nitric oxide, which is used mainly in persistent pulmonary hypertension of the newborn, has the particular benefit of being pulmonary selective, due to its route of administration and rapid inactivation. Anticoagulants have a specific role in the treatment of pulmonary thromboembolic pulmonary hypertension and are also used routinely in patients with primary pulmonary hypertension. Nondrug treatments for pulmonary hypertension include (i) supplemental oxygen (> or = 15 h/day), which is the primary therapy in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease and (ii) heart-lung or lung transplantation, which nowadays is regarded as a last resort. Different types of pulmonary hypertension require different treatment strategies. Future advances in the treatment of pulmonary hypertension may come from the use of drug combinations, the development of new drugs, such as endothelin antagonists, nitric oxide donors and potassium channel openers, or the application of gene therapy.     

A lung ultrasound sign allowing bedside distinction between pulmonary edema and COPD: the comet-tail artifact

OBJECTIVE: Acute cardiogenic pulmonary edema and exacerbation of chronic obstructive pulmonary disease (COPD) can have a similar clinical presentation, and X-ray examination does not always solve the problem of differential diagnosis. The potential of lung ultrasound to distinguish these two disorders was assessed. DESIGN: Prospective clinical study. SETTING: The medical ICU of a university-affiliated teaching hospital. PATIENTS: We investigated 66 consecutive dyspneic patients: 40 with pulmonary edema and 26 with COPD. In addition, 80 patients without clinical and radiologic respiratory disorders were studied. MEASUREMENTS: The sign studied was the comet-tail artifact arising from the lung wall interface, multiple and bilaterally disseminated to the anterolateral chest wall. RESULTS: The feasibility was 100%. The length of the examination was always under 1 min. The described pattern was present in all 40 patients with pulmonary edema. It was absent in 24 of 26 cases of COPD as well as in 79 of 80 patients without respiratory disorders. The sign studied had a sensitivity of 100% and a specificity of 92% in the diagnosis of pulmonary edema when compared with COPD. CONCLUSIONS: With a described pattern present in 100% of the cases of pulmonary edema and absent in 92% of the cases of COPD and in 98.75% of the normal lungs, ultrasound detection of the comet-tail artifact arising from the lung-wall interface may help distinguish pulmonary edema from COPD.     

Tricuspid valve disease. Clinical evaluation, physiopathology, and management

The tricuspid and mitral valves are homologous whose function depends on coordination among components. Isolated tricuspid valve abnormalities are relatively uncommon. Rheumatic disease, chemicals, immunologic and degenerative disorders alter leaflet anatomy and may result in either stenosis, insufficiency or a combination. More often, tricuspid disorders present as a component of congenital syndromes or secondary to pulmonary vascular or let heart disease which alter geometry and function of nonleaflet components.     

The development of the blood hyperviscosity syndrome in patients with a history of pulmonary artery thromboembolism

Examination of 64 patients with prior pulmonary artery thromboembolism revealed high blood viscosity in 88% of males and 77% of females. Polycythemia and disturbed erythrocyte deformability were the causes of increased blood viscosity. The degree of disturbed blood viscosity correlated with the degree of hemodynamic disorders. The development of the blood hyperviscosity syndrome was determined by the extent of the affected lungs rather than by the duration of the disease.     

0.9% sodium chloride injection with and without heparin for maintaining peripheral indwelling intermittent-infusion devices in infants

PURPOSE: Tachypnea in children is associated with respiratory disorders and nonrespiratory disorders such as cardiac disease, metabolic acidosis, fever, pain, and anxiety. Pulmonary embolism is seldom considered by pediatricians as a cause of tachypnea. PATIENTS AND METHODS: Three children of various ages with persistent tachypnea are described: a girl after orthopedic surgery for kyphoscoliosis, a boy with nephrotic syndrome, and a neonate with Hirschsprung disease. Other causes of tachypnea were diagnosed and treated before pulmonary embolism was considered. RESULTS: Ventilation-perfusion scanning appeared to be highly probable for pulmonary embolism in these patients. Anticoagulant therapy was started. CONCLUSION: Pulmonary embolism should be kept in mind in children with tachypnea, especially when other risk factors for venous thromboembolism are present, to avoid delay in anticoagulant treatment and a fatal outcome.     

Culturally competent healthcare

External respiratory function (ERF) was studied in 129 patients with restrictive pulmonary processes (tuberculomas, infiltrative and cavernous tuberculosis) before and after surgery. All the patients underwent saving lung resections. Changes in ERF were examined by conventional and the new method telespirography. This technique detects general and individual pulmonary ventilation disorders, which underlie criteria for assessing whether patients with pulmonary tuberculosis can be operated on. The authors show that the outcomes of surgical treatment are determined by the baseline status of the respiratory apparatus generally and each lung specifically. Distinctive features of complicated and uncomplicated postoperative periods are identified. The benefits of the new method are demonstrated.     

Using mutual information to measure coupling in the cardiorespiratory system

Approximately 2,000 infants with sickle cell disease are born each year in the United States. Sickle cell disease is an inherited disorder of red blood cell hemoglobin. Sickle cells increase adhesion and cause blockage in the small blood vessels, resulting in tissue damage. The cells' production of hemoglobin S results in two major pathophysiologic features of sickle cell disorders: chronic hemolytic anemia and vaso-occlusion. These disorders cause ischemic tissue damage and acute and chronic organ failure. Potential complications for children with sickle cell disease include vaso-occlusive events, splenic sequestration, bacterial septicemia from splenic hypofunction, aplastic crisis, pulmonary compromise including acute chest syndrome, renal tubular dysfunction and renal failure, priapism, aseptic necrosis, gallstones, delayed growth and development, leg ulcers, stroke and premature death. Three major sickle cell complications during the first years of life are dactylitis, splenic hypofunction and splenic sequestration. The risk for pneumococcal meningitis is 36 times greater in children with sickle cell anemia than for black children without the disease, and 314 times greater than for white children.     

The role of thrombosis in severe pulmonary hypertension

Considering the important surface in pulmonary circulation where blood can interact with the endothelium, the maintenance of blood fluidity through the lung, by antithrombotic pathways and products of the endothelium, is essential. This function appears to be ineffective in primary pulmonary hypertension and in severe secondary pulmonary hypertension. Thrombotic lesions are frequently found in pulmonary arteries in these diseases. Thrombin activity appears to be increased in severe pulmonary hypertension. Antithrombotic pathway disorders may account for this abnormality, particularly in chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension. Injured endothelium, a constant feature in severe pulmonary hypertension, either primary or secondary, enhances thrombus formation in pulmonary vessels. This is probably related to thrombomodulin and tissue factor imbalance, impairment of prostacyclin and nitric oxide release, as well as inefficiency of fibrinolysis. Moreover, platelets appear to be activated in the pulmonary circulation of these patients. They release several mediators acting on vascular tone and as mitogenic agents, and may also contribute to thrombin and clot generation. Long-term oral anticoagulant and continuous infusion of prostacyclin, treatments which impede thrombosis, are known to improve the survival rate in patients with primary pulmonary hypertension. These are the strongest arguments, so far, in favour of the role of thrombosis in severe pulmonary hypertension. However, we do not know whether these abnormalities result from a previous vascular injury or represent the primary disturbance.