Signs Of Right Ventricular Failure Research Articles

Severe cardiac failure in newborns with VGAM. Prognosis significance of hemodynamic parameters in neonates presenting with severe heart failure owing to vein of Galen arteriovenous malformation.

Neonatal vein of Galen malformation complicated by severe cardiac failure is a rare disease. The purpose was to assess the outcome of this life-threatening malformation and identify hemodynamic prognostic factors. Retrospective study. Twenty-four newborns with cardiac failure requiring mechanical ventilation were consecutively admitted from 1986 to 2000. Cardiovascular evaluation including echocardiogram was performed in all cases. Eighteen transarterial shunt occlusions with glue were applied by the same team of three physicians. Twelve babies survived and underwent one endovascular session at least (median age 20 days) with a mean 63 months follow-up. Embolization was not performed in 6 of the 12 nonsurvivors because of severe brain damage or profound hypotension Cardiogenic shock occurred in all nonsurvivors, but also in one long-term survivor (p<0.0001). Echocardiogram showed signs of right ventricular failure, most often in the dead babies (p=0.005). The pulmonary systemic arterial pressure ratio was significantly higher in the nonsurvivor group (p=0.031), and it decreased significantly after the first embolization only in patients who survived (p=0.01). Patent ductus arteriosus and a diastolic aortic reversed-flow were present in all nonsurvivors in contrast to 30% of the long-term survivors (p=0.003 ). There was no difference in the left ventricular contractility and mean cardiac output between the two groups. The outcome of vein of Galen malformation complicated by severe cardiac failure requiring mechanical ventilation remains poor. Neonatal embolization seems to be beneficial only in babies without suprasystemic pulmonary hypertension.

Modern treatment of pulmonary embolism.

Modern treatment of acute pulmonary embolism requires rapid and accurate diagnosis followed by risk stratification to devise an optimal management strategy. Patients at low risk have good outcomes simply with intensive anticoagulation treatment. Higher-risk patients may require more aggressive intervention with thrombolysis or embolectomy. Clinical risk factors for an adverse outcome include increasing age, cancer, congestive heart failure, systemic arterial hypotension, chronic obstructive pulmonary disease and right ventricular dysfunction. A promising approach is the Geneva Prognostic Score, which is based upon a rapid clinical assessment. On physical examination, signs of right ventricular failure, including distended jugular veins and a right-sided S3 gallop, should be looked for. The electrocardiogram may show evidence of right ventricular strain with a new right bundle branch block or T wave inversion in leads V1-V4. The troponin level may be elevated as a marker of cardiac injury and right ventricular microinfarction, even in the absence of coronary artery disease. The most useful imaging marker of high risk is the presence of moderate or severe right ventricular dilatation and hypokinesis on the echocardiogram, especially with progressively worsening right ventricular function despite intensive anticoagulation treatment. Patients at high risk should be considered for thrombolytic therapy or embolectomy rather than management with anticoagulation therapy alone. Special care must be taken to avoid thrombolytic therapy among patients who might be susceptible to intracranial haemorrhage. Intracranial haemorrhage reached a surprisingly high rate of 3.0% in the International Cooperative Pulmonary Embolism Registry of 2,454 prospectively evaluated acute pulmonary embolism patients at 52 hospitals in seven countries. An alternative approach to patients at high risk is a catheter-based or open surgical embolectomy. It is crucial to refer these patients as quickly as possible, rather than delaying intervention until cardiogenic shock has ensued. Fortunately the current tools for risk stratification provide an "early window" for prognostication and can help the coordination of a definitive treatment plan with optimal results.

Idiopathic Dilated Cardiomyopathy in Children: Prognostic Indicators and Outcome

To determine the outcome of Finnish children and adolescents with idiopathic dilated cardiomyopathy (IDCM) and factors that might be useful as prognostic indicators. The clinical profile and course of 62 Finnish children and adolescents (median age, 13 months; range, 1 day to 20 years) with IDCM in 1980 to 1991 were evaluated to detect factors that might predict outcome. Factors studied included age, gender, family history, previous viral illness, and symptoms and signs at presentation. Furthermore, data on serial electrocardiographic, echocardiographic, and chest x-ray examinations, histologic findings, and treatments were analyzed. During a mean (+/-SD) follow-up of 3.9 +/- 4.5 years (range, 1 day to 25 years), 10 patients (16%) recovered, 17 (27%) had residual disease, 4 (6.4%) underwent heart transplantation, and 31 (50%) died. Infants (<1 year of age) and adolescent (>/=15 years of age) male patients with progressing symptoms of left ventricular failure after initiation of medical therapy tended to have the poorest outcome. However, in multivariate analysis, only histologic evidence of endocardial fibroelastosis, clinical signs of right ventricular failure at presentation, and the need for anticoagulative therapy during follow-up, the last an expression of a severely impaired left ventricular systolic function, appeared to be significant predictors of long-term outcome. Our study confirms that the outcome of children with IDCM still remains poor. However, a group of patients, mainly infants, make a full recovery. Adolescent male patients as well as infants suffering from endocardial fibroelastosis with persisting symptoms of congestive heart failure after initiation of medical therapy tend to have the poorest outcome. These patients need a careful follow-up at short time intervals and, in the case of lacking response to medical treatment with resulting growth failure and/or poor quality of life, should be offered urgent heart transplantation.

Changes in contractile and non-contractile proteins, intracellular Ca2+ and ultrastructures during the development of right ventricular hypertrophy and failure in rats.

Whether cardiac hypertrophy is a compensatory response or a cause of decompensation has been an interesting and important controversy in cardiology. The purpose of this study is to assess qualitative and quantitative changes in biological factors involved in the evolution and the development of right ventricular hypertrophy (RVH) and right ventricular failure in response to pressure overload in rats with pulmonary hypertension induced by monocrotaline injection, and to clarify the process from compensation to deterioration in cardiac hypertrophy biochemically and morphologically. Significant RVH was produced in rats at 2 weeks after single subcutaneous injection of monocrotaline, and signs of right ventricular failure became obvious at 4 weeks as RVH became more severe. In the right ventricle of these rats, we found that: 1) myosin isoenzymes shifted from V1 to V3 both at 2 and 4 weeks; 2) total collagen content increased, and type III and type V collagens increased with a relative decrease in type I collagen at both 2 and 4 weeks; 3) intracellular Ca2+ transient recorded from isolated myocytes showed a lower peak and slower descent slope compared to those of control rats; 4) ultrastructural changes observed by scanning electron microscopy at 1 and 2 weeks disappeared gradually as heart failure developed, and degeneration or destruction of mitochondria or sarcoplasmic reticulum became remarkable at 3 and 4 weeks. These findings suggest that cardiac hypertrophy might be an ominous sign of cardiac failure rather than a benign adaptive process, at least in this model.

Plasma atrial natriuretic peptide in carcinoid heart disease

Plasma atrial natriuretic peptide (ANP) concentration was determined and cardiac ultrasound studies were performed in 50 patients with malignant midgut carcinoid tumors. The extent of carcinoid-related heart disease varied among the patients. The patients with the most severe right-sided heart disease, who often had signs of right ventricular failure, had significantly (p < 0.001) higher plasma ANP concentrations than either patients with less or no abnormal ultrasound findings or age- and sex-matched healthy control subjects. ANP levels were serially determined for 0.5 to 4 years (median 2.1) in 12 patients. The levels increased above the reference range in patients with clinical findings of right ventricular failure. In patients without cardiac decompensation the levels remained within the reference range. In 3 patients who had successful tricuspid and pulmonary valve replacements, signs and symptoms of right ventricular failure disappeared and plasma ANP levels declined and normalized. Five patients with progressive right ventricular failure and increasing plasma ANP levels during follow-up eventually died from cardiac decompensation. This study demonstrates the predictive value of serial determinations of plasma ANP in carcinoid heart disease. Such measurements can be an additional guide in the clinical management of these patients.

Circulatory Effects of Isoflurane during Acute Hypercapnia

Acute respiratory acidosis results in increases in cardiac output and in systemic and pulmonary arterial blood pressures. The aim of this investigation was to determine if isoflurane modifies these effects. Nine patients (ASA II or III) scheduled for major surgery took part in the investigation. After the induction of general anesthesia, CO2 was added to the inspiratory gas mixture. After 15 min, ventilation with addition of CO2 (PaCO2 8-9 kPa) isoflurane (3%) was added. Hemodynamic measurements were made to study the effects of acute hypercapnia and the effects of isoflurane during hypercapnia. The addition of carbon dioxide resulted in increases in cardiac output, systemic and pulmonary arterial blood pressures, and right and left ventricular stroke work. The addition of isoflurane during hypercapnia decreased systemic arterial blood pressure, but pulmonary arterial blood pressure was unaffected, cardiac output and stroke volume did not change, and left but not right ventricular stroke work decreased. In conclusion, acute pulmonary hypertension induced by hypercapnia was not affected by isoflurane but, despite increased right ventricular stroke work, there were no signs of right ventricular failure.

On the differential diagnosis of cardiac and pulmonary insufficiency according to instrumental research

Differential diagnosis of cardiac and pulmonary insufficiency in a routine clinical trial is often difficult or impossible, especially in acute conditions or with a combination of heart and lung diseases. These difficulties are due to the fact that many clinical signs of cardiac and pulmonary insufficiency are identical, for example, shortness of breath, cyanosis, tachycardia, hard breathing, wheezing in the lungs, accent 11 of the top and its cleavage over the pulmonary artery. Even instrumental invasive studies (measurement of pulmonary artery pressure and venous pressure) do not allow differentiating these conditions. In this regard, in the presence of pronounced signs of right ventricular failure, the question arises whether they are symptoms of a pulmonary heart or a primary disease of the left heart.

Simultaneous assessment of right ventricular ejection fraction and central haemodynamics at rest and during exercise in patients with pulmonary hypertension.

In 10 patients, aged 55-73, with pulmonary hypertension, right ventricular ejection fraction (RVEF) was measured simultaneously with central haemodynamics twice, at rest and during exercise. In the first investigation, RVEF was measured with first pass (FP) radionuclide angiocardiography using 133Xe and 99Tcm as tracers. In the second investigation after 1 h's rest, RVEF was measured with equilibrium (EQ) radionuclide angiocardiography. Significant correlations were found between RVEF and pulmonary artery pressure (r = -0.76 to -0.88) and between RVEF and right arterial pressure (r = -0.76 to -0.84) at rest and during exercise. RVEF was low or decreased during exercise in all patients with haemodynamic signs of right ventricular failure. Good correlations were found between the FP and EQ techniques for measuring RVEF both at rest, r = 0.86, and during exercise, r = 0.91. RVEF, measured with the FP technique, showed better reproducibility and better correlation to haemodynamic variables and to history of right ventricular failure than the EQ technique. Thus, the FP technique seemed to be the method of choice for assessment of RVEF.

Essai D'Un Inhibiteur De L'Anhydrase Carbonique, Le Dichlorphenamide, Dans Le Traitement De L'Acidose Respiratoire*

Summary1.Dichlorphenamide (150 mgr daily) was administered during 10 days to 6 patients with alveolar hypoventilation. Five patients suffered from emphy-sema, one from « Pickwick Syndrome ». None of them presented signs of right ventricular failure. They were hospitalized for at least one month, on a constant sodium intake.Before, during and after treatment, urinary volume and electrolytes, blood electrolytes, CO„ combining power, pH and oxygen, total and alveolar ventilation have been determined.2.This drug produces, within the hour of its administration, an increased urinary output of sodium, potassium and bicarbonates with elevation of urinary pH, as described for acetazolamide. Its action, however, is more potent and sustained : at the end of the treatment, sodium and potassium excretion are still increased. No significant chloruresis was observed.3.The treatment produces a decrease of the CO„ combining power and, in some cases, hyperchloremic acidosis; natremia and kalemia remain unchanged. Hypercapn...

Clinical and physiological correlations in patients with mitral stenosis. V.

1. 1. The area of the mitral valve and the degree of pulmonary vascular disease have been calculated from physiological data in thirty patients with pure mitral stenosis without evidence of active rheumatic carditis. 2. 2. From a hydraulic point of view, a valve area of 1.0 cm. 2, one-quarter to one-sixth normal, appears to be a critical one, for at that level of stenosis the pressure head needed to maintain a normal cardiac output approaches the plasma osmotic pressure. 3. 3. Probably from the stimulus of an increased pulmonary “capillary” pressure, a variable degree of vascular obstruction develops in patients when the mitral valve area becomes reduced to about 1.0 cm. 2 or smaller. This results in a lower cardiac output, which may protect the capillary bed from sudden increases in pressure. 4. 4. The clinical picture in mitral stenosis can be explained in a large measure by the interplay of the degree of stenosis with the degree of pulmonary vascular obstruction. 5. 5. The combination of a narrow valve with only a slight increase in pulmonary arteriolar resistance is associated with predominantly respiratory symptoms, exertional dyspnea, hemoptysis, and paroxysmal nocturnal dyspnea, the right ventricle not becoming dilated. 6. 6. The effect of a narrow valve and a high pulmonary arteriolar resistance appears to be additive in causing electrocardiographic evidence of right ventricular hypertrophy and roentgenographic signs of cardiac enlargement. 7. 7. The combination of a narrow valve and great increases in pulmonary arteriolar resistance is associated with severe dyspnea, cardiac enlargement, and signs of right ventricular failure. 8. 8. Most patients with mitral stenosis can be divided into four general categories by their signs, symptoms, and physiological adjustments.