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PubMed1995

[Severe pulmonary embolism: value of clinical findings and complementary investigations].

Pulmonary embolism is severe when pulmonary arterial obstruction affects right heart haemodynamics and gas exchanges. The clinical signs are not very discriminating in the assessment of the severity of pulmonary embolism: shock, neurological signs and cyanosis are the most suggestive signs of severe embolism. Of the routine complementary investigations, normal blood gases does not exclude the diagnosis of even severe pulmonary embolism but when the pO2 is less than 50 mmHg the vascular obstruction is severe. The risk of haemorrhage due to thrombolysis, commonly used in severe pulmonary embolism, is greater after invasive investigations. This makes it preferable to resort to non-invasive investigation initially, echocardiography, spiral computed tomography or pulmonary scintigraphy, depending on which technique is available in an emergency. In a suggestive clinical setting, echocardiographic signs of right ventricular overload and visualisation of a thrombus in the right heart chambers or pulmonary artery on echocardiography or spiral computed tomography practically confirms the diagnosis of severe pulmonary embolism. Transoesophageal echocardiography is more sensitive than transthoracic echocardiography for the visualization of a thrombus in the pulmonary outflow tract, but is not always inoffensive in those patients in an unstable condition. Lung scintigraphy, when interpretable, provides the diagnosis of pulmonary embolism, shows the anatomic extension and allows follow-up of the outcome. However, the specificity of this investigation is problematic. Pulmonary angiography, coupled with catheterisation of the right heart, remains the reference investigation in the diagnosis of pulmonary embolism and its anatomical diffusion. It is reserved to situations in which echocardiography is difficult and scintigraphy is uninterpretable, notably in patients with previous cardiopulmonary disease.

Blood Gas Analysis↗
PubMedDate not supplied

[Development of a canine model of chronic progressive right ventricular hypertension].

INTRODUCTION: Several animal models of right ventricle hypertension (RVH) have been produced through pulmonary artery banding with linen, tygon or teflon. Nevertheless few devices attempting a progressive, step by step graduated chronic development of RVH have been reported. The present study describes the results in our animal model of chronic RVH. MATERIAL AND METHODS: We designed a software programmed to obtain hemodynamic data and installed a small occlusive hydraulic device (OHD) at the pulmonary artery trunk producing a raise in the right ventricular systolic pressure (RVSP); this pressure can be modified externally through the OHD. We studied 12 healthy mongrel dogs (18 to 28 kg of weight) in the course of 6 months. Hemodynamic measurements were performed at different RVSP at two months intervals; (Baseline, 40 mmHg and 60 mmHg). RESULTS: The software was useful to analyze several hemodynamic variables at each RVSP. At 60 mmHg, the end diastolic pressure of the right ventricle (RVEDP) increased from 4.2 +/- 0.4 mmHg to 13.2 +/- 1.1 mmHg, p < 0.000, accompanied with a fall in cardiac output adjusted to the dogs weight from 0.16 +/- 0.03 L/min/kg to 0.09 +/- 0.01 L/min/kg, p > 0.000. Also an increase of the end diastolic pressure of the left ventricle (LVEDP) from 7.4 +/- 0.8 mmHg to 16.3 +/- 2.8 mmHg, p < 0.000, was observed. RVSP was maintained in chronic condition and the intraclass correlation coefficient was 0.83, P < 0.005. CONCLUSIONS: Right ventricular chronic hypertension is created. The device is useful and reliable to maintain chronic increments of RVSP. The software permits a versatile analysis.

Animals↗
PubMed2004

Pathophysiology of severe pulmonary hypertension in the critically ill patient.

Pulmonary hypertension (PH) is a threatening condition that can be associated with a great variety of both pulmonary and extrapulmonary diseases. In all forms of severe PH the pulmonary vascular bed looses its physiological features of a "high flow-low pressure system", putting an increased afterload on the right ventricle (RV). Acute pulmonary hypertension in the intensive care unit often represents a clinical problem secondary to acute respiratory failure, left heart failure, pulmonary embolism, or decompensation of prior PH by concurrent pulmonary or cardiovascular disease. Right ventricular failure (acute cor pulmonale) occurs when relevant increases in pulmonary vascular resistance overwhelm its compensatory mechanisms, both abruptly on a previously normal RV, or gradually on a chronic cor pulmonale. This review addresses the main pathophysiological aspects of severe PH, focusing on the hemodynamic derangements occurring in the setting of acute cor pulmonale, and emphasizing the role of ventricular interdependence (the way right ventricular failure greatly affects diastolic and systolic function of the left ventricle), the risk of RV ischemia (the end stage of RV failure) and systemic organ hypoperfusion (caused by antegrade and retrograde heart failure). The understanding of the peculiar features of this type of cardiovascular insufficiency is necessary to both provide effective monitoring and adequate supportive therapy.

Critical Illness↗
PubMed1993

The efficiency of pulmonary blood transport following single lung transplantation.

Perioperative right ventricular (RV) dysfunction remains a significant problem following single lung transplantation (SLT), especially in patients with pulmonary hypertension. Total RV power (Wt), a determinant of RV function, is the sum of the mean component (Wm) which contributes to actual blood flow and the oscillatory component (Wo) which is the energy expended on arterial pulsation. Calculation of Wo is possible only through harmonic analysis of pulmonary arterial (PA) pressure and flow waveforms, and as much as 33% of RV power is attributed to it. The purpose of this study was to precisely quantify changes in RV power output using Fourier analysis of PA pressure and flow waveforms after SLT. Fourteen dogs (donors) were instrumented with a PA ultrasonic flow probe, PA and left atrial (LA) micromanometers, and LA epicardial pacing leads. Control (Pre-Tx) pressure-flow data were acquired during transient occlusion of the right PA at a heart rate of 140. The PA was cannulated, the lungs were flushed with 1 liter of modified Euro-Collins solution at 4 degrees C, and the left lung was harvested and transplanted to 14 recipient dogs in a standard manner. After 1 hr of reperfusion, PA (Post-Tx) pressure-flow data were acquired as above. All recipient animals survived SLT with a mean ischemic time of 183 +/- 3 min. Following SLT, both the mean, Wm, (69 +/- 9 to 161 +/- 23 mW) and oscillatory, Wo, (23 +/- 3 to 46 +/- 10 mW) components of RV power output increased significantly after SLT (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Arrhythmogenic right ventricular cardiomyopathy: a survey of the investigations at the University of Padua.

The purpose of this paper is to review the history of the clinico-pathologic investigations performed at the University of Padua on an old morbid entity ("parchment heart"), which, in the 1960s, led to the clinical description of the disease, in the 1980s to the revival of the scientific interest, and in the mid 1990s to the understanding of the genetic background. All the steps of the progressive knowledge are reviewed: necropsy of young people who died suddenly, in vivo diagnosis by ECG, echocardiography, angiocardiography, endomyocardial biopsy, nuclear magnetic resonance, and diagnostic criteria. Familial occurrence with autosomic dominant transmission and various penetrance was documented. Gene defects were recently mapped both to chromosome 14q23-q24 and 1q42-q43, thus providing evidence for genetic heterogeneity. The pathologic substrates of arrhythmogenic right ventricular cardiomyopathy pointed to an acquired progressive myocardial atrophy with fibro-fatty replacement of dying myocytes. Nowadays the disease is definitively regarded as a primary myocardial disorder and it has been included in the revised WHO classification of cardiomyopathies.

Arrhythmias, Cardiac↗
PubMed1992

Preoperative prostaglandin E1 treatment to prevent right ventricular failure after orthotopic heart transplantation.

Elevated pulmonary vascular resistance (PVR) and pulmonary hypertension (PH) are high risk factors for early graft failure in orthotopic heart transplantation (oHTx). The need for an oversized donor in patients with elevated PVR aggravates the shortage of suitable donor organs. To decrease the elevated PVR to values suitable for orthotopic heart transplantation prostaglandin E1 (PGE1) was administered in 11 patients (11 male, mean age 49.2 years, mean dosage 35 ng/kg per min over 6-8 days). Ten days after the discontinuation of the PGE1 therapy, recatheterization was done. All haemodynamic data were determined by right heart catheterization using a Swan Ganz catheter and thermodilution technique before, and 10 days after, PGE1 treatment. The Wilcoxon signed ranks test was used for statistics. PVR significantly decreased in all patients (5.5 to 2.8 Wood units, P < 0.005). All patients were considered to be suitable for oHTX and put on the waiting list. At the time of writing, in eight of these patients (eight male, mean age 49.6 years; four ischemic, four dilatative CMP) oHTX had been successfully performed. No right ventricular failure occurred in the postoperative phase. These results sugest that long-term moderation of elevated PVR by PGE1 therapy weeks or months before transplantation enables oHTX in patients with elevated PVR.

Adult↗
PubMed2003

Effects of endotoxic shock on right ventricular systolic function and mechanical efficiency.

OBJECTIVE: To investigate the effects of endotoxin infusion on right ventricular (RV) systolic function and mechanical efficiency. METHODS: Six anesthetized pigs (Endo group) received a 0.5 mg/kg endotoxin infusion over 30 min and were compared with six other anesthetized pigs (Control group) receiving placebo for 5 h. RV pressure-volume (PV) loops were obtained by the conductance catheter technique and pulmonary artery flow and pressure were measured with high-fidelity transducers. RESULTS: RV adaptation to increased afterload during the early phase of endotoxin-induced pulmonary hypertension (T30) was obtained by both homeometric and hetereometric regulations: the slope of the end-systolic PV relationship of the right ventricle increased from 1.4+/-0.2 mmHg/ml to 2.9+/-0.4 mmHg/ml (P<0.05) and RV end-diastolic volume increased from 56+/-6 ml to 64+/-11 ml (P<0.05). Consequently, right ventricular-vascular coupling was maintained at a maximum efficiency. Ninety minutes later (T120), facing the same increased afterload, the right ventricle failed to maintain its contractility to such an elevated level and, as a consequence, right ventricular-vascular uncoupling occurred. PV loop area, which is known to be highly correlated with oxygen myocardial consumption, increased from 1154+/-127 mmHg/ml (T0) to 1798+/-122 mmHg/ml (T180) (P<0.05) while RV mechanical efficiency decreased from 63+/-2% (T0) to 45+/-5% (T270) (P<0.05). CONCLUSIONS: In the very early phase of endotoxinic shock, right ventricular-vascular coupling is preserved by an increase in RV contractility. Later, myocardial oxygen consumption and energetic cost of RV contractility are increased, as evidenced by the decrease in RV efficiency, and right ventricular-vascular uncoupling occurs. Therefore, therapies aiming at restoring right ventricular-vascular coupling in endotoxic shock should attempt to increase RV contractility and to decrease RV afterload but also to preserve RV mechanical efficiency.

Animals↗
PubMed2002

Pulmonary haemodynamics in obstructive sleep apnoea.

In patients with obstructive sleep apnoea syndrome (OSAS), pulmonary haemodynamics can show both transient perturbations during sleep and permanent alterations. During sleep, repeated fluctuations in pulmonary artery pressure and pulmonary wedge pressure, coincident with apnoeas, can be observed. Calculation of transmural pressure values is preferable to intravascular pressures in OSAS, due to the marked swings in intrathoracic pressure associated with obstructive apnoeas. Pulmonary artery pressure may progressively increase during sleep, particularly in close sequences of highly desaturating apnoeas. Apnoea-induced hypoxia appears as the most important determinant of this pulmonary artery pressure behaviour. Stroke volume and cardiac output during obstructive apnoeas show changes mainly related to intrathoracic pressure variations. Permanent precapillary pulmonary hypertension at rest is observed in <50% OSAS patients, and is poorly reversible after OSAS treatment. It correlates best with diurnal respiratory function parameters. However, the finding of pulmonary hypertension in some patients with near normal diurnal lung function led to suggest that sleep respiratory disorders may contribute to permanent pulmonary haemodynamic impairment in predisposed subjects. Knowledge on right ventricle hypertrophy in OSAS is inconsistent. As to right ventricle failure, it is clinically evident in subjects with associated lung disease or morbid obesity, while it may be detected instrumentally in subjects without such alterations, presumably as effect of apnoeas themselves. Besides, it appears more fully reversible after long-term OSAS treatment than pulmonary hypertension.

Hemodynamics↗
PubMedDate not supplied

Neonatal hemangiomatosis and atrial septal defect: a rare cause of right heart failure in infancy.

Neonatal hemangiomatosis is a well-recognized cause of left ventricular failure. We describe an infant with neonatal hemangiomatosis and an ostium secundum atrial septal defect who developed severe right heart failure. This was due to the combination of increased flow through the right heart as a result of the atrial septal defect, and the background high cardiac output from the massive arteriovenous shunting and multiple hemangiomas. In addition, the multiple hepatic hemangiomas may exert a vasoactive influence on the pulmonary vasculature.

Diseases in Twins↗
PubMed2005

[Variant angina mimicking right ventricular infarction--a case report].

A case of a 59-year-old man with recurrent angina associated with ST-segment elevation in leads II, III, aVF and V4R-V6R, cardiogenic shock and complete atrio-ventricular block, is presented. Coronary angiography was normal. Therapy with calcium channel blockers was effective. Difficulties in the treatment of patients with variant angina are discussed.

Angina Pectoris, Variant↗
PubMed1997

PEEP-induced tricuspid regurgitation.

OBJECTIVE: To determine the presence of tricuspid regurgitation (TR) in patients affected by acute lung injury (ALI) and the adult respiratory distress syndrome (ARDS) during mechanical ventilation with positive end-expiratory pressure (PEEP). DESIGN: A prospective clinical study. SETTING: 10-bed general intensive care unit in a University Hospital. PATIENTS: 7 consecutive patients an age 44.7 +/- 8.6 years with a diagnosis of ALI or ARDS were studied. All were on mechanical ventilation with PEEP. INTERVENTIONS: PEEP was increased in steps of 5 cm H2O until the appearance of TR or up to a limit of 20 cm H2O. MEASUREMENTS AND RESULTS: Right atrial pressure, pulmonary artery pressure, and wedge pressure were measured and cardiac output was determined by thermodilution. TR was graded from 0 to 3. Standard 2D echocardiographic and pulsed-wave images were obtained at each level of PEEP. PEEP was increased from 4 +/- 3 to 17 +/- 2 cm H2O. Mean PAP increased from 27.7 +/- 2.9 to 36.7 +/- 3.5 mm Hg (p < 0.02) when PEEP was increased. Five patients had competent valves and two had mild TR at baseline. In six out of the seven, TR either developed or increased when PEEP was increased. CONCLUSIONS: Our study demonstrated the development of TR after the use of PEEP in patients with ALI and ARDS as a consequence of pulmonary hypertension and right ventricular overloading. Since TR may randomly affect cardiac output values and derived parameters, the assessment of cardiac performance by some techniques such as thermodilution should be used with caution.

Adult↗
PubMed2005

[The role of an objective assessment of the heart right vientricle function for the anesthesiological maintenance and intensive therapy of surgical patients].

Latent dysfunction of the heart right ventricle and hypovolemia were assessed in 50 patients divided into 4 groups, operated on the heart, abdominal aorta and lungs. It was found that after revascularization of the myocardium the diastolic disorders prevailed. In patients operated for the heart valve (mitral and aortal) diseases prevailing were the systolic and pump dysfunction of the right ventricle. Insufficiency of the right ventricle in these groups was 13% and 22% respectively. After operations on the abdominal aorta a combination of the systolic and diastolic impairments of the right ventricle were observed. After extended resections of the lungs there was a characteristic combination of systolic, diastolic and pump dysfunctions. When the operation was followed by a decreased minute volume of circulation, its cause was hypovolemia in 29% of cases in the examined surgical patients. The investigation of the right ventricle functions with the help of pulmonary arterial volumetry can reveal their latent dysfunctions as well as hypovolemia in a considerable part of surgical patients.

Anesthesia↗
PubMed2001

Two cases of right ventricular ischemic injury due to massive pulmonary embolism.

In general, massive pulmonary embolism induces severe right ventricular overload, but pathological changes in the right ventricle due to pulmonary embolism is rarely seen. In this report, we describe two autopsy cases of massive pulmonary embolism without pre-existing cardiopulmonary disease. Both cases were accompanied by myocarditis-like changes in the right ventricle and infiltration of a number of polymorphonuclear neutrophils and mononuclear cells into the dilated right ventricular wall. Transmural or subendocardial coagulation necrosis was not apparent. Almost all of the mononuclear cells were immunohistochemically revealed to be CD68-positive macrophages. We speculated that these findings resulted from ischemia due to massive pulmonary embolism.

Accidents, Traffic↗
PubMed2000

Use of nitric oxide for decompensated right ventricular failure and circulatory shock after cardiac arrest.

We describe a case of peri-operative cardiac arrest, severe right ventricular failure and pulmonary hypertension in a 60-yr-old woman with interstitial pulmonary fibrosis. Inhaled nitric oxide therapy rapidly improved arterial oxygenation and haemodynamic variables, allowing recovery and weaning from mechanical ventilation. Subsequently, the patient was discharged from the cardiac intensive care unit.

Anesthesia, General↗
PubMed2003

Right ventricular myocardial responses to chronic pulmonary regurgitation in lambs: disturbances of activation and conduction.

Patients after repair of tetralogy of Fallot are at increased risk of arrhythmic death. Clinical data suggest that pulmonary regurgitation predisposes to these arrhythmias, although the cellular electrophysiologic effects of pulmonary regurgitation are unknown. We induced pulmonary regurgitation in lambs, and 3 mo later, having quantified the pulmonary regurgitant (PR) fraction, studied right ventricular mechanical and electrophysiologic properties in vivo and in vitro. The PR fraction was greater in PR (75 +/- 10%) than in sham-operated animals (8 +/- 4%; p < 0.01). In vivo, monophasic action potential duration and activation time, at rest and during acute right ventricular stretch, were similar in both groups. However, the dispersion of activation time was greater in PR animals at rest (13 +/- 1.1 versus 8 +/- 1.1 ms; p < 0.05). Furthermore, the dispersion of activation increased during right ventricular stretch in PR, but not in sham-operated animals. In vitro, myocardial force-frequency responses were similar in both groups, indicating preserved systolic performance, but mechanical restitution studies showed a prolonged refractory period (447 +/- 22 versus 370 +/- 26 ms; p < 0.05) and a decreased recovery time constant (184 +/- 19 versus 265 +/- 20 ms; p < 0.001) in PR animals, indicating altered calcium cycling. Furthermore, the myocardial conduction velocity was reduced in PR animals (31 +/- 3.58 versus 47.9 +/- 5.1 cm/s; p < 0.01), resulting from a 2-fold increase in intracellular resistance (437.25 +/- 125.93 versus 194 +/- 43.27 Omega. cm; p = 0.025). Chronic PR leads to inhomogeneity of right ventricular activation, alters myocardial calcium cycling, reduces conduction velocity, and increases intracellular resistivity. These may contribute to the development of arrhythmias associated with PR, including those in patients after tetralogy repair.

Animals↗
PubMed1994

A case of arrhythmogenic right ventricular dysplasia with atrial flutter.

A 57-year-old male who had arrhythmogenic right ventricular dysplasia (ARVD) with recurrent atrial flutter (AF) is reported. The patient had more frequent episodes of AF than of ventricular arrhythmias. Magnetic resonance imaging, echocardiography and right ventriculography revealed dilatation of the right ventricle and endomyocardial biopsy specimens from the right ventricle showed findings which were compatible with ARVD. The left ventricular specimen, however, also revealed a loss of myocytes and interstitial fibroelastic changes. The present case demonstrates an overlap of post-inflammatory or primary endomyocardial fibroelastic changes with ARVD.

Aged↗
PubMed2006

Arrhythmogenic right ventricular cardiomyopathy is a life-threatening disease at high risk for cardiac arrest during effort. Minor forms are as dangerous as major forms?

The aim of the present study was the evaluation of physical activity likely to lead to the onset of life-threatening ventricular arrhythmias in subjects affected by arrhythmogenic right ventricular cardiomyopathy. In particular, strenuous physical activity can be dangerous in patients with minor or 'concealed' forms of the disease, in whom no previous diagnosis has been made. In these patients preventive strategies cannot be adopted due to the lack of a clinical diagnosis, and so physical effort can be responsible for the first noticeable symptom of the disease.

Cardiomyopathies↗