Why protect the right ventricle in patients with acute respiratory distress syndrome?

Even a slight increase in pulmonary vascular resistance can overload a normal right ventricle, which ejects blood through a low-pressure circuit. In a clinical setting, a persistent increase in pulmonary vascular resistance produces acute cor pulmonale. From an echocardiographic point of view, may be defined as the combination of a paradoxical septal motion, reflecting systolic overload, with right ventricular enlargement, reflecting diastolic overload. In patients with acute respiratory distress syndrome, this complication reflects the severity of the pulmonary disease involving the microvasculature but may also be caused or exacerbated by an aggressive ventilatory strategy. In the past, conventional respiratory support used in acute respiratory distress syndrome to obtain normocapnia was associated with a poor prognosis and a high frequency of acute cor pulmonale, suggesting some relation between the two findings. This prognosis has greatly improved with protective ventilation. At the same time, the incidence of acute cor pulmonale has diminished in acute respiratory distress syndrome, and the prognosis of this specific complication has also improved, suggesting that the right ventricle may develop some adaptation against persistent overload. Past lessons, however, have taught us that this potential may be limited and lead us to recommend right ventricular protection during mechanical ventilation.     

Electrocardiographic considerations in right ventricular infarction.

Right ventricular infarction frequently occurs in the setting of infarction of the inferior wall of the left ventricle. Although there are several protective mechanisms that may limit the size of the infarction, right ventricular damage can result in right ventricular failure and cardiogenic shock. ECG manifestations of right ventricular infarction can facilitate the early recognition of this syndrome. The standard 12-lead ECG may provide some evidence of infarction of the right ventricle. ST-segment elevation in right precordial leads, however, is far more reliable in establishing a diagnosis. These leads should be recorded immediately if the standard 12-lead ECG reveals an acute inferior wall MI. Continuous ST-segment monitoring may be useful in the early detection of ongoing right ventricular ischemia. ECG markers can aid in the prompt institution of appropriate treatment. It is clear that early recognition of right ventricular infarction can have important diagnostic and therapeutic implications.     

An increase of BNP levels in massive pulmonary embolism and the reduction in response to the acute treatment

Type B Natriuretic Peptide (BNP) is a neurohormone that is secreted from the cardiac ventricles in response to dilatation or an increase of pressure. Right ventricle dysfunction is seen in pulmonary embolism patients, but it may be hard to diagnose. Echocardiography is the most sensitive means of diagnosis for acute right ventricle dysfunction. However, echocardiography is also limited in some ways. BNP levels may increase with right ventricle dysfunction when the patients is in bed and decrease with treatment. We presented a case study in which diagnosed with mitral valve regurgitation, pulmonary embolism and pregnant for 1.5 months. Initial BNP levels of 633 pg/ml decreased to 233, 65.2, 58.4 levels respectively which was parallel to improvements in the clinical state and right ventricle function detected in echocardiography. We used a rapid bedside test for determination of BNP.     

急性肺血栓栓塞症患者右室长轴应变及应变率变化的初步研究

目的：观察急性肺血栓栓塞症（APTE）患者右室压力负荷增加后右室长轴应变、应变率变化特点,并寻找可能判断右心功能不全的有效参数。方法：采集21例APTE患者及30例健康自愿者心尖四腔切面的二维图像,在组织速度显像（TV I）模式下应用应变、应变率成像技术测量右室游离壁及室间隔的基底段、中间段、心尖段心内膜下心肌收缩期峰值应变、应变率,进行分析研究。结果：APTE患者肺动脉压中度增高后,右室游离壁及室间隔基底段、中间段收缩期应变和应变率代偿性增强,左室收缩功能变化不大,而舒张功能轻度减低;APTE患者肺动脉压重度增高后,右室各节段收缩期应变和应变率较对照组均明显减小,以右室游离壁中间段变化最为明显,同时左室、右室收缩功能均减低。以右室游离壁中间段作为代表节段,以收缩期应变小于-15%,应变率小于-1.2s^- 1作为APTE时右心功能可能失代偿的参考指标。结论：应变、应变率技术是评价急性肺血栓栓塞症患者右室收缩功能变化的一种敏感、有效的方法。     

Anomalous coronary arteries of aortic origin

Anomalous coronary arteries cause only uncharacteristic symptoms and are therefore often an incidental finding during conventional coronary angiography, with an incidence of 0.3-0.8%. The commonest anomaly is an aberrant origin of the main left or right coronary artery from the wrong sinus of Valsalva. Rarely there is a fistula draining into one of the cardiac cavities (right ventricle, right atrium, left ventricle or, rarely, superior vena cava) or displaced connection, as seen in anomalous origin of coronary artery from the pulmonary artery, resulting in a left-to-right shunt. In congenital heart disease, especially Fallot's tetralogy, the incidence of abnormal coronary arteries may be 2% or more. The proximal course in the former category may be misdiagnosed in up to 50% of cases. Aortic root injection with subtraction angiography, further detailed investigation with transoesophageal echocardiography or magnetic resonance angiography are therefore required as these have potential implications on subsequent surgery. Because of the abnormal course between aorta and pulmonary artery/outflow tract of the right ventricle and acute angulation there is a risk of angina, acute myocardial infarction or sudden death during or after exercise. It is therefore important to identify the exact cardiac anatomy, particularly in patients undergoing angioplasty, stenting or cardiac surgery.     

急性右室心肌梗塞的二维超声心动图特征

目的：研究右心室梗塞（ＲＶＩ）的二维超声心动图特征;方法：１０例于发病第一周或第二周的急性右室梗塞患者应用二维超声心动图检查,结果：７例右室下后壁节段异常;４例右室游离壁无运动;３例室间隔运动异常,其中１例矛盾运动,２例运动增强,４例右室扩大,４例右房扩大;同时伴有左室壁节段运动异常。结论：右室梗塞多与左室梗塞并存,在右室壁节段运动异常存在的同时,并有左室壁节段运动异常。     

急性下壁合并右室梗死的早期判断及观察要点

目的 探讨单纯急性下壁心肌梗死和合并右室梗死在临床观察，处理等方面的差异，以便护士及早发现右室梗死先兆，及时采取预防措施。方法 对150例急性下壁心梗的病历进行回顾性研究，并自设问卷了解CCU护士对这一疾病知识的掌握程度。结果 急性下壁合并右室梗死心前区不适发作持续间断时间，发作次数比单纯下壁的长，心电图V2导ST段压低，／aVF导ST抬高≤0．5，以及ST段抬高Ⅲ／Ⅲ＞1是急性下壁合并中室梗死心电图的特征（P＜0．01，P＜0．05），护士对可疑右室梗死时应观察的项目认识不够，缺乏相关的记录。结论 我们应加强对CCU护士专科知识技能的训练。对急性下壁心肌梗死的护理，尤其要掌握观察的内容并给予恰当的护理，以挽救这部分病人的生命。     

Predominant right ventricular infarction in malignant renovascular hypertension in rats

Malignant hypertension was induced in Wistar rats of both sexes by complete aortic ligature just above the origin of the left renal artery. An acute and a late phase of hypertension, 4 days and 28 days after the aortic ligature respectively, were defined to study the relationship between the severity of hypertension and injury of the small arteries and myocardial necrosis. The most frequent finding in the heart was the presence of right ventricular infarction. In acute-phase hypertension most of the animals showed acute infarction of the right ventricle, but only focal left ventricular infarction was found. Lesions in the large coronary arteries were not observed. However, the small arteries and arterioles of the right ventricle presented fibrinoid necrosis lesions. In late-phase hypertension, the intramyocardial small vessels showed proliferative endarteritis and fibrinoid necrosis lesions, but this time they appeared in both ventricles. The severity of the myocardial infarcts and the percentage of small arteries and arterioles injured in the right ventricle were significantly higher than in the left ventricle despite the maintenance of blood pressure almost to the same level. No changes in the right ventricular pressure were observed in either phase. These observations suggest that in malignant renovascular hypertension the intramyocardial arteriolar lesions appear to be an important factor in the production and the severity of myocardial infarcts with predominance in the right ventricle.     

Right ventricular strain in pulmonary embolism by Doppler tissue echocardiography.

For patients with submassive pulmonary embolism, failure of the right ventricle can often be visualized by 2-dimensional echocardiography. We used strain analysis to demonstrate changes in the regional right ventricular free wall performance during the acute and recovery stages of pulmonary embolism.     

Evaluation of the function of the left heart ventricle during the modeling of right ventricular hyperfunction using a pulsatile pump

Left ventricular function was studied in 11 acute experiments on dogs during right ventricular hyperfunction modelling using an artificial heart ventricle (AHV). The right ventricle was excluded from circulation and replaced by AHV. First the baseline condition with regard to the cardiac index was recovered. The right ventricle was considered to be completely functionally replaced when no hemodynamic changes were observed. When the AHV output increased by 26% there were no considerable changes in hemodynamics and the functional condition of the left ventricle remained adequate. If the output was 56% higher certain hemodynamic changes and a tendency towards deterioration of the left ventricular function have been observed. The final stage of the experiments was characterized by twice as high ANV output, as compared to the initial one, which caused considerable hemodynamic changes and greater left ventricular weakness.     

Massive pulmonary embolism with anterolateral ST-segment elevation: electrocardiogram limitations and the role of echocardiogram

Although acute pulmonary embolism (PE) may give rise to certain electrocardiographic (ECG) changes, most of these changes have low sensitivity and specificity and are of limited value alone in the diagnosis. Possible ECG changes with acute PE include S(1)Q(3)T(3) pattern, atrial tachyarrhythmias, incomplete right bundle-branch block, or negative T wave over right and midprecordial leads. Elevation of ST segment is a rare ECG manifestation with PE. We present a case of PE that went unrecognized in the emergency department (ED). The patient presented with anterior chest pain and dyspnea, and ECG showed ST elevation in V3 through V6. The differential diagnosis included acute coronary syndrome and acute pericarditis. Echocardiography revealed dilatation and dysfunction of right ventricle. Emergent computed tomographic pulmonary angiography showed bilateral pulmonary artery thrombosis and confirmed the diagnosis. Thrombolytic therapy with tissue plasminogen activator was initiated, and symptoms subsided dramatically. We proposed that the ST elevation in anterolateral leads might be the reciprocal changes of myocardial strain in the interventricular septum or right ventricle lateral wall. In a patient with such a critical condition and a confusing ECG, echocardiography played an important role in the diagnostic procedure, enabling prompt therapeutic intervention.     

Isolated right ventricular infarction: a rare complication of coronary artery dissection

Infarction of the right ventricle generally occurs in association with posterior left ventricular infarction, and isolated right ventricular infarction is unusual. We have reported a case of acute infarction of the right ventricle unassociated with infarction of the left ventricle in a patient with type I aortic dissection that extended into the right coronary artery, resulting in near-complete occlusion of its lumen. We believe that poor collateral circulation of the myocardium played a major role in the pathogenesis of isolated right ventricular infarction after sudden occlusion of the right coronary artery.     

Protein-losing enteropathy in association with constrictive pericarditis

Although acute pericarditis is a common and usual benign disorder, sometimes evolution to constrictive pericarditis may occur. We present a case of constrictive pericarditis late after coronary bypass grafting, complicated by right sided heart failure. Edema formation was aggravated due to protein-losing enteropathy, resulting in hypoalbuminemia. Imaging of constrictive pericarditis was done by ultrasound as well as simultaneous pressure recording of the right and left ventricle. Imaging of intestinal protein loss was possible using intravenous Technetium-99m-labelled human serum albumin.     

Right ventricular infarction: specific requirements of management.

The principal cause of right ventricular infarction is atherosclerotic proximal occlusion of the right coronary artery. Proximal occlusion of this artery leads to electrocardiographically identifiable right-heart ischemia and an increased risk of death in the presence of acute inferior infarction. Clinical recognition begins with the ventricular electrocardiographic manifestations: inferior left ventricular ischemia (ST segment elevation in leads II, III and aVF), with or without accompanying abnormal Q waves and right ventricular ischemia (ST segment elevation in right chest leads V3R through V6R and ST segment depression in anterior leads V2 through V4). Associated findings may include atrial infarction (PR segment displacement, elevation or depression in leads II, III and aVF), symptomatic sinus bradycardia, atrioventricular node block and atrial fibrillation. Hemodynamic effects of right ventricular dysfunction may include failure of the right ventricle to pump sufficient blood through the pulmonary circuit to the left ventricle, with consequent systemic hypotension. Management is directed toward recognition of right ventricular infarction, reperfusion, volume loading, rate and rhythm control, and inotropic support.     

Thoracic epidural anesthesia impairs the hemodynamic response to acute pulmonary hypertension by deteriorating right ventricular-pulmonary arterial coupling

OBJECTIVE: Thoracic epidural anesthesia is increasingly used in critically ill patients. This analgesic technique was shown to decrease left ventricular contractility, but effects on right ventricular function have not been reported. A deterioration of right ventricular performance may be clinically relevant for patients with acute pulmonary hypertension, in which right ventricular function is an important determinant of outcome. In the present study, we tested the hypothesis that thoracic epidural anesthesia decreases right ventricular contractility and limits its capacity to tolerate pulmonary hypertension. DESIGN: Prospective, placebo-controlled study using an established model of acute pulmonary hypertension. SETTING: University hospital laboratory. SUBJECTS: A total of 14 pigs (mean weight, 35 +/- 2 kg). INTERVENTIONS: After instrumentation with an epidural catheter, biventricular conductance catheters, a pulmonary flow probe, and a high-fidelity pulmonary pressure catheter, seven pigs received thoracic epidural anesthesia and seven pigs served as control. Hemodynamic measurements were performed in baseline conditions and after induction of pulmonary hypertension via hypoxic pulmonary vasoconstriction (Fio2 of 0.15). MEASUREMENTS AND MAIN RESULTS: Ventricular contractility was assessed using load- and heart rate-independent variables. Right ventricular afterload was characterized with instantaneous pressure-flow measurements. In baseline conditions, thoracic epidural anesthesia decreased left but not right ventricular contractility. In untreated animals, pulmonary hypertension was associated with an increase in right ventricular contractility and cardiac output. Pretreatment with thoracic epidural anesthesia completely abolished the positive inotropic response to acute pulmonary hypertension. As a result, ventriculo-vascular coupling between the right ventricle and pulmonary-arterial system deteriorated, and cardiac output was significantly lower in animals with thoracic epidural anesthesia than in untreated controls during hypoxia-induced pulmonary hypertension. CONCLUSIONS: Thoracic epidural anesthesia inhibits the native positive inotropic response of the right ventricle to increased afterload and deteriorates the hemodynamic effects of acute pulmonary hypertension.     

Assessment of the functional state of the right ventricle by radionuclide tomoventriculography

The aim of this work was to evaluate the potential of radionuclide tomoventriculography (RTVG) for the study of the functional state of right ventricle (RV) in patients with thromboembolism of branches of the pulmonary artery (TEPA) or ventricular arrhythmias. A total of 96 patients were admitted for examination to the clinics of Research Institute of Cardiology, Siberian Division of Russian Academy of Medical Sciences in 2006-2008. They were divided into 3 groups. Group 1 (n = 40) included patients of mean age 62 +/- 11 years with non-massive TEPA, group 2 (n = 15) patients with coronary heart disease NYHA class I-II (50 +/- 9 years), group 3 (n = 4) children and adolescents 13.2 +/- 3.7 years with ventricular extrasystole and/or monomorphic ventricular tachycardia. All patients were examined by ECG-synchronized RTVG. The study showed that this method can be used to efficaciously determine volume characteristics of right ventricle, ejection fraction, relationship between fast and slow filling phases, and intreventricular dyssynchronism. The functional ability of the right side of the heart in patients with minor lesions in the pulmonary vasculature should be regarded as a sign of acute thromboembolism and marked systole-diastolic dysfunction of right ventricle (under similar conditions) as a manifestation of chronic post-thromboembolic hypertension. The number of areas of asynchronous myocardial contractions and the degree of intraventricular dyssynchronism detected by RTVG positively correlate with the degree of contractile dysfunction of right ventricle. Scintiographic signs of intraventricular dyssynchronism suggest predominance of contractile heterogeneity of right ventricle over physiological one.     

中心静脉压监测在救治急性右室心肌梗死中的应用价值

目的探讨急性右室心肌梗死扩容治疗时中心静脉压（CVP）应维持的最佳范围。方法将68例急性右室心肌梗死并低血压休克患者采用随机对照的原则分为3组（A组、B组、C组）,3组均予相同的基础治疗,如休息、吸氧、镇静、止痛、抗凝、抗血小板及再灌注治疗,在此治疗的基础上给予扩容治疗,使A组患者CVP维持在6~12 cm H2O,B组患者CVP维持在13-19 cm H2O,C组患者CVP维持在20-26 cm H2O,监测患者的心率、平均动脉压、心输出量、尿量及肺水肿发生率,比较各组疗效。另分别计算出单纯右室心肌梗死与非单纯右室心肌梗死患者的CVP值并进行比较。结果B组和C组在心率、平均动脉压、心输出量、尿量方面均优于A组（P〈0.05）,而B组和C组比较,差异无统计学意义;A组和B组的肺水肿发生率明显低于C组（P〈0.05）,而A组和B组比较,差异无统计学意义;单纯右室心肌梗死组的CVP明显高于非单纯右室心肌梗死组的CVP（P〈0.05）。结论急性右室心肌梗死扩容治疗时中心静脉压（CVP）应维持的最佳范围为13-19 cm H2O。     

The right ventricular myocardium in Ebstein's anomaly: a morphometric histopathologic study.

Ebstein's anomaly of the tricuspid valve is associated with right ventricular dilatation in approximately two-thirds of cases. Dilatation may be massive. It involves not only the right ventricular wall proximal to the tricuspid valve (atrialized ventricle) but also the right ventricle distal to the valve (funtional right ventricle), including the right ventricular infundibulum. For further definition of the pathogenesis of dilatation of the functional right ventricle (distal chamber), a morphometric histopathologic study was performed on 10 hearts with Ebstein's anomaly and 10 normal age-matched control hearts. In the group with Ebstein's anomaly, five hearts exhibited dilated ventricles and five did not. The study demonstrated that dilatation of the right ventricle in Ebstein's anomaly was associated not only with thinning of the wall but also with an absolute decrease in the number of myocardial fibers counted through the thickness of the wall from endocardium to epidcardium.     

右心室-肺动脉耦合在肺动脉高压中的应用进展

肺动脉高压患者的临床预后与右心功能密切相关。病变早期,右心室可通过增加收缩力的方式维持肺循环正常血供,随病情进展,右心室后负荷持续升高,右心室逐渐失代偿,甚至发生右心衰竭。右心室-肺动脉耦合是指右心室收缩力与后负荷之间的匹配关系,耦合受损可作为右心室功能障碍的早期标志。本文就右心室-肺动脉耦合的评估方法及其在肺动脉高压中的应用进展作一综述,以期为临床诊疗提供参考。     

Two-dimensional echocardiographic evaluation of right ventricular size and contractility in acute respiratory failure

Right ventricular size and contractility were evaluated using two-dimensional echocardiography during the first days of respiratory support in 23 patients requiring mechanical ventilation for acute respiratory failure. Nine patients had normal echocardiographic right ventricular function, and nine other patients had a slightly enlarged right ventricle with normal systolic function. The remaining five patients had a severely enlarged right ventricle with abnormal contractile pattern. In these five patients, two-dimensional echocardiography also showed a reduction in left ventricular size suggesting detrimental ventricular interdependence. All 23 patients had normal left ventricular systolic function by two-dimensional echocardiography.