Postcardiotomy right ventricular failure: experience with pulmonary arterial balloon counterpulsation and pulmonary arterial venting

From 1981 through 1985, 3,057 patients underwent cardiac operations using cardiopulmonary bypass (CPB) at our institution. When we reviewed these cases, we found that in ten cases (0.32%) right ventricular or biventricular failure had prevented weaning from CPB. All ten patients were also refractory to pharmacologic intervention and to systemic intraaortic balloon pumping. Two patients had isolated right ventricular failure, and the other eight had biventricular failure. Four patients had had previous pulmonary hypertension. Of the ten patients who could not be weaned, three were treated with pulmonary arterial balloon counterpulsation (PABC), and seven underwent pulmonary arterial venting (PAV). Procedures performed concomitantly with PABC included left heart bypass in one case and creation of an atrial septal defect in another case. All of the PAV group underwent concomitant intraaortic balloon pumping. One PABC patient and four PAV patients could be weaned from CPB. All who were treated with PABC eventually died, but there are three long-term survivors in the PAV group. In light of this study, biventricular unloading with PAV appears to be a valid method of treating right ventricular or biventricular failure.     

Pulmonary (venous) air embolism

Pulmonary (venous) air embolism is a catastrophe which may occur under a variety of circumstances in medical practice. It must be distinguished from arterial air embolism. Our studies in the experimental animal have shown that important factors in determining whether death or survival will occur are: (1) the amount of air which gains admission to the circulation, (2) the speed with which it enters, (3) the position of the body at the time of the embolic accident, and (4) the efficacy of the respiratory excretory mechanism. Death, when it occurs, is due to circulatory obstruction resulting from an air trap in the right ventricular outflow tract. Displacement of the air trap by turning the body into the left lateral position may be life saving even after the right ventricular contractions have become feeble and death seems imminent.Pulmonary air embolism provides a valuable means of studying experimentally the effects of acute right ventricular dilatation produced by obstruction. The rapid and profound electrocardiographic changes which occur under these circumstances include an excellent demonstration of the effects of myocardial ischemia, and also, in some instances, the demonstration of right ventricular conduction defects. The observations of Bayley and LaDue concerning the ischemia-injury pattern are confirmed.     

上腔静脉逆行灌注救治体外循环期间动脉大量气栓(附7例报告)

本文报告７例心脏直视手术体外循环期间动脉大量气栓,经上腔静脉逆行灌注等抢救,４例存活。随防１～６年,３例无永久性中枢神经系统损害。采用的逆灌压力４．０～８．０ｋＰａ,略高于以往文献报道。作者认为：上腔静脉逆行灌注能排除脑血管内气体,再经右心房逆行灌注可排除冠状血管内气体。这对解除或减轻中枢神经系统和心肌损伤、防止严重低心排综合征的发生、增加心脑复苏机会十分重要。应在气栓发生后即刻采用。高压氧可促进脑气栓吸收,增加脑组织氧供,改善脑损伤后遗症。应在病人循环功能稳定后及早进行。     

Incidence and cardiac effects of systemic venous air embolism. Echocardiographic evidence of arterial embolization via noncardiac shunt

Central nervous system dysfunction in venous air embolism may result from air entering the arterial circulation. Using two-dimensional and pulsed-wave Doppler echocardiography, this study not only documented the frequent presence of air in the right heart chambers of patients undergoing upright neurosurgery or pacemaker insertion, but also documented the presence of air in the left atrium and left ventricle of one patient via noncardiac shunt. Studies in dogs confirmed paradoxical air embolism in the absence of anatomic communications between right and left heart chambers. Systemic venous air also produced a dose-dependent increase in pulmonary artery pressure and diastolic flattening of the ventricular septum with increase in left ventricular filling pressure despite preserved systolic function.     

Acute Right Ventricular Failure in the Setting of Acute Pulmonary Embolism or Chronic Pulmonary Hypertension: A Detailed Review of the Pathophysiology, Diagnosis, and Management

The right ventricle (RV) is integral to normal cardiac function, but receives little attention in the medical literature. The etiologic causes of acute RV failure often differ from those encountered in left ventricular dysfunction. Thus, RV failure frequently requires diagnostic procedures and management strategies that differ from those routinely used in the management of intrinsic left ventricular dysfunction. In this summary, the structure and function of the RV will be reviewed, concentrating on the pathophysiologic mechanisms behind the development of RV dysfunction. We will then focus on two distinct populations of patients who are at risk for acute RV failure: those with chronic pulmonary arterial hypertension (PAH) and those with acute pulmonary embolism. In chronic PAH, we will examine clinical circumstances common to hospitalized patients that may provoke acute RV decompensation, as well as pharmacologic therapies that are unique to RV failure management in PAH. Individuals with acute RV failure in the setting of pulmonary embolism represent a group with particularly high mortality, and the specific diagnostic and management strategies that are important for improved survival will be discussed.Key Words: Right ventricular failure, shock, pulmonary hypertension, pulmonary embolism.     

Transoesophageal echocardiography for definitive diagnosis of haemodynamically significant pulmonary embolism

Transoesophageal echocardiographic evaluation of right and leftpulmonary arteries, up to the origin of their lobar branches,was prospectively performed with a single plane probe in 32consecutive patients (18M, 14F, aged 55.5 ± 14.6, from32 to 80 years) with clinical or echocardiographic suspicionof pulmonary embolism, who met transthoracic echocardiographiccriteria of right ventricular overload Transoesophageal echocardiographyshowed unequivocal (20 patients) or suspected (three patients)intraluminar thrombi in 88.5% of 26 patients with haemodynamicallysignificant acute or chronic pulmonary embolism, confirmed withreference methods. The sensitivity of the unequivocal transoesophagealechocardiographic diagnosis was 80% for acute and 73% for chronichaemodynamically significant pulmonary embolism. No false-positiveresults were found (specificity 100%). Additionally, in three cases, transoesophageal echocardiographydisclosed the cause of the right ventricular overload revealinga previously undiagnosed atrial septal defect or Ebstein anomaly. Direct visualization of proximal pulmonary arterial thrombiby transoesophageal echocardiography emerges as a useful newmethod of prompt and definite diagnosis of haemodynamicallyimportant pulmonary embolism.     

Pulmonary embolism: impact of right ventricular dysfunction

PURPOSE OF REVIEW: The appropriate treatment of patients with acute pulmonary embolism who present with right ventricular dysfunction but normal arterial blood pressure, and particularly the potential benefits of thrombolytic treatment in this setting, continue to be highly controversial. In the past year, several well designed studies improved our understanding of subclinical right ventricular dysfunction in pulmonary embolism, and emerging risk stratification algorithms now appear to identify high-risk patients reliably. RECENT FINDINGS: A meta-analysis confirmed that echocardiographically diagnosed right ventricular dysfunction is an independent predictor of early mortality in normotensive patients with pulmonary embolism. Retrospective studies suggest that similar information can also be obtained by multidetector-row chest computed tomography. Recent data indicate that biomarker (particularly troponin) testing followed by echocardiographic imaging of the right ventricle is an efficient and reliable strategy both for excluding (ruling out) and for predicting (ruling in) a poor outcome in patients with pulmonary embolism. SUMMARY: Novel risk stratification algorithms may help identify possible candidates for early thrombolytic treatment in pulmonary embolism and thus provide the background for a large international multicenter study that will hopefully resolve the 30-year-old debate on the benefits of thrombolysis in normotensive patients with pulmonary embolism and right ventricular dysfunction.     

Intensive care unit management of patients with severe pulmonary hypertension and right heart failure

Despite advances in medical therapies, pulmonary arterial hypertension (PAH) continues to cause significant morbidity and mortality. Although the right ventricle (RV) can adapt to an increase in afterload, progression of the pulmonary vasculopathy that characterizes PAH causes many patients to develop progressive right ventricular failure. Furthermore, acute right ventricular decompensation may develop from disorders that lead to either an acute increase in cardiac demand, such as sepsis, or to an increase in ventricular afterload, including interruptions in medical therapy, arrhythmia, or pulmonary embolism. The poor reserve of the right ventricle, RV ischemia, and adverse right ventricular influence on left ventricular filling may lead to a global reduction in oxygen delivery and multiorgan failure. There is a paucity of data to guide clinicians caring for acute right heart failure in PAH. Treatment recommendations are frequently based on animal models of acute right heart failure or case series in humans with other causes of pulmonary hypertension. Successful treatment often requires that invasive hemodynamics be used to monitor the effect of strategies that are based primarily on biological plausibility. Herein we have developed an approach based on the current understanding of RV failure in PAH and have attempted to develop a treatment paradigm based on physiological principles and available evidence.     

Pulmonary Embolism with Right Ventricular Dysfunction: Who Should Receive Thrombolytic Agents?

Background

Appropriate management of pulmonary embolism patients with right ventricular dysfunction is uncertain. Recent guidelines have stressed the need for more data on the use of thrombolytic agents in the stable pulmonary embolism patient with right ventricular dysfunction. The objective of this study is to investigate the hypothesis that thrombolytic therapy in hemodynamically stable pulmonary embolism patients with right ventricular dysfunction is not associated with improved mortality.

Der intensivpflichtige Patient mit Lungenembolie oder arteriellem Gefäßnotfall

Acute pulmonary embolism requires ICU management only for patients with hemodynamic instability who need artificial ventilation, or for hemodynamically stable patients with significant right ventricular dysfunction. For both patient groups, echocardiography is the most relevant diagnostic method. The main therapeutic consideration is on systemic thrombolysis. It is indicated in almost all patients with hemodynamic instability but only in selected cases of right ventricular dysfunction. All other patients receive standard anticoagulation only. A second vascular emergency scenario is type 2 heparin-induced thrombocytopeniae (HIT II) which may cause venous as well as arterial complications. Alternative anticoagulation has to be established from the first moment of clinical suspicion. It has to be continued in a therapeutic dosage if HIT II is confirmed, and has to be stopped if the diagnosis is refuted. The latter case is by far more frequent. Regarding arterial occlusions (acute limb ischemia, acral gangrene, iatrogenic vascular trauma) hints are given for the management in the setting of intensive care.     

Echocardiographic characteristics of venous air embolism presenting as reversible pulmonary atresia in a premature neonate

Air embolism secondary to mechanical ventilation is a rare but well-described complication in premature infants. We describe the echocardiographic appearance of venous air embolism manifesting as acute obstruction of the right ventricular outflow tract in such a premature infant, and review the pathophysiology of acute obstruction of the right ventricular outflow tract secondary to the "air lock" phenomenon. Awareness of the pathophysiology and echocardiographic appearance of venous air embolism may aid in prompt recognition and potential therapy for this lethal complication of mechanical ventilation.     

心脏直视手术心搏骤停26例原因分析及救治体会

对26例（38次）体外循环心脏直视手术中和术后早期心搏骤停病人进行病因分析，总结救治经验。病因有动脉大量空气栓塞、鱼精蛋白过敏性休克、电解质紊乱、严重缺氧、低心排综合征、畸形矫治不良等。主要救治措施：心脏按压、心肺机辅助循环、心血管兴奋药物、上腔静脉及右心房逆行灌注、纠正电解质紊乱等。作者认为要重视镁缺乏导致的心律失常、心搏骤停。对体外循环手术病人，尤其有慢性心功能不全者，围术期应注意补镁、监测血清镁浓度，及时纠正镁缺乏。     

Results of thrombo-endarterectomy of chronic pulmonary embolism

Between 1973 and 1987, 33 patients underwent pulmonary thromboendarterectomy for chronic pulmonary embolism. Twenty-six patients were in Class III of the NYHA Classification, 5 in Class IV with overt right ventricular failure and 2 in Class II. The average pO2 was 60 mmHg under basal conditions without oxygen therapy. The amputation of the pulmonary vascular tree was greater than 50 per cent in all patients. The average systolic pulmonary artery pressure was 70 mmHg. Twenty patients were operated by a lateral thoracotomy without CPB and 6 by sternotomy with CPB under normothermia with or without cardiac fibrillation. The later method avoids having to open the pleura and seemed to give better haemodynamic control. Interruption of the inferior vena cava was systematic in all cases. The global operative mortality was 20 per cent but this seemed to be less in the patients operated by sternotomy under normothermic CPB (no deaths in 6 patients). The authors consider that this technique should be studied in a larger series of patients. Eighteen patients are still being followed up; the clinical and scintigraphic and/or angiographic improvement is clearcut in the majority of cases.     

Acute circulatory failure caused by primary pulmonary hypertension or pulmonary embolism

Patients with acute massive pulmonary embolism or primary pulmonary hypertension may develop acute circulatory failure and are therefore admitted in the intensive care. The mortality rate of patients with pulmonary embolism and shock varies between 25 and 35% whereas the corresponding figure in patients with submassive embolism is less than 10%. Spiral computed tomography may be the most convenient test for diagnosing pulmonary embolism in the setting of acute circulatory failure. In the few patients who remain unstable despite adequate symptomatic treatment, transthoracic echocardiography combined with clinical judgement is appropriate. Inotropic support and thrombolytic therapy are clearly indicated for patients with massive embolism and shock. The role of the latter is more controversial in patients with right ventricular distension and normal blood pressure. The optimal duration of anticoagulant therapy for pulmonary embolism remains to be defined. Most patients are adequately treated with a six-month course of oral anticoagulants. A shorter duration may be sufficient when a transient risk factor is the cause of the initial event whereas patients with cancer or antithrombin deficiency may require a life long treatment. Primary pulmonary hypertension is a much more uncommon disease which can also lead to right ventricular failure. Symptomatic treatment combines oxygen, inotropic drugs, as well as the optimisation of right ventricular filling pressure. Specific treatment includes inhaled nitric oxide or intravenous epoprostenol followed by anticoagulants with either calcium channel blockers in patients responding acutely to vasodilators or a continuous infusion of epoprostenol in those who do not respond to acute challenge or who are not improving with calcium channel blockers. Although the long term survival has markedly improved as a result of epoprostenol treatment, some patients with refractory primary pulmonary hypertension remain candidates for lung transplantation.     

Streptokinase and heparin versus heparin alone in massive pulmonary embolism: A randomized controlled trial

To test the efficacy of thrombolytic therapy in massive pulmonary embolism, we conducted a prospective randomized controlled trial. Eight patients were randomized to receive either 1,500,000 IU of streptokinase in 1 hour through a peripheral vein followed by heparin or heparin alone. All patients had major risk factors for deep vein thrombosis (DVT) and were considered to have high clinical suspicion for pulmonary embolism (PE). At baseline all patients had a similar degree of systemic arterial hypotension, pulmonary arterial hypertension, and right ventricular dysfunction. The time of onset of cardiogenic shock in both groups was comparable (2.25 ±0.5 hours in the streptokinase group and 1.75 ±0.96 hours in the heparin group). The four patients who were randomized to streptokinase improved in the first hour after treatment, survived, and in 2 years of follow-up are without pulmonary arterial hypertension. All four patients treated with heparin alone died from 1 to 3 hours after arrival at the emergency room (p=0.02). Post-thrombolytic therapy the diagnosis of PE was sustained in the streptokinase group by high probability V/Q lung scans and proven DVT. A necropsy study performed in three patients in the heparin group showed massive pulmonary embolism and right ventricular myocardial infarction, without significant coronary arterial obstruction. The results indicate that thrombolytic therapy reduces the mortality rate of massive acute pulmonary embolism.     

High Dose and Short-Term Streptokinase Infusion in Patients with Pulmonary Embolism: Prospective with Seven-Year Follow-Up Trial

Background: High dose and short-term streptokinase infusion has proved to improve survival among few patients with pulmonary embolism and cardiogenic shock, without increasing hemorrhagic complications. However its efficacy and safety in terms of long follow-up and in major number of patients requires to be established. Methods: Patients with pulmonary embolism proved through high probability V/Q lung scan, suggestive echocardiogram, or deep venous thrombosis were enrolled. All were assigned to receive 1,500,000 IU in one-hour streptokinase infusion. The primary end point was efficacy and safety of streptokinase regimen in terms of pulmonary arterial hypertension, right ventricular dysfunction, perfusion abnormalities, recurrence, mortality and hemorrhagic complications. In long-term follow-up, we assessed functional class, recurrence, chronic pulmonary arterial hypertension, postthrombotic-syndrome and mortality. Results: A total of 40 consecutive patients (47.3±15.3 years of age) with large or massive pulmonary embolism were enrolled. In 35 patients high dose and short-term streptokinase regimen reversed acute pulmonary arterial hypertension, clinical and echocardiographic evidence of right ventricular dysfunction and improved pulmonary perfusion without increasing hemorrhagic complications. In acute phase 5 patients died, necropsy study performed in 4 patients showed massive pulmonary embolism and right ventricular myocardial infarction, without significant coronary arterial obstruction. Risk factors for mortality and recurrence were: right ventricular global hypokinesis (p<0.0001), 6 hours or over between onset symptoms and streptokinase regimen (p=0.02), severe systolic pulmonary arterial hypertension (p=0.001) right ventricular hypokinesis (p=0.001), hypoxemia (p=0.02) and right ventricular acute myocardial infarction (p<0.0001). Right ventricular hypokinesis (p=0.02) was the only independent risk factor for recurrence. In a seven-year follow-up of the original 35 patients who survived in acute phase, 2 patients were lost and 33 are alive, in functional class I, without recurrence or chronic pulmonary arterial hypertension. Conclusions: Our report indicates that among properly selected high-risk PE patients, short-term streptokinase infusion is effective and safe.     

Cerebral air embolism as a complication of computed tomography-guided marking of the lung: depiction of air inflow route from a pulmonary vein to the left atrium

Air embolism in the arterial system is a very rare but potentially fatal complication of percutaneous transthoracic needle biopsy or marking. We report a case of a patient with interstitial pneumonia associated with Sj?gren syndrome, who presented with systemic arterial air embolism as a complication of computed tomography-guided marking of the lung. The air inflow route was depicted clearly on computed tomography from the peripheral pulmonary vein that crossed the needle pathway to the left atrium.     

Entropy score, patent ductus arteriosus (PDA), and cardiopulmonary bypass (CPB): ligation of PDA on CPB can compromise cerebral blood flow

A patent ductus arteriosus (PDA) is often present in patients undergoing correction of congenital heart disease. It is well appreciated that during cardiopulmonary bypass (CPB), a PDA steals arterial inflow into pulmonary circulation, and may lead to systemic hypoperfusion, excessive pulmonary blood flow (PBF) and distention of the left heart. Therefore, PDA is preferably ligated before initiation of CPB. We describe acute decreases of arterial blood pressure and entropy score with the initiation of CPB and immediate increase in entropy score following the PDA ligation in a child undergoing intracardiac repair of ventricular septal defect and right ventricular infundibular stenosis. The observation strongly indicates that a PDA steals arterial inflow into pulmonary circulation and if the PDA is dissected and ligated on CPB or its ligation on CPB is delayed the cerebral perfusion is potentially compromised.     

肺动脉血栓切除术治疗急性危重肺动脉栓塞症-单中心45例报告

目的 探讨肺动脉血栓切除术在急性危重肺动脉栓塞症（Pulmonary embolism,PE）治疗中的作用。方法 收集了我院2010年-2018年行肺动脉血栓切除术的45例急性危重PE患者的临床资料,比较患者术前、术后及随访期间的心脏彩超右心室直径、右心房直径、三尖瓣返流压差、肺动脉直径,比较术前、术后的动脉血氧分压（PaO2）、动脉血氧饱和度（SaO2）。结果 45例急性危重PE患者中3名术前心脏骤停的患者术后因严重缺血缺氧性脑病、多器官功能衰竭死亡或放弃治疗。其余42例病人均存活,随访期间无死亡病例（存活率93.3%,中位随访时间32月）。术后患者的PaO2、SaO2均高于术前（P<0.05）;术后、随访期间末次超声的右心房直径、右心室直径、三尖瓣返流压差、肺动脉直径均较术前明显减小（P<0.05）。结论 对于急性危重PE患者,肺动脉血栓切除术是一种安全的手术方式,死亡率低,可显著改善患者右心室功能及肺动脉压力,中远期效果良好。对于大面积肺动脉栓塞的危重患者,应该更为积极的考虑进行肺动脉血栓切除术。     

CentriMag left ventricular assist system: cannulation through a right minithoracotomy

The CentriMag left ventricular assist system can be used for perioperative or postcardiotomy circulatory support of the failing heart. The device resides at the patient's bedside, and the cannulae are usually inserted through a midline sternotomy, with the inflow cannula in the left ventricle or right superior pulmonary vein and the outflow cannula in the aorta. In a patient whose chest has been closed and who has a delayed need for temporary mechanical support, a less invasive method of left ventricular assist device cannula insertion is preferred. In these cases, the CentriMag cannulae can be inserted through a right minithoracotomy with the inflow cannula in the right superior pulmonary vein and the outflow cannula in the aorta, with no heparinization. Herein, we describe this approach in a patient who experienced postcardiotomy cardiogenic shock after aortocoronary bypass surgery. This technique may facilitate ambulation and recovery in selected patients.