Episodes Of Acute Pulmonary Edema Research Articles

Abstract 11693: When a Parachute Fails: A Rocky Landing to Heart Transplant

A 71 year-old man with heart failure, porcelain aorta, and mitral regurgitation presented for heart transplant evaluation. He was in cardiogenic shock requiring inotropic support. An echocardiogram showed a dilated left ventricle, severely reduced systolic function, restricted mitral valve leaflet motion, an elevated mean transmitral gradient, and severe mitral regurgitation. The differential of mixed stenotic and regurgitant mitral valve pathology included rheumatic heart disease and congenital mitral valve anomaly. Hemodynamic management of cardiogenic shock in the setting of mixed mitral valve disease presented unique challenges due to a narrow therapeutic window of optimal preload, afterload reduction, inotropic support, and chronotropic control. He was not a candidate for percutaneous mitral valve interventions or surgery. A porcelain aorta made him high risk for vascular complications with mechanical circulatory support. His course was complicated by worsening shock requiring escalation of inotropes, rapid atrial fibrillation, and recurrent episodes of acute pulmonary edema. Ultimately, he underwent an orthotropic heart transplant. A transesophageal echocardiogram at the time of transplant suggested a parachute mitral valve, where all chordae appeared be originating from one papillary muscle. However, additional views revealed the presence of two papillary muscles with asymmetric, shortened anterior chordae and a hypertrophied anterior papillary muscle. Findings were consistent with a rare parachute-like asymmetric mitral valve complicated by mild mitral stenosis and severe mitral regurgitation. Examination of the explanted native heart confirmed these findings.This case highlights: 1) complex management of mixed valvular disease in the setting of cardiogenic shock, 2) echocardiographic evaluation of mixed valvular heart disease, and 3) a rare congenital malformation of a parachute-like mitral valve presenting in adulthood.

Systemic Markers of Monocyte Activation in Acute Pulmonary Oedema

Hydrostatic lung injury followed by pulmonary remodelling variably complicates cardiogenic acute pulmonary oedema (APO). Pulmonary remodelling may be regulated by the balance between distinct phenotypes of pulmonary macrophages; activated/inflammatory (M1), and reparative/anti-inflammatory (M2), derived from circulating monocyte populations. The aim of this study was to identify biomarkers in peripheral blood that are consistent with hydrostatic lung injury and pulmonary remodelling in APO and which follow the variable clinical course. To examine peripheral markers of lung inflammation, resolution and remodelling, 18 patients, admitted to the intensive care unit (ICU) with a clinical diagnosis of APO, were enrolled. Admission, 12- and 24-hour post-admission bloods were assayed for cytokines by ELISA (R&D Systems, Minneapolis, MN, USA) and leukocyte surface markers by flow cytometry. Admission PaO2 to FiO2 ratio was positively correlated with Mon 2 (intermediate) monocyte prevalence, through increasing ratio of CD16+ monocytes to CD11b+ and CD40+ monocytes, and negatively correlated with Mon 1 (classical) monocyte prevalence, through decreasing ratio of CD16+ monocytes to CD62L+. Secondary cohort analysis compared 10 APO patients with established chronic heart failure (CHF) to eight without CHF. An increase in monocyte chemotactic peptide (MCP)-1, monocyte prevalence, and CD16-CD62L+ monocytes with CHF, all characteristic of monocyte activation to a Mon 1 phenotype, were found in the CHF APO patients. Increased systemic monocyte prevalence and expression of cell surface markers suggest a Mon 1 profile in CHF patients during episodes of APO. Future studies should define the role of systemic monocyte prevalence and activation in decompensated CHF.

Eclipsed mitral regurgitation successfully treated with a combination of surgical and pharmacological therapies: a case report.

BackgroundEclipsed mitral regurgitation (MR), which is characterized by a transient and reversible massive functional MR, usually causes recurrent episodes of acute pulmonary oedema in patients with a preserved left ventricular ejection fraction. The pathophysiological mechanism and optimal treatment of eclipsed MR are not yet fully understood.Case summaryA 72-year-old woman was hospitalized with cardiogenic shock and takotsubo cardiomyopathy. After hospitalization worsening dyspnoea again appeared, and urgent transthoracic echocardiography revealed severe MR, which spontaneously resolved in a few minutes. At this point, eclipsed MR was detected for the first time. Diagnostic examination revealed that the eclipsed MR was caused by a left ventricular afterload increase. Ultimately, the patient began medical therapy and underwent mitral valve replacement. The subsequent clinical course was favourable.DiscussionThis case illustrates the importance of early intervention for eclipsed MR. A combination of surgical and pharmacological therapies can serve as one treatment option for an eclipsed MR.

Chronic Atrial Fibrillation Ablation with Harmonic Scalpel during Mitral Valve Surgery.

ObjectiveTo evaluate surgical treatment of chronic atrial fibrillation with ultrasound in patients with mitral valve disease, considering preoperative clinical characteristics of patients undergoing surgical procedure and follow-up in the immediate postoperative period, in hospital and up to 60 months after discharge.MethodsWe studied 100 patients with chronic atrial fibrillation and mitral valve disease who underwent surgical treatment using ultrasound ablation. Patient data were reviewed by consulting the control reports, including signs and symptoms, underlying disease, functional class, hospital stay, surgical procedure time, ablation time, immediate complications, and complications at discharged and up to 60 months later. Actuarial curve (Kaplan-Meier) was used for the study of permanence without recurrence after 12, 24, 36, 48 and 60 months.Results86% of the patients had rheumatic mitral valve disease, 14% had degeneration of the mitral valve, 40% had mitral regurgitation, and 36% had mitral stenosis. Main symptoms included palpitations related to tachycardia by chronic atrial fibrillation (70%), congestive heart failure (70%), and previous episodes of acute pulmonary edema (27%). Early results showed that 94% of the patients undergoing ultrasound ablation reversed the rate of chronic atrial fibrillation, 86% being in sinus rhythm and 8% in atrioventricular block. At hospital discharge, maintenance of sinus rhythm was observed in 86% of patients and there was recurrence of chronic atrial fibrillation in 8% of patients. At follow-up after 60 months, 83.8% of patients maintained the sinus rhythm.ConclusionSurgical treatment of chronic atrial fibrillation with ultrasound concomitant with mitral valve surgery is feasible and satisfactory, with maintenance of sinus rhythm in most patients (83.8%) after 60 months of follow-up.

Recurrent non-st elevation myocardial infarction: An unusual cause

Pheochromocytoma is a rare, catecholamine-secreting tumor derived from chromaffin cells. It usually presents with palpitations, diaphoresis, headache, and paroxysmal hypertension. Rarely, it may associate with acute myocardial infarction (MI) and other cardiovascular complications. Here, we are reporting a case of a 40-year-old male with adrenal pheochromocytoma presented with a history of repeated episodes of acute pulmonary edema along with electrocardiographic changes and serum cardiac marker elevation, suggestive of MI, with complete reversal of these abnormalities after surgical removal of the tumor.

Complications Associated With Nitrate Use in Patients Presenting With Acute Pulmonary Edema and Concomitant Moderate or Severe Aortic Stenosis

We evaluate the incidence of complications associated with the use of nitrates in patients presenting with acute pulmonary edema and concomitant moderate or severe aortic stenosis compared with patients without aortic stenosis. Nitrates are contraindicated in severe aortic stenosis because of the theoretical yet unproven risk of precipitating profound hypotension. A cohort design with retrospective chart review study was conducted at two Canadian hospitals. Patients with aortic stenosis (moderate or severe) and without aortic stenosis were included if they presented with acute cardiogenic pulmonary edema, received intravenous or sublingual nitroglycerin, and had an echocardiography report available. The primary outcome was clinically relevant hypotension, defined as hypotension leading to any of the following predefined events: nitroglycerin discontinuation, intravenous fluid bolus, vasopressor use, or cardiac arrest. The secondary outcome was sustained hypotension, defined as a systolic blood pressure less than 90 mm Hg and lasting greater than or equal to 30 minutes. The cohort consisted of 195 episodes of acute pulmonary edema, representing 65 episodes with severe aortic stenosis (N=65) and an equal number of matched episodes with moderate aortic stenosis (N=65) and no aortic stenosis (N=65). Nitroglycerin was administered intravenously only in 70% of cases, intravenously and sublingually in 25%, and sublingually only in the remaining 5%. After adjustment for sex, initial systolic blood pressure, furosemide dose, and use of noninvasive ventilation, moderate and severe aortic stenosis were not associated with clinically relevant hypotension after receipt of nitroglycerin (adjusted odds ratio [OR] 0.97, 95% confidence interval [CI] 0.40 to 2.37 for moderate aortic stenosis; adjusted OR 0.99, 95% CI 0.41 to 2.41 for severe aortic stenosis). The incidence of clinically relevant hypotension was 26.2% for moderate and severe aortic stenosis and 23.1% in the no aortic stenosis reference group. The secondary outcome of sustained hypotension occurred in 29.2% of patients with severe aortic stenosis, 16.9% with moderate aortic stenosis, and 13.8% in the no aortic stenosis group (adjusted OR for severe aortic stenosis 2.34; 95% CI 0.91 to 6.01). In this retrospective study, neither moderate nor severe aortic stenosis was associated with a greater risk of clinically relevant hypotension requiring intervention when nitroglycerin was used for acute pulmonary edema. Future studies should investigate safety and efficacy of nitroglycerin for patients with aortic stenosis because this study was limited by a small sample size and design limitations. Cautious use of nitroglycerin in patients with moderate or severe aortic stenosis and presenting with acute pulmonary edema may be a safer strategy than traditionally thought.

Coexistence of dynamic mitral regurgitation and dynamic left ventricular dyssynchrony in a patient with repeated episodes of acute pulmonary edema: Improvement with cardiac resynchronization therapy

A 69-year-old woman with idiopathic dilated cardiomyopathy and chronic heart failure experienced repeated hospital admissions for acute pulmonary edema with no recognizable precipitating factor. Worsening mitral regurgitation was triggered by exercise echocardiography and significant intraventricular dyssynchrony was elicited by low-dose dobutamine stress echocardiography. After cardiac resynchronization therapy she remained free of hospitalizations for 12 months. This case highlights the dynamic nature of both functional mitral regurgitation and left ventricular dyssynchrony and illustrates how in some patients stress echocardiography can help to clarify clinical scenarios and help with the challenging task of selecting patients who will benefit from cardiac resynchronization therapy.

Coexistence of dynamic mitral regurgitation and dynamic left ventricular dyssynchrony in a patient with repeated episodes of acute pulmonary edema: Improvement with cardiac resynchronization therapy

A 69-year-old woman with idiopathic dilated cardiomyopathy and chronic heart failure experienced repeated hospital admissions for acute pulmonary edema with no recognizable precipitating factor. Worsening mitral regurgitation was triggered by exercise echocardiography and significant intraventricular dyssynchrony was elicited by low-dose dobutamine stress echocardiography. After cardiac resynchronization therapy she remained free of hospitalizations for 12 months. This case highlights the dynamic nature of both functional mitral regurgitation and left ventricular dyssynchrony and illustrates how in some patients stress echocardiography can help to clarify clinical scenarios and help with the challenging task of selecting patients who will benefit from cardiac resynchronization therapy.

Paramedic Identification of Acute Pulmonary Edema in a Metropolitan Ambulance Service

Introduction. Acute pulmonary edema (APE) is a common cause of acute dyspnea. In the prehospital setting, it is often difficult to differentiate APE from other causes of shortness of breath (SOB). Radiography and echocardiography aid in the identification of APE but are often not available. There is little information on how accurately ambulance paramedics identify patients with APE. Objectives. This study aimed to 1) describe the prehospital clinical presentation and management of patients with a clinical diagnosis of APE and 2) compare the accuracy of coding of APE by paramedics against the emergency department (ED) medical discharge diagnosis. Methods. This study included a retrospective cohort of all patients who had episodes identified as APE by ambulance paramedics and were transported to a metropolitan hospital ED in 2011. Two databases were used: an ambulance database and the Emergency Department Information System. The ED medical discharge diagnosis (using International Statistical Classification of Diseases and Related Problems, 10th Revision, Australian Modification [ICD-10-AM] codes) was used as the comparator with paramedic-assigned problem codes for APE. The outcomes for the study were the positive predictive value, i.e., the proportion of patients identified as having APE in the ambulance database who also had an ED discharge diagnosis of APE, and the sensitivity of paramedic identification of APE, i.e., the proportion of patients with an ED discharge diagnosis of APE that were correctly identified as APE by the ambulance paramedics. Results. Four hundred ninety-five patients were transported to an ED with APE identified by the paramedics as the primary problem code. Shortness of breath, crepitations, high systolic blood pressure, and chest pain were the most common presenting signs and symptoms. Pink frothy sputum was rare (3% of patient episodes of APE). One hundred eighty-six patients received an ED discharge diagnosis of APE, i.e., a positive predictive value of 41%. Of 631 ED presentations with APE, paramedics identified 186, i.e., a sensitivity of 29%. Conclusion. Acute pulmonary edema is difficult to identify in the prehospital setting because of the variability in the signs and symptoms associated with this condition. Improved identification of APE is essential in the initiation of appropriate and timely care. Ambulance paramedics need to be aware of such variability when considering patients who may be suffering from APE. Key words: pulmonary edema; acute pulmonary edema; emergency medical services; ambulance; paramedics

The value of using fractional flow reserve measurements in helping to diagnose acute left ventricular failure in the presence of normal left ventricular systolic function

1. Case history A 57-year-old female smoker with a longstanding history of hypertension and diabetes presented to hospital with sudden onset of severe breathlessness in the absence of chest pain. Examination revealed sinus tachycardia, hypertension (blood pressure 200/120) and pulmonary oedema. Routine blood investigations and 12-h troponin measurements were normal, and a diagnosis of acute decompensated heart failure secondary to hypertensive crisis was made. She was treated with diuretics and betablockers and made a good recovery. Transthoracic echocardiography demonstrated left ventricular hypertrophy with preserved left ventricular systolic function and Grade 2 diastolic dysfunction. Renal ultrasound confirmed structurally normal kidneys with no evidence of renal artery stenosis. The patient was able to exercise to Stage 3 of a standard Bruce protocol exercise test without symptoms or electrocardiographic changes and subsequent coronary angiography demonstrated a 50% tubular stenosis of the proximal left anterior descending (LAD) artery and 60% stenoses of the mid LAD and origin of the second diagonal (D2) (Fig. 1). Consequently, moderate non-flowlimiting coronary disease was diagnosed, and the patient was discharged with appropriate medical therapy. Unfortunately, the patient re-presented on three subsequent occasions with further episodes of acute pulmonary oedema. The haemodynamic significance of the LAD disease was therefore reassessed, with additional measurements of fractional flow reserve (FFR). This revealed an FFR of 0.71 distal to the mid LAD bifurcation. The D2 and LAD/ D2 bifurcation was therefore stented resulting in a post-stent FFR of 0.85 with a pressure “jump” of 0.08 over the proximal vessel on pull-back (Fig. 2). This led to an additional stent being deployed at the site of the proximal LAD stenosis with complete restoration of flow and perfusion in the distal LAD and a post-stent FFR of 0.9 in the distal LAD. Following discharge the patient has remained well and over 18 months, there have been no further episodes of acute pulmonary oedema.

Rheumatic mitral valve disease in pregnancy

A 32-year-old Nepalese woman with known rheumatic mitral valve disease presented 17 weeks into her first pregnancy with exertional breathlessness and wheezing, leading to expectoration of foamy pink liquid. Her history included percutaneous balloon mitral valvotomy at the age of 25 years, after which she had remained asymptomatic and fully active. She had three episodes of acute pulmonary oedema and was transferred to a tertiary centre for further management. An echocardiogram suggested severe mitral stenosis (mitral valve area 1.0 cm2) and pulmonary hypertension (mean pulmonary artery pressure 87 mmHg). She had further episodes of pulmonary oedema despite maximal medical therapy with diuretics, cardioselective beta blockers (dose limited because of systolic hypotension), digoxin, nitrates and anticoagulation. At 21 weeks' gestation, an emergency St Jude metallic valve was implanted. Unfortunately, intrauterine death occurred 2 days postoperatively, likely caused by pre-eclampsia or haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome. The patient recovered well and continues on warfarin and a small dose of beta blocker.

Recurrent Severe Acute Pulmonary Edema Caused by Transient Left Ventricular Insufficiency With Mitral Regurgitation Related to Severe Coronary Artery Spasm

A 64-year-old diabetic and dyslipidemic woman was admitted to our hospital with a history of 3 episodes of acute pulmonary edema in the past 4 months, without evidence of organic heart disease. She was affected by a hypopituitarism and was treated with levothyroxine and desmopressin. She had atypical chest pain 1 year before, but 2 exercise stress tests were negative. In the past 4 months, she had been admitted 3 times for severe dyspnea at rest of sudden onset without chest pain, requiring endotracheal intubation because of severe acute pulmonary edema. Basal physical examination was normal. ECGs and serial troponin levels were normal. Clinical treatment was successful with early extubation. Echocardiography (echo) at rest was completely normal with normal left ventricular systolic and diastolic function and no valvular regurgitations. Coronary angiography revealed normal coronary arteries and normal global and regional left ventricular systolic motion. Thoracoabdominal computerized tomography was normal; and pulmonary thromboembolism, aortic disease, and suprarenal tumor were ruled out. Pulmonary biopsy also was normal. Laboratory tests including hemoglobin, electrolytes, autoantibodies, catecholamine, and thyroid hormones were also normal. Holter and telemetry did not reveal arrhythmias. Gated single-photon emission computed tomography and stress echo were negative for ischemia. Most of …

Recurrent acute pulmonary oedema after aortic and mitral valve surgery due to trachea malacia and obstructive sleep apnoea syndrome.

In this report we describe a patient with recurrent episodes of acute pulmonary oedema after aortic and mitral valve surgery. The first episode of pulmonary oedema was caused by mitral valve dysfunction. The second episode of pulmonary oedema was not clearly associated with a mitral valve problem, but reoperation was performed in the absence of another explanation. After the third episode of acute pulmonary oedema occurred, the diagnosis of obstructive sleep apnoea syndrome (OSAS) was considered and confirmed. After starting treatment with continuous positive airway pressure (CPAP) during his sleep the patient had no further episodes of acute respiratory failure. Our case demonstrates that acute pulmonary oedema after cardiothoracic surgery can be caused or at least be precipitated by OSAS and should be suspected in patients with unexplained episodes of (recurrent) pulmonary oedema. (Neth Heart J 2008;16:310-2.).

Induction immunosuppression after heart transplantation: monoclonal vs. polyclonal antithymoglobulins. Is there a difference?

Induction immunosuppression after heart transplantation is believed to reduce the risk of acute graft rejection. While monoclonal and polyclonal antithymoglobulins are considered the optimal induction agents, controversy remains regarding their relative superiority. This article presents a systematic review of the literature and a meta-analysis in order to assess the relative benefits and side-effects of monoclonal vs. polyclonal antithymoglobulins as induction immunosuppression agents. Pooled analysis demonstrated a small but statistically insignificant difference in the average time to first rejection between the groups (6.7+/-15.5 days, P=0.39). No statistically significant differences in the proportion of patients who developed rejection or infection episodes at 6 months were observed (Relative Risk 0.97, P=0.82 and Relative Risk 0.85, P=0.14, respectively). In addition, no statistically significant difference in survival was found between the groups at 6 months (Relative Risk 0.98, P=0.58). A greater number of drug related side-effects was observed, however, in the monoclonal group, including episodes of acute pulmonary edema and hypotension. In conclusion, this review revealed no statistically significant differences in rejection, infection, or survival rates between the monoclonal and polyclonal groups. The increased rate of side-effects with monoclonal antibodies might suggest a superiority of polyclonal over monoclonal antibodies.

Outcome of renal transplantation in children with pericardiopleural effusion

Introduction Children with end-stage renal disease may present with pericardiopleural effusion secondary to volume overload and overhydration. The present study was designed to investigate the efficacy and safety of renal transplantation in these pediatric patients. Methods From 1981 to 2001, six of 20 patients (30%) under 18 years old who received renal transplants showed pericardiopleural effusion after serial pretransplant imaging studies. These patients also displayed associated diseases, such as congestive heart failure ( n = 3), ascites ( n = 2), and splenomegaly ( n = 2). The recipients included five boys and one girl of mean age of 12.7 years (range, 8 to 17 years), all of whom had undergone hemodialysis before transplantation. The waiting time for grafts ranged from 1.3 to 6 years (mean = 2.6 years). Episodes of acute pulmonary edema had been observed in three patients pretransplant. Results One recipient died with a functioning graft due to heart failure with acute pulmonary edema at 4 months after transplantation. Acute rejection episodes were observed in three, and chronic rejection in two children. The median follow-up was 11 years (range = 6 to 16 years) in the other five recipients, all of whom presently survive with functioning grafts. The posttransplant mean serum creatinine levels at 1 year, 3 years, and 5 years were 1.54 ± 0.44, 1.74 ± 0.56, and 1.92 ± 0.56 mg/dL, respectively. Conclusion Renal transplantation in children displaying pericardiopleural effusion was associated with a high success rate. However, these patients must be followed closely with regular cardiopulmonary evaluation since their condition may deteriorate.

Transplant Renal Artery Stenosis Presenting with Recurrent Acute Pulmonary Edema

Renal artery stenosis of the transplant kidney occurs in approximately 6% of renal allograft recipients. Severe bilateral renal artery stenosis and unilateral renal artery stenosis to a single functioning kidney have been described as causes of recurrent pulmonary edema in nontransplant patients with normal cardiac function. We report 2 patients with severe transplant renal artery stenosis who presented with recurrent episodes of acute pulmonary edema. Successful revascularization in 1 patient prevented the recurrence of pulmonary edema. In renal allograft recipients who present with unexplained recurrent episodes of acute pulmonary edema, who do not have an obvious cardiac cause, transplant renal artery stenosis should be considered as a possible etiology.

Pathophysiology of Dynamic Cardiomyoplasty: A Clinico-Pathological Case Study

A 58-year-old man with end-stage ischemic cardiomyopathy underwent dynamic cardiomyoplasty. "On" and "off" studies with the cardiac assist device failed to show any significant hemodynamic changes despite improvement in functional status. The patient's late postoperative course was complicated by two episodes of acute pulmonary edema followed by cardiac arrest. These events were precipitated by ventricular tachycardia. The last episode led to myocardial infarction requiring diastolic counterpulsation and inotropic support. He died 4 1/2 months following the cardiomyoplasty. Postmortem findings revealed an anterior left ventricular infarct with aneurysm. There was fusion of skeletal muscle to the epicardium with minimal fibrosis and atrophy. The latissimus dorsi (LD) flap was viable, but myofibrillar ATPase stain revealed incomplete transformation. Several clinical observations have emerged from the early experience with dynamic cardiomyoplasty: (1) Important arrhythmias and cardiac arrest compromise the vascular supply and thus power of the muscular flap; (2) Resting ejection fraction does not correlate with exercise tolerance, therefore, other parameters must be sought to explain improved functional status; (3) Uniform muscle transformation in humans may be unpredictable with current clinical stimulation protocols. The conformation of LD to the epicardium underscores a potential remodeling phenomenon which may ultimately spare the diseased myocardium by altering its oxygen supply/demand ratio and thus the natural history.

Prevention of Acute Pulmonary Edema after Bone Marrow Transplantation

In a retrospective review of 21 bone marrow transplantation procedures (BMT), we identified ten episodes of acute pulmonary edema coinciding with significant weight gain in the second week after BMT. When we prospectively observed nine consecutive BMT recipients, six patients developed acute pulmonary edema associated with significant (p less than 0.05) weight gain and an increase in echocardiographically determined left ventricular end diastolic diameter. These findings led to a prospective prophylactic intervention study of 30 consecutive BMT patients. Prophylactic intervention consisting of reduced fluid volume of parenteral alimentation, and diuretic therapy was instituted at any clinical sign of fluid overload. No episode of pulmonary edema occurred. The dramatic difference--acute pulmonary edema occurred in 16/30 untreated vs 0/30 treated cases--suggests that this post-BMT complication is critically related to fluid balance and can be prevented by careful clinical examination, close monitoring of weight change, avoidance of fluid overload and the appropriate use of diuretic therapy.

Acute Pulmonary Edema of Altitude

Three separate episodes of acute pulmonary edema are described that developed in two otherwise healthy individuals during heavy exertion at high altitudes. Detailed physical examination and laboratory studies failed to demonstrate pulmonary infection or cardiac disease. Data obtained by cardiac catheterization during one of these episodes revealed elevation of the pulmonary artery pressure and a normal left atrial pressure. This syndrome appears to be the consequence of pulmonary vascular obstruction distal to the capillary bed, presumably in the pulmonary veins. It is brought about by exposure of susceptible individuals to high altitudes, and is completely reversed by oxygen administration.