Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema.

Nifedipine induces vascular smooth muscle relaxation through a calcium antagonistic action. The possibility of clinical use of the drug as a ventricular unloading agent has been explored in this study. In patients with hypertensive (seven cases), primary (seven cases) or rheumatic (aortic insufficiency five cases, mitral regurgitation five cases) cardiac disease, nifedipine, administered in a single sublingual dose (10 mg), relieved acute pulmonary edema. Circulatory variations from control were the following: decrease of systemic and pulmonary arterial pressures, and of vascular resistances, of pulmonary wedge pressure, of left ventricular diastolic and systolic dimensions (echocardiography); increase of cardiac and stroke index, of left ventricular mean rate of circumferential fiber shortening, of left and right mean pre-ejection delta P/delta t and mean rate of ejection; improvement of forward output in primary and rheumatic disease. Nifedipine benefits acute congestive heart failure by sustained fall of both preload and afterload and, possibly, by an enhanced contractility. It seems to have an appropriate indication in cases in which left ventricular afterload reduction is desirable.     

Mechanisms of action of morphine in the treatment of experimental pulmonary edema

The hemodynamic effects of morphine were correlated with the course of acute pulmonary edema in 18 dogs. Pulmonary edema was produced by various technics designed to simulate the clinical cardiovascular disorders in which pulmonary edema most commonly occurs. Morphine (0.5 mg./kg.) resulted in subsidence of pulmonary edema in all animals, and improvement was concomitant with striking and parallel decreases in pulmonary arterial flow and pressure and in left atrial and left ventricular enddiastolic pressures.

Total pulmonary vascular resistance was measured before and after morphine administration in 12 normal dogs. A preparation was utilized in which left atrial pressure and pulmonary and systemic arterial flows were maintained constant. A slight to moderate decrease in resistance usually occurred, but the changes were variable and not of significance.

The experiments indicate that the beneficial effects of morphine in pulmonary edema may be principally attributed to the effects of the drug on the capacitance vessels of the peripheral circulation. Capacity of the peripheral vascular bed is increased, systemic venous return is reduced, and improvement results from a “pharmacologic phlebotomy.”     

A comparison of nesiritide vs. epoprostenol in a patient with precapillary pulmonary hypertension due to scleroderma complicated by postcapillary pulmonary hypertension

To the best of our knowledge, acute decompensated left-sided heart failure with preserved left ventricular ejection fraction in a patient with scleroderma has not been previously reported. We describe a patient with severe pulmonary hypertension due to limited scleroderma in whom nesiritide led to marked reductions in pulmonary arterial and capillary wedge pressure as well as resolution of symptoms and pulmonary edema. Subsequent epoprostenol use was associated with an increase in pulmonary capillary wedge pressure and a recurrence of pulmonary edema. Thus, nesiritide may be the preferred agent in scleroderma patients with severe pulmonary hypertension and preserved left ventricular systolic function since epoprostenol may lead to adverse hemodynamic effects.     

A 64-year old man who sustained many episodes of acute cardiogenic pulmonary edema successfully treated with Boussignac continuous positive airway pressure: a case report

Continuous positive airway pressure (CPAP) is standard treatment for patients with acute cardiogenic pulmonary edema. We describe a patient who had 21 episodes of acute cardiogenic pulmonary edema due to very poor patient compliance. This 64-year old man had end-stage congestive heart failure based on systolic left ventricular dysfunction following two myocardial infarctions. In addition to routine medical treatment 15 episodes of pulmonary edema were successfully treated with Boussignac continuous positive airway pressure (BCPAP). The BCPAP system is a simple, disposable, FDA-approved device that delivers positive pressure without a ventilator. This extraordinary case underscores the utility of the BCPAP system to avoid repeated intubation and mechanical ventilation in patients with cardiogenic pulmonary edema.     

无创双水平正压通气治疗急性左心衰竭15例疗效观察

目的 对经鼻面罩双水平正压通气在急性心源性肺水肿的临床疗效进行观察。方法15例均为危重急性左心衰竭发作，在常规治疗基础上，加用无创机械通气治疗，观察病情好转率。结果 应用无创机械通气治疗的患者，病情好转11例(70％)，2例死亡，气管插管2例。结论 经鼻面罩双水平正压通气治疗重度急性左心衰竭疗效显著。     

Quantitative two-dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement

In 14 patients requiring aggressive therapy for circulatory failure resulting from massive pulmonary embolism, hemodynamic and two-dimensional echocardiographic data were obtained at bedside (acute phase) and again after circulatory improvement (intermediate phase) and during recovery. The acute stage was characterized by a low cardiac output state despite inotropic support (cardiac index 1.9 +/- 0.6 liters/min per m2) associated with increased right atrial pressure (12.4 +/- 4.2 mm Hg), increased right ventricular end-systolic and end-diastolic area (12.4 +/- 3.4 and 15.4 +/- 4.1 cm2/m2, respectively) and reduced right ventricular fractional area contraction (20.1 +/- 8.6%). Two-dimensional echocardiography also revealed interventricular septal flattening at both end-systole and end-diastole and markedly decreased left ventricular end-diastolic dimensions. Left ventricular fractional area contraction remained normal. Hemodynamic improvement occurred during the intermediate phase as shown by restoration of cardiac index (3.3 +/- 0.6 liters/min per m2), decrease in right atrial pressure (8.3 +/- 4.8 mm Hg), reduction in right ventricular end-systolic area (9.0 +/- 3.6 cm2/m2 at the intermediate stage and 6.1 +/- 1.8 cm2/m2 at recovery) and end-diastolic area (10.5 +/- 3.6 cm2/m2 at the intermediate stage and 8.9 +/- 2.9 cm2/m2 at recovery) and improvement in right ventricular fractional area contraction (31.5 +/- 16.4%). The interventricular septum progressively returned to a more normal configuration at both end-systole and end-diastole, and left ventricular diastolic dimension steadily increased. It is concluded that circulatory failure secondary to massive pulmonary embolism was mediated through a profound decrease in left ventricular preload, resulting from both pulmonary outflow obstruction and reduced left ventricular diastolic compliance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of afterload reduction on plasma volume during acute heart failure

Previous investigations in our unit indicated that acute cardiogenic pulmonary edema is associated not only with an increase in left ventricular end-diastolic pressure and pulmonary arterial wedge pressure but also with a relative increase in colloid osmotic (oncotic) pressure and peripheral hemoglobin concentration. This combination of changes suggested that acute congestive heart failure with pulmonary edema, unlike chronic congestive heart failure, is associated with a contraction of intravascular blood volume. In this study, plasma volume changes were measured before and during the treatment of acute cardiogenic pulmonary edema in 14 patients with arteriosclerotic heart disease. The plasma volume measurement in all 14 patients before the initiation of treatment was either normal or decreased. After treatment with the alpha adrenergic blocking agent phentolamine, the plasma volume increased rather than decreased when measured 4 and 12 hours after the initiation of treatment. During this time colloid osmotic pressure and peripheral hemoglobin concentration progressively decreased. These findings suggest that acute cardiogenic pulmonary edema is associated with the extravasation of large quantities of plasma water from the intravascular compartment into the interstitial compartment and contraction of the intravascular plasma volume. The treatment of acute cardiogenic pulmonary edema is associated with the return of hypo-oncotic fluid from the interstitial compartment back into the intravascular compartment with expansion of plasma volume and reduction of colloid osmotic pressure and hemoglobin concentration.     

Acute heart failure: a novel approach to its pathogenesis and treatment

Acute heart failure (HF) is one of the most common syndromes in emergency medicine, however, its exact pathogenesis has remained largely unknown. Based on clinical and hemodynamic data we have sub-divided acute HF into four syndromes: cardiogenic shock, pulmonary edema, hypertensive crisis and exacerbated HF. Cardiogenic shock is caused by a severe reduction in cardiac power which is not met by an adequate increase in peripheral vascular resistance leading to significant decrease in blood pressure and end organ perfusion. Hence the treatment of cardiogenic shock should be directed at improving cardiac performance (by optimizing filling pressure, intra-aortic balloon pump and immediate revascularization) and administration of peripheral vasoconstrictors. The other acute HF syndromes (pulmonary edema, HTN crisis and exacerbated HF) are caused by a combination of progressive excessive vasoconstriction superimposed on reduced left ventricular functional reserve. The impaired cardiac power and extreme vasoconstriction induce a vicious cycle of afterload mismatch resulting in a dramatic reduction of CO and elevated left ventricular end diastolic pressure, which is transferred backwards to the pulmonary capillaries yielding pulmonary edema. Therefore, the immediate treatment of these acute HF syndromes should be based on the administration of strong, fast-acting intravenous vasodilators such as nitrates or nitroprusside. After initial stabilization, therapy should be directed at reducing recurrent episodes of acute HF, by prevention of repeated episodes of excessive vasoconstriction along with efforts to optimize cardiac function.     

Relationship between colloid osmotic pressure and pulmonary artery wedge pressure in patients with acute cardiorespiratory failure

Close relationships between progressive respiratory failure, roentgenographic signs of pulmonary opacification and decreases in the difference between colloid osmotic pressure of plasma and the pulmonary artery wedge pressure (colloid-hydrosatic pressure gradient) were demonstrated in 49 critically ill patients with multisystem failure, in patients in shock. The potential importance of this relationship is underscored by the observation that fatal progression of pulmonary edema was related to a critical reduction in the colloid-hydrostatic pressure gradient to levels of less than 0 mm Hg. More often, reduction in colloid osmotic pressure rather than increases in left ventricular filling pressure (pulmonary artery wedge pressure) accounted for the decline in colloid-hydrostatic pressure gradient. Routine measurement of colloid osmotic pressure, preferably in conjunction with pulmonary artery wedge pressure, is likely to improve understanding of the mechanisms of acute pulmonary edema.     

Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema.

Twenty-two patients with clinical signs of pulmonary edema (orthopnea, cyanosis, profuse sweating and pulmonary rales1) were studied and separated into two groups. In seven patients (Group A), hemodynamic studies were performed. Pulmonary arterial pressure and cardiac output were measured during the emergency condition of severe pulmonary edema. Within 10 minutes after sublingual administration of nitroglycerin, 1.6 mg, left ventricular filling pressure decreased from 33 ± 10 (mean ± 1 standard deviation) to 24 ± 8 mm Hg, and cardiac output increased significantly from 3.3 ± 0.8 to 3.7 ± 0.8 liters/min. In one patient with recent myocardial infarction, left ventricular filling pressure decreased from 50 to 27 mm Hg within 5 minutes. Orthopnea and pulmonary rales disappeared rapidly.In 15 patients (Group B), the clinical course was observed and documented. These patients received one to six doses of 0.8 to 2.4 mg of nitroglycerin sublingually at intervals of 5 to 10 minutes. Five minutes after administration, the first evidence of clinical improvement was observed in seven of these patients. After 15 to 20 minutes, pulmonary rales disappeared or decreased in 11 and dyspnea decreased in 14. The elevated arterial blood pressure and heart rate decreased significantly. Only one patient with terminal pulmonary edema remained refractory to therapy. Thus, sublingual nitroglycerin had beneficial effects in the emergency treatment of classic pulmonary edema. Elevated left ventricular filling pressure decreased and cardiac output increased within 5 minutes. These hemodynamic changes produced immediate clinical improvement.     

Acute pulmonary edema provoked by psychologic stress. Report of two cases

Emotional stress has been considered responsible for life-threatening ventricular arrhythmias but acute stress-induced heart failure has not been reported in man. Two patients with recent uncomplicated myocardial infarction presenting acute pulmonary edema immediately after psychologic stress testing are the object of this report. Four stressors, mental arithmetic, 30 emotionally involving questions (Sacks' test modified), an image quiz (Raven's matrices) and white noise were administered during hemodynamic monitoring (Swan-Ganz catheter) in a 3-min stress-5-min recovery sequence. Response to the stressors was not unusual; greatest cardiovascular response occurred during mental arithmetic, least during noise and intermediate patterns were induced by the other stressors. Heart rate and systemic blood pressure, markers of autonomic activation, increased moderately. Neither ventricular arrhythmias nor ischemic electrocardiographic changes were observed during or after stress testing. Complete recovery followed each stress-induced cardiovascular response. About 10 min after completing stress testing, acute pulmonary edema occurred in both patients neither of whom had presented other episodes of acute pulmonary edema, suggesting that psychologic stress may induce pump dysfunction in patients with latent heart failure.     

Estenose aórtica grave e choque cardiogénico: um desafio terapêutico

Acute heart failure in patients with severe aortic stenosis and left ventricular systolic dysfunction is well known for its dire prognosis and limited therapeutic options.The authors describe the case of a man admitted for non-ST-elevation myocardial infarction. Diagnostic exams revealed severe aortic stenosis, with good left ventricular systolic function, and two-vessel coronary artery disease. The development of cardiogenic shock with left ventricular systolic dysfunction on day four led to changes in the therapeutic strategy. Percutaneous aortic balloon valvuloplasty coupled with complete myocardial revascularization was performed with a view to future surgical intervention. After discharge, the patient was readmitted with acute pulmonary edema, cardiogenic shock and cardiopulmonary arrest. Ventilator weaning was not possible due to acute heart failure and so it was decided to administer levosimendan, which resulted in substantial clinical and echocardiographic improvement. The patient subsequently underwent successful aortic valve replacement.This case highlights the challenge that characterizes the management of patients with concomitant coronary artery disease, left ventricular systolic dysfunction and severe aortic stenosis. Percutaneous aortic balloon valvuloplasty and levosimendan were safe and effective in the treatment of acute heart failure, acting as a bridge to surgery.     

Afterload reduction with phentolamine in patients with acute pulmonary edema

Phentolamine in amounts of 10 to 40 μg/kg/min was infused intravenously for the emergency treatment of acute pulmonary edema due to left ventricular failure. Fourteen patients with arteriosclerotic heart disease, ranging in age from 52 to 87 years, had clinical and roentgenographic signs of pulmonary edema. The pulmonary artery wedge pressure was increased to an average of 24 mm Hg and the cardiac index was decreased to 1.9 liters/min/m² or less prior to the administration of phentolamine. A reduction in the pulmonary artery wedge pressure to 14 mm Hg and an increase in the cardiac index to 2.5 liters/min/m² was observed in response to this alpha adrenergic blocking agent. Reduction in peripheral resistance with phentolamine was associated with reversal of pulmonary edema.     

Reperfusion pulmonary edema after thrombolytic therapy of massive pulmonary embolism

We report here the occurrence of acute focal pulmonary edema after thrombolytic therapy for massive pulmonary embolism. Symptomatic pulmonary edema developed in a 75-yr-old man after streptokinase infusion for a massive pulmonary embolism. Repeat radiographic studies demonstrated that the edema occurred in an area of early reperfusion. Right heart catheterization showed pulmonary hypertension, and there was no clinical evidence of left ventricular failure. The edema spontaneously resolved during a second course of thrombolytic therapy that successfully lysed the remaining thrombus. We conclude that reperfusion pulmonary edema is a potential, albeit rare, complication of thrombolytic therapy for pulmonary embolism.     

Right ventricular failure following placement of a percutaneous left ventricular assist device

Right ventricular (RV) dysfunction following surgical implantation of a left ventricular assist device (LVAD) is a well-documented phenomenon, and it is associated with poor outcomes. We are reporting a 25-year-old male patient who presented to the hospital with flu-like symptoms, hypotension and acute hypoxic respiratory failure. The patient's Laboratory data was significant for elevated troponin, and his Chest X-ray showed acute pulmonary edema. Echocardiogram revealed reduced left ventricular (LV) ejection fraction and normal RV function. Coronary angiography was normal, and the cardiac index was 1.3?L/min/m². Impella 5.0 (Abiomed, MA) was placed through the left axillary artery graft and 4.5?L/min flow was achieved with an improvement in blood pressure. Thirty minutes later, he developed hypotension, the device flow dropped to 3.0?L/min, and right atrial pressure increased. The Pulmonary artery pulsatility index was consistent with RV failure. Possible causes of RV failure include unmasking of RV dysfunction with high LVAD flow and altered RV geometry due to ventricular septum shift. Impella RP (Abiomed, MA) was placed for RV support achieving a flow of 3.8?L/min with a significant improvement in impella LV flow, cardiac output and blood pressure (mean 90?mmHg). Ventricular support devices were weaned off on day 9. The patient was discharged on day 15. Conclusion: our case highlights the risk of RV failure following percutaneous LVAD placement. Early identification and appropriate mechanical support is imperative.     

Cardiovascular management in acute hypoxemic respiratory failure

This paper reviews recent data concerning the interactions among pulmonary edema, intrapulmonary shunt and cardiac output in acute hypoxemic respiratory failure. In canine oleic acid edema, a 5 mm Hg reduction in pulmonary wedge pressure significantly reduces edema, but a corresponding increase in colloid osmotic pressure does not. When pulmonary wedge pressure is lowered, cardiac output can be maintained with infusions of nitroprusside, dopamine or dobutamine. Each vasoactive agent improves ventricular pumping function, and the increase in cardiac output is due in part to peripheral circulatory actions of the drugs. Although pulmonary shunt increases with these vasoactive agents, increased shunt is due not to their pulmonary vasoactivity but to the associated increase in pulmonary blood flow. Positive end-expiratory pressure reduces venous return by raising right atrial pressure, and it does not depress ventricular pumping function. Rather, positive end-expiratory pressure increases ventricular filling pressure at a given end-diastolic volume; it does not reduce and probably increases edema, yet it reduces shunt by redistributing the edema. These interpretations suggest several goals for cardiovascular management in acute hypoxemic respiratory failure: (1) the lowest pulmonary wedge pressure consistent with adequate cardiac output; and (2) the least positive end-expiratory pressure consistent with saturation of adequate circulating hemoglobin on nontoxic inspired oxygen.     

Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.     

Successful treatment of acute circulatory failure of unknown cause using critical ultrasound-guided reverse fluid resuscitation: A case report

Rationale:Fluid resuscitation manages shock effectively. However, shock is not always caused by hypovolemia; various types of shock have variable volumetric reactivity. Combined echocardiography and lung ultrasound (LUS) is a new technique for assessing volume status and pulmonary edema in these patients. We report a case of unexplained acute circulatory failure and acute kidney injury (AKI) aggravated by active fluid resuscitation. We used the critical consultation ultrasonic examination (CCUE) protocol for evaluation, and successfully revived the patient with reverse fluid resuscitation.Patient concerns:An 82-year-old man with hypertension, atrial fibrillation, and left ventricular diastolic dysfunction (LVDD) was admitted with abdominal distention and lower extremity edema. He developed symptoms of acute circulatory failure, including low blood pressure, anuria, and skin spots. After positive fluid resuscitation, the blood pressure lowered further, and moist rales were audible over both lungs.Diagnosis:We performed bedside critical ultrasound for evaluation. The differential diagnoses based on the findings included left atrial and right heart dilatation, low cardiac output owing to reduced left ventricular ejection consequent to excessive circulatory capacity, right heart dilation, and left ventricular compression, and pulmonary edema caused by volume overload.Interventions:Infusion was withheld, and tracheal intubation and mechanical ventilation were instituted to assist breathing; reverse fluid resuscitation was initiated, using continuous renal replacement therapy (CRRT) to maintain a negative fluid balance.Outcomes:Within 72 hours of fluid withdrawal, the blood pressure reverted to normal, symptoms of pulmonary edema were alleviated, and the circulation and tissue perfusion were restored. The symptoms of acute renal injury are relieved and allowing urine formation without support.Lessons:Not all patients with acute circulatory failure require positive fluid resuscitation. Fluid balance should be closely monitored and managed. Potential intolerance to the rapid increase in volume may lead to biventricular interaction, ultimately leading to acute circulatory failure. The shock caused by volume overload should be treated with reverse fluid resuscitation. Combined echocardiography and LUS is a powerful tool for the differential diagnosis of circulatory and respiratory dysfunction.     

Œdème aigu du poumon secondaire à l’administration intraveineuse de β2 mimétiques pour asthme aigu grave

We report the case of a severe acute pulmonary edema secondary to the administration of salbutamol to a patient admitted for severe asthma. The diagnosis of acute pulmonary edema was suspected on the clinical examination, chest radiography, biological (plasmatic Pro-BNP rate) and echocardiographic findings. Rapid improvement under dobutamine and mechanical ventilation argue in favour of cardiogenic pulmonary edema. The young age of our patient, the absence of history of cardiovascular disease and the chronology of this complication onset regarded to salbutamol infusion could suggest β2 agonist involvement in this event. The improvement of cardiac function on echocardiography and the normal results obtained with myocardial perfusion scintigraphy performed 35 days later show the left ventricular reversible dysfunction.     

老年重症急性左心衰竭及心源性休克的主动脉内气囊反搏治疗

目的　观察主动脉内气囊反搏救治老年重症急性左心衰竭及心源性休克的临床疗效。方法　使用 8F、9F容量 40ml的反搏导管紧急经皮穿刺 ,治疗 5例老年重症急性左心衰竭及心源性休克。结果　 4例有效 ,1例好转。结论　主动脉内气囊反搏通过有效的心脏辅助作用 ,对老年重症急性左心衰竭及心源性休克有迅速提高血压、消除肺水肿、改善心功能的效果