Non-cardiac Origin Research Articles

Chest Pain in an Urban Pediatric Cardiology Practice 133

Evaluation of chest pain is the second most common reason for referral to our pediatric cardiology clinics. Chest pain generates anxiety for patient and parent, as well as frequent diagnostic testing. We sought to determine diagnostic testing patterns and their economic implications in the evaluation of chest pain in children and adolescents. We conducted a retrospective chart review of children and adolescents referred to our practice for initial evaluation of chest pain between 1992 and 1997, who had no pre-existing cardiac conditions. Of 347 children referred, 200 met these criteria. The mean age was 11.5 yrs. (3-19 yrs.), with 51% males. Pertinent past medical history included asthma (17%) and pectoral deformities (2%); pertinent family history included mitral valve prolapse (MVP) (5%), and early sudden death (3%). Chest pain was acute (<1 month) in 15%, chronic in 48%, and of unspecified length in 35%. Other chronic illnesses, primarily asthma, were present in 20%. Associated symptoms were present in 40%; most common were tachycardia (10.5%), dizziness (8%), and palpitations (7%). Chest pain occurred equally with activity and at rest. In only 7 cases (3.5%) was a cardiac abnormality identified: MVP (1%), benign arrhythmia (1.5%), hypertension (0.5%), and small secundum atrial septal defect (0.5%). In only 1 case was the chest pain thought to be related to a cardiac abnormality (mild MVP), and in no case was a serious or life-threatening condition identified. Other causes of chest pain identified included muscloskeletal pain (40.5%), asthma (5%), and obesity(2.5%). All but 1 patient had some diagnostic test: 69 (34.5%) had electrocardiogram (ECG) only; 66 (33%) had ECG and echocardiogram (ECHO),and the remainder had various combinations of ECG, ECHO and a variety of other tests, including Holter monitoring, stress testing, and event monitoring. Total charges were $210,300, or $1,051 per patient, including the outpatient visit, and technical and professional fees for tests performed (except charges for event monitoring, for which complete data were not available). Conclusions: Our data agree with previous studies that chest pain is not a harbinger of serious cardiovascular disease. In general, young patients who have life-threatening cardiac events do not have chest pain as a premonitory symptom. The cost of diagnostic testing in the evaluation of chest pain is high, and the yield is nearly zero. We believe no additional tests are required if the history and physical reveal a non-cardiac origin of chest pain, and that ECG alone should suffice if further testing is desired.

Out-of-hospital cardiac arrests of non-cardiac origin. Epidemiology and outcome.

The aim of the study was to determine the epidemiology of out-of-hospital cardiac arrests of non-cardiac origin and survival following resuscitation, using the Utstein method of data collection. The study was of prospective cohort design and was conducted in a middle-sized urban city (population 525000) served by a single emergency medical services system. Consecutive out-of-hospital cardiac arrests of non-cardiac origin occurring between 1 January 1994 and 31 December 1995 were included. Survival from cardiac arrest to hospital discharge, and factors associated with survival were considered as main outcome measures. Of the 809 patients, 276 (34.1%) had a cardiac arrest of non-cardiac origin. The mean (SD) age of the patients was 49.8 (20.9) years. Resuscitation was attempted in 204 cases, 82 of whom (40.2%) were hospitalized alive and 23 (11.3%) were discharged. Thirteen (56.5%) of the survivors were discharged neurologically intact or with mild disability (overall performance category I or II). The survivors, during the study period, who suffered an out-of-hospital cardiac arrest of non-cardiac origin comprised 19.2% of all out-of-hospital cardiac arrest survivors. Trauma (62), non-traumatic bleeding (36), intoxication (31), near drowning (22) and pulmonary embolism (18) were the most common aetiologies, comprising 61.2% of cases. The non-cardiac aetiology was suspected pre-hospital in 176 (63.8%) cases; in the remaining cases, the aetiology was revealed only after in-hospital investigations or autopsy. In a logistic regression model, time interval to first responding unit, collapse outside the home, and aetiologies of near-drowning, airway obstruction, intoxication and convulsions were associated with survival. These results indicate that sudden out-of-hospital cardiac arrest more often has a non-cardiac cause than previously believed. Although survival is not as likely as from cardiac arrest of cardiac origin, since non-cardiac-cause survivors comprise one fifth of all out-of-hospital cardiac arrest survivors, resuscitation efforts are worthwhile.

High-frequency pressure-control ventilation with high positive end-expiratory pressure in children with acute respiratory distress syndrome

OBJECTIVE: Animal models suggest that high-frequency ventilation with low tidal volumes and high positive end-expiratory pressure (PEEP) minimize secondary injury to the lung. We hypothesized that using a high-frequency pressure-control mode of ventilation with high PEEP in children with severe acute respiratory distress syndrome (ARDS) would be associated with improved survival. DESIGN: The study was a retrospective and prospective clinical study at a 24-bed tertiary care pediatric critical care unit. Fifty-three patients with severe ARDS were studied during a 37-month period, 30 prospectively and 23 retrospectively. Severe ARDS was defined as (1) rapid onset of severe bilateral infiltrates of noncardiac origin, (2) partial pressure of oxygen (arterial)/fraction of inspired oxygen less than 200 on PEEP of 6 cm H 2O or more for 24 hours or longer, and (3) Murray disease severity score greater than 2.5. All patients meeting these criteria underwent ventilation in the pressure-control mode; the protocol for ventilation had the following general guidelines: (1) fraction of inspired oxygen limited to 0.5, (2) mean airway pressure titrated with PEEP to maintain arterial partial pressure of oxygen at 55 mm Hg or greater (7.3 kPa), (3) peak inspiratory pressure minimized to allow hypercapnia (arterial partial pressure of carbon dioxide, 45 to 60 mm Hg [6.0 to 8.0 kPa]), and (4) ventilator rates of 40 to 120/min. Percutaneous thoracostomy and mediastinal tubes were placed for treatment of air leak. RESULTS: The survival rate was 89% (47/53) in children with severe ARDS. Nonsurvivors had significantly higher peak inspiratory pressures (75 vs 40 cm H 2O, p = 0.0006), PEEP (23 vs 17 cm H 2O, p = 0.0004), mean airway pressure (40 vs 28 cm H 2O, p = 0.04), alveolar-arterial oxygen gradient (579 vs 540 mm Hg, p = 0.03), and oxygenation index (43 vs 19, p = 0.0008) than survivors. Air leak was present in 51% of patients; there was no difference in the incidence of air leak between survivors and nonsurvivors ( p = 0.42). CONCLUSIONS: The high-frequency positive-pressure mode of ventilation was safe and was associated with an improved survival rate (89%) for children with severe ARDS. Limitation of both inspired oxygen and tidal volume, along with aggressive treatment of air leak, may have contributed to the improved survival rate. (J P EDIATR 1996;129:566-73)

Variance cardiography for emergency department evaluation of chest pain patients.

To determine the test performance of 24-lead variance cardiography (VC), an ECG technique that measures QRS morphologic variability, for ED evaluation of chest pain associated with coronary artery disease (CAD). A prospective, single-blind study of VC was performed in a community teaching hospital ED. All chest pain patients (> 30 years of age) who, after initial emergency physician evaluation, were believed to have pain of potential cardiac etiology and were admitted to the hospital were eligible. Exclusion criteria included obvious noncardiac etiology for discomfort, bundle-branch block, atrial fibrillation, and incomplete subsequent cardiac evaluation. After initial evaluation and stabilization, VC was obtained. The numerical output of VC was a CAD index (CADI). Serum myoglobin and creatine kinase (CK)-MB levels were obtained at the time of presentation and after one, two, and six hours. Hospital records were reviewed to determine final diagnosis and in-hospital evaluation results. Fifty-two of 75 eligible patients had complete data. Final diagnoses were as follows: 27/52 (52%), noncardiac; 13/52 (25%), acute myocardial infarction (AMI); and 12/52 (23%), unstable angina due to CAD. Twenty-three percent (12/52) of the patients had CADIs < 75. Eleven of these were found to have noncardiac origins for their chest pain. The twelfth patient had a 12-lead ECG revealing AMI and had been given thrombolytic therapy with subsequent reperfusion prior to VC. Using a CADI < 75 as the cutoff for a negative study, VC alone had a negative predictive value of 92%, a sensitivity of 96%, a positive predictive value of 60%, and a specificity of 41%. A CADI < 75, in addition to clinical impression and initial ECG, may identify chest pain patients who do not have significant CAD. Further prospective assessment of VC is warranted.

The size of territorial brain infarction on CT relates to the degree of internal carotid artery obstruction.

We studied the relationship between infarct size and degree of internal carotid artery stenosis in 227 stroke patients without a source of embolism in the heart, who had a CT-verified territorial brain infarct. We used logistic regression analysis adjusting for differences between groups in co-associated variables such as age, sex, hypertension, diabetes mellitus, and a history of ischaemic heart disease. Ipsilateral carotid stenosis greater than 50% was more strongly associated with large than small infarcts; adjusted odds ration [(a)OR]: 4.56; 95% confidence interval (CI): 1.21-17.2; P = 0.02. For ipsilateral carotid occlusion the association was even stronger--(a)OR: 36.80; 95% CI: 2.54-533; P = 0.007. When large infarcts were compared with infarcts of small and moderate size together the ORs were 2.29, 95% CI 1.14-4.58 and 2.57, 95% CI 1.17-5.67 for carotid stenosis or occlusion, respectively. Our data show a relationship between greater than 50% carotid stenosis or occlusion and large brain infarcts. We suggest that haemodynamic impairment may contribute to infarct size in territorial infarcts of non-cardiac origin.

Training Room Evaluation of Chest Pain in the Adolescent Athlete

A physician or athletic trainer will often be faced with an athlete complaining of chest pain during or after an event. Chest pain in children and adolescents is usually of a noncardiac origin; only 5% of cases are due to cardiac problems. With a properly documented history and physical evaluation, one can usually identify the etiology of the chest discomfort or at least rule out any serious difficulties. The various diagnostic possibilities include cardiac, musculoskeletal, pulmonary, gastrointestinal, and psychiatric causes of pain. We discuss several specific conditions, as well as the signs, symptoms, and basic management.

Drugs and surgery in the prevention of ischemic stroke.

Randomized clinical trials have proved that warfarin therapy decreases the risk of stroke in patients with nonvalvular atrial fibrillation and in those who have had a myocardial infarction. In patients who are not candidates for long-term anticoagulant therapy, aspirin is beneficial, but the reduction in risk is smaller with aspirin than with warfarin. In patients with cerebral ischemic symptoms of noncardiac origin, aspirin and ticlopidine reduce the risk of stroke, but the benefit is modest. Given alone, neither dipyridamole nor sulfinpyrazone prevents stroke. The question remains whether either of these drugs plus aspirin is better than aspirin alone. The optimal dose of aspirin for stroke prevention has not been established. Carotid endarterectomy reduces the risk of stroke in symptomatic patients with at least 70 percent stenosis, as determined by arteriography. Current trials are addressing the question of whether endarterectomy is beneficial for patients with moderate degrees of carotid stenosis. The benefit of endarterectomy for patients with asymptomatic carotid lesions remains unclear.

FV-ARG-506-GLN-Mutation-associated resistance to activated protein C in ischemic stroke

A recently described coagulation disorder [FV-Arg-506-Gln-mutation-associated resistance to activated protein C (APC-resistance)] leads to a five- to tenfold increased risk for venous thromboembolism. The aim of the study was to determine if this disorder also predisposes to ischemic stroke. Ninety-nine consecutive patients with ischemic stroke of noncardiac origin were screened for APC-resistance and tested for the FV-Arg-506-Gln mutation. The FV-Arg-506-Gln mutation was found in 5 of the 99 stroke patients and in 6% of a pool of blood donors. FV-Arg-506-Gln mutation is not a major cause of ischemic stroke. However, a minor predisposing effect cannot be excluded. Further studies with larger stroke populations and subpopulations are indicated to determine the exact impact of this condition on ischemic stroke.

Out-of-hospital cardiac arrest in an oriental metropolitan city

To investigate the epidemiology of out-of-hospital cardiac arrest in Taipei City, Taiwan, a prospective chart review and follow-up study was conducted by collecting the prehospital cardiac arrest record from 10 designated responsible emergency departments (EDs) from August 1, 1992 through May 31, 1993. Cases with the restoration of spontaneous circulation (ROSC) were followed up until discharged from hospital. The information gathered included age, sex, bystander cardiopulmonary resuscitation, response time (time elapsed from receiving the call to arrival on the scene), advanced cardiac life support (ACLS) time (time elapsed from receiving the call to arrival at the ED), initial cardiac rhythm in the ED, ROSC, survival to discharge from the hospital, underlying disease, past history, personal history, and neurological outcome at discharge. Of 638 out-of-hospital cardiac arrests, 554 (86.7%) were nontraumatic. Response time, ACLS time, ROSC rates, and survival rates were 7.4 minutes, 21.6 minutes, 15.8%, and 1.4%, respectively. In comparing the trauma and nontrauma group, there were significant differences in age, sex, response time, and ACLS time. Between cases of patients who had ROSC and those who died, the data were statistically significant, P = .0143, showing that ACLS time was shorter in the ROSC group (19.5 v 21.9 minutes). In analysis of underlying disease, definite and probable cardiac-origin sudden deaths were found in only 120 patients, which may extend the annual sudden cardiac death rates to be 0.0053%. In conclusion, the low resuscitation and survival rates in this country were because of delayed initiation of both basic life support and ACLS. Out-of-hospital arrests of noncardiac origin had an extremely low survival rate

Diagnoses, symptoms, and attribution of symptoms among black and white inpatients admitted for coronary heart disease.

This study examined health care-seeking behaviors to elucidate factors that contribute to differences in patterns of coronary heart disease between African Americans and Whites. The prevalence of diagnosed coronary heart disease, patients' perceptions of symptoms and attribution of symptoms, and predictors of painful symptoms and attribution of cardiac symptoms were examined. The study involved 2416 patients admitted with diagnoses of coronary artery disease, ischemic heart disease, or myocardial infarction or to rule out myocardial infarction. Structured interview questions were used to obtain demographic information, symptoms precipitating admission, and patients' attribution of their symptoms. Discharge diagnoses were obtained from hospital records. Acute myocardial infarction, unstable angina, nonacute ischemic heart disease, and atherosclerosis were more frequent in White patients. For Blacks, the odds of reporting painful symptoms were only 64% of the odds found for Whites when other factors were controlled, and the odds of attributing symptoms to cardiac origins were almost 50% lower for Blacks than for Whites. The tendency of Blacks to report fewer painful symptoms and to attribute their symptoms to noncardiac origins may contribute to differences in care-seeking and in medical management of heart disease in Blacks.

Umbilical pressure measurement in the evaluation of nonimmune hydrops fetalis

Nonimmune hydrops fetalis continues to have a perinatal mortality rate > 50%. Although many abnormalities are associated with nonimmune hydrops fetalis, the direct mechanism by which the hydrops occurs is often obscure, even after delivery. There are at least three possible mechanisms for hydrops: heart failure (whether primary or a secondary effect of obstructed venous return), lymphatic malformation, and liver or peritoneal disease. The development of safe access to the fetal circulation by cordocentesis allows for the measurement of the umbilical venous pressure, which is closely related to the fetal central venous pressure. The premise that nonimmune hydrops fetalis of cardiac origin could be distinguished from that of noncardiac origin was examined by measuring the umbilical venous pressure. Umbilical venous pressure was measured during indicated diagnostic cordocentesis in three groups of fetuses: 20 with nonimmune hydrops fetalis, four with a cardiac malformation but without nonimmune hydrops fetalis, and eight with immune hydrops (fetal hemolytic disease). In 16 of 20 fetuses with nonimmune hydrops fetalis the serum total protein and albumin concentrations were also measured. Presumed inadequate cardiac output, as indicated by an elevated umbilical venous pressure, was the mechanism of nonimmune hydrops fetalis in 13 of 20 (65%). The pathologic condition included arrhythmia, cardiothoracic abnormalities, severe polycythemia and hyperviscosity, viral infection, and severe anemia. Successful antenatal treatment normalized the umbilical venous pressure. Nonimmune hydrops fetalis secondary to noncardiac mechanisms did not progress in severity and was not amenable to antenatal therapy. Hypoproteinemia and hypoalbuminemia were found in only six of 16 cases and were similarly distributed between cardiac and noncardiac mechanisms. This is the first report where the measurement of umbilical venous pressure was applied to the evaluation of nonimmune hydrops fetalis. Cardiac dysfunction was the most common mechanism causing hydrops. The finding of a normal umbilical venous pressure greatly reduces the likelihood that the heart is the cause of the hydrops, even when there is a coexistent heart malformation. This immediate information allows the practitioner either to focus on therapeutic interventions that might lower the umbilical venous pressure or to look for noncardiac causes for the hydrops.

Beat-to-beat morphologic variability of the electrocardiogram for the evaluation of chest pain in the emergency room

The value of electrocardiographic, morphologic variability in the early diagnosis of acute myocardial infarction (AMI) and myocardial ischemia was evaluated in 49 nonselected patients presenting to the emergency room with chest pain. High-resolution electrocardiography was used to determine the morphologic variability of consecutive electrocardiographic complexes, and the ratio of the variance of the QRS onset to that of the entire electrocardiogram was calculated. A final diagnosis of AMI was confirmed in 8 patients, acute coronary insufficiency in 8, angina pectoris in 19, and a noncardiac origin for chest pain in 14. Patients with AMI had a significantly higher beat-to-beat electrocardiographic morphologic variability of the QRS onset (1.4 ± 0.2) than did those with acute coronary insufficiency (1.1 ± 0.2), angina pectoris (0.9 ± 0.1) or noncardiac chest pain (0.8 ± 0.1) (p < 0.05). The sensitivity of the clinical presentation, typical electrocardiographic changes and creatine phosphokinase levels for the diagnosis of an acute ischemic event on admission to the emergency room was 62, 25 and 37.5%, respectively. Relative variance of the QRS onset of >0.86 had a sensitivity of 75% and a specificity of 61% for diagnosing an acute ischemic event. Logistic regression of these variables showed that the QRS onset relative variability is an independent predictor for an acute ischemic event. It is concluded that an increased beat-to-beat electrocardiographic variability in patients with AMI is present on admission to the emergency room and may assist in establishing the diagnosis in this setting.

The oxygen dependence of mitochondrial oxidative phosphorylation and its role in regulation of coronary blood flow.

The oxygen dependence of mitochondrial oxidative phosphorylation measured in isolated cells of cardiac and non-cardiac origin are affected by the metabolic state of the cells. The contribution of oxygen diffusion to the measured P50 value in resting cells is small. In cardiac myocytes, and possibly in the other cells as well, this contribution may become significant near maximal levels of respiration. The influence of cellular energy metabolism on the oxygen dependence of respiration in cardiac myocytes suggests strongly that mitochondrial oxidative phosphorylation in these cells is an oxygen sensor for adjusting coronary vascular tone during normal cardiac function.

Recurrent Noncardiac Pulmonary Edema Accompanying Pregnancy-induced Hypertension

Severe pulmonary edema occurred in a patient during the third trimester of two consecutive pregnancies, 17 months apart. Noncardiac origin of the pulmonary edema was demonstrated by normal pulmonary capillary wedge pressures, normal roentgenographic cardiac dimensions with absence of effusions, normal echocardiographic ejection fraction, and elevated thermodilution cardiac outputs; moderate reduction in serum albumin levels may have contributed. In the setting of pregnancy-induced hypertension, the development of ARDS on each occasion suggests a pathophysiologic link.

Calcium-channel blocking agents and chest pain.

Calcium-channel blocking agents can relieve anginal and chest pain associated with hypermotility of the esophagus. Although calcium-channel antagonists differ in their effects on the esophageal body and the lower esophageal sphincter, reduction of lower esophageal sphincter pressure theoretically could result in gastroesophageal reflux and pain. This pain may be difficult to differentiate from chest pain of cardiac origin. An association between calcium-channel blocking agents and chest pain is speculative at this time. However, the possibility of such an effect should be considered by clinicians in the total management of patients. Future clinical studies are warranted to address the issue of the incidence of such an effect and to define more precisely the potential interrelationship among the calcium-channel antagonists, their efficacy in relieving cardiac pain, and their potential liability in inducing chest pain of noncardiac origin.

Left Ventricular Aneurysm Repair with Myocardial Revascularization: An Analysis of 246 Consecutive Patients over 15 Years

From 1970 to 1985, 246 consecutive patients with left ventricular (LV) aneurysm underwent repair and concomitant myocardial revascularization at Ochsner Foundation Hospital. The overall incidence of perioperative death was 7.3%. Although the deaths were mainly cardiac related (10/18) with congestive heart failure (CHF) as the leading cause (6/10), 8 deaths were of noncardiac origin. Perioperative mortality increased significantly in patients with mitral regurgitation (MR) (22%; p = 0.0008); perioperative mortality for patients without MR was 4.8%. The overall 5-year survival was 69%. Late deaths were caused most commonly by myocardial infarction (20/32) with only 7 due to CHF. Predictors of long-term survival were related to LV function preoperatively: absence of CHF ( p = 0.001); LV end-diastolic pressure less than or equal to 20 mm Hg ( p = 0.03); and ejection fraction greater than or equal to 35% ( p = 0.02). Factors that did not significantly affect long-term survival were type of aneurysm repair (resection or plication), morphology of left anterior descending coronary artery (occlusion or stenosis), and size of the aneurysm.

A comparison of blood, crystalloid and oxygenated crystalloid cardioplegia solutions on myoglobin and creatine kinase release following cardiac surgery

Oxygenated crystalloid cardioplegia was found not to produce better cardioprotection than blood or crystalloid cardioplegia, as assessed by myoglobin and creatine kinase MB (CPK-MB) isoenzyme, in patients undergoing coronary artery surgery. Myoglobin and CPK-MB levels were found to peak at 1 and 3 h, respectively, following release of the aortic cross-clamp. There was a good correlation between peak myoglobin and CPK-MB levels. CPK-MB of non-cardiac origin was found to represent a substantial proportion of total CPK-MB 4 h after the release of the aortic cross-clamp.

7 Angina-like chest pain of oesophageal origin

Angina-like chest pain of non-cardiac origin is a major diagnostic and therapeutic problem. The oesophagus is frequently suspected to be the cause of the chest pain in these patients. However, a positive statement for the oesophageal origin of the pain can only be made when during manometry or pH-monitoring the familiar pain attack appears to be accompanied by reflux, severe motor disorders or a combination of both. Due to the intermittent nature of the pain this is only rarely the case during short-listing conventional examinations. Provocation tests have been used to induce the familiar chest pain. The Bernstein acid perfusion test and the edrophonium test yield the best results. Prolonged (24-hour) ambulatory recording of intra-oesophageal pressure and pH to increase the chances of recording chest pain concomitantly with an episode of reflux and/or motor disorders appears to be the most sensitive and also the most physiological test. It is the only test that provides reliable information on the underlying mechanism of the pain, especially in patients with the syndrome of irritable oesophagus, thus contributing in establishing the appropriate therapy for these patients.

Cardiac-specific troponin-l radioimmunoassay in the diagnosis of acute myocardial infarction

The cardiac isotype of the myofibrillar contractile protein, troponin-I, is located specifically in the mammalian heart. A sensitive radioimmunoassay has been developed to detect human and nonhuman primate cardiac troponin-I in serum down to 10 ng/ml. Immunochemical cross reactivity with skeletal troponin-I was only 2% and was species nonspecific. Normal patient levels of cardiac troponin-I are about 10 ng/ml. In patients with acute myocardial infarction (n = 32), serum cardiac troponin-I was elevated within 4 to 6 hours, reached a mean peak level of 112 ng/ml (range 20 to 550 ng/ml) at 18 hours, and remained above normal for up to 6 to 8 days following infarction. Peak cardiac troponin-I correlated with peak creatine kinase (CK) MB isoenzyme (r = 0.75). In subjects (n = 34) with skeletal muscle damage (total CK = 338 to 5384 IU/L), cardiac troponin-I levels were not elevated above normal, although CK-MB isoenzyme was elevated in some patients. Cardiac troponin-I levels were normal or slightly elevated in patients with ischemic heart disease and were normal in patients with chest pain of noncardiac origin. Immunoassay of cardiac troponin-I could be a valuable diagnostic aid in the cardiac-specific detection of cell necrosis.

Pulmonary Edema Associated With Subarachnoid Hemorrhage

A 56-year-old woman with no history of cardiac disease developed acute pulmonary edema following a subarachnoid hemorrhage. A constellation of findings, including elevated creatine kinase MB isoenzyme activity in the absence of electrocardiographic or scintigraphic evidence of acute myocardial infarction, elevated pulmonary artery wedge pressure, segmental wall motion abnormalities, and depressed ejection fraction of the left ventricle demonstrated by two-dimensional echocardiography and radionuclear ventriculography, pointed to a direct myocardial injury leading to cardiac failure. The evidence for cardiogenic origin of pulmonary edema provided by this case is in contrast to the belief that "neurogenic" pulmonary edema is of noncardiac origin.