Cardiogenic pulmonary edema

Hypotension, tachycardia, tachypnea, confusion, and oliguria are common symptoms. Myocardial and cerebral ischemia, pulmonary edema (cardiogenic shock), and multisystem organ failure often follow. Significant hypotension (systolic blood pressure [SBP] less than 90mmHg) with reflex sinus tachycardia (greater than 120 beats/min) and increased... 

Pulmonary edema with some mucosal irritation (greater water solubility of agent is equal to greater mucosal irritation) leading to ARDS or non-cardiogenic pulmonary edema. Pulmonary infiltrate. 

Suggested Alternatives for Differential Diagnosis Acute respiratory distress syndrome, congestive heart failure, pulmonary edema, AIDS, pneumonia, cardiogenic shock, septic shock, phosgene toxicity, phosphine toxicity, salicylate toxicity with pulmonary edema, influenza, plague, tularemia, and anthrax. 

Contraindications Bronchial asthma or related bronchospastic conditions, cardiogenic shock, pulmonary edema, second- or third-degree atrioventricular (AV) block, severe bradycardia, overt cardiac failure, hypersensitivity to penbutolol or any component of f he formulafion... 

In 40 patients with atrial fibrillation, some with severe heart disease (including cardiogenic shock in eight and pulmonary edema in 12), amiodarone 450 mg was given through a peripheral vein within 1 minute, followed by 10 ml of saline 21 patients converted to sinus rhythm, 13 within 30 minutes and another 8 within 24 hours (21). There were two cases of hypotension, but in those that converted to sinus rhythm there was a slight increase in systolic blood pressure. There were no cases of thrombophlebitis. Efficacy is hard to judge from this study, because it was not placebo-controlled. 

There have been reports of non-cardiogenic pulmonary edema in three adolescent renal transplant recipients, one of whom died (4). 

Non-cardiogenic pulmonary edema has been reported after a single dose of buprenorphine (SEDA-19, 89). 

Dextrans can also cause non-cardiogenic pulmonary edema and/or respiratory distress syndrome. 

Although thromboprophylaxis of microvascular anastomoses seems advisable theoretically, there is little clinical evidence to support the use of dextran for this purpose. The pulmonary edema in these cases was thought to be non-cardiogenic, similar to that caused by heroin, methadone, propoxyphene, and salicylates, due to a direct adverse effect on the pulmonary vasculature, rather than anaphylaxis, cardiac pump failure, or volume overload. 

The syndrome of acute hypotension, adult respiratory distress syndrome, non-cardiogenic pulmonary edema, anemia, coagulopathy, and anaphylactic reactions after the administration of dextran 70 is referred to as the dextran syndrome (36-39). Factors other than acute volume overload due to intravascular absorption of dextran are thought to account for the syndrome. A combination of diverse pathophysiological factors may be responsible, namely direct pulmonary toxicity, activation of the coagulation cascade, release of vasoactive mediators, hypotension, pulmonary edema, intravascular intravasation of fluids, dilution of blood, and impaired renal and hepatic clearance. Cases of pulmonary edema are described under the section Respiratory. 

Cardiac failure, pulmonary edema, and cardiogenic shock (with and without ischemic symptoms) (13-16). 

Acute pulmonary edema leading to lethal cardiogenic shock has been reported with fluorouracil. This occurred despite the fact that the patient had received eight infusions of leucovorin 100 mg/m at weekly intervals (26). 

Non-cardiogenic pulmonary edema has been seen several times after contrast media in patients with a prior history of myocardial infarct (SEDA-16, 531) it can also be a component of anaphylactic shock. Non-cardiogenic pulmonary edema has been reported as a complication of intravenous injection of iomeprol (71). 

A 68-year-old man with chronic obstructive pulmonary disease underwent CT examination of the abdomen with intravenous infusion of iomeprol for suspected hepatocellular carcinoma and 2 hours later developed severe dyspnea. A chest X-ray showed bilateral diffuse shadowing of the lungs and the heart shadow was not enlarged. A diagnosis of non-cardiogenic pulmonary edema was made and he improved with glucocorticoids. 

Accidental inhalation of hypertonic contrast media during oral administration can cause fatal non-cardiogenic pulmonary edema (75). 

A 42-year-old woman suffered an acute anterior myocardial infarction, initially associated with pulmonary edema. After hemodjmamic stabilization she was given lisinopril 10 mg oraUy. Two hours later she developed circulatory failure in conjunction with acute renal insufficiency. Right heart catheterization showed markedly reduced systemic vascular resistance but a normal cardiac index. After the usual causes of cardiogenic shock had been ruled out, repeated fluid challenges and intravenous noradrenaline failed to improve her hemodynamic status. She was therefore given angiotensin II intravenously (5-7.5 pg/minute), which immediately and markedly raised the systematic vascular... 

Non-cardiogenic pulmonary edema has been reported with monoctanoin after appropriate intra-biliary use (6). If monoctanoin is injected intravenously in error, fatal respiratory and cardiac arrest can occur (7). 

Non-cardiogenic pulmonary edema occurred in three cancer patients, all of whom had received rapidly escalating doses of morphine over a short period (15). 

Bruera E, Miller MJ. Non-cardiogenic pulmonary edema after narcotic treatment for cancer pain. Pain 1989 39(3) 297-300. 

Dyspnea and pleurisy have been described. Of 52 travellers with adverse reactions to Fansidar in Sweden, six had pulmonary infiltrates accompanied by fever (SEDA-13, 241). Such infiltrates have also been described in the past, and in one case a diagnosis of eosinophilic infiltration was made (SEDA-11, 590). A case of non-cardiogenic pulmonary edema was reported in 1989 (SEDA-13, 813). 

Bowden FJ. Non-cardiogenic pulmonary edema after ingestion of chlorothiazide. BMJ 1989 298(6673) 605. 

Several mechanisms may be involved in non-cardiogenic pulmonary edema subsequent to verapamil intoxication, including leaky capillary syndrome attributable to inhibition of prostacyclin, a cellular membrane protector. Prolonged hypotension and a shock-like state may also contribute. The authors recommended pressor/inotropic therapy and mechanical ventilation as therapy. 

A 37-year-old man with a history of ethanol abuse presented with hepatic failure and non-cardiogenic pulmonary edema after an overdose of paracetamol, codeine, ibuprofen, and diazepam. He received two... 

Because the initial bronchitis following respiratory exposure is not infectious, patients will not benefit from administration of antibiotics. However, routine laboratory evaluation shonld include daily sputum cultures. Within the first several days after exposure, patients may develop a chemical pnenmonitis, reflected by fever, elevated white blood cell connts and pulmonary infiltrates, bnt this pnenmonitis is typically sterile. An infectious etiology is uncommon until the third or fourth day after exposure. Patients should receive antibiotics only after identification of a causative organism, not prophylactically (8,25,26). Patients with pnlmonary edema should not receive diuretics, because vesicant-caused pulmonary edema is not cardiogenic (3). 

Bauer P, Weber M, Mur JM, et al. 1992. Transient non-cardiogenic pulmonary edema following massive ingestion of ethylene glycol butyl ether. Intensive Care Med 18(4) 250-251. 

LeConte P, Countant V, N Guyen JM, et al. Prognostic factors in acute cardiogenic pulmonary edema. Am J Emerg Med 1999 17 329-332. 

Pulmonary edema may result from the failure of any of a number of homeostatic mechanisms. The most common cause of pulmonary edema is an increase in capillary hydrostatic pressure because of left ventricular failure. Excessive fluid administration in compensated and decompensated heart failure patients is the most frequent cause of iatrogenic pulmonary edema. Besides hydrostatic forces, other homeostatic mechanisms that may be disrupted include the osmotic and oncotic pressures in the vasculature, the integrity of the alveolar epithelium, interstitial pulmonary pressure, and the interstitial lymph flow. The edema fluid in cardiogenic pulmonary edema contains a low amount of protein, whereas noncardiogenic pulmonary edema fluid has a high protein concentration. This indicates that noncardiogenic pulmonary edema results primarily from disruption of the alveolar epithehum. The reader is referred to Chap. 28 for a detailed discussion of this topic. 

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