Myocardial edema

M. Hori, K. Gotoh, M. Kitakaze, K. Iwai, K. Iwakura, H. Sato, Y. Koretsune, M. Inoue, A. Kitabatake and T. Kamada, Role of oxygen-derived free radicals in myocardial edema and ischemia in coronary microvascular embolization, Circulation 84, 828-840 (1991). 

Loss of membrane permeability caused by ischemia leads to cellular sodium accumulation and myocardial edema. After prolonged coronary occlusion and complete reflow, the rate of myocardial sodium accumulation may be governed by microvascular integrity. Three-dimensional Na MRI was used to monitor myocardial sodium content changes over time in an in vivo closed-chest canine model of myocardial infarction and reperfusion. 

Performing a standard coronary CTA, CT density values within the myocardium can give insight into pathologic ischemia of the myocardium, i.e., hypoperfusion or myocardial infarction, both reflected by a reduced CT density or hypoattenuation. Ischemic changes in the myocardium after coronary arterial occlusion consist of disruption of cell membrane function and integrity and increased permeability of small vessel walls. In contrast-enhanced CT, the initial area of low attenuation primarily reflects myocardial edema, i.e., a pronounced water content of the myocardium, which is followed by infiltration of inflammatory cells. Subsequently, necrotic myocardium is replaced by fibrous and/or fatty... 

Myocardial edema with consequent regional wall thickening has been seen using magnetic resonance imaging [39 ]. 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

While epinephrine is usually well tolerated in young and healthy individuals, there may be problems in elderly patients with cardiac arrhythmia or previous myocardial infarction episodes [31-33]. Pharmacological effects of epinephrine include rapid rise in blood pressure, pallor, anxiety, tachycardia, headache and tremor as well as vertigo. Most commonly these effects occur after intravenous injection or after overdosing epinephrine. Cardiac arrhythmia or pulmonary edema may develop in serious cases [33, 34]. 

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

Terbutaline has been shown to prolong pregnancy but has not been associated with decreased neonatal morbidity.36 It is contraindicated for use in women with preexisting cardiac arrhythmia. Potentially serious adverse effects include pulmonary edema, cardiac arrhythmia, or myocardial ischemia in the mother. Reported fetal and neonatal adverse effects include tachycardia, hyperglycemia, and hyperinsulinemia.41... 

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

Beyer et al. (1998c) aver that the most reliable indicators of lead poisoning in waterfowl include impactions of the upper alimentary tract, submandibular edema, myocardial necrosis, biliary discoloration of the liver, and hepatic lead concentrations of at least 38 mg/kg DW or 10 mg/kg FW. 

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... 

Elevated blood pressure should remain untreated in the acute period (first 7 days) after ischemic stroke because of the risk of decreasing cerebral blood flow and worsening symptoms. The pressure should be lowered if it exceeds 220/120 mm Hg or there is evidence of aortic dissection, acute myocardial infarction, pulmonary edema, or hypertensive encephalopathy. If blood pressure is treated in the acute phase, short-acting parenteral agents (e.g., labetalol, nicardipine, nitroprusside) are preferred. 

Edema can occur in patients with decreased myocardial contractility, nephrotic syndrome, or cirrhosis. 

Bradykinin b2 Human cDNA Asthma, arthritis, cancer, hypertension, inflammation, migraine, myocardial ischemia, pain, rhinitis, diabetes, cystic fibrosis, nociception Vasodilatation, stimulation of natriuresis-diuresis in kidney, smooth muscle contraction, induction of hyperalgesia, edema, neuroprotection... 

Cardiovascular Effects. One of the patients described by Letz et al. (1984) (see Section 2.2.3.1) who had a terminal cardiopulmonary arrest had acute myocardial interstitial edema, myocardial inflammation, and Gram-positive sporulating rods at necropsy. The second patient initially had a normal electrocardiogram, but as his renal and hepatic function deteriorated, eventually developed supraventricular tachycardia and asystole. 

Several serious toxicities have been observed, with a fatahty rate of 5% in the initial studies. The major adverse effect is severe hypotension in as many as 85% of patients, which may lead to myocardial infarctions, pulmonary edema, and strokes. This hypotension is thought to be due to a capillary leak syndrome resulting from extravasation of plasma proteins and fluid into ex-travascular space and a loss of vascular tone. Patients with significant cardiac, pulmonary, renal, hepatic, or CNS conditions should not receive therapy with aldesleukin. Other adverse reactions include nausea and vomiting, diarrhea, stomatitis, anorexia, altered mental status, fevers, and fatigue. 

Arrhythmias, stroke, transient ischemic attacks, congestive heart failure (CHF), pulmonary edema, and myocardial infarction (Ml) occur rarely with interferon alfa-2a,... 

IV administration of furosemide produces prompt relief in acute pulmonary edema (acute left ventricular failure, following myocardial infarction). This is due to the vasodilator action that precedes the saluretic action. 

Diuretics are the mainstay of heart failure management and are discussed in detail in Chapter 15. They have no direct effect on cardiac contractility their major mechanism of action in heart failure is to reduce venous pressure and ventricular preload. This results in reduction of salt and water retention and edema and its symptoms. The reduction of cardiac size, which leads to improved pump efficiency, is of major importance in systolic failure. Spironolactone and eplerenone, the aldosterone antagonist diuretics (see Chapter 15), have the additional benefit of decreasing morbidity and mortality in patients with severe heart failure who are also receiving ACE inhibitors and other standard therapy. One possible mechanism for this benefit lies in accumulating evidence that aldosterone may also cause myocardial and vascular fibrosis and baroreceptor dysfunction in addition to its renal effects. 

Yanagawa et al Infusion of adrenomedullin improves acute myocarditis via attenuation of myocardial inflammation and edema. Cardiovasc Res 2007 76 110. [PMID 17599815]... 

The relief produced by intravenous morphine in dyspnea from pulmonary edema associated with left ventricular heart failure is remarkable. Proposed mechanisms include reduced anxiety (perception of shortness of breath), and reduced cardiac preload (reduced venous tone) and afterload (decreased peripheral resistance). However, if respiratory depression is a problem, furosemide may be preferred for the treatment of pulmonary edema. On the other hand, morphine can be particularly useful when treating painful myocardial ischemia with pulmonary edema. 

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