naloxone and Ventricular-Dysfunction--Left

Morphine is an opiate alkaloid characterized by various clinical effects, among which the most prominent are its analgesic and psychoactive effects. It also has a prominent depressive effect on the respiratory and cardiovascular system. Because of its psychoactive effect, morphine is very addictive and often used as a recreational narcotic. As a medication, it has found its use as an analgesic agent in chronic pain treatment, in hemorrhagic shock, and in acute heart failure with pulmonary edema. Albeit, morphine use in heart failure is controversial, based on many observational studies showing the negative effect on the outcomes of the patients treated with morphine during acute cardiovascular incidents. In this report, the authors present a case of cardiogenic shock (CS) with transient left ventricular ejection fraction reduction, occurring in a patient attempting suicide using a high dose of intravenous morphine sulphate administration. Other CS causes were ruled out. To the best of the authors' knowledge, this is the second case of a morphine-related CS reported in literature. Int J Occup Med Environ Health. 2021;34(1):133-8.

Topics: Administration, Intravenous; Adult; Analgesics, Opioid; Humans; Hypotension; Male; Morphine; Naloxone; Narcotic Antagonists; Norepinephrine; Shock, Cardiogenic; Suicide, Attempted; Ventricular Dysfunction, Left; Ventricular Function, Left

Although animal and human models suggest that direct suppression of myocardial contractility may occur with morphine administration, to our knowledge, clinical observation of this potentially important effect has not been reported. This case report presents a unique case of morphine-induced transient reversible cardiogenic shock.. A 44-year-old woman with a history of hypertension, diabetes, and asthma presented with a 3-day history of epigastric pain. Initial investigation results revealed elevated serum lipase level and computed tomography imaging that was consistent with a diagnosis of mild acute pancreatitis. Intravenous fluids and morphine, via patient-controlled analgesia, were started and the patient was admitted. The next day, she developed cardiogenic shock with a globally reduced left ventricular ejection fraction (LVEF) of 26% and was admitted to the intensive care unit. Morphine was discontinued and norepinephrine and naloxone were concurrently administered. Over the next 24 hours her clinical status improved, and an echocardiogram 29 hours after the initial echocardiogram showed normal LV function (LVEF 62%).. To our knowledge, this represents the first reported case of clinically significant morphine-induced cardiogenic shock. An objective causality assessment using the Naranjo probability scale suggests that the cardiogenic shock was probably related to morphine. Other causes of shock were ruled out. Additionally, the fact that the transient nature of the observed LV dysfunction reversed with discontinuation of morphine and administration of naloxone provides further support, particularly with the evidence that opiates may depress cardiac myocytes and cardiac output in animal and human models.. Opiates can cause severe LV dysfunction. Physicians should consider emergent evaluation for myocardial depression in patients who are receiving opioids and present with persistent hypotension or pulmonary edema without other known etiology.

Topics: Adult; Analgesics, Opioid; Echocardiography; Female; Humans; Morphine; Naloxone; Narcotic Antagonists; Norepinephrine; Shock, Cardiogenic; Ventricular Dysfunction, Left

Ten-minute perfusion of intact isolated rat heart with Krebs-Henseleit solution containing delta-opioid receptor agonists (DPDPE, (-)-TAN-67) or delta-opioid receptor antagonists (naltrindole, TIPP[psi], ICI 174,864) at a final concentration of 0.1 mg/liter decreased HR, blood pressure in the left ventricle, and the rates of myocardial contraction and relaxation. Intravenous injection of delta-agonists (DPDPE, (-)-TAN-67, deltorphin II) or delta-antagonists (naltrindole, TIPP[psi], ICI 174,864) decreased HR in narcotized rats. Naloxone and naltrexone produced no effect on contractility and HR both in vivo and in vitro. Preliminary injection of naloxone and naltrexone did not prevent the negative chronotropic effect of ICI 174,864 in vitro. The negative inotropic and chronotropic effects of delta-opioid receptor antagonists are mediated by unknown non-opioid receptors in the heart.

Topics: Animals; Blood Pressure; Cardiotonic Agents; Ligands; Myocardial Contraction; Myocardium; Naloxone; Naltrexone; Perfusion; Rats; Rats, Wistar; Receptors, Opioid; Receptors, Opioid, delta; Ventricular Dysfunction, Left