naloxone and Shock--Cardiogenic

In summary, naloxone has proved to be effective and safe during its years of use for narcotic antagonism. Its usefulness in non-narcotic coma and shock remains controversial, although some encouraging but inconclusive evidence exists. The final answer lies on the horizon of medicine; it awaits further delineation of the role of endogenous opioids in health and disease and clear statistical verification of naloxone's efficacy in such disease states.

Topics: Animals; Arousal; Coma; Humans; Naloxone; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Shock, Septic

In a canine model of congestive heart failure beta endorphin concentrations were high and opioid receptor antagonists exerted beneficial haemodynamic effects. In humans previous studies have suggested that opioid peptides may modify the perception of breathlessness and fatigue in heart failure.. Plasma concentrations of beta endorphin were measured in patients with acute and chronic heart failure and cardiogenic shock. A subgroup of eight patients with New York Heart Association (NYHA) class III-IV heart failure was assessed for acute haemodynamic effects of naloxone, an opioid receptor antagonist. A separate group of 10 patients with class II-III heart failure, was randomised to a double blind placebo controlled study of the effects of intravenous naloxone on cardiopulmonary exercise performance.. Plasma concentrations of beta endorphin were usually normal in patients with chronic heart failure and did not correlate with severity as assessed by NYHA class. In 29% of patients with acute heart failure and 71% of those with cardiogenic shock beta endorphin concentrations were high. The median concentration in the cardiogenic shock group was significantly higher than in either of the two heart failure groups and there was some evidence of a relation between beta endorphin concentrations and survival. At the doses tested, naloxone was unable to modify systemic haemodynamics, exercise performance, or symptoms in patients with chronic congestive heart failure.. Circulating concentrations of beta endorphin are usually normal in patients with chronic congestive heart failure. Inhibition of the endogenous opioid system is unlikely to have therapeutic potential in heart failure.

Topics: Acute Disease; Adult; Aged; beta-Endorphin; Chronic Disease; Double-Blind Method; Exercise Test; Female; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Naloxone; Shock, Cardiogenic; Stroke Volume; Ventricular Function, 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

Methadone overdoses are increasing in parallel with the increased frequency of opiate substitution therapy in adults. Although unintentional methadone intoxication in children is rare, it is becoming more frequently recognized. We report 3 cases of unintentional methadone overdose in toddlers who initially displayed central nervous system depression associated with severe nonketotic hyperglycemia and discuss the possible pathophysiologic mechanisms of an underrecognized symptom of opiate intoxication in young children.

Topics: Accidents, Home; Animals; Brain Damage, Chronic; Child, Preschool; Diabetes Mellitus, Type 1; Diagnostic Errors; Dobutamine; Drug Packaging; Epinephrine; Female; France; Humans; Hyperglycemic Hyperosmolar Nonketotic Coma; Infant; Insulin; Islets of Langerhans; Male; Methadone; Mice; Multiple Organ Failure; Myocardial Infarction; Naloxone; Receptor, Insulin; Receptors, Opioid, mu; Shock, Cardiogenic; Sweetening Agents; Time Factors

Endogenous opioid peptides subserve regulatory roles in cardiovascular function and are released upon myocardial ischemia contributing to the development of ischemic arrhythmias and cardiogenic shock, which are reversed by the opioid antagonist naloxone. Since the hallmark of myocardial infarction is the impairment of hemodynamics and ventricular function, we evaluated further if blockade of opioids reverses the ischemia induced hemodynamic compromise, and if the effects are mediated by opioid receptors. Thirty-two mongrel dogs were anesthetized and artificially ventilated. Median thoracotomy was performed, the heart exposed, and the left anterior descending coronary artery isolated for subsequent occlusion and reperfusion. All cardiac parameters were recorded on an Electronics for Medicine recorder through the intracardiac catheters advanced from femoral vessels. Results indicate that naloxone significantly reversed the ischemic and reperfusion induced reduction in aortic, left ventricular and pulmonary arterial pressures, and left ventricular dp/dt. The inactive (+) stereoisomer of naloxone was without effect. These data demonstrate that opioids may have a role in the pathophysiology of myocardial infarction, mediated by opioid receptors, and provide new insight and strategies for the understanding and treatment of ischemic heart disease.

Topics: Animals; Arrhythmias, Cardiac; Dogs; Female; Hemodynamics; Male; Myocardial Ischemia; Myocardial Reperfusion Injury; Naloxone; Narcotic Antagonists; Opioid Peptides; Receptors, Opioid; Shock, Cardiogenic; Stereoisomerism

The endogenous opioid peptide (EOP) dynorphin and opioid receptors have been found in the heart. This opioid system plays important roles in cardiovascular regulation and is involved in the pathophysiology of shock, heart failure and myocardial ischaemia. The aim of this study was to evaluate whether the EOP dynorphin modulates or potentiates ischaemia-induced arrhythmias and whether its effects are prevented by the opiate antagonist naloxone. Following coronary artery occlusion, all rats in the control group developed ischaemia-induced arrhythmias, bradycardia and hypotension, which were significantly potentiated by pre-treatment with dynorphin and attenuated by treatment with naloxone. The results clearly indicate that EOPs may be released when myocardial ischaemia occurs, thus causing arrhythmias, bradycardia and hypotension. Dynorphin and naloxone, by virtue of their opioid agonistic and antagonistic actions, respectively, potentiate and attenuate these fatal complications secondary to myocardial ischaemia. This suggests that EOPs play an important part in ischaemic heart disease.

Topics: Animals; Arrhythmias, Cardiac; Bradycardia; Dynorphins; Female; Heart Conduction System; Hypotension; Male; Myocardial Ischemia; Naloxone; Rats; Rats, Sprague-Dawley; Shock, Cardiogenic

Topics: Adult; beta-Endorphin; Case-Control Studies; Female; Humans; Male; Middle Aged; Myocardial Infarction; Naloxone; Shock, Cardiogenic

The effect of naloxone (4.4-5.9 mg i.v.) was evaluated in 10 patients with circulatory shock (sepsis, n = 7; intoxication, n = 1; cardiogenic shock, n = 2) not responding to full conventional therapy. In addition, we measured plasma ACTH and immunoreactive beta-endorphin before and 60 min after administration of naloxone and compared the results with hormone concentrations in 10 intensive care patients without shock. Only in two patient with septic shock a transient increase (duration 15 min and 60 min, respectively) of systolic blood pressure was observed, while naloxone was ineffective in the remaining eight patients. No adverse effects of naloxone were found. Plasma ACTH and immunoreactive beta-endorphin concentrations in patients with shock were not different from those in controls (ACTH, 79 +/- 28 vs 120 +/- 60 pg/ml; immunoreactive beta-endorphin, 952 +/- 262 vs 1,070 +/- 378 pg/ml). Our findings suggest that naloxone in a single dose of 4.4-5.9 mg i.v. does not improve the management of circulatory shock unresponsive to conventional treatment. beta-endorphin seems to play no major role in the hypotension of shock.

Topics: Adrenocorticotropic Hormone; Adult; Aged; beta-Endorphin; Endorphins; Female; Humans; Infusions, Intravenous; Male; Middle Aged; Naloxone; Shock; Shock, Cardiogenic; Shock, Septic

Topics: Humans; Naloxone; Shock, Cardiogenic; Shock, Septic

Topics: Humans; Naloxone; Narcotic Antagonists; Shock, Cardiogenic