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Published on: July 7, 2016
Cardiovascular effects of atropine in postoperative cardiac patients receiving digoxin for ventricular dysfunction
Insights
Blocking digoxin's cholinergic effects with atropine significantly increased cardiac output in postoperative patients. This intervention offers a potential method to enhance cardiovascular function in this population.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Digoxin is a key cardiac medication for arrhythmias and inotropic support.
- Its therapeutic actions involve the cholinergic nervous system, which can depress ventricular function.
- The study explored augmenting digoxin's effects by antagonizing its cholinergic pathways.
Purpose of the Study:
- To investigate the impact of atropine, a cholinergic blocker, on the cardiovascular effects of digoxin.
- To determine if blocking digoxin's cholinergic effects can enhance cardiac output in postoperative cardiac patients.
Main Methods:
- Ten postoperative cardiac patients received 1 mg of intravenous atropine.
- Cardiovascular parameters including cardiac output were monitored for 8 hours using ECG and advanced hemodynamic monitoring.
- Statistical analysis was performed to assess changes in cardiovascular metrics.
Main Results:
- A significant increase in cardiac output (CO) was observed within 2 hours post-atropine administration (p < 0.05).
- Cardiac output rose from 5.98 L/min to 6.60 L/min.
- No significant changes were noted in heart rate, systemic vascular resistance, pulmonary artery wedge pressure, or systemic blood pressure.
Conclusions:
- Cholinergic blockade of digoxin with atropine acutely enhances cardiac output in postoperative cardiac patients.
- This strategy may offer a method to improve cardiovascular performance in specific patient groups.
- Further research could explore the sustained effects and broader applications of this intervention.
Abstract:
Digoxin is clinically useful as a cardiac antiarrhythmic and inotropic agent. Its antiarrhythmic actions are mediated through the cholinergic nervous system. The cholinergic system, when activated, can depress ventricular function. We have sought to further increase the cardiovascular effects of digoxin by blocking its cholinergic effects with atropine. Atropine, 1 mg intravenously, was given to 10 postoperative cardiac patients. The cardiovascular time course was monitored by an ECG, radial arterial line, and pulmonary artery thermodilution catheter for 8 hours. A significant increase (p less than 0.05) in the cardiac output (CO), from 5.98 +/- 0.24 L/min to 6.60 +/- 0.34 L/min, was evident within 2 hours after atropine administration. The CO returned to control levels by 6 hours. There were no significant changes in heart rate, systemic vascular resistance, pulmonary artery wedge pressure, or systemic blood pressure. The results indicate that the cholinergic blockade of digoxin with atropine will acutely increase the cardiac output in postoperative cardiac patients.
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