AI Insight
A study in 25 anesthetized female pigs examined the hemodynamic effects of a standard 300 mg intravenous bolus of amiodarone administered over 30 minutes during normal sinus rhythm. Amiodarone reduced systolic and mean arterial blood pressure by 12%, driven by a 24% decrease in cardiac output resulting from combined reductions in both heart rate and stroke volume. The drug also impaired left ventricular contractility, as shown by decreased end-systolic elastance, while systemic vascular resistance remained unchanged, leading to ventriculo-arterial decoupling and reduced blood flow to the carotid arteries and kidneys.
Why it matters
These findings provide mechanistic insight into why intravenous amiodarone causes hypotension, which may help clinicians better anticipate and manage cardiovascular deterioration in critically ill patients receiving the drug for acute arrhythmia management.
by Laura Svanekjær, Emma Illum, Peter H. Frederiksen, Louise Linde, Anika Klein, Karoline Korsholm Jeppesen, Ann Banke, Sarah Holle, Lisette O. Jensen, Henrik Schmidt, Jens F. Lassen, Jacob E. Møller, Hanne B. Ravn
Background
Intravenous amiodarone is used for acute management of severe arrhythmias and can cause hypotension. However, amiodarone’s direct hemodynamic and myocardial effects during sinus rhythm are not well characterized.
Methods
Twenty-five anesthetized female pigs (75–80 kg) received a 300 mg intravenous bolus amiodarone over 30 minutes. To assess hemodynamic effects, animals were instrumented with a left ventricular conductance catheter, a pulmonary artery catheter, a carotid artery Doppler flow probe, and a renal vein catheter. Data were recorded at baseline, after 15 and 30 minutes and presented as median with interquartile ranges.
Results
Amiodarone reduced systolic and mean arterial blood pressure by 12% (p < 0.001) after 30 minutes infusion, primarily driven by 24% reduction in cardiac output due to combined deceased heart rate (87 (79; 99) beats per minute (bpm) to 72 (62; 81) bpm, p < 0.001) and stroke volume (69 (64; 79) mL to 64 (48; 73) mL, p = 0.004). End-systolic elastance (EES) decreased (0.54 (0.33; 0.63) mmHg/mL to 0.43 (0.29; 0.51) mmHg/mL, p < 0.001), while systemic vascular resistance and arterial elastance (EA) remained unchanged, resulting in an increased EA/EES ratio from 2.45 (2.01;3.53) to 3.26 (2.55; 4.30) (p < 0.001). This impaired cardiac function led to reduced carotid artery blood flow and renal perfusion pressure.
Conclusion
Infusion of 300 mg amiodarone intravenously in anesthetized pigs in sinus rhythm impaired left ventricular contractility and caused ventriculo-arterial decoupling with increased EA/EES ratio. This led to reduced cardiac output, blood pressure, and reduced carotid- and renal blood flow.