Hemodynamic effects of nitroglycerin-induced vasodilation in acute heart failure
J Lukoschewitz, F F Lau, E Seven, J Kjaergaard, J Hove, N B Foss, J G GrandAbstract
Background
Acute heart failure is a life-threatening syndrome associated with high 1-year mortality. Intravenous nitroglycerin is recommended in selected patients for reducing cardiac filling pressures and afterload. However, its hemodynamic effects in this syndrome are not fully understood. This study evaluated the acute hemodynamic effects of nitroglycerin-induced vasodilation in patients hospitalised with acute heart failure.
Methods
In this interventional study, patients hospitalised with acute heart failure and a systolic blood pressure >85 mmHg were enrolled. Nitroglycerin was per protocol titrated to achieve a 20–30% reduction in mean arterial pressure (MAP) for 90 minutes, followed by a 90-minute control phase. Hemodynamic parameters were continuously monitored using the lithium dilution cardiac output system (LiDCO). The primary outcome was change in stroke volume. Secondary outcomes included changes in MAP, cardiac output, heart rate, systemic vascular resistance (SVR) and urine output. Exploratory outcomes included echocardiographic measurements. Repeated measures were analysed using mixed-effects models.
Results
Twenty-one patients were included (mean age, 78 ± 11 years; 48% women). Pulmonary oedema was the cause of admission in 24%, while 76% presented with acute decompensated heart failure. Of all patients, 48% had heart failure with reduced ejection fraction, and 52% had heart failure with preserved ejection fraction. The median total nitroglycerin dose administered was 38 mg (range, 6–87 mg). Stroke volume decreased during nitroglycerin infusion from 79 mL (95% CI, 66–92) at baseline to 70 mL (95% CI, 57-84) at 90 minutes (−9 mL, −11%), and increased to 79 mL (95% CI, 65–92) during the control phase. Stroke volume remained significantly lower throughout the vasodilation phase compared with the control phase (−15 mL at 90 minutes; p < 0.001). Echocardiography confirmed this reduction and demonstrated significant decreases in estimated cardiac filling pressures and central venous pressure. MAP declined during vasodilation from 79 mmHg (95% CI, 73–84) to 69 mmHg (95% CI, 64–75), a reduction of 10 mmHg (−13%). During the control phase, MAP increased to 74 mmHg (95% CI, 68–80) (p < 0.001). Cardiac output decreased by 7% during vasodilation. Heart rate increased during vasodilation with approximate 4 beats per minute but there was no statistically significant difference from the control phase. No significant differences in SVR were observed between phases. Urine output increased more rapidly during vasodilation than during the control phase (89 mL/h vs 44 mL/h), corresponding to an additional 45 mL/h (p = 0.002).
Conclusion
In patients with acute heart failure, nitroglycerin-induced vasodilation reduced stroke volume assessed by LiDCO and was possibly associated with lower cardiac filling pressures based on echocardiographic estimates, reflecting a complex hemodynamic response to vasodilator therapy.Figure 1:Changes in HemodynamicFor image description, please refer to the figure legend and surrounding text.