Overexpression of the HCN2 channel increases the arrhythmogenicity induced by hypokalemia.

Hypokalemia, an abnormally low level of potassium (K), is a electrolyte imbalance that commonly occurs in heart failure patients. Hypokalemia is well known to induce lethal ventricular arrhythmia. However, the effects of hypokalemia in failing hearts that have undergone electrophysiological remodeling, i.

HCN4 pacemaker channels attenuate the parasympathetic response and stabilize the spontaneous firing of the sinoatrial node.

Key Points: The contribution of HCN4 pacemaker channels in the autonomic regulation of the sino-atrial node (SAN) has been a matter of debate. The transgenic overexpression of HCN4 did not induce tachycardia, but reduced heart rate variability, while the conditional knockdown of HCN4 gave rise to sinus arrhythmia. The response of the SAN to β-adrenergic stimulation was not affected by overexpression or knockdown of HCN4 channels.

A significant complication that occurred during insertion of dual guidewires into the right internal jugular vein for central venous catheterization.

We report a significant complication that occurred during double guidewire insertion. The first guidewire (GW1) was inserted under ultrasonographic guidance, whereas the second guidewire (GW2) was inserted by the landmark-based method. Subsequently, GW2 penetrated and entangled with GW1, which caused difficulty in removing both guidewires.

A case of delayed emergence from anesthesia caused by postoperative brain edema associated with unexpected cerebral venous sinus thrombosis.

Cerebral venous sinus thrombosis (CVST) is rare but displays various and often dramatic clinical symptoms. Few cases of CVST have been reported in the field of anesthesiology. We encountered an unexpected case of CVST that presented with delayed emergence from anesthesia after resection of a brain tumor.