Clinical hypokalaemia is associated with acquired electrocardiographic QT prolongation and arrhythmic activity initiated by premature ventricular depolarizations and suppressed by lidocaine (lignocaine). Nevertheless, regular (S1) pacing at a 125 ms interstimulus interval resulted in stable waveforms and rhythm studied using epicardial and endocardial monophasic action potential (MAP) electrodes in Langendorff-perfused murine hearts whether under normokalaemic (5.2 mM K + ) or hypokalaemic (3.0 mM K + ) conditions, in both the presence and absence of lidocaine (10 μM). Furthermore, the transmural gradient in repolarization time, known to be altered in the congenital long-QT syndromes, and reflected in the difference between endocardial and epicardial MAP duration at 90% repolarization (ΔAPD 90 ), did not differ significantly (P > 0.05) between normokalaemic (5.5 ± 4.5 ms, n = 8, five hearts), hypokalaemic (n = 8, five hearts), or lidocaine-treated normokalaemic (n = 8, five hearts) or hypokalaemic (n = 8, five hearts) hearts. However, premature ventricular depolarizations occurring in response to extrasystolic (S2) stimulation delivered at S1S2 intervals between 0 and 22 ± 6 ms following recovery from refractoriness initiated arrhythmic activity specifically in hypokalaemic (n = 8, five hearts) as opposed to normokalaemic (n = 25, 14 hearts), or lidocaine-treated hypokalaemic (n = 8, five hearts) or normokalaemic hearts (n = 8, five hearts). This was associated with sharp but transient reversals in ΔAPD 90 in MAPs initiated within the 250 ms interval directly succeeding premature ventricular depolarizations, from 3.3 ± 5.6 ms to −31.8 ± 11.8 ms (P < 0.05) when they were initiated immediately after recovery from refractoriness. In contrast the corresponding latency differences consistently remained close to the normokalaemic value (−1.6 ± 1.4 ms, P > 0.05). These findings empirically associate arrhythmogenesis in hypokalaemic hearts with transient alterations in transmural repolarization gradients resulting from premature ventricular depolarizations. This is in contrast to sustained alterations in transmural repolarization gradients present on regular stimulation in long-QT syndrome models.
Cardiovascular and respiratory systems are anatomically and functionally linked; inspiration produces negative intrathoracic pressures that act on the heart and alter cardiac function. Inspiratory pressures increase with heart failure and can exceed the magnitude of ventricular pressure during diastole. Accordingly, respiratory pressures may be a confounding factor to assessing cardiac function. While the interaction between respiration and the heart is well characterized, the extent to which systolic and diastolic indices are affected by inspiration is unknown. Our objective was to understand how inspiratory pressure affects the hemodynamic assessment of cardiac function. To do this, we developed custom software to assess and separate indices of systolic and diastolic function into inspiratory, early expiratory, and late expiratory phases of respiration. We then compared cardiac parameters during normal breathing and with various respiratory loads. Variations in inspiratory pressure had a small impact on systolic pressure and function. Conversely, diastolic pressure strongly correlated with negative inspiratory pressure. Cardiac pressures were less affected by respiration during expiration; late expiration was the most stable respiratory phase. In conclusion, inspiration is a large confounding influence on diastolic pressure, but minimally affects systolic pressure. Performing cardiac hemodynamic analysis by accounting for respiratory phase yields more accuracy and analytic confidence to the assessment of diastolic function.
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