Ming H. Hwang

Regional changes in blood flow, extracellular potassium and conduction during myocardial ischemia and reperfusion

OBJECTIVESnWe postulated that ventricular arrhythmias may arise from the heterogeneous washout of ischemic metabolites. Our objective was to investigate the distribution of extracellular potassium concentration ([K+]o) during myocardial ischemia and reperfusion and to correlate this distribution with regional differences in myocardial blood flow.nnnBACKGROUNDnOur previous study showed that reperfusion after a brief period of ischemia resulted in heterogeneous reflow of the ischemic myocardium.nnnMETHODSnThe changes in regional myocardial blood flow, midmyocardial [K+]o and electrogram duration were quantitated in 14 dogs undergoing 20 min of left anterior descending coronary artery occlusion and 1 min of reperfusion. Regional myocardial blood flow was measured by using 15-microns radioactive microspheres in 1- to 1.5-g full thickness myocardial samples. The [K+]o was measured with intramyocardial K(+)-sensitive electrodes.nnnRESULTSnDuring coronary occlusion, the ischemic zone exhibited a reduction in regional blood flow to 0.13 +/- 0.06 ml/g per min and increases in [K+]o to 9.3 +/- 2.6 mmol/liter and electrogram duration to 131.8 +/- 38.6% of control. Heterogeneous reduction in regional blood flow at various sites in the ischemic zone had fair correlations with variable increases in [K+]o (r = -0.70) and electrogram duration (r = -0.75). During min 1 of reperfusion, regional blood flow ranged from two to more than seven times baseline, resulting in a disorganized spatial distribution of perfusion with islands of high and low blood flows. Associated with the heterogeneous early reperfusion regional myocardial blood flow, [K+]o and electrogram duration changed at different rates toward normal. Whereas correlation between regional blood flow and [K+]o or standardized electrogram duration was fair during ischemia, this correlation was poor during early reperfusion.nnnCONCLUSIONSnSpatial heterogeneity in regional myocardial blood flow during myocardial ischemia and early reperfusion is associated with heterogeneity in [K+]o and electrophysiologic characteristics, which in turn may play an important role in the genesis of arrhythmias arising from the ischemic and reperfused myocardium.

Effect of acute pericardial tamponade on the relative contributions of systolic and diastolic pulmonary venous return: A transesophageal pulsed Doppler study

The effect of acute pericardial tamponade on pulmonary venous return was assessed by transesophageal pulsed Doppler echocardiography. In 14 open-chest anesthetized dogs peak pulmonary venous flow velocities in systole (VJ) and in diastole (VK) were measured during apnea and atrial pacing while acute tamponade was induced by intrapericardial instillation of 0.9% sodium chloride solution. Before intravascular volume expansion, induction of acute tamponade resulted in a significant decline in VK (43 +/- 17 to 19 +/- 8 cm/sec; p < 0.05) but no change in VJ or the ratio VJ/VK. After intravascular volume expansion, induction of acute tamponade resulted in significant reductions in VJ (43 +/- 9 to 29 +/- 10 cm/sec; p < 0.001) and VK (37 +/- 19 to 15 +/- 11 cm/sec; p < 0.001). The effect was disproportionately greater on VK, however, resulting in a significant increase in VJ/VK (1.51 +/- 0.84 to 2.58 +/- 1.41; p < 0.001). The disproportionate effect of acute tamponade on VK suggests that increased pericardial pressure directly constrains diastolic filling of the left atrium as a conduit to the left ventricle and that it does not decrease the systolic and diastolic phases of pulmonary venous return uniformly. Intravascular volume expansion increases cardiac output before acute tamponade, but during acute tamponade it amplifies the disproportionate impact of increased pericardial pressure on left ventricular diastolic filling as the left ventricle is constrained within the fluid-filled pericardial sac.

Various Electrocardiographic and Electrophysiologic Presentations of Normal and Abnormal Sinus Node

Electropbysiology of the Sinus Node. Differentiation of normal from abnormal sinus nodal function is frequently difficult because the electrocardiographic and electrophysiologic presentations of abnormal and normal sinus nodal function are quite diverse. The autonomic nervous system greatly influences sinus nodal function, making this differentiation even more complicated. Data obtained from the recording of sinus nodal electrogram in animals and humans have helped in elucidating changes in automaticity and conduction of the sinus node. In this review, we provide examples of rhythms related to normal and abnormal sinus nodal function. (J Cardiovasc Electrophysiol, Vol. 3, pp. 187–197, April 1992)

Impairment of myocardial vascular responsiveness after transient myocardial ischemia and reperfusion

Coronary vascular responses after brief periods of myocardial ischemia are impaired. Whereas some studies suggest that the ischemic insult selectively depresses endothelium-dependent vasodilator mechanisms, other studies indicate that even responses to direct vascular smooth-muscle relaxants such as adenosine may be decreased. This study was undertaken to measure regional myocardial blood flow (RMBF) responses to adenosine (a direct coronary vasodilator) and serotonin (an indirect, endothelium-dependent vasodilator) in myocardium subjected to regional ischemia followed by reperfusion. Temporary regional ischemia was achieved by 20 minutes of occlusion of the left anterior descending coronary artery (LAD) followed by 20 minutes of reflow in 10 open-chest anesthetized dogs. In the left circumflex coronary artery (LCX) territory, which served as a nonischemic control, RMBF (measured with radioactive microspheres) increased significantly in response to left atrial infusions of adenosine (1.29 +/- 0.27 to 3.89 +/- 3.89 +/- 2.15 ml/min/gm; p < 0.001) and serotonin (1.29 +/- 0.27 to 3.29 +/- 1.49 ml/min/gm; p < 0.001) and the percent reduction in coronary vascular resistance (% delta CVR) was comparable for these two pharmacologic probes (65% +/- 26% vs 62% +/- 19%; difference not significant [NS]). In contrast, in the myocardium supplied by the LAD, which was subjected to ischemia followed by reperfusion, the augmentation of RMBF by adenosine (1.07 +/- 0.29 to 1.82 +/- 1.35 ml/min/gm; p < 0.001) and serotonin (1.07 +/- 0.29 to 2.37 +/- 1.21 ml/min/gm; p < 0.001) was blunted.(ABSTRACT TRUNCATED AT 250 WORDS)

Pacemaker Malfunction Simulated by Amplifier Saturation

In this case report, pacemaker malfunction is simulated by prolonged pauses after each pacemaker discharge. The pauses were due to saturation of the input of the telemetry monitor amplifier by the discharge voltage of the pacemaker. It is important to recognize amplifier saturation as a form of artifact that can mimic pacemaker malfunction.