T-wave

Figure 8.3. Wave interactions in planar tensile fracture experiment, (a) Shows the distance-time plot of interacting compression C , rarefaction R , and tension T , waves (b) Shows the corresponding particle-velocity profiles including the initial compressive shock wave (tj, tj), the pull-back signal (tj, tj), and subsequent reflection >h).

Electrocardiogram (ECG) May be normal or could show numerous abnormalities including acute ST-T-wave changes from myocardial ischemia, atrial fibrillation, bradycardia, and LV hypertrophy. 

After an electrical impulse is initiated and conducted, there is a period of time during which cells and fibers cannot be depolarized again. This period of time is referred to as the absolute refractory period (Fig. 6-2),2 and corresponds to phases 1,2, and approximately half of phase 3 repolarization on the action potential. The absolute refractory period also corresponds to the period from the Q wave to approximately the first half of the T wave on the ECG (Fig. 6-2). During this period, if there is a premature stimulus for an electrical impulse, this impulse cannot be conducted, because the tissue is absolutely refractory. 

Hyperkalemia is defined as a serum potassium concentration greater than 5 mEq/L (5 mmol/L). Manifestations of hyperkalemia include muscle weakness, paresthesias, hypotension, ECG changes (e.g., peaked T waves, shortened QT intervals, and wide QRS complexes), cardiac arrhythmias, and a decreased pH. Causes of hyperkalemia fall into three broad categories (1) increased potassium intake (2) decreased potassium excretion and (3) potassium release from the intracellular space. 

ECG may indicate prolonged PR interval, shortened QT interval, and widened T wave. 

Acute coronary syndromes Ischemic chest discomfort at rest, most often accompanied by ST-segment elevation, ST-segment depression, or T-wave inversion on the 12-lead electrocardiogram. Furthermore, it is caused by plaque rupture and partial or complete occlusion of the coronary artery by thrombus. Acute coronary syndromes include myocardial infarction and unstable angina. Former terms used to describe types of acute coronary syndromes include Q-wave myocardial infarction, non-Q-wave myocardial infarction, and unstable angina. 

Figure 13.4 Electrocardiogram. The electrocardiogram (ECG) is a measure of the overall electrical activity of the heart. The P wave is caused by atrial depolarization, the QRS complex is caused by ventricular depolarization, and the T wave is caused by ventricular repolarization.

Second, the area under the curve of the P wave is small compared to that of the QRS complex. This is related to the muscle mass of the chambers. The ventricles have significantly more muscle than the atria and therefore generate more electrical activity. Furthermore, although it may not appear to be the case given the spike-like nature of the QRS complex, areas under the QRS complex and the T wave are approximately the same. This is because these recordings represent electrical activity of the ventricles even though one is caused by depolarization and the other by repolarization. Either way, the muscle mass involved is the same. 

ECG TP segment P wave PR segment QRS complex ST segment T wave... 

Harrison GR (1939) M. I. T. wave-length tables of 100,000 spectrum lines. New York... 

Figure 1. Experimental waveforms from excitation (266 nm) of 2-hydroxybenzophenone (T-Wave, and acetone in air-saturated (E-Wave(l)) and argon-saturated (E-Wave(2)) cyclohexane. (With permission from Joshua L. Goodman.)...

ECG changes include increased heart rate, flattened T waves, ST-segment depression, prolongation of QT and PR intervals, and torsade de pointes. Torsade de pointes has been reported with thioridazine, which may be a cause of cardiac sudden death. 

Electrocardiogram (ECG) changes include shortening of the QT interval and coving of the ST-T wave. 

Cardiovascular manifestations include hypertension and cardiac arrhythmias (e.g., heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, and digitalis-induced arrhythmias). In severe hypokalemia (serum concentration <2.5 mEq/L), ECG effects include ST-segment depression or flattening, T-wave inversion, and U-wave elevation. 

The earliest ECG change (serum potassium 5.5 to 6 mEq/L) is peaked T waves. The sequence of changes with further increases is widening of the PR interval, loss of the P wave, widening of the QRS complex, and merging of the QRS complex with the T wave resulting in a sine-wave pattern. 

ECG changes include widened QRS complexes and peaked T waves in mild deficiency. Prolonged PR intervals, progressive widening of the QRS complexes, and flattening of T waves occur in moderate to severe deficiency. 

Time to incapacitation for the 100, 102, 123, 147, and 156 ppm concentrations were 19, 16, 15, 8, and 8 min, respectively the relationship between exposure and time to incapacitation was linear. During exposures, effects consisted of hyperventilation (within 30 s), loss of consciousness, and bradycardia with arrhythmias and T-wave abnormalities recoveries were rapid after exposure. The animal inhaling 147 ppm stopped breathing after 27 min and required resuscitation. Two additional exposures were terminated prior to the end of the 30 min due to severe signs. Animals rapidly recovered and were active during the first 10 min after exposure even though blood cyanide remained at levels that initially caused incapacitation. Purser (1984) states that the hyperventilatory response followed by incapacitation occurs at >80 ppm, but neither paper (Purser 1984 Purser et al. 1984) provides the experimental data for the 80 ppm concentration. At 180 ppm, hyperventilation occured almost immediately, and at 90 ppm the response was delayed for 20 min. 

The Lord is not worshipped with material things, but with one s own consciousness. Don t wave lights and incense, or offer flowers and food. He is found effortlessly when worshipped through self-realisation alone. The continuous and unbroken awareness of the indwelling Presence, the inner light of consciousness, is the supreme meditation and devotion. 

The QT interval (measured from the beginning of the Q wave to the end of the T wave of the surface electrocardiogram) reflects the duration of individual action potentials in cardiac myocytes (Figure 3.1) indeed, a prolongation of the action potential duration (APD) of myocytes will result in a prolonged QT interval. 

Changes in heart rate require correction different formulas may optimize correction in different species Definition of the end of the T wave is problematic in some species such as the dog, having a variable morphology of the T wave... 

Measurement of QT interval Definition of the end of the T wave. Changes in T wave morphology and occurrence of U waves (these may be important warning signs and precede the occurrence of TdP) Errors in manual measurement in QT interval Variability in the heart rate (need to correct the QT value for heart rate) Lack of reliable correlation between readings from Holter recordings and standard ECG Lack of standardization of automated ECG readings (computerized methods are often unreliable) Need for a central core laboratory to analyze data... 

Figure 4.2 Cartoon representation of an ECC trace and ventricular cardiac action potential, (a) A representation of an ECC trace with its five typical deflections (PQRST) arising from the spread of electrical activitythrough the heart. The QRS wave denotes the ventricular depolarization, while the T wave represents ventricular repolarization. The QT interval therefore estimates the duration of a ventricular action potential, (b) Schematic of the five phases of a ventricular action potential. Phase 0 is the rapid depolarization phase due to a large influx of Na+ ions (Ina). Phase 1 occurs with the inactivation of Na+ channels and the onset of transient outward (repolarizing) currents (/to)...

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