Will drinking cold water prior to an ECG alter the T wave reading?

Answer 1

No the T wave represents repolarization and is only altered by changes to the myocardium such as anoxia.

Answer 2

Not to my knowledge and I look at ECG's everyday.

Answer 3

The electrical activity forms a series of waves and complexes separated by regularly occurring intervals. These waves and complexes have been arbitrarily labeled as the P wave, the QRS complex, and the T wave. The P Wave is formed as the electrical impulse spreads across the atria (depolarization) and causes both atria to contract The QRS Complex is the deflection that is formed as the electrical impulse spreads from the Purkinje fibers to the ventricles (depolarization), causing both ventricles to contract. The T Wave is the wave formed after ventricles contract, which represents the ventricular resting period (repolarization). During the resting period the chambers fill with blood for the next contraction. Graph PaperThe graph paper moves through an ECG machine at a standard speed. This allows each vertical line to represent time. Each Small Box = 0.04 seconds and the Large Box = 0.20 seconds. Three-second time intervals are marked at the top of the ECG paper for your convience. The graph paper is usually started and stopped by a control button placed on the top or front of the monitor.

The T wave is the most labile wave in the ECG. T wave changes including low-amplitude T waves and abnormally inverted T waves may be the result of many cardiac and non-cardiac conditions. The normal T wave is usually in the same direction as the QRS except in the right precordial leads (see V2 below). Also, the normal T wave is asymmetric with the first half moving more slowly than the second half. In the normal ECG the T wave is always upright in leads I, II, V3-6, and always inverted in lead aVR. The other leads are variable depending on the direction of the QRS and the age of the patient.

Survive:

Ten subjects (6 males, 4 females) aged between 24 and 34 years were studied. All subjects were normotensive, non-smokers, on no medication and were screened by history and physical examination to exclude cardiovascular or neurological dysfunction. In addition four cardiac transplant recipients were recruited (2 males, 2 females) aged between 50 and 62 years and between 2 and 9 years post- transplant. In each patient persistent cardiac vagal dennervation had been confirmed by power spectral analysis of ECG recordings and lack of measurable baroreflex sensitivity by the phenylephrine bolus method.

Subjects were studied in a random-order crossover design and all studies were commenced at 08.00 hours after a 12-h fast. Subjects were asked to avoid alcohol for at least 24h before each study and to empty their bladder before starting the study. Transplant recipients withheld their regular medication on the morning of each study, with the exception of immunosuppressive therapy. The laboratory temperature was kept constant at 23±1 °C and subjects rested in the semi-supine position throughout. A standard three-lead ECG signal was amplified, processed [high frequency (HF) signal noise filter >500Hz], and digitized at 500Hz with the use of a National Instruments NB/MI0/16XH/18 analog-to-digital converter board (National Instruments Corporation, Newbury, Berks., U.K.). A continuous arterial pressure signal was obtained with the Portapres device (TNO Biomedical Instrumentation, Amsterdam, The Netherlands) and was similarly digitized. Respiratory excursion was recorded from the amplified output of a standard strain gauge attached to an elastic strap around the subject's chest. All signals were displayed on the screen of a personal computer running Laboratory View 5.0 software (National Instruments Corporation). In addition, blood pressure was recorded throughout the protocol at 5min intervals, taking the mean for three consecutive measurements using automated arm cuff sphygmomanometry.

Subjects were rested for 30min, after which 5-min segments of the three digital signals were recorded during breathing at the predetermined frequency and stored to disk. Subjects were then asked to drink tap water at 18°C as quickly as was comfortable. All subjects were randomly assigned to drinking 500ml or 20ml (control) of water during the first of two studies. The second volume was given during a separate study visit 7 to 14days later. ECG and blood pressure monitoring continued for a further 45min whilst 5min recordings for analysis of heart rate variability were stored at 5, 20 and 35min after drinking during fixed frequency respiration.

Data analysis:

The ECG series for analysis were coded so that the investigator performing the analysis was blinded to the nature of the study. All ECG series were reviewed and if necessary edited to exclude ectopic and artifact signals. The RR intervals before and after any ectopic beats were replaced by interpolation from the previous and following sinus intervals. No signal containing >1% of ectopic beats was used for analysis. R waves were detected by an individually adjusted threshold. Heart rate variability (HRV) was analysed off-line on data lengths of 256 RR intervals.

Time domain analysis:

Using the standard time domain measures of root-mean-square of successive RR interval differences (RMSSD), and percentage of successive RR interval differences exceeding 50ms (pNN50). These indices, based on successive differences in RR intervals, assess HF ('beat-to-beat') variation associated with respiratory sinus arrhythmia mediated principally by the vagus nerve.

Statistical analysis

Data for arterial blood pressure and RR interval in the water and control arms of the study were compared by a two-tailed paired Student's t test. Differences between groups for time and frequency domain indices of HRV were determined with the Wilcoxon signed rank test for paired data. Statistical significance was defined by a value of P<0.05. Numerical values are expressed as mean±S.E.M.

RESULTS

The frequency of metronomic breathing was within the range 0.18 to 0.22Hz. Baseline values for mean arterial pressure, RR interval, and indices of HF HRV were not significantly different in the group before drinking 500ml or 20ml of water. Drinking 500ml of water did not result in any change in arterial blood pressure measured by Portapres or brachial sphygmomanometry. After ingesting 500ml of water there was, however, a fall in the heart rate in each of the ten subjects. This decrease was maximal at 20min after ingestion. The heart rate returned to a level not statistically different from baseline values at 40min. In contrast, in the control arm of the study, with the same subjects drinking 20ml of water, there was no significant change in the heart rate.

The physiological response to water drinking in normal subjects appears to be complex, involving both limbs of the autonomic nervous system. Only when the normal response to water drinking is clearly understood will we be able to explain the powerful and potentially useful effects of water ingestion on blood pressure in subjects with autonomic dysfunction.