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- Fri Aug 13, 2010 11:41 am
How many Milli-Volts (mV) is generated by Sinoatrial Node in the heart [not using an EKG or ECG machine, the acctual Volts given off during a heart beat (P wave) measured off of the heart its self]. This may seem like just a trivial question but the implications of the answer is quite important.
-Thank You to all who can help me with this.
| Dr.M.Aroon kamath
- Mon Aug 30, 2010 8:38 am
The voltages of the action potentials recorded from for example, the SA node are a lot different than those voltages seen on surface electrocardiograms. In a surface EKG, the various waves that you see are a sum of the electrical waves of depolarization and repolarization and not from the individual cells.
The voltages recorded at the surface are modified by many factors including,
- the thickness of the myocardium,
- the pericardium,
- overlying lung tissue and pleurae,and
- the thicknesss of the chest wall.
Pacemaker action potentials: In contrast to the other excitable tissues such as the skeletal muscle and the neurons whose action potential lasts for only a few milliseconds, the cardiac action potential in general exhibits a duration exceeding 150 milliseconds and generally displays a prominent plateau. The time spent by the action potential above 0 mV is called the overshoot.The SA nodal (pace maker) action potential is different from that of the cardiac myocytes in that there are no "fast" sodium (Na+) channels in the SA nodal cell membranes. Rather, there are "slow" calcium (Ca++) channels which are of 4 types(A,B,C and D). The calcium channels open one after the other allowing a slow influx of calcium ions into the cell. Because of this, the pacemaker action potential begins slowly. SA nodal cells do not have a stable resting membrane potential and that is the reason why they automatically generate action potentials.The "resting potential" of -60mV, the voltage slowly increases to -30 to -40 mV("pacemaker potential") at which point ("threshold potential"), the depolarization speeds up with an upstroke in the tracing which can rise upto +10 to +20 mV.
In contrast, the surface ECG records a P wave of approximately + 2.5 mV.
It is well known that low voltage complexes can occur in several conditions including,
- obese individuals,
- in myxedema,
- in COPD,
- pleural effusion,
- pleural effusions etc.
It has been seen in cases of congestive cardiac failure, that the voltages on surface EKG become attenuated.One study which studied this phenomenon objectively, concludes thus:
"Drawing on the experience from patients with a diversity of edematous states it now appears that the underlying common mechanism of this phenomenon is extracardiac, mediated by the decrease in the electrical impedance of the body volume conductor enveloping the heart and resulting from the fluid engorged interstitium (interstitial fluid has the lowest possible special resistance in the body). The lowering of electrical impedance of the body volume conductor is translated in turn into attenuated body surface ECG potentials. As expected, amelioration of the PERED results in augmentation of the QRS complexes, P waves, and T waves".
. Geddes LA, Baker LE. The specific resistance of biological material -- a compendium of data for the biomedical engineer and physiologist. Med Biol Eng 1967; 5:271-293.
. Madias JE, Bazaz R, Agarwal H, Win M, Medepalli L. Anasarca-mediated attenuation of the amplitude of electrocardiogram complexes: A description of a heretofore unrecognized phenomenon. J Am Coll Cardiol 2001; 38:756-764.
. Madias JE. P waves in patients with changing edematous states: Implications on interpreting repeat P wave measurements in patients developing anasarca or undergoing hemodialysis. Pacing Clin Electrophysiol 2004; 27:749-756.
. Madias JE. T-wave amplitude attenuation/augmentation in patients with changing edematous states: Implications for patients with congestive heart failure.
Congestive Heart Failure Volume 13, Issue 5, pages 257–261, September/October 2007
I hope this information is of use to you.