It would be well beyond the scope of this single page to undertake to provide a more complete discourse on electrocardiography. Instead, we will focus on the core electrocardiographic conversations around our PICSI product (physiological intuitive computer system interface). With a better understanding of ECG, you can better discern the differences between the majority of sensors and the PICSI/Bionet project.


Electrocardiology Basics
ECG as it relates to the heart






The electrocardiogram waveform is a representation of the electrical activity from within the heart.
When the electrical signal of a depolarization reaches the contractile cells, they contract. When the repolarization signal reaches the myocardial cells, they relax. Thus, the electrical signals cause the mechanical pumping action of the heart.

The Sinoatrial (SA) node is the normal pacemaker of the heart, initiating each electrical and mechanical cycle. When the SA node depolarizes, the electrical stimulus spreads through the atrial muscle causing the muscle to contract. Thus, the SA node depolarization is followed by atrial contraction.

The SA node impulse also spreads to the atrioventricular node (AV node) via the internodal fibers. (The wave of depolarization does not spread to the ventricles right away because there is nonconducting tissue separating the atria and ventricles.) The electrical signal is delayed in the AV node for approximately 0.20 seconds when the atria contract, and then the signal is relayed to the ventricles via the bundle of His, right and left bundle branches, and Purkinje fibers. The Purkinje fibers, relay the electrical impulse directly to ventricular muscle, stimulating the ventricles to contract (ventricular systole). Repolarization of the SA node is also spread throughout the atria, and then the ventricles, starting the relaxation phase (ventricular diastole).

Although the heart generates its own beat, the heart rate, measured in beats-per-minute or (BPM) and strength of contraction of the heart are modified by the sympathetic and parasympathetic divisions of the autonomic nervous system.

The sympathetic system acts as an accelerator, speeding up and increasing the contractile force of the heart. Whenever oxygen demands increase, e.g., during exercise or if blood pressure drops, the sympathetic input increases, causing heart rate and strength of contraction to increase. Sympathetic influence increases during inhalation.
The parasympathetic input acts as a brake, slowing down the heart. When you relax, the parasympathetic input becomes dominant and the heart rate slows. Parasympathetic influence increases during exhalation.

The Electrocardiogram

Just as the electrical activity of the pacemaker is communicated to the cardiac muscle, “echoes” of the depolarization and repolarization of the heart are sent through the rest of the body. By placing a pair of very sensitive receivers (electrodes) on other parts of the body, the echoes of the heart’s electrical activity can be detected. The record of the electrical signal is called an electrocardiogram (ECG). You can infer the heartís mechanical activity from the ECG.

The electrical events of the heart are usually recorded on the ECG as a pattern of a baseline broken by a P wave, a QRS complex, and a T wave.

  • The baseline (isoelectric line) is a straight line on the ECG. It is the point of departure for the electrical activity of depolarizations and repolarizations of the cardiac cycles.
    The P wave results from atrial depolarization.
    The QRS complex is a result of ventricular depolarization and indicates the start of ventricular contraction.
    The T wave results from ventricular repolarization and signals the beginning of ventricular relaxation.

The electrical signal for atrial repolarization is masked by the larger QRS complex.

ECG Morphology
Atrial Fibrillation
Myocardial Infarct
ST Segment
Reference Documents

Recommendations for the Standardization and Interpretation of the Electrocardiogram – Part I: The Electrocardiogram and Its Technology: A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology