Introduction to Electrophysiology;

What are they doing in there?

ECG Complexes and Intervals As Related To The Ventricles:

QRS Complex Represents Ventricular Depolarization

Labeling:

• If the first deflection is negative it is the Q
• All upright deflections are R waves
• A negative deflection following an  R is an S
• Capital letters are used to label tall waves, small letters for small waves

T Wave represents ventricular repolarization:

Direction:

• Upright in I,II, V3-6
• Variable in III, AVL, AVF, V1, V2
• Inverted in AVR may be related to one of the following; myocardial ischemia, ventricular hypertrophy, BBB, pericarditis, cor pulmonale, cardiomyopather, electrolyte imbalance, metabolic deficiency, digitalis intoxication

Shape:

• Normally slightly rounded
• Slightly asymmetrical
• Sharply pointed or notched may be normal and is common in children; also found in pericarditis.  A sharply pointed T wave, either upright or inverted, is suspicious for an MI

Height:

• Normally not above 5 mm in any standard lead and not above 10 mm in any precordial lead
• Tall ususally indicative of MI or elevated potassium
• Tall T can also bbe seen in myocardial ischemia without an infarction, ventricular overload, psychotics and CVA
• Flat T wave can be seen in obesity with the normal amplitude returning after weight loss.

Q-T Interval is the time between onset of ventricular depolarization and end of ventricular repolarization.:

• Beginning of the QRS to the end of the T wave
• Affected by autonomic influences and catecholamines
• Fluctuates diurnally becoming longer during sleep
• Varies with heart rate, sex, age
• Ashman chart or nomogram for QTc – corrected QT interval
• QT should be less than half the preceding R-R interval except if the HR <65 or > 90
• Proportionate to the preceeding cycle
• U wave may merge with QT – presence of U wave is abnormal and may be related to hypokalemia, hypomagnesemia, ischemia

Prolonged QT:

• Lengthened by ischemic heart disease, rheumatic fever, MI, myocarditis, mitral valve prolapse
• Electrolyte disturbances, hypocalcemia, hypokalemia, hypomagnesemia, hypothyroidism
• Subarachnoid or intracerebral hemorrhage, stroke
• Antiarrhythmics – eg: sotolol Trade Name BETAPACE amiodarone Trade Name CORDARONE quinidine Trade Names CARDIOQUIN QUINAGLUTE - tricyclic antidepressants, phenothiazines, other drugs
• Hypothermia
• Stringent dieting

Shortened QT:

• Digitalis
• Hyperkalemia
• Hypercalcemia
• Hypermagnesemia

U Wave:

• Low voltage, small wave
• Polarity usually same as T wave
• Best seen in V3
• Taller with hypokalemia
• Inverted with myocardial ischemia aortic or mitral regurg, and left ventricular overload from HTN.
• Negative U in resting ECG may show significant stenosis of left main or LAD
• Affected by digitalis, quinidine, epinephrine, hypercalcemia, thyrotoxicosis, intracranial hemorrhage and exercise - all of which will increase the amplitude of the U wave.  Size may vary with cycle length – the longer the cycle length, the taller the U wave

Want to know more about the U wave?  Go Here

Refer to the discussion on the the heart’s conduction system.

From the ECG Learning Center
Dr. Alan Lindsay. Excellent site for learning to read ECGs.

P Wave:

• Normally upright in Lead I, II, V4-6 and AVF
• Normally inverted in AVR
• Variable in Lead III, AVL and other chest leads
• Amplitude should not exceed 2 -3 mm in any lead
• Normal conture gently rounded rather than pointed and notched

P Wave  Abnormalities

• Inversion when shouldbe upright (ectopic atrial or junctional)
• Increased amplitude: atrial hypertrophy or dilation, valve disease, HTN, cor  pulmonale
• Increased width: Left atrial enlargement P< 0.11
• Diphasic LAE (Lead III, or V1)
• Notching P. mitrale I.  III signifcant when peak distance > 0.04
• Peaking P-Pulmonale III>I
• Absence of P waves

Tp Wave (Ta)

• Represents atrial recovery
• Opposite direction of P wave

P – R Interval

• 0.12 – 0.20 seconds
• Varies with heart rate
• If conduction system is diseased or affected by digitalis, P-R may lengthen as if conducting system as the rate increases.

Prolonged PR Interval

• AV block due to coronary disease, rheumatic disease,
• In some cases of Hyperthyroidism
• As a normal varriation (1.3%)

Shortened PR Interval

• AV junctional and low atrial rhythms
• WPW
• Normal variation
• Glycogen storage issue
• Pheochromocytoma
• Some hypertensive patients
• Fabry’s disease

PR Segment

• Normally isoelectric
• May be displaced in atrial infarction and acute pericarditis 

Atrial Fibrillation Electrophysiology

The normal electrical conduction system of the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to and stimulate the myocardium (muscle of the heart). When the myocardium is stimulated, it contracts. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped to the body.

In atrial fibrillation, the regular impulses produced by the sinus node for a normal heartbeat, are overwhelmed by rapid electrical discharges produced in the atria and adjacent parts of the pulmonary veins. Sources of these disturbances are either automatic foci, often localized at one of the pulmonary veins, or a small number of reentrant sources (rotors) harbored by the posterior wall of the left atrium near the junctions with the pulmonary veins. The pathology progresses from paroxysmal to persistent AF as the sources multiply and localize anywhere in the atria. Because recovery of the atria from excitation is heterogeneous, the electrical waves generated by the AF sources undergo repetitive, spatially distributed breakup and fragmentation in a process known as “fibrillatory conduction”.

AF can be distinguished from atrial flutter (AFL), which appears as an organized electrical circuit usually in the right atrium. AFL produces characteristic saw-toothed F-waves of constant amplitude and frequency on an ECG whereas AF does not. In AFL, the discharges circulate rapidly at a rate of 300 beats per minute (bpm) around the atrium. In AF, there is no regularity of this kind, except at the sources where the local activation rate can exceed 500 bpm.

Although the electrical impulses of AF occur at a high rate, most of them do not result in a heart beat. A heart beat results when an electrical impulse from the atria passes through the atrioventricular (AV) node to the ventricles and causes them to contract. During AF, if all of the impulses from the atria passed through the AV node, there would be severe ventricular tachycardia resulting in severe reduction of cardiac output. This dangerous situation is prevented by the AV node since its limited conduction velocity reduces the rate at which impulses reach the ventricles during AF.

Resources: ^ Klabunde, Richard (2005). Cardiovascular Physiology Concepts. Lippincott Williams & Wilkins. pp. 25, 28. ISBN 978-0781750301.

Definitions of the Properties of Cardiac Function:

Automaticity:  the ability of certain cells in the heart to initiate electrical impulses spontaneously

Excitability:  the ability of the cardiac cells to respond to stimulation

Conductivity:  the ability to transmit an impulse through specialized conduction system and atrial / ventricular muscle

Refractoriness:  the inability to undergo repeat stimulation until after a certain period of time has elapsed

Contractility:  the ability of the fibers to shorten when stimulated, resulting in the contraction of muscle creating a pump action

Depolarization and Repolarization:

Polarized Cell:  The cell at rest.  The interior of the cell has a negative charge with respect to the outside.  Normal distribution of K+ and Na+ is maintained.

Depolarization:  The cardiac cell is stimulated when Na+ enters the cell and an inward electricla current is produced.

Repolarization:  The cell recovers as K+ leaves and outward electrical current is produced

Click Here  for animation of this process.

Refractory Periods:

Absolute Refractory Period (ARP):  a relatively long period following excitation during which cells cannot respond to another stimulus, regardless of its strength.  This period of time is roughly the duration of systole.

Relative Refractory Period (RRP):  a narrow window of time near the beginning of the ARP during which stimulus strength must be above normal and the response from which is less than normal.

Vulnerable Period:  not a refratory period but a window of time during the refractory phase that the heart is prone to develop fibrillation in response to a premature beat delivered at that time; generally corresponds to the top of the T wave.

Supernormal Period (SNP):  also not a refracctory period, but is an interval of time during which it may be possible for a premature stimulus to conduct with better than expected behavior.

A review of the action potential of the heart is appropriate here. You will love these instructional videos!