Chapter 10 Flashcards
PR depression
Normal variant is up to 0.8mm of depression, due to atrial repolarization which pulls the PR segment down. It is called the Tp wave but normally not seen.
PR depression indicates
Pericarditis or rarely atrial infarct/ischemia
Pericarditis signs and symptoms
Tachycardia
PR depression (greater than 0.8mm)
Scooped out ST elevation in limb leads (I II III aVF aVL and V2-V6) with reciprocal changes in V1 aVR.
Notching of the terminal portion of the QRS complex, especially in lateral precordial leads
Sharp chest pain which increases on inspiration, coughing, lying back. Pain is relieved when sitting forward
Why are atrial infarcts rare
Relatively small pressures encountered in the atria and thinness of the atrial walls. Also, thesbian veins that carry blood directly to the tissues. These small veins originate in the atrial or ventricular cavities and bypass the coronary system.
Thesbian veins
Minute, valveless veins in the walls of all four chambers which drain the myocardium. Most prominent on the right atrium, least prominent in the left ventricle. They connect directly to the medium and larger coronary veins.
Where should the PRI be measured
In the lead with the widest p wave and widest QRS in order to avoid the inadvertent omission of an isoelectric portion of the P wave.
PRI shortened in
Sinus tach and kids, longer in geris
Three major mechanisms that cause shortened PRI
Retrograde junctional P wave
Lown-Ganong-Levine syndrome (LGL)
Wolff-Parkinson-White pattern and syndrome (WPW)
Lown-Ganong-Levine (LGL)
Shortened PRI is caused by the impulse being transmitted through a bypass tract called James fibres. James fibres bypass the upper and central portions of the AV node where the normal physiologic block occurs. PSVT is a possibility with LGL. QRS will be normal as the impulse is still transmitted through the bundle of His and proceeds to the ventricles normally
Mahaim fibers
Connect the lower AV node or the bundle of His to the interventricular septum. A normal PRI is seen. Associated with a delta wave.
Wolff-Parkinson-White ECG presentation
Shortened PRI with a normal P wave (12% have normal PRI) Wide QRS Presence of a delta wave ST-T wave changes or abnormalities Association with PSVT
Kent bundle
A tract in WPW which bypasses the AV node. The impulse from the atria reaches the Kent bundle and AV node at the same time, the AV node slows conduction as normal. The Kent bundle bypasses the AV node and depolarizes the ventricles before the normal pathway. The transmission is slow and creates the start of a wide QRS, the AV node then depolarizes the rest of the ventricles which the Kent bundle has not already.
First degree AV block
Prolongation of the normal physiologic block usually at the AV node itself. It can be caused by organic heart disease, digoxin, calcium channel blockers, TCAs, hypercalcemia, hypothermia, and increased vagal stimulation such as inferior wall MIs
Mobitz I
Wenkebach. Defective AV node with a long refractory period. The lengthening PRI is caused by the SA node sending impulses at a regular rate which is too fast for the defective AV node. The AV keeps lagging further behind until it cannot conduct another impulse and a QRS is dropped. The R-R will get shorter until the dropped beat. The distances between the QRS with the dropped beat is less than twice the shortest R-R interval.
Mobitz II
PRI remains constant, but there are intermittent dropped QRS. Harbinger of complete block. If there is a 2:1 P wave to QRS ratio you cannot tell if it is a Mobitz I or II.
