Exam I Cardio III Flashcards
Where are the three bipolar limb leads of an EKG placed?
Lead I: neg terminal on R arm, pos on L arm
Lead II: neg terminal on R arm, pos terminal on L leg
Lead III: neg terminal on L arm, pos terminal on R leg
Define a vector. What direction does the arrow point (pos or neg) and to what is the arrow length proportional?
What is the arrow known as in terms of EKG? What does it represent?
Because the average person’s mean QRS is 59 degrees, what does this tell us about depolarization wave?
Starting with the idea of a vector- defined as an arrow or indicator pointing in the direction of a potential generated by current flow, with the arrow by convention pointing in the positive direction & the arrow length proportional to voltage.
The arrow then is the ‘instantaneous mean vector’, which represents the sum of the currents as they flow from the base to the apex.
A vertical vector then is ±90, etc. The average person’s mean QRS vector is 590. This shows that the during most of the ventricular depolarization wave, the apex is positive relative to the base and the depolarization travels from base to apex.
What is the projected vector? How do you determine it? How does vector A’s perpendicularity to the axis affect the voltage?
The projected vector is the vector that is on the axis of the lead NOT the dotted line that is drawn from the tip of the arrow to the axis. You draw a dotted line from the tip to the axis in order to project the correct projected vector. The projected vector will also have an arrow.
The more perpendicular A vector is to a lead axis, the smaller the voltage recorded in that lead. i.e. it will make projected vector B shorter.
Why does the Q wave typically have a slight negative value?
Q wave typically has slight negative value due to initial depolarization on the left side of the septum, a brief left to right vector develops.
What causes the ventricular T-wave? What is the first area of the heart to repolarize? Why? (Why is this unexpected?) What does this do to the vector/T-wave?
After ventricle muscle has depolarizied, .15 sec later repolarization begins and lasts until @ .35sec. This repolarization is responsible for the T-wave. Due to the way the contraction lasts longer at the septum, this isn’t the first area to repolarize (even though it depolarized first), but rather the outer surface around the apex repolarizes first.
The idea is that the high blood pressure in the ventricles slows perfusion of the septal tissue, thereby slowing repolarization. This leaves the vector pointing to the apex of the heart (remember the vector points in the positive direction), so the T wave records as positive in all leads.
How is repolarization of the atria different from repolarization in the vetricles? What is the cause of this? How does it affect the atrial repolarization vector?
When does the atrial T-wave occur?
The atria have no Purkinje system to facilitate the spread of depolarization, so it spreads much more slowly in the atria than in the ventricles. Since the atria depolarization spreads more slowly than in ventricles, there is a (relatively long) delay between the depolarization of the sinus nodal region and the distal atria. So, when repolarization begins, it tends to follow the path of depolarization, starting at the sinus node and moving distally (Opposite of the ventricles). This reverse direction of repolarization results in a ‘backward’ vector, which is recorded as a negative wave in the different leads. When repolarization begins, the region around the sinus node becomes positive with respect to the rest of the atria (becomes positive because the vectors are measuring the charges of the extracellular spaces which are becoming more positive as repolarization occurs, and get more negative as depolarization occurs). Therefore, the atrial repolarization vector is backward to the vector of depolarization. (Note that this is opposite to the effect that occurs in the ventricles.)
the so-called atrial T wave follows about 0.15 second after the atrial P wave, but this T wave is on the opposite side of the zero reference line from the P wave; that is, it is normally negative rather than positive in the three standard bipolar limb leads.
The atrial T wave occurs during the QRS complex and therefore is rarely seen.
How can you differentiate bundle branch block from axis deviation caused by hypertrophy?
Because of slowness of impulse conduction when the Purkinje system is blocked (due to bundle branch block), in addition to axis deviation, the duration of the QRS complex is greatly prolonged because of extreme slowness of depolarization in the affected side of the heart. One can see this by observing the excessive widths of the QRS waves. This extremely prolonged QRS complex differentiates bundle branch block from axis deviation caused by hypertrophy.
What are some examples that can cause bizarre QRS patterns?
Bizarre QRS patterns can result from multiple causes, usually:
1. Loss of muscle in cardiac tissue, which is replaced with scar tissue.
2. multiple small blocks in conduction in the Purkinje system.
These result in irregular impulse conduction, rapid voltage shifts, axis deviations, multiple peaks in some leads
Describe what occurs during a right bundle branch block.
Right bundle branch block. This means the left ventricle depolarizes more rapidly than the right ventricle, meaning the left side becomes electronegative before the right side. This results in a vector developing with the negative end toward the left ventricle, positive end toward the right ventricle, producing a right axis deviation. This figure shows an electrical axis of 1050 (rather than the normal 59).
What is a high voltage EKG and what could likely cause a high voltage EKG? What about low voltage EKG?
In QRS complex, normal voltages from R peak to bottom of S in standard bipolar limb leads varies between .5 and 2 mV, w/ lead II highest and lead III lowest. If the three leads sum to greater than 4mV, it is considered to be a high-voltage EKG. This is usually caused by hyperthrophy of the heart muscle, often indicating the heart is working against an excessive load.
You can also have a decrease in voltage, which is usually due to decreased muscle mass from old myocardial artery infarctions.
Fluid in the pericardium is another important cause of low-voltage QRS. This fluid effectively short-circuits the electrical signal so that less reaches the surface to be recorded.
Pulmonary emphysema can also lower QRS voltage through increasing the air in the lungs acting as an insulator around the heart.
What are currents of injury? How are they oriented on the axis and why? What can cause them?
Current of Injury
Some cardiac abnormalities cause heart tissue to remain depolarized all the time, this results in current flowing from depolarized to polarized areas- this is “Current of Injury”. Injured area is always “negative” (interior is positive). Can be due to:
1) Mechanical trauma > making membranes too permeable to repolarize.
2) Membrane damage due to infectious processes.
3) Ischemia from local coronary occlusions (most common).
The injured part of the heart is negative, because this is the part that is depolarized and emits negative charges into the surrounding fluids, whereas the remainder of the heart is neutral or positive polarity.
J point: when depolarizing wave has passed through all the tissue, everything is depolarized and no current flows. This is the zero potential level (J point).
A small area in the base of the left ventricle is newly infarcted (loss of coronary blood flow), how will this change the T-P interval?
A small area in the base of the left ventricle is newly infarcted (loss of coronary blood flow). Therefore, during the T-P interval— that is, when the normal ventricular muscle is totally polarized (depol. hasnt occured yet, happens at P)— abnormal negative current still flows from the infarcted area at the base of the left ventricle and spreads toward the rest of the ventricles.
How to locate the J point in a current of injury.
The J point of each of these two electrocardiograms (leads I and III) is not on the same line as the T-P segment. In the figure, a horizontal line has been drawn through the J point to represent the zero voltage level in each of the two recordings. The injury potential in each lead is the difference between the voltage of the electrocardiogram immediately before onset of the P wave and the zero voltage level determined from the J point.
How can arrhythmia occur? (5) What are 4 kinds of arrhythmia? Explain
Arrhythmias can occur from 1) abnormality in pacemaker 2)shift in pacemaker away from SA node (an “ectopic pacemaker”) 3) impulse blocks 4) abnormal impulse transmission pathways and/or 5) spontaneous generation of spurious impulses.
A. Tachycardia: fast heart rate (over 100 beats/min). Normal is @ 72/min. EKG is normal other than rate, which is 150/min. Caused by increased temp., sympathetic stimulation, toxins.
You get 10 beats/min for each degree F increase up to 105F due to increased metabolism in Sa node.
B. Bradycardia: slow heart rate (less than 60). Athlete’s resting rate is lower than average due to larger stroke volume, so it takes fewer strokes to pump enough blood.
C. Changes in heart rate with normal and then deep respiration. Deep breathing can change rate dramatically (30%).
D. SA Block. Note loss of P waves. Ventricles will beat at slower rhythm with impulses from A-V node.
What can cause abnormal T-waves? How will this affect the vector of repolarization? Explain. How can overdosing on digitalis cause an abnormal T-wave? (When is digitalis used?)
Abnormal T waves due to shortened depolarization of ventricular base, causing repolarization to start there in lieu of apex. Caused by ischemia in base muscle.
If base of ventricles has shortened depolarization, repolarization won’t begin in apex as normally is the case, and base repolarizes sooner. Vector of repolarization will then point from apex toward base, making the T-waves in leads negative rather than positive.
Mild ischemia is most common cause of shortening of depolarization of cardiac muscle.
Effects of digitalis. Digitalis used during cardiac insufficiency to increase cardiac contraction. If overdosed, depolarization duration may be prolonged in one part of ventricle, producing non-specific changes in T-wave. Shown here is biphasic T-wave.
