Test 7 Flashcards
PR interval
TIme from beginning of P wave to beginning Q wave. Represents beginning and end of atrial depolarization.
QT interval
Entire time ventricles remain depolarized
PP interval
TIme between each atrial depolarization or contraction.
RR interval
Time between each ventricular depolarization or contraction.
What is the hexagonal lead system and why is it used?
Superimposed standard and augmented leads that midpoints of lead coincide with each other forming a circular field used to determine the direction and magnitude of the net electrical axis during a ventricular depolarization.
What is the triaxial lead system?
Transposing Lead I, II and III to form a triangle with a center point of zero potential.
What are the six steps taken when evaluating an ECG printout?
- Heart rate
- Measure complexes (mV) and intervals (sec)
- Is rhythm regular or irregular?
- P-wave for very QRS complex, QRS complex for every p-wave?
- Origin of QRS complex (supraventricular or ventricular)
- Mean electrical axis
If there is a long P-R interval, what are some problems associated?
First degree AV node block
If there is a discrepancy between the number of P waves and QRS waves, what are some problems associated?
Second and Third degree AV node blocks
If we see deep S waves, what may be occurring?
Ventricular hypertrophy
Bundle branch blocks
Delays depolarization in part of ventricle after the block which takes away dipole because electrical signal go through more slowly in the affected side.
What can an ECG give us information about?
- Heart rate
- Relative sizes of heart chambers
- Rhythm or conduction disturbances
- Origin of the pacemaker
- Effects of altered electrolytes like K+
- Effects of certain drugs
- Anatomical orientation of heart
What can an ECG not give us information about?
- Cardiac output
2. Mechanical performance
What is electrical mechanical dissociation? Can an ECG detect this?
When you see normal heart rhythm but no palpable pulse or measurable blood pressure…NO
T/F: Each cardiac cell has an electrical dipole and can be characterized as a vector with magnitude and direction and each can be summated to represent one single dipole of the heart.
True
In order for an ECG to detect an electrical signal, what must occur?
There must be a wave of electrical charges moving over the heart
Why would we see lower amplitude ECG recordings in larger, fatter, or deeper chested animals or animals with a small heart (cats)?
The heart is further away from the electrodes and the lung field is larger.
If a wave of electrical potential moves towards a positive electrode, what kind of deflection will occur?
Positive
If a wave of electrical potential moves towards a negative electrode, what kind of deflection will occur?
Negative
What occurs if there is no deflection in the electrical signal?
The electrical potential wave is perpendicular to the electrode axis
Why would there be high plasma K+ but not noticeable electrical problems on ECG?
Hypercalcemia
How can be protect an animal from hyperkalemia?
Give bicarbonate, calcium, insulin, or glucose to drive K+ back into cells out of the plasma
What do we see on an ECG from hyperkalemia and why?
- Bradycardia-due to the depressive effects K+ has on the rate of diastolic depolarization.
- P wave becomes broad and flattened-due to depressed excitability of atrial myocardium
- 1st and 2nd degree AV node block
- Duration of QRS complex increases
- Spiked T wave
* Imagine ECG is a string and you pull on it, what happens? -stretch it all out, except for T wave*
What must happen to the cardiac cell membrane in order for diastolic depolarization to occur? How does hyperkalemia mess with this process?
Cell membrane must become less permeable to K+. Increases permeability of cell membrane to K+ even though the concentration gradient favors K+ leaving the cells. This change in permeability slows down diastolic depolarization.
If K+ continued to increase in the plasma, after we observed the first few signs on the ECG, what would we observe next?
P-wave disappears because atrial myocardium is at a standstill as it is more affected by potassium than ventricles which leads to a sinoventricular rhythm.
How can hyperkalemia lead to ventricular tachycardia and fibrillation?
Re entry pattern in ventricles due to slow propagation velocity ( if this doesn’t occur, ventricles can just slow down more and more until cardiac arrest occurs)
What happens to the resting membrane potential, action potential, and upstroke in ventricular cardiac cells or purkinje fiber cells as extracellular K+ rise?
RMP becomes less negative, action potential velocity and amplitude diminish, and steepness of the upstroke diminishes which all slow the conduction velocity and cause RMP level to get so high that it inactivates all the M and H gates leaving slow Ca+ channels to start slow wave response to get back to normal.
Would a respiratory sinus arrhythmia be considered normal? When would we see the the P-P interval increase over the normal amount? Decrease?
Yes, due to respiration. During expiration, the P-P interval gets longer, but during inspiration, it gets shorter.
If the P wave is too wide, what could be happening?
Left atrial enlargement because it takes longer for the depolarization to get over to the left atrium ( also called P mitrale) or there is some digitum toxicity going on so need to adjust dose.
If the P wave is too tall, what could be happening?
There is right atrial enlargement or P pulmonale
If the P-R interval is too long, what could be happening?
First degree AV node block
If you are looking at an ECG and notice that the pacemaker is ventricular in origin instead of supraventricular, what condition is probably occurring?
Ventricular tachycardia possibly leading to fibrillation
If there is a bundle branch block in the right side of heart what will we see on the ecg and why?
We could see a deep S wave due to right ventricular hypertrophy. Due to the block on the right side, the left side of heart is done depolarizing before the right causing there to be no electrical dipole present which would culminate in higher electrical activity in the right side of heart.
What are five reasons that could account for supraventricular tachycardia?
- Junctional tachycardia
- Sinus tachycardia
- Atrial tachycardia
- Atrial fibrillation
- Atrial flutter
Explain the dicrotic notch.
A small decrease followed by increase in the aortic pressure at the end of reduced ventricular ejection and isovolumetric ventricular relaxation when the aortic valve closes causing retrograde blood flow sloshing blood up against valve. Blood moves away decreasing pressure and then moves back increasing pressure.
Stroke volume
End diastolic volume- end systolic volume
Cardiac output
Stroke volume X Heart rate
If you increase venous or arterial pressure, how does this affect cardiac output?
Increase preload of ventricles-Increase EDV-increase stroke Volume- increase cardiac output
If sympathetic activity increases, how does this affect the stroke volume and cardiac output?
Increased contractility-decreased ESV-increased stroke volume-increased cardiac output
If ventricular compliance decreases, what does this do to cardiac output?
Decreased EDV-decreased stroke volume- decreased cardiac output
What are the five most common congenital heart defects found in dogs?
- Patent Ductus Arteriosus
- Pulmonic stenosis
- Aortic stenosis
- Ventricular septal defect
- Tetralogy of Fallot
During aortic or pulmonic stenosis, what is occurring?
The aortic or pulmonic valves have a narrow valve opening that creates restriction of blood flow out of the ventricles into the aorta or pulmonary artery during ventricular systole. This causes systolic heart murmurs.
If the aortic or pulmonary valves are not closing completely and allowing regurgitation of blood back into the ventricles, what type of murmur will we hear?
Diastolic murmur
You hear a diastolic murmur and have determined that the defect is not at the aortic or pulmonary valves. What else could be happening?
There is stenosis of the AV valves which is creating a narrow opening for blood to pass through during ventricular diastole or filling of blood from the atria to the ventricles.
You hear a systolic murmur and have determined that the defect is not in the aortic or pulmonary valves. What else could be happening?
There is insufficient AV valves..allowing regurgitation of blood from ventricles to the atria when the ventricles are in systole and contracting to push blood through the aortic and pulmonary valves.
Explain what is occurring during ventricular diastole.
Ventricles are passively filling with blood from the atriums (rapid ventricular filling). The tricuspid and mitral valves are open because pressure in atrias is higher than ventricles. Ventricles are relaxed and pressure is gradually increasing as more blood fills the chambers.
Explain what is occurring during atrial systole.
The atriums contract due to SA node pacemaker cells depolarizing. Ventricles are almost at their end diastolic volume at this point so atrium is “topping off”the ventricles.
Explain what is occurring during isovolumetric ventricular contraction.
At this point, all the valves are closed because atrias relax and pressure drops below ventricles causing backflow of blood. First phase of ventricular systole with unchanging ventricular volume (isovolumetric) until pressure builds enough in ventricles to overcome aortic/pulmonary pressure.
Explain what is occurring during ventricular ejection.
Pressure in ventricles exceeds pressure in aorta/pulmonary artery and pushes semilunar valves open causing rapid ejection of blood. Reduced injection follows as ventricular pressure begins to drop and falls below aortic/pulmonary pressure.
Explain what occurs during isovolumetric ventricular relaxation.
As pressure in ventricles drop below aortic/pulmonary pressures, backflow of blood closes semilunar valves. The pressure drops but does not drop below atrial pressure so AV valves remain closed with no change in volume of blood (isovolumetric). Once pressure drops below atrial pressure, AV valves will open and the next phase of ventricular diastole will occur.