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.
During which phases of the mechanical cardiac cycle do we hear the first and second heart sounds?
S1= At end of atrial systole and during all of Isovolumetric ventricular contraction (marks beginning of ventricular systole) “lub”
S2=Between reduced ventricular ejection and isovolumetric ventricular relaxation (marks beginning of ventricular diastole) ““dub”
If you wanted to auscultate a dog to hear the mitral and tricuspid valve heart sounds (S1), where would you place stethoscope?
Mitral= left 5th intercostal space, at apex, low at costal-chondral junction
Tricuspid=right 4th intercostal space, at apex, low at costal-chondral junction
If you placed your stethoscope on the left side, near base of heart in the 3rd intercostal space, what valve sound would you hear?
Pulmonic valve second heart sound
If you placed your stethoscope on the left side high in the intercostal space, what heart sound would you hear and from where?
A second heart sound of the aortic valve near the base of heart
When would you hear a split heart sound? ( 2 reasons)
- The pulmonic valve tends to close later than the aortic valve because the right ventricle is weaker than the left.
- During inspiration , blood venous return to right ventricle increasing delaying closure of pulmonic valve
How are calcium and end diastolic volume related?
As end diastolic volume increases, the stretch on the walls of the ventricle stimulates calcium release during next contraction creates a stronger contraction force and increased stroke volume.
What are the similarities between the right and left side of heart in regards to mechanics?
Blood volume
Rate of blood flow
How does the thermodilution technique measure cardiac output?
Use saline colder than blood temperature and inject into right atrium. If the temperature change when measured at pulmonary artery is large, there is small blood flow (small CO) versus small temperature change equaling higher blood flow (high CO).
How do we measure the left ventricular preload? (pulmonary wedge pressure)
Insert a swan-ganz catheter into jugular or femoral vein and advance it to right atrium-right ventricle-pulmonary artery and into branch of pulmonary arter. Backup of blood (downstream segment) against balloon is a good approximation of left side pressure.
What is preload?
The pressure within a ventricle at the end of diastole . It is the pressure associated with end diastolic volume.
How do we measure preload in the right heart versus left heart?
Right ventricular preload=central venous pressure via a central venous catheter
Left ventricular preload= pulmonary wedge pressure via swan-ganz catheter
If preload decreases, what happens to the EDV, stroke volume, and cardiac output?
EDV decreases-stroke volume decreases-cardiac output decreases
Frank Starling Law of Heart
If pressure in right ventricle increases, stroke volume increases which increases more return to left ventricle which increases left ventricular pressure with an increase in stroke volume…keeps stroke volumes of ventricles balanced.
If there is a stiff/non-compliant ventricle, how would the heart maintain the same end diastolic ventricular volume?
A higher preload or pressure in the ventricles would be required
What is cardiac compliancy?
The ease with which ventricular walls stretch to accommodate incoming blood during diastole. Measured by dividing change in volume by the change in pressure. A higher compliance means that the heart requires less pressure in the ventricles in order to obtain a normal EDV. A lower compliance means that the heart requires more pressure in ventricles in order to obtain a normal EDV.
If a dog is hemorrhaging, what is occurring in the heart?
Preload or pressure in the ventricles decreases which decreases the EDV and the stroke volume which would decrease the cardiac output.
How does diastolic filling time affect the EDV?
If the diastolic filling time decreases due to a higher heart rate, the EDV will decrease causing stroke volume and cardiac output to decrease. This can be compensated by the influence of the sympathetic nervous system.
Why is a lower end systolic volume a good thing and why does it lead to a higher stroke volume and cardiac output?
A lower end systolic volume means that the ventricles are pumping out blood more efficiently because less blood is left in ventricles after contraction.
What is the biggest factor that affects the end systolic volume?
Contractility of ventricles. If there is high contractility due to increases in sympathetic nerve stimulation, there will be a lower end systolic volume, Therefore, higher contractility= higher stroke volume and cardiac output.
What is the hallmark of heart failure?
Decreased contractility
What is the ejection fraction? What does it tell us?
Stroke volume divided by end diastolic volume. The fraction of end diastolic blood volume ejected during ventricular systole. If the fraction is 80%, that means 80% of total blood in ventricle is ejected out during a heartbeat. Crude estimate of contractility.
If there is a high ejection fraction, what could be going on? What about a low ejection fraction?
If the ejection fraction is too high, this could indicate hypertrophic cardiomyopathy which can cause sudden cardiac arrest. If it is too low, could indicate heart failure.
Afterload
Pressure in the aorta that the ventricle must overcome to pump blood into the aorta.
If there is a high afterload, how would this affect the pumping system of heart?
ESV will increase because not as much blood can leave ventricle which would decrease stroke volume and decrease cardiac output.
What is the 4th heart sound associated with?
Atrial systole, when the blood vibrates on the walls of atrium
WHat is the 3rd heart sound associated with?
Rapid ventricular filling when blood fall into ventricle
When are cardiac muscle cells at their maximum stretch and tension?
At the end of isovolumetric ventricular contraction as the aortic valve opens.
When are cardiac muscle cells at their shortest length and lowest tension?
At the end of isometric ventricular relaxation before mitral/tricuspid valves open and ventricular fills with blood.
When are cardiac muscle cells at their shortest but still have quite a bit a tension?
When the ventricles reach end systolic volume at the end of ventricular ejection.
When are cardiac muscle cells at their stretch capacity and most relaxed?
At the end of ventricular diastolic filling at the point when the ventricle reaches end diastolic volume.
What happens to the stroke volume as the mitral/tricuspid valve opens and the ventricles fill with blood to the point when the end diastolic volume is reached?
Increases along with the intraventricular volume
With regards to increased preload, there will be ________ EDV, _______peak pressure, _______ESV, and _______ stroke volume.
Increased; the same; the same; increased
With regards to increased afterload, there will be ______ EDV, _______peak pressure, _______ ESV, and _______ stroke volume.
the same; increased; increased; decreased
With regards to increased contractility, there will be _______ EDV, ________ peak pressure, _______- ESV, and _______ stroke volume.
the same, increased, decreased, and increased
What occurs to systole and diastolic filling time during exercise? How does this affect cardiac output?
Systole shortens and most diastolic filling time is preserved. CO will increase as the heart rate increases because stroke volume is maintained. Even though there is less time for the ventricles to fill and get to the desired end diastolic volume, this is remedied by the decrease in the end systolic volume and increased contractility brought on by the sympathetic nervous stimulation of exercise.
What occurs to systole and diastolic filling time when there is a pacemaker in the heart?
The diastolic filling time is not preserved because the systole stays the same. Only 1/3 of time systole is occurring while 2/3 of time heart is in diastolic filling time.
At the molecular level, how does sympathetic nervous system increase contractility and cardiac output?
Catecholamines bind to beta adrenergic receptors- ATP change to cAMP via adenylyl cyclase- cAMP phosphorylates calcium channels on sarcoplasmic reticulum- calcium triggered calcium released from SR for myosin-actin crossbridges which increases contractility and decreases ESV, increases stroke volume and cardiac output.
How does sympathetic stimulation cause the contraction to end faster so a new contraction can occur thereby increasing contractility and cardiac output of heart?
Ca+ transported back into SR via Ca+ pump that was activated by the phosphorylation of phospholamban AND Troponin I phosphorylates and reduces the Ca+ myofilament sensitivity, increases rate of Ca+ dissociation from troponin C thereby accelerating relaxation so that a new contraction can occur faster.
How does sympathetic tone influence end systolic volume and the complete emptying of the ventricles?
It decreases ESV due to more efficient emptying of the ventricles into the aorta and pulmonary artery giving the ventricles more time to remain in diastole.
Negative chronotropic effect on heart and drug examples?
Decreases heart rate due to increase in parasympathetic activity
Digitalis
Positive chronotropic effect on heart and drug examples?
Increase heart rate due to increase in sympathetic activity
Beta adrenergic agonist
What do we call a substance that increases contractility of the heart? Example?
Positive inotropic substance like digitalis
What is a calcium channel or beta blocker drug considered in respect to heart contractility?
Negative inotropic drug because it decrease contractility of the heart
What is a calcium channel or beta blocker drug considered in respect to heart contractility?
Negative inotropic drug because it decreases contractility of the heart
Where is a patent ductus arteriosus and what does it cause?
Persistent connection after birth of the opening between the aorta and pulmonary artery. It causes a continuous heart murmur in systole and diastole.
Where is a ventricular septal defect and what does it cause?
Connection between the left and right ventricle causing a systolic heart murmur as blood rushes from left to right ventricle during contraction (higher pressure in left ventricle).
If an artery is connected to a vein in the systemic circulation, what could this cause?
Arteriovenous fistula between a high pressure and low pressure vessel can cause a murmur.
What are three clinically important pathological changes in body that can occur as a result of cardiac murmurs?
- Abnormally high/low blood flow to one region of body
- Abnormally high/low blood pressure in particular region of body
- Excessive hypertrophy of cardiac muscle due to an increased workload for one or both ventricles
What can cause systolic heart murmurs? ( 4 )
Av valve incompetence/insufficiency
Pulmonic/aortic stenosis
Patent ductus arteriosus
Ventricular septal defect
What can cause diastolic heart murmurs? (3)
Av valve stenosis
Pulmonic/aortic incompetence/insufficiency
Patent ductus arteriosus
What pathological consequence does ventricular septum defect cause?
Abnormally high blood flow into the right ventricle
What pathological consequence does PDA cause?
Abnormally high pressure in the pulmonary arteries
When comparing a PDA to a VSD in the heart, which would cause there to be a higher total work on the heart? Why?
During a VSD, a volume of blood is pumped from the left ventricle into the right ventricle causing the right ventricle to do more work to eject the extra volume. During a PDA, there is a higher afterload in the pulmonary artery which causes the right ventricle to have to work harder to pump blood into the pulmonary artery. Volume work is easier for the heart and causes less hypertrophy than pressure work therefore, PDA causes a higher total work on the heart.
What is the equation for the work of the left ventricle?
Pressure generated by pump x volume of fluid pumped in one stroke x number of pump strokes
What occurs in the heart if there is a pressure overload in a heart chamber?
Concentric hypertrophy due to increased systolic pressure and wall stress which causes parallel addition of new myofibrils and wall thickening reducing the size of chamber.
If there is a volume overload in the heart, what happens to the heart chamber?
Eccentric hypertrophy due to increased diastolic pressure and increased wall stress which causes the series addition of new sarcomeres thereby enlarging the chamber and the heart in general, but keeping the wall thin.
If there is mitral regurgitation( insufficiency), what kind of workload on the heart will there be and how bad will the hypertrophy of left ventricle be?
Volume work which will cause mild/moderate left hypertrophy (because pressure is more work and causes more hypertrophy than volume work)
If there is a PDA, what kind of workload and how bad will hypertrophy of the left ventricle be? Right ventricle?
Left ventricle: volume work with moderate hypertrophy
Right ventricle: pressure work with severe hypertrophy
If there is mitral stenosis, which chamber of the heart will be most affected and what will occur in that chamber?
(LEFT ATRIUM) The pressure in the left atrium will increase because the mitral valve opening is narrow into the left ventricle. This causes a backup in pressure to the pulmonary veins causing pulmonary edema. The atria can also stretch out causing a bigger chamber (seen as a long p-wave on ecg) which can lead to reentry rhythms which can cause atrial fibrillation.
If the P wave has a higher than normal amplitude on ECG, what is a likely cause?
Atrial enlargement
If the R wave has a higher than normal amplitude on ECG, what is the likely cause?
Left ventricular enlargement
If the R wave is increased in duration on ECG, what is the likely cause?
Left bundle branch block
If the S wave is increased in amplitude on ECG, what is the likely cause?
Right ventricular enlargement
If the S wave is increased in duration on ECG, what is the likely cause
Right bundle branch block
What drugs can be used to treat Av node blocks?
Atropine
Beta adrenergic agonists
What drug can be used to treat ventricular fibrillation after electrical cardioversion is accomplished?
Lidocaine
In which of the following arrhythmias will the ECG not characteristically show the same number of P waves and QRS complexes?
A. Third degree AV node block B. First degree AV node block C. Ventricular tachycardia D. Atrial Flutter E. A, B and D F. None of the above
E.
The time required for the conduction of the cardiac action potential through the AV node would be approximately equal to the:
A.QT interval B.ST interval C. PR interval D. RR interval E. PP interval
C.
The T wave in a normal ECG is:
a. Always negative.
b. Always positive if the R wave is positive.
c. Also known as the pacemaker potential.
d. Caused by the delay between atrial and ventricular
depolarization.
e. Caused by ventricular repolarization.
E.
You examine a 7-year-old poodle and find evidence of a systolic murmur (no diastolic murmur), pulmonary edema (indicated by rapid, noisy respiration and cough), left ventricular hypertrophy (no right ventricular hypertrophy), and exercise intolerance. The most likely explanation for the symptoms is:
a. Mitral regurgitation.
b. Mitral stenosis.
c. Aortic regurgitation.
d. Pulmonic stenosis.
e. Ventricular septal defect.
A.
Systolic murmurs can involve a ventricular septal defect, mitral regurgitation, or pulmonic/aortic stenosis.
Since we have left ventricular hypertrophy, this means the left ventricle is trying to pump out more blood than normal which means there is an access of volume in the left ventricle ( excess volume work). The only way excess volume is in the left ventricle is because blood is leaking into it from the left atrium through an insufficient mitral valve. The pulmonary edema occurs because the left atrium pressure increases causing an increase in pulmonary venous pressure,
Which statement is true for a normal heart?
a. Sympathetic activation causes end-systolic ventricular volume to increase.
b. An increase in ventricular preload causes end diastolic ventricular volume to decrease.
c. An increase in ventricular contractility causes systolic
duration to increase.
d. An increase in ventricular contractility causes the external work of the heart to decrease.
e. Pacing the heart at a high rate causes stroke volume to decrease.
E.
In the normal cardiac cycle:
a. Ventricular systole and ventricular ejection begin at the same time.
b. The second heart sound coincides with the beginning of isovolumetric relaxation.
c. The highest left ventricular pressure is reached just as the aortic valve closes.
d. Aortic pressure is highest at the beginning of ventricular systole.
e. Atrial systole occurs during rapid ventricular ejection.
B.
You examine a puppy and hear a systolic murmur when auscultating on left side of dog in the 4th intercostal space. On the ECG, you see deep, wide S waves with shorten QRS intervals. What could be going on?
When there are deep S waves on a ECG, there usually is a right ventricular hypertrophy occurring. Hearing a murmur on the left side in the 4th intercostal space is where the pulmonic valve is located. A systolic murmur suggests that there stenosis of a semilunar valve. Pulmonic stenosis
ST Elevation (TP segment depression)
Ischemic caudal part of ventricle
Ischemia in cranial part of ventricle
ST Depression (TP segment Elevation)
If the EDV decreases, how does this effect ejection fraction and contractility?
Ejection fraction will increase
