17 and 18 - Cardiac Cycle I and II Flashcards
What is TRUE regarding the RELATIVE refractory period of the ventricular action potential:
a. A new stimulus cannot generate another action potential.
b. The inactivation gate of all fast sodium channels is open.
c. The channel pore of all fast sodium channels is open.
d. The inactivation gate of some fast sodium channels is open, some are closed.
e. The relative refractory period occurs during Phase 0 of the cardiac (ventricular) action potential.
d. The inactivation gate of some fast sodium channels is open, some are closed.
What is the first period of the cardiac cycle?
Atrial systole
This is the only period where the atria are contracted
What is the second period of the cardiac cycle?
Isovolumic contration
What is the third period of the cardiac cycle?
Rapid ejection
What is the fourth period of the cardiac cycle?
Reduced ejection
What is the fifth period of the cardiac cycle?
Isovolumic relaxion
What is the sixth period of the cardiac cycle?
Rapid ventricular filling
What is the seventh period of the cardiac cycle?
Reduced ventricular filling
Describe the state of the ventricles and atria during atrial systole (1)
- Atria are contracted
- Ventricles are relaxed
Describe the state of the ventricles and atria during isovolumic contraction (2)
- Ventricles contract with NO change in volume
- Atria are relaxing
Describe the state of the ventricles and atria during rapid ejection (3)
- Ventricles are contracting
- Atria are relaxed
Describe the state of the ventricles and atria during reduced ejection (4)
- Ventricles are still contracting
- Atria are still relaxed
Describe the state of the ventricles and atria during isovolumic relaxation (5)
- Ventricles are relaxing with NO change in volume
- Atria are relaxed
Describe the state of the ventricles and atria during rapid ventricular filling (6)
- Ventricles are relaxed
- Atria are NOT contracting to fill the ventricles (this is done by the pressure differential as ventricle expands, sucking blood in)
Describe the state of the ventricles and atria during reduced ventricular filling (7)
- Ventricles are relaxed
- Atria are relaxed (filling occurs by positive pressure from the vena cavas)
Describe the state of the AV valves, the pulmonic valve and the aortic valve during atrial systole (1)
- AV valves are open
- Aortic and pulmonic valves are closed
Describe the state of the AV valves, the pulmonic valve and the aortic valve during isovolumic contraction (2)
- AV valves are closed
- Aortic and pulmonic valves are closed
Describe the state of the AV valves, the pulmonic valve and the aortic valve during rapid ejection (3)
- AV valves are closed
- Aortic and pulmonic valves are open
Describe the state of the AV valves, the pulmonic valve and the aortic valve during reduced ejection (4)
- AV valves are closed
- Aortic and pulmonic valves are open
Describe the state of the AV valves, the pulmonic valve and the aortic valve during isovolumic relaxation (5)
- AV valves are closed
- Aortic and pulmonic valves are open
Describe the state of the AV valves, the pulmonic valve and the aortic valve during rapid ventricular filling (6)
- AV valves are open
- Aortic and pulmonic valves are closed
Describe the state of the AV valves, the pulmonic valve and the aortic valve during reduced ventricular filling (7)
- AV valves are open
- Aortic and pulmonic valves are closed
What are the three atrial pressure waves?
A wave
C wave
V wave
where can you measure and record the a, c and v waves?
The internal jugular vein
Are they formed from the atrial pressure on the right side or the left side?
RIGHT side
What exactly will this information tell us?
It will give an indicator of the total (mean) pressure in the right atrium
What is the mechanism that is responsible for the production of the A wave?
- There is an increase in atrial pressure, accompanied by a decrease in the size of the atrial cavity
- This creates the force of expulsion of the blood into the ventricle and gives us the A wave
What is the mechanism that is responsible for the production of the C wave?
- There is an increase in atrial pressure during isovolumetric contraction
- The C wave is an overall result from ventricular contraction
- The AV valves close as the ventricles depolarize
- Depolarization begins at the interventricular septum and the result is that the heart is temporarily shortened
- The shortening forces of the AV valves into the atria leads to an increase in atrial pressure
- The subsequent contraction of the rest of the ventricular myocardium results in the heart lengthening
- This allows the AV valves to “pull out” of the atria and decrease the pressure
What is the mechanism that is responsible for the production of the V wave?
- A pressure increase in the atria is associated with venous return
- This occurs during isovolumic relaxation of the ventricle
- At the end of isovolumic relaxation, the AV valves open and the rapid filling of the ventricles begins
- This process leads to a decrease in atrial pressure
What does the P wave correspond to?
Period 1 of the cardiac cycle (atrial systole)
What does the QRS complex correspond to?
The isovolumic contraction of the ventricle
What does the ST interval correspond to?
The rapid ejection phase
The ventricle is still contracting to expel blood
What does the T wave correspond to?
The reduced ejection as the ventricle begins to relax and pressure decreases
Describe the pressure in the aorta during atrial systole (1)
Decreasing
Describe the pressure in the aorta during isovolumic contraction (2)
Still decreasing
Describe the pressure in the aorta during rapid ejection (3)
Rapid increase
Describe the pressure in the aorta during reduced ejection (4)
A peak in pressure has been reached and the pressure begins to rapidly decrease
Describe the pressure in the aorta during isovolumic relaxation (5)
There is a slight peak after the aortic and pulmonic valves close, then the pressure begins to steadily decrease
Describe the pressure in the aorta during rapid ventricular filling (6)
Steadily decrease
Describe the pressure in the aorta during reduced ventricular filling (7)
Still a steady decrease
Describe the pressure in the left ventricle during atrial systole (1)
Much lower than aortic pressure, but slightly increasing
Describe the pressure in the left ventricle during isovolumic contraction (2)
Rapid increase in pressure, to the point where is reaches the same pressure as the aorta
This rapid increase occurs after the closing of the tricuspid and mitral valves and before the opening of the aortic and pulmonic valves
Describe the pressure in the left ventricle during rapid ejection (3)
Pressure remains the same as the aortic pressure and continues to rapidly increase
Describe the pressure in the left ventricle during reduced ejection (4)
A peak in pressure has been reached and the pressure begins to rapidly decrease (same pressure as aorta)
Describe the pressure in the left ventricle during isovolumic relaxation (5)
Rapid decrease in pressure continues
(at this point the aortic pressure remains somewhat high, while the left ventricle pressure continues to decrease to a much lower pressure)
Describe the pressure in the left ventricle during rapid ventricular filling (6)
The pressure continues to drop before reaching a minimum pressure
Describe the pressure in the left ventricle during reduced ventricular filling (7)
The pressure begins to slightly increase back up to the starting pressure
Describe the volume of blood in the left ventricle during atrial systole (1)
High, increasing volume
Describe the volume of blood in the left ventricle during isovolumic contraction (2)
Plateau of peak blood volume
Describe the volume of blood in the left ventricle during rapid ejection (3)
Rapid decrease in the blood volume
Describe the volume of blood in the left ventricle during reduced ejection (4)
Decrease in blood volume continues
Describe the volume of blood in the left ventricle during isovolumic relaxation (5)
Plateau of minimum blood volume
Describe the volume of blood in the left ventricle during rapid ventricular filling (6)
Blood volume begins to rapidly increase
Describe the volume of blood in the left ventricle during reduced ventricular filling (7)
Blood volume continues to increase, but at a slower rate
What is the equation for calculating the stroke volume?
Stroke volume = LVEDV - LVESV
Left ventricular end diastolic volume (LVEDV)
Left ventricular end systolic volume (LVESV)
What does the stroke volume represent?
The volume of blood discharged into circulation during each cycle
When in the cardiac cycle is the first heart sound heard?
S1 - Heard during the closing of the mitral and tricuspid valves at the beginning of isovolumic contraction
“Lub”
When in the cardiac cycle is the second heart sound heard?
S2 - Head during the closing of the aortic and pulmonic valves at the end of cardiac ejection
“Dub”
When in the cardiac cycle is the third heart sound heard?
S3 - Occurs at the transition between rapid ventricular filling and reduced ventricular filling
- This results from the sudden tensing of the chordae tendinae as the relaxing ventricle pulls on these
- This is an early diastolic sound
When in the cardiac cycle is the fourth heart sound heard?
It is NOT a normal noise
- It is an abnormal sound made in the ventricules after the peak of the A wave (atrial systole) as ventricular pressure is increasing
What is an opening snap?
It is NOT a normal sound
- It is heard in cases of mitral senosis at the beginning of ventricular filling
There are two types of murmur classifications. What are they and what determines their classification?
Diastolic murmurs
Systolic murmurs
This is determined by the timing of the murmur in relation to S1 and S2
What is a diastolic murmur?
A murmur that occurs AFTER S2, but before the next S1
- This is a time when the ventricles are relaxed
- This is often a result of mitral valve stenosis
What is a systolic murmur?
A murmur that occurs AFTER S1, but before S2
- S2 marks the beginning of ventricular relaxation, so after S1 and prior to S2, the ventricles are in systole
- This sound is heard in the case of mitral valve regurgitation
What is mitral valve regurgitation?
The cusps do not completely close, so during ventricular systole, some blood is forced back up into the atria
There are three mechanisms that are involved in the physiologic splitting of the second heart sound. What are they?
Mechanism I: delayed closing of the pulmonary valve
Mechanism II: sustained opening of the pulmonary valve
Mechanism III: aortic valve closes sooner
Describe mechanism I of the physiologic splitting of the second heart sound
- Inhalation results in expansion of the pulmonary artery
- This leads to more flow through the artery
- The effect increases the time that blood flows through the pulmonary valve
- The result is a delayed closing of the pulmonary valve
Describe mechanism II of the physiologic splitting of the second heart sound
- With inhalation, the favorable pressure gradient (more negative) increases venous return
- The result is that the right ventricle end diastolic volume (RVEDV) will be increased compared to exhalation
- More time is therefore required to empty the right ventricle
- The end result is that the pulmonary valve remains open longer
Describe mechanism III of the physiologic splitting of the second heart sound
- With inhalation, a small amount of blood is trapped in the lungs
- This is because as the lungs expand, so do the vessels in the lungs
- This decreases venous return to the left side of the heart
- This results in less blood being expelled from the left ventricle
- Because less blood is expelled, the aortic valve closes sooner
What can result from severe hypertension and a left bundle branch block (LBBB)?
A paradoxical splitting (reverse splitting) of S2
In normal conditions, the aortic valve closes ___________ the pulmonary valve
BEFORE
So, in the case of a left bundle branch block (LBBB), what happens to the left ventricle?
It takes longer to depolarize
What is the mechanism of this slow depolarization?
The depolarization impulse is not traveling through the fast pukinje fibers, but just through the cell-to-cell gap junctions of the myocardial cells
In this case, would the right ventricle be functioning normally?
Yes
This means the pulmonary valve will close as it should, however what happens to the closing of the aortic valve?
It is delayed due to the delayed contraction of the ventricle
When would you be able to hear this paradoxical splitting (reverse splitting) of S2?
On exhalation
What can you hear on inhalation?
The pulmonic valve remains open longer, so only one audible sound is heard
Why does tachyarrhythmias, such as atrial fibrillation with rapid ventricular response, often result in reduced cardiac output
- 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
Explain how a drug that slows conduction through the AV node could reduce ventricular response rate and increase cardiac output during atrial fibrillation
- Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, in effect decreasing the number of impulses that conduct into the ventricles, therefore giving the ventricles enough time to fill before contracting and therefore increasing cardiac output
Beta blockers can accomplish this
Describe the distribution of Beta-one receptors in the heart
Beta-1 receptors are found in the SA node and the ventricular muscles
Explain how an increase in sympathetic tone can increase force of contraction of the atria and the ventricles
In the SA node…
- Beta-1 receptors work to increase the heart rate, and therefore increase the cardiac output
In the ventricular muscles…
- Beta-1 receptors work to increase the force of contraction and therefore increase the cardiac output
What are all the ways that beta-1 receptors can increase cardiac output?
- Increase heart rate in SA node (chronotropic effect)
- Increase atrial cardiac muscle contractility. (inotropic effect)
- Increases contractility and automaticity of ventricular cardiac muscle
- Increases conduction and automaticity of AV node
