Chpt 4- Heart probs

In a physical exam, Rachel's heart rate was rapid and very irregular. Furthermore, her heart rate, determined directly by listening to her heart with a stethoscope, exceeded the pulse rate taken concurrently at her wrist. No definite P waves could be detected on Rachel's ECG. The QRS complexes were normal in shape but occurred sporadically. Given these findings, what is the most likely diagnosis of Rachel's condition?

Atrial fibrillation

Decrease in cardiac output causes what change to Mean arterial pressure?

It causes MAP to decrease

Diltiazem is a non-DHP calcium channel blocker, a negative inotropic agent (as well as other effects). Would this be a good drug for congestive heart failure? Why or why not?

It is not. Contractility in heart is already decreased in heart failure. Adding a negative inotropic agent will make it even lower, causing an increase in the mismatch of SVs, thereby increasing congestion.

the conducting system of the heart refers to ...

SA node, AV node, bundle of His and Purkinje fibers

What do histamines do to blood vessels?

cause vasodilation

what is the effect of PKA phosphorylating Ca channels?

increases Ca for contraction

atrial flutter

rapid electrical signals travelling in circles from the SA node to the AV note and back to the SA node. Because of the refractory period of AV node cells, not every signal reaching the AV node causes firing.

An insufficient AV valve will sound from which steps in the cardiac cycle and will sound like a (whistle) (gurgle).

ventricular contraction, ventricular relaxation and un until the beginning of late diastole An insufficient valve doesn't close proper. The sound will happen when it should be closed. The AV valve should be closed as soon as ventricular diastole starts (Z) and continue until it opens when the pressure in the atrium is greater than the ventricle (X). The sound will be a gurgle. (Note: the video described this sound ending as the semilunar valve closes, at W, while the text describes it as lasting as long as the valve should be closed, which is until X. I accepted both.)

Mary suffers from atrial flutter, a disease related to atrial fibrillation (A-fib). Instead of the random electrical activity seen in A-fib, atrial flutter involves rapid electrical signals travelling in circles from the SA node to the AV note and back to the SA node. Because of the refractory period of AV node cells, not every signal reaching the AV node causes firing. Is Mary likely to have sufficient O2 delivered to her tissues? Why or why not?

A heart rate in the ventricles (which is what matters for O2 delivery to tissues) of 80 bpm is in the normal range, so Mary's tissues should receive sufficient O2.

An increase in heart rate can lead to what change in stroke volume?

An increase in heart rate can lead to a decrease in stroke volume because the increased contraction due to increased HR causes the ventricles to not have enough time to fill with blood. This in turn decreases the amount of blood leaving the ventricles, so a decrease in SV.

In a physical exam, Rachel's heart rate was rapid and very irregular. Furthermore, her heart rate, determined directly by listening to her heart with a stethoscope, exceeded the pulse rate taken concurrently at her wrist. No definite P waves could be detected on Rachel's ECG. The QRS complexes were normal in shape but occurred sporadically. Would cardiac output be seriously impaired by this condition? Why or why not?

Atrial fibrillation causes increased HR, but probably decreased SV since the ventricles might not have enough time to fill. The answer would depend on whether these two balanced each other out. (The truth is that CO is usually not adversely affected with atrial fibrillation)

David has developed complete (or third-degree) heart block. Describe how his ECG will look compared to an unaffected person. If David's complete heart block goes untreated, what compensations will his body make? That is, which homeostatic reflex will operate and what are the steps and outcome of this reflex?

Decreased CO leads to lower mean arterial pressure (MAP), which is detected by baroreceptors in the aorta and carotid arteries. Lower MAP means less frequent firing by the baroreceptors, which send their axons to the cardiovascular control center (CVCC). The CVCC sends output to lower parasympathetic nervous system activity, increasing HR, and increases sympathetic nervous system activity, further increasing HR, increasing contractility, thus SV, causing vasoconstriction (thereby increasing TPR) and increasing venous return, also increasing SV. Even though increased sympathetic input is attempting to increase ventricle contractions, it only increases atrial ones (with accompanying atrial depolarizations and P waves).

True or False: Every artery in a healthy body contains relatively well oxygenated blood.

False The pulmonary arteries are an important exception

Herb had a heart attack that damages the papillary muscles of his left ventricle, leading to mitral valve prolapse, meaning that his mitral valve is open part of the time it should be closed. He survives the heart attack, but a year later shows signs of pulmonary edema. Why?

He is probably suffering from heart failure as his left ventricle has to work harder continually to increase SV. This, together with mitral valve prolapse, lead to back up first in the left atrium, then the pulmonary circulation. This leads to an in pressure (thus PH/PC) in the pulmonary system which leads to excess filtration that the lymphatics can't handle.

Mary suffers from atrial flutter, a disease related to atrial fibrillation (A-fib). Instead of the random electrical activity seen in A-fib, atrial flutter involves rapid electrical signals travelling in circles from the SA node to the AV note and back to the SA node. Because of the refractory period of AV node cells, not every signal reaching the AV node causes firing. Is it more or less likely that Mary will have a stroke than a patient who has A-fib, all else being equal?

In A-fib, atrial depolarization and thus contractions are disorganized so the 20% of ventricle filling due to atrial contraction likely doesn't happen. In A-flutter, these contractions seem to be happening, and even if the timing is wrong so not all of the 20% gets to the ventricle each time, it seems less likely in A-flutter that there will be the blood pooling that causes clots which can cause a stroke.

Atropine is muscarinic receptor antagonist. What effect would it have on heart rate? Increase it, decrease it or leave it unchanged

Increase it

In a physical exam, Rachel's heart rate was rapid and very irregular. Furthermore, her heart rate, determined directly by listening to her heart with a stethoscope, exceeded the pulse rate taken concurrently at her wrist. No definite P waves could be detected on Rachel's ECG. The QRS complexes were normal in shape but occurred sporadically. Explain why the condition is characterized by a rapid, irregular heartbeat.

The AV node will relay all the signals it gets (unless it's in its refractory period). Because signals sporadically, arrhythmically, reach the AV node, it sends these arrhythmic signals down the AV bundle, bundle branches, and Purkinje fibers, leading to ventricular contractions.

In atrial flutter, is each P wave coupled to an organized atrial contraction? Explain.

The atrial depolarization is organized enough to give a normal looking P wave, so it seems likely that each one is coupled to an atrial contraction. Note: the atrial contractile cells are unlikely to be in their refractory period because they seem to depolarize again as indicated by the next P wave. Note also, the normal timing of the atrial contraction is in the P-R segment, but the flatness is due to this point in the normal cycle being electrically silent not a necessity for contraction

Herb had a heart attack that damages the papillary muscles of his left ventricle, leading to mitral valve prolapse, meaning that his mitral valve is open part of the time it should be closed. Before compensation, what will happen to Herb's BP? (increase) (decrease) (stay the same)

decrease In a ventricular contraction, all the blood that leaves should go to the aorta, but if the mitral valve isn't closed properly, some will go back to the left atrium instead. This will lower the stroke volume. Since CO = SV x HR, if HR doesn't change, CO will also decrease. Decreased CO means that MAP will decrease.

Herb had a heart attack that damages the papillary muscles of his left ventricle, leading to mitral valve prolapse, meaning that his mitral valve is open part of the time it should be closed. Before compensation, what will happen to Herb's CO? (increase) (decrease) (stay the same)

decrease In a ventricular contraction, all the blood that leaves should go to the aorta, but if the mitral valve isn't closed properly, some will go back to the left atrium instead. This will lower the stroke volume. Since CO = SV x HR, if HR doesn't change, CO will also decrease. Decreased CO means that MAP will decrease.

Herb had a heart attack that damages the papillary muscles of his left ventricle, leading to mitral valve prolapse, meaning that his mitral valve is open part of the time it should be closed. What will happen to Herb's SV? (increase) (decrease) (stay the same)

decrease In a ventricular contraction, all the blood that leaves should go to the aorta, but if the mitral valve isn't closed properly, some will go back to the left atrium instead. This will lower the stroke volume. Since CO = SV x HR, if HR doesn't change, CO will also decrease. Decreased CO means that MAP will decrease.

Left-sided systolic heart failure is associated with stroke volume that is (increased) (decreased) (unaffected).

decreased Weakened heart muscle leads to decreased contractility, meaning the heart contracts with less force, decreasing the amount of blood that leaves per beat (i.e., the stroke volume)

Left-sided systolic heart failure is associated with contractility that is (increased) (decreased) (unaffected).

decreased Weakened heart muscle leads to decreased contractility, meaning the heart contracts with less force.

David has developed complete (or third-degree) heart block. Describe how his ECG will look compared to an unaffected person. The R waves of David's ECG will have a frequency that is [increased, decreased, the same], AND this frequency is determined by [SA node, AV node, internodal fibers, bundle of His, Purkinje fibers].

decreased AND purkinje fibers Because of issues with the AV node, signals don't get to the ventricles. Thus the only autorhythimic left to set the pace are the Purkinje fibers, which fire at a slower rate than the SA and AV nodes.

During exercise (relative to at rest), the end diastolic volume (increases/decreases). In spite of this, the stroke volume during exercise (increases/decreases). This means the end systolic volume must (increase/decrease). What changes in order for this to happen?

end diastolic volume decreases stroke volume during exercise increases end systolic volume must decrease With exercise, an increase in heart rate (HR) leads to incomplete filling of the ventricles, thus a decrease in EDV. But because of an increase in contractility, more blood is squeezed out during contractions, and the stroke volume increases, and a decrease in the amount of blood left in the ventricle after contraction (i.e., ESV).

Left-sided systolic heart failure is associated with end diastolic volume that is (increased) (decreased) (unaffected).

increased Weakened heart muscle leads to decreased contractility, meaning the heart contracts with less force, decreasing the amount of blood that leaves per beat (i.e., the stroke volume). This leaves behind more blood, which increases the end-diastolic volume.

David has developed complete (or third-degree) heart block. Describe how his ECG will look compared to an unaffected person. The P waves of David's ECG will have a frequency that is [increased, decreased, the same], AND this frequency is determined by [SA node, AV node, internodal fibers, bundle of His, Purkinje fibers].

increased/the same AND SA node In complete heart block the damage is to the AV node. The SA node and atrial depolarization (thus P waves) are normal. *increased after compensation also accepted

What is another way of thinking about prolapse?

insufficient valve murmur -valve doesn't properly close

Occasionally a child is born with a defective aortic valve that is both stenotic and insufficient. The abnormally shaped valve leaflets neither open nor close properly. List the sequence of sounds that would be heard when listening to the heart with a stethoscope, taking into account the timing and type of murmur(s).

lup-whistle-dup-swish Stenosis (whistle) is heard when the valve should be open, which is during ventricular systole, and insufficiency (swish) is heard when the valve should be closed, which is during ventricular diastole.

how do you know is a p wave is coupled with an organized artial contraction in an ECG?

the p wave looks normal regardless of how many or how few there are

Complete heart block is also known as ...

third degree heart block

Mary suffers from atrial flutter, a disease related to atrial fibrillation (A-fib). Instead of the random electrical activity seen in A-fib, atrial flutter involves rapid electrical signals travelling in circles from the SA node to the AV note and back to the SA node. Because of the refractory period of AV node cells, not every signal reaching the AV node causes firing. How is atrial flutter different from complete heart block (also known as third-degree heart block)?

Both appear to have P waves that are independent of R waves, but for different reasons. In CHB, the AV node is nonfunctional, so R waves (and then ventricle contractions) happen when Purkinje fibers fire - at their slower rate of ~35bpm. P waves (and atrial contractions) are pretty normal since the SA node is fine. In A-flutter, R waves are still under the control of the atrial conducting system - just not every signal gets through. Thus, the rate of ventricle contraction is higher in A-flutter. Of course, the atrial conducting system is out of whack in A-flutter. [See notes for more A-flutter info]

Which is more serious: atrial fibrillation or ventricular fibrillation? Why?

Both of these leads to a loss of contractions in the affected chamber, without affecting the other chamber. Without atrial contractions, 80% filling of the ventricles still take place; without ventricle contractions, the body (especially the brain!) doesn't get its blood supply. This leads to death very quickly.

It is possible to study skeletal, cardiac, and smooth muscle in vitro. In these preps, it is possible to vary the constituents of the ECF. What will happen to contraction in each case when Ca2+ is removed from the ECF and the muscle is activated, relative to activating the muscle in the presence normal levels of ECF Ca2+. cardiac contractile cell

Cardiac contractile cells will not contract without Ca2+ in the ECF. In this case, the DHPR (aka L-type Cav channel) is acting as a channel, and it allows Ca2+ to enter from the ECF when the cell membrane depolarizes. This Ca2+ binds RyRs, causing them to open, thereby releasing SR stores of Ca2+.

Herb had a heart attack that damages the papillary muscles of his left ventricle, leading to mitral valve prolapse, meaning that his mitral valve is open part of the time it should be closed. Describe the compensatory response in the cardiovascular system, including the stimulus, sensor, integrating center and three targets/effectors.

Carotid and aortic baroreceptors (the sensors) will detect ̄ BP (the stimulus), due to ̄ stretch, and fire less to the CVCC (the integrating center). The CVCC will decrease output through the parasympathetic nervous system going the SA and AV nodes, thereby decreasing HR. The CVCC will increase output through the sympathetic nervous system, increasing the HR by its action on the SA and AV nodes, increasing contractility by its action on contractile cells of the ventricles, and increasing vasoconstriction of arterioles, increasing TPR. All of these go to increasing BP, restoring it to its normal range. (SA and AV nodes, contractile cells, and arterioles are targets/effectors).

David has developed complete (or third-degree) heart block. Describe how his ECG will look compared to an unaffected person. What treatment will David likely receive?

David needs a pacemaker to increase rate of ventricular contractions.

Herb had a heart attack that damages the papillary muscles of his left ventricle, leading to mitral valve prolapse, meaning that his mitral valve is open part of the time it should be closed. Will Herb's arterial PO2 (increase) (decrease) (stay the same) AND will his arterial PCO2 (increase) (decrease) (stay the same)

Decrease AND Increase Because of in diffusion distance at alveolar-pulmonary capillary interface, there will be less diffusion of both O2 and CO2, leading to ̄ arterial O2 and arterial CO2. (Note: O2 is affected more but both are affected.)

David has developed complete (or third-degree) heart block. Describe how his ECG will look compared to an unaffected person. Because of the complete heart block, David has [increased, decreased, the same] cardiac output, assuming no compensation. Explain.

Decreased Because the ventricles are contracting at a slower rate, blood is leaving the heart at a slower rate. CO = SV x HR, so CO would be decreased. SV might also be lower because the 20% of blood that atrial contraction send to the ventricles might not be properly coordinated.

Mitral valve prolapse is sometimes associated with a murmur. During which parts of the cardiac cycle will the murmur occur? After which heart sound, S1 (lub) or S2 (dup), does the sound occur? Explain.

Mitral valve prolapse will be like an insufficient valve; that is, open when it should be closed. For an atrioventricular valve, this would be during isovolumic ventricular contraction and ventricular ejection. (The valve should also be closed during isovolumic ventricular relaxation, but the pressure wouldn't likely be high enough to force the valve open). The murmur would be happening during ventricular systole; i.e., after S1 and before S2 during each cycle. The sound would be a swish rather than a whistle, so lub-swish- dup. (Note: with prolapse enough pressure has to build for the valve to open during systole, and it often opens with a click in mid systole, after which the swish is heard.)

David has developed complete (or third-degree) heart block. Describe how his ECG will look compared to an unaffected person. Would either the R or P waves be arrhythmic?

Neither would be arrhythmic. The rhythm in each would have consistent spacing, they would just be out of sync with each other.

What treatment would you give someone who has no P wave showing up on their ECG and few QRS complexes?

No P waves means no atrial contraction means pooling in the atria, which can lead to clotting. I would prescribe an anticoagulant. This HR is a bit low, so maybe a pacemaker. Or maybe something to increase contractility, like a b1 agonist.

It is possible to study skeletal, cardiac, and smooth muscle in vitro. In these preps, it is possible to vary the constituents of the ECF. What will happen to contraction in each case when Ca2+ is removed from the ECF and the muscle is activated, relative to activating the muscle in the presence normal levels of ECF Ca2+. skeletal muscle

The skeletal muscle will contract normally without Ca2+ in the ECF because all the Ca2+ necessary for contraction is coming from inside the SR. The DHPR in this case is acting as a voltage-sensor, not a Cav channel, and opens RyR, which it is directly coupled to, by voltage induced conformational change.

Occasionally a child is born with a defective aortic valve that is both stenotic and insufficient. The abnormally shaped valve leaflets neither open nor close properly. During which of the following stages of the cardiac cycle (steps numbered below) would you hear a murmur if the aortic valve is stenotic? Steps of cardiac cycle: 1. atrial systole 2. isovolumic ventricular contraction 3. ventricular ejection 4. isovolumic ventricular relaxation 5. late diastole/ventricular filling

The stenosis would be heard during ventricular ejection (step 3), i.e., when the aortic valve isopen, but not open enough.

What is the possible diagnosis if ECG has more P waves than QRS complexes, but each QRS complex is paired with a P wave?

This suggests that there is a conduction problem (heart block), signals are likely not making it through the AV node. Each QRS complex looks normal and is paired properly with a P wave, however, suggesting that the conduction problem is intermittent, and not as severe as the third degree block we looked at in class. I suspect that the atria are contracting faster because with fewer ventricular contractions, not enough oxygen is reaching the body and the ANS is signaling to the SA node to increase HR.

True or False: The left and right ventricles contract at the same time.

True

In a physical exam, Rachel's heart rate was rapid and very irregular. Furthermore, her heart rate, determined directly by listening to her heart with a stethoscope, exceeded the pulse rate taken concurrently at her wrist. No definite P waves could be detected on Rachel's ECG. The QRS complexes were normal in shape but occurred sporadically. What type of drug might you use to treat the rapid heart rate?

You would want to slow the heart rate. Ivabradine, the If antagonist, would work, as would muscarinic agonists or b1 adrenergic antagonists (b1 blockers).