Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Guyton & Hall Physiology > Ch 9-12 Cardio > Flashcards

Ch 9-12 Cardio Flashcards

1
Q

Where is the SA node located?

A

In the superior posterolateral wall of the right atrium, immediately below and slightly lateral to the opening of the superior vena cava

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the resting membrane potential of the sinus nodal fibers? Why is it this way?

A

-55 to -60 mv

The cell membranes are leaky to Na and Ca, so positive charges of these cations neutralize some negativity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What three types of membrane ion channels does cardiac muscle possess?

A

Fast sodium channels, slow sodium channels, and potassium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What causes the rapid upstroke spike in the action potential of ventricular muscle?

A

Opening the fast sodium channels for a brief period, which causes rapid positive influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes the plateau of a ventricular action potential?

A

Slower opening of the slow Na/Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What brings the membrane potential back to resting level in a ventricular action potential?

A

Opening K+ channels, which allows outflux of positive ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Opening of which ion channels causes an action potential in sinus nodal fibers?

A

Slow sodium-calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can sinus nodal fibers keep from being in a state of constant depolarization?

A
  1. Na/Ca channels inactivate/close shortly after opening
  2. At the same time, many K+ channels open
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does hyperpolarization occur in a nodal fiber?

A

K+ channels remain open for another few tenths of a second to continue movement of positive charges out of the cell. Then they close soon after, and Na and Ca leak back into the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the anterior interatrial band? What others are like it?

A

a band of atrial fibers passing through the anterior atrial walls to the left atria (also have the middle and posterior pathways).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is the AV node located?

A

The posterior wall of the right atrium immediately behind the tricuspid valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes the slow conduction in the transitional, nodal, and penetrating AV bundle fibers?

A

Fewer gap junctions between successive cells in the conducting pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are action potentials rapidly transmitted between Purkinje fibers?

A

high levels of permeability of the gap junctions at the intercalated discs between successive cells. AND the action potentials cannot travel backward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the order in which cardiac impulses spread throughout the heart?

A
  1. SA node
  2. AV node
  3. Ventricular septal AV bundle
  4. Purkinje fibers
  5. Ventricular endocardium
  6. Through ventricular muscle to the epicardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How many times per minute do the AV nodal fibers discharge?

A

40-60 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How frequently do the purkinje fibers discharge?

A

15-40 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why does the SA node control heartbeat in a normal patient?

A

It discharges more rapidly than the AV or PF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Stokes-Adam syndrome?

A

Delayed pickup of the heart beat b the Purkinje system after AV bundle block caused by the temporarily suppressed state of the Purkinje fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Briefly, how are the nerves of the PSNS and the SNS distributed throughout the heart?

A

SNS: all over the heart, especially ventricular muscle
PSNS: SA and AV nodes, a little to atrial muscle, least to ventricular muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is/are the effect(s) of acetylcholine on the heart, overall?

A

Decreased rate of SA node, decreased excitability of AV junctional fibers, (slowing transmission)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the action of acetylcholine on the heart at a cellular level?

A

ACh increases fiber membrane permeability to K+ ions, so K+ leaks out, so the fibers hyperpolarize and become LESS excitable.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In general, what are the effects of SNS stimulation on the heart?

A
  1. increases rate of sinus nodal discharge
  2. increases rate of conduction
  3. increases level of excitability in all portions of the heart
  4. increases force of contraction of all cardiac muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

At a cellular level, how does NorEpi cause the effects described above?

A

Stimulates beta-1 adrenergic receptors, which mediate effects on heart rate
At the sinus node, Sodium-calcium permeability increases, so the membrane is more excitable
Also the increased permeability to calcium contributes to increased contractile strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which aspects of the ECG are depolarization waves? Which are repolarization waves?

A

The P wave and parts of the QRS.
Repol is T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Briefly, describe the events associated with each segment and wave in an ECG. Start with the SA node firing

A
  1. P wave: Atrial depolarizaton
  2. PR segment: AV nodal delay
  3. QRS complex: ventricular depolarization and the atria is simultaneously repolarizing
  4. ST segment: ventricles contracting and emptying
  5. T wave: ventricular repolarization
  6. TP segment: time during which ventricles are relaxing and filling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why is the p wave smaller than the QRS complex?

A

because the atria have a smaller muscle mass compared to ventricles, so create less electrical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

For how long do the ventricles remain contracted (by ECG timeline, not seconds)?

A

Until after the end of the T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is the T wave prolonged compared to the QRS?

A

Because ventricular repolarization takes longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do you determine heart rate from an ECG?

A

Recipricol of the time interval between two successive heart beats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why does depolarization spread more slowly through the atria than through the ventricles?

A

Because atria lack a purkinje system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does increased cardiac muscle mass impact an ECG?

A

It causes high voltage QRS complexes. Diminished muscle mass does the opposite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the three main causes of decreased voltage in ECG leads?

A
  1. Pericardial fluid
  2. Pleural fluid
  3. Pulmonary emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the three main causes of a prolonged QRS complex?

A
  1. Ventricular hypertrophy
  2. Ventricular dilation
  3. Purkinje fiber blockage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the main causes of Bizzare QRS complexes?

A

Cardiac muscle destruction and multiple small blockages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Briefly, what are the effects of Digitalis on the heart?

A

It increases strength of cardiac muscle contraction
The T wave may invert or become biphasic
When overdosed, depolarization duration increases disproportionately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does body temperature influence heart rate?

A

For each degree F, HR increases about 10 bpm (in humans)

37
Q

Why does fever cause tachycardia?

A

Incr temp increases rate of metabolism of the sinus node, thereby increasing excitability and rhythm

38
Q

What are the 4 main causes of an AV block?

A
  1. AV node or AV bundle fiber ischemia
  2. AV bundle compression
  3. Inflammation, which dcrs conductivity
  4. Extreme vagal excitaton
39
Q

Briefly, what is the main non-pathologic cause of sinus arrhythmia?

A

“Respiratory” type: results from “spillover” of signals from the medullary resp center into the adjacent vasomotor center during insp and expr cycles of resp. THis causes alternate increases and decreases in the number of impulses transmitted through the sns and vagus nerves

40
Q

What is a 1st degree AV block?

A

Prolonged PR/PQ interval (> 0.20 sec)

41
Q

What is a 2nd degree AV block?

A

When the action potential is not strong enough to pass through the bundle into the ventricles. There’s a p wave but no QRS

42
Q

What is a 3rd degree AV block?

A

When the condition causing poor conduction in the AV node or bundle is severe enough to completely block the atrial impulse from reaching the ventricles.
In these, there is no relation between the rhythm of the atria and that of the ventricles

43
Q

What is ventricular escape?

A

When, after a few seconds of overdrive suppression of the ventricles, the purkinje system begins rhythmically discharging and acting as a ventricular pacemaker

44
Q

What is electrical alternans?

A

Partial intraventricular block: partial intraventricular block every other heartbeat

45
Q

What are the main causes of premature ventricular contractions?

A

Usually ectopic foci
1. local areas of ischemia
2. small calcified plaques
3. toxic irritation of the AV node, purkinje system, or myocardium via drugs/nicotine/caffeine

46
Q

What effects do premature ventricular contractions cause in the ECG?

A
  1. prolonged QRS complex
  2. High voltage QRS complex because the impulse only travels in one direction, so one entire side of the ventricles depolarizes ahead of the other
  3. After most PVCs, the T wave’s electrical potential is almost opposite the QRS because of slow conduction of the impulse through the cardiac muscle
47
Q

Why is long QT syndrome of concern?

A

It can lead to torsades de pointes ventricular arrhythmia. Why? because of delayed repolarization. Can be treated with MgSO4 or Beta adren blockers

48
Q

What are the main two implications when ventricular paroxysmal tachycardia develops?

A
  1. Represents considerable ischemic ventricular damage
  2. Often initiates the lethal even of V-fib
49
Q

What are the main causes of V Fib?

A
  1. Sudden electrical shock of the heart
  2. Ischemia of the heart muscle or its conducting system
50
Q

What are the three abnormalities of circus movement of an impulse through the ventricular muscle that can cause V Fib?

A
  1. The conduction pathway is too long
  2. Velocity of conduction becomes decreased
  3. The muscle refractory period greatly shortens
51
Q

Describe the three main events that transpire and culminate in VFib

A
  1. Some depolarization waves are transmitted in some directions, but not in others
  2. Rapid stimulation of the heart causes decreased velocity of conduction, and the refractory period of the muscle shortens
  3. Impulses divide: when a depolarization wave reaches a refractory area in the heart, it travels to both sides around the refractory area, becoming two impulses that create many routes that lengthen the conduction pathway
52
Q

Why does defibrillation need to be initiated rapidly?

A

The heart muscle is too weak after about 1 minute due to insufficient coronary blood flow

53
Q

What commonly causes atrial fibrillation?

A

Atrial dilation/enlargement from valve lesions preventing complete atrial emptying

54
Q

Briefly, describe the pathophys of atrial fibrillation

A

Numerous small depol waves spread in all directions through the atria. THe waves are weak and often of opposite polarity and so can neutralize each other. The atria cannot function as a pumping unit, and blood flow to the ventricles has to occur mostly by passive flow. Also, the interval between successive ventricular contractions varies and causes irregular heartbeat (usually a faster rate too)

55
Q

Why is the action potential of a cardiac myocyte so long?

A
  1. Unlike skeletal muscle, cardiac action potentials involve both opening of fast Na channels and slow Ca channels (Na/Ca channels). The Ca channels are slower to open remain open for several 10ths of a second, allowing a lot of Ca and Na to flow into the myocyte and maintain a plateau of depolarization
  2. Immediately after the action potential begins, cardiac muscle membrane’s permeability to K+ decreases fivefold, decreasing K+ outflux and preventing early return to resting voltage
56
Q

What event in a cardiac action potential brings on the END of the action potential?

A

Closing of the slow Ca/Na channels. Once this happens, membrane permeability to K+ increases rapidly and thus membrane potential returns to resting level

57
Q

How does the refractory period of atrial muscle compare to that of ventricular muscle?

A

Atrial muscle RP is shorter

58
Q

In summary, how are cardiac myocytes adapted to utilize calcium for action potentials?

A

Calcium is released from longitudinal sarcoplasmic tubules when acted upon by action potentials from T tubules (like skel muscle) AND Ca++ diffuses from the T-tubules themselves into the sarcoplasm at the time of the action potential…which opens voltage-gated Ca channels in the T tubules

Ca enters the cell, activates Ca release channels aka Ryanodine Receptor Channels in the sarcoplasmic reticulum membrane.

This triggers Ca release into the sarcoplasm, which is now available to interact with Troponin and cause cross-bridge formation and contraction

59
Q

Why are T tubules so essential for Cardiac APs?

A

Because the sarcoplasmic reticulum of cardiac muscle is less developed than in skel muscle and doesn’t store enough Ca.
SO the T tubules compensate by having a diameter 5x that of skel muscle and binding Ca inside T tubules using negatively charged mucopolysaccarides

60
Q

Complete the sentence : “The duration of contraction of cardiac muscle is a function of…”

A

…The duration of the action potential, including the plateau

61
Q

Finish the sentence: The strength of contraction of cardiac muscle depends greatly on the …

A

… concentration of calcium ion in the extracellular fluids

62
Q

In relation to systolic or diastolic events, when does the qrs complex begin? What about the T wave?

A

QRS is just before the onset of ventricular systole. T wave is slightly before ventricular contraction

63
Q

What percentage of ventricular fill does active atrial contraction contribute?

A

ONly about 20%. 80% flows directly from A to V

64
Q

Which phase of the cardiac cycle decreases the most in duration when heart rate increases?

A

Diastole (relaxation phase)

65
Q

What three ‘events’ are denoted by the a, c, and v waves, and what do they represent as far as pressure changes in the atria?

A

a wave: atrial contraction. L > R atrial pressure
c wave: ventricles contract and slightly backflow of blood into the atria and bulging of the AV valves backward increases atrial pressure slightly
v wave: end of ventricular contraction, when slow flow of blood into the atria from the veins while AV valves are closed increases atrial pressure

66
Q

When does rapid ventricular filling occur?

A

the first 1/3 of diastole

67
Q

What occurs during isovolumic/isometric contraction?

A

the ventricles contract but are closed, so there’s no emptying. Incr tension but no change in muscle fiber length

68
Q

What occurs during isovolumic relaxation?

A

aka isometric.
End of systole, after blood has been shoved into the great vessels, A and P valves close and the ventricular muscle keeps relaxing, with no change in volume

69
Q

What causes end systolic volume to decrease?

A

Increased strength of cardiac contraction

70
Q

When do the papillary muscles contract?

A

when the ventricular walls contract but do NOT help the valves to close. They pull the vanes inward to prevent bulging

71
Q

What is the “incisura” of the aortic pressure curve?

A

During a short period of backward blood flow immediately before closure of the valve, causing mild increase in aortic pressure before it decreases

72
Q

What is the first heart sound?

A

Closure of the AV valves. Low pitch, long lasting, occurs when the ventricles contract

73
Q

What is the second heart sound?

A

Rapid snapping sound, caused by closure of the aortic and pulmonary valves closing at the end of systole

74
Q

What comprises work output of the heart?

A
  1. Volume-pressure work/external work: used to move blood from low pressure veins to high pressure arteries
  2. Kinetic energy of blood flow: accelerates blood to this velocity of ejection through the aortic and pulmonary valves
75
Q

What is end systolic volume?

A

vol of blood remaining in the ventricle after the previous heartbeat

76
Q

What happens to the area of the work diagram when the heart pumps large quantities of blood?

A

It enlarges.

77
Q

What is meant by the term “preload” ?

A

The end-diastolic pressure when the ventricle has become filled. It is the degree of tension on the muscle when it begins to contract.
Pressure during ventricular filling.

78
Q

What is meant by the term “afterload”?

A

Afterload of the ventricle is the pressure in the aorta leading from the ventricle. It is the load against which the muscle exerts its contractile force.
Arterial pressure against which the ventricle must contract

79
Q

What is the equation that explains the contributors to cardiac muscle tension during contraction?

A

Heart muscle tension in contraction= pressure x diameter of the ventricle

80
Q

How is the volume pumped by the heart regulated?

A
  1. Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing in the heart
  2. Control of heart rate and strength of heart pumping by the ANS
81
Q

Briefly, what does the Frank Starling mechanism state?

A

The greater the heart muscle is stretched during filling, the greater the force of contraction and the greater the quantity of blood pumped into the aorta

aka

Within physiologic limits, the heart pumps all the blood returned to it by the veins

82
Q

How does stretch of the right atrial wall influence heart rate?

A

It increases the heart rate by 10-20 percent

83
Q

What effect does vagal stimulation have on the heart?

A

Decreases rate but not strength of contraction

84
Q

What are the effects of potassium ions on the heart’s activity?

A

-Excess K+ in the ECF causes the heart to dilate, become flaccid, and slows HR. Lg amounts can block conduction from the A to V’s

-Because…it decreases the resting membrane potential, partially depolarizing the cell membrane and causing it to become less negative , which leads to less intense action potentials and weakens the heart

85
Q

What are the effects of calcium ions on the heart’s function?

A

Since Ca directly initiates the cardiac contractile process, it causes the heart to go toward spastic contraction

Ca deficiency though causes cardiac flaccidity

86
Q

What are the effects of temperature on heart function?

A

Increased temp: increases HR , increased contractile strength temporarily. Increases cardiac myocyte membrane permeability ions that control HR
Decreased temp: HR falls

87
Q

In a nutshell: during normal function of the heart, what determines cardiac output?

A

Ease of blood flow through the body’s tissues, which in turn controls venous return

88
Q
A

Guyton & Hall Physiology (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions