Cardiovascular ll Flashcards

1
Q

Where do the atria receive blood from?

A

The venous system.

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2
Q

Where do ventricles deliver blood to?

A

The arterial system.

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3
Q

What prevents the mixture of blood from the two sides of the heart?

A

The septum.

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4
Q

What is the path of pulmonary circulation?

A

Right ventricle to left atrium

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5
Q

What is the path of systemic circulation?

A

Left ventricle to right atrium

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6
Q

Review cardiac anatomy and the pathway of blood/ the chambers of the heart and their characteristics.

A

Slides 10-15

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7
Q

Which ventricle in the heart does more work, left or right?

A

The left ventricle performs more work by a factor of 5-7 than that of the right ventricle.

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8
Q

Which ventricle, left or right, is thicker and why? By how much?

A

The left ventricle is thicker because it performs more work and it is required to be thicker because it uses stronger contractions. The left ventricle is approximately 8-10 mm thick versus the right ventricle wall which is about 2-3 mm thick.

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9
Q

Atria and ventricles are separated into two functional units by a sheet of connective tissue and there are one way _________ values.

A

Atrioventricular

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10
Q

What is the purpose of the atrioventricular valves?

A

Prevent backflow of blood into the atria. They are affected by pressure differences in the atria and ventricles.

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11
Q

The AV valve between the RA and RV has how many flaps? What is this called?

A

Three flaps = Tricuspid valve

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12
Q

The AV valve between the LA and LV has how many flaps? What is this called?

A

Two flaps = Bicuspid valve or “mitral valve”

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13
Q

One-way semilunar valves are located where?

A

One way semilunar valves are located at the origin of the pulmonary artery and aorta.

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14
Q

What is the function of the pulmonary valve?

A

Pumps deoxygenated blood to the lungs.

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15
Q

What is the function of the aortic valve?

A

Pumps oxygenated blood to the body.

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16
Q

What happens when ventricles contract?

A

The valves open so blood is pumped through them.

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17
Q

What happens during ventricular relaxation?

A

The semilunar valves snap shut so that blood doesn’t flow back into the ventricles.

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18
Q

Review the heart valves.

A

Slide 16 and Slide 17

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19
Q

What does diastole mean?

A

When both atria and ventricles are relaxed.

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20
Q

Describe the events during diastole.

A

When both the atria and the ventricles are relaxed, venous return fills the atria, atrial pressure increases, the AV valves open, and blood flows into the ventricles. Both atria then contract sending blood to the ventricles.

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21
Q

What does systole mean?

A

Simultaneous contract of both ventricles.

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22
Q

Describe the events during systole.

A

Simultaneous contraction of both ventricles about 0.1-0.2 seconds after diastole. One ventricle sends blood to the lungs or pulmonary system and the second ventricle sending blood to the body or systemic system.

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23
Q

Review the diagrams on systole and diastole.

A

Slide 20

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24
Q

Define end-diastolic volume?

A

The volume of blood in the ventricles at the end of diastole right before the ventricles contract.

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25
Q

Contraction of the ventricles in systole ejects about ___ (ejection fraction) of the blood they contain.

A

2/3

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26
Q

What is the stroke volume?

A

The volume of blood pumped per beat by each ventricle. 2/3 of the blood left in the ventricles before they contract.

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27
Q

What is the end systolic volume?

A

1/3 of the blood left in the ventricles. 1/3 of the end total diastolic volume.

28
Q

Define end-diastolic volume.

A

Volume in the ventricles at the end of diastole.

29
Q

Define end-systolic volume.

A

Volume in ventricles following their contraction.

30
Q

At an average cardiac rate of 70 bpm, how long does each cycle of the cardiac cycle last?

A

0.8 seconds

31
Q

During the cardiac cycle how much time is send in diastole ?

A

0.5 sec

32
Q

During the cardiac cycle how much time is send in systole?

A

0.3 sec

33
Q

Define cardiac output.

A

The volume of blood pumped per minute by each ventricle.

34
Q

What is the formula for cardiac output?

A

Cardiac output = SV (mL/beat) x HR (beats per min)

SV= Stroke Volume
HR = Heart Rate

Average resting HR = 70 bpm
Average SV = 70-80 mL/beat

Therefore, the average CO = 5000 to 5500 mL/min

35
Q

Describe the electrical activity of the heart that facilitates its pumping ability.

A
  • Myocardial cells interconnected by gap junctions (electrical synapses).
  • An entire mass of interconnected cells if referred to as myocardium (functional syncytium)
36
Q

What are the three regions of the heart that can spontaneously generate action potentials?

A
  1. Sinoatrial node (SA node) -> Pacemaker located in the right atrium, near the opening of the superior vena cava

** Note that the vagus nerve innervates the SA node and can adjust HR**

  1. AV node
  2. Purkinje fibres
37
Q

Where do action potentials originate in the heart? How often?

A

SA node (Review slide 30). Cause muscle contraction about every 0.8 seconds because one cell cycle is about 0.8 seconds.

38
Q

Action potentials spread to adjacent ________ in the right atrium and left atrium through gap junctions between these cells.

A

Myocytes

39
Q

The atria and ventricles are separate, so specialized electrical cells called _____________ (conducting tissue) are needed to move the impulse atria to the ventricles in the AV node.

A

Myocardial cells

40
Q

Describe the pathway of electrical activity in the heart and timing of these steps. There are 5 steps.

A
  1. Impulse starts the at SA node (atria contract) –> Spreads quickly (0.8-1.0 m/s)
  2. Goes to the AV node (inferior inter arterial septum) –> Conduction rate slows (0.03 to 0.05 m/s): The delay in excitation between the atria and ventricles allow the ventricles to fill with blood)
  3. Continues through the AV bundle (“bundle of His”) –> Conduction rate increases
  4. Descends down he intraventricular septum, dives right and left with Purkiinje fibres in the ventricle wall –> Conduction rate peaks at 5 m/s
  5. Spreads from endocardium (inner) to epicardium (outer) causing both ventricles to contract simultaneously

**Review slides 32-35

41
Q

Identify the electrical activity of the heart based on the diagram.

A

Reviewslide 33

42
Q

SA node cells (pacemaker cells) directly contact ______________.

A

Atrial muscle cells

43
Q

The atrioventrical node is located in the _________ wall of the right atrium, conduction rate slows, allowing the atria to contract and fill the ventricles.

A

Posterior septal

44
Q

The action potential moves to the atrioventricular bundle (His) and the conduction rate starts to increase. _______ and ______ are the only connection between the atria and ventricles.

A

AV bundle and AV node

45
Q

At the _______, the conduction rate peaks. Rapid conduction occurs caused by more positive resting membrane potential and many gap junctions.

A

Purkinje fibrers/ Bundle branches

46
Q

Describe the echocardiogram and how it works.

A
  • Potential differences generated by the heart are conducted to body surfaces where they can be recorded by surface electrodes placed on the skin.
  • ECG is not the recording of a single action potential, but it does result from the production and conduction of action potentials in the heart.
47
Q

ECG: What is the P-Wave?

A

Depolarization of atria in response to SA node triggering.

48
Q

ECG: What is the PR Interval?

A

Delay of AV node to allow filling on the ventricles.

49
Q

ECG: What is the QRS Complex?

A

Depolarization of ventricles, triggers main pumping contractions.

50
Q

ECG: What is the ST Segment?

A

Beginning of ventricle depolarization, should be flat.

51
Q

ECG: What is the T-Wave?

A

Ventricular depolarization

52
Q

The Echocardiogram: Review the graph and area of the heart interacted with.

A

Slide 41

53
Q

A heart attack, known as schema deals with which segment of the ECG graph?

A

S-T segment (Review slide 43)

S-T segment depression is caused by the health myocytes being more depolarized than the cells in the infarct region leading to a potential difference

54
Q

What is bradycardia?

A

Bradycardia is a slow heart rate. The hearts of adults at rest usually beat between 60 and 100 times a minute. If you have bradycardia, your heart beats fewer than 60 times a minute.

55
Q

What is tachycardia?

A

Tachycardia is the medical term for a heart rate over 100 beats a minute. Many types of irregular heart rhythms (arrhythmias) can cause tachycardia. A fast heart rate isn’t always a concern.

56
Q

Right bags (EACh) innervates SA node and ______________ can lead to bradycardia. (Vagus slows down HR)

A

Hyperstimulation

57
Q

Ventricles receive direct innervation from ___________ when circulating catecholamines.

A

Adrenergic neurons

58
Q

Where is epinephrine released from?

A

The adrenal medulla

59
Q

Where is norepinephrine released from?

A
  • Released from cardiac sympathetic nerve endings
  • Some from the adrenal medulla (~15% of catecholamine release)
60
Q

When are the release of catecholamines activated?

A

Times of stress (exercise, heart failure, hemorrhage, emotional stress, pain).

61
Q

Describe the characteristics of epinephrine.

A
  • B -adrenergic receptors are most sensitive.
  • B1 (75-80%) and B2 receptors are present in the myocardium.
  • Increased heart rate and ionotropy (contractilit) –> Increased CO
  • Vasodilatation of arterioles(effects are masked by dominant alpha-recpetor-mediated constriction
  • Relaxation and dilation of bronchioles
62
Q

Describe the characteristics of norepinephrine.

A
  • Alpha-adrenergic receptors are most senestive.
  • Alpha receptor predominant in smooth muscle and the wall of blood vessels
  • Vasoconstriction in systemic arteries and veins
  • Overall, increased systemic vascular resistance and increased arterial BP
63
Q

Antagonists are used as _____________.

A

Blockers

64
Q

Alpha blockers such as prazosin may be used to treat _________.

A

High blood pressure

65
Q

Beta blockers such as propranolol may be used to lower ______________.

A

Heart rate and blood pressure

66
Q

Review the vicious cycle of sympathetic activation in chronic heart failure.

A

Slide 52