Chapter 25 (Test #3) Flashcards

1
Q

During Phase 0 of cardiac action potentials, how do the myocytes in the heart become stimulated to depolarize? is it slow or rapid?

A

The myocytes are stimulated to depolarize by sodium entering into the cell, this is a fast response action potential.

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2
Q

During Phase 0 of cardiac action potentials, how do the SA and AV nodal cells get stimulated to depolarize? IS this a fast or slow process?

A

These cells are stimulated to depolarize when calcium enters the cells. This is a slow response action potential.

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3
Q

What happens during Phase 0 of the cardiac action potential?

A

Positive ions influx into the cells, causing depolarization.

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4
Q

What happens during Phase 1?

A

Early cellular repolarization begins as potassium exits the intracellular space.

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5
Q

What happens during phase 2?

A

The plateau phase occurs

Rate of repolarization slows, calcium ions enter the cell.

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6
Q

What happens during phase 3?

A

This is when the completion of repolarization occurs and the cell enters its resting state again. (potassium and sodium leave the cell)

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7
Q

What happens during phase 4?

A

This is the resting phase before another depolarization occurs. (potassium enters cell again)

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8
Q

`Describe automaticity.

A

This is the ability to generate an electrical impulse.

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9
Q

Describe excitability.

A

This is an ability to respond to an electrical impulse.

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10
Q

Describe conductivity.

A

This is the ability to transmit an electrical impulse from one cell to another.

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11
Q

At what rate does the SA node fire? What is another name for the SA node?

A

60-100

primary pacemaker

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12
Q

At what rate does the AV node fire? What is another name for the AV node?

A

40-60

Secondary pacemaker

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13
Q

At what rate does the bundle of his, bundle branches, and purkinje fibers conduct impulses?

A

30-40

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14
Q

Why is there a slight delay between the time the AV node receives the impulse from the SA node, and the time it relays the impulse to the ventricles?

A

This slight delay allows time for the atrias to contract to complete ventricular filling.

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15
Q

Does is special about the left bundle branch?

A

The left bundle branch has to stimulate the largest chamber of the heart to contract, so it actually branch again into the left anterior and left posterior bundle branches.

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16
Q

What is the terminal point of the cardiac conduction system? What does it specialize in?

A

The terminal point is the purkinje fibers, these purkinje cells rapidly conduct impulses through the walls of the ventricles to allow for an almost synchronous contraction.

17
Q

Does atrial systole account for most of the ventricular filling?

A

NO, it only accounts for 15-25%

passive ventricular filling is where its at

18
Q

Describe the the cardiac cycle (in detail!), starting with diastole.

A

The atrias are now filling the ventricles with blood through the AV valves that is returning through the vena cavae and the pulmonary vein, as this is happening the pressure inside the ventricles is increasing. At the end of passive filling the atrias will contract due to the transfer of an impulse from the SA to the AV node. After the last of the blood is filled into the ventricles the ventricles will begin to contract, as the pressure increases in the ventricles the AV valves will close, preventing regurg. As the pressure continue to increase the semilunar valves will open once the pressure exceeds that of the systemic or pulmonary circuit. At the the ejection of the blood will be rapid becuase of the large difference in pressurs, but eventually the pressures will decrease and then equalize at the end of ventricular systole. This will then cause the semilunar valves to close. The process is then repeated.

19
Q

What is cardiac output? Whats the normal value?

A

The amount of blood ejected by one of the ventricles per minute. 4-6L/min

20
Q

What is stroke volume? What is the normal value?

A

This is the amount of blood ejected by the heart per beat. 60-130 ml

21
Q

How is CO calculated?

A

CO= SV x HR

22
Q

How does the parasympathetic nervous system stimulate the SA node?

A

Vagus nerve (slows the HR)

23
Q

How does the the sympathetic nervous system innervate the SA node? What stimulates them?

A

beta-1 receptors in the SA node (increases HR)

Stimulated by catecholamines (secreted by the adrenal gland) and thyroid hormone that has catecholamine-like effects.

24
Q

How do baroreceptors affect CO?

A

In response to HTN, baroreceptors will send impulses to the cerebral medulla which will initiate parasympathetic activity and inhibit sympathetic response. This will lower HR and BP.

and the opposite is true for hypotension

25
Q

What are some ways pre-load is decreased?

Increased?

A

Decreased: reduction of volume entering the ventricles, diuresis, venodilating agents, excessive loss of blood, dehydration.

Increased: increasing return of blood to ventricles, controlling blood loss or body fluid loss, replacing fluids (IV fluids or blood transfusion)

26
Q

What is after load?

What is the resistance against the left ventricle called?

Right ventricle?

A

Afterload is the resistance of blood ejection from the ventricle, or what the ventricles have to push against.

Left: systemic vascular resistance

Right: Pulmonary vascular resistance

27
Q

What do preload and afterload dewtermine?

A

stroke volume

28
Q

What happens to afterload and SV during vasoconstriction?

A

Afterload increases and SV decreases.

29
Q

What happen to afterload and SV during vasodilation?

A

Afterload decreases and SV increases

30
Q

How is contractility depressed?

A

hypoxemia

acidosis

certain medicaitons

31
Q

How is contractility enhanced?

A

circulating catecholamines, sympathetic neuronal activity, certain medications

32
Q

In relation contractility, afterload, and preload, how would the heart achieve the highest SV?

A

Increased preload, increased contractility, and decreased afterload.

33
Q

What is ejection fraction? What is the normal value?

A

This is the percentage of end-diastolic volume that is ejected with each heartbeat.

55-65%

34
Q

At what ejection fraction should a patient be treated for HF?

A

less than 40%

35
Q

What are some age-related changes in cardiac function?

A

The heart will hypertrophy (causes a decrease in chamber size and contractility)

The valves stiffen (cause backflow which causes murmurs)

The heart cant compensate as well to metabolic needs, and may become fatigued, short of breath, and have palpitations due to stress, exercise, or illness.

LOOK AT TABLE 25-1 ON p. 660

36
Q

What are some gender related characteristics of cardiac function?

A

Womens hearts are smaller and have more narrow coronary vessels, this makes procedures done with atheroscerosis more difficult (caths or angioplasty)

Women have increased estrogen which increases HDL, decreases LDL, and dilates blood vessels (enhances blood flow to heart), this decreases their risk of getting CAD until menopause at around 50, then their estrogen slowly decreases until 65 when they are at an equal risk to men.

women usually get CAD 10 years later than men

37
Q

Is hormone therapy in postmenopausal women a good idea to deter the development of CAD?

A

In the past it was thought to have been, but NO NO NO