The Heart as a Pump Flashcards

1
Q

Veins vs arteries

A

Veins carry blood to the heart

Arteries carry blood away from the heart

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2
Q

Which artery carries less oxygenated blood?

A

Pulmonary artery

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3
Q

Why does a vein contain fewer layers of smooth muscle and connective tissue than an artery?

A

Blood is under lower pressure in veins so the vessel does not require as much protection and veins don’t constrict so no smooth muscle is required.

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4
Q

Where is blood at highest pressure in the body?

A

Left atrium —> aorta

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5
Q

Where is the only place gas/material exchange?

A

Capillary beds

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6
Q

Materials entering the body moved by the CV system

A

Oxygen, nutrients, water

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7
Q

Materials moving from cell to cell by the CV system

A

Wastes, immune cells, antibodies, clotting proteins, hormones, stored nutrients

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8
Q

Materials leaving the body moved by the CV system

A

Metabolic wastes, heat, CO2

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9
Q

What is blood pressure?

A

Force exerted by blood on the walls of a vessel

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10
Q

What is the primary reason blood pressure falls as we move further from the heart?

A

Friction

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11
Q

Where is blood pressure lowest in the body?

A

Venae cavae

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12
Q

Fluid flows only if there is a ______ pressure gradient.

A

Positive (delta P is > 0)

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13
Q

3 factors that influence the movement of fluid through a tube

A

Radius of the tube (most important for blood vessels)
Length of the tube
Viscosity of the liquid

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14
Q

Examples of changing the radius of a blood vessel and effect on pressure

A

Vasodilation & vasoconstriction apportions blood to different parts of the body.

Atherosclerosis prevents vessels from expanding.

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15
Q

Flow rate vs. velocity

A

Flow rate = measure of volume output / minute

Velocity = change in position of a point/ time

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16
Q

How is the cross-sectional area of a vessel related to the velocity of blood flow?

A

Higher cross-sectional area (ex: in capillaries) causes slower linear velocity of blood

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17
Q

Why is blood flow unidirectional?

A

Valves

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18
Q

Why is muscle thicker in ventricles than atria?

A

Must pump blood with greater force

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19
Q

How are autorhythmic cells related to the nervous system?

A

No input needed from the NS for these cells to fire but can be regulated by the NS - ex: heart beating faster when nervous

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20
Q

Why don’t autorhythmic cells contribute to contractile force of the heart?

A

They do not contain sarcomeres (don’t contain actin/myosin)

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21
Q

Process of cardiac muscle contraction

A
  1. AP from neighboring cell/pacemaker depolarizes membrane of cardiac cell via gap junction
  2. VG Ca2+ channels open allowing Ca2+ into the cell
  3. Entry of Ca2+ induces Ca2+ release via RyR
  4. Ca2+ spark
  5. Summed sparks creates a Ca2+ signal
  6. Ca2+ binds to troponin & initiates contraction
  7. Ca2+ unbinds from troponin leading to relaxation
  8. Ca2+ is pumped back into the SR for storage, exchanged with Na+ via NCX antiporter
22
Q

Rapid depolarization of the cell membrane is caused by________.

A

The rapid opening of VG Na+ channels

23
Q

What causes the prolonged plateau of depolarization? (2 things)

A
  1. Slow but prolonged opening of VG Ca2+ channels

2. Closure of K+ channels

24
Q

What causes repolarization of the membrane?

A

TBD (closure of K+ channels)

25
Q

In cardiomyocytes, the AP largely overlaps with the contraction. What does this prevent?

A

Tetanus - this creates a long refractory period to avoid tetanus

26
Q

How does an electrical signal travel through the heart?

A

Originates at the SA node, travels to the atria, atria contract, travels to AV node, pauses, travels down septum to apex, ventricles contract

27
Q

Steps in the AP of a pacemaker cell

A
  1. Funny channels allow Na+ to leak into cells depolarizing the cell
  2. This depolarization activates the VG Ca2+ channels that allow Ca2+ influx depolarizing the cells to threshold
  3. Repolarization occurs when K+ channels open and Ca2+ channels close.
  4. AP of SA node is communicated to contractile cells via gap junctions
28
Q

The signal is held at the AV node briefly to allow…?

A

Ventricles to fill with blood before receiving a signal to contract

29
Q

P wave

A

Atrial depolarization

30
Q

P-R segment

A

Conduction through AV node and AV bundle

31
Q

QRS complex

A

Ventricular depolarization

32
Q

T wave

A

Ventricular repolarization

33
Q

S-T segment

A

Ventricles contract

34
Q

Systole

A

Ventricular contraction ejects blood from ventricles into the pulmonary artery and aorta

Systolic pressure is maximum pressure

35
Q

Diastole

A

Post-systole when muscle relaxes and atria fill with blood

36
Q

End diastolic volume

A

Volume at the end of filling

37
Q

Stages of systole and diastole

A
  1. Late diastole - both sets of chambers are relaxed & passively filling with blood
  2. Atrial systole - atrial contraction forces a small amount of additional blood into the ventricles
  3. Isvolumic ventricular contraction - first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
  4. Ventricular ejection - ventricular pressure rises and exceeds pressure in arteries; semilunar valves open and blood is ejected
  5. Isovolumic ventricular relaxation - ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed
38
Q

Cardiac output

A

Heart rate x stroke volume (amount of blood pumped from the left ventricle)

Amount of blood moved per unit time

Heart rate is variable but stroke volume is largely static though can be improved by strengthening the heart

39
Q

Ways to increase the strength of contraction

A
  1. Add epi or epi agonist
  2. Stretch the heart (frank-starling; increased venous return)
  3. Increase the extracellular concentration of calcium (works mostly in vitro)
40
Q

How does the nervous system regulate pacemaker potential?

A

Both parasympathetic and sympathetic neurons synapse with the SA node to slow and increase heart rate.

Parasympathetic stimulation hyperolarizes the membrane potential to slow depolarization and thus heart rate.

Sympathetic stimulation and epi depolarize the membrane, speed up potential, and increase the heart rate.

Parasympathetic is the dominating influence. A heart removed from the body beats faster without that parasympathetic effect.

41
Q

What type of receptor does epi/norepinephrine bind to?

A

Adrenergic GPCRs

42
Q

The cAMP second messenger system results in the phosphorylation of?

A

VG-Ca2+ channels which allows Ca2+ entry from the ECF —> contraction

Phospholamban which increases Ca2+ ATPase on SR which ultimately releases Ca2+ from SR and leads to more forceful contraction and shortens Ca2+-troponin binding time which shortens the duration of a contraction

43
Q

How does sympathetic stimulation increase the force and velocity of contraction?

A
  1. Allowing cytosolic Ca2+ to increase more quickly
  2. Allowing cytosolic Ca2+ to return the the SR more quickly
  3. Increasing the rate of cross-bridge cycling
44
Q

Which proteins in the cells does PKA affect?

A

L-type Ca2+ channel in the membrane, RyR, Ca2+ binding to troponin

45
Q

Describe the overlap of actin and myosin in cardiac muscle at rest

A

More overlap than is ideal, so stretching the muscle moves overlap into ideal stretch for the most forceful contraction

Cardiac muscle has a much larger tension range (25-100% of maximum tension)

46
Q

Starling Curve

A

Stroke volume increases as end-diastolic volume increases. The heart pumps all the blood it contains.

Relationship between stretch (indicated by end-diastolic volume) and force (indicated by stroke volume)

47
Q

How does epinephrine affect the starling curve?

A

Epi shifts the starling curve such that the heart pumps more blood (higher stroke volume) for the same stretch (end-diastolic volume)

48
Q

How do the events leading to threshold potential differ in cardiac contractile and non-contractile cells?

A

In contractile cells, depolarization enters via gap junctions.

In non-contractile/autorhythmic cells, Net sodium entry through funny channels plus calcium entry depolarizes the membrane to threshold.

49
Q

How does the source of the rising phase of the action potential differ in cardiac contractile and non-contractile cells?

A

Contractile cells - Na+ entry

Non-contractile cells - Ca2+ entry

50
Q

Which type of cardiac cell has an extended potential plateau caused by Ca2+ entry?

A

Contractile

51
Q

Why don’t contractile cardiac cells hyperpolarize?

A

Contractile cardiac cells are primarily leaky to K+ ions so their resting membrane potential is -90 mV.

52
Q

Why do contractile cells have a relatively long action potential (200+ ms)?

A

To avoid tetanus

VG-Na+ channel inactivation gates wait to reset until the end of an AP to avoid tetanus