Cardiac Flashcards

1
Q

Fibrous pericardium

A

Outermost layer made of dense CT

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2
Q

Function of fibrous pericardium

A

Stabilizes heart in position, protects heart from infection, and prevents overfilling with blood

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3
Q

What are the 2 layers of the serous pericardium? What are their locations?

A

Parietal (outer)and visceral (inner)

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4
Q

What separate the parietal and visceral layer of serous pericardium? Function?

A

Pericardial fluid, lubricates heart-pericardium interaction

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5
Q

The visceral pericardium is continuous with ___?

A

Epicardium

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6
Q

What are the 3 heart wall layers from outermost to innermost?

A

Epicardium, myocardium, endocardium

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7
Q

Pericardium

A

Collagenous sac that encloses heart

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8
Q

What separates the superior chambers of the heart?

A

Interatrial septum

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9
Q

What separates the inferior chambers of the heart?

A

Interventricular septum

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10
Q

Oxygenated blood enters the heart via the ___ and enters the ___.

A

Pulmonary veins, left atrium

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11
Q

What are the 3 locations that feed the right atrium?

A

SVC, IVC, and coronary sinus

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12
Q

The pulmonary veins contain ___ blood.

A

Oxygenated

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13
Q

Why is the LV more muscular?

A

The systemic circuit is a longer, higher pressure circuit

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14
Q

The LV pumps more blood per beat than the RV. T/F

A

False, they pump the same amount of blood per beat

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15
Q

The LV is the pump for the ___.

A

Systemic circuit

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16
Q

The ___ circuit is a longer, higher pressure circuit than the ___ circuit, which is shorter and lower pressure.

A

Systemic, pulmonary

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17
Q

The left atrium receives ___ blood from the ___

A

oxygenated, pulmonary veins

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18
Q

___ is the key molecule that links electrical and mechanical in cardiac muscle excitation

A

Calcium

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19
Q

What are the 2 main types of cardiac cells? What is the percentage of each type?

A

Cardiac muscle cells (99%) and cardiac nodal cells (1%)

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20
Q

What is the function of desmosomes in the heart?

A

Hold the cardiac cells together, used for structural integrity

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21
Q

Where does the automaticity of the heart begin?

A

SA node in the upper right atrium

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22
Q

Which of the nodal cells is the first to depolarize?

A

SA nodal cells

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23
Q

What is considered the pacemaker of the heart?

A

SA node

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24
Q

The SA node contains the only pacemaker cells in the heart that can spontaneously depolarize. T/F

A

False, the AV node also contains these cells

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25
Q

Why is the SA node considered the pacemaker of the heart instead of the AV node?

A

The SA nodal cells spontaneously depolarize faster than the cells of the AV node, so they determine the heart rate.

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26
Q

Pathway of electrical current in heart

A
  1. SA node
  2. Internodal pathways
  3. AV node
  4. Bundle of His
  5. Bundle branches
  6. Purkinje fibers
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27
Q

The AV node ___ the conduction velocity, which is called the ___. What is the importance of this?

A

Slows, AV delay
Allows time for the atria to depolarize, contract, and eject their blood into the ventricles before the ventricles contract

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28
Q

Where is the heart located?

A

Mediastinum (medial thoracic cavity)

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29
Q

The apex of the heart points towards the ___ and the base of the heart is directed towards the ___.

A

Left hip, right shoulder

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30
Q

Which layer of the heart is muscular layer where the contractile cells are?

A

Myocardium

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31
Q

Outline the pulmonary circuit

A

RV ->Pulmonary Trunk ->L&R Pulm Arteries ->Pulmonary Capillaries -> Pulmonary Veins -> LA

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32
Q

___% of oxygen is depleted per beat.

A

25%

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33
Q

The ___ receives oxygenated blood from the ___.

A

Left atrium, pulmonary veins

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34
Q

What is the valve between the pulmonary veins and the left atrium?

A

No valve, trick question

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35
Q

The ___ septum is thick than the ___ septum.

A

Interventricular, interatrial

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36
Q

The ___ prevents backflow into the right ventricle.

A

Pulmonary semilunar valve

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37
Q

The ___ prevents backflow in the right atrium.

A

Tricuspid valve

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38
Q

___ prevents backflow into the left ventricle.

A

Aortic semilunar valve

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39
Q

___ prevents backflow into the left atrium.

A

Bicuspid / mitral valve

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40
Q

The conduction velocity of the atria is ___ and ___ for the AV node.

A

1 m/s, 0.01 m/s

1/100 of speed in AV node

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41
Q

Cardiac muscle cells are innervated by alpha motor neutrons. T/F

A

False

Pacemaker cells spontaneously depolarize

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42
Q

Intercalated discs

A

Made of desmosomes and gap junctions, connect both muscle cells and nodal cells

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43
Q

What is the function of gap junctions in the heart?

A

Join adjacent cardiomyocytes, allow fast conduction

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44
Q

Only pacemaker cells in the SA or AV node can spontaneously depolarize. T/F

A

False, under pathological conditions, damaged muscle cells can depolarize, but at a much slower rate.

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45
Q

Which component of the electrical system of the heart has the fastest depolarization rate? Which has the slowest?

A

SA node, muscle fiber

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46
Q

A patient has their sinoatrial node damaged. Predict the new pacemaker.

A

Atrioventricular node

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47
Q

What currents do the ventricular cardiomyocytes have?

A

Sodium, calcium, and potassium

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48
Q

What currents do the nodal cells have?

A

Calcium, potassium, and pacemaker current

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49
Q

Both ventricular cardiomyocytes and nodal cells have sodium currents. T/F

A

False, nodal cells lack fast voltage-gated sodium channels

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50
Q

Phase 0 Ventricular AP

A

Upstroke
Sodium and calcium current is involved in depolarization of ventricular cardiomyocytes
Fast voltage-gated sodium channels open, an inward sodium current occurs, and the cell depolarizes. During late depolarization, voltage-gated L-type calcium channels (DHPR) open, leading to CICR

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51
Q

Phase 1 Ventricular AP

A

Initial repolarization

At 20 mV, the voltage-gated sodium channels inactivate and voltage-gated potassium channels open

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52
Q

The voltage-gated sodium channels involved in Phase 0 and Phase 1 Ventricular AP open rapidly but inactivate slowly. T/F

A

False, the sodium channels open fast and inactivate fast.

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53
Q

During Phase 1 of Ventricular AP, potassium efflux out of the cell is down its concentration gradient but against its electrical gradient. T/F

A

False, the inside of the myocytes are positive due to sodium efflux (depolarization) during Phase 0, so potassium exits the cell down its electrical gradient as well as chemical.

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54
Q

What is the membrane potential at peak of the upstroke in ventricular AP?

A

+20 mV

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55
Q

Phase 2 Ventricular AP

A

Plateau
A stable, depolarized membrane potential occurs due to the isoelectric balance of outward potassium current and inward calcium current

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56
Q

Phase 3 Ventricular AP

A

Repolarization

L-type calcium channels are closing while potassium efflux ramps up

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57
Q

Phase 4 Ventricular AP

A

RMP / Electric diastole

Potassium current decreases, inward current equals outward current

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58
Q

Phase 4 Nodal AP

A

Spontaneous depolarization / pacemaker potential
Repolarization (from preceding AP) opens non-selective cation channels, which causes an inward sodium current (funny current). The funny current and slow depolarization will bring the membrane potential to threshold, opening the calcium channels for upstroke

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59
Q

Which phase of the nodal action potential accounts for the automaticity of SA nodal cells?

A

Phase 4 / spontaneous depolarization / pacemaker potential

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60
Q

The funny current is caused by fast, voltage-gated sodium channels in nodal cells. T/F

A

False, the funny current is an inward sodium current, but from voltage-gated non-selective cation channels, so potassium moves out of the cell too.

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61
Q

Phase 0 Nodal AP

A

Upstroke
Depolarization due to calcium influx through voltage-gated L-type calcium channels
Nodal AP upstroke not as rapid/steep as ventricular AP upstroke

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62
Q

The upstroke of the ventricular AP is steeper than the upstroke of the nodal AP. T/F

A

True

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63
Q

Why is the slope of depolarization in nodal action potential less steep than the depolarization in ventricular action potential?

A

Calcium is moving through L-type calcium channels, which are slower to open and close than fast, voltage-gated sodium channels

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64
Q

Phase 3 Nodal AP

A

Repolarization due to potassium efflux down its electrochemical gradient

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65
Q

The absolute refractory period is caused by what?

A

Inactive sodium channels

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66
Q

What phases are included in the absolute refractory period?

A

Upstroke (Phase 0), initial repolarization (Phase 1), plateau (Phase 2), and part of repolarization (Phase 3)

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67
Q

Supranormal period

A

Ranged from when membrane potential is -70 until fully repolarized -85 mV
The cell is more excitable than normal, thus less inward current is required to depolarize the cell to threshold

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68
Q

The relative refractory period is caused by what?

A

Sodium channels transitioning from inactivated to closed

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69
Q

What phases are included in the relative refractory period?

A

Repolarization (Phase 3)

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70
Q

What is the maximum diastolic potential?

A

-65 mV, the most negative value of membrane potential

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71
Q

During phase 2 of the non-pacemaker cell action potentia, all cystolic calcium enters the cardiomyocyte via the L-type calcium channels. T/F

A

False, only 20% enters via DHPR, 80% enters via RYR from SR

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72
Q

When comparing action potentials of pacemaker and non-pacemaker cells, both display a plateau phase. T/F

A

False

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73
Q

Pacemaker cells have no ___ after repolarization, instead they have a ___.

A

RMP, maximum diastolic potential

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74
Q

___ cells have a positively sloping phase 4.

A

Pacemaker cells / nodal cells

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75
Q

Which phases do the pacemaker cells have?

A

Phase 0, phase 3, phase 4

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76
Q

The nodal action potential does not include phases ___ and ___.

A

1, 2

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77
Q

Non-pacemaker cells are considered to be in a state of high excitability (low refractoriness) when most fast sodium channels have transitioned from the inactivated state to the closed state. T/F

A

True

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78
Q

If a drug increases the potassium permeability of pacemaker cells, what effect does it have on the maximum diastolic potential?

A

It is more negative

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79
Q

If a drug increases the calcium permeability of L-type calcium channels in the pacemaker cells, what effect does it have on the amplitude of phase 0 of the action potential?

A

It increases

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80
Q

If a drug increases the permeability of potassium permeability of non-pacemaker cells, what effect does it have on the cell’s RMP?

A

It is more negative

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81
Q

If a drug increases the calcium permeability of a non-pacemaker cell, what effect does it have on the cell’s action potential duration?

A

It is longer

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82
Q

A drug increases the permeability of the sinus node pacemaker cells. What effect does it have on heart rate?

A

It decreases

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83
Q

What turns on the funny current?

A

Repolarization from preceding action potential

normally channels are triggered by depolarization of membrane potential becoming more positive

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84
Q

What is the function of the chordinae tendineae?

A

Provide structure to the AV valves to prevent the ventricles from ejecting blood into the atria, linked to papillary muscles

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85
Q

AV valves

A

Prevent backflow of blood into atria when ventricles contract
Tricuspid between RA/RV
Bicuspid / mitral between LA/LV
Linked to chordae tendineae

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86
Q

The ___ valve is between the left atrium and left ventricle.

A

mitral / bicuspid

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87
Q

The ___ valve is between the right atrium and right ventricle.

A

Tricuspid

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88
Q

Semilunar valves

A

Prevent backflow of blood into the ventricles from the large arteries
Pulmonary and aortic

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89
Q

The heart valves open and close due to ___.

A

Blood pressure gradients

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90
Q

When the pressure in the atria is ___ than the ventricles, the AV valves open.

A

higher

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91
Q

When pressure in the ___ is higher than in the atria, the AV valves close.

A

Ventricles

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92
Q

The ___ side valves open first, while the ___ side valves close first.

A

Right, left

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93
Q

The left side valves are open for a ___ time than the right.

A

Shorter

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94
Q

Why is the aortic valve open for a shorter time than the pulmonary valve?

A

Aortic / systemic pressure is greater than pulmonary pressure, so the LV takes longer to generate enough pressure to open

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95
Q

Why is the mitral valve open for a shorter time than the tricuspid valve?

A

For the mitral valve to open, the pressure in the LA has to exceed the pressure of the LV. The left ventricle is higher pressure than the right ventricle, so the mitral valve opens later than the tricuspid valve and closes quicker

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96
Q

Chordae tendineae

A

Collagenous strings that link AV valves to papillary muscles, prevent AV valves from swinging upward from ventricle power

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97
Q

The tricuspid valve is open when the RA pressure is ___ than RV pressure.

A

Greater

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98
Q

The mitral valve is open when the LA pressure is ___ than LV pressure.

A

Greater

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99
Q

The tricuspid valve is closed when the RA pressure is ___ than RV pressure.

A

Less

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100
Q

The bicuspid valve is closed when LA pressure is ___ than LV pressure.

A

Less

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101
Q

The pulmonary semilunar valve is open when the RV pressure is ___ than pulmonary trunk pressure.

A

Greater

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102
Q

The pulmonary semilunar valve is closed when RV pressure is ___ than pulmonary trunk pressure.

A

Less

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103
Q

The aortic semilunar valve is open when LV pressure is ___ than aortic pressure.

A

Greater

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104
Q

The aortic semilunar valve is closed when LV pressure is ___ than aortic pressure.

A

Less

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105
Q

Frank-Starling relationship

A

The volume of the blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole
Cardiac output equals venous return

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106
Q

Frank-Starling mechanism

A

As the ventricle fill, the myocytes stretch, getting closer to the optimal length / overlap of myosin and actin, which increases the systolic force generated resulting in increased stroke volume

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107
Q

Overfilling the heart, where there is too much load, decreases the systolic force due to suboptimal overlap of myosin and actin. T/F

A

True

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108
Q

The closer the cardiomyocytes get to optimal overlap, the more the stroke volume is.

A

True, optimal overlap means increased systolic force generated during contraction

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109
Q

Normal heart sounds

A

Lup-Dup-Pause

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110
Q

What are heart sounds generated by?

A

The turbulence of blood vibrating chamber walls

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111
Q

The heart sounds are caused by valves closing. T/F

A

False

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112
Q

Lub (S1)

A

Closing of AV valves and beginning of ventricular systole

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113
Q

Dup (S2)

A

Closing of semilunar valves and beginning of ventricular diastole

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114
Q

S3

A

Recoil of ventricular walls in children and adults, can be normal or pathological

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115
Q

S4

A

Always pathological, coincides with atrial contraction, atrial trying to fill stiffened ventricle

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116
Q

Physiological splitting of ___ occurs during ___.

A

S2, inspiration

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117
Q

Why does physiological splitting of S2 occur during inspiration?

A

S2 splits due to the aortic valve closing before the pulmonary valve. Inspiration accentuates this by decreasing intrathoracic pressure, which increases venous return. This increases end-diastolic volume of RV, increasing RV stroke volume, prolonging RV ejection time, thus delaying pulmonary valve closure relative to aortic valve closure

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118
Q

S1 can be split under pathological conditions. T/F

A

True

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119
Q

The ___ atrium and the ___ ventricle contract first.

A

Right, left

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120
Q

Which atrium contracts first? Why?

A

The right atrium contracts first since the SA node is located in the RA.

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121
Q

Which ventricle contracts first? Why?

A

The left ventricle contracts first since the left bundle branch is larger in diameter than the right, so conducts electrical signal faster

122
Q

The isovolumetric contraction time is ___ on the left side than the right. Why?

A

Longer since the aortic diastolic pressure is much greater than the pulmonary diastolic pressure

123
Q

The ventricular ejection time is ___ on the left side than the right. Why?

A

Shorter since the time that left ventricular pressure exceeds aortic pressure is shorter than the time that right ventricular pressure exceeds pulmonary artery pressure

124
Q

Blood moves from one place to another because of a ___.

A

Pressure gradient

125
Q

Pulmonary valve stenosis would affect the workload of the right ventricle how? Why?

A

RV would have increased workload, thus becoming hypertrophied

126
Q

Jugular vein pressure changes caused by cardiac cycle

A

Pressure in RA sends pressure back up veins
Has 3 peaks:
A peak - contraction of right atria
C peak - bulging of tricuspid into RA (from ventricular systole)
V peak - filling of right atria

127
Q

Order the 3 events of the cardiac cycle that impact the jugular vein pressure from greatest to least pressure

A

RA contraction (A peak) > Tricuspid bulging (C peak) > RA filling (V peak)

128
Q

Jugular vein distension

A

Indicates increased central venous pressure

Could mean that RV isn’t working properly to eject blood into pulmonary circuit, causing backflow

129
Q

90% of movement of blood from atria to ventricles is ___. How?

A

Passive, atria stretched from filling retract

130
Q

Rapid ventricular filling and reduced ventricular filling account for ___% of ventricular filling.

A

90%

131
Q

The atrial systole accounts for ___% of ventricular filling.

A

10%

132
Q

Atrial systole (atrial kick)

A

Atria actively contracts to remove last 10% of blood out to ventricle

133
Q

Isovolumetric contraction

A

In between time where ventricle pressure has exceeded atrial pressure (AV valves closed) but not pulmonary artery or aortic pressure (SL valves closed)

134
Q

Isovolumetric relaxation

A

Ventricular pressure greater than aortic pressure, AV valves closed

135
Q

When the mitral valve first opens, passive filling of the LV begins, but the LV pressure continues to decrease slightly. T/F

A

True, even though blood is rapidly entering the left ventricle, the muscle is continuing to relax during diastole.

136
Q

Ventricular pressure is at its lowest in the cardiac cycle during ventricular filling. T/F

A

True, since the muscle continues to relax during diastole, even while being rapidly filled, the pressure is at its lowest

137
Q

The heart is completely relaxed during ___% of ventricular filling.

A

80%

138
Q

The atrial systole accounts for the last ___% of time spent in ventricular filling and ___% of final stroke volume.

A

20%, 10%

139
Q

End-diastolic volume is around ___.

A

130mL

140
Q

End-diastolic volume

A

The volume of blood in the LV at the end of ventricular filling

141
Q

During ventricular filling, ventricular volume is ___.

A

Increasing

142
Q

During ventricular filling, atrial pressure is ___ than ventricular pressure.

A

Greater

143
Q

During ventricular filling, both ventricles are in ___.

A

Diastole

144
Q

During ventricular filling, RV pressure is ___ than pulmonary trunk pressure.

A

Less

145
Q

During ventricular filling, LV pressure is ___ than aortic pressure.

A

Less

146
Q

During ventricular filling, both AV valves are ___.

A

Open

147
Q

During ventricular filling, both semilunar valves are ___.

A

Closed

148
Q

During isovolumetric contraction, ventricular volume is ___.

A

Constant

149
Q

During isovolumetric contraction, ventricular pressure is ___.

A

Increasing

150
Q

During isovolumetric contraction, atrial pressure is ___ than ventricular pressure.

A

Lower

151
Q

During isovolumetric contraction, both ventricles are in ___.

A

Systole

152
Q

During isovolumetric contraction, RV pressure is ___ than pulmonary trunk pressure.

A

Less

153
Q

During isovolumetric contraction, LV pressure is ___ than aortic pressure.

A

Less

154
Q

During isovolumetric contraction, both AV valves are ___.

A

Closed

155
Q

During isovolumetric contraction, both semilunar valves are ___.

A

Closed

156
Q

The aorta pressure typically goes to ___ during systole then recoils to ___ during diastole before the next contraction occurs.

A

120 mmHg, 80 mmHg

157
Q

End systolic volume is typically around ___.

A

50 mL

158
Q

The ventricles eject all of their blood, leaving no remaining. T/F

A

False, about 50 mL remain, called the end systolic volume

159
Q

Stroke volume

A

Volume of blood ejected

70 mL

160
Q

LV pressure decreases immediately after ejection. T/F

A

False

161
Q

Cardiac output

A

Total volume of blood ejected per unit time
5000 mL/min
CO=HR*SV (heart rate x stroke volume)

162
Q

What is the formula for cardiac output?

A

CO = HR * SV

163
Q

Ejection fraction

A

The percentage of blood in ventricle ejected each beat
Measure of ventricular efficiency
Around 65-70%

164
Q

Ejection fraction is a measure of ___.

A

Ventricular efficiency

165
Q

What is the formula for ejection fraction?

A

EF= (EDV-ESV) / EDV

166
Q

Athletes can increase their cardiac output up to ___ the resting cardiac output, which is ___L/min.

A

7x, 35 L/min

167
Q

Normal people have a maximum output of ___ their resting cardiac output.

A

4-5x

168
Q

What is the formula for stroke volume?

A

SV = EDV-ESV

169
Q

Cardiac reserve

A

The difference between the resting and maximum cardiac output

170
Q

End systolic volume

A

The remaining blood in the ventricle after ejection

50 mL

171
Q

During ventricular ejection, ventricular volume is ___.

A

Decreasing

172
Q

During ventricular ejection, atrial pressure is ___ than ventricular pressure.

A

Less

173
Q

During ventricular ejection, both ventricles are in ___.

A

Systole

174
Q

During ventricular ejection, RV pressure is ___ than PT pressure.

A

Greater

175
Q

During ventricular ejection, LV pressure is ___ than aortic pressure.

A

Greater

176
Q

During ventricular ejection, both AV valves are ___.

A

Closed

177
Q

During ventricular ejection, both semilunar valves are ___.

A

Open

178
Q

Isovolumetric relaxation

A

Ventricles done contracting, atria filling, all valves closed

179
Q

During isovolumetric relaxation, ventricular volume is ___.

A

Constant

180
Q

During isovolumetric relaxation, ventricular pressure is ___.

A

Decreasing

181
Q

During isovolumetric relaxation, atrial pressure is ___ than ventricular pressure.

A

Less

182
Q

During isovolumetric relaxation, both ventricles are in ___.

A

Diastole

183
Q

During isovolumetric relaxation, RV pressure is ___ than PT pressure.

A

Less

184
Q

During isovolumetric relaxation, LV pressure is ___ than PT pressure.

A

Less

185
Q

During isovolumetric relaxation, both AV valves are ___.

A

Closed

186
Q

During isovolumetric relaxation, both semilunar valves are ___.

A

Closed

187
Q

How much blood is ejected per minute?

A

5 liters

188
Q

What 3 factors regulate stroke volume?

A

Preload, contractility, and afterload

189
Q

Preload

A

The degree of stretch of cardiac muscle fibers before contraction
Exercise increases venous return stretches ventricles and increases contraction force

190
Q

___ is a great indicator of preload.

A

EDV

191
Q

___ increases preload by increasing venous return.

A

Exercise

192
Q

Preload impacts stroke volume based on what principle? How?

A

Frank-Starling Mechanism
With increased venous return, the ventricle is stretched, so there is a more optimum overlap of actin and myosin, so more systolic force is generated and more blood is pumped out

193
Q

Contractility

A

Force of contraction directly related to calcium availability

194
Q

Contractility impacts the stroke volume due to the Frank-Starling mechanism. T/F

A

False

195
Q

What role does calcium play in muscle contraction?

A

Increased calcium being released from SR means increased calcium binding to troponin, causing more actin and myosin crossbridge formation

196
Q

NoEP and EP ___ contractility.

A

Increase

Beta 1 adrenergic stimulus

197
Q

Glucagon ___ contractility.

A

Increase

Stimulates cardiac calcium current by activation of adenylyl cyclase and inhibition of phosphodiesterase

198
Q

Thyroxine ___ contractility.

A

Increase

Increase transcription of contractile proteins

199
Q

Digitalis ___ contractility.

A

Increase

200
Q

Acidosis ___ contractility.

A

Decrease

Competitive inhibition of slow calcium current by hydrogen ions

201
Q

Increased extracellular potassium ___ contractility.

A

Decreases

Inactivates sodium channels and opens potassium channels causing cells to become refractory, messes with gradient

202
Q

Calcium channel blockers ___ contractility.

A

Decrease

203
Q

If contractility decreases, stroke volume ___.

A

Decreases

204
Q

If contractility increases, end systolic volume will ___.

A

Decrease

205
Q

Afterload

A

Pressure the ventricles must overcome to eject blood into major arteries

206
Q

Afterload is important in hypertensive individuals. Why?

A

The LV has a greater load to overcome (pressure in aorta is higher), so it takes longer to open semilunar valves and ejection time decreases

207
Q

As afterload increases, stroke volume ___.

A

Decreases

208
Q

As afterload increases, end systolic volume will ___.

A

Increase

209
Q

With increased contractility, ESV ___ and ___ pressure is generated.

A

Decreases, more

210
Q

With increased preload, EDV ___ and ___ pressure is generated.

A

Increases, more

211
Q

With increased afterload, LV pressure is ___ and aortic valve closes ___.

A

Higher, quicker

212
Q

The automatic nervous system is controlled by the ___.

A

Medulla oblongata

213
Q

There is parasympathetic influence on the heart at resting heart rate. T/F

A

True

Like brakes at stoplight

214
Q

The effects of the ANS on heart rate are called ___.

A

Chronotropic effects

215
Q

Sympathetic control on heart

A

Increased cardioacceleratory center in medulla oblongata sends AP down sympathetic cardiac nerves causing catecholamines (NE) to be released on SA and AV nodes and myocardium, so HR and contractility increased
Rate of phase 4 depolarization is increased and threshold potential decreased (funny current increased and more calcium channels available)

216
Q

Sympathetic activation results in a ___ rate of depolarization of the nodal AP.

A

Increased

217
Q

What are the 2 ways that sympathetic activation increases contractility and rate of depolarization?

A

Increase in funny current (less depolarization needed to reach threshold) and calcium current (more functional calcium channels decreases threshold)

218
Q

___ released from sympathetic nerve fibers activates ___ receptors on SA and AV nodes.

A

NoEP, beta 1 adrenergic

219
Q

Parasympathetic control on the heart

A

Increased cardioinhibitory center in medulla oblongata sends APs down vagus nerve causing ACh to be released on SA and AV nodes and myocardium, so HR declines
The rate of nodal phase 4 depolarization is slowed, the maximum diastolic potential is hyperpolarized, and the threshold potential is increased

220
Q

What are the 3 ways that parasympathetic activation decreases rate of depolarization and contractility?

A
  • -Rate of nodal phase 4 depolarization is slowed (funny current is decreased)
  • -Hyperpolarization of maximum diastolic potential (potassium current/efflux increased)
  • -Threshold potential increased (less functional calcium channels)
221
Q

___ released from parasympathetic nerve fibers activates ___ receptors on SA and AV nodes.

A

ACh, muscarinic cholinergic

222
Q

Electrocardiogram

A

Electrical recording of the heart

223
Q

EKG waves generated by the ___ electrical activity of the heart.

A

Cumulative

224
Q

The amplitude of the ___ ventricle is the largest. Why?

A

Left has more cardiomyocytes

225
Q

The vertical axis of an EKG measures ___. A little square is ___ and a bigger square is ___.

A

Voltage, 0.1 mV, 0.5 mV

226
Q

The horizontal axis of an EKG measures ___. A little square is ___ and a bigger square is ___.

A

Time, 0.04s, 0.2s

227
Q

An EKG flatline is ___.

A

Isoelectric

228
Q

When you have a depolarization wave going towards an electrode, you will get a ___ deflection.

A

Positive

229
Q

When you have a depolarization wave going away from an electrode, you will get a ___ deflection.

A

Negative

230
Q

If a wave of depolarization is moving perpendicular to a electrode, you will get a ___.

A

Biphasic wave

231
Q

A repolarization wave first coming towards, passing, then going away from an electrode will record what type of deflection?

A

Negative then positive biphasic wave

232
Q

How do you know what the mean electrical axis (MEA) on an EKG is?

A

Wherever the highest deflection occurs

233
Q

Mean electrical axis

A

Vector that shows where the most depolarization occurs, usually at 60 degrees, goes to Lead II

234
Q

Where is the MEA directed usually?

A

60 degrees, towards Lead II

235
Q

How can the MEA change?

A

If heart has changed shape, hypertrophy / dilation in response to cardiac disease

236
Q

The angle of orientation of Lead I is ___.

A

0

Left arm positive and right arm negative

237
Q

The angle of orientation of Lead II is ___.

A

60

Right arm negative and legs positive

238
Q

The angle of orientation of Lead III is ___.

A

120

Left arm negative and legs positive

239
Q

The angle of orientation of Lead aVL is ___.

A

-30

Left arm positive, all other limbs negative

240
Q

The angle of orientation of Lead aVR is ___.

A

-150

Right arm positive, all other limbs negative

241
Q

The angle of orientation of Lead aVF is ___.

A

90

Legs positive, all other limbs negative

242
Q

6 Precordial leads

A

Go from anterior to posterior of heart

Electrodes put on chest, thus depolarization

243
Q

P wave

A

Atrial depolarization

244
Q

___ occurs from endocardium to epicardium. What does this look like on EKG due to precordial leads?

A

Depolarization, positive deflection (depolarization going towards electrode)

245
Q

___ occurs from epicardium to endocardium. What does this look like on EKG due to precordial leads?

A

Repolarization, positive deflection (repolarization going away from electrode

246
Q

T wave

A

Ventricular repolarization

247
Q

QRS complex

A

Ventricular depolarization

248
Q

Inferior leads

A

Lead II, Lead III, Lead aVF

249
Q

Left lateral leads

A

Lead I, Lead aVL

250
Q

Right sided lead

A

Lead aVL

251
Q

Why is T wave a positive deflection?

A

Ventricular repolarization is heading away from the electrodes

252
Q

Why is Q wave a negative deflection?

A

LV depolarizes first and does so left to right, so the left lateral leads read a small negative deflection

253
Q

Why is S wave a larger negative deflection?

A

LV is bigger so the cumulative vector swings leftward and Lead aVR reads a large negative deflection

254
Q

PR interval

A

Start of atrial depolarization to start of ventricular depolarization, including isoelectric AV delay

255
Q

ST segment

A

End of ventricular depolarization to start of ventricular repolarization
Isoelectric or upsloping

256
Q

QT interval

A

Start of ventricular depolarization to the end of ventricular repolarization

257
Q

What two leads are used to calculate the MEA?

A

Lead I and aVF

258
Q

Calculate MEA:
Lead I +
aVF +

A

Normal axis

259
Q

Calculate MEA:
Lead I +
aVF -

A

Left axis deviation

260
Q

Calculate MEA:
Lead I -
aVF +

A

Right axis deviation

261
Q

Calculate MEA:
Lead I -
aVF -

A

Indeterminate / extreme right axis deviation

262
Q

Cardiac hypertrophy shows what 3 characteristics on an EKG?

A

Increased duration, increased amplitude, and left axis deviation

263
Q

What affect will hypertrophy have on the MEA?

A

Left axis deviation

264
Q

Ischemia

A

Low bloodflow to a tissue

265
Q

Myocardial infarction

A

Blocking of the coronary arteries

266
Q

EKG evolution of ischemia to infarction

A
  1. Peaked T-waves transitioning to inverted T-waves
    - -sign of ischemia, reversible damage
  2. ST segment elevation (tombstone)
    - -Close to permanent damage
  3. Large Q-wave
    - -Permanent damage, presents years later
267
Q

What is an EKG sign of a person undergoing ischemia?

A

Peaked T-waves transitioning to inverted T-waves

Damage is reversible

268
Q

What is an EKG sign of an imminent myocardial infarction and permanent damage?

A

ST segment elevation

269
Q

If an individual already had a myocardial infarction, what EKG sign could be seen?

A

Large Q-waves

270
Q

An EKG shows the electrical activity of the nodal cells. T/F

A

False

271
Q

R-R interval

A

From ventricular depolarization to ventricular depolarization

272
Q

Arrhythmias

A

Alterations to rhythm or conduction of heartbeat

Symptoms: palpitations and sudden light-headedness

273
Q

How to calculate heart rate?

A

60 / time between each peak

274
Q

What are the 2 common SA nodal arrhythmias?

A

Sinus bradycardia (>60) and sinus tachycardia (>100)

275
Q

Sinus bradycardia

A

HR under 60 BPM

Everything else normal

276
Q

Sinus Tachycardia

A

HR over 100 BPM

Everything else normal

277
Q

Which SA nodal arrhythmias is the more worrisome?

A

Tachycardia because the heart has to work harder

278
Q

What are the 2 common atrial arrhythmias?

A

Atrial flutter and atrial fibrillation

279
Q

Atrial flutter

A

Rapid, regular depolarizations in sawtooth pattern

280
Q

Atrial fibrillation

A
No coordination of atrial depolarization 
Irregular QRS (AV node fires once it's no longer refractory)
281
Q

For atrial arrhythmias, the QRS complex would be regular in ___, but irregular in ___.

A

Atrial flutter, atrial fibrillation

282
Q

Ectopic foci

A

Abnormal pacemaker sites (outside SA node)

283
Q

Cardioversion

A

Trying to get all the cells of the heart into an absolute refractory phase by contracting all cells
Used to treat AFib

284
Q

___ is used to remedy AFib.

A

Cardioversion

285
Q

Why is AFib not life threatening?

A

90% of ventricular filling is passive

286
Q

AV Conduction blocks

A

When depolarization is not conducted from atria to ventricles properly (AV node and bundle branches)

287
Q

First degree heart block

A

Prolonged PR interval

Increased AV nodal delay

288
Q

Second degree heart block

A

Not all APs are conducted by AV node, dropped beats
More P-waves than QRS complexes (ratio > 1:1)
Mobitz Type I + II

289
Q

Mobitz Type I block - Wenckebach

A

PR interval gets progressively longer until a beat is dropped

290
Q

Mobitz Type II block

A

PR interval set but randomly dropped beats

291
Q

___ is when there are randomly dropped beats in the EKG, and ___ is when the PR interval gets longer until a beat is dropped.

A

Mobitz Type II block, Mobitz Type I (Wenckebach)

292
Q

Third degree heart block

A

No conduction between atria and ventricles
P-waves and QRS have regular rhythm, but aren’t in sync
QRS can be wide (ventricular origin of depolarization)

293
Q

Ventricular tachycardia

A

Fast depolarizations, ischemic event, can lead to ventricular fibrillation

294
Q

Ventricular fibrillation

A

Uncoordinated depolarization, rapid death

295
Q

Where do the disturbances arise in ventricular arrhythmias?

A

Below the AV node

296
Q

What is characteristic of ventricular arrhythmias?

A

Wide QRS

297
Q

What is the most lethal of the arrhythmias?

A

Ventricular fibrillation

298
Q

Digitalis / digitoxin

A

Increases contractility but decreases HR

Sodium potassium pump inhibitor

299
Q

How does digitalis function?

A

By inhibiting the sodium potassium pump, intracellular sodium increases. The sodium calcium exchanger (3 sodium in, 1 calcium out), which relies on that sodium gradient doesn’t work as well, so more calcium in the cell, which means more calcium in SR, which leader to more release and stronger contraction
Affects funny current and calcium takes longer to be resequestered, so longer time between depolarizations, decreased HR

300
Q

Digitalis ___ contractility and ___ HR.

A

Increases, decreases

301
Q

Wolff-Parkinson-White Syndrome

A

Extra electrical pathway in heart, leads to tachycardia (in children)

302
Q

What effect would a severe anaphylatic reaction have on the Starling Fluid Flux?

A

Histamines (vasodilators) are released, arterioles are dilated, increasing blood flow through arteries

Blood cell clefts are widened, the reflection coefficient for plasma proteins is decreased and they escape into IF

BCOP decreases, IFCOP increases significantly

Water is attracted osmotically to proteins in IF, so fluid rushed out of capillaries into IF, causing edema (increased by vasodilation too)

BHP decreases as fluid continues to leave vasculature, IFHP increases with edema

Large amount of filtration, little resorption

Arterial blood pressure drops (leads to anaphylatic shocks / death)

Epi-Pen treatment - vasoconstrictor of arteries and bronchodilator