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A&P 2 > Heart > Flashcards

Heart Flashcards

1
Q

Location of Heart

A

from the second rib to the 5th intercostal space. 60% on the left side of the chest. Sits in the mediastinal cavity.

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2
Q

3 chambers of thoracic cavity

A

two pleural chambers with lungs and the mediastinal cavity

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3
Q

weight of the heart

A

300g

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4
Q

where is the apex of the heart and why

A

Apex of the heart is at the bottom left, has to do with how the heart is form

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5
Q

where is the base of the heart

A

posterior side of heart is the base

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6
Q

pericardium

A

serous membrane surrounding the heart

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7
Q

fibrous pericardium

A

not part of serous membrane, made of dense connective tissue

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8
Q

two layers of serous pericardium and their location

A

a. Parietal—the layer that lines the cavity

b. Viscera—the layer that lines the heart itself

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9
Q

what is pericardial fluid where does it hang out and how much of it is there

A

serous fluid between the parietal and visceral layers, 50ml

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10
Q

cardiac tamponade

A
  1. Excess fluid or blood in the pericardial sac prevents the heart from expanding fully, so it cannot adequately fill and pump blood
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11
Q

3 layers of the heart

A

epicardium
myocardium
endocardium

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12
Q

epicardium

A

Epicardium: outer layer. The same thing as the visceral pericardium

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13
Q

myocardium

A

middle layer, the cardiac muscle

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14
Q

endocardium

A

inner layer, made from simple squamous epithelium (endothelium)

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15
Q

auricles

A

right and left, purple fleshy structures at the top of the heart. Extra spaces for blood. The atria are deep to the auricles

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16
Q

Fossa Ovalis and PFO: function in utero, what happens when baby is born, what can happen when disease processes affect this on adults

A

When baby is still in uterus, lungs are filled with amniotic fluid which creates a lot of resistance. There is a hole between right and left article called Patent Foramen Ovale (PFO) where blood can move between RA and LA. Patent means open. When baby is born, pressure changes causes a “door” to shut across the PFO, this is referred to as the Fossa Ovalis. In 75% of people the fossa ovalis is sealed shut, but in 25% it is only closed, and being kept closed by the relatively higher pressure in the left atrium. Disease processes may cause the pressure to be higher in the right atrium, which may cause the fossa ovalis to leak which could lead to a stroke.

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17
Q

pectinate muscles

A

only in the right atrium. “Shaggy carpet” at the top left right atrium. Function unknown.

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18
Q

crista terminalis

A

C-shaped structure that divides atrium into posterior and anterior

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19
Q

Flow of blood through the heart

A
  1. Deoxygenated blood from the body enters the heart on the right side in the RA, exits through RV to go to the lungs, comes back from the lungs through the LA, exits from the LV through the aorta to the body.
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20
Q

atrioventricular (AV) valves location

A

between the atria and ventricles

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21
Q

tricuspid valve location and number of cusps

A

has three cusps, is on the right side b/w RA and RV

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22
Q

bicuspid valve location, number of cusps, common name

A

has two cusps, b/w LA and LV. Also commonly known as mitral valve

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23
Q

AV valves function

A

the atrioventricular valves are open most of the time, they only close as the ventricles contract.

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24
Q

stenosis

A

when an atrioventricular valve is too narrow, making it hard for blood to drain into the ventricle, making the heart have to work harder.

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25
Q

regurgitation

A

when the valves are too loose, causing blood to leak from the ventricle to the atrium. Also known as “incompetent valve”.

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26
Q

ventricles

A

chambers on the bottom of the heart

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27
Q

wall thickness atria vs ventricles

A

ventricles have Thicker walls than the atria because they work harder. Left ventricle is thicker than right for the same reason

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28
Q

Papillary muscles

A

attached to ligaments (chordae tendineae), which are attached to the cusps on the AV valves. These contract just before the ventricle contracts to anchor the valves in order to overcome the pressure of the ventricular contraction and prevent the valve from opening upwards into the atrium

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29
Q

carnae trabeculae

A

“cross-bars of flesh” inside the ventricles

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30
Q

5 great vessels

A 
superior vena cava
inferior vena cava
pulmonary artery
pulmonary veins
aorta
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31
Q

superior vena cava function and valves

A

drains blood from the head, neck, certain parts of the thorax, into the RA. no valves.

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32
Q

inferior vena cava function and valves

A

drains blood from the rest of the body to the RA. No valves.

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33
Q

pulmonary artery function and valves

A

takes blood from the RV to the lungs. Semilunar valve: pulmonary valve

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34
Q

pulmonary veins number, function, valves

A

(4), two of them bring blood from left lung, two from right lunh, all to the LA. No valve.

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35
Q

aorta function, valves

A

biggest artery in body, attaches from LV. semilunar valves

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36
Q

semilunar valves

A

closed most of the time. Only open when ventricles contract. Like 3 tea cups together. They move away from each other when the ventricle contracts and the blood pushes past, but come back together as soon as the pressure subsides.

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37
Q

ligamentum arteriosum (PDA)

A

When baby is in uterus, there is a connection between pulmonary artery and aorta called patent ductus arteriosus (PDA) that serves to decrease pressure on the circulatory system (same as PFO). Eventually closes after birth, creating the ligamentum arteriosum

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38
Q

3 circulations/circuits

A

pulmonary
systemic
coronary

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39
Q

pulmonary circulation

A

deoxygenated blood leaving the right ventricle, going into the pulmonary system, becoming oxygenated in the lungs and then coming back to the heart via left atrium. low resistance.

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40
Q

systemic circulation

A

oxygenated blood leaving from left ventricle going out to the body and then returning as deoxygenated blood to the right atrium. high resistance.

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41
Q

coronary circulation function

A

delivers nutrients to cardiac muscle.

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42
Q

coronary circulation pathway

A

L and R coronary arteries come right off the aorta, travels behind the pulmonary trunk to the front of the heart.
L coronary a. descends anteriorly and becomes the anterior interventricular a., (aka anterior descending a.) and sits in the anterior ventricular sulcus. The anterior descending artery continues down and rounds the bottom of the heart and starts ascending on the posterior side, to form an anastomosis with posterior inter ventricular a.
c. R coronary a. travels from the aorta underneath the R auricle.
d. R marginal a. branches off from the R coronary a. to supply the right ventricle.
e. R coronary a. also continues down, rounds the bottom of the heart and ascends posteriorly and forms an anastomosis joining up with the circumflex artery.
f. Posterior interventricular artery travels down from the anastomosis between the R coronary a. and circumflex a. and forms the anastomosis with the anterior interventricular a.
g. All of the coronary veins drain to the coronary sinus which is on the posterior side of the heart. The coronary sinus drains straight into the right atrium.

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43
Q

Which artery is called the widow-maker and why

A

the anterior interventricular a., (aka anterior descending a.) supplies blood to the left ventricle so it is very deadly to have blockages or issues with this artery

44
Q

3 factors affecting resistance of blood vessels

A

i. Viscosity of blood
ii. Diameter of the vessel
iii. Length of vessel. Pulmonary circulation has less resistance because it’s shorter than systemic.

45
Q

angina pectoris

A

a. Pain in the chest usually caused by blockages in coronary vessels leading to ischemia in parts of the cardiac muscle, causing injury to the tissue. When a vessel is blocked for long enough, the tissue around it dies, and cardiac muscle doesn’t repair itself. This is called infarction.
b. Sometimes the pain will be referred to the shoulder, jaw or back

46
Q

characteristics of cardiac muscle

A

a. Striated, 1 or 2 nuclei

b. Short, branched (as opposed to skeletal muscle fibers which go the entire distance of the muscle).

47
Q

purpose of branching muscle fibres in cardiac muscle

A

c. The branching allows the heart’s fibers contract all at once, as opposed to skeletal muscle in which the amount of fibers activated is matched to the load being lifted.

48
Q

how much mitochondria in cardiac muscle

A

f. Lots and lots of mitochondria—25% of cardiac muscle is made up of mitochondria

49
Q

2 types of cardiac muscle cells

A

contractile

pacemaker

50
Q

pacemaker cells function and what % of cardiac muscle cells are pacemaker cells

A

has the ability to spontaneously fire. This is called automaticity or autorhythmicity. 1% of cells are pacemaker cells

51
Q

refractory period definition and what it looks like in cardiac muscle

A

a period of time when cells cannot be stimulated. The refractory period of cardiac muscle is much longer than skeletal muscle, it lasts almost the entire contraction, preventing new impulses from changing the contraction or causing a cramp.

52
Q

contractile action potentials

A

i. Depolarization happens rapidly due to many fast voltage Na+ channels opening and Na+ entering the cell.
ii. When the Na+ channels deactivate, the membrane potential does not immediately return to its resting potential as in a skeletal muscle cell. Instead, slow Ca2+ channels open, which keeps the cell depolarized and creates a slightly downward sloping plateau in the action potential.
iii. Repolarization happens when Ca2+ channels inactivate, and K+ channels open, allowing K+ to exit the cell, which returns the cell to its resting potential.

53
Q

pacemaker action potentials

A

ii. Pacemaker cells have initially slow depolarization from opening of slow Na+ channels. When it reaches threshold the action potential begins, with the opening of fast Ca2+ channels.
iii. When the pacemaker potential reaches its peak, that is what causes the contractile cells to contract. This communication between pacemaker and contractile cells is due to the branching nature of cardiac muscle cells.
iv. Repolarization starts when Ca2+ channels inactivate and K+ channels activate, causing efflux of K+, bringing it down below the threshold and hyperpolarizes the cell
v. Hyperpolarization activates the “funny channels” (hyperpolarization-activated cyclic nucleotide gated channels), which allow for slow entry of Na+, starting the cycle over again with slow depolarization.

54
Q

difference between contractile cardiac cells and skeletal muscle cells

A

Contractile cells are very similar to skeletal muscle cells, they both have sarcoplasmic reticulum and t-tubules. The difference is that 10-20% of the Ca2+ in contractile cells comes from outside the cell and the rest of it comes from the sarcoplastic reticulum. Basically a small amount of calcium comes from outside the cell and triggers a greater amount of calcium being released from the sarcoplastic reticulum

55
Q

5 nodes in order

A 
sinoatrial (SA)
atrioventricular (AV)
bundle of his (atrioventricular bundle)
L and R bundle branches
perkinje fibers (subendocardial conducting network)
56
Q

Sinoatrial node location and function

A

right atrium. “The general”. Every other node follows the SA node. The SA node sends out impulses about 70 times per minute, it sends them to contractile cells in the atrium but also to the next node, atrioventricular (AV) node.

57
Q

atrioventricular node location and function

A

right atrium. “The captain”. If AV node doesn’t get impulses from SA node, it sends out impulses on its own but at a slower rate—60bpm.

58
Q

bundle of his (AV bundle) location and function

A

between the ventricles. “The sergeant”. If bundle of his doesn’t receive impulse from captain, it fires on its own at 50bpm.

59
Q

L and R bundle branches location and function

A

Left and right bundle branches: between the ventricles inferior to bundle of his. If no impulse from above it will fire at 40bpm

60
Q

perkinje fibers location and function

A

innervate the cardiac muscle itself. If no impulses from above, the fire at 30bpm.

61
Q

how to know what node impulses are coming from

A

look at EKG

62
Q

what can happen with perkinje fibres and how fast can they beat

A

Perkinje fibers can get pissed off sometimes and start firing at 140bpm if they’re not getting directions.

63
Q

what could happen if one of the nodes in the middle go out

A

If one of the nodes in the middle go out, it’s possible for the SA node to be firing at 70bpm and ones below it at 50 or 40bpm.

64
Q

ANS innervation of the heart

A

The heart is innervated by both parasympathetic and sympathetic nerves. The parasympathetic nerve (vagus nerve) innervates only the SA and AV nodes and decreases heart rate. The sympathetic cardiac nerves innervate all the nodes and increase heart rate and force of contraction

65
Q

P-wave

A

atrial depolarization, immediately preceeds atrial contraction

66
Q

R-wave

A

R-wave: ventricular depolarization

67
Q

T-wave

A

T-wave: ventricular repolarization

68
Q

r-wave vs p-wave size

A

h. Ventricular depolarization is much bigger than atrial depolarization due to the larger amount of muscle present in the ventricles relative to the atria.

69
Q

QRS complex

A

results from ventricular depolarisation and immediately precedes ventricular contraction

70
Q

why does atrial depolarisation not show up on EKG

A

Atrial repolarization has such a small output that it doesn’t get recorded

71
Q

segment definition

A

A segment is a section of the isoelectric line that doesn’t have any waves

72
Q

S-T segment

A

between S-wave and T-wave should not have any waves. If there is S-T elevation/depression it’s indicative of disease

73
Q

Interval definition

A

One segment and at least one wave is an interval

74
Q

P-R interval

A

how long it takes an impulse to travel from the atria to the ventricles. Changes in this number inform diagnoses

75
Q

Q-T interval

A

total amount of time the ventricle is contracting or in the process of relaxing

76
Q

arrhythmia definition and aka

A

without a rhythm. Aka dysrhythmia.

77
Q

long Q-T syndrome

A

a type of channelopathy where one of the ion channels isn’t working. This causes the refractory period to last too long, risking the contractile impulse to fail, causing potentially lethal arrhythmia.

78
Q

heart sounds lub dup

A

Heart Sounds are valves closing

a. First (lub): AV valves.
b. Second: (dup): semi-lunar valves.

79
Q

heart murmurs

A

blood moving in a direction it’s not supposed to, or at a time it’s not supposed to

80
Q

where to listen to each valve

A

a. Aortic valve: listen just to the right of the sternum at the second intercostal space
b. Tricuspid valve: listen just to the right of the sternum at the 5th intercostal space
c. Mitral valve: listen over the heart apex, in 5th intercostal space in line with middle of left clavicle
d. Pulmonary valve: sounds heard in 2nd intercostal space at mid clavicular line

81
Q

systole

A

a. Systole: the contractile part of the cardiac cycle.

82
Q

diastole

A

b. Diastole: the relaxing and resting phase.

83
Q

4 steps in cardiac cycle

A

Ventricular filling
Isovolumetric contraction
Ventricular ejection
Isovolumetric relaxation

84
Q

ventricular filling process (mid-to-late diastole)

A

Passive process: AV valves (bicuspid and tricuspid) are open most of the time, so blood that enters the atria flows down into the ventricles.

85
Q

atrial kick definition and amount of blood it contributes

A

The atria only contract just before the ventricles contract, in order to squeeze out the last bit of blood present—called “atrial kick”. This contraction accounts for 10-15% of the blood volume in the ventricles.

86
Q

End diastolic volume (EDV)

A

the amount of blood left at the end of diastole: the greatest amount of blood ever found in the ventricle. At this point the pressure in the ventricles is going to be greater than the pressure in the atria and that’s going to push the AV valves closed.

87
Q

ventricular systole & isovolumetric contraction

A

the pressure slowly increases in the ventricle as the contractile cells make lots of tiny little contractions, until the pressure inside the ventricle is higher than outside the semilunar valve, at which point the valve opens and ventricular ejection takes place.

88
Q

isovolumetric relaxation: early diastole

A

all valves are closed and the contractile cells are relaxing

89
Q

End systolic volume (ESV)

A

the amont of blood left in the ventricle after contraction. The smallest amount of blood ever found in ventricle, though the heart is not 100% effective so it’s never empty.

90
Q

Stroke volume definition and formula

A

amount of blood ejected out of the ventricle at each beat (difference between EDV and ESV: SV=EDV-ESV)

91
Q

dicrotic notch

A

the closure of the semilunar valves which causes a dip in the pressure of the aorta just before ESV.

92
Q

Cardiac output (CO) definition, formula and normal levels

A

a. The amount of blood pumped out of heart each minute
b. Stroke volume (SV) * heart rate (HR)
c. Normal CO is 5-6 L per minute

93
Q

3 factors affecting stroke volume

A

preload
contractility
afterload

94
Q

preload

A

frank sterling law. i. Stretch: The more the cardiac muscle fibers are stretched, the bigger the contraction, the bigger the stroke volume.
Amount of venous return affects this, as the primary way the muscles stretch is with blood.

95
Q

contractility

A

i. Contractility independent of the preload.

ii. Sympathetic nervous system impacts the amount of Ca2+ present, which affects the force of the contraction.

96
Q

afterload

A

the pressure on the outside of the valve that the contraction needs to overcome. A decrease in afterload increases stroke volume because less pressure is needed to open the valve, and that pressure is instead used to pump out blood

97
Q

sympathetic regulation of heart rate

A

beta 1 receptors on the heart

  1. Causes quicker depolarization and relaxation—the diastolic phase gets shorter which means the filling time decreases
  2. Easier Ca2+ entry also allows for faster contraction
98
Q

parasympathetic regulation of heart rate

A

acetylcholine. Easier K+ efflux hyperpolarizes and lowers membrane potential of the contractile cells
2. Endurance athletes have more prominent vagal tone which is why they have a lower HR

99
Q

atrial reflex

A

aka bainbridge reflex. baro receptors in the atria (mostly RA) detect increases in pressure, usually due to an increase in blood. This is interpreted by the heart as a need to speed up so that the blood doesn’t get backed up. This effect is generally very small.

100
Q

chemical regulation of heart rate

A

catecholamines (epi, norepi)
thyroxine (thyroid hormone)
ions

101
Q

other factors affecting heart rate

A

age, exercise, temperature

102
Q

bradycardia

A

<60bpm

103
Q

tachycardia

A

> 100bpm

104
Q

congestive heart failure

A

contractile muscles are not functioning well enough

105
Q

cor pulmonale

A

right ventricular failure

A&P 2 (8 decks)

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