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BS453: Physiology > Chapter 4: The Cardiovascular System > Flashcards

Chapter 4: The Cardiovascular System Flashcards

1
Q

(1) pericardium, aka (2), covers and adheres closely to the outer surface of the heart

A
  1. visceral
  2. epicardium
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2
Q

() pericardium lines the inner surface of the pericardial sac

A

parietal

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3
Q

parietal pericardium is composed of (1) and (2)

A
  1. areolar tissue
  2. mesothelium
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4
Q

(1), aka the (2) pericardium stabilizes the position of the heart and associated vessels within the mediastinum

A
  1. pericardial sac
  2. fibrous
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5
Q

space in the chest that holds the heart and other organs

A

mediastinum

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6
Q

fills the pericardial cavity to act as a lubricant

A

pericardial fluid

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7
Q

inflammation of the pericardium

A

pericarditis

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8
Q

caused by fluid (e.g. blood from heart) accumulation in the pericardial cavity

A

cardiac temponade

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9
Q

muscular wall of the heart

A

myocardium

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10
Q

inner surface of the heart

A

endocardium

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11
Q

left atrioventricular valve

A

mitral valve (bicuspid)

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12
Q

right atrioventricular valve

A

tricuspid valve

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13
Q

protrusions in the atrial walls that give the blood turbulence

A

pectinate muscles

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14
Q

protrusions in ventricular walls that give blood turbulence

A

trabeculae carneae

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15
Q

(1) refers to an open hole between atria of a growing fetus; becomes (2) once it closes after birth

A
  1. foramen ovale
  2. fossa ovalis
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16
Q

(1) muscles contract when the ventricular muscles contract; however, they do not help to close the valves

A

papillary

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17
Q

papillary muscles are attached to () and together they prevent bulging of the tricuspid/bicuspid valve into atria during ventricular contraction

A

chordae tendinae

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18
Q

region between pulmonary valve and right ventricle

A

conus arteriosus

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19
Q

part of the heart conduction system and connects intraventricular septum to anterior papillary muscle

A

moderator band

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20
Q

the pulmonary valve is (attached/not attached) to chordae tendinae and papillary muscles

A

not attached

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21
Q

() valves are thin anf filmy -> require almost no backflow to cause closure

A

A-V (tricuspid and bicuspid)

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22
Q

() valves are heavier and are snapped closed due to higher pressure in the arteries

A

semilunar valves (aorta, pulmonary artery)

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23
Q

the right coronary artery branches into:

A
  1. marginal arteries
  2. posterior descending (PD) artery
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24
Q

the left coronary artery branches into:

A
  1. left circumflex artery (LCX)
  2. left anterior descending (LAD) artery
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25
Q

interconnections between arteries that serve as a safety measure -> if one artery is blocked, these connections allow blood to still reach the blocked-off tissue through a different artery

A

arterial anastomoses

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26
Q

arterial anastomoses exist between the (1) and (2)

A
  1. posterior descending (PD) artery
  2. left anterior ascending (LAD) artery
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27
Q

cardiac veins return to the heart via the ()

A

coronary sinus

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28
Q

condition characterized by (chronic or transient) shortage of blood supply

A

ischemia

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29
Q

ischemic heart disease is also called ()

A

coronary artery dieases

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30
Q

transient shortage of blood -> transient contraction of coronary vessels -> causes chest pain

A

angina pectoris

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31
Q

if angina persists, cardiac tissue dies due to lack of blood supply

A

acute myocardial infarction

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32
Q

flow of cardiac electrical impulses

A

SA node → AV node → His bundle → His bundle branches → Purkinje fibers

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33
Q

fibers directly innervating and exciting ventricular muscle

A

purkinje fibers

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34
Q

heart contracts on its own, in absence of neural or hormonal stimulation

A

automaticity

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35
Q

refractory period in cardiac muscle where AP is generated, but cannot be conducted to cause contraction

A

effective refractory period

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36
Q

at the end of repolarization, almost all the Na+ channels in cardiac muscle have recovered from inactivation + membrane is still a bit depolarized -> membrane potential is more excitable that usual

A

supranormal

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37
Q

major current responsible for phase 4 (RMP) of fast cardiac action potential

A

inward rectifier K+ current (IK1)

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38
Q

major current responsible for phase 1 (upstroke) of fast cardiac action potential

A

inward Na+ current (INa)

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39
Q

major current responsible for phase 1 (transient repolarization) of fast cardiac action potential

A

transient outward current (Ito) of K+ ions

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40
Q

major currents responsible for phase 2 (plateau) of fast cardiac action potential

A
  1. delayed rectifier K+ outward current (IK)
  2. inward Ca2+ current (ICa)
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41
Q

major currents responsible for phase 3 (repolarization) of fast cardiac action potential

A
  1. delayed rectifier K+ outward current (IK)
  2. inward rectifier K+ current (IK1) -> accelerates recovery
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42
Q

pacemaker depolarization in slow APs in the SA node is caused by

A

IK decay, Ih, ICa

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43
Q

hyperpolarization-activated inward current passes through () channels

A

hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels; aka pacemaker channels

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44
Q

example of HCN channel blocker -> action results in delayed pacemaker activity

A

ivabradine

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45
Q

major current responsible for phase 0 (upstroke) of slow cardiac action potential

A

inward Ca2+ current (ICa)

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46
Q

due to the absence of (), repolarization in slow cardiac APs is caused only by IK

A

IK1

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47
Q

in physiological conditons, the SA node pacemaker activity suppresses all other (latent) pacemaker activities

A

overdrive suppression

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48
Q

chronotropic effects deal with ()

A

heart rate

49
Q

inotropic effects deal with ()

A

cardiac muscle contractility

50
Q

which limbs were submerged in salt bath during Einthoven’s ECG experiment

A

both arms, left foot

51
Q

causes upward projection in ECG graph

A
  1. depolarization heads towards (+) pole
  2. repolarization heads away from (+) pole
52
Q

causes downward projection in ECG graph

A
  1. depolarization moves away from (+) pole
  2. repolarization heads towards (+) pole
53
Q

part of ECG graph that corresponds to atrial depolarization

A

P wave

54
Q

part of ECG graph that corresponds to ventricular depolarization

A

QRS complex

55
Q

part of ECG graph that corresponds to ventricular repolarization

A

T wave

56
Q

describe poles of bipolar lead I

A

(-): right arm
(+): left arm

57
Q

describe poles of bipolar lead II

A

(-): right arm
(+): left leg

58
Q

describe poles of bipolar lead III

A

(-): left arm
(+): left leg

59
Q

Einthoven’s Law

A

lead I + lead III = lead II

60
Q

describe poles of unipolar lead aVR

A

(-): left arm + left leg
(+): right arm

61
Q

describe poles of unipolar lead aVL

A

(-): right arm + left leg
(+): left arm

62
Q

describe poles of unipolar lead aVF

A

(-): both arms
(+): left leg

63
Q

ECG parameter: determines heart rate

A

R-R interval

64
Q

normal values for heart rate

A

60-100

65
Q

HR > 100 bpm

A

tachycardia

66
Q

HR < 60 bpm

A

bradycardia

67
Q

how to determine if heart rhythm is normal

A

R-R intervals are the same

68
Q

the cardiac axis is determined from the vector sum of (1) as the x-axis and (2) as the y-axis

A
  1. lead I
  2. aVF
69
Q

() axis deviation occurs if lead I QRS amplitude is negative

A

right

70
Q

() axis deviation occurs if aVF QRS amplitude is negative

A

left

71
Q

right or left atrial enlargement causes bigger () in ECG graph

A

P wave

72
Q

larger QRS complexes in ECG graph may indicate () in the ventricles

A

hypertrophy

73
Q

larger T wave may indicate increased [K+] in blood -> can be used to diagnose (1), (2)

A
  1. hyperkalemia (increased blood [K+])
  2. myocardial infarction/ischemia
74
Q

caused by the presence of an abnormal accessory electrical conduction pathway between atria and ventricles -> may cause ventricles to prematurely contract, resulting in decreased PR interval

A

Wolff-Parkinson-White (WPW) syndrome

75
Q

the accessory electrical bundle in WPW syndrome is called

A

Bundle of Kent

76
Q

most of the conduction time between the atrium and ventricle is the ()

A

delay at AV junction (AV node + His bundle)

77
Q

delays in AV junction cause increased ()

A

PR interval

78
Q

if QRS complex doesn’t appear regularly, we can suspect ()

A

AV block

79
Q

myocardial ischemia may cause () of the ST segment

A

depression

80
Q

myocardial infarction may cause () of the ST segment

A

elevation

81
Q

increased QT interval in long QT syndrome is caused by delay in (1); this is caused by mutations in (2)

A
  1. ventricular repolarization
  2. delayed rectifier channels
82
Q

treatment principle for long QT syndrome

A

decreasing delayed rectifier K+ channel activity to decrease HR -> decreases likelihood long QT episodes that lead to dangerous arrhythimas

83
Q

cAMP and pKa signalling downstream of (1) receptors augments inward Ca2+ current -> increased contractility -> (2)

A
  1. beta 1 receptors
  2. positive inotropic effect
84
Q

signaling via (1) receptors inhibit ICa via (2), which binds to GIRK channels -> results in overall ()

A
  1. M2 muscarinic
  2. beta-gamma subunit
  3. negative inotropic effect
85
Q

protein that inhibits SERCA

A

phospholamban

86
Q

phospholamban is inhibited when it is (1) -> leads to activation of (2)

A
  1. phosphorylation by sympathetic stimulation
  2. SERCA
87
Q

because cardiac glycosides have an overall effect of increasing intracellular [Ca2+], they are useful treatments for (), which are characterized by the heart not pumping enough blood due to weak cardiac contractions

A

congestive heart failure

88
Q

in the left ventricle, preload = (1), afterload = (2)

A
  1. left ventricular end-diastolic volume
  2. aortic pressure
89
Q

systole starts when (1) and ends when (2)

A
  1. mitral valve closes
  2. aortic valve closes
90
Q

diastole starts when (1) and ends when (2)

A
  1. aortic valve closes
  2. mitral valve closes
91
Q

inward rectifier channel class for strong inward rectifier current (IK1)

A

Kir2.1

92
Q

inward rectifier channel for G protein-gated rectifier K+ current

A

Kir3.1 and Kir3.4

93
Q

GIRK channels are activated by () binding

A

ACh

94
Q

inward rectifier channel for ATP-sensitive K+ current

A

Kir6.2

95
Q

specific name of Kir6.2 channel expressed in heart and skeletal muscle; contribute to lowering heart activity in case of ischemia/low [ATP]

A

SUR2A

96
Q

Na+ channel responsible for inward Na+ current (INa) in heart muscle

A

Nav1.5 (SCN5A)

97
Q

K+ channel responsible for transient outward K+ current in heart

A

Kv4.3 (KCND3)

98
Q

type of Ca2+ channel responsible for inward Ca2+ current (ICa) in heart

A

L-type Ca2+ channel

99
Q

inorganic Ca2+ channel blockers

A

Mn, Co, Ni

100
Q

organic Ca2+ channel blockers

A

verapamil, amlodipine, diltiazem, nifedipine

101
Q

plateau lasts longer if (1) is greater than (2)

A
  1. ICa
  2. IK
102
Q

2 types of delayed rectifiers K+ channels

A
  1. Rapid Delayed Rectifier Current (IKr)
  2. Slow Delayed Rectifier Current (IKs)
103
Q

K+ channels responsible for rapid delayed rectifier current

A

HERG, KCNH2

104
Q

K+ channels responsible for slow delayed rectifier current

A

KvLQT1, KCNQ1

105
Q

total volume of blood that is pumped out of heart during a single contraction

A

stroke volume

106
Q

Eqn for stroke volume

A

End Diastolic Volume - End Systolic Volume

107
Q

describe the Frank-Starling Relationship

A

volume of blood ejected by the ventricle depends on the volume present in the ventricle

108
Q

first sound of heart (‘Lub’) is caused by ()

A

closing of AV valves

109
Q

2nd sound of heart (‘Dubb’) is caused by ()

A

closing of semilunar valves

110
Q

weak sounds in heart (S3 and S4)

A

S3: rapid ventricular filling
S4: atrial contraction

111
Q

the ff conditions cause systolic murmur

A
  1. aortic stenosis
  2. mitral regurgitation
112
Q

the ff conditions cause diastolic murmur

A
  1. aortic regurgitation
  2. mitral stenosis
113
Q

() causes continuous murmur because blood continuously leaks between heart chambers

A

patent ductus arteriosus

114
Q

an additional connection in the heart that bypasses fetal lungs to connect the pulmonary artery and aorta

A

ductus arteriosus

115
Q

patent ductus arteriosus is frequently observed in preterm babies born before () gestational age

A

34 weeks

116
Q

() are used to facilitate closing of patent ductus arteriosus

A

prostaglandins

117
Q

openings between atria

A

atrial septal defect

118
Q

opening between ventricles

A

ventral septal defect

119
Q

both ASD and VSD cause () due to blood leaking into pulmonary circulation

A

pulmonary hypertension

BS453: Physiology (6 decks)

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