Chapter 4: The Cardiovascular System Flashcards
1
Q
(1) pericardium, aka (2), covers and adheres closely to the outer surface of the heart
A
- visceral
- epicardium
2
Q
() pericardium lines the inner surface of the pericardial sac
A
parietal
3
Q
parietal pericardium is composed of (1) and (2)
A
- areolar tissue
- mesothelium
4
Q
(1), aka the (2) pericardium stabilizes the position of the heart and associated vessels within the mediastinum
A
- pericardial sac
- fibrous
5
Q
space in the chest that holds the heart and other organs
A
mediastinum
6
Q
fills the pericardial cavity to act as a lubricant
A
pericardial fluid
7
Q
inflammation of the pericardium
A
pericarditis
8
Q
caused by fluid (e.g. blood from heart) accumulation in the pericardial cavity
A
cardiac temponade
9
Q
muscular wall of the heart
A
myocardium
10
Q
inner surface of the heart
A
endocardium
11
Q
left atrioventricular valve
A
mitral valve (bicuspid)
12
Q
right atrioventricular valve
A
tricuspid valve
13
Q
protrusions in the atrial walls that give the blood turbulence
A
pectinate muscles
14
Q
protrusions in ventricular walls that give blood turbulence
A
trabeculae carneae
15
Q
(1) refers to an open hole between atria of a growing fetus; becomes (2) once it closes after birth
A
- foramen ovale
- fossa ovalis
16
Q
(1) muscles contract when the ventricular muscles contract; however, they do not help to close the valves
A
papillary
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
18
Q
region between pulmonary valve and right ventricle
A
conus arteriosus
19
Q
part of the heart conduction system and connects intraventricular septum to anterior papillary muscle
A
moderator band
20
Q
the pulmonary valve is (attached/not attached) to chordae tendinae and papillary muscles
A
not attached
21
Q
() valves are thin anf filmy -> require almost no backflow to cause closure
A
A-V (tricuspid and bicuspid)
22
Q
() valves are heavier and are snapped closed due to higher pressure in the arteries
A
semilunar valves (aorta, pulmonary artery)
23
Q
the right coronary artery branches into:
A
- marginal arteries
- posterior descending (PD) artery
24
Q
the left coronary artery branches into:
A
- left circumflex artery (LCX)
- left anterior descending (LAD) artery
25
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
arterial anastomoses
26
arterial anastomoses exist between the (1) and (2)
1. posterior descending (PD) artery
2. left anterior ascending (LAD) artery
27
cardiac veins return to the heart via the ()
coronary sinus
28
condition characterized by (chronic or transient) shortage of blood supply
ischemia
29
ischemic heart disease is also called ()
coronary artery dieases
30
transient shortage of blood -> transient contraction of coronary vessels -> causes chest pain
angina pectoris
31
if angina persists, cardiac tissue dies due to lack of blood supply
acute myocardial infarction
32
flow of cardiac electrical impulses
SA node → AV node → His bundle → His bundle branches → Purkinje fibers
33
fibers directly innervating and exciting ventricular muscle
purkinje fibers
34
heart contracts on its own, in absence of neural or hormonal stimulation
automaticity
35
refractory period in cardiac muscle where AP is generated, but cannot be conducted to cause contraction
effective refractory period
36
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
supranormal
37
major current responsible for phase 4 (RMP) of fast cardiac action potential
inward rectifier K+ current (IK1)
38
major current responsible for phase 1 (upstroke) of fast cardiac action potential
inward Na+ current (INa)
39
major current responsible for phase 1 (transient repolarization) of fast cardiac action potential
transient outward current (Ito) of K+ ions
40
major currents responsible for phase 2 (plateau) of fast cardiac action potential
1. delayed rectifier K+ outward current (IK)
2. inward Ca2+ current (ICa)
41
major currents responsible for phase 3 (repolarization) of fast cardiac action potential
1. delayed rectifier K+ outward current (IK)
2. inward rectifier K+ current (IK1) -> accelerates recovery
42
pacemaker depolarization in slow APs in the SA node is caused by
IK decay, Ih, ICa
43
hyperpolarization-activated inward current passes through () channels
hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels; aka pacemaker channels
44
example of HCN channel blocker -> action results in delayed pacemaker activity
ivabradine
45
major current responsible for phase 0 (upstroke) of slow cardiac action potential
inward Ca2+ current (ICa)
46
due to the absence of (), repolarization in slow cardiac APs is caused only by IK
IK1
47
in physiological conditons, the SA node pacemaker activity suppresses all other (latent) pacemaker activities
overdrive suppression
48
chronotropic effects deal with ()
heart rate
49
inotropic effects deal with ()
cardiac muscle contractility
50
which limbs were submerged in salt bath during Einthoven's ECG experiment
both arms, left foot
51
causes upward projection in ECG graph
1. depolarization heads towards (+) pole
2. repolarization heads away from (+) pole
52
causes downward projection in ECG graph
1. depolarization moves away from (+) pole
2. repolarization heads towards (+) pole
53
part of ECG graph that corresponds to atrial depolarization
P wave
54
part of ECG graph that corresponds to ventricular depolarization
QRS complex
55
part of ECG graph that corresponds to ventricular repolarization
T wave
56
describe poles of bipolar lead I
(-): right arm
(+): left arm
57
describe poles of bipolar lead II
(-): right arm
(+): left leg
58
describe poles of bipolar lead III
(-): left arm
(+): left leg
59
Einthoven's Law
lead I + lead III = lead II
60
describe poles of unipolar lead aVR
(-): left arm + left leg
(+): right arm
61
describe poles of unipolar lead aVL
(-): right arm + left leg
(+): left arm
62
describe poles of unipolar lead aVF
(-): both arms
(+): left leg
63
ECG parameter: determines heart rate
R-R interval
64
normal values for heart rate
60-100
65
HR > 100 bpm
tachycardia
66
HR < 60 bpm
bradycardia
67
how to determine if heart rhythm is normal
R-R intervals are the same
68
the cardiac axis is determined from the vector sum of (1) as the x-axis and (2) as the y-axis
1. lead I
2. aVF
69
() axis deviation occurs if lead I QRS amplitude is negative
right
70
() axis deviation occurs if aVF QRS amplitude is negative
left
71
right or left atrial enlargement causes bigger () in ECG graph
P wave
72
larger QRS complexes in ECG graph may indicate () in the ventricles
hypertrophy
73
larger T wave may indicate increased [K+] in blood -> can be used to diagnose (1), (2)
1. hyperkalemia (increased blood [K+])
2. myocardial infarction/ischemia
74
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
Wolff-Parkinson-White (WPW) syndrome
75
the accessory electrical bundle in WPW syndrome is called
Bundle of Kent
76
most of the conduction time between the atrium and ventricle is the ()
delay at AV junction (AV node + His bundle)
77
delays in AV junction cause increased ()
PR interval
78
if QRS complex doesn't appear regularly, we can suspect ()
AV block
79
myocardial ischemia may cause () of the ST segment
depression
80
myocardial infarction may cause () of the ST segment
elevation
81
increased QT interval in long QT syndrome is caused by delay in (1); this is caused by mutations in (2)
1. ventricular repolarization
2. delayed rectifier channels
82
treatment principle for long QT syndrome
decreasing delayed rectifier K+ channel activity to decrease HR -> decreases likelihood long QT episodes that lead to dangerous arrhythimas
83
cAMP and pKa signalling downstream of (1) receptors augments inward Ca2+ current -> increased contractility -> (2)
1. beta 1 receptors
2. positive inotropic effect
84
signaling via (1) receptors inhibit ICa via (2), which binds to GIRK channels -> results in overall ()
1. M2 muscarinic
2. beta-gamma subunit
3. negative inotropic effect
85
protein that inhibits SERCA
phospholamban
86
phospholamban is inhibited when it is (1) -> leads to activation of (2)
1. phosphorylation by sympathetic stimulation
2. SERCA
87
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
congestive heart failure
88
in the left ventricle, preload = (1), afterload = (2)
1. left ventricular end-diastolic volume
2. aortic pressure
89
systole starts when (1) and ends when (2)
1. mitral valve closes
2. aortic valve closes
90
diastole starts when (1) and ends when (2)
1. aortic valve closes
2. mitral valve closes
91
inward rectifier channel class for strong inward rectifier current (IK1)
Kir2.1
92
inward rectifier channel for G protein-gated rectifier K+ current
Kir3.1 and Kir3.4
93
GIRK channels are activated by () binding
ACh
94
inward rectifier channel for ATP-sensitive K+ current
Kir6.2
95
specific name of Kir6.2 channel expressed in heart and skeletal muscle; contribute to lowering heart activity in case of ischemia/low [ATP]
SUR2A
96
Na+ channel responsible for inward Na+ current (INa) in heart muscle
Nav1.5 (SCN5A)
97
K+ channel responsible for transient outward K+ current in heart
Kv4.3 (KCND3)
98
type of Ca2+ channel responsible for inward Ca2+ current (ICa) in heart
L-type Ca2+ channel
99
inorganic Ca2+ channel blockers
Mn, Co, Ni
100
organic Ca2+ channel blockers
verapamil, amlodipine, diltiazem, nifedipine
101
plateau lasts longer if (1) is greater than (2)
1. ICa
2. IK
102
2 types of delayed rectifiers K+ channels
1. Rapid Delayed Rectifier Current (IKr)
2. Slow Delayed Rectifier Current (IKs)
103
K+ channels responsible for rapid delayed rectifier current
HERG, KCNH2
104
K+ channels responsible for slow delayed rectifier current
KvLQT1, KCNQ1
105
total volume of blood that is pumped out of heart during a single contraction
stroke volume
106
Eqn for stroke volume
End Diastolic Volume - End Systolic Volume
107
describe the Frank-Starling Relationship
volume of blood ejected by the ventricle depends on the volume present in the ventricle
108
first sound of heart ('Lub') is caused by ()
closing of AV valves
109
2nd sound of heart ('Dubb') is caused by ()
closing of semilunar valves
110
weak sounds in heart (S3 and S4)
S3: rapid ventricular filling
S4: atrial contraction
111
the ff conditions cause systolic murmur
1. aortic stenosis
2. mitral regurgitation
112
the ff conditions cause diastolic murmur
1. aortic regurgitation
2. mitral stenosis
113
() causes continuous murmur because blood continuously leaks between heart chambers
patent ductus arteriosus
114
an additional connection in the heart that bypasses fetal lungs to connect the pulmonary artery and aorta
ductus arteriosus
115
patent ductus arteriosus is frequently observed in preterm babies born before () gestational age
34 weeks
116
() are used to facilitate closing of patent ductus arteriosus
prostaglandins
117
openings between atria
atrial septal defect
118
opening between ventricles
ventral septal defect
119
both ASD and VSD cause () due to blood leaking into pulmonary circulation
pulmonary hypertension
