unit 3: heart Flashcards
(142 cards)
1
Q
heart sounds are produced by
A
closing valves
2
Q
losing of AV valves; occurs at
ventricular systole
A
lub
3
Q
closing of semilunar valves; occurs
at ventricular diastole
A
dub
4
Q
what are the valveslocated btwn atria and corresponding ventricles
A
tricuspid and bicuspid
-responsible for blood flow btwn atria and ventricles
5
Q
makes a sound bc thats how fast and sharp the valves slam shut.
A
lub
6
Q
happens after T wave
A
dub
7
Q
Abnormal heart sounds produced by
abnormal blood flow through heart.
1) Many caused by defective heart valves
A
heart murmurs
8
Q
Mitral valve calcifies and
impairs flow between left atrium and
ventricle
A
mitral stenosis
9
Q
what can mitral stenosis cause
A
pulmonary hypertension
10
Q
occurs when the valve isnt completely closed and regurgitation. hearing blood do different things
A
heart murmur
11
Q
high bp in arteries of lungs. puts strain on right side of heart, which pumps blood into lungs
A
pulmonary hypertension
12
Q
what are the point of tricuspid and bicuspid
A
close bc of pressure in ventricles, prevents backflow.
13
Q
where on ecg does lub happen
A
btwn s and t
14
Q
when is heart in diastole on ecg
A
after t wave
15
Q
why does blood in arteries want to go back during diastole
A
pressure; blood wants to go to low pressure. this is generated by myocardium
16
Q
to listen
A
auscultation
17
Q
issues with electric circuit of heart
A
arythmia
18
Q
what are the valves made of
A
CT
-av valves(facing atria)= areolar ct
-ventricles (facing high pressure)= dense ct
19
Q
why would mitral stenosis result in pulmonary hypertension
A
blood cant move thru the valves as efficiently and it pulls it back up towards the lungs. so pulmonary circuit becomes hypertensive
20
Q
prevents regurgitation fromm the ventricles to atria
A
av valve
21
Q
what are the valves located btwn ventricles and corresponding arteries and why do we have them
A
aortic semilunar valves and pulmonary semilunar valve
-regurgitation
-regulate the flow of blood leaving the heart
22
Q
flow of blood thru heart right side
A
deoxygenated blood
-superior/inferior vena cava(from body)
-right atrium
-tricuspid valve
-right ventricle
-pulmonary semilunar valve
-pulmonary artery (to lungs)
23
Q
flow of blood thru heart left side
A
oxygenated blood
-pulmonary veins (from lungs)
-left atrium
-bicuspid valve
-left ventricle
-aortic semilunar valve
-aorta (supplies body)
24
Q
incompetent valves do not close properly. this could be due to:
A
damaged papillary muscles, mitral valve prolapse, septal defects
25
this is a cone shaped muscles located in the ventricles. each muscle connects to the heart valves via chordae tendinae.
papillary muscles
26
this muscle functions in contracting during ventricular contraction, prevent valves from regurgitation
papillary muscles
27
what is the most common cause of chromic mitral regurgitation
mitral valve prolapse
28
backflow of blood. dont want bc inefficient to oxygenate new blood
regurgitation
29
this occurs when mitral valve in heart does not close properly. instead of sealing shut during contraction, valves flaps bulge up in left atrium. this happens in left atrium and left ventricle
mitral valve prolapse
30
our blood goes in one direction. this is efficient bc
simplicity, prevent backflow, maintain pressure, support oxygen delivery (keep from mixing)
31
what is it called when blood is not going in the only direction its supposed to go
regurgitation
32
anytime a structure pushes into an area its not supposed to push into (in the opposite direction)
-this is when the chordae tendinae or papillary muscles fail
prolapse
33
holes in interventricular or
interatrial septa which allows blood to cross
sides
spetal defects
34
walls that seperate chambers of the heart. they allow blood to flow abnormally btwn left and right sides of heart
septa
35
results from a failure of
the foramen ovale to close after birth.
patent ductus arteriosus
36
pulmonary circuit and aortic circuit artery connection
foramen ovale
37
types of septal defects
-atrial septa defects (hole in btwn L&R atria)
-ventricular sd (hole in btwn L&R ventricle)
-atrioventricular sd
38
begins with contraction of atria and ends with relaxation of ventricles
cardiac cycle
39
flow of how heart beats and pumps blood
cardiac cycle
40
contraction of heart muscles. this pumps blood out of heart.
systole
41
what is contracting during systole
the myocardia= layer of heart
42
relaxation of the heart muscles. heart fills with blood
diastole
43
three layers of heart muscle walls
(inner) endocardium, pericardium, epicardium (outer)
44
what are the 2 seperate parts of myocardia
atrial myocardia and ventricular myocardia
45
why cant the atrial and ventricular myocardia contract at the same time
bc the ventricles would overpower the atria
46
total volume of
blood in the ventricles at the end of diastole
-the heart is fully filled and ready to pump
end diastolic volume
47
the amount of blood
left in the left ventricle after systole
-whats left behind after the heart gives its best effort
end systolic volume
48
intercallated discs communicate thru
gap junctions
49
Ventricles begin contraction, pressure rises, and
--- close (lub); what type of contraction is this
av valves; isovolumetric contraction
50
why is 'lub' an isovolumetric contraction
bc the ventricles contract, volume pressurize, but volume does not change
51
what happens during isovolumetric contraction
Pressure builds, semilunar valves open, and
blood is ejected into arteries
52
Pressure in ventricles falls; ----
close (dub); what is this called
semilunar valves; isovolumetric relaxation
53
what happens due to isovolumetric relaxation
-Pressure in ventricles falls below that of atria, and
AV valve opens. Ventricles fill
-Atria contract, sending last of blood to ventricles
54
pressure drops which is not enough to open av valves to let blood flow to atria
isovolumetric relaxation
55
short period of time follwoing the start of ventricular systole where the ventricles start to contract and build enough pressure to 'lub; but not enough pressure to overcome pressure of arteries.
-both valves are still closed, so actual amount of volume does not change
isovolumetric contraction
56
what happens during atrial systole (when it begins)
-pushing the last bit of blood into ventricles
-av valves open
-semilunar valves are closed
-happens after p wave
57
what happens durong ventricular systole
-isovolumetric contraction. ventricles begin to contract, all valves are closed, pressure builds.
-ventricular ejection. pressure opens semilunar valves, blood pumped into aorta from LV, pulmonary artery from RV, AV valves stay closed to prevent backflow
58
what happens during ventricular diastole
-isovolumetric relaxx. ventricles relax, all valves closed, pressure drops inside ventricles
passive filling. pressure in atria increases more than ventricles, av valves open and blood flows passively, semilunar valves close
59
what is the meaning of the sound 'dub'
semilunar valves closing
60
Cardiac muscle cells are interconnected by
gap junctions called
intercalated discs
61
The area of the heart that contracts from
one stimulation event is called a
myocardium or functional syncytium
62
The atria and ventricles are separated
electrically by the
fibrous skeleton
63
muscle layer of the heart wall. made up of cardiac tissue
myocardium
64
function as a single unit. behavior of myocardium
syncytium
65
This means that the individual cells work with adjacent cells for coordinated action. Rapid transmission of electrical impulses transfers between cells to trigger simultaneous contraction of the heart muscle.
functional syncytium in the heart
66
made of dense collagen CT located between atria and ventricles. functions in structural support, electrical insulation, anchors cardiac muscle, prevent valves from overstretching
fibrous skeleton
67
how do we get signals from atria to ventricles?
-the eletrical signal pathway
sa node, av node, bundle of his, right and left bundle branches, purkinje fibers
68
automatic nature of the
heartbeat
automaticity
69
“pacemaker”;
located in right atrium
sinoatrial node (sa node)
70
are described
as potential/secondary or ectopic
pacemakers; can be faster or slower than
sinus rhythm and is abnormal
av node and purkinje fibers
71
what does ectopic mean
not in the right place/ abnormal
72
step 1 of conducting tissues of the heart:
Action potentials spread via intercalated discs
(gap junctions)
73
step 2 of conducting tissues of the heart:
SA node to AV node to stimulate atrial
contraction
74
step 3 of conducting tissues of the heart:
AV node at base of right atrium and bundle of
His conduct stimulation to ventricles.
75
step 4 of conducting tissues of the heart:
In the interventricular septum, the bundle of His
divides into right and left bundle branches
76
step 5 of conducting tissues of the heart:
Branch bundles become Purkinje fibers, which
stimulate ventricular contraction
77
Action potentials from the SA node spread ---
rapidly
78
At the AV node, things ---. this accounts for the majority of the time delay btwn atrial and ventricular contraction
slow down
79
--- records the
electrical activity of the heart by picking
up the movement of ions in body tissues
in response to this activity
electrocardiograph
80
what ions does the electrocardiograph record the movt of
na, k ,ca
81
the electrocardiograph Does not record action potentials, but results
from ---
waves of depolarization
82
the electrocardiograph Does not record contraction or relaxation,
but records the---
electrical events leading to
contraction and relaxation
83
this wave shows atrial depolar. initial electrical excitation of atrial muscle cells, initiated by sa node, which triggers this wave
p wave
84
this wave shows atrial systole. this is the actual contraction of atrial muscle fibers. thos pushes blood from atria into ventricles
P-R interval
85
this wave shows ventricular depolar. ventricles preparing to contract
qrs complex
86
this wave is the plateau phase, ventricular systole. ventricles are contracted but no electrical activity occuring. flat, isoelectric line represents plateau
S-T seg
87
this wave shows ventricular repolar. heart muscles return to their resting state after contraction. completion of electrical cycle
T wave
88
what happens physically after qrs
-lub
89
why do the semilunar valves close after qrs (lub)
pressure in ventricles (ventricular depolarization)
90
different viewpoints from which the electrical activity of the heart is recorded. help spot abnormalities in different parts of the heart
electrocardiograph leads
91
this means as electricity flows thru bundle of his and bundle branches, its going to be picked up by specific leads (specifically right arm and left leg)
electrocardiograph leads
92
between right arm and left arm
lead 1
93
between right arm and left leg
lead 2
94
between left arm and left leg
lead 3
95
record voltage between a single
electrode on the body and one built into the
machine (ground)
unipolar leads
96
where do unipolar leads go
Limb leads go on the right arm (AVR), left arm (AVL), and
left leg (AVF)
-there are 6 chest leads
97
why do semilunar valves close
pressure higher in aortic artery and pulmonary artery. lower pressure in ventricles
98
occurs after qrs wave as the av valves close
lub
99
occurs att he beginning of the t wave as SL valves close
dub
100
--- are abnormal patterns of electrical
activity that result in abnormalities of the
heartbeat
arrhythmias
101
Drugs used to treat arrhythmias affect the nature
and conduction of
cardiac action potentials
102
drugs used to treat arrhythmias are classified into 4 different group to slow the heart and block
sodium, beta-blockers, potassium, slow calcium channels
103
if blocked, slows down the heart bc prevents ap and contraction.
- these channels depolarize during contraction. by blocking, we prevent this
sodium channels
104
this prevents beta from being stimulated bc adrenaline increases heart rate.
-located on sa node
-beta= adrenaline/ epinephrine
drugs that are beta-blockers
105
blocking this prevents repolarization and reset of electric concentration. blocking this takes longer to repolarize and cant get an ap
drugs that block potassium channels
106
increase rate of ap (refractory period). heart has this to prevent contraction over and over again. only in sa node
-this slows the rate of repolarization
drugs block the slow ca2+ channels
107
type of arrhythmia thats too slow
bradycardia
108
type of arrhythmia thats too fast
tachycardia
109
what is the danger of atherosclerosis
plaque, heart failure, stroke
110
what is the issue with high blood pressue
your heart has to work harder to pump blood and your blood vessles are under constant strain. over time, this damages the entire cardiovascular system
111
Most common form of arteriosclerosis
(hardening of the arteries)
atherosclerosis
112
during atherosclerosis, --- protrude into the lumen and ---
plaques; reduce blood
flow
113
plaque serves as sites for
thrombus formation
114
the process of a blood clot forming inside a blood vessel or the heart. It’s a normal part of healing after injury, but when it happens inappropriately (like inside an intact vessel), it can become dangerous.
thrombus formation
115
form in response to damage done to the
endothelium of a blood vessel
plaques
116
what causes plaques/ atherosclerosis
smoking, high blood pressure, diabetes,
high cholesterol
117
btwn tunica intima and tunica media. leads to stress in endothelium and smooth muscle responses
plaque
118
layers of BV
-tunica intima
-tunica media
-tunica externa
119
is a fat like substance found in the blood. we need it to build cell membranes, make hormones, produce vitamin d, and help with digestion
cholesterol
120
why is cholesterol good
-liver makes it naturally
-cell function, hormone prod, and nerve insulation
-carries thru blood by proteins called lipoproteins
121
why is cholesterol bad
too much can
-stick to artery walls
-cause plaque buildup
-increase risk of heart attack, stroke, poor circulation
122
this is good. it carries cholesterol awat from arteries to the liver for removal
high density lipoprotein
123
this is bad. delivers cholesterol to the tissues, but can deposit in artery walls
low density lipoprotein
124
what is the func of tunica intima and what is the endothelium
-provide smooth lining for blood flow and release chemicals that control vasodilation, clotting, inflammation
-simple squam
125
what is the func of tunica media and what is the endothelium
controls vasoconstriction and vasodilation, regulates blood blow and pressure
-smooth muscle, elastic fibers
126
what is the func of tunica externa and what is the endothelium
protects and anchors the vessel. provides structural support
-connective tissue
127
when a tissue or organ doesn’t get enough blood flow, which means it’s not getting enough oxygen and nutrients to function properly.
-results in narrow vessels
ischemia
128
steps 1 of developing atherosclerosis
Lipid-filled macrophages and lymphocytes
assemble at the site of damage within the
vessel wall (fatty streaks)
-under endothelium
129
steps2 of developing atherosclerosis
layers of smooth muscle are added
130
steps 3 of developing atherosclerosis
a cap of connective tissue covers the
layers of smooth muscle, lipids, and cellular
debris
131
steps 4 of developing atherosclerosis
Progress promoted by inflammation stimulated
by cytokines and other paracrine regulators
132
what do macrophages become when they store too musch inside them
-fat and full of lipids
foam cells
133
carry
cholesterol to arteries
Low-density lipoproteins (LDLs)
134
People who consume or produce a lot of
cholesterol have more
ldl
135
high LDL level is associated with
increased
development of atherosclerosis
136
carry
cholesterol away from the arteries to the
liver for metabolism
high density lipoproteins (hdl)
137
This takes cholesterol away from the
macrophages in developing plaques (foam
cells)
hdl
138
Statin drugs (for example, Lipitor), fibrates, and
niacin increase
hdl levels
139
Atherosclerosis is now believed to be an
inflammatory disease
140
---is a better predictor for
atherosclerosis than LDL levels
C-reactive protein (a measure of
inflammation)
141
is a marker of systemic inflammation—so high levels suggest your body is actively responding to vascular injury or plaque
C reactive protein
142
When endothelial cells engulf LDLs, they
become oxidized LDLs that ---
damage the
endothelium bc oxidized ldl triggers a toxic inflammatory response (plaque build up/ atherosclerosis)
