LEC EXAM #3 CHP 11 Flashcards
(95 cards)
1
Q
Cardiac muscle tissue characteristics: (4)
A
- automaticity
- extended contraction time
- long absolute refractory period
- nervous system alters contraction force and rate
2
Q
Automaticity:
A
- contraction without neural stimulation
- controlled by pacemaker cells (SA node)
3
Q
In what way does cardiac muscle tissue have a long absolute refractory period?
A
Prevention of wave summation and tetanic contractions of cell membranes
4
Q
Does cardiac or skeletal muscle tissue have a longer contraction time?
A
Cardiac
5
Q
2 kinds of cardiac cells:
A
- pacemaker cells (auto rhythmic/myogenic cells)
- contractile cells
6
Q
Intercalated discs:
A
Hold cells together
7
Q
Gap junctions:
A
Ports that allow ions to spread from one cell to another
8
Q
Pacemaker cells are found:
A
- SA node (sets pace/rate)
- AV node
- Bundle of HIS
- Purkinjee fibers
- Bundle branches
9
Q
What do pacemaker and contractile cells have in common?
difference?
A
- both rely on K+, Ca2+, Na+, and CI-
- different AP’s
10
Q
4 characteristics of pacemaker cells:
A
- spontaneously depolarize
- slow to depolarize/hit threshold
- autorhythmic
- do NOT contract
11
Q
Pacemaker cell AP
Phase 0: (2)
A
- Ca rushes in
- increases depolarization
12
Q
Pacemaker cell AP
Phase 3:
A
K leaves
13
Q
Pacemaker cell AP
Phase 4:
A
Na rushes in
14
Q
Pacemaker cells depolarized by:
A
Ca rushing in
15
Q
Contractile cells characteristics:
A
- low RMP= -96 mv
- gets impulse from pacemaker cells via gap junctions
- depolarize-> contract
- long absolute refractory period
16
Q
Do pacemaker cells or contractrile cells have a longer absolute refractory period (depol)?
A
Contractile
17
Q
Why do contractile cells have a longer absolute refractory period?
A
Because Ca is rushing in at the same time as K is leaving, leading to a plateau PHASE 2
18
Q
Cardiac muscle cell contraction occurs:
A
In contractile cells only
19
Q
Provides Ca for cardiac muscle contraction:
important bitch
A
ECF and SR
20
Q
Main function of sarcoplasmic reticulum?
A
To store Ca
21
Q
Less Ca (in cardiac muscle cell contraction) =
A
less force generated
22
Q
Heart failure channel blocker would be:
A
Calcium
23
Q
What is the secondary active transport in cardiac muscle cell relaxation?
A
Calcium being forced out by Na coming in
sodium-calcium antiport
24
Q
Cardiac tissue is innervated by:
A
Autonomic nervous system at SA node
25
What is absolute refractory period responsible for?
Not generating an AP
26
How do contractile cells communicate?
SA node spreads through the atria
27
AV node is responsible for what during contraction?
Takes the impulse from the atria to the ventricles
28
Why do we need relaxation to occur?
To refill with enough blood
29
Once contractile cells get an impulse, what happens?
- Ca from skeletal muscle is released from endoplasmic reticulum
- binds troponin to move tropomyosin out of the way
- myosin binds to active site
30
Where do we get Ca for skeletal muscle contraction?
Sarcoplasmic reticulum
31
Alpha and beta adrenergic cardiac tissue receptors bind:
Nor-epi + Epi (hormone) and increase depolarization of pacemaker cells
32
Epi has higher affinity for:
Beta adrenergic receptors
33
What happens to your HR when nor-epi and epi bind to alpha and beta receptors?
- increase in HR
- increase in SV
- increase in CO
34
Nor-epi has higher affinity for:
Alpha adrenergic receptors
35
Sympathetic hormones:
receptors:
Parasympathetic hormones:
receptors:
NE + Epi
Alpha + Beta adrenergic
Ach
Muscarinic cholinergic
36
What happens to your HR when Ach bind to muscarinic cholinergic receptors?
- decrease in HR
- decrease in SV
- decrease in CO
37
Phenoxybenzamine:
Antagonistic drug that binds to alpha adrenergic receptors
38
Propranolol:
Antagonistic drug that binds to beta adrenergic receptors
39
Atropine:
(from deadly night shade)
| antagonistic drug that binds to muscarinic cholinergic receptor
40
How would phenoxybenzamine effect HR?
Unable to bind to alpha adrenergic receptor to nor-epi so slight decrease in HR
41
Lead 1:
RA (-) LA (+)
42
How would atropine effect HR?
blocks Ach and causes an increase in HR
43
How would propranolol effect HR?
Since we have more beta receptors, greater decrease in HR
44
Lead 2:
RA (-) and LL (+)
45
Lead 3:
LA (-) and LL (+)
46
Which lead shows the bulk of the electrical current?
Lead 2
47
"0" on an EKG represents:
Isoelectric line= no electrical activity
48
When waveform deflects up (pos deflection)->
Electrical activity is going towards positive lead (lLL)
49
When waveform defects down (neg deflection)->
Electrical activity is going towards negative lead (RA)
50
P wave shows:
Atrial depol
51
Before the atria depolarizes, what has to depolarize?
SA node
52
QRS interval shows:
Ventricle depol
53
T wave shows:
Ventricle repol
54
Where is the P wave depolarizing towards?
LL
| Positive deflection
55
Interval has ____
| Segments have no ____
Waves
56
If SA node is damaged, can the heart still beat?
Yes, but the rate will be slower and the AV node takes over
57
Cardiac cycle:
period between the start of one heartbeat and the beginning of the next
58
Cardiac cycle consists of:
Systole + diastole
59
Atria cardiac cycle:
1. atria passively fill (end of diastole)
2. atria contract (start of systole)
3. atria eject blood into ventricles (end of systole)
4. atria relax (start of diastole)
60
Ventricular cardiac cycle:
1. ventricles passively fill as atria fill and contract (end of diastole)
2. atria contract (start of systole)
3. atria eject blood into ventricles (end of systole)
4. atria relax (start of diastole)
61
What is happening at diastole?
Blood is filling into the atria and ventricles
62
What is the "lub" sound in the heart?
Blood hitting the closed AV valves, pressure is built up
63
What is the "dub" sound in the heart?
Blood hitting the shut semilunar valves
64
During systole, what happens to BP?
increases
65
During diastole, what happens to BP?
decreases
66
Blood flows from:
high -> low pressure
67
What dictates blood flow throughout the heart?
Contractions and valves
68
Does all the blood get ejected from the ventricles when it contracts?
NO
69
Where is pressure higher?
Ventricles
70
Ventricles contract every:
270 milliseconds (0.2 secs)
71
Contraction for heart time:
370 milliseconds
72
How is SV calculated?
EKG, ultrasound, prob into neck
73
Tachycardia:
Fast rhythm
74
Bradycardia:
Slow rhythm
75
Be able to talk through the steps of the Wigger diagram:
- P wave depolarizes
- Increase in atrial pressure-> atrial systole
- blood is pushed into ventricles as a result of the LA contracting
- increase in ventricular volume
- QRS complex causes ventricular depol
- isovolumetric contraction occurs resulting in the AV and semilunar valves closing as the ventricles build up in pressure
- semilunar valve opens causing ejection
- causes a decrease in ventricular volume
- T wave causes ventricles to repolarize
- ventricle relaxation + isovolumetric relaxation
- ventricles able to fill again
76
Ventricular filling (phase 1)
- blood->relaxed atria->av valves->ventricles
| - atria contract-> blood going into ventricles
77
Isovolumetric contraction (phase 2)
- ventricles begin contracting
- all valves closed
- no blood flowing=same volume
78
Ventricular ejection (phase 3):
- ventricles contract
| - blood ejects into aorta + pulmonary arteries
79
Isovolumetric relaxation (phase 4)
- semilunar shut
| - AV valves open and ventricles passively fill with blood until they contract again
80
During ventricular contraction the aorta:
Stores energy by stretching (pressure reservoir)
81
Aortic pressure is higher than ventricular pressure during:
Diastole
82
During ventricular diastole the aorta:
Releases pressure to maintain blood flow to body
83
MAP=
profusion pressure to organs
84
EDV:
End-diastolic volume
85
ESV:
End-systolic volume
86
Equation to get SV?
EDV-ESV=SV
87
Starling's law:
Increase EDV by increasing venous return via:
- skeletal muscle pump
- respiratory pump
- sympathetic nervous system
- arterial vasoconstriction
88
Dicrotic notch shows:
Semilunar valves closing
89
Equation to get CO?
SVxHR=CO
90
What does increasing venous return result in? (starling's law cont.)
- increase stretch of cardiac fibers
- increase strength of contraction
- increase SV
91
Starling's law causes:
Stroke volume to increase
92
How do we measure resting HR? (3)
3 sec method
6 sec method
R-R method
93
PT interval:
heart contracts, systole
94
PT segment:
heart resting, diastole
95
Why is an AP not possible during absolute refractory period?
Because Na v.g.v. are sealed shut
