Week 3- Cardiovascular Physiology Flashcards
1
Q
Properties of the Heart
A
- Automaticity
- Excitability
- Conductivity
- Contractility
2
Q
Automaticity
A
- Cells depolarize without any impulse from an outside source
- Self-excitation
3
Q
Excitability
A
Cells respond to an electrical stimulus
4
Q
Conductivity
A
Cells propagate the electric impulse from cell to cell
5
Q
Contractility
A
Specialized ability of cardiac muscle cells to contract
6
Q
What occurs to produce mechanical activity?
A
Electrical activity
7
Q
Do action potentials appear the same for all parts of the heart?
A
No, the shape will vary depending on where the action potential is taking place
8
Q
Phases of a cardiac action potential
A
- Phase 0
- Phase 1
- Phase 2
- Phase 3
- Phase 4
9
Q
How to the action potentials taking place at the ventricle and atrium differ?
A
The ventricle AP takes longer
10
Q
Which phases are missing from the sinoatrial node?
A
- Phase 1
- Phase 2
11
Q
Types of cardiac action potentials
A
- Fast response
- Slow response
12
Q
Where do the fast response action potentials occur?
A
- Atrial and ventricular myocytes
- Purkinje fibers
13
Q
Where do the slow response action potentials occur?
A
SA and AV nodes
14
Q
Phase 0 of Fast Cardiac Action Potential
A
- Fast Na+ channels open (influx), then slow Ca++ channels
- Results in fast depolarization
15
Q
Phase 1 of Fast Cardiac Action Potential
A
- K+ channels open (efflux)
- Results in initial repolarization
16
Q
Phase 2 of Fast Cardiac Action Potential
A
- Ca++ channels open more (influx)
- Delays repolarization, resulting in a bit of a plateau
17
Q
Phase 3 of Fast Cardiac Action Potential
A
- K+ channels open more, causing a quick repolarization
- Ca++ channels close
18
Q
Phase 4 of Fast Cardiac Action Potential
A
- Resting membrane potential
19
Q
What happens to open Na+ channels in phase 0?
A
- Depolarization from -90 to -65 mV
- Depolarization results in increased Na+ conductance
20
Q
How long does it take for the Na+ channels to activate?
A
~0.1 msec
21
Q
How long does it take for the Na+ channels to inactivate?
A
1-2 msec
22
Q
How long will Na+ channels remain closed?
A
- Until membrane potential is returned to resting values
- Underlies the refractory periods
23
Q
What drives phase 0 in slow response action potential?
A
Ca++ conductance
24
Q
What is the effect of tetrodotoxin on fast Na+ channels
A
- They block them
- Makes the action potential look like that of a slow response AP
25
What kind of Ca++ channels open in Phase 2 of fast response AP?
- L-type Ca++ channels
| - Inactivated much more slowly than fast Na+ channels
26
Effect of Ca++ channel blockers
- Block Ca++ influx
| - Result in reduced contractility from lack of CICR
27
Calcium induced calcium release
Ca++ from the ECF stimulates more release of Ca++ from the sarcoplasmic reticulum
28
Examples of Ca++ channel blockers
- Verapamil
| - Amlodipine
29
What can increase Ca++ conductance?
- Beta-adrenergic stimulation (from catecholamines)
| - Results from increased CICR
30
When does phase 3 of fast response cardiac AP occur?
When efflux of K+ exceeds Ca++ influx
31
Is duration of the plateau longer in atrial muscle or ventricular muscle?
Ventricular muscle
32
What role do specialized K+ channels play in repolarization?
The more the membrane potential polarizes the more K+ they contribute
33
What is another name for phase 4 of the cardiac action potential?
Maximum diastolic potential
34
How are Na+ and Ca++ concentrations restored to resting conditions?
- Na+: Na+/K+ ATPase
| - Ca+: Na+/K+ ATPase provides an electrochemical gradient which drives Ca++ transport through the NCX, as well as SERCA
35
NCX
Sodium/Calcium Exchanger
36
What channels are mainly responsible for this phase?
Inward rectifying K+ channels
37
When do inward rectifying K+ channels come into play?
- Come into play when potential is hyperpolarized
| - They allow K+ to influx, bringing the potential back to resting levels
38
What is ischemia?
Inadequate blood supply to an organ or part of the body, especially the heart muscles
39
What happens as a result of ischemia in the heart?
Decreased O2 to tissues --> decreased energy due to decreased ATP --> decreased Na+/K+ ATPase
40
What will happen if the Na+/K+ ATPase stops working?
- Increased [Na+] in the ICF
- Increased [K+] in the ECF
- Increased osmolarity inside cells --> cells burst and die
41
What are the major differences between the slow and fast response cardiac AP?
In slow response AP:
- Phase 1 (early repolarization) is absent
- Phase 2 (plateau) is absent
- Ca++ conductance is responsible for phase 0 (depolarization)
- Resting membrane potential is -55 to -65 mV
42
What drives the slower response in slow response AP?
- The mechanics of Ca++ channels are slower than the fast Na+ channels
- Causes the electrical delay between atrial and ventricular contraction occurring at the AV node
43
What happens if extracellular [Ca++] is low?
- Action potentials are weaker
| - Weaker contractility
44
What causes the automaticity of the SA node?
The funny current
45
Where is the funny current found?
- SA and AV nodal cells
| - Purkinje fibres
46
What channels undergird the funny current?
Na+ channels
47
What stimulates these channels?
- Hyperpolarization at the end of phase 3
| - Largely responsible for heart rate
48
Types of refractory periods inn the heart
- Absolute refractory period (ARP)
- Effective refractory period (ERP)
- Relative refractory period (RRP)
- Supranormal period (SNP)
49
Absolute refractory period (ARP)
- No stimulus is large enough to generate a new AP
| - Concludes at -50 mV
50
Effective refractory period (ERP)
- A new AP may be generated
| - No conduction will occur
51
Relative refractory period (RRP)
- Greater than normal stimulus needed to generate an AP
| - Will have abnormal configuration
52
Supranormal period (SNP)
- Begins at -70 and concludes at -85 mV
| - Na+ channels are restored and the cell is more excitable
53
In a fast response AP, at what phase can you get a new action potential?
Phase 3
54
In slow response APs, what phase does the refractory period extend into?
Well beyond phase 3 and into phase 4
55
What can these long refractory periods lead to?
Conduction blocks (AKA heart blocks)
56
How does the sarcoplasmic reticulum in cardiac muscle differ from that of skeletal muscle?
- Not well developed in cardiac muscle
| - This is why Ca++ from the ECF plays such a big role in cardiac excitation-contraction coupling
57
How to the T-tubules in cardiac muscle differ from skeletal muscle?
- Cardiac T-tubule diameter is 5x that of skeletal muscle T-tubules
- Opens directly into the ECF, passing through the muscle
58
Where does the conduction of a cardiac action potential start?
SA node --> AV node
59
What are the pathways from the SA node to the AV node called?
The internodal pathways are high conduction pathways
60
What connects the right atrium with the left atrium?
Bachman's bundle
61
Conduction pathway for cardiac action potential
1) Depolarize atria
2) Depolarize septum from left to right
3) Depolarize ventricular septum toward the apex
4) Depolarize bulk of ventricular myocardium (endocardium to epicardium)
5) Depolarize posterior base of left ventricle
6) Ventricles are completely depolarized
62
Conduction velocity in atrial muscle
0.3 m/s
63
Conduction velocity in internodal pathways
1 m/s
64
Conduction velocity in AV node
0.01 to 0.05 m/s
65
Conduction velocity in Purkinje fibers
2-4 m/s
66
What determines conduction velocity
Time to spread to neighboring cells, not AP duration
67
How long is the delay from the SA node to the AV node?
0.16 seconds
68
How long does the AP stay in the AV node?
0.09 seconds
69
How long does it take for the AP to cross the penetrating portion of the AV bundle?
0.04 seconds
70
What is the delay at the AV node?
0.13 seconds
71
What is the initial conduction delay?
0.03 seconds
72
What causes the conduction delay to the AV node?
- Slow response AP
| - Decreased # of gap junctions
73
What is the consequence of the delay to the AV node?
- Time for ventricular filling
- AV node acts as gatekeeper of conduction, limiting rate of ventricular stimulation in case the atrium contracts too much
74
What is overdrive suppression?
The pacemaker with the fastest firing rate will control HR
75
Order of pacemaker cells
- SA node (70-80 impulses/min)
- AV node (40-60)
- Bundle of His (40)
- Purkinje fibers (15-20)
76
What conditions must be met in order for latent pacemakers to drive HR?
- SA node suppression
- Firing rate of a latent pacemaker is higher than the SA node
- Conduction block
77
Which parts of the heart receive sympathetic NS innervation?
All parts, but especially the ventricles
78
Which parts of the heart receive parasympathetic NS innervation?
- Mostly SA and AV node
| - Atria slightly
79
Which nerve provides parasympathetic innervation?
- Vagus nerve
| - Almost does not innervate the ventricles
80
Autonomic effects on the heart
- Chronotropic
- Dromotropic
- Inotropic
- Lusitropic
81
Chronotropic effects
Heart rate
82
Dromotropic effects
Conduction velocity
83
Inotropic effects
Contractility
84
Lusitropic effects
Relaxation
85
Mechanisms behind heart rate modulation
- Decreased rate of polarization
- Shifting maximum diastolic potential (resting potential)
- Shift in threshold potential
86
Effect of ACh on SA node and AV node
- Same b/t these 2 nodes, but different results
- Slower depolarization in SA node
- Slower conduction in AV node
87
What causes a shift down in resting membrane potential?
- ACh
| - Causes increase in K+ conductance, hyperpolarizes the membrane
88
What causes a shift up in threshold potential?
- ACh
| - Causes decrease in Ca++ conductance, so more depolarization is needed to reach threshold
