1
Q
What are cardiac autorhythmic cells and how do they differ from typical cardiac muscle cells?
A
- Autorhythmic cells are specialized cardiac muscle cells that generate action potentials on their own
- They lack a constant resting potential and instead slowly depolarize until threshold is reached
2
Q
What channels are responsible for depolarization in autorhythmic cells?
A
- They contain If channels, allowing Na⁺ and K⁺ to enter, causing slow depolarization
- These may belong to the HCN family or involve T-type Ca²⁺ channels
3
Q
What causes the upstroke of the action potential in autorhythmic cells?
A
The upstroke is due to L-type Ca²⁺ channels
4
Q
Where are autorhythmic cells found?
A
- Sinoatrial node
- Atrioventricular node
- Bundle of His
- Purkinje fibres
5
Q
Sinoatrial node (SA node)
A
Small area located in the right atrial wall near the opening of the superior venae cavae
6
Q
Atrioventricular node (AV node)
A
Small area located in the right atrium where the right atria and right ventricle come together
7
Q
Bundle of His
A
- Consists of specialized cells that come from the AV node
- It splits into two bundle branches that run down each side of the septum to the heart’s bottom, then curve around and travel back toward the atria
8
Q
Purkinje fibres
A
Small fibres that branch off the bundle of His and spread along the inner surface of the ventricles
9
Q
What is the role of the SA node in normal pacemaker activity of the heart?
A
- The SA node’s autorhythmic cells depolarize fastest, making them the heart’s pacemaker
- They set the heart rate at about 70–80 beats per minute and override slower autorhythmic cells
- As long as the SA node works, it controls the heartbeat, without it, the heart wouldn’t beat at all
10
Q
In order for an efficient cardiac contraction to take place, what 3 criteria must be satisfied?
A
- Atrial contraction and excitation should be complete before the onset of ventricular contractions
- Excitation of the cardiac muscle fibres needs to be coordinated
- The pair of atria and ventricles must be functionally coordinated
11
Q
Atrial contraction and excitation should be complete before the onset of ventricular contractions
A
- During heart relaxation, low ventricular pressure opens the AV valves, allowing 80% of blood to flow passively from atria to ventricles
- The remaining 20% is pushed in when the atria contract about 160 msec before the ventricles, preventing incomplete filling
12
Q
Excitation of the cardiac muscle fibres needs to be coordinated
A
- The heart must contract in a coordinated way for effective pumping
- If different ventricular regions depolarize at different times, blood can’t be ejected properly
- Uncoordinated depolarization is called ventricular fibrillation
13
Q
The pair of atria and ventricles must be functionally coordinated
A
- The right and left sides of the heart must pump the same amount of blood simultaneously
- Both atria contract together, followed by both ventricles contracting together, ensuring coordinated blood flow through the body
14
Q
What are the two main mechanisms by which excitation spreads through the atria after the SA node fires?
A
- Gap junctions
- Interatrial and internodal pathways
15
Q
Gap junctions
A
The gap junctions between atrial cells
16
Q
Interatrial and internodal pathways
A
Move the excitation wave faster than by the gap junctions alone
17
Q
Interatrial pathway
A
- Extends from right atrium to the left atrium
- Ensures the wave of excitation spreads across both atria at the same time
18
Q
Internodal pathway
A
Connects the SA node to the AV node
19
Q
Why can’t the ventricles rely only on gap junctions for excitation?
A
- Because the ventricles are large and hollow, gap junctions alone would cause the top to contract before the bottom
- The bundle of His and Purkinje fibres ensure excitation reaches all regions efficiently
20
Q
How does excitation spread through the ventricles to ensure coordinated contraction?
A
After the AV nodal delay, excitation travels through the right and left bundles of His and Purkinje fibres, then spreads via gap junctions to remaining muscle cells, ensuring both ventricles contract simultaneously
21
Q
How does the cardiac action potential differ from those in nerve and pacemaker cells?
A
- The cardiac action potential has a different shape because ventricular muscle cells contain different voltage-gated ion channels
- Their resting potential is around –80 mV and remains steady until the cell is excited
22
Q
Cardiac action potential - Step 1
A
When a cardiac myocyte is excited and reaches threshold, voltage-gated Na+ channels open and the membrane potential rapidly depolarizes towards +50mV
23
Q
Cardiac action potential - Step 2
A
- Rapid depolarization activates a transient outward K⁺ channel, L-type Ca²⁺ channels, and a delayed rectifying K⁺ channel
- The opposing Na⁺ influx, Ca²⁺ influx, and K⁺ efflux balance each other, keeping the membrane potential steady at the plateau potential
24
Q
Cardiac action potential - Step 3
A
- The transient outwards K+ and L-type Ca2+ currents inactivate, and continued K⁺ efflux through delayed rectifier channels hyperpolarizes the cell
- Returning it to its resting membrane potential
25
5 steps of how a myocyte is activated to initiate contraction
1. Action potential in cardiac contractile cell
2. Release of Ca2+
3. Interaction with contractile apparatus
4. Large release of Ca2+ from SR
5. Contraction
26
Action potential in cardiac contractile cell - Step 1
During the plateau phase of the action potential, L-type Ca2+ channels, found within the T tubules open
27
Release of Ca2+ - Step 2
The opening of L-type Ca2+ channels allow Ca2+ to enter the cell
28
Interaction with contractile apparatus - Step 3
This Ca2+ can directly interact with the contractile apparatus
29
Large release of Ca2+ from SR - Step 4
- When Ca²⁺ enters the cell, it binds to ryanodine receptors on the sarcoplasmic reticulum (SR), activating them and triggering a large additional release of Ca²⁺ from internal stores
- Process is called Ca²⁺-induced Ca²⁺ release (CICR)
30
Contraction - Step 5
- Influx of Ca2+ initiates cardiac muscle contraction
- When Ca2+ is removed from the cytosol, either by moving it across the plasma membrane or pumping it back into the SR, contraction ends
31
Why can’t cardiac muscle undergo summation or tetanus like skeletal muscle?
because the long duration of its action potential prevents twitch overlap, avoiding dangerous, inefficient contractions
32
What causes the long refractory period in cardiac myocytes?
- During the plateau phase, depolarization keeps voltage-gated Na⁺ channels inactivated, preventing re-stimulation
- This refractory period lasts long enough for the contraction to finish before another can start
33
What does an electrocardiogram (ECG) measure and why is it useful?
- An ECG measures the summed electrical activity of the heart detected at the skin’s surface
- It records changes in electrical potentials transmitted through body fluids, allowing observation of excitation spread and detection of cardiac abnormalities
34
Who invented the first ECG and what was the Einthoven Triangle?
- Willem Einthoven invented the first ECG using three electrical limb leads with a ground on the right leg
- These formed the Einthoven Triangle, which detects heart electrical activity between the leads and serves as the basis for modern ECGs
35
Lead 1
Right arm to left arm
36
Lead 2
Right arm to left leg
37
Lead 3
Left arm to left leg
38
How does the modern ECG differ from Einthoven’s original design?
The modern ECG uses the same principles but expands from three limb leads to a 12-lead system based on 9 physical leads
39
9 physical leads from modern day ECG
- 3 limb leads (I–III)
- 6 chest (precordial) leads
- 3 mathematically derived leads from I, II, and III
40
What does a standard ECG recording show?
- It’s usually taken from Lead II, showing voltage changes around the isoelectric line (0 mV)
- Depolarization appears as upward (positive) deflections and repolarization as downward (negative) ones
41
P wave
- Represents atrial depolarization triggered by the SA node
- The SA node’s own electrical activity is too small to detect at the body’s surface, so only the excitation of the atria is seen
42
QRS complex
- Shows ventricular depolarization
- After the AV node delay, excitation travels through the bundle of His and Purkinje fibres to depolarize the ventricles
- The ECG is flat before this because no net charge movement occurs during atrial depolarization
43
T wave
- Represents ventricular repolarization
- The ECG remains flat while the ventricles stay depolarized, then shows the T wave as they repolarize
- After this, no net current occurs until the SA node fires again to begin the next heartbeat
44
PR segment
Indicates AV node delay
45
ST segment
Indicates the time during which ventricles are contracting and emptying
46
TP interval
Indicates the time during which ventricles are relaxing and filling
47
QT segment
Indicates electrical depolarization and depolarization of the ventricles
48
Atrial repolarizationWhy isn’t atrial repolarization seen on an ECG?
Atrial repolarization occurs while the ventricles are depolarizing, and because ventricular muscle mass is much larger, the electrical signal from atrial repolarization is masked by the stronger ventricular depolarization in the ECG
49
Tachycardia
- Heart rate over 100 bpm in adults
- It can result from factors like exercise, caffeine, or electrical abnormalities
- It decreases cardiac output by reducing ventricular filling
- ECGs classify tachycardia as wide or narrow based on the QRS complex.
50
Extrasystole
- A premature heartbeat initiated by the Purkinje fibres instead of the SA node
- The ventricles contract before the atria, reducing blood filling and cardiac output
- It can cause palpitations and be harmless in healthy people but dangerous if frequent
51
Ventricular fibrillation (V-fib)
- Occurs when the heart quivers instead of pumping due to abnormal ventricular electrical activity, causing cardiac arrest, loss of consciousness, and no pulse
- It can result from coronary artery disease or intracranial bleeds
- On an ECG, it appears as irregular, unformed QRS complexes with no clear P waves
52
Complete heart block (third-degree AV block)
- Impulses from the SA node fail to reach the ventricles, so AV node pacemaker cells independently activate them
- The ECG shows two rhythms: regular P–P intervals and QRS complexes that don’t always follow P waves
- Causes low heart rate and blood pressure
PHGY 215
flashcards
Decks in class (28)
# Cards
-
Module 1: Section 1 + 256
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Module 1: Section 316
-
Module 1: Section 413
-
Module 1: Section 531
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Module 2: Section 120
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Module 2: Section 216
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Module 2: Section 332
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Module 2: Section 451
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Module 2: Section 511
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Module 4: Section 127
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Module 4: Section 235
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Module 4: Section 333
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Module 4: Section 426
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Module 4: Section 59
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Module 4: Section 628
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Module 5: Section 115
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Module 5: Section 234
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Module 5: Section 352
-
Module 5: Section 47
-
Module 5: Section 533
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Module 5: Section 67
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Module 6: Section 121
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Module 6: Section 223
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Module 6: Section 344
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Module 6: Section 428
-
Module 6: Section 512
-
Module 6: Section 613
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Module 6: Section 743
