Electrophysiology of the Heart Flashcards
3 Muscles of the Heart
- Atrial Muscles2. Ventricular Muscles3. Conductive Muscle Fibers
Intercalated Discs
Connection of heart muscle cells
Desmosomes
Structural element that combines them
Gap Junctions
Ion channels that allow ions to move freely between cells, allowing electrical impulse
Contractile Cells
- Compose most of the heart2. Contract when stimulated
Auto-rhythmic Cells
- Comprise the conducting system2. Self-stimulating and can contract/depolarize without external stimulus
Fast Response Cells
- Atrial and Ventricular Myocytes2. Purkinje Fibers
Examples of Slow Response Cells
- SA Node2. AV Node
Resting Membrane Potential
-80-90mV Interior Negative
Phase 0
- Higher K insid ethe cell- Sudden opening of fast and slow Na+ channels- Rise in Na+ permeability- Drop in K+ permeability
Tetrodotoxin
Blocks Na+ Channels
Phase 1 (Also called?)Blocked by?
Repolarization- K+ channels open- Primarily caused by closing of Na+ ion channels and opening of K+ ion channelsBlocked by 4-aminopyridine
Phase 2 Activators and Blockers
A: Catecholamines: Increase ECF-Ca2+ ConcentrationB: Ca2+ Antagonists and Mn2+
Phase 2 (Or?)1. What changes to voltage?2. What channels are open?3. What’s happening?
Plateau Phase1. Voltage is constant2. Ca2+ channels are open (Some K+ leaking out, causing balance)3. Prolongs duration of contraction, prevent overstimulation
Phase 3 (Or?)What channels are open?
Genesis/Final RepolarizationOnly K
Phase 4 (Or?)1. What is working in this stage?2. What happens to Ca2+?
Rest Phase
- Na-K ATPase pump works to remove Na+ and returns K+
- Ca2+ exchanged for Na+
Major Differences of Skeletal and Cardiac Muscles?
- Presence of both fast Na+ and slow Ca2+ channels in Cardiac Muscles2. Decreased K+ channel permeability after action potential: Prevents premature return to resting levels
Absolute Refractory Period
Cannot be stimulated no matter what
Effective Refractory Period
Can only be stimulated by a larger than normal stimulus
Only a local response can be produced
No action potential generated
Relative Refractory Period
Action Potential can only be stimulated by a larger than normal stimulus
Supernormal Period
More excitable than normal; ala a weaker stimulus can cause depolarization
Full Recovery Time in Fast Response and Slow Response cell is dependent on?
Fast-Response: Voltage-DependentSlow-Response: Time-Dependent
Effects of VMAX
More VMAX :: More Conduction
Diameter
Fatter Cell : Faster
Changing Resting Membrane Potential
More Negative :: More Quicker
Conducting System Pathway
SA Node -> Atrium -> AV Node -> Bundles of His -> Purkinje Fibers -> Ventricular Muscles
SA Node Resting Potential
-55 to -60mV
Why is the SA Node Membrane Naturally Leaky to Sodium Ions?
- Enter through slow sodium channels- More permeable to Na due to higher extracellular concentration- Faster heart rate : More Sodium
Fast, Slow, or both Na+ channels for SA Nodes?
Only slow, fast channels are blocked due to less negativity
Threshold Voltage of SA Node
-40 mV
Bachmann’s Bundle
Conducts impulse from SA node -> Left Atrium
AV Node Function
Delays the impulse from the atria to the ventricle to allow for more contraction time
Purkinje System Transmission Rate
1.5-4m/s (Fastest)
Hierarchy of Pacemakers
- SA Node: 70-80 bpm2. AV Node: 40-60 bpm3. Purkinje Fibers: 15-40 bpm
Which pacemaker is most dominant and why?
The SA Node, because it has the fastest rate of depolarization preventing others from self-exciting
Stokes-Adam Syncope
Occurs when SA node fails and takes time for the AV node to take over; causes you to faint
Parasympathetic Nerves:1. Innervates2. Secretes
- Mainly sinus and AV node, some parts of the two atria and little to the ventricular muscles2. Acetylcholine
Acetylcholine Effects
- Decreases rate of rhythm of sinus node2. Decreases excitability of the AV junctional fibers between atrial musculature and AV node3. Slows down heart rate
Mechanism of Parasympathetic Nerves
Increases permeability of K+ ions out of cell, causing hyperpolarization
Sympathetic Nerves1. Innervates2. Secretion
- All parts of the heart2. Norepinephrine
Norepinephrine Effects
- Increases rate of sinus node discharge2. Increases rate of conduction and excitability3. Increases force of contraction
P Wave
Atrial Depolarization
QRS Complex
Ventricular Depolarization
T Wave
Ventricular Repolarization
ECG X and Y Axis
X: TimeY: Voltage
ECG Small Box, Big Box
Small Box: 0.04sBig Box: 0.2s (equal to 5 small boxes)
Normal QRS Axis
Between -30 and +90 degrees
Increased Voltage in ECG
- Normal 0.5 to 2.0mV- Commonly caused by ventricular hypertrophy
Decreased Voltage in ECG
- Decreased Muscle Mass- Pericardial Effusion: Fluid shorts the currents- Pulmonary Emphysema: Excessive air in lungs act as insulators
Prolonged QRS Complex
- Cardiac Hypertrophy or Dilation: Increased distance for current to travel to depolarize- Purkinje System Blocks
T Wave Abnormality
Caused by conduction blocks, premature contractions or prolonged depolarizatoin
Tachycardia
> 100 BPM- Increased temperature- Sympathetic Stimulation
Bradycardia
< 60 BPM