3 - Cardiac Excitation (Kim) Flashcards
Why do the Atria and Ventricles not contract simultaneously?
What is automaticity?
What is Rhymicity?
To allow atria to empty prior to ventricle contraction
Automaticity = Ability to initiate own beat
Rhyhmicity = Regularity of pacemaking activity
**What is the conduction pathway and the major players in the heart?**
Start: Sinoatrial (SA) Node - “Pacemaker”
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Atrioventricular (AV) Node - “Relay”
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Bundle of His - “Tunnel”
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Bundle Branches (R/L)
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End: Purkinje Fibers - “Fastest!”
What is the only electrical conduction between the atria and ventricles?
AV Node
How do depolarizations spread in the heart?
Cell to Cell
What is the purpose of the Anterior and Middle Tracts?
What is the purpose of the Brachmann Bundle?
Connect SA to AV Node
Connects the Right and Left Atria
Bundle of His
Continuous with AV node; gives off left bundle branch at top of interventircular septum and continues as right bundle branch
Left and Right Bundle Branches
Contact Purkinje System, whose fibers spread to all parts of ventricular myocardium
Purkinje Fibers
Transmits electrical impulses through ventricular system
Fastest signal transduction, synchronized contraction of both ventricles
What ais the fastest and slowest signal transduction in the cardiac conduction system?
Fastest = Purkinje Fibers
Slowest = AV Node
Within the cardiac tissue, how does the conduction spread in the heart?
Depolarizations spread from Endocardium to Epicardium
Sympathetic Control of Heart
Increased activity Raises heart rate
NT: Norepinephrine stimulates B-1 Adrenergic Receptors
Inreases rate of Phase 4 Depolarizations
Parasympathetic Control of Heart
Increased parasympathetic activity diminishes heart rate
NT: Acetylcholine (ACh) activates Muscarinic (M2) receptors in SA node.
Decrease in rate of Phase 4 Depolarizations
Increases OUTWARD K+ current; hyperpolarizing maximum diastolic potential (makes it harder to fire Action Potentials)
Temperature influence on SA Node?
Increase rate with increase in temperature
Tachycardia associated with fever
Digitalis (drug) influed on SA node?
Strengthen contractility; increase AV node conduction velocity
Latent Pacemakers
AV Node / Bundle of His and Purkinje Cells exhibit automaticity less than SA Node
Blocked by Overdrive Supression
Overdrive Suppression
SA Node initiates 70-80 BPM; which is faster than Latent Pacemakers (AV Node/Bundle of His/Purkinje); thus supressing their firing rate
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If SA Node (or downstream) get’s broke, it can dork this up
Mechanisms of Tachyarrythmias (increased firing rate)
Increased Automaticity of SA Node (pacemaker)
Increased Autmaticity of Latent Pacemakers (AV/Bundle of His/Purkinje)
Abnormal Automaticity (disease state)
Triggered Activity
Unidirectional Block and Reentry
Mechanisms of Bradyarrhythmias (decreased firing rate)
Altered Impulse Formation: Decrease Automaticity of SA Node (pacemaker)
Altered Impulse Conduction: Conduction Block
How can Sinus Node Automaticity be altered?
Increase: Increase Sympathetic Activity (normal during exercise)
Decease: Increas Parasympathetics, or Decrease Sympathetic
B-Blockers slow heart rate
Escape Rhythms
Escape Beat
If SA Node becomes too suppressed, Latent Pacemakers may take over (overdrive supression lost)
Continued series of escape beats = Escape Rhythm
Escape Beat = impulse initiated by latent pacemaker
Junctional Escape
Escape beats arise from AV Node or proximal Bundle of His
Moderate Parasympathetic Stimulation slows the SA Rate, and allows pacemaker to shift to the AV Node
Ventricular Escape
Beats arise from distal end of conduction system
Very strong Parasympathetic stimulation suppresses both SA and AV Nodes
Usually 15-40 BPM
What can enhance automaticity of latent pacemakers?
(Ectopic Beat, Rhythm)
High Catecholamine Concentrations
Hypoxemia, Ischemia, Electrolyte Disturbances
Certain drug toxicities
How may myocytes play a role in Ectopic Beat or Ryhthm formation?
When myocytes become injured (ischemia, etc), their membranes become leaky
Unable to maintain gradients, become easily depolarize
