Term
the pathway of electrical conduction of the heart |
|
Definition
SA node--> depolarize the ventricles--> AV node--> through the AV bundle-->to the left and right bundle branches--> to the purkinje fibers-->to the cells of the ventricles |
|
|
Term
What occurs during the AV node bottleneck delay? |
|
Definition
the ventricles fill with blood |
|
|
Term
what physically causes the AV nodal delay? |
|
Definition
decreased numbers of gap junctions in the AV node, also the fibrous tissues between the atria and ventricles act as a insulator |
|
|
Term
Where is cardiac impulse conduction the fastest? |
|
Definition
|
|
Term
the fast conduction of the purkinje fibers promotes what? |
|
Definition
coordinated ventricular contraction |
|
|
Term
Where the cardiac impulse is conducted the slowest? |
|
Definition
|
|
Term
the ion that causes the plateau period during ventricular AP |
|
Definition
|
|
Term
the ion that causes promotes repolarization during ventricular AP |
|
Definition
|
|
Term
WHat cases the large spike during ventricluar AP |
|
Definition
|
|
Term
THese occur during which phase Slow voltage-gated Ca++ channels (L-type) open Ca++ influx Voltage-gated K+ channels close reduce K+ efflux, however ungated K+ channels still open Inward Ca++ current is balanced by outward K+ current Ca++ influx contraction + release Ca++ from SR |
|
Definition
Phase 2 plateau period of ventricular contraction |
|
|
Term
What occurs during the Phase 1 dip of ventricular AP |
|
Definition
Partial repolarization due to close Na+ channels and opens of K+ channels |
|
|
Term
The conduction of the action potential through the heart is slowest in the |
|
Definition
|
|
Term
A patient received a heart transplant from a healthy donor and it is routine that the surgeon leaves the transplanted heart unconnected to the patient’s autonomic nervous system. What do you predict will be the patient’s resting heart rate when fully recovered from the operation? |
|
Definition
|
|
Term
What causes the phase 2 in ventricular action potenital |
|
Definition
Slow voltage-gated Ca++ channels (L-type) open Ca++ influx Voltage-gated K+ channels close reduce K+ efflux, however ungated K+ channels still open Inward Ca++ current is balanced by outward K+ current Ca++ influx contraction + release Ca++ from SR |
|
|
Term
what causes phase 1 (dip) in ventricular AP |
|
Definition
partial repolariztion due to the closing of Na channels and the opening of K channels |
|
|
Term
Phase 3 repolarization of ventricular AP |
|
Definition
Ca++ channels close stop Ca++ influx Voltage-gated K+ open K+ efflux |
|
|
Term
Phase 4 AP is caused by (rest/ reload) |
|
Definition
Stable resting membrane potential due to high K+ permeability |
|
|
Term
why can't cardiac musle go into tetani |
|
Definition
because the absolute and the relative refractory preriod are almost as long as the AP |
|
|
Term
what is a common mechanism for arrhythmia |
|
Definition
abnormal waves of conduction through the heart |
|
|
Term
Long QT syndrome leads to |
|
Definition
ventricular tachycardia and sudden death |
|
|
Term
What can the physician do to prevent sudden death in these patients with Long QT syndrome ? |
|
Definition
|
|
Term
What symptoms is a patient with ventricular tachycardia likely to experience? |
|
Definition
light headed, heart flutter, decreased pump efficiecny |
|
|
Term
for which part of the heart is the resting potential losest to threshold |
|
Definition
|
|
Term
|
Definition
Phase 0: upstroke phase Phase 3: repolarization Phase 4: spontaneous depolariztion and pacemaker potential |
|
|
Term
what happens during phase 0 of SA node AP? |
|
Definition
slow voltage gated Ca channels T-type open and calcium enters the cell |
|
|
Term
what happens at phase 3 of SA node AP? |
|
Definition
voltage gated K channels open and K leaves the cell |
|
|
Term
what occurs during phase 4 of SA node AP |
|
Definition
there are multiple mechanisms 1. FUnny sodium current 2. Calcium current 3. Potassium current |
|
|
Term
hyperpolarization-activated Na channels open causing Na to enter and is modulated by cAMP, ACH, and NE |
|
Definition
|
|
Term
L-type and T-type channels cause an inward calcium current SR-mediated ----- channels |
|
Definition
|
|
Term
decreased K conductance promotes depolarization |
|
Definition
|
|
Term
If your patient does not have a normally functioning ‘funny’ (If) current (hyperpolarization-actived sodium channel); what do you expect the patient’s resting heart rate to be ? |
|
Definition
there would be a decreasein heart rate because less Na channels are available to cause depolarization |
|
|
Term
Why does the SA node set the pace or rate of electrical impulses through the heart ? |
|
Definition
because it has the most rapid phase 4 depolarization |
|
|
Term
Given the intrinsic rate of the SA node; what keeps the normal heart rate 60-90 bests/minute ? |
|
Definition
the vagus nerve of the parasympathetic autonomic nervous system |
|
|
Term
An Atrial Tachycardia is causing too rapid a ventricular rate and causes fainting. What site along the conduction pathway is the best target to slow the ventricular response? |
|
Definition
the best place to control is the AV node because there are multiple autorhymic sites in the atria |
|
|
Term
Based on your knowledge of the cellular physiology of SA and AV node Phase 4 depolarization ; what do you predict may happen to the patient’s A-V conduction when you administer a drug for an atrial tachyarrhythmia that: |
|
Definition
blocks nodal L-type calcium channels ? reduces nodal cAMP levels ? |
|
|
Term
Patient symptomatic due to rapid ventricular response to atrial tachyarrhythmia. Application of Physiology Principles Therapy -- further delay A-V node conduction |
|
Definition
the target would be the Phase 4 channels
Adenosine (reduces cAMP) this reduces Na influx frim the funny channels and enhances K efflux
Verapmil block L tpye calcium channels reducing Ca influx |
|
|
Term
What is the mechanism underlying the effect of parasympathetic nerve activation and acetylcholine release on the SA node rate ? |
|
Definition
Ach slows the heart rate by activating the G-protein coupled muscarinic receptor to modulate several pathways in the SA nodal cells: Decreases Na+ influx via If ‘funny current’ (If current reduced by Ach-induced decrease in cAMP) Decreases Ca + + influx Increases K + efflux |
|
|