Trachte/Nordgren Week 3 Flashcards
What do sympathetic nerves innervate to elevate HR, SV and TPR?
atria, ventricle, arterioles and veins
What is the major effect of the sympathetic nervous system?
elevate blood pressure
What is the equation for BP?
HR x SV x TPR
Steps to synthesis of norepinephrine?
Tyrosine to DOPA to Dopamine to Norepinephrine to Epinephrine (adrenal medulla)
What is the rate limiting step in norepinephrine production?
tyrosine hydroxylase (cystolic)
What is an inhibitor of DOPA carboxylase?
carbidopa
What are the 3 deviations that can cause an arrhythmia?
change in rate of impulse, impulse site of origin or conduction of the impulse
What is the equilibrium potential of K?
-90mv (wants to move out of cell)
What is the equilibrium potential of Na?
+70mv (wants to move into cell)
What is the key factor in pathophysiology of arrhythmias and the drugs that treat them?
relation between RESTING potential of a cell and the number of ACTION POTENTIALS that can be evoked
What is the range where Na channel inactivation gates close?
75 to -55mV
What is the time between Phase 0 and sufficient recovery of Na+ channels in Phase 3 to allow another action potential?
Refractory Period
In what phase do Na channels recover from inactivation and become available?
During repolarization in phase 3
What happens at optimal conditions when you add a drug that blocks Na channels?
total number of channels available at optimal conditions will be decreased
What happens at suboptimal conditions when you add a drug that blocks Na channels?
Na channels will be unavailable dt inactivation gate closure AND drug blockade
What happens to Na channel recovery time with depolarization of membrane potential? Why?
Increases; depolarized cells recover more slowly and increases the refractory period of the cell
What phase of a pacemaker cell is the more important factor of the two on HR?
diastolic interval
What 2 things can you do to slow the pacemaker?
- alter slope of diastolic interval 2. hyperpolarize diastolic interval
What can you do to speed the pacemaker?
alter slop of diastolic interval
What are membrane voltage oscillations that result in transient, abnormal depolarizations of cardiac myocytes during phase 2, 3, or 4 of the cardiac AP
Afterdepolarizations
Define an early afterdepolarization
occur during action potential and interrupt orderly repolarization of myocyte
What is the cause of a late phase 2 early afterdepolarization?
opening of more Ca channels
What is the cause of a late phase 2 early afterdepolarization?
opening of sodium channels
What can happen dt inhibition of K channels?
early afterdepolarization
If early afterdepolarization is exacerbated at slow heart rates what can occur?
torsades des pointes and tachycardias
Define a delayed afterdepolarization
occur after action potential, when nearly or fully repolarized, but before another action potential would normally occur
What causes a delayed afterdepolarization?
elevated cytosolic Ca levels dt overload of SR spontaneous release of Ca and leads to depolarizing current
When is a delayed afterdepolarization exacerbated?
at fast heart rates
When do blocks occur?
if the electrical signal is slowed or disrupted as it moves through the heart
Define a partial blockage of impulse conduction?
electrical impulses are delayed and/or occasionally stopped
Define a complete blockage of impulse conduction?
electrical impulses are completely stopped
Define reentry impulse conduction disturbance? What is another name for this?
impulse reenters and excites areas of the heart more than once; aka circus movement
What type of block prevents passage of an impulse when it approaches form one direction but not from the other?
unidirectional block
What type of block prevents passage of an impulse in both directions?
bidirectional block
What 3 things must happen in order for reentry to occur?
- obstacle (anatomic or physiologic) to homogenous conduction 2. unidirectional block at some point in the circuit 3. conduction time must exceed the effective refractory period
Name an abnormal electrical accessory connection b/w atria and ventricle
bundle of kent
A form of reentry that is strictly anatomical?
Wolff-Parkinson-White Syndrome
What happens dt Bundle of Kent?
allows for impuls to be conducted without going through AV node, causing ventricle to prematurely contract; conduit for reentry to the atria
How does slow conduction lead to no reentry?
bidirectional block
How does too fast conduction (almost normal) lead to no reentry? why?
bidirectional block; impulse travels around unidirectinoal block too quickly and reaches tissue that is still refractory so no reentry
What causes slowing conduction?
decreased Ca current or decreased Na current
What is the action of Na channel blockade (Class 1 drugs)?
alters AP duration and kinetics of Na channel blockade
What is the action of B-adrenoceptor blockade (Class II drugs)?
blockade of SNS effects in the heart
What is the action of K channel blockade (Class III drugs)?
prolongation of the effective refractory period
What is the action of Ca channel blockade (Class IV drugs)?
slows conduction where depolarization is Ca dependent
When do use or ‘state dependent’ drugs bind?
bind to activated (phase 0) or inactivated (phase 2); bind poorly or not at all to rested channels
When do ‘use’ or ‘state dependent’ drugs block electrical activity?
fast tachycardia (many channel activations), significant loss of resting potential (many inactivated channels during rest)
What happens as a result of Na and Ca channel blockade?
slow conduction speed to bidirectional block to no reentry (steady state reduction in # of available unblocked channels which reduces excitatory currents to a level below that required for propagation)
What happens as a result of K channel blockade?
slow conduction speed to bidirectional block to no reentry (prolongation of recovery time of the channels still able to reach the rested and available state, which increases refractory period)
