9/1 Electrochemistry of the heart Flashcards
what are the waves of the normal heart EKG
P,R,Q,S,T
what is the normal activation sequence of the heart?
SA node — Atria — AV node — His bundle — bundle branches — Purkinje fibers — ventricles.
what are the two types of cells in anormal heart
working cells and the specialized cells
working cardiac cells
contract and impart energy and import a stroke volume
what are the specialized cells in the heart:
SA, AV, His, BB, Perkinje fibers
job of Specialized cells in the heart
to initiate the electrical signal and to propigate that electrical signal through the cell.
what is the SA node
the node of speical cells on top of the right atrium that is the dominant pace-maker of the heart.
How could the signal get to the rest of the heart form the SA node
the AV node in the bottom of the Right atrium into the ventricle. The only path from the atrium to the ventricle.
why delay the activation of the ventricle
to time the distole/systole correct
what is the path from the RA to the RV/LV electricly
SA node, then AV node, then His bundle then bundle branches then purkinje fibers
where is the electrical signal slow or rapid in the heart?
slow in the SA to AV node, and fast everywhere else
what is automaticity
the ability to fire spontaniousley
what cardio cells have automaticity?
the Specialized cells: SA, AV, His, BB, Purkinje fibers
what are the phases of cardiac action potentials?
phase 0: upstroke, rapid dpolarization; Phase 1: rapid repolarization following the peak; Phase 2: the plateau; Phase 3: rapid repolarizatio following the plateau; Phase 4: period between the maximum negativity (diastolic potential) and the upstroke of the next action potential.
how do the activation sequence of cardiac specialization cells look different than working cells?
the specialization cells depolarize during phase four of the cycle, leading to spontaneous APs and pacemaker activity
what is the dominant pace maker of the heart?
the SA node
what property of the SA node make it a pace maker
phase four of the activation sequence is shortest among the specialized cells.
describe the sequence of electrical activation in the heart.
P2
how does the sypathetic nervous system or epinepherin/neuroepinephrin change the activation of the SA node
it increases the rate of depolarization
how does a lower pacemaker represent a safety mechanism
the lower pacemaker has a lower fate of spontaneous firing, that will take over the rate if the SA node doesn’t fire
what is less than 60 beats per minute in heart
bradycardia
what is greater HR than 100
tachycardia
where does the electrical activity recorded on the skin come form in the heart
the depolarization of the atrium (P); the depolariztion of the ventricle (QRS) the repolariztion of the ventricle (T)
what is the p wave
depolarization of the atrium
what is the q, R, S wave
depolarization of the ventricle
what is the T wave
the repolarization of the ventricle cells
what are the two big parts of info in an EKG
how long does it take to get to different parts of the heart. How does the signal move through the heart (vector direction)
what does the width of the P and QRS wave tell us
the atrial and ventricale cells take time to depolarize, and wider peak is a longer delay
where does the activation sequence fit into the ECG signal and what are the common intervals of the ECG?
P1
why do we have a space between the P and QRS? (P-R interval)
the activation of the AV node
what would the time interval between P and QRS tell us
the conduction through the AV node is properly timed
what woud the S-T segment tell us
reflect action potential duration. elevation or depression frequently occurs during acute myocardial infarction.
what would the Q-T interval tell us
action potential duration, where a block of potasium flux to depolarize the AP would lead to a long Q-T syndrome!
what if we block Na channels in heart cells
prolong QRS duration since the QRS duration reflects the action potential propagation through the ventricles.
what would highper cholemia do to the ECG
slow the action potential duration and get long long Q-T syndrome!
whould would bundle branch block, ventricular hypertrophy, and severe hyperkalemia lead to?
prolonged QRS duration due to a longer time to electrically activate the ventricles.
what is the basis of the electrical dipole that is measured by the ECG
dipoles form in the cells due to cells of different Vm and therefore different membrane potentials being near another; and these will then sum together to give an average dipole as the difference in potential propagates.
wwhat is the direction of the dipole
towards the resting cells or towards the positive extracellular potential.
what is the dipole once all of the cells are depolarized
ZERO!!! there is only a dipole when cells of different external membrane potential are in close proxcimony.
when do you get an EKG signal
when the depolarization wave moves through the cell so that some of the cell is depolarized and some is not. This difference in polarization in the cell makes the dipole whose magnitude is measured by the ECG
what if the dipole signal is in the same direction as your leads are oreinted, or in the opposite, or half way between?
maximum signal; minumum signal; Isoelectric signal
as the cell depolarizes and is half way depolarized what is the EKG signal doing
the signal is at its peak
