How is the basis for an AP different for an SA node than other cardiac cells?
1. Automaticity: spontaneous generation of AP without neuronal input
2. Unstable resting membrane potential: Phase 4 (because of constant Na+ leak out that depolarizes cell)
3. No sustained plateau
Difference in the SA node phases than other cardiac cells
-upstroke is not as steep as in other cardiac cells
-results in inward Ca++ current NOT Na+ current
Phases 1 and 2 are absent
Phase 3: is a result of K+ flow OUT
-longest portion of the SA AP
-also called the "PACEMAKER POTENTIAL" since it accounts for the automaticity of the SA node
What is the "pacemaker potential"
Membrane potential in SA node only goes down to -65 mV and it does not remain a constant at this value
*instead there is a slow depolarization produced by opening of Na+ channels and an inward current
How is the inward flow of Na+ in the SA node upheld?
Inward current is turned on by the repolarization phase of the preceding AP, ensuring that each AP in the SA node is followed by another AP
each AP automatically sets up next AP so that the heart constantly beats - keeps going
What phase in the SA node determines the heart rate?
Rate of phase 4 depolarization sets the heart rate
when rate of depolarization increases, the threshold potential is reached sooner, and the heart rate increases
Normally phase 4 is slow, the sympathetic stimulation increases the depolarization whereas parasympathetic decreases this polarization rate
Cardiac Pacemakers: SA node
Cells that undergo spontaneous Phase 4 depolarization can function as pacemakers in the heart
SA node is the normal pacemaker since it has the fastest rate of phase 4depolarization
Also has the shortest AP (and therefore the shortest refractory period) --> so recovers faster and is ready to fire another AP before other cell types are ready
When the SA node drives the HR, other potential pacemakers are suppressed (this is called overdrive suppression)
When the SA node drives the HR, other potential pacemakers are suppressed
Pacemakers other than the SA node can also drive the heart (ie AV node, Bundle of His, Purkinje fibers)
*Latent pacemakers can drive the heart rate if:
1. the SA node is suppressed
2. the intrinsic firing rate of the latent pacemaker becomes faster than the SA node (ie due to injury)
Intrinsic rates of latent vs SA pacemakers
The intrinsic rate of latent pacemakers are slower than the SA node (slower the further down the path you go): as a result the heart will beat at a lower rate than if the SA node was in charge
when a latent pacemaker takes over and becomes the pacemaker of the heart
(so either because SA becomes below resting threshold, or during injury one of the latent pacemakers has acquires a threshold that goes above that of the SA)
Positive Chronotropic effects
Release of norepinephrine from the sympathetic nerve fibers activates Beta1 R in the SA node
POSTIVE CHRONOTROPIC EFFECTS RESULT IN INCREASED HR
increased rate of Phase 4 depolarization
cells are less depolarized (takes less time to reach threshold potential)
Negative Chronotropic effects
Release of ACh from parasympathetic nerve fibers activates M2 muscarinic R in the SA node
NEGATIVE CHRONOTROPIC EFFECTS RESULT IN DECREASED HR
decreased rate of phase 4 depolarization
cells are more hyperpolarized (take more time to reach threshold potential)
threshold potential is increased
Define the refractory Periods and which is the most important for ECG arrhythmia
ARP: absolute refractory period - NO stimulus can contract an AP again at this pont
ERP: effective refractory period - can not be stimulated again with a normal impulse only with a high one
RRP: relative refractory period - normal impulse can activate an increase in HR again
SNP: supranormal refractory period - a less than normal impulse can stimulate a reaction again * (worry about R on T phenomina in ECG)
Measurement of tiny potential differences on the surface of the body that reflect the electrical activity of the heart since the entire myocardium is not depolarized all at once we are able to measure depolarization and repolarization
What are the steps to contraction?
1. Atria depolarize before the ventricles
2. Ventricles depolarize
3. Atria repolarizes (while ventricles are depolarizing)
4. ventricles repolarize
as a result of the timing and spread of the action potentials in the heart, we are able to measure the potential differences that are established between different portions of the heart
Represents Atrial depolarization
duration corresponds with conduction through the atria
repolarization is not usually seen (hidden in QRS complex)
usually a positive deflection on lead 2 ECG
What does width of an ECG indicate?
width means the time it takes for AP to conduct through that part of the heart
Consists of 3 waves: Q, R, and S waves
Represents ventricular depolarization
Usually a positive deflection on lead 2 ECG
T - Wave
Represents ventricular repolarization
can be positive or negative deflection on lead 2 ECG
What does body position do to waves?
cant change duration
BUT changes the size of the wave
usually measured using a unipolar lead (1 direction)
uses an "exploring" electrode connected to an "indifferent" electrode
Depolarization that moves towards an exploring electrode produces a positive (+) deflection on the ECG --> depolarization in opposite direction produces a (-) deflection
Normally the AP travel from the base of the heart (SA node) towards the apex (ventricles)
as a result, we generally see positive deflections on lead 2 for most of the waves
Where do the three leads go?
Lead 1: right forelimb to Left forelimb
Lead 2: Right forelimb to left hindlimb
Lead 3: Left forelimb to left hindlimb
- 2 categories of abnormalities
-how it can happen
Abnormalities in: Heart rate, regularity, or site of origin of cardiac impulse
Disturbance in conduction of the impulse, such that normal sequence of activation of the atria and ventricles is altered
Conduction may be *altered or *ectopic pacemakers can "take over"
What are the three steps to ECG interpretation?
Step 1: Determine the HR
Step 2: determine if it is supraventricular or aventricular rhythm
Step 3: determine how regular the rhythm is
Goal of an ECG
The goal is to diagnose the rhythm and decide if any therapy is required
How to achieve step 1 of an ECG interpretation
Step 1: what is the heart rate?
"ticks" are 3 seconds apart when printed at 25 mm/s (pr at 50 mm/s but always 3 s apart)
Count the number of QRS complexes over 6 seconds and multiply by 10
Is the rate fast? slow? normal?
Tachycardia: too fast HR (conduction = faster than normal)
Bradycardia: too slow HR (conduction = slower than normal)
How to achieve step 2 of an ECG interpretation
Step 2: supraventricular or ventricular?
It is important to determine where the beats are coming from since the prognosis and treatment are different
Is there a P wave for every QRS complex, and a QRS complex for every P wave?
There needs to be a P wave for rhythm to be supraventricular (atria contraction, if there is no P wave then contraction is coming from ventricles)
IF there is no P wave we need to find out where the QRS complex is coming from
Supraventricular are usually not as serious
-cardiac output not as compromised
-less chance for fatal arrhythmia
-usually only treated if severe or patient is showing signs
Ventricular are usually serious
- compromises cardiac output, can lead to cardiac arrest
- worry more about risk of "R on T phenomenon"
- monitor patient closely, treat sooner than later
when are heart attacks prone?
Heart attack is prone when ventricles are repolarizing and get an impact from another area
"R on T impulse" ***
Happens in supranormal refractory period
when impulse from somewhere else in heart comes and impacts current impulse: sets out of order contraction
How to achieve step 3 of an ECG interpretation
Step 3: is the rhythm regular or not?
Look at the R to R intervals on the ECG trace
-can also auscultate the heart or palpate the pulses
Is the rhythm regular?
If it is irregular is it: regularly irregular (regular with breathing)? or irregularly irregular (cant predict rhythm)?
ST segment depression
look at the duration of the PR interval to determine how long it takes for the AP to travel from the SA node to the ventricles
ST segment depression
Does not become "isoelectric" (resting electrical level) between the S wave and the T wave
Sign of myocardial hypoxia (inadequate oxygenation of the heart muscle itself)