Exam 4 - Lecture 7 Flashcards
If the APs are generating faster than normal, this means we have a
abnormal pacemaker
Definition of arrhythmias
problems with conduction system of the heart or how the APs travel through the heart
5 causes of cardiac arrythmias
Abnormal rhythmicity of pacemaker
Shift of pacemaker from sinus node
Blocks at different points in transmission of cardiac impulse
Abnormal pathways for transmission
Spontaneous generation of abnormal impulses from any part of the heart
ectopic pacemaker
site within heart other than SA node that is generating heartbeats
Moving the VRm closer to threshold potential in pacemaker cell can
fire an early AP
Generally speaking, increase VRm causes
the heart to not completely reset itself
If VRm increaes at AV node, it may
fire an AP early before the SA node does, causing an arrythmia
Anything that increases VRm, will
increase risk of arrythmia
Tachycardia is due to a
abnormal SA node
Sinus tachycardias will have _____ in the normal orientation with a ____ PR interval.
P-wave; short
NSR officially becomes sinus tach at
101bpm
Why does increased body temp cause a abnormal rhythm?
sinus tach, due to increased energy demands
Causes of sinus tach in relation to nervous system?
overactive SNS, underactive PNS
If you have co-arrythmias, what can you do to combat the sinus tach associated with them?
d/t decreased stroke volume from arrythmia, heart may try to speed up to compensate. Need a beta blocker to combat that as long as a med to help with arrythmia.
Toxic conditions of heart leading to sinus tach (SA node)
Acidosis, nicotine, alcohol
Why do athletes have bradycardia?
Large stroke volume
physiologically large heart d/t athletic training
3 Causes of bradycardia
athletes
vagal stim
nerual reflex to drugs
Generally speaking, the higher your resting heart rate, the
worse off your heart bc it probably has a lower stroke volume
High heart rate is usually d/t
hyperthyroidism
What usually accomplishes bradycardia? vagaling or decreasing SNS?
increasing vagal stimulation
If you pump someone full of phenylephrine to drive the BP up, the baroreceptors detect that and will
slow heart rate down, reflex bradycardia.
Paroxysmal atrial tachycardia characteristics
Abnormal atrial excitation, SA nodes are firing irregularly, P and T waves overlap d/t timing, morph into eachother.
What are drug tx for paroxysmal atrial tachycardia?
Vagal reflex, beta blocker, digoxin
Sinoatrial block
impulses from SA node are blocked, may be from ischemia and cant reset its VG ion channels.
Causes cessation of P-waves, or inverted p-wave
usually results in AV node controlling heart rate.
What determines whether P-wave is inverted or absent?
Where it comes from in the AV node.
Early part of AV node: inverted
Late part of AV node: absent
Why is the p-wave absent if it comes from later part of AV node?
takes so long for the retrograde current to reach the rest of the tissue, it gets masked by ventricular current.
Main issues that arrythmias cause physiologically with the heart
reduces stroke volume from abnormal beats
AV valves aren’t in correct timing, so they may be closed, causes turbulence, may damage/calcify the valves, cause blood clots.
Atrioventricular block
AV node and AV bundles of his are slowed or blocked.
normal PR interval
0.16
Causes of atrioventricular block (5 things)
-Ischemia of AV node or AV bundle (raises VRm, less VG ion channels participating in AP)
-Compression of AV bundle by scar tissue or calcified tissue, maybe from CHF or an MI from fiberblasts laying down scar tissue, also creates a smaller inner diameter, causing slower APs
-AV nodal or AV bundle inflammation
-Excessive vagal stimulation (such as five and dien)
-Excess digitalis/beta blockers
How does digitalis work
Sodium/K ATPase inhibitor, causing excess sodium in heart cell, decreasing the sodium gradient, increased VRm
Last HF drug you get put on is
digitalis, because it affects such an important mechanism of the heart, and it affects other systems.
1st degree heart block
Increases PR interval to > 0.20 seconds.
- just a delay, not losing any QRS complexes or anything like that.
2nd degree heart block
PR interval increases to 0.25 - 0.45 seconds
- some impulses pass through AV node, some dont.
- Dropped beats.
- Atria has a faster rate than Ventricles.
- wenkebach, mobitz type I
Mobitz type I/wenkebach
type of 2nd degree heart block, irregular PR interval,
1st PR interval after dropped beat is normal
2nd degree heart block
- mobitz type II, fixed P-wave to QRS complex ratio, fixed PR interval on the the QRS complexes we do have. (may be 2:1, 3;2, 3:1, etc.)
- 0.25 - .45 seconds
- dropped beats
- need a pacemaker
Which of the heart blocks is more dangerous?
2nd degree
How do you treat 2nd degree heart block?
Pacemaker
Complete heart block: 3rd degree
Total AV nodal or bundle of his block
-complete dissociation of QRS from P waves
- Ventricular escape @ 15-40bpm
- Atrial rate elevated
why is the atrial rate elevated in complete heart block?
Body senses decreased cardiac output from low heart rate, speeds up the atrial rate in response.
Atrial flutter
Circular reentry in atria that is completely separate from SA node
- really slow conduction rate in atria with circular movements, and the AP are going around in a slow circle and not waiting around for SA node to fire AP.
- it’s a slower conduction rate, cause if it was faster, the AP would run into tissue that’s in refractory period, and if it’s in complete refractory period it wouldn’t allow circular movement.
What increase likelihood of a-flutter?
When the conduction is slow, and When the atria is all stretched out, the electricity has a longer pathway to take, and less likely to hit refractory period/makes it a slower conduction rate.
The net result of a-flutter is
High atrial and high ventricular heart rates
Does A-flutter have a P wave?
No, there’s no normal pathway for the P-wave to exist.
Atrial fibrillation
Stretched out atria, No defined pathway for electrical current, bunch of ectopic pacemakers, and all firing on their own. It’s uncoordinated and irregular. Causes lots of turbulence in atria, causing blood clots in the atria.
What can cause a PE?
Blood clot in right atria, dislodging and being sent into right ventricle, into pulmonary circulation.
Factors to cause A-fib
Usually age, stretching out the atrias
Treatments for A-fib
Ablation, blood thinners for blood clots, anti-arrhythmics
What are circus movements?
During a-fib, got action potentials running in all different directions
Stokes-Adams syndrome
HEREDITARY, causing fainting/syncope d/t low BP/stroke volume.
-irregular complete AV block at random times. Ventricular pacing has to take over, takes 5-30 seconds for that to kick in and help you regain consciousness.
Takes 7-8 seconds to pass out
What does your heart rate return to after stokes-adams syncope episode?
15-40 as the ventricles are taking over pacing.
Incomplete intraventricular block
Called Alternans.
- slowed conduction in purkinje system.
- occurs every other heart beat, the abnormal beats are smaller and wider QRS complexes
- more likely during ventricular tachycardia
- tissue is not fully repolarizing itself as fast as it normally would, so that’s why they’re smaller.
- ischemia and digitalis prevent full resetting of purkinje system
- p-wave being hidden in T-wave
Premature contractions: atrial source
Ectopic tissue in atria firing early APs
-result from ischemia, irritation, or calcified plaques
-radial pulse deficits, early depolarizations result in less filling time, lower SV
Premature contractions: AV nodal/bundle source
Missing P wave during premature beat cause it’s coming from AV mode, originates from middle AV junction and P-wave gets obscured by QRS complex
For premature contractions from AV node/bundle source, p-wave early and inverted means it came from ______. Late and inverted came from ______.
High AV junction; Low AV junction (but should be hidden in QRS)
PVCs
Prolonged QRS due to slower conduction speed of ventricular muscle
Taller QRS due to ventricles pumping at separate times, causing an additive affect on the current reading.
T-wave is usually inverted after PVC QRS
caused by caffeine, nicotine, stress, lack of sleep
Ventricular tachycardia: paroxysmal
QRS originating within ventricles, high voltage prolonged QRS, No normal QRS interspersed, dangerous and usually requires infarction, initiates V-fib. P-waves are not visible or inverted.
Ventricular premature depolarization
EAD, DAD, early AP initiation, very inefficient pumping, looks like a long QT interval.
What predisposes ventricular premature depolarization?
Beta adrenergic agonists, mACh-r antagonists
Taking too much Benadryl will cause
Long QT prolongation
What looks like mACh-r?
Histamine receptors, so the anti/histamine Benadryl binds to mACh-r
Repetitive ventricular premature depolarization can lead to
Torsades de pointes
Torsades de pointes is a precursor to
V-fib
If the stroke volume is low enough, what happens to coronary arteries?
Coronary blood flow comes from the aorta, so if that blood pressure is low from low ventricular output, then none of the tissues repolarize and are ischemic
Re-entry sources
Accessory pathways, bundles of Kent (extra tissue that connects ventricles to atria, is in 0.2% of the population).
