Lecture 11/1: EKG interpretations Flashcards
End test 4
What is an arrhythmia?
A problem with the conduction system or APs going through muscle of the heart
What are some causes of arrhythmias?
- Abnormal firing of pacemaker (faster or slower)
- Shift of pacemaker from sinus node
- Blocks at different points of transmission
- Abnormal pathway transmission
- Spontaneous generation of abnormal impulses
T/F: increasing Vrm closer to threshold potential, especially in pacemaker cells, increases the likelihood of firing a spontaneous AP from etopic pacemakers and cauing an arrhythmia.
T
______ K+ will decrease the concentration gradient. This will _______ the Vrm, which will increase HR.
Increasing
Increase
T/F: Things that increase Vrm prevent the heart from reseting/repolaring correctly
T
Keep looking at this card
When will the AP fire if the Vrm is raised?
Early
This will cause an arrhythmia
T/F: in a healthy heart, the ventricles generates the AP
F
SA node does
What increases the likelihood of in arrhythmia?
Increasing Vrm
What are 2 things that can cause an increase in Vrm?
- Ischemia/Infarct
- Increase K+
Sinus Tachycardia: where does it originate?
SA node
Sinus Tachycardia: what is a characterized by?
Fast HR
P waves at a rate of greater than 100 bpm
Sinus Tachycardia: Causes:
- Increased body temp
- sympathetic stimulation
- loss of vagal stimulation of PNS
- Toxic conditions in heart
How does increased body temperature cause increase HR?
Increased body temp –> increase metabolic demands –> increased HR
Why does blood loss initially increase HR?
BP will drop –> info in fed to CNS –> ANS will tell heart to beat faster.
What compensatory mechanism do some arrhythmias have? What medication can you give to combat this?
Reflex activation of the SA node resulting in reflex sinus tachycardia
Beta blocker (-olol)
Sinus Tachycardia: describe the P & QRS complexes
RR intervals
There is a P for every QRS complex
Short RR intervals
What are toxic conditions in the heart that can increase Vrm?
Nicotine
Alcohol
Increased K+
Acidosis
NAKA
(create toxic conditions at SA node)
Sinus Bradycardia: where does it originate?
SA node
Sinus Bradycardia: what is a characterized
Slow HR
P waves at a rate of less than 60 bpm
Describe why Sinus Bradycardia is normal in athletes
D/t training, physiologically, they have a larger heart. Because of this, their SV is larger as well causing them to have a larger CO. The CNS senses this and the ANS slows down the heart rate so the body can have the proper CO needed (and not more than needed)
T/F: if you are healthy and have a lower resting heart rate, this is a problem
F
This is a good thing, unless dangerously low.
If your resting heart rate is _____, this is bad.
high
What are some common problems associated with high resting heart rate?
Hyperthyroidism
Valve problem
Sinus Bradycardia: Causes:
- Vagal stimulation (PNS)
- Decreases SNS tone
- Neural reflex to drugs (Ex. Lots of phenephrine –> vasoconstriction –> ANS decreases HR to decrease CO)
Sinus Bradycardia: describe the P & QRS complexes
RR intervals
There is a P for every QRS complex
Long RR intervals
What is another name for paroxysmal atrial tachycardia?
Supraventricular Tachycardia
What is a normal RR interval?
0.83 seconds
Atrial Tachycardia (SVT): Describe
SA node firing in an irregular way
RR intervals are regular then irregular
Atrial Tachycardia (SVT): Causes
Temporary decrease in vagal tone
When it stops, rhythm should go back to normal
Atrial Tachycardia (SVT): describe the P & T waves
May overlap and cant distingish them
Atrial Tachycardia (SVT): Treatments
Vagaling down
Beta blocker
SA node block: Causes:
Severe dysfunction
Ischemia
This causes the SA node to not be able to reset any VG L-type Ca++ channels
SA node block: what happens to the P wave?
May be inverted
may not have one
SA node block: where is the new pacemaker
- AV node
- then purkinje fibers
SA node block: describe how the p wave will look and why?
- No p wave: deep within the AV node or within the purkinje fibers (takes awhile to travel backwards through AV node, QRS is happening. P wave hidden within QRS)
- inverted p wave: at the beginning/front of AV node
Describe what happens in the heart when you move the pacemaker or have ectopic pacemakers (specifically SA node blocks)
Ventricles depolarizes early causing early closure of AV valves. Atria is contracting, while AV valves are closed –> pushing blood against close valves = blood turbulence –> damage the heart valves; generates blood clots; moves blood clots that are already there; calcified heart valves
What medication should you be on if you have a fib or a flutter? Why?
Anticoagulant
Syncytiums are not having coordinated contractions causing blood turbulence against heart valves causing increase risk of blood clots and calcified valves
What is the purpose of the delay at the AV node?
Coordinated contractions between syncytiums
To filter unwanted electrical activity
What is the normal PR interval?
0.16
AV node block: How does this present?
PR interval greater than 0.16
AV node block: causes:
- Ischemia of AV node or bundle of His d/t increase in Vrm (increasing Vrm decrease ion channels involved in AP)
- Compression of AV bundle (by scar tissue or calcification)
- inflammation of AV bundle
- excessive vagal stimulation
- Excessive digitalis/beta blocker
T/F: The more narrow an area is the faster it conducts an AP
F
Narrow = more resistance –> slower
What is digitalis?
Na+/K+ ATPase inhibitor
Digoxin
What does digitalis do in the heart?
Increases Vrm by inhibiting the Na/K ATPase pump. This causes more Na to be in the cell which decreases the rate of Ca++ removal from the cell during an AP. This can be helpful during HF as a last resort
Why is digitalis dangerous?
It is non selective for Na+/K ATPase not just in the heart but everywhere
What is a last resort effort for HF?
Digitalis
Digoxin
Describe a 1st degree heart block
Regular rhythm with PR interval greater than 0.20 seconds
Describe a 2nd degree type I heart block
Dropped QRS complexes
Atria has a faster rate than ventricles
PR intervals 0.25-0.45 seconds
PR intervals progressively increases until QRS is dropped
What is the nickname for 2nd degree type I heart block?
Mobitz Type I
Wenckebach periodicity
Which 2nd degree HB is more dangerous?
Type II
Describe 2nd degree type II heart block
Dropped QRS complexes
Atria has a faster rate than ventricles
PR intervals 0.25-0.45 seconds
Fixed PR interval with randomly dropped QRS complex
What could be the ratio of P/QRS to dropped QRS complexes?
2:1
3:2
3:1
What is the treatment for symptomatic 2nd degree type II heart block?
Pacemaker
What is the nickname for 2nd degree type II heart block?
Motiz Type II
Ventricular escape =
purkinje fibers
Describe 3rd heart block
Total AV node/bundle block
Nothing is getting through the AV node
Sinus node doing 1 thing
Purkinje fibers doing another….
Complete dissociation of P waves from QRS
Relying on Ventricular escape for HR at 15-40bpm
Increased atria rate d/t decreased CO
Describe A flutter
Circular reentery AP in atria completely separate from SA node (atria is contracting separate from SA node)
Somes AP able to hit during refractory period
High atria & ventricle rate
Which atrial arrhythmia is worse? Why?
Afib
Circus movement
What is circular reentry?
AP going around in a circle
Part of atria contracting & part is relaxed
Not effective priming for ventricles
What causes circular and circus reentry movements?
- slow conduction rate
- hypertropy (stretched out atria/ventricle)
Describe Afib
circus movement from etopic pacemakers in atria
Somes AP able to hit during refractory period
High ventricle rate
No p waves only “fibrillation”
T/F: there are p waves in aflutter
F
Afib is _______ movement while A flutter is _______ and has a defined pathway.
uncoordinated
coordinated
What is circus movement?
A bunch of ectopic pacemakers firing AP in a bunch of different directions
What is fibrillation?
Shaking his where parts of the heart are contracting while other parts are relaxing
results in no blood being pumped to that part of the heart
Which atria gets stretched out easier? What does this mean?
R atria
Predisposes R atria to flutter and fibrillation easier
Circus/circular movement causes ________ in the atria. Which increases the risk for clots in the ______ atria! This can cause the clot to go into that respective ventricle and go into the _________ and cause a ______
turbulence
Right
Pulmonary artery
Pulmonary embolism (PE)
What is the treatment if you have some really bad etopic pacemakers?
Ablation for a few of them
If you random faint, you may have what? Describe this
Stokes-Adam Syndrome
Random complete AV node block
Lag of about 30 seconds d/t purkinje fibers getting to threshold –> faints d/t low BP
T/F: Stokes-Adam syndrome is a virus that you catch and never fully goes away
F
This is a hereditary condition that causes fainting
Describe Alternans
Problem with conduction of the purkinje fibers
Irregular QRS every other heartbeat: ventricles cant depolarize like normal (larger&shorter every other)
Happens during tachy rhythms
What causes alternans?
Ischemia of the purkinje fibers
Digitalis
Describe Premature Atrial Contractions (PACs)
Ectopic tissue in atria fires AP early –> early depolarization of ventricles –> less filling –> decreased SV –> radial pulse deficit (sound)
Causes of PACs
Ischemia
Irritation
Calcified plaques
T/F: PACs cause Radial pulse deficits
T
Describe Premature AV node contractions
Random AP generating from AV node
Describe Premature Ventricular Contractions (PVCs)
Random AP happening in the ventricular muscle tissue!!! (not AV node or Purkinje but the muscle tissue baby!!!!!)
Prolonged QRS (Muscle tissue slow)
High voltage QRS (1 ventricle depolarizes while both depolarizing; they dont cancel out)
T-wave usually inverted
T/F: PAC are worse than PVC
F
PVCs are dangerous and worse
Causes of PVCs include:
CRNA school….
Caffeine
Nicotine
Stress
Lack of sleep
What does Paroxysmal mean?
Brief & intermittent
temporary
Describe Paroxysmal Ventricular Tachycardia
QRS originating within the venticular muscle tissue
Prolonged QRS
High voltage
Accelerated QRS complexes
no p waves
Paroxysmal Ventricular Tachycardia can cause __________
V-fib
Causes of Paroxysmal Ventricular Tachycardia include:
Infarction
What drug can cause long QT syndrome?
Benadryl
What is Early afterdepolarization?
AP hitting a cell before it had time to fully reset. We have less ion channels involved, so AP doesn’t look the same. Also less Ca++ coming in so heart wont contract as much –> decreased HR –> decreased CO
What 2 drugs can increase EAD and DAD?
Atropine (antimuscarinic)
Epi (Beta agonist)
Both increase cAMP –> increase PKA –> increase phosphorylation of of L-type Ca++ channels –> increases their sensitivity –> increases likelihood of pacemaker cells in the ventricles wanting to fire AP early
What does Early afterdepolarization look like on an EKG? Why?
A long QT interval
Cells are not able to reset
EAD can lead to ________ which can lead to ________
torsades de pointes
V-fib
T/F: You can last in V-fib for a long time
F
It can kill quickly even with CPR and defibrillation….
Describe Ventricular Fibrillation
Circus movement in ventricles
What can cause V-fib?
- EAD/torsades
- Hyperkalemia
- Lidocaine
- Benadryl (causes long QT syndrome)
Describe Lidocaine and its effects on the heart
It can slow conduction system in heart and cause circus movements –> increase risk for V fib
Generally lidocaine is safe, but if you dont need it, dont use it.
What is the Bundles of Kent?
Connective tissue that allows for an extra pathway on the lateral walls between the L atria and L ventricles & vice versa
Bypasses the ventricular conduction system
What percent of people have Bundles of Kent?
0.2%
What is the treatmet for Bundles of Kent if they become problematic?
Ablation
