Exam 4 Lecture 7 Flashcards
What are the 3 Ratios of PR-Int to QRS Complexes in a 2nd Degree Type 2 HB
2:1
3:1
3:2
If P wave is Inverted, where is this source?
Retrograde AP from AV junction
Define PVC
*Why is the QRS duration longer?
*Why is the Amplitude of the QRS higher?
*Describe the T-Wave
Ventricle contraction before normal, as Ventricular muscle conduction is slower than the Purkinje System
*Longer b/c the AP starts in ventricular muscle, which takes longer to depolarize the Purkinje Fibers
*Higher b/c if the depolarization starts on the high lateral side of the L or R ventricle, this leads to increased magnitude
*T-Wave after PVC is usually inverted
List Pathway for Blood Clot in R atria to Lungs, per lecture
R atria, R ventricle, L ventricle, Pulmonary System
What is Cardiac Turbulence?
*What 2 things can this lead to
Blood swishing and hitting closed valves or walls, leading to increased blood clots and Ca++ deposits
Premature Ventricle Contraction
What is a normal CO?
5L/min
What are cranial nerves V and X
Trigeminal and Vagus
Atrial Flutter
Define Paroxysmal Ventricular Tachycardia
*Is this dangerous?
*What is this a precursor to?
*Talk about P waves, if any
Over active ventricle conduction system
*Yes, can lead to VFIB
*VFIB
*If any, probably inverted
What can cause Paroxysmal VTACH: 2 Things
Ischemia or Infarct
What are the Bundles of Kent
*What % of the population has this?
*How to treat if needed
Connections that bypass the normal connections such as the internodal system
*0.2%
*Cardiac Ablasion
Premature Contract: AV node Source: Talk about P wave
AV node ectopic issues, so missing P-Wave
3 Tx for SVT [Paroxysmal Atrial Tachycardia]
Vagal Reflex, BB, Digoxin
Sinus Tachycardia
SinoAtrial Block: Define what happens when the ventricles are depolarized early, in terms of creating “turbulence”
During contraction, AV valves are open. If you depolarize the ventricles early, the Atrium pushes blood against closed AV valves, leading to damage and more turbulence
Define PAC: Talk about SV
*What 3 things does this result from
*What is a Radial Pulse Deficit
Ectopic issues in atria fire early AP; Lower SV
*Ischemia, Irritation, Calcification
*Lower SV from less filling time in early depole = less noise when auscultating
Define Sinus Tachycardia
*How long is PR-Int
*BPM?
Abnormal SA node firing P-Waves faster than normal
*PR-Int<0.16 sec
*>100BPM
What does the Bundles of Kent do?
Connect R Atria with R vent or L atria with L vent
How to get out of VFIB, per lecture
Shocking
Define Paroxysmal Atrial Tachycardia[SVT]
*Talk about P and T waves
*Is this a permanent state of the Heart?
High HR driven by abnormal Atrial Excitation
*P waves and T waves may overlap
*No, usually this comes and goes
Atrial Flutter
Define Sinoatrial Block: Is this common?
*Talk about P-Waves, SV, and CO
*What becomes the New PM?
*PM if the new PM is blocked?
SA Node Blocked completely; Rare
*NO P waves, decreased SV and CO
*AV Node: 40-60 BPM
*Purkinje Fibers: 15-30 BPM
If P wave is late and Inverted, where is this source?
*can we see this?
Low AV Junction
*Mostly hidden by QRS complex, so probably not
If P wave is early and Inverted, where is this source?
HIGH AV Junction
- Premature Depolarization
- Repetitive Premature Depolarization
Sinus Bradycardia
What drug classes does Benadryl fall into?
*What heart arrhythmia can it cause
Antihistamine and Anticholinergic
*Tachycardia and PVC
Premature Contraction: Atrial Source
Predisposed to Afib: 2 Things
Age around 70 and Atrial Hypertrophy
Which is more dangerous: 2nd Degree Type 1 or Type 2?
*Tx for the more dangerous one?
*When do we usually “find” this Arrhythmia
Type 2
*Possible Pacemaker
*Preop EKG on Pt who hasn’t had one in a while
Ventricular Fibrillation
Torsades de Pointes
How does Digoxin work
Block NaKATPase Pump, which increases Vrm by increased Na+ and Ca++ w/in the cell
Sinoatrial Block
What 3 things can cause a PAC
1.Ischemia
2. Irritation
3. Calcification
Define Complete HB: 3rd degree
*What is the Ventricular Escape
*Is Atrial Rate faster or slower than normal? Why?
No correlation between P-Wave and QRS complex; total AV node or Bundle of His block
*15-30 BPM
*Faster than normal, as ANS tells heart to speed up Atrial contractions to compensate for poor CO
Paroxysmal Atrial Tachycardia
5 Causes of Cardiac Arrhythmias
- Abnormal Rhymic of PM [ectopic PM]
- Shift of PM from Sinus Node
- Blocks in cardiac transmission
- Abnormal Pathways of Transmission [hitting relative refract period]
- Spontaneous Generation of Abnormal Impulses
What is a Cardiac Arrhythmia?
Problem with the Heart’s conduction system
Ventricular Fibrillation
2 Causes of Sinus Bradycardia
Vagal stimulation by PNS [can also decrease SNS, but not common]
Neural Reflex to Drugs [phenylephrine]
Define A-Flutter: What type of Pathway
*Is this coordinated or uncoordinated
*Talk about P-Waves
*Is this a good or bad primer for the ventricles? Why
Circular reentry Pathway in Atria
*Coordinated
*NO P-Waves
*Bad Primer - leads to increased atrial and ventricle rates [cannot sync properly]
Define a 2nd Degree Type 2 HB
*How long is the PR-Interval
*Which have fast rate: Atria or Ventricle?
*Describe the PR-Intervals
AV block that drops QRS complexes
*0.25-0.45 sec
*Atria rate is faster, as dropping QRS complexes
*PR-Intervals are FIXED RATIO
Define a 1st degree HB
PR>0.20 seconds; longer time for atria to reach ventricles
Incomplete Intraventricular Block: Alternans
Atrial Fibrillation
3 Causes of Sinus Tachycardia
- Hyperthermia [increased energy]
- Sympathetic Stimulation [loss of vagal tone, loss of blood, reflex stimulation]
- Toxic Conditions [Things that increase Vrm]
If you have an increased resting HR, what could be 2 causes per lecture?
Hyperthyroidism or Valve issues
Define Sinus Bradycardia
*What Pt. Pop is this commonly seen in? Why?
*BPM?
Abnormal SA nodal firing beats slower than normal
*Athletes who have a large SV; ANS tells Heart to slow down HR, as it has enough CO
*<60BPM
6 Things that can cause Increased Vrm
- Hyperkalemia [decreased CG]
- Acidosis <7.4; Increased H, Increased Protons
- MI*
4.Infarct* - Ischemia*
- Drugs/Medications
Define A-Fib
*What type of “movements”
*Is this coordinated or uncoordinated
*Talk about P-Waves
*Talk about Turbulence
Irregular “flutter” type electrical conductance in the Atria
*Ectopic PM and Circus Movements
*Uncoordinated
*No P-Waves
*Increased turbulence due to muscles contracting and relaxing in different “flutter” manner: Increased clot risk
Complete Heart Block: 3rd Degree
Incomplete Heart Block: 1st Degree
What are PVC Precursors To?
Torsades, VFIB
Overall, is having a higher or lower resting HR better?
Lower
Define Stokes-Adams Syndrome
*Why do we pass out?
*What ventricular escape do we resume HR at?
*What is our seconds delay threshold until we pass out?
Fainting/Syncope due to an AV block that happens time to time
*We pass out due to the heart not pumping, so from hypotension
*15-30 BPM
*7-8 second threshold
Incomplete Heart Block: 2nd Degree Type 2
Which is worse: Afib or Aflutter? Why
*What medication type must the worst arrhythmia be “treated” with?
Afib, as it is uncoordinated, irregular electrical conductance
*Blood thinners
How much longer does it take to depolarize the L ventricle compared to the R ventricle?
*Why
0.01 seconds
*More tissue
Atrial Fibrillation
Premature Contraction: AV Nodal/Bundle
How do we end up in VFIB: No ventricular repolarization
*Talk about BP and BF
Atria BP low - Ventricle Output low - coronary BF low = No ventricular repolarization
What are the 5 Things that can cause an AV Block
*Expand on Fibroblasts
*Expand on V and X reflex
*Expand on the meds listed
- Ischemia of AV node
- Compression of AV bundle [scar tissues from Fibroblasts in CHF/MI] = compression, which lowers AP conductance
- AV node inflammation
- Excessive Vagal Stimulation: V and X reflex
- Excess digitalis/BB: D - block NaKATPase Pump, leading to increased Vrm by Na+ and Ca++
BB - inhibit cAMP, PKA
- SA node
- Anterior Internodal System
- Middle Internodal System
- Posterior Internodal System
- AV node
- Interatrial Bundle [Bachman’s Bundle]
- Left Bundle Branch
- Right Bundle Branch
- Purkinje Fibers
Incomplete Heart Block: 2nd Degree Type 1 Wenckebach
Define IV Block: Alternans
*At which heartbeat does this occur
*What other arrhythmia will you most likely see this one?
*Causes of this?
*Talk a/b scar tissue and conduction speed in terms of QRS
Slowed conduction @ Purkinje System, as trouble repolarizing
*Every other HB
*VTACH
*Ischemia and Digitalis preventing the full repolarization of the Purkinje System
*Scar tissue/chronic depolarized = decreased conduction speed [longer QRS but less amplitude]
Main difference between 2nd Degree Type 1 and Type 2 HB
Type 1: Variable PR-Int
Type 2: Fixed PR-Int
Predisposed to AFlutter: 2 things
Slow conduction rate and Atrial Hypertrophy
Ventricular Premature Depolarization:
*What does this look like on an EKG
*Talk about CO/SV
*3 Causes
Long QT syndrome
*Decreased CO/SV
*How sensitive Ca++ channels are [increased Beta agonist activity], mACh-R antagonists, Benadryl
What are 4 Causes of PVCs
Caffeine, Nicotine, Stress, Lack of Sleep
Any Increase in Vrm can cause what?
*What does this do to repolarization?
Risk of ectopic PM firing AP on its own
*delays it/prevents it
Paroxysmal Ventricular Tachycardia
Define a 2nd Degree Type 1 HB
*How long is the PR-Interval
*Which have fast rate: Atria or Ventricle?
*Describe the PR-Intervals
*Another Name for this?
AV block that drops QRS complexes
*0.25-0.45 sec
*Atria rate is faster, as dropping QRS complexes
*PR-Intervals are VARIABLE
*Wenckebach Periodicity
Causes of R Axis Deviation
- Pulmonary Stenosis (R Vent Hypertrophy)
- RBBB
- Deep Breath (inspiration)
- R Vent Hypertrophy
- COPD
Causes of L Axis Deviation
- LBBB
- L Vent Hypertrophy
- Decreased Lung Volume (expiration)
- Aortic Stenosis (L Vent Hypertrophy)
Phrenic Nerve: Definition and Which Part of the Spine Involved
Bundle of Axons in the PNS
*C3, C4, C5
Beta Agonist, in terms of inotropy, chrono, etc..
+ ino, chrono, dromo, luso
Atenolol in terms of inotropy, chrono, etc..
- ino, chrono, dromo, luso
What 2 Main Things can Cause Circular Reentry, leading to VFIB
Slowed Conduction and Shorter Refractory Period
