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Equipment and Monitors: Cardiac Rhythms

Terms in this set (202)

Conduction System Anatomy
-Sinoatrial (SA) node
-Internodal tracts
-Atrioventricular (AV) node
-Bundle of His
-Bundle branches
-Purkinje fibers
know locations
3 internodal tracts that connect the SA to the AV node
-Anterior internodal tract (Bachmann bundle)
-Middle internodal tract (Wenckebach tract)
-Posterior internodal tract (Thorel tract)
Which internodal tract extends into the left atrium?
Anterior internodal tract (Bachmann bundle)
Conduction velocity definition
Quantifies how fast an electrochemical impulse propagates along a neural pathway
Conduction velocity is a function of...(3)
-Resting Membrane Potential
-Amplitude of the action potential
-Rate of change in membrane potential during phase 0 (how fast it will depolarize)
Conduction velocity is affected by (5)
-ANS tone
-Hyperkalemia induced closure of fast Na+ channels
-Ischemia
-Acidosis (K+ moves out and trades places with H+)
-Antiarrhythmic drugs
Conduction velocity of the SA and AV nodes
0.02-0.1 m/sec (slow conduction)
Conduction velocity of the His bundle, bundle branches, and purkinje fibers
1-4 m/sec (fast conduction)
Conduction velocity of myocardial muscle cells
0.3-1 m/s (intermediate conduction)
The only electrical pathway between the cardiac chambers
AV node

*AV node is the gatekeeper of electrical transmission between the atria and the ventricles
Accessory pathways that bypass normal conduction pathways
James fiber
Atrio-hisian fiber
Kent's bundle
Mahaim bundle
James fiber connects...
atrium to AV node

"S - bypasses SA node"
Atrio-hisian fiber connects...
atrium to His bundle
Kent's bundle connects...
atrium to ventricle
Mahaim bundle connects...
AV node to ventricle
Phase 0 of the ventricular action potential
-Event
-Ion Movement
-EKG event
-Event: Depolarization
-Ion Movement: Na+ In
-EKG event: QRS
Phase 1 of the ventricular action potential
-Event
-Ion Movement
-EKG event
-Event: Initial repolarization
-Ion Movement: Cl- In and K+ Out
-EKG event: QRS
Phase 2 of the ventricular action potential
-Event
-Ion Movement
-EKG event
-Event: Plateau
-Ion Movement: Ca+2 In and K+ Out
-EKG event: ST segment
Phase 3 of the ventricular action potential
-Event
-Ion Movement
-EKG event
-Event: Final repolarization
-Ion Movement: K+ Out
-EKG event: T wave
Phase 4 of the ventricular action potential
-Event
-Ion Movement
-EKG event
-Event: Resting Phase
-Ion Movement: Na+ Out
-EKG event: End of T wave --> QRS
What is the absolute refractory period and when is it located?
-Period where no stimulus can depolarize the myocyte
-Q wave to first 1/3 of T wave
What is the relative refractory period and when is it located?
-Period where a strong stimulus is required to depolarize the myocyte
-Last 2/3 of the T wave
Electrical Events during EKG
-P wave
-PR interval
-QRS
-ST segment
-T wave
-After T wave
-P wave: Atrial depolarization begins
-PR interval: Atrial depolarization complete
-QRS: Atrial repolarization AND beginning of ventricular depolarization
-ST segment: Ventricular depolarization complete
-T wave: Ventricular repolarization begins
-After T wave: Ventricular repolarization complete
P wave
-Duration (sec)
-Amplitude (mm)
-Prolonged with ___
P wave
-Duration (sec): 0.08-0.12
-Amplitude (mm): <2.5
-Prolonged with 1st degree heart block
PR Interval
-Duration (sec)
-Amplitude (mm)
-PR interval depression with ___
PR Interval
-Duration (sec): 0.12-0.20
-Amplitude (mm): X
-PR interval depression with pericarditis
Q Wave
-Duration (sec)
-Amplitude (mm)
Q Wave
-Duration (sec): <0.04
-Amplitude (mm): <0.4-0.5
Consider MI if the Q wave...
amplitude > 1/3 of R wave
duration > 0.04 seconds
depth > 1mm
QRS Complex
-Duration (sec)
-Amplitude (mm)
QRS Complex
-Duration (sec): <0.10
-Amplitude (mm): Progressively increases from V1-6 (normal R wave progression)
What should you consider if QRS complex increased?
LVH, bundle branch block, ectopic beat, WPW

All of these are below the AV node
Normal QTc
< 0.45s (men)
< 0.47s (women)
Consider MI if ST segment elevation or depression greater than ___.
-Elevation is also caused by ___ and ___
1mm
Hyperkalemia or endocarditis
T wave
Duration:
Amplitude:
T wave
Duration: X
Amplitude: <10 precordial leads, <6 in limb leads
*T wave usual points in the same direction as QRS
When would the T wave point in the opposite direction of the QRS?
If repolarization is prolonged by myocardial ischemia or a BBB
Intracranial bleed, myocardial ischemia, LVH effects on T wave?
Peaked T waves
If a U wave is present and >1.5mm, consider...
hypokalemia
*U wave is usually absent
At what point do you measure ST changes?
J point
Order of EKG changes (early to late) with hyperkalemia
Narrow peaked T
Short QT
Wide QRS
Low P amplitude
Wide PR
Nodal block
Sine wave fusion of QRS and T
VF or asystole

Hyper = EKG bunched up "hyper"
Hypo = EKG drawn out "slow"
EKG changes with hypokalemia
U wave
ST depression
Flat T wave
Long QT
EKG changes with hypercalcemia
Short QT
EKG changes with hypocalcemia
Long QT
EKG changes with hypermagnesemia
No significant effect unless very high
Heart block + cardiac arrest
EKG changes with hypomagnesemia
No significant effect unless very low
Long QT
Mean electrical vector definition
-Measured on?
-The average current flow of all the action potential at a given point in time
-The wave form on an EKG is a measure of the mean electrical vector

*each myocyte generates an action potential and each of these potentials can travel in any direction
How does the EKG measure the mean electrical vector?
-Each lead consists of a negative electrode and a positive electrode

*The positive electrode acts as a "camera" that monitors the path of the mean electrical vector
Vector of Depolarization on EKG
QRS Complex
Direction of vector of depolarization (direction of heart depolarization)
From base to apex
From endocardium to epicardium
Polarity of myocytes in the QRS complex (vector of depolarization)
Internally negative to internally positive
Produces positive electrical current
Vector of Depolarization
-Positive deflection when the vector travels ____ the positive electrode
-Negative deflection when the vector travels ___from the positive electrode
-Biphasic defection when the vector travels ___ to positive electrode
-Positive deflection when the vector travels TOWARDS the positive electrode
-Negative deflection when the vector travels AWAY from the positive electrode
-Biphasic defection when the vector travels PERPENDICULAR to positive electrode
Which direction does the heart repolarize (vector of repolarization)?
From the apex to base
From the epicardium to endocardium

*Opposite of depolarization
Vector of Repolarization on EKG
T wave
Polarity of myocytes in the T wave (vector of repolarization)
Internally positive to internally negative
Produces a negative electrical current

*Positive deflection occurs when the wave travels AWAY from the positive electrode
Why do T waves point in the same direction as R wave?
-Vector of repolarization travels in the opposite direction as the vector of depolarization
-Vector of repolarization produces a negative current
-"Double negative" explains why T wave usually points in the same direction as the R wave
Leads are divided into 3 groups:
Bipolar leads (I, II, III)
Limb leads (aVR, aVL, aVF)
Precordial leads (V1 - V6)
Lateral CxA leads
I, aVL, V5, V6
LAD leads
-Septum
-Anterior
LAD: V1-V4
-Septum V1, V2
-Anterior: V3, V4
Inferior/RCA leads
II, III, aVF
In axis deviation, the axis represents...
-The direction of the mean electrical vector in the frontal plane
Axis Deviation Lead I
-Normal
-Left axis deviation
-Right axis deviation
-Extreme right axis deviation

*positive or negative - draw out wave form
Axis Deviation Lead I
-Normal: +
-Left axis deviation: +
-Right axis deviation: -
-Extreme right axis deviation: -

Leave each other Left
Reach for each other Right
Axis Deviation Lead aVF
-Normal
-Left axis deviation
-Right axis deviation
-Extreme right axis deviation

*positive or negative - draw out wave form
Axis Deviation Lead aVF
-Normal: +
-Left axis deviation: -
-Right axis deviation: +
-Extreme right axis deviation: -
If the QRS is positive in both lead I and aVF, axis deviation is...
normal
If the QRS is positive in lead I and negative in aVF, axis deviation is...
Left axis deviation
Leads are "Leaving" each other
If the QRS is negative in lead I and positive in aVF, axis deviation is...
Right axis deviation
Leads are "Reaching" toward each other
If the QRS is negative in both leads I and aVF, axis deviation is...
extreme right axis deviation
Normal axis is between _____ and _______ degrees
-30 and +90

"think of apex as top"
Left axis deviation is... (number)
more negative than -30 degrees
Right axis deviation is... (number)
more positive than 90 degrees
The mean electrical vector tends to point __________ hypertrophy and _________ areas of MI
-Toward hypertrophy (there is more tissue undergoing depolarization)
-Away from MI (vector has to move around these areas)
Causes of right axis deviation (5)
COPD
Acute bronchospasm
Cor pulmonale
Pulmonary HTN
Pulmonary embolus
Causes of left axis deviation (5)
Chronic HTN
LBBB
Aortic stenosis
Aortic insufficiency
Mitral regurgitation
Sinus arrhythmia occurs when...
-The SA node's pacing rate varies with respiration
-Usually benign

-Inhalation →↓intrathoracic pressure →↑venous return →↑HR
-Exhalation →↑intrathoracic pressure →↓venous return →↓HR
What reflex can cause sinus arrhythmia?
Bainbridge reflex (increased venous return stretches RA and SA node causing increased HR)
-Define sinus bradycardia
-When is it common
-Increased ___ tone is often the source
-HR < 60 bpm
-Common in athletes
-Increased vagal tone is often the source
First line treatment for bradycardia?
What happens if you under dose the treatment?
-Atropine
-Under dosing (<0.5 mg IV) can cause paradoxical bradycardia
Paradoxical bradycardia when giving atropine is probably mediated by...
presynaptic muscarinic receptors
Treatment for severely symptomatic patients with bradycardia?
Severely symptomatic patients (syncope or chest pain) should receive immediate transcutaneous pacing
What is glucagon useful for?
How does glucagon work on the heart?
-BB or CCB overdose
-Stimulates glucagon receptors on the myocardium, increasing cAMP and leading to increased HR, contractility, and AV conduction
Dose of Glucagon and Infusion rate
-Initial dose: 50-70mcg/kg q3-5min
-Infusion: 2-10mg/hr
Sinus Tachycardia Definition
-Caused by
-Etiologies
-Treatment
HR > 100 bpm
-Caused by increased intrinsic firing rates of the SA node or sympathetic stimulation
-Etiologies: hypovolemia, hypoxia, infection, pain, thyrotoxicosis, malignant hyperthermia
-Treat underlying cause and/or rate control (BB, CCB)
Tachycardia increases/decreases myocardial O2 demand and increases/decreases O2 supply.
This can precipitate ___ and __ in patients with poor cardiac reserve or CAD.
Tachycardia increases myocardial O2 demand and decreases O2 supply.
This can precipitate myocardial ischemia/infarction and congestive heart failure in patients with poor cardiac reserve or CAD.
Atrial fibrillation definition
Irregular rhythm with the absence of a P wave
-Chaotic electrical activity in the atrium is conducted to the ventricle at a varied and irregular rate
In atrial fibrillation, ___ is lost and reduces CO. Patients have an increased risk of ___ and ___
In atrial fibrillation, atrial kick is lost and reduces CO. Patients have an increased risk of perioperative mortality and atrial thrombus formation (stroke)

*rapid ventricular response reduces diastolic filling and leads to severe reduction in CO (syncope, chest pain, shortness of breath)
Treatment for a-fib includes...
-Acute onset treatment
Rate control: beta blockers, CCBs, digoxin, and anticoagulation

Acute onset - cardioversion starting at 100J

*new onset is older than 48 hours (or undetermined onset) a TEE must be performed to rule out atrial thrombus
*new onset or undiagnosed AF is an indication to cancel surgery
Most common postop tachydysrhythmia and when does it usually occur?
A-fib
Postop day 2-4

*most common in older patients after cardiothoracic surgery
Atrial flutter definition
Atrial flutter is an organized supraventricular rhythm (saw tooth pattern)

*each atrial depolarization produces an atrial contraction but not all atrial depolarizations are conducted past the AV node to ventricles
*usually a defined ratio of atrial to ventricle contractions (3:1)
*Indication to cancel surgery
What prevents all atrial impulses from being transmitted to the ventricles?
-What can a rapid ventricular rate lead to?
-Refractory period
-Rapid ventricular rate can lead to hemodynamic instability
The rate with a-flutter is usually...
250-350bpm
Atrial flutter treatment
Rate control or cardioversion
-Hemodynamically unstable atrial flutter should be treated with cardioversion (start at 50J)

*Onset is older than 48 hours or undetermined onset, a TEE must be preformed to rule out atrial thrombus
Why is the QRS wide during a PVC?
-Because PVCs originate from foci below the AV node
-PVCs that arise from a single location are unifocal (morphology is the same on EKG)
-PVCs that arise from multiple locations are multifocal (different QRS morphologies on EKG)
Conditions that are associated with PVCs
-SNS stimulation (hypoxia, hypercarbia, acidosis, light anesthesia)
-Myocardial ischemia/infarction
-Valvular heart disease
-Cardiomyopathy
-Prolonged QT interval
-Hypokalemia
-Hypomagnesemia
-Digitalis toxicity
-Caffeine
-Alcohol
-Mechanical irritation (central line insertion)
A PVC that lands on the second half of the T wave (during the relative refractory period) can precipitate...
R on T phenomenon
When to treat PVCs
-Treatment
-Treat when they are frequent (>6/min), polymorphic, occur in runs of 3+

-Treat underlying cause
-Lidocaine 1-1.5mg/kg, then infusion of 1-4mg/min
Brugada syndrome definition
-Common cause of sudden nocturnal death d/t __ and __
-Most common in males/females from ___
-Sodium ion channelopathy in the heart
-Common cause of sudden nocturnal death d/t VT or VF
-Most common in males from southeast Asia
Diagnostic EKG findings in Brugada syndrome
RBBB and ST elevation in V1-V3
Considerations for patients with Brugada syndrome during surgery
Patient may require ICD or pad placement during surgery
First Degree Heart Block
-Key Characteristic
-Affected Region
-Etiology
-Treatment
-Key Characteristic: PR interval > .2 sec
-Affected Region: AV node or His bundle
-Etiology: Age related degenerative changes, CAD, digoxin, amiodarone
-Treatment: Monitor (usually asymptomatic)

"R is far from the P, you have 1st degree"
What area is affected if a first degree heart block is seen?
AV node or bundle of His
Second Degree heart block is also called:
Mobitz Type 1 or Wenckebach
Where is the affected region of a 2nd degree heart block?
AV node
Why does the second degree heart block type 1 occur?
Each successive depolarization increases the duration of the refractory period in the AV node, but the last P is dropped because it arrives at the AV node while it's in the absolute refractory period
What is the etiology of a 2nd degree heart block?
Conduction defect
Myocardial injury/infarct
Beta blockers
CCBs
digoxin
sympatholytic agents
What is the treatment for 2nd degree block?
Asymptomatic-monitor
Symptomatic- give atropine
Another name for 2nd degree block type 2
Mobitz type II

"if some Ps dont get thru you have mobitz type II"
What happens in a type II 2nd degree block?
Some Ps conduct to ventricles while others don't usually 2:1 OR 3:1 ratio

QRS drops and then the next P is usually on time
Affected regions with second degree heart block type 2
His bundle or bundle branches
Etiology 2nd degree type 2?
Is it symptomatic?
Conduction defect or infarction
Usually symptomatic- palpitations and syncope
Treatment for 2nd degree type 2?
Pacemaker
Atropine often not effective
Is there a risk of a 2nd degree type II progressing into a complete heart block?
Yes- high risk
What is a 3rd degree block?
Atria and ventricles have their own rate (AV dissociation)
3rd degree Block at the AV node has a __________ QRS (rate ___-____bpm)
3rd degree Block at the AV node has a narrow QRS (rate 45-55bpm)
Block below the AV node has a _____ QRS (rate ___ -___bpm)
Block below AV node has a wide QRS (rate 30-40bpm)
What is the etiology of a 3rd degree block?
Fibrotic degeneration of atrial conduction system
Lenegre's disease
Symptoms associated with 3rd degree heart block?
Dyspnea, syncope, weakness, vertigo
Treatment for third degree heart block
Pacemaker or isoproterenol
What can a 3rd degree block lead to?
CHF d/t decreased HR and CO
Stokes-adams attack
Can occur d/t third degree heart block
Decreased CO --> decreased cerebral perfusion --> syncope
Class 1 antidysrhythmics block...
sodium channel
Effects of class 1 antidysrhythmics on the action potential
Depression of phase 0
1a prolongs phase 3 repolarization
1b shortens phase 3 repolarization
1A Na+ channel blockers cause:
Moderate depression of phase 0
prolongs phase 3 repolarization (K+ channel block increases QT)
Examples of class 1a antidysrhythmics
Quinidine, procainamide, disopyramide
IB Na+ channel blockers cause:
-Weak depression of phase 0
-Shortened phase 3 repolarization
Examples of class 1b antidysrhythmics
Lidocaine, phenytoin
IC Na+ Channel blockers cause:
-Strong depression of phase 0
-little effect on phase 3 repolarization
Examples of class 1c antidysrhythmics
Flecainide, propafenone
Class II antidysrhythmics are...
beta blockers
Effect of class II antidysrhythmics on the action potential
Slow phase 4 depolarization in the SA node
Class III antidysrhythmics are...
potassium channel blockers
How do class III antiarrythmics affect the action potential?
Prolong phase 3 repolarization (increased QT)
Increase effective refractory period
Examples of class III antidysrhythmics
Amiodarone, bretylium
Class IV antidysrhythmics are:
calcium channel blockers
How do class IV antidysrhythmics work?
Decrease conduction velocity through the AV node
Examples of class IV antidysrhythmics
Verapamil, diltiazem
How does adenosine work?
Stimulates the cardiac adenosine-1 receptor, causing potassium to move into the cell, hyperpolarizing the cell membrane
Slows conduction through the AV node (hyperpolarizes cell membrane and reduces action potential)
Half life of adenosine
5 seconds (rapidly metabolized by plasma)
When is adenosine useful?
SVT, WPW with narrow QRS
NOT for afib/flutter or VT
Side effect of adenosine
Bronchospasm in asthmatics
1st and 2nd dose of adenosine when given peripherally
6mg, then 12mg
1st and 2nd dose of adenosine when given centrally
3mg, then 6mg
Impulse conduction- Normal Pathway
SA node--> AV node-->HIS bundle-->Bundle Branches--> purkinje fibers
-cardiac impulse cant go back d/t absolute refractory period in the tissues behind impulse
-1:1 ratio of SA depolarization and cardiac contraction

-impulses meet along connecting pathways, but cancel each other out so reentry doesn't happen
Most common cause of tachyarrhythmias
Reentrant pathways
Reentry
The process where a single cardiac impulse can move backwards and excite the same part of the myocardium over and over
How do you break the reentry circuit?
1. Slow conduction velocity
2.increase refractory period of the cells at the location of the unidirectional block
Left atrial dilation d/t mitral stenosis may cause reentry by...
conduction occurring over a long distance
Ischemia or hypokalemia can cause reentry by...
conduction velocity too slow
Epi or electric shock can cause reentry by...
shortening the refractory period
WPW is the most common
Pre-excitation syndrome
Defining feature of WPW
Accessory conduction pathway (Kent's bundle) bypasses the AV node
No delay at the AV node, so the impulse quickly moves from the atrium to the ventricle
Definitive treatment of WPW
Ablation of accessory pathway
Common characteristics of the EKG with WPW
Delta wave caused by ventricular preexcitation
Short PR interval
Wide QRS
Possible T wave inversion
Origin of delta waves
SA node depolarizes, electrical impluse travels thru AV node/accessory pathway at same time

Accessory pathway doesnt delay the impulse and it arrives early at ventricle

when the impulse from the AV node catches up, you will then see the rest of QRS
Afib and WPW
Since there is no delay in accessory pathway, a rapid atrial rate can be conducted to ventricles in a ____:____ ratio
1:1
What must you monitor during radio frequency ablation for WPW?
Esophageal temperature - risk of thermal injury to the LA and esophagus

notify surgeon if esophageal temp rises during ablation
Afib and WPW
During afib atria can depolarize up to ____ per min.

Combination of AF an WPW can precipitate:
300 per min

CHF, Vfib, death
Treatment of choice in afib with WPW
Procainamide (1A) - increases refractory period in the accessory pathway

Cardioversion if unstable

WPW with afib - procainamide--> Antidromic?
Most common tachydysrhythmia associated with WPW
AV nodal reentry tachycardia
Most AV nodal reentry tachycardias with WPW are classified as...
orthodromic (90%)
Orthodromic AVRNT pathway
Atrium --> AV node --> ventricle --> accessory pathway --> atrium
QRS with orthodromic AVRNT
Narrow

(ventricular depolarization occurs normally via His-purkinje system)
Treatment of orthodromic AVRNT
Block conduction at AV node (increase refractory period)
Vagal, amio, adenosine, BBs, verapamil, cardioversion
Antidromic AVRNT pathway
Less common (10%)
Atrium --> accessory pathway --> ventricle --> AV node --> atrium
QRS with antidromic AVRNT
Wide (His-purkinje is bypassed- slower ventricular depolarization)
Treatment of antidromic AVRNT
Block conduction at accessory pathway

Procainamide, cardioversion
(WPW w/ afib)

Do not give any agents that increase the AV node refractory period- will favor conduction through the accessory pathway
What drugs must you avoid with antidromic AVRNT? Why?
Adenosine, digoxin, CCBs (diltiazem and verapamil), BBs, lidocaine

-Forces conduction along the accessory pathway and may induce VF
Which type of AVRNT is more dangerous?
Antidromic
-gate keeper function of AV node is bypassed and heart can pump well beyond the hearts ability (very reduced filling times)
Is cardioversion a safe option for orthodromic and antidromic?
yes
Torsades is associated with:
Long QT interval
Prolonged QT interval defined as:
Men >0.45
Women >0.47
Underlying cause of torsades
Delay in ventricular depolarization (phase 3 of the action potential)

self limiting, but can progress to vfib
PVC or poorly times pacer discharge during the relative refractory (during 2nd half of t wave) period can cause:
Torsades via R on T phenomenon
Mnemonic POINTES for causes of torsades
Phenothiazines, Other meds, Intracranial bleed, No known cause, Type 1 anyarrhythmics, Electrolyte disturbances, Syndromes
Metabolic disturbances that prolong QTc and may precipitate torsades
Hypokalemia
Hypocalcemia
Hypomagnesemia
Drugs that prolong QTc and may precipitate torsades
Methadone
Droperidol, haloperidol
Ondansetron
Halogenated anesthetics
Amio
Quinidine

"Anything that chills/prolongs people"
Genetic syndromes that prolong QTc and may precipitate torsades
Romano-Ward syndrome
Timothy syndrome
Conditions that prolong QTc and may precipitate torsades
Hypertrophic cardio Myopathy
Subarachnoid hemorrhage
Bradycardia
Acute treatment for torsades
Magnesium sulfate
Cardiac pacing to increase the HR - reduces action potential duration and QT interval
Indications for pacemaker insertion
Symptomatic diseases of impulse formation (SA node disease)
Symptomatic diseases of impulse conduction (AV node disease)
Long QT
Dilated cardiomyopathy
Hypertrophic obstructive cardiomyopathy
What is the most important information to have preoperatively for a patient with a pacemaker?
Underlying rhythm so if it fails you can treat accordingly

-consider isoproterenol, epi, and/or atropine
Epicardial leads stimulate
Transvenous leads stimulate...
surface of heart
the cardiac chambers (RA and/or RV)
Single chamber demand pacing
ex: AAI, VVI
Back up mode- only fires if native HR falls below predetermined rate
Dual- chamber demand pacing
ex) DDD
most common mode
makes sure atrium contracts first followed by ventricle
improves AV synchrony
Examples of asynchronous pacing and what does it mean?
AOO, VOO, DOO
Delivers a constant rate without sense or inhibition
A pacer spike during ventricular repolarization can result in R on T
Position 1 of the pacer code
Chamber that is paced
O = none, A = atrium, V = ventricle, D = both A and V
Position 2 of the pacer code
Chamber that is sensed
O = none, A = atrium, V = ventricle, D = both A and V
Position 3 of the pacer code
"Inhibits"
Response to the sensed native cardiac activity
T = sensed activity tells pacer to fire
I = sensed activity tells pacer NOT to fire
D = inhibits if native activity is sensed, but fires if not
Position 4 of the pacer code
Indicates the programmability of the pacemaker
Ability to adjust the HR based on physiologic need
O = none, R = rate modulation
Position 5 of the pacer code
Indicates that the pacer can pace multiple sites
O = none, A = atrium, V = ventricle, D = dual
If the atrium is paced, where does the electrical signal travel?
Though the AV node
QRS maintains its normal narrow appearance
If the ventricle is paced, where does the electrical signal travel?
Beyond the AV node
QRS takes on a wide appearance
By placing a magnet over a pacemaker...
it usually converts the pacer to an asynchronous mode
Best answer is to consult with the manufacturer
By placing a magnet over an ICD...
it suspends the ICD and prevents shock delivery
Pacemaker function can be impaired because of...
electromagnetic interference (electrocautery or radiofrequency ablation) or conditions that make the myocardium more resistant to depolarization
By placing a magnet over a pacemaker that also has ICD function...
it suspends the ICD and prevents shock delivery but has NO effect on the pacemaker function
Which setting on electrocautery causes more electromagnetic interference?
Coagulation more so than cutting
Does monopolar or bipolar cautery/ ultrasonic harmonic scalpel cause more electromagnetic interference (EMI)?
Monopolar
If the surgeon insists on monopolar cautery in the presence of a pacemaker, they should...
limit to short bursts ≤0.5 seconds
How far should the electrocautery tip be from a pacemaker?
15cm
(risk of EMI is highest <15cm of pulse generator)
Where should the electrocautery return pad be placed?
Far from pulse generator in a location that prevents direct line of current thru pulse generator
Is succs contraindicated in pts with pacemaker?
no
in theory could make myocardium less resistant to depolarization (transient increase in serum K+/ skm contraction could confuse pacemaker)- but doesn't seem to be a clinical issue
Is electroconvulsive therapy contraindicated in pts with pacemaker?
no
Is lithotripsy contraindicated in pts with pacemaker/ICD?
No- beam just needs to be directed away from pulse generator
What imaging is contraindicated in pts with pacemaker/ICD?
MRI
Pacemaker failure:
Conditions that make the myocardium more resistant to depolarization, possibly causing failure to capture
Hyperkalemia, hypokalemia
Hypocapnia (intracellular K+ shift H+ going out)
Hypothermia
MI
Fibrotic tissue buildup around pacing leads
Antiarrhythmic meds
Three causes of pacemaker failure:
1. pulse generator failure
2. lead failure
3. failure to capture
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