EQUIPMENT-cardiac rhythm monitors Flashcards
What are the 3 internodal tracts that travel from the SA node to the AV node
- Anterior internodal tract (Bachmann bundle)
- Middle internodal tract (Wenckebach tract)
- Posterior internodal tract (Thorel tract)
Compare the conduction velocities of the cardiac conduction pathway from fastest to slowest
SA node AV node His Bundle Bundle branches Purkinje fibers Myocardial muscle cells
Conduction velocity is a function of what 3 factors
- Resting membrane potential
- Amplitude of the AP
- Rate of change in the membrane potential during phase 0
What 5 factors affect conduction velocity
- ANS tone
- Hyperkalemia induced closure of Na+ channels
- Ischemia
- Acidosis
- Antiarrhythmic drugs
Atrial depolarization occurs during which EKG events (2)
P wave (begins) Pr interval (ends)
Atrial repolarization occurs during which EKG event
QRS complex
Ventricular depolarization occurs during which EKG events
QRS complex (begins) ST segment (ends)
Ventricular repolarization occurs during which EKG events
T wave (begins) After T wave (ends)
P wave:
Duration=
Amplitude=
Duration= 0.08 - 0.12 sec Amplitude= <2.5 mm
PR interval
0.12 - 0.20 sec
Q wave:
Duration=
Amplitude=
Duration= < 0.04 sec Amplitude= <0.4 - 0.5 mm
QRS complex:
Duration=
Amplitude=
Duration= <0.10 sec Amplitude= progressive increase from V1 to V6
What does a biphasis P wave indicate
- Mitral stenosis
2. LA enlargement
What does a tall P wave suggest
- Cor pulmonale
2. RA enlargement
What does a prolonged PR interval indicate
1st degree HB
What does PR interval depression indicate
- Viral pericarditis
2. Atrial infarction
What 3 alterations in the Q wave can indicate MI
- Amplitude greater than 1/3 of R wave
- Duration > 0.04 sec
- Depth > 1 mm
What 4 abnormalities occurs with increased QRS complex duration
- LVH
- BBB
- Ectopy
- WPW
QTc interval:
Duration =
Men <0.45
Women < 0.47
What are 3 causes of elevated ST segment
- MI (> 1 mm)
- Hyperkalemia
- Endocarditis
Describe causes of negative T wave
- MI
2. BBB
What are 3 causes of peaked T wave
- MI
- LVH
- ICH
When is a U wave present
hypokalemia?
How is ST segment elevation or depression determined
By measuring the beginning (J point) relative to the PR segment
+/- 1 mm is significant
What 6 EKG changes occur with elevated K+
From early to late appearance
- Narrow, peaked T
- Short QT
- Wide QRS
- Low amplitude P
- Wide PR
- Nodal block
What 4 EKG changes occur with low K+
- U wave
- ST depression
- Flat T wave
- Long QT interval
What EKG changes occur when Ca++ is abnormal
High=
Low=
High= short QT Low= Long QT
What EKG changes occur when Mg++ is severely abnormal
High=
Low=
High= heart block, cardiac arrest Low= Long QT
What does a positive deflection indicate in EKG
Depolarization travels TOWARD positive electrode
What does a negative deflection indicate for EKGs
Depolarization travels AWAY from positive electrode
What does a biphasis deflection indicate for EKGs
Depolarization travels PERPENDICULAR to the positive electrode
What is the directionality of depolarization
Base to apex
Endocardium to epicardium
How does polarity of the myocyte change during depolarization
Myocyte goes from internally NEG to internally POS
This produces positive electrical current
What is the directionality of repolarization
Apex to base
Epicardium to endocardium
How does polarity of the myocyte change during repolarization
Myocyte foes from internally POS to internally NEG
Produces negative electrical current
Why is the T wave positively reflected during repolarization
Because repolarization travels in the opposite direction with a negative current (double negative)
What are the bipolar leads
Leads I, II, III
What are the limb leads
Leads aVR, aVL, aVF
What are the precordial leads
Leads V1 - V6
What do leads II, III, aVF monitor
Vessel and location
Inferior
RCA
What do leads I, aVL, V5, V6 monitor
Vessel and location
Lateral
CxA
What do leads V1 - V4 monitor
Vessel and location
Septum
LAD
What does the EKG axis represent
The direction of the mean electrical vector in the frontal plane
What is the easiest method to determine axis deviation
Examine lead I aVF
What does normal axis deflection look like
Lead I = +
Lead aVF= +
What does left axis deviation look like
Lead I = +
Lead aVF= -
What does right axis deviation look like
Lead I = -
Lead aVF=+
What does extreme right axis deviation look like
Lead I = -
Lead aVF= -
What are 5 common causes of right axis deviation
- COPD
- Cor pulmonale
- Acute bronchospasm
- PE
- Pulm HTN
What are 5 common causes of left axis deviation
- Chronic HTN
- LBBB
- AS
- AI
- Mitral regurg
What is normal axis deviation measurement
Left axis=
Right axis=
Normal= -30 to +90 degrees Left= more neg than -30 Right = more pos than +90
Where does the mean electrical vector tend to point
- TOWARDS areas of hypertrophy
- more tissue to depol - AWAY from areas of infarction
- vector moves around MI
What reflex mediates sinus arrhythmia
Bainbridge reflex
SA node pacing varies with respirations (d/t changes in intrathoracic pressure)
How is glucagon useful in some bradycardias
Useful for BB or CCB overdose
Glucagon receptors are stimulated on myocardium, increasing cAMP and HR
What is the dose for glucagon for BB/CCB OD
Initial = 50 - 70 mcg/kg Infusion = 2-10 mg/hr
1st line treatment for bradycardia
Treatment for symptomatic bradycard
1st line = atropine
Symptomatic = transcutaneous pacing
1 physiologic causes of ST
- increased intrinsic firing of SA node
2. SNS stimulation
How does ST affect myocardial O2 supply and demand
Demand = increased Supply = decreased
Why is ST not tolerated in pts with poor cardiac reserve or CAD
Poor reserve = Precipitate MI or CHF
CAD = precipitate ischemia or infarction
How does AFib affect CO
- Loss of atrial kick
- Reduced diastolic filling time with RVR
- Decreased CO
What medications are used to treat afib
- BB
- CCB
- Digoxin
- Anticoags to prevent thrombus
Initial cardioversion energy for acute onset a-fib
100 joules
How does a-flutter differ from a-fib
A-flutter has an organized supraventricular rhythm
Atrial rate >250
Describe a-flutter
Each atrial depolarization produces an atrial contraction
Not all atrial depolarization conduct past AV node
Initial cardioversion energy for a-flutter
50 joules
When does a junctional rhythm occur
When AV node functions as dominant pacemaker
Rate 40 - 60 bpm
Why is junctional rhythm slower
Rate of phase 4 depolarization of the AV node is slow
2 causes of Junctional rhythm
- SA node depression (volatile anesthetics)
- SA node block
- Prolonged conduction at the AV node
What are premature ventricular contractions (PVCs)
Contractions that originate from foci below the AV node
-reason for wide QRS
What are 7 conditions that can develop PVCs
- SNS stimulation
- MI
- Valvular dz
- Cardiomyopathy
- Prolonged QT interval
- Hypokalemia
- Hypomagnesemia
- Digitalis tox
- CVC
How can PVCs lead to further dysrhythmias
If PVC lands on second half of T wave, can precipitate R on T phenomenon
What medication can be given for symptomatic PVCs
Lidocaine 1.0 - 1.5 mg/kg
Treatment for V fib
Immediate CPR
Defibrillation
Treatment for asystole
CPR
NO shocks
What is Brugada syndrome
Na+ ion channelopathy in heart
Can lead to V-Tach or V-Fib
What are diagnostic EKG changes of Brugada syndrome
RBBB w/ ST-segment elevation in leads V1-V3
Treatment and considerations for patients with Brugada syndrome
ICD placement
Pad placement during surgery
Describe a 2nd-degree Mobitz type 1 block
PR interval progressively longer
P wave drops QRS
Describe a 2nd-degree Mobitz type 2 block
Some Ps conduct to ventricle, other Ps drop QRS
NO PROLONGATION
Treatment for 2nd-degree blocks
Type 1
Type 2
Type 1 = atropine
Type 2 = pacing (atropine NOT useful)
Describe a 3rd-degree heart block
The atria and ventricle each have their own rates
AV dissociation
Treatment for 2rd-degree heart block
- pacemaker
2. Isoproterenol
What altered conduction regions produce the following block
2nd degree T1
2nd degree T2
2nd degree T1 = AV node
2nd degree T2 = His bundle or bundle branches
What is the mechanism of class 1 antiarrhythmic drugs Ex:
Inhibition of fast Na+ channels
Ex: lidocaine, procainamide, phenytoin
What is the mechanism of class 2 antiarrhythmic drugs Ex:
Decrease the rate of phase 4 depol
Ex: BB
What is the mechanism of class 3 antiarrhythmic drugs Ex:
Inhibits K+ ion channels and prolongs phase 3 repol
Ex: amiodarone
What is the mechanism of class 4 antiarrhythmic drugs Ex:
Inhibits slow Ca++ channels, slows conduction velocity through AV node
Ex: CCB, diltiazem, verapamil
What is the mechanism of action and dose for adenosine
MOA = Slows conduction through AV node by stimulating adenosine-1 receptor, causing K+ efflux and hyperpolarizing the cell membrane
Dose = 3 mg - 12 mg IVP
In which dysrhythmic conditions is adenosine useful
SVT
WPW w/ narrow QRS
In which pts should adenosine be used with caution and why
Asthma pts
Can cause bronchospasms
What are 3 causes of re-entry pathways
- Conduction occurs over a long distance
- Conduction velocity is too low
- Refractory period is shorter
What are 2 ways to disrupt a reentry circuit
- Slow the conduction velocity through the circuit
2. Increase the refractory period of the cells at the location of the unidirectional block
What is the most common cause of tachydysrhythmias
Re-entry pathway
How can mitral stenosis cause a re-entry pathway
Conduction must occur over a longer distance
how can ischemia cause a reentry pathway
Conduction velocity through the affected region is too slow
How can epinephrine cause a reentry pathway
It shortens the duration of the refractory period
What is the defining feature of WPW
An accessory conduction pathway (Kent’s bundle) that bypasses the AV node (connect atrium and ventricle)
There is a conduction delay
What is a key diagnostic feature of WPW on EKG
delta wave
What is the most common tachydysrhythmia associated with WPW
AV nodal reentry tachycardia
What is the morphology and treatment (6) for orthodromic AVNRT
Morphology = narrow QRS
Treatment = increase refractory period at AV NODE
-vagal maneuver, amio, adenosine, BB, CCB, cardiovert
What is the morphology and treatment (2) for antidromic AVNRT
Morphology = wide QRS complex
Treatment = increase refractory period of the ACCESSORY pathway
-procainamide, cardiovert
What agents (5) should be avoid when treating antidromic AVNRT
Medications that increase the refractory period (opposite of orthodromic AVNRT)
-adenosine, digoxin, CCB, BB, lidocaine
What do each of the following positions categorize in pacemakers Position 1 Position 2 Position 3 Position 4 Position 5
Position 1 = chamber paced Position 2 = chamber sensed Position 3 = response to sensed activity Position 4 = programmability options Position 5 = PM can pace multiple sites
How are the following pacing modes indicated in their settings
Asynchronous =
Single-chamber=
Dual-chamber=
Asynchronous = AOO, VOO, DOO Single-chamber= AAI, VVI Dual-chamber= DDD
What does failure to capture indicate
The PM delivers an electrical stimulus but fails to trigger myocardial depolarization
What does magnet placement do to a PPM
Converts the PM to asynchronous mode
What does a magnet placement do to an ICD
Suspends the ICD and prevents shock delivery
What does a magnet placement do to a PM/ICD
Suspends ICD
No effect on PM function
Which setting of electrocautery causes more EMI with a PM
coag > cutting
What type of cautery causes more EMI in pts with PM
Monopolar > bipolar=US harmonic
When is EMI risk highest in the presence of electrocautery
When tip is used w/in 15 cm radius of pulse generator
Where should the cautery ground pad be placed in pts with PM/AICD
As far away from pulse generator and in location that prevents a direct line of current through PM
