Apex- Monitors and Equipment > Cardiac rhythms Flashcards
Which pathway depolarizes the left atrium
A. Thorel tract
B. Bachmann bundle
C. Kent bundle
D. Wenckebach tract
B. Bachmann bundle
There are 3 internodal tracts that travel from the SA to aV node:
1. Anterior internodal tract (gives rise to the Bachmann bundle)
2. Middle internodal tract (wenkebach tract)
3. Posterior internodal tract (thorel tract)
Kent’s bundle is a pathologic accessory pathway that is responsible for Wolff-Parkinson-White syndrome
Where does the electric signal go from the SA node
SA node → internodal tracts → AV node → Bundle of His → Bundle Branches → Purkinje fibers
Match each phase of the ventricular AP to its corresponding component on the EKG waveform
-QRS complex, QT interval, T wave
-Phase 3, 0, 2
Phase 0 → QRS complex
Phase 2 → Qt interval (plateau phase)
Phase 3 → T wave (final repolarization)
Phase 4 → T > QRS (resting phase)
P wave →
PR interval →
QRS complex →
ST segment →
T wave→
P wave → atrial depolarization begins
PR interval → atrial depolarization is complete
QRS complex → Atrial repol + ventricular depol starts
ST segment → Ventricular depolarization complete
T wave → ventricular repolarization begins
What is the absolute refractory period?
Where does it start and end on the EKG
From what phase to what phase
Period where NO stimulus - no matter how strong - can depolarize the myocyte
QRS > Mid- T wave
What is the relative refractory period?
where does it start/end?
It’s a period of time wehre a larger than normal stimulus is required to depolarize the myocyte
second half to end of T-wave
label events occuring in whited out boxes
also label stars - which waves
label phases, event, and the ionic movement during each
Phase 0 → ventricular depolarizaion →Sodium in
Phase 1 → initial repolarization → cloride (-) in, K+ out
Phase 2 → Plateau (ST) → CA++ in, K+ out
Phase 3 → Final repolarization → K+ out
Phase 4 → resting phase K+ leak
What portion of the ventricular action potential occurs during the ST segment?
end of ventricualr depolarization
Match each disease with the EKG abnormality that it is MOST likely to cause:
WPWS, Pericarditis, ICH, Hypokalemia
PR interval depression, U-wave, Peaked T wave, Delta wave
WPWS → Delta wave
Pericarditis → PR interval depression
ICH → Peaked T- Wave
Hypokalemia→ U- Wave
T/F- pericarditis can casue PR-interval prolongation
False- depression
Q waves suggest MI if the:
amplitude is >
duration is >
or depth is >
amplitude > 1/3 the R wave
duration > 0.04 seconds
depth > 1mm
4 things that can cause peaked T-waves
- Hyperkalemia
- Myocardial ischemia
- LVH
- Intracranial bleeding
My measuring _ , we can quantify the amount of ST elevation and depression.
As a general rule of thumb, changes greater than or less than what are significant
The J-point
>
- 1.0 or < -1.0
4 EKG changes seen with HYPOkalemia
Vs 6 changes seen with HYPERkalemia
- increased PR interval
- increased QT interval
- flattened T-waves
- U-wave
- Prlonged PR (same) + 2. prolonged QRS
- PEAKED T-waves + 4. flattened P-waves
- Sinus wave pattern + 6. Vfib
Match each lead to the cardiac region it monitors:
aVF, V3, Lead 1, V1
Lateral wall, septum, inferior wall, anterior wall
aVF → Inferior
V3 → Anterior
V1 → Septum
Lead 1 → Lateral
On the EKG, what are the:
Bipolar leads:
Limb leads:
Precordial leads:
Bipolar leads → I, II, III
Limb leads → aVR, aVL, aVF
Precordial leads → V1-V6
RCA supplies the _ heart & is monitored by leads:
Circ supplies the _ heart & is monitored by the leads:
LCA/LADsupplies the _ heart & is monitored by leads:
RCA - inferior heart - II, III, aVF
Circ supplies- left lateral heart - I, AvL, V5, V6
LCA/LAD supplies antierior heart - V1-V4
explain this image
a positive deflection occurs when the vector of depolarization travels towards the positive electrode
A negative deflection occurs wehn the vector of depolarization travels away from the positive electrode
A Biphasic deflection occurs wehn the vector of depolarization travels perpendicular to the positive electrode
The heart depolarizes from the (apex to base or base to apex)
&
from the (endocardium to epicardium or epicardium to endocardium)
Base → apex
&
Endocardium → epicardium
The mean electrical vector tends to point: (select 2):
-towards areas of hypertrophy
-towards areas of myocardial infarction
-away from areas of hypertrophy
-away from areas of myocardial infarction
Towards areas of hypertrophy
and away from areas of infarction
Towards hypertrophied areas (more tissue to depolarize)
away from areas of infarction (vector travels around these areas)
The easiest way to determine axis devation is to examine which 2 leads?
What’s normal, left vs right deviation, & extreme right deviation
I & avF
Normal : Lead 1 +, aVF +
Left: Lead 1 +, aVF -
Right: Lead 1 -, aVF +
Extreme right: Lead 1 -, aVF -
What are right and left axis deviations typically caused by?
right axis devation - things that affect the right heart : COPD, acute bronchospasm, cor pulmonale, PE
left axis devation- things that affect the left heart: chornic HTN, LBBBB, AS, AI, MR
What types of axis deviations are these
Orange - extreme right (2 thumbs down)
Green = normal (2 thumbs up)
Red = Left axis devation (leads Leaving eachother)
Blue = Right axis devation (leads Reaching for eachother)
All of the following are effective for treatment of afib EXCEPT:
A. Verapamil
B. Digoxin
C. Metoprolol
D. Adenosine
Adenosine
-it slows conduction through the AV node
- stimulates cardiac adenosine-1 receptor; adenosine activates K+ currents → hyperpolarizes cell membrane and reduces AP duration
not efficaious for afib, flutter, torsades, or VT
works well for SVT and WPW with a narrow QRS
what’s this rhythm and what is one thing that can cause it
sinus arrhythmia → occurs wehn the SA node’s pacing rate varies with respiration (usually benign)
Bainbridge reflex can cause this!
Inhalation → decreased intrathoracic pressure → increased venous return → increased HR
Exhalation → increased intrathoracic pressure → decreased venous return → decreased HR
What is often the source of sinus bradycardia
increased vagal tone
What is the first line treatment for sinus bradycardia
what should you be careful of and why
Atropine
underdosing it (<0.5mg IV) can cause paradoxical bradycardia which is thought to be mediated by presynaptic muscarinic receptors
THEN WHY TF DOES IT COME IN 0.4mg/ml VIALS?
What should you do with a severely symptomatic bradycardic patient
immediate transcutaneous pacing
What drug can be given in the setting of beta-blocker or CCB overdose.
Dosage
How does it work?
Glucagon
initial dose = 50-70mcg/kg q 3-5min
can be followed by infusion of 2-10mg/hr
it stimulates glucagon receptors on the myocardium, which increases cAMP → increased HR, contractility, AV conduction
What is acute onset a-fib treated with?
what should you start at
Cardioversion - start at 100j
When does a TEE need to be done prior to cardioverting afib?
why?
if afib onset is >48hrs ago or if onset is unknown
to r/o atrial thrombus
T/F- new onset or undiagnosed afib is an indication to cancel surgery
True
What is the most common postop tachydysrthymia
when does it usually occur
what population is at greatest risk?
afib
POD 2-4
older patients after CT sugery
TF- volatile anesthetics are a known cause of junctional rhythm
treatment for junctional rhythm if it impacts hemodynamics?
What junctional rhythm progress to? issue?
True
*Atropine 0.5mg IV can be given if hemodynamics are affected
can progress to junctional tachycardia (narrow complex tachycardia) > can produce hemodynamic instability
PVCs should be treated in what 3 circumstances
how should they be treated?
- Frequency > 6/min
- polymorphic
- runs of 3 or more
- Reverse underlying cause : hypoxia, hypercarbia, d/c QT prolonging drugs, tx lytes
- If symptomatic - Lidocaine 1-1.5mg/kg followed by a gtt @ 1-4mg/min if continues
What is the most common dysrythmia of sudden cardiac death
vfib
What is the syndrome associated with a sodium ion channelopathy in the heart?
Who is it most commonly seen in?
What are the diagnostic EKG findings and considerations for someone with this?
Brugada Syndrome
males from southeast asia
Right BBB and persistent ST elevation in precordial leads V1-V3
-pt may require ICD or pad placement during surgery
Brugada syndrome type 1 vs type 2
1 & 2 > ST elevations >/= 2mm
1 → DOWNSLOPING ST segment & INVERTED T-wave
2 → “saddle back” (think 2 words = 2) ST-wave configuration & UPRIGHT or Biphasic (2) T wave
What rhythm
Second degree heart block- Mobitz 2
Some P’s conduct to the ventricles, while others don’t (usually there is a set ratio of 2:1 or 3:1). After the dropped QRS, the next P arrives right on time
What rhythm
Second degree heart block- Mobitz 2
Some P’s conduct to the ventricles, while others don’t (usually there is a set ratio of 2:1 or 3:1). After the dropped QRS, the next P arrives right on time
What is 1st degree heart block
treatment?
PR > 0.20
usually asymptomatic and no treatment required
Mobitz 1 vs 2
treatments
1 → wenchebach- PR longer longer drop
2 → Some P’s conduct to the ventricles while others dont (usually set ratio of (2:1 or 3:1)
often asympomatic
1 → atropine if symptomatic
2 → pacing
True/False: Atropine is treatement of choice for 2nd-degree heart block- Mobitz 2
False - Mobitz 1
Mobitz 2 often does not respond to Atropine and pacing is required
3 causes of 1st degree heart block
- age related degenerative changes
- CAD
- drugs: dig/amio
What rhythm
treatment
1st degree heart block
monitor (usually asymptomatic)
Rhythm
tx
Second degree- Mobitz 1 (Wenkebach)
asymptomatic - nothing
symptomatic - atropine
What causes 3rd degree heart block? (2)
- fibrotic degeneration of the atrial conduction system
- Lenegres Disease
What rhythm
2 treatments
CHB
mechanical pacemaker (transcutaenous, transvenous, implantable)
chemical pacemaker (isoproterenol)
What rhythm is associated with Stokes-Adams attack and what is that?
CHB
- decreased CO → decreased cerebral perfusion → syncope
Which type of heart blocks may require a pacemaker?
Mobitz 2 & CHB
Which inotrope best treats 3rd degree heart block?
Isoproterenol
Match each antiarrhythmic agent with it’s drug class (1-4)
-propanolol, lidocaine, amiodarone, verapamil
1 → Lidocaine
2 → Propanolol
3 → Amiodarone
4 → Verapamil
1 → inhibit fast sodium channels
2 → decrease rate of depolarization
3 → inhibit potassium ion channels
4 → inhibit slow calcium channels
What are the 4 classes of antiarrhythmics and their MOA
1 → Sodium channel blockers
2 → Beta blockers
3 → K+ channel blockers
4 → Calcium channel blockers
1 → quinidine, procainamide, disopyramide; lidocaine & phenytoin; flecainide, propafenone
2 → obvious ones
3 → amiodarone & bretyium
4 → verapamil & diltazem
What phases of the action potentials do each class of antiarrhythmic agents affect?
1 → depression of phase 0 & phase 3 repolarization
2 → slows phase 4 depolarization in the SA node
3 → prolongs phase 3 repolarization
4 → decreases conduction velocity through the AV node
1→ sodium channel blockers (lido)
2 → betablockers
3 → k+ channel blockers (amio)
4 → calcium channel blockers (verapamil and cardizem)
How does amiodarone work?
It prolongs phase 3 repolarization (increases Qt), increases effective refractory period
K* channel blocker
bretium also in this class (class 3)
Difference between class 1A, B, C antiarrhythmics, examples of each (3,2,2 respectively)
class 1 = sodium channel blockers (phases 0 and 3)
1A: mod ↓phase 0; prolonged phase 3 (increased Qt)
1B: weak ↓phase 0;** shortened **phase 3
1C: STRONG ↓phase 0, little effect on phase 3
1A → quinidine, procainamide, disopyramide
1B → lidocaine, phenytoin
1C → flecainide, propafenone
What class of antiarrythmic agent and how the AP is affected
answer from left to right
- Slowing of phase 4 depolarization → Class 2→ betablockers
- Strong depression of phase 0, little effect on phase 3 repolarization → class 1c → Na channel blockers - flecanide & propafenone
- Prolonged phase 3 repolarization → K+ channel blocker (increased QT) → amio & bretyium
- Moderate depression of phase 0 depolarization + prolonged phase of phase 3 repolarization (increased QT) → Class 1A → quinidine, procainamide, disopyramide
- Decreased conduction velocity trhough AV node → Class 4 → Ca++ channel blockers → verapamil and diltazem
- Weak depression of phase 0, shortened phase 3 repolarization → class 1B (NA++ blockers) → lidocaine and phenytoin
*When thinking about how antidysrhythmics work, ask yourself:
1. Are they depressing phase 0 (class 1)
2. Are they effecting phase 3 repolarization (class 1, 3)
3. Or are they slowing phase 4 depolarization (class 2)
We have andenosine naturally circulating in our bodies?! what does it do?
Yep, it slows conduction through the AV node
it stimulates the cardaic adenosine-1 receptors and promotes potassium efflux, hyperpolarizing hte cell membrane, and slowing conduction
How is adenosine metabolized?
1/2 life?
rapidly in the plasma
5 seconds
T/F - Adenosine can be used for rapid AFIB
FALSE
not useful for afib/flutte – only SVT and WPW with narrow complex
T/F- Adensosine can cause bronchospasm in the asthmatic patient
True
peripheral vs central line dosing of adensoine (1st and 2nd doses)
what peripheral site is preferred?
Peripheral 6mg → 12mg
Central 3mg → 6mg
*AC preferrerd for peripheral - closest to heart
Wolff- Parkinson- White syndrome is associated with:
A. Atrial re-entry
B. SA nodal re-entry
C. A-V re-entry
D. Ventricular re-entry
C. A-V reentry
- WPW occurs when an accessory pathway joins the atrium to the ventricles (kent’s bundle)
What is the most common cause of tachyarrhythmias?
Re-entry pathways
A patient with WPWS develops afib during surgery. Select the BEST treatment for this situation (select 2)
- Cardioversion
- Verapamil
- Digoxin
- Procainamide
Cardioversion and Procainamide
In the normal conduction pathway, the cardiac impulse is delayed at the AV node, meaning it has a long ……
how does this relate to accessory pathways?
refractory period
in the accessory pathway, there is no delay, so the impulse quickly moves from the atrium to the ventricle → there is no gate keeper (slowed movement thru the AV node)
What is the diagnostic feature of WPWS?
3 other things that can be commonly seen
- Delta wave
Short PR (<0.12), Wide QRS, Possible T-wave inversion
After the SA node depolarizes, the electricle impulse travels through the accessory pathway and the same time as the AV node; the accessory pathway route is not delayed like the AV route and arrives at the ventricle earlier, causing the delta wave.
Orthodromic AVNRT vs Antidromic AVNRT
incidence →
reentry pathway route →
QRS →
treatment →
which one is more dangerous and why
antidromic is more dangerous bc the gatekeeper function of the AV node is bypassed and the heart rate can increase well beyond the heart’s pumping ability (dramatically reducing filling time)
Drugs to avoid with a patient with an antidromic AVNRT (5)
why?
Lidocaine
Adenosine
Beta-blockers
Calcium channel blockers
Digoxin
(L-ABCD) (Love ABCD)
Bc if you give a drug that preferentially blocks the AV node to an antidromic AVNRT, then you’ll force conduction along the acessory pathway which can induce vfib!
why is it bad news if a patient with WPW goes into Afib?
how do you want to treat it and why?
bc during afib the atria can depolarize up to 300 times a mintue, and combining this with WPW can preciptate CHF, vfib, and death.
*Procainamide is the treatment of choice bc it increases the refractory period in the accessory pathway. If the patient is hemodynamically unstable, then cardioversion is the best option
*avoid drugs that increase the refractory period of the AV node
What is the definitive treatment for WPWS?
radiofrequency ablation of the accessory pathway
What is the only narcotic known to increase the QT interval?
Methadone
How can furosemide affect the QT interval?
it can cause hypokalemia and hypomagnesia which both can prolong the QT
when asked about how something affects the QT interval - think does it affect the lytes? low lytes = long qt
how does hyperventilation affect the QT interval?
hyperventilation shifts K+ into the cells
→ decreased serum K can prolong the QT interval
2 acute treatments for torsades?
mag sulfate and cardiac pacing
What 2 genetic syndromes are associated with Torsades?
Romano Ward & Timothy
Timothy Romano Ward
Normal QT interval for men vs women
men > 0.45
women > 0.47
Why do we used corrected QT?
bc the QT interval varies inversely with HR
Match the NBG pacemaker identification code to its designated function:
Postion 1 →
Position 2 →
Position 3 →
Postion 4 →
Mneumonic?
Chamber sensed, Progamability, Response to sensed event, chamber paced
Postion 1 → chamber Paced
Position 2 → chamber Sensed
Position 3 → Response to sensed event
Postion 4 → Programability
PaSeR
Chamber Paced
Chamber Sensed
Response of pacmaker if native activity is sensed
What kind of pacing modes are AAI, VVI ?
What does the pacemaker do?
Single-chamber demand pacing
BACKUP MODE
only fires wehn the native HR falls below a pre-determinded level
AAI - atria paced, atria sensed, inhibition
VVI - ventricle paced, ventricle sensed, inhibition
*inhibition = if natative activity is sensed, the pacemaker is inhibited (won’t fire – unless under a certain rate)
What is the most common mode of modern day pacemakers?
How does it work?
DDD
dual paced, dual sensed, dual response
ensures the atrium contracts first, followed by the ventricle and improves AV-synchrony
Describe AOO pacing
risk?
Asynchrounous pacing
-Atrium is paced, no chamber is sensed, and no response to native cardaic electricle activity
R-on-T
Describe VVI pacing
Single-chamber demand pacing
Ventricle is paced and sensed & the pacer is inhibited if native electric activity is sensed
A patient undergoing bunionectomy has a VOO pacer with a rate of 80bmp. during the procedure, there is failure to capture and the HR decreases to 50bmp. Which of the following BEST explains why this complication occured?
A. EtCO2 was 20mmHg
B. An ultrasonic Harmonic scalpel was used
C. The patient was hyperthermic
D. The electrocautery setting was changed from “coag” to “cutting”
A. EtCO2 was 20mmHg
The pacer failed to capture because hypocarbia (which caused hypokalemia) made the myocardium more resistant to depolarization. The same electrical stimulus from the pacer was no longer sufficent to depolarize the heart. You’ll see the pacer spikes, but you wont see capture
-when compared to ESU, the use of a ultrasonic harmonic scalpel decreases the risk of electromagnetic interference
-changes from “coag to cutting” also reduces the risk of EMI
-hypothermia makes the myocardium more resistant to to depolarization (also explains why hypothermia causes bradycardia)
What does putting a magnet on a pacemaker vs. ICD vs. Pacer+ICD combo
Pacer → converts it to asynchronous mode (usually but not always) > asynchonous = delivers a constant rate despite underlying native activity
ICD → suspends ICD and prevents shock delivery
PACER+ICD: suspends ICD and prevents shock delivery; no effect on pacemaker function (interesting?)
What is the most critical information to have preop in someone with a pacemaker?
what’s their underlying rhythm - so you know how to prepare for device failure
-can be treated with isoproterenol, epi, or atropine (depends on the underlying rhythm)
what’s going on here….concern?
failure to sense
-pacer is sending sporatic impulses
-concern for R on T
not sure wtf i would do other than consult cardiology to interrogate it?
whats going on
6 conditions that could lead to this
failure to capture
conditions that can hyperpolarizing the myocardium, making it more resistant to depolarization (electrical stimulus)
- hyperkalemia, hypokalemia
- hypocapnia (intracellular K shift)
- hypothermia
- MI
- Fibrotic tissue builiding up on leads
- Antiarrythmic meds
can also be from electrode displacement or wire fracture
What gives off more EMI, coag or cutting setting on the bovie?
coag
The risk of EMI is highest when electrocautery tip is used within how man cm radius of the pulse generator
15cm
(i read somewhere that concern should be have when operating above umbilicus)
where should the bovie pad be placed on someone with a pacer?
far away from the generator, in a location that prevents a direct line of current thru it
T/F- a pacemaker is a contraindication for lithotripsy
False - the beam should be directed away from the generator
T/F- ECT is contraindicated in a person with a pacemaker
false
MRI is the only contraindication (even though some newer ones are MRI safe)
The EKG in this image is due to injury of the:
A. His bundle
B. AV node
C. SA node
D. Bachmann’s bundle
A. Bundle of His
It’s Mobitz 2 - affected regions of this are the His bundle or bundle branches
The EKG in this image is due to injury of the:
A. His bundle
B. AV node
C. SA node
D. Bachmann’s bundle
A. Bundle of His
It’s Mobitz 2 - affected regions of this are the His bundle or bundle branches
Which EKG change is associated with ICH?
A. short PR
B. peaked T waves
C. Deep Q waves
D. U waves
B. Peaked T’s
- PR depression > pericarditis
- Deep Q waves > MI
- U waves > hypokalemia
What kind of axis devation?
Left axis devation
Lead 1 is postive and AVF is negative
Which Bipolar limb lead is ALWAYS positive
Bottom left
Which Bipolar limb lead is ALWAYS positive
Bottom left
click on tha area of hexagonal reference system that correlates with left axis devation
-90 to -30 degrees
Normal = -30 to +90
Left axis = < -30 (L , to the Left)
Right = > +90 (R, to the right)
T/F- Sinus tachycardia is the MOST common cause of acute MI
TRUE!
Which of the following if the reference point for measuring changes in the ST segment?
A. PR Segment
B. ST Segment
C. J Point
D. Qt interval
A. PR segment
The J point is where the QRS complex ends and the ST segment begins. By measuring this point relative to the PR segment, we can quantify the amount of elevation and depression
Which of the following if the reference point for measuring changes in the ST segment?
A. PR Segment
B. ST Segment
C. J Point
D. Qt interval
A. PR segment
The J point is where the QRS complex ends and the ST segment begins. By measuring this point relative to the PR segment, we can quantify the amount of elevation and depression
T/F- the bovie pad is a gounding pad
FALSE - no one in the OR should be grounded, not even the patient
it is a return electrode where electricty flows after it flows through the tip of the electrocautery > pt > exits patient through the return electrode
Word association game:
Lengres disease
CHB
Word association game:
Romano ward disease/syndrome
What other disease is associated w it
Torrsaddes
(+Timothy disease)
DISOPYRAMIDE
CLASS 1A antidysrhythmic w procainamide and quinidine
Mod phase 0, prolonged phase 3(qt)
