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
What rhythm
treatment
1st degree heart block
monitor (usually asymptomatic)
Rhythm
tx
Second degree- Mobitz 1 (Wenkebach)
asymptomatic - nothing
symptomatic - atropine
What rhythm
2 treatments
CHB
mechanical pacemaker (transcutaenous, transvenous, implantable)
chemical pacemaker (isoproterenol)
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)
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)
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
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
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)
