Review of Dysrhythmias - Dr. McNeill Flashcards
What does a narrow QRS complex indicate regarding heart electricity
running through intrinsic circuitry (SA to AV to bundle of His, etc.
Definition of sinus rhythm
- even R to R
- P before every QRS
- QRS < 0.12 seconds
Asystole
- EKG appearance
- best chance of recovery
- flat line
- if d/t drug overdose and have narcan/naloxone on hand
Two types of vfib
course
fine
What causes the courseness of line in course vfib
- differing amts of myocardium fibrillation
- myocytes in diff states of excitation and refraction (not working together) so have multiple points of excitation
What is important about fine vfib
can look like asystole and the treatments for asystole is very different than vfib
Is there a pulse in vfib?
never !
what happens to rhythm at the end of vfib?
- see little blibs (agonal) that sort of look like PVCs
- is myocardium dying
Agonal/idioventricular rhythm
- treatment
- length can stay in this rhythm
- treat like asystole, stop the code (take leads off so family doesn’t get upset)
- can stay in this stage for 30-40 minutes until all myocardium dies
What rhythms does AED recognize?
V fib
V tach
What is width of QRS in all heart blocks?
narrow - means electricity flows through AV node
First degree AV block
- EKG findings
- prolonged PR, conduction delay
- P to Q is >0.2 seconds
- SA node is fine but extra long slow down in AV node
- does not progress to 2nd or 3rd degree blocks
Second degree AV block Mobitz type I
- EKG findings
- pulse
- PRI is short, longer, longest, dropped QRS
- pulse will feel abnormal
Second degree AV block Mobitz type II
- EKG findings
- pulse
- PRI always the same except when a QRS is dropped
- All QRS have a P
- Not all P have a QRS
- Pulse will feel abnormal
- can progress to 3rd degree block
Third degree AV block
- EKG findings
- rate
- R to R the same
- P to P the same
- Rs not related to Ps, atrium and ventricle doing their own thing
- rate usually brady <40
STAT treatment for 3rd degree AV block
pacemaker
What happens with P on T (R on T) phenomena
- when does it happen
- causes fibrillation
- why cardiovert doesn’t fire until after the T wave
- can happen in 3rd degree block
Sinus bradycardia
- cause
- SA node is slowed down
- often due to BB or CCB overdose, thyroid issues, low cortisol, etc
PEA
organized rhythm on EKG but no pulse
A fib
- EKG findings
- biggest worry
- no P waves
- narrow QRS (still using AV node)
- irregular rhythm bc AV node fires erratically
- biggest worry is thrombus/embolus formation
A flutter
- EKG findings
- what’s happening with atria
- Sawtooth or picket fence waves
- organized atrial contraction at a regular rate
- only certain atrial contractions result in QRS
Causes of PEA trick to remember
Hs and Ts
H’s (correctable) causes of PEA
- Hypovolemia (#1)
- Hypoxia (#2)
- Hypothermia
- Hypo/hyperkalemia
- Hydrogen ion (acidosis)
- Hypoglycemia
- Tension pneumo
- Tamponade
- Toxins
T’s (not correctable) causes of PEA
- thrombosis (MI, PE)
- Trauma (increased cranial pressure ICP)
When do you stop a code when person is in PEA
NEVER
- will turn into vfib if don’t fix underlying cause
Sinus tachycardia
- EKG findings
- rate
- narrow QRS
- P before every QRS
- rate usually not greater than 150
Supraventricular tachycardia
- EKG findings
- rate
- narrow QRS
- no P wave
- rate can go above 150
ventricular tachycardia
- EKG findings
- three types
- wide QRS
- can be pulseless, stable, unstable
Pulseless vtach treatment
treat like vfib, defibrillate
Unstable vtach
likely to have low bp, wet lungs full of fluid, likely to pass out
AED and three types of vtach
can’t distinguish between all three types, will shock them all. Don’t want to shock stable vtach…
Monomorphic vs. polymorphic QRS
- monomorphic means one foci, all electrical impulses from same place outside of intrinsic circuitry, all QRS will look the same
- polymorphic means multiple foci, all outs intrinsic circuitry, QRS will look different
Junctional rhythm
- EKG findings
- Narrow QRS
- No P, no atrial contractions
- AV node is pacemaker, why rate is so slow
Multifocal PVCs
- how serious
- how treat
- more ominous sign than random PVC here or there
- need to suppress/stabilize myocardium to raise vfib threshold… usually via medication
How many PVCs a minute are ok
6 or fewer - as long as look the same (monomorphic)
Premature atrial contractions (PAC)
- EKG
- pulse
- how common
- early SA node firing
- irregular rate
- not common
What two things feel like “my heart just skipped a beat”
- PAC
- PVC
Torsades de pointes
- associated with long QT and drugs
- if stable, mag sulfate
- if not stable, treat like vfib even if pt has a pulse
Where is P wave in re-entry phenomena
- often hidden in QRS
- inverted bc atria are depolarizing from AV node and moving up atria
What is super important in reentry
timing - myocytes have to be excitable, if still in refractory period, won’t get reentry
Are most reentry local or global? Where do they enter?
Local
Enter at AV node
What causes reentry
- one example
- QRS and rate
- most d/t ischemic changes from aging
- ex. SVT
- narrow but rapid QRS
WPW
- local or global reentry
- what is the bypass called
- life expectancy
- global
- Bundle of Kent
- 42 yo if untreated
How to treat global or local reentry?
change the ANS input, vagal stimulation for example
what do you not give to someone with WPW
BB, CCB, adenosine - will wipe out normal pathway and make things worse.
Three things required for reentry
- unidirectional block with conducting pathway
- critical timing
- length of effective refractory period of normal tissue
To know more about reentry…
… read the long slide at the end of Dr. McNeill’s lecture :)
