Basic ECG Flashcards
pacemaker cell
determine heart rate and initiate heart beats
SA and AV
electrical conducting cell
deliver the impulse to the myocardial cells
mycardial cells
contract and pump blood out of the heart
SA node
primary pacemaker of the heart (sets HR)
60-100 bpm
AV node
becomes the pacemaker if for some reason the SA node fails
AV node rate= 40-60bpm
narrow QRS complex means what for conduction
rapid conduction
normal pathway of conductance
do electrical conducting cells transmit current slow or fast?
quickly
What is the electrical conducting cells pathway? (6)
SA node anterior, posterior, middle fascicles AVN Bundle of His RBB and LBB Purkinje fibers
myocardial cells can initiate heat beats in what two situations?
1- SA and AV nodes fail
2- myocardium is irritated
what causes the myocardium to become irritated?
ischemia
electrolyte abnormality
acidosis
caffine
Do myocardial cells or electrical conducting cells transmit current quickly and more effectively?
electrical conducting cells
Wide QRS complex means what for conductance
slow conductance
current travels through the muscle, not normal pathway
what do ECG leads detect?
the electrical difference (voltage) between two limbs
Lead I provides a picture from what angle?
180 degrees
lead II provides a picture from what angle?
60 degrees
Where are the leads on a 3 lead ecg?
right arm, left arm, left leg
what is the limitation for the 3 lead system?
not as sensitive for detecting myocardial ischemia in the left ventricle
What does Lead I detect? What is the color-to-color for Lead I?
detects electrical difference between the right arm (-) and left arm (+)
white to black
What does Lead II detect? What is the color-to-color for Lead II?
electrical difference between right arm (-) and left leg (+)
white to red
What does Lead III detect? What is the color-to-color for Lead III?
electrical difference between the left arm (-) and left leg (+)
black to red
The green lead
neutral or ground lead
completes electrical circuit and doesn’t have anything to do with the EKG itself
brown lead
additional precordial lead
more sensitive for detecting LV ischemia
what helps make higher quality signal for the ECG electrodes
better connection
conductive gel on electrode
can clean skin
try not to place on hair
ECG paper 1mV= ___ small boxes?
10small boxes
ECG paper 1 large box
200msec
5mm
1 small box= ____ mseconds
40 msec
1mm
5 large boxes
1 second
300 large boxes
1 min
two ways to estimate the HR?
- count number of beats within a certain number of time (2 sec or 6 sec) and multiply to get number of beats in minute
- count # large boxes between beats
do segments or intervals of the ECG have waves?
intervals
P wave
atrial depolarization
duration <120msec (3 small boxes)
QRS complex
ventricular depolarization
duration <120msec (3 small boxes)
premature ventricular contractions are causes by what?
if the heart gets irritated and the ventricles start their own heart beat
ventricular escape rhythm
electrical conductance fails and ventricles take over as pacemaker
potential cause for wide QRS complex (not irritation or electrical failure)
current travels across myocardium instead of through purkinje fibers
Wolf Parkinson White Syndrome (WPW)
Right bundle branch block (RBBB)
Left bundle branch block (LBBB)
T wave
ventricular repolarization
height <5mm in leads I,II,III
U wave
follows t wave
not seen unless hypokalemia
J point
point at which S wave returns to baseline
Delta wave
upward slurring of Q wave seen in WPW syndrome
J wave (osborne wave)
“bump” on the S wave
seen in hypothermia
PR interval start
beginning of p wave
PR interval end
start of Q wave
PR interval normal time
120-200msec (3-5 small boxes)
Why is the PR interval time important?
shows conduction is delayed in the AV node and allows atria to finish contract before ventricles contract
OPTIMAL VENTRICLE FILLING
QT interval start
q wave
QT interval end
end of the t wave
What medications prolong the QT interval? When should these be avoided?
Zofran and Phenergan (antiemetics)
avoided in pts with prolonged QT syndrome
PR segment start
end of p wave
PR segment end
beginning of Q wave
ST segment start
J point
ST segment end
start of T wave
premature beat
heart beat that happens before it is expected to
examples of premature beats
premature atrial contraction
premature junctional contraction
premature ventricular contractions
escape beat
heart beat that comes after a long pause
examples of escape beats
ventricular escape beat
junctional escape beat
during systole what is and is not perfused?
Perfused: organs of the body
Not perfused: the heart (coronary arteries are closed by valve)
During diastole what is and is not perfused?
Perfused: the heart (coronary arteries drain blood from backflow)
Not perfused: everything else
Do patients with high or low heart rates have better coronary perfusion? why?
slower HR
- longer time coronary arteries open
- greater diastolic filling time
What is cardiac output determined by?
ventricular filling prior to contraction
What are the two ways that ventricular filling occurs and which is better?
active filling (atria contract)** BETTER passive filling (atria dont contract)
If the ventricular filling is passive will the volume be lower or higher than active filling?
lower
factors that can reduce ventricular filling (3)
1- heart beat that occurs without an atrial contraction (no P wave; passive)
2- premature heart beats (ventricles contract before being filled)
3- rapid HR (atrial or ventricular)
what happens when atria contract too quickly?
not enough time to fulling contract so reduces amount of blood forced to ventricles
What happens when ventricles contract too quickly?
dont have enough time to fill before contraction
Rapid heart rate leads to (3)
decreased cardiac output
hypotension
pulseless pt
ECG description of sinus bradycardia
p wave present
HR <60bpm
benefits of sinus bradycardia
normal/good for these patients:
healthy pt who exercises
CAD patients
sinus brady cardia in healthy patients
higher stroke volume
maintains adequate cardiac output
sinus brady cardia in patients with CAD
increased oxygen supply (diastolic filling)
decreased oxygen demand
What do patients with CAD normally take to maintain a slow HR?
beta blockers
what does the level of concern with sinus bradycardia depend on? (3)
1- age (children very bad)
2- severity (50 could be normal; 30 always concern)
3- how fast the drop in HR occured
treatment for bradycardia
1- drugs (glyco, atropine, epi)
2- if unresponsive to drugs then initiate cardiac pacing with pacemaker
temporary transcutaneous pacing
use defibrillator to pace the heart
set a HR and it will stimulate at that pace
permanent implantable pacemaker
permanent, under clavicle, delivers current to the pacing wires that are inside the heart
only works when the HR falls below a certain point
ECG description of sinus tachycardia
P wave present
HR > 100 bpm
etiology (causes) of sinus tachycardia
hypovolemia/hypotension
pain/light anesthesia
anesthetic concerns with sinus tachycardia (3)
increased cardiac oxygen demand (bad in CAD)
decreased cardiac oxygen supply (decreases diastolic filling; bad CAD)
indicates possible hypovolemia
treatment for sinus tachycardia
depends on cause:
1- fluids if bc hypovolemia
2- deepen anesthetic if light
3- consider beta blocker if not hypovolemic or light
ECG description of irregular sinus rhythm
looks like sinus but rate is irregular
faster during inspiration
slower during expiration
during spontaneous inspiration what happens to the intrathoracic pressure and preload
intrathoracic pressure decreases
preload increase
HR speeds up to pump excess out
during spontaneous expiration what happens to the intrathoracic pressure and preload?
intrathoracic pressure increases
preload decreases
HR slows does bc it doesnt have to pump out as fast
anesthetic concerns with irregular sinus rhythm
not as concerned
seen in healthy pts with deep breaths
ectopy
any heart beat that originates outside the SA node
ectopy is activated where? (3)
AV node
atrial myocardium
ventricular myocardium
Supraventricular ectopy (6)
premature atrial contraction (PAC) atrial flutter atrial fibrillation (Afib) Premature junctional contraction (PJC) Junctional rhythm junctional escape beat
ventricular ectopy (5)
premature ventricular contraction (PVC) escape ventricular contraction ventricular escape (idioventricular) rhythm ventricular tachycardia (Vtach) ventricular fibrillation (Vfib)
Premature Atrial Contraction (PAC) ECG
premature beat has:
upright p wave
normal/narrow QRS complex
physiology of PAC
artrial myocardium node got irritated and initiated a beat without signal from SA node
Anesthetic concerns with PACs
depends on the frequency
associated with less ventricular filling and will cause problems if they happen often
Atrial flutter ECG
saw tooth pattern ~250-300 P waves/min
more p waves than QRS complexes
physiology of atrial flutter
atrial myocardium contracts regularly ~250-300 times/min
decreased ventricular filling
AV node blocks some signals thus ventricular rate is much slower
anesthetic concerns with atrial flutter
ventricular filling and CO decreased
heart has higher oxygen metabolism
NO ELECTIVE SURGERIES
treatment for atrial flutter
medications (digoxin, amiodarone)
unstable then use synchronized cardioversion
what does sychronized cardioversion treat?
“shocking” the heart (cardioversion or defibrillation) treats unstably fast rhythms
what does pacing treat?
unstably slow rhythms
fibrillate definition
quiver rapidly
Atrial fibrillation (afib)
electrical impulses originate from irregular spots in the atrium and radiate through the atrium walls in an uncoordinated manor
afib EKG
no p waves
irregularly irregular rhythm
(may look like junctional rhythm but the afib is irreg irreg)
physiology of afib
atria chaotically quivering up to 500 atrial impulses a minute
AV allows occasional impulse to pass
clinical implications of afib
risk of clot formation in left atrium increases
cardiac output decreases 25-30%
what does afib cause in acute cases?
hypotension
anesthetic concerns with afib
a lot of patients have afib thats unresponsive to therapy- their bodies compensate
developing acute afib then they suffer from decreases CO (more concerning)
treatment for afib
treatment the same as with atrial flutter:
medications
synchonized cardioversion
special concern for treatment of afib prior to cardioversion
if afib present for more than 2 days then clot can form in left ventricle and needs to be on anticoagulants for at least 3 weeks prior to cardioversion
premature junctional contraction (PJC) ECG
premature beat has:
missing or inverted p wave (some cases inverted p wave can come after QRS complex)
normal QRS complex
physiology of PJC
AV node gets irritated and initiated a heartbeat without signal from SA node
impulse travels retrograde direction for the atria (none or inverted p wave)
anesthetic concerns with PJC
level of concern proportional to the frequency of PJC
junctional rhythm
beat or rhythm originated in the AV node
junctional rhythm ECG
inverted or absent p wave
normal QRS complex
normal junctional rhythm
40-60bpm
accelerated junctional rhythm
60-100bpm
junctional tachycardia
> 100bpm
physiology of junctional rhythms
SA node not working
AV node is primary pacemaker
do the atria contract during junctional rhythm?
yes but delayed
atrial and ventricular contractions occur at similar times so decreases ventricular filling
anesthetic concerns with junctional rhythm
HR is slow and less ventricular filling; concerning if BP is low
**converts back to sinus rhythm after robinul
escape beat
a beat that comes after a long pause
junctional escape beat ECG
escape beat that has junctional properties
inverted or absent p wave
normal or narrow QRS
physiology of junctional escape beat
SA node temporarily failed
av node jumps in to initiate heat beat
SA node works again
¯_(ツ)_/¯
anesthetic concerns with junctional escape beats
the frequency in which this occurs is proportional to level or concern
treatment for junctional escape beats
robinul, atropine, pacing if frequently or pauses are prolonged
premature ventricular contractions (PVC) EKG
no p wave
a wide or bizarre or different QRS complex
physiology of PVC
ventricular myocardium initiates single beat prematurely
anesthetic concerns with PVC
concerning if frequent
PVC dont produce pulse (if bigeminal then pulse is half of EKG rate)
bigeminy
cardiac rhythm where a normal beat is followed by irregular beat
What can PVCs develop into?
Vtach if their frequency continues to increase
treatment of PVC
antiarrhythmics (lidocaine, amiodarone)
Robinul or atropine
what are the three types of premature beats?
premature atrial contraction (PAC)
premature junctional contraction (PJC)
premature ventricular contraction (PVC)
ventricular escape beat EKG
long pause followed by ventricular beat (wide QRS)
no p wave
similar to junctional escape beat but no p wave
physiology of ventricular escape beat
SA and AV node fail
ventricular myocardium initiates beat
SA node starts to work
¯_(ツ)_/¯
anesthetic concerns with ventricular escape beats
concern increases as frequency increases
consider robinul or atropine if it occurs frequently
what are the two types of escape beats?
junctional escape beat
ventricular escape beat
ventricular escape rhythm (idioventricular) EKG
no pave
wide QRS complex
slow HR <60bpm
physiology of ventricular escape rhythms
SA and AV nodes failed
ventricular myocardium starts initiating beats
anesthetic concerns with idioventricular rhythm
no active ventricular filling
HR slow
low CO
NO ELECTIVE CASE
treatment for ventricular escape rhythm
cardiac pacing
epi if unstable
When should you avoid lidocaine?
ventricular escape rhythm
3rd degree AV node block
idoventricular rhythm pace
<60 bpm
accelerated idioventricular rhythm pace
60-100bpm
vtach
> 100bpm
EKG ventricular tachycardia (Vtach)
no p wave
wide QRS complex
HR >100bpm
physiology of vtach
ventricular myocardium initiating beats at rapid rate
high oxygen consumption
minimal ventricular filling
anesthetic concerns with vtach
MEDICAL EMERGENCY
immediate cardioversion/defibtrillation
what are the two treatments of vtach?
antiarrhythmics
electrical cardioversion
ventricular fibrillation (vfib) EKG
just deflections from the baseline
no p wave or QRS complex
physiology of vfib
ventricles are quivering at rapid rate
heart consuming a lot of oxygen
no pulse or cardiac output
anesthetic concerns with vfib
MEDICAL EMERGENCY
(more than vtach)
requires immediate defibrillation
treatment for vfib
defibrillation
CPR until perfusing rhythm returns
1st degree AV block
long PR interval
>1 large box
physiology of 1st degree AV block
conduction through the AV node is slower than normal
anesthetic concern with 1st degree AV block
don’t need to worry
2nd degree AV block (mobitz)
dropped QRS complex (sometimes can be two in a row)
what are the two types of 2nd degree blocks?
mobitz type I (wenckebach)
mobitz type II
mobitz type I 2nd degree block EKG
dropped QRS complex
increasingly longer PR intervals before the ORS is dropped
physiology of mobitz type I 2nd degree block
wenckebach
partial block in AV node that is bad enough to fully block sometimes
mobitz type II 2nd degree block EKG
dropped QRS complex
constant PR interval before the QRS is dropped
physiology of mobitz type II 2nd degree block
block below the AV node thats bad enough to completely block some impulses
anesthetic concerns with 2nd degree AV block
NO ELECTIVE CASES
more concerning the more dropped beats
potentially require pacing
3rd degree AV block (complete heart block) EKG
have p waves and QRS complexes that are not associated with eachother
“atrioventricular dissociation”
what is the normal ventricular rate for 3rd degree AV block
~30-40bpm
physiology of 3rd degree AV block
atria are contracting no impulse goes through AV though
ventricles also initiate their own beats
contracting independently
For a 3rd degree AV block are the QRS complexes normal or wide?
they can be either
(we dont know why)
¯_(ツ)_/¯
clinical effects of complete heart block
atria may try to empty into full ventricles
ventricles may contract when empty
serious reduction in cardiac output
anesthetic concerns with 3rd degree AV block
NO ELECTIVE CASES
CO low
treatment for complete heart block
cardiac pacing
epi if unstable
signs of ischemia/infarction (3)
ST segment changes
abnormal T waves
Abnormal Q waves
ST depression vs ST elevation (what does each indicate)
ST depression: ischemia
ST elevation: infarction
what are the two abnormal T waves
peaked T wave
T wave inversion
Myocardial ischemia treatment
increase oxygen supply
decrease oxygen demand
ways to increase oxygen (5)
1-100% FiO2 2-decrease HR (beta blocker) 3-maintain normal BP (avoid hypotension) 4-administer NTG 5-administer aspirin
ways to decrease oxygen demand (3)
1-decrease HR (beta blocker)
2-avoid pain /anxiety
/tachycardia (narcotics/sedatives)
3- avoid high afterload (Htn)
Why is it important to compare preoperative EKG to intraoperative EKG?
signs of ischemia and infarction can be present in an EKG due to an old MI
