cardiac rhythm monitors and equipment Flashcards
which pathway depolarizes left atrium
bachmann bundle (anterior internodal)
outline the conduction system pathway in the heart
SA node –> internal tracts –> AV node –> bundle of his –>bundle branches –> purkinje fibers
outline the internal tracts
anterior internodal tract
middle internodal tract (winkebach)
posterior internodal tract (thorel tract)
conduction velocity in SA and AV nodes
0.02-0.1 m/sec (slow conduction)
conduction velocity in myocardial muscle cells
.3-1 m/sec (intermediate conduction)
conduction velocity in his bundle, bundle branches, and purkinje fibers
1-4 m/sec (fast conduction)
conduction velocity is a function of (3)
- RMP
- amplitude in the AP
- rate of change in membrane potential during phase 0
conduction velocity is affected by (5)
ANS tone
hyperkalemic induced closure of fast Na channels
ischemia
acidosis
anti arrhythmic drugs
what does the james fiber accessory pathway connect
atrium to AV node
what does the atrio hisian fiber accessory pathway connect
atrium to his bundle
what does the kents bundle accessory pathway connect
atrium to ventricle
what does the mahaim bundle accessory pathway connect
av node to ventricle
review 5 phases of ventricular AP and how it corresponds to EKG
0= rapid depol (QRS)
1= initial repol (QRS)
2=plateau phase (QT interval)
3= final repol (T wave)
4= resting phase (T–> QRS)
when does the absolute and relative refractory period occur during ventricular AP?
ion movement during each phase
ID the electrical event
atrial depol begins
ID the electrical event
atrial depol complete
ID the electrical event
atrial repol, ventricular depol begins
ID the electrical event
ventricular depol complete
ID the electrical event
ventricular repol begins
ID the electrical event
repolarization complete
ID red, blue, green lines on wiggers diagram
review left ventricular volume in relation to mechanical events in the heart
biphasic p waves in lead II suggests
left atrial enlargement. think mitral stenosis
tall P waves suggests
RA enlargement. think cor pulmonale
duration and amplitude of
P wave
PR interval
Q wave
QRS complex
PR interval depression suggests
pericarditis
atrial infarction
Q wave: consider MI if
amplitude is > 1.3 of R wave
DOA > .04 seconds
depth is >1mm
if QRS complex increased, consider
LVH, BBB, ectopic beat, WPW
duration and amplitude for
QTc
ST segment
T wave
U wave
Osborn wave
ST segment: consider MI if
elevation or depression >1mm
ST segment elevation also caused by (2)
endocarditis
hyperkalemia
T wave points in opposite direction of QRS if repolarization is prolonged by
MI, RBBB
peaked T waves are caused by (3)
ischemia, LVH, intracranial bleed
if U wave is > 1.5mm, consider
hypokalemia
describe osborn wave
small positive deflection immediately after QRS complex (at beginning of ST segment), may occur with hypothermia
you measure J point relative to
PR segment. isoelectric line
J point and ST elevation/depression
greater than 1.0mm increase or decrease is significant
how does hyperkalemia affect EKG
narrow and peaked T
short QT
wide QRS
low p amplitude
wide PR
nodal block
sine wave fusion of QRS and T –> VF or asystole
how does hypokalemia affect EKG
U wave
ST depression
flat T wave
long QT interval
hypercalcemia versus hypocalcemia and the EKG
hypercalcemia –> short QT
hypocalcemia –> long QT
hypermagnesemia and EKG
no significant effect unless very high. heart block, cardiac arrest
hypomagnesemia and EKG
no effect unless very low, long QT
review positive, negative, biphasic vector of depolarization and where the current travels
(+) deflection occurs when vector of depol travels towards positive electrode
(-) deflection occurs when vector or depol travels away from positive electrode
biphasic deflection: vector of depol travels perpendicular to positive electrode
vector of depolarization - QRS complex
heart depolarizes from base to apex and endocardium to epicardium
polarity: myocytes go internally (-) to internally (+). produces a positive electrical current
which are the bipolar leads
I, II, III
limb leads
aVr, aVL, aVF
precordial leads
V1-V6
outline where aVR, aVL, lead I-III, aVF are
outline V1-V6
correlate each lead with the region of the heart it monitors
vector of repolarization - T wave
heart repolarizes in opposite direction of depol (QRS complex)
from apex–> base and from
epicardium–> endocardium
polarity:
myocytes go from internally (+) to internally (-). produces negative electrical current
what does lead I and aVF look like during:
right axis deviation
extreme right axis deviation
normal axis
and left axis deviation
normal: lead 1 (+) and lead aVF (+)
left axis deviation: lead 1 (+) and lead aVF (-)
right axis deviation: lead 1 (-) and lead aVF (+)
extreme right axis deviation: lead 1 (-) and lead aVF (-)
“if the leads are reaching toward each other, right axis deviation
if theyre both facing up, two thumbs up (normal)
if the leads are leaving each other, left axis deviation
two thumbs down, extreme right axis deviation”
normal axis is between (degrees)
-30 and +90
left axis deviation is (degrees)
more negative than -30
right axis deviation is (degrees)
more positive than 90 degrees
the mean electrical vector tends to point
towards areas of hypertrophy (there is more tissue undergoing depolarization)
away from areas of MI (vector has to move around these areas
causes of right axis deviation
COPD
acute bronchospasm
cor pulmonale
pHTN
PE
causes of left axis deviation
chronic HTN
LBBB
aortic stenosis
aortic insufficiency
mitral regurg
how does inhalation affect heart rate
decreases intrathoracic pressure, increases venous return, increases HR (bainbridge, stretching of right atrium and SA node)
how does exhalation affect heart rate
increased intrathoracic pressure, decreased venous return, decreased HR
when does this rhythm occur
occurs when SA node pacing varies with HR (sinus arrhythmia).
what is the source of this rhythm
increased vagal tone is usually the source of bradycardia
how is glucagon useful in the setting of BB or CCB OD (MOA) and dose
stimulates glucagon receptors in the myocardium and increases cAMP which increases HR, contractility, and AV conduction.
initial dose 50-70mcg/kg q3-5m
infusion 2-10mg/h
how to treat acute onset, onset >48h old
surgical considerations
acute onset: 100j cardioversion
>48h, need TEE to r/o thrombus
new onset afib is an indication to cancel surgery. (there is an increased risk of periop mortality in general with afib)
how to treat, specific characteristics
atrial rate usually 250-350bpm, flutter is an organized supra ventricular rhythm
onset older than 48h, need TEE before cardioversion
cardiovert with 50j if hemodynamically unstable
this is an indication to cancel surgery
cause, tx of this rhythm
junctional rhythm caused by AV node acting as pacemaker. 40-60bpm. because phase 4 depol of AV node is slow
-caused by SA node depression (volatiles), SA node block, prolonged conduction at AV node
-can give atropine .5mg IV
rhythm origination, conditions that precipitate this, when to treat
origination: from foci below av node. as such, QRS complex is wide
caused by: SNS stimulation (hypoxia, hypercarbia, acidosis, light anesthesia), MI, valvular heart disease, cardiomyopathy, prolonged QT interval, hypokalemia, hypomagnesemia, digitalis toxicity, caffeine, cocaine, alcohol, mechanical irritation (CVC insertion).
-tx when frequent (>6/min), polymorphic, or occur in pairs of 3 or more. reverse underlying cause, lido 1-1.5mg/kg. if they continue, follow with infusion of 1-4mg/h
describe when R on T phenomenon occurs
PVC that lands on the second half of the T wave
most common cause of?
sudden cardiac death. CPR and defibrillator my boi
define brugada syndrome including
EKG findings
type 1 v 2
who it commonly afflicts
etiology
tx
sodium ion channelopathy in the heart.
most common in males from southeast asia
most common cause of nocturnal death due to vtach or fib
diagnostic EKG findings include RBBB and ST segment elevation in precordial leads (V1-V3)
-may require ICD or pad placement during surgery
affected region
etiology
tx of this rhythm
1st degree block (PR >.2)
affected region: AV node or his bundle
etiology: age related degenerative changes, CAD, dig, amio
tx: monitor (usually asymptomatic)
affected region/the “why”
etiology
tx
2nd degree type 1
the “why”: each depol increases rate of refractory period in AV node. the last P cycle is dropped because the AV node is in absolute refractory period
etiology: structural conduction defect, MI, BB, CCB, dig, sympatholytic agents
tx: symptomatic: atropine. asymptomatic: monitor
affected region
etiology
tx
2nd degree type 2
affected region: his bundle or bundle branches.
etiology: structural conduction defect or infarction
tx: often symptomatic (palpitations and syncope), pacer is effective but atropine is NOT*
HIGH risk of progressing to complete heart block
affected region
etiology
tx
3rd degree
affected region: SA and AV have their own rates
etiology: fibrotic degeneration of atrial conduction system. lenegres disease
tx: pacer or isoproterenol (chemical pacer) because usually symptomatic
can lead to CHF
4 classes of anti arrhythmic drugs and what they do
class 1 inhibits fast sodium channels
class 2 decreases rate of depol
class 3 inhibit potassium ion channels
class 4 inhibits slow calcium channels
MOA, examples of this antiarrhtyhmic class
class 1A sodium channel blocker
MOA: moderate depression of phase 0, prolongs phase 3 depol (K channel block, increase in QT)
examples: quinidine, procainamide, disopyramide
MOA, examples of this antiarrhtyhmic class
class 1B sodium channel blocker
MOA: weak depression of phase 0, shortened phase 3 repol
examples: lido, phenytoin
MOA, examples of this antiarrhtyhmic class
class 1C sodium channel blocker
MOA: strong depression of phase 0, little effect on phase 3 repol
examples: flecainide, propafenone
MOA, examples of this antiarrhtyhmic class
class 2 beta blocker
MOA: slows rate of phase 4 depol in SA node
examples: esmolol, metoprolol, atenolol, propanolol
MOA, examples of this antiarrhtyhmic class
class 3 potassium channel blockers
MOA: prolongs phase 3 repolarization (increase in QT), increase in effective refractory period
examples: amiodarone, bretyium
MOA, examples of this antiarrhtyhmic class
class 4 calcium channel blockers
MOA: decrease in conduction velocity through AV node
examples: verapamil, diltiazem
MOA of adenosine
metabolism
uses/what its not useful for
cautions
first dose/second dose in PIV v CVC
slows conduction through AV node. by stimulating the cardiac adenosine 1 receptor, adenosine causes potassium efflux, hyper polarizes the cell membrane, slows AV node conduction.
rapidly metabolized in the plasma
useful for SVT as well as WPW with narrow QRS. not useful in afib, aflutter, or vtach. can cause bronchospasm in asthmatic patients
first dose: 6mg, second 12 (in PIV)
first dose: 3mg, second 6mg (in CVC)
two ways to disrupt a re entry circuit
- slow conduction velocity through circuit
- increase refractory period of cells at the location of unidirectional block
example of a re re entry pathway where conduction occurs over a long distance
left atrial dilation due to mitral stenosis
example of a re re entry pathway where conduction velocity is too low
ischemia or hyperkalemia
example of a re re entry pathway where refractory period is shorter
epinephrine
electric shock from alternating current
most common pre excitation syndrome
WPW
describe WPW MOA
defining feature is accessory pathway (kents bundle) that bypasses AV node
-forms direct line of communication between atrium and ventricle
-in the normal conduction pathway, cardiac impulse is delayed in AV node. aka AV node has long refractory period
-in the accessory pathway there is no delay so impulse quickly moves from atrium to ventricle.
-there is no gate keeper function
common characteristics of observed WPW EKG
-delta wave caused by ventricular pre excitation
-short PR interval (<.12 seconds)
-wide QRS complex
-possible T wave inversion
most common tachydysrhythmia associated with WPW and types
orthodromic AVNRT
antidromic AVNRT
orthodromic AVNRT
incidence
reentry conduction pathway
QRS morphology
tx
incidence: more common (90% of cases)
reentry conduction pathway: atrium–> AV node –> ventricle –> accessory pathway –> atrium
QRS morphology: narrow. ventricular depol occurs normally via his purkinje system
tx: block conduction in AV node by increasing AV node refractory period
-cardiovert, vagal maneuvers, adenosine, BB’s, verapamil, amio
antidromic AVNRT
incidence
reentry conduction pathway
QRS morphology
tx
incidence: less common
reentry conduction pathway: atrium–> accessory pathway –> ventricle–> AV node –> atrium
QRS morphology: wide. ventricular depol is slower because his purkinje is bypassed
tx: block conduction in accessory pathway by increasing accessory pathway refractory period: cardioevrt, procainamide
-do NOT give meds that increase refractory period through AV node- this will favor conduction through accessory pathway.
which AVNRT pathway is more dangerous
antidromic. since it bypasses AV, dramatically reduces filling time
drugs to avoid with antidromic AVNRT
adenosine, digoxin, CCB’s (dilt and verapamil), BB’s, lido
tx of afib and WPW
procainamide–> increases refractory period in accessory pathway. if patient is hemodynamically unstable, cardioversion is best option.
- avoid drugs that increase refractory period over AV node
definitive tx for WPW and anesthetic considerations
radio frequency ablation
-risk of thermal injury to left atrium and esophagus. if temp rises during periods of ablation, alert cardiologist
underlying cause of this rhythm
delay in ventricular repol (phase 3 of AP), associated with long QT interval
conditions that prolong the Qtc
metabolic disturbances (hypokalemia, hypocalcemia, hypomagnesemia)
drugs (methadone, droperidol-get 12 lead first, haldol, ondansetron, halogenated agents, amio, quinidine)
genetic syndromes (romano ward, timothy)
misc (hypertrophic cardiomyopathy, SAH, bradycardia)
QTc > what is prolonged
> 0.4
causes of torsades: POINTES
penothiazines
other meds (see conditions that prolong Qtc)
intracranial bleed
no known cause
type 1 anti arrhythmic drugs
electrolyte disturbances
syndromes
prevention and tx of torsades
prevention: BB prophylaxis and/or ICD, avoid SNS stimulation
tx: mag sulfate and pacing to increase HR and decrease QTc
EKG appearance for atrial pacing and capture versus ventricular pacing and capture
mnemonic PaSeR
Pa= chamber paced
Se= chamber sensed
R=response
position 1: the chamber that is paced- options
O=none
A=atrium
V-ventriccle
D=dual (A+V)
position 2: the chamber that is sensed- options
O=none
A=atrium
V-ventriccle
D=dual (A+V)
position 3: response to sensed native cardiac activity: options
O=none
T= triggered (tells pacer to fire)
I= inhibited (tells pacer not to fire)
D= dual (T+I) if native activity is sensed, pacing is inhibited. if native activity is not sensed, pacer fires
position 4 on pacer
indicated programmability, can adjust HR based on RR, acid base status, vibration, etc
O=none
R= rate modulation
position 5 on pacer
indicates that the pacer can pace multiple sites
O=none
A= atrium
V= ventricle
D= dual (A+V)
what is happening on this EKG
dual chamber pacing
examples of asynchronous pacing modes specs and examples
AOO, VOO, DOO
-pacer delivers constant rate
-no sense or inhibition
-can be a competitive underlying rhythm
examples of single chamber demand pacing specs and examples
AAI, VVI
-think of it as a back up mode, only fires if HR falls below pre determined rate
examples of dual chamber AV sequential demand pacing specs and examples
DDD
-very flexible, most common mode of pacing
-makes sure the atrium contracts first, followed by ventricle
-improves AV synchrony
what happens when you place a magnet over a pacer
usually (not always) converts pacer to asynchronous mode
what happens when you place a magnet over an ICD
suspends ICD, prevents shock delivery
what happens when you place a magnet over a pacer/ICD
suspends ICD and prevents shock delivery but has NO effect on pacer function
-this means pacer will be subject to electromagnetic interference. if this is likely, have pacer reprogrammed by manufacturer before surgery
types of pacer failure (3)
failure to sense
failure to capture
failure to output
explain what is happening in this rhythm strip
failure to sense underlying cardiac rhythm
-pacer sends impulse at sporadic times
-undersending results in asynchronous pacing
explain what is happening in this rhythm strip
failure to capture. occurs when ventricle does not depol in response to pacing stimulus
-pacing spikes not followed by QRS
causes of failure to capture include
electrode displacement, wire fracture, and conditions that make the myocardium more resistant to repolarization including hyper and hypokalemia, hypocapnea (intracellular K shift), hypothermia, MI, fibrotic tissue build up around pacing leads, anti arrhythmic meds
explain what is happening in this rhythm strip
failure to output
-pacing stimulus not produced when it should be
-caused by oversensing, pulse generator failure, or lead failure
ways to reduce EMI during electrocautery
-cutting setting causes less EMI than coagulation setting
-monopolar cautery causes more EMI than bipolar or ultrasonic harmonic scalpel
-if they insist on monopolar, insist on short bursts (<.5 sec)
-risk of EMI is highest when electrocautery is being used with 15cm of pulse generator
-place electrocautery return pad far away from pulse generator
contraindications for patient with pacer/ICD
MRI
where are V leads on eichmanns triangle in terms of degrees and what part of the heart do they correlate to
V1-2 anteroseptal
V3-4 anteroapical
V5-6 anterolateral
