Class 22: Arrythmias Flashcards
what is the difference between a 12-lead ECG and cardiac monitoring
- 12-lead ECG = moment in time, very detailed
- cardiac monitoring = continuous, less detailed
what is the path of transmission for conduction
SA –> AV –> Bundle of His (splits into R and L) –> purkinje fibers
“save his kin”
where is the SA node located? how does correlate to this function
- RA
= causes atria to contract
what does it mean that the SA node is the pacemaker? what does it conduct impulses?
- sets the pace (HR) of the heart
- it is also the fastest pacing
- 60-100 bpm
where is the AV node located
- in the septum
- how you get from the atria to ventricles
what is meant by the AV node being the gatekeeper? why is this important?
- at the AV node, it causes a slight delay
- this is important because it allows the atria to fully empty into the ventricles
- also prevents the atria & ventricles from contracting at the same time
where is the bundle of his located
- in between the ventricles
- branches off into R and L bundle braches
where are the purkinje fibers located
- in the ventricles
where does contraction of the heart begin? describe how contraction spreads?
- at the apex
- it then fans out & up the ventricle wall to push blood up so it can leave the aortic & pulmonic valve
describe the difference between where conduction vs contraction begins
- conduction = base of heart (SA node)
- contraction = apex
what is the difference between depolarization & repolarization
- depolarization = contraction
- repolarization = relaxation
why is it important that electrical conduction follows the normal pathway
- it is the most efficient
- impulses travel fast down the septum
how does SNS and PSNS effect the SA rate
- SNS = increased
- PSNS = decreased
is it only certain cardiac cells that can initiate cardiac depolarization? what does this mean?
- any cardiac cell can spontaneously depolarizae & initiate cardiac depolarization
= although SA node is the pacemaker, cell in the AV node, etc. also have the capacity to become the pacemaker
how fast do SA cardiac cells depolarize compared to other cardiac cells
- they are faster
what is overdrive suppression
- the faster frequency in SA node cells suppresses other pacemaker sites thru this
explain how overdrive suppression works
- the faster conduction of the SA node causes all the other myocytes to contract
- after they contract, they enter a refractory period where they cannot contract again
- this means that the other myocytes do not have a chance to fire at their own rate
what is ectopic focus
- when a conraction is initiated by different cells other than the SA node cells
what is ectopic focus
- when a contraction is initiated by different cells other than the SA node cells
what can cause an ectopic beat
- ischemia
- stretch
- drugs
- electrolyte imbalance
what can cause an ectopic beat
- ischemia
- stretch
- drugs
- electrolyte imbalance
how are the atria & ventricles electrically insulated from each other
- by the AV valves
what is the only electrical path from the Atria to ventricles?
- AV node
what is wolfe parkinson white syndrome
- syndrome in 1 in 1000 individuals where they have a second electrical pathway between teh atria & ventricles`
how does SNS affect the AV node
- decreases the delay by increasing the speed
- decreased refractory period = speeds recovery
how does PSNS affect the AV node
- increases the delay
- increasing the refractory period = slows recovery
what are vagal maneuvers
- stimulation of the vagal nerve to lower HR by causing PSNS stimulation
who are vagal maneuvers used in
- pts with bursts or rapid HR
what are examples of vagal manuevers
- bearing down (“giving birth feeling”)
- coughing, gagging
- cold stimulus to face (ex. cold water)
- carotid massage (physician only)
what contraction/conduction correlates with the P wave
- SA node fires
= atria contract
what occurs druing the PR interval
- AV node delay
what occurs during the QRS complex
- ventricles contract
what occurs during the T wave
- ventricles repolarize (rest)
what influences the size of waves during an ECG
- more cells involved = bigger wave
- why P wave is smaller than QRS, because atria are smaller
why dont we see atrial repolarization in an ECG
- occurs at the same time as ventricles contracting =
it is hidden by the QRS wave because ventricles are bigger
explain the action potential in 1 myocyte
- depolarization = Na & Ca into cell
- repolarization = K+ leave the cell (?)
what is an electrocardiogram (ECG)
- when electrodes are placed on the skin to capture & map electrical activity of the heart on continuously running paper
how many electrodes vs leads are used?
- 10 electrodes
- 12 leads
think: 10 windows on a house, but can see 12 different views of the house
what are the electroduces
- the pads place directly on the skn
what are the leads
- the specific angle of electrical activity captured by the electrodes
what can a ECG detect
- abnormalities in cardiac conduction
- hypertrophy
- electrolyte abnormalities
what is normal sinus rhythmn (NSR)
- term used to describe a normal ECG rate and rhythmn
- generated in the SA node
what does each different lead do
- gives info about a very specific area of the heart
what happens if we see ST changes in a specific view of an ECG
- since different areas of the heart are supplied by a specific coronary artery, if see ST changes in a specific view, we can tell which artery in being blockedq
what is an ECG rhythm strip
- simple, single view of the hearts electrical conduction
- may only have 3 or 5 leads attached
what is a positive or upward deflection
- electrical activity moving toward an electrode
what is a negative or downward deflection
- electrical activity moving aware from the lead
ex. from atria to ventricle
what do upward and positive deflections cause
- some views are mirror of each other
ex. lead II and aVR
what are the 2 primary purposes of an ECG
- identify ischemia = ST changes
2. identify arrhythmias –> abnormal beating
when is ST change present? what does this mean?
- only during active ischemia or angina
= must get a STAT 12-lead ECG during angina to capture it - may always use cardiax monitoring
each is lead is in the ____ moment of time
same –> like a snapshot in time
what do we use if we want continuous monitoring
- cardiac monitoring
- 3 or 5 leads & let it run continuously
what are 3 different ways that ECGs are used
- telemetry
- holter monitor
- stress/exercise test
what is a telemetry
- where a pt has ECG monitoring that is transmitted to a local receiver and played on a monitor
- like a portable ECG
- often used in acute care wards
what are the benefits of telemetry
- allows patients to get up & move around
- allows them to test their heart function b4 going home
what is a holter monitor
- at home monitor
- record an ECG 24 h a day & patient will keep a log book of activity which can be matched to the ECG recording and any changes
what is a stress/exercise test
- patient will exert themselves & the ECG will record ant changes
what are stress/exercise tests used for
- determine if meds are controlling angina well
- or for intial diagnosis of stable angina
- only on stable patients
what happens if the SA node fails to fire
- the next fastest node will become the pacemaker
- in this case, the AV node
what is the intrinsic rate of the SA, AV, and purkinje fibers
- SA= 60-100
- AV = 40-40
- purkinje = 20-40
what might sinus brady & tachy be used for
- functional compensation = useful
when might sinus tachycardia be used
- during activity
ex. if running, need increased cardiac output = HR increases
when might sinus bradycardia be used full
- at rest
ex. when sleeping at night
what is ST elevation a sign of
- stemi
when do we see ST depression
- Non-STEMI
- unstable angina
- stable angina
why do we get ST depression with unstable angina & Non-STEMI
- get ischemia caused by partial occlusion of a coronary artery
why do we get ST elevation with STEMI
- bc get complete occlusion of the coronary artery & the entire thickness of the myocardium becomes ischemic
describe the evoluation of a STEMI
- NSR
- ST elevation peaked T-wave
- ST elevation lessons & deep Q-wave, inverted T-wave
- resolving ST elevation, inverted T wave
- pathological Q wave (may be permanent)
(look at pics in slides)
what might pathological Q wave indicate
- past MI bc may be permanent
describe the PR interval
- starts with atrial contraction
- end before ventricular contraction
= during the delay of AV nodes
describe the ST segment
- starts at end of ventricular contraction
- ends before ventricular repolarization
is the inside of the cell (+) and (-) during resting membrane potential
(-) bc 3 Na out and only 2 K+ in
what occurs during depolarization
- Na coming in = membrane potential becoming more (+)
= ventricular contraction = QRS complex
what occurs during repolarization
- K+ coming out of the cell = becomes more (-)
= ventricular relaxation = T wave
what occurs during the plateau of action potential
- Ca flows in
- K+ starts to flow out
= correlates with ST segment
what are arrhythmias
- alterations in cardiac rhythm
what are dysarrhythmias
- loss of rhythm
what is sinus bradycardia
- sinus rhythm with a resting rate less than 60 per min
who do we see sinus bradycardia in
- trained athletes
- during sleep
- MI
- resp. depression
- hypothyroidism
- drug toxicity
- can be compensation for an underlying disorder
what is sinus tachycardia
- sinus rhythm above 100 per min
when do we see sinus tachycardia
- w exercise
- fever
- CHF
- MI
- hyperthyroidism
- drug toxicity
- hypovolemia
do we usually directly treat sinus brady and tachy
- no bc usually occur secondary or as compensation
- will treat the underlying cause tho
what does excitability mean
- ability of a cell to respond to an impulse & generate an AP
what does conductivity mean
- ability to conduct impulses
what does refractoriness mean
- extent to which the cell is able to respond to an incoming stimulus
what are the 3 main mechanisms of arrhythmias
- increased automaticity
- triggered activity
- re-entry
what is increased automaticity? when does this occur? what does it cause?
- increase in the natural depolarization rate of nodal cells
- occur in response to SNS
= uncontrolled electrical activity
what is triggered activity
- when after depolarization of an action potential, a myocyte depolarizes spontaneously
“twitchy”
what are 2 types of after depolarization
- early
- delayed
what can cause triggered activity
- ischemica or fibrosis
- or HF
what does triggered activity cause
- ectopic or premature beats
what occurs with reentry
- in injured tissue, it sets up a condition for a recurrent circuit
- this causes an area of muscle to repeatedly contract
- so instead of the impulse leaving, it just re-enter to where it came from
explain how conduction moves in normal tissue
- electrical waves move & when meet in the middle they cease due to the absolute refractory period
explain what happen with conduction in necrotic tissue
- when an impulse runs into necrotic tissue, the impulse is blocked bc necrotic tissue does not have intact cell membranes for an action potential
what does a pacemaker do
- helps to control ur hearbeat
- primarily for bradycardia
what is cardiac resynchronization therapy
- used when ventricles are out of sync to resync them
- form of pacemaker
who is an implantable cardioverter defibrillator used in
- pts with frequent fatal arrhythmias
- or HF pts with EF of <30%
ex. VT and VF
what is cardioversion
- procedure using external electrical shocks to restore a normal heart rhythm
- often done in synchronization to R wave = must be able to recognize QRS
- lower energy used
- delay in delivery
- may be planned or scheduled
what is defibrillation
- emergency life saving procedure using electrical shocks
- not synchronized to R wave
- immediate delivery
- higher energy
what is an AED
- automated external defibrillator
when is an AED used
- in public buildings
what is CPR
- cardiopulmonary resuscitation
describe use of an external pacemaker
- for short term emergency use only
- for unstable, symptomatic, slow rhythmns
- very uncomfortable & painful
describe use of a temporary pacemaker
- wire inserted thru large blood vessel
- tip goes to apex of heart and delivers and electrical stimulus to pace the ventricle
what is a capture
- anytime an artificial stimulus is used & the heart responds by contracting
what is a non-capture
- when a stimulus does not respond in contraction
describe use of an internal pacemaker
- permanent, surgically implanted device w 2 wires
- one to pace the atria & one for the ventricle
where is the generator of an internal pacemaker placed
- below the clavicle
- under the skin but above the muscle wall so it can be accessed for replacement but also less invasive
describe how cardiac resynch therapy work
- adds a pacing lead to each ventricle (and the usual atrial) to recoordinate the ventricles & increase patient’s CO
what do we see on an ECG before CRT
- a bundle branch block = jagged look in the R wave
what is an implantable cardioverter defibrillator
- when lead is place on the heart to allow for monitoring of fatal arrhythmias
- when the arrhythmias occur, the heart sends a jolt of electricity to reset the hearts electrical conduction & return to NSR
- can be synchronized to R wave with cardioversion or random with defibrillation
who is cardioversion used in
- sustained SVT
- A-fib
- monomorphic VT
what is defibrillation used in
- v-fib
- polymorphin VT
- pulseless VT
- for emergencies & fatal arrhythmias
what is meant by avoid R on T when shocking
- shocking the heart causes depolarization
- want to avoid doing this during T wave bc it can initiate an arrhytmias, specifically a bad one like VT/VF
how do we avoid shocking the T wave?
- find the R waves, easy to see bc tall
- the machine will also calculate when the T waves are
is defibrillation synchronized?
- no, often no R wave present bc no ventricular contraction w VF
what are 3 concerns with arrhytmias
- sustainability
- cardiac workload & ischemia
- thrombus/emboli formation
describe the concern of sustainability with increased Hr
- increased HR = increased workload & decreased filling
describe the concern of sustainability with decreased HR
= decreased CO
describe hemodynamic instability with arrhytmias
= decreased CO = decreased bp = decreased perfuson = multiorgan failure (shock)
describe cardiac workload & ischemia in arrhythmias
increased workload = ischemia & angina
acute MI = further ischemia = extended MI
why is there a concern for thrombus/emboli formation w arrhythmias
- weak contraction = blood stasis
- atrial fibrillation = blood statis in the atria
what part of an ECG do we use to calculate HR/min
- R wave to r wave = ventricle rate (usually match pulse)
how do measure atrial rate
- P to P
what is an artifact rhythm on ECG
- extra activity on ECG from either
1. skeletal muscle activity (person moving around)
2. loose electrodes
what is sinus arrhythmia
- variation of NSR
- includes R to R variation that changes with breathing
- not pathological, otherwise normal
describe sinus arrhythmias during inspiration vs expiration
- inspiration = faster due to less vagal tone
- expiration = slower due to increased vagal tone = PSNS
what is a way to estimate vent or atria rate off an ECG
- 15 boxes = 3 sec & usually 2 per strip = 6 sec
- count how many R or P waves during 6 sec & multiply by 10
what is the box method to determine HR
- measure how many big boxes between R and R
- use formula: (60sec/1m) (1 beat/ (0.2 x # of boxes))
what is sinus bradycardia
- heart rhythmn regular
- but HR <60 beats/min
- everything else normal
what is sinus tachycardia
- heart rhythm normal
- but HR >100 beats/min
- everything else normal
what does sinus mean in sinus brady, tachy, etc.
sinus = originates from SA node
what is a key characteristic of atrial rhythmns
- abnormal P wave
what is premature atrial contraction
- abnormally early P wave
- looks like it kinda interupts the T wave
- otherwise everything else looks normal for the most part
what causes a PAC?
- premature atrial beats that originates in the atria but outside of the Sinus node
- automaticity or triggering
- stimulants: emotion, tobacco, coffee
- hypoxia/ischemia, electrolyte imbalances, cardiac condition
what are key ECG features of a PAC
- underlying NSR
- P-P interval shorted on premature beat
- narrow QRS
what are key assessment of a PAc
- pulse primarly regular
- occassional early beat
- otherwise asymptomatic
describe treatment for PAC
- remove stress/stimulant
- otherwise, no treatment
what is paroxysmal supraventricular tachy
- starts and stops aruptbly
what causes PSVT
- re-entry at the AV node
what are key ECG features of PSVT
- narrow QRS
- P hidden/distorted
- 170-250 rate
- starts & stops abruptly
- burst
- self limiting
what can we do to treat stable PSVT
- vagal maneuvers
how can we treat unstable PSVT
- adenosine IV bolus
- cardioversion
what is long term control for PSVT
- CCB/BB
- alblation therapy
what symptoms may be seen in PSVT
- drop in CO
- palpitations
- dizziness
- angina & dyspnea if +CAD
what is atrial flutter
- atria contract much quicker than should ~300 bpm
- creates F waves with a saw like appearance
- get increase in A:V ratio ex. 4:1
describe cause of atrial flutter
- fleeting
- re-entry
- ischemic, stretch
- usually resolves or converts to A fib
what are key ECG features of Atrial flutter
- sawtooth
- A-rate up to 300
- ratio of A:V changes
- narrow QRS
- regular/irregular variable
what are key assessments for atrial flutter
- senses flutter in chest = palpitation
- possible drop in CO with S/S from low perfusion –> weak pulses, low BP, sluggish cap refill, cyanosis, pale, syncope, low urine output
what is atrial fibrillation
- chaotic atrial contraction
- sometimes dont contract or signals do or not go to ventricles
- multiple uncontrolled re-rentry circuits
what determines our CO
- ventricles
what can cause atrial fibrillation
- acute or chronic
- multiple uncontrolled re-entry
- ischemia, stretch
- HTN/volume
- no a-kick
describe key ECG features in A-fib
- irregular V rate (due to contraction sometimes go thru, sometimes not)
- narrow QRS
- pulse deficit
- cant determine A rate
- bunch of F waves before QRS
- can be tachy or brady response
what are key assessment for afib
- rapid V response then drop in CO
- increased pulse deficit
what kind of meds for afib
- pre rate control meds: ex. digoxin, BB, CCB
- risk of thrombus = anticoag, antiplt
- rhythm-control with cardioversion and/or antiarryhthmics
