Basic Arrhythmia
Review
L E AV I T T, 2 0 2 0
Coronary circulation (plumbing)
(epicardial arteries, detail)
Systole & Diastole
Mechanical contraction occurs with
electrical depolarization
Systole: contraction=ejection of blood
◦ Atrial systole: contraction of atria
◦ Ventricular systole: contraction of
ventricles
The word SYSTOLE usually refers to
VENTRICULAR SYSTOLE or CONTRACTION
Diastole: relaxation= ventricles fill with
blood
SA Node
Bundle of pacemaker
cells located in the
upper right atrium
Discharges impulses at
rate of 60-100/minute
Dominant pacemaker of
the heart
Most automaticity
(ability to generate its
own impulses)
AV Node & Bundle of His
Located in lower right
atrium, near septum
2 Functions
◦ Slows impulse
conduction from atria to
ventricles (gatekeeper)
◦ Back-up pacemaker of
heart, if SA node fails
Discharges impulses at
rate of 40-60/minute
The AV Node and
Bundle of His together
are known as the A-V
Junction
& Bundle of His
Bundle Branches
& Purkinje Fibers
At Bundle of His, conduction
pathways split into the right
and left bundle branches to
conduct to each ventricle.
Bundle branches end in tiny
conduction network called
Purkinje Fibers
Ventricles can be a back-up
pacemaker at rate of 2040/minute
Purkinje Fibe
Purkinje Fibers
Note that the general
direction of the flow of
electrical impulses is from
the right arm towards the
left foot
Eintoven’s Triangle
& waveforms
Electrical current
moving toward a positive
electrode will result in a
positive deflection
Electrical current
moving toward a negative
electrode will result in a
negative deflection
Biphasic deflections are
both positive and
negative
• Vertical axis =
voltage
• One small box
is 0.1 mV &
1mm.
• Elevation or
depression is
measured in
millimeters
EKG graph paper
• Horizontal axis =
time
• One small box is
.04 seconds
• One large box is
.20 seconds
• Tic marks on EKG
paper occur
every 3 seconds
The cardiac cycle waveform
One complete heartbeat
KNOWLEDGE CHECK
Electrical impulses moving toward a
positive electrode will have a ________
deflection.
a. Negative
b. Positive
c. Biphasic
d. Neutral
P wave: atrial depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
P wave: atrial depolarization
• Starts in SA node and travels through
atrium to AV node
• Smooth, round and positive deflection
in lead II
• PR interval is the time of atrial
depolarization to ventricular depolarization
• .12-.20 seconds (3-5 small boxes)
QRS complex: ventricular depolarization
• Large wave because it is passing through
large ventricular muscle
• May have up to 3 deflections
• Q wave: negative wave before R wave
• R wave: 1st positive deflection
• S wave: negative wave after R wave
• QRS may not have all components
• .06-.10 seconds (1½ - 2½ small boxes)
ST segment: early ventricular
repolarization
• Line btwn end of QRS and beginning
of T wave. Look for change in slope.
• May be elevated or depressed
• J point: place where QRS meets ST
and the place we look for
ST elevation or depression
T wave: ventricular repolarization
• Begins at change in slope after ST
segment
• Ends when wave returns to baseline
• Don’t measure T wave, but can measure
Q-T interval for some medication effects
• Peaked in hyper K+ and hypo Mg++
K+ and Mg++ are monitored closely
after cardiac surgery
U Wave: Prolonged repolarization
Sometimes noted in hypokalemia
How to analyze a strip
5 steps to rhythm analysis
1.
Determine regularity?
◦ Measure R wave to R wave
2. Calculate the rate?
3. Examine P waves?
◦ P wave for each QRS?
◦ How is the morphology of the P wave?
4. Measure the PR interval
◦ .12-.20 seconds (3-5 small boxes)
5. Measure the QRS interval
◦ .06-.10 seconds (1.5-2.5 small boxes)
Then you can name the UNDERLYING rhythm
and any abnormalities
Determine regularity
Using calipers or paper, look at the distance between each
complex. (between R waves or any other constant point on the
cardiac cycle)
What is the rate?
Methods to determine rate
First method: Rapid rate calculation: Count the number of R
waves in a 6-second strip and multiply by 10 (Example 6 sec
X10 =60 HR per Minute)
◦
◦
◦
◦
Approx HR in beats per minute, is fast and simple
Can be used for both regular and irregular rhythms
Each 3 sec equals 15 boxes of.20 sec
Each small box is .04 in the EKG paper
Look at the P waves
One P wave for every QRS?
Are they upright?
Are they the same size and shape?
SHAPE = MORPHOLOGY
Measure the PR interval
Measure from beginning of P wave to the beginning of the
QRS
.12-.20 seconds
3-5 small boxes
Measure the QRS complex
Measure from where the beginning of the QRS leaves the iso-electric
line until the ST segment starts.
Less than 3 small boxes (1½-2½ small boxes)
KNOWLEDGE CHECK
This time interval represents the onset
of atrial depolarization to the onset of
ventricular depolarization:
a. P-R interval
b. QRS interval
c. ST segment
d. J Point
KNOWLEDGE CHECK
This time interval represents ventricular
depolarization:
a. P-R interval
b. QRS interval
c. ST segment
d. T wave
KNOWLEDGE CHECK
This time interval represents ventricular
repolarization:
a. P-R interval
b. QRS interval
c. ST segment
d. T wave
Sinus Rhythm
Rhythm: Regular
Rate: 60-100
P waves: normal size & shape
PR interval: normal (.12-.20)
QRS complex: Normal (.06-.10)
Sinus Bradycardia
Rhythm: Regular
Rate: < 60
P waves: normal size & shape
PR interval: normal (.12-.20)
QRS complex: Normal (.06-.10)
Sinus Tachycardia
Rhythm: Regular
Rate: 101-150/min
P waves: normal size & shape
PR interval: normal (.12-.20)
QRS complex: Normal (.06-.10)
Sinus Arrhythmia
Rhythm: irregular (at least 2 small boxes)
Rate: 60-100 or <60
P waves: normal in size and shape
PR interval: normal (.12-.20)
QRS complex: Normal (.06-.10)
Sinus Arrhythmia
CAUSES
Normal phenomenon, usually associated with
phases of respiration
◦ SA node speeds up with inspiration
◦ SA node slows with expiration
Common in infants & children, but may occur at
any age
TREATMENT
None required unless very slow rate causes
symptoms
Atrial Arrhythmias
Originate from ectopic sites in the atria
◦ WAP: Wandering Atrial Pacemaker
◦ PAC: Premature Atrial Contraction
◦ Conducted
◦ Non-conducted
◦ PAT or SVT: Paroxysmal Atrial Tachycardia or
Supraventricular Tachycardia
◦ A Flutter: Atrial Flutter
◦ A Fib: Atrial Fibrillation
Premature atrial contraction (PAC): Ectopic
atrial foci
Premature Atrial Contraction (PAC)
CAUSES
• Ectopic pacemaker cells in atrium fire faster than sinus node and the
beat comes in EARLY and moves down the normal conduction
pathways
• Increased vagal tone
• Increased automaticity of ectopic atrial cells
• Anxiety or excess caffeine
• Key word is Premature
TREATMENT
• No treatment needed if they are rare
• Check and correct underlying cause
• May be a clue that patient is going into another atrial arrhythmia,
such as atrial fibrillation
Premature Atrial Contraction (PAC)
Rhythm: irregular
Rate: same as underlying rhythm
P wave: premature, positive, shape is different, may be
hidden in previous T wave
PR interval: normal or maybe longer
QRS interval: normal. QRS looks the same as other
complexes
KNOWLEDGE CHECK
The P wave in a PAC looks different from the
sinus P wave – Why?
a. Impulse originates in a different part of
the atria
b. P waves always look different
c. Respiratory variation causes the change
d. It is rate-dependent
Paroxysmal Atrial Tachycardia
(PAT or SVT)
Paroxysmal Atrial Tachycardia (PAT or
SVT) characteristics
Rhythm: regular
Rate: 150-250 /min
P waves: often hidden in previous T wave
PR interval: may not be measurable
QRS: normal – narrow complex
Patients may feel palpitations
Paroxysmal Atrial Tachycardia -> SR
• PAT: Paroxysmal means “a burst”
• Has a start and stop
• If sustained, may be called SVT =
SUPRAVENTRICULAR TACHYCARDIA
Paroxysmal Atrial Tachycardia
(PAT or SVT)
CAUSES
Hyperthyroidism, COPD, valvular heart disease
Medications: albuterol treatments
Caffeine, alcohol, tobacco
SYMPTOMS
Palpitations
Anxiety
Hypotension, SOB, chest pain, syncope – signs of decreased
cardiac output…WHY?
Heart rate is too fast to allow for adequate filling during
diastole
PAT/SVT treatment
TREATMENT
Decrease heart rate
◦ Vagal maneuvers:
Cough, bear down, other
Valsalva maneuvers
◦ Medications: Adenosine,
Diltiazem, Beta blockers
◦ Synchronized
cardioversion if unstable
Atrial Flutter
Atrial Flutter characteristics
Rhythm: regular or irreg, depending on conduction ratios
Rate: Atrial: 250-400/min
Ventricular: whatever the AV node allows through. May be constant or variable
P waves: none. Sawtooth “F” flutter waves are baseline. DOES NOT RETURN TO
ISOELECTRIC LINE
PR interval: not measurable
QRS: normal – narrow complex
Patients may feel palpitations if rate is fast
Atrial Flutter – variable conduction
• AV node does not let all the impulses from
flutter waves conduct through to ventricles.
• Rate of conduction can be constant (2:1, 4:1) or
variable, as seen below
Sawtooth “F” flutter waves are the baseline.
They do not return to isoelectric line
Atrial Flutter
CAUSES
Re-entry, due to valvular heart disease
Post-op CV surgery
CAD
TREATMENT
Control rate of ventricles
Check hemodynamic effects of loss of atrial contraction (fatigue, hypotension,
SOB, CP?)
Medication to control rate or convert to SR
◦ Diltiazem, amiodarone, beta-blocker
Antigoagulation: because blood pools in atria
◦ Heparin (acute), Coumadin, Pradaxa, Xarelto, Eliquis
Synchroniczed Electrical Cardioversion
◦ Anticoagulation or TEE prior (if >48 hours duration)
Atrial Fibrillation characteristics
Rhythm: ALWAYS irregularly irregular
Rate: Atrial: usually >400/min. Atria are quivering
Ventricular: whatever the AV node allows through.
P waves: wavy baseline (fibrillatory waves)
PR interval: not measurable
QRS: normal – narrow complex
If ventricular rate is 60-100, the rhythm is called
“A fib with controlled ventricular response.”
A Fib = atrial chaos
Atrial Fibrillation with RVR or SVR
If rate >100/min.,
Atrial fibrillation with rapid ventricular response
If rate <60/min,
Atrial fibrillation with slow ventricular response
Atrial Fibrillation
A fib is very common. Some causes are…
◦ Post op CV surgery
◦ CAD, Htn, HF, COPD
May be transient
May be controlled with medication
Loss of “atrial kick” causes decreased cardiac output
◦ Fatigue, SOB, chest pain
Patients are at risk for stroke, due to stasis of blood in
atria
◦ Atria are “quivering” and not contracting, so blood
swirls and clots
Physiology of Stroke Risk
in Atrial fib & Atrial flutter
Rapid impulses cause the atria to quiver instead of
contracting regularly producing irregular wavy deflections.
Stasis of blood can lead to clot formation. Clot (thrombus) is
most likely to form in the atrial appendages.
Clot in the left atrial appendage is particularly important
since the left side of the heart supplies blood to the entire
body.
Clot that dislodges from left atrial appendage can embolize
to the brain
BIG STROKE!
Atrial Flutter/Fibrillation
& Risk of Stroke
Coronary Sinus
Vein
Pulmonary Veins
Left Atrial
Appendage
Clot formation in Left Atrial Appendage
Atrial Fibrillation
TREATMENT
Anticoagulation: because blood pools in atria
◦ Heparin (acute), Coumadin, Pradaxa, Xarelto, Eliquis
Medication to control ventricular rate or convert to SR
◦ Diltiazem, amiodarone, beta-blocker, ibutilide (Corvert)
Synchronized electrical cardioversion
◦ Anticoagulation or TEE prior (if >48 hrs duration)
EP catheter ablation if medication cannot control
Refractory A Fib Management
(A Fib that is not responsive to other treatments)
EP Catheter ablation of pulmonary veins, source of A fib
◦ Radiofrequency ablation - heat
◦ Cryo ablation – cold
Maze procedure: open heart surgery creating atrial scar tissue
Mini-maze procedure: minimally invasive surgery, incision between
ribs
◦ Encircles pulmonary veins with surgical incisions in left atrium
Left atrial appendage (LAA) occlusion
◦ Watchman device
Cardiac monitoring is a priority after ALL of these procedures
KNOWLEDGE CHECK
Which of the following atrial arrhythmias
put a patient at risk for stroke?
a. Paroxysmal atrial tachycardia
b. Atrial flutter
c. Atrial fibrillation
d. Both b & c
Junctional Rhythm
Originate in AV junction (area
around the AV node and the
Bundle of His)
2 Functions
◦ Slows impulse conduction from
atria to ventricles (gatekeeper)
◦ Back-up pacemaker of heart, if
SA node fails
Discharges impulses at rate of
40-60/minute
Junctional Rhythm
Rhythm: regular
Rate: 40-60/min
P wave: absent (hidden in QRS), inverted, or after QRS
PR interval: if present, it is <.12
QRS: normal
absent (hidden in QRS),
inverted
after QRS
Junctional rhythm
◦ Remember that
horizontal axis of EKG
paper measures time
◦ It takes less time for
impulse to move from
junctional area to
ventricle
◦ (From SA node to
ventricle is a longer
route!)
Accelerated Junctional Rhythm &
Junctional Tachycardia
Accelerated junctional rhythm
60-100/minute
Junctional tachycardia
>100/minute
KNOWLEDGE CHECK
In any Junctional Rhythm, the P wave can
be
a. Inverted in Lead II
b. Occurring just before the QRS
c. Occurring just after the QRS
d. Hidden in the QRS
e. All of the above
KNOWLEDGE CHECK
This strip is an example of
a. junctional rhythm
b. accelerated junctional rhythm
c. junctional tachycardia
d. premature junctional contraction
What are Heart Blocks?
DELAYED conduction or NO conduction through AV node to
ventricles
AV node is the bridge between that impulses cross to get from atria
to ventricles
PR Interval measures the time it takes the impulse to cross that
bridge
The site of pathology of the AV Blocks may be at the level of the:
◦ AV Node
◦ Bundle of His
◦ Bundle Branches
Steps to Interpret Heart
Blocks
Look for the P wave
◦ Is there one P for every QRS?
Measure the P-P interval (atrial rhythm)
◦ Is it regular? LOOK FOR HIDDEN P WAVES
Measure the R-R interval (ventricular rhythm)
◦ Is it regular?
Measure the PR Interval
◦ Is it CONSISTENT? Or does it CHANGE?
Measure the QRS complex
◦ Is it narrow or wide?
First Degree AV Block
Rhythm: Regular
Rate: same as underlying
P wave: sinus (normal)
PR interval: Consistently prolonged (>.20)
QRS: normal
Second Degree AV Block
Type I (Wenckebach, Mobitz I): block is within the AV node
Some of the sinus impulses are not conducted to the ventricles
P waves are regular
PR interval progressively lengthens...then drops QRS
Can be confused with non-conducted PAC or third degree heart block
Second Degree AV Block
Type I (Mobitz I, Wenckebach)
CAUSES
Ischemia to AV node
Medication effect
Increased vagal tone
TREATMENT
None required
 Usually temporary
and resolves spontaneously
Note meds, change if necessary
Monitor for further conduction problems
Second Degree AV Block
Type I (Mobitz I)
Second Degree AV Block
Type II (Mobitz II)
Type 2 (Mobitz II): block below the AV node within His-Purkinje system
Some of the sinus impulses are not conducted to the
ventricles
More P waves than QRS complexes (ratio)
P waves are regular
PR is fixed with dropped QRS
Patient condition related to ventricular rate
Second Degree AV Block
Type II (Mobitz II)
CAUSES
Anterior wall myocardial infarct (AWMI)
Degeneration of the electrical conduction system in the elderly
Assess your PT (Asymptomatic or Symptomatic)
TREATMENT
May SUDDENLY degenerate into complete heart block or
ventricular standstill and will usually require pacemaker
implantation
Atropine not effective
Transcutaneous pacer, Dopamine or Isuprel Drip.
Transfer to High Acuity of care ICU.
Second Degree AV Block
Type II (Mobitz II)
Third Degree AV Block
(Complete Heart Block)
Complete AV block: failure of any atrial impulses to be conducted to the
ventricles
Block is at AV node or Bundle of His
Atria and Ventricles beat independently of each other, which is called…
A-V Dissociation: P-P interval is fixed; R-R interval is fixed, but
they have no relation to each other
P waves are usually sinus at 60-100 bpm
QRS complexes are either from AV junction (narrow) at 40-60
bpm or from ventricles (wide) at 20-40 bpm
Third Degree AV Block
(Complete Heart Block)
CAUSES
Acute MI
Conduction system disease
Digoxin toxicity
TREATMENT
Rhythm can progress to ventricular standstill, so
pacemaker needed emergently
If patient decompensates, use trancutaneous
pacer while awaiting transvenous pacer
Third Degree AV Block
(Complete Heart Block)
QRS complexes are either from AV junction
(narrow) at 40-60 bpm or from ventricles
(wide) at 20-40 bpm
KNOWLEDGE CHECK
In which of the following heart blocks will
you see a P wave with no QRS complex?
a. 1st degree AV block
b. 2nd degree, Type I
c. 2nd degree, Type II
d. b & c
KNOWLEDGE CHECK
In which of the following heart blocks is there
consistently NO ELECTRICAL COMMUNICATION
between the atria and ventricles?
a. 1st degree AV block
b. 2nd degree, Type I
c. 2nd degree, Type II
d. 3rd degree
What is an Escape beat?
An escape beat occurs when the primary pacemaker of
the heart (the sinus node) does not initiate an impulse
and one of the back-up pacemakers (atrium, junction or
ventricle) takes over.
And escape rhythm is when one of the back-up
pacemaker sites takes over for an extended time, not just
1-2 beats.
Escape beats always follow a pause
ESCAPE BEATS ARE NEVER PREMATURE…THEY ALWAYS
OCCUR LATE IN THE CARDIAC CYCLE
Atrial escape
Junctional escape
Ventricular escape
Bundle Branches
& Purkinje Fibers
At Bundle of His, conduction
pathways split into the right
and left bundle branches to
conduct to each ventricle.
Bundle branches end in tiny
conduction network called
Purkinje Fibers
Ventricles can be a back-up
pacemaker at rate of 2040/minute
Purkinje Fibe
Purkinje Fibers
Bundle Branch Block
BBB can occur anywhere in R or L Bundle
system
The right bundle branch (which distributes
the electrical impulse across the right
ventricle) and the left bundle branch (which
distributes the impulse across the left
ventricle).
Ventricular depolarization (QRS) is wider,
because it takes longer
QRS .12 or greater = intraventricular
conduction delay
Differentiating between a RBBB and LBBB
requires a 12 lead ECG
Right & Left BBB
Bundle Branch Block
Rhythm: regular
Rate: same as underlying rhythm
P waves: sinus (Sinus P wave distinguishes BBB from PVC)
PR interval: normal
QRS: Wide (>.12)
KNOWLEDGE CHECK
Bundle branch blocks are
a. a block of one of the ventricular
conduction pathways
b. the same as ventricular escape
rhythms
c. a result of too much caffeine or
alcohol
d. all of the above
Ventricular arrhythmias
Premature Ventricular Contractions
Ventricular Tachycardia
◦ Monomorphic
◦ Polymorphic (Torsade de pointes)
Ventricular Fibrillation
Idioventricular Rhythm
Accelerated Idioventricular Rhythm
Ventricular Standstill
Agonal Rhythm
[Pulseless Electrical Activity]
PVC
PVCs
Premature Ventricular Contractions
CAUSES
CAD, ischemia, MI, hypoxia
MVP, CHF, Cardiomyopathy
Electrolyte imbalances (hypokalemia)
Medication effects (digoxin, epinephrine, dopamine) or substances
(caffeine, alcohol, tobacco)
TREATMENT
No treatment if rare PVCs
Anti-arrhythmic meds for significant PVCs (>6/min, VT, R-on-T…but
check your MD orders)
Treat cause
PVC
Variations
R-on-t PVCs
The relative refractory period
is an electrically vulnerable
interval in the cardiac cycle.
R-on-T PVC’s may result in
Ventricular Tachy or V Fib.
KNOWLEDGE CHECK
Following are differences between PVCs and PAC’s:
a. PVC’s are initiated in the ventricle, PAC’s are
initiated in the atrium
b. PVCs usually have wider QRS than PACs
c. PVCs and PACs both have premature P
waves
d. All of the above are true
e. Only a & b
Ventricular Tachycardia
Ventricular rhythm of 140-250/minute
No P waves
A series of wide QRS complexes in short runs or a continuous rhythm
Monomorphic: QRS complexes have same morphology – all
complexes look alike
Polymorphic: QRS complexes have different morphology
◦ Torsade de Pointes is a form of polymorphic VT
◦ QRS complex changes polarity, twisting around isoelectric line
◦ Treatment is Magnesium, even if Mg++is normal
Ventricular Tachycardia
Rhythm: regular, or might be slightly irregular
Rate: 140-250/min
P waves: None
PR interval: not measurable
QRS complex: WIDE (>.12)
Ventricular Tachycardia
Monomorphic: QRS
complexes have same
morphology – all
complexes look alike
Polymorphic: QRS
complexes have
different morphology
Polymorphic VT -> Sinus rhythm
Torsade de pointes
◦ Torsade de Pointes is a form of polymorphic VT
◦ QRS complex changes polarity, twisting around isoelectric line
◦ Only treatment is Magnesium 2 Gm slow IV push to stabilize the
cardiac membrane, even if Mg++is normal. Other antiarrhythmics have no effect. Cardioversion if pulse, defib if not.
Ventricular Tachycardia
CAUSES
CAD, ischemia, MI, hypoxia
MVP, CHF, Cardiomyopathy
Electrolyte imbalances (hypokalemia)
Medication effects (digoxin, epinephrine, dopamine)
This is a life-threatening arrhythmia!
RAPID RATE AND LOSS OF ATRIAL KICK REDUCES
CARDIAC OUTPUT!
MAY LEAD TO VENTRICULAR FIBRILLATION
Ventricular Tachycardia
TREATMENT (if patient has a pulse, treat as below – if no pulse,
treat like V. Fib)
Unstable patient?
◦ Hypotension, chest pain, SOB, skin cool, clammy, LOC change
◦ Cardioversion
Stable patient?
◦ Patient BP acceptable
◦ No chest pain or SOB
◦ No LOC decrease
◦ Give Amiodarone 150 mg over 10 min and/or Cardioversion
VT variations
R on T PVC -> VT, polymorphic
VT -> V Fib
KNOWLEDGE CHECK
The monitor room calls and says your patient is in ventricular tachycardia, rate
155. Which of the following actions are appropriate for the med-surg RN?
a. assess patient’s LOC, pulse, BP
b. cardiovert immediately
c. ask patient to cough or bear down
d. call Code Indigo
e. all of above
f. a, c, d
g. a, b, d
Ventricular Fibrillation
Lethal rhythm!
Disorganized, chaotic, electrical activity in the ventricles
No organized depolarization/repolarization cycle
Results in “quivering” of ventricles with no effective
contraction
No cardiac output
Most common cause of sudden death
The only way to save this patient is CPR and
DEFIBRILLATION!
Ventricular Fibrillation
Rhythm: None
Rate: None
P waves: None
PR interval: not measurable
QRS complex: none
Ventricular Fibrillation
Coarse or fine VF?
Fine VF may look
like asystole…
Change the lead
to check.
Ventricular Fibrillation Videos
Heart in Ventricular Fibrillation
What is Ventricular Fibrillation? (Play first)
Ventricular Fibrillation
SR->VT -> shock->VF -------------------> shock -> SR!!!
Defibrillation
IDIOVENTRICULAR RHYTHM
Very slow back-up ventricular rhythm
Sinus node and AV node are not initiating and
impulse OR are blocked.
IVR takes over
This is an “Escape rhythm”
This may be all the heart has left!
May occur in single “escape” beats, in short runs
or be sustained
IDIOVENTRICULAR RHYTHM
Rhythm: regular
Rate: 20-40/min
P waves: none
PR interval: not measurable
QRS complex: WIDE
ACCELERATED IDIOVENTRICULAR
RHYTHM
Rhythm: regular
Rate: 40-100
P waves: none
PR interval: not
measurable
QRS complex: WIDE
Agonal Rhythm
If Idioventricular rhythm rate is less than 20, the QRS
may widen and continue to slow
Deterioration of electrical system
Often called a “dying heart”
Ventricular Standstill
Rhythm: if atrial rhythm present, it may be regular,
ventricular rhythm will not be present
Rate: no ventricular rate, essentially this is asystole
P waves: present if atrial activity
PR interval: not measurable
QRS complex: none
CAUSES
Ventricular Standstill
(Asystole)
Hypovolemia
Massive MI
Complete heart block
Hypoxia
Tension pneumothorax
Pulmonary embolism
Hyper/Hypokalemia
Hypo/Hyperthermia
Drug overdose
Cardiac trauma
TREATMENT
ACLS protocol: CPR, Epi
Pulseless Electrical
Activity
Monitor shows organized rhythm, but patient has no
pulse
Most Common causes are Hypoxia and Hypovolemia
Same causes and treatment as Asystole
ACLS protocol
PACEMAKERS
Why do we use pacemakers?
The body’s intrinsic pacemaker is the Sinus node (SA node)
If the SA node is not functioning properly, the patient may need an
artificial pacemaker
This is a generator (for automaticity) that produces impulses that
are conducted through hard-wired leads which are placed in the
heart
Pacemaker indications
◦ Sinus bradycardia, sinus arrest, sinus exit block
◦ A Flutter or A Fib with slow ventricular response
◦ Mobitz II (Second degree, type II)
◦ Complete Heart Block (Third degree)
Pacemakers:
temporary or permanent?
Temporary pacing
◦ Symptomatic bradycardia
◦ Symptomatic Mobitz II or CHB
◦ Some invasive cardiac procedures
◦ Overdrive pacing to “break” SVT
◦ Post CV surgery
Permanent pacing
◦ Symptomatic bradycardia or heart block that is
not transient
◦ AV node ablation for tachy-brady syndrome
Symptomatic patient: what to
do before the pacer is placed
If patient is symptomatic, anticipate the use of
pharmacologic therapy and transcutaneous
pacing while waiting to place a temporary wire
If medications are the cause, withdrawal of
offending drugs is the first treatment for heart
block
Be vigilant: time is of the essence
Transcutaneous pacing for symptomatic bradycardia and heart blocks
Chest leads must be on for pacer to work!
EMERGENCY Temporary Pacing
Procedure
(done in ICU, or Cath Lab)
Permanent pacemaker pulse
generator & leads
Micra pacer: FDA approved 2016
Inserted percutaneously transcatheter
Ventricular pacing only
3 functions of pacemakers
FIRE
◦ Pulse generator produces energy impulse
◦ Indicated on EKG by a spike
CAPTURE
◦ Electrical impulse stimulates the cardiac myocytes, causing
depolarization
◦ Indicated on the EKG by the P wave (atrial) or the QRS complex
(ventricular)
SENSE
◦ Pacer “sees” the patient’s own intrinsic (native) beats and DOES NOT
FIRE OR Pacer does not “see” a rhythm, so it DOES FIRE
◦ Indicated on the EKG by patient’s native beat with NO paced beats until
the next appropriate interval
V-pacing!
But Check the pulse!
V-pacing: look for the spike!
Review: what kind of heart block
do you see in Strip A?
Intrinsic beats
Single and dual chamber
Chest PA and LATERAL
with implanted device
KNOWLEDGE CHECK
Dual chamber pacemakers
A. Have one lead in the right atrium and one lead in the right
ventricle
B. Have one lead in the right atrium and one lead in the left
ventricle
C. Can pace the atrium, the ventricle, or both if needed
D. Can pace twice as fast as single chamber pacemakers
E. A, C, D
F. B & C
G. A & C
3 functions of pacemakers
any malfunction will be in one of these 3 areas
FIRE
◦ Pulse generator produces energy impulse
◦ Indicated on EKG by a spike
CAPTURE
◦ Electrical impulse stimulates the cardiac myocytes, causing depolarization
◦ Indicated on the EKG by the P wave (atrial) or the QRS complex
(ventricular)
SENSE
◦ Pacer “sees” the patient’s own intrinsic (native) beats and DOES NOT FIRE
◦ OR Pacer does not “see” a rhythm, so it DOES FIRE
◦ Indicated on the EKG by patient’s native beat with NO paced beats until
the next appropriate interval
Failure to fire
Failure to capture
Failure to sense:
undersensing
Pacer did not “see” the patient’s native beats
Fusion
Native
Native
Fusion
Paced
Failure to sense:
oversensing
Pacer “saw” the P wave and treated it as a QRS, so it did not pace
KNOWLEDGE CHECK
What are the three main functions of a
pacemaker?
A. Pace, fire, capture
B. Fire, capture, fuse
C. Pace, sense, fire
D. Fire, capture, sense
Internal
Cardioverter/
Defibrillator
(ICD)
Implantable device that will act
as a pacemaker for SLOW
rhythms, but will also cardiovert
or defibrillate fast rhythms as
needed. The device is therefore
capable of correcting most lifethreatening cardiac
arrhythmias.
ICD
Types of defibrillators
ICDs can be
◦Single chamber: one lead in ventricle
◦Dual chamber: two leads, one in atrium &
one in ventricle)
◦Biventricular: two leads in ventricle; may also
have atrial lead
Subcutaneous ICD
◦Subcutaneous: no leads delivers enough energy to
defibrillate the heart without
leads! (no pacing function)
- THIS IS NEW!
Care of patient after cardiac
device implantation
VS, pain control
Observe heart rhythm: Is
pacer capturing and sensing
appropriately?
Observe for bleeding or
hematoma
Keep affected arm
immobilized 24 hours
Patient education: Limit range
of motion for 2-4 weeks
Electrical & mechanical function
of the heart = Cardiac Output!!!!
And it is ALL ABOUT the
Cardiac Output!!!