Download CV part 4

Patients with Cardiac Dysrhythmias
Lisa Pearson, RN MSN
Leads
• Most cardiac monitors used for patients are in
lead II.
• The pads (red dots) are placed on the chest at
certain spots and lead wires are connected to
the pads (usually 5).
• The pads and wires placement includes: 1 to
right lower chest (green),1 to right upper chest
(white), 1 to left upper chest (black), 1 to left
lower chest (red), and one in the center of chest
(brown).
Grass, Salt, Pepper, Ketchup, Ant
this picture has black and white mixed up!
Cardiac Monitor
Cardiac Conduction
Cardiac Conduction
• The purpose of the heart’s electrical conduction system
is to initiate an impulse to stimulate the cardiac muscle to
contract.
• The electrical activity can be viewed on a cardiac
monitor or recorded on an ECG/EKG.
• Just because the ECG records activity does not
necessarily mean that the heart contracted in response
to the electrical impulse. (VS and pulses verify a
contraction occurred).
Cardiac Conduction
• SA node is the heart’s pacemaker and normally fires at 60-100 bpm.
• If the SA node does not fire or does not fire enough, the AV node
initiates impulse of 40-60 bpm which is known as nodal or
junctional rhythm.
• If the AV node is unable to initiate an impulse, then the Bundle of
His/Purkinje fibers (ventricles) initiate the impulse at 20-40 bmp
which is known as third-degree block/complete heart block or
ventricular escape rhythm.
• The ventricular rhythms are the heart’s last attempt to compensate
for loss of SA and AV node impulse initiation. 20-40 bpm is not
adequate to meet the body’s oxygen needs…signs of inadequate
CO develop such as dyspnea, abnormal VS, and changes in LOC.
• Will need pacing/pacemaker.
Cardiac Conduction
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When the atria contract it is atrial systole.
When the ventricles contract it is ventricular systole.
Relaxation of the atria is atrial diastole.
Relaxation of the ventricles is ventricular diastole.
When atria contract, the ventricles are relaxed.
When the ventricles contract, the atria are relaxed.
When the atria and ventricles are each contracting, they are
squeezing blood to the next chamber.
• When the atria and ventricles are each relaxed, they are receiving
blood. (right atria=vena cava; right ventricle=right atria; etc…).
Cardiac Cycle
• We have learned that a cardiac cycle is one
heart beat.
• Each cardiac cycle begins with the impulse of
the SA node and ends when the ventricles
complete their contraction.
• Each normal cardiac cycle has a P wave, a QRS
complex, and a T wave.
ECG
EKG
• The P wave is the first wave of the cardiac cycle
and represents atrial depolarization (atrial
contraction).
• Only one P wave should be represented on the
EKG strip in a normal cardiac cycle.
• There are some disorders that change the atrial
size and cause alternations in P wave shape
and size (a-fib; atrial flutter).
EKG
• QRS Complex represents ventricular depolarization (contract) and is
composed of three waves, the Q, R, and S.
• The Q wave is the first downward deflection after the P wave.
• The R wave is the first upward deflection after the P wave and it
follows the Q wave.
• The S wave is a downward deflection after the R wave.
• All three waves are not always present in every QRS complex;
however, the QRS is still referred to as the QRS complex and can
be considered normal.
ECG
• During the QRS complex, the ventricles are contracting and the atria
are relaxing (repolarization); however, the ventricle activity with their
contractions are powerful and atrial repolarization is not seen on the
ECG.
• The next P wave proves that repolarization of the atria occurred.
• The T wave represents ventricular repolarization, the resting state of
the heart, when the ventricles are refilling and the SA node is getting
ready to fire again to begin another cardiac cycle.
• The T wave is when the heart is “Taking a break.”
• The T wave can indicate ischemia of the heart.
T Wave Figure
U Wave
• The U wave-form is usually not present.
• The U wave represents the recovery period of the
Purkinje or ventricular conduction fibers.
• It is seen in patients with hypokalemia (low K+),
hypercalcemia (high calcium), or digoxin toxicity.
• Occurs shortly after the T wave and can distort the
configuration of the T wave.
U Wave
ECG Graft Paper
ECG Graft Paper
• The graft paper is calibrated in a grid with small squares
divided into heavy lined blocks of 25 (5 squares wide
and 5 squares high).
• Each small square is 0.04 seconds wide equaling 0.20
per heavy lined block. (0.04 x 5 = 0.20).
• 5 heavy lined blocks = 1 second.
• 30 heavy lined blocks = 6 seconds.
• To read or interpret an ECG strip with the recorded
activity, we look at the information recorded in 6 seconds
(i.e. HR can be counted in the 6 seconds and multiplied
by 10 for bmp).
Intervals
• Using the ECG graft paper, we can count how
much time it takes for the ventricles to contract
after the atria have contracted.
• We can also count how long the ventricles
contracted and how long the heart repolarizes
(relaxes) before the next impulse is fired to
begin the cardiac cycle again.
• These are known as PR Interval, QRS Interval,
ST Segment, and ST Interval.
PR Interval
• The PR Interval represents how long (time) it takes for the impulse
that is initiated in the SA node to travel down (and around) the atria
to the AV node, down the bundle of His, through the right and left
bundle branches.
• It starts at the beginning of the P wave and ends at the beginning of
the QRS complex.
• The normal PR Interval is 0.12 to 0.20 second.
• You have to count the number of small boxes (0.04 second per
small box) horizontally that this interval covers to determine the
length of the PR Interval.
PR Interval
• The normal PR Interval is 0.12-0.20 second.
• Changes in the PR interval indicate an altered impulse formation or
a conduction delay (AV block).
• Short PR intervals (< 0.12 second) indicates the impulse originated
somewhere other than the SA node (junctional arrhythmias).
• Prolonged PR intervals (> 0.20 second) may represent a conduction
delay through the atria or AV junction due to digoxin toxicity or heart
block (slowing related to ischemia) or conduction tissue disease.
PR Interval
Counting for Intervals
• You would try to find a wave that begins with a
small box; however, if you find the first wave you
need to count falls halfway between a small box
(0.04) starting counting it but count it as half of
the box time (0.02).
QRS Interval
• To measure the QRS Interval, start counting the number
of boxes (0.04) from the wave that begins the QRS
complex to the end of the wave that ends the QRS
complex.
• This is measuring how long (time) it takes for the
ventricles to contract (beginning to end of contraction).
• Normal QRS Interval is <0.12 seconds.
QRS Interval
QRS Interval
• If no P wave is present before the QRS complex, this could indicate
the impulse may have originated in the ventricles.
• Deep, wide Q waves may represent MI.
• A “notched” R wave may signify a bundle branch block.
• A widened QRS complex (> 0.12 second) may signify a ventricular
conduction delay.
• A missing QRS complex may indicate AV block or ventricular
standstill.
ST Segment
• The ST segment reflects the time from
completion of a contraction (depolarization) to
the recovery (repolarization) of myocardial
muscle for the next impulse (beginning of next
cardiac cycle).
• The ST segment starts at the end of the QRS
and ends at the beginning of the T wave.
• The duration (time) of the ST segment varies
from person to person.
ST Segment
ST Segment
• The ST segment is examined for patients
experiencing chest pain.
• Changes in the ST segment can indicate the
presence of ischemia or an injury pattern
suggestive of myocardial damage.
• Ischemia = ST segment can be inverted or
depressed.
• Cardiac injury= ST segment elevates.
ST Segment Inverted or Depressed
Ischemia
ST Segment Elevated
Cardiac Injury
6 Second Strip
6 Second Strip
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5 steps to reading strips.
1- Regularity of Rhythm
2- Heart Rate
3- P Wave
4- PR interval
5- QRS Complex
6 Second Strip
Step 1 Regularity of Rhythm
• 1- Regularity of Rhythm is the regularity or rhythm of the heart beat
can be determined at the R-R interval.
• R-R should have the same amount of space between them…can
count spaces (boxes) between each R wave; however, variation
should be no greater than 2 small boxes for a regular rhythm.
• May use calipers or mark a sheet of paper to measure from top of
one R wave to another R wave to see if distance is the same.
• If the distance is the same, then rhythm is regular.
• Pattern can be regularly irregular which means it has a predictable
pattern of irregularity.
• Pattern may be irregularly irregular which is without any pattern of
irregularity.
Normal cardiac waves are equal distance apart
a- R-R waves
b- P-P waves
Step 2 Heart Rate
• After the rhythm regularity is determined, the heart rate is counted.
• The 6 second method is used for irregular rhythms and when a rapid
estimate of regular rhythm is needed.
• Although it is not the most accurate method of regular rhythms, this
is what is used.
• 5 big boxes = 1 second…15 big boxes = 3 seconds…30 big boxes =
6 seconds.
• Another method is to count the number of small boxes and divide by
1500 or count large boxes and divide by 300.
• Count number of large boxes between two R waves and divide into
300; large boxes, 300/5 = 60 beats per minute.
Counting R waves in a 6 second strip
6 x 10 = 60 beats per minute
Step 3: P Wave
• The P waves on the ECG strip are examined to see if
there is one P wave in front of every QRS, the P waves
are regular, and the P waves all look alike.
• If all the P waves meet these criteria, they are
considered normal.
• If they do not, further examination of the strip is
necessary to determine the dysrhythmia.
Step 4: PR Interval
• All PR intervals are measured to determine
whether they are normal and constant.
• If the PR is found to vary, it is important to note
whether there is a pattern to the variation.
Step 5: QRS Complex
• The QRS intervals are measured to determine whether
they are all normal and constant.
• Then the QRS complexes are examined to see if they all
look alike.
Normal Sinus Rhythm
NSR
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NSR is the normal cardiac rhythm.
It begins in the SA node and has complete, regular cardiac cycles.
Rules for NSR
1- rhythm is regular
2- HR 60-100 bpm
3- P waves: rounded, precede each QRS complex, and are alike
4- PR interval 0.12 to 0.20 seconds
5- QRS interval < 0.12 seconds.
NSR
Dysrhythmias/Arrhythmias
• Arrhythmia is an irregularity or loss of rhythm of the heart beat.
• Dysrhythmia is an abnormal, disordered, or disturbed rhythm.
• Each of these words are interchangeable; however, dysrhythmia is
the most accurate term for the discussion of abnormal rhythms.
• Several mechanisms can cause irregularity or dysrhythmia such as
disturbance in the formation of an impulse and a disturbance in the
conduction of the impulse (could be from atria, AV node, or
ventricles).
• These disturbances from the formation of an impulse can be seen
as an increased or decreased HR, early or late beats, or atrial or
ventricular fibrillation.
Dysrhythmias/Arrhythmias
• With a disturbance in conduction, there may be normal formation of
the impulse, but it becomes blocked within the electrical conduction
system, resulting in abnormal conduction such as in heart block or
bundle branch blocks.
SA Node Dysrhythmias
• Rhythms arising from the SA node are referred
to as sinus rhythms.
• Disturbances in conduction from the SA node
can cause irregular rhythms or abnormal heart
rates.
• These dysrhythmias are RARELY dangerous;
however, patients with heart, lung, or kidney
disease may not be able to tolerate a rapid or
slow HR and may need treatment.
Sinus Bradycardia
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Sinus bradycardia is a slower than normal HR.
Has same cardiac cycle components as NSR.
Only difference is HR is slower < 60 bpm.
Causes: medications (digoxin), MI, electrolyte imbalances, finetuned athletes (heart works better/more efficiently).
• S/S: rare…unless HR is so slow that it reduces CO. (fatigue or
fainting spells).
• Treatment: none if asymptomatic. O2, IV access, pacemaker…if
symptomatic…atropine, transcutaneous pacing, dopamine,
epinephrine, or isoproterenol.
Sinus Bradycardia
Sinus Tachycardia
• HR greater than 100 bpm.
• Has same components as NSR.
• Causes: physical activity, hemorrhage (often 1st sign of
hemorrhage), shock, medications (epinephrine, atropine, nitrates),
dehydration, fever, MI, electrolyte imbalances, fear, and anxiety.
• May occur to compensate for hypoxia when more CO is needed to
deliver O2 to organs and tissues.
• S/S: may not be present. If HR is very rapid and sustained for long
periods, the patient may experience angina or dyspnea.
• Treatment: depends on cause and s/s. Meds (digoxin, calcium
channel blockers, or beta blockers). O2.
Sinus Tachycardia
Dysrhythmias originating in the atria
• The SA node is the primary pacemaker; however, if the atria initiate
impulses faster than the SA node, they become the primary
pacemaker.
• Atrial rhythms are usually faster than 100 bpm and can exceed 200
bpm.
• When the impulse originates outside the SA node, the P waves
produced look different from the rounded P waves from the SA node
which indicates the SA node is not controlling the HR.
• These atrial impulses travel to the ventricles to initiate a normal QRS
complex after each P wave.
Premature Atrial Contractions
PACs
• Premature refers to an “early” beat.
• When the atria fire an impulse before the SA node fires,
a premature beat occurs.
• If the underlying rhythm is sinus rhythm, the R-R interval
is the same except where the early beat occurs.
• Looking at a EKG strip, a shortened R-R interval is seen
where the premature beat occurs.
Premature Atrial Contractions
PACs
Premature Atrial Contractions
PACs
• Causes: hypoxia, smoking, stress, myocardial ischemia, enlarged
atria in valvular disorders, medications (digoxin), electrolyte
imbalances, atrial fibrillation onset, and heart failure.
• S/S: can occur in health people. No s/s are usually present. If many
PACs occur in succession, the patient may report sensation of
palpitations.
• Usually not dangerous and often no treatment is needed other than
correcting the cause.
• Frequent PACs indicate atrial irritability and can worsen into other
atrial dysrhythmias.
• Quinidine or procainamide can be given for frequent PACs to slow
the heart rate.
Atrial Flutter
• With atrial flutter, the atria contract or flutter at a rate of 250 to 350
bpm.
• The very rapid P waves or F waves appear to flutter and look like
“saw-toothed” pattern on EKG strip.
• Some of the impulses get to the AV node and a normal QRS
complex occurs.
• Can be 2-4 F waves between QRS complexes.
• If impulses pass through the AV node at a consistent rate, the
rhythm is regular.
• Classic characteristics include more than one P wave before QRS,
saw-toothed pattern of P waves, and atrial rate of 250-350 bpm.
Atrial Flutter
Atrial Flutter
• Causes: rheumatic or ischemic heart diseases, CHF, HTN,
pericarditis, PE, and post-op CABG. Also some medications.
• S/S: presence of s/s depends on ventricular rate. If ventricular rate is
normal, usually no s/s are present. If the rate is rapid, the patient
may experience palpitations, angina, or dyspnea.
• Treatment: Goal is to control ventricular rate and convert the rhythm.
Cardioversion may be scheduled ahead of time. If rate is > 150,
immediate cardioversion is needed. Calcium channel blockers and
beta blockers can slow the heart rate. Digoxin can be used for
rhythm conversion to slow conduction through the AV node and
increase cardiac contractility. Quinidine, procainamide, or
propranolol can be used to slow HR.
Atrial Fibrillation
A-Fib
• The atrial rate is extremely rapid and chaotic.
• Atrial rate of 350-600 bpm can occur.
• AV node blocks most of the impulses so the ventricular rate is much
slower than the atrial rate.
• No definable P waves because the atrial is essentially quivering.
• R waves are irregular.
• Ventricular rate varies from normal to rapid.
• A-fib can be self-limiting, persistent, or permanent.
• A complication is an increased risk of thrombus formation from the
blood stasis in the atria (stroke, PE).
Atrial Fibrillation
A-fib
A-Fib
• Causes: aging, rheumatic or ischemic heart diseases, HF, HTN,
pericarditis, PE, and post-op CABG. Also some medications.
• S/S: most patients feel the irregular rhythm and describe it as
palpitations or a skipping heart beat. Radial pulse may be faint.
• Treatment: If patient is unstable, cardioversion is done ASAP. If
patient is stable, meds to restore and maintain NSR and control
ventricular rate are used such as digoxin, beta blockers, or calcium
channel blockers. Meds to convert a-fib and maintain NSR include
dofetilide, quinidine, flecainide, propafenone, and ibutilide IV. May
be given anti-coagulants. Dual-chamber pacing and implantable
cardioverter defibrillators (ICDs). Ablation can be done. Maze
procedure (surgical).
Ventricular Dysrhythmias
PVCs
• Premature ventricular contractions (PVCs) orignate in the ventricles
from an ectopic focus (site other than the SA node).
• Ventricles are irritable and fire prematurely, before the SA node.
• When the ventricles fire first, the impulses are not conducted
normally through the electrical pathway which results in a wide
bizarre QRS complex on EKG strip.
• PVCs occur in different shapes.
• A unifocal PVCs all look the same because they stem from same
area of ventricle.
• Multifocal PVCs do not all look the same because they originate
from several irritable areas in the ventricle.
PVCs
PVCs
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Bigeminy is a PVC that occurs every other beat.
Trigeminy is a PVC that occurs every third beat.
Quadrigeminy is a PVC that occurs every fourth beat.
When two PVCs occur together, they are called a
couplet or a pair.
• If three or more PVCs occur in a row, it is called a run of
PVCs or ventricular tachycardia.
PVCs
PVCs
• Causes: use of caffeine, alcohol, anxiety, hypokalemia,
cardiomyopathy, ischemia, and MI.
• S/S: patient describes as skipped beat or palpitations. Frequent
PVCs can cause decreased CO, leading to fatigue, dizziness, or
more severe dysrhythmias.
• Treatment: depends on type and number of PVCs and if s/s occur. A
few PVCs do not usually need treatment. If PVCs are more than six
per minute, regularly occurring, multifocal, falling on the T wave (Ron-T) which can trigger life-threatening dysrhythmias, or caused by
an acute MI, they can be dangerous. Anti-dysrhythmic meds that
depress myocardial activity are used to treat PVCs such as lidocaine
(Xylocaine) and procainamide (Procan) IV.
Ventricular Tachycardia
V-tach
• The occurrence of three or more PVCs in row is referred
to as V-tach.
• Is a result from the continuous firing of an ectoptic
ventricular focus.
• During v-tach, the ventricles rather than the SA node
become the pacemaker of the heart producing a wide,
bizarre QRS complexs.
• Causes: myocardial irritability, MI, cardiomyopathy are
common causes. Also respiratory acidosis, hypokalemia,
digoxin toxicity, cardiac catheters, and pacing wires.
V-Tach
V-Tach
• S/S: seriousness depends on duration. Compromises
CO. Patients are aware of a sudden onset of rapid heart
rate and can experience dyspnea, palpitations, and lightheadedness. Angina commonly occurs. Left ventricle
can fail and complete cardiac arrest results.
• Treatment: is patient is pulseless or not breathing, CPR
and immediate defibrillation are required. ACLS
protocols. Meds given such as amiodarone,
procainamide, sotalol, lidocaine, phenytoin, or beta
blockers. Magnesium is mag level low (helps stabilize
ventricle muscles).
Ventricular Fibrillation
V-Fib
• V-fib occurs when many ectopic ventricular foci fire at
the same time.
• Ventricular activity is chaotic with no discernible waves.
• Ventricle quivers and is unstable to initiate contraction.
• There is a complete loss of CO.
• If this rhythm is not terminated immediately, death
ensues.
V-Fib
V-Fib
• Causes; hyperkalemia, hypomagnesemia, electrocution, CAD, and
MI.
• S/S: patients lose consciousness immediately. NO heart sounds,
peripheral pulses, or BP (circulatory collapse). Also, respiratory
arrest, cyanosis, and pupil dilation occur.
• Treatment: immediate defibrillation is the very best treatment. CPR
until defibrillation is available. AEDs, ET intubation, ventilator
support. Meds given according to ACLS protocol such as
epinephrine, vasopressin, amiodarone, lidocaine, magnesium, and
procainamide.
Asystole
• Asystole (the silent heart) is the absence of electrical activity in the
cardiac muscle.
• A straight line appears on the EKG strip.
• V-fib usually precedes this rhythm and must be reversed
immediately to help prevent asystole.
• Causes: v-fib and loss of majority of functional cardiac muscle due
to an MI are common causes. Also, hyperkalemia.
• Treatment: CPR is started ASAP. ACLS protocols. ET intubation,
transcutaneous pacing is considered, then epinephrine and atropine
are administered.
Asystole
Cardiac Pacemakers
• Can be external and temporary or internal and permanent.
• They are used to override dysrhythmias or to generate an impulse
when the heart is beating too slowly.
• Trascutaneous pacemakers are used in emergency situations
because they are quick and easy to apply with impulses delivered to
the heart through the skin from the external generator via electrodes
that are attached to the chest and back.
• Temporary pacemakers are used for bradycardia or tachycardia that
do not respond to medications or cardioversion. Can be inserted
during valve or open heart surgery or in the cardiac cath lab or
critical care unit at the bedside as emergency treatment until
permanent pacemaker can be placed surgically.
Pacemakers
• Permanent pacemaker insertion is a surgical procedure in which
fluroscopy is used.
• The pacemaker generator is implanted SQ and attached to one or
two leads that are inserted via a vein into the heart.
• Lead can deliver the impulse directly to the heart wall.
• A single-lead pacemaker paces either the right atrium or right
ventricle.
• Dual-chamber pacemakers have two leads, with one in the right
atrium and the other in the right ventricle.
• Pacemakers are usually set at a prescribed rate of 72 bpm.
• A small spike is seen on the EKG strip before the paced beat. The
spike is the electrical stimulus. It can precede the P wave, QRS
complex, or both. May have all paced beats, a mixture, or all their
own beats.
Pacemakers
Pacemakers
Pacemakers
• Problems with pacemakers include: failure to sense the
patient’s own beat, failure to pace because of a
malfunction of the pulse generator, or failure to capture
which is lack of depolarization.
• Nursing care: cardiac monitor and rest for several hours
after insertion. Monitor apical pulse for irregular rhythms
or rate slower than the pacemaker’s set rate can indicate
pacemaker malfunction. Dressing site monitored every
2-4 hours for s/s of bleeding. Report ASAP any chest
pain or changes in vital signs. May have a sling on
affected side for 24-48 hours.
Pacemakers
• Teach patients to check radial pulse and report rate less than set
paced rate. Report s/s of dizziness, fainting, irregular heart beats, or
palpitations to physician. Medial alert bracelets and carry pacemaker
information card. Avoid radiation, magnetic fields (MRI), high
voltage, anti-theft devices, and large running motors.
• May trigger alarm at airport security.
• Avoid lifting more than 10 pounds, making major arm movements, or
participating in contact sports for 6 weeks after surgery.
• Periodic pacemaker checks will be done by the physician or over the
phone.
• Re-programming of the pacemaker can be done by the physician if
needed.
Defibrillation
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AEDs:
Implantable cardioverter defibrillators:
Cardioversion:
Ablation: