Patients with Arrhythmias and Conduction Problems Flashcards
process of cardiac conduction
- electrical impulse generated at the SA node stimulates the atria to contract
- the impulse travels to the AV node, where there is a brief delay
- it then sweeps to the bundle of his and divides into the left and right bundle branches
- conduction to the purkinjie fibers causes contraction of the ventricles
signs and symptoms of decreased cardiac output
tachypnea
SOB
orthopnea
DOE
hypoxemia
crackles
wheeze
dry or productive cough
edema
JVD
S3
murmurs
hypotension
decreased MAP
delayed cap refill
tachycardia
decreased urinary output
oliguria
abd distention
ascites
dizziness
syncope
fatigue
anxiety
restlessness
purpose fo electrocardiogram (ECG)
Provides a picture of cardiac electrical activity, including contraction and relaxation of the heart chambers
purpose of a lead on ECG
provides one view of heart; multiple can be used
Best lead to identify/interpret a rhythm for atria:
for ventricular:
Lead II for atria
Lead V1 for ventricles (mimics natural direction of a healthy heart)
Electrical impulses move b/w positive and negative pole
Moves toward from positive= waveforms upright on ECG
Moves away from positive = waveforms have negative deflection
positioning of electrodes
Crucial to obtaining an accurate ECG
Position the client supine with HOB 30-40⁰
Debride the skin with soap and water as necessary
Clip (DO NOT SHAVE) the hair if necessary
Avoid diaphoretic area
Connect electrodes to lead wires before placing them on the chest
Locate the landmarks for placement in the light
Change electrodes every 24-48 hours
Use hypoallergic electrodes if necessary
Who is responsible for obtaining an ECG?
Who is responsible for interpreting an ECG?
continuous ECG monitoring
Indications for use
– Risks of unnecessary monitoring
Electrodes placed on the trunk of the body in five locations
Ensure proper placement of leads
Always assess the patient first!!
Signals transmitted to bedside monitor or from a transmitter box to a central monitoring station (telemetry)
When should the monitoring be suspended? Who determines this?
ambulatory electrocardiography
Continuous form of monitoring used in the outpatient setting
Wears a portable recording device that is connected to the chest by electrodes
Monitoring period can be 24-48 hours (Holter) or weeks
Client records any symptoms
interpreting ECG strip paper
Rhythms are printed on special graph paper
Measures amplitude and time
–Time/rate is on horizontal axis (in sec); amplitude/voltage (in mm) is on the vertical axis
Each small box is 1 mm and 0.04 sec;
Each large box is 0.20 sec
–Small box X 5 = large box
–Five large blocks = 1 sec
–Thirty large blocks = 6 sec
interpretation of a P wave
SA Node sending out electrical impulse
**Atrial depolarization/contraction (generation of an impulse from SA node)
Should be upright and rounded
Should not be longer than 0.10 sec and no higher than 2.5 mm
interpretation of the PR interval
- Measure of time it takes for sinus node stimulation,
atrial depolarization, and conduction through AV node - Measured from beginning of P wave to the beginning
of QRS - Electrical activity from atria to ventricles
- Should be 0.12 – 0.20 seconds
interpretation of QRS complex
Ventricle contraction
* Time required for depolarization of both ventricles
* Hides atrial repolarization
* Pointy, skinny
* A wide QRS indicates ventricular as pacemaker or block in ventricles delaying impulse going to ventricles
* Normally <0.10 seconds
interpretation of T wave
Ventricles relax
* Represents ventricular repolarization; electrical recovery
* Positive, rounded, and upright; follows QRS
* Can become inverted, peaked, or flat from myocardial ischemia, potassium imbalances, meds, or ANS effects
interpretation of ST segment
- Represents early ventricular repolarization (resting state)
- Length can vary
- ST-Depression = ischemia
- ST Elevation = injury
- Q wave = necrosis/infarction
interpretation of U wave
- Represents repolarization of Purkinje fibers
- May or may not be present
- Seen in hypokalemia, HTN, or heart disease
- Follows T wave
QT interval
- Time it takes ventricles to depolarize, contract and then repolarize
**Start of Q to the end of T wave - Medications can prolong
- < 0.50 sec.
steps for interpreting arrhythmias
- determining the HR
- determine the rhythm regularity
- determine if the rhythm originated in the SA node
- evaluate conduction
- evaluate the appearance of the rhythm
- interpret the rhythm
- if a change is noted from pts baseline, evaluate the patient, consider obtaining a 12-lead ECG, and report the change to the provider as appropriate
3 ways to determine the HR (step 1)
First
* Use a 6 second strip to determine rate
** Count number of QRS complexes and multiply by 10
** More commonly used to assess irregular rhythms
Second
* Count number of small boxes between 2 R waves
** Divide into 1500
** More commonly used for accuracy
Third
* Count number of large boxes between 2 R waves
** Divide into 300
how to determine regularity of rhythm (step 2)
- Count boxes between waveforms being measured
- From P wave to P wave (atrial)
- From QRS complex to QRS complex (ventricular)
- Regular rhythm has equal space b/w waveforms
- Can be regularly irregular or irregularly irregular
how to analyze the P waves (step 3)
Check the P-wave shape is consistent and existent
Determine if there is one P wave for each QRS
Ask:
–Are P waves present?
–Are the P waves occurring regularly?
–Is there one P wave for each QRS complex?
–Are the P waves smooth, rounded, and upright in appearance?
–Do all the P waves look similar?
how to measure the PR interval (step 4)
- measure from beginning of P wave to end of PR segment
- should be 0.12-0.20 sec
- should be consistent
- if there are no P waves, this cannot be calculated
how to measure the QRS duration (step 5)
Measure at the beginning to the end of QRS complex
Normally measures 0.04 – 0.10 sec
–If QRS is narrow, indicates impulse was not formed in ventricles
–If QRS is wide, indicates impulse is ventricular (abnormal)
Should be consistent
how to examine the ST segment and T wave
ST segment:
–Monitor for depression and elevation
–ST elevation: MI, pericarditis, hyperkalemia
–ST Depression: Hypokalemia, MI, ventricular hypertrophy
T wave:
–Note shape and height
–Abnormal T waves (peaking or inversion) indicate MI or ventricular hypertrophy
Originates from the SA Node
–Rate: 60-100
–Rhythm: Regular
–P Wave: Present, consistent, one P wave for each QRS
–PR interval: 0.12-0.20 sec and constant
–QRS duration: <0.10 sec and constant
normal sinus rhythm
Results from changing with breathing (increases with inspiration; decreases with expiration)
Same characteristics as NSR, but it is irregular
Not clinically significant
Sinus Arrythmia
what is a dysrhythmia
Disruptions in the cardiac conduction pathway
Can cause decreased cardiac output
clinical manifestations that MAY be present with dysrhythmias
Palpitations,
hypotension,
anxiety,
diaphoresis,
SOB,
syncope,
lightheadedness,
weakness/fatigue,
dizziness
possible causes of dysrhythmias
Cardiac disease: HTN, HF, Cardiomyopathy, MI
Electrolyte Imbalances
Hypoxia
Infections
Drug toxicity
Hypovolemia
Stress
Fear
Anxiety
Recreational drug use: Substance abuse, tobacco, alcohol
components of sinus bradycardia
Regular rhythm same as NSR but HR
<60
Can be caused by a variety of things
s/s of sinus bradycardia
syncope,
dizziness,
weakness,
confusion,
hypotension,
diaphoresis,
SOB,
chest pain
interventions for sinus bradycardia
- Treat underlying cause when symptomatic
- Nursing: notify the MD; assess LOC, pulse, BP, ECG; educate about s/s
- Atropine IV (if cause unknown), epi, IV Fluids, O2, discontinuance of causative agent
- Pacing
Rate: Less than 60
* Rhythm: regular
* P wave: present and consistent in size and shape
* PR interval: WNL
* QRS: normal
Sinus Bradycardia
what is sinus tachycardia
Similar characteristics of NSR, but rate is >100
Over a long period of time, can cause inadequate perfusion
Different causes
Assess for reduced cardiac output; can be asymptomatic
symptomatic treatment of sinus tachycardia
treat underlying cause,
beta blockers,
vagal maneuvers (carotid massage ONLY MD),
IVF,
pain management,
anxiety reduction techniques,
treat infection,
control thyroid,
administer blood,
change medication regiment
Adenosine 6 mg (first dose) followed by 20 ml sale flush
repeat in 1-2 min with 12 mg (second dose)
o2, CCB, or BB, possible cardioversion
client teaching for sinus tachycardia
Avoid substances causing increase in heart rate,
stress management
Rate: Greater than 100
Rhythm: regular
P wave: present and consistent in size and shape
PR interval: WNL
QRS: normal
Sinus tachycardia
what is premature atrial contractions (PAC)
Electrical impulse starts in the atrium earlier than expected
Can be hidden in the T wave and is usually followed by a pause to reset and resume regular rhythm
causes of premature atrial contractions (PAC)
hypoxia,
excessive stimulant ingestion like caffeine/alcohol/nicotine, hypervolemia,
anxiety,
hypokalemia,
atrial ischemia/injury/infarction
s/s of premature atrial contractions (PAC)
asymptomatic
sometimes palpitations
treatment of premature atrial contractions (PAC)
treat causes,
monitor frequency,
eliminate coffee,
manage stress,
avoid substances
If frequent, further work-up
Rate: depends on underlying rhythm
Rhythm: irregular
P wave: premature beat different; others WNL
PR interval: premature beat >0.12
QRS: normal
premature atrial contraction (PAC)
what is atrial flutter
Produced by a pacemaker cell other than the SA Node (so no P waves seen)
Flutter waves present, described as a saw-tooth pattern with F waves
Atria beat too fast, with rates of 250-300 but with a regular rhythm
- Atrial rate is faster than AV node can conduct not all atrial impulses go to the ventricle
causes of atrial flutter
CAD,
HTN,
pulmonary emboli,
cardiomyopathy,
MI,
severe mitral valve disease,
thyroid storm,
COPD
complication of atrial flutter
emboli
tx of atrial flutter
Like A-fib
Cardioversion, but not first line treatment unless symptomatic. Patient needs to have SOB, chest pain, and hypotension for use
Rate: atrial rate 220-350; ventricular rate 75-150
Rhythm: usually regular
P wave: flutter waves in a characteristic sawtooth pattern
PR interval: not measurable
QRS: normal
atrial flutter
what is atrial fibrillation
Most common dysrhythmia
Rapid, disorganized, and uncoordinated electrical activity within the atria; atria quiver
Can lead to pooling of blood in atria
embolism
Can be chronic or short-term
Can be controlled (<100), uncontrolled (100-149), or with RVR (>150)
risk factors of atrial fibrillation
age,
valvular heart disease,
CAD,
HTN,
HF,
cardiomyopathy,
DM,
OSA,
obesity,
hyperthyroid,
pulmonary disease,
chronic lung disease,
surgery;
hypoxia,
infection,
hypoglycemia,
caffeine,
alcohol,
smoking,
sympathomimetics
assessment of afib
Chaotic rhythm with no clear P waves, irregular ventricular response/rhythm, narrow QRS, atrial rate 300-600 bpm
Characterized as irregularly irregular
Can cause impaired perfusion
Can be symptomatic or asymptomatic
Monitor for s/s of thromboembolism
s/s of afib
fatigue,
malaise,
dizziness,
lightheadedness,
fainting,
SOB,
Sweating,
anxiety,
palpitations;
s/s of poor tissue perfusion
goal of managing afib
control ventricular rate and achieve rhythm conversion to NSR
medical management of afib
Can use CCBs (diltiazem) and amiodarone to convert rhythm to NSR, Beta blockers (metoprolol and esmolol) to slow ventricular response, Digoxin for HF and afib, anticoagulants (warfarin, apixaban/eliquis, dabigatran/pradaxa, rivaroxaban/xarelto)
Client teaching?
Teaching with anticoagulants?
Cardioversion with new-onset and unstable after TEE (but can’t have clots in atrium)
Catheter Ablation for no response to meds (electrical system is mapped out and problem area is burned with a laser to prevent conduction going to that area)
what is supraventricular tachycardia
Tachycardias where the atrial and/or ventricular rate >100 at rest; electrical impulse originates above ventricles
s/s of supraventricular tachycardia
Palpitations,
chest pain,
fatigue,
SOB,
nervousness,
anxiety,
hypotension,
syncope for SUSTAINED
Not sustained may be asymptomatic
Rate: over 100
Rhythm: regular
P wave: if visible, may see it merged with QRS or T wave
PR interval: not measurable
QRS: normal generally depending on type
SVT
SVT Treatment
Treatment (goal to decrease ventricular response, convert to NSR, and treat cause)
Remove cause
Vagal maneuvers are temporary and may cause rebound effects
–Carotid massage: MD massages carotid artery over a few seconds.
–Monitor ECG before, during, and after.
–Monitor for complications bradydysrhythmias, asystole, Vfib, cerebral damage. Have emergency equipment ready!
–Valsalva: asking client to bear down
Adenosine 6 mg (first dose) terminates acute episode and given rapidly followed by 20 mL NS.
–Repeat in 1-2 min with 12 mg (second dose) if needed
–Causes bradycardia with pause, nausea, and vomiting
–Have emergency equipment available because it can cause asystole for a brief period (expected response)
Cardioversion
CCBs (diltiazem and verapamil) and BBs for ongoing management
what are premature ventricular contractions
Wide and atypical QRS complexes firing earlier than expected in ventricles
Can occur in bigeminy, trigeminy, or quadrigeminy, couplet; Can be unifocal or multifocal
Three or more successive PVCs are called ventricular tachycardia (VT)
Occur with MI (can trigger VT or VF), stress, nicotine, caffeine, alcohol, infection, exercise, dig toxicity, hypoxia, acidosis, hypokalemia
Modifiable risk factor for HF
Decrease cardiac output
s/s of premature ventricular contractions
asymptomatic mostly; can have palpitations or chest discomfort; decreased stroke volume occurs which leads to decreased peripheral perfusion
treatment of premature ventricular contractions
eliminating or managing cause
assess perfusion
what is ventricular tachycardia
Repetitive firing of QRS complex >100
Can be monomorphic or polymorphic
LIFE THREATENING due to decreased CO!
Can be intermittent or sustained
Occurs with hypovolemia, hypoxia, acidosis, hypokalemia, hyperkalemia, hypoglycemia, hypothermia, toxins, cardiac tamponade, after MI, PE, trauma
Common rhythm seen before Vfib and can cause cardiac arrest
S/S depend on if pulse is present or not; generally decreased cardiac output
Rate: 100-250
Rhythm: regular
P wave: usually not visible, if visible, not associated with QRS
PR interval: not measurable
QRS: Greater than 0.12
Ventricular tachycardia
medical management of vtach with a pulse
Patient remains conscious
S/S dizziness, lightheadedness, fainting, SOB, sweating, anxiety, palpitations
Check ABCs
Cardioversion for symptomatic s/s
Administer Oral antidysrhythmic
Electrolyte replacements
ACLS protocol
Treat causes
Stay with the patient
Obtain 12 lead ECG
Frequent assessment
medical management of vtach without a pulse
S/S: unresponsive, no pulse, no BP, apnea
Cardiac arrest
Follow ACLS protocol
-Initiate CPR/Defib/Code blue
–CAB approach (30:2)
–Maintain a patent airway
–Be aware of complications
–Do NOT stop while defibrillator is being set up
–Can do for about 5 cycles
Stay with client
Emergency meds: Epi and vasopressin
what is torsade de pointes
Polymorphic VT
Congenital or acquired
-Acquired causes – drug therapy, hypokalemia, hypomagnesemia
Immediate treatment required
treatment of torsade de pointes
Antiarrhythmics with temp pacing
IV mag initial treatment of choice for acquired
what is ventricular fibrillation
Electrical chaos in the ventricles; ventricular contraction does not occur; quivering
Life threatening if not fixed in 3-5 minutes
No cardiac output or systemic perfusion
when does ventricular fibrillation happen
hypovolemia,
hypoxia,
acidosis,
hypokalemia,
hyperkalemia,
hypoglycemia,
hypothermia,
toxins,
cardiac tamponade,
after MI, PE, trauma
s/s of ventricular fibrillation
unresponsive, no pulse, no BP, apnea; cardiac arrest imminent
treatment vfib
CODE BLUE,
Defib immediately,
CPR with chest compressions immediately,
epi
Rate: often undetermined; >220
Rhythm: irregular
P wave: not measurable
PR interval: not measurable
QRS: not measurable
ventricular fibrillation
what is asystole
No measurable electrical activity indicating no tissue perfusion
asystole results from:
myocardial hypoxia,
hyperkalemia,
acidosis,
drug overdose,
hypovolemia,
cardiac tamponade,
tension pneumo,
coronary or pulmonary thrombosis, trauma,
hypothermia
s/s of asystole
cardiac arrest (no pulse, BP, or resp), unconscious
treatment of asystole
Call CODE BLUE, CPR, stay with patient, ensure IV access, administer epi as ordered
ASSESS PATIENT FIRST!!!!
NEVER SHOCK ASYSTOLE!!!!!!!!!
Be aware of complications from CPR
Be aware of when to “call it”
Rate: not measurable
Rhythm: not measurable
P wave: not measurable
PR interval: not measurable
QRS: not measurable
Asystole
what is pulseless electrical activity (PEA)
Electrical conduction system on the monitory is organized, but heart muscle doesn’t respond with a contraction; client is unresponsive, not breathing, pulseless
causes of PEA
hypoxia, hypovolemia, hypo/hyperkalemia, acidosis, hypoglycemia, hypothermia, drug toxicities, cardiac tamponade, MI, PE
treatment of PEA
CPR
Epi
Treat causes
Do not assume the patient has a pulse because you see a rhythm on a monitor! Palpate carotid pulse!!!
assessment of patients with dysrhythmias
Vitals Q4 hours and PRN
Peripheral circulation
Change in LOC
Electrolytes and cardiac enzymes
respiratory difficulty
general care of patients with dysrhythmias
Monitor for further development and complications and treat as appropriate
Evaluate and document response to dysrhythmias
Encourage client to notify of chest pain and document quality of chest pain
Provide antidysrhythmic therapy according to unity policy as appropriate and monitor response
Schedule exercise/rest periods appropriately
Monitor relevant labs
Promote stress reduction and decrease causative factors if possible
Offer spiritual support
Education
Prevention?
Care for older adult?
purpose of cardioversion and defibrillation
Used to treat tachyarrhythmias by giving an electrical current that depolarizes, then repolarize, allowing SA node to take over again
Usually cardioversion has < amount of joules than defib
Electrically current done with paddles or electrode pads (used more frequently) OR internally or externally
Follow safety measures for both!!!
what does cardioversion do
Delivery of electrical current is synced with client’s intrinsic rhythm
Used for tachy Afib, SVT, Vtach with pulse
Patient awake and sedated
with QRS
Consent form
what does defib do
Emergency
Only corrects a rhythm, does not restart the heart
Not if the patient is conscious
Delivery of electrical current is not synced (delivered independent) of client’s intrinsic rhythm
Used for vfib or vtach without pulse
No cardiac output
performing cardioversion
Delivery of timed electrical current for tachydysrhythmias
IV moderate sedation and analgesic/anesthesia
Defibrillator set in synchronous mode
Make sure area is clear; Turn 02 off and away from patient and bed (causes fire)
Never shock on T wave!! May cause VT or Vfib
Lower electricity
D/C dig 48 hours before elective cardioversion
May need anticoags few weeks before to prevent emboli during procedure
Don’t eat or drink 4 hours before
performing defib
Used in emergencies for vtach w/o pulse and vfib
NOT used for clients that are conscious with pulse
After defib, immediately restart/start CPR
AED use
Stimulus stops the rhythm allowing the SA node to take over
Before, loudly and clearly command all personnel to CLEAR the area
Allow ACLS team to follow protocol
Never shock on T wave!! May cause Vfib
Maintain safety
D/C 02 near patient temporarily
Implantable cardioverter/defibrillator (ICD)
Terminates life-threatening episodes of tachycardia or fibrillation
Used for those that have survived cardiac arrest, vfib, symptomatic vtach, right ventricular dysfunction
Programmed to automatically charge and deliver a shock when abnormality is present
Some have pacemaker function
Wearable cardioverter/defibrillator (LifeVest)
–Worn 24 hours a day except bathing
–Monitors for VF and VT; if patient conscious can press a button to deliver a shock
teaching for Implantable cardioverter/defibrillator (ICD)
Shock can feel like a blow to the chest
Report to HCP swelling, fever, redness, soreness or drainage at incision site
Do not manipulate generator
Avoid rough contact and strenuous exercise
Do not wear tight clothing
Know function of device; emotional support
Avoid strong magnetic fields
Lie down or sit if dizzy or if they feel a shock
Wear medical alert bracelets and notify providers
Ensure family/friends know CPR
pacemaker therapy
Electronic device that delivers electrical stimulation to the heart to regulate heart rate with slower than normal rate
Can be temporary or permanent
Consist of:
–Generator: contains energy source to determine the rate and strength of electrical stimulus to the heart
–Leads: deliver the settings from generator
Can be in fixed or demand mode
–Fixed (asynchronous) – fires at a constant rate regardless of heart’s electrical activity
–Demand (synchronous) – detects heart rate and fires only if rate is below a certain level
what is temporary pacing
Nonsurgical technique providing a timed electrical impulse to the heart to regulate the heart
transcutaneous pacing (temporary)
Electrodes are attached to the skin and a generator emits electrical impulses
Done for emergencies used for profound bradycardia and asystole when atropine has failed
Can cause discomfort; may need sedation and analgesia
Inspect skin for thermal burns
Obtain CXR for placement
pacemaker leads attached directly to heart during open heart surgery
epicardial
wires threaded through large vein and logged in chamber walls
endocardial
permanent pacemaker
Treat conduction disorders that are chronic/recurrent AV node conduction disorders
Most last for 10 years
After procedure, monitor for: bleeding, swelling, redness, tenderness, and infection; teach ROM restrictions
Report failure to pace and capture
Complication of Pacemakers
Local infection
Bleeding and Hematomas
Hemothorax or Pneumothorax
Ventricular ectopy and tachycardia
Movement or dislocation of electrode
Phrenic nerve stimulation (hiccups s/s)
Cardiac tamponade
Failure to sense/pace
Client Teaching with Permanent pacemaker
With permanent pacemaker, restrict activity on side of implantation for 2-4 weeks
Wear sling when out of bed; avoid raising arm above shoulder for 1-2 weeks
Keep record of pacemaker settings
Monitor for s/s of bradycardia and decreased cardiac output
Objects that contain magnets should not be near the generator for longer than a few seconds
Keep cellphones 6 inches away from generator and do not keep in pocket
Keep identification card in wallet and wear medical alert bracelet
Don’t apply pressure to site
Take pulse for 1 minute every day at the same time; notify provider if there is a difference
Inform airport personnel
Follow up with pacemaker clinic
treatment of PEA
CPR and epi
