Dysrhythmias and Conduction Problems

Dysrhythmias
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Disorders of the formation or conduction (or both) of the electrical impulse within the
heart.
Disturbance in heart rate, heart rhythm or both
Uses ECG analysis
Named according to the site of origin of the impulse and the mechanism formation or
conduction involved. (ex. Sinus bradycardia originating at SA Node)

*sinus rhythm electrical activity of the heart initiated by the sinoatrial (SA) node
*refer to other notes for conduction system
Electrocardiogram (ECG)
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The electrical impulse that travels through the heart can be viewed by means of
electrocardiography.
Number and placement of electrodes depends on the type of ECG needed.
Electrodes creates imaginary lines (LEAD) reference point from which the electrical
activity is viewed. (LEAD like an eye of a camera; narrow peripheral field of vision
looking only at the electrical activity directly in front of it!)

Obtaining an Electrocardiogram
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Standard 12-lead- for Immediate recording (at patients side) ECG (10 electrodes; 6
on chest 4 on limbs)
Hardwire Monitoring continuous monitoring (found in ICU)
Telemetry small box that the patient carries that continuously transmits the ECG
information by radiowaves to a central monitor located elsewhere
Ambulatory/Holter monitor small lightweight tape recorder-like machine that
patients wears and that continuously records the ECG on a tape, later viewed and
analyzed with a scanner

Standard 12-Lead ECG reflects the electrical activity primarily in the left ventricles
Limb electrodes place on areas that are not bony and that do not have significant movement
- provides the first 6 leads: I, II, III, aVR, aVL and aVF.
*locating specific intercostal spaces is very crucial for errors may arise if incorrectly placed.

Interpreting an ECG
*ECG waveform moves towards the top of the paper POSITIVE DEFLECTION; bottom
NEGATIVE DEFLECTION

Waves, Complexes and Intervals

*Waveforms P wave, QRS Complex, T wave, and possibly U wave
*Segments and Intervals PR interval, ST Segment, QT interval
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P wave electrical impulse from the SA node and spreads through the ATRIA; ATRIAL
DEPOLARIZATION
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Normal: 2.5 mm or less in height; 0.11 seconds or less in duration

QRS Complex represents the VENTRICULAR DEPOLARIZATION; less than 0.12 sec in
duration
*Q wave- first negative deflection after P wave (Normal: less than 0.04 sec in duration and less
than 25% of the R wave amplitude)
*R wave first positive deflection after P wave; S wave- first negative deflection after R wave.
*wave less than 5mm small letters are used; waves taller than 5 mm Capital letters are
used
*T wave represents VENTRICULAR REPOLARIZATION
*Atrial repolarization occurs but is not visible in the monitor
*U Wave thought to be repolarization of the Purkinje fibers;
*PR Interval time needed for sinus node stimulation, atrial depolarization and conduction
through the AV node before ventricular depolarization
*ST segment early ventricular repolarization; should be isoelectric (otherwise a sign of
cardiac ischemia)
*QT interval total depolarization and repolarization; varies with age, heart rate, gender
Normal Sinus Rhythm electrical impulse stars at a regular rate and rhythm in the sinus node
and travels through the normal conduction pathways.
Ventricular and atrial rate: 60 to 100 in the adult
Ventricular and atrial rhythm: regular
QRS Shape and duration: usually normal but may be regularly abnormal

TYPES OF DYSRHYTHMIAS
I.

Sinus Node Dysrhythmias

a. Sinus Bradycardia sinus node creates an impulse at a SLOWER-THAN-NORMAL rate

Causes:
*Lower metabolic needs (sleep, athletic training, hypothyroidism)
*Vagal Stimulation (vomiting, suctioning, severe pain, extreme emotions)
*medications (calcium channel blockers, amiodarone, beta blockers)
*idiopathic sinus node dysfunction
*increased Intracranial pressure
Rate: below 60
characteristics: weak and thready
Drug of Choice: Atropine Sulfate, 0.5mg given rapidly as IV bolus every 3 to 5 min to a
max dose of 3 mg (symptomatic)
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b. Sinus Tachycardia sinus node creates an impulse at a FASTER-THAN-NORMAL RATE

Cause:
*Physiologic or Psychologic stress (acute blood loss, anemia, shock, hypervolemia,
hypovolemia, heart failure, pain, hypermetabolic states, fever, exercise and anxiety)
*Medications that stimulate sympathetic response (cathecolamines, aminophylline,
atropine), stimulants (caffeine, alcohol, nicotine) and illicit drugs (amphetamines,
cocaine, ecstasy)
*Enhanced automaticity of the SA node and/or excessive symphathetic tone with
reduced parasympathetic tone (inappropriate sinus tachycardia)
*Autonomic dysfunction resulting in Postural Orthostatic Tachycardia Syndrome
(POTS).
POTS patients have tachycardia without hypotension within 5-10min of standing
or with head-upright tilt testing
Rate: above 100 decrease vagal stimulation

characteristics: Rapid and bounding

pulse
Drug of choice: Beta blockers/ calcium channel blockers
POTS: increased fluid and sodium intake, use of antiembolic stockings to prevent
pooling of blood in the lower extremities

c. Sinus Arrhythmias sinus nodes creates an impulse at an irregular rhythm

Rhythm increases with inspiration and decrease with expiration; usually doesnt have
hemodynamic effect
Nonrespi causes includes Heart Disease and Valvular Disease
Rate: 60 to 100
Rhythm: irregular
DOC: Tachy = CCB
Brady: Atropine SO4
II.

Atrial Dysrhythmias

a. Premature Atrial Complex single ECG complex that occurs when an electrical impulse
starts in the atrium before the next normal impulse of the sinus node.
Causes: intake of caffeine, alcohol, nicotine, stretched atrial myocardium
(hypervolemia), anxiety, hypokalemia, hypermetabolic states (e.g., pregnancy) or atrial
ischemia, injury or infarction
- common in normal hearts. MY HEART SKIPPED A BEAT
- a pulse deficit may exist (apical radial pulse ; difference)
- infrequent, no tx necessary However, if frequent (more than 6/min) may worsen
disease states or onset
b. Atrial Flutter occurs because of a conduction defect in the atrium and causes a rapid,
regular atrial rate usually between 250 and 400 times per minute
*Atrial rate is faster than AV node can conduct = not all atrial impulse are
conducted into the ventricle causing a therapeutic block at the AV node
*if all atrial impulse were conducted to the ventricle, the ventricular rate would
also be 250-400 and may result in V-Fib!
Common in: COPD, Valvular Disease and thyrotoxicosis, open heart surgery and repair
of congenital defects
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ECG: saw tooth

Management:
*Vagal Manuevers and Administration of Adenosine
- sympathetic block and slowing of conduction in the AV node
*adenosine administration rapidly administered via IV followed by a 20mL saline flush
and elevation of the arm with the IV line to promote rapid circulation of medication
*electrical cardioversion last resort
*anticoagulants if lasted longer than 48hrs and transesophageal echocardiogram has
not confirmed the absence of atrial clots
*beta blockers, calcium channel blockers and digitalis slows ventricular response rate
*Catheter Ablation (rather than antiarrhythmic meds) is now the long-term treatment of
choice
c. Atrial Fibrillation uncoordinated atrial electrical activation that causes a rapid,
disorganized and uncoordinated twitching of atrial musculature. Life threatening!
- The ventricular rate response is dependent on the ability of the AV node to conduct the
atrial impulse, level of sympathetic and parasympathetic tone, presence of accessory
pathways & effects of any medications.
- May be transient, stop and occurring (paroxysmal dysrhythmias) or may be persistent
kaya mahirap tlaga siya ilabel and hanapan ng comparative assessment of treatments
- Linked siya sa increased risk of stroke and premature death
- Neurogenic atrial fibrillation sa subarachnoid ang hemorrhage
- No underlying pathophysiology lone atrial fibrillation
- Kay ang AF kay maka wala sa AV synchrony (dli dungan ang atria and ventricles mo
contract), and atrial kick (last part of diastole and ventricular filling) kay mawala sab.
- Result: irregular palpitations and symptoms of HF; short ang time sa diastole reduced
pud ang time for coronary artery perfusion = increased risk for myocardial ischemia.
- The erratic atrial contractions and atrial myocardial dysfunction promotes formation of
emboli
III.

Ventricular Dysrhythmias

a. Premature Ventricular Complex - skipped a beat

- an impulse that starts in a ventricle and is conducted through the ventricles before the
next normal sinus impulse.
- may occur in healthy people: intake of caffeine, nicotine or alcohol
-may be caused by: cardiac ischemia or infarction, increased workload to the heart, F&E
imbalance(hypokalemia), acidosis
- not serious IN THE ABSENCE of disease
-frequent and persistent: Amiodarone or Sotalol
-PVC accompanied with MI: Lidocaine; patients who did not receive thrombolytics and
had more than 10 PVCs ; received thrombolytics and had more than 25PVCs per hour
found to be at greater risk for sudden cardiac death
b. Ventricular Tachycardia three or more PVCs in a row, occurring at a rate exceeding
100bpm
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- patients with larger MIs and lower ejection fractions are at higher risk of lethal
ventricular tachycardia
- an emergency because the patient is usually unresponsive and pulseless
- No P and T wave, purely QRS
v rate: 100-200 times/min
- Factors determining initial treatment:
1. identify the rhythm
*monomorphic consistent QRS shape and rate
*polymorphic having varying QRS shape and rhythms ex. Torsades de pointes
2. existence of prolonged QT interval
3. ascertain heart condition
With Pulse
(-)
(-)
(+)
(-)
(+)

Ventricular Tachycardia
CC
Endotracheal intubation
Vent
Defibrillation
Medications

Without Pulse
(+)
(+)
(+)
(+)
(+)

Management:
*antiarrhythmic meds Procainamide IV (stable MI with VT)
- Amiodarone IV (unstable VT or impaired cardiac function)
- Lidocaine immediate, short term therapy;
no short/long term efficacy in cardiac arrest
*antitachycardia pacing
*direct cardioversion tx of choice for monophasic VT in symptomatic patient.
*Defibrillation tx of choice for pulseless VT
c. Ventricular Fibrillation most common in patients with cardiac arrest; rapid,
disorganized ventricular rhythm that causes ineffective quivering of the ventricles.
-No atrial activity is seen in ECG
-Cause: CAD and resulting MI; Brugada Syndrome (Asian descent) normal structure of
heart, few or no factors for CAD and a Family Hx of sudden cardiac death.
-Rate: Greater than 300/min
Rhythm: Extremely irregular without specific
pattern
-Characteristic: absence of audible heartbeat, a palpable pulse and respirations
-no coordinated cardiac activity, cardiac arrest and death are imminent if not corrected.
H
Management:
*CPR until defibrillation is available
*Epinephrine (immediately before or after the second defib) then 3 to 5 min
*Vasopressin (1 dose) may be administered instead of Epi if Cardiac arrest
persists
*other antiarrhythmic meds
*induced hypothermia (unconscious adults experiencing cardiac arrest &received
CPR w/in 10min)
- 32C to 34C core body temp
- induction started as soon as possible after circulation is restored(within
60min) and maintained for 12 to 24 hours
- icepack on axilla or groin; admin of iced saline gastric lavage until cooling
machine is avail
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-NSG ACTION: monitor appropriate level of cooling, sedation and

neuromuscular paralysis to prevent seizures, myoclonus and shivering
d. Ventricular Asystole - flatline cardiac standstill isoelectric line
- absence of QRS complexes confirmed in 2 different leadss
- no heartbeat, no palpable pulse and no respiration
Management:
*high-quality CPR with minimal interruptions
*rapid assessment to identify possible cause
*establishment of intubation and IV access
*after 2 min or 5 cycles of CPR, a bolus of IV Epinephrine is given
*Vasopressin admin for the first or second dose of epi
*atropine IV bolus asap after rhythm check
*NO DEFIB!
IV.

Pulseless Electrical Activity (known before as Electromechanical Dissociation)

- clinical diagnosis of cardiac arrest; unresponsiveness and lack of palpable pulse in the
presence of organized cardiac electrical activity
-most dangerous; treatment with asystole
Causes:
*Profound Cardiovascular Insult (always) ex. Severe prolonged hypoxia or acidosis ,
extreme hypovolemia or flow-restricting pulmonary embolus)
Prognosis: poor unless a rapidly reversible cause is identified and corrected
Management:

1. Initial evaluation

Activate emergency response system

Basic life support (BLS) algorithm
2. Initial intervention

Start high-quality cardiopulmonary resuscitation (CPR)

Administer oxygen if hypoxemic
Attach monitor/defibrillator
Monitor blood pressure and oximetry
Identify and treat reversible causes
3. Check rhythm

Shockable rhythm = VF/VT

Nonshockable rhythm = asystole/PEA
4. Initial treatment of asystole/PEA

Continue CPR for 2 minutes

Obtain intravenous (IV)/intraosseous (IO) access
Consider advanced airway, end-tidal carbon dioxide tension (PETCO2)
5. Administer vasopressor (epinephrine q3-5min)
6. Check pulse and rhythm (every 2 minutes)

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If nonshockable, return to step 4

If shockable, follow ventricular tachycardia (VT)/ventricular fibrillation (VF) algorithm
Rotate chest compressors
Drug therapy
See the list below:

Epinephrine 1 mg IV/IO q3-5min

Vasopressin 40 units IV/IO can replace first or second dose of epinephrine
Flush medications with 20 mL fluid after and elevate extremity for 10-20 seconds
Combining medications is not recommended and may cause harm
Routine use of sodium bicarbonate is not recommended
CPR quality
See the list below:

Push hard and fast (>100/min)

Allow complete chest recoil
Minimize interruptions in compressions
Avoid excessive ventilation
Rotate compressor every 2 minutes
Compression-to-ventilation ratio of 30:2
Continuous compressions if advanced airway present
If PETCO2 < 10 mm Hg, attempt to improve CPR quality
If diastolic pressure < 20 mm Hg, attempt to improve CPR quality
Advanced airway
See the list below:

Supraglottic advanced airway or endotracheal (ET) intubation

Waveform capnography to confirm and monitor ET tube placement
Ventilation every 6-8 seconds asynchronous with compressions
Stop CPR for no longer than 10 seconds for the placement of an advanced airway
Reversible causes
See the list below:

H's: hypovolemia, hypoxia, H+ (acidosis), hypokalemia, hyperkalemia, hypothermia

T's: toxins, tamponade (cardiac), tension pneumothorax, thrombosis (pulmonary, coronary)
Return of spontaneous circulation
See the list below:

Pulse and blood pressure present

Abrupt sustained increase in PETCO2 (typically >40 mm Hg)
Spontaneous arterial pressure waves with intra-arterial monitoring

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