Module 2: Dysrthymias Flashcards
Properties of Heart Cells
Automaticity
Excitability
Conductivity
Contractility
Nervous System Control of Heart
Autonomic nervous system controls
Parasympathetic nervous system - vagus nerve
* Decreases firing of SA node
* Slows impulse conduction of AV node
Sympathetic nervous system
* Increases SA node firing
* Increases impulse conduction of AV node
* Increases cardiac contractility
Calculating HR from ECG
Count
Number of QRS complexes in 1 minute
Number of QRS complexes in 6 seconds and multiply by 10
Number of small squares between one R-R interval, and divide this number into 1500
Number of large squares between one R-R interval, and divide this number into 300
ECG Monitoring
Graphic tracing of electrical impulses of heart
*Waveforms represent electrical activity produced by movement of charged ions across membranes of heart cells
Telemetry Monitoring: 2 Types
Two types
Assessing heart rhythm off site
Centralized monitoring system
Advanced alarm system alerts provides different
levels of detection of dysrhythmias, ischemia, or
infarction
Normal Sinus Rhythm
SA node fires 60 to100 beats/min
Follows normal conduction pattern
P wave is normal and precedes QRS
QRS has normal shape and duration
PR interval is normal
Sinus Bradycardia
SA nodes fires at less than 60 beats/min
Normal rhythm in aerobically trained athletes
and during sleep
Can occur in response to parasympathetic nerve
stimulation and certain drugs
Also associated with some disease states
Sinus Brady Manifestations
Manifestations
Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath
Sinus Brady Treatment
Stop offending drugs
IV Atropine
Pacemaker
Dopamine or epinephrine infusion
Sinus Tachycardia
Sinus rate is 101 to 180 beats/min.
Caused by vagal inhibition or sympathetic
stimulation
Associated with physiologic and psychologic
stressors
Drugs can increase rate
Sinus Tachy Manifestations
Manifestations
Dizziness
Dyspnea
Hypotension
Angina in patients with CAD
Sinus Tachy Treatment
Treatment
Guided by cause (e.g., treat pain)
Vagal maneuvers
β-blockers, adenosine, or calcium channel blockers
Synchronized cardioversion
Premature Atrial Contraction
Contraction starting from ectopic focus in atrium
in location other than SA node
Travels across atria by abnormal pathway,
creating distorted P wave
May be stopped, delayed, or conducted normally
at the AV node
Premature Atrial Contraction Causes
Emotional stress
Fatigue
Caffeine
Tobacco
Alcohol
Hypoxia
Electrolyte imbalances
Disease states
Premature Atrial Contractions Manifestations + Treatment
Manifestations
-Palpitations
-Heart “skips a beat”
Treatment
-Monitor for more serious dysrhythmias
-Withhold sources of stimulation
-β-blockers
Paroxysmal Supraventricular
Tachycardia
Reentrant phenomenon: PAC triggers a run of
repeated premature beats
Paroxysmal refers to an abrupt onset and
ending
May occur with overexertion, stress, deep
inspiration, stimulants, disease, digitalis toxicity
Paroxysmal Supraventricular
Tachycardia - Manifestations
Manifestations
HR is 151 to 220 beats/min
HR greater than 180 leads to decreased cardiac
output and stroke volume
* Hypotension
* Palpitations
* Dyspnea
* Angina
Paroxysmal Supraventricular
Tachycardia - Treatment
Treatment
Vagal stimulation
IV adenosine
IV β-blockers
Calcium channel blockers
Synchronized cardioversion
Atrial Flutter
Typically associated with disease
Symptoms result from high ventricular rate and
loss of atrial “kick” associated with atrial flutter
decrease CO; can cause heart failure
Atrial rate 200 to 350 beats/min
Increases risk of stroke
Atrial Flutter Treatment
Treatment
Pharmacologic agent
Electrical cardioversion
Radiofrequency ablation
Atrial Fibrillation
Paroxysmal or persistent
Most common dysrhythmia
Prevalence increases with age
Usually in patients with underlying heart disease
Can occur with other disease states
As with atrial flutter—causes a decrease in CO
and an increased risk of stroke
Atrial rate may be as high as 350 to 600
beats/min. with chaotic, fibrillatory waves
replacing P waves
AFib Treatment
Drugs to control ventricular response, prevent stroke, and/or convert to sinus rhythm (amiodarone most common)
Electrical cardioversion
Anticoagulation
Radiofrequency ablation
Maze procedure with cryoablation
Left Atrial Appendage Occlusion
(LAA)
Pouch that extends off left atrium
Common source of blood clots with atrial
fibrillation
LAA occlusion done to prevent blood clots,
decrease risk of stroke
Alternative treatment is oral anticoagulation
Junctional Dysrythmias
Dysrhythmias that start in the AV junction
SA node does not fire, or impulse is blocked at
the AV node
AV node becomes pacer—retrograde
transmission of impulse to atria
Abnormal P wave; normal QRS
Associated with disease, certain drugs
Serves as safety mechanism—do not suppress
If rhythms are rapid, may result in reduction of CO
Treat if patient is symptomatic
Atropine for escape rhythm
Correct cause
Drugs to reduce rate if tachycardia
First Degree AV Block
Associated with increasing age, disease states,
and certain drugs
Usually not serious
Patients asymptomatic
No treatment
Monitor for changes in heart rhythm
Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
May result from drugs or CAD
Typically associated with ischemia
Usually transient and well tolerated
Treat if symptomatic
Atropine
Pacemaker
If asymptomatic, observe closely
Second-Degree AV Block,
Type 2 (Mobitz II)
Associated with heart disease and drug toxicity
Often progressive and results in decreased CO
Treat with pacemaker
Treatment
Transcutaneous pacing or temporary pacemaker
Third-Degree AV Heart Block
(Complete Heart Block)
Associated with severe heart disease, some
systemic diseases, certain drugs
Usually results in decreased CO, ischemia, HF,
and shock
Can lead to syncope
Treat with pacemaker
Drugs to increase heart rate if needed while
awaiting pacing
Premature Ventricular Contractions
Associated with stimulants, electrolyte
imbalances, hypoxia, heart disease
Not harmful with normal heart but may reduce
CO, lead to angina and HF in diseased heart
Assess hemodynamic status
Treatment
Correct cause
β-blockers, lidocaine, or amiodarone
Accelerated Idioventricular Rhythm
(AIVR)
Develops when the intrinsic pacemaker rate (SA
node or AV node) becomes less than that of
ventricular ectopic pacemaker
Rate is between 40 and 100 beats/min
Atropine if patient symptomatic
Temporary pacing
Do not suppress rhythm
Ventricular Tachycardia
Ectopic foci take over as pacemaker
-Normally, the heart’s rhythm is controlled by the sinus node, located in the right atrium. In VT, ectopic foci (abnormal pacemaker sites within the ventricles) take over the role of the pacemaker.
This results in rapid and often inefficient contractions of the ventricles.
Types of VTach:
Monomorphic VT: This is the most common type. “Monomorphic” means the heartbeats look similar to each other on an ECG. It occurs due to a single ectopic focus in the ventricles.
Polymorphic VT: In this type, the ECG appearance of the heartbeats varies, indicating multiple ectopic foci within the ventricles. A subtype of this is Torsades de Pointes, which is often related to prolonged QT interval on ECG and can be very dangerous.
Sustained VT: This refers to VT that lasts for more than 30 seconds. It is a medical emergency that requires immediate treatment, as it can lead to hemodynamic instability and progress to more serious conditions like ventricular fibrillation.
Nonsustained VT: This form of VT lasts for less than 30 seconds and stops on its own. While it may not be immediately life-threatening, it often requires evaluation to assess the risk of more serious arrhythmias or underlying heart disease.
Considered life-threatening because of
decreased CO and the possibility of
development to ventricular fibrillation
Ventricular Tachycardia
Torsades de Pointes
VTach Causes
Associated with heart disease, long QT
syndrome, electrolyte imbalances, drug toxicity,
CNS disorders
Can be stable (patient has a pulse) or unstable
(pulseless)
Sustained VT causes severe decrease in CO
Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest
Precipitating causes must be identified and
treated (e.g., hypoxia)
VT with pulse (stable) treated with
antidysrhythmics or cardioversion
Treatment for polymorphic VT with prolonged
baseline QT interval includes IV magnesium,
isoproterenol, phenytoin, or antitachycardia pacing
Pulseless VT treated with CPR and rapid
defibrillation
Ventricular Fibrillation
Associated with acute MI, ischemia, chronic disease
states, cardiac procedures
Unresponsive, pulseless, and apneic
If not treated rapidly, death will result
Treat with immediate CPR and ACLS
Rapid defibrillation
Drug therapy (epinephrine, amiodarone)
Asystole
Total absence of ventricular electrical activity
No ventricular contraction
Patient unresponsive, pulseless, apneic
Must assess in more than one lead
Usually result of advanced cardiac disease, severe
conduction system problem, or end-stage HF
Treat with immediate CPR and ACLS measures
Epinephrine
Intubation
Poor prognosis
Pulseless Electrical Activity
Electrical activity can be observed on the ECG,
but no mechanical activity of the heart is evident,
and the patient has no pulse
Prognosis is poor unless underlying cause
quickly identified and treated
H’s and T’s Mnemonic
Hypovolemia
Hypoxia
Hydrogen ion
(acidosis)
Hyper-/hypokalemia
Hypoglycemia
Hypothermia
Toxins
Tamponade (cardiac)
Thrombosis (MI and
pulmonary)
Tension
pneumothorax
Trauma
Treatment
CPR followed by intubation and IV epinephrine
Treatment is directed toward correction of the
underlying cause
SCD (sudden cardiac death)
Death from a cardiac cause
Most SCDs result from ventricular dysrhythmias
Ventricular tachycardia
Ventricular fibrillation
Prodysrhythmia
Life-threatening dysrhythmias caused by
antidysrhythmia drugs
Severe LV dysfunction increases risk
Digoxin and class IA, IC, and III antidysrhythmic
drugs
Most susceptible first few days of drug therapy
Defibrillation
Treatment of choice for VF and pulseless VT
Most effective when completed within 2 minutes
of dysrhythmia onset
Passage of electrical shock through the heart to
depolarize myocardial cells
Allows SA node to resume pacemaker role
Monophasic defibrillators deliver energy in one
direction
Biphasic defibrillators deliver energy in two
directions
Use lower energies
Fewer post shock ECG dysrhythmias
Output is measured in joules or watts per second
Recommended energy for initial shocks in
defibrillation
Biphasic: 120 to 200 J
Monophasic: 360 J
Immediate CPR after first shock
Synchronized Cardioversion
Therapy of choice for ventricular or
supraventricular tachydysrhythmias (VT with a
pulse)
Synchronized circuit delivers a shock on the R
wave of the QRS complex of the ECG
Procedure similar to defibrillation except sync button turned ON
If patient stable, sedate prior
Initial energy lower
50 to 100 J (biphasic)
100 J (monophasic)
If patient becomes pulseless, turn sync button off
and defibrillate
Implantable Cardioverter-
Defibrillator
Appropriate for patients who
Have survived SCD
Have spontaneous sustained VT
Have syncope with inducible ventricular
tachycardia/fibrillation during EPS
Are at high risk for future life-threatening
dysrhythmias
Decreases mortality
Implantable Cardioverter-
Defibrillator Set Up
Consists of a lead system placed via subclavian
vein to the endocardium
Battery-powered pulse generator is implanted
subcutaneously
Sensing system monitors HR and rhythm—
delivering 25 J or less to heart when detects
lethal dysrhythmia
Includes antitachycardia and antibradycardia
pacemakers
Overdrive pacing for tachycardias
Backup pacing for bradycardias
Pre-procedure and postprocedure care same as
pacemaker
S-ICD
Pacemakers
Used to pace the heart when the normal conduction
pathway is damaged
Pacing circuit consists of
Power source *battery-powered pulse generator)
Programmable circuitry
Pacemaker Mechanism
Pace atrium and/or one or both of ventricles
Most pace on demand, firing only when HR drops
below preset rate
Sensing device inhibits pacemaker when HR
adequate
Pacing device triggers when no QRS complexes
within set time frame
Antitachycardia pacing: delivery of a stimulus to
the ventricle to end tachydysrhythmias
Overdrive pacing: pacing the atrium at rates of
200 to 500 impulses/min to try to stop atrial
tachycardias
Cardiac resynchronization therapy (CRT)
Resynchronizes the heart cycle by pacing both
ventricles
* Biventricular pacing
Used to treat patients with heart failure
Can be combined with ICD for maximum therapy
Transcutaneous Pacing
For emergency pacing needs
Noninvasive
Bridge until transvenous pacer can be inserted
Use lowest current that will “capture”
Patient may need analgesia/sedation
Epicardial Pacing
Leads placed on epicardium during heart
surgery
Passed through chest wall and attached to
external power source
Leads placed prophylactically to treat
dysrhythmias postoperatively
Radiofrequency Catheter
Ablation Therapy
Electrode-tipped ablation catheter “burns”
accessory pathways or ectopic sites in the atria,
AV node, and ventricles
Nonpharmacologic treatment of choice for
several atrial dysrhythmias
Postcare similar to cardiac catheterization
Syncope
Brief lapse in consciousness accompanied by a loss
in postural tone (fainting)
Noncardiovascular causes
Stress
Hypoglycemia
Dehydration
Stroke
Seizure
Cardiovascular causes
Cardioneurogenic or “vasovagal” syncope
* Carotid sinus sensitivity
Dysrhythmias (tachycardias, bradycardias)
Prosthetic valve malfunction
Pulmonary emboli
HF
