N418 – Exam 1
NURS 418 UNIT 3 (PT. 3) – DYSRHYTHMIAS: SVT’s,
PVC’s, A. FIB LATEST UPDATED EXAM WITH
COMPLETE VERIFIEDSOLUTIONS
DYSRHYTHMIAS
• Abnormal cardiac rhythms are termed dysrhythmias
• Prompt assessment of dysrhythmias & the pt. response to the rhythm is
critical
EVALUATION OF DYSRHYTHMIAS Regular EKG monitoring
Holter monitoring: o External box that records a 24-hour
EKG tracing or to a week (pt. keeps daily activity diary) Event
recorder monitoring: o Pt. activates recorder during periods of
lightheadedness or chest pain o Put in at cath lab under skin
o Continuous monitor for potentially
months o Basically a high-tech Holter Exercise
treadmill testing: o Performed to elicit
dysrhythmias
o If pt. is unable to physically do this,
perform a cardiolight stress test (pt. is given a
substance like Adenosine to stimulate their heart
& see what the EKG reads) Signal EKG: o Does
NOT allow for all views of the heart o Provides a
one time snap-shot of dysrhythmia
Serial 12-Lead EKG (always
compare to a previous lead) o
Usually taken in series
o Use on pt with chest pain and suspected of MI
Electrophysiological (EP) study: o Performed by
specialized cardiologist in cath lab (venous access also looks
1
, N418 – Exam 1
at pressures) o Stimulate the pt. to go into an arrhythmia
by introducing different catheters
o Used to identify focal points of irritability/re-entry &
can evaluate effectiveness of drugs o Very time-consuming
study
SINUS TACHYCARDIA
• Discharge rate from the SA
(sinus) node is increased as
o a result of vagal inhibition
• Not a dysrhythmia o Rate is > 100 bpm; P-wave is present;
QRS is normal
Sinus tachycardia will NOT have a rate >140-150 bpm
>150 = arrhythmia
< 150 = sinus tachycardia
• Clinical Associations: (physiological stressors)
o Exercise o Pain
o Hypovolemia
o MI
o Heart failure
o Fever, infection, thyroid disorders o Usually caused as
compensatory mechanism Clinical Significance: o
Dizziness & Hypotension due to decreased CO
o Increased myocardial O2 consumption may cause angina
• Treatment: (determined by underlying cause) o Sinus
tachycardia usually accompanies a primary cause, so treatment
is focused on figuring out the underlying cause so we can treat
that
o Beta-blockers (reduce HR & myocardial O2 consumption -
Lopressor) -Adrenergic blockers to reduce HR and
myocardial oxygen consumption
2
, N418 – Exam 1
If sinus tach is due to MI or other
disease processes, we treat it with
beta-blockers – decreases sympathetic
system stimulation & reduces work
load of the heart with the ultimate
goal of decreasing
HR
Beta-blocker act as a negative
chronotropic (decreases rate) o
Antipyretics to treat fever o
Analgesics to treat pain o Fluids to
treat volume depletion
VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS
• Class I: Sodium-Channel Blockers (atrial & ventricular) – most
cardiotoxic group o IA: moderately slow conduction,
moderately prolonged duration of action potential Ex:
Qunidine, Procainamide, Disopyramide
Prolongs QT
interval o IB: minimally slowed
Active in both atrial conduction, shortened duration of
and ventricular action potential – accelerated
repolarization Ex: Lidocaine, Mexiletine, Tocainamide,
Phenytoin (Dilantin)
Active only in o IC: markedly slowed conduction,
ventricles minimally duration of action potential
Ex: Flecainide, Encainide, Propafenone, Moricizinze
Prolongs QT interval
Active in both atrial
and ventricular • Class II: Beta-Blockers- slow
conduction through AV node o Active in AV nodes, ventricles
BETA-BLOCKERS (3 CLASSES)
3
, N418 – Exam 1
• Non-selective Beta-Blockers: stimulates both beta-1(heart) &
beta-2 (lungs) o Propranolol (Inderal) o Sotalol (Beta-pace) –
pro-dysrhythmic Class II and class III characteristics
Cardioselective Beta- doesn’t cause issues in pt. with
Blockers: beta-1 pulmonary conditions
o Atenolol (Tenormin)
o Acebutolol (Sectral)
o Metoprolol
(Lopressor, Toprol XL) o
Bisoprolol (Zebeta) o
Esmolol (Brevibloc) o
Nebivolol (Bystolic)
Combination Alpha [peripheral] & Beta-
Blockers: decreases both BP & HR
o Labetalol (Trandate)
o Carvedilol (Coreg) o
Virtually no pro-
arrhythmic effects
• Class III: Potassium-Channel Blockers (prolonged duration of
action potential)
o Prolong QT =
tordeas de pontez
POTASSIUM CHANNEL BLOCKERS
• Anytime a pt. is started on a new anti-arrhythmic drug, they
need to be monitored in a hospital setting even though they
are not physically ill – antidysrhythmic medications are
“prodysrhythmia” meaning they are used to treat dysrhythmias
BUT they can also cause dysrhythmias
• Amiodarone (Cordarone) o Most widely used K-channel
blocker; used for atrial & ventricular dysrhythmias
• Azimilide (Stedicor)
4
NURS 418 UNIT 3 (PT. 3) – DYSRHYTHMIAS: SVT’s,
PVC’s, A. FIB LATEST UPDATED EXAM WITH
COMPLETE VERIFIEDSOLUTIONS
DYSRHYTHMIAS
• Abnormal cardiac rhythms are termed dysrhythmias
• Prompt assessment of dysrhythmias & the pt. response to the rhythm is
critical
EVALUATION OF DYSRHYTHMIAS Regular EKG monitoring
Holter monitoring: o External box that records a 24-hour
EKG tracing or to a week (pt. keeps daily activity diary) Event
recorder monitoring: o Pt. activates recorder during periods of
lightheadedness or chest pain o Put in at cath lab under skin
o Continuous monitor for potentially
months o Basically a high-tech Holter Exercise
treadmill testing: o Performed to elicit
dysrhythmias
o If pt. is unable to physically do this,
perform a cardiolight stress test (pt. is given a
substance like Adenosine to stimulate their heart
& see what the EKG reads) Signal EKG: o Does
NOT allow for all views of the heart o Provides a
one time snap-shot of dysrhythmia
Serial 12-Lead EKG (always
compare to a previous lead) o
Usually taken in series
o Use on pt with chest pain and suspected of MI
Electrophysiological (EP) study: o Performed by
specialized cardiologist in cath lab (venous access also looks
1
, N418 – Exam 1
at pressures) o Stimulate the pt. to go into an arrhythmia
by introducing different catheters
o Used to identify focal points of irritability/re-entry &
can evaluate effectiveness of drugs o Very time-consuming
study
SINUS TACHYCARDIA
• Discharge rate from the SA
(sinus) node is increased as
o a result of vagal inhibition
• Not a dysrhythmia o Rate is > 100 bpm; P-wave is present;
QRS is normal
Sinus tachycardia will NOT have a rate >140-150 bpm
>150 = arrhythmia
< 150 = sinus tachycardia
• Clinical Associations: (physiological stressors)
o Exercise o Pain
o Hypovolemia
o MI
o Heart failure
o Fever, infection, thyroid disorders o Usually caused as
compensatory mechanism Clinical Significance: o
Dizziness & Hypotension due to decreased CO
o Increased myocardial O2 consumption may cause angina
• Treatment: (determined by underlying cause) o Sinus
tachycardia usually accompanies a primary cause, so treatment
is focused on figuring out the underlying cause so we can treat
that
o Beta-blockers (reduce HR & myocardial O2 consumption -
Lopressor) -Adrenergic blockers to reduce HR and
myocardial oxygen consumption
2
, N418 – Exam 1
If sinus tach is due to MI or other
disease processes, we treat it with
beta-blockers – decreases sympathetic
system stimulation & reduces work
load of the heart with the ultimate
goal of decreasing
HR
Beta-blocker act as a negative
chronotropic (decreases rate) o
Antipyretics to treat fever o
Analgesics to treat pain o Fluids to
treat volume depletion
VAUGHAN WILLIAMS CLASSIFICATION OF ANTIARRHYTHMIC DRUGS
• Class I: Sodium-Channel Blockers (atrial & ventricular) – most
cardiotoxic group o IA: moderately slow conduction,
moderately prolonged duration of action potential Ex:
Qunidine, Procainamide, Disopyramide
Prolongs QT
interval o IB: minimally slowed
Active in both atrial conduction, shortened duration of
and ventricular action potential – accelerated
repolarization Ex: Lidocaine, Mexiletine, Tocainamide,
Phenytoin (Dilantin)
Active only in o IC: markedly slowed conduction,
ventricles minimally duration of action potential
Ex: Flecainide, Encainide, Propafenone, Moricizinze
Prolongs QT interval
Active in both atrial
and ventricular • Class II: Beta-Blockers- slow
conduction through AV node o Active in AV nodes, ventricles
BETA-BLOCKERS (3 CLASSES)
3
, N418 – Exam 1
• Non-selective Beta-Blockers: stimulates both beta-1(heart) &
beta-2 (lungs) o Propranolol (Inderal) o Sotalol (Beta-pace) –
pro-dysrhythmic Class II and class III characteristics
Cardioselective Beta- doesn’t cause issues in pt. with
Blockers: beta-1 pulmonary conditions
o Atenolol (Tenormin)
o Acebutolol (Sectral)
o Metoprolol
(Lopressor, Toprol XL) o
Bisoprolol (Zebeta) o
Esmolol (Brevibloc) o
Nebivolol (Bystolic)
Combination Alpha [peripheral] & Beta-
Blockers: decreases both BP & HR
o Labetalol (Trandate)
o Carvedilol (Coreg) o
Virtually no pro-
arrhythmic effects
• Class III: Potassium-Channel Blockers (prolonged duration of
action potential)
o Prolong QT =
tordeas de pontez
POTASSIUM CHANNEL BLOCKERS
• Anytime a pt. is started on a new anti-arrhythmic drug, they
need to be monitored in a hospital setting even though they
are not physically ill – antidysrhythmic medications are
“prodysrhythmia” meaning they are used to treat dysrhythmias
BUT they can also cause dysrhythmias
• Amiodarone (Cordarone) o Most widely used K-channel
blocker; used for atrial & ventricular dysrhythmias
• Azimilide (Stedicor)
4
