Transcript Arrhythmias: Hyperfunction

Arrhythmias:
By Kelle Howard
From the notes of : Nancy Jenkins
The EKG is the electrical activity
of the heart.
Electrical precedes mechanical
(Without electricity, we have no pump!!)
How is electricity generated?
By action potentials (view on own)
Na, K and Ca very important for this
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Na K pump
Calcium channels
Depolarization
Repolarization
YouTube - How the Body Works : A Nerve Impulse
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ECG waveforms are produced by the movement
of charged ions across the semipermeable membranes
of myocardial cells.
EKG waveforms
• P wave associated with atrial depolarization (stimulation)
• QRS complex associated with ventricular depolarization
(stimulation)
• T wave associated with ventricular repolarization
(recovery)
• Atrial recovery wave hidden under QRS wave
• Stimulus causes atria to contract before ventricles
• Delay in spread of stimulus to ventricles allows time for
ventricles to fill and for atrial kick -25-30% CO
Cardiac Cycle
Conduction system- Pacemakers
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SA node -- 60-100 bpm
AV node -- 40-60 bpm
Bundle of His
Left and Right Bundle Branch
Purkinge Fibers -- 15-40 bpm
• Each beat that is generated from the same
pacemaker will look identical.
• Impulses from other cardiac cells are called _______
and look different (___________, _________)
• Primary and secondary pacemakers
EKG graph paper
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Horizontal measures time
Vertical measures voltage
Helps us determine rate
Width of complexes- intervals (_______)
Duration of complexes- intervals (_________)
EKG graph paper
Definitions:
PR Interval: time the electrical impulse takes to travel
from the sinus node to the AV node where it enters the
ventricles.
The PR interval is a good estimate of AV node function.
QRS Complex: depolarization of the right and left
ventricles
QT Interval: represents electrical depolarization and
repolarization of the left and right ventricles.
T Wave: absolutely refractory period
ST Segment: represents the period when the ventricles
are depolarized.
Intervals:
PR .12-.20
QRS .04-.12
QT .34-.43
Monitoring leads- based on 12 lead EKG
• Each lead is either unipolar or bipolar.
• Each lead looks at a different area of the heart.
• This can be diagnostic in the case of an MI
RNCEU’s
We monitor using 3 leads or 5 leads
Best for arrhythmiaslead II and MCL(if using 3 leads) or V1 leads- easy to see P waves
MCL or V1 easy to see ventricular rhythms.
If impulse goes toward positive electrode complex is positively deflected or
_____________
If impulse goes away from positive electrode complex is negatively deflected or
goes __________ from baseline
How to place leads
HINTS:
White is right
clouds over grass (white over green) & smoke over fire (black over red)
In 5 lead **V1 is 4th ICS right of sternum – brown or ground
(most important)
Cardiac cells are either:
contractile cells
pacemaker cells
4 Characteristics of Cardiac Cells
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Automaticity-_____________
Excitability- ______________
Conductivity- _____________
Contractility- _____________
Refractoriness
– relative
– absolute
Refractory Period
Risk Factors for Arrhythmias
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Hypoxia
Structural changes
Electrolyte imbalances
Central nervous system stimulation
Medications
Lifestyle behaviors
Steps in Assessment of Rhythms
• **Calculate rate
– Big block- big blocks in R-R divide into 300
– Little block - little blocks in R-R into 1500
– Number of R waves in 6 sec times 10
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Calculate rhythm
Measure PR interval
QRS interval
P to QRS relationship
How is the rate controlled?
Autonomic Nervous System
• Parasympathetic nervous system:
– i.e. Vagus nerve
• Decreases rate
• Slows impulse conduction
• Decreases force of ____________
• Sympathetic nervous system:
• Increases rate
• Increases force of _____________
Rate Calculation
1 lg box= .20
5 lg boxes =1 sec
30 lg boxes =6sec
Therefore there are 300 lg boxes in 1 min.
Sinus Rhythm
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Normal P wave
PR interval <.20
QRS .04-.12
T wave for every complex
Rate is regular 60-100
What is common to all arrythmias?
• Decreased Cardiac Output
– Neuro
– Cardiac
– Respiratory
– GI
– Renal
– Skin
Characteristics for ST include:
If rate >100: Sinus Tachycardia
Causes-anxiety, hypoxia, shock, pain, caffeine, drugs
Treatment-eliminate cause
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Regular rhythm
PR interval less than .20 secs.
QRS < .12
Rate greater than 100
• Rate<60: Sinus Bradycardia
– (can be relative)
– Cause-vagal stimulation, athlete, drugs
(Blockers and digoxin), head injuries, MI
– Watch for syncope and falls
– Treatment- if ____________: atropine or pacer
Sinus Arrhythmia (SA)
• Rate 60-100
• Irregular rhythm- increases with
inspiration, decreases with expiration
• P, QRS,T wave normal
• Cause- drugs (morphine), MI
• Treatment- _________
Sinus Arrest
• See pauses
• May see ectopic beats (PAC’s PVC’s) do not
treat
• Cause MI
• Treatment
– Atropine
– Isuprel
– Pacemaker
Atrial Arrythmias
• Atria is the pacemaker
• Atrial rate contributes 25-30% of cardiac
reserve
**Medications used to treat the atrial
rhythms
• Cardizem and Verapamil
– calcium channel blockers
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Digoxin
Amiodarone or dronedarone- (Multaq)
Corvert- (ibutilide)
Metropolol and Propanalol
– beta blockers
Premature Atrial Contraction (PAC’s)ectopic
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P wave abnormally shaped
PR interval shorter
QRS normal
Cause-age, MI, CHF, stimulants, dig,
electrolyte imbalance, stress, fatigue
• Treatment- remove stimulants and watch
for SVT
(Paroxysmal) Supraventricular
Tachycardia (PSVT/SVT)
• Rate is 150-300, regular, p often hidden
• Atria is pacemaker (may not see p waves)
reentrant phenomenon
• Cause-SNS stimulation, MI, CHF, sepsis
• Treatment- vagal stimulation, * ________,
digoxin, verapamil, inderal, cardizem, tikosyn,
or ____________
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Atrial Flutter
Rate of atria is 250-300, vent rate varies
Regular rhythm- single focus in RA
P waves saw tooth, ratio 2:1, 3:1, 4:1
Flutter waves- No PR interval
Cause-diseased heart, dig
Treatment- cardioversion, calcium channel
blockers and beta blockers, amiodorone, ablation,
ALSO: __________, __________, __________
3:1 flutter
Atrial Fibrillation –
most common
• Rate of atria 350-600- (disorganized rhythm)
• Problem arises when:
– Ventricular response becomes irregular
– (RVR) – rapid ventricular response
• No P waves, “garbage baseline”
• Cause: #1 arrhythmia in elderly
– heart disease- CAD, rheumatic fever, CHF, alcohol
• Complications: __________________
• Treatment:
– ___________________
– Prevent cerebral embolic events
– Convert to SR if possible
Treatment Afib
• Rate control-
– start with digoxin, ca channel blockers, beta
blockers, (multaq-too many side effects no
longer use)
• Convert to SR– amiodorone and ibutilide (corvert), pronestyl,
cardioversion (TEE to see if clots before)
Coumadin- check PT and INR, ablation and
Maze
• Prevent embolic events– Coumadin, Pradaxa, Xarelto, Lovenox
– (ASA if low risk)
Atrial Fibrillation
Arrhythmias of AV Node
**AV Conduction Blocks- important
to check HR and hold blockers
First Degree AV Block
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Transmission through AV node delayed
Regular rhythm
Rate <100
PR interval >.20
QRS normal and regular
Cause-dig toxicity, MI, CAD vagal, and blocker
drugs
• Treatment- none but watch for further blockage,
monitor meds (_____________)
Second Degree AV Block
more P’s than QRS’s
• A. Mobitz I (Wenckebach) YouTube - Diagnosis
Wenckebach
– PR progressively longer then drops QRS (long, longer,
longest, drop)
– Cause- MI, drug toxicity, ischemia
– Treatment- watch for type II and 3rd degree
• B. Mobitz II
– More P’s but skips QRS in regular pattern 2:1,3:1,
4:1(QRS usually greater than .12-BBB)
– Constant PR interval- can be normal or prolonged
– Treatment-Pacemaker
– Occurs in HIS bundle with bundle branch block
Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
• Clinical significance
– Usually a result of myocardial ischemia or
infarction
– Almost always transient and well tolerated
– May be a warning signal of a more serious
AV conduction disturbance
Second-Degree AV Block,
Type 2 (Mobitz II)
• Clinical significance
– Often progresses to third-degree AV
block
– Associated with a poor prognosispacemaker
– Reduced HR often results in decreased
CO with subsequent hypotension and
myocardial ischemia
3rd Degree AV Block
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Atria and ventricles beat independently
Atrial rate- 60-100
Slow ventricular rate 20-40
No PR interval
Wide or normal QRS (depends on where block is)
Cause- severe heart disease, blockers elderly, MI
Complications- dec. CO, ischemia, HF, shock, and
syncope
• Treatment- __________, _________
Third-Degree AV Heart Block
(Complete Heart Block)
• Clinical significance
– Decreased CO with subsequent
ischemia, HF, and shock
– Syncope may result from severe
bradycardia or even periods of asystole
(patient may present with history of
fall)
3rd Degree
Bundle Branch Blocks
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Left BBB
Right BBB
QRS .12 or greater
Rabbit ears- RR
No change in rhythm
Right Bundle Branch Block
Junctional Rhythm
• AV node is pacemaker- slow rhythm (40-60) but very regular impulse goes
to atria from AV node- (backward)
• P wave patterns
– Absent
– P wave precedes QRS inverted in II, III, and AVF
– P wave hidden in QRS
• P wave follows QRS
• PR interval
– Absent or hidden
– Short <.12
– Negative or RP interval
• QRS normal
• No treatment
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Ventricular Arrythmias
most serious
Easy to recognize
Premature Ventricular Contractions
(PVC’s)-ectopic
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QRS wide and bizarre
No P waves
T opposite deflection of PVC
Cause- 90% with MI, stimulants, dig,
electrolyte imbalance
• Treatment- O2, amiodarone, lidocaine,
pronestyl
Premature Ventricular Contractions
• Clinical significance
– In normal heart, usually benign
– In heart disease, PVCs may decrease CO and
precipitate angina and HF
• Patient’s response to PVCs must be monitored
• PVCs often do not generate a sufficient
ventricular contraction to result in a _________
___________
• Apical-radial pulse rate should be assessed to
determine if pulse deficit exists
Premature Ventricular Contractions
• Clinical significance
– Represents ventricular irritability
– May cause HF, angina, and dec CO
– May occur
• After lysis of a coronary artery clot with
thrombolytic therapy in acute MI—
reperfusion dysrhythmias
• Following plaque reduction after
percutaneous coronary intervention
PVC’s
PVC’s multi-focal
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Multifocal- from more than one foci
Bigeminy- every other beat is a PVC
Trigeminy- every third beat is a PVC
Couplet- 2 PVC’s in a row
Treat if:
• >5 PVC’s a minute
• Runs of PVC’s
• Multi focal PVC’s
Ventricular Tachycardia (VT)
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Ventricular rate 150-250, regular or irregular
No P waves
QRS>.12
Can be stable- pulse or unstable –no pulse
Cause- electrolyte imbalance, MI, CAD, dig
Lifethreatening, dec. CO, watch for V-fib
Treatment– same as for PVC’s
– __________ for sustained/pulseless
– __________ for wide complex
Ventricular Tachycardia
• Clinical significance
– Treatment for VT must be rapid
– May recur if prophylactic treatment is not
initiated
– Ventricular fibrillation may develop
• Sustained VT: Severe decrease in CO
Ventricular Tachycardia is worse than
Ventricular Fibrillation.
1. True
2. False
VT- Torsades de Pointes- polymorphic VT
(Magnesium)
French for twisting of the points
Ventricular Fibrillation
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Garbage baseline-quivering
No P’s
No QRS’s
No CO
Cause-MI, CAD, CMP, shock, K+, hypoxia,
acidosis, and drugs
• Treatment- code situation, ACLS, CPR,
**__________- if available no delay
Complications of Arrhythmias
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Hypotension
Tissue ischemia
Thrombi
Heart failure
Shock
Death
Diagnostic Tests
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Telemetry- 5 lead( lead II and V1)
12 lead EKG
Holter monitor- pt. keeps a diary
Event monitoring- pt. records only when
having the event
• Exercise stress test
• Electrophysiology studies- induce arrhythmias
under controlled situation
Nursing Assessment
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Apical rate and rhythm
Apical/radial deficit
Blood pressure
Skin
Urine output
Signs of decreased
cardiac output
Nursing Diagnoses
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Decreased cardiac output
Decreased tissue perfusion
Activity intolerance
Anxiety and Fear
Knowledge deficit
Medications
• Classified by effect on action potential
• Class I- fast Na blocking agents-ventricular
– Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol
• Class II-beta blockers (esmolol, atenolol, inderal)
atrial- SVT,Afib,flutter
• Class III- K blocking (amiodorone, tikosyn, sotalol,
corvert) both atrial and ventricular
• Class IV- Ca, channel blockers (verapamil
cardizem)SVT,Afib,flutter
• Other- adenosine, dig, atropine, magnesium
Medications
• Classified by effect on action potential
• Class I– fast Na blocking agents-ventricular
– Quinidine, Pronestyl, Norpace, ___________, Rhythmol
• Class II– beta blockers - atrial- SVT,Afib,flutter
– esmolol, ________, _________
• Class III– K+ blocking - both atrial and ventricular
– _______, _________, sotalol, corvert
• Class IV– Ca, channel blockers - SVT, Afib, A flutter
– verapamil, __________
• Other- adenosine, dig, atropine, magnesium
Comfort Measures
• Rest
• O2
• Relieve fear and anxiety
Invasive procedures
• Defibrillation
– Emergency- start at 200 watt/sec, go to 400
– Safety precautions
– AED’s
• Synchronized Cardioversion- for vent. or SVT
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Can be planned- if stable
Get permit
Start at ________ watt/sec (depending on wide/narrow)
Awake, give O2 and sedation
Have to synchronize with rhythm
cardioversion
• Implanted Cardiac Defibrillator (ICD)
– Senses rate and width of QRS
– Goes off 3 times, then have to be reset
– Combined with pacemaker- overdrive pacing or
back up pacing
Implantable Cardioverter- Defibrillator
(ICD)
Fig. 36-22
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
http://www.vmth.ucdavis.edu/cardio/cases/case14/pacemaker.htm
Pacemaker
• Permanent- battery under skin
• Temporary- battery outside body
• Types
– Transvenous
– Epicardial- bypass surgery
– Transcutaneous- emergency
• Modes
– Asynchronous- at preset time without fail
– Synchronous or demand- when HR goes below set rate
• Review classifications
Pacemaker Classification
Most pacemakers are
1. Atrial
2. Ventricular
3. Dual
Pacemakers
Fig. 36-27
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Pacemaker Problems:
Failure to sense
Failure to capture
Ablation
• Done in special cardiac procedures lab
• Use a laser to burn abnormal pathway
EKG changes associated with an MI or ACS
include:
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Q waves
ST segment elevation or
depression
T wave inversion
3 ECG Changes Associated with
Acute Coronary Syndrome (ACS)
• Ischemia
– ST segment depression and/or T wave
inversion
– ST segment depression is significant if it is
at least 1 mm (one small box) below the
isoelectric line
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
• Injury/Infarction- ST elevation
– ST segment elevation is significant if
mm above the isoelectric line
>1
• If treatment is prompt and effective,
may avoid infarction
–If serum cardiac markers are
present, an ST-segment-elevation
myocardial infarction (STEMI) has
occurred (code stemi)
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
• Infarction/Necrosis- Q wave
– Note: physiologic Q wave is the first negative
deflection following the P wave
• Small and narrow (<0.04 second in duration)
– Pathologic Q wave is deep and >0.03 second in
duration
ECG Changes Associated with Acute
Coronary Syndrome (ACS) FYI only
Fig. 36-29 A
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Fig. 36-29 B
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Fig. 36-30
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Syncope
• Brief lapse in consciousness
• CausesVasovagal
– Cardiac dysrhythmias
– Other- hypoglycemia, seizure, hypertrophic
cardiomyopathy
• 1-year mortality rate as high as 30% for
syncope from cardiovascular cause