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Henderson County EMS 3 lead class

EMS ECG Review
by

John Fiveash

on 16 October 2012

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Transcript of Henderson County EMS 3 lead class

P-R Interval (PRI) *0.12-0.20 Seconds

Treatment
None if patient is asymptomatic
Treat symptomatic bradycardia Multifocal Atrial tachycardia COMMON EMS DYSRHYTHMIAS - Analyze the rate
six second method
heart rate calculator
R-R Interval
Triplicate Method Back to the basics-THE PROCESS regular
occasionally Irregular
regularly irregular
irregularly irregular Are they present?
P waves regular?
Is there one P for each QRS?
Are the p waves upright or inverted? 2 Analyze the rhythm Step 2 1st step Spark Cardiac Physiology (cc) image by nuonsolarteam on Flickr Step 3 Analyze the P-Wave The FIVE STEPS STEP 4 Analyzing the P-R Interval .12- .20 STEP 5 Analyzing the QRS Complex Do all the QRS complexes look alike ?
What is the QRS duration ? Henderson county ems ecg review Cardiac conductive system Components Sinoatrial Node
Internodal Atrial Pathways
Atrioventrical Node
Atrioventrical Junction
Bundle of His
Left and Right Bundle Branches
Purkinje Fibers The Electrocardiogram Routine Monitoring Information from a single lead shows: Last step
Rate & regularity
Time to conduct an impulse
A single lead cannot:
Identify/ locate an infarct
Identify axis deviation or chamber enlargement
Identify right to left differences in conduction
The quality or presence of pumping action MEASUREMENTS Time intervals Q-T Interval (cc) image by nuonsolarteam on Flickr QRS Interval
*0.08-0.12 Seconds S-T Segment *0.33-0.42 seconds Last step step one 1 Sinus Arrest Etiology
Often a normal finding, sometimes related to the respiratory cycle.
May be caused by enhanced vagal tone Sinus Dysrthyhmia Sinus Arrest Sinus Bradycardia Rate- Less than 60
Rhythm- Regular
Pacemaker Site- SA Node
P Waves- Up Right & normal
PRI- Normal
QRS- Normal Sinus Brady Rate- Greater than 100
Rhythm- Regular
Pacemaker Site- SA Node
P Waves- Up Right & normal
PRI- Normal
QRS- Normal Sinus Tachycardia Atrial Rhythms Sinus Tachycardia Rate- 60-100
Rhythm- irregular
Pacemaker Site- SA Node
P Waves- Up Right & normal
PRI- Normal
QRS- Normal Dysrhythmias Originating in the SA Node Rate- Normal to slow
Rhythm- Irregular
Pacemaker Site- SA Node
P Waves- Up Right & normal
PRI- Normal
QRS- Normal Etiology
results from an increased rate of SA node discharge
Potential causes include exercise, fever, anxiety, hypovolemia, anemia, pump failure, increased sympathetic tone, hypoxia, or hypothyroidism. Etiology-
Increased parasympathhetic (vagal) tone, intrinsic disease of the SA node, drug affects.
May be a normal finding in healthy, well conditioned persons Etiology
Occurs when the sinus node fails to discharge
May result from ischemia of the SA node, digitalis toxicity, excessive vagal tone, or degenerative fibrotic disease Dysrhythmias
originating in the Atria Rate- more than 100
Rhythm- irregular
Pacemaker Site- Ectopic sites in atria
P Waves- organized, nonsinus p waves;at least 3 forms
PRI- varies depending on source of impulse
QRS- variable Supraventricular Tachycardia Rate- 150-250
Rhythm- Regular
Pacemaker Site- Atrial (outside SA node
P Waves- Often buried in preceding T wave
PRI- Usually normal
QRS- Usually normal Treatment
Vagal Maneuvers
Pharmacological Therapy
Adenosine
Verapamil
Electrical Therapy
Consider if Pt symptomatic with HR>150
Synchronized cardioversion starting at 85J Atrial Flutter Rate- Atrial Rate 250-350 Ventricular rate varies
Rhythm- Usually regular
Pacemaker Site- Atrial (outside SA node)
P Waves- F waves are present
PRI-usually normal
QRS- usually normal Etiology
Results when the AV node cannot conduct all the impulses.
Impulses may be conducted in fixed or variable ratios.
Usually associated with organic disease such as congestive heart failure (rarely seen in MI) Treatment
Electrical Therapy
Consider if ventricular rate >150 and symptomatic.
Synchronized cardioversion starting at 85J.
Pharmacological Therapy
Diltiazem
Verapamil, digoxin, beta-blockers, Amiodaron, and quinidine Atrial fibrillation Rate- 350-50
Rhythm- Irregularly irregular
Pacemaker Site- Atrial (outside SA node)
P Waves- none discernible
PRI- none
QRS- normal
Clinical Significance
Atria fail to contract effectively, reducing cardiac output.
well tolerated with normal ventricular rates
high to low ventricular can result in cardiac compromise Etiology
Often seen in acutely ill pts
May result from pulmonary disease, metabolic disorders, ischemic heart disease, or recent surgery.
Clinical Significance
Presence of multifocal atrial tachycardia often indicates a serious underlying illness.
Treatment
Treat the underlying illness Etiology
Rapid atrial depolarization overrides the SA node.
May be precipitated by stress, overexertion, smoking, caffeine. Clinical Significance
May be tolerated well by healthy pt for short periods
marked reduction in cardiac output can precipitate angina, hypotension, or congestive heart failure.
Treatment
Typically, none required Clinical Significance
normal variant
Clinical Significance-
May result in decreased cardiac output, hypotension, agina, or CNS symptoms. Treatment-
Generally unnecessary unless hypotension or ventricular irritability is present.
Otherwise:atopine,TCP, Dopamine, Epi drip
Treatment-
Treatment is directed at the underlying cause
Clinical Significance
Decreased cardiac output for rates >140 very rapid rates can precipitate ischemia or infarct
Clinical Significance
Frequent or prolonged episodes may decrease cardiac output and cause syncope
Prolonged episodes may result in escape rhythms
Clinical Significance
Generally well tolerated
Rapid ventricular rates may compromise cardiac output and result in symptoms.
May occur in conjunction with atrial fibrillation Etiology
Results from multiple ectopic foci; AV conduction is random and highly variable
Often associated with underlying heart disease. Treatment
Electrical Therapy
Consider if ventricular rate >150 and symptomatic.
Synchronized cardioversion starting at 85J
Pharmacological Therapy
Diltiazem
Verapamil, digoxin, beta-blocker, procainamide, and quinidine.
Anticoagulant AV BLOCKS Dysrhythmias Originating Within the AV AV BLOCKS LOCations At the AV Node
At the Bundle of His
Below the Bundle of His Classifications
First Degree AV block
Type I Second Degree AV Block
Type II Second Degree AV Block
Third Degree AV Block First Degree AV Block Rate- Depends on underlying rhythm
Rhythm- Usually regular
Pacemaker Site- SA node or atrial
P Waves- Normal
PRI- >0.20 Seconds
QRS- Usually <0.12 seconds First Degree AV Block Etiology-
Delay in the conjunction of an impulse through the AV node.
May occur in healthy hearts, but often indicative of ischemia at the AV junction Clinical Significance
Usually not significant, but new onset may precede a more advanced block Treatment
Generally, none required other than observation.
Avoid drugs that may further slow AV conduction
Rate- Atrial, regular; ventricular, normal to slow
Rhythm- Atrial, regular; ventricular, irregular
Pacemaker Site- SA node or atrial
P Waves- Normal, some P waves not followed by QRS
PRI- Increased until QRS is dropped, then repeats
QRS- usually <0.12 seconds Type I Second degree AV block Type I Second Degree Etiology
Also called Mobitz I, or Wenckebach
Delay increases until an impulse is blocked
Indicative of ischemia at the junction Clinical Significance
Frequently dropped beats can result in cardiac compromise. Treatment
Generally, none required other than observation.
Avoid drugs that may further slow AV conduction.
Treat symptomatic bradycardia The Main Difference is the HR In most cases: 100-160
Can be seen as high as: 220 BPM
Max is different for every one MAX HR= 220 bpm - Age Sinus Dysrhytmia Atrial Fibrillation Supraventricular tachycardia Multifocal atrial tachycardia Atrial Flutter type II Second degree av block Rate- atrial, normal; ventricular,slow
Rhythm- may be regular or irregular
Pacemaker Site- SA node or atrial
P Waves- Normal,some P waves not followed by qrs
PRI- constant for conducted beats, may be > 0.21 seconds
QRS- normal or >0.12 seconds Etiology
Also called Mobitz II or infranodal
Intermittent block of impulses
Usually associated with MI or septal necrosis Clinical Significance
May compromise cardiac output and is indicative of MI.
Often develops into full AV block. Treatment
Avoid drugs that may further slow AV conduction.
Treat symptomatic bradycardia
Consider transcutaneous pacing Third Degree AV Block Rate- Atrial, normal;ventricular,40-60
Rhythm- Both atrial and ventricular are regular
Pacemaker Site- SA node and AV junction or ventricle
P Waves- Normal with no correlation
PRI-No relationship to QRS
QRS- 0.12 seconds or greater type II Second degree av block Third Degree AV Block Etiology
Absence of conduction between the atria and the ventricles.
Results from AMI, digitalis toxicity, or degeneration of the conductive system Clinical Significance
Severely compromised cardiac output Treatment
Transcutaneous pacing for acutely symptomatic Patients
Treat symptomatic bradycardia.
Avoid drugs that may further sloe AV conduction Ventricular Arrhythmias Dysrhythmias originating in the Ventricles ventricular escape complexes and rhythms Rate- 15-40
Rhythm- Escape complex, irregular;escape rhythm, regular
Pacemaker Site- ventricle
P Waves- none
PRI-none
QRS- >0.12 seconds, bizarre ventricular escape complexes and rhythms Etiology
Safety mechanism to prevent cardiac standstill.
Results from failure of other foci or high degree AV block. Clinical Significance
Decreased cardiac output,possibly to life threatening levels Treatment
For perfusing rhythms, administer atropine and or TCP.
For nonperfusing rhythms, follow pulseless electrical activity (PEA) protocols Accelerated idioventricular rhythm Etiology
A subtype of ventricular escape rhythm that frequently occurs with mi Clinical Significance
May cause decreased cardiac output if the rate slows Treatment
Does not usually require treatment unless the patient becomes hemodynamically unstable
The goal is to treat the underlying MI. Premature ventricular contractions Rate- Underlying rhythm
Rhythm- Interrupts regular underlying rhythm
Pacemaker Site- ventricle
P Waves- none
PRI-none
QRS- >0.12 seconds, bizarre Etiology
Single ectopic impulse resulting from an irritable focus in either ventricle
Causes may include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid base disturbances, electrolyte imbalances, or as a normal variation of the ECG
May occur in patterns
bigeminy, trigeminy, or quadrigeminy.
couplets and triplets Clinical Significance
Malignant PVCs
more than 6 minute, R on T phenomenon, couplets or runs of ventricular tachycardia, multifocal PVCs, or PVCs associated with chest pain.
Ventricles do not adequately fill, causing decreased cardiac output Treatment
Non malignant PVCs do not usually require treatment in patients without a cardiac history.
Cardiac patients with nonmalignant PVCs.
Administer oxygen and establish IV access
Malignant PVCs
Lidocaine or Amiodarone.
If PVCs are not suppressed, repeat doses.
If PVCs are suppressed, administer Lidocaine drip or Amiodarone Drip Rate- 100-250
Rhythm- Usually regular
Pacemaker Site- ventricle
P Waves- If present, not associated with QRS
PRI-none
QRS- >0.12 seconds, bizarre Ventricular Tachycardia Ventricular Tachycardia Etiology
3 or more ventricular complexes in succession at a rate of >100.
Causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid-base disturbances, or electrolyte imbalances.
VT may appear monomorphic or polymorphic Clinical Significance
Decreased cardiac output, possibly to life threatening levels.
May deteriorate into ventricular fibrillation Treatment
Perfusing patients
Administer oxygen and establish IV access.
Consider immediate synchronized cardioversion starting at 85j for hemodynamically unstable patients.
Initially administer Lidocaine 0.5-0.75 mg/kg to the max dose of 3.0 mb/kg, or until VT is suppressed.
Amiodarone 150-300 mg IV>
Nonperfusing patient
follow ventricular fibrillation protocol. Torsade de pointes Polymorphic VT
caused by the use of certain antidysrhythmic drugs
Exacerbated by antihistamines, azole antifungal agents and macrolide antibiotics, erythromycin, azithromycin,
and clarithraycin. Typically occurs in nonsustained bursts.
QRS rates from 166-300
RR interval highly variable. Treatment
Do not treat as standard VT.
Administer magnesium sulfate 1-2g diluted in 100 ml D5W over 1-2 minutes
Amiodarone 150-300 mg is also effective Torsade de Pointes Ventricular fibrillation Rate- no organized rhythm
Rhythm- no organized rhythm
Pacemaker Site- Numerous ventricular foci
P Waves- Usually absent
PRI-none
QRS- none Ventricular fibrillation Etiology
Wide variety of causes, often resulting from advanced coronary artery disease Clinical Significance
Lethal dysrhythmia with no cardiac output and no organized electrical pattern Artificial pacemaker Rate- Varies with pacemaker
Rhythm- may be regular or irregular
Pacemaker Site- Depends upon electrode placement
P Waves- none produced by ventricular pacemakers; pacemakers spike
PRI-If present, varies
QRS- >0.12 seconds, bizarre Artificial pacemaker Etiology
Single vs. dual chambers pacemakers.
Fixed rate vs. demand pacemakers. Clinical Significance
Used in patients with a chronic high-grade heart block, sick sinus syndrome, or severe symptomatic bradycardia. AV sequential pacer Both Atria & Ventricals are controlled by the device Note the two Pacer spikes Practice By: Jim Teague
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