Transcript Document

BASIC ECG
N240 – Advanced Med-Surg
K. Brooks, RN, MSN
Starting with the Basics …
► What are the functions of the heart?
►Electrical: “impulse”
►Mechanical: “pump” “contraction”
► What is the normal blood flow through
the heart?
► What is the normal electrical pathway conduction?
►Nodes (SA, AV, Bundle)
►Inherent Rates
Electrical Conduction Pathway
SA Node – “pacemaker” of
the heart (60-100bpm)
AV Node – junction of the
atria and ventricles (40-60bpm)
Bundles – Bundle of His
connects the AV node to the
bundle branches (20-40bpm)
Normal Cardiac Cycle
Systole
Diastole
Electrical
Depolarization
“activate”
Repolarization
“recovery”
Mechanical
Contract
“empty”
Relax
“fill”
“EKG” - Electrocardiogram
An EKG is a useful tool for diagnosing a
variety of cardiac abnormalities. It displays the
activity of the heart’s electrical impulse flow through
the conduction system.
What does it tell us?
• the electrical conduction through the heart
• areas of ischemia or myocardial damage
• LV Hypertrophy
• electrolyte disturbances / drug toxicity
• ECG PAPER
EACH E.C.G PAPER DIVIDED TO SMALL SQ
WITH LENGTH 1mm BOTH VERITICALLY
AND HORIZONTALLY ,,,,,,,,,,,EVERY 5
SMALL SQ FORM ONE LARGE SQ ALSO
HORIZONATLY AND VERTICALLY
VERTICAL MEASURMANT
VOLTAGE SMALL SQ=0.1MV ,,,,,,,,,,,LARGE SQ
=0.5mv ANY ECG MACHINE STANDARDIZED IN
SUCH MANNER THAT IMPUSLE OF MILLIVOLT
WILL CAUSE A DEFLECTION OF 10 SMALL
SQUARE OR 2 LARGE SQ . Or 1 mvolt THIS NORMAL
VOLTAGE FOR ALL EVERY ECG
WHAT CLINICAL APPLICATION FOR THAT
• HORIZONTAL MEASURMENT
• 1mm = SMALL SQ = 0.04 SECOND AND
5mm= ONE LARGE SQ = O.20 SECOND
THEN 1 SECOND = 5 LARGE SQ OR
25mm and 1 minute = 300 large square
• What is benefit for that ???
EKG Tracing ……….
• Grid Paper
• Each small box = 0.04 seconds
• Each large box = 0.20 seconds (5 small boxes
across)
• One second is 5 large boxes
• Three seconds is 15 large boxes
• Six seconds is 30 large boxes
• Each minute has 300 large boxes
• 300\R-R the heart regular
• If the heart rate iirugular
• Count R falling in 30 L sq XXX 10
• Or count R in 15 LS XXXX20
• Anther method
• Every 5mm (L S )= 0.20 sec >>>>>>> 1
second = 25mm=2.5cm every 3second =
7.5cm every 6 second 15cm
• By ruller count R in 15 cm XXXXby 10
The Concept of a “Lead”
By combining certain limb leads into
a central terminal, which serves as
the negative electrode, other leads
could be formed to "fill in the gaps"
in terms of the angles of directional
recording. These leads required
augmentation of voltage to be read
and are thus labeled.
What Is In Each Beat?
(the cardiac cycle in waves, complexes, and intervals)
• P Wave – atrial contraction or depolarization, (usually upright)
• QRS Complex – time for ventricular contraction or depolarization
(usually upright) (0.04 - 0.12sec) (delays in the bundle branches will widen the
QRS)
• T Wave – ventricular repolarization “recharging” (usually upright)
• PR Interval – time between atrial depolarization to ventricular
depolarization (beginning of P wave to beginning of QRS)(0.12 - 0.20sec)
(prolonged PR = delays in the AV node conduction)
• QT Interval – represents one complete ventricular depolarization and
repolarization (beginning of QRS to the end of the T wave) (0.32 – 0.44sec)
(disturbances are usually due to electrolyte disturbances or drug effects)
Reading a Rhythm Strip
What Do I Look For?
► Regularity - What is the R – R Interval?
► Rate - Is the rate normal (60-100), slow, or fast?
***Six-second strip method - (30 big boxes) &
multiply times ten
► P Wave – Is there a P wave before every QRS? Is it
upright?
► QRS Complex – Is there a normal QRS complex
following each P wave? Wide or normal?
► T wave – How does your T wave look? Upright?
► Measure your intervals – PR Interval, QRS, QT
“Practice Strip”
“Check Your Pulse”
Match the Rhythm with the Pt
• After assessing the EKG strip in a
systematic method, gather the information
about your pt’s assessment: med hx, s/sx,
labs.
• Does the rhythm make sense for the pt?
• What is going on with the pt?
2nd level assessment
• The following should be considered when
interpreting ECG
• NEVER GIVE IMPRESSION ON SINGLE
ECG PARTICULARLY IF THE RESULT
NOT FIT WITH CLINICAL DATA
What is Normal?
“Normal” Sinus Rhythm
The electrical impulse originates in the SA Node
1) Rhythm ► Regular
2) Rate ► Regular
(R to R Interval)
(60 – 100 beats/minute)
3) P wave ► before every QRS complex
4) QRS complex ► narrow, not wide (0.04-0.10sec)
A Slight Deviation from “Normal”
“too slow and too fast”
Sinus Bradycardia
1st Level Assessment
►Rate? (less than 60bpm)
►Symptoms? (subjective and objective)
2nd Level Assessment
►Reasons? Etiology?
Nursing Interventions
Pharmacology
Sinus Tachycardia
1st Level Assessment
►Rate? (> than 100)
►Symptoms? (subjective and objective)
2nd Level Assessment
►Reasons? Etiology?
Nursing Interventions
ECG ABNORMALITIES MAY BE SEEN IN NORMAL HEALTHY PERSON
IN ABSENCE OF ORGANIC HEART DISEASE
1 – EARLY REPOLARIZATION
2- HIGH LV VOLTAGE
3-JUVENILE T WAVE
4-ATHLETIC T WAVE
5-INSIGNIFICANT Q WAVES IN AVL , 1 V5 AND V6
6-RIGHT AXIS DEVIATION
7-SHORT PR INTERVAL
8-FIRST DEGREE HEART BLOCK
9-RBBB
ECG MAY NORMAL OR UNINTERPRETED IN
PRESENCE OF ORGANIC HEART DISEASE IN
FOLLOWING SITUATION
1-ACUTE MI ESPECIALLY EARLY PRESENTATION
OR MASKED BY WPW ,LBBB AND PACE MAKER
2-PATIENT WITH SEVER CORONARY ARTERY
DISEASE
3-WITH ACUTE PULMONARY EMBOLISM NORMAL
ECG OR NON SPECIFIC
4- IN SOME CASE OF LV OR RV HYPERTROPHY
5-ECG MAY NORMAL IN BETWEEN ATTACK OF
a-PAROXYSMAL AF
b-PAROXYSMAL SVT
SOME MEDICAL DISEASE
MAY BE MANIFEST WITH ECG
1-CVA ( INTRACERBRAL Hage
)
2-DRUGS TOXISITY
3-ELECTROLYTE DISORDER
4-ENDOCRINE DISEASE
TIFECT & ECG
1-LIMB REVERSAL
2-VOLTAGE CALIBRATION
3-INCORRECT PAPER SPEAD
4-EXTERNAL ELECTRICAL
INTERFERENCE
5-PATIENT MOVEMENT (
VULONATARY OR BY
DIEASE e.g. PARKINSONS
• P –WAVE
• ABSENT( AF, SINUS NODE ARREST
, HYPERK+)
• INVERTED( LEAD
MALPLACEMT,DEXTROCARDIA)
• TO TALL (…..P PULMONALE ….)
• TOO WIDE (…..P MITRALE….)
PR INTERVAL
SHORT
1-NORMAL VARIENT
2-L.G.L SY NDROME
3-WPW SYNDROME
4-AV- JUNCTION RHTYUM
LONG
1- HEART BLOCK
2-DRUGS
-VARY
1- SECOND DEGREE HB
4-DEPRESSED
PERICARIDITIS
ELEVATED
ATRIAL INFARCTION
QRS
1-ABNORMAL SHAPE
BBB & FASCICLUR BLOCK
2-ABNORMAL DURATION
AND SHAPE
WPW , HYEPK+
,VENTRICULAR RHYTHUM ,
PACE MAKE
AMPILTUDE
LOW IN HYPOTHRYRDISM ,
CALBIRATION
PERICARIDAIL EFFUSION
HIGH AMLITUDE
CALBIRATION
L.V.H AND RVH
POST. MI
Q- WAVES
PHYSIOLOGICAL SMALL IN
AVL , I, V5 AND V6
PATHOLOGICAL 25% OF R
HIGHT
ST
DEPRESSION
1- ISHEMIA
2-POST MI
3-DRUGS
4-STRIAN PATTERN
5-RESIPROCAL CHANGES
ST- ELEVATION
1-MI
2-PERICARIDITIS
3-ANUERYISM
4-EARLY REP
5-PRINZMATEAL ANGINA
6-METASTASIS
MYCARDIUM
T WAVES
TO TALL
HYPERKALMEAI
MI
TOOSMALL
INVERTED
…DISTURBANCE
REPOLARIZTION ( ISHEMIA
,
INFLAMATION ,DRUGS
,HYPOXIA TOXINS))
QT INTERVAL
LONG
1-DRUGS
2-ISHEMIA
3- MI
4-HCMP
5-HYPOTHERMAI
6-CVA
U- WAVES
S
??????
What is an Arrythmia anyways?
► Definition: a disorder of impulse formation. An
abnormal electrical conduction that changes the
heart rate and rhythm. A disturbance in the
heart’s rhythm.
► Why? Causes?
1) Classified according to their origin
2) Some are mild, asymptomatic – require no treatment
3) Some are catastrophic – require immediate emergency
response
4) They can influence cardiac output and blood pressure
“Clinical Significance”
•
Thousands of people suffer with
arrythmias
•
Dysrhythmias are responsible for over
44,000 deaths each year.
•
There site of origin can often lead us to
the problem area
•
About 15% of strokes occur in patients
with atrial arrythmias
•
A large majority of sudden cardiac
deaths are thought to be caused by
ventricular dysrhythmias.
What is The Big Deal?
Why are we so concerned with Arrythmias?
SV x HR = CO
► SV dependent on filling time, adequate volume, and
myocardial muscle function
► HR dependent on electrical stimulus, Autonomic NS,
Parasympathetic NS
►Too Fast
►Too Slow
►Too Irregular
NOT GOOD!!!
Some of you might be feeling a bit
overwhelmed at this time ….
Atrial Arrythmias
• Atrial arrythmias occur because there are
other pacemakers in the atria competing to
be the “commander”
• SA Node is not healthy and unable to lead
Atrial Fibrillation
Results from disorganization of atrial electrical
activity without effective atrial contraction.
Repetitive, irregular, uncontrolled depolarization.
Atrial rate ~ 350-600 bpm, Ventricle - varies
► No P Wave! Very “jiggly” baseline wave
► No PR Interval
► Irregular with a wavy baseline
► Rate - Controlled vs. Uncontrolled
► Loss of “Atrial Kick”
► Emboli Potential
Atrial Fibrillation
•
•
•
•
1st Level Assessment
2nd Level Assessment
Nursing Consideration
Pharmacologic Consideration
–
–
–
–
Digoxin
Ca+ Channel Blockers
Beta Blockers
Coumadin
On Your Own ….
You are responsible for reviewing pharmacology re: arrhythmias:
• Please know the actions, doses, side effects, nursing
considerations, monitoring, precautions, therapeutic drug
levels, s/sx toxicity for the following drugs:
•
•
•
•
Digoxin
Ca+ Channel Blockers (verapamil, diltiazem)
Beta Blockers (atenolol, metoprolol)
Anticoagulants (warfarin)
Atrial Flutter
Results from the atria stimulated to contract 250-350
bpm in a circuit fashion around the atrium
► No true P waves – F waves larger than P
waves (flutter waves)
► Sawtooth-shaped waves
► Usually a regular rhythm D/T AV Node filter
► Ventricular Rate – atria to ventricle ratio (2:1 or
4:1)
Assessment and treatment the same as Atrial Fib
The “Basic Blocks”
• First Degree AV Block
• Third Degree Block
(AKA) Complete Heart Block
Etiology, 1st and 2nd Level Assessment, Intervention
Check Your Pulse!
“From the Bottom of My Heart”
Arrythmias stemming from the ventricles. Occurs when a
pacemaker in the ventricles initiate a beat or a whole rhythm
►Premature Ventricular Contraction (PVC) “FLB”
QRS wide and bizarre
►Ventricular Tachycardia (V Tach)
3 or more ventricular ectopic complexes (PVCs)
Rate greater than 140-250bpm
QRS complex wide and aberrant
3 or More PVCs =
Ventricular Tachycardia
“Sustained V Tach”
Treatment for PVCs / V Tach
• Dependent on patient’s condition
• How frequent are the PVCs: unifocal, multifocal,
healthy heart?
• Pulse? No Pulse?
• Labs? Particularly K+ and Mg+ levels?
• Sustained ? Non-sustained?
►Ventricular Fibrillation (V Fib)
Results from part of the ventricle depolarizing at a
rapid and erratic uncontrolled manner. There are no
recognizable waves and complexes and segments
► Nursing Considerations:
► 1st Level Assessment
► 2nd Level Assessment
► Nursing Intervention
V Fib is the most lethal arrhythmia and will be fatal!
Patient assessment is crucial! Early Defibrillation! CPR!
Bundle Branch Block
“The Road Detour”
Interruption of conduction
in one of the main branches
of the Bundle of His
• Normal conduction
through the bundles?
• Why interruptions?
• QRS wide – greater than
0.12 seconds
Don’t Just Stand There!
ASYSTOLE
(please, not on my shift )
AKA “flatline”, “cardiac standstill”
►Etiology
►Nursing Assessment and Intervention
►Pharmacological Considerations
And you may feel like all rhythms look alike
Look Closely and you will see the differences!
ST Segment Depression –
“Infarcted”
“Check Your Pulse”
? Immediate Nursing Question ?
“How does my patient look?”
“Do they have any symptoms?” (what are symptoms of low CO?)
“Do they have a normal or diseased heart?”
This can buy you time!!!
(to assess and gather more information about the patient’s condition)
Top Nursing Priorities
►Check the patient (LOC?)
►ABC – airway, breathing, circulation
►Oxygen administration
►IV Access / Patency
►Electrode placement
►Associated Symptoms? Chest pain, SOB,
dyspnea, vertigo, nausea
►Fluids
►Monitor VS
Fast Assessment and Identification of the
problem are key Nursing Priorities
In the cardiac world, time is
oxygen. The longer you delay
reaction to arrhythmias, the
longer the heart suffers. Don’t
let your patient “circle the
drain”!
Pharmacologic Considerations
Above the AV NODE (Atrial) (ABCD)
• Too Slow
Atropine
• Too Fast
Beta Blockers
Calcium Channel Blockers
Digoxin
Amiodarone
Below the AV NODE (Ventricular) (LAP)
• Too Fast
Lidocaine
Amiodarone
Procainamide
Too Slow …..
• Treatment for Symptomatic Bradycardia
is Atropine (check your patient first)
Classification: Antidysrhythmic/Anticholinergic
Common dose: 0.5mg – 1.0mg – up to 2mg IVP
How to give: given every 3-5 minutes
SE: hypotension, angina, tachycardia, PVCs, dry mouth
Too Fast …
• Uncontrolled Atrial Fibrillation
- Beta Blockers (Lopressor, Labetolol)
- Calcium Channel Blockers (Cardizem,
Verapamil)
- Glycosides/Inotropes (Digoxin)
• Ventricular Arrhythmias
- Antiarrythmics (Lidocaine, Procainamide,
Amiodarone)
Practice on your Own …
Antiarrhythmic IV Drips
• Lidocaine bolus of 50-100mg (1mg/kg) over 2-3 minutes
• IV Drip: (1gm/250ccs) or (2Gm/500ccs) to run at
1-4mg/min
How to figure that in ml/hr for a pump …..
Know nursing considerations / monitoring and
s/sx of toxicity
Non – Pharmacologic Treatment
• Electroshock – Cardioversion
Unstable “tachy” rhythms
• Ablation
• Defibrillation (and internals)
Nursing Consideration and Care
*** Look at Patient Teaching in Table 35-9
Pacemakers
I. External Pacing – noninvasive
temporary with patches on chest wall
II. Internal Pacing – invasive
temporary internal through the femoral
arteries
III. Permanent Pacemaker – inserted through the chest
wall – open heart
IV. Modes: Demand or Override
*** Review Pt Teaching with a pacemaker
Case Study Example
Mrs. Taylor has become more forgetful lately.
She has trouble managing her medications. She
is supposed to take (1) Digoxin in the morning,
but sometimes she takes one at night. As a
result, her Digoxin level has reached toxic
levels. She comes to the ER with nausea,
vomiting, fatigue, vision changes. You put her
on the EKG monitor and she is in 3rd degree
heart block with a HR of 32. Her blood pressure
is 70/40. The ER doctor orders for you to put
her on an external pacemaker. She will remain
on this pacemaker to maintain an adequate HR
and CO until her Dig toxicity resolves.
We are done for the day!
Additional References
http://medlineplus.gov
http://www.nurse411.com
click on: educational links
click on: basic EKG tutorial, put in your name,
and push play
Adams, M., Josephsen, D., Holland, L. (2005).
Pharmacology for Nurses: A pathophysiologic
approach. New Jersey: Prentice Hall.
Further Study on Your Own
Taking it a step further …..
Challenge yourself
The Health of the Heart Walls
The heart is composed of four walls and each
of the walls is fed oxygen through direct
and indirect blood flow.
This blood flow is delivered by coronary
arteries and through collateral circulation.
Heart Walls
• Anterior Wall
Includes most of the left ventricle, the intraventricular
septum
• Inferior Wall
Includes most of the right ventricle and some of the
left ventricle, extends down to the apex
• Lateral Wall
Located on the left side of the heart (no right heart
involvement)
• Posterior Wall
Lies along the back of the heart
Coronary Artery Supply
Right Coronary Artery
Left Main Coronary Artery
Left Circumflex Coronary Artery
Left Anterior Descending
Right Coronary Artery
feeds the right atrium and ventricle
inferior wall
posterior wall
SA Node and AV Node (in most people)
Left Anterior Descending
anterior wall and intraventricular septum
apex of the heart
papillary muscles
bundle branches
Circumflex
lateral and posterior wall of L Ventricle
How Does This Tie To The EKG?
When one looks at an EKG and
notices disturbances or problems
in certain areas of the heart, it
is useful to understand which
coronary artery supplies that
area. This can help you identify
the vessel where blood supply is
possibly compromised
(arteriosclerotic changes)
Example
A patient that came into the hospital with Sick Sinus
Syndrome (SA Node is not feeling well) and was in
Symptomatic Sinus Bradycardia may go for a Coronary
Angiogram. During this procedure, the MD may find that
they have atherosclerotic changes and blocks in their Right
Coronary Artery that feeds blood supply (and O2) to that
node. Without proper blood supply, that area is unable to
perform normal electrical conduction and begins to show
disturbances (arrhythmias). This patient may need to have
an angioplasty or stent placement or CABG to open up that
area to better blood supply.
Additional References
http://medlineplus.gov
http://www.nurse411.com
click on: educational links
click on: basic EKG tutorial, put in your name,
and push play
Adams, M., Josephsen, D., Holland, L. (2005).
Pharmacology for Nurses: A pathophysiologic
approach. New Jersey: Prentice Hall.