ECG

What is the voltage measured at (units)

0.1mV/mm

How many seconds is a small square

0.04 sec

How many seconds is one large block (5 small blocks)

0.2 seconds

Hoe many large blocks occur in 1 second

5 large blocks

What is the paper speed set at

24mm/second

Standard 12-lead ECG set up (2 types of leads)

-6 limb leads

-6 chest leads

What are the 6 limb leads

-I

-II

-III

-aVR (augmented vector, right wrist)

-aVL (augmented vector left wrist)

-aVF (augmented factor, left foot)

6 chest leads

-V1 placed over R side of heart

-V2 placed over R side of heart

-V3 placed over ventricular septum

-V4 placed over ventricular septum

-V5 placed over L side heart

-V6 placed over L side heart

How many electodes are in a 12-lead ECG

-10 lelectrodes

-A lead means “view”, NOT electrode. the different views provides the additionat views to make a 12-lead (view) ECG

V1 anatomic placement

R 4th intercostal space

V2 anatomic placement

L 4th intercostal space

V3 anatomic placement

midway between V2 and V4

V5 anatomic placement

follow fingers alongs 5th intercostal space to beginning of axilla

V6 anatomic placement

5th intercosal space directly below midline of axilla

Limb electrode anatomic placement

-aVR: anterior right superior

-N: anterior right inferior (neutral lead, only there to complete circuit)

-aVL: anterior left superior

-aVF: anterior left inferior

Unipolar lead

Looks at the heart with tunnel vision, only see what is directly in front of them

Bipolar lead

-aVR, aVL, aVF make a triangle “Einthoven’s triangle”

-considered to be bipolar because they form a line of the site, not just what is underneath them

-Each electrode can see 2 leads5

5 electode ECG

-used on telemetry, cardiac rehab, ICU, or where continuous monitoring is required

-5 electrodes conmbine to form one view

-Used to monitor view

-NOT as sensitive as 12-lead ECG, therefore CANNOT detect ST segment changes

Cardiac muscle has 6 characteristics, what are they

-Automaticity

-Rhythmicity

-Conductivity

-Excitability

-Contractility

-Refractoriness

Automaticity

cardiac mucle cells can ischarge and contract without being stimulated by a nerve

-most noted in SA node, primary pacemaker of the heart, has most amount of automaticity

-unfortunately, other cardiac cells can fire at anytime due to this phenomenom

Rhythmicity

regularity of which pace making acitivity can occur

Conductivity

-cardiac cells can spread impulses to adjoining cells very quickly

Excitability

-cardiac cells have the ability to respond to an electrical impulse

Contractility

ability to contract once an electrical impulse is recieved

refractoriness

the cells inability to respond to another electrical impulse

Compared to skeletal muscle cells, cardiac cells are unique in that they have gap junctions between the cells that allow the heart to pump in a sequential manner. What is this phenomenom called?

Functional syncytium

What is the catch 22 of functional syncytium?

Due to the gap junctions, once cell that may fire without being told to do so may cause other cells around it to fire as well, causing dysfunction

How does symoathetic nervous system (SNS) control cardiac activity

-excites

-releases norepinepherine which increases HR, conduction velocity, irritability of the heart, and strength of contraction

How does parasympathetic nervous system (PNS) control cardiac activity

-depresses

-releases acetylcholine which decreases HR, decreases conduction

-Vagus nerve is the main control of the PNS

The right electrode is considered what charge?

-(-) or cold leadTh

The left electrode is considered what charge?

-(+) or hot lead

When a (+) signal hits the hot lead or a (-) signal hits the cold lead, what direction is te spike on the isoelectric line?

-positive waveform made

-signal goes up

If a signal that is oppositely charge than the lead, what direction of the spike is made?

-Negative waveform

-Signal goes down

Depolarization is what charge

POSITIVELY charges

Repolarization is what charge

NEGATIVELY charged

4 most common MI locations

-Lateral MI (Circumflex artery)

-Inferior MI (R coronary artery)

-Septal Wall MI (L coronary artery)

-Anterior MI (L coronary artery)

-Lateral MI (circumflex artery)

The primary pacemaker that initiates the electrical impulse for the heart?

SA node

SA node impulse represents what in the ECG

P wave

Once the impulse reaches the AV node, what do it do?

Delays electrical impulse to the ventricles for 1/10 second allowing for ventricles to fill, allowing ATRIAL KICK

AV node shows up as what in an ECG

isoelectric line aka PR segment

What occurs when the impulse reaches Bundle of His and Bundle branches?

-R bundle branch: responsible for depolarization of R ventricel

-L bundle branches: responsible for depolarization of L ventricle

Depolarization of R and L ventricles is shown in the ECG as what?

QRS complex

ST segment

-isoelectric line after QRS complex to the beginning of the T wave

T wave

ventricular depolarization occurs. no contraction takes place, the ECG records return of K+ inward and Na+ outward of the cardiac cells

Single lead, or multiple lead ECG

-telemtry floor

-electrodes hooked to box, transportable, which sends reading to main area where practitioner monitors HR, rhythm, potential for ischemia

-# views depends on how many electrode on pt

Holter monitor

-record for 24 hrs

-pt may c/o dizziness here or therm the MD will rx holter monitor to monitor ECG activity for 24 hours

-when pt feels dizzy, pt records time sxs occurred

-practitioner can correlate sxs with time recorded on ECG

ECG rate and rhythm abnormalities

-HR 60-100 BPM

-SA node in control

-Regular rhythm (the distance between R waves are symmetrical)

What does “sinus” refer to

-the rate we are talking about is from the SA node

Normal sinus rhythm

-60-100 BP<, regular, originates in SA nodeS

Sinus tachycardia

-normal with exercise, rate between 100-160

-we know it originates in SA node because P wave is nomal, followed by QRS, and space between Ps and QRS are regular

Sinus bradycardia

-normal if pt sleeping

-we know it originates in SA node because P wave is nomal, followed by QRS, and space between Ps and QRS are regular

Sinus arrythmia

-Irregular (HR speeds up with inspiration and slows with expiration, due to increased intrathoracic pressure)

--we know it originates in SA node because P wave is nomal, followed by QRS, and space between Ps and QRS are regularS

Sinus block

-can occur if someone scare your, “skipped beat” hiccup may cause skipped beat

-rate varies on frequency of blocks

-we know it originates in SA node because P wave normal followed by normal QRS complex

-irregular (complete skip of PQRST complex, pause length IS a multiple of P-P interval)

Sinus arrest

-rate varies upon frequency of arrest

-we know it originates in SA node bc P wave normal followed by normal QRS complex

-irregular (complete skip of PQRST complex, CANNOT predict multiple of p-p interval)

-could faint, SOB, dizziness, depending on how long pause is or how frequent

Sick sinus syndrome

-indicating SA node is failing (MI, angina)

-rate varies betwen bradycardia and tachycardia

-we know it originates in SA node because P was normal followed by normal QRS

dysrhythmia

-can be seen as an abnormal rhythm, an abnormal heart rate, or both

-due to an ectopic focus/foci

→irritable cell “all it takes is one bad apple”

→ gap junction causes numerous cardiac cells to misfireca

causes of ectopic foci

-ischemia or hypoxia to myocardium

-acidosis in general: lactic acidosis; diabetic ketoacidosis (increased acidic environment causes cell membranes to increase their permeability causing imbalances with ions)

-sympathetic discharge: exercise; stress; caffeine

-electrolyte imbalane

-hypoxia (desaturation_

-Hypotension/hypertension

common signs of dysrhythmia

-decreased CO can be life threatening (bradycardia, tachycardia)

-hypotension

-pallor

-temperature changes

-decreased urinary output

-SOB

-dizziness

-desaturation

How to calcular HR off ECG

-6 second rule

-Rule of 300 (find where a QRS touches a vertical line, see where the next consecutive QRS lands on vertical line, then use 300, 150, 100, 75, 60, 50, 43 rule to calculate)

How long should PR interval be

-less than 0.2 seconds (one large block)

-if greater than 0.2 s =200 msecs conduction block in AV node

R wave should be how long?

-should go up AND down within 3 small blocks

-this is where a wild rope would be seen: possibly a PVC

St segment depression

-myocardial ischemia

-measured in mm, each small box is 1 mm

ST segment elevation

-acute myocardial infarction

-elevation measured in mm

bradycardia

-HR below 60 BPM

-if rhythmical: Sinus bradycardia

tachycardia

-HR above 100

-If rate rhythmical: sinus tachycardia

Inherent rates:

-SA node: 100 BPM

-Atria: 75 BPM

-AV node: 60 BOM

-Ventricles 30-40

How does vagus nerve slow down HR (what inherent rate does it affect)

-Slows the SA node, keeping it in check

Protective mechanism to control HR

-If the SA node does not fire, the atria can fire at ~75BPM and so on down the chain

Premature beats

Pre-mature atrial contraction (PAC)

-ectopic beat comes from atrium and not SA nofde

-in L atrium: P wave would be flipped due to electrical impulse coming from left AV node

-in R atrium: P wave would be earlier than normal if the ectopic foci cam from right of AV node

Pre-mature node contraction (PNC)

-ectopic beats fires prior to SA node and atrium (P wave would be absent)

Pre-mature ventricular contraction (PVC)

-DO NOT calculate ST segemt elevation or depression with PVC

-ectopic beats fires from ventricle, looks like wild rope

PVC univocal vs multifocal

-unifocal PVCL one ectopic foci occurs and may occur again repeatedly (the same ectopic foci firing loos similar on ECG)

-multifocal PVC: one ectopic foci occurs followed by a different ectopic foci (viewed differently on ECG from the first ectopic foci; wild rope present but look different)

Patterns (normal/abnormal) can be seen with PAC, PNC, and mostly PVC

-Geminy pattern: pattern of normal and abnormal beats

-bigeminy: one normal, one abnormal

-trigeminy: two normal, one abnormal

-quadrigeminy: 3 normal, one abnormal

Couplet

two PVCs in a row

Ventricular tachycardia

>3 PVCs in a row

PVC landing on T wave

-very dangerous

-during a T wave we should have ventricular repolarization

-during a PVC, ventricular depolariztion is demonstrated

-when repolarization meets depolarization, people can go into fibrillation

→most serious rhtyhm disturbance

→ventricles quiver and heart cannot pump any blood cauding cardiac arrest

Paroxysmal atrial tachycardia

-paroxysmal = “sudden occurrence”

-atrial tachycardia > 3 PAC in a row

-so there is a sudden >3 PACs in a row

Supraventricular tachycardia

-P waves and T waves form together

-Unsure of where ectopic foci could be, so we label it supraventricular (above the ventricle somewhere)

-Clinically pt feels like heart racing, no S&S of dizziness or LOC

—>Have patient perform valsalva maneuver (inspiratory hold) to increase CO2 temporarily to decreased HR and maintain COVen

Ventricular tachycardia

-More than 3 PVCs in a row

-100-200 bpm

-not supraventricular becuase we see wild rope, indicating a ventricle issue

-pt looses consciousness, and a code/defibrillatir is the only this that will correct this

The only two pathologies you would shock for

-Ventricular tachycardia

-Ventricular fibrillationa

atrial flutter

-one ectopic foci firing out of control

-looks like saw took on ECGa

atrial fibrillation

-uncontrolled a-fib demonstrates a HR>100 bpm

-normally atrium squeezed blod down into the ventricle

-numerous ectopic foci contracting simultaneously

-no detectable P-wave on an ECG

-QRS complexes come at various rates

-heart does not contract normally (prone to stasis of blood flow, clots)

ventricular flutter

-one ectopic foci firing uncontrollable

-rate of200-300 bom, usually ineffective pumping from the heart

-may not be able to palpate pulse, pt may go unconscious, begin CPR

-Torsades De Point TdP (when the ECG jus looks like sinusoidal wave)

Ventricular fibrillation

-multiple ectopic foci firing at same time in ventricles

-CO is 0

-HR is 0

-heart os not working

-call a code, start CPR, use AED to defibrillate, sending an electrical impule hoping to get SA node to take over again

What do we do with patients who have dysrhythmias while performing activity

-when in doubt, stop, rest, and get help

-If sxs get better:

→do they have aprior dx? continue

→Never been dx? → contact MD

-If sxs worsen

→potential emergency situation, call for help

AV blocks

-Due to MI damaging AV node

→1st degree AV block

→2nd degree AV block type 1 (Wennkebach)

→2nd degree AV block Type 2

→3rd degree AV block (the worst, a complete block)

1st degree AV block

-prolonged PR segment past 0.2 sec

-PR duration is the same length evry time

-P wave: one for every QRS complex

-Regular whythm

-Originates in SA node

-Patients usually not symptomatic and should tolerate PT intervention just fine

1st degree vs 2nd degree

-1st degree always has QRS complex following P wave

-whenever QRS complex is dropped following p wave. you have a 2nd degree

2nd degree AV block type 1 (Wenckebach)

-Missing QRS complex (irregular rhythm)

-Distance of PR interval is NOT the same each time→longer, longer, longer .. DROP QRS

-Still a P wave is present, so originating from SA node

-May require use of a pacemaker

-Irregular P-P, irregukar Q-Q (no longer rhythmical)

2nd degree AV block type 2

-Missing QRS complex (irregular rhythm)

-Distance of PR interval IS the same each time

-Still a P wave is present, so originating from SA node

-May require use of a pacemaker

-Regular PP, Irregular Q-Q

3rd degree AV block

-complete block, no communication btwn SA node, atrium and ventricles

-heart still beats at about 20-60 beats per minute due to automaticity of AV node (junction) (40-60 bpm or ventricles (20-40 bpm)

→HR is too slow, not efficient

-Patient reuires a pacemaker

-P-P regular, Q-Q regular

-Atrium still filling normally from SA node because there are regular P waves, and ventricles are contracting regular normally due to normal Q waves, however, the atrium and ventricles are not communicating

-These pts are symptomatic

Escape beat

-named because they actually escape you from death

→heart stops, something kicks in to restart the heart

→more concerning than pre-mature beats

-ther are atrial, nodal, and ventricular escape beats

Wolff-Parkinson-White syndrome

-rare phenomenom: have an accessory bundle of kent

-two ways of conducting from atrium down into ventricle

-shown on an ECG by P wave going right up into QRS complex without flat lining

-S&S: non, extra PVCs, rapid ventricular rates

→sometimes remove extra bundle of kent via surgery