EKG reading the basics Flashcards
how does a beat happen
-cardiac cells inside are neg charged at rest
-K, Na, Cl, Ca keep them at electronegative resting state -> ion channels make this possible
-depolarization! -> wave we see on EKG
-repolarization- return to neg state
pacemaker cells
-sinus node and AV node
-power source
-less negative resting potential
-not seen on EKG
-neurohormonal input:
-sympathetic accelerates / adrenalin
-parasympathetic decelerates / vagal stimulation
conducting cells
-bachman’s bundle - interatrial conduction
-purkinje system
-hard wiring -> PNS only affects SA and AV node -> this influences PR interval (not QRS)*
-rapid conduction
myocardial cells
-contractile machinery
-actin and myosin
-slower conduction, wave like across myocardium
-most of electrical activity thats seen on EKG
-contraction happens after electrical signal
different waves
-myocardial depolarization and repolarization
-P wave is atrial depolarization
-QRS depolarization of ventricle
-T wave is repolarization of ventricle
p wave
-right atrium then the left atrium
-pause after wave is slow at the AV node (fraction of second)
QRS
-bundle of his -> all or nothing (no PNS influence here and on)
-bundle branches- right and left
-left bundle branches -> septal, anterior, posterior fascicles
-you can have bundle branch blocks
-purkinje fibers
-Q WAVE- 1st downward deflection- septal contraction
-R WAVE- 2st upward deflection
-R’ (R prime) - 2nd upward deflection (if there is one) -> right bundle branch block
-S WAVE- 1st downward deflection after upward tick
left bundle branches
-septal fascicle- interventricular septum -> first part to depolarize
-anterior fascicle- anterior wall of left ventricle
-posterior fascicle- posterior wall of left ventricle
-septal fascicle is not seen on EKG - not as relevant
j point
-after QRS when you return back to isoelectric line
T wave
-restoring the electrical negativity
-repolarization
U wave
-wave appearing after T wave, normal or pathological
-usually same axis as the T wave -> if opposite, consider that there are two p waves
-physiologic meaning not understood
segments
-straight line connecting two waves
-ST segment- from end of ventricular depolarization to start of repolarization
-PR segment- pause at the AV node -> end of atrial and start of ventricular depolarization
intervals
-are a wave and the straight line
-PR interval- from start of atrial and start of ventricular depolarization
-QT interval- from start of ventricular depolarization to end of ventricular repolarization
-PR interval
boxes
-1 tiny box = 1mm
time:
-1 tiny box = 0.04s (40ms)
-5 tiny boxes (1 big box) = .2s (200ms)
-5 big boxes = 1s
voltage: vertical axis: amplitude
-1 tiny box = .1mv
-5 tiny boxes = .5mv
heart rate
-sinus rhythm should be 60-100 bpm at rest
-count number of boxes then divide into 300
-if not even large boxes count the small boxes .2
-ex. 4.40 boxes -> 300/4.4 = 68 bpm
how long is the pause (PP)
-3.6s
-2.6s (HR 58)
electrode
-towards (electrode?) is a positive deflection
-away is a negative deflection (down)
-reached it…..cancel each other out!!! -> baseline
-10 stickers and 12 views
6 limb leads
-view heart from frontal plane
-record electrical forces moving up, down, left, right
-leads 1-3 -> bipolar
-augmented leads -> unipolar
-lead 1- neg (RA) to pos (LA)
-lead 2- neg (RA) to pos (LL)
-lead 3- neg (LA) to pos (LL)
-aVR, aVL, aVF
-inferior view- lead 2, 3, aVF
-left lateral view- lead 1 and aVL
-aVR- only right view of heart
pericordial leads
-measures electrical forces moving anterior and posterior
-horizontal plane
V1 is placed in the fourth intercostal space to the right of the sternum.
V2 is placed in the fourth intercostal space to the left of the sternum.
V3 is placed between V2 and V4.
V4 is placed in the fifth intercostal space in the midclavicular line.
V5 is placed between V4 and V6.
V6 is placed in the fifth intercostal space in the midaxillary line.
normal measurements for intervals
-PR - 120-200ms -> .12s-.2s
-QRS - 60-100ms -> > 120 is pathologic
-QT - 40% of the R to R interval (QTc formula):
-faster the HR the shorter the QT interval
-slower HR the long the QT interval
hypertrophy
-increased muscle mass
-caused by increased pressure load
-HTN
-aortic stenosis
-can coexist with enlargement -> ways heart tries to increase CO
-increase muscle thickness -> compromise ability to pump -> demands more blood supply but has reduced density of capillaries -> more susceptible to ischemia
enlargement
-dilatation of a chamber
-caused by volume overload -> valvular disease
-can coexist with hypertrophy -> ways heart tries to increase CO
hypertrophy/enlargement EKG changes
-duration of wave increases (more tissue to move through)
-larger voltage*
-more current through the bigger chamber so vector can change -> axis shift
-add up all the directions of depolarization -> mean electrical axis….hypertrophy shifts this axis
-axis moves towards hypertrophy and away from an an infarction
axis shift
-more current through bigger chamber so vector can change -> axis shift
-add up all directions of depolarization, mean electrical axis….hypertrophy shifts this axis
-axis moves toward hypertrophy and away from an infarction
-left axis deviation (left up)- LV hypertrophy
-horizontal axis (left)- LV hypertrophy
-right axis deviation (down/right)- RV hypertrophy
-right axis deviation (down/right)- LV infarction
axis deviation
-not always pathological
-can be rotational
-obesity
-emphysema (diaphragm flattened)
normal axis
-mean QRS axis is leftward and inferior
-+90 to -30 degrees
-lead 1 & aVF -> if POSITIVE then normal axis
possible LAD
0 to -90 degree
-lead 1 POSITIVE
-lead aVF NEGATIVE
RAD
+90 to 180 degree
-lead 1 NEGATIVE
-lead aVF POSITIVE
extreme axis
(-90) to 180 degree
-lead 1 and lead aVF NEGATIVE
right atrial enlargement
-leads 2 and 6
-right enlargement the 1st half of p wave amplitude increases
-P pulmonale - caused by lung disease
-I dont think you need to know this!
left atrial enlargement
-2nd portion of p wave may increase and that portion drops more than 1mm below the isoelectric line in 6
-p wave duration increases because it is the 2nd half of wave
-p mitrale from mitral disease common cause
-I dont think you need to know this!
right ventricular hypertrophy
-90 to 180 degrees
-lead 1 more negative than positive
-larger R waves in the early precordial leads (V1), small in V5 and V6
-rules:
-V1 R wave > S wave
-V6 S wave > R wave
-pulmonary disease and congenital heart disease
left ventricular hypertrophy (LVH)
-Increased R wave amplitude in precordial leads over LV.
-Increased S wave over precordial leads over RV
-Systemic HTN, Valvular Disease
50% of pts with LVH will have EKG changes, 90% of those with the changes have LVH on echocardiogram.
There can be secondary changes ( T wave inversions, down slopping ST segment depressions)
-Rules:
-R wave amplitude in V5 or V6 plus he S wave in V1 or V2 is >35 mm ( most predictive)*******
-R wave amplitude in lead V5 >26 mm
-R wave amplitude in V6 > 20 mm
-R wave amplitude in V6 exceeds the R wave amplitude in lead V5
arryhthmia
-sinus rhythm 60-100 bpm
-disturbance in rate, rhythm, site of origin or conduction
-single beat or sustained
-slight irregularity during breathing
-not every arrhythmia is a problem to be fixed
-however…some can cause sudden death
symptoms of arrhythmia
-palpitations
-light headedness
-syncope
-chest pain
-heart failure
-sudden death
arrhythmia causes: HIS DEBS
-hypoxia- pulmonary disorders including COPD and PE
-Ischemia & Irritability- MI, angina, myocarditis
-Sympathetic Stimulation- hyperthyroidism, CHF, anxiety, exercise
-Drugs- Antiarrhythmics, Z- pack, tricyclic antidepressants
-Electrolytes- Hypokalemia, calcium or magnesium
-Bradycardia- Sick Sinus Syndrome, Lymes Disease
-Stretch- enlargement and hypertrophy. CHF & valvular
arrhythmia diagnosis
-rhythm strip
-EKG
-holter monitor
-event monitor
-implanted loop recorder
5 types of arrhythmias
-sinus origin
-ectopic origin- diff part of heart is trying to set rhythm
-reentrant arrhythmias- loops in AV node
-conduction blocks
-preexcitation syndromes- getting signal too fast
sinus origin- sinus bradycardia
-< 60 bpm
-normal in athletes
-hypothyroidism
-vagal tone or sleep apnea
-ischemia
sinus origin: sinus tachycardia
->100 bpm
-normal during exertion
-pain
-CHF
-COPD
-anemia
-hyperthyroidism
sinus arrest
-stops firing
-asystole
escape beats
-atrial 60-100 bpm
-junctional 40-60 bpm- pause, no p wave, QRS -> AV node fires on its own -> wide
-ventricular 30-45 bpm - has to be bradycardic -> random cell from ventricle fires
-escape beats are bradycardic -> ventricular escape beat is the bradycardic PVC
ectopic rhythms
-arise from area other than sinus node
-single or sustained
-single cell is stimulated to depolarize faster and faster overdriving the sinus node
-premature atrial contraction (PAC)
-scars, congenital, MI can cause this
reentrant rhythms
-impulse transmission disorder
-2 tracts with different conduction speeds
-uninterrupted revolving circuit
-electrical racetrack
-loop back
-either in AV node or tricuspid valve (flutter)
4 questions to ask yourself
-1. are P waves normal?
-normal- in atria
-none- AV node or ventricles
-abnormal P wave- atrial focus or retrograde
-2. are QRS complexes narrow or wide?
-narrow is usually pathway. at or above AV node
-wide is within the ventricles
-3. what is relationship between P waves and QRS complexes?
-1:1 with P before every QRS then sinus or atrial
-lack of correlation is AV dissociation
-4. is the rhythm regular or irregular?
supraventricular early beats
-single ectopic atrial beat - premature atrial contractions (PACs)
-junctional premature beats (PJC)
supraventricular arrhythmias
-1. paroxysymal supraventricular tachycardia
-2. atrial flutter
-3. atrial fibrillation
-4. multifocal atrial tachycardia
-5. wandering atrial pacemaker
-6. paroxsymal atrial
paroxsymal supraventricular tachycardia
-Usually AV nodal re-enterant tachycardia
-Sudden onset
-Usually initiated by a premature beat
-Regular rhythm
-150-250 bpm
-p waves are buried in QRS
-tx- Carotid massage increases vagal tone to slow conduction OR Adenosine
atrial flutter
-Regular
-P waves at 250 bpm
-Reentrant around tricuspid valve annulus
-“Saw toothed pattern”
-2:1, 3:1, 4:1 conduction
-Axis of P waves can tell you which direction around the valve
-can be brady, regular, or tachy
-this is a type of SVT
atrial fibrillation
-Electrical chaos, confused AV node
-No true P wave
-**Irregularly irregular rate
-Ventricular rate can be slow, normal or fast.
-MC sustained arrhythmia
-Stroke risk*
-type of SVT
-quivering
-clot - stroke, ischemic limb
multifocal atrial tachycardia vs wandering atrial pacemaker
-P waves present
-Three P wave morphologies
-Irregular rhythm
-100- 120 bpm
-WAP is the same but less than 100 bpm
-common in lung disease or thyroid issues
supraventricular arrhythmia common in severe lung disease
-multifocal atrial tachycardia and wandering atrial pacemaker
paroxsymal atrial tachycardia
-regular
-100-200 bpm
-automaticity (warm up and cool down seen) or reentry (early beat)
-p waves are abnormal compared to sinus but they are all the abnormal waves are the same
-single ectopic site in atria is going rapid
ventricular arrythmias
-premature ventricular contractions (PVCs)
-ventricular tachycardia
-ventricular fibrillation
premature ventricular contractions (PVCs)
-Wide complex
-Can be pattern
-1:1 bigeminy
-2: 1 trigeminy
-Concerning when frequent
-Multiform
-On the T wave “R on T”
-During acute MI
-PVC on long QT -> can put someone into torsade
ventricular tachycardia
-3 or more PVC’s
-120-200 bpm
-Non-sustained VT, 3 beats up to < 30s
-Sustained VT (>30sec) is emergency and requires immediate treatment
-Cardiac arrest
-you can pop out of this on your own
-poor filling
-Can have monomorphic morphology or changing (Polymorphic VT).
-Monomorphic seen in old infarct site -> reentrant -> usually due to scar
-PMVT can be seen in ischemia, infarction, electrolyte abnormalities & QT prolongation
-you can count clear complexes with VT
ventricular fibrillation
-Preterminal event
-Dying heart
-Sudden death
-Course to fine
-No true QRS
-No cardiac output-> no BP or pulse
-Start CPR!
-Defibrillation!
-Causes:
-MI or ischemia
-Heart failure
-Hypoxia or hypercapnea
-Hypotension
-Shock
-Electrolyte imalance
-Overdose
