ECG's Rules Flashcards
Where is the p wave originated from -
Atrial contraction generated by SA ( sino-atrial) node
Where is the PR wave originated from-
AV ( atrio ventricular) node delay
Where is the QRS wave originated from -
ventricular contraction ( generated by the Purkinje Fibres )
Where is the T wave wave originated from -
from the ventricular relaxation / repolarisation.
What is the complex in-between the s and t segment that crucial in diagnostic of a stemi
J point
Explain or describe the electrical conductivity of the heart - all electric pathways and follow of blood and how does this correspond to complexes seen on ECG
SA node( positioned in right atrial ) fires - across the atria
Atria contracts * P WAVE **
Signal pass through to AV NODE this delay the signal allowing blood to fill the ventricals *** PR INTERVAL ””””
Signal passes from AV NODE to bundle of his, which splits into the bundle branches ( left and right)
This passes to the Purkinje fibre @ the apex of the heart.
The signal passes up the walls from bottom up via the Purkinje fibre - causes ventricular contraction **** QRS COMPLEX
The centrical then repolarisation occurs ** T WAVE **
THE Atrial repolarization occured during the QRS COMPLEX. - not visible due to the high charge at ventricles
What is the duration of the p wave -
0.08s ( 2-2.5 sq)
What is the duration of the PR wave -
0.12s to 0.20s (equal to 3-5sq)
What is the duration of the QRS complex -
less than 0.12s ( 3sq)
What is the duration of the QT interval -
Bonus points what is the normal QTC
0.36s to 0.44s (equal to 9-11 sq)
QTC sgpuld be less than 500ms
What is PPCI criteria for STEMI 🚨🚨
Limb lead - 2+ lead with elevation in 1 small box plus
Chest lead - 2+ lead with elevation in 2 small boxes plus
What are the lead views on a 12 lead ECG
Lateral - L1 avl v5 V6
Inferior - L2, L3 avf
Septal - v1, V2
Anterior- v3, v4
Non - avr
What should be suspected if st depression is seen in the anterior lead
1) what are the anterior lead cover
2) suspected is
3) test we can conduct
1) v3v4 V2 v1
2) posterior MI
3) v7, V8،v9
What test should be conducted if ST elevation is seen in the inferior lead
1) what are inferior leads
2) answer to question - how to conduct
3) why - how does this effect the treatment plan
1) L2, L3 , AVF
2) V4R , take v4 and place on right side same spot.
3) if ST elevation see this mean right ventricular involvement (RMCA) therefore caution in give GTN +morphine due to high risk of bp drop reduced cardiac output + venous return therefore cardiac arrest
What are the two sub branches that come off the LMCA ( left main cononary artery)
LCF - left circumflex
LAD - left anterior descending
What does the LMCA ( left main coronary artery ) feed
Left ventriculal
Left atrial
And the septum
What does the right main cononary artery feed (RMCA)
Bothe ventricles
Right atrium
And the posterior portion of the heart
What is the molecules that great a electrical charge in the heart and how do they get affected once a charge arrives
Potassium ( INSIDE) the cell - maintained by pump and gated channel ( acting as a door)
Calcium + sodium outside the cell
Electric current arrives
Sodium in - causes more sodium channels to open which inturn cause positivity and open calcium channels
Calcium come bind = contraction
Cardiac axis - what lead are need to determine cardiac axis
Lead 1
Avf
Cardiac axis - what is the cardiac axis if both L1 and Avf are positive
Normal cardiac axis
What do the lead look like when it’s a normal cardiac axis
Lead 1 & avf are positive
if lead 1 is positive and and avf is negative what is the cardiac axis
Left axis deviation as the leads are ** leaving**
What does left axis deviation look like
The lead are leaving
L1 is positive
Avf is negative
What does right axis deviation look like
L1 is negative
Avf is positive
** Reaching for each other **
If L1 is negative and avf is positive
What is the axis deviation
Reaching towards each other
Right axis deviation
What does extreme axis deviation look like
Both L1 & avf are negative
If both L1 and Avf are negative what is the axis deviation
Extream axis deviation
How can you identify a right bundle branch
All 3 thing must be true
1) wide qrs complex - 0.12s +
2) upright QRS complex in v1
3) slurred s waves in V6
Can turn paper on it’s right side
If the r wave faces right if not it’s facing left it’s left
How can you identify a left bundle branch block
All 3 things must be true
1) broad qrs complex - 0.12s +
2) mainly downward facing ( negative ) QRS COMPLEX in v1
3) with broad upward facing r waves in V6
4) no Q waves in v6
Turn it on it’s side ( right side ) - it’s be facing left
How can you identify a sinus tachycardia
1) heart rate above 100 but below 140
2) normal p qrs and t waves
How can you identify re- entrant tachycardia also know as narrow complex tachycardia or SVT
HR above 140
Normal qrs length
Constant rate
no p waves - as we are flying 🕊️
What is the pathophysiology of re- entrant tachycardia / svt / narrow complex tachycardia
There is a backflow of electrical activity in the atria
What is the treatment for re -enterant tachycardia / svt / narrow complex tachycardia
STOPPIT- mnemonic
Vasovagal manovour - blow into something and tilt
??? Can we do as paramedic
Defibb Pads on
PRE - ALERT
What is the pathophysiology of wolff Parkinson white syndrome
The heart creates a new pathway from atria to centrical call the bundle of Kent which bypasses the bundle of his and av node
This causes an early depolarisation from the centrical seen as the Dela wave
What is an indicator of wolf Parkinson white syndrome on an ECG
A delta wave
This is due to early repolarisation of ventricles
This is a slight upward curve at the start of the qrs then it fly’s up
How do you identify a broad complex tachycardia or VT or ventricular tachycardia
Ventrical originating rhythm
Qrs size is 0.12s + ++++
Regular
Above 100bpm
What is known as an ectopic beat or escaped beat
This is a beat which is not generated by the SA node but from secondary cardiac pacemakers
How do you identify a 1st degree AV block
1) the PR interval has to be 0.20+ (5sq)
2) this distance must be constant, regular rhythm
What is an incomplete bundle branch block
A bundle branch block which has the morphology of a block however has a duration of less than 0.12s
What is first degree AV Block
- pr interval 0.20+
- this is constant
- followed by a qrs complex
Can be a normal variant
What is 2nd degree type 1. AV block
- pr interval 0.20+
Pr interval gradual increases distance before QRS goes missing
Type 1 runs along
What is 2nd Degree type 2 AV block
(2:2)
Pr interval longer than 0.20+
- pr interval constant before a random QRS complex drop off
How do you identify a broad complex tachycardia
Rate of above 100bpm
Qrs length larger than 0.12s
Regular
What is torsade debpoint and what is the key in idefinificstion
Has Long qt syndrome
R on t ( repolarisation and deoperisation happen as same time
R waves have different amplitude
What is long Qt syndrome ( cause of sudden cardiac arrest)
- what medication can prolonge the QT syndrome
- what rhythm can originate from prolonged QT
Duration between q wave and t wave is 0.44+ or 11 sq +
Ondansatron can further elongate this
- VF or torsades
What is atrial fibrillation
Eptopic side of heart takes over as SA node loses control ( random depolarisation at different voltages ) some go through some don’t
- no p waves
- irregularity irregular
- no flat base line ( fibrillation)
- irregular pulse
What is fast AF or AF with rapid ventricular contraction
It’s is AF which is tachycardiac above 110bpm
What is atrial flutter
Right atrial is damage
No isoelectric line
Jagged p waves ( f waves) ( teeth shark)
What is wap ( wandering atria pacemaker
3 + atrial pacemaker conduct ectopic beats
- different p waves morphology
Different pr intervals
Rate less than 100bpm ( above =multi atria tachycardia
What is the job of an eptopic pacemaker cells
- act as a back up for the SA node if it fails
- not affected by sympathetic or parasympathetic nerve system
What is a junctional rhythm
What is the rate set
- what are the characteristics of this rhythm
- escaped beat oreiginting from the AV site
40-60 BPM
normal qrs
Absent inverted or diassosuwed “ P WAVES”
What are the causes of escaped rhyms
3rd degree AV block
Sinus arrest
Bradycardia
Drugs - beta blockers, CCB, DIGOXIN
What are the factors that are identifiable of a ventricular escaped rhythm
Beats originating from below BOH
rate - 15 to 40BPM
**QRS bizarre and wide ( may look like BBB)
P WAVES - dissaosited or absent
What is an agonal Rhythm
- seen before aystole
- below 20 BPM
- wide bizarre qrs complexes
What is a PVC
- how does it display on ECG
Wide abnormal QRS complex
Larger amplitude than other qrs
Followed by a pause= reset then normal
Occurs because of 2 pathways in heart after BOH - FAST = NORMAL
SLOW = PVC
What is a bigemany
Every second beat = pvc
What is couplets
What is this dangerous
2 PVC right after each other
3 + pvc = VT
PAD ON - get ready patient may arrest
What is the 3 classification of angina
Stable - exception
Unstable - random
And prinzaomental - vasoconstriction spasms
What is the pathophysiology of stable and unstable angina
- why does pain occur
Atheocrosis layer on the contrary arterioles - reduces diameter = less to flow when need = pain
What is the pathophysiology of prinzmental angina
Vasoconstriction spasm of the cononary ateryes
Can show ST elevation - which quickly resolves with GTN
What is a STEMI Vs non stemi
A full major occasion - causing ischemia and necrosis
Non stemi - minor full occlusion - no st segment changes on ECG
What is de winters signs
Sloped (upwards) st depression with hyper acute (upwards) t waves in the precordial leads
Treat as MI
SIGN OF PROXIMAL LAD occlusion
- What is biphasic t waves
- what does it suggest
- upward a d downwards t waves
Ischemia or hypokalemia + wellen sign
Inverted t waves can be a normal variant in which leads
3
Avl
V1 & v2
What is wellens syndrome and it’s significants
Biphasic t waves - t wave starts positively ends negatively
No st changes
Deeply inverted T waves
Seen in precordial anterior lead and avl
This is a sign of stenosis of the LAD - increasing the risk of MI or post MI
If a patient has a new onset of a LBBB with how should this be treated
IF THERE IS ACS symptoms treat
as a STEMI
Otherwise normal road - call PPCI
What are the different variations of at depression
Horizontal
Upward sloping
And downward sloping
What are the 3 different ECG changes which indicates ischemia to the heart
St depression - 2+ leads
T waves - , hyperactue, biphasic or flipped
Stemi - but shuttle (not PPCI criteria)
Pathological q waves (old ischemia )
When discussing T waves ischemia what should I look for
T waves inverion - 2 lead same view of the heart
Biphasic t waves - goes positive to negative or the other way
Hyperacute ts
When discussing T waves ischemia what should I look for
T waves inveted - 2 lead same view of the heart
Biphasic t waves - goes positive to negative or the other way
Hyperacute t waves
Deeply inverted t’s
If you see biphasic T waves on an ECG - clinically what does this mean
Ischemia
Hypokalemia (signs )
Wellen syndrome (+2-)
What is the nmenonic for finding for understanding where to look for respical changes in a STEMI
pails
Got stemi - look at the next letter for the resipical changes
Posterior
Anterior
Inferior
Lateral
Septal
What is the progression of a stemi in terms of ECG visual visually looking
In the first stage you see by phasic or inverted t waves
-hyper acute t waves which are equal to or longer than the qrs in terms of amplitude next you will see the semi appearance
Pathological key waves with lots of r shape
The morphology stays the same but with added inverted t waves
Pathological key waves remain but rest of the ECG turns back to normal
What is the visual st changes caused by
Electrical activity passing through ischemic or dead myocardiocytes - they have a shorter contraction phase alongside potential for deoplerisation
Ischemia is the the shape of st changes
Why Is some with st elevatoin whilst others depression
Elevation - MI facing the lead
Depression - MI FACING away
What are the ECG changes seen in PT with pericarditis
Global st elevation
Pr segment depression
St depression in AVR
What are the ECG changes seen in PT with pericarditis
Global st elevation
Pr segment depression
St depression in AVR
How can you distinguish LEFT main artery occulsion
ST elation in AVR
WITH
st depression in inferior or lateral leads
What is a sign of Lad occlusion
ST elevation in AVR
WITH RBBB OR v1 st elevation
What is early polerisatrisation / high take off - see it on a ECG
1) quick repolarisation
2) look like st elevation ( 1-3mm) = if chest pain treat it as stemi - or do it anyways - treat worst case
What is early polerisatrisation / high take off - see it on a ECG
1) quick repolarisation
2) look like st elevation ( 1-3mm) = if chest pain treat it as stemi - or do it anyways - treat worst case
What is brugada syndrome
2) how do you identify it
3) alongside ECG changes what else must be present
2) ST elation in (v1 to V3), with coved ST elevation at least 2mm which leads to inverted T wave
3) Syncopy witnessed VT /VF or history of sudden adult death
What are the signs you should look for in an ECG which is representative of ACS
ST ELEVATION OR DEPRESSION
T WAVE INVERTION
PATHOLOGICAL Q WAVES
What are the signs you should look for in an ECG which is representative of ACS
ST ELEVATION OR DEPRESSION
T WAVE INVERTION
PATHOLOGICAL Q WAVES
What is the most important lead to identify right-sided involvement in an inferior stemi
V4r
When assessing an inferior stemi what signs on an ECG could be indicative of right ventricular involvement
Lead 3 bigger than lead 2
One mil of st elevation in v1 or AVR
St elevation of 0.5 millimeter in a in v4r
When assessing an inferior stemi what signs on an ECG could be indicative of right ventricular involvement
Lead 3 bigger than lead 2
One mil of st elevation in v1 or AVR
St elevation of 0.5 millimeter in a in v4r
What is the inferior stemi right ventricular involvement triad
Hypertension
Jugular vein distention
Clear lungs
What is the inferior stemi right ventricular involvement triad
Hypertension
Jugular vein distention
Clear lungs
Why can right entricular involvements in various stemi cause RVI triad
As there’s an effect on preload due to death of cardiac muscle
Thus reduced blood flow to the lungs
Hence reduced blood flow to the left ventricle that’s reduced cardiac output
What is the management for an inferior stemi with right ventricular involvement
Clinical decision on whether to give morphine or gtn as they can affect preload
Maintaining systolic blood pressure of 100 mmgh
What is the management for an inferior stemi with right ventricular involvement
Clinical decision on whether to give morphine or gtn as they can affect preload
Maintaining systolic blood pressure of 100 mmgh
What is the general management of STEMIS
ACS bundle- aspirin gtn opioid
Defibrillator pads
Pre alert to ppci
What are the indicators for posterior stemi
St depression in the septal leads
This is confirmed by st elevation of 0.5 mm in v7 v8 and v9
What is the importance of pathological Q waves
How do you identify this on a ECG
2mm in depth or 1mmin length - in lead v1 to V3
Sign of previous cardiac muscle death or current mi
-
What are the ECG changes for left ventricular hypertrophy
Amplitude to the t and s waves
Increase R waves in L1 avl V4 v5 V6
Increased s wave in v1 V2
What are the clinical signs shown for right ventricular hypertrophy
QRS R wave increases V1 AVR
QRS S WAVE WAVE INCREASE IN LATERAL LEADS 1 AVR V5 V6
Why do bunder branch occur
Blockages occur in the affective branch
Electrical activity has to flow through opposite ventricle or through septum = takes more time
What are the clinical ECG signs of left bundle branch block
QRS larger than 0.12 seconds
V1 DOMINANT S WAVES
V6 UPRIGHT R WAVES WITH NO Q WAVES
What is an incomplete bunch of branch block
Bundle branch block meets the criteria
Butch the qrs complex is shorter than 0.12 seconds
What are the clinical signs of a right bundle branch block
Qrs larger than 0.12ms
V1 qrs complex positive in rsr pattern
V6 slurred s-waves
What is the predominant pattern (qrs) in a right bundle branch block v one and why
Rsr
Second r is the right ventricle contraction after delay
What is the predominant pattern (qrs) in a right bundle branch block v one and why
Rsr
Second r is the right ventricle contraction after delay
What is the ECG change for right ventricular strain/ McGinn-White sign
S1 Q3 T3
-dominet S wave in lead 1
- deep Q wave in lead 3
- Inverted T in lead 3
How do you know if a patient has a atrial pacemaker on ECG
Pacing spike before p wave
What may a paced rhythm look like and why
What must also be present
BBB - as paced ventrical depolerises before other one
- look for pacing spike
What are the early stages of hyperkalemia on an ECG
Peaked t waves
What is the second change of hyperkalemia after peaked tvwavea
Increased pr interval
Widening and eventually loss of p waves
Turning to af widening qrs and heart blocks
What is the ECG changes seen in mild to moderate hypokalemia
Increased pr interval
Increased hight and length of p waves
St depression
Inverted and flattened t waves
What are the changes seen in hypercalcaemia
Decreased qt and st segment duration
Osborn waves
What are the change seen on an ECG for hypothermia
Bradycardia
atrial fibrillation
Osborne waves
increased prqrs
and qt interval
What is refractory VF
Recurrent Vf despite multiple deffibulation attempts
What should you assess for during a cardiac arrest whereby PEA is the dominant rthym
The qrs
Wide qrs ( mechanical problem = tensions, tamponade, pe
Narrow qrs ( metabolic - hyperkalemia, sodium channel blocker toxicity, mi pump failure
How do you recognise WOLFF Parkinson White syndrome
- short PR interval
- Sloped upwards on QRS = (delta wave)
- Deep S waves or TALL R’s in. septal leads
What is a shark MI
