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Introduction to ECGs

The basics of electrocardiograms, how to read them & what they tell us about the heart

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/22

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Learning Objectives

Explain, in depth, the conduction system of the heart, emphasizing the importance of the fibrous annulus
Explain, in depth, the cardiac vectors and how they relate to the normal ECG
Explain the unipolar and bipolar limb leads and how they visualize the heart in the frontal plane
Explain the chest leads and how they visualize the heart in the horizontal plane
Explain underlying physiology of the pathological features of an MI on ECG

Jerrid Archutik adapted from Manvir Parmar, Doctorials 2021/2022

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Cardiac Anatomy Review

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Tortora (2012)

Heart located in middle mediastinum
Apex (inferolateral part of left ventricle) at left 4^th – 5^th intercostal space
4 chambers:

Right atrium (RA)
Right ventricle (RV)
Left atrium (LA)
Left ventricle (LV)

4 valves between chambers:

Tricuspid (RA 🡪 RV)
Pulmonary (RV 🡪 pulmonary trunk)
Mitral/bicuspid (LA 🡪 LV)
Aortic (LV 🡪 aorta)
Cusps of valves connected to chordae tendineae 🡪 papillary muscles

SVC/IVC 🡪 RA🡪 RV 🡪 Pulmonary Arteries 🡪 Lungs 🡪 Pulmonary Veins 🡪 LA 🡪 LV 🡪 Aorta 🡪 Systemic Circulation

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Cardiac Cells

Costanzo (2014)

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Contractile cells (“working cells”, 99% of all cardiac cells)

Atrial & ventricular myocytes
Contractility, conductivity & excitability
Contraction 🡪 generation of force
Intercalated disks and gap junctions allow rapid electrical impulse transmission to adjacent cells

Conducting cells (“electrical cells”, 1% of all cardiac cells)

Pacemaker cells
Specialized cells to generate and conduct action potentials
Automaticity, conductivity & excitability
Found throughout cardiac conduction system

Sinoatrial (SA) Node (60-100 BPM)
Atrioventricular (AV) Node (40-60 BPM)
Purkinje Fibres (20-40 BPM)

Latent Pacemakers (overdrive suppression from SA node)

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Cardiac Myocyte Action Potential

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

McMaster Pathophysiology

Phase 4 (resting phase): Resting membrane potential is -90 mV from constant leak of K+ via inward rectifier channels (Na+ and Ca++ channels are closed)
Phase 0 (depolarization): Action potential from nearby cardiomyocyte or pacemaker cell is propagated (gap junctions allow Na+ and Ca++ to leak into the cell) until the cell reaches threshold potential (-70 mV) 🡪 fast voltage-gated Na+ channels open allowing Na+ into the cell and rapid depolarization occurs 🡪 overshoots to a slightly positive potential (~ +20 mV)

At ~ -40mV, L-type Ca++ channels (long-opening) open and cause small but steady influx of Ca++ down its concentration gradient

Phase 1 (early repolarization): Voltage-gated Na+ channels closed and some voltage-gated K+ channels open
Phase 2 (plateau): Around 0 mV, L-type Ca++ channels are still open (still allowing for constant inward flux of Ca++) & K+ leaks out down its concentration gradient through delayed-rectifier K+ channels 🡪 causes excitation-contraction coupling and plateau is maintained
Phase 3 (repolarization): L-type Ca++ channels close, and there is persistent K+ outflow exceeding Ca++ inflow 🡪 brings cell back to -90 mV resting transmembrane potential
Normal transmembrane ionic concentration gradients are restored by returning Na+ and Ca++ ions to extracellular environment and K+ ions inside the cell via Na+/Ca++ exchanger, Ca2++ ATPase and Na+/K+ ATPase in sarcolemma

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Pacemaker Cell Action Potential

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Phase 4 (pacemaker potential): Most negative value of membrane potential (-65 mV) = maximum diastolic potential (no technical “resting membrane potential” because cells are always firing)

Slow depolarization via opening of Na+ channels and inwards Na+ current (I_f, “funny current”)
I_f is turned on by repolarization from the preceding action potential 🡪 ensures each action potential will be followed by another
I_f and Na+ channels bring membrane to threshold potential (-40 mV) 🡪 T-type Ca++ channels opened for upstroke
Phase 4 depolarization sets heart rate!! Can be increased/decreased via influence of autonomic nervous system!!

Phase 0 (upstroke): depolarization via inward Ca++ current carried by L-type (primarily) and T-type Ca++ channels

Not as rapid depolarization as myocytes

Phase 3 (repolarization): Ca++ channels shut, K+ ion channels open (favoring electrochemical gradient) 🡪 repolarizes membrane potential
Phase 1 & 2 are absent

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Cardiac Electrophysiology

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Toronto Notes (2017)

Electrical activation of the heart:

Creates cardiac action potentials
Conduction of action potentials along specialized conducting tissues
Modulating effects of autonomic nervous system on heart rate, conduction velocity & excitability
ECG

Initiation & distribution of electrical impulses through the heart:

Sinoatrial (SA) Node
Internodal tracts (anterior, middle, posterior)
Bachmann’s Bundle
Atrioventricular (AV) Node
Bundle of His
Bundle Branches (left anterior, left posterior, right)
Purkinje Fibres

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Cardiac Electrophysiology

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Toronto Notes (2017)

Electrical system controls each heartbeat by regulating:

Rate (# beats per minute)
Rhythm (synchronized pumping action of chambers)

Sinoatrial (SA) Node:

Located in upper RA wall, under SVC opening
Blood supply: RCA (60%), Cx of LCA (40%)
Pacemaker cells produce action potentials
60-100 BPM
Surrounding cardiac myocytes depolarize & transmit

Q: What is the purpose of Bachmann’s Bundle?

Q: How do cardiac cells propagate action potentials from pacemaker cells?

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Cardiac Electrophysiology

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Toronto Notes (2017)

Atrioventricular (AV) Node:

Located on floor of RA, above interventricular septum
Blood supply: RCA (80%), Cx of LCA (20%)
Electrical relay point between atria & ventricles
Slowing of impulse conduction (0.1s delay)

Atrioventricular Bundle (of His):

Traverses through fibrous annulus
Continuation of AV node
Bundle of His is the ONLY electrical connection between atria & ventricles
Specialized one-way conduction of action potentials which prevents re-entry of impulses from ventricular myocytes back to atria

Q: Why is there a delay in impulse conduction between SA and AV node?

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Cardiac Electrophysiology

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Toronto Notes (2017)

Bundle Branches:

Divisions of Bundle of His 🡪 spread towards apex down interventricular septum
Left bundle branch 🡪 anterior & posterior fascicle transmitting conduction to LV
Right bundle branch transmits conduction to RV

Purkinje Fibres:

Transmit impulses from bundle branches to cardiac muscle cells
Very large fibres 🡪 HIGH VELOCITY impulse transmission
Ends of fibres penetrate muscle mass for continuous and rapid communication with muscle fibres
Rapid propagation of impulses important for effective ventricular contractions

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Cardiac Skeleton

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Tortora (2012)

Fibrous Annulus (fibrous skeleton of the heart)

4 dense collagen rings that surround valves of the heart
Annuli around valves connecting trigones (triangular mass of fibrous tissue)
Fuse with one another

Functions of annulus fibrous:

Attachment points for valves
Prevents overstretching of valves as blood passes through
Separates atrial myocardium from ventricular myocardium 🡪 insulation to electrically isolate impulses between atria & ventricles

Bundle of His = ONLY electrical conducting point between atria & ventricles

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Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

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Electrocardiography

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

GeekyMedics (2020)

ECG is a composite recording of all action potentials produced by the nodes and cells of myocardium from atrial and ventricular depolarization & repolarization in one cardiac cycle

Does not assess contractility of the heart

Important tool for diagnosis (and therefore management) of cardiac abnormalities and pathologies
Indications:

Abnormal rhythms (arrythmias)
Chest pain/MI
Dizziness, syncope, breathlessness
Drug monitoring

A 12-lead ECG provides a look at the heart’s electrical activity from 12 different “views”

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ECG Waveform

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

GeekyMedics (2020)

ECG wave complex has 5 wave forms

P, Q, R, S, T
QRS generally referred to as one unit (QRS complex)

Segments = sections of ECG that connect two waves (without including either wave)

PR segment
ST segment

Intervals = portions of ECG that contain a segment and one or both waves

PR interval
QT interval

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ECG Waveform

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

The ECG Made Easy (2013)

	Represents	Location	Amplitude (height)	Duration (length)	Configuration
P	Atrial depolarization	Precedes QRS complex	2-3 mm	0.06-0.12s	Round & Upright
QRS	Ventricular depolarization - Q = conduction through bundle branches - R = Depolarization of ventricular walls - S = Ventricular depolarization at base of heart	Following PR interval	5-30 mm (differs per lead)	0.12s (duration shows how long excitation takes to spread through ventricles)	- Negative deflection in aVR, V1-V3 - Positive deflection in I, II, III, aVL, aVF, V4-V6
T	Ventricular repolarization	Following S wave	- 0.5 mm (I, II, III) - Up to 10 mm in precordial	0.1-0.2s	Round & Upright

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ECG Waveform

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

The ECG Made Easy (2013)

	Represents	Location	Duration (length)
PR Interval	Impulse passing from atria 🡪AV nodes 🡪 bundle of His 🡪 bundle branches	Beginning of P wave to beginning of QRS complex	0.12-0.20s
ST Segment	- End of ventricular depolarization and beginning of ventricular repolarization - Ventricular contraction - Isoelectric (but can vary -0.5-+1mm in precordial leads)	- End of S wave to beginning of T wave - J-point = end of QRS complex	0.05-0.15s
QT Interval	Ventricular depolarization & repolarization	Following S wave	- Length usually depends on HR (faster = shorter interval) - Generally 0.42s

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ECG Waveform

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

The ECG Made Easy (2013)

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ECG Paper

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

GeekyMedics (2012)

Generally, ECG paper is standardized across most hospitals
Small squares = 0.04s
Large squares = 0.2s
There are 5 large squares per second & 300 large squares per minute

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Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Boards & Beyond (2020)

Mean Direction of ALL Electrical Forces

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Electrodes Placement

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

The ECG Made Easy (2013)

4 Limb electrodes 🡪 leads give view of heart in vertical plane

Right Arm (RA)
Left Arm (LA)
Left Leg (LL)
Right Leg (RL) = neutral

6 Chest electrodes 🡪 leads give view of heart in horizontal plane

V1 & V2 = faces at right ventricle
V3 & V4 = faces at septum
V5 & V6 = faces at anterior and lateral

walls of left ventricle

* Ride Your Green Bike *

(clockwise from RA)

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Electrodes & Leads

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

The ECG Made Easy (2013)

ELECTRODES are the conductive pads attached to the body

Pair of electrodes can measure the electrical potential difference between the two locations 🡪 forms a LEAD
AP towards positive electrode = positive deflection
AP away from positive electrode = negative deflection
Opposite for repolarization (towards is negative, away from is positive)

Electrode leads can be unipolar (one pole) or bipolar (2 poles)
3 types of leads:

Limb leads (I, II, III)
Augmented limb leads (aVR, aVL, aVF)
Chest/precordial leads (V1-V6)

In a standard 12-lead ECG, 10 electrodes (9 polar, 1 neutral) are used to produce 12 leads

Limb leads are all bipolar
Precordial leads are all unipolar

* You have 1 chest (unipolar chest leads) and 2 arms/legs (bipolar limb leads)

=

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Limb Leads – Einthoven’s Triangle

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

Lead I = RA 🡪 LA

Lateral view of the heart

I

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Limb Leads – Einthoven’s Triangle

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

Lead II = RA 🡪 LL

Inferior view of the heart

I

II

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Limb Leads – Einthoven’s Triangle

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

Lead III = LA 🡪 LL

Inferior view of the heart

II

I

III

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Augmented Limb Leads

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

aVR = towards right

Lateral view of the heart

II

I

III

aVR

Q: What do you suspect if aVR is showing positive deflection?

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Augmented Limb Leads

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

aVL = towards left

Lateral view of the heart

II

I

III

aVL

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Augmented Limb Leads

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

aVF = towards feet

Inferior view of the heart

II

I

III

aVF

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Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

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Jerrid Archutick adpated from Manir Parmar

V1

V2

V3

Correlation of Leads & Areas of Left Ventricle

(RV)

(V9)

(V8)

V5

V6

Posterior =

non-standard

leads

Antero-lateral

(V4R)

V4

(RV)

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Summarizing Leads

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Boards & Beyond (2012), The ECG Made Easy (Year), Toronto Notes (2017)

Lead	Electrode 1 Placement (-)	Electrode 2 Placement (+)	QRS Waveform Deflection
I	RA	LA	Positive (0°)
II	RA	LL	Positive (60°)
III	LA	LL	Positive (120°)
aVF	RA + LA (average)	LL	Positive (90°)
aVR	LA + LL (average)	RA	Negative (-150°)
aVL	RA + LL (average)	LA	Negative (-30°)

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Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Boards & Beyond (2020)

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How to Read an ECG

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Easy as 1, 2, 3…

Calculate Rate
Assess Rhythm & Waves
Determine Cardiac Axis

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Calculating Heart Rate and Regularity

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

GeekyMedics (2020)

What is the heart rate?

R-R Interval on rhythm strip (lead II)
How many large squares are present within one R-R interval?

TIP: Try to pick an R-R interval with peaks on (or close to) margins of large boxes

Calculate HR (beats per minute) by dividing # of squares in R-R interval by 300 (large boxes that make up 1 minute)
If patient’s rhythm strip is too irregular, count # of complexes and multiply by 6

Is heart rate normal?

60-100 bpm = normal for adults
< 60 bpm = bradycardia
> 100 bpm = tachycardia

What is the character?

Regular, irregular (regularly-irregular, irregularly-irregular)
Measure # of small squares between R-R intervals
TIP: Take a small strip of paper and mark one R-R interval 🡪 use this and match up the remainder of your R-R peaks along the rhythm strip

Q: What is meant by “normal sinus rhythm”?

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Let’s Practice!

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Calculate the heart rate:

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Assessing Rhythm

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

GeekyMedics (2020)

Lead II first 🡪 then the rest
Are P waves present?

If yes, is each P wave followed by a QRS complex?
How does the P wave look?
If P wave absent, is there atrial activity? (flutter, fibrillation, flat line?)

What is the PR interval?

Is it between 0.12 and 0.2s? (3-5 small squares)
Widening? Shortening?

How does the QRS complex look?

What is the width, height & morphology?

Is ST segment isoelectric?

Is elevation or depression present?

How do the T waves look?

Peaked? Inverted? Biphasic? Flattened?

What is the QT interval?

Shortened? Prolonged?

Are U waves present?

Not common finding
Accompany flattened T wave?

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Let’s Practice!

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

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Cardiac Axis

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

Can be determined for any waveform (P, QRS, T)
Standard ECG reports QRS axis (mean axis of frontal plane) 🡪 Indicates average direction of electrical activity of the heart during ventricular depolarization

Normal cardiac axis range = -30° to +90°
Right axis deviation = +90° to +180°
Left axis deviation = -30° to -90°
Extreme axis deviation = -90° to -180°

+/- 180°

-90°

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Cardiac Axis

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Boards & Beyond (2020)

Note: there are many different methods out there to determine cardiac axis

2 Lead Analysis using leads I and aVf 🡪 deflection of QRS complex

Look at Lead 1 and aVF

If both are positive = normal axis
If lead I is positive & lead aVF is negative = LEFT axis deviation
If lead I is negative & lead aVF is positive = RIGHT axis deviation

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Let’s Practice!

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

This ECG shows normal axis, no deviation

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Let’s Practice!

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

This ECG shows right axis deviation

Lead I = (net) negative deflection
aVF = Positive deflection

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Myocardial Infarction

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

MI occurs when cardiac myocytes die due to prolonged myocardial ischemia
Causes:

Coronary atherosclerosis +/-

Thrombosis superimposed on atheroma (90%)
Hemorrhage into plaque
Associated vasoconstriction

Signs & symptoms:

Chest pain (does not resolve to sublingual GTN)
Pain radiating to left arm, neck, jaw
Autonomic symptoms (sweating, pale & clammy)
Atypical symptoms (dyspnea, fatigue, presyncope or syncope)

ECG & serum cardiac markers can be used to diagnose (ECG alone cannot diagnose an MI)
Extent of infarct depend on different factors:

Duration
Extent
Anatomical location
Patient baseline

Q: What serum cardiac biomarkers would you be looking for in a suspected MI?

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Myocardial Infarction

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

NSTEMI (Subendocardial Infarct):

Limited to inner 1/3 of ventricular wall
Caused by increased cardiac demand with limited supply due to atherosclerotic plaques
Incomplete blockage of coronary artery
Diffuse coronary atherosclerosis and borderline perfusion (vasospasm hypotension)
Persistent ischemia 🡪 subendocardial necrosis

STEMI (Transmural Infarct):

Complete occlusion of a major extramural coronary artery
Consequence of atherosclerosis
May lead to rupture of myocardium
Most transmural infarcts affect left ventricle

Early recognition & treatment is important to save myocardium from further death!!

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Myocardial Infarction – ECG Changes

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Kumar & Clark (2012)

Ischemia:

ST depression
T wave inversion (commonly in V1-V6)

NSTEMI 🡪 Partial occlusion

ST depression in affected areas
T wave inversion

ST Elevated MI (STEMI) 🡪 complete occlusion & transmural ischemic injury

ST elevation of at least 1 mm in 2 adjacent limb leads OR
1-2 mm elevation in adjacent precordial leads

Typical evolving MI ECG changes:

Hyperacute (tall) T waves in leads facing infarct +/- ST elevation
ST elevation
Significant Q waves >0.4s or >1/3 total QRS
Inverted T waves (days to weeks post-infarct)

Q: How is an NSTEMI pathologically different from a STEMI?

Q: How would you diagnose an NSTEMI?

Transient coronary artery spasm (Prinzmetal angina) can be slight or very prominent ST elevation (up to 10mm)

Recall that cause of acute coronary syndrome is mismatch in myocardial oxygen demand and myocardial oxygen consumption

STEMI mismatch cause = almost always coronary plaque rupture 🡪 thrombosis formation 🡪 occlusion of coronary artery

NSTEMI has several causes which lead to flow-limiting conditions (stable plaques, vasospasm in Prinzmetal angina, coronary embolism, coronary arteritis) or unrelated coronary arteries/myocardium itself (hypotension, hypertension, tachycardia, aortic stenosis, coronary arteritis)

Diagnosis of NSTEMI based on history, cardiac biomarkers & ECG (can still show transient ST elevation/depression and/or T wave abnormalities)

A NORMAL ECG DOES NOT RULE-OUT ACS/NSTEMI

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Myocardial Infarction – ECG Changes

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

The ECG Made Easy (2013)

MI ECG changes generally occur in the leads that overlay the areas of ischemia, injury and/or infarction
Key is to identify what leads contain ST segment elevations

View of the Heart	Leads	Supplying Coronary Artery
Inferior	II, III, aVF	Right Coronary
Lateral	I, aVL, aVR, V5, V6	Left Circumflex
Anterior	V3, V4	Left Anterior Descending
Septal	V1, V2	Left Anterior Descending

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Tying Everything Together…

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

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Questions?

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

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EXTRA: Common ECG Pathologies

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Torsades de Pointes

Atrial Fibrillation

Atrial Flutter

First Degree Heart Block

Second Degree Heart Block (Mobitz I)

Third Degree (Complete) Heart Block

Ventricular Fibrillation

Ventricular Tachycardia

Premature Ventricular Contraction

Torsade de Pointes

Prolonged QT interval 🡪 can lead to cardiac arrest
Drugs (antiarrhythmic), hypokalemia, hypomagnesemia
Rarely from hypocalcemia

Atrial fibrillation (A. fib)

Quivering (fibrillatory waves
No distinct P wave, irregularly irregular rhythm

Atrial Flutter

Characteristic sawtooth pattern
Less common than A. fib

Ventricular Fibrillation (V. fib)

Multiple ectopic electrical impulses
Quivering (fibrillatory) ventricles

Ventricular Tachycardia (T. tach)

“Tombstoning” pattern
Broad complex tachycardia in ventricles
Loss of coordinated atrial contraction

Premature ventricular contractions (PVCs)

”extra” beats from ventricles (ectopic)
Ectopic beats can be atrial, junctional or ventricular

1^st Degree Heart Block = increased PR interval with no hemodynamic disturbance

2^nd Degree Heart Block = progressive prolongation of PR interval 🡪 nonconductive P wave (Mobitz I) or intermittent non-conducting P waves without progressive prolongation of PR interval (Mobitz II)

3^rd Degree Heart Block = absence of AV conduction, severe bradycardia

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Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022

Thank You QTs ☺

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References

Boards & Beyond (2020)
Costanzo Physiology (2014)
GeekyMedics (2020)
McMaster Pathophysiology (2012-2018)
Kumar & Clark’s Clinical Medicine (2012) 8^th Edition
The ECG Made Easy (2013)
Toronto Notes (2017)
Tortora Principles of Anatomy & Physiology (2012) 13^th Edition

Useful Resources:

Jerrid Archutick adapted from Manvir Parmar, Doctorials 2021/2022