interventricular

artery (PIVI

I

Acute marginal

Figure 1. Anatomy of the coronary arteries (right anterior oblique projection)

Posterior view of llio mitral valve appuratus

Anterior initiQl annulus

Anterior mitral leaflet

Lateral v

commissure

Med jl commissure

Left circumflex -

- coronary artery S

2

c — Posterior

mitral leaflet

Posterior mitral

annulus Lerfetlcuip)

S ’

.otutiu Hf |unct)on

Conttnumto

Coronary artory

(tna coronary ost a)

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d•

•

5

K

o

Snus of Valsalva

Irter *

a1lei inaoQlo

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lea'

iei attaclimont Posteiomedial

papillary m.

Aortic valvo: Three leaflets only

I

Aortic root: All components iSmutas ol Valsalva.iniarbiallat tnanglas, :

stnulubulur function.teattui alluchmunts. ballots,

annulusI

Loft ventricle

1

Antotolalorol

papillary m.

Figure 2a. Aortic root

Modified from SevenH-H,Hummer W.The ever yd.iyusednomeridatuie olthe aoillc root

components:the towel ol Babel

’

.European Joutnal ol Cdtdio.ThoriKlc Surgery.2012.41.3.478.82.

by peimlssion olOcloidUniversity Pie»

Figure 2b. Mitral valve apparatus

Anterior semilunar cusp

Right semilunar cusp..

Loft semilunar cusp

Pulmonary

valve Conus arteriosus

Right coronary artery Right coronary

Isemilunar) cusp

Loft coronary_

(semilunar) cusp

Noncoronary

Ipostcnor — semilunarl cusp /

Left coronary artory

Aortic

valve

Jt- Anterior cusp

-— Soptal cusp

UPostorior cusp

Tricuspid

valve Loft fibrous trigone

Circumflex artory'

Mitral [

AntBriorcusp,

valve Posterior cusp

ri

L J

^ Right fibrous ring

Right fibrous trigone

Left fibrous ring

Coronary sinus

+

Postonor interventricular artery

3lesia Siyca 2021

Figure 2c. Fibrous skeleton of the heart

Of Cardiology and Cardiac Surgery Toronto Notes 2023

Cardiac Anatomy

• layers of the heart

• endocardium, myocardium, epicardium, visceral pericardium, pericardial cavity, parietal

pericardium

• valves

• semilunar valves:3 leaflets separating outflow tractsfrom the great arteries

aortic valve: noncoronary cusp, LCC, RCC;RCC and LCC have coronary ostia;separates LVOT

and ascending aorta

pulmonary valve: anterior cusp, left cusp, right cusp;separates RVO'

l and PI

atrioventricular valves:subvalvular apparatus present in the form of chordae tendineae and

papillary muscles

mitral valve: anterior (2/3 valve area, 1/3 valve circumference) and posterior leaflets (1/3 valve

area, 2/3valve circumference);separates LA and LV

tricuspid valve:anterior, posterior, and septal leaflets;separates RA and RV

• conduction system

• SA node

located at the junction of SVC and roof of RA

governs pace-making;heartbeat originates here

anterior-, middle-,and posterior-internal nodal tracts carry impulsesin the RA with the

atrial impulses converging at the AV node and along Bachmann's bundle in the LA

• AV node

located within the triangle of Koch which is demarcated by:superior margin of the coronary

sinus, tendon of Todaro,and hinge of the septal leaflet of the tricuspid valve

AV node is the conduit for electrical impulsesfrom atria to ventricles, unless an accessory AV

pathway (c.g. WPW syndrome) is present

bundle of His

AV node connects to the bundle of His, which divides into LBB and RBB

- LBB furthersplits into anterior and posterior fascicles

- RBB and fascicles of LBB give off Purkinjc fibres which conduct impulses into the

ventricular myocardium

SA node _ _ Bachmann'

s bundle

Internodal

pathways:

- Anterior tract

' '

AV node

.Bundle of His

1 - Middle tract

.Lett bundle branches

- Posterior fascicle •Posterior tract'll

Myocardium tnducardiuir

Left bundle branches

Epicardium V\ - Anterior fascicle

/

Right bundle branch

© Young M. Kim 2010

Figure 3. Conduction system of the heart

Systole Djastole Legend:

AV -aortic valve

LA -left atrium

LV — left ventricle

MV-mitral valve

AV closes Aortie

essure

120 -|

AV opens "

* • •

1 LVpressure F.

60 - ;.u LA V

S

-

closes /pressure MV opens

0 -

I X ,.LY

.LV end-diastolic

volume

120

H 80 -

.LV end-systolic

volume 4^

« -i

n

L J

ECG

Heart S.SJS

Sounds -t-

$ .

O D C C 3

+

Time (sec) © Anas Nader 2009

Figure 4. Cardiac cycle

Grey shaded bars indicate isovolumic contraction (left) and isovolumic relaxation (right)

AL GRAWANY

C5Cardiology and Cardiac Surgery Toronto Notes 2023

• cardiovascular innervation

• sympathetic nerves

» innervate the SA node, AV node, ventricular myocardium, and vasculature

increased activity of the SA node via the pi receptor leads to increased HR via more frequent

impulse from pacemaking cells (increased chronotropy - increased HR)

cardiac muscle (pi ) fibres increase contractility (inotropy - leads to increased SV)

stimulation of pi- and p2-receptors in the skeletal and coronary circulation causes

vasodilatation

parasympathetic nerves

innervate the SA node, AV node, and atrial myocardium but few vascular beds

at rest, vagal tone dominates the tonic sympathetic stimulation of the SA node and AV node,

resulting in slow AV' conduction,and consequently a prolonged PR interval or second or third

degree AV block (i.e. reduced dromotropy (if only affecting AV' node conduction))

parasympathetics have very little impact on total peripheral vascular resistance

Differential Diagnoses of Common

Presentations

Note: bold text indicates most common, underlined text indicateslife threatening condition

Chest Pain

• often described as pressure, heaviness, discomfort

note: ischemic pain is usually dull and diffuse while chest wall and pericardial pain are often

sharp,localized, and worse on inspiration (i.e. pleuritic)

• cardiac

• Ml,stable myocardial ischemia (angina), myocarditis, and pericarditis/Dressler’

s syndrome,

tamponade, aortic valve disease

• pulmonary

• PE, pneumothorax/hemothorax, tension pneumothorax, pneumonia, empyema, pulmonary

neoplasm, bronchiectasis, pleuritis, asthma,COPD, pleuritis, sarcoidosis, pulmonary

hypertension, and TB

• gastrointestinal

esophageal: GEKD. esophageal rupture, spasm,esophagitis, ulceration, achalasia, neoplasm, and

Mallory-Weiss syndrome

• otherstructures:PUD, gastritis, pancreatitis, and biliary colic

• mediastinal

• lymphoma, thymoma

• vascular

dissecting aortic aneurysm, aortic rupture

• drug use: methamphetamine or cocaine intoxication

• surface structures

• costochondritis

• rib fracture

• skin (bruising, herpes zoster)

• breast

• anxiety/psychosomatic

• referred pain

• trauma

Loss of Consciousness

1. causes of true syncope (impaired cerebral perfusion )

reflex mediated/rellex dysfunction

vasovagal (most common;also known as reflex mediated syncope, neurocardiogenic syncope)

situational (micturition, cough, carotid hypersensitivity)

autonomic dysfunction (often associated with neurologic diseases)

postural hypotension (e.g. central nervoussystem disorders, antihypertensive drugs)

inadequate circulating volume (bleeding, hypovolemia with orthostasis)

obstruction to blood flow

tamponade

pulmonary embolism

severe pulmonary HTN

severe obstructive valve disease (MS and AS)

left ventricular outflow obstruction (HCM)

cerebrovascular events (e.g. cerebrovascular accident)

arrhythmia leading to sudden loss of CO

tachyarrhythmia, (e.g. Al-ib, SVT, VT, Vl'

ib)

severe bradycardia (sinus arrest, AV block)

r1

»

C6 Cardiology and Cardiac Surgery Toronto Notes 2023

2.loss of consciousness NOT due to impaired cerebral perfusion

• seizure

hypoglycemia

severe hypoxia or hypercarbia

psychiatric

head trauma

Local Edema

• venous or lymphatic obstruction

thrombophlebitis/deep vein thrombosis, venous insufficiency, chronic lymphangitis, lymphatic

tumour infiltration, filariasis

• inflammation/infection

• trauma

Generalized Edema

• increased hydrostatic pressure/fluid overload

HT, pregnancy, drugs (e.g. CCBs), iatrogenic (e.g.IV fluids)

• decreased oncotic pressure/hypoalbuminemia

• liver cirrhosis, nephrotic syndrome, malnutrition

• increased interstitial oncotic pressure

myxedema

• increased capillary permeability

• severe sepsis

• hormonal

hypothyroidism,exogenous steroids, pregnancy, estrogens

Palpitations

• subjective sense of abnormal/irregular heartbeats

• palpitations that may have continuous rapid heart action:

conditions causing sinus tachycardia:endocrine (thyrotoxicosis, pheochromocvtoma, and

hypoglycemia),systemic (anemia, fever),drugs (stimulants and anticholinergics), and psychiatric

(panic attacks, generalized anxiety disorder, and somatization)

• conditions causing pathologic tachycardia:SVT (atrial tachycardia, Al'

ib, and atrial flutter) and

re-entrant SVT, VT

• palpitations that may have irregular/intermittentsensations (e.g. FACs, PVCs)

Dyspnea

• exercise

elevated pulmonary venous pressure

poor Hb-oxygen dissociation curve kinetics

• cardiovascular

due to elevated pulmonary venous pressure: acute Ml, CH17LV failure, aortic/mitral stenosis, AS/

MS, AR/MK,arrhythmia, cardiac tamponade, constrictive pericarditis,and left-sided obstructive

lesions (e.g.left atrial myxoma)

• respiratory

airway disease

asthma,COPD exacerbation, and upper airway obstruction (anaphylaxis,foreign body, and

mucus plugging)

parenchymal lung disease

pneumonia, interstitial lung disease

• pulmonary vascular disease

Pt, pulmonary'HTN, and pulmonary'vasculitis

• pleural disease

pneumothorax, pleural effusion

• neuromuscular and chest wall disorders

cervicalspine injury

polymyositis, myasthenia gravis,Ciuillain-Barre syndrome, and kyphoscoliosis

• anxiety/psychosomatic

• hematological/metabolic

• anemia,acidosis, and hypercapnia

r->

LJ

+

C7 Cardiology and Cardiac Surgery Toronto Notes 2023

Cardiac Diagnostic Tests

Electrocardiography Basics

Description

• a graphical representation (amplitude of electrical vector projection over time) of the heart'

s electrical

activity

• on the ECG graph

• the horizontal axis represents time (at usual paper speed of 25 mm/s)

1 mm (1 smallsquare)

= 40 msec

5 mm (1 large square)

= 200 msec

the vertical axis represents voltage (at usual standard gain setting of 10 mm/mV )

I mm (1 small square)

= 0.1 mV

10 mm (2 large squares)

= 1 mV

standard leads of 12-lead ECG

limb (bipolar) leads: 1, 11, 111, aVL, aVK, aVE

precordial (unipolar) leads: VI-V6 (V1-V2 (septal), V3-V4 (anterior), and V5-V6 (lateral))

additional leads

right-sided leads: V3R-V6R (useful in RV infarction and dextrocardia)

posterior leads: V7-V9 (useful in posterolateral infarction)

leads that indicate specific regions of the heart:

lateral wall

= 1, aVL, V5, V6

inferior wall

= II, 111, aVF

anterior wall= VI-V4

Figure 5. ECG lead placement

Indications for brief (12-lead ECG) or prolonged (24 h or more) monitoring

• myocardial injury,ischemia,or history of prior infarction

• conditions associated with palpitations or risk of serious arrhythmias (e.g. WFVV, long QT, HCM,

heart block, and bradycardia)

• conduction abnormalities (e.g. LBBB/RBBB)

• electrolyte abnormalities (e.g. hyperkalemia/hypokalemia)

• investigation ofsyncope, near syncope, or palpitations (“symptom/rhythm correlation”)

• can be used for:

recording of cardiac rhythm during symptoms or antiarrhythmic drug monitoring

assessment of cardiac structure and function (e.g.RVH/LVH and cardiomyopathy)

detection of non-sustained arrhythmias that require prophylactic intervention

DURATION

(msec)

120-200 1/2 RR

Figure 6. ECG waveforms and normal

values

For more examples and practice visit Approach to ECGs www.ecgmadesimple.com

Introduction

Below, we are presenting both the classical approach and the newer PQRSTU approach to provide

students with different ways to view'the ECG.Despite methodological differences, the rigor and final

result is the same.

Classical Approach to ECG

• Rate

. Rhythm (defined by R-R or P-P

Classical intervals between beats) Approach to ECGs • Axis

• Conduction abnormalities

• Hypcrtrophy/chamber enlargement

Ischemia/infarction

• Miscellaneous ECG changes(e.g.OT

interval)

RATE

• normal = 60-100 bpm

• atrial rates above normal range:

150-250 bpm = paroxysmal tachycardia

• 250-350 bpm atrial flutter

>350 bpm = AFib (note: atrial “rate"

is not discernible)

• regular rhythm (defined by equal R-R or P-P intervals between beats)

rate can be calculated using either of the following two methods:

divide 300 by the number of large squares between 2 QRS complexes (there are 300 large

squares in 1 min:300 x 200 msec

= 60 s)

use the square counting method by counting the number of big boxes between the R waves

using the following sequence of numbers:300 (1 box)-150 (2 boxes)-100 (3 boxes)-75 (4

boxes)

-60 (5 boxes)

-50 (6 boxes)

Differential Diagnosisfor Left Axis

Deviation

• Normal variant (physiologic, often

age-related change)

• Left anterior hemiblock

. LVH

• Inferior Ml

. WPW

• RV pacing

• Elevated diaphragm

• Lead misplacement

• Congenital heart disease (e.g.

prlmum ASD. endocardial cushion

defect)

• Hyperkalemia

• Emphysema

• irregular rhythm

rate = 6 x number of R-R intervals in 10 s (a standard ECG is 10 s)

• atrial escape rhythm in case ofsinus node failure = 60-80 bpm, junctional escape rhythm = 40-60

bpm, ventricular escape rhythm 20-40 bpm +

C8Cardiology and Cardiac Surgery' Toronto Notes 2023

RHYTHM

• regular: R-R interval is the same across the tracing

• irregular: R-R interval varies across the tracing

• regularly irregular: repeating pattern of varying R-R intervals (e.g. atrial flutter with variable block)

• irregularly irregular: R-R intervals vary erratically (e.g. Al:

ib, VI ib)

• normal sinus rhythm (NSR)

• P wave precedes each QRS; QRS follows each P wave

P wave axis is normal ( positive in 2 of the following 3 leads: I, II, aVF)

• rate between 50-100 bpm

Differential Diagnosisfor Right Axis

Deviation

• Normal variant (vertical heart with an

axis of 90°)

. RVH

• Left posterior hemiblock

• Pulmonary embolism

. C0PD

t Lateral Ml

. WPW

• Dextrocardia

• Septal defects

AXIS

• mean axis indicates the direction of the mean vector

• can be determined for any waveform ( P, QRS, T)

the standard EC(i reported QRS axis usually refers to the mean axis of the frontal plane it

indicates the mean direction of ventricular depolarization forces

• QRS axis in the frontal plane

• normal axis:-30° to 90°(i.e. positive QRS in leads I and 11)

• left axis deviation (LAD): axis <-30°

right axis deviation (RAD): axis >90°

• QRS axis in the horizontal plane is not routinely calculated

transition from negative to positive is usually in lead V3

Table1. Conduction Abnormalities

Left Bundle Branch Block (LBBB) Right Bundle Branch Block (RBBB) Figure 7.Axial reference system

Each lead contains a (

*

) area

displayed by the bold arrows.

Impulses traveling toward the positive

region of the lead result in an upward

deflection inthat lead.Normal QRS

axis is between -30° and < 90°

Complete LBBB

ORS duration >120msec

Broad notched R navesIn leads I. aVl.VS, and V6

Deep broad S waves in leads VI-2

Secondary SI

-T changes|

-ve in leads with broad notched R waves.-*ve

in VI-2) are usually present

IBBB can mask ECG signs of Ml

IBBB:lead VI negative. V6 positive and notched

Complete RBBB

ORS duration >120 msec

Positive ORS in lead V1 (rSR' or occasionally broad R wave)

Broad S wavesin leads I. V5-6 ( -40 msec)

Usually secondary I wave inversion in leads V1- 2

Frontal axis determination using only the first GO msec

RBBB:VI is positive (rSR '

l

, V6 has broad S wave

Left Bundle

Branch Block Left Anterior Fascicular Block (LAFB) Left Posterior Fascicular Block (LPFB) Bifascicular Block

(Left Anterior Hemiblock) (Left Posterior Hemiblock)

VI V5

Right Axis Deviation (110°to 180°)

Small 0 and prominent R in leads I and aVl Small R and prominent S in leads I and aVl

Small R and prominent S in leads II.III. and aVF Small 0 and prominent R in leads II.III. and aVF The lirsl 60 msec (1.Ssmall squares) of the ORS

shows the pattern of LAFB or LPFB

Bifascicular block refers to impaired

conduction in two ol the three fascicles, most

commonly a RBBB and left anterior hemiblock:

the appearance on an ECG meets the criteria

for both types of blocks

left Axis Deviation (-30° to -90*| RBBB Pattern

Small 0 and prominent R r*

Right Bundle

Branch Block

Nonspecific VI V5 Intraventricular Block

• QRS duration >120 msec

• absence of definitive criteria for LBBB or RBBB

Table 2. Hypertrophy/Chamber Enlargement

Lett Ventricular Hypertrophy Right Ventricular Hypertrophy

S in Vt * R in V5or V6 >3S mm above age 40. (»40 mm tor age 31-40.

»45 mm for age 21-30)

RinaVL »11 mm

Rini-*Sin III >25 mm

Additional criteria

IV strain pattern (asymmetric SI depression and I wave inversion in

leads I.aVL.and V4- V6)

Left atrial enlargement

N.B.The greater the number of criteria,the more likely the diagnosis

is IVH. II only one voltage criteria present, it is called minimal voltage

criteria lor IVH (may be a normal varianl)

left Atrial Enlargement

Brphasic P wave with the negative terminal component of the P wave in P wave »2.5 mm in height in leads il.Ill, or aVf (“P pulmonale”)

lead V1»1mm wide and »1mm deep

P wave »100 msec, could be notched in lead II ("P mitrale")

Right axis deviation

R /S ratio »1or qR in lead Vt

RV strain pattern:SIsegment depression and I wave inversion in leads

Left Ventricular

Hypertrophy

VI VI V5

-2

Right Vontricular

Hypertrophy Right Atrial Enlargement

r

l

I

I

l

©

+

Figure 8. Complete LBBB.RBBB,

LVH,and RVH (please see online

examples for the full range of

waveforms and the text for additional

characteristics)

C9 Cardiology and Cardiac Surgery Toronto Notes 2023

ISCHEMIA/INFARCTION

• look for the anatomic distribution of the following ECG abnormalities (see Table 3)

• ischemia

• ST segment depression

T wave inversion (most commonly in V1-V6)

injury/infarct

• transmural (involving the epicardium)

- ST elevation in the leads facing the injured/infarcted area

subendocardial

- marked ST depression in the leads facing the affected area

may be accompanied by enzyme changes and other signs of Ml

Left Atrial Enlargement

I

LEAD II

It -y.rRight Atrial Enlargement

LEAD II

"

"

T1

'Vfv VI

JL J

I

Acute

days

(avg.3-5 hours)

ST segment elevation

Recent

weeks-months

T wave inversion

Old

months-ycars

(avg. >6 months)

Persistent Qs

Figure 10. LAE, RAE (please see

online examples and the text for

characteristics)

Figure 9. Typical ECG changes with infarction

Note that 0 waves may gradually appear over time (not shown here)

• ST elevation

new ST elevation in two contiguous leads of >0.1 mV (in all leads other than leads V2-V3)

for leads V2-V3: £0.2 mV in men £40 yr, £0.25 mV in men <40 yr, or £0.15 mV in women

• “typical"sequential changes of evolving Ml

1.hyperacute T waves (tall,symmetric T waves) in the leadsfacing the infarcted area, with or without

ST elevation

2.ST elevation (injury pattern) in the leadsfacing the infarcted area

usually in the first hours post-infarct

in acute posterior MI, there is ST depression in V 1-V3 (reciprocal to ST elevation in the

posterior leads that are not recorded in the standard 12-lead ECG) hence get a 15-lead ECG

3.significant Q waves:>40 msec or >1/3of the total QRS amplitude and present in at least 2

consecutive leads in the same territory (hours to days post-infarct)

Q waves of infarction may appear in the very early stages, with or without ST changes

non-Q wave infarction:there may be only ST or T changes despite clinical evidence of

infarction

4.inverted T waves (one day to weeks after infarction)

• completed infarction

abnormal Q waves (Q waves may be present in lead 111 in normal individuals due to initialseptal

depolarization)

duration >40 msec (>30 msec in aVE for inferior infarction)

Q wave is >1/3of the total QKS amplitude

present in at least 2 consecutive leads in the same territory

abnormal R waves (RIS ratio >1, duration >40 msec) in VI, and occasionally in V2, are found in

posterior infarction (usually in association with signs of inferior and/or lateral infarction)

Table 3. Areas of Infarction/Ischemia (right dominant anatomy)

Vessel Usually Involved Infarct Area (LAD and LCx) Leads (LAD and LCx)

&

LAO AnteroscpUl V1. V2

Anterior

Anterolateral

Extensive anterior

Inferior

Right ventricle

Posterior Ml (associated with inferior Ml)

Lateral

Isolated posterior Ml

Pacemakers

• Atrial pacemaker has discharge

(“spike”) prior to P wave

• Ventricular pacemaker has a

pacemaker spike prior to the 0RS

which is usually broader with a LBB8

morphology

V3. V4

l.aVL, V 3-6

I.aVL, V1-6

RCA II.lll. aVF

V3R . V4R (right-sided chest leads)

VI,V2 (prominent R waves)

I.aVL, V5-6

VI. V2 (prominent R waves)

LCx

MISCELLANEOUS ECG CHANGES

n

Electrolyte Disturbances

• hyperkalemia

mild to moderate (K +5-7 tnmol/L):tall, peaked T waves

severe (K +

>7 mmol/L):progressive changes whereby P waves flatten and disappear, QRS

widens and may show abnormal morphology, axisshiftsleft or right,ST shift with tall T waves,

eventually becomes a “sine wave" pattern

• hypokalemia

ST segment depression, prolonged QT interval (with risk for Torsades de Pointes VT if extreme),

low T waves, prominent U waves (U>T)

enhances the toxic effects of digitalis

LJ

+

CIO Cardiology and Cardiac Surgery' Toronto Notes 2023

• hypercalcemia

• shortened QT interval (more extracellular Ca -'

meansshorter plateau in cardiac action potential)

• hypocalcemia

• prolonged QT interval (less extracellular Ca 2+means longer plateau in cardiac action potential)

T wave 1 I K

-

4A

Figure 11. Hyperkalemia

L- J

I Uwave

U/V

Figure 12. Hypokalemia

Hypothermia

• sinus bradycardia

• when severe, prolonged QRS and QT intervals

• Al;

ib with slow ventricular response and other atrial/ventricular dysrhythmias

• Osborne ) waves: “hump-like” waves at the junction of the|point and the ST segment

Pericarditis

• early: diffuse ST segment elevation ± PR segment depression, upright T waves

• later: isoelectric ST segment, flat or inverted T waves

• ± tachycardia

Drug Effects

• digitalis (cardiac glycoside) poisoning rare in 2021; <1/1000 cardiac patients overall

therapeutic levels may be associated with “digitalis effect"

ST downsloping or “scooping”

T wave depression or inversion

QT shortening ± U waves

slowing of ventricular rate in Al'

ib

most common rhythm disturbance: PVCs

• toxic levels associated with:

arrhythmias:paroxysmal atrial tachycardia (PAT) with conduction block,severe bradycardia

in Al'

ib, accelerated junctional rhythms, PVCs, VT (seeArrhythmias, Cl 9)

“regularization" of ventricular rate in Al'

ib due to complete heart block with junctional

escape rhythm

• amiodarone,quinidine, phenothiazines, mood stabilizing medications (including tricyclic

antidepressants and antipsychotics),some antihistamines, antifungals, and some antibiotics

prolonged QT interval, U waves

Figure 13. Osborne J waves of a

hypothermic patient

Mlm

J

ill: lit::: ::]_ jig« 1 :

Digitalis Side Effects

Palpitations,fatigue, visual changes

(yellow vision),decreased appetite,

hallucinations,confusion,and

depression

Si TtT

Figure 14. AFib, ST change due todigitalis (“digitalis effect”)

Pulmonary Disorders

•cor pulmonale (often secondary to CQPD)

low voltage, right axis deviation (RAD), poor R wave progression in precordial leads

- RAE and RVH with strain

multifocal atrial tachycardia

•massive pulmonary embolism

sinus tachycardia and Al'

ib/atrial flutter are the most common arrhythmias

RAD, RVH with strain

mostspecific sign isS1Q3T3(S in 1, Q and inverted T wave in 111) but rather uncommon

ri

+

Cl1Cardiology and Cardiac Surgery Toronto Notes 2023

Alternative PORSTU Approach to ECGs

Note:the PQRSTU Approach is organized a different way based on the anatomy of the ECG

PORSTU

<D

Approach to ECGs

Pwave

P-R interval

ORS complex

ST segment

T wave

O-T interval

Uwave

ventriu _ ar

repolarization

t

ECG

LEAD II

© Ashley Hui 2015

Figure 15.ECG correlations with heart activity

PWAVE

•the P wave represents atrial contraction, best seen in leads:11 and V1

lead 11:the P wave should be rounded, <120 msec and <2.5 mm in height

• lead V 1: the P wave is biphasic with a positive phase slightly greater than the negative phase

•atrial flutter: “sawtooth” P wave with continuous atrial activity at 300 bpm indicates the interval

(Hints:flip the ECG upside-down and check inferior leads (II, III, and aVP) to see it better)

•APib:absent P wave, may have fibrillatory wave, irregular rhythm

•RAE: tall P w'

ave (>2.5 mm) in II or VI (P pulmonale)

•LAE: biphasic P wave with negative deflection >1 mm deep

notched P wave in II may be present (P mitrale)

or >1 mm wide in VI, wide (>100 msec)

P-R INTERVAL

•the P-R interval indicatesthe interval between sinus node activation and the start of ventricular

depolarization

includes the impulse traveling through the atria, the AV node, and the bundle of His. The

magnitude of the conduction velocity is referred to as “dromotropy" (faster = positive

dromotropy,slowrer = negative dromotropy)

positive dromotropy associated with increased conduction velocity (e.g.sympathetic stimulation),

while negative dromotropy is associated with decreased velocity (e.g. vagal stimulation)

•P-R intervalshould be 120-200 msec

•long P-R interval (>200 msec)

heart block (may be due to disease, delay in the AV node, or delay in distal (His-Purkinje)

conduction system)

first degree: fixed, prolonged P-R interval (though every P wave has a QRS following)

second and third degree AV block:some P waves are NOT followed by a QRS

second degree Mobitz I (Wenckebach):gradual prolongation of the P-R interval precedes a

dropped P wave

second degree Mobitz 11 (Hay):fixed P-R interval with ratio of atrial to dropped ventricular

beats (e.g.for every 3 atrial beats, there is one ventricular beat (3:1))

third degree/complete: constant P-P and R-R intervals but variable P-R intervals

Significant ECG Changes

• Look for ST changesstarting at 60

msec from J point

• J point-the junction between the

ORS complet and theST segment

• ST elevation:at least1mm in 2

adjacent limb leads, or at least 1-2

mm in adjacent precordial leads

• ST depression:downsloping or

horizontal

• 0Wave: pathological if 0wave >1

smallsquare (>40 msec) or >1/3of

the total ORS amplitude

+

C12 Cardiology and Cardiac Surgery Toronto Notes 2023

hypokalemia

• “trifascicular"

block:long PR segment (first degree AV block) and bifascicular block

•short P-R interval (<120 msec)

pre-excitation syndrome (delta wave:upsloping of the first part of the QRS complex) due to

accessory pathways

• low atrial rhythm, P waves inverted in 11, 111, and aVP

QRS COMPLEX

•represents ventricular contraction

•rate: check if R-R interval matches the P-P interval

•amplitude:check for hypertrophy (see Table 2, CS )

• narrow QRS (<120 msec) means that the His-Purkinje system is being used

•wide QRS (>120 msec) means that the His-Purkinje system is being bypassed or is diseased

BBB, VT, ventricular hypertrophy, cardiomyopathy, WPVV, ectopic ventricular beat,

hyperkalemia, or drugs (e.g.tricyclic antidepressants, antiarrhythmics)

•

Q wave: the first downward deflection of the QRS complex

• significant Q wave (>40 msec or >1/3 of total QRS amplitude) indicates myocardial necrosis (new

or old)

•R and S wave abnormalities typically show pathology in terms of BBB or intraventricular

abnormalities

Insignificant 0 Wave

• Septal depolarization by the left

bundle

. Seen in leadsI,II,III,aVL,V5, and V6

. <40 msec

• 0 wave <V3 of the total QRS

amplitude

ST SEGMENT

•located between QRS complex and the beginning off wave

• corresponds to the completion of ventricular depolarization

• normally at the same level as baseline (T'

-P segment)

•ST elevation:see Infarction,C9

•ST depression:ischemia

• ischemia that causes ST depression can result in myocardial damage (NSTEMI)

lateral ST depression (leads 1, aVL, V5, V6) may actually indicate a STEM!in the right heart

ST depression may be nonspecific,or associated with remote MI or ischemia

T WAVE

• repolarization phase of ventricles (repolarization of the atria is obscured by the QRS complex)

•typically positive (except in aVR and V 1) on ECG but normal isolated negative T waves may be present

(especially in VI and V2)

•T wave variation in consecutive leads may indicate pathology

inversion:BBB, ischemia, hypertrophy, drugs (e.g.digitalis), pulmonary embolism (lead HI as

part ofSlQ3T3sign)

• elevation: infarction (STEM!, Prinzmetal, hyperacute), hyperkalemia (wider, peaked)

• flattened: hypokalemia, pericarditis, drugs (e.g. digitalis), pericardial effusion

flat T waves are nonspecific with no clinicalsignificance (common)

variations:T wave alternans;beat-to-beat variations due to PVC overlap (R on T phenomenon

which may precipitate VT or Vl-

'

ih)