1. The document discusses various abnormalities that can be seen on preoperative electrocardiograms (EKGs), including chamber hypertrophies, conduction defects, arrhythmias, and signs of ischemia/infarction. 2. Chamber hypertrophies covered include left and right atrial and ventricular hypertrophies, each with characteristic EKG patterns. 3. Conduction defects discussed are right and left bundle branch blocks, along with their typical EKG presentations and common causes.

1. D R S Y E D S H A H E E R
F C P S
F E L L O W C A R D I O T H O R A C I C A N E S T H E S I A
I S L A M A B A D
PREOPERATIVE EKG

2. CHAMBER HYPERTROPHY
1. Left atrial Hypertrophy (P-Mitrale)
• Bifid p waves in I, II, avl and avF
• Biphasic p wave in v1
• Mitral stenosis, regurgitation, hypertension,
hypertrophic cardiomyopathy
2. Right atrial enlargement (P-Pulmonale)
• Tall p waves >2mm in II and v1
• Pulmonic stenosis, raised PAP, hypetrophic
cardiomyopathy

4. CHAMBER HYPERTROPHY
3. Left Ventricular Hypertrophy (LVH)
• HTN, AVD, MR, Hypertrophic cardiomyopathy, coarctation
of aorta, myocardial fibrosis
• Cornell criteria (specificity 95%)
Men: S(v3) + R(avL) >28mm
Women: S(v3) + R(avL) >20mm
• Old index
R waves in v5 v6 > 26mm
S waves in v1 v2 >25mm
Sum of R + S > 35mm
• LV Straining: if ST depression and T inversion in lateral chest
leads (secondary ST-T changes)

6. CHAMBER HYPERTROPHY
4. Right Ventricular Hypertrophy (RVH)
• HTN, PHTN, COPD, Transposition, PVS, ASD,
VSD, TR
• Must be pronounced before come to EKG
expression
• Sum of R(v1) + S(v6) >10mm
• Secondary ST-T changes in v1v2 v3
• Mandatory right axis deviation and p-pulmonale is
very common

8. CONDUCTION DEFECTS
5. Right bundle branch block(RBBB)
• QRS > 120ms with M or rSR pattern in v1v2 and
broad S waves in v5 v6 >40ms
• where “r” comes from LV and R comes RV
• Fibrosis, TOF, IHD from LAD, Acute cor pulmonale,
COPD, Previous cardiac surgery, sometimes PCI,
HOCM, Aberrancy, atheletes
• Asymptomatic- no significance
• Dyspnea- suspected pulmonary embolism
• Chest pain- Suspect occlusion of LAD

10. CONDUCTION DEFECTS
6. Left bundle branch block(LBBB)
• Left sided impulses transmitted from right sided branches either
partially or completely
• No Q waves in v5v6
• QRS > 120ms, Broad S waves v1v2, Broad and notched R waves in
v5v6
• Secondary ST-T depressions in v5v6 and elevations in v1v2
• Causes include HTN, LVH, AVD, Myocarditis, IHD, HF,
Cardiomypathies.
• LBBB complicates EKG diagnosis of AMI
a. May imitate acute STEMI- common reason of false
catheterization
b. May conceal ischemia due to disturbance of repolarisation
which usually prevents ST-T changes of ischemia
c. May be caused by ischemia- LBBB mask significant ST-T
changes

11. CONDUCTION DEFECTS
6. Left bundle branch block(LBBB) contd….
• ACC recommends: Patients with clinical suspicion of
ongoing myocardial ischemia and LBBB should be managed
in a similar way to acute STEMI
• Sgarbossa criteria for acute ischemia with LBBB
(specificity 98%)
a. ST elevation >1mm in any (v4v5v6 avL I) – 5points
b. St depression >1mm in any (v1v2v3) – 3 points
c. St elevation >5mm in any (v1v2v3) – 2 points
Cut of points is 3 with high specificity
• Remembrance: Incomplete LBBB with QRS<120ms may
tend to progress to complete bundle branch block.

14. ARRHYTHMIAS
7. Atrial Extrasystoles (PAC)
• Virtually harmless but can proceed to sustained SVTs like A-
fib, AVNRT and AVRT.
• P waves morphology depends on ectopic focus in atria but
PR interval remains static due to regular AV conduction.
• Resetting of SA node so usually no compensatory pause
(Hallmark)
• With sinus tachycardia- may resemble False A-Fib (always
look for p waves)
• Causes include: stress, coffee, smoking, straining of atria.
• Treatment only in feeling excessive palpitations or
tachyarrythmias with Bisoprolol 5-10mg or Ca Channel
blockers.

16. ARRHYTHMIAS
8. Ventricular Extrasystoles (PVCs)
• QRS complex >120ms with compensatory pause
(Hallmark) so increased ventricular filling time
• If 3-30 PVCs occur consecutively, it is called non-
sustanined VT and if 30 or more, it is sustained VT.
• Same morphology- same focus (monomorphic)
• Changing morphology- Polymorphic
• Positive PVCs in v1 – Focus is in left ventricle
• Negative PVCs in v1- Focus is in right ventricle
• Causes include: Males, stress, hypokalemia, infection,
alcohol, sleep deprivation, increasing age, Ischemic
myocardium

18. ARRHYTHMIAS
• For Healthy: If >15% of all beats are PVCs – risk of PVC
induced cardiomyopathy and LV dysfunction – needs ablation
therapy
• For IHD: Treat if
a. Symptomatic – Palpitations
b. > 10 PVCs per minute
c. Negative hemodynamic effects
Rule out: Hypokalemia & Hypomagnesemia
Treat: B Blocker (DOC) Bisoprolol 5-mg OD or metoprolol
50-100mg OD  Amiodarone  Ablation
Remembrance: Watch PVC distance from T wave (R on T
phenomenon)

19. ARRHYTHMIAS
9. Atrial Fibrillation (A-Fib)
• Most common pathological tacharrhythmia
• Risk: Male, HTN, LVH, LVD, any valve disease (Mitral
common), Coronary artery disease, CHF, DM, Obesity,
Smoking, OSAS, COPD.
• Low recurrences: Thyrotoxicosis, alcohol overdosage,
AMI, Pericarditis/Myocarditis, Pulmo embolism
• 5 times risk of stroke and 2 times risk of mortality
specially if LA appendage has a clot
• Long periods of tachy and desynchronised atrial/vent
activity– more adverse effects
• Early anticoagulants reduce risk of stroke by 70%

20. ARRHYTHMIAS
9. A-Fib Contd….
• Absence of p waves and irregularly irregular rhythm (Hallmark),
between QRS complexes are f-waves (300-600/minute). Vent rate
>100/min
• When indoubt apply unilat carotid massage
• Ashmann phenomena frequently associated(abberant vent
conduction in which BBB occurs as result of change in cardiac cycle)
• Types: a. New/Lone A-Fib
b. Paroxysmal-lasts <48hrs
c. Persistent- >7days
d. Long standing - >12months
e. Permanent – Cant be reverted
• Trigger and Driver mechanism—Transition betwn atria and
pulmonary veins is most common trigger and variable excitible
myocytes are common drivers.

22. ARRHYTHMIAS
9. A-Fib Contd….
• Treat: For Acute A-Fib
a. 60% revert spontaneously <16hrs
b. Cardioversion should be performed within 48hrs (>90%
success rate with >200J Biphasic)
c. Chemical cardioversion: Amiodarone, Flecainide, Ibutilide
d. If hemodynamic compromise suspected- electric
cardioversion preferred
• Long Term Treatment:
a. Control Vent rate(Mortality benefit <100/min)
B-Blocker, Ca-Blocker, Digoxin
b. Rhythm Control
Amiodarone, Flecainide, sotalol
c. Ablation therapy

23. ARRHYTHMIAS
• Recent meta-analysis Euro heart journal 2016:
Paroxysmal A fib has lower risk of stroke than persistent
one.
• CHAD scoring for anticoagulation
C= H/O CHF
H= HTN
A= Age >75
D= DM
S= Previous stroke or TIA
Score >3  Significant

24. ISCHEMIA/INFARCTION
Classification of MI by AHA, ACC & ESC:
Type-1:Spontaneous MI
Due to: Plaque rupture, thrombosis, disection
Type-2: MI secondary to ischemic imbalance
Due to: Anemia, Hypo/Hypertension, embolism,
tachy/brady arrhythmias, Resp failure
Type-3: MI resulting in sudden cardiac death
Type-4a: MI secondary to PCI
Type-4b: MI secondary to stent thrombosis
Type-5: Perioperative MI
Due to: CABG

25. NSTEMI
• Subendocardial ischemia, ST depressions, T wave
inversions, elevated troponins and in majority of cases
leads to non Q wave infarction.
• Current guidelines (Nov, 2017 on ESC):
New horizontal or downsloping ST segments
>0.5mm in atleast two anatomically contiguous leads.
• Other causes(frequent)of ST depressions:
Digoxin, Sympathetic stimulation, Hypokalemia,
SVT, Heart failure

27. STEMI
• Transmural ischemia, ST elevations, elevated troponins and
in majority of cases leads to Q wave infarction
• Current guidelines (Nov, 2017 on ESC):
New ST elevations in atleast two anatomically
contiguous leads
Men >40yrs: >2mm in v2v3 & >1mm in all other leads
Men <40yrs: >2.5mm inv2v3 & >1mm in all other leads
Women (any age): >1.5mm in v2v3 & >1mm in all other
leads

29. STEMI
Two areas are normally missed on 12 leads:
a. Posterolateral wall of LV
b. Right Ventrical infarction (v4R and v5R is advised)

31. THANK YOU