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PAT with
3:1 block
Multifocal Atrial Tachycardia
(MAT)
Irregular rhythm
≥3 different P wave morphologies
Rate >100/min (if rate
<100/min=Wandering pacemaker)
Ventricular Tachycardia
(VT)
•Irregular rhythm
•Not seen P wave (fibrillate baseline)
•Atrial rate ~350-500/min
•Ventricular rate variable
Ventricular Fibrillation
Multipleventricular foci rapidly discharge
producing a totally erratic ventricular
rhythm without identifiable waves
Bradyarrhythmia
Sinus bradycardia
Sinus rhythm
Rate<60/min
Sinus Arrest
and SA Exit Blo
ck
Tachy-brady syndrome
Escape Rhythms
Escape beats= rescuing beats
originating outside the sinus node
AV Node (junctional rhythm): 40 to 60
beats/minute
Ventricles: 30 to 40 beats/minute
Junctional rhythm
Junctional rhythm
Rate 40-60/min
Most often not seen P wave (Occasional
retrograde P wave)
Narrow QRS complex
Idioventricular rhythm
Rate30-40 /min
Wide QRS complex
Accelerated Idioventricular
rhythm
Rate50-100/min
Regular wide QRS complex
AV Block
First
degree AV block
Second degree AV block
Type I (Wenchkebach)
Type II
2:1 second degree AV block
Advanced second degree AV block
Third degree AV block
1 DEGREE AV BLOCK
st
≥ 3:1 AV block
Constant PR interval
Third degree AV block
3º degree AV block
(AV dissociation)
Normal conduction
The Electrical Conduction System
Normal Bundle Branch
Conduction
Ventricular depolarization
V1 V6
Right Bundle Branch Block (RBBB)
Right Bundle Branch Block
(RBBB)
Lead V1 QS or rS
Lead I, V6 Monophasic R wave, no Q
RBBB, LBBB, IVCD
Secondary ST-T change
Left Anterior Fascicular
Block
LAFB
1. Left axis deviation (usually>-60º)
2. Small Q in leads I & aVL, small R
in II, III, aVF
3. Usually normal QRS duration
Left Posterior Fascicular
Block
LPFB
1. Right axis deviation (usually> +120º)
2. Small R in leads I & aVL, small Q in II,
III, aVF
3. Usually normal QRS duration
Axis change in fascicular
block
Abnormal morphology
Abnormal P wave
LAE (P mitrale)
RAE (P pulmonale)
Abnormal P wave Axis
Abnormal P wave axis
Non-sinus P wave
Arm lead reversal
Dextrocardia
Abnormal P wave axis
LAE RAE
PR interval
Short PR interval
Prolongation of PR interval (AV block)
Preexcitation syndrome
In the preexcitation
syndrome, there are
accessory
pathways by which
the current can
bypass the AV node
and arrive at the
ventricles ahead of
time
Acces
sory
Pathw
WPW pattern
•Short PR interval
•Wide QRS complex with delta wave
•WPW syndrome= history of PSVT +
WPW pattern ECG
AF with WPW
Abnormal QRS complex
Abnormal Q wave
Abnormal R wave
Abnormal S wave
Normal ECG
Abnormal Q wave
Significant Q wave is 1 mm wide (0.04
sec in duration) or Q wave ≥1/3 of the
QRS complex
Exclude lead aVR
Significant Q wave = Infarction
Leads that may normally
display moderate to large-si
zed Q waves
Lead III
Lead aVF
Lead aVL
Lead V1 (and sometimes also lead V2)
Lead aVR
Tall R in V1
Posterior wall MI
Pre excitation
Dextrocardia
Duchene Muscular Dystrophy
Right Bundle Branch Block
Right Ventricular Hypertrophy
Rotation of heart
Normal ECG
RVH
Dextrocardia
1. Ischemia
2. “Strain”
3. Digitalis effect
4. Hypokalemia /
Hypomagnesemia
5. Rate-related changes
6. Any combination of the above
Various type of
ST segment depression
ST elevation
Acute myocardial injury
Myocardial aneurysm
Pericarditis
Early repolarization pattern
Myocarditis
Repolarization abnormality
chanellopathy : Brugada syndrome
electrolyte abnormality
drugs
Severe chest pain in a 45 yo
man
Acute IWMI with
ST depression V1-V3
Myocardial injury
Early repolarization
LBBB with STT changes
Acute pericarditis
Evolution of acute
pericarditis
ST segment elevations
Concave=pericarditis Convex=MI
Brugada pattern
T wave morphology
Inverted T abnormality
Cardiac ischemia /injury
Cardiomyopathy
Brain pathology
Repolarization abnormality
secondary repolarization
chanellopathy : LQTS
electrolyte abnormality
drugs
Leads that may normally
display
T wave inversion
Lead III
Lead aVF
Lead aVL
Lead V1 (and sometimes also lead V2)
Lead aVR
Causes of nonspecific ST-T
changes
Ischemia Hyperventilation
LVH Severe medical illness
Cardiomyopathy Severe emotional stress
Mitral valve prolapse Exercise
Drug effect (digitalis, Hypoxemia
antiarrhythmic agents) Acidosis
Electrolyte disorder Temporature extremes
(i.e.,hypokalemia, (hypothermia,hyperthermi
hypomagnesemia) a)
CNS disorder (stroke, Many others...
intracerebral bleed,etc.)
Hyperkalemia
Tall peak T: HyperK
Hyper K
Hyper K: Tall T, wide QRS,
bradycardia
QT prolongation
Common causes of QT
prolongation
1. Drugs
○ Type I A & Type III antiarrhythmic agents
○ Tricyclic antidepressants
○ Phenothiazines
2. “Lytes”
○ Hypokalemia
○ Hypomagnesemia
○ Hypocalcemia
3. CNS
○ Stroke
○ Intracerebral or brainstem bleeding
○ Seizure
○ Coma
Hypokalemia
ECG in ischemic heart
disease
Q wave= infarction
ST elevation= acute injury (transmural)
ST depression= acute injury
(subendocardial)
Inverted T wave =Ischemia
Heroin
Methadone
Perphenazine
Disease
Corticosteroids
Drugs displacing thyroxine binding sites
- Salicylate
- Diphenylhydantoin
- Furosemide
Disease
Cushing’s syndrome
Severe (Cirrhotic) liver diseases
Active acromegaly
Nephrotic syndrome
Protein-losing enteropathies
Genetic
TSH
Aminotransfera
Most types of liver disease
: ALT>AST activity
AST come from non hepatic tissue
: heart ,skeletal tissue and red blood cell
ALT is low concentrations in tissue other than
liver
Specific for hepatocellular injury
Non hepatic conditions etc myopathic disease1-2 and
kidney
1
Scola RH, et al. Arg Neurosiquiatr 20
2
Lin YC, et al. Taiwan Erch Ko I Hsueh Hut Tsa Chili 19
Test Normal Mild Moderate Marked
Body mass 40-50% higher with high BMI 40-50% higher with high BMI
index (BMI)
Meals No effect No effect
Exercise 3-fold increase with strenuous exercise 20% lower in those who exercise at
usual levels than in those who do not
exercise or exercise more strenuously
than usual
Specimen Stable at room temp for 3 d, in refrigerator for Stable at room temp for 3 d, in
storage 3 wks (<10% decrease); stable for years refrigerator for 3 wks (10-15%
frozen (10-15% decrease) decrease). Marked decrease with
freezing/thawing
Hemolysis, Significant increase Moderate increase
hemolytic
anemia
Muscle injury Significant increase Moderate increase
Viral 10-40
Hepatitis
X- times, URL - upper reference limit
Alcoholic 2-8
2. Predominant AST elevation
Alcoholic liver disease
Extrahepatic source of AST:
Hemolysis
Skeletal muscle disease
Cardiac muscle
Cirrhosis
AST > ALT activity
Alcohol induces release of mitochondrial AST
from cells without visible cell damage 1
Pyridoxine deficiency decreases hepatic ALT
activity 2
1
Zhov S-L, et al. Hepatology 19
2
Luding S, et al. Gastroenterlogy 19
3. Rate of aminotransferase declination
Rapid declination of aminotransferase
Ischemic hepatic injury
Drug induced hepatitis : short half life drug
Acute biliary tract obstruction
Fulminant hepatitis
Slow declination of aminotransferase
Acute viral hepatitis
Drug induced hepatitis : long half life drug
Autoimmune disease,Metabolic disease
The patients had a rapid striking elevation of AST and LDH, with rapid resolutio
10000
8000 AST
LDH
U/L 6000
4000
2000
0
1 2 3 4 5 6 7 8 9 10 Days
Biopsy
Test of the capacity of the liver to
transport organic anions and
metabolize
Albumin drugs
• Bilirubin Aminotransferases
Blood-clothing • Alkaline
factors
phosphatas
e
• GGT
Heme
Oxygenase
Hem Biliverdin
e IXα
Biliverdin
reductase
NADPH
5
(relative to 25-35 yrs, Males)
Upper reference limit
Female
3 Male
0
0 10 20 Age 40 60
80
Age and Gender effects on URL for ALP:
The URL for 25-35 year old male is set at 1.0.ALP is many fold higher in
children and adolescents,reaching adult activities by about age 25.
Factor Change Comments
Day to day 5-10% Similar in liver disease and
health, and in elderly and young
*
Hedworth-Whitty RB,et al,Brit Heart J,196
Mild elevation ALP
History and PE
Repeat to confirm Hepatic image
ERCP
GGT normal ↑GGT Specific disease
bone continue work up accordingly
Drug or alcohol
repeat 2-8 wks Parenchymal disease
after withdrawal
Infiltrative lesion
• TBc, fungal, other granulomatous, malignancy
• PBC
Liver mass (s)
Partial biliary tract obstruction (Stone, PSC)
Drugs – Anti - convulsants, Warfarin