Guide in Reading ECG

1. Standardization & technique V1 = 4th ICS at the right sternal border

2. Rhythm V2 = 4th ICS at the left sternal border
3. Rate: atrial & ventricular V3 = Halfway between V2 and V4
4. P wave morphology & duration V4 = 5th ICS at the left midclavicular line
5. P-R interval V5 = 5th ICS at the left anterior axillary
6. QRS complex morphology & duration V6 = 5th ICS at the left mid-axillary line
7. ST segment
8. T-wave V3R = Halfway between V1 & V4R
9. U wave V4R = 5th ICS at the right midclavicular line
10. Q-T interval

Indications for Ordering an ECG

 To determine cardiac rate

 To accurately define cardiac rhythm
 To diagnose old or new myocardial infarction
 To identify conduction disturbances
 To aid in the diagnosis of ischemic heart disease,
pericarditis, myocarditis, electrolyte abnormalities, and
pacemaker malfunction
 To determine the effects of medications specially
antiarrhythmic drugs
3. Turn on the machine.
1. Preparing the patient. Check the stylus (if any)
Make sure the patient is comfortable in lying down position Routine speed at 25 mm/sec.
Expose contact areas adequately but provide privacy 4. Introduce a 1 mV standardization pulse.
Rub each contact area with EKG cream or solution A square wave should consist of 10 small squares
(Do not smudge to adjacent areas.) 5. Record limb leads first then the chest leads.
6. Each lead should contain at least 3 to 5 complexes.
2. Attach the cable and electrodes. 7. All ECG complexes should be within the printed lines.
Limb leads: 8. Use appropriate sensitivity;
Right arm : RA (red) for small complexes use 2 mV &
Left arm : LA (yellow) for tall complexes use 5 mV
Right Foot : ground (black) 8. Label all tracings :
Left foot : L F (green) - patients’ name incl.middle name
- location or ward
- date and time ECG was taken

Normal Electrocardiogram

Normal electrocardiograms recorded from the six standard chest leads.

Normal electrocardiograms recorded from the three standard

electrocardiographic leads

Normal electrocardiograms recorded from the three augmented

unipolar limb leads.
 Determination of Rhythm Determination of Rate

RHYTHM (Sinus? Regular? Irregular?) Formula 1: 300

# big squares between R-R

Formula 2: 1500

# small squares between R-R

Normal rate? Bradycardia? Tachycardia?

 Determination of Axis Using the previous ECG tracing compute for the following:

1. atrial rate
2. ventricular rate
3. PR interval
4. QRS interval
5. QT interval
6. Axis

Chamber Enlargement

Right Atrial Enlargement (RAE)

TALL P WAVE IN LEAD 2,

AND LEAD AVF >=2.5 mm

Determine the axis of the ff:

Left Atrial Enlargement (LAE)

P WAVE IN LEAD 1 >=0.11 sec,

TERMINALLY NEGATIVITY OF
P WAVE IN LEAD 6 >=1 mm2

Left Ventricular Hypertrophy (LVH)

HIGH VOLTAGE IN LIMB LEADS (LEAD 1-3, aVF, aVL, aVR):

(R + S3 > 25mm)
OR PRECORDIAL LEADS: (S V6 + R V5, or S V1 + R V6, >=35 mm)
Often LAE, ST-T abnormalities
Right Ventricular Hypertrophy (RVH)

Sokolow-Lyon Criteria: Additional Criteria:

R in V1 + S in V5-V6 > 11 mm QR in V1
R in V1 > 7mm S1 Q3 pattern
R: S in V1 > 1 S1 S2 S3 pattern
RAD > +90 degrees p pulmonale

Identify chamber enlargements and hypertrophies.

 Positive caloric balance Genetic predisposition Sedentary Lifestyle

Adiposity & adiposopathy

OBESITY

Lipid deposition in liver & muscle

Increase adiponectin &
increase local TNF

NO RAAS INSULIN RESISTANCE Inflammation Oxidative Stress

Hyperinsulinism

DIRECT EFFECTS Inadeqaute

 Hyperuricemia B-cell compensation
HYPERTENSION  Acanthosis nigricans (B-cell lipotoxicity)
 Hyperandrogenism
 Polycystic ovary
syndrome

HYPERGLYCEMIA DYSLIPIDEMIA
 Impaired glucose tolerance  Hypertriglyceridemia
 Impaired fasting glucose  Low HDL
 Dense LDL  Dense LDL

Oxidative stress
Protein kinase C-activation SMOKING
Receptor for advanced glycation end
product (RAGE) activation

IL-6, TNF, IL-18

C-reactive protein
Endothelial Dysfunction

VASCULAR
INFLAMMATION
NO NO NO
Leakage of plasma
Endothelin NF-KB activation Tissue factor
component across
Angiotension II Angiotensin II Plasminogen activator Inhibitor-I
vessel walls
Activation of activator protein 1 Prostacyclin

MCP-1, VCAM-1,
ICAM-1

VASOCONSTRICTION INFLAMMATION THROMBOSIS

HYPERTROPHY OF  HPN  Release of chemokines & cytokines  Hypercoagulation

MEDIA  Vascular smooth  Expression of cellular adhesion  Platelet activation
Smooth Muscle muscle cell growth molecules  Decrease fibrinolysis
Extracellular matrix

Hyaline arteriosclerosis
ATHEROSCLEROSIS
HEART FAILURE Systolic Heart Failure or Dysfunction
TYPICAL PRESENTATION
• A complex of clinical syndrome that can result from any structural • History
or functional cardiac disorders that impairs the ability of the – breathlessness
ventricle to fill with or eject blood. – -fluid retention
– -fatigue
Spectrum of heart failure
•Physical examination
– congested lungs-gallop rhythm
– distended neck veins
– fluid retention or edema

•Chest x-ray
– enlarged heart, congested lungs

•Echocardiogram
– dilated LV, low EF

Diastolic Heart Failure or Dysfunction

TYPICAL PRESENTATION

•History & PE
– history of breathlessness & fatigue
– clear lungs
– no venous distention
– no edema

•Chest x-ray -small heart

– no lung congestion

•Echocardiogram
– non or slightly dilated LV
– normal or slightly decreased LVEF
– impaired LV relaxation

Differential Diagnosis of Systolic Heart Failure and Diastolic Heart

Failure

Systolic Heart Failure Diastolic Heart Failure

- Large, dilated heart - Small LV cavity, concentric

- Normal or low blood pressure
- Broad age group; more common
common in men
- Low ejection fraction (< 40%)
ejection fraction (> 40%)
- S3 gallop
- Systolic & diastolic impairment
- LV hypertrophy
- Systemic hypertension
- Elderly women more
- Normal or increased
- S4 gallop
- Systolic & diastolic
impairment by echo by
various echo measurements

- Treatment well-established - Treatment not well-

established
Classification of Heart Failure In Adults - Poor prognosis - Prognosis not as poor
•Acute heart failure
•Chronic heart failure
PATHOPHYSIOLOGY OF HEART FAILURE
•Systolic heart failure
•Diastolic heart failure
Compensatory Mechanisms

Acute heart failure in adults usually presents as: • Sympathetic nervous system stimulation
• Renin-angiotensin system activation
• Acute cardiogenicpulmonary edema • Myocardial hypertrophy
• Cardiogenicshock • Altered cardiac Rhythm
• Acute decompensationof chronic heart failure
Pathophysiology

 Systolic LV Dysfunction/Failure • In order to maintain normal cardiac output, several compensatory

- reflects a decrease in normal emptying capacity shown mechanisms play a role as under: Compensatory enlargement in
usually with an ejection fraction (EF) of 45% or less the form of cardiac hypertrophy, cardiac dilatation, or both.

 Isolated Diastolic Ventricular Dysfunction/Failure • Tachycardia (i.e. increased heart rate) due to activation of
- is present when the filling of one or both ventricles is neurohumoral system e.g. release of norepinephrine and atrial
impaired while the emptying capacity is normal. natroureticpeptide, activation of renin-angiotensin aldosterone
mechanism.
 STARLING’S LAW
Within limits, the force of ventricular contraction is a function
of the end-diastolic length of the cardiac muscle, which in turn
is closely related to the ventricular end-diastolic volume.

 This is achieved by increasing the length of sarcomeres in dilated

heart

 Increases the myocardial contractility and thereby attempts to

maintain stroke volume.

 COMPENSATION in the form of stretching of myocardial fibers

results
 Stretching leads to cardiac dilatation which occurs when the left
ventricle fails to eject its normal end diastolic volume