Fig. 10C.2: Arteriovenous fistula (AV) created for dialysis.

D: Hypothyroidism

History Lethargy, somnolence, weight gain, goiter, cold intolerance, and

hoarse voice

Family history

Drug history

Vitals Bradycardia, nonpitting edema, diastolic hypertension, and

thyromegaly

Pallor

Anemia

Anthropometry Obesity

Skin Myxedema (Fig. 10D.1) (non pitting edema of the skin of hands,

feet, and eyelids), dry flaky skin and hair, alopecia, vitiligo,

purplish lips and malar flush, carotenemia, erythema ab igne,

xanthelasmas, and madarosis (thinning of lateral one-third of

eyebrows)

Cardiovascular Angina, bradycardia, hypertension (diastolic), cardiac failure,

pericardial effusion, dyslipidemia and hyperhomocysteinemia

Respiratory Pleural effusion and OSA

Neurological Aches and pains, muscle stiffness, delayed relaxation of tendon

reflexes (Woltman’s sign), carpal tunnel syndrome, depression,

psychosis, cerebellar ataxia, deafness, myotonia, proximal

myopathy, pseudohypertrophy of muscles, and Hashimoto

encephalopathy

Gastrointestinal Reduced appetite, constipation, ileus, ascites, and macroglossia

Musculoskeletal Carpal tunnel syndrome

Others Menorrhagia, infertility, galactorrhea (hyperprolactinemia),

impotence and hyponatremia

Complete

diagnosis

Primary hypothyroidism possibly secondary to Hashimoto’s

disease with bilateral carpal tunnel syndrome and infertility

Investigations TSH, free thyroxine (FT4), thyroid peroxidase (TPO) antibodies,

FBS, lipid profile, CBC with smear, and ECG

Treatment plan Thyroxine supplementation

Monitoring with TSH

Referral Endocrinology

Fig. 10D.1: Non pitting pedal edema-myxedema.

E: Hyperthyroidism

History Weight loss, heat intolerance, fatigue, gynecomastia, apathy, and

thirst

Vitals Tachycardia, irregularly irregular pulse [atrial fibrillation (AF)], and

hypertension

Anemia

Thyroid: Diffuse or nodular enlargement, warmth and bruit (due to

increased vascularity)

Anthropometry Low BMI

Skin Soft, warm, and moist. Increased sweating, pruritus, palmar

erythema, spider nevi, onycholysis, pretibial myxedema (Graves’),

pigmentation, alopecia, and clubbing (thyroid acropachy)

Cardiovascular Exertional dyspnea, palpitations, angina, sinus tachycardia, atrial

fibrillation, wide pulse pressure, cardiac failure, cardiomyopathy,

and “scratchy” midsystolic murmur (Means–Lerman scratch)

Neurological Nervousness, irritability, psychosis, emotional lability, and fine

tremors

Inability to concentrate, hyperreflexia, proximal myopathy, bulbar

myopathy, ill-sustained clonus

Gastrointestinal Increased appetite, vomiting, diarrhea, and steatorrhea

Others Menstrual disturbances (amenorrhea or oligomenorrhea),

repeated abortions, infertility, loss of libido, and impotence.

Eye signs (Figs. 10E.1A to D): Lid lag, exophthalmos, proptosis,

extraocular diplopia, exposure keratitis, and lagophthalmos

(classically seen in Graves’ disease)

Complete

diagnosis

Primary hyperthyroidism due to Graves’ disease with thyroid

ophthalmopathy and atrial fibrillation

Investigations TSH, FT4, FT3, TSH receptor antibody, radioactive iodine (RAI)

scan, USG neck, ECG, and CBC

Treatment plan Antithyroid drugs

Surgery/radioactive iodine ablation ablation

Follow-up

Referral Endocrinology, nuclear medicine, ophthalmology, and surgery

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Figs. 10E.1A to D: (A and B) Exophthalmos (front and side view);

(C) Infiltration of extraocular muscles in hyperthyroidism; (D) Eye

signs and enlarged nodular goiter (arrow).

F: Cushing’s Syndrome (Fig. 10F.1)

History Onset

Duration

Any complications—cardiovascular system (CVS) and

respiratory system (RS)

Other coexistent diseases

• Treatment history—chronic steroid use with indication

Vitals Hypertension

Pedal edema

Anthropometry BMI—truncal obesity

Skin

(Figs. 10F.2A to

D)

Moon face, buffalo hump, plethora, and purple striae.

Easy bruisability, and ecchymosis.

Thinning of hair, skin infections, and acne

Cardiovascular Hypertension, coronary artery disease, and heart failure

Respiratory Infections—pneumonia and tuberculosis

Neurological Proximal myopathy, emotional lability, nervousness, irritability, and

psychosis

Gastrointestinal Pain abdomen and peptic ulcer disease

Musculoskeletal Backache, osteoporosis, and fractures

Others Females: Hirsutism, acne, and menstrual disturbances

Male: Gynecomastia, impotence, and loss of libido

Complete

diagnosis

For example, Cushing’s syndrome probably due to glucocorticoid

therapy

Investigations Serum electrolytes (hypokalemia and hypochloremia), glucose

tolerance test (GTT), CT/MRI abdomen (adrenal lesion) and brain

(pituitary tumor), serum cortisol and adrenocorticotropic hormone

(ACTH), low dose/high dose dexamethasone suppression test,

and 24-hour urinary free cortisol excretion

Treatment plan Adrenal adenoma/carcinoma—surgical resection

Ectopic ACTH—treatment of primary and medical/chemical

adrenalectomy

Management of complications

Referral Endocrinology and surgery

Fig. 10F.1: Clinical features of Cushing’s syndrome.

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Figs. 10F.2A to D: Features of Cushing’s syndrome. (A) Cushing’s

habitus, obesity and moon facies; (B) Buffalo hump; (C and D)

Pigmented striae.

G: Acromegaly (Figs. 10G.1 to 3)

History Onset

Duration

Any complications—CVS and RS

Other coexistent diseases

• Husky voice to be noted

Vitals Hypertension

Anthropometry BMI

Gigantism

Skin Thick skin with hypertrichosis and exaggerated nasolabial fold

Hyperhidrosis, skin tags, and acanthosis nigricans

Cardiovascular Hypertension, cardiomegaly, cardiomyopathy, and congestive

cardiac failure (CCF)

Respiratory OSA

Neurological Proximal myopathy, bitemporal hemianopia, blindness (optic

atrophy), headache, and cranial nerve palsy

Gastrointestinal Organomegaly

Musculoskeletal Prognathism, carpal tunnel syndrome, osteoporosis,

kyphoscoliosis, dental malocclusion, and frontal bossing

Others Macroglossia, spade-shaped hand, and increased heel pad

thickness

Females: Mild hirsutism, menstrual disturbances, and

galactorrhea

Male: Impotence and loss of libido

Complete

diagnosis

Acromegaly due to pituitary tumor with impaired glucose tolerance

(IGT)

Investigations

(Figs. 10G.3A to

C)

Basal fasting growth hormone (GH) levels, insulin-like growth

factor-1 (IGF-1) level, X-ray (skull, hand, and feet), GTT, MRI

brain (pituitary tumor), and visual field examination

Treatment plan Medical: Octreotide, pegvisomant, and bromocriptine

Transsphenoidal surgical removal of pituitary adenoma

Management of complications

Referral Endocrinology, neurosurgery, and ophthalmology

Fig. 10G.1: Summary of various clinical features of acromegaly

(diagrammatic).

Figs. 10G.2A and B: Acromegalic facies and thick and spadeshaped hands.

Figs. 10G.3A to C: X-ray findings in acromegaly. (A) Lateral X-ray

skull showing sellar enlargement, thickening of the calvarium,

enlargement of the frontal and maxillary sinuses, and enlargement of

the jaw; (B) X-ray ankle shows increased thickness of the heel pad in

acromegaly; (C) X-ray of hand showing increased soft tissue bulk and

“arrowhead” tufting of the distal phalanges.

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Simplified Approach to ECG

(Reading and Diagnosis)

C H A P T E R

11

CONDUCTION SYSTEM OF THE HEART (FIG. 11.1)

The rate and rhythm of the heart are controlled by the sinoatrial node (SA node) situated at the junction

of superior vena cava and right atrium.

The impulse from the SA node spreads through the atrial musculature and down to the atrioventricular

(AV) node that is situated above the tricuspid valve.

Passage through the AV node is relatively slow, accounting for the normal physiological delay in

ventricular depolarization.

The impulse then travels downward to the bundle of His and through its branches (right bundle branch

and left bundle branch) to the Purkinje network of fibers that convey the impulse to the ventricular

endocardium and then epicardium.

The SA node is the normal pacemaker of the heart as it has the fastest inherent discharge rate.

However, potential pacemaking properties also exist in the cells of the AV node, bundle of His, and

Purkinje fibers.

Sinoatrial node—dominant pacemaker with an intrinsic rate of 60–100 beats/minute.

Atrioventricular node—back-up pacemaker with an intrinsic rate of 40–60 beats/minute.

Ventricular cells—back-up pacemaker with an intrinsic rate of 20–45 bpm.

ECG WAVEFORMS AND INTERVALS

The electrocardiogram (ECG) ordinarily is recorded on special graph paper that is divided into 1-mm2

grid-like boxes. Since the ECG paper speed is generally 2 mm/s, the smallest (1 mm) horizontal

divisons correspond to 0.04 (40 ms), with heavier lines at intervals of 0.20 s (200 ms). Vertically, the

ECG graph measures the amplitude of a specific wave or deflection (1 mV = 10 mm with standard

calibration; the voltage criteria for hypertrophy are given in millimeters) (Fig. 11.2).

Fig. 11.1: Conduction system of the heart.

Fig. 11.2: ECG grid and standardization.

The ECG waveforms are labeled alphabetically (Fig. 11.3), beginning with the P wave, which

represents atrial depolarization. The QRS complex represents ventricular depolarization, and the ST-T-U

complex (ST segment, T wave, and U wave) represents ventricular repolarization. The J point is the

junction between the end of the QRS complex and the beginning of the ST segment. Atrial repolarization

is usually too low in amplitude to be detected, but it may become apparent in conditions such as acute

pericarditis and atrial infarction.

There are four major ECG intervals; R-R, PR, QRS, and QT. The heart rate (beats per minute) can

be computed readily from the inter beat [R-number of small (0.04 s) units into 1,500]. The PR interval

measures the time (normally 120–200 ms) between atrial and ventricular depolarization, which includes

the physiologic delay imposed by stimulation of cells in the AV junction area. The QRS interval (normally

100–110 ms or less) reflects the duration of ventricular depolarization. The QT interval incudes both

ventricular depolarization and repolarization times and varies inversely with the heart rate. A rate-related

(“corrected” Bazett’s correction) QT interval, QTc, can be calculated as QT/Type equation here. R-R and

normally is 0.44 s (some references give QTc upper normal limits as 0.43 s in men and 0.45 s in women.

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Also, a number of different formulas have been proposed, without consensus, for calculating the QTc).

The QRS complex is subdivided into specific deflections or waves. If the initial QRS depletion in a

particular lead is negative, it is termed a Q wave; the first positive deflection is termed an R wave. A

negative deflection after an R wave is an S wave. Subsequent positive or negative waves are labeled

“R” and “S”, respectively. Lowercase letters (qrs) are used for waves of relatively small amplitude. An

entirely negative QRS complex is termed a QS wave.

U Wave:Small, rounded, and upright wave following T wave. Most easily seen with a slow heart rate.

Indicates repolarization of Purkinje fibers.

ECG Leads (Figs. 11.4A and B)

The 12 conventional ECG leads record the difference in potential between electrodes placed on the

surface of the body. These leads are divided into two groups: Six limb (extremity) leads and six chest

(precordial) leads. The limb leads record potentials transmitted onto the frontal plane, and the chest

leads record potentials transmitted onto the horizontal plane.

The spatial orientation and polarity of the six frontal plane leads are represented on the hexaxial

diagram. The six chest leads are unipolar recordings obtained by electrodes in the following positions;

lead V1, fourth intercostal space, just to the right of the sternum; lead V2, fourth intercostal space, just to

the left of the sternum; lead V3, midway between V2 and V4: Lead V4, midclavicular line, fifth intercostal

space; and lead V5, anterior axillary line, same level as V4; and lead V6, midaxillary line, same level as

V4 and V5.

Fig. 11.3: Normal waves, segments and Intervals.

Figs. 11.4A and B: Anatomical relation of leads.

Anatomic Groups of ECG Leads

1.

2.

3.

4.

5.

6.

7.

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Together, the frontal and horizontal plane electrodes provide a three-dimensional representation of

cardiac electrical activity. Each lead can be likened to a different video camera angle “looking” at the

same events—atrial and ventricular depolarization and repolarization—from different spatial

circumstances. For example, right precordial leads V3R, V4R, etc. are useful in detecting evidence of

acute right ventricular ischemia. Bedside monitors and ambulatory ECG (Holter) recordings, usually

employ only one or two modified leads. The ECG leads are configured so that a positive (upright)

deflection is recorded in a lead, if a wave of depolarization spreads toward the positive pole of the lead,

and a negative deflection is recorded, if the wave spreads toward the negative pole. If the mean

orientation of the depolarization vector is at right angles to a particular lead axis, a biphasic (equally

positive and negative) deflection will be recorded.

READING 12-LEAD ECGS

The best way to read 12-lead ECGs is to develop a step-by-step approach (just as we did for analyzing

a rhythm strip). In these modules, we present a seven-step approach:

Calculate RATE

Determine RHYTHM

Determine QRS AXIS

Check individual WAVES

Calculate INTERVALS

Assess for HYPERTROPHY

Look for evidence of infarction/dyselectrolytemia.

Step 1: Determining the Heart Rate (Fig. 11.5A)

Rule of 300/1500

Count the number of “big boxes” between two QRS complexes, and divide this into 300 (smaller boxes

with 1,500) for regular rhythms.

Fig. 11.5A: Calculation of heart rate.

6 Second Rule

ECGs record 6 seconds of rhythm per page

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Count the number of beats present on the ECG in 6 seconds

Multiply by 10

This is useful for irregular rhythms.

Interpretation bpm Causes

Normal 60–

99

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Bradycardia <60 Hypothermia, increased vagal tone (due to vagal stimulation or drugs), athletes (fit people)

hypothyroidism, beta blockade, marked intracranial hypertension, obstructive jaundice, uremia, structural

SA node disease, or ischemia

Tachycardia >100 Any cause of adrenergic stimulation (including pain); thyrotoxicosis; hypovolemia; vagolytic drugs (e.g.

atropine) anemia, pregnancy; vasodilator drugs, including many hypotensive agents; fever, myocarditis

Step 2: Determine Regularity

Look at the R-R distances (using a caliper or markings on a pen or paper).

Regular (are they equidistant apart)? Occasionally irregular? Regularly irregular?

Irregularly irregular?—atrial fibrillation (AF).

Sinus rhythm

Cardiac impulse originates from the sinus node. Every QRS must be sinus node. Every QRS must be preceded by a P wave.

Sinus bradycardia

Rhythm originates in the sinus node. Rate of less than 60 beats per minute.

Sinus tachycardia

Rate >100 bpm, otherwise, normal

Sinus pause

In disease (e.g. sick sinus syndrome), the SA node can fail in its pacing function. If failure is brief and recovery is prompt, the

result is only a missed beat (sinus pause). If recovery is delayed and no other focus assumes pacing function, cardiac arrest

follows.

Atrial fibrillation

Atrial rate approximately 400–600; Ventricular rate approximately 150 bpm; irregularly irregular, baseline irregularity, no visible p

waves, QRS occurs irregularly with its length usually <0.12 s, fibrillary waves.

Atrial flutter

Atrial rate =~300 bpm, P waves absent but have flutter waves, ECG baseline adapts “saw-toothed” appearance.

Ventricular fibrillation

Rate cannot be discerned, rhythm unorganized, QRS broad >0.12 s

Ventricular tachycardia

Rate = 100–250 bpm, broad QRS, regular

Torsades de Pointes

Literally meaning twisting of points is a distinctive form of polymorphic ventricular tachycardia characterized by a gradual change

in the amplitude and twisting of the QRS complexes around the isoelectric line.

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