Search This Blog


Types of hysterectomy

Abdomen Hys
  • TAH
  • - Sub total hysterectomy
  • Total hysterectomy with b/l salpingoophorectomy
  • Extended hysterectomy
  • Radical hysterectomy

Vagina hyst. (VH)


Benign disease

Abn bleeding
Ut prolapse
Chronic PID with tuboovarian mass
Caesarean Hyst.
Molar preg >40 age
Septic abortion
Chronic inversion of Ut


Ca Cx
Ca ovary
Ca fallopian tube
Gestational TD


Complete physical and anesthetic evaluation

Routine blood test
  • Full blood count
  • CXR
  • ECG
  • Bowel preperation

Technique for TAH

  • Supine position
  • Abdo wall open in layers
  • Self retaining retractors
  • Trendelenberg position
  • Pack intestine

Complication of operation

Immediate complications

Anasthesia compl
Bleeding, haemotama
Injury to the surrounding structure
Intestine, bladder, ureter,

Early complications

Atelactasis, UTI, DVT, wound Infection, burst abdomen, vault prolapse

Remote complication

keloid, vault granulation, vault prolapse, incisional hernia, psy and emotional problem

Follow up

Histo path


  • Common gynecological problem
  • Affect reproductive age group
  • Difficult to treat
  • Adolescents girls – mullaerian anomaly
  • Postmenopausal - HRT

Presence of viable Endometrial tissue
(Glands surrounded by stroma)
outside the uterine cavity.

Sites of endometriosis

Pelvic and extra pelvic

Endometriosis of POD-(pouch of douglas)

Endometriosis of peritoneum

Ruptured endometriotic cyst

Ectopic Endometrial tissue

Tissue Contents

Endometrial Glands

Endometrial Stroma surrounding the glands


Respond to hormonal stimulation

Benign tissue that invades other surrounding tissues

Menstruation within the ectopic endometrial tissue

Inflammatory response


Endometriosis Theories
  1. Implantation theory (sampson)
  2. Coelomic metaplasia theory
  3. Scar endometriosis

Other factors
  1. Immunological
  2. Genetic
  3. Hormonal

Samson’s Implantation theory:
  1. Reflux of endometrial tissue
  2. Endometriosis in girls with cryptomenorrhoea

Scar endometriosis-following
  1. Classical Caesarean section
  2. Hysterotomy
  3. Myomectomy.
  4. Episiotomy

Unusual sites:
  1. Umbilicus,
  2. Ureters,
  3. Lung,
  4. Pleura,
  5. Episiotomy scar
  6. Extremities

Hormonal Influence

+ Estrogen

- Progseteron


Pregnancy causes atrophy of endometriosis
Regression following oophorectomy and irradiation
Rarely before puberty and after menopause


Usual sites

Lower pelvis
Uterosacral ligaments
Peritoneum over bladder
Back of uterus
Sigmoid / Appendix

Surgical sites


Cx stump

Abdominal scar after uterine surgery

Gross appearence

Small black dots (Gun Powder Burns)
Scarring and puckering
Yellowish brown fluid in peritoneal cavity

Chocolate cysts of ovary


Vascular red adhesions on surface of ovary

Inner surface of cyst wall is vascular with dark brown tissue


Endometrial glands & stroma

Granulation tissue

Hemosiderin laden phagocytic cells

Laproscopic findings

Powder Burn-puckered black spots
Red vascular
Bluish/blackish/chocolate cysts
Dense adhesions in pelvis
Yellow brown peritoneal fluid
Early lesions-red flame like raised areas

Clinical Features





Dyschezia and tenesmus

Infertility tubal blockage/ovulation dysfunction

Acute abdomen (rupture of chocolate cyst)

Chronic Pelvic Pain

Dysuria, Hematuria, Hematochezia, Hemoptysis

Physical Findings
  • P/A: Cystic swelling-simulates an ovarian tumor (Chocolate cyst)-fixed, tender
  • P/V: Tender fixed R/V uterus, Adnexal mass, POD-Nodular

Endocrinology Abnormalities
  1. Anovulation
  2. Abnormal follicular development
  3. Luteal insufficiency
  4. Premenstrual spotting
  5. Lutenized unruptured follicle


Ovarian tumours(benign+malignancy)
Rectal carcinoma
Acute abdomen


is not much of help because small lesion can not be detected. Useful in case of chocolate cyst of ovary.
lesions can be seen and tissue biopsy as well as treatment can be done.
Diagnosis is only by HPE examination.
Ca 125

Endometriosis vs. PID

  1. Pelvic pain
  2. Congestive dysmen.
  3. Menorrhagia
  4. Sterility
  5. Response to hormones

  1. Pelvic pain
  2. Congestive dysmen.
  3. Menorrhagia
  4. Sterility
  5. Response to antibiotics

Basis of treatment

Depends on
Desire to conceive
Need for conserving reproductive function
Extent of Disease
Response to Medical treatment

Objectives of Rx

To give comfort from disease

Facilitate child bearing


For pain

For mass

For infertility

4. Combined

Management plan

Medical Treatment

  • Oral contraceptive pills
  • Progestogens
  • Androgens
  • GnRH analogues

Combined OCPs

1. Continuous 2tabs per day may need to increase for 6-9 months

Warnings; High incidence of side effects, risk of thromboembolism

Oral progestogens

Mode of action: Antiestrogenic effect. Continuous administration– endometrial atrophy

Duration: 6 to 9 months daily

Medroxyprogesterone acetetate
  • Dose– Given Intramuscular
  • Long acting depot preparation
  • 100mgs im every two weeks—3 months
  • 200mgs monthly for 3 to 6 months
  • ORAL- 30mgs daily

Results of Progestational Agents

50 to 70% symptomatic relief

SIDE EFFECTS: Weight gain

Irregular bleeding. Reduced libido. Mental depression. Breast tenderness.


Synthetic derivative of Ethinyl testosterone
Action: Inhibits Pituitary gonadotrophins
Also, mildly anabolic, antioestrogenic and anti progestational
Effective though expensive
Dose: 200 to 800mgs daily for 6 to 8 months-start on first day of menses
If > 8 months symptoms of menopause
Lesions regress but side effects
Weight gain, hirsuitism, sweating, muscle cramps, depression, atrophy of breasts and vaginal epithelium, liver and renal damage

Antinflammatory drugs

Mefenamic acid 500mgs thrice a day

Helps dysmenorrhoea in 70 to 80% patients


Gonadotrophin releasing hormone-
given continuously to supress pituitary
gonadotrophins --- causes atrophy of the endometriotic tissue
Cost is a limiting factor
Ablation of endometriotic implants <3cms Laparoscopy



CO2 vaporization



For advanced cases/larger lesions
  1. Dissection/excision of chocolate cyst
  2. Salphingo-ophorectomy
  3. Abdominal hysterectomy
Pre/post operative medical Rx


Islands of endometrium (endometrial glands surrounded by stroma) found in the myometrium
Uterus up to14 wks size

Diffuse, non-capsulated involvement of myometrium with tiny dark haemorrhagic areas interspersed in between.

  1. Parous around 40 yrs
  2. Menorrhagia, increasing dysmenorrhoea
  3. Pelvic discomfort
  4. Backache
  5. Dyspareunia

  1. Symmetric enlargement of uterus (seldom>14 wk)
  2. Menorrhagia
  3. Dysmenorrhoea

Surgery is the treatment of choice

Final diagnosis is on the histopathology



Most common gynaecological carcinoma in
developed countries
Japan and Asia have 5 times lower incidence

Most cases are post-menopausal
< 5% under age of 40 ( hyperestrogenic )
At diagnosis 75% have Stage 1 disease
OBESITY strong link as peripheral conversion to Estrone
SHBG(sex hormone binding globulin) decrease with an increase in FREE estrogen for uptake in target tissues

Lifetime risk: 1.1%
Lifetime risk of dying: 0.4%
5-year survival rates are considered to be
good at around 75%

The prognosis is generally good because the majority
of patients are diagnosed in an early stage

Role of hormones (estrogen)

Estrogen dependent disease
Prolonged exposure without the balancing effects of progesterone

Conditions of Estrogen excess

Early Menarche and Late Menopause

Associated with more estrogen exposure

Estrogen Replacement Therapy

Place women at high risk
Risk reduced when + progesterone


Anti-estrogenic drug for breast cancer
Side effect
Induces non-cancerous uterine tumors
Some may develop into endometrial cancer
Long term use => endometrial cancer
Only 1 in 500 develop endometrial cancer

Reduced Risk

Oral Contraceptives

Combined OC => 50% reduced rate
Actual reduction number small because uncommon in women of child bearing age
Long term offers protection
Reduced risk presumably => progesterone

Physical exercise and fruit vegetables diet

Endometrial Carcinoma: aetiology

Hyperoestrogenic states

Age - mainly 60-70 years (late menopause)
Parity - nulliparity, relative infertility
Metabolic disorders [Cancer Triad]
Obesity, Diabetes, Hypertension
Ovarian tumours
granulosa cell tumour, PCOD
unopposed Exogenous oestrogens [HRT]

other conditions
leiomyomas; adenomyosis, endometriosis, breast Ca

Risk factors
  • Usually in postmenopausal women
  • Unapposed estrogen stimulation
  • Preceded by endometrial hyperplasia
  • Simple hyperplasia

Adenomatous hyperplasia

Cellular Atypia

Clinical Features

Abnormal bleeding
mainly postmenopausal
intermenstrual or pre-menstrual

Lower abdominal pain
abnormal vaginal discharge / pyometra

Endometrial Carcinoma


Endometrial sampling
Dilation and curettage / Endometrial aspiration

TVS / CT scan / MRI

Hysteroscopy + targeted biopsy

Tumor marker
Ca 125 / 199

Cystoscope / Proctoscope


Early detection is best prevention
Treating precancerous hyperplasia
Hormones (progestin)
10 ~ 30% untreated develop into cancer

Histology/ grade

90% endometrial adenocarcinoma
Arise from the epithelium

Tumor grading
Grade 1
Well differentiated
Grade 2
Moderately differentiated with solid component
Grade 3
Poorly differentiated with solid sheets of tumor

Rare cell types

10% rare cell types
Papillary serous carcinoma
Clear cell carcinoma
Papillary endometrial carcinoma
Mucinous carcinoma
Rarer cancers
Onset at later age
Greater risk for metastases
Poorer prognosis
50% of treatment failure


Direct spread
Through endometrial cavity to the cervix
Through fallopian tubes to ovary / peritoneum
Invade myometrium reaching serosa
Rare: invasion to pubic bone
Lymphatic spread
Pelvic and para-aortic LN
Inguinal LN ( rare )
Hematogenous spread
Rare but may spread to lungs

Adenocarcinoma uterus

Intraoperatively obtained gross specimen of the uterus, bivalved in a sagittal plane, shows deep invasion (50% of the myometrial thickness) of endometrial carcinoma

Stage 1 Tumour confined to corpus
Stage 1a <50% myometrial invasion
Stage 1b >50% myometrial invasion

Stage 2 Tumour invades Cx stroma

Stage 3 Local/regional tumour spread

3a Invades serosa/+- adnexa
3b Vaginal or parametrial spread
3c1 Positive pelvic nodes
3c2 Positive para-aortic nodes
Stage 4 Invades bladder/bowel/distant

Treatment of endometrial hyperplasia/ carcinoma

Endometrial hyperplasia

Excessive stimulation of the uterine endometrium results in endometrial hyperplasia

Imbalance of hormones or hormonal changes can happen around the time of menopause, and contribute to the development of hyperplasia in some women.

Endometrial hyperplasia of the uterus, by itself, is not cancerous, but requires treatment and monitoring to prevent the risk of cancer.

Managing endometrial hyperplasia

Uterine hyperplasia can get worse, leading to atypical and precancerous cellular changes.

This is why any woman with hyperplasia is considered to be at a higher risk for cancer than one without hyperplasias.

investigate thickened endometrium,
hyperplasia can lead to uterine cancer —
early identification and intervention for uterine abnormalities is highly successful.

The evaluation process begins with a
speculum and bimanual exam
(internal exam and external palpation of the pelvic organs)

An ultrasound and tissue sampling
with endometrial biopsy, hysteroscopy and/or D&C

Hormonal treatment of endometrial hyperplasia

hyperplasia without atypia
progesterone/progestin therapy for three months,
then to retest the endometrium.
micronized natural progesterone at high doses

Atypia present
option for women who want to wait or avoid surgery altogether is Megace (megestrol acetate), a very potent, orally administered hormonal agent.

Ca Endometrium Treatment Algorithms

Clinical Stage I

( Grade? Depth? Cell type ?)

Low Risk ~ 75%

High Risk ~ 25%
EBRT to pelvis
(but~13% have PA nodes)

Treatment of endometrial cancer

Stage II
Consider radical hysterectomy
With macroscopic tumor on cervix:

Consider a cervical cancer

Intra-abdominal spread:
Remove all tumor if possible

Advanced stage

Debulking surgery


+/- hormone / chemotherapy


Likely in women with advanced disease
Within 3 years of original diagnosis
Hormone therapy can be considered
External beam pelvic radiation or brachytherapy.



Amenorrhea is defined as absence or cessation of menses

Types : Physiological - prepubertal
Pathological - Primary

PRIMARY AMENORRHEA is defined as absence of menses by 16 years of age in the presence of secondary sexual characteristics
or by 14 years in the absence of secondary sexual characteristics
Incidence 1-2% of women
SECONDARY AMENORRHEA is defined as the absence or cessation of menses for 6 months in a women who had previously menstruated

Normal menses
  • XX chromosome
  • intact functioning hypothalamo –pituitary axis
  • functioning ovary
  • responsive endometrium
  • patent outflow tract

At puberty there are a series of changes where there is physical growth-breast development-pubic & axillary hair growth- dev of ovaries and genital organs- growth spurt and menstruation.
Average age of menarche in Indo-Pakistani girls 13.5 yrs


intact hymen
vaginal agenesis
vaginal septa
cervical agenesis
cervical os stenosis

  • primary amenorrhea in a teenage girl
  • cyclic pain abdomen
  • palpable lower abdominal mass
  • possible urinary difficulty
  • Bluish bulging membrane at lower end of vagina


Mullerian agenesis/dysgenesis:
Rokitansky Syndrome
Androgen insensitivity (XY)

Asherman Syndrome secondary to curretage /infections like TB
damaged by RT

removed surgicaly
Congenitaly absent endometrium (v rare)

Rokitansky syndrome
  • 46XX geneticaly female
  • Mullerian agenesis(absent uterus or small rudimentary bulb with blind vagina)
  • phenotypically female
  • normal ovaries
  • Presents with primary amenorrhea
  • associated with other cong anomalies :urinary 47%, skeletal 12%,heart disease

Testicular feminization syndrome
  • Genotype male 46XY
  • Absence of cytosol androgen receptors
  • phenotypicaly female : tall with long hands and feet
  • breasts developed : peripheral conversion of testerone
  • pubic and axillary hair not well developed
  • blind vagina
  • testes are in abdomen or inguinal region


Agenesis /dysgenesis
Turners Syndrome (XO),mosaics
Pure gonadal dysgenesis
partial deletion of X chromosome(46xx)

exposure to RT /chemo (destroys the follicles)
surgical removal
premature ovarian failure ? Autoimmune cause
Resistant Ovary Syndrome
Polycystic ovarian disease
galactosemia : galactose has toxic effect on ovarian follicles

Turners Syndrome
  • gonadal dysgenesis 45XO
  • primary amenorrhea
  • short stature
  • absence of Sec. sexual characteristics
  • streak ovaries
  • webbed neck
  • increased carrying angle
  • shield chest
  • associated with heart and renal defects
  • Growth hormone before epiphysis close; estrogen replacement therapy later


Tumours : non functioning adenomas
hormone producing eg prolactinomas , hyperthyroidism etc
Empty sella syndrome :hypo pituitary function
Destruction of pituitary by
necrosis : Sheehans syndrome
infiltrative lesion eg lymphocytic hypophysitis ,
granulomatous lesions
RT or surgery

  • Due to drugs: haloperidol ,metochlorpramide ,phenothiazine, reserpine, methyldopa : decrease dopamine which inhibits prolactin
  • adenomas (micro and macro)
  • Hypothyroidism : Increased TRH stimulates PL release
  • present with galactorrhea, anovulation, oligo and amenorrhea (20%), subfertility
  • CT/MRI

Hypothalamus (decrease secretion or synthesis of GnRH)
  • physiological delay (most common)
  • Kallmanns Syndrome : insufficient secretion of GnRH
  • Tumours : craniopharyngioma ,tubercular granuloma, dermoid etc
  • anorexia nervosa, extreme exercise ,stress
  • drugs : phenothiazine,reserpine,ganglion blocking agents affect hypothalamus

Congenital adrenal hyperplasia
  • congenital defect in enzymes needed for formation of cortisol – increased ACTH production
  • increased androgen : causing ambigous genitalia, amenorrhea, virilism
  • normal looking uterus and ovaries
  • can be XY or XX
  • serum levels of 17 OH progesterone levels are raised
  • supplement small doses of corticosteroid to suppress the ACTH
  • function of ovaries and uterus possible with eraly treatment

Clinical history


detailed menstrual history
secondary sexual development
associated symptoms : pain
pregnancy related symptoms
headache, visual disturbances
discharge from breast
menopausal symptoms
diet ,recent change in weight or voice

Parity , recent birth related haemorrhage,need for curretage for abortion or PPH
contraceptive history : post pill or depo related amenorrhea
Past medical : TB,DM(vasculitis can damage pituitary), psychological disorders with medications, Cushings syndrome, adrenal disorders,thyroid disorders ,cancers needing RT/Chemo
Past Surgical history : oopherectomy or hysterectomy, D/C , cranial surgeries etc

Personal : use of any drugs, exercise
Family history : mother and sisters age of onset of menses


General habitus : cachexic ,obese, truncal obesity, enlarged facial features and hands and feet
height and weight

Limbs : cubitus valgus
Secondary sexual characteristics ; breast , pubic and axillary hair
Neck : short webbed neck, LN, thyroid
Chest : shield chest ,widely spaced nipples, milky discharge from breast

PA : mass perabdominal or in inguinal region

PV: ambiguos genitalia, labial fusion, absent or short vagina, imperforate hymen(bluish bulge at introitus), absence of uterus, palpable ovarian mass

PR : confirm mass anteriorly or absence of uterus/vagina . Finger can easily feel a metal catheter in the urethra in case of vaginal agenesis ,but not in case of crptomenorrhoea


From the examination outflow tract obstruction is evident .eg agenesis of vagina,uterus
In cases of vaginal agenesis the presence of uterus and ovaries need to be confirmed .
USG - uterus ovaries presence,size
collection within uterus
collection within vagina
endometrial thickness

absent present
Mullerian agenesis vaginal agenesis
True hermaphrodite septa
Androgen insenstivity Cervical stenosis
Ashermans Syndrome

Karyotyping ,especially in case of ambigous genitalia

No anatomical defect, pregnancy ruled out , uterus present

Serum Prolactin functioning uterus
Serum TSH estrogenized or not

Progestin Challenge Test
5mg MPA daily for 5 days –withdrawl bleeding within a week
bleeding present No bleeding
Endogenous estrogen present No estrogen production

Estrogenized endometrium estrogen/progesterone
Patent outflow supplementation
No bleeding withdrawl
PCOD endometrial damage
positive withdrawl
* Low FSH (<40iu/L) constituitional delay
Low LH (<5iu/L) Hypothalamic causes
(hypoGn,hypo gonadism)
* High FSH (>40iu/L) ovarian failure
(hyper Gn ,hypogonadism)
* PL increased hyperprolactinaemia
* TSH increased hypothyroidism


Based on the cause
outflow tract obstruction :
cryptomenorrhea : hymenectomy using cruciate incision
septa : excision
haematometra : cervical dilation/drainage
vaginal agenesis : vaginoplasty

Mullerian agenesis : counseling, adoption

Ashermans syndrome : hysteroscopic breakdown of adhesions ,IUCD kept for 10-12 months to deter reformation

Ovarian dysgensis or failure : HRT supplementation in case of Y chromosome testes is to be removed,as there is 50% chance of malignancy arising from such a gonad
PCOD : medicaly ovulation induction, progesterone supplementation
Testicular feminization : treat patient as female, remove gonads , estrogen suplementation

Hyperprolactinaemia :
lateral skull Xray : enlargement of pit fossa, destruction of clinoid process - CT scan
medicaly : bromocryptine /cabergoline (D agonist)
Surgicaly : macroadenomas with pressure symptoms

Importance of amenorrhea
  • psychosocial development delays, physical sexual abnormalities
  • ? Problems with identity : ?male? Female
  • coital difficulty
  • Pain /Mass
  • infertility
  • risk of malignancy in XY cases: 50%
  • hypoestrogenic status : risk of osteoporosis
  • Hyperestrogenic status : risk of endometrial cancer


Abnormal bleeding from the uterus in the absence of any organic disease in the genital tract

10 % of women attending gynecologycal OPD


According to functional abnormality

Anovulatory DUB

Ovulatory DUB

Clinical time of presentation

5-7 yrs following menarche (puberty menorrhagia)

20-25 yrs of mature reproductive life (corpus luteum dysfunction)

5-7 yrs preceding menopause (perimenopausal DUB)

Pathophysiology of DUB :

Anovulatory DUB

Dysfunction of hypothalamo-pituitary ovarian axis due to impaired response of hypothalamus or immaturity of estrogen feedback mechanism

Under the estrogenic influence
Hyperplasia of endometrium
Fragile supporting stromal tissue of endometrium
Endometrium outgrow the estrogen support
Estrogen threshold bleeding – not enough estrogen to support endometrial growth

Causes local disturbance in the endometrium due to imbalance in the production of vasodilator and vasoconstrictor prostaglandin (↑ PG E2- ↑ vasodilatation)

Ovulatory DUB

Corpus luteum hypo function (insufficiency/ irregular ripening)- disordered growth of endometrium
Corpus luteum hyper function (persistent corpus luteum)- continued secretion of estrogen and progesterone - absence of sharp fall- irregular shedding
↑ PGF2α -↑vasoconstriction- endothelial damage
↑ plasminogen/ fibrinolytic activity -↑ bleeding

Normal endometrium
Proliferative endometrium/Secretory endometrium
Disordered growth, irregular ripening, irregular shedding
Atrophic endometrium

After menarche
Immaturity of hypothalamic –pituitary-ovarian axis – anovulatory DUB

In the mature reproductive age group
Hypo or hyperfunction of corpus luteum
Local disturbance in the endometrium -ovulatory DUB

In the perimenopausal group
Increased resistance of ovarian follicles
Decreased number of follicles - anovulatory DUB


Abnormal bleeding P/V
Excessive, prolonged duration, irregular bleeding, with clots
Irregular cycle/ preceded by a variable period of amenorrhoea
Symptom of anemia
Change in daily routine activity

Clinical examination

Normal pelvic finding
Signs of anemia if bleeding is severe

Rule out secondary causes (normal pelvic findings)
IUCD, Norplant, Depo provera
Thyroid problem
Coagulation disorder

Differential diagnosis of abnormal bleeding PV

Pregnancy related bleeding
Fibroid uterus
Adenomyosis, endometriosis
Endometrial / endocervical polyps, hyperplasia,
Malignancy of cervix / uterus
Hormone producing ovarian tumor


To assess severity of condition
Hb, PCV, Blood grp Rh typing

To exclude organic pathology and confirm diagnosis
Endometrial biopsy
Platelet, BT, CT
Thyroid function test


General measures
Oral iron capsule / menstrual calendar
Blood transfusion

Medical treatment

Non hormonal – prescribed during menstruation
Tranexamic acid- Anti fibrinolytic agent
Ethamsylate- increases capillary wall strength, anti fibrinolytic activity
Anti prostaglandins-mefenamic acid


Progesterone for anovulatory bleeding

Reverses effect of estrogen mediated endometrial proliferation
Induce endometrial maturation
For acute control of bleeding
Cyclically for 21 days
Progesterone containing IUCD

Estrogen and Progesterone ( COCP), for needing contraceptive as well

Danazol ( testosterone derivative)-competitive inhibitor of sex steroid

GnRH analogues- suppresses gonadotropin release from pituitary

Surgical management

Therapeutic D and C

Conservative surgery or minimal invasive
surgery under hysteroscopy
Endometrial resection and endometrial ablation

Non conservative surgery

ECG Interpretations

Aortic valve replacement

Asymptomatic patient

Cardiac surgery

Cerebral vascular accident

Coronary heart disease and Hypertension
Chest Discomfort

Congestive heart failure
Elective colon surgery
Elective hip Surgery
Forearm rash

Mitral valve replacement

Paroxysmal Atrial Fibrillation


Pulmonary edema


Severe Dyspnea

ECG Interpretations

Rheumatic Fever

Atrial fibrillation with Nausea and Dehydration

Recurrent Chest pain

Chronic Dyspnea on Exertion

Diaphoresis and Dyspnea

Atrial Fibrillation and Atrial flutter


Diastolic murmur

Mild indigestion

Myocardial infarction

ECG Interpretations

ECG of Atypical Chest pain

ECG of CCU-coronary care unit- include Medication

ECG of Preoperative evaluation

ECG of CCU -coronary care unit

ECG of Chest pain

ECG of Congestive heart failure (a)

ECG of Congestive heart failure (b)

ECG of Chest discomfort