1. Length of Vas deferens or ductus deferens
2. Length of thoracic duct
3. Length of Spinal cord
4. Femur (for 6 feet person)
5. Length of transverse colon
6. Distance from the incisor teeth to the cardiac end of the stomach
7. Umbilical cord at birth
8. Length of sartorius muscle

All are about 25 cms or 10 inches:

1. Length of Esophagus
2. Length of Ureter
3. Length of Duodenum
4. Length of Descending colon

All are about 10 cms or 4 inches:

1. Length of Trachea
2. Length of Fallopian or Uterine tube
3. Length of Common bile duct
4. Length of 3rd part of Duodenum (Transverse Duodenum)
5. Length of Posterior wall of Vagina
6. Anteroposterior measurement of Inlet of Pelvis
7. Transverse measurement of Outlet of Pelvis

All are about 4 cms or 1.5 inches:

1. Length of Auditory tube
2. Length of Anal canal
3. Length of Female urethra
4. Length of Cystic duct
5. Length of Common hepatic duct
6. Length of External acoustic/auditory meatus when measured from tragus
7. Length of Optic nerve
8. Length of Ovary
9. Length of Inguinal canal
10. Length of Femoral sheath
11. Thickness of Kidney
12. Width of Pons

All are about 1 inch or 2.5 cm

1. Length of Medulla
2. Length of Midbrain
3. Length of Pons
4. Length of 4th part of Duodenum (Ascending Duodenum)
5. Length of Ducts of Bartholin’s gland (Greater vestibular glands)
6. Diameter of Trachea
7. Diameter of Right main bronchus
8. Distance between Ureteric orifice in Empty bladder

Structures whose width is greater than length:

1. Pons varioli
2. Cecum
3. Prostate

Descent of Testis:

1. 3rd month: Reaches Iliac fossa
2. 6th month: Rests at Deep Inguinal ring
3. 7th month: Traverses Inguinal canal
4. 8th month: Reaches Superficial Inguinal ring
5. 9th month: Descneds into Scrotum

Rule of 2s for Meckel’s Diverticulum:

Meckel’s Diverticulum is a congenital outpouching of the ileum that is a normal variant and is the remnant of omphalomesenteric (vitellointestinal) duct. It is a true diverticulum, that consists of all the layers of the intestinal wall (mucosa, submucosa and muscularis).

1. Occurs in 2% population
2. 2 times more common in male
3. 2 feet proximal to ileocecal valve
4. 2 inches in length
5. 2 years of age is typical for onset of symptoms
6. 2 % are symptomatic
7. 2 types of mucosa possible (Small intestine and Gastric)

Rule of 2s: 2nd week of Development (Embryology)

1. Trophoblast differentiates into 2 layers: Cytotrophoblast and Sycytiotrophoblast
2. Embryoblast forms 2 layers: Epiblast and Hypoblast
3. Extraembryonic mesoderm splits in 2 layers: Somatopleure and Splanchnopleure
4. 2 cavities are formed: Amniotic cavity and Yolk sac cavity

Rule of 3s: Thoracic spine levelling

1. T1-3 (and T12) transverse processes are at the level of the corresponding thoracic spine.
2. T4-6 (and T11) transverse processes lie superiorly between its level’s spine and the spine of the thoracic segment above it.
3. T7-9 (and T10) transverse processes lie superiorly at the level of the superior segment’s spine.

Rule of 3s: 3rd week of Development

1. Bilaminar germ disc changes into trilaminar germ disc with 3 layers ectoderm, mesoderm and endoderm
2. Formation of 3 important structures: Notochord, Neural plate and Primitive streak
3. 3 layered chorionic villi
4. 3 carnegie stages

Dalley/Voss Rule of 3s of 2s: Sacral Plexus

For 3 sets of 3 nerves:

• 1st set of 3 nerves will all have 3 spinal contributions (3,3,3)
• 2nd set of will have 2 nerves with 3 spinal contributions and 1 nerve with 2 spinal contributions (3,3,2)
• 3rd set will have 1 nerve with 3 spinal contributions and 2 nerves with 1 spinal contribution (3,2,2)

1st set of nerves (3,3,3):

1. Superior gluteal nerve: 3 spinal contributions beginning from L4 (L4,L5,S1)
2. Inferior gluteal nerve: 3 spinal contributions beginning from L5 (L5,S1,S2)
3. Posterior femoral cutaneous nerve: 3 spinal contributions beginning from S1 (S1,S2,S3)

2nd set of nerves (3,3,2):

1. Nerve to Quadratus femoris: 3 spinal contributions beginning from L4 (L4,L5,S1)
2. Nerve to Obturator internus: 3 spinal contributions beginning from L5 (L5,S1,S2)
3. Nerve to Piriformis: 2 spinal contributions beginning from S1 (S1,S2)

3rd set of nerves (3,2,2):

1. Pudendal nerve: 3 spinal contributions beginning from S2 i.e. where you left off with pyriformis (S2,S3,S4)
2. Nerve to levator ani: 2 spinal contributions beginning from S3 (S3,S4)
3. Nerve to coccygeus:2 spinal contributions beginning from S4 (S4,S5)

Gate’s Rule of 4s: For Detecting Brainstem Lesion

There are 4 rules in Rules of 4s:

1. 4 structures in the “M“idline begins with “M“: Motor pathway (Corticospinal Tract), Medial Lemniscus, Medial longitudinal fasciculus, Motor nucleus and nerves (CN 3,4,6,12)
2. 4 structures to the “S“ide begins with “S“: Spinothalamic, Spinocerebellar tract, Sensory nucleus of CN V, Sympathetic pathway
3. 4 Cranial nerves in Each of:
• Medulla: 9,10,11,12
• Pons: 5,6,7,8
• Above Pons: 1,2,3,4
4. The 4 midline motor nuclei can exactly divide 12 (excluding 1 and 2 which are purely sensory) – 3, 4, 6 and12 (Remaining 4 motor nuclei are on sides/laterally i.e 5, 7, 9 and 11).

Associated deficits of 4 Midline “M” structures:

1. Motor pathway (or corticospinal tract): contralateral weakness of the arm and leg.
2. Medial Lemniscus: contralateral loss of vibration and proprioception in the arm and leg.
3. Medial longitudinal fasciculus: ipsilateral internuclear ophthalmoplegia (failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally).
4. Motor nucleus and nerve: Ipsilateral loss of affected cranial nerve function (3, 4, 6 or 12).

Associated deficits of 4 Side “S” structures:

1. Spinocerebellar pathways: ipsilateral ataxia of the arm and leg.
2. Spinothalamic pathway: contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk.
3. Sensory nucleus of 5th Cranial nerve: ipsilateral alteration of pain and temperature on the face in the distribution of the 5th cranial nerve (this nucleus is a long vertical structure that extends in the lateral aspect of the pons down into the medulla).
4. Sympathetic pathway: Ipsilateral Horner’s syndrome i.e ptosis, miosis, anhydrosis.

Associated deficits of 4 Cranial nerves in Medulla:

1. 9th or Glossopharyngeal: ipsilateral loss of pharyngeal sensation
2. 10th or Vagus: ipsilateral palatal weakness
3. 11th or Spinal accessory: ipsilateral weakness of the trapezius and sternocleidomastoid muscles
4. 12th or Hypoglossal: ipsilateral weakness of the tongue

Associated deficits of 4 cranial nerves in Pons:

1. 5th or Trigeminal: ipsilateral alteration of pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw
2. 6th or Abducens: ipsilateral eye abduction weakness
3. 7th or Facial: ipsilateral facial weakness
4. 8th or Auditory: ipsilateral deafness

Associated deficits of 4 cranial nerves above Pons:

1. 1st or Olfactory: not in midbrain.
2. 2nd or Optic: not in midbrain.
3. 3rd or Occulomotor: impaired adduction, supraduction and infraduction of the ipsilateral eye (eye is turned out and slightly down)
4. 4th or Trochlear: eye unable to look down when the eye is looking in towards the nose

Applying the knowledge:

Pathways and tracts pass through the entire length of brainstem and can be likened  to “meridians of longitude” whereas the cranial nerves can be likened to “parallels of latitude”. To establish the site of brainstem lesion, you need to detect the point of intersection of the meridians of longitude and parallels of latitude. Thus a medial brainstem syndrome will consist of the deficits of 4 “M”s and the relevant motor cranial nerve, and a lateral brainstem syndrome will consist of the deficits of 4 “S”s and either the 9–11th cranial nerve if in the medulla, or the 5th, 7th and 8th cranial nerve if in the pons.

Example:

58 years old lady with left hemiparesis, Left side loss of proprioception and right sided tongue deviation.

1. Left hemiparesis is associated with deficit of Motor or corticospinal pathway of Right side which lies medially
2. Left sided loss of proprioception is associated with deficit of medial lemniscus of Right side which lies medially
3. Right sided tongue deviation is associated with deficit of Cranial nerve 12 on Right side which lies medially in medulla

Diagnosis: Medial medullary syndrome due to lesion in right vertebral artery

Rule of 7s: For Orbit

There are 7 bones, 7 intraorbital muscles and 7 nerves in orbit

• 7 Bones: Frontal, Ethmoid, Lacrimal, Sphenoid, Zygomatic, Palatine, Maxilla
• 7 intraorbital muscles: Levator palpebrae, 4 recti (Superior, Inferior, Medial and Lateral), 2 oblique (Superior and Inferior)
• 7 orbital nerves: Optic (CN II), Occulomotor (CN III), 3 branches of Opthalmic nerve (CN V1) – Frontal, Nasociliary, Lacrimal, Abducens nerve (CN VI)

• Mycobacterium tuberculosis
• Mycobacterium bovis
• Mycobacterium microti
• Mycobacterium africanum
• Mycobacterium canettii

General Characteristics:

• Nonmotile, nonsporing and noncapsulated bacillus arranged singly or in group
• Has a complex peptidoglycan arabinogalactan mycolate cell wall that is approximately 60% lipid, resulting in acid-fastness, poor Gram staining (weakly gram positive), and resistance to drying and many chemicals
• Mycobacterium tuberculosis appears slender, straight or slightly curved rod with beaded or barred appearance in ZN stain while Mycobacterium bovis appears straighter, stouter and shorter with uniform staining.
• A slow grower (generation time 12-24 hours) because it has single copies of ribosomal genes.
• Obligate aerobe and Facultative intracellular

Determinants of pathogenecity (Mycosides):

Mycosides are glycolipid derivatives of mycolic acid. Following mycosides are pathogenic determinants:

1. Cord factor (Trehalose mycolate):

• inhibits neutrophil migration and causes the organism to grow in a cord or serpentine fashion in culture
• elicits granuloma formation
• disrupts mitochondrial membranes, interfering with respiration and oxidative phosphorylation
• immunogenic
• release of TNF (cachectin) resulting in rapid weight loss in mice experiments

2. Sulfatides (Sulfur containing glycolipid):

• potentiates action of Cord factor
• permits intracellular survival in macrophages by inhibiting phagolysosome formation and by suppressing superoxide formation

3. Wax D (complex mycoside):

• activation of cell mediated immunity

Mnemonic: Mike WaxeD his SUrfboard and Corded (leashed) it
Mike: Mycoside
Waxed: Wax D
Surfboard: Sulfatide
Corded: Cord factor

Tuberculosis

Tuberculosis (TB) is an infectious bacterial disease caused by Mycobacterium tuberculosis, which most commonly affects the lungs. However, no organ is known to be spared by Tuberculosis, but it is extremely rare in pancreas, thyroid and muscles and unheard of in hair and nail.

Causative agent:

• Mycobacterium tuberculosis (hominis)
• Mycobacterium bovis
• Mycobacterium avium intracellulare (MAI)

Mode of transmission:

• Person to person transmission of airborne droplets of organisms from an active case to a susceptible host
• Oropharyngeal and intestinal TB due to drinking of M.bovis contaminated milk or swallowing sputum
• Transplacental route

Risk factors:

• Poverty, crowding and chronic debilitating illness
• Elderly
• Transplant recepient, AIDS, malignant disease, Diabetes Mellitus, Silicosis, Chronic renal failure, Malnutrition, Alcoholism, Immunosuppression due to corticosteroid

Pathogenesis:

A. Primary Pulmonary tuberculosis:

Less than 3 weeks (Sensitization):

1. Primary infection usually occurs in lungs of immunologically naive individuals. Inhaled bacteria land in the areas of the lung that receive the highest air flow: the middle and lower lung zones.
2. Inhaled bacteria cause a local infiltration of neutrophils and macrophages
3. The mycobacteria are picked up by phagocytic cells (macrophages) but the bacteria survives and replicates intracellularly due to endosomal manipulation mediated by virulence factors and kills the phagocytic cells.
4. The bacteria spread through the lymphatics and bloodstream to to seed regional lymph nodes, other sites of lung and distant sites.

More than 3 weeks (Type 4 Delayed Hypersensitivity):

1. Some macrophages succeed in phagocytosing the and breaking the invading bacteria.
2. These macrophages then run toward a local lymph node and present bacterial antigens to T-helper cells.
3. The sensitized T-cells leads to activation of macrophages which releases Nitric oxide and free radicals having bactericidal activity and mediators like TNF, chemokines which leads to granuloma formation.
4. Caseous necrosis occurs in the center of the epitheloid granuloma. Viable organisms often remain on the outer edges of the necrosis, inside the granuloma.

Lesion: Ghon (Primary) complex comprising of Ghon focus (small focus of tuberculous pneumonia in lung parenchyma usually lower part of upper lobe or upper part of lower lobe) and nodal involvement (hilar lymphnodes and lymphangitis of draining lymph vessels). Ghon complex undergoes progressive fibrosis often followed by radiologically detectable calcification to form Ranke complex.

Clinical presentation: Mostly asymptomatic but symptomatic less frequently in children, the elderly, and the immunocompromised.

Fates:

1. Healed lesions
2. Latent lesions which can reactivate to progress to secondary TB
3. Progressive primary TB leading to Milliary TB (small milliary tubercles containing numerous organisms but no caseous necrosis in different organs) due to massive lymphatic and hematogenous dissemination.

B. Secondary Pulmonary Tuberculosis:

1. Secondary TB occurs either due to Reactivation of Latent lesion or Reinfection
2. The infection can occur in any of the organ systems seeded during the primary infection. It is presumed that a temporary weakening of the immune system may precipitate reactivation.
3. It normally reactivates in the upper lobe because oxygen tension is the highest there, due to decreased pulmonary circulation, and Mycobacterium tuberculosis is an aerobic bacterium.
4. An old granuloma may weaken and erode into a bronchus or blood vessel (Progressive TB) and spread to take the form of Milliary TB.

Clinical presentation: Cough with hemoptysis (blood in sputum), night sweats, fever, anorexia and weight loss

Extrapulmonary Tuberculosis:

1. Endobronchial, Endotracheal and Laryngeal TB
2. Pleural and Pericardial effusion
3. Tuberculous lymphadenitis or Scrofula (Commonest in cervical lymph nodes)
4. Renal tuberculosis often presenting with sterile pyuria
5. Pott’s disease of vertebra
6. Tuberculous osteomyelitis
7. Tuberculous meningitis
8. Tuberculous salpingitis of fallopian tubes

Rule of 5 for Tuberculosis

1. Droplet nuclei are 5 micrometers and contain 5 Mycobacterium tuberculosis bacilli.
2. Patients infected with Mycobacterium tuberculosis have a 5% risk of reactivation in the first 2 years and then a 5% lifetime risk.
3. Patients with HIV will have a 5+5% risk of reactivation per year.

Laboratory Diagnosis of TB

Specimen:

A. Pulmonary TB:

1. Expectorated Sputum
2. Induced Sputum
3. Bronchoalveolar lavage
4. Gastric lavage (Choice in children who cannot cough up the sputum)
5. Lung biopsy

About collection of expectorated sputum:

• Early morning sputum with minimal saliva content of 3 consecutive days.
• Spot-Morning-Spot Timing is recommended now for non-hospitalized patients (i.e. Spot collection during initial visit to the clinic, Early morning sputum in the morning and Spot collection at second visit to the clinic) as it is more convenient.

B. Extrapulmonary TB:

1. Urine: First-morning urine at least 50 mL, obtained by catheterization or from the midstream clean catch on
2. three consecutive days for suspected Renal TB
3. Fluids: spinal, pleural, pericardial, synovial, ascitic, blood, pus, and bone marrow
4. Blood
5. Tissue

Transport and Storage:

• Storage: 4 c for not more than 5 days
• Transport: Cetylpyridinium chloride (CPC) method

Detection

A. Microscopy:

1. ZN staining:
Reagents and Technique of ZN stain
Observation: Acid Fast Bacilli (AFB) appear as pink brightened rods
Significant bacterial count: 50,000 to 100,000 bacilli per ml of sputum

Quantitation scale recommended by WHO and International Union Against TB and Lung Disease

• 0: Report as Non AFB observed
• 1-9/100 fields: Report Exact count
• 10-99/100 fields: Report as 1+
• 1-10/field: Report as 2+
• >10/field: Report as 3+

2. Fluorescent staining:

• Stain: Auramine-rhodamine fluorescent stain
• Observation: Bright rods against dark background when examined under uv light

B. Concentration and Decontamination of Specimens:

Use: Smear, animal inoculation, culture

Techniques:

1. Petroff’s method: sputum is liquefied with NaOH (4%), concentrated by centrifugation and then neutralized with HCl (8%)
2. Homogenisation method: H2SO4, HCl or oxalic acid
3. Trisodium phosphate method: Trisodium citrate, Sodium hydroxide, N-acetyl-L-cysteine (NALC)

C. Culture

Traditional Method:

1. Solid Medias: examined for growth twice a week for the first four weeks starting on day 3 to 5 postinoculation, and thereafter, once a week until the eighth week
Egg-based Lowenstein Jensen (LJ) media: Components of LJ media: To cook egg you need Egg (enhances growth), Salt (Mineral salt), Chilli (Malachite green inhibits contaminants), Sugar (Glycerol)
Agar-based Middlebrook 7H10 and 7H11 media

2. Incubation: 36-37 c in dark and light upto 12 weeks (Usually grow in 2 to 8 weeks)

3. Colony: Rough, tough and buff colored

4. Liquid medias: Liquid Media like Middlebrooke 7H9 media (Recovery of bacteria is quicker)

Newer method:

• Culture in Automated or Semi-automated liquid culture media like (Bactec 460)
• Radiolabeled broth demonstrating the metabolism of 14C-labeled palmitic acid with release of CO2
• Faster and more sensitive

D. Identification

Morphological properties: Microscopy and Colony characteristics

Biochemical tests

1. Niacin test: Only M.tuberculosis produces niacin in sufficient quantities in egg medium to give positive test indicated by a canary yellow color.
2. Catalase test: Tubercle bacilli (M.tuberculosis and M.bovis) are peroxidase positive and weakly catalsae positive while atypical mycobacteria are strongly catalase positive and peroxidase negative.
3. Nitrate reduction test: Positive for M.tuberculosis but Negative for M.bovis
4. Pyrazinamidase test: Positive for M.tuberculosis but Negative for other MTC species except M.cannetii
5. Susceptibility to TCH (Thiopen-2-carboxylic acid hydrazide): M.tuberculosis is resistant but other MTC species except M.cannetti are susceptible
6. Oxygen requirement: M.tuberculosis is aerobic but M.bovis is microaerophilic

E. PPD Skin Test:

• Reagent: Purified Protein Derivative (PPD) – purified preparation of antigenic tuberculoprotein
• Method: Mantoux test i.e. intradermal injection of 0.1 ml of PPD into flexor aspect of arm
• Purpose: A positive test indicates infection at some time but not necessarily current disease. This is important because many infected individuals will not manifest a clinical infection for years. When a positive PPD test occurs, you can treat and eradicate the disease before it significantly damages the lungs or other organs.
• Result: Read after 2-3 days
1. Positive: Determined by measure of zone of induration
• 15 mm in a healthy person (not known to have exposure)
• 10 mm in individuals from countries of high risk, healthcare workers or after BCG vaccination
• 5 mm in HIV infected or with recent known exposure
2. Flase negative:
• Milliary TB
• Aergic patients (Corticosteroids, malnutrition, Hodgkin’s disease, Sarcoidosis)
3. False positive:
• BCG vaccination
• Atypical mycobacterium

F. Drug Sensitivity Testing: Using antitubercular drugs like Rifampicin, Isoniazid, Ethambutol, Pyrazinamide, Streptomycin, etc.

Rheumatic fever (RF) is an acute, immunologically mediated, multisystem inflammatory disease involving heart, joints, CNS, skin and other tissues that occurs a few weeks after an episode of group A β-hemolytic streptococcal pharyngitis. Acute rheumatic heart disease (RHD) is the cardiac manifestation of RF and is associated with inflammation of the valves, myocardium, or pericardium. Rheumatic fever is said to “lick the knee but bite the heart”.

Pathogenesis:

Phase 1:

1. β-hemolytic streptococci (Group A) pharygitis
2. Formation of antistreptococcal antibodies which cross reacts with endogenous tissue antigens in heart (Antibody against Streptococcal M protein cross reacts with Cardiac myosin and Sarcolemma), joints (Antibody against Streptococcal hyaluronic acid cross reacts with connective tissue proteoglycans) and other tissues

Phase 2 (2 weeks Post-infection):

1. Joints: Acute febrile polyarthritis
2. Heart: Pancarditis
3. Eye: Uveitis
4. Kidney: Acute glomerulonephritis
5. Brain: Sydenham chorea (rare)

Morphology:

A. Acute Rheumaic Heart Disease:

1. Aschoff bodies or Rheumatic granuloma: Fibrinoid necrosis demarcated by:

• Antischkow cells (Specialized histiocytes resembling Epithelioid cells which appears catterpillar like in cross section and owl’s eye in longitudinal section)
• Lymphoplasmacytic infiltrate (Sparse)
• Rarely Aschoff cells (Inflammatory Giant cells)

2. Pancarditis: Diffuse inflammation and Aschoff Bodies in any of the 3 layers of heart – pericardium, myocardium, endocardium (including valves)

• Pericardium: “Bread and Butter” Pericarditis (Fibrinous or Serofibrinous)
• Myocardium: Myocarditis (Scattered Aschoff bodies within interstitial connective tissue)
• Endocardium: Fibrinoid necrosis along the lines of closure of valves forming 1 to 2 mm vegetations (verrucae); Macculum plaques usually in left atrium

B. Chronic Rheumatic Heart Disease:

1. Organization of Acute Inflammation and Subsequent Fibrosis:

• Valve leaflet thickening
• Commisural fusion and shortening
• Thickening and fusion of chordae tendinae
• “Fish mouth” or “Button hole” Stenoses: Fibrous bridging across the valvular commisures and calcification

2. Microscopical Examination:

• Diffuse fibrosis and neovascularization
• Aschoff bodies replaced by fibrous scar

Functional Consequences:

1. Valvular stenosis and regurgitation
2. Stenosis > Regurgitation
3. Involvement of Mitral valve alone: 70%
4. Involvement of both Mitral and Aortic valve: 25%
5. Mitral stenosis: 99% (Left atrium dilate and may harbor mural thrombi)
6. Long-standing congestive pulmonary changes: Leads to Right ventricular hypertrophy

Jone’s Criteria:

A. Major: “SPACE”

1. Subcutaneous nodules
2. Pancraditis
3. Migratory polyArthritis
4. Sydenham Chorea
5. Erythema Marginatum of Skin

B. Minor: LEAF

1. Fever
2. Arthralgia
3. Leukocytosis and Raised ESR (Erythrocyte Sedimentation Rate)

Diagnosis: Either of the following

1. Essential criteria (serologic evidence of a previous streptococcal infection) + 2 or more Major Criteria
2. 1 Major Criteria + 2 Minor Criteria

Notes:

• The clinical course of rheumatic fever involves a childhood infection with complications in adulthood (cardiac defect).
• Myocardial scarring following ischemia occurs far from vascular structures but in rheumatic fever scarring occurs close to vascular structures.
• Rheumatic fever in children proceeds from the myocardium to the endocardium to the joints; in adults, it proceeds from the joints to the endocardium to the myocardium.

Important terms:

1. Diastole: a period of relaxation during which heart fills with blood
2. Systole: a period of contraction during which the blood is ejected from the heart.
3. Isovolumetric: a phase when all valves are closed and ventricle behaves as a closed chamber and volume within ventricle remains constant

Time period of various events of cardiac cycle:

A)     Atrial Cycle: 0.8 sec

1. Systole: 0.1 sec

2. Diastole: 0.7 sec

B)      Ventricular Cycle: 0.8 sec

1. Systole: 0.3 sec

• Isovolumetric contraction: 0.05 sec
• Rapid ejection phase: 0.1 sec
• Reduced ejection phase: 0.15 sec

2. Diastole: 0.5 sec

• Isovolumetric relaxation: 0.1 sec
• Rapid filling phase: 0.1 sec
• Reduced filling phase (Diastasis): 0.2 sec
• Last Rapid filling phase (Atrial systole): 0.1 sec

Points to understand:

• Normally, atrial and ventricular systoles never coincide. Ventricular systole occurs during atrial diastole and atrial systole occurs during ventricular diastole.
• For a period of about 0.4 sec (Isovolumetric ventricular relaxation, Rapid ventricular filling phase and Reduced ventricular filling phase), both the ventricles and atria relax.

Events in Cardiac Cycle:

1. Atrial Systole:

• Preceded by ECG “P” wave  which begins due to spontaneous generation of action potential in SA node
• Contributes to last rapid phase of ventricular filling (20% filling) but is not essential for ventricular filling
• Filling of ventricle by atrial systole gives rise to 4^th Heart sound, which is not audible in normal adults
• “a” wave appears on atrial pressure curve due to increase in atrial pressure (4 to 6 mmHg in right atrium and 7 to 8 mmHg in left atrium)

2. Isovolumetric ventricular contraction:

• Ventricles are filled with blood: 80% filling occurred before atrial systole and 20% filling occurred during atrial systole
• Begins after onset of ECG “QRS” complex
• Immediately after ventricular contraction begins, pressure rises abruptly
• When Ventricular pressure > Atrial pressure, Atrioventricular (AV) valve closes giving rise to 2^nd heart sound (As mitral valve closes before tricuspid valve, 1^st heart sound may split)
• Since AV valves and semilunar valves (aortic and pulmonary valves) are both closed, isovolumetric contraction occurs and there is rapid rise in ventricular pressure.

3. Rapid Ventricular Ejection:

• When the left ventricular pressure rises above the aortic pressure (~80 mmHg), aortic valve opens and there is rapid ejection (70% ejection) of blood into the aorta.
• When the right ventricular pressure rises above the pulmonary pressure (~8 mmHg), pulmonary valve opens and there is rapid ejection (70% ejection) of blood into the pulmonary trunk.
• “c” wave appears on atrial pressure curve due to bulging AV valve on atria due to increasing ventricular pressure
• Pressure rise in the ventricles is slower because the blood flows into the arteries. The entry of blood into the arteries causes arteries to stretch and pressure increases. During this period, the pressure in the left ventricle and aorta reaches a maximum of 120 mmHg (systolic pressure) and that in right ventricle and pulmonary trunk reaches a maximum of 24 mmHg.
• Atrial filling begins
• Onset of ECG “T” wave marks end of both ventricular contraction and rapid ejection.

4. Reduced Ventricular Ejection:

• Ejection of blood (30% ejection) from the ventricles continues, but is slower
• Ventricular pressure begins to decrease
• Aortic and Pulmonary pressure also decreases because of runoff of blood from larger arteries into smaller arteries
• Atrial filling continues

5. Isovolumetric ventricular relaxation:

• Repolarization of Ventricles is now complete (marked by end of ECG “T” wave)
• Ventricular pressure begins to fall
• When the pressure in respective ventricles < pressure in aorta and pulmonary trunk, the semilunar valves close (closure of aortic valve followed by pulmonary valve) giving rise to 2^nd heart sound. Inspiration causes splitting of 2^nd heart sound.
• Dicrotic notch or incisura appears on aortic pressure curve as a “blip” after closure of aortic valve due to short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of the backflow.
• Since, AV valves and semilunar valves are both closed; isovolumetric relaxation
• Ventricular falls rapidly but the elastic walls of the arteries maintain a high pressure in the arteries, even during diastole although there is a fall in arterial pressure.
• “v” wave appears on atrial pressure curve due to accumulation of blood in atria against closed AV valves
• When ventricular pressure < atrial pressure, AV valves (Mitral and Tricuspid) open.

6. Rapid Ventricular Filling:

• Rapid flow of blood, long accumulated in the atria to the ventricles gives rise to the 3^rd heart sound, which is normal in children but pathologic in adults.

7. Reduced ventricular filling (Diastasis):

• Longest phase of cardiac cycle
• Only a small amount of blood flows into the ventricles at a slower rate from the great veins via atria.
• During this period, the blood in both atrium and ventricle becomes continuous as if a single cavity.
• Time required for diastasis and ventricular filling depends on the heart rate. Increase in heart rate decreases the time available for ventricular filling.

8. Last rapid filling phase:

• Coincides with the atrial systole

Summary:

Phases in Left Ventricle:

• Isovolumetric contraction: period between mitral valve closure and aortic valve opening; period of highest O2 consumption
• Systolic ejection: period between aortic valve opening and closing
• Isovolumetric relaxation: period between aortic valve closing and mitral valve opening
• Rapid filling: period just after mitral valve opening
• Reduced filling: period just before mitral valve closure

Heart Sounds:

• S1: mitral and tricuspid valve closure; loudest at mitral area.
• S2: aortic and pulmonary valve closure; loudest at left sternal border.
• S3: in early diastole during rapid ventricular filling phase.
• Associated with ↑ filling pressures and more common in dilated ventricles (but normal in children and pregnant women).
• S4: in late ventricular diastole or atrial systole.
• Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall.

Jugular venous pulse (JVP):

• a wave: atrial contraction
• c wave: RV contraction (tricuspid valve bulging into atrium).
• v wave: ↑ atrial pressure due to filling against closed tricuspid valve.

Flowchart: