Pulmonary Circulation

•The pulmonary circulation originates from the right ventricle. The main pulmonary arteries branch into lobar arteries and enter the lungs with the lobar bronchi.

 

  •The arteries branch in tandem with the airways and additionally feature right-angle bifurcations in order to reach peribronchiolar alveoli.

  •The amount of blood ejected by heart into pulmonary circulation is same as the amount ejected into systemic circulation.

 

   •Pulmonary vascular bed handles cardiac output in such a way that pressure is not high for the same volume.

   •Systemic circulation is a high pressure circulation due to greater resistance offered by the blood vessels ( mainly arterioles ) of the systemic vascular bed.

  •The pulmonary circulation on the other hand is a low pressure circulation due to less resistance offered by the pulmonary vessels.

  •The total resistance in pulmonary circulation is about one tenth of systemic circulation.

FUNCTIONAL ORGANISATION

   •Branch of pulmonary arteries and airway branch run parallel to each other.

 

  •Pulmonary capillaries are large in diameter and have multiple anastomoses.

 

  •Each alveolus is surrounded by a capillary basket.

  •Pulmonary artery branch divides to form arterioles making an extensive capillary lattice around a single alveolus.

 

  •Drains into pulmonary veins.

 

  •Pulmonary vessels are having blood which is about 40% of total weight of lungs.

FUNCTIONS OF PULMONARY CIRCULATION 

•Gas exchange – brings venous blood from various parts of body in contact with alveoli for exchange of gases.

 

•Filter – filter thrombi and emboli that originate from venous compartment and right side of the heart.

•Endothelial cells of pulmonary vessels release fibrinolytic agents that lyse blood clots(thrombi) and thus prevent the entry of these thrombi and emboli into coronary, cerebral and other important vessels.

 

•Metabolic functions-  vasoactive hormones are metabolized.

•Angiotensin I is converted to Angiotensin II in the lungs by ANGIOTENSIN CONVERTING ENZYME (ACE).

 

•Serves as blood reservoir - 500 ml of circulating blood is present in pulmonary circulation.

SPECIAL FEATURES OF PULMONARY CIRCULATION 

    •Pulmonary circulation is a low pressure and low resistance system.Pulmonary artery has thin walls and more compliant.

 

   •Due to their high compliance pulmonary vessels can accommodate a relatively large amount of blood.

  •Pulmonary arterioles are thin walled and contain less smooth muscle. Hence the ability to constrict is less and are highly compliant.

 

  •Capillaries form lattice in the alveolar wall and they collapse if local alveolar pressure exceeds capillary pressure.

 

  •Change in pulmonary venous and left atrial pressures profoundly affects gas exchange.

Wedge pressure reflects left atrial pressure

 

PULMONARY VASCULAR RESISTANCE (PVR)– 

Its very low, 1/10th of systemic vascular resistance.

•Reasons- 

A) Pulmonary resistance vessels (arterioles) are thin, short and wide with high compliance.

B) Resting vasoconstrictor tone is very low and arterioles are mostly dilated.

PVR falls with increased pulmonary arterial pressure and increased cardiac output 

•Mechanisms  -

1.Capillary recruitment – when blood flow increases , the collapsed vessels in lungs are opened. This decreases the overall PVR.

 

2. Capillary distension in response to increased pressure. This occurs due to thin and highly compliant pulmonary capillaries.

PHYSIOLOGICAL SIGNIFICANCE OF LOW PVR

   •When the flow rate is high, decreased PVR decreases velocity. This gives more time for capillary blood to take up O2 and remove CO2.

 

  •Capillary distension decreases PVR, increases capillary surface area. This facilitates diffusion of gases along the alveolar capillary membrane.

 

  •The decrease in PVR decreases the load on Right ventricle and decreases the capillary pressure that prevents pulmonary edema.

PULMONARY BLOOD FLOW 

•10% of circulating blood volume – 500 mL.

 

     •In pulmonary arteries- 150 mL

     •In pulmonary veins – 270 mL

     •In pulmonary capillaries – 80mL

FACTORS AFFECTING PULMONARY BLOOD FLOW 

•Pulmonary vascular resistance (PVR)

 •Gravity

 •Alveolar pressure

 •Arterial to venous pressure gradient

PULMONARY VASCULAR RESISTANCE 

PVR is affected by lung volumes, hormones and oxygen tension.

1.Lung volumes - 

pulmonary vessels are of two types-

 

Alveolar vessels (arterioles, capillaries , venules) subjected to alveolar pressure and

Extra-alveolar vessels( pulmonary arteries and veins) subjected to pleural pressure.

•High lung volumes –pleural pressure is more negative. Alveolar vessels are compressed and pulmonary vascular resistance is increased.

 

•Low lung volumes – pleural pressure is positive. It increases PVR. PVR is lowest at functional residual capacity and increases at both higher and lower lung volumes.

 

2.Hormones – 

Vasoconstrictors increase PVR. Vasodilators decrease PVR

 

3. Oxygen tension – 

low O2 tension decreases PVR by causing vasoconstriction.

4. Effects of gravity

•Upright posture pulmonary blood flow increases from apex to base of the lungs.

 

•Physiologically , lung is divided into three zones with perfusion changes.

•Alveolar pressure – depends on lung volumes and changes pulmonary blood flow

 

•Arterio venous pressure gradient – affected by alveolar pressure and determines rate of blood flow.

REGULATION OF PULMONARY BLOOD FLOW

•Regulated by active and passive factors.

 

•Active factors are neural , hormonal and chemical.

Neural regulation

•Richly innervated by sympathetic nerves.

•Resting sympathetic tone of pulmonary circulation is  almost absent.

•Unaffected by ANS in normal conditions.

Hormonal regulation

Vasoconstrictors decreases pulmonary blood flow , some of them include

   •Serotonin

   •Norepinephrine

   •Endothelin

   •Angiotensin

   •Thromboxane A2

   •Leukotrienes

 

Vasodilators increases pulmonary blood flow, some of them include

•Adenosine

•Acetylcholine

•Prostacyclin

•Bradykinin

•Nitric oxide

•Increase pulmonary blood flow

CHEMICAL REGULATION 

•Hypoxemia or alveolar hypoxia causes vasoconstriction of small pulmonary arteries.

 

•Hypoxia directly causes contraction of pulmonary vascular smooth muscles.

 

•High CO2 and low blood pH – vasoconstriction.

 

•Hypoxia inhibits K+ channels and opens the voltage gated Ca+2 channels .

 

• Influx of Ca+2 causes vasoconstriction.

 

Passive factors

•Cardiac output – higher Cardiac output increases pulmonary circulation

 •Gravity

 •Lung volumes

FILTRATION ACROSS PULMONARY CAPILLARIES

•Starling forces governs filtration of fluid across capillary walls in pulmonary circulation.

 

•Surface tension favors filtration  and alveolar pressure opposes filtration

 

1.Hydrostatic and osmotic pressure gradients- hydrostatic pressure lesser than osmotic pressure favors net absorption of fluid from interstitial space into capillary blood.

2.Alveolar surface tension favors filtration.

 

3.The extensive and well developed in lungs.

 

• The lymphatics in terminal bronchioles drain the excess fluid from peribronchial space.

APPLIED PHYSIOLOGY 

PULMOMARY EDEMA 

•Develops when excess of free fluid accumulates in interstitial spaces and alveoli.

 

•Causes – 

   1. Increased capillary hydrostatic pressure

   2.Increased alveolar surface tension.

   3.Decreased oncotic pressure.

   4. Increased capillary permeability.

Effects of pulmonary edema

•Decreases gas exchange resulting in hypoxemia, hypercapnia.

 

•Obstructs small airways and it increases airway resistance.

 

•Lung compliance decreases due to interstitial swelling and increased alveolar surface tension.

 

•Work of breathing increases due to decreased compliance and airway obstruction.

Physiological basis of treatment of pulmonary edema

•Aim of treatment is to reduce pulmonary capillary hydrostatic pressure.

 

•1. Diuretics – decrease blood volume.

•2. Digitalis – increases left ventricular function.

•3. Vasodilators – relaxation of systemic blood vessels

DROWNING

•Fresh - water drowning : Aspiration of water occurs into the lungs, death doesn’t occur due to pulmonary edema.

 

•Death is due to ventricular fibrillation.

 

•Entry of water into blood causes hypotonicity and hemolysis.

 

•Hemolysis  causes hyperkalemia and hyponatremia.

 

•Ventricular fibrillation occurs due to hyperkalemia and hypoxemia.

Salt water drowning

•Aspirated water is hypertonic due to high sodium and chloride content of sea water.

 

•Hypertonic fluid in alveoli produces pulmonary edema.

 

•Cause of death is asphyxia.

PHYSIOLOGY OF LACTATION | DEVELOPMENT OF BREAST

PHYSIOLOGY OF  LACTATION  

DEVELOPMENT OF BREAST 

 Present in both the sexes but rudimentary in males and well developed in females.

PHASES OF DEVELOPMENT OF BREAST 

In intrauterine life

At birth

At puberty

In pregnancy

During lactation

BREAST IN INTRA UTERINE LIFE ( EMBRYOGENESIS )

•Mammary bud – at 18-19 weeks of gestation  thickened mass of epithelium develop.

•16-20 solid outgrowths  arises and project into dermis.

•Then this thickened mass andoutgrowth canalized – form  Rudimentary duct system.

•Terminal part of outgrowth  proliferate into secretory  elements, Occurs at puberty.

•Proximal end of each duct  opens into common pit by  cavitation of thickened  mass

•Growth of mesodermal  tissue pushes wall of the pit  outwards as Nipple.

 

 

BREAST AT BIRTH 

* At birth rudimentary as tiny nipples and few ducts radiating from it.

BREAST AT PUBERTY

*Upto puberty remain quiescent and then changes occurs.

1)Thelarche – (9-11 yrs of age) at the time of  puberty before menses.

*Breast gets enlarged and only duct system proliferate and shows branching.

2) At Menarche – after menses cyclical growth correspond with menstrual cycle.

*In proliferative phase – duct cells proliferate.

*In luteal phase – progesterone stimulate proliferation of terminal ductules – glandular  tissue forms.

*At Menstruation –as both oestrogen and progesterone levels , no proliferation of  duct cells and glandular tissue.

*With further cycles progressive growth  occurs with fat deposition in adipose tissue.

BREAST IN PREGNANCY 

*Growth of both - Glandular & Ductal tissue occurs.

*Only during first pregnancy glandular tissue  develops fully.

*In first half – Duct system proliferate and shows sprouting and branching along with  growth of stroma and deposition of fat.

*In second half – growth of glandular tissue  occurs.

BREAST DURING LACTATION

*After child birth alveolar cells get enlarged and distended and starts forming milk  (Lactogenesis)

*Involution – after normal period of lactation  (7-9 months) alveolar epithelium undergoes  apoptosis and glands revert back to non-  pregnant state.

FUNCTIONAL ANATOMY OF BREAST 

Gross anatomy –  round elevated structure present over pectoral region, with central dark pigmented area areola and projected  above surface - Nipple.

 

Histological structure.

*The fascia covering mammary gland is  connected by suspensory ligaments to  overlying skin and underlying muscle.

*It Consists of 15-20 lobes and each lobe has  number of lobules.

*Glandular tissue – consists of alveoli having  secretary cells.

*Secretion – Apocrine in nature by exocytosis  into ducts.

*About 15-20 ducts opens at summit of nipple, just before opening lactiferous ducts shows  dilatation called – Lactiferous sinus.

*Smaller ductules lined by single columnar  epithelial cells and near opening at nipple lined  by squamous cells.

*Around alveoli ductules and lobules are  present in myoepithelial cells – so squeeze  and pour content into ductules.

Electron microscopically

*Secretory cells contains rough and smooth  endoplasmic reticulum, numerous  mitochondria, Golgi apparatus and Lysosomes.

*Protein as membrane bound vesicles & fat as  large globule.

CONTROL OF BREAST DEVELOPMENT AND GROWTH 

OESTROGEN –

It is essential mainly for ductal growth and fat deposition, also causes thickening of nipple.

PROGESTERONE 

It is essential for Glandular tissue development.

Other hormones – Growth hormone, thyroxine, cortisol and insulin cause growth and development.

Corpus luteal & placental hormones – during pregnancy

PROLACTIN 

Structure and secretion :

Single peptide chain secreted by acidophilic cells of anterior pituitary  gland.

 

Placental concentration

Pulsatile

Shows diurnal variations

During pregnancy – start at 8th week & peak  (200-400 ng/ml) at term

Sources – placenta, amniotic fluid & maternal  anterior pituitary gland.

During pregnancy & lactation – affected by  oestrogen.

Control of prolactin secretion

Hypothalamic control – Prolactin  inhibitory factor from  Arcuate nucleus of  hypothalamus acts on  anterior pituitary  gland.

PHASES OF LACTATION 

1)Mammogenesis

2)Lactogenesis

3)Galactokinesis

4)Galactopoiesis.

MAMMOGENESIS 

•Breast develops fully and prepared for milk secretion after delivery.

•Hyperplasia of ductal & alveolar tissue

•Areola – Pigmented.

•Sebaceous glands becomes prominent in areola.

•Nipples become larger and pigmented.

LACTOGENESIS 

 

Human milk contains

Colostrum – Deep yellow colour fluid during  postpartum

Contains – high protein, immunoglobulins & lactoferrins

Granular bodies – colostrum corpuscle (alveolar cells,  Leucocytes with fats)

Transition milk or intermediate milk – 6-15th day.

Mature milk – after 15th day

 

FORMATION OF MILK 

Mammary gland – metabolically active

Amino acids , FA, glucose & Ca derived from  plasma into alveolar cells.

Process involved are :

1)Fat synthesis and secretion

2)Ion and water secretion

3)Transcytosis of immunoglobulins

4)Exocytosis.

GALACTOKINESIS 

It is nothing but expulsion of milk

   Milk ejection

   Milk expulsion

   Milk let down

   Suckling effect.  (Psychological

component)

GALACTOPOIESIS 

It is nothing but maintenance of milk secretion.

Depend on surge in prolactin secretion.

In nursing mothers reflex causes 10-20 fold  rise in prolactin secretion for 1 hr & it occurs  at every feeding.

It depend on infants demand.

IMPORTANCE OF LACTATION 

Advantages of breastfeeding to the baby

Advantages of breastfeeding to the  mother.

ADVANTAGES OF BREAST FEEDING TO BABY 

1)Balanced diet – contains proteins, minerals, fats, carbohydrates and vitamins

2)Protection against infection – high lymphocytes, neutrophils, macrophages, lysozymes & immunoglobulins.

3)Easily digestible.

4)Growth factors – epidermal growth factors, insulin and somatostatin C are present.

5)Other – sterile, convenient, inexpensive, no allergy.

ADVANTAGES OF BREAST FEEDING TO MOTHER 

•Lactational ammenorrhoea (natural contraception)

•Involution of uterus.

•Protection against breast engorgement.

•Protection against obesity – body fat used for milk synthesis.

•Emotional bonding.

•Protection against cancer.

FEMALE REPRODUCTIVE SYSTEM

Female gonads are the ovaries where the female sex cells or ova are formed. 

    Female reproductive tract includes :

    1)An organ (uterus) to hold and nourish a developing infant.

    2)Various passageways

    3) External genital organs

   

OVARIES

   

     Small, somewhat flattened oval body.             Ovaries descend but only as far as the pelvic portion of the abdomen. 

    Held in place by ligaments that attach them to the uterus and body wall.

   

OVA AND OVULATION

   Ovaries of a newborn female contain a large number of potential ova.

   Each month during the reproductive years, several ripen but only one is released.

   

   Maturation of the ovum takes place in a small fluid-filled cluster of cells called the ovarian follicle. (graffian follicle)

  As the follicle develops, cells in its wall secrete estrogen which stimulates growth of the uterine lining.

  

   When an ovum has ripened, the ovarian follicle may rupture and discharge the egg cell from the ovary surface.

   The rupture of follicle allowing the escape of an ovum is called ovulation. 

  

   Any ova that are not released degenerate.

   Released egg cell makes its way to the nearest oviduct i.e. a tube that arches over the ovary and leads to the uterus.

   

CORPUS LUTEUM

    After the ovum is expelled, the remaining follicle is transformed into a solid mass called the corpus luteum.

   Corpus luteum secretes estrogen and progesterone.

   Which eventually shrinks and is replaced by scar tissue.

   When a pregnancy occurs, however, the structure remains active for three months.

   Sometimes during a normal ovulation, the corpus luteum persists and forms a small ovarian cyst, (fluid filled sac) which resolves without treatment

   

ACCESSORY ORGANS

They include :

    oviducts

    uterus

    vagina

    greater vestibular glands 

    vulva

    perineum

  

OVIDUCTS

   Tubes that transport the ova in the female reproductive system.

   Also known as the uterine tubes or fallopian tubes. Their is no direct connection between ovary and this tube.

   Ovum is swept into oviduct by a current in the peritoneal fluid

  

   Peritoneal fluid produced by fimbriae. (small, fringelike extensions located at the edge of the tube’s opening into the abdomen). 

   Ova cannot move on own.

   Movement depends on sweeping action of cilia in the oviduct’s lining and on peristalsis of the tube.

   Takes 5 days for an ovum to reach the uterus form the ovary

  

UTERUS

   Organ in which a fetus can develop to maturity.

  Oviducts lead to the uterus.

  Superior portion rests on upper surface of the urinary bladder and inferior portion embedded in the pelvic floor between the bladder and the rectum.

   

 WALLS OF UTERUS

The walls of the uterus include:

    1) Muscular layer (myometrium)    

    2) Inner layer called endometrium

      

The inner layer changes during menstrual cycle

   

VAGINA

    Distal part of the birth canal which opens to the outside of the body.

    Cervix (opening of the uterus) leads to the vagina.

   Muscular tube connecting the uterine cavity with outside.Lining of the vagina is a wrinkled mucous membrane similar to that found in the stomach.

  

    Rugae (folds) permit enlargement so that childbirth usually does not tear the lining.

   Vagina is an organ for child birth and also receives the penis during sexual intercourse.          A fold of membrane, called the hymen, may sometimes be found near the vaginal canal opening.

  

GREATER VESTIBULAR GLANDS

   Just superior and lateral to the vaginal opening are the two mucus-producing greater vestibular glands.

   These glands secrete into an area near the vaginal opening known as the vestibule.

  These glands provide lubrication during intercourse.

   

PUBERTY IN FEMALES

   The onset of puberty is caused by an alteration in brain function that increases the secretion of GnRH.

   This hormone in turn stimulates the secretion of pituitary gland gonadotropins,which stimulate follicle development and estrogen secretion.

   

   The adipose-tissue hormone leptin is known to stimulate the secretion of GnRH and may play a role in puberty. This may explain why the onset of puberty tends to correlate with the attainment of a certain level of energy stores(fat) in the girl’sbody.

AMENORRHEA 

   

    The failure to have a normal menstrual cycle is called amenorrhea. Primary amenorrhea is the failure to initial normal menstrual cycles at puberty(menarche), whereas secondary amenorrhea is defined as the loss of previously normal menstrual cycles(common causes pregnancy and menopause).

   

     Excessive exercise and anorexia nervosa can cause both primary and secondary amenorrhea.

  

PRECOCIOUS PUBERTY

    The age of normal onset of puberty is controversial. However, puberty onset before the age of 6-7 in girls and 8- 9in boys warrants clinical investigation.

    Precocious puberty is defined as the premature appearance of secondary sex characteristics and is usually caused by an early increase in gonadal steroid production.

    This leads to an early onset of the puberty growth spurt, maturation of the skeleton, breast development(in girls) and enlargement of genitalia in boys. 

    True precocious is caused by the premature activation of GnRH and LH and FSH secretion.         Which is often caused by tumors or infections in the area of the central nervous system that control GnRH release. 

    Treatments that decrease LH and FSH release are important to allow normal development.

  

CONTROL OF OVARIAN FUNCTIONS

THE OVARIES HAVE SEVERAL FUNCTIONS

▪ Oogenesis-the production of gametes during the fetal period.

▪ Maturation of the oocyte.

▪ Expulsion of the mature oocyte(ovulation)

▪ Secretion of the female sex steroid hormones (estrogen and progesterone). It also secretes the peptide hormone inhibin.

 

The major factors controlling the ovaries are:

1.GnRH – Gonadotropin-releasing hormone 2.FSH-Follicle stimulating hormone

3.LH- leutinizng hormone

4.Estrogen 

5.Progesterone

  

GONADOTROPIN-RELEASING HORMONE IS SECRETED FROM THE HYPOTHALMUS AND IT STIMULATES THE ANTERIOR PITUITARY GLAND TO SECRETE LH AND FSH.

    LH is released form the pituitary gland. Its main function is to cause ovulation and it causes the formation of the corpus luteum.

    FSH is primarily responsible for stimulating the growth of the ovarian follicle.

   Estrogen is secreted from the ovary and it is involved in the thickening of endometrium of the uterus and the growth of the uterus

   Progesterone causes the endometrium to secrete special proteins during the second half of the menstrual cycle, preparing it to receive and nourish an implanted fertilized egg.

  

   During early in uterine development, the primitive germ cells, or oogonia, undergo numerous mitotic divisions. Around the seventh month after conception, the fetal oogonia cease dividing. 

   

   During fetal life, all the oogonia develop into primary oocytes, which then begin a first meiotic division by replicating their DNA. 

   They do not complete division in the fetus. The cells are said to be in a state of meiotic arrest. This state continues until puberty and the onset of renewed activity in the ovaries.

 

   Only those primary oocytes destined for ovulation will complete the first meiotic division,it occurs just before the egg is ovulated.

    Each daughter cell receives 23 chromosomes, each with two chromatid. In this division, one of the two daughter cells, the secondary oocyte, retains virtually all the cytoplasm.

    The other called the first polar body is small and non-functional. Thus, the primary oocyte, which is already as large as the egg will pass on to the secondary oocyte just half of its chromosomes but almost all of its nutrient-rich cytoplasm.

      The second meiotic division occurs in the fallopian tube after ovulation, but only if the secondary oocyte is fertilized. 

     As a result of this second meiotic division, the daughter cells receive 23 chromosomes, each with a single chromatid.

  

   Once again, the daughter cell, now called an ovum, retains nearly all the cytoplasm. The other daughter cell, the second polar body is very small and non-functional.

   The net result of oogenesis is that each primary oocyte can produce only one ovum.

      

    GnRH is secreted from the hypothalmus. This causes the secretion of LH and FSH from the anterior pituitary gland. 

    LH and FSH levels increase (slightly elevated levels of estrogen and inhibin exhibit little negative feedback)

   

     Multiple follicles begin to enlarge and secrete estrogen. Estrogen concentration increase markedly.

    FSH secretion and FSH plasma concentration decrease.

     The increasing plasma estrogen concentration exerts a “positive” feedback on gonadotropin secretion.

 

   An LH and FSH surge is triggered and ovulation occurs.

   The corpus luteum forms and begins to secrete large amounts of both estrogen and progesterone.

   

    Plasma concentrations of estrogen and progesterone increase.

 FSH and LH secretion are inhibited and their plasma concentrations decrease.

 The corpus luteum begins to degenerate and decrease its hormone secretion.

 Plasma estrogen and progesterone concentrations decrease.

 FSH and LH concentrations begin to increase and a new cycle begins.

  

EFFECTS OF ESTROGEN

▪ Stimulates the growth of the ovary and follicles.

▪ Stimulates external genitalia.

▪ Stimulates breast growth, particularly ducts and fat deposition in puberty.

▪ Stimulates female body configuration development during puberty: narrow shoulders, broad hips, female fat distribution. (deposition on hips and breasts)

▪ Stimulates prolactin secretion but inhibits prolactin’s milk-inducing action on the breasts.

  

EFFECTS OF PROGESTERONE 

▪ It Converts the estrogen primed endometrium to an actively secreting tissue suitable for implantation of the embryo.

▪ Decreases contraction of the fallopian tubes and myometrium.

▪ Increases body temperature.

▪ Decreases proliferation of vaginal epithelial cells.

▪ Induces thick, sticky cervical mucus.

▪ Inhibits milk producing effects of prolactin.

▪ Stimulates breast growth, particularly glandular tissue.

PHYSIOLOGY OF MENSTRUAL CYCLE

FOLLICULOGENESIS

SELECTION

•10-15 primordial follicles start maturing but only one  matures fully dominant  ( Graffian )  follicle  &  rest undergo atrophy

 

• Selection occurs at day 5-7

• It depends on  

       -  intrinsic capacity of follicle to  synthesize estrogen.

        - no. of FSH receptors.

       

• Follicle with  highest no. of FSH receptors will continue  to thrive.

 

• These changes are under influence of  (mainly) FSH and LH  from anterior pituitary.  

 

•FSH ACTIONS

   

   -Recruitement

   -Mitogenic effect which leads to 

       Increase in  No.of granulosa cells

OVULATION

• Release of secondary oocyte from  ovary (following  rupture  of Graffian  follicle)  into  peritoneal cavity is called ovulation 

 

• Occurs at 14th  day   ( 28-day cycle )

 

• 36 hrs after mid-cycle LH surge.

 

PREOVULATORY PERIOD

• NEGATIVE FEEDBACK  ON  PIUITARY

 

-Estradiol and inhibin have negative feed back on pituitary secretion of FSH

 

 • POSITIVE FEEDBACK ON PITUITARY

•Estradiol (reaching a threshold concentration) have +ve feed back on pituitary (facilitated by low levels of progestrone) which leads to LH surge and  secretion of progestrone.

•Operates after puberty.

•+ve feed back on pituitary secretion of FSH.

 

OVULATION

• During follicular phase, low level of estrogen suppresses production of LH. (Negative feedback )

 

• When ovum is almost matured, estrogen levels reaches threshold above which they stimulate production of LH , LH SURGE (Positive feedback )

 

• FSH surge occurs .

 

• Gonadotropin surge causes ovulation after 36 hrs.

 

POSTOVULA TORY  PHASE

 

•Remarkably  constant  period  - 14 days.

 

 •Development of Corpus  luteum - luteal  phase.

 

 

          Ovulation

                ↓

Corpus  haemorrhagicum

                ↓

      Corpus luteum

                ↓

          1. Corpus albicans

     2. Corpus  luteum of pregnancy.

 

•FORMATION OF CORPUS HEMORRHAGICUM

•It is  Graafian  follicle  is  filled with blood . Minor  bleeding  from  follicle  into  abdominal  cavity  may  cause  peritoneal  irritation  and  lower  abdominal   pain (mittelschmerz).

 

•FORMATION OF CORPUS LUTEUM

•Ruptured follicle heals &  forms corpus luteum (Yellow body)  .

• LH is responsible  for  this.

•They  secrete progesterone and to a lesser  extent estrogen . Progesterone has negative  feedback effect on anterior pituitary and  decreases secretion of both LH & FSH.

     The fate of corpus  luteum  depends  on conception.

 

•FORMATION OF CORPUS ALBICANS

•If  no fertilization  ,it involute after 24th  day  and is replaced  by a whitish  scar tissue,  called  corpus  albicans.  

      

      This is  due to falling levels  of  FSH  and  LH  and inhibin secreted  by lutein cells.  With   involution  of corpus luteum, on 26th  day , levels of oestrogen,  progesterone and  inhibin fall.   

     

      This removes feedback inhibition of   anterior pituitary consequently FSH and in a few days LH secretion begins  and next cycle  is initiated.

 

•CORPUS LUTEUM OF PREGNANCY 

  •If  ovum  is  fertilized ,corpus luteum  persists and secretes  oestrogen  and  progesterone  till 3rd month of pregnancy   when placenta takes over its endocrine   function.

 

  •An embryo in the uterus will secrete a HCG . 

  •It prevents  corpus luteum from decomposing which maintains progesterone levels so that endometrium is not shed.

 

LUTEAL PHASE

    •Corpus luteum  produces significant amounts of  progesterone, which  makes  endometrium receptive to implantation of  blastocyst.

    •High levels of estrogen and progesterone suppress production of FSH and LH that  corpus luteum needs to maintain itself.

 

UTERINE  CHANGES   

ENDOMETRIAL CYCLE

 

•Cyclic  changes  occurring in  endometrium   during  reproductive period  in females.

 

PHASES  OF ENDOMETRIAL  CYCLE

•1st day  of bleeding - first  day of cycle

 

•Three  phases

    1)Menstrual  phase      :    1st - 5th day

    2)Proliferative  phase  :    6th - 14th day

    3)Secretory   phase      :   15th - 28th day

 

FOLLICULAR OR PROLIFERATIVE PHASE 

    Estrogen leads to increase in mitotic activity in the glands and in stroma.

    Endometrial thickness increases from 2 to 8 mm. (from basalis to opposed basalis layer)

LUTEAL OR SECRETORY PHASE

    Progestrone increases which leads to restriction of  Mitotic activity.

    Endometrial glands secrete glycogen rich vacoules and the following changes are seen

              -Stromal edema

              -Stromal cells enlargement

              -Spiral arterioles develop, lengthen and coil

                                     

MENSTRUATION

•Periodic desquamation of the endometrium.

•The external hallmark of the menstrual cycle

     •Just before menses the endometrium is infiltrated with leucocytes

    •Prostaglandins are maximal in  the endometrium just before menses.

    •Prostaglandins increases which leads to constriction of the spiral arterioles leading to ischemia and desquamation.

   Followed by arteriolar relaxation, bleeding and tissue breakdown.

 

SECRETORY PHASE 

• 15th to 28th day.

 

•Changes - due to both estrogen and progesterone secreted by corpus luteum .

 

• It coincides with luteal phase of ovarian cycle.

 

CHATRESTERIC CHANGES IN SECRETORY PHASE 

   

   1. Prominent corkscrew-shaped glands  

   

    2. Increased vascularity

    3. Endometrial glands –

    Increases in size and thickness of endometrium and become tortuous.

    They secrete thick viscous fluid containing glycogen.

    4. Blood supply of endometrium further  increases. 

    5. Thickness of endometrium increases to 5-6 mm.

   6. These changes provide appropriate conditions for implantation.

   7. If their is no fertilization then corpus luteum involutes and oestrogen and progesterone level falls.

 

MENSTRUAL PHASE 

 

26th or 27th day of  previous cycle

               ↓

reduction in  estrogen  & progesterone  from ovary

              ↓

    menstruation

 

Average duration -  3-5 days .

 

CHANGES IN CERVIX

•PROLIFERATIVE PHASE 

  Cervical secretions become thin.  

  •At ovulation , it is thinnest and its elasticity  is maximum.It can be stretched like elastic thread  (spinnbarkeit  effect) which favours    transport of sperms.

  •When Mucus is spread on slide it shows fern-like pattern.

SECRETORY PHASE

  

  Cervical secretions decrease in quantity and  becomes thick.

  It make a plug and prevent entry of sperm  through cervix.

CYCLIC CHANGES IN VAGINA

PROLIFERATIVE PHASE 

  

Epithelium becomes thickened and cornified.

and contain glycogen granules.

 

SECRETORY PHASE 

  

Epithelium proliferates and infiltrated with leucocytes.  

Secretions become thick and viscid which   increases resistance to infection.

 

HORMONAL CONTROL OF MENSTRUAL  CYCLE

•Hormones involved are:

1.Hypothalamic hormone - GnRH

2.Anterior pituitary hormones – FSH and LH

3.Ovarian hormones – Estrogen and progesterone.

Physiology of Transport of Gases | Gas Exchange

GAS EXCHANGE

SITES OF GAS EXCHANGE 

It occurs in two places mainly 

       -At tissues

(between blood & tissues).

       -At the lungs

(between blood & air).

MECHANISM OF GAS EXCHANGE

Gaseous exchange occurs by simple diffusion.

SIMPLE DIFFUSION

The movement of gases occur down the partial pressure gradient i.e from high partial pressure to low partial pressure.

IN LUNGS 

 

• O2 diffuses from alveoli to blood  down its pressure gradient.

 

• CO2 diffuses from blood to alveoli  down its pressure gradient.

TOTAL AND PARTIAL PRESSURES OF GASES

1)Alveolar PO2 = 100 mmHg

2)Pulmonary Artery  PO2 = 40 mmHg

(Pulmonary artery conatins venous blood)

3(Pulmonary Vein PO2 = 100 mmHg

(Pulmonary vein contains arterial blood)

Alveolar-Capillary membrane

(Respiratory membrane)

FACTORS THAT AFFECT GASEOUS DIFFUSION 

1)Partial pressure gradient of the gas across the alveolar- capillary membrane. (60 mmHg for O2 & 6 mmHg for CO2).

2)Surface area of the alveolar-capillary membrane. (about 70  m2).

3)Thickness of the alveolar-capillary membrane. (about 0.5 μ).

4)Diffusion coefficient of the gas that depends on the following parameters :

    •Gas solubility. (CO2 is 24 times soluble than O2).

     •Molecular weight of the gas. (CO2 M.W. is 1.4 times greater than O2).

     •Net effect: CO2 diffusion is 20 times faster than O2

TRANSPORT OF OXYGEN IN BLOOD

•O2 is transported by the blood mainly in two forms:

     -Physically dissolved  in blood = 1.5%

     -Chemically bound  to haemoglobin = 98.5%

PHYSICALLY DISSOLVED OXYGEN 

    

     •Only 1.5 % of total O2 in blood.

     •Dissolved in plasma and water of  RBC. (because solubility of O2 is  very low)

     •It is about 0.3ml of O2 dissolved in  100ml arterial blood (at PO2 100  mmHg).

     •Its amount is directly proportional  to blood PO2.

     •Can not satisfy tissue needs.

CHEMICALLY COMBINED OXYGEN 

    

     •98.5 % of total O2 in blood.

     •Transported in combination with Hb.

     •It is about 19.5 ml of O2 in 100 ml of arterial blood.

    •Can satisfy tissue needs.

OXYGEN COMBINED TO HEMOGLOBIN 

     •Hb is formed of 4 subunits.

     •Each subunit contains a heme group attached to a  polypeptide chain (α or β).

     •O2 binds to the ferrous iron atom in the heme group in a  rapid oxygenation reaction (HbO2).

     •The connection between iron and O2 is weak and reversible.

     •The iron stays in the ferrous state.

     •Thus, each Hb molecule can carry up to 4 O2 molecules.

OXYGEN CONTENT OF BLOOD 

      •It is the total amount of Oxygen carried by blood.

     Which is nothing but the sum of dissolved O2 and O2 combined with Hb ( 0.3 ml/100ml + 19.5 ml/100ml )

Plasma (0.3 ml) + Hb of RBCs (19.5 ml)

= 19.8 ml/100 ml blood.

 

      •It depends mainly on the O2 bound to Hb, as it represents the main component.

OXYGEN CARRYING CAPACITY OF THE BLOOD 

    

     •It is the maximum amount of O2 that can be carried by Hb.

     •Each gram Hb, when fully saturated with O2, can carry 1.34  ml O2.

     •As Hb content = 15 gm/100 ml blood.  So, O2 carrying capacity = 1.34 x 15

= 20.1 ml O2/100 ml blood.

(Hb = 15 gm  Each gm: 1.34 ml O2)

                  

Hb SATURATION WITH OXYGEN 

(%  Hb saturation)

•It is an index for the extent to which Hb can be combined with oxygen.

 

•When all Hb molecules are carrying their maximum O2 load,  Hb is said to be fully saturated (100 % saturated).

 

•PO2 of the blood is the primary factor that determines % Hb saturation.

Importance of Hb saturation

•In arterial blood (High PO2 ):

97% of Hb is saturated with O2

•In venous blood (Low PO2 ):

75% of Hb is saturated with O2

 

•At the lung: high alveolar PO2 (100 mmHg)

Hb automatically loads up (binds) O2.

•At the tissues: low tissue PO2  (40 mmHg)

Hb automatically unloads (releases) O2.

OXYGEN HEMOGLOBIN DISSOCIATION CURVE

•It is a curve that represents the relationship between  blood PO2 (on the horizontal axis) and % of Hb saturation (on the vertical axis) .

Because the % of haemoglobin saturation depends on the PO2 of  the blood.

•It is not linear , it is an S-shaped curve that has 2 parts:

     -upper flat (plateau) part.

     -lower steep part.

In the pulmonary capillaries (lung, PO2 range of 100-60 mmHg).

97% of Hb is saturated with O2.

90% of Hb is saturated with O2 (small change in % Hb

-At PO2 100 mmHg

-At PO2 60 mmHg  saturation).

The upper flat (plateau)  part of the curve

•PHYSIOLOGICAL SIGNIFICANCE

- Drop of arterial PO2 from 100 to 60 mmHg

little decrease in Hb saturation to 90 % which will be sufficient to  meet the body needs.

This provides a good margin of safety against blood PO2

changes in pathological conditions

- Increase arterial PO2 (by breathing pure O2

)little increase in % Hb saturation (only 2.5%) and in total O2 content

of blood.

In the systemic capillaries (tissue, PO2 range of 0-60 mm Hg).

70% of Hb is saturated with O2

- At PO2 40 mmHg (venous blood)  (large change in % Hb saturation).  

The steep or lower part  of the curve

•Physiologic significance:

- In this range, only small drop in tissue PO2

rapid desaturation of Hb to release large amounts of O2

- If arterial PO2 falls below 60 mmHg

Hb occurs very rapidly  tissues.

This is very important at tissue level.

FACTORS AFFECTING O2 HB DISSOCIATION CURVE 

Factors that shift O2-Hb Curve to the right =

decreased affinity of Hb to O2 & increase  O2 release to tissues.

Factors that shift O2-Hb Curve to the left =

increased affinity of Hb to O2 & decrease  O2 release to tissues.

Factors affecting O2-Hb dissociation curve

FACTORS THAT SHIFT O2 Hb CURVE TO RIGHT

•Decreased PO2.

•Increased blood PCO2.

•Increased blood H+ concentration.

•Increased blood  temperature.

•Increased concentration of 2,3 DPG.

FACTORS THAT SHIFT O2 Hb CURVE TO LEFT

•Increased PO2.

•Decreased blood PCO2

•Decreased blood H+

concentration.

•Decreased blood  temperature.

•Decreased concentration of

2,3 DPG

CHANGES IN O2 Hb DISSOCIATION CURVE DURING EXERCISE

There will be:

    •Decreased PO2 in capillaries of active muscles.

     •Increased temperature in active muscles.

     •Increased CO2

     •Decreased pH due to acidic metabolites.

     •Increased 2, 3 DPG in RBCs by anaerobic glycolysis.

All these factors lead to:

      •Shift of O2-Hb dissociation curve to the right.

      •Decrease affinity of Hb to O2.

      •More release of O2 to tissues.

P-50

    •It is the PO2 at which 50% of Hb is saturated with O2.

    •It is an index for Hb affinity to O2.

    •Normally, P50 is 27 mmHg

(At PCO2=40mmHg, pH=7.4, 37°C).

BOHRS EFFECT 

•Represents the effect of PCO2 and H+ (acidity) on the  O2-Hb dissociation curve.

-At tissues: Increased PCO2 & H+ concentration  shift of O2-Hb curve to the right.

-At lungs: Decreased PCO2 & H+ concentration

shift of O2-Hb curve to the left.

So, Bohr's effect facilitates

   i)O2 release from Hb at tissues.

   ii)O2 uptake by Hb at lungs.

Other factors

•CO2: combine reversibly with Hb (at sites other than O2 binding sites)  change in the molecular structure of Hb    decrease in affinity of Hb to  O2.

•H+: combine reversibly with Hb (at sites other than O2 binding sites)

decrease in affinity of Hb to

change in the molecular structure of Hb

O2.

•2,3 DPG:

-Produced by anaerobic glycolysis inside RBCs.

-Binds reversibly with Hb (at β polypeptide chain) decrease Hb affinity to O2.

-Increased by: exercise, at high altitude, thyroid hormone, growth hormone  and androgens.

-Decreased by: acidosis and in stored blood.

O2 DISSOCIATION CURVE OF FETAL Hb

•Fetal Hb (HbF) contains 2 alpha and 2 beta polypeptide chains  and has no  chain which is found in adult Hb (HbA).

 

•So, it cannot combine with 2, 3 DPG that binds only to  chains.

 

•So, fetal Hb has a dissociation curve to the left of that  of adult Hb.

 

•So, its affinity to O2 is high    increased O2 uptake by the fetus from the mother.

O2 DISSOCIATION CURVE OF MYOGLOBIN 

•One molecule of myoglobin has one ferrous atom (Hb has 4  ferrous atoms).

 

•One molecule of myoglobin can combine with only one  molecule of O2 .

 

•The O2–myoglobin curve is rectangular in shape and to the left of the O2-Hb dissociation curve.

 

•So, it gives its O2 to the tissue at very low PO2.

 

•So, it acts as O2 store used in severe muscular exercise when  PO2 becomes very low.

CHLORIDE SHIFT PHENOMENON

•Definition: It is the movement of Cl- in exchange  with HCO-3 across RBC membrane.

•It is responsible for carrying most of the tidal  CO2 in the bicarbonate form.

•It prevents excessive drop of blood pH.

MECHANISM OF CHLORIDE SHIFT PHENOMENON

•Mechanism:

    -CO2  entering the blood diffuses into RBCs    rapidly hydrated to H2CO3 in the presence of the carbonic anhydrase enzyme.

    -H2CO3 dissociates into H+ and HCO-3.

    -H+ is buffered by the reduced (not oxygenated) Hb.

    -HCO-3 concentration in RBCs increases.

    -Some of the HCO-3 diffuses out to the plasma.

    -In order to maintain electrical neutrality, chloride ions (Cl-)  migrate from the plasma into the red cells.

NET EFFECT OF CHLORIDE SHIFT PHENOMENON 

-Increased HCO-3 in both the RBCs and plasma.

-Increased Cl- inside the RBCs.

-Increased osmotic pressure inside RBCs  shift from the plasma.

-Increase RBCs volume increase in the hematocrit  value.

-Buffering of the tidal CO2 with very little change in the  pH.

REVERSE CHLORIDE SHIFT PHENOMENON

•Definition: It is the movement of Cl- in exchange  with HCO-3 across RBC membrane.

•It is responsible for removal of the tidal CO2 by  lungs.

•CARBON DIOXIDE DISSOCIATION CURVE 

•It is a curve which represents the relationship between the total CO2 content and CO2 tension.

•It is linear, in the physiological range of PCO2.

•The normal PCO2 range is:

-40 mmHg in arterial blood with CO2 content of 48 ml/100 ml blood

-46 mmHg in venous blood with CO2 content of 52 ml/100 ml blood.

•This linear relationship means that any change in PCO2 will  produce a great change in CO2 content of the blood.

•Also, at any given CO2 tension, reduced Hb carries more CO2 than  oxyHb.

CO2 dissociation curve

HALDANE EFFECT 

1. Release of O2 in the tissues from HbO2 with formationof deoxygenated haemoglobin stimulates uptake of Co2 by RBC . This is know as Haldane effect

 

2. Co2 dissociation curve various with the partial pressure of O2. As the partial pressure of 02 raises , the Co2 dissociation curve shifts to the right .

CARBON MONOXIDE POISONING

•CO + Hb  forms  carboxyhemoglobin (HbCO).

•CO and O2 compete for the same binding sites on Hb.

•The affinity of Hb for CO is 240 times more than its affinity for  O2.

•CO can interfere with both the combination of O2 with Hb in the lungs and the release of O2 at tissues by:

-Presence of of CO (even in small amounts) binds to a large portion  of Hb preventing its binding to O2.

-CO shifts  O2-Hb  dissociation curve to the left.

 

 APPLIED ASPECTS 

•CYANOSIS :

•This is the bluish discoloration of skin & mucous membranes.

•It is an very important sign in clinicals.

•It denotes the amount of saturation of haemoglobin.

 

•SHORTNESS OF BREATH or SOB or DYSPNOEA :

•Another important sign in clinicals

•Air hunger or consciousness of breathing or laboured breathing.

 •treat the cause or underlying disease

Physiology of Microcirculation and Lymphatic Circulation

MICRO CIRCULATION

•Microcirculation is the blood flow through blood vessels smaller than 100 µm (i.e. arterioles, capillaries, and venules).

• Function: Transport of cells, oxygen and other substances to or from the tissues and helps in regulation of body temperature

Microcirculation depends of two main forces 

     1) Capillary hydrostatic pressure

     2) Capillary osmotic pressure 

CAPILLARY HYDROSTATIC PRESSURE 

• This pressure drives fluid out of the capillary (i.e., filtration), and is highest at the arteriolar end of the capillary and lowest at the venular end.

• Depending upon the organ, the pressure may drop along the length of the capillary (axial pressure gradient) by 15-30 mmHg.

• The axial gradient favors filtration at the arteriolar end (where PC is greatest) and reabsorption at the venular end of the capillary (where PC is the lowest).

• The average capillary hydrostatic pressure is determined by arterial and venous pressures (PA and PV), and by the ratio of post-to- precapillary resistances (RV/RA).  PC is more sensitive to changes in PV than by changes in PA.

 

CAPILLARY OSMOTIC PRESSURE 

• Osmotic pressure is the hydrostatic pressure produced by a solution in a space divided by a differentially permeable membrane due to a differential in the concentrations of solute.

• Because the capillary barrier is readily permeable to ions, the osmotic pressure within the capillary is principally determined by plasma proteins that are relatively impermeable.

• Therefore, instead of speaking of “osmotic" pressure, this pressure is referred to as the "oncotic".

• Albumin generates about 70% of the oncotic pressure. This pressure is typically 25-30 mmHg.

• The oncotic pressure increases along the length of the capillary, particularly in capillaries having high net filtration (e.g., in renal glomerular capillaries), because the filtering fluid leaves behind proteins leading to an increase in protein concentration.

 

ENDOTHELIUM

• The endothelium (0.5 μm) is the layer of thin specialized epithelium, comprised of a single layer of flat cells that line the interior surface of blood vessels, forming an interface between circulating blood in the lumen and the rest of the vessel wall.

•Space between cells 6-7 nm (little bit less than albumin)  Endothelial cells line the entire circulatory system, from the heart (endocardium) to the smallest capillary. Both blood and lymphatic capillaries are composed of a single layer of endothelial cells

FUNCTIONS OF ENDOTHELIUM 

• vasoconstriction and vasodilation, and hence the control of blood pressure

• blood clotting (thrombosis & fibrinolysis)

•formation of new blood vessels (angiogenesis)

• inflammation and swelling (oedema)

• transit of white blood cells

• Pathology

•Atherosclerosis (patients with diabetes mellitus, hypertension and hyperlipidemia)

ARTERIOLES

• An arteriole is a small diameter (<20 μm, up to 5-9 μm) blood vessel that extends and branches out from an artery and leads to capillaries.

• Arterioles have thin muscular walls (usually only one to two layers of smooth muscle) and are the primary site of vascular resistance.

• In a healthy vascular system the endothelium, inner lining of arterioles and other blood vessels, is smooth and relaxed.

• This healthy condition is promoted by the production of nitric oxide in the endothelium.

• The mean blood pressure in the arteries supplying the body is a result of the interaction between the cardiac output (the volume of blood the heart is pumping per minute) and the vascular resistance, usually termed total peripheral resistance.

• Any pathology which constricts blood flow, such as stenosis, will increase total peripheral resistance and lead to hypertension.

 

TOTAL PERIPHERAL RESISTANCE

• Total peripheral resistance refers to the cumulative resistance of the thousands of arterioles in the body, or the lungs, respectively.

• It is approximately equal to the resistance of the arterioles, since the arterioles are the chief resistance vessels in the body.

 

TOTAL PERIPHERAL RESISTANCE FORMULA

• Total Peripheral Resistance = Mean Arterial Pressure / Cardiac Output.

• The total peripheral resistance of healthy lung arterioles is typically about 0.15 to 0.20 that of the body, so pulmonary artery mean blood pressure are typically about 0.15 to 0.20 of aortic mean blood pressures.

 

CAPILLARIES 

• Capillaries, are the smallest of a body's blood vessels, measuring 5-10 μm .

• They connect arteries and veins, and most closely interact with tissues.

• Capillaries have walls composed of a single layer of cells, the endothelium.

• This layer is so thin that molecules such as oxygen, water and lipids can pass through them by diffusion and enter the tissues.

• Waste products such as carbon dioxide and urea can diffuse back into the blood to be carried away for removal from the body.

• Capillary permeability can be increased by the release of certain cytokines.

 

• The "capillary bed" is the network of capillaries supplying an organ.

• The more metabolically active the cells, the more capillaries it will require to supply nutrients.

• The capillary bed usually carries no more than 25% of the amount of blood it could contain, although this amount can be increased through autoregulation(i.e. active muscle cells) by inducing relaxation of smooth muscle.

• Any signaling molecules they release (such as endothelin for constriction and Nitric oxide for dilation) act on the smooth muscle cells in the walls of nearby, larger vessels, e.g. arterioles.

ENDOTHELIN 

• Endothelin is a 21-amino acid vasoconstricting peptide that plays a key part in vascular homeostasis and it is one of the strongest vasoconstrictors.

• In a healthy individual a delicate balance between vasoconstriction and vasodilation is maintained by endothelin, calcitonin (vasoconstrictors) and by nitric oxide, prostacyclin (vasodilators).

• Overproduction of endothelin can cause pulmonary artery hypertension.

NITRIC OXIDE 

• The chemical compound nitric oxide is a gas with chemical formula NO.

• In the body, nitric oxide (the 'endothelium-derived relaxing factor', or 'EDRF') is synthesized from arginine and oxygen by various nitric oxide synthase (NOS) enzymes and by sequential reduction of inorganic nitrate.

FUNCTIONS OF NITRIC OXIDE (NO)

• The endothelium (inner lining) of blood vessels use nitric oxide to signal the surrounding smooth muscle to relax, thus dilating the artery and increasing blood flow.

• Nitric oxide is a key biological messenger, playing a role in a variety of biological processes (vessel dialatation, neurotransmission, penile erections, hair growth / loss).

•"Nitro" vasodialators such as nitroglyceric are converted to nitric oxide.

• Immune system: generated by macrophages, toxic to bacteria 

 

CAPILLARY PRESSURES VALUES

•Middle pressure is about 25 mm Hg

           •30-40 mm Hg by arterioles

           •10-15 mm by venules

•Oncotic pressure is about 28 mm Hg

           •19 mm Hg because of proteins

           •9 mm Hg because of some cations

• As their are differences in capillary pressures by arterioles and venules.

• Venous end has lower pressure, but there is higher permeability - therefore 90 % of liquid that goes out at arterial end comes back at venous end. 

•Increase of capillary pressure of 20 mmHg, increases filtration pressure and  Lymphatic system is not able to accomodate the increase of IC liquid which results in oedemas.

 

PRESSURES IN THE ARTERIAL END OF CAPILLARY

• Pressures going out of the capillary:

     Capillary pressure  - 30mmHg                  

     Pressure of interstitial fluid  - 3mmHg

     Oncotic pressure of ISF   -  8mmHg                 

      Total pressure outwards is - 41mmHg

• Pressures going into the capillary:

     Oncotic pressure of plasma  -  28mmHg

•Together 41-28=13 mmHg in direction out of the capillary (0.5 % of plasma)

PRESSURE IN THE VENOUS END OF CAPILLARY 

• Pressures going out of the capillary:

       Capillary pressure - 10mmHg                      .    Pressure of interstitial fluid  -  3mmHg

       Oncotic pressure of ISF  - 8mmHg

        Total pressure going out - 21mmHg                                                        

• Pressures going into the capillary:

      Oncotic pressure of plasma    -   28mmHg

•Together 28-21=7 mmHg in direction into the capillary (0.5 % of plasma)

TYPES OF CAPILLARIES :

CONTINUOUS CAPILLARIES

Continuous capillaries have a sealed epithelium and only allow small molecules, water and ions to diffuse.

FENESTRATED CAPILLARIES

 Fenestrated capillaries (as their name implies "fenster") have openings that allow larger molecules to diffuse.

SINUSOIDAL CAPILLARIES

 Sinusoidal capillaries are special forms of fenestrated capillaries that have larger openings in the epithelium allowing RBCs and serum proteins to enter.

 

* One of the two major types of capillaries,         found in muscle, skin, lung, central nervous     system and other tissues, characterized by the presence of an uninterrupted endothelium and a continuous basal lamina, and by fine filaments and numerous pinocytotic vesicles.

* One of the two major types of capillaries, found in the intestinal mucosa, renal glomeruli, pancreas, endocrine glands and other tissues and characterized by the presence of circular fenestrae or pores that penetrate the endothelium;

• These pores may be closed by a very thin diaphragm.

 

SINUSOIDAL CAPILLARIES 

• A sinusoid is a type of a capillary with a fenestrated endothelium.

• Located in: liver, lymphoid tissue, endocrine organs, and hematopoietic organs (bone marrow, spleen).

Their highly permeable in nature, which is due to larger inter-cellular clefts which allows small and medium-sized proteins such as albumin to enter and leave the blood stream.

•Some spaces are large enough for blood cells to pass.

•Liver sinusoids are equipped with Kupffer cells that can take up and destroy foreign material such as bacteria entering the sinusoids.

 

VENULES 

• A venule is a small blood vessel that allows deoxygenated blood to return from the capillary beds to the larger blood vessels called veins.

•Venules have three layers:

➢ An inner endothelium composed of squamous epithelial cells that act as a membrane.

➢ A middle layer of muscle and elastic tissue.      (poorly developed so that venules have thinner walls than arterioles)

➢ An outer layer of fibrous connective tissue.

LYMPHATIC SYSTEM 

• The lymphatic system is a complex network of lymphoid organs, lymph nodes, lymph ducts, and lymph vessels that produce and transport lymph fluid from tissues into the circulatory system.

• The lymphatic system is a major component of the immune system.

 

FUNCTIONS OF LYMPHATIC SYSTEM 

➢Removal of excess fluids from body tissues.

➢Absorption of fatty acids and subsequent transport of fat and chyle to the circulatory system.

➢Production of immune cells (such as lymphocytes, monocytes, and antibody producing cells called plasma)

 

LYMPH

• Lymph originates as blood plasma that leaks from the capillaries of the circulatory system, becoming interstitial fluid, and filling the space between individual cells of tissue.

• Plasma is forced out of the capillaries by hydrostatic pressure, and as it mixes with the interstitial fluid, the volume of fluid accumulates slowly.

• Most of the fluid is returned to the capillaries by osmosis (about 90% of the former plasma).

• The excess interstitial fluid is collected by the lymphatic system by diffusion into lymph capillaries, and is processed by lymph nodes prior to being returned to the circulatory system.

• Once within the lymphatic system the fluid is called lymph, and has almost the same composition as the original interstitial fluid.

 

LYMPH NODE 

• A lymph node is an oval or kidney- shaped organ of the lymphatic system, distributed widely throughout the body including the armpit and stomach and linked by lymphatic vessels. Lymph nodes are major sites of B, T, and other immune cells.

• Lymph nodes are important for the proper functioning of the immune system, acting as filters for foreign particles and cancer cells. Lymph nodes do not deal with toxicity, which is primarily dealt with by the liver and kidneys.

CLINICAL SIGNIFICANCE OF LYMPH NODES

• They become inflamed or enlarged in various infections and diseases which may range from trivial throat infections, to life- threatening cancers.

• The condition of the lymph nodes is very important in cancer staging, which decides the treatment to be used, and determines the prognosis. When swollen, inflamed or enlarged, lymph nodes can be hard, firm or tender.

LYMPHATIC CIRCULATION

• The lymphatic system acts as a secondary circulatory system, except that it collaborates with white blood cells in lymph nodes to protect the body from being infected by cancer cells, fungi, viruses or bacteria.

• Unlike the circulatory system, the lymphatic system is not closed and has no central pump; the lymph moves slowly and under low pressure due to peristalsis, the operation of semilunar valves in the lymph veins, and the milking action of skeletal muscles.

 

• Like veins, lymph vessels have one-way, semilunar valves and depend mainly on the movement of skeletal muscles to squeeze fluid through them.

Rhythmic contraction of the vessel walls may also help draw fluid into the lymphatic capillaries.

• This fluid is then transported to progressively larger lymphatic vessels culminating in the right lymphatic duct (for lymph from the right upper body) and the thoracic duct (for the rest of the body);

• These ducts drain into the circulatory system at the right and left subclavian veins.

• The thoracic duct, is an important part of the lymphatic system—it is the largest lymphatic vessel in the body.

• It collects most of the lymph in the body (except that from the right arm and the right side of the chest, neck and head, which is collected by the right lymphatic duct) and drains into the systemic (blood) circulation.

• The thoracic duct drains into the left subclavian vein.

• In an adult, the thoracic duct transports up to 4 L of lymph per day. When the thoracic duct is blocked or damaged a large amount of lymph can quickly accumulate in the pleural cavity, this situation is called chylothorax.

 

FATTY ACID TRANSPORT SYSTEM 

• Lymph vessels are present in the lining of the GIT.

• While most other nutrients absorbed by the small intestine are passed on to the portal venous system to drain, via the portal vein, into the liver for processing, fats are passed on to the lymphatic system, to be transported to the blood circulation via the thoracic duct.

• The enriched lymph originating in the lymphatics of the small intestine is called chyle. 

• The nutrients that are released to the circulatory system are processed by the liver.

Lymphoid organs

• The thymus, spleen, lymph nodes, peyer's patches, tonsils, vermiform appendix, and red bone marrow are accessory lymphoid tissues that comprise the lymphoid organs.

• These organs contain a net that support circulating B- and T- lymphocytes and other immune cells like macrophages and dendritic cells.

• Another sub-component of the lymphatic system is the reticuloendothelial system.

• When micro-organisms invade the body or the body encounters other antigens, those are transported from the tissue to the lymph circulation. The lymph nodes filter the lymph fluid and remove foreign material, such as bacteria and cancer cells. Specialized cells called macrophages and dendritic cells phagocytose pathogens and present antigens to lymphocytes.

• When these pathogens are recognized, the lymph nodes enlarge and additional immune cells are produced to help fight the infection.

Thymus

• The thymus is an organ located in the upper anterior portion of the chest cavity.

• The thymus plays an important role in the development of the immune system in early life, and its cells form a part of the body's normal immune system.

• It is most active before puberty, after which it shrinks in size and activity in most individuals and is replaced with fat.

•Function: Production (maturation) of T cells.

SPLEEN

• The spleen is located in the upper left part of the abdomen, behind the stomach and just below the diaphragm.

• The spleen is the largest collection of lymphoid tissue in the body.

• It is regarded as one of the centres of activity of the reticuloendothelial system.

• Its absence leads to a predisposition to certain infections.

FUNCTIONS OF SPLEEN

➢Acts as Blood reservoir

➢Helps in destruction of old red blood cells

➢It even has some immune functions

➢Helps in blood cells production in embryogenesis

HEART RATE

•Pulse rate represents heart rate.

 

•With each stroke output, blood is ejected into circulation which produces arterial pulsation

 

•Arterial pulse rate coincides with ventricular ejection rate.

NORMAL HEART RATE 

• Normal heart rate is 60-100 beats per minute in adults.

 

•HR less than 60 bpm is called bradycardia.

 

•HR more than 100 bpm is called tachycardia.

 

•HR is the rate of discharge of SA node.

PHYSIOLOGICAL VARIATIONS OF HEART RATE 

•Age 

HR is more in infants and children .

HR is less after sixty years age.

 

•Gender 

Its less in females due to their high parasympathetic tone and less basal metabolism.

 

•Diurnal variation 

More in the day time and less in sleep due to less physical activity and less stress.

 

•Respiration 

HR is more during inspiration and less during expiration (sinus arythmia)

 

•Body temperature 

Higher temperature favours higher heart rate.

 

•Environment 

HR is more in summer

 

•Food intake 

It increases HR by increasing body metabolism.

•Posture 

On standing from supine , heart rate increases due to decreased stimulation of baroreceptors.

 

•Exercise

HR increases with exercise due to sympathetic stimulation.

 

REGULATION OF HEART RATE (HR)

•HR is primarily controlled by autonomic nervous system.

 

•Vagus nerve (Parasympathetic-PNS) inhibits and sympathetic nerves (SNS) stimulates HR.

 

•HR is primarily a vagal function.

 

•Neural and humoral mechanisms are involved in regulation of HR.

AUTONOMIC REGULATION  (medullary CV center)

 

Receives input from higher brain centers and variety of sensory receptors.

       •Proprioreceptors

       •Chemoreceptors

       •Baroreceptors

 

•Sympathetic output increases HR and contractility.

 

•Parasympathetic impulses decreases HR.

•PNS has little effect on contractility ( because

 it does not innervate ventricular myocardium)

•Several factors contribute to regulation of heart rate:

CHEMICAL REGULATION 

•Cardiac activity is depressed by.    

       •Hypoxia

       •Acidosis

       •Alkalosis

PARASYMPATHETIC NERVOUS SYSTEM 

•Vagus nerve (via ACh) decreases HR by decreasing or slowing down the inflow of Na+ and Ca++ and by increasing the subsequent outflow of potassium (K+).

 

•Acts at SA and AV nodes.

 

•May treat SNS-driven heart attack by gagging or massage of carotid arteries and activates vagal reflexes. 

PNS counteracts SNS.

CARDIVASCULAR RESPONSE TO STRESS 

•It leads to increase in heart rate which is due to increase in SNS tone and decrease in PNS tone

 

•Norepinephrine (NE) and epinephrine (Epi) increases which leads to increase in inflow of Na+ and Ca++

Which increase rate of re-excitation in SA node.

 

•This increase in intracellular  Ca++ also increases contractility.

 

•SNS terminals also excite AV node and whole myocardium therefore enhances contractility everywhere.

REFLEX CONTROL 

•Cardiovascular reflexes that regulate BP also control HR , which is part of integrated control mechanisms.

 

• Reflexed includes -

        •Baroreceptor reflex

        •Chemoreceptor reflex

        •Bainbridge reflex

        •Cushing’s reflex

BARORECEPTOR REFLEX 

•Baroreceptors are located in the carotid sinus and aortic arch.

 

•They are stimulated when BP rises and this stimulates Nucleus Tractus Solitarius(NTS) in medulla via 9th and 10th cranial nerves

 

•NTS inhibits Vasomotor center(VMC)

BAINBRIDGE REFLEX 

•The receptors are present in the atria at the venoatrial junction . They are known as tachycardia producing receptors.

 

•This reflex accounts for tachycardia produced following saline infusion or blood transfusion.

 

•It is more observable when initial HR is low.

CHEMORECEPTOR REFLEX 

•Chemoreceptors responds to hypoxia, hypercapnia and acidosis.

 

•Activation of chemoreceptors primarily produces bradycardia.

CUSHING'S REFLEX 

• Activated in gross hypotension that decreases blood flow to the VMC .

 

•Direct stimulation of VMC  produces vasoconstriction and tachycardia.

 

 REGULATION OF HEART RATE BY HIGHER CENTRES 

•Stimulation of motor cortex, frontal lobe, and thalamus increases HR.

 

•Increase in HR in emotional states, anxiety and excitement is due to stimulation of limbic system.

HUMORAL AND CHEMICAL CONTROL OF HR 

It is mediated by .

    •Hormones

•Catecholamines and thyroid hormones increase HR and contractility

     •Cations

•Alterations in balance of K+, Na+ and Ca2+ alter HR and contractility

 

MAREY'S LAW 

•Muscular exercise and anxiety are exception for Marey’s law. Both BP and HR increases

HEART RATE VARIABILITY 

•Heart rate variability is the physiological phenomenon of variation in the time interval between heartbeats.

 

• It is measured by the variation in the beat-to-beat interval

 

•Other terms used include: "cycle length variability", "RR variability", and "heart period variability"

Heart rate variability or HRV is the physiological phenomenon of the variation in the time interval between consecutive heartbeats in milliseconds.

PHYSIO LOGICAL IMPORTANCE OF HEAR RATE VARIABILITY ( HRV)

•HRV is regulated by the autonomic nervous system (ANS), and its sympathetic and parasympathetic branches.

 

• It is commonly accepted as a non-invasive marker of autonomic nervous system activity.

•The sympathetic branch activates stress hormone production and increases the heart’s contraction rate and force (cardiac output) and decreases HRV.

 

• It  is needed during exercise and mentally or physically stressful situations.

•The parasympathetic branch slows the heart rate and increases HRV to restore homeostasis after the stress passes.

 

• This natural interplay between the two systems allows the heart to quickly respond to different situations and needs.

Study of HRV in time and frequency domain

•The HRV was evaluated by both time domain and frequency domain analysis.

 

•Mean heart rate, standard deviation of all R–R intervals (SDNN) and root-mean-square of successive differences (RMSSD) were measured in the time domain analysis of HRV.

 

•Done with holter monitoring for 24 hrs

EFFECT OF RESPIRATION ON HEART RATE

•While breathing normally, heart rates usually increase during inhalation and decrease during exhalation.

 

•This cyclic change in heart rate, that is driven by breathing, is known as Respiratory Sinus Arrhythmia (RSA).

RESPIRATORY SINUS ARRHYTHMIA (RSA)

Clinical importance of RSA

•Sinus arrhythmia is a commonly encountered variation of normal sinus rhythm.

 

•Sinus arrhythmia characteristically presents with an irregular rate in which the variation in the R-R interval is greater than 0.12 seconds.

 

•Additionally, P waves are typically monoform and in a pattern consistent with atrial activation originating from the sinus node.

 

•During respiration, the intermittent vagus nerve activation occurs, which results in beat to beat variations in the resting heart rate.

 

•When present, sinus arrhythmia typically indicates good cardiovascular health.

•Sinus arrhythmia is a common rhythm variation. It is seen more often in children and young adults.

 

•Respirations lead to vagal stimuli resulting in R-R interval variations.

 

•Typically its presence is an indicator of good cardiovascular health.

 

• Loss of sinus arrhythmia may indicate underlying heart failure or structural heart disease.

JUGULAR VENOUS PRESSURE(JVP)

•The jugular venous pressure (JVP, sometimes referred to as jugular venous pulse) is the indirectly observed pressure over the venous system via visualization of the internal jugular vein.

 

•It can be useful in the differentiation of different forms of heart and lung disease.

•Classically three upward deflections and two downward deflections have been described.

 

•The upward deflections are the "a" (atrial contraction), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumetric systole) and "v" = venous filling.

 

•The downward deflections of the wave are the "x" (the atrium relaxes and the tricuspid valve moves downward) and the "y" descent (filling of ventricle after tricuspid opening) .

VISUALISATION OF JVP

 

•The veins of the neck, are viewed from in front.

 

•The patient is positioned at a 45° incline, and the filling level of the external jugular vein determined.

 

•Visualize the internal jugular vein when looking for the pulsation.

 

•In healthy people, the filling level of the jugular vein should be less than 3 centimeters vertical height above the sternal angle.

 

•A pen-light can aid in discerning the jugular filling level by providing tangential light.

 

 •The JVP is easiest to observe if one looks along the surface of the sternocleidomastoid muscle  as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90 degree angle).

 

•Pulses in the JVP are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the right atrium.

 

DIFFERENCES BETWEEN JVP AND CAROTID PULSE 

 

•The JVP and carotid pulse can be differentiated in several ways:

•Multiphasic - the JVP "beats" twice (in quick succession) in the cardiac cycle. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart.

 

•The first beat represents that atrial contraction (termed a) and second beat represents venous filling of the right atrium against a closed tricuspid valve (termed v) and not the commonly mistaken 'ventricular contraction'.

 

• The carotid artery only has one beat in the cardiac cycle.

 

•Varies with respiration - the JVP usually decreases with deep inspiration.

 

•Physiologically, this is a consequence of the Frank–Starling mechanism as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the pulmonary circulation.

 

JVP RECORD

•There is no valve at the junction of superior venacava and right atrium.

 

•Hence right atrial pressure changes are transmitted to the jugular vein in the neck , producing 3 characteristic waves.

 

•“a” wave – due to atrial systole. Some blood regurgitates into the great veins when atria contracts , even though the orifices of ‘IVC’ and ‘SVC’ are constricted.

 

•In addition, venous inflow stops , causing rise in venous pressure , contributing to the

a wave’.

 

•‘ c wave’ – it is the transmitted manifestation of the rise in atrial pressure produced by the bulging of the tricuspid valve into the right atrium during isovolumetric ventricular contraction phase.

 

•‘v wave’ – it is due to rise in atrial pressure before the tricuspid valve opens during diastole.

JVP WAVE FORM

 

•The jugular venous pulsation has a biphasic waveform.

 

•The " a " wave corresponds to right Atrial contraction and ends synchronously with the carotid artery pulse. The peak of the 'a' wave demarcates the end of atrial systole.

 

•The " c " wave corresponds to right ventricular Contraction causing the triCuspid valve to bulge towards the right atrium.

 

 •The " x' " (x prime) descent follows the 'c' wave and occurs as a result of the right ventricle pulling the tricuspid valve downward during ventricular systole.

 

•(As stroke volume is ejected, the ventricle takes up less space in pericardium ,  allowing relaXed atrium to enlarge).

 

•The x' (x prime) descent can be used as a measure of right ventricle contractility.

 

•The " x " descent follows the 'a' wave and corresponds to atrial relaXation and rapid atrial filling due to low pressure.

 

•The " v " wave corresponds to Venous filling when the tricuspid valve is closed and venous pressure increases from venous return - this occurs during and following the carotid pulse.

 

•The " y " descent corresponds to the rapid emptYing of the atrium into the ventricle following the opening of the tricuspid valve.

 

INTERPRETATION

 

•Certain wave form abnormalities, include Cannon a-waves - increased amplitude 'a' waves, are associated with AV dissociation (third degree heart block),when the atrium is contracting against a closed tricuspid valve, or even in ventricular tachycardia.

 

•Another abnormality, "c-v waves", can be a sign of tricuspid regurgitation. The absence of 'a' waves may be seen in atrial fibrillation.

 •An elevated JVP is the classic sign of venous hypertension (e.g. right-sided heart failure). JVP elevation can be visualized as jugular venous distention, whereby the JVP is visualized at a level of the neck that is higher than normal.

 

•Kussmaul sign - paradoxical increase of the JVP with inspiration (instead of the expected decrease).

•It indicates impaired filling of the right ventricle.

 

•Differential diagnosis of Kussmaul's sign includes constrictive pericarditis , restrictive cardiomyopathy , pericardial effusion,  and severe right-sided heart failure.

 

•An exaggerated "x" wave or diastolic collapse of the neck veins from constrictive pericarditis is referred to as Friedreich's sign

 

•Parodoxical JVP (Kussmaul's sign): JVP rises with inspiration, drops with expiration) occurs in the following conditions

        •Pericardial effusion

        •Constrictive pericarditis

        •Pericardial tamponade

 

•Raised JVP, normal waveform occurs when their is one of the following 

       •Bradycardia

       •Fluid overload

       •Heart Failure

       •Raised JVP, absent pulsation

       •Superior vena cava syndrome

 

•Large 'a' wave (increased atrial contraction pressure) occurs in following conditions 

       •tricuspid stenosis

       •Right heart failure

       •Pulmonary hypertension

 

•Cannon 'a' wave (atria contracting against closed tricuspid valve) can be seen in the following conditions 

        •Atrial flutter

        •Premature atrial rhythm (or tachycardia)

        •third degree heart block

        •Ventricular ectopics

        •Ventricular tachycardia

 

CARDIAC MURMURS 

•A number of different adventitious sounds or heart murmurs , may also be detected.

 

•These abnormal sounds are usually associated with turbulence of blood generated as blood passes through the leaking valves or a valve that has a narrowed orifice resulting from a disease.

 

•HS3 and HS4 are less important , being normally inaudible.

BLOOD PRESSURE AND ITS REGULATION

BLOOD PRESSURE

•Arterial blood pressure is defined as  the lateral pressure exerted by the contained column of blood on  the wall of arteries.

•Generally , the term blood pressure refers to  arterial blood pressure.

•Normal blood pressure  is 120 /80 mmHg

                  Systolic 120 mmHg

                  Diastolic 80 mmHg

 

•The arterial blood pressure is expressed mainly in four ways.

 

1.Systolic blood pressure

2.Diastolic blood pressure

3.Pulse pressure

4.Mean arterial pressure  

SYSTOLIC BLOOD PRESSURE 

•Systolic blood pressure is defined as the maximum pressure exerted in the arteries during  systole of the heart

      •Normal value     - 120 mm Hg

      • Normal range    - 110  to 140 mm Hg

DIASTOLIC BLOOD PRESSURE

•Diastolic blood pressure is the minimum pressure in the arteries during diastole of the heart

 

        •Normal value.    - 80 mmHg

        • Normal range   -  60 – 80 mmHg

 

PULSE  PRESSURE

•Pulse pressure is the difference between the Systolic  and   Diastolic pressure.

 

         •Normal value  – 40 mmHg

MEAN ARTERIAL PRESSURE

•It is the average pressure existing in the arteries .

•It is the diastolic pressure plus one - third of pulse pressure.

 

         •Normal value  - 93 mmHg

BLOOD PRESSURE – VARIATIONS

1. Age

2.Sex

3.Body built

4.Diurnal variation

5.After meals

6.During sleep

7.Emotional conditions

8.After exercise

 

 

AGE :

Arterial blood pressure increases as age advances

Systolic blood pressure at various ages 

In newborn baby  - 40 mmHg

After 15 days         - 70 mmHg

After one month      - 90 mmHg

At puberty                 - 120 mmHg

At 50 years                 - 140 mmHg

At 70 years                  -160mmHg

At 80 years                 -180 mmHg

 

•Diastolic blood pressure at various ages 

 

At puberty        - 80 mmHg

At 50 years       - 85 mmHg

At 70 years        -90 mmHg

At 80 years        - 95 mmHg

SEX 

•In females ,up to the period of menopause , the arterial pressure is low up to 5mmHg  as compared to the males  of same age.

 

•After menopause the blood pressure  in the females becomes equal to that in the  males of same age .

BODY BUILT

•The arterial blood pressure is more in the obese persons than lean persons  

DIURNAL VARIATION

•In the early morning blood pressure is low.

•IN the afternoon  it reaches maximum.

•In the evening  blood pressure becomes low again.

AFTER MEALS

•The blood pressure is increased for few hours after meals.

•This  is due to increase in cardiac out 

DURING  SLEEP

•The blood pressure is reduced up to 15 to 20 mmHg during deep sleep.

EMOTIONAL CONDITIONS

•The blood pressure increases during excitement or anxiety.

•This is due to release of ADRENALINE in the blood circulation

AFTER EXERCISE

•After moderate exercise systolic pressure increases by 20 -30 mmHg.

•This is due increase in force of contraction and stroke volume.

•Normally diastolic pressure is not effected by moderate exercise , Its  because  diastolic pressure depends upon the peripheral resistance.

•After sever exercise the systolic pressure rises by 40 – 50 mmHg above the basal level.

•But the diastolic pressure reduces because the peripheral resistance decreases in severe muscular exercise.

REGULATION BY BLOOD VESSELS

It occurs by following mechanisms :

• Alteration in the diameter of arterioles which changes peripheral resistance and blood pressure.

 

•Alteration in diameter  of  veins which changes venous return and cardiac output eventually blood pressure.

 

NEURAL  REGULATION

•It  is very important.

•It  responds with in seconds .

•Redistribution of blood flow  to the body.

•Increasing the heart rate .

•Rapid control of the blood pressure.

 

NEURAL  REGULATION COMPONENTS

 

•Medullary CVR control center.

•ANS  supplying the heart & blood vessels

•Afferent impulses to medulla

•Role of skeletal muscles

 

MEDULLARY CVR CONTROL CENTRE

•It is popularly known as VASOMOTOR center.

•It is medullary sympathetic center .

•Located in the M.O. of BRAIN STEM.

•It consists of groups  of neurons at the floor of Fourth ventricle

PRESSOR AREA

•Pressor area is located at  RVLM.

•It contains glutaminergic neurons .

•This has the excitatory effect on neurons.

Continuous sympathetic vasoconstrictor tone

•Shows continuous tonic activity in the  body

•The discharge rhythmically *1  impulse/ sec

MEDULLARY PARA SYMPATHETIC CENTER

•Cardiac vagus center.

•Earlier also called Cardiac inhibitory center.

•Now it is called as NUCLEUS AMBIGUOUS 

•N.A. receives  afferents via  NTS.

•To decrease heart  rate  F.C.

•It is a relay station  cardio respiratory afferents.

•It gets afferents from Baroreceptors &  Chemoreceptors.

VAGUS  EFFECT

PARA SYMPATHETIC CENTER

BARORECEPTOR MECHANISM

• High- pressure baroreceptors are present in following areas 

1.Carotid sinus 

2.Aortic arch

3.Walls of left ventricle

4.Root of left subclavian artery

5.Junction of thyroid artery

BARORECEPTOR MECHANISM

• Low- pressure baroreceptors are present in following areas 

 

1.Walls of right & left atrium

2.Entrance of S.V & I.V

3.Walls of pulmonary trunk

4.Right & left pulmonary artery

 AUTOREGULATION OF BLOOD PRESSURE

•In any tissue of the body, an acute increase in arterial pressure causes immediate rise of blood flow but with in no time the blood flow in most tissues returns normal.

HUMORAL  REGULATION

Humoral control means control by substances

secreted into the body fluids.

  Ex : Hormone & ions

        •Vasoconstrictor agents

        •Vasodilator agents

Vasoconstrictor agents include :

1.Vasopressin

2.Endothelin - A

3.Epinephrine

4.Norepinephrine

5.Angiotensin - II

 

Vasodilator agents include 

1.Bradykinin

2.Histamine

 

VASOCONSTRICTORS

•Epinephrine  & Nor-epinephrine are two important vasoconstrictors.

•During stress,fright they are released in ample amounts 

•They have same effect as sympathetic stimulation.

•They lead to contraction of veins & arterioles.

Adrenal medulla secretes  these hormones.

 

ANGIOTENSIN ǁ 

• As little as 1 millionth of a gram can increase

arterial pressure by 50mm of Hg.

•It constrict small arterioles powerfully.

•It increase total peripheral resistance , thus it plays important role in the regulation of arterial pressure.

VASOPRESSIN or ANTI DIURETIC HORMONE 

•It is also  called antidiuretic hormone (ADH)

•It is more powerful than angiotensin II.

•MOST POTENT vascular constrictor.

•It is formed in nerve cells, in hypothalamus.

and is transported downwards though nerve axons to get stored in posterior pituitary.

•It acts mainly by increasing water reabsorption from renal tubules.

ENDOTHELIN-A

•It is large 21 amino acids containing peptide .

•This substance is present in endothelial cells.

•Causes powerful vasoconstriction.

•After severe blood vessel damage , endothelin-a is released from endothelial cells.

•It prevent  bleeding of arteries by constricting them.

 

VASODILATORS

      •Bradykinin

      •Histamine 

BRADYKININ

•Several substances called KININ, causes powerful vasodilatation.

•Kinins are small peptides, Kallikrinin which is its inactivate form.

•When their is tissue inflammation it  becomes activated.

HISTAMINE

•In allergic reaction histamine is released.

•Histamine is derived from MAST cells and 

from the BASOPHILS in the blood.

•POWERFUL VASODILATOR in the tissue .

•Due to action of histamine fluid leaks out in the tissue and causes OEDEMA

VASCULAR CONTROL BY IONS AND   CHEMICALS

•Calcium ion con causes vasoconstriction.

 •Potassium ion causes vasodilatation .

•Magnesium ion is powerful vasodilator.

•Hydrogen  ion is powerful vasodilatatior.

HYPERTENSION

•DEFINITON :

•Hypertension is defined as sustained elevation of systemic arterial pressure .

 

Usually hypertension means rise in diastolic pressure .

When Systolic Pressure is elevated above  150 mmHg and  Diastolic Pressure is elevated  above  90mmHg

TYPES OF HYPERTENSION

 

1.Primary (or ) Essential Hypertension

2.Secondary Hypertension  

 

PRIMARY (OR ) ESSENTIAL HYPERTENSION

•The blood pressure is elevated in the absence of any underlying disease.

•It is also known as essential hypertension

•The arterial blood pressure increased because of increased peripheral resistance due to some unknown causes.

It is again of two types :

      1. Benign Hypertension

      2. Malignant Hypertension  

BENIGN HYPERTENSION

•In early stages of condition, 

There is moderate increase in blood pressure

systolic to 200mmHg and the diastolic pressure of about 100mmHg.

In resting conditions and sleep the BP returns to normal level.

Later there is further increase in blood pressure and it does not come back to normal  level.

 

MALIGNANT HYPERTENSION 

•It is also called accelerated hypertension.

•In this case the blood pressure is increased to 250 mmHg systolic pressure and 150 mmHg diastolic pressure

•It always develops due to the combined effect of primary and secondary hyper tension

•Malignant hypertension produces renal diseases ,retinal hemorrhage.

•It is fatal disease and causes death with in few years

SECONDERY  HYPERTENSION

•It is due to some underlying disease

•CVS DISORDERS 

             Atherosclerosis 

             coarctation of aorta

•Endocrine disorders like  – 

             Tumors in adrenal medulla 

             Hyper aldosteronism                                            

             Cuishings syndrome

•RENAL DISORDERS         

             Stenosis of renal artery

             Glomerulonephritis

•CNS DISEASES             

             increased intra cranial pressure

             lesion in tractus solitarius

HYPOTENSION

•DEFINITION :

•The low blood pressure is called hypotension.

When the systolic pressure is less than 90 mmHg then it is considered as hypotension .

Types :

1.Primary hypotension

2.Secondary hypotension