All 3 venous systems drains into sinous venosus at the septum transverses.

Vitelline + Umbilical vein = Liver sinusoid → septum transverusus

Right Umbilical vein atrophic and left Umbilical vein develop Ductus venosus

Ductus venosus carried oxygenated placental blood. To heart with out passing to liver sinusoid, because Liver at this time main blood forming orgon required low-tension oxygen.

Superior vena cave → cervical to heart major ventral anastamosis → left brachiocephalic vein between left and right cardinal vein.

Left cordial vein loses its connection. Now left common cardial vein isoletd form cardial system and remain as cororary sinsus

Right common cardinal vein displaced cranially and form vertical superior vena cava and right nodal tissue – sinoatrial node.

The great arteries – five arch arteries 1, 2, 3, 4, 6 (5^th transient) in pair each side of developing pharynal unit in the dorsal and ventral aortae. I and II disappear early leaving plexus which external cardiac arteries developing, dorsal aortae between III, IV (ductus caroticus) disappear and replaced by other longitudinal arteries verterbral cervical etc.

Heart: the straight heart tube formed by the fusion of the two separate tube of sinusus venosus in septum transvesus.

Contraction strart at sinus venosus and cardial tissue make muscle contract effective and presents the reflex of blood.

Heart tube fold by loss of dorsal wall of the ventricle and ventral wall of atrium and sinous venosus move in to pericardial cavity to lie in atrioventricular sulcus.

Fibrous atrioventicular ring (AV) which separate sinus and arterial muscle except at left nodal tissue.

Atrium expand right and sinusus venosus with pulmonary vein absorbed and form posterior smooth walled and 4 separate pulmonary vein open left side.

Vanae cavae and coronary sinus open into right side of smooth wall.

On right smooth wall area limited by Cristaterminalis

Inter artrial septum divide atrium first form septum primum I between sinusus venosus and pulmonary vein toward AV opening at AV orifice anterior and posterior endocardial cushion fuse and now combined in forman seccedum II formed. Forman I and second septum II formed digital septum directs the inferior vena caval blood toward septum I and blood pass in to and through foramen II into left atrium. This oblique root between two septa is formen ovale, septum II also separate the superior venacaval blood from formen II, it passes directly to AV orifice.

Before birth very little flow of blood through pulmonary vein. Hence, pressure in right atrium is being keeping septum I displaced and formen ovale open. AV fistula = increase cardiac output

Heavy exercise = increase cardiac output, stimulation of sympathetic nervous system = increase blood supply to muscles increase metabolism = vasoconstriction of other organ.

Low cardiac output = obstruction of vein, decrease blood volume, acute venous dilatation, circulation shock, myocardial infraction, severe valvular heart disease, myocarditis, cardiac temponade, cardiac metabolism, cardiac shock,

Hyper effective heart = sympathetic stimulation, hypertrophy of heart, inhibition of parasympathetic of heart.

Hypo effective heart = MI, VHD, increase atrial pressure, increase parasympathetic, decrease sympathetic, CHD, myocarditis, cardiac anorexia, diphtheria

Sympathetic inhibition by = total spinal anesthesia, by injection Hexamethonium

Measurement of cardiac out put

oxygen flick method = O₂ absence in lung ml/mt / AV O₂ diffusion ml/mt

indicator dilution method (cardio green dye)

Pulmonary circulation = pulmonary vessel, bronchial vessel, lymphatics

Pressure 25mmhg right ventricle

Diastole – 8 mmhg

Mean 15mmhg

Venous pressure – 2 mmhg

Arterial pulse pressure= 17mmhg

Capillary pressure = 7mmhg

Blood volume = 450 ml 9% = 250ml resurve

Three zone include

Zone I = area of Zero flow

Zone II = area of Zero flow during part of the heart cycle

Zone III = area of continuous flow

LHF = increase left atrial pressure → increase blood volume in pulmonary vein → transudation of fluid into pulmonary tissue → pulmonary edema → intra alveolar edema

Pulmonary capillary pressure = 7 mmhg

Blood stay in lungs = 0.8 – 0.3 sec

Sifting factor = 23mmhg – increase – 30mmhg → pulmonary edema

Pulmonary edema → capillary damage

Massive pulmonary embolism = long bed ridden → sluggish blood flow → massive clots.

Diffuse pulmonary embolism – (1) fat embolism, (2) air embolism

Emphysema = increase in cigarette smoking

Treatment = O₂ inhalation

Diffuse sclerosis of lungs – silicosis tuberculosis, Syphilis, anthrosis

Atelectasis = collapse of a lung or part – open chest in atmospheric pressure.

Coronary circulation – 225ml/mt = 0.2 – 0.8 ml/gm/mt = 4 – 5 %

Ischemic heart disease – atherosclerosis – acute occlusion of coronary artery

Collateral circulation in heart – myocardial infraction

Cause of death fallowing acute coronary occlusion → decreased cardiac output→ cardiac shock → damming of blood in venous system → rupture of infraction area – cardiac tamponade → fibrillation of ventricle

Non function area → dead tissue → scar tissue.

Cellular death = degree of ischemia X degree of metabolism of heart muscles

Treatment = total bed rest

Pain in coronary disease – angina pectoris = lactic acid, histamine, kinine, drug induce (vasopressine, oxytocin, ergotamine, methysergide, propranol withdrol, thyronine, alpha blocker, hydralagine) cigarette, hypertension, diabetes, hypercholesterole.

Treatment = vasodilator drugs nitroglycerine, rest, isosorbided diuretics, beta blocker, calcium antagonist (diltagine 30-90, nephedapine, verapramil)

Surgical treatment = aortic coronary by pass, coronary angioplasty

Investigation = during angina ST & T wave abnormality

Stress testing = treadmill

Coronary arteriography

Embolism

Effect of embolism on defferent orgon:

Retina →Amauresis fugax = fleeting blindness of central Artery ± Pennus

Mesentry = Engorgment ± Gangreen

Spleen = Local pain with increase in size.

Kidney = Loin pain, Haematuria

Lungs = Pulmonary embolism

Embolic arterial occlusion is an emergency and immediately diagnosis made (not for reassment the next morning)

Treatment = Heparin 5000 – 10000, Embolectomy and thrombectomy and Fogarty catherisation, Harman’s Solution 1000 heparin in 150 ml, Papavarin Sulphate to relive post operative spasm,Long term warferin

Congenital Heart Disease:

Three type:

(1) Stenosis, (2) Left to Right Shunt, (3) Right to Left Shunt.

Stenosis:

(1) Co arctation of aorta: hypertension in upper extremity, delayed femoral pulse, decrease in blood pressure in lower extremity, ECG = LVH, X ray Chest shows Notching of ribs due to collateral arteries and figure 3 appearance.

(2) Congenital pulmonary stenosis: JVP with α wave with S₂ Split, Diamond shaped murmur systole, ECG = RVH, RAH, Treatment = Valve replacement, valvularplasty, balloon dilatation.

(3) Congenital Aortic stenosis

Left to right shunt:

PPA

IASD

IVSD: Roger’s disease: direct communication between aorta and pulmonary artery at their basses.

Right to left shunt:

Tetralogy of Fallot: stenosis of pulmonary artery, Dilatation of right ventricle, VSD, Aortic displacement.

Tranportation of aorta and pulmonary artery.

Pericarditis = Picks disease

Rheumatic pericarditis = Bread and battil disease.

Tubercular pericarditis = Milk Spot.

Circulatory Shock: generalized inadequacy of blood flow throughout the body: abnormal tissue perfusion pattern, excessive metabolism of body.

Decrease Cardiac output: (1) Cardiac abnormalities: the ability of heart to pump blood, (2) factor that decrease venous return.

Intestinal obstraction, burn, dehydration, Hemorrhagic shear → hypovoluemia → shock

Shock is following type:

Neurological shock: increase vascular capacity may be due to deep general anesthesia, spinal anesthesia, brain damage, depressed vasomotor centre.

Anaphylactic shock: Histamine shock: it is an allergic condition in which cardiac output and arterial pressure often fall drastically.

Septic shock: May be due to peritonitis, generalized infection, gangrene = high fever, vasodilatation, sledging of blood, DIC,

Endotoxin shock: due to Gram negative bacteria

Effect of shock: decrease in metabolism in hypovoemic shock, muscular weak ness, body temperature rise, mental function altered, decrease renal fucntion

Treatment = Blood and plasma transfusion. Sympathotomimitic drug (norepinepharin, epinepharin), sympatholytic drug, head down position (in decrease in blood pressure), O₂, glucocorticoid, antihistaminic, pain reliving drug in trauma.

xje, xq: Hkkstu, d"kk;, dVq inkFkZ, Je, eksg, fpUru, v/kkj.kh; osx /kkj.kA

okrkfn nks"k jl dks nqf"krdj gn; esa vofLFkr gksdj gn; esa fodkj mRiUu djrs gsA

lkekU; y{k.k% oSo.;Z ewPNkZ Toj dkl fgDdk 'oklkL; oSjL; r`"kk izeksgk%A

NfnZ% dQksRDys’k:tks·:fp’p gnzksxtk% L;qfoZfo/kLrFkk ·U;sA

Okkfrd gn;jksx% Angina Pactoris: Coronary thrombosis: gn; esa f[kpkoV, lqfpdkos/kuor ihM+k, M.Ms ls eFkuk, nks VqdMs+ vkfj, dqYgkM+h ls phjkA pjd us tdMk+gV, ePNkZ, os"BuA

Okfrd gn; jksx es agn;dEiu ¼palpitation½ vkSj LrEHk ¼irrythmia and heart block½ feyrs gSaA

iSfrd gnzksx (inflammation, myocarditis, pericarditis) & I;klxehZ, nkg, pksl, gn; O;kdqyrk, /kwe izfrfr, ewPNkZ ilhuk,

dQt gnzksx%hypertrophy, pericardial effusion: Hkkjhiu, ykykizlsd, v:fp, tdM+kgV, vfXueka|, e/kqj LoknA

Formation of Hemoglobin:

2 succinyl – CoA + 2 glycine → Pyrrole

4 pyrrole → Protoporphyrin 1x

Protoporphyrin 1x + Fe⁺⁺→ Heme

4 Heme + Polypeptide → Hemoglobin Chain (α / β)(molecular weight 16000)

2 α chain + 2 β → Hemoglobin A (adult type)

1 heme carries 1 molecule of O₂

1 hemoglobin carries 4 molecule of O₂ = 8 atom of Oxygen.

Molecular weight of Hemoglobin = 64458

Iron Metabolism:

60% in liver(soluble → Ferritine, wt = 460000 and insoluble → Hemosiderine )

Daily loss of iron in male 1mg and in female 2mg.

Average life of RBC = 120 days, Hemoglobin destructed by Macrophages in tissue liver (Kupffer’s cells), spleen, bone marrow.

Iron deficiency = spoon shape, dry brittle nail.

plummar vinson syndrome = hypochromic microcytic anemia, dysphasia, crack angled mouth

Chlorosis =young working girl

Anemia =

(1) Blood loss anemia (1) Rapid – return normal in 3 – 4 weeks, (2) Chronic → microcytic Hypochromic anemia ¼jDrfir, jDrk’kZ½

(2) Aplastic anemia =pancytopanemia =panmyelopathy → Bone marrow aplasia may due to X ray, Pb, Hg, S, (vfLFkeTtkfod`fr tU; ik.Mq), fever, ulcer of mouth

ik.Mw jksx 5 izdkj ¼1½ okfrd, ¼2½ iSfrd, ¼3½ dQt, ¼4½ lfUuikfrd, ¼5½ e`frdk tU;A pjd

lqJqr us ik.Mw 4 izdkj dk ekuk gS ¼ e`frdk tU; ugh ekuk½

O;k;kEeYya yo.kkfu e|a e`na fnokLoIuerho rh{.keA

fu"ksoek.kL; iznq"; jDra nks"kkLRop ik.Mwjrka U;fUrA

lqJqr jDr dks nq"V rFkk pjd o okXHkV~ Ropk, ekal, jDr dks nq"V ekurs gSA

ik.Mwjksx esa fir nqfCV, fiRroxhZ; jDr dh n`f"V gksrh gS

Extrinsic factor: Fe, Cu, Mg, Vitamine

Intrinsic factor: Bile, Gastric juice, Thyroxin, other intrinsic factor.

Primary: aplastic anemia etc.

Secondary: Malaria, Hemorrahge, Hookworm etc.

vk;qosZn lksE; jl gh ;d`r xr jatd fir ds la;ksx ls jDr curk gSA ;g vk/kqfud dk Anti anemic principal or intrinsic factor gSA

vk;qosZn ;d`r Iyhgk dks jDr fuek.kZ dzsUnz ekurk gSA lqJqr us ljDr esn ¼bone marrow½ dks Hkh ekuk gSA

iw.kZ:i& RodLQksVu "Bhou xk=lkn e`}{k.k izs{k.k dwV 'kksFkk%A fo.ew= ihr RoeFkk foikdks Hkfo";rL; iqj%ljkf.k AA

okfrd ik.Mq & Ropk, ew=, us=, u[k, eq[k, ey, :{k d`".k, v:.k, lwfpdk os/kuor ihM+k, dEiu, vkukg, Hkze, esn 'kwyA

iSfrd ik.Mq & Toj, r`"kk, fiiklk, vUukfHkyk"kk vEyksnxkj, reizos’k, nkg ¼peripheral neuritis½, ey, ew= ihrrk, dVqdkL;rk vfrlkjA

dQt ik.Mq & xkSjo, rUnzk, NfnZ, izlsd, xk=lkn, 'okldkl, vkyL;, e/kqjkL;rk, 'osrkoHkklrk, ykseg"kZ, Hkze, ewPNkZ, v:fp, 'kksFk, ey, ew=, us= ’osro.kZA

f=nks"kt ik.Mq & Toj, vjkspd, oeu, I;kl DyeA

e`frdkHk{k.k% e`frdk lsoukuqlkj & d"kk; ¾ okfrd ik.Mq, mlj ¾ iSfrd ik.Mq, e/kqj ¾ dQt ik.MqA

jDrfuek.kZ es fod`fr ¼1½ jDr/kkRokfXu fod`fr ls & macrocytic, normochromic anemia, (2) jatd fir fod`fr ls & Normocytic hypochromatic anemia.

Treatment = iapxO;?k`r, egkfrDr ?k`r, dY;k.k ?k`r, nkfMek| ?k`r, dVqdk| ?k`r, iF;k?k`r, nUrh?k`r, nzk{kk?k`r, gfjnzk?k`rA vf/kd vke dQ & /kkekxZo }kjk oeuA

fojspu & okfrd ik.Mq esa nq/k ;k xksew=, nUrhQyDokFk $ equDdk lsouA

iSfrd ik.Mq esa f=o`rpw.kZ, iF;k?k`r ls rFkk dQt esa gjhrdh p.kZA

iquuZok e.Mwj, ykSg HkLe, dklhlHkLe, 'kq) e.Mwj, vkjksX;o/kZuh ofV, ?k`rdqekjh, rkez, dqekjhvklo, /kkÿ;kfj"V, chtdkfj"V, /kkÿ;koysg, f=Qyk|oysg, yksgklo, O;ks"kkfn ?k`r, xksew=, gjhrdhA

iF; & xks/kwe, ;okuh, eqnx, elwj, tkaxyekal puk, rqoj Rest.

nks"k & firiz/kku, nq"; & jDr ¼Rod, ekal½, esn, vkstA

lzksrl & jDroglzksrl ¼jlog½, lzksrksnqf"V izdkj & laxA

vf/k"Bku & Rod, vkek’;ksRFk O;kf/k, fpjdkjhA

Leucocytes = White blood cells (WBC): count 7000/m³ (6 types)

a. Polymorphonuclear Neutrophils 62%

b. Polymorphonuclear Eosinophiles 2 – 3%

c. Polymorphonuclear Basophiles 04%

d. Monocyte 5.3%

e. Lymphocyte 30%

f. Plateles (megakaryocytes) 300000

g. #9; ± plama cells

Genesis of Mylocyte:

Polymor and monocyte form in bone marrow and stay up to requirement.

Lymphocytes and plasma cells form in lymph node, thymus, spleen, tonsils.

Myelocytes → Myeloblast → promyleocytes → Megakaryocytes
Myelocytes → Myeloblast → promyleocytes → Basophil myelocyte → Polymorph basophiles.

Myelocytes → Myeloblast → promyleocytes → Eosinophiles myelocyte → Eosinophil metamyelocyte → Polymorphonuclear Eosinophiles

Myelocytes → Myeloblast → promyleocytes → Neutrophillmyelocyt → Young Neutrophill metamyelocyte → band neutrophil

Myelocytes→Monocytes

Life span of WBC: 4 – 8 hour in blood, 4 -5 days in tissue, in severe infection few hours.

Lymphocyte: few hours to 100 – 300 days → years

Platelets = 10 days, 30000/mm³ platelets form each day
properties of neutrophil, monocytes and macrophages

(1) Diapedesis, (2) Ameboid motion, (3) Chemotaxis, (4) Margination & Diapedesis of leukocytes throw capillary membrane, (5) Phagocytosis (neutrophil & macrophage)

Process of inflammation: Tissue injuries (By bacteria, Trauma, Chemical, Heat) → vasodilatation with excess local blood flow → increase permeability of capillary with leakage of large amount of fluid in to interstitial spaces → clotting of fluid in these space because of excessive amount of fibrinogen and other protein, leaking from capillaries → swelling of cells → walling off effect of inflammation at area of injuries from the remain tissue & inflamed area becoming invaded by Neutrophils and macrophages.

1^st line of defense: Tissue macrophages

2^nd line of defense: Neutrophile → Neutrophilia,

Movement of Neutriphil by margination → Diapedic → Chemotaxis

Colony stimulating factor (CSF) = collection of Glycoprotein (20000 – 50000 wt) → with in several hour increase production of Neutrophil by bone marrow.

3^rd line of defense: Macrophages proliferation and monocyte response:

slow and long term chronic infection: there is progressively increasing production of Monocyte.

Macrophages play an important role in initiating development of antibiotics.

Formation of pus: after several days a cavity is often excavated in the inflamed tissue containing varying portion of necrotic tissue, dead neutrphil and dead macrophages such mixture is commonly known as Pus.

Neutrophilia is caused by → Tissue destruction, acute hemorrhage, poisoning, operative procedure, very slight hemorrhage into the peritoneal cavity, and injection of foreign protein in to body and one of the diagnostic feature of coronary thrombosis, Myocardial infraction.

Physiological Neutrophilia = Hard exercise, inj. Norephiderine.

Eosinophile: 2 – 3% weak phagocyte & exhibits chemo-taxis, esionophilia (parasitic infection ), attach to parasite & release substance (deactivated by Heparin) that kill many of them (like in Schistosomiasis, Trichinosis).

Basophile: circulate with mast cell & librate Heparin (a member of lysosomal enzyme), Bradykinine, Serotinine, Histamine.

Agranulocytosis: Bone marrow stop production of WBC (bone marrow aplsia, X ray, γ ray, radiation, radio active products)

Leukemia: uncontrol production of WBC

Acute leukemia (1) ALL-child hood , (2) AML- any age

Chronic leukemia:

Lymphogenic leukemia(CLL =age of 45to 70 , cervical axillary, inguinal lymph node enlargement, TLC =100000, 80 – 90%

Monocytic leukemia

Myelogenrous leukemia (CML= age of 35 to 50 year )

a. Neutrophilic leukemia (age of 20 to 50 years Neutrophil 500000)

b. Eosionphilic leukemia

c. Basophilic leukemia

Aleukamic leukemia = fails to appear peripheral circulation. Decrease TLC, decrease Platelets

A typical leukemia =leucosarcoma

Agronulocytosis = decrease TLC, increase platelets

Thrombo cytopenia WBC (20000 – 50000), primitive cells (30 – 90)

Important notice

Dear friend,

These very tiny parts of notes are taken form various sections form Chotiwala's Notes. For complete notes and guidance please order today.

Best of luck

Tomorrow is yours

Yours truly,

Dr. Sanjay Kr. Singh

M.S. (Ay), D.Yo., I.M.S. B.H.U., Gold Medalist

Consultant Surgeon & Oncologist

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