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Fetal CirculationFetal Circulation
- Dr. Chintan
Circulatory Readjustments
First, loss of the tremendous blood flow through the
placenta, which approximately doubles the SVR at birth.
This increases the aortic pressure as well as the pressures
in the left ventricle and left atrium.
Second, the PVR greatly decreases as a result of
expansion of the lungs. In the unexpanded fetal lungs, the
blood vessels are compressed because of the small
volume of the lungs.
Immediately on expansion, these vessels are no longer
compressed and the resistance to blood flow decreases.
Circulatory Readjustments
Also, in fetal life, the hypoxia of the lungs causes
considerable tonic vasoconstriction of the lung
blood vessels, but vasodilation takes place when
ventilation of the lungs eliminates the hypoxia.
All these changes together reduces the pulmonary
arterial pressure, right ventricular pressure, and
right atrial pressure.
Closure of the Foramen Ovale
The low right atrial pressure and the high left atrial pressure
cause blood now to attempt to flow backward through the
foramen ovale; that is, from the left atrium into the right atrium.
The small valve that lies over the foramen ovale on the left side
of the atrial septum closes over this opening, thereby preventing
further flow through the foramen ovale.
In 2/3rd
of all people, the valve becomes adherent over the
foramen ovale within a few months to a few years and forms a
permanent closure.
But even if permanent closure does not occur, the left atrial
pressure throughout life normally remains 2 to 4 mm Hg greater
than the right atrial pressure, and the backpressure keeps the
valve closed.
Closure of the Ductus Arteriosus
↑ SVR elevates the aortic pressure while ↓ PVR reduces the pulmonary
arterial pressure. So, after birth, blood begins to flow backward from the
aorta into the pulmonary artery through the ductus arteriosus.
After only a few hours, the muscle wall of the ductus arteriosus constricts
markedly, and within 1 to 8 days - functional closure of the ductus
arteriosus.
Then, during the next 1 to 4 months, the ductus arteriosus ordinarily
becomes anatomically occluded by growth of fibrous tissue into its
lumen.
The degree of contraction of the smooth muscle in the ductus wall is highly
related to availability of oxygen.
In one of several thousand infants – PDA. The failure of closure result from
excessive ductus dilation caused by vasodilating prostaglandins in the
ductus wall – indomethacin role
Closure of the Ductus Venosus
In fetal life, the portal blood from the fetus’s abdomen joins
the blood from the umbilical vein, and these together pass
by way of the ductus venosus directly into the vena cava
bypassing the liver.
Immediately after birth, blood flow through the umbilical
vein ceases, but most of the portal blood still flows through
the ductus venosus, with only a small amount passing
through the channels of the liver.
Within 1 to 3 hours the muscle wall of the ductus venosus
contracts strongly and closes this path of flow. As a
consequence, the portal venous pressure rises from near 0
to 6 to 10 mm Hg, which is enough to force portal venous
blood flow through the liver sinuses.
Thank You…Thank You…
Splanchnic CirculationSplanchnic Circulation
- all the blood that courses through the gut, spleen,
and pancreas
- - portal vein
- – liver
- - millions of minute liver sinusoids
- - hepatic veins
- - vena cava of the general circulation
- This allows the reticuloendothelial cells that
line the liver sinusoids to remove bacteria and
other particulate matter that might enter the
blood from the GIT
Splanchnic CirculationSplanchnic Circulation
- The nonfat, water-soluble nutrients absorbed from the
gut (such as carbohydrates and proteins) are transported in
the portal venous blood
- fats absorbed from the intestinal tract are absorbed into the
intestinal lymphatics and then conducted to the systemic
circulating blood by way of the thoracic duct, bypassing the
liver.
- Blood supply - celiac artery, superior mesenteric and
inferior mesenteric arteries
- during active absorption of nutrients, blood flow increased
as much as eightfold. Likewise, blood flow in the muscle
layers of the intestinal wall increases with increased
motor activity in the gut
Splanchnic CirculationSplanchnic Circulation
- Sympathetic stimulation, by contrast, has a
direct effect on essentially all the gastrointestinal
tract to cause intense vasoconstriction of the
arterioles with greatly decreased blood flow.
- After a few minutes of this vasoconstriction, the
flow often returns almost to normal by means of a
mechanism called “autoregulatory escape.”
- That is, the local metabolic vasodilator
mechanisms that are elicited by ischemia become
prepotent over the sympathetic vasoconstriction -
redilate the arterioles – return of blood flow to
the gastrointestinal glands and muscle.
Splanchnic CirculationSplanchnic Circulation
- sympathetic vasoconstriction allows shut-off of gastrointestinal
and other splanchnic blood flow for short periods of time during
heavy exercise, when increased flow is needed by the skeletal
muscle and heart.
- In circulatory shock, when all the body’s vital tissues are in danger
of cellular death for lack of blood flow — especially the brain and the
heart — sympathetic stimulation can decrease splanchnic blood flow
to very little for many hours.
- Sympathetic stimulation also causes strong vasoconstriction of the
large-volume intestinal and mesenteric veins. This decreases
the volume of these veins, thereby displacing large amounts of blood
into other parts of the circulation.
- In hemorrhagic shock or other states of low blood volume, this
mechanism can provide as much as 200 to 400 milliliters of extra
blood to sustain the general circulation.
ECG Machine
ECG Machine
ECG Machine
ECG Machine
ECG Machine
ECG Machine
ECG Machine
holter monitor
holter monitor
holter monitor
holter monitor
T - ECG
Limb leads
Chest leads
Chest electrodes
Intracardiac electrodes
Esophageal electrodes
Esophageal electrodes
Cardiac jelly
1. What is Monroe Kellie Doctrine law? 2. Cerebral circulation. 3. Define arterial blood pressure. Describe the
nervous regulation of arterial blood pressure. 4. Pacemaker Potential. 5. Regulation of coronary circulation. 6.
Windkessel effect. 7. Phonocardiogram. 8. VO2 Max. 9. Define cardiac cycle. Describe in detail with the help of a
diagram - The mechanical changes during cardiac cycle. Add a note on heart sounds. 10. Draw a labeled diagram of
arterial pulse and explain. 11. Draw a normal E.C.G. and label it. 12. Refractory period. 13. Atrial natriuretic
peptide. 14. Jugular venous pulse. 15. Kirchhoff’s law and Einthoven’s law. 16. Tracing of arterial pulse. 17.
Reynolds’s number. 18. Pre load and after load in the heart. 19. Discuss the short term and long term regulation of
Arterial blood pressure. Add a note on Neurogenic Hypertension. 20. Endothelins. 21. Cardiac Index. 22. Unipolar
limb leads. 23. Define Cardiac output. Discuss the factors regulating the cardiac output. Add a note on Fick’s
principle. 24. Normal ECG in Lead II. 25. Regulation of coronary blood flow. 26. State Frank Starling’s law of the
heart. 27. List short term regulation of blood pressure. 28. Describe the structure and function of the conducting
system of the Heart. List the properties of cardiac muscle. 29. Special features of coronary circulation. 30. Cardiac
pacemaker potential. 31. Draw a labeled diagram of a normal ECG in lead II. Write a brief note on PR interval. 32.
Non progressive shock. 33. Dicrotic notch. 34. Cardiac reserve. 35. J point. 36. Extrasystole. 37. Define cardiac
output. Discuss the factors affecting cardiac output and any one method of determination. What is the significance
of ejection fraction in ventricular functioning? 38. Hypovolemic shock 39. Heart Sounds 40. PR interval in ECG 41.
Phasic changes in coronary circulation 42. Define cardiac cycle. Describe in detail the pressure volume changes that
occur during a Cardiac cycle with suitable Diagram 43. End diastolic volume 44. Define cardiac output. What are
the methods to measure the cardiac output? 45. SA node as pacemaker. 46. PR interval 47. Define the term Blood
pressure. Discuss the determinants and regulation of blood pressure 48. Ionic basis of the pace-maker potential 49.
Windkessel effect of aorta 50. Illustrate with a diagram, the left ventricular volume and pressure changes during a
cardiac cycle. 51. List the calcium transporters on the sarcoplasmic reticular membrane in the ventricular Muscle
52. State Starling’s law of the heart 53. Define the terms Cardiac output and Total Peripheral resistance and
discuss their Determinants. 54. Describe the 3 bipolar limb leads of ECG. What is the significance of (a) PR interval
(b) ST segment in an ECG? 55. Discuss the changes in ventricular volume during different phases of the cardiac
cycle with a diagram. 56. List the types of shock 57. Define Preload and state its effect on cardiac function 58.
Baroreceptor reflex 59. What is myocardial infarction? State one ECG change in this condition. 60. Define blood
pressure. Discuss in brief the various factors which influence the pressure. Add a note on hypertension. 61. Heart
sounds 62. Waves of ECG in Lead II 63. Define cardiac cycle. Describe the sequence of events during cardiac cycle
in detail with suitable diagrams. 64. Korotkoff sounds 65. Define cardiac output. Explain the factors regulating
cardiac output. Add a note on ejection fraction. 66. Conducting system of the heart 67. Features of Shock. 68.
Determinants of Blood pressure. 69. Phasic changes in coronary blood flow. 70. AV nodal delay. 71. Splanchnic
circulation. 72. Starling forces and oedema. 73. Mechanism of edema in congestive cardiac failure. 74. Extracellular
edema 75. Describe formation, circulation and functions of cerebrospinal fluid (C.S.F.).

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Fetal circulation

  • 2.
  • 3. Circulatory Readjustments First, loss of the tremendous blood flow through the placenta, which approximately doubles the SVR at birth. This increases the aortic pressure as well as the pressures in the left ventricle and left atrium. Second, the PVR greatly decreases as a result of expansion of the lungs. In the unexpanded fetal lungs, the blood vessels are compressed because of the small volume of the lungs. Immediately on expansion, these vessels are no longer compressed and the resistance to blood flow decreases.
  • 4. Circulatory Readjustments Also, in fetal life, the hypoxia of the lungs causes considerable tonic vasoconstriction of the lung blood vessels, but vasodilation takes place when ventilation of the lungs eliminates the hypoxia. All these changes together reduces the pulmonary arterial pressure, right ventricular pressure, and right atrial pressure.
  • 5. Closure of the Foramen Ovale The low right atrial pressure and the high left atrial pressure cause blood now to attempt to flow backward through the foramen ovale; that is, from the left atrium into the right atrium. The small valve that lies over the foramen ovale on the left side of the atrial septum closes over this opening, thereby preventing further flow through the foramen ovale. In 2/3rd of all people, the valve becomes adherent over the foramen ovale within a few months to a few years and forms a permanent closure. But even if permanent closure does not occur, the left atrial pressure throughout life normally remains 2 to 4 mm Hg greater than the right atrial pressure, and the backpressure keeps the valve closed.
  • 6. Closure of the Ductus Arteriosus ↑ SVR elevates the aortic pressure while ↓ PVR reduces the pulmonary arterial pressure. So, after birth, blood begins to flow backward from the aorta into the pulmonary artery through the ductus arteriosus. After only a few hours, the muscle wall of the ductus arteriosus constricts markedly, and within 1 to 8 days - functional closure of the ductus arteriosus. Then, during the next 1 to 4 months, the ductus arteriosus ordinarily becomes anatomically occluded by growth of fibrous tissue into its lumen. The degree of contraction of the smooth muscle in the ductus wall is highly related to availability of oxygen. In one of several thousand infants – PDA. The failure of closure result from excessive ductus dilation caused by vasodilating prostaglandins in the ductus wall – indomethacin role
  • 7. Closure of the Ductus Venosus In fetal life, the portal blood from the fetus’s abdomen joins the blood from the umbilical vein, and these together pass by way of the ductus venosus directly into the vena cava bypassing the liver. Immediately after birth, blood flow through the umbilical vein ceases, but most of the portal blood still flows through the ductus venosus, with only a small amount passing through the channels of the liver. Within 1 to 3 hours the muscle wall of the ductus venosus contracts strongly and closes this path of flow. As a consequence, the portal venous pressure rises from near 0 to 6 to 10 mm Hg, which is enough to force portal venous blood flow through the liver sinuses.
  • 8.
  • 10. Splanchnic CirculationSplanchnic Circulation - all the blood that courses through the gut, spleen, and pancreas - - portal vein - – liver - - millions of minute liver sinusoids - - hepatic veins - - vena cava of the general circulation - This allows the reticuloendothelial cells that line the liver sinusoids to remove bacteria and other particulate matter that might enter the blood from the GIT
  • 11. Splanchnic CirculationSplanchnic Circulation - The nonfat, water-soluble nutrients absorbed from the gut (such as carbohydrates and proteins) are transported in the portal venous blood - fats absorbed from the intestinal tract are absorbed into the intestinal lymphatics and then conducted to the systemic circulating blood by way of the thoracic duct, bypassing the liver. - Blood supply - celiac artery, superior mesenteric and inferior mesenteric arteries - during active absorption of nutrients, blood flow increased as much as eightfold. Likewise, blood flow in the muscle layers of the intestinal wall increases with increased motor activity in the gut
  • 12.
  • 13.
  • 14. Splanchnic CirculationSplanchnic Circulation - Sympathetic stimulation, by contrast, has a direct effect on essentially all the gastrointestinal tract to cause intense vasoconstriction of the arterioles with greatly decreased blood flow. - After a few minutes of this vasoconstriction, the flow often returns almost to normal by means of a mechanism called “autoregulatory escape.” - That is, the local metabolic vasodilator mechanisms that are elicited by ischemia become prepotent over the sympathetic vasoconstriction - redilate the arterioles – return of blood flow to the gastrointestinal glands and muscle.
  • 15. Splanchnic CirculationSplanchnic Circulation - sympathetic vasoconstriction allows shut-off of gastrointestinal and other splanchnic blood flow for short periods of time during heavy exercise, when increased flow is needed by the skeletal muscle and heart. - In circulatory shock, when all the body’s vital tissues are in danger of cellular death for lack of blood flow — especially the brain and the heart — sympathetic stimulation can decrease splanchnic blood flow to very little for many hours. - Sympathetic stimulation also causes strong vasoconstriction of the large-volume intestinal and mesenteric veins. This decreases the volume of these veins, thereby displacing large amounts of blood into other parts of the circulation. - In hemorrhagic shock or other states of low blood volume, this mechanism can provide as much as 200 to 400 milliliters of extra blood to sustain the general circulation.
  • 35. 1. What is Monroe Kellie Doctrine law? 2. Cerebral circulation. 3. Define arterial blood pressure. Describe the nervous regulation of arterial blood pressure. 4. Pacemaker Potential. 5. Regulation of coronary circulation. 6. Windkessel effect. 7. Phonocardiogram. 8. VO2 Max. 9. Define cardiac cycle. Describe in detail with the help of a diagram - The mechanical changes during cardiac cycle. Add a note on heart sounds. 10. Draw a labeled diagram of arterial pulse and explain. 11. Draw a normal E.C.G. and label it. 12. Refractory period. 13. Atrial natriuretic peptide. 14. Jugular venous pulse. 15. Kirchhoff’s law and Einthoven’s law. 16. Tracing of arterial pulse. 17. Reynolds’s number. 18. Pre load and after load in the heart. 19. Discuss the short term and long term regulation of Arterial blood pressure. Add a note on Neurogenic Hypertension. 20. Endothelins. 21. Cardiac Index. 22. Unipolar limb leads. 23. Define Cardiac output. Discuss the factors regulating the cardiac output. Add a note on Fick’s principle. 24. Normal ECG in Lead II. 25. Regulation of coronary blood flow. 26. State Frank Starling’s law of the heart. 27. List short term regulation of blood pressure. 28. Describe the structure and function of the conducting system of the Heart. List the properties of cardiac muscle. 29. Special features of coronary circulation. 30. Cardiac pacemaker potential. 31. Draw a labeled diagram of a normal ECG in lead II. Write a brief note on PR interval. 32. Non progressive shock. 33. Dicrotic notch. 34. Cardiac reserve. 35. J point. 36. Extrasystole. 37. Define cardiac output. Discuss the factors affecting cardiac output and any one method of determination. What is the significance of ejection fraction in ventricular functioning? 38. Hypovolemic shock 39. Heart Sounds 40. PR interval in ECG 41. Phasic changes in coronary circulation 42. Define cardiac cycle. Describe in detail the pressure volume changes that occur during a Cardiac cycle with suitable Diagram 43. End diastolic volume 44. Define cardiac output. What are the methods to measure the cardiac output? 45. SA node as pacemaker. 46. PR interval 47. Define the term Blood pressure. Discuss the determinants and regulation of blood pressure 48. Ionic basis of the pace-maker potential 49. Windkessel effect of aorta 50. Illustrate with a diagram, the left ventricular volume and pressure changes during a cardiac cycle. 51. List the calcium transporters on the sarcoplasmic reticular membrane in the ventricular Muscle 52. State Starling’s law of the heart 53. Define the terms Cardiac output and Total Peripheral resistance and discuss their Determinants. 54. Describe the 3 bipolar limb leads of ECG. What is the significance of (a) PR interval (b) ST segment in an ECG? 55. Discuss the changes in ventricular volume during different phases of the cardiac cycle with a diagram. 56. List the types of shock 57. Define Preload and state its effect on cardiac function 58. Baroreceptor reflex 59. What is myocardial infarction? State one ECG change in this condition. 60. Define blood pressure. Discuss in brief the various factors which influence the pressure. Add a note on hypertension. 61. Heart sounds 62. Waves of ECG in Lead II 63. Define cardiac cycle. Describe the sequence of events during cardiac cycle in detail with suitable diagrams. 64. Korotkoff sounds 65. Define cardiac output. Explain the factors regulating cardiac output. Add a note on ejection fraction. 66. Conducting system of the heart 67. Features of Shock. 68. Determinants of Blood pressure. 69. Phasic changes in coronary blood flow. 70. AV nodal delay. 71. Splanchnic circulation. 72. Starling forces and oedema. 73. Mechanism of edema in congestive cardiac failure. 74. Extracellular edema 75. Describe formation, circulation and functions of cerebrospinal fluid (C.S.F.).