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REGULATION OF HEARTBEAT AND BLOOD PRESSURE

REGULATION OF HEARTBEAT AND BLOOD PRESSURE. MUC – IB TRANSPORT NOVEMBER 24, 2009. REGULATION OF HEART RATE. Basic rate of heart beat is controlled by the activity of the SAN.

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REGULATION OF HEARTBEAT AND BLOOD PRESSURE

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  1. REGULATION OF HEARTBEAT AND BLOOD PRESSURE MUC – IB TRANSPORT NOVEMBER 24, 2009

  2. REGULATION OF HEART RATE • Basic rate of heart beat is controlled by the activity of the SAN. • However since heart rate is constantly changing as the body goes through different activities, the heart rate is controlled by two control systems: • Nervous • Chemical (hormonal)

  3. REGULATION OF HEART RATE • These two systems ensure that constant conditions are maintained within the bloodstream even though external conditions are constantly changing.

  4. CARDIAC OUTPUT • This is the amount of blood flowing from the heart over a given period of time. • Cardiac output = stroke volume x heart rate • Stroke volume is the volume of blood pumped out of the heart at each beat and the heart rate is number of beats per minute. • One way of controlling cardiac output is to control the heart rate.

  5. QUESTION

  6. NERVOUS CONTROL OF HEART RATE • First let us look at the divisions of the nervous system of the human body.

  7. NERVOUS CONTROL OF HEART RATE • Centre for control of heart rate in the brain is in the medulla. • The medulla has two regions affecting heart rate: • Cardiac inhibitory center (reduces heart rate) • Cardiac accelerator centre (increases heart rate)

  8. NERVOUS CONTROL OF HEART RATE • Two parasympathetic nerves called the vagus nerves, leave the inhibitory center and run, one on either side of the trachea to the heart. • Nerve fibres lead to the SAN, AVN and bundle of His (which branch into the pair of Purkinje fibres) to trigger a release of neurotransmitter acetylcholine. • This substance reduces the heart rate.

  9. VAGUS NERVES

  10. NERVOUS CONTROL OF HEART RATE • Other nerves, part of the sympathetic nervous system, originate in the cardiac accelerator region. • These run parallel to the spinal cord and enter the SAN and cardiac cells to cause a release of neurotransmitter substance norepinephrine. • The substance results in an increase in the heart rate.

  11. NERVOUS CONTROL OF HEART RATE • These two sets of nerves from the inhibitory and acceleratory regions in the medulla co-ordinate to control the heart rate.

  12. NERVOUS CONTROL OF HEART RATE • The aorta, carotid arteries and vena cava have stretch receptors that respond to the stretching of the tissue. • Sensory nerve fibres from these recptors run to the cardiac inhibitory centre in the medulla.

  13. NERVOUS CONTROL OF HEART RATE • As the volume of blood flowing through these vessels fluctuate, the stretch receptors register the changes. • Impulses received from the aorta and carotids decrease the heart rate (a fail-safe mechanism so that the heart does not work too hard). • Those from the vena cava stimulate the accelerator center which increases the heart rate.

  14. STRETCH RECEPTORS FROM THE VESSELS TO THE MEDULLA

  15. HORMONAL CONTROL OF HEART RATE • Adrenaline and noradrenaline / norepinephrine (secreted by the adrenal glands) stimulate the heart rate. • Cardiac output and blood pressure are increased by increasing the heart rate.

  16. HORMONAL CONTROL OF HEART RATE • The hormone thyroxine (secreted by the thyroid gland) raises basal metabolic rate. This is the rate at which energy is used by an organism at complete rest. • This leads to greater metabolic activity with greater demand for oxygen and production of more heat.

  17. HORMONAL CONTROL OF HEART RATE • Vasodilation increases. • Blood flow then increases. • Hence cardiac output increases. • Thyroxine therefore can indirectly or directly stimulate heart rate.

  18. OTHER FACTORS THAT CONTROL HEART RATE • High pH decelerates heart rate. • Low pH accelerates the heart rate. • Emotions, sights and sounds can increase the heart rate by increasing sympathetic activity. • Low temperature decelerates heart rate. • High temperature accelerates heart rate.

  19. LONG TERM EFFECTS OF EXERCISE ON HEART RATE • Heart gets stronger with exercise because muscles are worked out. • Heart chambers get larger and there is a 40% increase in cardiac output.

  20. MEASURING BLOOD PRESSURE • Blood pressure is the force developed by the blood pushing against the walls of the blood vessels. • Usually measured in the brachial artery in the arm using a sphygmomanometer. • Systolic pressure is high and is placed at top • Diastolic pressure is low and placed at bottom. • Normal pressure is around 120mmHg / 80mmHg.

  21. REGULATION OF BLOOD PRESSURE • Blood pressure depends on several factors: • Heart rate • Stroke volume • Resistance to blood flow by the blood vessels (peripheral resistance) • Strength of heartbeat

  22. REGULATION OF BLOOD PRESSURE • Resistance altered by vasodilation and vasoconstriction. • Controlled by vasomotor centre in the medulla • Nerve fibres run from this centre all over the body. • Vasomotor centre activity is regulated by impulses coming from pressure receptors in the walls of the aorta and carotids.

  23. BLOOD CLOTTING Blood clotting serves two main purposes: It prevents the body from losing too much blood from a wound It keeps invading organisms from entering a wound and causing infection.

  24. Blood disorders Thrombosis: A blood clot in a blood vessel or within the heart. Embolism: When an object migrates from one part of the body and blocks a blood vessel at another part of the body. Haemophilias: bleeding disorders that arise from a missing or mutant blood clotting protein/factor.

  25. BLOOD GROUPS There are four blood groups: A, B, AB and O.

  26. BLOOD GROUP INTERACTIONS

  27. Deficiency Anemia • Iron Deficiency (helps make haemoglobin) • Folate Deficiency (helps make DNA) • Pernicious (lack of Vitamin B12) (helps make folate) • Copper Deficiency (iron absorption decreases) • Vitamin C Deficiency (iron absorption decreases)

  28. Sickle Cell Anemia Genetic disorder so cannot be cured as deficiency anemia. A base glutamic acid is replaced by valine in the beta-proteins that helps make up heamoglobin. The red blood cells adopt a sickle shape and lodge in the blood vessels instead of flowing through freely.

  29. OXYGEN TRANSPORT, DISSOCIATION CURVES AND THE BOHR EFFECT DECEMBER 1, 2011

  30. OXYGEN DISSOCIATION CURVES • Release of oxygen from haemoglobin is dissociation. • The amount of oxygen that can combine with haemoglobin is determined by the oxygen concentration or partial pressure. • The more oxygen in the air the higher the partial pressure.

  31. OXYGEN DISSOCIATION CURVES • The higher the partial pressure of oxygen, the more saturated haemoglobin becomes with oxygen.

  32. The degree to which haemoglobin is saturated is illustrated by a sigmoid curve.

  33. Over the steep part of the curve a small decrease in the oxygen partial pressure of the environment will bring about a large fall in the percentage saturation of haemoglobin.

  34. The oxygen given up by the pigment in such a situation is available to the tissue.

  35. FOETAL AND MATERNAL HAEMOGLOBIN • Foetal haemoglobin (HbF) is structurally different from normal haemoglobin (Hb). • The foetal dissociation curve is shifted to the left relative to the curve for the normal adult.

  36. FOETAL AND MATERNAL HAEMOGLOBIN • At the placenta there is a higher concentration of a certain chemical compound (2,3-DPG) is formed. • This binds more readily to adult haemoglobin but not to foetal haemoglobin. • This causes the adult Hb to release more oxygen at the placenta to be taken up by the foetus. • Foetal Hb is made up of gamma chains not beta ones, and 2,3-DPG does not bind readily to gamma chains, hence it does not give up its oxygen.

  37. The foetal haemoglobin saturates more readily than that of the mother under the same conditions of partial pressure. This saturation also falls less rapidly than for the mother when oxygen levels decrease.

  38. This is because, typically, fetal arterial oxygen pressures are low, and hence the leftward shift enhances the placental uptake of oxygen.

  39. FOETAL AND MATERNAL HAEMOGLOBIN

  40. THE BOHR EFFECT • This states that at lower pH, haemoglobin will bind to oxygen with less affinity. • Since high carbon dioxide levels in the blood form carbonic acid, this effect has its roots in carbon dioxide concentration. • Hence high respiratory levels are associated with high carbon dioxide levels.

  41. THE BOHR EFFECT • In regions with an increased partial pressure of carbon dioxide, the oxygen dissociation curve is shifted to the right. • This is the Bohr effect and has a physiological advantage. • Increasing the carbon dioxide concentration results in oxygen being released from haemoglobin.

  42. THE BOHR EFFECT • Vertical line represent 29 mmHg or the partial pressure which gives 50% oxygen saturation in red blood cells.

  43. MYOGLOBIN • Red pigment similar to one of ht epolypeptide chains in haemoglobin. • Found in skeletal muscles and gives meat its red colouration. • Shows a great affinity for oxygen and oxygen dissociation curve is displaced well to the left of haemoglobin.

  44. MYOGLOBIN • It will only release its oxygen when oxygen in the environment is below 20mm Hg. • Hence myoglobin is a store of oxygen in resting muscle.

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