Cardiovascular physiology


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Brief overview of cardiac physiology

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Cardiovascular physiology

  1. 1. Cardiovascular Anatomy andPhysiology
  2. 2. Cardiovascular Anatomy•Weighs between 200-400 grams•By the end of a normal life it may have beat more than 3.5billion times•Each day the heart beats 100,000 times•Pumping about 7,751 litres of blood.
  3. 3. Cardiovascular Anatomy•Located between lungs•Behind and slightly to the leftof sternum•Double layered membranecalled pericardium surroundsheart•Outer layer of pericardiumattached by ligaments tospinal column and diaphragm•Coating of fluid separatesthe two membranes
  4. 4. Cardiovascular AnatomySuperior vena cava takesdeoxygenated blood frombodyPulmonary artery sendsdeoxygenated blood to thelungsPulmonary veinstake oxygenatedblood from the lungsInferior vena cava takesdeoxygenated blood frombodyAorta sendsoxygenated bloodaround the body
  5. 5. Cardiovascular AnatomyThe tricuspid valve regulates blood flowbetween the right atrium and right ventricle.The mitral valve lets oxygen-richblood from your lungs pass from theleft atrium into the left ventricle.
  6. 6. Cardiovascular AnatomyThe pulmonary valve controls blood flowfrom the right ventricle into the pulmonaryarteries, which carry blood to your lungs topick up oxygen.The aortic valve opens the way foroxygen-rich blood to pass from theleft ventricle into the aorta, yourbodys largest artery, where it isdelivered to the rest of the body.
  7. 7. Cardiovascular Anatomy
  8. 8. Cardiovascular Anatomy
  9. 9. Cardiac muscle•Contractileproteins•Contractionachieved throughrelease of calcium•Rich inmitochondria-aerobicdependent•Fibres connect toeach otherthroughintercalcateddiscs
  10. 10. Action PotentialsResting membranepotential -90mVRapiddepolarisation to+20mVPartial repolarisation to5-10mVSlowRepolarisationRapidrepolarisation
  11. 11. Action PotentialsCardiac cells absolutely refractory tostimulation for whole duration of actionpotentialSecond action potentialcannot be generated for upto 350msProlonged action potentialprotects against pumpfailure caused by sustainedcontractionSets upper rate ofcontraction 3-4 beats persecond.
  12. 12. Membrane potentialDepolarisation opens sodiumchannelsInward sodium current causesfurther depolarisationCalcium channels open moreslowlyOnce open keeps membranedepolarised and maintainsplateau.Initially less outward flow ofPotassiumThen outward flow increases repolarising themembrane
  13. 13. Membrane potentialRapid depolarisationSodium rushes inCalcium inflowslowerMaintains plateauPotassium outflowreduced, then risesThis repolarisesmembrane
  14. 14. Automaticity• Action potentials are generatedspontaneously within the cellsthemselves- myogenic.• Known as pacemaker cells• Instead of constant resting potentialthere is a steady depolarisingpotential• Once action potential is generated atone site it is rapidly conducted.• Driven by fastest pacemaker cells inheart- normally SA node.
  15. 15. Conducting pathways in the HeartAP’s conducted away from SA node by atrialfibres.Made possible by low resistance junction atintercalcated discsProduces atrial contractionAV node capable of pacemaker activity butnormally driven by SA node.Slow conduction which ensures ventricularcontraction does not take place until atrialcontraction complete.Action potential travels down left and right sideof Bundle of HisTransmission through Bundle and Purkinjefibres rapid to promote synchronisedcontraction of ventricles.
  16. 16. Cardiac Cycle- Ventricular pressureDuring ventricular diastoleventricular pressure is low-1mmHgRises to about 5mmHg at endof atrial systole as blood isforced into ventricle.Ventricular systolecommences raisingpressures rapidly to about120mmHgPeak pressure in rightventricle about 25mmHgAs heart rate increasesdiastole shortens.Inadequate filling in shortdiastole compromises heartif heart rate too high.
  17. 17. Cardiac Cycle- Atrial pressureAtrial pressure remains constant atabout 1mmHg until....Atrial systole when pressure risesto about 6mmHgThis is the a wave.Atrium relaxes and AV valve closes(mitral valve, tricuspid valve)Causes back pressure on valvecusps.Rise in pressure results in c wave.Aortic and pulmonary valves openand atrial pressure falls to almostzero.Blood enters atria from venoussystem.AV valves are closed so pressurerises.This is v wave
  18. 18. Cardiac Cycle- Aortic pressureDuring ventricular diastole there isa gradual decline in aortic pressureto about 80mmHgDuring this time aortic pressurehigher than ventricular pressureso AV remains closedDuring systole ventricularpressure rises opening valveAortic pressure peaks at about120mmHgPressure drops and aortic valvecloses causing small rise inpressure.....Dicrotic notch
  19. 19. Cardiac Cycle- Heart SoundsFirst heart sound- lub-caused by closure ofmitral and tricuspidvalves at start of systoleSecond heart sound-dub- caused by closure ofaortic and pulmonaryvalves at end of systole
  20. 20. Ventricular VolumeAt the end of systole there isabout 80mls of blood inventricleThis increases to about130mls during diastole dueto passive filling from theatriumActive filling from the atriumonly increases this by about25% to 150mlsApproximately 70mls ofblood ejected during systoleThe dominant effect of passive fillingexplains why ventricular filling is still possiblein the absence of coordinated atrialcontraction e.g. Atrial fibrillation
  21. 21. Cardiac OutputCardiac output = heart rate X stroke volumeAt rest:Cardiac output = 70bpm X 70ml/beat=4900ml/minOr5 Litres per minute.
  22. 22. Intrinsic control of cardiac outputIncreased force ofcontraction as restinglength of cardiac musclesincreasedResults in increasedin increases in strokevolume as volume ofventricle immediatelybefore contractionwas increased
  23. 23. Intrinsic control of cardiac outputPreload-Refers to level of stretch in a relaxed muscle justbefore it contracts.In the heart this is largely dictated by the venousreturn.So increased venous return increases stretch inmuscle which increases cardiac out put.Afterload-Refers to the force that the muscle mustgenerate during contraction.Most affected by changes in arterialpressure
  24. 24. Extrinsic control of cardiac output•Nervous control•Sympathetic•Parasympathetic•Can alter heart rate- chronotropic effects•Can alter force of contractility- inotropic effects.
  25. 25. Extrinsic control of cardiac output•Nervous control•Sympathetic.•Controlled in a number of regions of the CNS•Postganglionic nerves release neurotransmitter noradrenaline•Stimulation of nerves leads to• increased heart rate (positive chronotropic effect)•Increased myocardial contractility (positive inotropic effect)•Leads to increased cardiac output at any given pressure•Limits to benefits of increased heart rate due to compromisedatrial filling.
  26. 26. Extrinsic control of cardiac output•Nervous control•Parasympathetic.•Come from medulla oblongata in the brain and reach heart viavagus nerve.•Supply SA and AV node and release acetylcholine whenstimulated•This slows heart (negative chronotropic effect) through itsinfluence on pacemaker activity.•Reduction in cardiac activity.
  27. 27. Extrinsic control of cardiac output•Hormonal Control•Catecholamines•Adrenaline•Noradrenaline•Released by adrenal medullary cells in response to sympatheticnervous stimulation•Increase both heart rate and myocardial contractility
  28. 28. Pi PoSo there are only two ways inwhich we can affect blood flowControl of arterial pressureFor fluid to flow through a pipe theremust be a pressure gradient betweenthe two ends of that pipe.The size of that gradient(arterialpressure) equals the rate offlow(cardiac output) times theresistance to that flow(SVR).OR Cardiac Output = Arterial Pressure X ResistanceChangingpressuredifferenceacross itsvascular bedChanging itsvascularresistance
  29. 29. Control of arterial pressureIf Cardiac output is constantthen pressure differencebetween two points will beproportional to theresistance.Pressure in aorta and largearteries is high and pulsatileand there is only a smalldrop in pressure along theirlength.Largest pressure drop occursin the arteriolesSo single largest contributionto peripheral resistancecomes from the arteriolesTherefore peripheralresistance can be controlledby constriction or dilation ofthese vessels
  30. 30. Regulation of arterial pressure.• Nervous control– Vasomotor centre- activates sympathetic nerves;• Stimulate heart rate and contractility• Release noradrenaline• Causes venules to constrict which increases venousreturn, increasing cardiac output.• Preganglionic sympathetic nerves stimulate release ofadrenaline and noradrenaline from adrenal medulla.
  31. 31. Regulation of arterial pressure.• Nervous control– Baroreceptor reflexes• Stretch receptors in carotid sinus and aortic arch• Increases in arterial pressure stretch aorta and carotid.• This stimulates sensory output from receptors• Which inhibits sympathetic outflow to thecardiovascular system and...• Stimulates parasympathetic nerves thereby...• Reducing cardiac output.• Respond very rapidly.
  32. 32. Regulation of arterial pressure.• Nervous control– Low pressure volume receptor reflexes• In walls of great veins, atria and pulmonary trunk.• Particularly sensitive to changes in blood volume• Increased blood volume stretches these receptors....• Which reduce blood pressure by...• Reducing vasoconstrictor sympathetic activity, reducingresistance..• Release of ADH is inhibited• ADH causes direct vasoconstriction and stimulateswater absorption from the kidney.
  33. 33. Regulation of arterial pressure.• Nervous control– Chemoreceptors• Found in aortic and carotid bodies• Sensitive to changes in tissue oxygen levels• So if arterial pressure is very low oxygen levels maydrop at the tissue level• Stimulate vasoconstrictor sympathetic nerves torestore blood pressure.
  34. 34. Regulation of arterial pressure.• Hormonal control– Catecholamines• Adrenaline/noradrenaline– ADH (vasopressin)• Vasoconstrictor– Renin-angiotensin-aldosterone system.
  35. 35. Renin-angiotensin-aldosterone system.
  36. 36. Requirements for effective operation• Contractions of cardiac muscle cells must occur atregular intervals and be synchronized (not arrhythmic).• Valves must be fully open (not stenotic)• Valves must not leak (not insufficient or regurgitant)• Muscle contractions must be forceful (not failing)• Ventricles must fill adequately during diastole.