Heart Physiology, Schleich
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Heart Physiology, Schleich

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Heart Physiology, Schleich Presentation Transcript

  • 1. A heartbeat is a two-part pumping action that takes abouta second. Cardiac Cycle: diastole PhaseThis part of the two-part pumping phase (the longer of thetwo) is called diastole.Diastole begins as the ventricles start to relax. Soon thepressures within the aorta and pulmonary artery exceedventricular pressures, causing the semilunar valves toclose (B2 murmur).As the ventricular pressure falls below the atrial pressurethe AV valves open and the ventricles fill with blood. Theventricles fill to about 80% of capacity prior to contractionof the atria, the last event in diastole.Atrial contraction forces the final 20% of the end-diastolic volume (the volume of blood that exists in theventricles at the end of diastole) into the ventricles. / SA nodecontractsSummary of Diastole:pulmonary and aortic valves closeVentricles relax => isovolumic relaxationAV valves openventricles fill (about 80% of capacity) => inflowatria contract (ventricles fill another 20%)Contraction reaches AV node…
  • 2. The second part of the pumping phase beginswhen the ventricles are full of blood. Cardiac Cycle: Systole PhaseThe electrical signals from the SA node travelalong a pathway of cells to theventricles, causing them to contract. This iscalled systole.As the ventricles start to contract, theventricular pressure soon exceeds the atrialpressure, causing the AV valves to close (B1murmur).As the ventricles continue to contract, theventricular pressure exceeds the arterialpressures causing the semilunar valves open.Blood is forcefully ejected out of the ventriclesand into the aorta and pulmonary artery.Summary of Systole :AV valves closeventricles contract => isovolumic contractionaortic and pulmonary valves openblood is ejected => ejection phaseatria relax and fill with blood
  • 3. Plan: Evaluation of the cardiac performance • On the cellular « scale » – muscular cells and cardiac myocytes – myofibril / « Sarcomere » – proteins: actin / myosin – role of Ca++ – => « cell’s performance » • Laws and principles of haemodynamic: – Poiseuille or Darcy – Starling : preload and post load – «heart’s performance » • On the scale of the organ: the heart – Cardiac cycle – Relation pressure-volume – The regulation of the cardiac output
  • 4. Physiology (1)All muscles derive from paraxial mesoderm.The three types of muscle (skeletal, cardiac and muscle cell orsmooth) have significant differences. However, allthree use the movement of actin against myosin tocreate contraction.Cardiac muscle is a type of involuntary striatedmuscles found in the walls of the heart, specificallythe myocardium.Cardiac and smooth muscle contractions arestimulated by internal pacemaker cells whichregularly contract, and propagate contractions toother muscle cells they are in contact with.Muscle is mainly composed of muscle cells. Withinthe cells are myofibrils; myofibrils containsarcomeres, which are composed of actin andmyosin.
  • 5. Muscle / Fasicle / Fiber (cell) / Fibril / sarcomere
  • 6. musclefiber or cellmyofibrilssarcomere
  • 7. 1:Axon / 2:neuromuscular junction / Physiology (2) 3:muscle cell / 4:myofibrilMyofibrils are cylindrical organelles. They are foundwithin muscle cells or fibers.They are bundles of actomyosin filaments that runfrom one end of the cell to the other and areattached to the cell surface membrane at each end.The filaments of myofibrils, ormyofilaments, consist of two types, thick and thin. Thin filaments consist primarily of theprotein actin, coiled with nebulin filaments. Thick filaments consist primarily of theprotein myosin, held in place by titin filaments.The filaments are organized into repeated subunitsalong the length of the myofibril.These subunits are called sarcomeres.The sarcomere is the “functional” basic unit ofcontraction.
  • 8. sarcomere sarcomeresarcomere
  • 9. Physiology (3)Cardiac muscle requires extracellular calciumions for contraction to occur. Like skeletalmuscle, the initiation and upshoot of the Sliding filament model of muscle contractionaction potential in ventricular muscle cells isderived from the entry of sodium ions across myosin relaxedthe sarcolemma in a regenerative process.Once the intracellular concentration ofcalcium increases, calcium ions bind to theprotein troponin, which initiates contraction actin filamentby allowing the contractile proteins, myosin contractedand actin to associate through cross-bridgeformation. Shortening of 1 µm / sarcomere If 10 5 sarcolemma (striated muscle) => Shortening of 10cm
  • 10. Neuromuscular junctionfor the next presentation… In contrast to skeletall muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular muscle cells is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. Once the intracellular concentration of calcium increases, calcium ions bind to the protein troponin, which initiates contraction by allowing the contractile proteins, myosin and actin to associate through cross-bridge formation.
  • 11. Poiseuille or Darcy’s law / (Ohm)– ∆P = Q x Rv / (Flow = Pressure/Resistance ) • ∆P => Mean gradient pressure – ∆Ps = PAo – POD – ∆Pp = PAP – PVP – Qs = SV x Hr (SV=> Stroke Volume = EDV – ESV )After birth: « serial circulation » without shunt => Qs=Qp => pressures in aorta and PA depend on ResistancesBefore birth: « parallel circulation »With shunts => Pao = PAP / Qs ≠ Qp Rp are high => Qp is low Rs are low (placenta) => Qs is high
  • 12. Frank-Starling law• The Frank-Starling law of the heart states that the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume).• This allows the cardiac output to be synchronized with the venous return, arterial blood supply and humeral length[1] without depending upon external regulation to make alterations.• As the heart fills with more blood than usual, the force of the muscular contractions will increase.• The stretching of the muscle fibres increases the affinity of troponin C for calcium, causing a greater number of cross-bridges to form within the muscle fibers; this increases the contractile force of the cardiac muscle.• The force that any single muscle fiber generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibers is related to the end-diastolic volume of the ventricle.
  • 13. TAToum
  • 14. TAToum
  • 15. Parameter Values• End-diastolic volume (EDV) 120 ml 290 l / hour• End-systolic volume (ESV) 50 ml 7 056 l / day 2 575 440 l / year• Stroke volume (SV) 70 ml 180 280 800 l / 70 years• Ejection fraction (Ef) 58%• Heart rate (HR) 70 bpm•• Cardiac output (CO) 4.9 L/mn• Cardiac index (CI) 2,5 -3,5 l/mn/m2
  • 16. End systolic volume (afterload volume)Pressure Contractility Starling lawmm Hg 140 Systolic phase Ejection phase Closure of the aortic valves 80 Opening of the aortic valves SV (35ml) Isometric relaxation Isometric contraction Compliance 30 Opening of the AV valves 10 Closure of the AV valves Filling 10 40 50 100 Volume ml Diastolic phase End diastolic volume (preload volume)
  • 17. the cardiac performance
  • 18. Regulation of cardiac output the rate of contraction can be changed by nervous or hormonal influences, exercise and emotions. For example, the sympathetic nerves to heart accelerate heart rate and the vagus nerve decelerates heart rate. Qs = SV x Hr (SV=> Stroke Volume = EDV – ESV )
  • 19. Evaluation of and for the « teacher » !• How do you define a muscular fiber and a sarcomere ?• Explain the mechanism of shortening of a muscle fiber ?• What is the Starling’s law ?• What happens during the isovolumic relaxation concerning the heart’s valves ?• Define the « compliance » of the heart• How many liters does the heart pump during one year ? (bonus)
  • 20. Physiopathology