HK 3810 Package 1 notes.docx

Amount of blood delivered to the heart is increased

Info icon This preview shows pages 5–7. Sign up to view the full content.

View Full Document Right Arrow Icon
amount of blood delivered to the heart is increased and contractility of heart stayed the same an extra 20 mL will be in the ventricle, but this cannot happen o In reality, if EDV increase contractility of the heart will increase strength of contraction increases increase volume ejected from the heart; heart function was changed in order to deal with the extra 20 mL Output from the heart - ESV – increase strength of contraction decrease ESV increase SV increase CO Intrinsic regulation – regulation by a factor originating from within the tissue o Frank-Starling Law of the heart – in crease in EDV leads to increase in strength of contraction of the heart o EDV is dictating stretch on the myocyte, which is dictating sarcomere length o Staircase phenomenon (Treppe) Increase in HR = increase in force If we increase frequency of contraction increase force development decrease ESV increase SV increase CO Extrinsic regulation – regulation by forces originating outside of the tissue o Nervous innervation – direct innervation to cardiac myocytes
Image of page 5

Info icon This preview has intentionally blurred sections. Sign up to view the full version.

View Full Document Right Arrow Icon
HK 3810 Package 1 SNS innervation causes the release of NE on to cardiac myocytes which have a B-adrenergic membrane population changes G protein increase AC increase cAMP increase protein kinases increases phosphorylation of: Voltage dependent Ca2+ channels (L-type, responsible for trigger calcium) increase # of channels that open per AP increase trigger Ca2+ increase contractility Ca2+ pumps on SR that use ATP to move Ca2+ into the SR increase activity decrease relaxation time increase speed of contraction PNS releases Ach onto cardiac myocytes which binds to a muscarinic cholinergic membrane receptor population stimulates an inhibitory G-protein decrease AC decrease cAMP decrease protein kinases decrease phosphorylation of: Voltage dependent Ca2+ channels (L-type) decrease in contractility Ca2+ pumps on SR decrease speed of contraction o More force causes ESV to go down, less force causes ESV to go up bc less volume is being ejected o Hormonal control SNS goes to the adrenal glands to release EPI/NE that will bind to the B-adrenergic membrane receptors of cardiac myocytes results are the same as SNS stimulation o Paracrine – endothelial cells line the heart Releases products such as endothelin which binds to ET1 or ET2 membrane receptors on cardiac myocytes increase IP3 increase Ca2+ available for contraction increase force of contraction decrease ESV Nitric oxide has unknown effects on force o Afterload – volume and pressure in the aorta that the ventricle has to work against High afterload decrease volume out/beat increase ESV decrease SV increase CO Output from the heart – HR Intrinsic control - neural control o PNS release Ach onto SA/AV node increase K+ permeability hyperpolarization
Image of page 6
Image of page 7
This is the end of the preview. Sign up to access the rest of the document.

{[ snackBarMessage ]}

What students are saying

  • Left Quote Icon

    As a current student on this bumpy collegiate pathway, I stumbled upon Course Hero, where I can find study resources for nearly all my courses, get online help from tutors 24/7, and even share my old projects, papers, and lecture notes with other students.

    Student Picture

    Kiran Temple University Fox School of Business ‘17, Course Hero Intern

  • Left Quote Icon

    I cannot even describe how much Course Hero helped me this summer. It’s truly become something I can always rely on and help me. In the end, I was not only able to survive summer classes, but I was able to thrive thanks to Course Hero.

    Student Picture

    Dana University of Pennsylvania ‘17, Course Hero Intern

  • Left Quote Icon

    The ability to access any university’s resources through Course Hero proved invaluable in my case. I was behind on Tulane coursework and actually used UCLA’s materials to help me move forward and get everything together on time.

    Student Picture

    Jill Tulane University ‘16, Course Hero Intern