A&P II Heart Final

  1. American College of Sports Medicine
    Seven Factors
    • Non Life Style Lifestyle
    • 1. Age
    • 2. Genetics
    • 3. Type I
    • Life Style
    • 4. Hypocholsterolimia
    • 5. Hypertension
    • 7. Sedentary Lifestyle
  2. Coronary Artery Disease Factors
    • Age
    • Genetics
    • Type I
    • Hypertension
    • Eating
    • Excercise
    • Smoking
    • Sedentary Lifestyle
  3. Emulsifiction stage I
    Fat enters the small intestine and sends out a hormone signal cholecyokinin to Gall Bladder to secrete bile into small intestine which surrounds the fat making it water soluble
  4. Emulsification Stage II
    The pancrease secretes Lipases to breakdown fat into a smaller form called Monoglycerides surrounded by gile now called Micells.
  5. Emulsification III
    Micells enter enterocytes by facillited diffusion and modified at he smooth endoplasmic reticulum and repackaged at the Golgi into CHYLOMICRON which is larger.
  6. Emulsification IV
    Chylomicron enters lymphatic system via lymp lacteals into circulation for fat delivery
  7. Emulsification V
    High density lipo protein (HDL) recognizes the Chylocicron remants after most of the delivery has been make and places a molecular tag on the remants for liver take up
  8. Emulsification VI
    Liver repackages chylomicron remants into a new smaller form called VLDL and sent out for delivery
  9. Emulsification VII
    HDL recognizes VLDL liver takes up and repackages into smaller IDL form sent out for delivery
  10. Emulsification VIII
    HDL recognizes IDL liver take up repackaged into LDL sent out for delivery
  11. Emulsificaton iX
    HDL recognizes LDL and liver takes up remants
  12. Lymphatic Safety Factors
    • Tissue pressure -6mm/hg
    • Lymphatic drain -7mm/hg
    • Wash down of proteins -7mm/hm

    Need to exceed -20mm/hg in order to have Edema
  13. Capillary Exchange Pressures
    • Arteriol end
    • BP out 30mm/hg Hydrostatic Pressure-heart pumping
    • TP out -6mm/hg Hyrostatic Pressure into interstial space cells creating a sucking effect
    • COPV in 28mm/hg osmosis toward albumin in vascular space
    • COPT out 4mm/hg sosmosi toward protein in interstitial space
    • Filtration

    • Venule end
    • BP out 10mm/hg muscle tonus
    • TP out -6mm/hg Hyrostatic Pressure into interstial space cells creating a sucking effect
    • COPV in 28mm/hg osmosis toward albumin in vascular space
    • COPT out 4mm/hg sosmosi toward protein in interstitial space
    • Osmosis
  14. Causes of Edema
    • any increase of BP on either the Arteriol end or Venule end
    • art-renal failure, hypertension
    • ven-hd increasing P1 pressure, decrease muscle tonus

    • decrease in COPV=decrease albumin
    • Kwashiakov, protein malnutrition, renal disease
    • natural way-histamine release by immune system creating local temporary edema for healing
    • increases the gap between cells
    • Lymphatic blockage-bacterial infection, elephantitus, surgical removal
  15. Tachycardia Drugs
    Class II
    • Beta receptors-blockers effect both heart and lungs
    • beta blocker inhibit EPI decreasing Sympathetic NS and allowing Parasympathic to lower BP
    • Increase HR- secrete EPI with Atropine blocking receptor onthe heart and lungs down regulating the parasympathetic NS
  16. Tachycardia Class I
    • Inhibit, block or slow
    • Na+ from entering cells extending depolarization
  17. Tachycardia III
    • Inhibit, block or slow
    • K+ from exiting cells during repolarization extending repolarization
  18. Tachycardia IV
    • Inhibit, block or slow
    • Ca2+ from entering cells during depolarization extending depolarization
  19. Tachycardia V
    • Adensine
    • Increase K+ ability to leave the cell during repolarization causing hyperpolarization
  20. Blood Flow
    Into the right atrium-oxygen-poor

    • The oxygen-poor blood flows from the right atrium through the tricuspid valve to the right ventricle.
    • From the right ventricle, blood is pumped through the pulmonary valve into the blood vessel that goes to the lungs. This blood then picks up oxygen (becomes oxygenated or oxygen-rich).
    • Oxygen-rich blood flows from the lungs through blood vessels back to the heart's left atrium.

    • From the left atrium, blood goes through the mitral valve and into the left ventricle.
    • The left ventricle pumps blood through the aortic valve to a major blood vessel called the aorta and out to the body.
    • The blood delivers oxygen to the body, then returns through veins to the right atrium and repeats the blood flow cycle.
  21. Chronotropic
    • Changes that effect the heart rate
    • SA node sets regular rhythm
  22. Resting membrane potential
    • electric stability
    • brief isoelectric line at -70 mv
    • K+ leak
    • Na+ bully
    • Na+/K+ pump
  23. Threshold
    • minimum valve needed to depolarize the nerve
    • dotted isolectric line at -50mv
    • set by channels of depolarization
  24. Trigger Zone
    • distance electrically from RMP to threshold
    • represented by the line from RMP to threshold
    • Na+ leak channel
  25. Depolarization
    • generation of electricity
    • distance from threshold to peak of amplitude
    • Ca2+ voltage gate channels
  26. Repolarization
    • reset electric potential back to RMP
    • distance electrical from end of depolarization until reaching RMP
    • K+ voltage gated channels
  27. Blood flow control
    Pre capillary sphincters smooth muscle collar at the end of arteries which can either vasoconstric or vasodialate hooked to CNS to control flow
  28. Systemic Circulation
    • arranged in parallel
    • provide equal delivery
    • ablility to regulate flow
  29. Pulmonary circulation anatomy
    • rt heart, atrium, ventricle
    • pulmonary artery and lungs
  30. Systemic Circulation Anatomy
    • pulmonary veins
    • left heart, atrium, ventricle
    • all tubing
  31. Poiseuille's Law
    • 4th Power law
    • change the diameter of the tube the flow rate changes by the 4th power
  32. Iontropic
    • increase of heart contraction
    • increase intercelluar Ca2+ release causing more actin myosin crossbridging
    • natural-release of EPI-binds to beta 1 receptors causing increasing intercellular Ca2+
    • cardiac glycosides-digitalis - digitoxin inhibitsa very small portion of Na+/K+ pump causing an increase in intracellular Na+
    • Na+ inhibits Na+/Ca2+ exchange increaseing intracellular Ca2+ increasing contraction strength
  33. EKG
    electrical representation of how electricity travels through the electrical conduction tissue SA node, AV node, bundle of hiss, bundle branches and perkiji fibers
  34. Components of EKG
    • P-wave-electricity as it travels through the SA node representing atrial contraction
    • QRS complex- electricity as it travels through AV node, bundle of hiss, bundle branches and perkinji fibers ventrical contraction
    • T-wave-electrical tissue of the QRS complex repolarizing ventrical relaxation
    • atrial relaxation not seen masked by QRS complex
    • PR interval time between atrial contraction and ventrical contraction
    • QT time between ventrical contraction and ventrical relaxation
  35. Cardiac Cycle Diagram
    • Stage I-Diastasis-Atrial&ventricular contraction relaxation filling with blood 75% ventricle at this time
    • Stage II-Atrial Systole-atrium contraction- atrial kick
    • Stage III Ventricular contraction-increase in left ventricular pressure with no change in volume-before aortic valve opens
    • Stage IV 2nd part of ventricular contraction-rapid ejection
    • Stage V Isovalumic relaxation-decrease in left ventricular pressure no change in left vent volume-beginning of relax b4 mitral valve opens
  36. Cardiac Function Evaluation using cardiac cycle
    • 1 determine stage effected
    • 2 EKG effected?
    • 3 pressure changes
    • 4 volume changes
    • 5 heart sounds
  37. Compensation from Edema
    • any increase in P1 pressure leads to Edema
    • any decrease in P3 pressure leads to Edema via renin release
    • any decrease in P3 pressure leads too LVH leading to CHF or chronic heart failure
    • heart rate increases ventilation rate increases
  38. cholesterol measures
    • total measures all chrylomicrons, vldl, idl, ldl
    • Individual-LDL less than 100mg/dl, HDL greater than 35mg/dl
    • Ratio-3:1 total vs HDL
    • Tri 130mg/dl
  39. Atherosclerosis process
    • How plaque happens in arteries
    • turbulent flow causes Eddy currents
    • Eddy currents damage epithial lining and immune system activated for healing
    • LDL answer the call invaginating into the damaged epithial cells
    • macrophages engulf LDL and encapsulate them causing an inward hypertrophy toward the lumen decreasing the diameter
    • anthroma protective cap is placed over tissue creating a positive feedback system
    • thrombus-a piece breaks off
    • complete occlusing-blocked
    • spasm- cocaine binding
  40. atherosclerosis signs and symtoms
    • 60-70% blockage-no symtoms
    • 80%-at excercise
    • 90%- at rest and excercise
  41. atherosclerosis therapy
    • diet and excercise-decreasing blood pressure and turbulent flow through excercise
    • decrease HCT by plasma volume increase
    • decrease viscosity
    • increase HDL
    • decrease LDL
    • decrease animal fat intake
    • increase veggies and fruit
    • eat more fiber
    • lower salt
    • take pharma
    • surgery-stent, shave, laser, angioplasty
    • CAB
  42. Cardiac measures after heart attacks
    • creatine kinase enzyme measures
    • PCR+H+ +ADP
    • Skeletal muscle CK-mm
    • Nervous tissue CK-BB
    • Cardiac muscle CK-mb 8-24 hrs

    • Tripoinin Complex Protein
    • 12-24 hrs
Card Set
A&P II Heart Final
Heart Anatomy and Physiology