physio mini 3

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sweetlu
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115198
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physio mini 3
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2011-12-04 12:15:43
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physio mini 3
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  1. right atrial mean pressure
    -4 to 4
  2. right ventricle pressure
    25/0
  3. pulmonary artery pressure
    25/8
  4. left atrial mean pressure
    7
  5. left ventricle pressure
    120/0
  6. aortic pressure
    120/80
  7. CO
    • ~ 5L/min
    • = SV x HR = (EDV-ESV) x HR
  8. ejection fraction
    • normal: 55-65%
    • =SV/EDV
  9. Fick principle
    CO= VO2/ (CA-CV)

    • -VO2: rate of O2 consumption
    • -CA: O2 content in peripheral artery
    • -CV: O2 content in mixed venous blood (RV, PA or RA)
  10. Pulse Pressure
    =Psys - Pdias

    ~SV/ arterial compliance
  11. MAP
    • normally around 100
    • = Pdias + 1/3(pulse pressure)
    • = CO x TPR
  12. wedge pressure
    • - normal : 8-10 mmHg
    • - used as an approximation of pressure in pulmonary veins and left atrium
    • - >15= mitral stenosis or regurg, severe aortic stenosis or regurg, ventricular failure, etc.
  13. Aortic stenosis
    • - narrowing of the aortic valve
    • - ausciltation at right 2 ICS:
    • ---mid-systolic murmur(later murmur=later stage of stenosis)
    • ---S4 will be present due to LV hypertrophy (differential from mitral regurg)
  14. S1
    • -closure of AV valves
    • - splitting may be caused by conduction problem, ie right bundle branch block
    • - heard at start or isovolumetric contraction
  15. S2
    • - closure of aortic and pulmonary valves
    • - splitting can be caused by inspiration(inc ven return)
    • ---if splitting is not accentuated by inhalation, then pathological (atrail septal defect or bundle branch block)
    • - heard at start of isovolumetric relaxation
  16. S3
    • - excessive ventricular dilation caused by atrial contaction
    • - physiological in younger patients
    • - pathological- aortic or mitral regurg
    • - heard at start of rapid ventricular filling
    • - "SLOSH'--ing-in"
  17. S4
    • - low ventricular compliance
    • - pathological- aortic stenosis or ventricular hypertrophy due to hypertension
    • - heard right before S1 during atrial systole
    • - "a-STIFF'--wall"
  18. mitral regurge
    • incompetent mitral valve causing regurgitation into the LA
    • - systolic murmur
    • - S3 heard (differential from aortic stenosis)
  19. mitral stenosis
    • - narrowing of the mitral valve
    • - causes diastolic murmur because of larger pressure gradient b/t atrium and ventricle
  20. PR interval
    - normal: .12-.20 seconds
  21. QRS complex
    • - normal < .10 seconds
    • - isovolumetric contraction (mechanical phase)
  22. QT interval
    • - > 1/2 of a complete cardiac cycle (~1/3)
    • - ventriclar systole
    • - starts IVC and ends after RE
  23. main metabolite vasodilators of SkM
    K and adenosine
  24. main metobolite vasodilators of CM
    adenosine and NO
  25. main metabolite vasodilator of brain
    PCO2
  26. primary factor that alters pulmonary resistance
    • hypoxia, causes vasocontriction
    • -this helps redirect blood flow to the areas of the lung that are better ventilated
  27. alveolar PO2
    PAO2= PIO2- (PACO2/R)

    • -Pi= PO2 of inspired air
    • -PACO2= PCO2 of alveolar air
    • -R= respiratory quotient (CO2 output/ O2 uptake)
  28. partial pressure of CO2 in alveolus
    PACO2= (VCO2/VA) x 863

    • -VCO2= vol of CO2 from metabolism
    • - VA= minute alveolar ventilation
  29. alveolar ventilation
    VA= (VCO2/PaCO2) x 863
  30. obstructive disease
    • - any disease that decreases the alveolus ability to create positive pressure (on expiration)
    • - ie, COPD,empysema, asthma, chronic bronchitis
  31. restrictive disease
    • -any disease that decreases the lungs ability to create a negative alveolar pressure on inspiration
    • - ie fibrosis, asbestosis
  32. respiratory system compliance
    1/CRS= 1/CL + 1/CCW
  33. respiratory exchange ratio
    CO2 output/O2 uptake
  34. arterial O2 content
    VaO2= O2 dissolved + (gm Hb x 1.34)

    .03 ml O2 dissolved/ 10mmHg PO2
  35. lowest PVR
    • -FRC
    • -PVR increase (and flow decrease) on either side of FRC
  36. stagnant hypoxia
    • - PO2 and [O2]a are both normal
    • -decreased blood flow
  37. anemic hypoxia
    • - PO2 normal, [O2]a is decreased
    • - decreased [Hb]
  38. histotoxic hypoxia
    • - PO2 and [O2]a are normal
    • - poisoning (CN) blocks O2 utilization on cellular level
  39. arterial hypoxemias with reduced PO2 and no change in (A-a)PO2
    • - low inspired PO2 (high altitude)
    • - hypoventilation
  40. decreased PaO2 and (A-a)PO2>0
    • -diffusion limitation
    • - R to L shunt
    • - V/Q mismatch
  41. steps to determining the cause of hypoxemia
    • 1- check PaCO2
    • a. high= hypoventilation
    • b. low= low PIO2 (high altitude)
    • c. normal-> continue to step 2
    • 2. Give 100% O2
    • a. PaO2<400 = R to L shunt
    • b. PaO2>400 continue to step 3
    • 3. CO2 diffusion capacity test
    • a. normal= V/Q defect
    • b. decreased= diffusion problem
  42. VRG
    • both inspratory and expiratory nuerons and is thought to be the rythm generator
    • -ramp signal
  43. pneumotaxic center
    • controls TV and breathing rate
    • -controls "switch off" point of the inspiratory ramp
  44. - Hering-Breur reflex
    -high lung volume (sensed via vagus nerve,via slowly adapting pulmonary stretch receptors in the smooth muscle of the airway) inhibits further inspiration, thus terminatin inspiration and begins expiration
  45. rapidly adapting pulmonary stretch receptors
    • location- airway epithelium
    • nerve- myelinated vagal
    • activation- lung distention and irritants
    • function- cough reflex, gasp and bronchoconstriction by high activity
  46. C- fibers or type J- receptors
    • - location- near capillaries
    • - nerve- non myelinated vagal
    • - activated by increase interstitial fluid and pulmonary embolism
    • -function-cause rapid shallow breathing, bronchoconstriction and CV depression(tachypnea and hyperventilation
  47. slowly adapting stretch receptors
    • - location- SM of airway
    • -nerve- myelinated vagal
    • -activation- lung distention, breath holding and deflation below FRC
    • -function- terminate inspiration and terminate large expiration
  48. central chemoreceptors
    • - stimulated by H+ (PCO2 responder)
    • - inhibited by cold and anesthetics
    • - defects can result in sleep apnea, SIDS, panic attacks, epilepsy and migraines
  49. peripheral chemoreceptors
    • - PO2 responder mainly
    • - located in the carotid body of ExCa
    • - mainly O2 sensitive via type 1 glomulus cells(threshold PO2~80mmHg, significant at PO2 of 65 mmHg)
    • - mildly CO2 and H+ sensitive
  50. chronic hypercapnea
    • - at first increase in CO2 causes increased ventilation via central CR, inc CO2 in CSF-> inc H+ in CSF
    • - increased CO2 and H+ increases respiration via peripheral CR as well
    • -kidney will compensate for inc H+, which decreases peripheral and central CR stim= dec respiration
    • -now only stim for inc resp is PO2, so if pt is given O2, this may cause cessation of breathing
  51. chronic hypoxia
    • - dec PO2 causes immedite hyperventilation (good low lower PCO2, thus raise PO2), but causes resp alkalosis
    • - resp alkalosis will inhibit P and C CR CO2/pH receptor response thus decreasing ventilation for the first few days
    • - once alkalosis is compensated for, ventilation increases
  52. cheynes-stokes breathing
    • -cycles of gradual increase in tidal volumes followed by a gradual decrease
    • -
  53. kussmaul breathing
    • -increased tidal volume seen in DKA anddiabetic coma
    • - aka air hunger
  54. range of BP for autoregulatory organs to keep blood flow normal
    60-180 mmHg
  55. at what heart rate will SV begin to decline
    180-200 bpm

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