Week 1: Physiology part 4 & 5 Flashcards

1
Q

Total O2 content

A
  1. bound to Hemoglobin
    - measured by pulse ox and ABG
  2. disolved PaO2
    - measured by ABG
  3. O2 dissociation curve -can’t be measured
    - Left shift (higher affinity): CO, MetHb, opposite of listed below
    - Right Shift (into tissue, less affinity): high temp, acid (low pH), high 2,3-DPG, Bohr effect (increased CO2 bound to Hgb)
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2
Q

Hemoglobin concentration effects on oxygen dissociation curve

A
  1. Anemia: shift down
    - decreased Hb conc., normal O2 per Hb, decreased O2 content
  2. polycythemia: shift curve higher
    - increased Hb conc., normal O2 per Hb, increased O2 content
  3. CO: has greater affinity for Hgb than oxygen. Shifts curve to the left and reduces carrying capacity, shift down
    - normal Hb conc., decreased O2 per Hb, decreased O2 content
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3
Q

Forms of carbon dioxide

A
  1. Dissolved CO2: PaCO2
    - 5% in this formed, measured by ABG
  2. carbamino compounds
    - Hb mostly
    - 10%
  3. Bicarbonate
    - 85% of Co2
    - measured by venous blood draw
    - carbonic anhydrase must be present to convert CO2 into bicarbonate or reverse
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4
Q

Transport of Co2

A
  • plasma contains no Carbonic anhydrase, Co2 moves into RBC to be converted to HCO3-
  • chloride shift: Cl- moves into RBC and HCO3- moves out of RBC to maintain electrical neutrality
  • HCO3- formed in RBC but carried in plasma
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5
Q

Regulation of Alveolar Ventilation

A
  1. Central Chemoreceptors
    - located in the CNS close to the surface of the medulla
    - directly monitor and stimulated by CSF [H+] and PaCO2
  2. Peripheral chemoreceptors: detect PaO2 and PaCO2. Strongly stimulated by dramatic decrease in PaO2 and less sensitive than central PaCO2 but still contributes to normal drive for ventilation
    a. carotid bodies
    b. aortic arch
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6
Q

What happens if you give supplemental oxygen in patients with COPD?

A
  • normal reaction to hypercapnia? in COPD is vasoconstriction of bad alveoli and vasodilation of good alveoli
  • If given supplemental O2:
    1. Worsened V/Q matching due to loss of hypoxic pulmonary vasoconstriction
  • increased dead space secondary to loss of vasodilation to good alveoli
    2. decreased binding affinity of Hg for CO2 (Haldane effect)
    3. Decreased minute ventilation
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7
Q

Central respiratory centers

A
  • Apneustic Center: located in caudal pons. Intrinsic constant stimulus to promote inspiration. inhibited by pulmonary stretch
  • Pneumotaxic Center: aka pontine respiratory group. Network of neurons that is located in rostral dorsal lateral pons. Cyclically inhibits inspiration by antagonizing apneusitic center. Regulates amount of air a person can take with each breath
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8
Q

Hering-Breuer Reflex

A
  • “inflation reflex”
  • triggered to prevent over-inflation of the lungs
  • pulmonary stretch receptors present in smooth muscle of the airways to excessive stretching of the lung during large inspirations by inhibiting the apneustic center
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9
Q

Acute and long term adaptations to high altitude

A
  1. Acute Changes
    - decreased PAO2, PaO2, PACO2 and PaCO2
    - increased systemic arterial pH
    - no change in Hb conchs
    - Hb sat decreased
    - systemic arterial O2 content decreased
  2. Acclimatization
    - decreased PAO2, PaO2, PACO2 and PaCO2
    - normal systemic arterial pH, decreased from elevated by renal compensation
    - Hb conc. increases
    - Hb sat remains decreased
    - systemic arterial O2 content increases to normal
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10
Q

Responses of chemoreceptors and CNS to high altitude

A
  • have low Patm, reduces PAO2 and PaO2. Low PaO2 will stimulate peripheral chemoreceptors.
  • Main drive for ventilation changes from PaCO2 on central chemoreceptors to low PaO2 drive of peripheral chemoreceptors. Leads to hyperventilation.
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11
Q

Response to high pressure environment (diving)

A
  • N2 normally inhaled and exhaled because no soluble at sea level
  • under high pressure (diving), can diffuse into the bloodstream
  • if diver surfaces too quickly, the N2 becomes not soluble anymore and forms N2 bubbles which can embolize
  • Rx with hyperbaric chamber or to redive and surface slowly
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12
Q

Regional differences in blood flow in the lung

A

Due to Gravity

  • Toward the Apex: arterial flow decreases towards the apex. vessels are less distended since alveoli are more distended, compressing the vessels. Higher resistance system
  • Toward the base: arterial flow increases. Vessels are more distended. Lower resistance system
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13
Q

Regional differences in ventilation in the lung.

A
  • Apex: least ventilation and blood flow. Ventilation is still to high for the very low blood flow, so it is OVER ventilated
  • Base: most ventilation and high blood flow. Ventilation not high enough for blood flow, so UNDER ventilated region
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14
Q

What is ARDS?

A
  • Acute lung injury characterized by increased permeability of the alveolar-capillary membrane
  • leads to pulmonary edema, severe hypoxemia, decreased pulmonary compliance
  • direct causes: aspiration, pneumonia, inhalation injuries
  • indirect causes: sepsis, pancreatitis, trauma
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15
Q

ARDS ventilator strategies.

A
  • ventilator induced lung injury: caused by over distended alveoli
  • recommended: low tidal volumes improve survival. 6ml/kg is optimal
  • don’t worry abut PaCO2, so long as adequate tissue oxygenation is maintained
  • ARDS has shunt physiology: to improve oxygenation, need to pop open fluid filled alveoli and avoid barotrauma and oxygen toxicity
  • use PEEP: valve shuts when patient is near end expiration while there is still positive intrathoracic pressure
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16
Q

ARDS: best positioning

A
  • lateral decubitus is tried first with good lung down so that good alveoli would get more perfusion
  • with hemoptysis: bleeding lung down so the blood won’t go into the good lung
17
Q

Pulmonary effects of positive pressure ventilation

A
  • increased physiologic dead space: increases ventilation in some regions without a corresponding increase in perfusion
  • decreased physiologic shunting: increase in mean airway pressure to maintain airway latency in patients with respiratory failure who have increased shunting due to focal atelectasis
18
Q

Hemodynamic effects of PPV

A
  1. Decreased venous return: intrathoracic pressure increases during PPV, reduces gradient for venous return
  2. Reduced right ventricular output: alveolar inflation during PPV compresses the pulmonary vascular bed, increases pulmonary vascular resistance and reduces RV output
  3. Reduced LV output: increased pulmonary vascular resistance can shift the intraventricular septum to the left and impair diastolic filling