week 1 - Friday lectures, O2, CO2, etc Flashcards

1
Q

Causes of Anaemic hypoxia

decrease in oxygen-carrying capacity of the blood. This occurs despite normal oxygen levels in the lungs. If Hb levels are too low or dysfunctional, the blood cannot carry enough O₂, leading to anaemic hypoxia.

A
  • vitamin B12 deficiency -> megalobalstic anaemua - DNA syntehsis
  • folic acid (B9) deficiency -> megalobastic anaemia - DNA synthesis
  • Sickle cell anaemia -> genetic mutation -> sickle shape RBCs, reduced lifespan
  • Iron deficiency -> microcytic hypochormic (reduced Hb production)
  • chronic blood loss -> progressive iron loss
  • fish oil -> omega 3 fataty acids can increase bleeding tendency by inhibiting platet aggregation -> iron depletion

KOILONYCHIA = spoon nails = sign of chornic iron deficiciency = low Hb = aneamic hypoxia

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2
Q

causes of toxic hypoxia

A
  1. Cyanide poisoining
  2. CO excess
  3. Oxidation of ferrous iron (Fe2+), normal in Hg, to ferric iron (Fe3+), creating met-haemoglobin which has a high afffinity for cyanide, and cannot bind to O2, causing reduced delivery to tissues. –> Methemoglobinemia

explore the causes of each of these - go to lecture slides and notes ++++ treatment

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3
Q

Causes of Alveolar Hypoventilation

A
  1. Central Respiratory depression from
    - opioid drug use
    - anaphylaxis (severe allaergic reaction) -> histamine release, causing airway swelling and bronchospasm
  2. mechanical restriction of breathing - reducign ability of the lungs to expand, and diaphragm movement
    - obesity, compressing the chest
    - scoliosis, restricting rib cage movement (spinal curvature, chest wall deformity). can lead to type 2 RR
  3. Airway + Lunug collapse
    lung collapse = atelectasis –> mucus plugs, inadequate ventilation, poor patient positioning

airway obstruction - upper(food, tumor, swelling) and lower (copd, asthma)

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4
Q

Causes of Type 2 RR

inadequate ventilation (hypoventilation), leading to:
✅ Low O₂ (Hypoxemia) PaO₂ < 60 mmHg
✅ High CO₂ (Hypercapnia) PaCO₂ > 50 mmHg

A
  • Airway obstruction (e.g., COPD, asthma, severe pneumonia).
    • Neuromuscular diseases (e.g., Guillain-Barré syndrome, myasthenia gravis).
    • Chest wall deformities (e.g., scoliosis, obesity hypoventilation syndrome).
    • Opioid overdose (respiratory depression).
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5
Q

Drug-induced bronchospasm

A
  • β-blockers (e.g., propranolol, atenolol) → Block β₂-receptors, preventing bronchodilation and triggering bronchospasm in asthmatics.
    • Aspirin & NSAIDs (Aspirin-Exacerbated Respiratory Disease, AERD) → Inhibit COX-1, leading to increased leukotrienes, which cause bronchoconstriction.
    • Anesthetic agents (e.g., desflurane, isoflurane) → Can induce airway irritation and bronchospasm during surgery.
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6
Q

Pathways to Atelectasis (Lung collapse) = alveolar deflation or inadequate air filling

Air pressure inside the alveoli (positive pressure) keeps them expanded.

✅Surfactant (reduces surface tension) prevents alveoli from collapsing.

Negative pressure in the pleural cavity (created by lung recoil & chest wall expansion) helps keep the lungs inflated. ⇒ Lung recoil = lung’s intrinsic tendency to deflate following inflation

If one or more of these forces is disrupted, the alveoli collapse, leading to atelectasis.

A

Obstructive Atelectasis - Blocked airway
prevents air entry, trapped air is absorbed, alveoli collapse.

Mucus plug (post-surgery, asthma, COPD) ✅ Foreign body aspiration (common in children) ✅
Tumors (bronchogenic carcinoma) ✅ Enlarged lymph nodes (e.g., TB, lymphoma)

Compressive - External pressure squeezes lung tissue, preventing expansion.
Adheesive - Lack of surfactant
→ High alveolar surface tension → Alveoli collapse.

Pleural effusion (fluid in pleural space) ✅ Pneumothorax
(air in pleural space) ✅ Tumors compressing the lung ✅ Diaphragmatic elevation (e.g., ascites, pregnancy)

Relaxation - Loss of negative pleural pressure, lung recoils and
collapses.

Pneumothorax ✅ Pleural effusion

Cicatricial(Fibrotic) - Lung scarring (fibrosis) causes irreversible collapse.

Tuberculosis (TB) ✅ Pulmonary fibrosis ✅
Radiation therapy

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7
Q

WHAT CAN CONTRIBUTE TO DECOMPENSATED RESPIRATOR ACIDOSIS in e.g. COPD patients when given high amounts of O2?

A

1️⃣ The Haldane Effect → Hemoglobin releases more CO₂ into the blood, increasing hypercapnia.
2️⃣ V/Q Mismatch → Blood is redirected to poorly ventilated alveoli, trapping CO₂.
3️⃣ Reduced Respiratory Drive → Slight reduction in ventilation leads to CO₂ retention

  • COPD patients should NOT receive excessively high oxygen (>92% SpO₂).
    • Target oxygen saturation is 88–92% to avoid CO₂ retention and acidosis.
      The main contributors to CO₂ retention are the Haldane Effect and V/Q mismatch rather than reduced respiratory drive.
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8
Q
A
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