week 1 - Friday lectures, O2, CO2, etc Flashcards
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.
- 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
causes of toxic hypoxia
- Cyanide poisoining
- CO excess
- 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
Causes of Alveolar Hypoventilation
- Central Respiratory depression from
- opioid drug use
- anaphylaxis (severe allaergic reaction) -> histamine release, causing airway swelling and bronchospasm - 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 - Airway + Lunug collapse
lung collapse = atelectasis –> mucus plugs, inadequate ventilation, poor patient positioning
airway obstruction - upper(food, tumor, swelling) and lower (copd, asthma)
Causes of Type 2 RR
inadequate ventilation (hypoventilation), leading to:
✅ Low O₂ (Hypoxemia) PaO₂ < 60 mmHg
✅ High CO₂ (Hypercapnia) PaCO₂ > 50 mmHg
- 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).
Drug-induced bronchospasm
- 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.
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.
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
WHAT CAN CONTRIBUTE TO DECOMPENSATED RESPIRATOR ACIDOSIS in e.g. COPD patients when given high amounts of O2?
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.
- Target oxygen saturation is 88–92% to avoid CO₂ retention and acidosis.