Hypoxia Flashcards
What are the different types of hypoxia?
Hypoxaemic = low paO2 due to poor oxygenation in lungs
e.g. low pO2 in atmosphere
Anaemic = decreased HbO2
e.g. reduced haemoglobin, CO poisoning
Ischaemic = oxygenated blood not reaching tissues
e.g. peripheral arterial disease
Histiocytic = inability to utilise O2
e.g. cyanide poisoning
Outline the pathway of oxygen from the air to the blood. Give examples of diseases which effect the different stages.
Air —> airways
(disease = ventilatory/pump failure)
Airways —> alveolar gas
Alveolar gas —> alveolar membrane
(disease = ventilation:perfusion mismatch)
Alveolar membrane (disease = poor diffusion across membrane)
Alveolar membrane —> arterial blood
(disease = ventilation:perfusion mismatch)
Arterial blood (disease = anaemia)
Arterial blood —> regional arteries
(disease = shock)
Regional arteries (disease = peripheral arterial disease)
Regional arteries —> capillary blood
Describe the aetiology, pathophysiology, and signs and symptoms of peripheral arterial disease.
Arterial narrowing or occlusion due to atheroma/embolism
Organs affected:
- regional artery (peripheral vascular disease)
- coronary artery (ischaemic heart disease)
- cerebellar artery (ischaemic stroke)
S&S:
- claudication (peripheral vascular disease) = pain on exercise, relieved by rest, weak/absent peripheral pulses, pale/blue discolouration, cold extremities, reduced capillary refill - assess by Doppler flow, treat with bypass
- angina (ischaemic heart disease)
- neurological deficit (ischaemic stroke)
- cyanosis = purplish discolouration of skin & mucous membranes due to the presence of desaturated Hb (present when ~1/3 of total Hb is desaturated)
Contrast central and peripheral cyanosis.
CENTRAL CYANOSIS:
- seen in tongue & oral mucosa (usually well perfused and warm)
- indicates severe arterial hypoxia
- peripheral cyanosis will usually be present as well (blood is already hypoxic when leaving the left ventricle)
note: if only one leg is affected, the cause is NOT central cyanosis (other leg is well perfused)
PERIPHERAL CYANOSIS:
- seen in extremities
- due to increased O2 extraction (more time for tissues to extract O2) caused by reduced capillary circulation
- can occur without central cyanosis (e.g. peripheral vascular disease, cold weather)
note: if all fingers are cyanosed, the cause is likely to be general (e.g. heart failure)
What is shock in general? What are the different types?
Arterial pressure is too low to perfuse all tissues
- hypovolaemic = reduced blood volume
e. g. blood loss - cardiogenic = reduced cardiac output due to pump failure
e. g. heart failure - mechanical = reduced filling of the heart due to outside obstruction
e. g. cardiac tamponade - septic = reduced peripheral resistance due to release of bacterial endotoxins
- anaphylactic = reduced peripheral resistance due to widespread release of histamine in response to environmental stimulus
Outline the pathophysiology of hypovolaemic shock.
Reduced volume —> reduced venous return —> reduced preload —> reduced cardiac output —> reduced arterial pressure
Baroreceptor-mediated sympathetic reflexes cause pale, cold, clammy skin & tachycardia
Vasoconstriction in veins in legs (attempt to increase venous return) & autotransfusion (more ECF enters due to reduced hydrostatic pressure —> attempts to increase BP & therefore increase cardiac output)
Blood loss —> RBCs & plasma lost
Fluid loss via GI tract —> ECF loss only
Outline the pathophysiology of cardiogenic shock.
Damage to myocardium —> heart pumps too little —> reduced arterial pressure
Baroreceptor-mediated sympathetic reflexes cause pale, cold, clammy skin & tachycardia
RAAS activation —> Na+ & water retention —> oliguria
Reduced brain perfusion causes confusion
Outline the pathophysiology of septic shock.
Endotoxins released by bacteria —> overwhelming vasodilatation (warm, red peripheries) —> reduced total peripheral resistance —> reduced arterial pressure
Outline the pathophysiology of anaphylactic shock.
Release of histamine from mast cells —> overwhelming vasodilatation —> reduced total peripheral resistance —> reduced arterial pressure
Mediators also cause bronchoconstriction & laryngeal oedema
Treated with adrenaline
What are the consequences of poor perfusion during shock?
Poorly perfused tissues —> anaerobic metabolism —> production of lactic acid —> metabolic acidosis —> tissue death —> release of vasodilator mediators —> circulatory collapse —> multiple organ failure
What is the pathophysiology of anaemia? Give some examples of causes. What are some consequences of anaemia?
Not enough haemoglobin in blood
OR RBC production rate does not match rate of RBC loss
OR carbon monoxide poisoning (binds to Hb instead of O2, so blood looks “cherry red” - therefore do not look cyanosed)
Causes:
- iron deficiency (dietary or chronic blood loss e.g. GI/colon cancer, fibroids causing menorrhagia)
- vitamin B12/folate deficiency (intrinsic factor produced by stomach & absorbed in terminal ileum)
- bone marrow disease e.g. leukaemia, aplastic anaemia
- excessive RBC breakdown e.g. sickle cell anaemia, G6PD deficiency causing haemolysis
Consequences:
- fatigue
- poor exercise tolerance
Give some examples of general causes of poor oxygenation of the blood.
Ventilatory failure (unable to move sufficient amounts of air in & out of the lungs)
- poor diffusion across alveolar membrane
- ventilation:perfusion mismatch
- combination of the above
What is the classification of respiratory failure? What are the different types?
paO2
How can the blood oxygenation be measured?
Oxygen saturation: pulse oximeter
- SaO2 should be > 95%
Arterial blood gas: arterial stab (radial artery)
note: check that ulnar artery is functional before carrying out arterial stab using Allen’s test
What should be done before carrying out an arterial blood gas?
Allen’s test (check radial artery is functioning)
Elevate hand and make fist for 30s —> apply pressure over ulnar & radial arteries to occlude both of them —> open hand whilst still elevated (should be blanched - pallor at fingernails) —> release ulnar pressure —> colour should return in 5s-15s
Negative test means you cannot safely cannulate or perform a radial arterial stab
Give some examples of causes of ventilatory failure.
Type 2 respiratory failure: low pO2 & high pCO2 (usually easy enough for enough CO2 to leave with normal bronchodilation therefore usually needs artificial ventilation)
Causes:
- poor respiratory effort due to respiratory centre depression e.g. narcotics, trauma
- poor respiratory effort due to muscle weakness (particularly of diaphragm) e.g. UMN or LMN damage
- chest wall problems due to scoliosis/kyphosis, trauma (flail chest), or pneumothorax
- stiff lungs e.g. end-stage fibrosis
- hard to ventilate lungs due to high airway resistance e.g. late stage COPD, severe asthma (exhaustion —> Type 2 resp. failure due to CO2 retention)
What is flail chest?
Ribs broken in 2 places —> segment of chest wall moves independently
Chest wall moves paradoxically (moves in on inspiration)
Give some examples of poor diffusion across alveolar membrane.
Type 1 respiratory failure as only diffusion of O2 affected (CO2 is more soluble)
Causes:
- (idiopathic/iatrogenic/dust inhalation) fibrous lung disease = thickened alveolar membranes slows gas exchange, affecting most alveoli, but normal chest wall expansion
- pulmonary oedema = presence of fluid in interstitial space increases the diffusion distance (normally oncotic pressure > hydrostatic pressure in a low pressure system)
- emphysema = destruction of alveoli reduces surface area for gas exchange
Give some examples of causes of ventilation:perfusion mismatch.
Ventilation:perfusion mismatch = some alveoli are poorly ventilated OR poorly perfused
Oxygen uptake cannot be compensated for in unaffected areas of lung, but carbon dioxide can still be removed (Type 1 resp. failure)
Causes:
- pulmonary embolism = some alveoli are poorly perfused, so blood is redirected to other parts of the lung, but ventilation of the affected alveoli is wasted (excess perfusion in rest of lung not matched by available ventilation)
- some alveoli poorly ventilated (e.g. pneumonia, acute asthma, respiratory distress syndrome) = poor oxygen uptake cannot be compensated for in rest of the lung, but carbon dioxide can still be removed
How does the body try to compensate for chronic hypoxia? What are some of the causes of chronic hypoxia?
Causes of chronic hypoxia:
- live at high altitude
- intermediate stage of lung disease (before muscle exhaustion & stiff lungs)
Compensations:
- increased erythropoietin synthesis —> increased haemoglobin synthesis (polycythaemia - purplish discolouration)
- increased 2,3-BPG synthesis
- pulmonary hypertension (increased flow to overcome resistance) —-> right heart failure (cor pulmonale)
How does the respiratory drive change in COPD?
Chronic type 2 resp. failure —> chronic CO2 retention —> CSF acidity corrected by choroid plexus —> central chemoreceptors reset to higher [CO2] —> persisting hypoxia —> respiratory drive governed by pO2
Therefore be careful about giving O2 (increased pCO2 on ABG indicates this —> put on ventilation)
Define hypoxia. In general, what is the difference in oxygen demand between tissues?
Oxygen deficiency at a tissue level
Brain & heart require oxygen immediately
Skin & gut require an AVERAGE amount of oxygen over minutes/hours
What are the six P’s of claudication?
Pulseless Pain Pallor Paraesthesia Paralysis Perishingly cold
Reminder: what is the mechanism of atherosclerosis.
- LDL oxidation
- Foam cell formation
- Plaque rupture
- Increased LDL deposition/thrombus formation
- Occlusion or emboli —> occlusion
Which artery is most likely to be affected in intermittent claudication in the calf? Describe its course.
Posterior tibial artery
Branch of popliteal artery —> posterior to medial malleolus —> sole of the foot
Describe where the peripheral pulses are palpated.
Femoral artery: inferior to the inguinal ligament midway between ASIS and pubic symphysis
Popliteal artery: medial to the midline in the popliteal fossa
Posterior tibial artery: posterior to medial malleolus
Dorsalis pedis: between extensor hallucis longus and extensor digitorum longus tendon to the 2nd toe
What mechanisms prevent severe postpartum haemorrhage?
Uterine contraction (+ve feedback; supported by oxytocin drugs)
Intercalating muscle fibres constrict arteries in myometrium (living ligature)
Clotting factors
Why does heart failure cause breathlessness?
Pulmonary hypertension —> pulmonary oedema —> reduced oxygen diffusion in interstitial fluid surrounding alveoli —> hypoxia —> increased respiration rate
