Respiratory Pathophysiology Flashcards
Definition of respiratory failure
When lungs fail to oxygenate the arterial blood adequately and or fails to prevent undue CO2 retention.
Hypoxic failure PaO2 < 60 mmHg
Hypercapnic failure PaCO2 > 50mmHg
O2 cascade, things that effect each stage PiO2 PAO2 PaO2 PtO2
PiO2: Altitude and FiO2
PACO2: Alveolar ventilation(can be altered in disease, increased dead space, decreased VA
PaCO2: Diffusion, V/Q mismatch, R-L shunt
PtissueO2: Blood flow, O2 content and extraction
Oxygen content, saturation and partial pressure
PP: The pressure exerted by dissolved oxygen in blood
Oxygen content: Total amount of O2 in blood, bound and unbound
Oxygen saturation: amount of O2 bound to Hb
What is hypercapnia?
relationship between PaCO2 and VA
Alveolar hypoventilation! (less O2 in, less CO2 out) or a V/Q mismatch. Could be combined with a metabolic acidosis
PaCO2 is inversely proportional to VA, so a decrease in VA will increase PaCO2.
Minute ventilation point (VE)
VE= VA + VD, so in disease, an increased dead space and lowered VA and thus making one hypercapnic will have an un changed MV
Three reasons why someone may be hypoventilating and thus hypercapnic
Decreased respiratory drive: from brainstem, interacts with phrenic nerve (diaphragm) and ant horn cells. Some drugs might interact here? (opioids, morphine etc)
Neuromuscular transmission/(in) competence: Disruption (GB syndrome), nerve damage, myasthenia gravis, muscular weakness or fatigue: dystrophy
Abnormal load: increased resistance, increased lung elastic load, MV load, obesity
Equation to calculate PAO2 as you can not measure
Thus A-a gradient
PACO2= (Patm-PH2O)x FiO2 - PACO2(PaCO2 as equal due to CO2 nature)/RQ (0.8 rough)
20- PaCO2/(0.8)
A-a gradient= 20-PaCO2/0.8 - PaO2
normal is 1-2kPa
Causes of hypoxaemia
Reduced PiO2; Hypoventilation; Diffusion; V/Q mismatch; R-L shunt
last three to do with gas exchange
Interstitial lung disease (pulmonary fibrosis) and how it effects diffusion
Extra fibrous tissues causes an alveolar capillary block, leading to hypoxia
Graph of time (x) and Po2 (y)
time in capillary versus Po2. Total time about .75s
Perfect PAO2 at 100mmHg
Red blood cell has certain P(mixed venous)O2 enters
ordinarily comes into equilibirum with PAO2 or close to it (about .25 seconds) plateaus.
with a thickened membrane, liner, and does not equilibrate. Reaches about 80mmHg. gets worse as disease progresses.
During exercise, time is shortened and an even smaller PO2
Lab test for diffusion
DLCO, using Co due to its avid binding to Hb, soluble, diffusion and not perfusion limited.
Will depend on gas; diffusion distance/thickness; SA; Hb; capillary volume
Abnormal diffusion conditions
Alveolar block- diffuse lung disease
SA loss/loss of diffusing surface- emphysema
capillary volume/Hb: pulmonary hypertension, anaemia
COPD defintion
Airflow limitation that is not fully reversible
limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles/gases
Effect of Smoking and FEV1
Ordinarily FEV1 decreases after 25
Steeper decline if a smoker. if you quit will level out a little bit
3 types of COPD
Chronic mucus secretion= chronic bronchitis: goblet cell hyperplasia and gland hypertrophy
Emphysema: imbalance of proteases and anti-proteases, made by neutrophils. Destroys elastin
Small airway inflammation: air flow obstruction
What is the most important cause, and how COPD causes hypoxaemia?
V/Q mismatch
3 compartment model
Dead space: V/Q=infinite, ventilated but not perfused
Perfect lung: V/Q 1, ventilated and perfused
Venous admixture, V/Q=0. perfused but not ventilated
- Content of oxygen and carbon dioxide in all the compartments
- What is the result of adding perfect lung and non ventilated lung (a V/Q mismatch!)
- How do we compensate with this added mixture and how does it affect content?
- 1) nil for both
2) C(oxygen): Normal, C(CO2): N
3) C(oxygen): very low; C(CO2): very high - Mixed: C(oxyen): low; C(CO2): high
- Compensation is the increase in alveolar ventilation due to being hypercapnic (response to hypercapnia before hypoxaemia, needs to be quite lowfor hypoxia); C(oxygen): low (does not correct as only 2nd compartment ventilated, not much change on content curve), C(CO2) Normal due to hyperventilation
What happens in the case where smoking disease worsens (sequelae very important)
Disease worsens due to smoking, increased V/Q mismatch (more 3rd compartment)-> unable to compensate with hyperventilation (too much load)-> PaCO2 high (pH normalises due to metabolic compensation)-> loss of CO2 drive, and respiration dependent on hypoxic drive
Dangers: high inspired O2, monitoring O2 sat only
(will abolish her hypoxic drive as hypercapnic drive switched off due to sustained hypercapnia (reflected by high bicarbonate), no ventilation)
What is a shunt?
Anatomical shunt is abnormal vessel that bypasses alveoli entirely. Can be an arterio-venous malformation in the lung or a cardiac abnormality, complex but moves from Right to left heart due to septal defect?
How to determine V/Q mismatch from R-L shunt (graph)
NB with shunt, even with a shunt, and PaO2 not increasing to 600mmHg, saturation will still be maximal at 200mHg, so don’t rely on oximeter
Administer 100% O2
Normally PaO2 rises to >600mmHg
-With V/Q mismatch, with 100% O2, there is enough alveolar ventilation to get PaO2 up to point of 600mmHg
-With shunt, blood does not ‘see’ added O2, so will increase just not to the same extent. e.g 20% stunt 250mmHg.