2.2 Oxygen & CO2 Flashcards
What causes a left shift in ODC in terms of Hb
what about a right shift
does low hb directly affect
Fetal haemoglobin,
methaemoglobin and
carboxyhaemoglobin all shift the curve to the left.
Haemoglobin S shifts the curve to the right. Androgen prenancy acclimitasion thyroxine
Anaemia affects the quantity not the characteristics of the haemoglobin. But severe anaemia may reduce oxygen delivery to tissues resulting in metabolic acidosis. This may cause a shift of the ODC to the right
Oxidation of pyruvate
can it be under anerobic conditaion
where does it occur
what regulates the reaction
what is cofactor for entry to the krebs cycle
Altough pyruvate can be broken down by aerobic and anaerobic respiration, oxidation requires oxygen and hence cannot occur under anaerobic conditions.
This takes place in the mitochondrion in eukaryotic cells, but at the cell membrane in prokaryotic cells.
Acetyl CoA, a product of the pyruvate dehydrogenase reaction, is a central compound in metabolism.
Thiamine is involved as a cofactor in numerous enzymes and is essential in every cell for ATP production via the Krebs’ cycle.
Oxygen content arterial blood - formula
Multiply by what gives what
Increased meatbolic demand do what which does what to arterial blood
The oxygen content of arterial blood is the sum of the oxygen bound to haemoglobin and the oxygen dissolved in the plasma:
(10 × haemoglobin × SaO2 × 1.34) + (PaO2 × 0.0225).
When multiplied by the cardiac output it gives the amount of oxygen delivered to the tissues in unit time (oxygen flux).
Factors which are associated with an increased metabolic demand encourage the offloading of oxygen from the haemoglobin in the tissues (oxygen dissociation curve shifted to the right) which subsequently reduces the oxygen content of arterial blood.
Thus a pyrexia and a metabolic or respiratory acidosis lowers the oxygen content (oxygen dissociation curve, ODC, shifted to the right), whereas a low level of 2,3 diphosphoglycerate (2,3-DPG) is usually related to an increased oxygen content due to less offloading (ODC shifted to the left).
Therefore in simple terms, for a given PaO2, a high blood oxygen content is related to factors which shift the ODC to the left (not right).
A low haematocrit usually denotes a decreased haemoglobin concentration, which is associated with decreased oxygen binding to haemoglobin.
Afinnity of CO for hb
Affect on ODC shift
- does what
What enzyme does it inhbiit
which does what
How does carboxy affect sats reading
what does this cause as a problem for the body
Whats most senstive to CO in brain
What level is fatal
CO had an affinity for haemoglobin which was 200 - 250 times that of oxygen.
Carboxyhaemoglobin (COHb) causes a leftward shift in the oxygen dissociation curve, inhibiting the peripheral release of oxygen. Carbon monoxide also inhibits the cytochrome oxidase system (cytochromae A3), which impairs metabolism at the mitochondrial level leading to histotoxic hypoxia.
The oxygen saturation measured by pulse oximetry tends to read close to 100% (not low), because the COHb is falsely interpreted as oxygenated haemoglobin. The arterial PO2 is unaffected and consequently the aortic and carotid bodies do not detect hypoxia.
The portions of the brain which are most sensitive to CO injury include the basal ganglia, hippocampus and cerebral cortex. Neurological and psychiatric symptoms may follow recovery from carbon monoxide poisoning.
COHb levels below 20% do not usually result in neurological impairment. However, neurological and cardiac ischaemia occurs with carboxyhaemoglobin (COHb) levels of 50%, which in most patients is fatal.
CO2 & plasma
RBC
CL movement
Rise CO2 does what to oxyhb curve
what effect is this
CO2 diffuses into plasma and the red blood cells; HCO3- is formed faster in the red blood cells because of carbonic anhydrase, and therefore HCO3- moves out of the cells into the plasma. To maintain electrical neutrality, Cl- ions move into the red blood cells (Hamburger shift).
The rise in CO2 shifts the curve to the right (Bohr effect), that is, with an increased PCO2, haemoglobin has a diminished ability to bind O2, and therefore gives it up to the tissue more readily.
Increasing temperature and a decrease in pH will also cause a rightward shift in the curve. Even though the volume must be the same as that in the aorta, the flow must be lower because the total cross sectional area is gre
ODC in carboxyhb - affect on P50
what else does it do
The ODC is shifted to the left (not right), which reduces the P50 (not increases) and results in tissue hypoxia.
An additional feature of carbon monoxide poisoning is that it binds to and inhibits other haemoproteins (myoglobin, cytochrome c and reduced cytochrome P450).
The pulse oximeter is not able to differentiate between oxyhaemoglobin and carboxyhaemoglobin.
Cortical blindness is a known and permanent complication with concentrations of carboxyhaemoglobin above 40%.
Oxygen cascade
What is it
Greatest drop is where
what are the valus here
How much does it drop betwen air and alveous
what is humidify po2 in trachea
capiliary
What is normal alveolar pco2
The oxygen cascade is a series of steps where the PO2 falls from atmospheric air to the intracellular mitochondria.
A fall in the PO2 at any stage will cause a decrease in the PO2 value at all subsequent steps, which may result in insufficient oxygen for aerobic metabolism.
The greatest drop in PO2 is indeed between the artery (13.3 kPa or 100 mmHg) and the mitochondria (1-5 kPa or 7.5-40 mmHg).
The PO2 does drop by about one third between the air (21 kPa or 160 mmHg) and alveolus (14 kPa or 106 mmHg).
Humidified tracheal gas has a PO2 of 19.8 kPa (150 mmHg) and capillaries has a PO2 of 6-7 kPa (45-55 mmHg).
The alveolar PCO2 is normally between 4.7-6.0 kPa (35-45 mmHg)
Cao2
Is what
normally how many ml dl
what is the calculation
What law is involved
Arterial oxygen content (CaO2) is the amount of oxygen carried by 100 ml of blood and is normally 17-24 ml/dL.
It can be determined by the following equation:
CaO2 = oxygen bound to haemoglobin + oxygen dissolved in plasma
CaO2 = (1.34 × Hgb × SaO2 × 0.01) + (0.003 × PaO2)
where:
1.34 = Huffner’s constant
Hgb is the haemoglobin level in g/dL
SaO2 is the percent oxyhaemoglobin saturation of arterial blood
PaO2 is (0.0225 = ml of O2 dissolved per 100 ml plasma per kPa, or 0.003 ml per mmHg).
Whilst important, quantitatively, the amount of oxygen dissolved in plasma is 0.3 mL/dL.
Henry’s law states that at constant temperature, the amount of gas dissolved at equilibrium in a given quantity of a liquid is proportional to the pressure of the gas in contact with the liquid.
Given a haemoglobin concentration of 15 g/dL and a SaO2 of 100% and a PaO2 of 13.3 kPa, the amount of oxygen bound to haemoglobin is 20.4 mL/100mL.
Cardiac output is an important determinant of oxygen delivery but does not influence the oxygen content of blood.
Huffner’s constant does not change and its magnitude relatively small.
ODC - plot of what and what
What type of shape
What is Po2 at 75%
97%
What causes right shift
whats the bohr affect
what shifts to left
The oxygen dissociation curve (ODC) is a plot of oxygen saturation of haemoglobin against PO2 at 37°C. It is sigmoid shaped (not hyperbolic) because of the increasing affinity of haemoglobin for successive oxygen molecules after the first.
Venous blood is 75% saturated and this normally corresponds to a PO2 of 5.3 kPa (40 mmHg), whereas arterial blood is 97% saturated and has a PO2 of 13.3 kPa (100 mmHg).
The ODC is shifted to the right by acidosis, hyperthermia, hypercapnia (Bohr effect) and increased 2,3-DPG levels, which favour the unloading of oxygen to the tissues.
The curve is shifted to the left in opposite situations to those that cause a rightward shift and with fetal haemoglobin, methaemoglobinaemia and carbon monoxide poisoning.
A left shift reduces oxygen release to the tissues.
Carotid body chemoreceptors
situated where relation to bifurc
Contain what type of cells
where do they pass info to
via what
how high is the blood supply
rate discharge increased x 3 things
Carotid bodies are chemoreceptors, which are situated above the carotid bifurcation on each side (not below).
They contain both glomus (type 1) and glial (type 2) cells, and afferent fibres pass to the brainstem via the glossopharyngeal nerve.
Each carotid body receives the highest blood flow of any tissue in the body. Thus they do not have a dedicated arterial blood supply, but rely on the oxygen dissolved in the blood to provide their oxygen requirements.
The rate of discharge is increased by:
A reduction in the arterial partial pressure of oxygen (pO2)
Increase in the arterial partial pressure of carbon dioxide (pCO2) and
Fall in arterial pH (increasing H+ concentration).
Nitric oxice produced from what by what
what does it cause
how is it inacitvated
what is the secondary messenger
Nitric oxide is produced from l-arginine by nitric oxide synthase and is produced by the vascular endothelium in response to haemodynamic stress. It produces smooth muscle relaxation and reduced vascular resistance.
Nitric oxide is a free radical and may be inactivated through interaction with other oxygen free radicals, e.g. oxidised LDL.
It causes the production of cGMP as a second messenger.
Oxygen consumption
ml min 100g
oxygen extraction ratios at rest
Organ Oxygen consumption (ml/minute/100g) Hepatoportal 2.2 Kidney 6.8 Brain 3.7 Skin 0.38 Skeletal muscle 0.18 Heart 11 Oxygen extraction ratios (at rest):
Heart - 60-70%
Brain - 33%
Kidney - 7.5%
Liver - 17%
Lactic acidosis
characterised by what
how does it happen
what removes lactate
two types
related to what
how rx
whhat about resitant cases
Lactic acidosis is characterised by an elevated arterial blood lactate level and an increased anion gap ([Na + K] - [Cl + HCO3]) of > 20 mmol. It can be a consequence of overproduction and/or reduced metabolism of lactic acid.
The liver removes 70% of lactate. Mitochondria-rich tissues such as skeletal and cardiac myocytes and proximal tubule cells remove the rest of the lactate by converting it to pyruvate.
There are two recognised types of lactic acidosis:
Type A is due to Tissue hypoxia Inadequate tissue perfusion and Anaerobic glycolysis which may be seen in cardiac arrest, shock, hypoxaemia and anaemia.
Management involves reversing the underlying cause of tissue hypoxia.
2. Type B occurs in the absence of tissue hypoxia.
The causes include:
Hepatic failure Renal failure Diabetes mellitus Pancreatitis Infection and Drugs (aspirin, ethanol, methanol, biguanides and intravenous fructose).
Optimising tissue oxygen delivery, correcting the cause and infusions of intravenous sodium bicarbonate (not methanol) form the mainstay of treatment.
Peritoneal dialysis has been used in resistant cases.
2,3 DPG
created where
during what
by what
Why is it prodecuded
2,3-diphosphoglycerate, or 2,3-DPG, is created in erythrocytes during glycolysis by the Rapoport-Luebering shunt.
The production of 2,3-DPG is likely an important adaptive mechanism, because the production increases for several conditions in the presence of diminished peripheral tissue O2 availability, such as:
hypoxaemia
chronic lung disease
anaemia, and
congestive heart failure.
High levels of 2,3-DPG shift the curve to the right, while low levels of 2,3-DPG cause a leftward shift, seen in states such as septic shock and hypophosphataemia.
What happens CO2 in RBC
Cl shift - is what
Whats the haldane effect
BOhr effect
How much co2 carried 100ml blood
what constitutients
what is the anrep effect
In the red blood cell carbon dioxide is converted by carbonic anhydrase to carbonic acid, which in turn dissociates to hydrogen and bicarbonate ions.
The chloride shift (or Hamburger shift) is the movement of chloride ions into red blood cells (not plasma) as bicarbonate ions enter the plasma, which maintain electrical neutrality. The hydrogen ions are buffered mainly by haemoglobin.
The Haldane effect refers to haemoglobin’s increased buffering ability as it becomes deoxygenated.
The Bohr effect is the rightward shift of the oxyhaemoglobin dissociation curve associated with a rise in arterial PCO2.
In arterial blood approximately 50 ml of carbon dioxide is carried per 100 ml of blood: 45 ml as bicarbonate, 2.5 ml as carbonic acid and 2.5 ml as carbamino compounds. Venous blood carries 54 ml of carbon dioxide and 47.5 ml of this is as bicarbonate.
The Anrep effect describes the intrinsic regulatory mechanism of the heart in response to an increased afterload.
