1.2 Respiratory Flashcards
NO is what
where and what is synthesisd by
half life
effects mediated via
what are those effects
production in pregnancy?
NO is a free radical which is synthesised by nitric oxide synthase in many tissues but particularly the endothelium.
Its half life is seconds and its effects are mediated through cyclic guanosine monophosphate (cGMP) production as the second messenger.
It produces vasodilatation through smooth muscle relaxation, this process being impaired in endothelial dysfunction.
NO production is increased in normal and even more so in abnormal pregnancies.
What are the varies RQ of substrates
The respiratory quotient (RQ) is the ratio of CO2 produced by the body to the volume of O2 consumed per unit time:
RQ = CO2 produced / O2 consumed.
Typically 200 mL/minute CO2 produced and 250 mL/minute O2 consumed.
A mixed diet will typically produce and RQ of about 0.8.
The RQ will vary with the energy substrates in the diet.
Granulated sugar is a pure refined carbohydrate and is 99.999% carbohydrate with no significant lipid, proteins, minerals or vitamin content.
Glucose and other hexose sugars:
RQ = 1
Fats:
RQ = 0.7. Lipids require more oxygen than carbohydrates for complete oxidation.
Proteins:
RQ is approximately 0.9.
Ethyl alcohol:
RQ = 0.67
An RQ can exceed 1.0 when carbohydrate is converted into fat. In these circumstances there is likely to be fat deposition and gain of weight.
A-a difference
what is it
what is it a measure of
What can cause an icnreased AA difference
Most likely causes of A-A difference in healthy adult breathing 100%
The alveolar-arterial (A-a) oxygen difference is the ‘ideal’ alveolar PO2 minus arterial PO2.
The ‘ideal’ alveolar PO2 is the PO2 which the lung would have if there were no ventilation-perfusion (V/Q) inequality and it was exchanging gas at the same respiratory exchange ratio as real lung, and is derived from the alveolar air equation.
Arterial PO2 is measured directly.
The A-a oxygen difference (or gradient) is a useful measure of shunt and V/Q mismatch, and in normal adults breathing air the A-a difference is less than 2 kPa (15 mmHg). When breathing 100% oxygen the A-a difference increases, because the shunt component is not corrected and it may be up to 15 kPa (115 mmHg).
An increased A-a difference may be caused both by abnormally low and abnormally high V/Q ratios within the lung, though chiefly the former. The most likely cause of an A-a difference in a healthy adult breathing 100% oxygen is atelectasis, which would give a low V/Q ratio.
Hypoventilation may result in a rise in alveolar (and hence arterial) CO2 which according to the alveolar air equation may lower the alveolar PO2.
High altitude will also lower the alveolar PO2.
A right to left shunt and an oxygen transport diffusion defect are unlikely to be found in healthy individuals.
What are deactivated travelling thru the lung
What are activated
What about injured lung
Bradykinin, 5-hydroxytryptamine and prostaglandin F2 alpha are deactivated on passage through the normal lung.
In the diseased lung this ability is reduced.
Angiotensin 1 is converted into the active angiotensin 2, whereas histamine is only inactivated on passage through an injured lung.
v/q plot
curve represent what
what is v/q in apex vs base
The V/Q ratio influences alveolar oxygen (PAO2) and carbon dioxide tension (PACO2) in any alveolar unit.
A Ventilation-Perfusion (V/Q) ratio graph plots the partial pressure of alveolar carbon dioxide (PACO2) against that of alveolar oxygen (PAO2). The curve itself represents all of the possible values for PACO2 and PAO2 that an individual alveolus may have given a set of model assumptions.
In theory a V/Q ratio of infinity (ventilation but no perfusion or dead space), the values the PACO2 of the alveolus will equal zero whereas the PAO2 will approach that of external air (150mmmHg). The V/Q ratio is 3.3 at the apex of the lung compared with 0.67 at the base.
In theory a V/Q ratio of zero (no ventilation but perfusion) the PACO2 and PAO2 approach the partial pressures for these gases in the venous blood. The V/Q ratio is 0.67 at the base of the lung compared with 3.3 at the apex.
Typical value for PAO2 at the apex is 132mmHg and the typical PACO2 28mmHg
Typical PAO2 at the base is 89 mmHg and the typical PACO2 42 mmHg
Inspiration - triggered where
expiration
all loacted where
what inhbits repirtaion
emotional states what imputs
where are periph chemo rec
what most important effector
Inspiration arises from activity within the dorsal respiratory group of neurones (not ventral) and expiration is thought to relate to activity in the ventral respiratory group of neurones. They are all located within the medulla.
In animals, stimulation of the pneumotaxic centre inhibits inspiration, which controls the volume and rate of respiration. In emotional states such as fear and rage the hypothalamus and limbic system alter the pattern of breathing.
The peripheral chemoreceptors are located in the carotid body (not the carotid sinus).
The diaphragm is the most important effector of respiration (not the intercostal muscles).
Principal preoxygenation
slow fast
o2 consumption
Hypoxia after depend on
The two principal pre-oxygenation techniques include the application of a tight fitting face mask connected to an appropriate anaesthetic circuit with an adequate fresh gas flow:
Slow technique - Normal tidal volume breathing for two to five minutes (TVB 2-5 min). Denitrogenation is 95% complete after three minutes.
Fast technique - The patient takes four to eight deep vital capacity breaths at FiO2 of 1.0 (100%) for 30 to 60 seconds (4-8 DB 30-60 s).
The oxygen consumption of an adult is approximately 250 mL per minute. The duration of apnoea before hypoxia develops following induction of anaesthesia will depend on a number of factors, these are:
Initial amount of oxygen stored
Tissue availability, and
Oxygen consumption.
Breathing 100% oxygen for three minutes will oxygenate the functional residual capacity (FRC) and provide the best reservoir of oxygen during apnoea. Sitting at 450 might increase the FRC and improve oxygen reserve but not compared with 100% oxygen. A study comparing 450 and supine pre-oxygenation positions in healthy individuals found no difference in “tissue” oxygenation in the two groups
Interstitial oncotic pressure acting across a normal pulmonary capillary
The interstitial oncotic pressure is relatively high in the pulmonary circulation due to the presence of lymph.
Explanation
The typical values of the Starling forces acting across normal pulmonary capillaries are as follows:
Interstitial oncotic pressure = 17 mmHg (estimated from measurements on pulmonary lymph)
Capillary hydrostatic pressure (Pc) is 13 mmHg (arteriolar end) to 6 mmHg (venous end) but variable because of the hydrostatic effects of gravity especially in the erect lung.
Interstitial hydrostatic pressure (Pi) - Variable but ranges from zero to slightly negative.
Capillary oncotic pressure = 25 mmHg.
Preoxygenation of the morbildy obese
why is hypoxia compunded in supine position
This patient is morbidly obese and is prone to the development of hypoxia. This will be compounded with the patient in the supine position secondary to:
Reduced functional residual capacity (FRC)
Increased closing capacity (CC)
Diminished tidal volume due to increased resistance of the airway, diminished compliance of the thoracic cage and diminished strength and endurance of respiratory muscles
A tendency towards atelectasis following induction of general anaesthesia and
Increased O2 consumption due to the increased workload of respiratory muscles and to the general increase in metabolism.
In normal circumstances, pre-oxygenation with 100% oxygen via a tight fitting mask can be carried out either using tidal volume breaths for three to five minutes or four vital capacity breaths. This patient is much more likely to be “adequately” pre-oxygenated in the head-up position and maximising the FRC and minimising the CC. The Mapleson A and circle systems are both efficient in spontaneously breathing patients but the Mapleson D requires 160-200 ml/kg/minute to prevent rebreathing
What lung pathology is unlikely to improve with 100% O2
What is a true one called
how much % of this normal physiology
When a V/Q ratio is zero, giving 100% oxygen is unlikely to improve oxygenation
A true shunt is sometimes called an anatomical or extra-pulmonary shunt. Blood enters the arterial system without passing through ventilated areas of the lungs.
Physiological shunt: normally 2-4% of the cardiac output bypasses the lungs.
Coronary arterial blood empties directly into the left ventricle via the thebesian veins
Some bronchial arterial blood empties directly into the pulmonary veins.
Pathological shunt:
Congenital heart disease with right to left shunt
Perfusion of non-ventilated areas of lung (V/Q ratio = zero). For example, areas of atelectasis or bronchial obstruction
Pulmonary arterio-venous shunts.
Severe bullous emphysema
How most accurately measure residual volume
Why is the other method less effective
What happens gas exhcnage in mild emphsyema
With severe diseases what happens with exertion
What are the changes with regards to compliance & recoil
what happens to alveolar pressure -
How do they prevent airway collapse
CO transfer factor
Whole body plethysmography also measures trapped gas, i.e. intrathoracic gas within bullae and other poorly ventilated areas, which barely communicates with the airway.
Standard gas-dilution (e.g. helium) only measures gas that communicates with the airway, and mixing during helium dilution is more difficult in airway obstruction requiring multibreath methods that last five minutes rather than a single breath test.
Exercise may actually improve gas exchange in subjects with mild emphysema, by improvement in V/Q ratios resulting from more even distribution of ventilation. With severe disease, V/Q mismatching and peripheral oxygen extraction are increased, and dynamic hyperinflation contributes to alveolar hypoventilation, with increased exertional hypoxemia.
The characteristic changes of severe emphysema are an increase in static compliance and a reduction in lung recoil pressure. Loss of lung recoil causes a reduction of alveolar pressure (elastic recoil pressure of lung and pleural pressure) leading to collapse of peripheral airways on exhalation.
Emphysematous patients purse their lips in expiration to increase airway pressure to prevent this collapse.
Carbon monoxide transfer factor is reduced (not normal).
Why do smokers have poorer o2 delivery
Carboxyhaemoglobin levels maybe up to 15% in smokers. Carbon monoxide and oxygen both bind to the alpha chain of haemoglobin, but the affinity of carbon monoxide is 250 times greater than oxygen. This results in a reduction in the availability of oxygen binding sites and a reduction in oxygen carrying capacity with left shift of the oxygen haemoglobin dissociation curve and reduced tissue oxygen delivery.
PEEP
how does it spare oxygen
what are the deleterious effects
Although positive end expiratory pressure (PEEP) may provide an oxygen sparing effect by reducing the intrapulmonary shunt and increasing alveolar recruitment it has many deleterious effects including:
Decreasing cardiac output
Increasing pulmonary artery pressure due to increased pulmonary vascular resistance
Increasing dead space
Increasing the distension of uninjured lung units increases the risk of barotrauma
Increasing extra-vascular lung water by decreasing pulmonary interstitial lymph drainage (although PEEP reduces oedema in left ventricular failure and in fluid overload).
The protective effects of PEEP on the lung are mediated not only through its ability to decrease the inspired oxygen requirements, but also due to a reduction in repeated alveolar collapse and re-inflation.
This limits the shear stress on the alveolar wall, which reduces the formation of pro-inflammatory mediators by the pulmonary vascular epithelium and alveolar macrophages.
What is dead space
How is it measured
What is it the sum of
how much is approx
can it be measured with fowlers
Difference between healthy and illness dead spaces
How is deadspace increased
What is the effect of neck extension
Dead space is defined as the volume of inspired air that takes no part in gas exchange.
The Bohr equation is used to measure the physiological dead space and is the sum of the anatomical dead space and the alveolar dead space. It is approximately 2-3 ml/kg which equates to about 30% of the tidal volume.
Fowler’s method is used to measure anatomical dead space.
In healthy subjects anatomical and physiological dead space measurements are approximately the same. However, in disease states the physiologic dead space increases because of ventilation and perfusion (V/Q) mismatch.
Salbutamol causes bronchodilation and increases physiological dead space due to its effect on increasing the anatomical dead space.
Neck extension similarly increases the physiological dead space by increasing the anatomical dead space.
Acute severe asthma:
What features
When is an ABG approp
When is a cxr approp
tachycardia ecg indicated
In a patient presenting with acute asthma any one of the following suggests acute severe asthma:
PEFR 33-50% best/predicted
Respiratory rate ≥25/min
Heart rate ≥110/min or
Inability to complete a sentence in one breath.
Saturations of less than 92% in this context suggest life threatening asthma.
Patients with oxygen saturations of less that 92% on or off oxygen warrant arterial blood gas analysis looking for normo- or hypercarbia.
A chest x ray should be performed in the following circumstances:
Presence of subcutaneous emphysema
Persisting unilateral signs suggesting pneumothorax
Signs of lobar collapse or consolidation
Life-threatening asthma not responding to treatment
If the patient requires mechanical ventilation
While PEF is one of the indicators for differentiating moderate, acute, severe and life threatening asthma, other clinical parameters can also be used to make the diagnosis as described above.
One criterion to suggest life threatening asthma is arrhythmia. Together with the tachycardia an ECG would be indicated. Although one of the defining criteria for moderate asthma is PEFR 50-75% best/predicted this patient already has features suggestive of acute severe asthma with tachycardia and tachypnoea.
Hypoxaemia arterial po2 of what
What is it caused by
What is hypoxia
WHat does CO cause
Hypoxaemia is an arterial PO2 below 12 kPa (90 mmHg) and is caused by:
Hypoventilation
Shunt
Ventilation/perfusion (V/Q) mismatch
High altitude, and
Diseases that impair diffusion across the alveolus (for example, pulmonary fibrosis and connective tissue diseases).
A reduced functional residual capacity (FRC) may also cause hypoxaemia if the closing capacity exceeds the FRC resulting in a V/Q mismatch.
Hypoxia is defined as the failure of oxygenation at tissue level.
Carbon monoxide poisoning causes anaemic hypoxia. Carbon monoxide (CO) preferentially binds to haemoglobin preventing the loading of oxygen onto binding sites. CO poisoning also causes a form of histotoxic hypoxia by inhibiting mitochondrial cytochrome (A3) involved with oxidative phosphorylation.
Surfactant comprieses of what
is it neutral lipid its main constituent
What produces
how is that controlled
how does it reduce surface tension
whats the half life
what does amphipathic mean
Surfactant is a complex material which comprises 80% dipalmitoyl phosphatidylcholine or DPPC (which is not neutral lipid), carbohydrate and protein. It is produced by type II pneumocytes, which is under some control of the hypothalamic-pituitary-adrenal axis, and prevents alveolar collapse at low lung volumes by reducing alveolar surface tension.
The reduction in surface tension is thought to be due to alignment of proteins SP-A and SP-D, which are the hydrophilic parts of the DPPC molecules on the surface of the alveoli. This causes repulsion between adjacent molecules and the repulsion increases as the molecules are compressed at low lung volumes.
Surfactant is amphipathic, which means it has a charged hydrophilic head (choline) and a hydrophobic tail (two palmitoyl groups).
Surfactant has a half life of two hours (not 50 minutes).
Lung compliance
how is it dertmenind
what shape is the curve
how does it change over volumes
how can it be measured
what is the normal complaince and the units its measured in
how is it affected by age
how does the dynamic compiance vary with frequency of vent
Compliance of the lung is determined by plotting a graph of volume (y axis) against pressure (x axis). The pressure-volume curve is sigmoid in shape. The relationship between lung volume and intra-pleural pressure is approximately linear in the middle range, which includes normal tidal ventilation.
Compliance is decreased at low and high volumes, with pulmonary oedema and pulmonary fibrosis. It increases with age.
Intrapleural pressure can be measured indirectly using an oesophageal manometer.
Respiratory volumes can be measure at the mouth using a pneumotchograph.
The normal compliance (Cl) of a normal lung is 200mL/cmH2O (range 100-400)
Total static compliance (Ct) includes the compliance of the chest wall (Ccw) that is also 200mL/cmH2O.
Summation of elastance = 1/compliance.
Ct = Cl + Ccw
1/Ct = 1/200 + 1/200 = 100mL/cmH2O
The dynamic compliance is inversely proportional to the frequency of ventilation.
