pulmonary function tests

pulmonary function tests

1. spirometry

spirometry is used to measure how much air can be taken in and out as wellas how fast air can move also in and out.
the spirometry is used for the following 3 tests:

• flow volume loops

flow volume loops provide a graphical illustration of a patient`spirometric efforts. flow is plotted against volume to display a contiuous loop from inspiration to expiration.
the loops show FVC and FEV1.
FEV1/ FVC is normally 80%.

COPD: decrease in expiratory flow rate at any giving lung volume, invrease in residual volume.
restrictive disease; decrease in all lung volumes.
fixed large airway ostruction: plateau in both ispiratory and expiratory cycles.
variable extrathoracic obstruction: plateau in the inpiratory limb.

• The severity of the abnormality might be graded as follows:
• May be a physiologic variant: Predicted FEV₁ ≥100%
• Mild: Predicted FEV₁ <100% and ≥70%
• Moderate: Predicted FEV₁ <70% and ≥60%
• Moderately severe: Predicted FEV₁ <60% and ≥50%
• Severe: Predicted FEV₁ <50% and ≥34%

case discussion

hi, here I post this case for open discussion. let us think together and try to answer these questions. I am waiting for your valuable contributions.


A 56-year-old coal miner requires sigmoid colectomy for carcinoma. He has a home nebuliser. His FEV1 is 0.68 litres, and he has 3% reversibility with salbutamol.

Observations/examination Shortness of breath 50 yards. 
Wheezy chest 
Respiratory rate 30/min 
Non-productive cough 
Chest X-ray: bullous lung disease and prominent pulmonary arteries 
ECG: normal 
Saturations: 93% on air. PO2 12 kPa; PCO2 4.5 kPa 
No FBC 
No electrolytes 

Drugs 
He is currently taking 2.5 mg prednisolone (the dose was recently reduced) 

Questions 1. Summarise the case. 
2. What are the main issues? 
3. How would you optimise this patient preoperatively? 
4. What is the likely cause of his COPD? 
5. Present the chest X-ray. 
6. What are the chest X-ray findings in pulmonary hypertension? 
7. Present the ECG. 
8. What ECG findings might you find? 
9. What are the ECG changes seen in heart strain (left and right)? 
10. What are the criteria for pathological Q waves? 
11. What is respiratory failure? 
- Give blood gas definitions of type 1 and 2 respiratory failure 
12. What are blue bloaters and pink puffers? 
- Which is this patient? 
13. How would you anaesthetise this man? 

ArticleDate:20070524 

Oxygen content of blood

The theoretical maximum oxygen carrying capacity is 1.39 ml O2/g Hb, but direct measurement gives a capacity of 1.34 ml O2/g Hb.
1.34 is also known as Hüfner’s constant.

The oxygen content of blood is the volume of oxygen carried in each 100 ml blood.
It is calculated by: (O2 carried by Hb) + (O2 in solution) = (1.34 x Hb x SpO2 x 0.01) + (0.023 x PaO2)

Where:

 SO2 = percentage saturation of Hb with oxygen
 Hb = haemoglobin concentration in grams pre 100 ml blood
 PO2 = partial pressure of oxygen (0.0225 = ml of O2 dissolved per 100 ml plasma per kPa, or 0.003 ml per mmHg)

For a normal adult male the oxygen content of arterial blood can be calculated:

Given arterial oxygen saturation (SpO2) = 100%, Hb = 15 g/100 ml and arterial partial pressure of oxygen (PaO2) = 13.3 kPa, then the oxygen content of arterial blood (CaO2) is:
CaO2 = 20.1 +0.3 = 20.4 ml/100 ml

Similarly the oxygen content of mixed venous blood can be calculated.  Given normal values of mixed venous oxygen saturation (SvO2) = 75% and venous partial pressure of oxygen (PvO2) = 6 kPa, so:
CvO2 = 15.2 + 0.1 = 15.2 ml/100 ml

Oxygen delivery (DO2) and oxygen uptake (VO2)

Oxygen delivery is the amount of oxygen delivered to the peripheral tissue, and is obtained by multiplying the arterial oxygen content (CaO2) by the cardiac output (Q).  For CaO2 = 20.1 ml/100 ml and Q = 5 l/min:

Oxygen delivery (DO2) = 1005 ml/min

The oxygen returned is given by the product of the mixed venous oxygen content (CvO2) and the cardiac output.  For CvO2 = 15.2 ml/100 ml and Q = 5.0 l/min:

Oxygen return = 760 ml/min

Oxygen uptake is the amount of oxygen taken up by the tissues that can be calculated from the difference between oxygen delivery and the oxygen returned to the lungs in the mixed venous blood.

Thus

Oxygen uptake (VO2)  = (oxygen delivery) – (oxygen return) = 1005 – 760 = 245 ml/min

To Summarise:

The primary goal of the cardio respiratory system is to deliver adequate oxygen to the tissues to meet their metabolic requirements, a balance between VO2 and DO2.
The balance between oxygen uptake by the body tissues and oxygen delivery to them is assessed by:

 The oxygen content of mixed venous blood CvO2, which is normally about 15 ml/100 ml
 The extraction ratio, which is the ratio of VO2 to DO2 expressed as a percentage.  Normally the extraction ratio is about 25% but can double to 50% if tissue demand increases

Both of the above indices are dependant on mixed venous saturation (SvO2), and cardiac output.

The figure shown below illustrates that if the level of haemoglobin is halved, the oxygen content of arterial blood will be halved.

Figure 1: Oxygen dissociation curve (ODC)



Carbon monoxide (CO) interferes with the O2 transport function of blood by combining with Hb to form carboxyhaemoglobin (COHb).  CO has about 240 times the affinity of O2 for Hb.  For this reason, small amounts of CO can tie up a large proportion of the Hb in the blood, thus making it unavailable for O2 carriage.  If this happens, the Hb concentration and PO2 of blood may be normal, but its O2 concentration is grossly reduced.  The presence of COHb also shifts the O2 dissociation curve to the left, thus interfering with the unloading of O2.  This is an additional feature of the toxicity of CO.

The sigmoid shape of the oxygen dissociation curve is a result of the cooperative binding of oxygen to the four polypeptide chains.  Cooperative binding is the characteristic of a haemoglobin to have a greater ability to bind oxygen after a subunit has bound oxygen. Thus, haemoglobin is most attracted to oxygen when three of the four polypeptide chains are bound to oxygen. 

Factors that Influence Oxygen Binding 

 Temperature- Increasing the temperature denatures the bond between oxygen and haemoglobin, which increases the amount of oxygen and haemoglobin and decreases the concentration of oxyhaemoglobin (Schmidt-Nielsen, 1997).  The ODC shifts to the right.

 pH- A decrease in pH by addition of carbon dioxide or other acids causes a Bohr Shift.  A Bohr shift is characterized by causing more oxygen to be given up as oxygen pressure increases. The ODC shifts to the right.

 Organic Phosphates:2,3-diphosphoglycerate (2,3-DPG) is a substance made in the red blood cells. It controls the movement of oxygen from red blood cells to body tissues. Haemoglobin uses 2,3-DPG to control how much oxygen is released once the blood gets out into the tissues. The more 2,3-DPG in the cell, the more oxygen is delivered to body tissues. 2,3 DPG binds to haemoglobin which rearranges the haemoglobin into the T-state, thus decreasing the affinity of oxygen for haemoglobin (T and R State).  The ODC shifts to the right.

Hyperbaric oxygen therapy (HBOT)

This is oxygen therapy at greater than atmospheric pressure, usually 2-3 atmospheres, HBOT increases the amount of dissolved O2 in the blood according to Henry’s law.  In 100 ml blood, 0.3 ml O2 dissolves at PO2 of 13.3 kPa (100mmHg).  Thus for 100% O2 at 3 atmospheres, dissolved O2 = 5.7 ml.  HBOT may be used in the treatment of carbon monoxide poisoning.

source: http://www.frca.co.uk/article.aspx?articleid=100175

lung function

Understanding lung function is vital for both intensivists and anaesthetists. Normal lung physiology is unfortunately extremely complex, and this complexity is further enhanced in sick lungs! Lacking smart and well-programmed supercomputers to simulate normal lung physiology, we tend to rely on gross over-simplification. The relationship between our current understanding of how lungs function, and what actually happens is perhaps similar to the relationship between counting on one's fingers and advanced matrix algebra! Unfortunately, many of the fruitful analogies that we use have been turned into dogma!

In most textbooks, you will encounter a vast array of "laws", which examination candidates in particular are encouraged to regurgitate, often with minimal understanding. For the record, here are some of them:-

A List of Laws Note that this mildly formidable table is mainly for reference purposes. The wise reader will skip over it, and come back from time to time. All equations are discussed in a friendly fashion in the body of the text! Those we are on "first name" terms with (Henry, Charles & Graham) will be used less extensively!
Name	Equation	Meaning
Boyle's Law	P.V = K	In a container filled with gas, if you decrease the volume, the pressure will correspondingly increase, and vice versa.
Dalton's Law		In a mixture of gases, each gas behaves as if it were on its own: it exerts a partial pressure that is independent of that exerted by other gases in the mixture.
Hooke's Law	L   T	The change in length of a spring is proportional to the tension exerted on the spring.
Laplace's Law	P = 2.T/r	The pressure inside a bubble exceeds the pressure outside the bubble by twice the surface tension, divided by the radius. In other words, the smaller a bubble, the more the pressure inside it exceeds the pressure on the outside.
Poiseuille's Law	R = 8.L.eta/(pi.r4)	Where laminar flow occurs, the resistance to flow decreases with the fourth power of the radius - if you double the radius, the resistance decreases sixteen times! Resistance also depends on the eta, (the viscosity of the gas or fluid), as well as the length of the tube being assessed (L). Note that with turbulent flow, things are completely different - we can't even talk about "resistance" as the drop in pressure is not directly related to flow, but to flow squared!
The Fanning Equation	P  1 / r5	With turbulent flow, for any particular flow rate, pressure drop depends on the fifth power of the radius of the tube.
Fick's Law	Vgas  A * P / L	Gas transfer through a membrane is proportional to membrane surface area (A) and partial pressure gradient across the membrane(P), and inversely proportional to thickness (L).
Graham's Law	D  sol / MW0.5	Diffusion of molecules is inversely proportional to the square root of their molecular weight, and directly proportional to their solubility.
Henry's Law		The number of molecules of gas dissolved in solution is proportional to the partial pressure of the gas.
Charles' Law	V = K'. T	As the temperature of an amount of gas increases, so does its volume (maintaining a constant pressure). We can combine this with Boyle's law to get: PV = nRT Where n is the number of moles of gas, and R is a constant, the universal gas constant. At standard temperature and pressure, a mole of gas occupies 22.4 litres. The actual value for CO2 and N2O is about 22.2 litres.
Reynold's number	linear gas velocity * diameter * density / viscosity	Reynold's number is dimensionless. Turbulence occurs if Reynold's number is over 1000, and flow is entirely turbulent if it exceeds 1500.

Basic Ideas

Atmospheric oxygen arose as a toxic by-product of the very first photosynthetic organisms, which were possibly quite similar to today's blue-green algae. Smarter organisms rapidly learned to use this oxygen, and minimise its toxic effects. When they possibly unwisely decided to abandon their individual identities and co-operate to form multicellular organisms, and moved onto land, then their problems really began! They needed:

1. Ways of acquiring atmospheric oxygen in large quantities;
2. A method to transport this O₂ to distant, oxygen- starved cells;
3. Processes for removal of carbon dioxide, the principal metabolic waste product.

All of these are more-or-less adequately fulfilled by the tightly entwined cardiovascular and respiratory systems. The respiratory system is a marvellous, efficient pump for passing air over the capillary bed of the lung, where oxygen moves into the blood and CO₂ is removed from the blood. The inefficient and failure-prone cardiovascular system then takes over, finally distributing oxygen to oxygen-hungry cells throughout the body. The inefficiency with which this occurs can be seen if we look at the oxygen cascade, which documents the changes in partial pressure of oxygen from inspired air down to the mitochondrion where the oxygen is actually used. Oxygen moves down a gradient, from a partial pressure of about 160mmHg in the atmosphere, down to about 4-20mmHg in the mitochondrion! The steps are:

Inspired oxygen	160 mmHg
Alveolar oxygen	~ 120 mmHg
Oxygen in the blood	~ 100 mmHg
Oxygen at tissue level	~ 4-20 mmHg

Considering these in more detail we find:

1. Atmospheric pressure at sea level is about 760mmHg, and the concentration of oxygen is 20.95%. Using Dalton's Lawwe calculate that in dry, inspired air, the partial pressure of oxygen is 159mmHg. Unfortunately, air within the lungs is 100% saturated with water. We need to re-think! If we know that the partial pressure of water vapour at 37 degrees Celsius is 47mmHg, we can work out that the partial pressure of the remaining gases is (760 - 47)mmHg. We'll call this barometric pressure that excludes water vapour pressure the 'dry barometric pressure', or P_Bdry. Applying Dalton's law yet again, we determine that the inspired PO₂ is therefore actually 149mmHg, once the air has become fully hydrated in the nose. Let's abbreviate the inspired PO₂ to PiO₂. But wait a bit..
   
2. Oxygen is taken up in the lung! This will decrease the amount of oxygen in the alveolar air. The decrease will be directly related to the amount of oxygen taken up, and inversely related to the alveolar ventilation. In other words, the greater the alveolar ventilation, the less the effect of this oxygen uptake on the fraction of oxygen in the alveolar air. This is an expression of the "universal alveolar air equation". We say:
   
   
   alveolar PO2     ~     P_Bdry * (FiO2 - fractional O2 uptake)
   
   Where the fractional O2 uptake is equal to: O2 uptake / alveolar ventilation
   
   We may abbreviate alveolar PO2 to P_AO2. Thus:
   
   
   P_AO2    ~    P_Bdry * (FiO2 - O2 uptake / alveolar ventilation)
   
   
   Note that this is only approximate - differences between inspired and expired volumes will affect the estimate. In addition, if you guessed that P_AO2 fluctuated with each breath, you would be correct, but this variation is normally only about 3mmHg. 
   (There are more convenient ways of estimating P_AO2, although many of these are fairly inaccurate!) Plugging values into the above, we might get something like:
   
   P_AO2 = (760 - 47) * ( 0.2095 - 250/5000)
   
   Where the true barometric pressure is 760mmHg - the partial pressure of water vapour at 37 degrees is 47mmHg, the inspired oxygen concentration is 20.95%, the oxygen consumption is say 250 ml/minute, and the alveolar ventilation is 5 litres/minute. This gives us a P_AO2 of about 114 mmHg. We rush on, inexorably down the oxygen cascade!
   
3. In a healthy young adult breathing air, the gradient from alveolus to capillary is minimal - under 15mmHg. In the 'normal' elderly person, this may rise to 37mmHg! (One convenient estimate of this gradient is simply 4 + age/4 mmHg)! In the critically ill, this alveolar/arterial oxygen difference may be hundreds of millimetres of mercury. Nevertheless, even in the normal young individual we still take a small step down, to an arterial partial pressure of oxygen (P_aO2) of about 100mmHg.
   
   Another useful estimate for PaO2 at sea level (in healthy subjects breathing air) is given as:
   
   
   PaO2    = 102 - 0.33 * (age in years)
   
   This is expressed in mmHg, and we stress that the confidence limits for this estimate are fairly wide: +- 10mmHg.
   
4. The big drop comes at the tissue level, where the PO2 within the mitochondrion has been estimated to be as low as 4-20mmHg! In some normally functioning cells this PO2 may even drop to 1mm Hg!
   Perhaps this is the PO2 that our ancient unicellular ancestors first found that they could effectively use, and there has been no (heh) pressure to subsequently change, or perhaps this low PO2 is a trade-off related to the number of capillaries needed to support the tissues, but we know one thing, and that is that we could sure use a bigger tolerance margin in critically ill patients!

source: http://www.anaesthetist.com/icu/organs/lung/Findex.htm#lungfx.htm

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PSYCHIATRIC DISORDERS AND ANESTHESIA

Psychiatric Disorders

Depression

        Depression is a mood disorder characterized by sadness and pessimism. Its cause is multifactorial, but pharmacological treatment is based on the presumption that its manifestations are due to a brain deficiency of dopamine, norepinephrine, and serotonin or altered receptor activities.

 Up to 50% of patients with major depression hypersecrete cortisol and have abnormal circadian secretion.

 Current pharmacological therapy utilizes three classes of drugs that increase brain levels of these neurotransmitters: tricyclic antidepressants, monoamine oxidase (MAO) inhibitors, and atypical antidepressants.

The mechanisms of action of these drugs result in some potentially serious anesthetic interactions.

 Electroconvulsive therapy (ECT) is increasingly used for refractory and severe cases and prophylactically once the patient returns to baseline. The use of general anesthesia for ECT is largely responsible for its safety and widespread acceptance.

Tricyclic Antidepressants

        Tricyclic antidepressants may be used for the treatment of depression and chronic pain syndromes.

All tricyclic antidepressants work at nerve synapses by blocking neuronal reuptake of catecholamines, serotonin, or both.

Desipramine (Norpramin and Pertofrane) and nortriptyline (Pamelor and Aventyl) are commonly used because they are less sedating and tend to have fewer side effects.

 Other agents are generally more sedating and include amitriptyline (Elavil [withdrawn from the U.S. market]), imipramine (Tofranil and Janamine), protriptyline (Vivactil), amoxapine (Asendin), doxepin (Sinequan and Adapin), and trimipramine (Surmontil).

Clomipramine (Anafranil) is used in the treatment of obsessive–compulsive disorders.

 Most tricyclic antidepressants also have significant anticholinergic (antimuscarinic) actions: dry mouth, blurred vision, prolonged gastric emptying, and urinary retention. Quinidine-like cardiac effects include tachycardia, T-wave flattening or inversion, and prolongation of the PR, QRS, and QT intervals. Amitriptyline has the most marked anticholinergic effects, whereas doxepin has the fewest cardiac effects.

Applications of ultrasound in anaesthesia

Applications of ultrasound in anaesthesia

The applications of ultrasound in anaesthesia include

1. Ultrasound for vascular access

2. Ultrasound guided regional anaesthesia

3. Trans-esophageal echocardiography

ULTRASOUNDFORVASCULARACCESS

Ultrasound can be used to reduce complications associated with the cannulation of veins and arteries.

ULTRASOUND GUIDED CENTRAL VENOUS CANNULATION

Indications for central venous catheter insertion

include:

 Haemodynamic monitoring

 Intravenous delivery of blood products and drugs

 Haemodialysis

 Total parenteral nutrition

 Cardiac pacemaker placement

 Difficult peripheral access

Commonly used sites for central venous cannulation

are

 The internal jugular vein (IJV)

 The subclavian vein (SV)

 The femoral vein (FV).

The traditional “landmark” method of central venous cannulation relies on surface anatomical landmarks. The literature failure rates for initial CVC insertion with this method have been reported to range between 10% and 35%.

The most common complications associated with CVC placement are:

 Arterial puncture

 Pneumothorax

 Nerve injury

 Multiple unsuccessful attempts

 Malposition of catheter

 Arteriovenous fistula formation

The risk of complications increases, depending upon:

 Difficult anatomy: obesity, short neck, scarring due to surgery or radiation

 Repeated catheterization: increased risk of

thrombus formation

 Coagulopathies

 Patients on mechanical ventilation

The advantages of ultrasound-guided central

venous catheterization include:

 Identification of the vein

 Detection of variable anatomy

 Detection of intravascular thrombi

 Avoidance of inadvertent arterial puncture.

Two types of ultrasound guidance are described:  two dimensional (2-D) imaging ultrasound guidance and audio guided Doppler ultrasound guidance.

Two-dimensional ultrasound provides a real-time image of the anatomy. Audio-guided Doppler ultrasound helps to localize the vein and differentiate it from its companion artery. However it does not give an idea about the depth of the vessel

The needle puncture may be made in two ways:

 Indirectly: after pre-procedure identification of the vessel by ultrasound. This technique may not have any advantage over conventional ‘landmark’ identification of vascular structures.

 Directly: under real-time visualization

Machines designed for vascular access (e.g.Siterite) usually provide B-mode 2-D real-time images; generally using 2.5 to 10 MHz probes. Needles are seen more easily in longitudinal section; however relationship of the needle to surrounding structures is better appreciated in transverse section. In the absence of direct view, tissue distortion produced by needle movement can indicate the direction.

A guide may be present on the ultrasound probe to

facilitate needle insertion. Sterile gel is used between the probe and the skin surface, and sterility of the probe is maintained by covering it with a transparent plastic sheath.

Arteries appear round in cross-section, are pulsatile, and not easily compressible with pressure applied by the probe.

Veins are more irregular, vary in size with respiration and are easily compressible. A meta-analysis of 12 randomized controlled trials evaluating the effect of realtime ultrasound guidance using regular or Doppler ultrasound for central venous catheter placementwas conducted and they found a reduction in placement failure, decreased need for multiple attempts, and decreased complications, as compared to the standard landmark technique.Another meta-analysis of 7 trials was carried out comparing the use of 2-D ultrasound versus landmark method for central venous cannulation in adults.5 It showed that for IJV cannulation, 2-D ultrasound guidance was associated with reduced risks of failed catheter placements, catheter placement complications, failure on the first catheter placement attempt, and fewer attempts to achieve successful catheterization.

The difference between the 2-D ultrasound method and the landmark method in the time taken to insert a catheter successfully was small and not statistically significant. For subclavian vein cannulation, 2-Dultrasound guidance was associated with reduced risks of catheter

placement failure and catheter placement complications.

In the cannulation of the IJV in infants, 2-D ultrasound guidance was significantly better than the landmark method in terms of reductions in the risk of failed catheter placements, the risk of catheter placement complications, and the number of attempts required before catheterization was successful. Using 2-D ultrasound guidance, successful cannulation was achieved more quickly than with the landmark method, although this result was not statistically significant.

2D ultrasound was also found to be superior to

Doppler ultrasound for IJV and subclavian vein procedures.

Based on this meta-analysis, the NICE (National

Institute for Clinical Excellence – NHS) has recommended that the use of two-dimensional (2-D) imaging ultrasound guidance should be considered in most clinical circumstances where CVC insertion is necessary.3, The use of ultrasound for vascular access may be particularly helpful in haemodialysis patients who need wide bore access, present for repeated cannulation, may not be able to lie supine, and may have underlying coagulopathy or platelet dysfunction.7Ultrasound can also be used as an alternative to X-ray to check for malposition of central venous catheters and peripherally inserted central catheters. Routine ultrasound examination of recently cannulated veins can also be done to rule out presence of thrombi, prior to re-cannulation.

Ultrasound for arterial cannulation

Arterial cannulae are inserted for blood pressure

monitoring and blood gas sampling. Studies comparing the use of ultrasound versus blind technique for radial artery cannulation have found that ultrasound guidance decreases the number of attempts, and improves the overall success

rate of cannulation.

Ultrasound guided regional anaesthesia

The features of any imaging technique used for regional anaesthesia should include:

 Good resolution

 Safety - for both patient and operator – minimal

exposure to radiation

 Offer real time guidance

 Portability

 Should not require additional personnel to operate

Among currently available imaging techniques, ultrasound is the most compatible with these criteria In routine anaesthetic practice, ultrasound can be used for

1. Peripheral nerve plexus blocks

2. Central neuraxial blocks in children and in difficult anatomical situations in adults

3. In procedures for chronic pain

Peripheral nerve blocks

A successful regional block requires optimum distribution of local anaesthetic around nerve and plexus structures.

Ultrasound imaging has the following advantages:

 Direct visualization of neural structures

 Direct visualization of related structures like blood vessels and tendons, which helps to identify nerves

 Guidance of the needle under real-time visualization

 Avoid complications like intravascular and

intraneuronal injection

 Monitor the spread of local anaesthetic

 Allows repositioning of the needle after an initial injection to allow better delivery of local anaesthetic to areas that may not be completely blocked with a single dose

 Can be used in patients with poor twitch response to nerve stimulation On high-resolution ultrasonography, nerves appear as honey comb structures with hypoechoic fascicles surrounded by hyperechoic tissue. 10-15MHz probes are used for the brachial plexus at the interscalene or supraclavicular level. Deeper nerves like the sciatic, infraclavicular and popliteal require the use of lower frequency – 4-8 MHz – probes.

For ultrasound-guided nerve block, all the anatomical structures in the target area have to be visualized.

The penetration depth, the frequencies, and the position of the focal zones are optimized. The visibility of the needle on ultrasound is affected by the angle of insertion – reduced at steep angles - and the gauge of the needle – large bore needles are easy to visualize. The out-of-plane needle approach involves inserting the needle so that it crosses the plane of imaging near the target. The needle is not visible during insertion. The in-plane needle approach the needle is inserted within the plane of imaging to visualize the entire shaft and tip.

Once the needle is optimally in place, the local anaesthetic is administered under direct sonographic visualization until the nerve structures are surrounded by local anaesthetic. If the local anaesthetic does not spread in the right direction, the needle can be repositioned accordingly.

Air bubbles can cause shadowing and have to be removed prior to injection. Bicarbonate containing solutions are avoided because of CO2 production, which can interfere with imaging.

Nerve stimulation may be combined with ultrasound guidance to confirm nerve- needle contact. However, this has not been shown to confer any advantages A number of clinical studies have examined block characteristics

with ultrasound guidance at different anatomical locations.

All studies found improved block characteristics,

including reduced onset time and improved quality of block.

The dose of local anaesthetic required was reduced. The incidence of paraesthesia was also decreased, which could minimize post-procedure neuropraxia. The block performance time was not significantly increased. Complications like neurological damage and vessel puncture were avoided.

Central neuraxial blockade

Ultrasound guidance for neuraxial anaesthesia is limited by the presence of bony structures like laminae, spinous processes and transverse processes, which do not allow the ultrasonic be amto pass through. Also, the depth of the epidural space in adults needs imaging with low frequency

probes, which gives poor resolution. Present studies indicate that ultrasonography should be used along loss of resistance techniques, to guide needle orientation, and to give an idea of the depth atwhich the ligamentum flavum should be encountered.11Studies on the use of ultrasound for lumbar epidurals have shown good correlation between ultrasonographically measured data on the depth of the lumbar epidural space and direct measurement at the time of lumbar puncture. Ultrasound guidance is associated with significant reduction of the puncture attempts, reduction in

the number of puncture levels, more precise application of the catheter, and improvement of analgesia quality and patient satisfaction. Ultrasound visibility has been shown to be higher in the paramedian as compared to the median

plane. Ultrasound imaging has been shown to be superior to clinical palpation as a method of identifying lumbar intervertebral level In one case series, ultrasound guidance was used to determine the least rotated vertebral body for epidural catheter insertion in patients undergoing scoliosis surgery. Ultrasound has also been used to identify landmarks prior to difficult lumbar subarachnoid puncture.

Ultrasound in paediatrics

Ultrasonography is particularly useful for neural blocks in children for the following reasons:

 Variability in anatomy according to age and

constitution of the patient.

 Regional blocks are usually performed under

anaesthesia or sedation - adverse effects may not

be detected.

 Because of the superficial location of most neural structures in children, one can use higher frequency ultrasonic probes, with better resolution.

Spinous interspaces and intervertebral foramina allow the ultrasonic beam to penetrate through, to visualize deeper structures.

Studies have shown that ultrasound provides

information on the distance of skin-to-ligament flavum in neonates, infants and children. Hence, the risk of dural puncture is reduced and the spread of local anaesthetic can also be visualized.

Pain interventions

The use of ultrasound has been shown to have 100% accuracy in locating the caudal space and guiding epidural needles for caudal injections for low back pain. Use of ultrasound for facet joint injections, lumbar sympathetic blocks, celiac plexus blocks, stellate ganglion blocks and

identification of myofascial trigger points has also been described.

Ultrasound for trans-oesophageal echocardiography

 Currently available TEE probes combine multiplanar ultrasound for cardiac imaging, with Doppler to view blood flows.

TEE is used in anaesthesia to:

 Assess adequacy of repair and detect residual

pathology or prosthetic valve dysfunction in patients undergoing surgery for valvular and congenital heart disease

 Diagnose ongoing ischemia by detecting fresh regional wall motion abnormalities in patients with ischemic heart disease

 Assess left and right ventricular function, and volume status in patients with severe haemodynamic instability

 As a sensitive tool for early detection of pulmonary embolism, especially in patients undergoing neurosurgery in the sitting position

 Transesophageal stress echocardiography to detect coronary artery disease and viability.

Newer applications

The use of laryngeal ultrasound to detect patients at risk of post-extubation stridor, by evaluating peri-cuff airflow has been described. Ultrasound has also been shown to be as effective as MRI to assess subglottic diameter, to calculate appropriate endotracheal tube size. Ultrasound has been used to visualize CSF leak in cases of post-dural puncture headache, and for the application of epidural blood patch under real-time depiction.