BT_RT 1.22 Outline the anatomy relevant to drainage of the pleural space

T/F   an emergency decompression of a tension pneumothorax can be performed with a 14 G cannula into the second intercostal space in the midclavicular line

T/F   the second rib attaches to the sternum at the same point as the sternal angle (angle of Louis) – this landmark is reliably palpable

T/F   IV cannulae can be too short to reach the pleural space

T/F   the neurovascular bundle runs in a groove on the superior surface of each rib

T/F    a chest drain (intercostal catheter) is usually inserted in the mid-axillary line in the 4th or 5th intercostal space (the nipple position in a male is usually the 5th intercostal space)

T/F   if a chest drain is placed too posterior, the long thoracic nerve may be injured – this results in weakness of the serratus anterior muscle, and a ‘winged scapula’

T/F   after insertion, the presence of a chest drain is usually not painful, because both the visceral and parietal pleura are poorly innervated

References:
1. Anatomy for Anaesthetists 9th ed, p 48-51
2. Moore Clinically Oriented Anatomy 7th ed, Chapter 1

Further Discussion

Can you name 6 procedures which can potentially cause a pneumothorax as a complication?

On the diagram below, draw and name the borders of the “triangle of safety” for lateral insertion of a chest drain.

chest drain

 

Soda Lime

BT_SQ 1.15  Outline how CO2 is absorbed in a circle system, and the hazards associated with CO2 absorption.

The other day I saw a picture of some jacaranda trees on a Facebook post, and (tragically) it reminded me of the colour of the ethyl violet pH indicator in our CO2 absorbers.

I also recently did a tutorial on equipment for the registrars at my hospital, who were all panicking about the chemistry of soda lime.

For both these reasons, I though I’d do a post on soda lime / CO2 absorption.

No doubt you’ve realised that the need for chemical CO2 absorption is unique to anaesthesia (i.e. it’s not needed/used in ICU). This is because we use circle breathing systems which permit rebreathing. And the reason for this is to conserve N2O and volatile agents, by allowing them to be rebreathed. Without a rebreathing circuit, the cost of N2O and volatiles would be astronomical. To permit safe rebreathing, the patient’s exhaled CO2 has to be eliminated.

When you first look at the soda lime equations, you can get a bit daunted. Your goal should be to look beyond the equations, so that you understand what is happening. Simply writing out equations in an exam, with no explanation, will score hardly any marks. You could pass a question on this topic without using the actual equations, but by providing an explanation in words of what is happening. (Ideally, you should be able to do both).

Soda Lime Reactions

T / F  fresh soda lime is about 15% water – without water, the reactions can’t start

T / F  A strong base (sodium hydroxide) is needed to speed things up. Reaction #1 is very slow. But #1 will go faster if its product (carbonic acid) becomes one of the reactants in a very fast reaction (reaction #2).

T / F  the product of reaction #2 is sodium bicarbonate, which reacts with calcium hydroxide (another strong base) in reaction #3

T / F  the NaOH produced in reaction #3 is recycled through reaction #2 to keep things going

T / F  the CO2 absorber becomes “exhausted” when all the calcium hydroxide is used up

T / F  the basic aim of the CO2 absorber is to turn CO2 into chalk (calcium carbonate)

Discussion Questions

Is NaOH really necessary? If you feel inspired by this post, you might like to read about “Amsorb”. What advantages does it have over soda lime? Is its CO2 absorption capacity the same?

Does soda lime really “absorb” CO2? Can you think of a better word?

BT_SQ 1.7 Electrical Safety

The other day, we had a power failure at my hospital. It occurred in the middle of the day with about 20 theatres running. And the backup generator failed to start!! 

T / F  devices plugged into RED power points are supplied by the hospital’s backup generator in the event of a blackout

T / F  the BLUE power points are the “uninterruptable power supply” (UPS) – supplied by the backup generator, or emergency batteries in the event that the generator fails to kick in

T / F  life-sustaining equipment such as anaesthetic machines, ventilators, cardiopulmonary bypass machines etc. should all be plugged into BLUE power points

T / F  any anaesthetic machine which requires mains power to operate must have its own internal battery that can last for at least 2 hours

T / F  only the BLUE power points offer cardiac electrical protection

 

Oxygen Delivery

The learning outcomes which are related to this SAQ include, but are not limited to:
BT_PO 1.23  Describe the oxygen cascade
BT_PO 1.31  Discuss the carriage of oxygen in blood …
BT_RT 1.4  Describe oxygen delivery …

All of the following statements are considered to be core knowledge, and the answers can be found in Nunn’s Applied Respiratory Physiology.

T / F  normal alveolar PO2 is 150 mmHg (the same as humidified inspired air)

T / F  hypoventilation causes hypoxaemia mainly because the rate of oxygen removal from alveoli exceeds its replenishment by ventilation. The dilution of alveolar O2 by the addition of CO2 plays a minor role.

T / F  the alveolar-capillary membrane has a total combined thickness of 0.3 micrometres

T / F  the difference between alveolar and arterial PO2 is mainly explained by diffusion block

T / F  each molecule of haemoglobin can carry 1.34 mL O2

T / F  when breathing room air, haemoglobin in arterial blood is normally 100% saturated. This gives an oxygen content of 20.3 mL O2 / 100 mL blood.

T / F  if blood pH falls, the affinity of haemoglobin for oxygen increases

 

2018.2 SAQ 15 prostaglandin effect on smooth muscle

Describe the physiological role of prostaglandins on smooth muscle throughout the body.

You may think this is an obscure question, however a group of drugs we use commonly (NSAIDS in case you were wondering) effectively counteract the physiological effects of these autacoids.

Vallecula recently posted  on prostaglandins if you would like to review some more statements

Interestingly Katzung’s Basic and Clinical Pharmacology has a very good chapter (Chapter 18) discussing, amongst other things, prostaglandins.

BT_PO 1.89 Outline the physiological effects of prostaglandins and other autacoids

PGF2α causes contraction of uterine muscle, but relaxation of bronchial smooth muscle T/F

Prostaglandins generally cause contraction of GIT smooth muscle T/F

Prostacyclin, PGI2, causes vasodilation of arterioles through the release of nitric oxide T/F

Thromboxane mediates vascular smooth muscle contraction via increasing intracellular calcium levels T/F

PGF2α is a potent constrictor of the pulmonary vasculature, contraindicating its use intravenously T/F

2018.2 SAQ 14 Describe the factors determining transdermal uptake of drugs. Briefly outline the advantages and disadvantages of transdermal administration of drugs.

As anaesthetists, we encounter many patients with “patches” on, and often apply them to patients. There are certainly advantages to using this route, but there can be serious disadvantages too. The transdermal route bypasses the liver and any first-pass metabolism, but there are many advantages related to the pharmacokinetics and pharmacodynamics of the drugs given via this route. 

1. The epidermis is the greatest barrier to transdermal transport. T/F

2. There are two drug reservoirs in the process of transdermal uptake, one in the patch and one in the stratum corneum. T/F

3. The drug’s context-sensitive half time is irrelevant to the plasma concentration of the drug after removal of the patch. T/F

4. The problem of inter-patient variability in drug absorption by the skin is managed using a slow rate of drug release from the patch. T/F

5. Fentanyl is ideal for transdermal application as it is soluble in both fat and water, has a low molecular weight and is potent. T/F

6. Only hydrophobic drugs can cross the skin. T/F

 

 

2018.2 SAQ 13 – drugs affecting uterine tone

List the drugs that affect uterine tone, and outline the adverse effects of these agents.

Most of us will administer a uterotonic every time we give an anesthetic for a Caesarian section. Furthermore, we will be exposed to a group of parturients requiring tocolytics or non routine utertonics, so it is reasonable that we know their side effects – some are not that benign…

SS_OB 1.10 Describe the pharmacology of oxytocic agents with special reference to oxytocin derivatives, ergot derivatives and prostaglandins

SS_OB 1.11 Describe the pharmacology of tocolytic agents with particular reference to beta 2 agonists, calcium antagonists, magnesium, inhalational anaesthetics, nitrates and NSAIDS

I would consider all of the statements below to be testing core knowledge. The answers can be found in most pharmacology textbooks, but Goodman and Gilman’s textbook covers the topic quite well.

Syntocinon is structurally similar to vasopressin and may result in water intoxication when given to patients for augmentation of labour T/F

All uterotonics pose the risk of uterine rupture when given antepartum T/F

Severe hypertension may be precipitated by BOTH Syntocinon and ergotamine T/F

Slow administration of Syntocinon reduces the risk of severe cardiovascular side effects T/F

Tocolytics increase the risk of post partum haemorrhage T/F

NSAIDs are tocolytic and pose NO risk to the fetus when given antepartum T/F

Propofol causes a dose dependent reduction in uterine tone T/F

 

 

 

Therapeutic cooking

Frequent readers of this blog will most likely know that I am a fan of baking and find the process of cooking relaxing (except if I have 10 people over for dinner and am trying to get multiple different things ready to serve at the same time – that I find stressful). My latest thing is making my own sourdough – it is great fun. The loaves above I baked this morning.

It seems that I am not the only one who derives this benefit from cooking.

I have recently purchased the new cookbook written by Annabel Crabb and her friend Wendy Sharpe, Special Guest. Whilst thumbing though my new copy, a recipe caught my eye and I thought I would share it with you.

Punched Cucumber Salad. Whilst the cucumber is not actually punched, it is beaten with a rolling pin. The resultant salad sounds deliciously refreshing and in the process of preparing it, you can release some study related stress. I have made an intentional decision to post something other my usual sweet treats (although you can find them at various places on this blog). I have not actually made this yet, but plan to soon (I suspect it will be good – I have tried several of the recipes from their other book and they have all worked well).

I like the wording of the recipe, so I have just included a photo of it here

I hope you all have a great weekend and manage a little bit of therapeutic cooking.

2018.2 SAQ 11 – midazolam

I rarely use this drug as I worry about the ethical implications of amnesia in a patient who believes they were unconscious. In an anxious patient I prefer to make the experience as pleasant as possible with such activities as talking, hand holding, my ‘Lullabies for Grown-ups’ playlist and making the theatre table up as a cosy bed with the forced air warmer already running. Even so, some people are so anxious that midazolam is totally appropriate as an anxiolytic, and it has a role in my practice when performing procedures. 

The time to peak effect of midazolam is 2 minutes    TRUE/FALSE

Midazolam is water soluble in an acidic solution    TRUE/FALSE

Midazolam can be given orally    TRUE/FALSE

Midazolam can be used as an anticonvulsant    TRUE/FALSE

Upper airway reflexes are preserved with midazolam    TRUE/FALSE

 

2018.2 SAQ 10 – positive inotropes

Outline the mechanisms of action of the drugs, with examples, which increase myocardial contractility.

BT_PO 1.52  Describe the mechanism of action of sympathomimetic … drugs used clinically
BT_PO 1.53  Describe the pharmacology and clinical application of adrenergic agonists
BT_PO 1.60  Describe the pharmacology of drugs used to manage acute or chronic cardiac failure, including: sympathomimetics, phosphodiesterase inhibitors, digoxin, ….

T / F  noradrenaline has no inotropic effect because it is a pure alpha-1 adrenergic agonist

T / F  adrenaline exerts a positive inotropic effect via beta-2 adrenergic receptors on the cardiac myocytes

T / F  milrinone is a phosphodiesterase inhibitor – it works by inhibiting the breakdown of phosphokinase A

T / F  glucagon is a positive inotrope – it works in this way by upregulating the numbers of adrenergic receptors

T / F  levosimendan works by ‘sensitising’ troponin C to the effect of calcium

T / F  digoxin’s positive inotropic effect stems from its inhibition of the Na/K-ATPase