BT_PO 1.44 Describe the physiology of cardiac muscle and the mechanism of excitation contraction coupling

T/F  cardiac muscle is not striated

T/F  acetylcholine is released from the terminal ends of the cardiac conduction system, where it binds to muscarinic acetylcholine receptors on the myocytes

T/F  cardiac myocytes are connected to each other via gap junctions, to increase the speed of electrical conduction and enable the heart to contract “as one”

T/F  an increase in the force of myocardial contraction is brought about by recruitment of additional myocardial motor units

T/F  contractility is proportional to intracellular calcium concentration

T/F  entry of extracellular calcium via T tubules triggers further calcium release from sarcoplasmic reticulum

References

  • Ganong
  • Pappano & Weir

BT_PO 1.59 Describe the pharmacology of drugs used to manage myocardial ischaemia/infarction, including: nitrates, beta blockers, calcium antagonists, anti-platelet agents, anti- coagulants and fibrinolytic agents

T/F  the main mechanism by which glyceryl trinitrate can treat myocardial ischaemia, is by direct coronary artery vasodilation

T/F  tachyphylaxis can develop if glyceryl trinitrate is given continuously (e.g. transdermal patch), without a ‘rest’ period

T/F  beta blockers help reduce myocardial ischaemia mainly by reducing contractility – the decreased wall tension corresponds to decreased oxygen demand

T/F  the calcium channel blockers most appropriate for angina, are from the dihydropyridine group

T/F  aspirin is useful with myocardial ischaemia because it decreases vascular endothelial prostaglandin synthesis – this reduces platelet adhesion

T/F  tirofiban can be used IV for unstable angina – this must be ceased at least 24 hours pre-operatively to reduce bleeding risk

References

  • various bits of Hemmings & Egan, Evers & Maze, Stoelting

BT_GS 1.69a Describe how a patients temperature is monitored and discuss the indications for temperature monitoring with the advantages and disadvantages of particular sites and methods (also refer to monitors and monitoring standards, which is covered in the Safety and quality in anaesthetic practice clinical fundamental)

T/F  a 1 degree increment on the Celsius scale equals a change of 0.1 Kelvin

T/F all anaesthetised patients being actively warmed, must have their core temperature continually monitored

T/F temperature probes commonly used in anaesthesia incorporate a thermocouple which consists of two wires joined together, each being a different metal

T/F  a temperature probe placed in the oropharynx can underestimate core temperature – it should be placed in the oesophagus

T/F  urinary catheters with a built-in temperature probe can be useful with head and neck surgery, or in patients destined for ICU

T/F  a tympanic thermometer emits a beam of infrared light onto the tympanic membrane – this is then reflected back to a sensor at a given wavelength which corresponds to temperature

T/F  digital thermometers (e.g. for use per axilla) incorporate a thermistor, which consists of a small bead of a metal oxide – its electrical resistance increases as temperature increases

References

  • ANZCA PS 15
  • Davis & Kenny
  • look at the equipment in your hospital

BT_PO 1.92 Outline the basic electrophysiology of nerve conduction

T/F  the resting membrane potential of a nerve is about minus 90 mV

T/F  in a nerve, voltage gated sodium channels are opened at a threshold of minus 40 mV

T/F  voltage gated potassium channels are also triggered to open at threshold

T/F  there is no refractory period with a nerve action potential (this is only seen in cardiac action potentials)

T/F  saltatory conduction (i) increases the speed of conduction, and (ii) decreases the energy expended by the nerve cells

T/F  repolarisation of a nerve cell occurs when the sodium-potassium pumps actively pump out the sodium which entered the cell during depolarisation

References

any standard physiology book, including Kam & Power, Ganong, Guyton

A bit of a glitch

Hi everyone.

There seems to be a bit of a problem in the land of “WordPress meets my computer” and I can’t access any of the site material, other than the already published posts. I also can’t write a new post ( I am currently on my phone which has limited functionality).

I’ll try again a bit later today….

This fabulous table top is constructed from materials found in the Great Pacific garbage patch (I can remember the creators name)

BT_PO 1.19 Describe altered lung mechanics in common disease states

Notre Dame Cathedral

Ok, well that is Murphy’s Law in action. After trying repeatedly to get the site working, as soon a I posted that last message, it was back in action!

Sorry for the absence of a post yesterday – lucky we had two on Monday.

I think this may be the last respiratory LO yet to receive a post!

 

BT_PO 1.19 Describe altered lung mechanics in common disease states

In patient’s with CPOD, the diaphragm becomes less efficient, worsening ventilatory capacity T/F

Loss of compliance of the chest wall is a significant contributory to respiratory failure in patients with circumferential chest wall burns T/F

Hyperinflation of the lungs, due to gas trapping associated with COPD, results in improved intercostal muscle efficiency T/F

There is a restriction to inspiratory flow more than expiratory flow with obstructive airways disease T/F

With Easter around the corner here is something to think about. It has been postulated that many people who were crucified died from asphyxia or ventilatory failure. Can you postulate how this might occur thinking about the mechanics of breathing?

  

BT_PO 1.13 Describe the elastic properties of the chest wall and plot pressure-volume relationships of the lung, chest wall and the total respiratory system

Vienna again. An apartment block designed by Otto Wagner in secessionist style – how fabulous!

One of the quirks of the LOs, is that some of them seem to cover half a textbook’s worth of information and then others, like this one, are very specific. This LO is closely related to yesterday’s post.

I was looking for a picture of the respiratory system compliance like the ones in West’s Respiratory Physiology and I came across a fascinating article discussing how difficult it is to teach the mechanics of breathing by John West himself. It includes the diagram I was looking for (fig 7) and also a little appendix on the requisite physics – bonus! It also has a discussion about dynamic compression of the airways (one of my pet topics)

BT_PO 1.13 Describe the elastic properties of the chest wall and plot pressure-volume relationships of the lung, chest wall and the total respiratory system

At FRC, the forces promoting chest wall expansion and those promoting lung collapse are in equilibrium T/F

Chest wall compliance is calculated by measuring the difference between intrapleural and alveolar pressure under conditions of respiratory muscle relaxation T/F

At high lung volumes, the chest wall has a tendency to collapse inwards rather than spring outwards T/F

A normally compliant chest wall is important for respiratory function T/F

With a large pneumothorax, the lung collapses and the thoracic cage expandsT/F

Something to think about. In the context of this topic, why does a flail segment caused by multiple fractured ribs compromise ventilation (apart from the fact is it very painful!)?

BT_PO 1.6 Discuss the structure of the chest wall and diaphragm and the implications for respiratory mechanics

Another picture from the Albertina, this one by Chagall. Reminds me of Notting Hill (which is not a bad study avoidance movie actually, if you need an excuse for a laugh and a few tears)

Well wasn’t yesterday a lucky day – thanks to a total brain fade on my behalf, there were two posts on the one day! I hope that you enjoyed them both.

This one sort of follows on from my post from yesterday, at least staying in the realm of the respiratory system. I am taking the chest wall to include the intercostal muscles because allows a bit more scope for statements.

I think you should know the answer to all of these. Answers in West Respiratory Physiology (at least my VERY old copy circa 1995 – I can’t imagine this is the sort of information which changes on a yearly basis) and Nunn’s Applied Respiratory Physiology.

BT_PO 1.6 Discuss the structure of the chest wall and diaphragm and the implications for respiratory mechanics

In normal people, the thoracic cage is an elastic body T/F

At FRC the intrapleural pressure is negative partly because the chest wall wants to spring outwards T/F

At high lung volumes (>75% TLC), the tendency for the chest wall to spring outwards disappears T/F

During inspiration, the ribs move upwards and forwards due to the effect of the external intercostal muscles T/F

During quiet expiration, the internal intercostals contract to draw the ribs back to a resting position T/F

The diaphragm has the capacity for an excursion of up to 10cm during forced respiration T/F

Contraction of the diaphragm results in an increase in the vertical dimension of the chest cavity only T/F

IV Fluids

T/F the lactate in Hartmann’s can worsen a lactic acidosis

T/F Hartmann’s is contraindicated in patients with diabetes

T/F 5% glucose is used to provide IV water without causing haemolysis

T/F the rationale of 4% and a fifth is to meet the normal daily requirement of sodium

T/F 4% and a fifth can cause hyponatrarmia in unwell patients

Discussion point – it is common practise in neuroanaesthesia to use 0.9% saline instead of Hartmann’s – can you think of a rationale for this? Is it routinely necessary?

BT_GS 1.60 Describe the physiological effects of anaesthesia on the respiratory system

“Arrival of the Flower” by Wolfgang Hutter, viewed at the lovely Albertina Museum, Vienna (if anyone is heading to Euroanaesthesia this year, I would recommend a visit)

I wonder if this is another LO which appears elsewhere under another name. I find it hard to believe it has not already been covered, although my quick search cannot find another post on this area.

Clearly quite important to know this area in detail! I have added a few extra statements for you to sink your teeth into, because there is so much to consider.

The answer to all of the statements below can be found in Nunn’s Applied Respiratory Physiology which has an excellent chapter on the respiratory effects of anaesthesia.

BT_GS 1.60 Describe the physiological effects of anaesthesia on the respiratory system

FRC reduces upon induction of anaesthesia T/F

The reduction in FRC with anaesthesia is greater if the patient is paralysed rather than unparalysed T/F

The ventilatory response to hypoxia is attenuated by 0.2 MAC of volatile anaesthetic T/F

The ventilatory response to hypoxia is maintained during a propofol based anaesthetic T/F

The ventilatory response to hypercarbia is attenuated at lower levels of volatile anaesthesia compared to the hypoxic response T/F

Lung compliance is increased during anaesthesia T/F

Both shunt and dead space increase in anaesthetised patients T/F

All potent volatile anaesthetics (so excluding N2O) are bronchodilators, resulting in lower airways resistance in anaesthetised compared with awake supine patients T/F (this one requires a little bit more thought – the first part of the statement is true. See if you can work the second part out from first principles before looking up the answer)