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 1.92 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

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

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)

BT_PM 1.12 Describe opioid receptors

I don’t have any nice new poppy photos, so we will go with a water lilly instead

I think this is another LO where you what you learn should be directed towards how it affects function rather than just memorising in detail the intricacies of the receptor itself.

The top 4 statements are core. The last one is the most interesting (I’ll try to find a good concise article on it for those who are interested and will update the post when I have). You will find the answers to the rest in, you guessed it, Hemmings and Egan 2e. There is also a nice summary article in BJA Education here.

BT_PM 1.12 Describe opioid receptors

Opioid receptors are G-protein coupled receptors  T/F

Opioid receptors are found only on post synaptic cell membranes T/F

Activation of opioid receptors increases potassium conductance and  causing membrane hyperpolarisaton T/F

All opioid receptor subgroups have their own endogenous ligand, with B endorphin the ligand for the mu opioid receptor T/F

Opioid receptors are subject to significant genetic polymorphism which effects nociception and analgesia T/F

BT_PO 1.117 Describe the changes that occur during blood storage and their clinical implications

T/F  during storage of a unit of packed cells, the potassium concentration progressively rises – it can reach 30 mmol/L at 28 days

T/F  during storage of a unit of packed cells, the 2,3-DPG concentration falls to almost zero, within 24 hours

T/F  as storage time increases, some red cells become spherical and rigid – 10-20% of these may be destroyed within 24 hours if transfused at the maximum storage time

T/F  during storage of a unit of packed cells, the calcium concentration progressively falls – it can reach 0.1 mmol/L at 28 days

T/F  to extend the storage time of packed cells (e.g. for use in remote areas), they can be frozen

T/F  once thawed, a unit of fresh frozen plasma (FFP) must be used within 24 hours

References

  1. Kam and Power 3rd edition, page 291-292
  2. Red Cross Transfusion Service website

BT_PO 1.86 Describe the role of the hypothalamus in the integration of neuro-humoral responses

T/F   osmoreceptors are located in the hypothalamus – when osmolality increass, ADH is released from the posterior pituitary

T/F   the hypothalamus can suppress appetite via the satiety centre, by sensing blood glucose levels

T/F    the posterior hypothalamus contributes to the control of the sympathetic nervous system

T/F   the hypothalamus integrates body temperature regulation – responses to a fall in body temperature are triggered by the anterior hypothalamus

T/F  fever occurs when pyrogenic cytokines alter the “set point” of the hypothalamus to higher than 37 degrees

T/F  the hypothalamus secretes thyroid stimulating hormone (TSH) which stimulates T3 and T4 release from the thyroid gland

References

  1. Kam & Power 3rd edition, page 66-67
  2. Ganong 24th edition, chapter 17

Preventing Hypoxia

IT_AM 1.9 Describe preoxygenation, including its physiological basis
BT_RT 1.10 Describe the causes of hypoxaemia

Some of you may have read this article Bag-Mask Ventilation during Tracheal Intubation of Critically Ill Adults, published in NEJM in Feb 2019.

Was this trial ever really necessary?

T / F the FRC of patients with pneumonia / pleural effusions / pulmonary oedema is greatly reduced (and will be below closing capacity)

T / F the FRC of obese patients is greatly reduced (and will be below closing capacity)

T / F inducing anaesthesia further reduces FRC

T / F the FRC is the only oxygen store in the body that can be meaningfully increased

T / F the rate of oxygen consumption in very sick patients is increased

T / F ventilation with a bag and mask prevents the oxygen store in the FRC becoming depleted (!)

T / F if the FRC is small, the oxygen consumption is high, and the patient is left apnoeic, hypoxaemia will ensue very quickly

What is your stance on the dogma of “no mask ventilation” during an RSI or emergency intubation? What do the difficult airway societies now say about it?

BT_PO 1.15 Explain the physics of gas flow and the significance of the relationship between resistance and flow in the respiratory tract



A multi-branched thing of beauty

Wow! That is a long winded LO. There is another LO on factors affecting airway resistance (the post in that link is one of our very first!), so I think in this post we will focus on something else.

The answers to these questions can again be found in either West Respiratory Physiology or Nunn’s Applied Respiratory Physiology.

BT_PO 1.15 Explain the physics of gas flow and the significance of the relationship between resistance and flow in the respiratory tract

Breathing a helium-oxygen mixture may helpful in patients with large airway obstruction as it reduces the risk of turbulent flow T/F

The likelihood of turbulent flow in the trachea is increased as peak flow rates increase ( for example with intense exercise) T/F

True laminar flow does not occur within the respiratory system T/F

A multi-branched system, such as the respiratory tree provides unfavourable conditions for laminar flow T/F

Turbulent flow is more effective for purging a system than laminar flow T/F

During laminar flow gas as the centre of the tube moves approximately twice as fast as the edges T/F

Have a think about apnoeic oxygenation. How does it work? What physical principles are at work and how will the gas be flowing?