BT_PO 1.47 Discuss the control of blood pressure and the distribution of blood volume and flow throughout the cardiovascular system including ….

BT_PO 1.47 Discuss the control of blood pressure and the distribution of blood volume and flow throughout the cardiovascular system including: 
– the factors determining systemic blood pressure and its regulation and control
– total peripheral resistance and factors affecting it 
– the relationship between organ blood flow and demand and the role of autoregulation 
– clinically significant features of the coronary, cerebral, skin, muscle, renal, hepatic and splanchnic circulations
– the essential features of the microcirculation including fluid exchange and its control

T/F autoregulation of blood flow requires neural input from the autonomic nervous system

T/F pressure (myogenic) autoregulation maintains constant flow despite changes in blood pressure, by altering arterial diameter

T/F metabolic autoregulation alters organ blood flow independently of pressure autoregulation

T/F coronary blood flow fluctuates throughout each cardiac cycle – therefore, it does not demonstrate pressure autoregulation

T/F skeletal muscle blood flow has neither pressure or metabolic autoregulation – it is entirely controlled by the sympathetic nervous system

T/F blood flow to the placenta is not autoregulated

T/F within the kidneys, tubuloglomerular feedback is an additional mechanism which autoregulates blood flow

T/F increased blood flow to the GIT after a meal is an example of metabolic autoregulation

BT_PO 1.47 Discuss the control of blood pressure and the distribution of blood volume and flow throughout the cardiovascular system including ….

BT_PO 1.47 Discuss the control of blood pressure and the distribution of blood volume and flow throughout the cardiovascular system including:
– the factors determining systemic blood pressure and its regulation and control
– total peripheral resistance and factors affecting it
– the relationship between organ blood flow and demand and the role of autoregulation
– clinically significant features of the coronary, cerebral, skin, muscle, renal, hepatic and splanchnic circulations
– the essential features of the microcirculation including fluid exchange and its control

T/F 30% of the blood volume is in the systemic veins

T/F mean arterial pressure is mainly determined by the volume within the systemic arteries

T/F pulse pressure is mainly determined by the stroke volume, and arterial compliance

T/F cardiac output is not directly sensed within the body – it is mainly determined by local tissue autoregulation

T/F adding a placenta to the circulation will increase systemic vascular res

T/F venodilation will decrease the resistance to venous return, and thereby cause an increase in venous return **

Reference – Guyton

** Simple application of Ohm’s law is a bit confusing for the venous side of the circulation. The above statement is false (e.g. we know that VR decreases after a spinal due to venous pooling of blood) – yet this seems to contradict Ohm’s law. To explain the effect of venous tone on VR we need to use the terms “stressed” and “unstressed” volume. I would highly recommend reading the following article – it also helps untangle the Guyton’s curves.

Funk D etal. The role of venous return in critical illness and shock – Part 1: Physiology. Crit Care Med, 2013; 41: 255-262.

Can you think of any circumstances which would increase RVR to the extent of decreasing VR?

BT_PO 1.47 Discuss the control of blood pressure anyway d the distribution of blood volume and flow throughout the cardiovascular system including ….

BT_PO 1.47 Discuss the control of blood pressure and the distribution of blood volume and flow throughout the cardiovascular system including:
– the factors determining systemic blood pressure and its regulation and control
– total peripheral resistance and factors affecting it
– the relationship between organ blood flow and demand and the role of autoregulation
– clinically significant features of the coronary, cerebral, skin, muscle, renal, hepatic and splanchnic circulations
– the essential features of the microcirculation including fluid exchange and its control

Wow!! This single LO encompasses about half of CVS physiology. This week, I will do 4 posts on this LO.

T/F high pressure baroreceptors are located in the carotid and aortic bodies

T/F the rate of firing of baroreceptors increases as blood pressure increases

T/F efferent signals from the carotid baroreceptors are transmitted via the glossopharyngeal nerves

T/F low pressure baroreceptors only respond to distension of the atria (i.e. an increase in blood volume)

T/F with chronic hypertension the baroreceptor response curve becomes right shifted

T/F in zero gravity the baroreceptors cease to function

Study tip – avoid getting too much of a good thing…

In case you were wondering what too much of a good thing looks like (turning 15 on Monday!)

I recently attended a workshop where the effects of stress on performance were discussed.

Some of you may be familiar with the Yerkes-Dodson law (I had not realised this phenomenon was named…) which is demonstrated graphically below.

Most of the time, only the bottom curve is drawn, which shows that some stress (arousal) improves performance, but at a certain point it becomes detrimental. For specific, short and simple tasks the drop in function is not observed, but studying for and sitting the exam are not such tasks.

The nature of specialist medical training (let alone other life factors that often coincide with this time of life), means that many registrars are operating near the peak, or perhaps just over the top of the curve on a daily basis. This is the optimal part of the curve to be functioning on, so where is the problem?

The problem arises when something happens – the exam (or in the case of the rats involved in the experiments, an increased intensity of electric shock 😬) – which increases stress levels acutely and you suddenly find yourself on the steep descent. On this part of the curve, problem solving ability, memory and attention all suffer.

You do not want to find yourself on the descending part of the curve on the day of the exam, but rather at the peak.

So what can you do to give yourself the best chance of hitting the peak of the curve at the right time? It is completely reasonable to expect that stress levels will rise on the day of the exam, so the key is to get yourself onto the left side of the curve in the lead up to the examination day.

There are several things which are easy to do, inexpensive, and not too time consuming which are known to reduce stress levels:

  • Take a break – those of you who are regulars here, know that I need little encouragement for a bit of time out. Give yourself permission to do something you enjoy
  • Exercise
  • Meditate
  • Smile – perhaps watch some of those funny cat videos which seem to be so popular on YouTube (I tried to find a good one but failed – please leave a link in the comments if you have seen one which made you smile)
  • Talk to someone – make time for a coffee, dinner, phone call with a friend or relative. You will be doing yourself and them a great deal of good.

Sometimes some specialist help may be needed to give you some extra strategies to help you actively decrease your stress levels.

You want to be at your best on the day of the exam, so if you haven’t done so before, now is the time to make changes to ensure that you don’t end up with too much of a good thing…

MCQ Preparation

Candidates often ask me how they should go about preparing for the MCQ section of the exam.

No doubt you are aware of various online repositories of remembered questions. These can be used to assist you – provided you are not trying to remember questions verbatim. The best approach is to read around the main fact or concept the question is addressing.

There are several published books of MCQs, all available as eBooks via the ANZCA library website, so you don’t need to buy any. To access all of the following books, I put “primary FRCA” in the search box.

  1. Nickells J. SBA and MTF MCQs for the primary FRCA.
  2. Rangarajan D. Get through primary FRCA: SBAs.
  3. Bahal N. Get through primary FRCA: MTFs.
  4. Elfituri K. MCQs for the primary FRCA.
  5. Ebrahim H. 1000 practise MTF MCQs for the primary and final FRCA.

All of the above books were written for UK (FRCA) exam. Although the curriculum for the UK primary is extremely similar to ours, there are some differences – check Appendix 2 of the curriculum if in doubt. Also, we do not use MTF (multi true/false) questions in the ANZCA exams. We only use SBA (single best answer). Even so, MTFs can be of much assistance to you with knowledge recall.

Some textbooks have good MCQs at the end of each chapter. One example is Ganong’s Medical Physiology.

The Primer for the Primary is an extremely useful document, which contains T/F statements, organised by topic. It also directs you to the references for each topic which the author found most useful.

And last, but by no means least, there is this blog – Primary LO of the Day.

Regular use of MCQs from a range of sources is a great way of revising, by actually testing your knowledge and understanding. Just don’t expect there to be a word-for-word reproduction of your practise MCQs, on the exam.

BT_PM 1.5 Describe the injury response to acute pain

Townsville again

Another languishing LO. My feelings about this were “Ugh” and I wasn’t going to touch it either until I was looking through Acute Pain Management:Scientific Evidence, for another reason, and saw that there was a figure with that exact title – yippee!!

All statements relate to the figure (Fig 1.2 pg 26) and the surrounding text

Pain results in an decrease in activity of the parasympathetic nervous system T/F

Increased insulin sensitivity occurs in response to pain T/F

Cortisol levels are elevated by pain T/F

Activation of nociceptors results in changes in gene coding and protein synthesis T/F

In the post-operative setting it can be hard to separate the effects due to tissue damage from those caused by pain T/F

BT_PM 1.23 Describe the prostaglandin pathways and their physiological role in the production of pain

Townsville

There have been quite a few of posts on topics related to this one, but generally looking at how blockade of the PG pathway causes analgesia (ie. the effects of NSAIDs). I marked an SAQ on the effect of NSAIDs a couple of years ago. Candidates were much better at describing how these drugs produced their adverse effects rather than their beneficial ones.

So, how is it that prostaglandin production results in the experience of pain? Let’s investigate.

Although it is a pharmacology textbook, Katzung’s Basic and Clinical Pharmacology has an excellent chapter on prostaglandins (Ch 18). All of these statements are taken from that chapter. For those of you without access to the textbook, the beginning of this article has a good summary of how prostaglandins can produce pain.

BT_PM 1.23 Describe the prostaglandin pathways and their physiological role in the production of pain

COX 1 isoenzyme has a greater role to play in pain production compared with the COX isoenzyme T/F

Tissue damage releases cytokines which induce the COX-2 enzyme T/F

Arachidonic acid (the precursor of all prostaglandins) is induced by tissue damage T/F

PGE2 is involved in the sensitisation of peripheral nerve endings to painful stimuli, by reducing the threshold for neural transmission T/F

PGE2 has a role at the level of the dorsal horn to promote central sensitisation T/F

Hyperaemia in damaged tissues results from increased vascular permeability mediated by prostacyclin T/F

Hyperaemia enables increased delivery of inflammatory mediators to the area of tissue damage, resulting in further prostaglandin release T/F

BT_GS 1.37 Describe the pharmacological differences between neuromuscular blocking agents and the clinical importance of these differences.

Street art Mile End, Montreal

This is another of the neglected LOs although there have been several posts on muscle relaxants previously which you will find links to from here. (**UPDATE – the links are now as up to date as I can make them)

When next in theatre and the consultant you are working with asks you why you chose to use a certain muscle relaxant, please use today’s statements to help you think of a better answer than, “It is the one I am most familiar with” 😉.

Hemmings and Egan and Miller are both good sources for this topic.

BT_GS 1.37 Describe the pharmacological differences between neuromuscular blocking agents and the clinical importance of these differences.

Rocuronium is less potent that vecuronium, which is why it works so much faster when given at 4X ED95 T/F

Sugammadex is equally effective at reversing both rocuronuim and vercuronium T/F

At equipotent doses, the duration of atracurium and cistratrcurium are similar T/F

The majority of rocuronium is metabolised in the liver, making its action markedly prolonged in patients with liver disease T/F

Histamine release is a more common side effect with vecuronium compared with atracurium T/F

Atracurium and suxamethonium both undergo organ independent elimination T/F

Dissimilar chemical structures mean than anaphylaxis to both rocuronium and suxamethonium is rare T/F

BT_PO 1.43 Electrolytes and arrhythmias

Today’s winter picture from the rain forest at Paluma, Far North Queensland.

Earlier in the week, posts on the SRAP and FRAP made you think about the importance of different ion fluxes in generating the cardiac action potential. Yesterday you were asked to consider how the action potential affects the ECG. Today we will consider how different electrolyte disturbances may produce arrhythmias.

Whilst I think that it important that you have an appreciation of why various electrolyte disturbances affect the cardiac action potential and cause characteristic ECG changes, some of today’s statements a a little more esoteric, but hopefully interesting than the ones from earlier in the week.

I have used Ganong’s Review of Medical Physiology Ch29 and and Henmings and Egan’s book Ch 42 for these statements. Here is a BJA education article which looks at some important cations in this area.

BT_PO 1.43 Discuss the physiological basis of electrical activity and its relationship to mechanical events including the physiological basis of the electrocardiograph in normal and common pathological states and factors that may influence cardiac electrical activity

Hyperkalaemia is associated with peaked T waves. This could be explained by a larger gradient for inward flux of potassium into the cell during repolarisation T/F

Low potassium levels, may result in a more negative resting membrane potential, making normal initiation of both fast and slow action potentials more difficult T/F

With severe hyperkalaemia, the cardiac membrane becomes un-excitable the heart arrests in diastole T/F

Severe hypocalcaemia will reduce the ability of the heart to generate SRAPs, as calcium is essential for phase 0 T/F

Hypocalcaemia prolongs the ST segment as the FRAP plateau is lengthened T/F

Lengthening of the cardiac action potential plateau will tend to prolong the QT interval T/F

Sodium channel blockade by local anesthetists will have more effect on the FRAP than SRAP (I know this isn’t actually an electrolyte abnormality) T/F