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 Q12 – physiological control of blood glucose

This topic is considered important because we routinely fast patients for surgery, and because diabetes now affects 5% of the Australian population.

T/F Insulin levels rise with fasting

T/F Insulin is required for brain cells to utilise glucose

T/F Glucagon reduces blood ketone levels

T/F Insulin release increases glycogen synthesis in the skeletal muscle

T/F Fasting for more than 18 hours causes the blood glucose level to fall to 2.0-2.5 mmol/L

The answers to these questions can be found in Ganong.

2018.2 SAQ Q9 – Autonomic innervation of the heart

This question covers some fundamental material which is built upon in other physiology, pharmacology and anatomy topics.

A de-innervated transplanted heart has an intrinsic rate of 20 bpm TRUE/FALSE

Sympathetic innervation is responsible for sinus arrhythmia   TRUE/FALSE

A right sided sympathetic block will cause negative chronotropy   TRUE/FALSE

A right sided vagal block will cause negative chronotropy   TRUE/FALSE

At rest, parasympathetic tone predominates   TRUE/FALSE

 

 

 

 

2018.2 SAQ 8 – functions of the kidneys

Briefly outline the functions of the kidneys.

The “renal and fluids/electrolytes” group of LO’s are BT_PO 1.61 to BT_PO 1.82. Quite a few of these are applicable to this SAQ.

The following are random facts about the kidneys – they are not an attempt to suggest a structure or outline for answering the SAQ.

 

T / F  in the absence of ADH, 20% of the glomerular filtrate would remain in the collecting ducts, producing a urine output of 30 L/day

T / F  erythropoietin is synthesised in the kidneys – this is the only endogenous source in the human body

T / F  some drug metabolism occurs in the kidneys, but this is limited to CYP450 enzymes only

T / F  the kidneys are important for long term regulation of blood pressure, via regulating sodium and water balance

T / F  during a metabolic acidosis, increased hydrogen ion excretion by the kidneys occurs mainly as ammonium

T / F  in response to hypotension, renin is released from the macula densa

T / F  the kidneys are capable of gluconeogenesis

T / F  aldosterone provides the main control over renal potassium excretion

References:
1. Kam & Power 3rd edition, Chapter 7
2. Vander 8th edition (use this book to supplement Kam & Power as needed to enhance understanding)

 

2018.2 SAQ 6 – massive transfusion

**You are in luck today; a bit of miscommunication resulted in two posts being written for this SAQ. They include different statements, so I thought you may as well enjoy them both. Have fun!!**

Outline the adverse effects that could occur following the rapid transfusion for ten (10) units of packed red cells.

It is not uncommon for us to have to give a massive transfusion. There are significant physiological consequences of this practice, in addition to the usual risks of red cell transfusion.

There is a lot you could write on this topic. It is covered comprehensively in Miller’s Anesthesia Ch 61 Patient blood management: transfusion therapy. This article from BJA Education has a lot of information not required to answer the question, but does have a good section of complication of massive transfusion.

BT_RT 1.9   Describe physiological consequences of massive transfusion

BT_PO 1.116  Outline the composition, indications and risks of use of  blood components and products including packed red cells

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

Hypothermia caused by the rapid infusion of cold blood may worsen any coagulopathy T/F

Provided haemoglobin is returned to normal levels, oxygenation at the tissue level  is unlikely to be compromised by a massive transfusion T/F

Immediate immune reactions to packed red cells include anaphylaxis T/F

Most people with normal liver function can metabolise the citrate in packed red cells, so citrate toxicity is uncommon T/F

Citrate binds calcium and thus citrate toxicity manifests with the signs of hypocalcaemia T/F

Metabolism of citrate produces bicarbonate and thus may induce a metabolic alkalosis T/F

Transfusion related lung injury (TRALI) may be minimised by only using packed cells from female donors T/F

TRALI is an acute reaction seen within the first hour or two of transfusion T/F

2018.2 SAQ 6 – massive red cell transfusion

Outline the adverse effects which could occur following the rapid transfusion of ten (10) units of packed red cells.

BT_PO 1.116  Outline the composition, indications, and risks of use of the following blood components and products …. packed red cells ….
BT_RT 1.9  Describe physiological consequences of massive transfusion

As anaesthetists, it is our responsibility to direct the volume resuscitation of patients with major haemorrhage. Doing this well requires a sound knowledge of physiology in a number of areas, including the consequences of ‘massive transfusion’.

In response to a number of adverse outcomes related to blood transfusions, an excellent e-learning resource is now available. In addition, Miller 8th edition Chapter 61 (Patient Blood Management – Transfusion Therapy), and Oh 7th edition Chapter 95 (Blood Transfusion) will provide all the basic science background needed to answer this SAQ. The Australian Red Cross website also has excellent information.

In answering this SAQ, you need to consider both (i) the complications of any PRC transfusion, and (ii) the complications of rapidly giving 10 units.

T / F  one definition of a “massive” transfusion is replacing the whole blood volume in 24 hours

T / F  using O negative packed cells will avoid the risk of any haemolytic transfusion reactions

T / F  the risk of transfusion-related acute lung injury (TRALI) correlates with the number of units of PRC given

T / F  one unit of PRC contains about 10% of the normal amount of platelets, and 50% of the normal amount of clotting factors

T / F  massive PRC transfusion can cause hyperkalaemia and hypercalcaemia

T / F  blood is stored at 4 degrees C, so rapid transfusion will cause hypothermia unless the blood is warmed

T / F  transfused red cells have a left shifted OHC causing impaired oxygen offloading due to depleted 2,3 DPG – it can take 24 hours for this to be corrected

T / F the risk of HIV transmission via a transfusion is estimated at less than 1 in 1 million in Australia

This is a good opportunity to remind yourself of the MTP in your hospital. How do you contact blood bank, and how do you activate the MTP? Are there wall charts in your OR’s reminding you of critical ratios of different blood products? Where do you get ‘Level 1’ pressure infusers and blood warmers? Have you observed a massive transfusion – what went well, and what didn’t?

2018.2 SAQ 5 – maternal CVS changes in pregnancy

SS_OB 1.1  Describe the physiological changes and their implications for anaesthesia that occur during pregnancy, labour and delivery, in particular the respiratory, cardiovascular, haematological and gastrointestinal changes
SS_OB 1.5  Describe the mechanism and consequences of aorto-caval compression in pregnancy

Answers to the following statements can be found in Kam & Power, and Miller.

T / F  there is no appreciable increase in HR during the first trimester

T / F  at term, the HR increases by at least 15%, and CO by about 50%

T / F  at term, utero-placental blood flow is about 750 mL/min – this increases the maternal SVR

T / F  maternal red cell volume increases by 20% at term – this increases maternal haemoglobin by a similar value

T / F  the risk of aortocaval compression is present from about 30 weeks gestation onwards

T / F  maternal CO and BP return to normal by about 2 weeks post delivery

2018.2 SAQ 2 – oxygen transport

Discuss the factors that affect oxygen transport from the alveoli to the tissues

No prizes for guessing why this is an important topic…

I have previously posted on the oxygen cascade and included a reference at that post which you may like to refer to. This topic is well covered in both of the respiratory physiology textbooks on the reading list.

BT_PO 1.23 Oxygen cascade

BT_PO1.24 Describe the alveolar exchange of oxygen and carbon dioxide

BT_PO 1.25 Discuss diffusion capacity and its measurement

BT_PO 1.31 Discuss the carriage of oxygen in blood, etc.

The first 4 of these are reasonably easy, as are the ones in my other post on this topic.

There is a linear relationship between PaO2 and oxygen content of arterial blood T/F

It is normal for the A-a gradient of oxygen to increase with increasing age T/F

Breathing a hypoxic mixture will generally result in hyperventilation, in an attempt to return alveolar oxygen levels to normal T/F

A patient breathing room air with a Hb of 15g/dL will have the same oxygen carrying capacity as a patient with a Hb of 10g/dL breathing 100% O2 T/F

A person with an oxygen consumption of 200ml/min, breathing room air, will require an alveolar ventilation rate of at least 1L/min to prevent alveolar PO2 reaching zero T/F        (the answer to this one can be found in a very interesting graph in Nunn’s Chapter on Oxygen)

BT_PO 1.10 Describe the properties of surfactant and its role in respiratory mechanics

Sunset last night, Hamilton Island

This is the LO number that the work of breathing post from yesterday was given by mistake, so surfactant fell through the gaps…

I am sure you would find the answers to these in either West or Nunn’s (Lumb) books. I used Nunn because I am still on holidays.

BT_PO 1.10 Surfactant properties and role in respiratory mechanics
Surface tension in the alveoli is reduced by the presence of surfactant T/F

Surfactant ensures that surface tension is equal throughout the lung T/F

Surfactant release is stimulated by high volume lung inflation T/F

Surfactant plays a role in keeping the alveoli free from transudate T/F

Surfactant has an important immunological function in the lung T/F

Why is surfactant important in preventing collapse of small alveoli? Which physical law determines pressure within a sphere? If you do a little mathematical equation looking an pressure within an alveolus with a 0.1mm sphere and one with a 0.2mm sphere assuming equal surface tension, you will be able to work out the answer to the second statement.

Again my best wishes for those of you with vivas today