Acute Medicine

Oliver Hart

Welcome to the Acute Medicine podcast. This episode recaps the most important aspects of each topic, so that you can feel confident in your knowledge.

Alys Davies

We've split the episode into two parts. First, we'll go through a breakdown of each topic. Then we'll move into our rapid-recall round, where we test your knowledge on everything we've covered.

Oliver Hart

There are six Acute Medicine topics in this episode, with tips and reminders dotted throughout.

Alys Davies

If you're using this podcast to revise for upcoming exams, please check the official exam websites for specifics on question weighting and structure. Throughout this episode, we'll explain each topic through realistic clinical scenarios and presentations. This helps you link up your knowledge within each topic, and it reflects the kinds of scenarios you're likely to meet in exams.

Oliver Hart

So, let's get started.

Alys Davies

Our first topic is cardiac arrest, and we'll start with the two categories of rhythm. The moment you confirm a cardiac arrest and attach a monitor, you need to answer one question: is this rhythm shockable or not?

Oliver Hart

The shockable rhythms are ventricular fibrillation and pulseless ventricular tachycardia, known as VF and pVT. The non-shockable rhythms are pulseless electrical activity, or PEA, and asystole.

Alys Davies

This distinction matters because shockable rhythms need defibrillation straight away, without delay. Non-shockable rhythms do not respond to a shock, so there is no benefit in trying.

Oliver Hart

For shockable rhythms, the ALS algorithm repeats a 2-minute cycle. You deliver a shock, give 2 minutes of CPR, and then check the rhythm again. You only repeat the cycle if the rhythm is still shockable.

Alys Davies

If return of spontaneous circulation has not been achieved after the third shock, you give adrenaline and amiodarone together, at the same time.

Oliver Hart

For non-shockable rhythms, the approach is different. You start CPR, gain IV access, and give adrenaline as soon as that access is in. There is no need to wait for three cycles. Adrenaline is given early and then repeated every 3 to 5 minutes throughout the resuscitation.

Alys Davies

Amiodarone, however, is not given in non-shockable rhythms. It is an antiarrhythmic, so it has no role when the problem isn't a shockable arrhythmia.

Oliver Hart

Next, let's look at CPR quality. Good-quality CPR means 100 to 120 compressions per minute at a depth of 5 to 6 cm, with full chest recoil between compressions and minimal interruptions.

Alys Davies

When CPR is done well, it generates around 25 to 30% of normal cardiac output. That is enough to sustain coronary and cerebral perfusion while you work on reversing the underlying cause.

Oliver Hart

This brings us to the reversible causes, known as the 4Hs and 4Ts. The four Hs are hypoxia, hypovolaemia, hypo- or hyperkalaemia, and hypothermia. The four Ts are tension pneumothorax, tamponade, thrombosis (which includes PE and coronary thrombosis) and toxins.

Alys Davies

You should actively look for these causes throughout the resuscitation, because if the underlying cause isn't found and fixed, you won't achieve sustained return of spontaneous circulation.

Oliver Hart

Now let's look at the drugs in a bit more detail, starting with adrenaline. Adrenaline acts on alpha-1 adrenoceptors to cause vasoconstriction. This increases coronary perfusion pressure, which is what makes it useful in cardiac arrest. However, there is an important caveat from the evidence.

Alys Davies

The PARAMEDIC2 trial showed that adrenaline improves your chances of achieving return of spontaneous circulation, but it did not improve neurologically intact survival. In other words, more patients survived to hospital, but not necessarily with good neurological outcomes.

Oliver Hart

This is an important nuance for exams: adrenaline improves ROSC, but it does not clearly improve neurological outcomes. It remains in the algorithm, even though the evidence isn't as clear-cut as we'd like.

Alys Davies

Amiodarone is a class 3 antiarrhythmic. It works by blocking potassium channels, which prolongs the action potential and raises the threshold for ventricular fibrillation. If amiodarone isn't available, the alternative is lidocaine 100 mg.

Oliver Hart

Two drugs are no longer part of the ALS algorithm: atropine and sodium bicarbonate. Atropine was removed because there is no evidence that it benefits patients in asystole or PEA. Sodium bicarbonate is not given routinely; instead, it's reserved for specific situations, such as cardiac arrest caused by hyperkalaemia or tricyclic antidepressant toxicity.

Alys Davies

Once you achieve return of spontaneous circulation, the work doesn't stop. Post-ROSC care is an important topic in its own right.

Oliver Hart

For years, standard practice was targeted temperature management, keeping the patient at 32 to 36°C for 24 hours. However, the TTM2 trial in 2021 compared cooling to 33°C with normothermia and found no significant difference in outcomes. The current approach, therefore, is to avoid hyperthermia, as the evidence for active cooling to 33°C is now less compelling.

Alys Davies

The blood glucose target post-ROSC is 6 to 10 mmol/L. Critically, ST elevation on the post-ROSC ECG means emergent PCI, regardless of the patient's GCS. You do not wait for the patient to wake up.

Oliver Hart

Remember. In shockable rhythms, adrenaline is withheld until after the third failed shock, and then given together with amiodarone. In non-shockable rhythms, adrenaline is given as soon as IV access is obtained.

Alys Davies

Our second topic is shock. Exams may test whether you can distinguish between four very different types of shock that look similar on the surface. In each case, the patient is hypotensive, tachycardic and poorly perfused, but the underlying mechanism is different, and that mechanism determines the correct treatment.

Oliver Hart

Let's start with the definition. Shock is inadequate delivery of oxygen to the tissues relative to their metabolic demand. In haemodynamic terms, MAP equals cardiac output multiplied by systemic vascular resistance, so shock happens when one or more of those components fails.

Alys Davies

There are four types of shock. The first is cardiogenic shock, where the pump fails. Cardiac output is low, and systemic vascular resistance is high as the body tries to compensate. Pulmonary capillary wedge pressure is raised because blood backs up behind the failing ventricle.

Oliver Hart

The second is distributive shock, where the blood vessels dilate. Systemic vascular resistance is low, while cardiac output is initially high because the heart is working harder to compensate. The classic example is septic shock, but anaphylaxis and neurogenic shock also fit into this category.

Alys Davies

The third is hypovolaemic shock, where there isn't enough fluid in the circulation. Cardiac output is low, SVR is high, and wedge pressure is low because the tank is empty. The main causes are blood loss, burns, and severe vomiting and diarrhoea.

Oliver Hart

The fourth is obstructive shock, where a mechanical block prevents adequate cardiac output. The heart and the circulating volume might both be normal, but something is physically obstructing flow. The main causes are massive PE, cardiac tamponade and tension pneumothorax.

Alys Davies

You can use the mnemonic RSVP to remember the haemodynamic profiles: Rate, SVR, Volume, and Pump. However, the exact mapping matters less than remembering the four categories and their mechanisms.

Oliver Hart

Cardiogenic shock is caused by acute myocardial infarction in about 80% of cases, and it complicates 5 to 8% of all STEMIs. The vasopressor of choice is noradrenaline, as the SOAP-II trial showed it was superior to dopamine and caused fewer arrhythmias.

Alys Davies

There has also been a lot of interest in mechanical circulatory support. The IABP-SHOCK II trial showed that an intra-aortic balloon pump does not reduce mortality in cardiogenic shock. However, the more recent DanGer Shock trial showed that the Impella device improved 180-day survival, so the landscape is changing.

Oliver Hart

In distributive shock, and septic shock in particular, noradrenaline remains first-line. If the noradrenaline dose keeps escalating and you're still not achieving an adequate MAP, vasopressin can be added as an adjunct in catecholamine-resistant septic shock.

Alys Davies

Hypovolaemic shock is classified using the ATLS system, which grades blood loss into classes 1 through 4. Class 3 represents 30 to 40% blood loss and marks decompensated shock. At this point, the compensatory mechanisms are overwhelmed and the patient deteriorates rapidly.

Oliver Hart

In massive haemorrhage, blood products are given in a 1:1:1 ratio, meaning 1 unit of red cells to 1 unit of fresh frozen plasma to 1 unit of platelets. This balanced approach prevents the coagulopathy that develops when blood is given without clotting factors.

Alys Davies

In obstructive shock, treatment is directed at the obstruction itself. Massive PE is treated with thrombolysis using alteplase 100 mg over 2 hours. Tamponade is treated with pericardiocentesis. Tension pneumothorax needs immediate needle decompression in the second intercostal space, midclavicular line, followed by a chest drain.

Oliver Hart

The key principle in obstructive shock is that fluids and vasopressors are, at best, temporary measures. The only definitive treatment is to relieve the obstruction.

Alys Davies

Remember. Under Sepsis-3, septic shock requires vasopressors to maintain a MAP of at least 65, and a lactate greater than 2 mmol/L despite adequate fluid resuscitation. Mortality exceeds 40%. Both criteria must be present; hypotension alone is not enough.

Oliver Hart

Our next topic is the unconscious patient. This topic is best approached systematically, as exams tend to test how quickly and efficiently you respond to broad clinical scenarios.

Alys Davies

The first tool in that systematic approach is the Glasgow Coma Scale, or GCS. It has three components: eyes, scored 1 to 4; verbal, scored 1 to 5; and motor, scored 1 to 6. This gives a maximum score of 15 and a minimum of 3.

Oliver Hart

A GCS of 8 or below defines coma, and it is the threshold at which you should consider the patient unable to protect their own airway. Importantly, the motor component carries the greatest prognostic weight within the GCS.

Alys Davies

AVPU is a simpler bedside tool, standing for Alert, Voice, Pain, Unresponsive. A patient who responds only to Pain is roughly equivalent to a GCS of 8. AVPU works well as a quick screen, but the GCS gives you more detail.

Oliver Hart

For the differential diagnosis, most people use the mnemonic AEIOU-TIPS. A is for alcohol and toxins. E is for epilepsy, specifically the post-ictal state or non-convulsive status epilepticus. I is for insulin, meaning hypoglycaemia, which is the most immediately correctable cause.

Alys Davies

O is for opiates. U is for uraemia and other metabolic causes, such as electrolyte disturbances and hepatic encephalopathy. T is for trauma, such as a subdural or extradural haematoma. I is for infection, such as meningitis and encephalitis. P is for psychiatric causes, although this is always a diagnosis of exclusion. Finally, S is for stroke and structural lesions.

Oliver Hart

Next, examine the pupils, as they are a key examination finding. Bilaterally fixed and dilated pupils suggest either brainstem herniation or exposure to atropine or tricyclic antidepressants. Bilaterally pinpoint pupils point to opioid toxicity or pontine pathology.

Alys Davies

A unilateral fixed and dilated pupil, however, is a surgical emergency, as it indicates uncal herniation. Here, the uncus of the temporal lobe is compressing the third cranial nerve, and the patient needs neurosurgery.

Oliver Hart

In every unconscious patient, check the blood glucose, because hypoglycaemia is the most reversible cause of coma.

Alys Davies

If the patient has IV access, give 100 ml of 20% dextrose IV, or 200 ml of 10% dextrose IV over 15 minutes. Either formulation is acceptable. Then recheck the glucose after 10 minutes.

Oliver Hart

If there's no IV access, give glucagon 1 mg intramuscularly. There is an important clinical caveat here, though. Glucagon works by stimulating the breakdown of glycogen in the liver. If the patient's glycogen stores are depleted (through malnutrition, alcohol misuse, liver disease, or repeated hypoglycaemic episodes), glucagon will be far less effective, or completely ineffective.

Alys Davies

Whenever you give glucose to a patient with alcohol misuse or malnutrition, you must give IV thiamine first, or at least at the same time, such as Pabrinex 200 mg IV. This prevents you from precipitating Wernicke's encephalopathy.

Oliver Hart

If opioid toxicity is suspected, for example because of pinpoint pupils, respiratory depression or a suggestive history, give naloxone. The dose is 0.4 to 2 mg IV or IM, and you can titrate it up in increments. Remember that naloxone's duration of action may be shorter than the opioid's, so the patient can become re-narcotised once the naloxone wears off.

Alys Davies

When it comes to imaging, a CT head should be performed before a lumbar puncture in most cases. However, the exceptions are important. If you strongly suspect bacterial meningitis and there are no focal neurological signs and no papilloedema, you should give antibiotics before the CT if the scan would cause any delay. In this scenario, antibiotics should never be delayed for imaging.

Oliver Hart

One final point concerns non-convulsive status epilepticus, or NCSE. NCSE can present as unexplained coma without any obvious twitching or jerking. So, if you have an unconscious patient and the cause is unclear, an EEG is essential to exclude it.

Alys Davies

Remember. Glucagon is less effective in patients who are malnourished, those with severe liver disease, and those who have had repeated hypoglycaemic episodes that have depleted their glycogen stores. Always establish IV access and use dextrose wherever possible.

Oliver Hart

Anaphylaxis is our next topic.

Alys Davies

Before we move on to treatment, let's make sure we understand the mechanism. The classic form of anaphylaxis is IgE-mediated. On first exposure to an allergen, IgE antibodies are produced and bind to mast cells. On re-exposure, the allergen cross-links those IgE antibodies, causing the mast cells to degranulate and release histamine, tryptase, leukotrienes and prostaglandins.

Oliver Hart

There is also non-IgE-mediated anaphylaxis, sometimes called an anaphylactoid reaction. In this case, mast cells are activated directly, without IgE involvement. Classic triggers include NSAIDs, opioids and radiocontrast media. Crucially, the management is the same regardless of the mechanism.

Alys Davies

Clinically, 80 to 90% of anaphylactic reactions involve the skin and mucosa, causing urticaria, angioedema, flushing and pruritus. Respiratory involvement causes stridor from laryngeal oedema, as well as bronchospasm. Cardiovascular collapse can also occur. Gastrointestinal symptoms, such as nausea, vomiting and cramping, appear in about 30 to 40% of cases.

Oliver Hart

Now let's move on to treatment, which is IM adrenaline: 0.5 mg of the 1:1000 solution, given into the anterolateral thigh. The thigh is preferred over the deltoid because it has a better blood supply, which gives faster absorption.

Alys Davies

The dose varies by age. Adults receive 0.5 mg, children aged 6 to 12 years receive 0.3 mg, and children under 6 years receive 0.15 mg. If there is no improvement, the dose is repeated after 5 minutes.

Oliver Hart

Adrenaline is the treatment of choice because it acts on every part of the reaction. Its alpha-1 action reverses vasodilation and reduces mucosal oedema, including laryngeal oedema. Its beta-1 action increases cardiac output and heart rate. Its beta-2 action causes bronchodilation and, crucially, also stops mast cells from releasing further mediators.

Alys Davies

There are also second-line treatments. Chlorphenamine 10 mg IV is an H1 antihistamine that helps with the skin symptoms. Hydrocortisone 200 mg IV reduces the risk of a biphasic reaction and helps with prolonged bronchospasm. However, hydrocortisone takes hours to work.

Oliver Hart

Biphasic reactions deserve a special mention. They occur in 5 to 20% of anaphylaxis cases and involve a second wave of symptoms anywhere from 1 to 72 hours after the initial reaction, even after the patient appears to have recovered. This is why a minimum of 6 hours of observation is required.

Alys Davies

Serum tryptase is a useful test to help confirm the diagnosis. It should be measured 1 to 2 hours after symptoms begin, with a baseline sample taken at 24 hours. A peak tryptase more than 11.4 micrograms/L above the baseline level supports a diagnosis of anaphylaxis.

Oliver Hart

Importantly, though, a normal tryptase does not rule out anaphylaxis. In food-induced anaphylaxis in particular, tryptase levels are often not raised, even when the reaction is severe.

Alys Davies

Before discharge, every patient who has had anaphylaxis needs three things. The first is a self-injectable adrenaline device, such as an EpiPen or Jext at 300 micrograms. The second is a written emergency action plan explaining when and how to use it. The third is a referral to an allergy clinic for formal testing and long-term management.

Oliver Hart

Remember. Antihistamines and corticosteroids are second-line treatments. They do not treat cardiovascular collapse or laryngeal oedema, so they must never replace or delay IM adrenaline, which is the only treatment that addresses the life-threatening components of anaphylaxis.

Alys Davies

Our next topic is acid-base.

Oliver Hart

Exams favour a systematic approach to acid-base, so we recommend working through it in this order: pH, carbon dioxide, bicarbonate, and then the anion gap, if indicated.

Alys Davies

To do this, you need to know three normal ranges, as they are the anchor for everything else. Normal pH is 7.35 to 7.45. Normal PaCO2 is 4.7 to 6 kPa. Normal bicarbonate is 22 to 26 mmol/L.

Oliver Hart

There are four primary disorders. In metabolic acidosis, the pH is low and the bicarbonate is low, because the body is either generating excess acid or losing base. In metabolic alkalosis, the pH is high and the bicarbonate is high. In respiratory acidosis, the pH is low and the CO2 is high, because the lungs aren't excreting enough CO2. Finally, in respiratory alkalosis, the pH is high and the CO2 is low, because the patient is hyperventilating.

Alys Davies

If you identify a metabolic acidosis, the next step is always to calculate the anion gap. The anion gap equals sodium minus the sum of chloride and bicarbonate, and the normal range is 8 to 12 mmol/L.

Oliver Hart

An elevated anion gap means there is an unmeasured anion in the blood, which tells you that acid has been added to the system. The causes can be remembered using the mnemonic MUDPILES: Methanol, Uraemia, Diabetic ketoacidosis, Propylene glycol and paracetamol, Isoniazid and iron, Lactic acidosis, Ethylene glycol, and Salicylates.

Alys Davies

A normal anion gap metabolic acidosis is different, because here bicarbonate is being lost or chloride is being retained. The classic causes are diarrhoea (which directly loses bicarbonate), renal tubular acidosis, Addison's disease and acetazolamide.

Oliver Hart

In respiratory acidosis, the underlying problem is hypoventilation, as the lungs are not clearing enough CO2. The body compensates by retaining bicarbonate via the kidneys, but this renal compensation takes hours to days, so an acute respiratory acidosis won't have much compensation yet. The main causes to look out for are COPD, obesity hypoventilation syndrome, neuromuscular disease and opioid toxicity.

Alys Davies

Respiratory alkalosis, on the other hand, is caused by hyperventilation. Here, the body compensates by excreting bicarbonate, again over hours to days. The main causes to look out for are anxiety, pulmonary embolism (which is an important one not to miss), early sepsis, pregnancy and high altitude.

Oliver Hart

To check whether the respiratory compensation for a metabolic acidosis is appropriate, you can use Winter's formula. The expected PaCO2, in mmHg, equals 1.5 multiplied by the bicarbonate, plus 8, plus or minus 2.

Alys Davies

If the measured CO2 is lower than predicted, there is a respiratory alkalosis on top of the metabolic acidosis. If it is higher than predicted, there is a concurrent respiratory acidosis. In this way, the formula tells you whether the lungs are compensating appropriately, or whether there is a mixed disorder.

Oliver Hart

Lactic acidosis deserves a specific mention, because it comes up so often and exams expect you to distinguish between its two types. Type A lactic acidosis is caused by tissue hypoxia, for example from poor perfusion, septic shock or cardiac arrest. Type B is not caused by hypoxia, and its causes include metformin, liver failure and haematological malignancy.

Alys Davies

This distinction matters because the management is completely different. In Type A, the priority is to restore perfusion. In Type B, you need to identify and treat the underlying cause; in metformin-associated lactic acidosis, that means stopping the metformin and considering haemofiltration in severe cases.

Oliver Hart

Remember. In lactic acidosis, Type A is caused by tissue hypoxia, such as sepsis, shock or cardiac arrest. Type B occurs without hypoxia, for example with metformin, liver failure or malignancy. This distinction directly drives management and is a common exam discriminator.

Alys Davies

Our final topic is sepsis, which is one of the most time-critical conditions in acute medicine. The evidence is clear that every hour of delay worsens outcomes. Exams test whether you know the definition, the recognition tools, and what the Sepsis Six involves.

Oliver Hart

Let's start with the definition, because Sepsis-3 changed things significantly and exams test the updated version. Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection.

Alys Davies

The key word there is "dysregulated", because the immune response itself contributes to the organ damage. Septic shock sits at the most severe end of the spectrum. It is defined as sepsis requiring vasopressors to maintain a MAP of at least 65, with a lactate greater than 2 mmol/L, despite adequate fluid resuscitation. Mortality exceeds 40%.

Oliver Hart

Outside the ICU, high-risk patients can be identified quickly using qSOFA, the quick Sequential Organ Failure Assessment. It has three criteria: a respiratory rate of 22 or more, altered mental state, and a systolic blood pressure of 100 or less. A score of 2 or more flags the patient as high risk and should prompt urgent assessment.

Alys Davies

There is an important caveat, however: qSOFA does not replace SOFA for the formal diagnosis of sepsis. Sepsis is defined by an increase in SOFA score of 2 or more from baseline, whereas qSOFA is simply a quick bedside screen.

Oliver Hart

The Sepsis Six is a bundle of interventions that should be delivered within 1 hour of recognition. It is made up of three things to take and three things to give. The three to take are blood cultures (before antibiotics), serum lactate, and urine output monitoring. The three to give are oxygen if saturations are low, IV antibiotics, and IV fluid resuscitation.

Alys Davies

Lactate is a particularly important number. A lactate of 4 or above means the patient is high risk regardless of their blood pressure, because a patient can have a normal blood pressure and still be in occult shock. A lactate of 2 to 4 is intermediate risk and should prompt reassessment after fluid resuscitation.

Oliver Hart

For fluid resuscitation in sepsis, the Surviving Sepsis Campaign recommends 30 ml/kg of crystalloid within the first 3 hours. However, you should reassess after every bolus by looking at the patient's response. Is the lactate coming down? Is the urine output improving? Is the patient tolerating the fluid?

Alys Davies

If vasopressors are needed, noradrenaline is first-line, again supported by the SOAP-II trial, with a target MAP of 65 mmHg. If noradrenaline requirements keep escalating, vasopressin can be added as an adjunct. Because it acts on different receptors, it can reduce the dose of noradrenaline needed.

Oliver Hart

IV antibiotics should be given within 1 hour of recognition, every time, using broad-spectrum empirical cover based on the likely source of infection. Source control is equally important. If there is a collection to drain, an infected line to remove, or necrotic tissue to debride, this needs to happen as soon as feasible.

Alys Davies

Hydrocortisone, at 200 mg per day in divided doses, is reserved for refractory septic shock, meaning shock that does not respond to vasopressors after adequate fluid resuscitation. It is not given routinely to all patients with sepsis.

Oliver Hart

The evidence for corticosteroids in sepsis is nuanced. However, current guidance supports hydrocortisone specifically in the refractory subgroup, meaning those patients who remain dependent on vasopressors despite optimal fluid and vasopressor management.

Alys Davies

Remember. Under Sepsis-3, septic shock requires BOTH vasopressors to maintain a MAP of at least 65 AND a lactate greater than 2 mmol/L, despite adequate fluid resuscitation. Hypotension alone is not enough. This definition comes from Singer et al., JAMA 2016, and it is directly tested, so make sure you know both criteria.

Oliver Hart

Now, let's move on to our rapid-recall round.

Alys Davies

This section is all about what you know, and how quickly you can recall it!

Oliver Hart

We'll ask you a question, give you a couple of seconds to answer, and then give you the correct answer. Just try to shout out your answer in time!

Alys Davies

Question 1. In shockable VF or pulseless VT, which two drugs are given together after the third failed shock?

Oliver Hart

Adrenaline 1 mg IV and amiodarone 300 mg IV, both given after the third failed shock.

Alys Davies

Question 2. What is the correct CPR compression rate and depth?

Oliver Hart

100 to 120 compressions per minute, at a depth of 5 to 6 cm.

Alys Davies

Question 3. In the RSVP mnemonic for shock haemodynamic profiles, what does P stand for?

Oliver Hart

Pipe blocked: obstructive shock, where outflow is mechanically obstructed.

Alys Davies

Question 4.

Oliver Hart

A patient is found unconscious with bilaterally pinpoint pupils and a respiratory rate of 8. What drug and dose do you give immediately?

Alys Davies

Naloxone, 0.4 to 2 mg IV or IM, titrated to response.

Oliver Hart

Question 5. What is the first-line treatment for hypoglycaemia in an unconscious patient with IV access?

Alys Davies

100 ml of 20% dextrose IV, or 200 ml of 10% dextrose IV over 15 minutes.

Oliver Hart

Question 6. What is the IM adrenaline dose in adult anaphylaxis? Give the dose, the concentration, the route, and the site.

Alys Davies

0.5 mg of the 1:1000 solution, given intramuscularly into the anterolateral thigh.

Oliver Hart

Question 7. Name two second-line treatments in anaphylaxis, and explain why they must never replace adrenaline.

Alys Davies

Chlorphenamine 10 mg IV and hydrocortisone 200 mg IV. They do not treat cardiovascular collapse or laryngeal oedema, so they must never delay or replace IM adrenaline.

Oliver Hart

Question 8. What is the anion gap formula, and what is the normal range?

Alys Davies

Sodium minus the sum of chloride and bicarbonate, with a normal range of 8 to 12 mmol/L.

Oliver Hart

Question 9. Give three causes of elevated anion gap metabolic acidosis from MUDPILES.

Alys Davies

Any three from: methanol, uraemia, diabetic ketoacidosis, paracetamol, isoniazid, lactic acidosis, ethylene glycol and salicylates.

Oliver Hart

Question 10. What is the Sepsis-3 definition of septic shock?

Alys Davies

Vasopressors required to maintain a MAP of at least 65, AND a lactate greater than 2 mmol/L, despite adequate fluid resuscitation. Mortality exceeds 40%.

Oliver Hart

That's the end of your Acute Medicine rapid recall.

Alys Davies

Thank you for joining us for this episode.

Oliver Hart

If you have any questions, or would like to recap any of the topics we've covered today, take a moment to look back over the module.

Alys Davies

We'll see you in the next episode. Bye!