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Answers

1. Answer: D

Acute Respiratory Distress Syndrome (ARDS) is a heterogenous syndrome with symptoms of tachypnea, refractory hypoxemia, and diffuse opacities on CXR or CT chest. More than 85% of patients with ARDS have risk factors such as pneumonia, aspiration of gastric contents, and sepsis. Other risk factors for ARDS include pulmonary contusion, inhalation injury, near drowning, non‐thoracic trauma, haemorrhagic shock, pancreatitis, major burns, drug overdose, transfusion of blood products, cardiopulmonary bypass, and reperfusion oedema after lung transplantation or embolectomy.

Direct or indirect insult to the alveolar structure causes alveolar macrophage activation. This leads to the release of pro‐inflammatory mediators and chemokines that attract neutrophils and monocytes. Toxic mediators are released by activated neutrophils causing alveolar injury, leading to loss of barrier function, interstitial, and intra‐alveolar flooding. Expression of tissue factor mediated by tumor necrosis factor then promotes platelet aggregation, intra‐alveolar coagulation, and hyaline‐membrane formation.

In patients with severe ARDS, mortality is up to 46%. Long‐term sequelae for the survivors of ARDS include depression, skeletal‐muscle weakness, post‐traumatic stress disorder, and cognitive decline. Identification and treatment of the underlying cause(s) of ARDS is the first priority in the care of the patients with this condition.

The volumes of the aerated lungs are reduced in patients with ARDS. Using lung‐protective invasive mechanical ventilation with lower tidal volumes and airway pressure has been reported to reduce ventilator‐associated lung injury and mortality. Avoidance of fluid administration following reversal of shock has been shown to reduce mortality in a large randomised trial. IV albumin administration was not associated with reduced mortality in a large randomised trial in patients with ARDS. Currently, no pharmacologic therapy has been shown to reduce short‐term or long‐term mortality in patients with ARDS. A recent trial shows that infusion of muscle relaxant for 48 hours may improve oxygenation but does not improve mortality. Placing the patient in the prone position for moderate to severe ARDS may reduce mortality. Introducing inhaled nitric oxide therapy improves oxygenation but does not improve mortality.

Distinguishing between initial fluid resuscitation for shock and maintenance fluid therapy is important. Early aggressive resuscitation for associated circulatory shock and its associated remote organ injury are essential. However, several small trials have demonstrated improved outcome for ARDS in patients treated with diuretics or dialysis to promote a negative fluid balance in the first few days. Primary ARDS due to aspiration, pneumonia, or inhalational injury can be treated with fluid restriction. Secondary ARDS due to sepsis or inflammation requires initial fluid and potential vasoactive drug therapy to stabilize the patient.

An ARDS Clinical Trials Network study of a fluid‐conservative strategy versus a fluid‐liberal strategy in the management of patients with ARDS found no statistically significant difference in 60‐day mortality between the two groups 72 hours after presentation with ARDS. However, patients treated with the fluid‐conservative strategy had an improved oxygenation index and lung injury score and an increase in ventilator‐free days, without an increase in non‐pulmonary organ failures.

Thompson B, Chambers R, Liu K. Acute Respiratory Distress Syndrome. New England Journal of Medicine. 2017;377(6):562–572.

https://www.ncbi.nlm.nih.gov/pubmed/28792873

2. Answer: C

This patient’s clinical presentation and signs are consistent with cardiac tamponade which is a rare complication after pacemaker insertion. The diagnosis of cardiac tamponade is clinical and requires prompt recognition. Echocardiogram is the best imaging modality to use at the bedside, as it can confirm the presence of a pericardial effusion, determine its size, and whether it is causing compromise of cardiac function such as right ventricular diastolic collapse, right atrial systolic collapse, plethoric inferior vena cava (IVC). The commonest ECG finding of cardiac tamponade is sinus tachycardia. ECG may show low voltages or electrical alternans, which is the classic ECG finding in cardiac tamponade. A CXR may show an enlarged heart and may strongly suggest pericardial effusion if a prior CXR is available for comparison. CT chest can also detect pericardial effusion.

Differential diagnosis includes large pleural effusion, pneumothorax, pulmonary embolism, constrictive pericarditis, CCF, and shock.

Cardiac tamponade is a medical emergency. The urgent treatment of cardiac tamponade is the removal of pericardial fluid/blood to relieve the pressure surrounding the heart. This can be done by performing a needle pericardiocentesis at the bedside, performed either using traditional landmark technique in a sub‐xiphoid window or using a point‐of‐care echocardiogram to guide needle placement in real‐time. Surgical options include creating a pericardial window or removing the pericardium.

Complications of pacemaker insertion may occur during the immediate or early post‐insertion period and can be related to (ii) venous access (pneumothorax, haemothorax, air embolism, haematoma, arterial puncture, wound healing problems, infection, pain), (ii) the pacemaker lead (cardiac perforation, tamponade, malposition or dislodgement of the lead), (iii) or the generator device. Late complications are related to infections, thrombosis, endocarditis, pulmonary embolism, superior vena cava (SVC) syndrome (due to thrombus formation and/or fibrosis of the pacing wires within the SVC), and pericarditis.

Mahadevan V, Agrawal H. Cardiac tamponade – Symptoms, diagnosis, and treatment | BMJ Best Practice [Internet]. Newbp.bmj.com. 2019 [cited 22 August 2019]. Available from: https://bestpractice.bmj.com/topics/en-gb/459

3. Answer: D

Carbon monoxide (CO) poisoning causes a large number of deaths due to intentional self‐injury and non‐intentional injury related to fires. Chronic CO poisoning is more commonly encountered as a result of faulty heating. CO binds to heme products with much greater affinity than oxygen and reduces oxygen delivery to tissues. However, this mechanism only accounts for some of the toxicity of CO, and as a result, carboxyhaemoglobin levels do not necessarily correlate with severity of toxicity. CO poisoning also produces toxicity by binding many intracellular heme products resulting in impaired cellular function. For example, CO inhibits mitochondrial respiration by binding ferrous heme, which is the active site on cytochrome c oxidase complex IV. CO inhibits platelet function, causes inflammation, central demyelination and global brain ischaemic injury, through acidosis and oxidative stress. CO poisoning can be diagnosed by consistent symptoms, history of recent CO exposure, and elevated carboxyhaemoglobin levels. Conventional pulse oximetry cannot distinguish between carboxyhaemoglobin and oxyhaemoglobin, so pulse oximetry usually returns normal values. Treatment focuses on accelerating the dissociation of CO through oxygen therapy. Whilst hyperbaric oxygen has been shown to accelerate this process faster than normobaric oxygen, it has not shown improved clinical outcomes. Long term sequelae of CO poisoning are common, with cardiovascular toxicity and neurological deficits occurring most frequently.

Rose J, Wang L, Xu Q, McTiernan C, Shiva S, Tejero J et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy. American Journal of Respiratory and Critical Care Medicine. 2017;195(5):596–606.https://www.atsjournals.org/doi/full/10.1164/rccm.201606‐1275CI

4. Answer: B

Disseminated intravascular coagulation (DIC) is an overactivation of the coagulation cascade resulting in consumption of coagulation factors, and disordered haemostasis, manifesting as either coagulation or bleeding. DIC affects about 35% of patients who have sepsis. Depending on the cause, DIC manifests in different ways. This is thought to be due to differential effects of the causative pathology on fibrinolysis and procoagulant factors. For example, DIC caused by trauma or acute promyelocytic leukaemia tends to result in bleeding, whereas sepsis most frequently causes multi‐organ dysfunction through microembolic damage. Obviously, the treatment of these differentially manifesting pathologies will differ. The typical laboratory parameters in DIC are decreased platelet count, increased prothrombin time, increased (often dramatically) D‐dimer, and decreased fibrinogen. However, the individual components of laboratory diagnosis are not all required and DIC can go undiagnosed if this possibility is not recognised. For example, low fibrinogen is only present in around 30% of DIC associated with sepsis. One of the most thoroughly validated scoring systems for the diagnosis of DIC is that of the International Society of Thrombosis and Haemostasis (ISTH), which gives weight to the above‐mentioned laboratory parameters and a score of 5 or more denotes DIC. There is still some controversy surrounding the supportive management of DIC (other than addressing the underlying cause), but treatment strategies in sepsis induced DIC include replacing factors, activated protein‐C and systemic anticoagulation.

Iba T, Levy JH, Warkentin TE et.al. Diagnosis and management of sepsis‐induced coagulopathy and disseminated intravascular coagulation. J Thromb Haemost. 2019; 17(11): 1989–1994.

https://onlinelibrary.wiley.com/doi/10.1111/jth.14578

5. Answer: B

Septic shock is a type of distributive shock and is the most common cause of circulatory shock among patients in the ICU (62% of the patients). It is followed by cardiogenic (16%), hypovolemic (16%), and obstructive shock (2%). Causes of shock may be obvious from history, clinical examination, and/or investigations. Patients who present with a history of trauma/gastrointestinal bleeding may have hypovolaemic shock; patients with massive pneumothorax/pulmonary emboli/cardiac tamponade are likely to have obstructive shock; patients with fever, symptoms/signs of infection, an elevated WBC count, a high CRP, and an elevated procalcitonin level may have septic shock; patients present after a recent acute coronary syndrome are likely to have cardiogenic shock, etc. Some patients may have mixed types of circulatory shock.

Initial presentations may be similar in patients with different types of shock. Depending on the organ involvement after circulatory shock, the patient may have mental status changes, hypotension, tachycardia, tachypnoea, reduced urine output, coagulation abnormalities, etc. Blood lactate levels are elevated in patients with impaired tissue perfusion.

Further investigations by performing a septic screen, assessing cardiac output by echocardiogram, monitoring mixed venous oxygen saturation (SvO2), monitoring of central venous pressure, or performing a CTPA can help to differentiate the underlying cause(s) of circulatory shocks. If an echocardiogram shows large ventricles and poor contractility, cardiogenic shock is likely. An echocardiogram may help to rule out pericardial effusion, cardiac tamponade, etc. some of the common causes of obstructive shock.

After failing initial intravenous fluid resuscitation, it may be appropriate to provide vasopressor support, intensive blood pressure monitoring via an arterial line, and central venous catheters in the ICU if patients wish to have more intensive monitoring and treatment. Broad spectrum antibiotics administration according to the possible sites of infections should be considered as soon as possible without delay after a septic screen is performed if there is suspicion of septic shock, to minimise morbidity and mortality associated with sepsis.

Vincent J, De Backer D. Circulatory Shock. New England Journal of Medicine. 2013;369(18):1726–1734.https://www.nejm.org/doi/10.1056/NEJMra1208943

6. Answer: A

The ECGs show

1 Left bundle branch block (LBBB)
2 ST change associated with severe left ventricular hypertrophy (LVH)
3 ST changes associated ‘Tented’ T wave in patient with hyperkalaemia
4 Widespread concave (‘saddleback’) ST segment elevation in a patient with pericarditis

The key point is that not all ST elevation is due to ST elevation acute myocardial infarction (STEMI). ECG A is typical for LBBB which is new. New LBBB alone is not necessarily an indication for immediate cardiac catheterisation. However, the following criteria are the indications for immediate cardiac catheterisation:

Unstable patient with hypotension, acute pulmonary oedema or electrical instability

Sgarbossa Criteria (electrocardiographic findings used to identify myocardial infarction (MI) in the presence of a LBBB)Concordant ST‐segment elevation of 1 mm in at least 1 leadConcordant ST‐segment depression of at least 1 mm in leads V1 to V3

Smith‐Modified Sgarbossa criteria – any single lead with at least 1 mm of discordant ST elevation that is ≥25% of the preceding S‐wave.

In patients with old LBBB, ST–T abnormalities are common, making it difficult to assess the presence of AMI. ST segment and T–waves are usually discordant with the QRS in LBBB, since they are directed in opposite directions. A concordant ST segment shift should always be presumed to be a myocardial lesion and considered as strongly indicative of AMI. On the other hand, a discordant ST segment displacement may be indicative of a myocardial lesion when specific standard criteria are exceeded. For example, discordant elevation of the J point ≥0.5 mV in V1–V2 is strongly suggestive of AMI in the presence of LBBB. Moreover, in LBBB, the QRS/T ratio appears to be more predictive than the amplitude of ST elevation. When this ratio is near to or less than 1, the probability that the repolarisation abnormality is related to an MI is high.

ECG B is typical of LVH with associated concave ST elevation not STEMI. In LVH, the repolarisation pattern is usually discordant to the QRS as in LBBB, The elevation is more commonly observed in leads V2–V3 and is usually <0.3 mV with minor abnormalities in V4–V6. ECG shows high voltage of R waves in antero‐lateral leads associated to Q waves in anterior and inferior leads. The T waves, usually being very deep and inverted in V2–V4, may resemble a non‐Q AMI.

ECG C has ST changes associated ‘Tented’ T wave in a patient with hyperkalaemia. Significant variations of potassium levels have dramatic effects on electrical activities and cause arrhythmias. Hyperkalaemia induces an ST elevation in right precordial leads that can resemble an AMI. Other ECG changes in hyperkalaemia include reduction in the amplitude of P waves, prolongation of the PQ interval, enlargement of QRS complex and concave ST segment elevation.

ECG D shows widespread concave (‘saddleback’) ST segment elevation in a patient with pericarditis. Although pericardium is electrically inactive, its infection and/or inflammation as seen in this case of uraemic pericarditis may affect the external part of epicardium and cause concave ST elevation in almost all leads, as pericarditis generally affects the whole pericardium.

Smith S, Dodd K, Henry T, Dvorak D, Pearce L. Diagnosis of ST‐Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST‐Elevation to S‐Wave Ratio in a Modified Sgarbossa Rule. Annals of Emergency Medicine. 2012;60(6):766–776. https://www.annemergmed.com/article/S0196‐0644(12)01368‐6/fulltext

7. Answer: D

Extracorporeal membrane oxygenation (ECMO) is an advanced form of temporary life support which helps to maintain respiratory and/or cardiac function. It diverts venous blood through an extracorporeal circuit and returns it to the body after gas exchange through a semi‐permeable membrane. ECMO can be used for oxygenation, carbon dioxide removal and haemodynamic support. Additional components allow thermoregulation and haemofiltration. The two most common forms of ECMO are: (i) veno‐arterial ECMO (VA‐ECMO) to support patients with a reversible cause of cardiogenic shock that is refractory to maximal therapy. VA‐ECMO can also be a salvage treatment option in the setting of cardiac arrest with unsuccessful advanced life support. (ii) veno‐venous ECMO (VV‐ECMO) is indicated for patients with a reversible cause of acute respiratory failure with refractory hypoxaemia or hypercapnia despite optimal ventilation. VV‐ECMO allows reduction in the ventilatory insult caused by mechanical ventilation.

The indications and contraindications for ECMO in critically ill patients are listed in Tables 2.1 and 2.2.

Table 2.1 Indications for ECMO.

Indications for VA‐ECMO	Indications for VV‐ECMO
Acute myocardial infarction	Reversible causes of acute respiratory failure
Fulminant myocarditis	ARDS
Acute exacerbations of chronic CCF	Trauma—extensive pulmonary contusion
Cardiac failure due to intractable arrhythmias	Massive pulmonary embolism with refractory shock and/or cardiac arrest
Primary graft failure following cardiac transplantation	Graft dysfunction following lung transplantation
Acute heart failure secondary to drug toxicity	Inability to provide adequate gas exchange without risk of ventilatory injury
Postcardiac arrest (as part of advanced life support)	Pulmonary haemorrhage

Table 2.2 Contraindications to ECMO.

Chronic respiratory or cardiac disease with no hope of recovery or transplant

Out‐of‐hospital cardiac arrest with prolonged down time

Severe aortic regurgitation or type A aortic dissection or severe peripheral vascular disease if using VA‐ECMO

Refractory septic shock in adults with preserved left ventricular function

ARDS with advanced multiorgan failure

ARDS in patient with advanced age

Prolonged pre‐ECMO mechanical ventilation

Therapeutic anticoagulation is a relative contraindication

Ali J, Vuylsteke A. Extracorporeal membrane oxygenation: indications, technique and contemporary outcomes. Heart 2019; 105:1437–43.

https://heart.bmj.com/content/105/18/1437.abstract

8. Answer: A

The most common cause of drowsiness in the admitted patient is a metabolic encephalopathy. Thorough neurological examination is needed, however, to rule out focal central nervous system pathology. Common causes of encephalopathy are infection, medications, decompensated hepatic failure, and hypercania. Less common causes include endocrine causes and electrolyte disturbance. In this case, type 2 respiratory failure is the most likely cause given the findings on history and examination.

Alpert J. Evaluation of the Poorly Responsive Patient. The Neurologic Diagnosis [Internet]. 2018 [cited 30 June 2020];163–206. Available from: https://link.springer.com/chapter/10.1007/978‐3‐319‐95951‐1_5

9. Answer: C

Intra‐aortic balloon pump (IABP) is a percutaneous temporary mechanical circulatory support that creates more favourable balance of myocardial oxygen supply and demand by using systolic unloading and diastolic augmentation.

The IABP, by inflating during diastole, displaces blood volume from the thoracic aorta. In systole, as the balloon rapidly deflates, this creates a vacuum effect, reducing afterload for myocardial ejection and improving forward flow from the left ventricle. The net effect is to decrease systolic aortic pressure by as much as 20% and increase diastolic pressure, but the MAP is usually unchanged. This subsequently results in decreased left ventricle wall stress reducing the myocardial oxygen demand. Overall, these haemodynamic changes indirectly improve the cardiac output by increasing stroke volume, particularly in patients with reduced left ventricular function. The augmentation of diastolic pressure by IABP leads to an increase in myocardial perfusion especially epicardial coronary circulation.

Indication for placement can include:

Myocardial infarction with decreased left ventricular function leading to cardiogenic shock

Myocardial infarction with mechanical complications causing cardiogenic shock, i.e., acute mitral regurgitation due to papillary muscle rupture or ventricular septal rupture

Acute congestive heart failure exacerbation with hypotension

As prophylaxis or adjunct treatment in high risk percutaneous coronary intervention

Low cardiac output state after coronary artery bypass grafting surgery

As a bridge to definitive treatment in patients with any of the following conditions: intractable myocardial ischaemia, refractory heart failure, or intractable ventricular arrhythmias

However, studies have not shown any survival benefits with the use of IABP and there is no convincing randomised data to support the routine use of IABP in infarct‐related cardiogenic shock.

Unverzagt S, Buerke M, de Waha A, Haerting J, Pietzner D, Seyfarth M et al. Intra‐aortic balloon pump counterpulsation (IABP) for myocardial infarction complicated by cardiogenic shock. Cochrane Database of Systematic Reviews. 2015.

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD007398.pub3/abstract

10. Answer: A

Advance care planning in a health care context can be described as the process by which an individual sets out their wishes for medical care in the event that they are unable to make decisions themselves. In addition, advance care planning can set out who they would like to assist in medical decision making such as family or close friends. Advance care planning has been shown in multiple studies as being valuable to patients and their families. Additionally, randomised controlled trials have shown significant improvement in several outcomes; decreased utilisation of healthcare and cost, increased satisfaction with care, decreased use of hospital resources, improved concordance with wishes. However, these trials have not been of sufficient rigour and size to evaluate whether advance care planning improves quality of end‐of‐life care such as by measures of individual comfort.

Weathers E, O’Caoimh R, Cornally N, Fitzgerald C, Kearns T, Coffey A et al. Advance care planning: A systematic review of randomised controlled trials conducted with older adults. Maturitas. 2016;91: 101–109.

https://pubmed.ncbi.nlm.nih.gov/27451328/

11. Answer: C

Necrotising fasciitis is a rapidly progressive infection of the fascia, with secondary widespread necrosis of the subcutaneous tissues. The frequency of necrotising fasciitis has been increasing because of an increase in immunocompromised patients with diabetes, peripheral vascular disease, alcoholism, organ transplants, and neutropenia. The causative bacteria may be aerobic, anaerobic, or mixed flora. The three most important types are as follows:

Type I, or polymicrobial

Type II, or group A streptococcal

Type III gas gangrene, or clostridial myonecrosis

The reported mortality in patients with necrotising fasciitis has ranged from 20% to as high as 80%. Early diagnosis is key and requires a high index of suspicion as the initial lesion is often trivial. In many cases of necrotising fasciitis, antecedent trauma or surgery can be identified. Necrotising fasciitis requires urgent surgical intervention, and the urgent initiation of broad spectrum antibiotics. Admission to the intensive care unit is likely required, as these patients are usually profoundly shocked.

While caring for critically ill patients with necrotising fasciitis the following complications should be close monitored:

Capillary leak syndrome: Circulating bacterial toxins and host cytokines cause diffuse endothelial damage. Intravenous fluid requirements may be extremely high (10 to 12 litres of normal saline per day). Profound hypoalbuminaemia is also common, and replacement with albumin is needed to maintain oncotic pressure.

Intravascular haemolysis: Bacterial haemolysins cause striking and rapid reductions in the haematocrit in the absence of DIC. Thus, the haematocrit may be a better indicator of the need for transfusion than the haemoglobin level.

Stress cardiomyopathy: necrotising fasciitis especially caused by streptococcal infection can cause global hypokinesia, severe systolic heart failure, low cardiac output. This cardiomyopathy is reversible, fully resolving in 3 to 24 months after infection.

Posterior reversible encephalopathy syndrome (PRES) is a clinico‐radiological syndrome characterised by headache, visual disturbances, seizures and altered consciousness. It is most commonly associated with accelerated and malignant hypertension. It can also be associated with eclampsia/preeclampsia, HUS, TTP, drug toxicity and very rarely sepsis. CT or/and MRI of the brain commonly show vasogenic oedema within the occipital and parietal regions, The oedema is usually symmetrical. PRES can be found in a non‐posterior distribution, mainly in watershed areas, including within the frontal, inferior temporal, cerebellar, and brainstem regions. Both cortical and subcortical locations are affected.

Stevens D, Bryant A. Necrotizing Soft‐Tissue Infections. New England Journal of Medicine. 2017;377(23):2253–2265.

https://www.nejm.org/doi/10.1056/NEJMra1600673

12. Answer: B

The updated paracetamol overdose management guidelines in 2019 recommend a two‐bag N‐acetylcysteine (NAC) infusion regimen (200 mg/kg over 4 hours, then 100 mg/kg over 16 hours) instead of the previous three‐bag regimen since they have similar efficacy and the two‐bag regimen has less adverse reactions. All patients with risks of hepatotoxicity secondary to paracetamol overdoses should receive NAC treatment. In patients with massive paracetamol overdoses which result in blood paracetamol level more than double the nomogram line should receive increased doses of NAC. In patients whose time of ingestion is unclear, it may be worthwhile to commence NAC infusion regardless given the unlikelihood of harm associated with the treatment.

The nomogram is only validated for a single ingestion of immediate release paracetamol. If extended‐release paracetamol is ingested, and or the overdose has occurred over a longer period of time, it is no longer validated. In these cases, NAC infusion should be commenced regardless, given the lack of harm. If there was co‐ingestion of opioids or anticholinergics, as they can affect gastric emptying and absorption of paracetamol, NAC should be given.

For patients who present within 2 hours of immediate release paracetamol overdoses or present within 4 hours of immediate release paracetamol ingestions greater than 30 gm, activated charcoal should be given in alert and co‐operative patients.

Only a small percentage of patients develop hepatotoxicity following acute paracetamol overdoses with symptoms that can include nausea, vomiting, abdominal pain, and right‐upper quadrant tenderness. Of these patients, a small number of patients develop fulminant hepatic failure. Most patients recover after standard treatment.

Liver transplant unit should be consulted if patients meet any of the following criteria:

INR >3.0 at 48 hours or >4.5 at any time.

Oliguria or serum creatinine is >200 μmol/L.

Persistent acidosis (pH <7.3) or arterial lactate >3 mmol/L.

Systolic blood pressure <80 mmHg, despite fluid resuscitation.

Hypoglycaemia, severe thrombocytopenia, or encephalopathy.

Any alteration of consciousness (GCS <15) not associated with concomitant sedative overdoses.

Chiew A, Reith D, Pomerleau A, Wong A, Isoardi K, Soderstrom J et al. Updated guidelines for the management of paracetamol poisoning in Australia and New Zealand. Medical Journal of Australia. 2019;212(4):175–183.

https://onlinelibrary.wiley.com/doi/abs/10.5694/mja2.50428

13. Answer: C

Pulseless electrical activity (PEA), previously known as electromechanical dissociation (EMD) is defined as the absence of a palpable pulse in an unconscious patient with organized electrical activity other than VT on ECG. The proportion of PEA among cases of sudden cardiac arrest increases with age. Females are more likely to develop PEA than males. Patients with PEA are more likely to have one or more co‐morbidities than those in the VF/VT group. However, PEA is less likely to occur in those with CCF. In one study, PEA was responsible for 68% of monitored in‐hospital deaths and 10% of all in‐hospital deaths.

PEA more commonly has an underlying cause of the arrest including the Hs and Ts listed below and the most frequent causes are hypoxemia secondary to respiratory failure and hypovolemia due to internal bleeding or a recent haemodialysis. This patient’s PEA is possibly due to hypoxia caused by his infective exacerbation of COPD. Tension pneumothorax also needs to be excluded.

Hypoxia

Hypovolemia

Hydrogen ion (acidosis)

Hypokalaemia/ hyperkalaemia, hypoglycaemia

Hypothermia

Toxins

Tamponade (cardiac)

Tension pneumothorax

Thrombosis (massive PE or AMI)

Trauma

The overall prognosis for patients with PEA arrest is dismal unless a rapidly reversible cause is identified and corrected. Only 11% of patients who have PEA as their first documented rhythm survives to hospital discharge. ECG characteristics are related to the patient's prognosis. The more abnormal the ECG characteristics, the less likely the patient is to recover from PEA; patients with a wider QRS (>0.2 sec) have worse prognosis.

PEA is treated in the same way as asystole. It is not a shockable rhythm. You should continue with CPR, administer epinephrine and begin to consider possible causes. Epinephrine can be given every 3 to 5 min.

Pulseless Electrical Activity: Background, Etiology, Epidemiology [Internet]. Emedicine.medscape.com. 2019 [cited 17 August 2019]. Available from: https://emedicine.medscape.com/article/161080‐overview

The Australian Resuscitation Council Guidelines [Internet]. Resus.org.au. 2019 [cited 17 August 2019]. Available from: https://resus.org.au/guidelines/

14. Answer: B

Patients with critical illness are at risk of upper gastrointestinal bleeding, a condition that may be associated with increased mortality. Clinically important gastrointestinal bleeding occurs in 3–5% of ICU patients. Until recently guidelines have recommended preventive therapy with either histamine H₂–receptor antagonists or proton‐pump inhibitors (PPIs) for patients in ICU who are at risk for stress ulceration and bleeding. However, any benefit from PPIs might be reduced by harmful events that are associated with the use of these agents, including nosocomial pneumonia, Clostridium difficile enteritis, and myocardial ischemia. The use of enteral feeding may also reduce the risk of gastrointestinal bleeding.

In a recent large trial, patients were randomly assigned to daily intravenous pantoprazole (40 mg) or placebo during their ICU admission. The patients were at high risk for gastrointestinal bleeding because of a history of liver disease, coagulopathy, shock, treatment with anticoagulant agents, renal replacement therapy, or mechanical ventilation that was expected to last for more than 24 hours. There was no significant difference between the groups in the rate of the primary outcome of death nor gastrointestinal bleeding, pneumonia, C. difficile infection, or myocardial ischemia. A further study of use with PPIs vs histamine H₂–receptor antagonists for stress ulcer prophylaxis among adults requiring mechanical ventilation did not result in a statistically significant difference for in‐hospital mortality.

Barkun A, Bardou M. Proton‐Pump Inhibitor Prophylaxis in the ICU — Benefits Worth the Risks? New England Journal of Medicine. 2018;379(23):2263–2264.

https://www.nejm.org/doi/full/10.1056/NEJMe1810021

15. Answer: D

AKI is a frequent complication associated with septic shock in patients who require ICU admission. AKI is also associated with an increased mortality rate in these patients.

In a large, multicenter, RCT, patients with early‐stage septic shock with severe AKI based on the failure stage of the risk, injury, failure, loss, and end‐stage kidney disease (RIFLE) system but without life‐threatening complications of AKI were randomised to either receive dialysis within 12 hours after documentation of AKI (early dialysis) or 48 hours after the AKI if no renal recovery was observed (delayed dialysis).

The failure stage of the RIFLE classification system is characterised by a serum creatinine level 3 times the baseline level (or ≥4 mg/dL with a rapid increase of ≥0.5 mg/dL), urine output less than 0.3 ml per kilogram of body weight per hour for 24 hours or longer, or anuria for at least 12 hours.

The trial was stopped early for futility after the second planned interim analysis showed no significant difference in overall mortality at 90 days in the early dialysis vs. delayed dialysis groups.

Barbar S, Clere‐Jehl R, Bourredjem A, Hernu R, Montini F, Bruyère R et al. Timing of Renal‐Replacement Therapy in Patients with Acute Kidney Injury and Sepsis. New England Journal of Medicine. 2018;379(15):1431–1442.

https://www.ncbi.nlm.nih.gov/pubmed/30304656

16. Answer: C

This patient is in septic shock, likely of urinary origin. Sepsis and septic shock are medical emergencies and treatment and resuscitation should begin immediately. Latest guidelines dictate that following initial fluid resuscitation, administration of additional fluids should be guided by frequent assessment of haemodynamic status. This includes thorough clinical examination including blood pressure, heart rate, respiratory rate, temperature, oxygen saturation and urine output.

Previous resuscitation guidelines in septic shock have recommended a protocolised approach, known as early goal‐directed therapy (EGDT) which described the use of goals that included central venous monitoring and serial haemoglobin monitoring. Previously, the EGDT dictated that early placement of a central venous catheter (CVC) improved outcomes in patients with septic shock. However, this approach has now been challenged following the results of three large, multicentre RCTs which showed no mortality benefit, as discussed in the Protocolised Resuscitation In Sepsis Meta‐Analysis (PRISM). New evidence found that the use of CVP alone to guide fluid resuscitation can no longer be justified given the limited ability of CVP to predict a response to a fluid challenge when the CVP is within a relatively normal range (8–12 mmHg).

Recommended volume of fluid resuscitation starts at 30 mL/kg; however, the balance of additional fluids and the use of vasopressors remains uncertain. Several clinical trials are underway which will evaluate this, however currently the goal of fluid resuscitation should be targeted at a mean arterial pressure (MAP) of 65 mmHg through the use of fluids and vasopressors, while normalising the lactate level. Two clinical trials show the potential for harm with starch‐related intravenous fluids, but limited evidence to support the use of colloids over crystalloids. (Starch trial: https://www.nejm.org/doi/full/10.1056/NEJMoa1204242 and ALBIOS trial: https://www.nejm.org/doi/full/10.1056/nejmoa1305727). There is emerging evidence for the use of balanced crystalloid solutions over 0.9% sodium chloride (SMART trial, https://www.nejm.org/doi/full/10.1056/NEJMoa1711584). There is also some emerging evidence for fluids potentially leading to higher mortality (FEAST trial, https://www.nejm.org/doi/full/10.1056/NEJMoa1101549).

In summary:

Septic shock is a medical emergency and resuscitation should begin immediately.

Initial fluid volume administered should start at 30 mL/kg.

Further fluid administration should be based on haemodynamic status as determined by physiologic parameters (BP, HR, urine output, oxygen saturation and temperature).

A target MAP of 65 mmHg may be used for vasopressor and fluid adjustment.

Serial measurement of CVP, Scvo2 and haemoglobin using a CVC is no longer recommended.

Berger R, Rivers E, Levy M. Management of Septic Shock. New England Journal of Medicine. 2017;376(23):2282–2285.

https://www.nejm.org/doi/full/10.1056/NEJMclde1705277?url_ver=Z39.88‐2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed

Rhodes A, Evans L, Alhazzani W, Levy M, Antonelli M, Ferrer R et al. Surviving Sepsis Campaign: International Guidelines for Management of for Management of Sepsis and Septic Shock: 2016. Critical Care Medicine: 2017; 45: 486–552.https://journals.lww.com/ccmjournal/Fulltext/2017/03000/Surviving_Sepsis_Campaign___International.15.aspx

17. Answer: B

Severe asthma is defined as uncontrolled asthma despite adherence to maximum optimised therapy and treatment of contributing factors or that exacerbates when high‐dose treatment is decreased. Patients with severe asthma suffer a substantial burden of symptoms, exacerbations, and side effects from medications. Patients with comorbidities such as severe sinus disease, recurrent respiratory infections, sleep apnoea, and gastroesophageal reflux experience more frequent recurrent exacerbations of severe asthma.

According to Global Initiative for Asthma (GINA) guidelines, approximately 50% of patients with severe asthma have type 2 inflammation which is characterised by eosinophils, increased fractional inhaled nitric oxide (FeNO), and cytokines such as interleukin [IL]‐4, IL‐5, IL‐13. GINA guidelines do not suggest use of exhaled nitric oxide to guide therapy in patients with severe asthma.

Mepolizumab is a humanised immunoglobulin G1 kappa monoclonal antibody specific for IL‐5. It binds to IL‐5 and stops IL‐5 from binding to its receptor on the surface of eosinophils. Therefore, it reduces blood, tissue, and sputum eosinophil levels. It is indicated for add‐on maintenance treatment of patients with severe asthma and with an eosinophilic phenotype.

Global Initiative for Asthma – Global Initiative for Asthma – GINA [Internet]. Global Initiative for Asthma – GINA. 2020 [cited 7 July 2020]. Available from: http://www.ginasthma.org

18. Answer: D

This patient has clinical evidence of severe and complicated Clostridium difficile infection (CDI). The incidence of CDI continues to rise. Oral vancomycin 125 mg four times daily is recommended as first‐line therapy for severe CDI. It can be administrated via nasogastric tube or per rectum. Oral metronidazole 400 mg three times daily for 10 days is recommended as first‐line therapy for first episode mild CDI. Fidaxomicin, a first‐in‐class macrocyclic bactericidal antibiotic, has targeted bactericidal activity against C. difficile through inhibiting clostridial RNA polymerase. Fidaxomicin demonstrates minimal impact on normal gut flora and spares Bacteroides spp., a major ‘protective’ constituent of faecal flora. Fidaxomicin has minimal oral absorption like vancomycin and a prolonged post‐antibiotic effect and has been approved by the Therapeutic Drug Administration (TGA) for use in CDI. Oral fidaxomicin 200 mg twice daily is a treatment alternative in recurrent CDI. Faecal microbiota transplantation (FMT) is a treatment option alternative in recurrent CDI for appropriately selected patients.

Trubiano J, Cheng A, Korman T, Roder C, Campbell A, May M et al. Australasian Society of Infectious Diseases updated guidelines for the management of Clostridium difficile infection in adults and children in Australia and New Zealand. Internal Medicine Journal. 2016;46(4):479–493.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/imj.13027

19. Answer: B

Sepsis is life‐threatening organ dysfunction caused by an infection‐induced dysregulated host response, which may be complicated by septic shock. Sepsis and septic shock are major causes of morbidity and mortality worldwide. The Surviving Sepsis Campaign (SSC) has strongly emphasised the importance of speed and appropriateness of therapy in improving outcomes. Since the application of the first SSC guidelines, a substantial reduction in mortality has been reported. Both sepsis and septic shock should be viewed as medical emergencies requiring rapid diagnosis and immediate intervention.

The hour‐1 bundle encourages clinicians to act as quickly as possible to obtain blood cultures, administer broad spectrum antibiotics, start appropriate fluid resuscitation, measure lactate, and begin vasopressors if clinically indicated. Ideally these interventions would all begin in the first hour from sepsis recognition but may not necessarily be completed in the first hour.

SSC Hour‐1 Bundle of Care Elements:

Measure lactate level, remeasure lactate if initial lactate is elevated (>2 mmol/L).

Obtain blood cultures before administering antibiotics.

Administer broad‐spectrum antibiotics.

Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate level ≥4 mmol/L.

Apply vasopressors if hypotensive during or after fluid resuscitation to maintain MAP ≥65 mm Hg.

Rhodes A, Evans L, Alhazzani W, Levy M, Antonelli M, Ferrer R et al. Surviving Sepsis Campaign. Critical Care Medicine [Internet]. 2017 [cited 21 June 2020];45(3):486–552. Available from: https://journals.lww.com/ccmjournal/Fulltext/2017/03000/Surviving_Sepsis_Campaign___International.15.aspx

20. Answer: B

The ECGs show

1 Left bundle branch block
2 Mobitz type II 2:1 heart block
3 Bifascicular block
4 Mobitz type I (Wenckebach) heart block.

Temporary transvenous pacing is necessary for patients with severe and symptomatic bradyarrhythmias. It should be considered for patients with second‐degree or third‐degree atrioventricular (AV) block associated with symptoms or hemodynamic compromise. Temporary transvenous pacing is necessary to increase heart rate and improve symptoms.

In summary, temporary transvenous pacing should be considered following an acute myocardial infarction (AMI), if there is:

Complete (third‐degree) heart block.

Mobitz type II second‐degree AV block.

New or age‐indeterminate bifascicular block (RBBB with LAFB or LPFB or LBBB) with PR prolongation.

Bradycardia‐induced tachyarrhythmias.

Symptomatic bradycardia of any aetiology if hypotension is present and the bradyarrhythmia is not responsive to atropine.

Despite reperfusion treatment, the incidence of intraventricular conduction disturbances post AMI has not changed, whereas the incidence of AV block post AMI has decreased but still remains high. AV block occurs in almost 7% of cases of AMI.

Kusumoto FM. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. Journal of the

American College of Cardiology. 2018.

https://www.sciencedirect.com/science/article/pii/S073510971838985X?via%3Dihub

21. Answer: D

Tranexamic acid has been shown to reduce surgical bleeding and decrease mortality in patients with mild to moderate traumatic extracranial bleeding. A 7‐year large randomised, placebo‐controlled, multi‐centre trial (CRASH‐3) with 12,737 patients in 29 countries has shown that tranexamic acid (loading dose 1 g over 10 min then infusion of 1 g over 8 h) is safe in patients with acute traumatic brain injury. The trial patients had a GCS score of 12 or lower or any intracranial bleeding on CT brain, and no major extracranial haemorrhage. Patients with a GCS score of 3 or bilateral unreactive pupils, severe brain injury, at baseline were excluded. Patients should be started on tranexamic acid as soon as possible after injury, within 3 hours of injury. Early treatment had more effect than later treatment in patients with mild and moderate head injury (p=0.005). There was no difference of the risk of vascular occlusive events and the risk of seizures in the tranexamic acid and placebo groups. It should be noted the benefit is mostly restricted to the moderate head injury group (and done as a subgroup analysis). However, given its low risk of causing harm, it may be beneficial to give to all groups of traumatic head injuries.

Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH‐3): a randomised, placebo‐controlled trial. The Lancet. 2019;394(10210):1713–1723.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6853170/

22. Answer: D

There is an increasing trend of using VBG instead of ABG to assess critically unwell patients in the emergency department, ICU, or when inpatients are acutely unwell. VBG can be obtained from the peripheral veins and is a safer, easier to obtain, and less invasive alternative. VBG blood test results can provide rapid and accurate information on acid‐base and CO2 status, along with SpO2, and provide direction on ventilation requirement and the need for ICU or high dependency unit admission. The pH of a VBG and ABG correlates closely and accurately measures the severity of an acidosis. The average VBG pH is 0.03–0.04 less than the ABG pH values. SpO2 values correlate well with PaO2 on ABG analysis as predicted by the standard oxygen–haemoglobin dissociation curve, but PaO2 level does not correlate well between the venous and arterial blood gases. PaO2 readings in VBG can significantly underestimate arterial oxygen level or miss patients with hyperoxia, a state in which oxygen supply is excessive. It is important to also recall that the oxygen‐haemoglobin dissociation curve is altered by arterial pH, PaCO2, and temperature. The bicarbonate (HCO3) correlates well between arterial and venous samples, and similar to the pH will closely approximate the arterial values, with a difference of 0.52–1.5 mmol/L. The lactate level correlates well between ABG and VBG, with a mean difference of 0.02–0.08. The venous lactic acid can be used determine trends in lactate during resuscitation.

In patients with a clinical suspicion of ARDS demonstrating signs and symptoms of dyspnoea, tachypnoea, hypoxaemia, and bilateral infiltrates on CXR, PaO2 in ABG results is required as part of the diagnostic criteria. A ratio of partial pressure of arterial oxygen to fraction of inspired oxygen (PaO2/FiO2) of 200 or less, regardless of positive end‐expiratory pressure, is supportive of the diagnosis of ARDS.

Please note that peripheral VBG may be skewed by prolonged tourniquet time. Central VBG or mixed VBG may be a useful marker in monitoring a patient’s cardiac function.

Zeserson E, Goodgame B, Hess J, Schultz K, Hoon C, Lamb K et al. Correlation of Venous Blood Gas and Pulse Oximetry With Arterial Blood Gas in the Undifferentiated Critically Ill Patient. Journal of Intensive Care Medicine. 2016;33(3):176–181.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5885755/

23. Answer: D

Azithromycin is considered to have minimal cardiotoxicity and is the safest of the macrolide derivatives due to divergent pharmacokinetic properties (e.g. minimal CYP3A4 metabolism/inhibition) and is limited in blockade of the rapid delayed rectifier potassium current (IKr) conducted by hERG‐encoded Kv11.1 potassium channel at therapeutic concentrations. There is a small absolute increased risk of ventricular arrhythmia and cardiovascular deaths, which is most pronounced among patients with a high baseline risk of cardiovascular disease and/or concomitant use of other QT‐prolonging drugs such as sotalol in this case. Prescribing physicians should carefully assess the risks and benefits of azithromycin use especially in patients with underlying cardiovascular disease and concomitant use of other QT‐prolonging drugs.

This patient has ongoing VT despite defibrillation three times. The next line of therapy is amiodarone.

According to the 2018 Australian and New Zealand Council of Resuscitation (ANZCOR) Advanced Life Support Guideline, intravenous amiodarone (300 mg) should be administered after the third failed attempt at defibrillation, at the time of recommencement of CPR. There is no evidence that giving any antiarrhythmic drug routinely during cardiac arrest increases rate of survival to hospital discharge. However, in comparison with placebo and lignocaine the use of amiodarone in shock‐refractory VF improves the short‐term survival. Despite the lack of long‐term outcome data, it is reasonable to continue to use antiarrhythmic drugs on a routine basis.

Magnesium sulphate is indicated only in the treatment of VF or pulseless VT arrest due to drug induced prolonged QT interval associated with torsades de pointes.

There are no placebo‐controlled studies that show that the routine use of any vasopressor at any stage during cardiac arrest increases survival to hospital discharge, though they have been demonstrated to increase return of spontaneous circulation. Current evidence is insufficient to support or refute the routine use of any particular drug or sequence of drugs. Despite the lack of human data, it is reasonable to continue to use vasopressors on a routine basis. Adrenaline (1 mg), when indicated, should be administered after rhythm analysis (± shock), at the time of recommencement of CPR.

Guidelines [Internet]. Resus.org.au. 2019 [cited 24 March 2019]. Available from: https://resus.org.au/guidelines/

24. Answer: D

This patient is in septic shock, likely due to urosepsis. Sepsis and septic shock are medical emergencies and treatment and resuscitation should begin immediately. Latest guidelines dictate that following initial fluid resuscitation, administration of additional fluids should be guided by frequent assessment of haemodynamic status. This includes thorough clinical examination including blood pressure, heart rate, respiratory rate, temperature, oxygen saturation and urine output. This patient is responding to initial fluid resuscitation; therefore, it is appropriate to continue monitor blood pressure and urine output and give additional fluid.

New evidence found that the use of CVP alone to guide fluid resuscitation can no longer be justified given the limited ability of CVP to predict a response to a fluid challenge when the CVP is within a relatively normal range (8–12 mmHg).

In summary:

‐ Septic shock is a medical emergency and resuscitation should begin immediately.

‐ Initial fluid volume administered should start at 30 mL/kg.

‐ Further fluid administration should be based on haemodynamic status as determined by physiologic parameters (blood pressure, heart rate, urine output, oxygen saturation and temperature).

‐ A target MAP of 65mmHg may be used for vasopressor and fluid adjustment.

‐ Serial measurement of CVP, Scvo2 and haemoglobin using a CVC is no longer recommended.

Berger R, Rivers E, Levy M. Management of Septic Shock. New England Journal of Medicine. 2017;376(23):2282–2285.https://www.nejm.org/doi/full/10.1056/NEJMclde1705277

Rhodes A, Evans L, Alhazzani W, Levy M, Antonelli M, Ferrer R et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Intensive Care Medicine. 2017;43(3):304–377.

https://link.springer.com/article/10.1007%2Fs00134‐017‐4683‐6

25. Answer: B

The latest guidelines from the Surviving Sepsis Campaign give detailed recommendations of initial resuscitation, screening and diagnosis of sepsis, antibiotic therapy, fluid administration, source control, administration of vasopressors and steroids, blood products, anticoagulants, immunoglobulins, mechanical ventilation, sedation, analgesia, glucose control, blood purification, renal replacement therapy, bicarbonate, venous thromboembolism and stress ulcer prophylaxis, and nutrition.

Specific recommendations in antimicrobial treatment include:

Administration of IV antimicrobials be initiated as soon as possible after recognition, and within one hour for both sepsis and septic shock.

Empiric broad‐spectrum therapy with one or more antimicrobials for patients presenting with sepsis or septic shock to cover all likely pathogens (including bacterial and potentially fungal or viral coverage) should be used initially.

Empiric antimicrobial therapy be narrowed once pathogen identification and sensitivities are established and/or adequate clinical improvement is noted.

Daily assessment for de‐escalation of antimicrobial therapy in patients with sepsis and septic shock should be performed.

Do not use systemic antimicrobial prophylaxis in patients with severe inflammatory states of non‐infectious origin such as severe pancreatitis, burn injury.

Dosing strategies of antimicrobials should be optimised based on accepted pharmacokinetic/pharmacodynamic principles and specific drug properties in patients with sepsis or septic shock.

Do not use combination therapy for the routine treatment of neutropenic sepsis/bacteraemia.

An antimicrobial treatment duration of 7 to 10 days is adequate for most serious infections associated with sepsis and septic shock.

26. Answer: E

27. Answer: B

28. Answer: D

29. Answer: F

30. Answer: A

31. Answer: G

Inotropes and vasopressors are used in shock states to improve perfusion by increasing BP. As BP is a function of both cardiac output and systemic vascular resistance, medications can increase BP by either increasing one or both of these parameters. Vasopressors induce vasoconstriction and thereby elevate BP. Inotropes increase cardiac contractility; however, many drugs have both vasopressor and inotropic effects.

One of the key mechanisms by which medications can improve BP is by stimulation of adrenoreceptors. Dobutamine predominantly stimulates beta adrenoreceptors and very short half‐life, thus having greater effect on cardiac output than systemic vascular resistance. Noradrenaline has a greater effect on peripheral resistance than cardiac output, through greater alpha than beta action. Phenylephrine has predominantly alpha adrenoreceptor action, resulting in increased BP through increased peripheral resistance. Dopamine is a precursor to both noradrenaline and adrenaline, but also acts independently on the renal arteries, resulting in renal arteriolar dilatation. Vasopressin also acts has vasopressor actions through stimulation of V2 receptors on peripheral vessels. Milrinone is a phosphodiesterase III inhibitor, which has its inotropic effect through decreasing metabolism of cAMP, leading to prolonged cardiac myocyte contraction – cAMP causes vasodilation both in the pulmonary arteries and peripheral arteries, which can be a useful by‐effect, for example in pulmonary hypertension. As adrenoreceptor agonists and phosphodiesterase inhibitors increase intracellular calcium, they have an unwanted effect of increasing myocardial oxygen demand and are potentially pro‐arrhythmic.

Levosimendan enhances the calcium sensitivity of troponin C, resulting in increased cardiac output, and also causes peripheral vasodilation, through activation of ATP‐sensitive potassium channels in peripheral vessels. Omecamtiv is a newer inotrope that acts as a selective cardiac myosin activator, which is currently being studied in relation to therapy for left ventricular dysfunction.

Arrigo M, Mebazaa A. Understanding the differences among inotropes. Intensive Care Medicine. 2015;41(5):912–915.

https://link.springer.com/article/10.1007/s00134‐015‐3659‐7

32. Answer: H

This patient has clinical features of life‐threating asthma. Please see the following criteria.

Near fatal asthma

Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures.

Life‐threatening asthma

Any one of the following in a patient with severe asthma:

Peak expiratory flow (PEF) <33% best or predicted

SpO2<92%

PaO2<60mmHg

Normal PaCO2

Silent chest

Cyanosis

Feeble respiratory effort

Bradycardia

Dysrhythmia

Hypotension

Exhaustion

Confusion

Coma

Acute severe asthma

Any one of:

PEF 33–50% best or predicted

Respiratory rate >25/min

Heart rate >110/min

Inability to complete sentences in one breath.

Initial management for life‐threatening asthma includes:

Take an ABG.

Give high concentrations of inspired oxygen aiming to achieve oxygen saturations >92%.

Give short‐acting β2‐agonists, salbutamol repeatedly in 5mg doses or by continuous nebulization at 10 mg/h driven by oxygen.

Add nebulized ipratropium bromide to nebulized salbutamol for all patients with life‐threatening asthma as it has been shown to produce significantly greater bronchodilation than β2 agonists alone.

Give high dose intravenous hydrocortisone to all patients with life‐threatening asthma as early as possible in the episode, as this may improve survival.

Give a single intravenous dose of magnesium sulphate 1.2–2g over 20 min if there is no improvement after performing the above. It has been shown to be safe and effective in acute severe asthma. Magnesium is a smooth muscle relaxant, producing bronchodilation. Rapid administration may be associated with hypotension. As this patient’s BP is low, it is better to be given after transfer to ICU.

Transfer to ICU for consideration of intravenous bronchodilators, epinephrine and mechanical ventilation.

Australian Asthma Handbook [Internet]. Asthmahandbook.org.au. 2020 [cited 7 July 2020]. Available from:

http://www.asthmahandbook.org.au/acute-asthma/clinical

33. Answer: C

This patient has collapse and VT due to hyperkalaemia after missing his regular haemodialysis. The best immediate treatment is intravenous administration of 10 ml 10% calcium chloride to stabilise the myocardial cell membrane and lower the risk of VF. Calcium chloride is preferred over calcium gluconate for a patient experiencing a cardiac arrest because the chloride formulation has approximately 3 times the amount of elemental calcium compared with the gluconate formulation. Furthermore, gluconate must be hepatically metabolized before its associated calcium becomes bioavailable, which is unlikely in the setting of hemodynamic instability or poor liver function during cardiac arrest. Calcium chloride is preferably given intravenously via a central or a large peripheral line to avoid any potentially harmful effects should extravasation occur.

Hyperkalaemia raises the resting membrane potential, causing a narrowing between resting membrane potential and threshold potential for action potential generation. Calcium restores this initial narrowing back towards 15 mV by raising the threshold potential to being ‘less negative’. Calcium results in improvement in ECG changes within minutes of administration.

Calcium is essential for normal muscle and nerve activity. It transiently increases peripheral resistance, myocardial excitability and contractility. Randomized control trials and observational studies have demonstrated no survival benefits when calcium was given in‐hospital or out‐of‐hospital cardiac arrest patients. In VF, calcium did not restore spontaneous circulation.

Ahee P. The management of hyperkalaemia in the emergency department. Emergency Medicine Journal. 2000;17(3):188–191.https://emj.bmj.com/content/17/3/188

34. Answer: J

This patient’s cardiac monitor demonstrates torsade de pointes. It is the result of QTc prolongation which can either be congenital or acquired. Acquired QTc prolongation is most often drug‐related. There are many medications that can predispose a person to torsades such as antiarrhythmics, antipsychotics, antiemetics, antifungals, and antimicrobials. Prolonged QTc and Torsades are also associated with hypokalaemia, hypocalcaemia, hypomagnesemia, bradycardia, and heart failure.

Magnesium is an electrolyte essential for membrane stability. Hypomagnesaemia causes myocardial hyperexcitability particularly in the presence of hypokalaemia and digoxin. Electrical cardioversion should be performed for patients with hypotension or in cardiac arrest from torsades de pointes. Intravenous magnesium is the first‐line pharmacologic therapy of torsades de pointes. The recommended initial dose of magnesium is a slow 2 g IV push. An infusion of 1g to 4 g/hr should be started to keep the magnesium levels >2 mmol/L. Once the magnesium level is >3 mmol/L, the infusion can be stopped. Severe magnesium toxicity is seen with levels >3.5 mmol/L which can cause confusion, respiratory depression, and cardiac arrest. It is important to remember to correct any hypokalaemia as well. There is insufficient data to recommend for or against its routine use in cardiac arrest.

There are many causes of hypomagnesaemia. Heavy binge alcohol intake can lead to a loss of magnesium from tissues and increased urinary loss. Chronic alcohol abuse has been reported to deplete the total body supply of magnesium. This is the most likely cause in this case.

Schwartz PJ. Predicting the Unpredictable Drug‐Induced QT Prolongation and Torsades de Pointes. J Am Coll Cardiol 2016; 67:1639–50.

https://www.sciencedirect.com/science/article/pii/S0735109716003387

35. Answer: K

This case is a very typical occurrence in hospital. The patient is in pain after the fracture and is waiting for surgery. He receives opioid analgesia regularly. Opiate toxicity should be suspected when the clinical triad of depressed level of consciousness (reduced GCS), respiratory depression, and pupillary miosis are present. It is important to remember opioid exposure/toxicity does not always result in miosis and that respiratory depression is the most specific sign. Respiratory failure and respiratory acidosis is due to hypoventilation.

Airway control and adequate oxygenation is the primary supportive treatment. Intravenous naloxone should be given in patient with reduced level of consciousness and/or respiratory depression. The usual dose is between 0.4 and 2 mg. The onset of effect following intravenous naloxone is 1–2 min; maximal effect is observed within 5–10 min. A repeat dose is indicated for partial response and can be repeated as often as needed. To avoid precipitous withdrawal (nausea, vomiting, agitation) and consequent aspiration, naloxone may be started with low doses such as 0.1 mg and titrated up gradually until reversal of respiratory depression is achieved.

Boyer E. Management of Opioid Analgesic Overdose. New England Journal of Medicine. 2012;367(2):146–155.

https://pubmed.ncbi.nlm.nih.gov/22784117/

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