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
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
