Regarding lactic acidosis, which ONE of the following is TRUE?
Answer: D: Adrenaline can cause hyperlactataemia and its use should be taken into account when interpreting blood lactate measurements.
Lactic acidosis is defined by convention as the combination of an increased blood lactate concentration >5 mmol/L and acidaemia (arterial blood pH < 7.35), whereas hyperlactaemia is defined as a blood lactate level ≥2 mmol/L. Critically ill patients with a lactic acidosis usually have a high mortality, and a blood lactate level >8 mmol/L predicts mortality. The initial degree to which lactate is elevated has been shown to correspond to the severity of shock. In addition, serial lactate measures can be used as a guide to assess the effectiveness of therapeutic intervention.
Bicarbonate therapy for lactic acidosis is controversial and its use is generally not recommended regardless of the degree of acidaemia. Cardiac dysfunction in patients is often due to other factors, with cytokines being the major cause in septic shock. There is no evidence to suggest that bicarbonate administration reverses myocardial depression or improves sensitivity to endogenous catecholamines.
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Regarding the management of septic shock in the ED, which ONE of the following statements is TRUE?
Answer: C: Adequate fluid resuscitation is fundamental in the management of patients with septic shock and should ideally be achieved before the use of vasopressors and inotropes. The crystalloid–colloid debate is still ongoing and so far there is no conclusive evidence that one is superior to the other. However, crystalloids are usually preferred as it is much cheaper.
Current recommendations are to maintain a mean arterial pressure (MAP) ≥65 mmHg to achieve minimal perfusion pressure and maintain adequate flow. Vasopressor therapy may be required, in addition to fluids, to achieve this. There is no high-quality evidence to recommend one catecholamine over the other. Animal and human studies suggest some advantages of noradrenaline and dopamine over adrenaline; adrenaline has the potential to cause tachycardia as well as deleterious effects on the splanchnic circulation and hyperlactataemia. However, there is no clinical evidence that adrenaline causes worse outcomes. Subsequently, the Surviving Sepsis Campaign advocates either noradrenaline or dopamine as the initial vasopressor to correct hypotension in septic shock. Adrenaline is recommended as the first chosen vasopressor if septic shock is poorly responsive to noradrenaline or dopamine.
The concept of relative adrenal insufficiency has led to the administration of low doses of hydrocortisone (200 mg/day) and is believed to decrease requirements for vasopressor agents and reduce mortality. However, in a recent multicentre, randomised, double-blind, placebo-controlled trial, hydrocortisone did not improve survival or reversal of septic shock. As a result, the Surviving Sepsis Campaign downgraded their recommendation on the use of steroids and suggests that intravenous hydrocortisone should be considered for adult septic shock when hypotension remains poorly responsive to adequate fluid resuscitation and vasopressors. An increased risk of infection and myopathy are known side effects of steroids.
Regarding haemodynamic monitoring in critically ill patients, which ONE of the following statements is TRUE?
Answer: C: The Trendelenburg position (supine head-down tilt of at least 45°) was originally intended to provide better surgical exposure for abdominal procedures. Over time, the Trendelenburg position has become popular in managing hypotension and shock, the proposed benefit being the shift of intravascular volume from the lower extremities and abdomen to the heart and brain therefore improving perfusion to these vital organs. However, current evidence does not support the use of the Trendelenburg position or head-down tilt in hypotensive patients because it does not appear to have any improvement in blood pressure or cardiac index. In addition, it may also have untoward effects on lung ventilatory mechanics and pulmonary gas exchange and is likely to increase intracranial pressure due to the effect on increased central venous pressure.
Passive leg raising (PLR) has been shown to be useful in predicting fluid responsiveness as it transiently increases venous return and causes an increase in cardiac output in patients who are preload responsive. It mimics an approximate equivalent of 300 mL blood bolus that persists for 2–3 minutes before resulting in intravascular volume redistribution. Furthermore, it has the advantage that this effect is reversible and can be used in the spontaneously breathing patient. The best way to perform a PLR manoeuvre is to elevate the lower limbs to 45° while at the same time placing the patient in the supine from a 45° semirecumbent position. Starting the PLR manoeuvre from a total horizontal position may induce an insufficient venous blood shift to elevate significantly cardiac preload. By contrast, starting PLR from a semirecumbent position induces a larger increase in cardiac preload because it induces the shift of venous blood not only from both the legs but also from the abdominal compartment.
Variations in arterial blood pressure can be observed during positive pressure mechanical ventilation as a result of changes in intrathoracic pressure and lung volumes. A large number of studies have demonstrated that the pulse pressure variation (PPV), derived from analysis of the arterial waveform, and the stroke volume variation (SVV), derived from pulse contour analysis, are accurate predictors of cardiac preload and highly predictive of fluid responsiveness. However, respiratory variability of haemodynamic signals cannot be used for predicting volume responsiveness in spontaneously breathing patients.
Early goal-directed therapy in sepsis has been associated with decreased mortality rates.
Regarding early goal-directed therapy in sepsis, which ONE of the following is NOT included in the end points of resuscitation?
Answer: C: Goal-directed resuscitation within the first 6 hours has been associated with decreased mortality rates in sepsis. It is aimed at restoring systemic perfusion and vital organ function. Patients are resuscitated to predefined physiological end points, which includes:
Regarding the use of vasoactive agents in shock, which ONE of the following is FALSE?
Answer: D: As Table below shows, dopamine’s actions are complex and dose-dependent. At low doses (<5 µg/ kg/min) dopamine causes vasodilation at vascular D1 receptors in renal, mesenteric and coronary beds. Dopamine might produce a diuresis but does not reduce the likelihood of renal failure. Therefore, the use of low-dose or ‘renal-dose’ dopamine to protect the kidneys is now discouraged and should not be used. At doses of 5–10 µg/kg/min, dopamine demonstrates activity at cardiac β1 receptors producing inotrope, whereas at higher doses (>10 µg/kg/min) it acts predominantly as an α-agonist, with a profile increasingly more like noradrenaline as the dose increases.
Noradrenaline is a potent α-agonist with significant activity at β1 receptors and minimal or no activity at β2 receptors. Due to the relative absence of β2 effect, noradrenaline causes an increase in both systolic and diastolic pressures. However, its effect on heart rate and cardiac output might be variable despite its positive inotropic and chronotropic actions as there is often a vagal mediated reduction in heart rate at low doses. Subsequently, despite the rise in MAP, cardiac output may remain the same or even fall. Metaraminol has an indirect effect by stimulating release of noradrenaline from sympathetic nerve terminals and is therefore a potent and selective α-agonist. Its duration of action is about 20 minutes; subsequently it is often administrated peripherally as a bolus for the short-term treatment of hypotension. However, metaraminol may induce a reflex bradycardia and increased ventricular afterload, which might be harmful in patients with cardiogenic shock or decompensated mitral regurgitation.
Isoprenaline is a synthetic non-selective β-agonist with β1 and β2 activities. The peripheral vasodilation due to β2 stimulation produces a marked reduction in peripheral vascular resistance with subsequent fall in diastolic and MAP, limiting its clinical utility.
ACTIONS OF VASOPRESSORS AND INOTROPES:
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