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Shock
Published in Ian Greaves, Keith Porter, Chris Wright, Trauma Care Pre-Hospital Manual, 2018
Ian Greaves, Keith Porter, Chris Wright
Hypovolaemic, cardiogenic and obstructive shock are all associated with vasoconstriction and increased systemic vascular resistance. In contrast, distributive or vasodilatory shock is associated with a failure of vasomotor tone and decreased systemic vascular resistance (4). The systemic release of histamine in anaphylaxis, the loss of sympathetic tone related to disruption of the autonomic pathways in spinal cord injury (neurogenic shock) and the systemic inflammatory response syndrome in sepsis are the commonest precipitants of distributive shock but other causes such as transfusion reactions and poisoning should be considered.
The management of major injuries
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Spinal fractures with spinal cord transection also disrupt the sympathetic nerve supply and cause distal vasodilatation. A high spinal transection will therefore cause neurogenic shock - this is vasodilatory shock and is characterized by hypotension, a low diastolic blood pressure, widened pulse pressure, warm and well-perfused peripheries and bradycardia. However, neurogenic shock can be complicated by hypovolaemic shock in multiply injured patients.
Acute coronary syndrome with haemodynamic instability
Published in K Sarat Chandra, AJ Swamy, Acute Coronary Syndromes, 2020
Davinder Singh Chadha, Keshavamurthy Ganapathy Bhat
Repeat haemodynamic assessment with insertion of haemodynamic (PCWP) catheter is done to guide therapeutic intervention (fluid replacement and vasopressor dosage). However, reperfusion therapy should not be delayed for the sake of insertion of a haemodynamic catheter [17,21,22]. Optimal PCWP for each patient is the lowest value that results in the highest cardiac output as long as the SaO2 is above 90%. The usual value in acute MI-related CS is between 18 and 25 mmHg [25]. Assessment of cardiac filling pressures so that hypovolemia and volume overload can be identified and corrected. Right ventricular (RV) MI often seen with inferior wall MI when complicated with CS may require more volume support as filling pressures are increased. Intravenous (IV) fluid replacement in these patients is indicated even if jugular (central) venous pressure is not elevated. Excess fluid replacement may, however, lead to RV dilatation with septal shift into the left ventricular and compromise its filling [26]. An early echocardiogram can be performed in this setting to guide clinical management.Evaluation of the response of cardiac output to therapeutic interventions, including volume management, sympathomimetics and mechanical support.Detection and quantification of intracardiac shunting in ventricular septal defect complicating acute MI.Calculation of systemic vascular resistance and discrimination of vasoconstrictive from vasodilatory shock.
The pharmacotherapeutic options in patients with catecholamine-resistant vasodilatory shock
Published in Expert Review of Clinical Pharmacology, 2022
Timothy E. Albertson, James A. Chenoweth, Justin C. Lewis, Janelle V. Pugashetti, Christian E. Sandrock, Brian M. Morrissey
High-dose hydroxocobalamin (vitamin B12a, trade name Cyanokit) is routinely used in the treatment of cyanide toxicity at a dose of 5 g IV over 15–30 min [136]. It is one of the active forms of vitamin B12 but it can also substitute a cyanide molecule for a hydroxyl group and bind the cyanide for urinary excretion [137]. Vasodilatory shock including vasoplegic shock is caused in part by vasodilation through NO-mediated mechanisms [138]. Hydroxycobalamin (HCB) is thought to be a potent binder/scavenger of NO (Table 2) [137,138]. Vasodilatory septic shock has elevated NO-mediated responses but may also have endogenous NO-mediated vasodilation and mitochondrial ‘intoxication’ mechanisms that contribute to vasodilation [136]. It is thought that HCB also scavenges, binds, and prevents formation of H2S in addition to NO [136].
Angiotensin axis antagonists increase the incidence of haemodynamic instability in dihydropyridine calcium channel blocker poisoning
Published in Clinical Toxicology, 2021
Jessica Huang, Nicholas A. Buckley, Katherine Z. Isoardi, Angela L. Chiew, Geoffrey K. Isbister, Rose Cairns, Jared A. Brown, Betty S. Chan
Dihydropyridine calcium channel blockers (CCBs) such as amlodipine, felodipine, lercanidipine and nifedipine are used as first-line treatment for essential hypertension [1]. In 2015, amlodipine was the fourth most commonly dispensed medication in Australia and the second most commonly prescribed antihypertensive medication by defined daily dose per day [2]. Dihydropyridine CCBs are perceived to be safer at therapeutic doses than non-dihydropyridine CCBs, such as verapamil and diltiazem, as they have more vascular selectivity and less negative chronotropy and inotropy [3]. Despite this, amlodipine is the leading contributor to cardiovascular drug related poisoning deaths (31.5%) in the USA [4]. Dihydropyridine overdose involves a loss of vascular selectivity [5,6] and a decrease in systemic vascular resistance to cause haemodynamic instability with hypotension and reflex tachycardia [7]. This may lead to vasodilatory shock [8,9].
Life-threatening triclopyr poisoning due to diethylene glycol monoethyl ether solvent
Published in Clinical Toxicology, 2021
K.Z. Isoardi, C.B. Page, M.S. Roberts, G.K. Isbister
A 66-year-old male with a past history of alcoholism and hypertension presented following a collapse in a nursing home. On arrival to hospital, he was confused with a GCS of 11 (M5), HR 89 bpm, BP 130/77 mmHg, RR of 20 and oxygen saturations of 97% on 4 litres of nasal prong oxygen. The arrival VBG revealed a high anion gap metabolic acidosis (pH 7.27, pCO2 29 mmHg, bicarbonate 13 mmol/L, AG 22 mmol/L, lactate 4.7 mmol/L) which progressed over the subsequent two and a half hours (pH 7.05, pCO2 33 mmHg, bicarbonate 9 mmol/L, AG 26 mmol/L, lactate 6.3 mmol/L). He had an acute kidney injury with a creatinine of 120 µmol/L (baseline 92 µmol/L [RR 64-108 µmol/L]). A provisional diagnosis of a toxic alcohol ingestion was made, and he was intubated, commenced on ethanol therapy and transferred to a tertiary hospital for dialysis. An osmolar gap performed 9 h post presentation was elevated at 33. He commenced continuous veno-venous haemodiafiltration 12 h following presentation. On day two, multiple boluses of sodium bicarbonate (600 mmol) and a bicarbonate infusion (100 mmol/h for 4 h) were given to treat metabolic acidosis. This was associated with vasodilatory shock treated with noradrenaline (peak dose 50 mcg/min) and vasopressin (peak dose 0.02 units/min). He had a four-hour course of high flux haemodialysis 29 h after presentation before switching back to haemodiafiltration that was continued up until 55 h after presentation (Figure 2).