Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.
AA severity characterisation of trauma (ASCOT).                    pressure via a bladder catheter or nasogastric tube, us...
2      ABO blood groups         men, the urethral meatus) for bruises, lacerations, entry          Abuse of anaesthetic ag...
Acetylcholinesterase           3                CH3                           O                      (a)                  ...
4      Acetylcholinesterase inhibitors    and choline, thus terminating its action. The N(CH3)3þ part        l   Dosage:  ...
Acidosis, metabolic          5metabolism of neutral substances, organic acids are produced        See also, Acid; Base; Bl...
6      Acidosis, respiratory    Acidosis, respiratory. Acidosis due to increased arterial                                 ...
Acute lung injury         7agents the energy may be provided by sparks, e.g. from build-     Acute demyelinating encephalo...
8      Acute phase response        result of damage caused by free radicals. Examples             Acute physiology, age, c...
Adrenal gland          9l   Dosage:                                                          Adenylate cyclase, see Adenos...
10      Adrenaline     respectively. Hyposecretion causes adrenocortical insuffi-          for general anaesthetics and hav...
Upcoming SlideShare
Loading in …5

Anaesthesia and Intensive Care A-Z | ElsevierAsia


Published on

This updated encyclopaedia of anaesthesia and intensive care medicine covers aspects relating to Anesthesia & critical care medicine. With extensive line diagrams & topic descriptions, this is a reference title that every post graduate should own.

If you would like to purchase this title, please visit Elsevier Asia Bookshop.

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

Anaesthesia and Intensive Care A-Z | ElsevierAsia

  1. 1. AA severity characterisation of trauma (ASCOT). pressure via a bladder catheter or nasogastric tube, using aTrauma scale derived from the Glasgow coma scale, sys- water column manometer.tolic BP, revised trauma score, abbreviated injury scale Management includes laparotomy and leaving the abdomenand age. A logistic regression equation is used to provide a open and/or using silastic material to cover the abdominalprobability of mortality. Excludes patients with a very poor or contents. Paracentesis may be effective if raised intra-abdom-very good prognosis. Has been claimed to be superior to the inal pressure is due to accumulation of fluid, e.g. ascites. Fulltrauma revised injury severity score system although more resuscitation must be performed before decompression as rapidcomplex. release of pressure may result in sudden washout of inflamma-Champion HR, Copes WS, Sacco WJ, et al (1996). J Trauma; tory mediators from ischaemic tissues, causing acidosis and40: 42–8 hypotension. Malbrain ML, Cheatham ML, Kirkpatrick A, et al (2006).A–adO2, see Alveolar–arterial oxygen difference Intensive Care Med; 32: 1722–1732, and Cheatham ML, Malbrain ML, Kirkpatrick A (2007). Intensive Care Med;ABA, see American Board of Anesthesiology 33: 951–62 See also, Compartment syndromesAbbott, Edward Gilbert, see Morton, William Abdominal decompression. Technique in obstetric anal-Abbreviated injury scale (AIS). Trauma scale first gesia whereby negative pressure is applied to the abdomen indescribed in 1971 and updated many times since. Comprises order to reduce labour pain and possibly shorten labour.a classification of injuries with each given a 6-digit code (the Thought to act by making the uterus more spherical duringlast indicating severity, with 1 ¼ minor and 6 ¼ fatal). The contractions, thus contracting with less force. Now rarelycodes are linked to International Classification of Diseases, thus aiding standardisation of records. The anatomical See also, Obstetric analgesia and anaesthesiaprofile is a refinement in which the locations of injuries aredivided into four categories; the AIS scores are added and the Abdominal field block. Technique using 100–200 ml localsquare root taken to minimise the contribution of less severe anaesthetic agent, involving infiltration of the skin, subcuta-injuries. neous tissues, abdominal muscles and fascia. Provides anal-Copes WS, Lawnick M, Champion HR, Sacco WJ (1988). gesia of the abdominal wall and anterior peritoneum, but notJ Trauma; 28: 78–86 of the viscera. Now rarely used. Rectus sheath block, trans- versus abdominis plane block, iliac crest block andAbciximab. Monoclonal antibody preparation used as an inguinal hernia field block are more specific blocks.antiplatelet drug and adjunct to aspirin and heparin inhigh risk patients undergoing percutaneous transluminal Abdominal sepsis, see Intra-abdominal sepsiscoronary angioplasty. Consists of Fab fragments ofimmunoglobulin directed against the glycoprotein IIb/IIIa Abdominal trauma. May be blunt (e.g. road traffic acci-receptor on the platelet surface. Inhibits platelet aggregation dents) or penetrating (e.g. stabbing, bullet wounds). Oftenand thrombus formation; effects last 24–48 h after infusion. carries a high morbidity and mortality because injuries mayCareful consideration of risks and benefits should precede use go undetected. May lead to massive intra-abdominal bloodsince risk of bleeding is increased. Licensed for single use loss or abdominal compartment syndrome. The abdomenonly. can be divided into three areas:l Dosage: 250 mg/min iv 10–60 min (up to 24 h in unstable w intrathoracic: protected by the bony thoracic cage. Con- angina) before angioplasty with 125 mg/kg/min (up to tains the spleen, liver, stomach and diaphragm. Injury 10 mg/min for 12 h afterwards). may be associated with rib fractures. The diaphragml Side effects: bleeding, hypotension, nausea, bradycardia. may also be injured by blows to the lower abdomen Thrombocytopenia occurs rarely. (which impart pressure waves to the diaphragm) or by penetrating injuries of the chest.Abdominal compartment syndrome. Combination of w true abdomen: contains the small and large bowel,increased intra-abdominal pressure and organ dysfunction, bladder and, in the female, uterus, fallopian tubes ande.g. following abdominal trauma or extensive surgery, ovaries.resulting from haemorrhage, leakage of oedema fluid and/or w retroperitoneal: contains the kidneys, ureters, pancreasmassive intestinal oedema. May also follow liver transplant- and duodenum. May result in massive blood loss fromation and acute pancreatitis. Intra-abdominal pressures retroperitoneal venous injury.above 20–25 cmH2O may be associated with reduced venous l Management:return and cardiac output, impaired ventilation, reduced renal w basic resuscitation as for trauma generally.blood flow and oliguria. Increased CVP may lead to raised w initial assessment: examination of the anterior abdom-ICP. Diagnosed clinically and by measuring intra-abdominal inal wall, both flanks, back, buttocks, perineum (and in I
  2. 2. 2 ABO blood groups men, the urethral meatus) for bruises, lacerations, entry Abuse of anaesthetic agents. May occur because of easy and exit wounds. Signs may be masked by unconscious- access to potent drugs by operating theatre or ICU staff. ness, spinal cord injury or the effects of alcohol or Opioid analgesic drugs are the most commonly abused drugs. Abdominal swelling usually indicates intra- agents, but others include benzodiazepines and inhalational abdominal haemorrhage; abdominal guarding or rigidity anaesthetic agents. Abuse may be suggested by behavioural usually indicates visceral injury. Absence of bowel or mood changes, or excessive and inappropriate requests for sounds may indicate intra-peritoneal haemorrhage or opioids. Main considerations include the safety of patients, peritoneal soiling with bowel contents. Colonic or rectal counselling and psychiatric therapy for the abuser, and legal injuries may cause blood pr. A high index of suspicion is aspects of drug abuse. May be associated with alcoholism. required for retroperitoneal injuries since examination is Berry CB, Crome IB, Plant M, Plant M (2000). Anaesthesia; difficult. 55: 946–52 w imaging: abdominal X-ray may reveal free gas under the See also, Misuse of Drugs Act; Sick doctor scheme; Substance diaphragm (erect or semi-erect; may also be visible on abuse chest X-ray) or laterally (lateral decubitus X-ray); other investigations include pelvic X-ray and urological radi- Acarbose. Inhibitor of intestinal alpha glucosidases and ology if indicated (e.g. iv urogram, etc.), CT and MRI pancreatic amylase; used in the treatment of diabetes melli- scanning and ultrasound. tus, usually in combination with a biguanide or sulfony- w peritoneal lavage is indicated in blunt abdominal trauma lurea. Delays digestion and absorption of starch and associated with: sucrose. Has a small blood glucose lowering effect. - altered pain response (head injury, spinal cord injury, l Dosage: 50 mg orally once daily, increasing up to 200 mg drugs, etc.). 8 hourly. - unexplained hypovolaemia following multiple trauma. l Side effects include flatulence and diarrhoea, and rarely - equivocal diagnostic findings. hepatic dysfunction. Contraindicated in pregnancy and w insertion of a nasogastric tube and urinary catheter (pro- inflammatory bowel disease. vided no urethral injury; a suprapubic catheter may be See also, Meglitinides; Thiazolidinediones necessary). w indications for laparotomy include penetrating injuries, Accessory nerve block. Performed for spasm of trapezius obvious intra-abdominal haemorrhage, signs of bowel and sternomastoid muscles (there is no sensory component to perforation or a positive peritoneal lavage. the nerve). 5–10 ml local anaesthetic agent is injected 2 cm See also, Pelvic trauma below the mastoid process into the sternomastoid muscle, through which the nerve runs. ABO blood groups. Discovered in 1900 by Landsteiner in Vienna. Antigens may be present on red blood cells, with Accident, major, see Incident, major antibodies in the plasma (Table 1). The antibodies, mostly type-M immunoglobulins, develop within the first few ACD, Acid–citrate–dextrose solution, see Blood storage months of life, presumably in response to naturally occurring antigens of similar structure to the blood antigens. Infusion of ACD-CPR, Active compression decompression CPR, blood containing an ABO antigen into a patient who already see Cardiac massage; Cardiopulmonary resuscitation has the corresponding antibody may lead to an adverse reac- tion; hence the description of group O individuals as universal ACE, Angiotensin converting enzyme, see Renin/angioten- donors, and of group AB individuals as universal recipients. sin system [Karl Landsteiner (1868–1943), Austrian-born US patholo- gist] ACE anaesthetic mixture. Mixture of alcohol, chloroform See also, Blood cross-matching; Blood groups; Blood trans- and diethyl ether, in a ratio of 1:2:3 parts, suggested in 1860 as fusion an alternative to chloroform alone. Popular into the 1900s as a means of reducing total dose and side effects of any one of the ABPI, see Ankle Brachial Pressure Index three drugs. Abruption, see Antepartum haemorrhage ACE inhibitors, see Angiotensin converting enzyme inhibitors Absolute risk reduction. Indicator of treatment effect in clinical trials. For a reduction in incidence of events from a% Acetaminophen, see Paracetamol to b%, it equals (a–b)%. Does not give an indication of the magnitude of a or b. Acetazolamide. Carbonic anhydrase inhibitor, which See also, Meta-analysis; Number needed to treat; Odds ratio; reduces bicarbonate formation and hydrogen ion excretion, Relative risk reduction thereby creating a metabolic acidosis. Also a weak diuretic, but rarely used as such. Used to treat glaucoma, metabolic alkalosis, altitude sickness and childhood epilepsy. Useful in Table 1 Antigens and antibodies in ABO blood groups the treatment of severe hyperphosphataemia because it leads to urinary excretion of phosphate. May be used to Group Incidence in UK (%) Red cell antigen Plasma antibody lower ICP by reducing CSF production. Has been used to alkalinise the urine in tumour lysis syndrome or to enhance A 42 A Anti-B excretion in drug intoxications, e.g. with salicylates. B 8 B Anti-A l Dosage: 0.25–0.5 g orally/iv, once/twice daily. AB 3 A and B None O 47 None Anti-A and anti-B Acetylcholine (ACh). Neurotransmitter, the acetyl ester of the base choline (Fig. 1). Synthesised from acetylcoenzyme
  3. 3. Acetylcholinesterase 3 CH3 O (a) Nicotinic CH3 N+ CH2 CH2 O C CH3 Somatic muscle CH3 Nicotinic Muscarinic ParasympatheticFig. 1 Structure of acetylcholine Nicotinic Adrenergic Most nervesA and choline in nerve ending cytoplasm; the reaction iscatalysed by choline acetyltransferase. Choline is actively To sweat Nicotinic Muscarinictransported into the nerve and acetylcoenzyme A is formed in Sympathetic glandsmitochondria. ACh is stored in vesicles.l ACh is the transmitter at: To adrenal Nicotinic w autonomic ganglia. medulla w parasympathetic postganglionic nerve endings. (b) w sympathetic postganglionic nerve endings at sweat glands and some muscle blood vessels. w the neuromuscular junction. ε δ α α w many parts of the CNS where it has a prominent role in β learning. 10 nmHas either muscarinic or nicotinic actions, depending on theacetylcholine receptors involved. ACh is hydrolysed to cho-line and acetate by acetylcholinesterase on the postsynapticmembrane. Other esterases also exist, e.g. plasma cholines-terase.See also, Muscarine and muscarinic receptors; Neuromuscu-lar transmission; Nicotine and nicotinic receptors; Parasym- Lipidspathetic nervous system; Sympathetic nervous system;Synaptic transmission CytoskeletonAcetylcholine receptors. Transmembrane proteins acti-vated by acetylcholine (ACh). ACh receptors may be mus- Fig. 2 (a) Types of acetylcholine receptors. (b) Structure of nicotiniccarinic or nicotinic (Fig. 2a). Injected ACh first stimulates acetylcholine receptormuscarinic receptors. As the dose is increased, nicotinicreceptors are stimulated; i.e. parasympathetic stimulationand sweating precedes effects at ganglia and the neuromus-cular junction (NMJ). The structure of the postsynaptic (nicotinic) receptors atthe NMJ has been identified largely through work on theelectric eel. Each receptor consists of five glycosylated pro- Acetylcholinetein subunits which project into the synaptic cleft. The sub- Ounits have been designated a (mw 40 000), b (mw 49 000), +g (mw 60 000) and d (mw 67 000). The g subunit is thought to (CH3)3 N CH2 CH2 O C CH3be replaced by an e subunit in mammals. The subunits span Hthe postsynaptic membrane and form a cylinder around a Ocentral ion channel (Fig. 2b). The two a subunits of eachreceptor carry the binding sites for ACh. Occupation ofthese sites causes a configurational change of the subunits, Anionic site Esteratic sitethus opening the ion channel; cations (mainly sodium, potas-sium and calcium) flow through the channel according to their Choline O Acetylatedconcentration gradients and thus generate an action potential. + enzymeNon-depolarising neuromuscular blocking drugs at normal (CH3)3 N CH2 CH2 OH C CH3doses reduce the number of receptors available to ACh. At Ohigher doses they may also block the ion channel. Muscarinicreceptors are G protein-coupled receptors. Neuronal forms of ACh receptors are more heterogenouswith a large number of subunit configurations.See also, Muscarine and muscarinic receptors; Neuromuscu- Olar transmission; Nicotine and nicotinic receptors; Parasym- Acetate C CH3pathetic nervous system; Sympathetic nervous system;Synaptic transmission O HAcetylcholinesterase. Enzyme present in the basement Opostsynaptic membranes of cholinergic synapses andneuromuscular junctions. Also found in red blood cellsand the placenta. Converts acetylcholine (ACh) into acetate Fig. 3 Action of acetylcholinesterase
  4. 4. 4 Acetylcholinesterase inhibitors and choline, thus terminating its action. The N(CH3)3þ part l Dosage: of ACh binds to the anionic site of the enzyme, and the w paracetamol poisoning: 150 mg/kg (to a maximum of acetate end of ACh forms an intermediate bond at the esteratic 12 g) in 200 ml 5% dextrose iv over 15 min, followed by site. Choline is liberated, and the intermediate substrate/en- 50 mg/kg in 500 ml dextrose over 4 h, then 100 mg/kg zyme complex is then hydrolysed to release acetate (Fig. 3). in 1 litre dextrose over 16 h. See also, Acetylcholinesterase inhibitors; Neuromuscular w to reduce viscosity of airway secretions: 200 mg transmission; Synaptic transmission 8 hourly, orally. Has been delivered by nebuliser. l Side effects: rashes, anaphylaxis. Has been associated with Acetylcholinesterase inhibitors. Substances which bronchospasm in asthmatics. increase acetylcholine (ACh) concentrations by inhibiting acetylcholinesterase. Used clinically for their action at the Achalasia. Disorder of oesophageal motility caused by idio- neuromuscular junction in myasthenia gravis and in the pathic degeneration of nerve cells in the myenteric plexus or reversal of non-depolarising neuromuscular blockade. vagal nuclei. Results in dysphagia and oesophageal dilatation. Concurrent administration of an antimuscarinic agent, e.g. A similar condition may result from American trypanosomal atropine or glycopyrronium, reduces unwanted effects of infection (Chagas’ disease). Aspiration pneumonitis or increased ACh concentrations at muscarinic receptors. Ef- repeated chest infections may occur. Achalasia is treated by fects at ganglia are minimal at normal doses. Central effects mechanical distension of the lower oesophagus or by surgery. may occur if the drug readily crosses the blood–brain bar- Heller’s cardiomyotomy (longitudinal myotomy leaving the rier, e.g. physostigmine (used to treat the central anticholi- mucosa intact) may be undertaken via abdominal or thoracic nergic syndrome). approaches. Preoperative respiratory assessment is essential. Have also been used to treat tachyarrhythmias. Patients are at high risk of aspirating oesophageal contents, l Classification: and rapid sequence induction must be performed. w prosthetic: competitive inhibition at the anionic site of [Carlos Chagas (1879–1934), Brazilian physician; Ernst Hel- the enzyme prevents binding of ACh, e.g. edropho- ler (1877–1964), German surgeon] nium, tetrahydroaminocrine. See also, Aspiration of gastric contents; Induction, rapid w oxydiaphoretic: acts as a substrate for the enzyme; the sequence reaction proceeds as far as the intermediate substrate/ enzyme complex. Hydrolysis of the complex and thus Achondroplasia. Skeletal disorder, inherited as an autoso- reactivation of the enzyme is slow. mal dominant gene, although most cases arise by spontaneous Examples: mutation. Results in dwarfism, with normally sized trunk and - neostigmine, physostigmine (few hours). shortened limbs. Flat face, bulging skull vault and spinal - pyridostigmine (several hours). deformity may make tracheal intubation difficult, and the - distigmine (up to a day). larynx may be smaller than normal. Obstructive sleep apnoea Organophosphorus compounds act as oxydiaphoretic may occur. Foramen magnum and spinal canal stenoses may inhibitors, but the substrate/enzyme complex is minimally be present. The former may result in cord compression on hydrolysed; inhibition lasts for weeks until new enzyme is neck extension; the latter may make central regional blockade synthesised. difficult and reduce volume requirements for epidural Acetylcholinesterase inhibitors augment depolarising anaesthesia. neuromuscular blockade and may cause depolarising block- ade in overdose. They may also cause bradycardia, hypoten- Aciclovir. Antiviral drug; an analogue of nucleoside sion, agitation, miosis, increased GIT activity, sweating and 2’-deoxyguanosine. Inhibits viral DNA polymerase; active salivation. against herpes viruses and used in the treatment of encephal- Centrally acting acetylcholinesterase inhibitors (e.g. done- itis, varicella zoster (chickenpox/shingles) and postherpetic pezil, rivastigmine, galantamine) are used for symptomatic neuralgia, and for prophylaxis and treatment of herpes infec- treatment of Alzheimer’s dementia. Of potential anaesthetic tions in immunocompromised patients. Treatment should relevance because of their side effects (including nausea, start at onset of infection; the drug does not eradicate the vomiting, fatigue, muscle cramps, increased creatine kinase, virus but may markedly attenuate the clinical infection. convulsions, bradycardia, confusion) and enhancement of the l Dosage: actions of suxamethonium. w as topical cream, 5 times daily. [Alois Alzheimer (1864–1915), German neurologist and w 200–800 mg orally, 2–5 times daily in adults. pathologist] w 5–10 mg/kg 8 hourly iv, infused over 1 h. See also, Neuromuscular transmission; Organophosphorus l Side effects: rashes, GIT disturbances, hepatic and renal poisoning impairment, blood dyscrasias, headache, dizziness, severe local inflammation after iv use, confusion, convulsions, N-Acetylcysteine. Derivative of the naturally occurring coma. amino acid, l-cysteine. A free radical scavenger, it acts as an antidote in paracetamol poisoning, probably by restoring Acid. Substance which yields hydrogen ions in solution. depleted hepatic stores of glutathione or by acting as an alternative substrate for a toxic metabolite of paracetamol. Acidaemia. Arterial pH < 7.35 or hydrogen ion concen- Also used as an ocular lubricant. tration > 45 nmol/l. Has been investigated for a possible role in protection See also, Acid–base balance; Acidosis against myocardial reperfusion injury, treatment of ful- minant hepatic failure, and treatment of MODS, acute Acid–base balance. Maintenance of stable pH in body fluids lung injury and neuropsychiatric complications of carbon is necessary for normal enzyme activity, ion distribution and monoxide poisoning. Has also been used as a mucolytic protein structure. Normally, blood pH is maintained at 7.35– because of its ability to split disulphide bonds in mucus 7.45 (hydrogen ion (Hþ) concentration 35–45 nmol/l); intra- glycoprotein. cellular pH changes with extracellular pH. During normal
  5. 5. Acidosis, metabolic 5metabolism of neutral substances, organic acids are produced See also, Acid; Base; Blood gas tensions; Breathing, controlwhich generate hydrogen ions. of; Davenport diagram; Siggaard-Andersen nomograml Maintenance of pH depends on: w buffers in tissues and blood, which minimise the in- Acid–citrate–dextrose solution, see Blood storage crease of Hþ concentration. Acidosis. A process in which arterial pH < 7.35 (or hydro- w regulation by kidneys and lungs; the kidneys excrete gen ion > 45 mmol/l), or would be < 7.35 if there were no about 60–80 mmol and the lungs about 15–20 000 compensatory mechanisms of acid–base balance. mmol Hþ per day. See also, Acidosis, metabolic; Acidosis, respiratoryBecause of the relationship between CO2, carbonic acid,bicarbonate (HCO3À) and Hþ, and the ability to excrete Acidosis, metabolic. Acidosis due to metabolic causes,CO2 rapidly from the lungs, respiratory function is important resulting in an inappropriately low pH for the measuredin acid–base balance: arterial Pco2. l Caused by: H2 O þ CO2 Ð H2 CO3 Ð HCOÀ þ Hþ 3 w increased acid production:Thus hyper- and hypoventilation cause alkalosis and acidosis - ketone bodies, e.g. in diabetes mellitus.respectively. Similarly, hyper- or hypoventilation may com- - lactate, e.g. in shock, exercise.pensate for non-respiratory acidosis or alkalosis respectively, w acid ingestion: e.g. salicylate poisoning. þby returning pH towards normal. w failure to excrete hydrogen ion (H ): Sources of Hþ excreted via the kidneys include lactic acid - renal failure.from blood cells, muscle and brain, sulphuric acid from me- - distal renal tubular acidosis.tabolism of sulphur-containing proteins, and acetoacetic acid - carbonic anhydrase inhibitors.from fatty acid metabolism. w loss of bicarbonate:l The kidney can compensate for acid–base disturbances in - diarrhoea. three ways: - gastrointestinal fistulae. À w by regulating the amount of HCO3 reabsorbed. 80– - proximal renal tubular acidosis. 90% of filtered HCO3À is reabsorbed in the proximal - ureteroenterostomy. tubule: l May be differentiated by the presence or absence of an - filtered sodium ion is exchanged for Hþ across the anion gap: tubule cell membrane. w anion gap metabolic acidosis occurs in renal failure, - filtered HCO3À and excreted Hþ form carbonic acid. lactic acidosis, ketoacidosis, rhabdomyolysis and fol- - carbonic acid is converted to CO2 and water by car- lowing ingestion of certain toxins (e.g. salicylates, bonic anhydrase on the cell membrane. methanol, ethylene glycol). - CO2 and water reform carbonic acid (catalysed again w non-anion gap (hyperchloraemic) metabolic acidosis is by carbonic anhydrase) within the cell. caused by the administration of chloride-containing - carbonic acid releases HCO3À and Hþ. solutions (e.g. saline) in large volumes, amino acid - HCO3À passes into the blood; Hþ is exchanged for solutions, diarrhoea, pancreatic fistulae, ileal loop pro- sodium ion, etc. cedures, after rapid correction of a chronically compen- w by forming dihydrogen phosphate from monohydrogen sated respiratory alkalosis or renal tubular acidosis. þ phosphate in the distal tubule (HPO42ÀþHþ!H2PO4À). l Primary change: increased H /decreased bicarbonate. The Hþ is supplied from carbonic acid, leaving HCO3À l Compensation: which passes into the blood. w hyperventilation: plasma bicarbonate falls by about w by combination of ammonia, passing out of the cells, 1.3 mmol/l for every 1 kPa acute decrease in arterial with Hþ, supplied as above. The resultant ammonium Pco2, which usually does not fall below 1.3–1.9 kPa ions cannot pass back into the cells. (10–15 mmHg). þIn acid–base disorders, the primary change determines w increased renal H secretion.whether a disturbance is respiratory or metabolic. The direc- l Effects:tion of change in Hþ concentration determines acidosis or w hyperventilation (Kussmaul breathing).alkalosis. Renal or respiratory compensation attempts to w confusion, weakness, coma.restore normal pH, not reverse the primary change. For w cardiac depression.example, in the Henderson–Hasselbalch equation: w hyperkalaemia. l Treatment: [HCOÀ ] pH ¼ pKa þ log 3 w of underlying cause. [CO2 ] w bicarbonate therapy is reserved for treatment of severeadjustment of the HCO3À/CO2 concentration ratio restores acidaemia (e.g. pH under 7.1) because of problemspH towards its normal value, e.g.: associated with its use. w primary change: increased CO2; leads to decreased pH If bicarbonate is required, a formula for iv infusion is: (respiratory acidosis). base excess  body weight (kg) À w compensation: HCO3 retention by kidneys; increased mmol ammonium secretion, etc. 3An ‘alternative approach’ suggested by Stewart in 1983 focuses Half this amount is given initially.on the strong ion difference to explain the underlying pro- w other agents under investigation include sodiumcesses rather than the above ‘traditional approach’ which con- dichloroacetate, Carbicarb (sodium bicarbonate andcentrates more on interpretation of measurements. It is based on carbonate in equimolar concentrations) and THAMthe degree of dissociation of ions in solution, in particular the (2-amino-2-hydroxymethyl-1,3-propanediol).effects of strong ions and weak acids, and the role of bicarbon- Morris CG, Low J (2008). Anaesthesia; 63: 294–301 andate as a marker of acid–base imbalance rather than a cause. 396–411[Peter Stewart (1921–1993), Canadian physiologist] See also, Acidaemia; Acid–base balance
  6. 6. 6 Acidosis, respiratory Acidosis, respiratory. Acidosis due to increased arterial (a) Pco2. Caused by alveolar hypoventilation. l Primary change: increased arterial Pco2. l Compensation: +40 w initial rise in plasma bicarbonate due to increased car- bonic acid formation and dissociation. w increased acid secretion/bicarbonate retention by the 0 kidneys. In acute hypercapnia, bicarbonate concentra- mV C tion increases by about 0.7 mmol/l per 1 kPa rise in B arterial Pco2. In chronic hypercapnia it increases by 2.6 mmol/l per 1 kPa. –55 l Effects: those of hypercapnia. –70 D l Treatment: of underlying cause. A E See also, Acidaemia; Acid–base balance ACLS, see Advanced Cardiac Life Support 0 1 2 3 Time (ms) Acquired immune deficiency syndrome (AIDS), see (b) Human immunodeficiency viral infection +20 1 2 Acromegaly. Disease caused by excessive growth hor- mone secretion after puberty; usually caused by a pituitary 0 adenoma but ectopic secretion may also occur. Incidence is 6–8 per million population. l Features: 3 w enlarged jaw, tongue and larynx; widespread increase in mV 0 soft tissue mass; enlarged feet and hands. Nerve entrap- ment may occur, e.g. carpal tunnel syndrome. w respiratory obstruction, including sleep apnoea. w tendency towards diabetes mellitus, hypertension and 4 –90 cardiac failure (may be due to cardiomyopathy). Thyroid and adrenal impairment may occur. Apart from the above diseases, acromegaly may present 0 100 200 difficulties with tracheal intubation and maintenance of Time (ms) the airway. Treatment is primarily pituitary surgery with or without sub- Fig. 4 (a) Nerve action potential (solid) showing changes in sodium (dotted) and potassium (dashed) conductance. (b) Cardiac action sequent radiotherapy. Some patients respond to bromocrip- potential (see text) tine or somatostatin analogues. Smith M, Hirsch NP (2000). Br J Anaesth; 85: 3–14 polarisation. Sodium permeability then falls. Potassium ACT, Activated clotting time, see Coagulation studies permeability increases slowly and helps bring about repolar- isation. Normal ion distribution is restored due to action of the Acta Anaesthesiologica Scandinavica. Official journal of sodium/potassium pump. The action potential is followed the Scandinavian Society of Anaesthesiology and Intensive by a refractory period. Care Medicine, first published in 1957. Action potentials in nerve and other cells involve similar changes; in cardiac muscle, however, a plateau follows ACTH, see Adrenocorticotrophic hormone depolarisation, brought about by calcium entry. The refractory period is thus lengthened (Fig. 4b). Actin. One of the protein components of muscle (mw l There are five phases of the cardiac action potential: 43 000). In muscle, arranged into a double strand of thin w phase 0: fast depolarisation and sodium entry. filaments (F-actin) with globular ‘beads’ (G-actin), to which w phase 1: onset of repolarisation due to sodium channel myosin binds, along their length. Present in all cells as micro- closure. filaments. w phase 2: plateau due to calcium entry. See also, Muscle contraction w phase 3: repolarisation. w phase 4: resting membrane potential. In pacemaker Action potential. Sequential changes in transmembrane cells, there is slow spontaneous depolarisation, due to potential that result in the propagation of electrical impulses decreased potassium permeability, leading to initiation in excitable cells (Fig. 4a). of impulses. l Stages involved are summarised as follows: See also, Nerve conduction w A: depolarisation of the membrane by 15 mV (threshold level). Activated charcoal, see Charcoal, activated w B: rapid depolarisation to þ40 mV. Activated clotting time, see Coagulation studies w C: repolarisation, rapid at first then slow. w D: hyperpolarisation. Activated protein C, see Drotrecogin alfa; Protein C w E: return to the resting membrane potential. Depolarisation causes opening of sodium channels and Activation energy. Energy required to initiate a chemical entry of sodium ions into the cell, which causes further de- reaction. For ignition of explosive mixtures of anaesthetic
  7. 7. Acute lung injury 7agents the energy may be provided by sparks, e.g. from build- Acute demyelinating encephalomyelopathy, see De-up of static electricity or electrical equipment. Combustion of myelinating diseasescyclopropane requires less activation energy than thatof diethyl ether. Activation energy is less for mixtures with Acute life-threatening events – recognition and treat-O2 than with air, and least for stoichiometric mixtures of ment (ALERT). Multiprofessional course developed in anreactants. effort to reduce the incidence of potentially avoidable car-See also, Explosions and fires diac arrests, admissions to ICU and in-hospital deaths. Aimed especially at pre-registration house officers, wardActive compression/decompression cardiopulmon- nurses and physiotherapists, but suitable for other clinicalary resuscitation, see Cardiac massage; Cardiopulmonary groups. Based on principles of many life-support trainingresuscitation programmes (e.g. ALS, ATLS, APLS, CCrISP), its devel- opment embraces both clinical governance and multiprofes-Active transport. Energy-requiring transport of particles sional education. Uses a structured and prioritised system ofacross cell membranes. Protein ‘pumps’ within the mem- patient assessment and management to assist ward staff tobranes utilise energy which is usually supplied by ATP recognise patients at risk of deterioration and those who aremetabolism, in order to move ions and molecules, often already seriously ill. Using a system of assessment similar toagainst concentration gradients. A typical example is the that of CCrISP, participants are taught to manage life-threat-sodium/potassium pump. ening events and to organise subsequent care. Smith GB, Osgood VM, Crane S (2002). Resuscitation; 52:Acupuncture. Use of fine needles (usually 30–33 G) to 281–6produce healing and pain relief. Originated in China thou- See also, Early warning scores; Medical emergency team;sands of years ago, and closely linked with the philosophy and Outreach teampractice of traditional Chinese medicine. Thus abnormalitiesin the flow of Qi (Chi: the life energy that circulates around Acute lung injury (ALI). Syndrome of inflammation andthe body along meridians, nourishing the internal organs) increased permeability of lung tissue associated with a varietyresult in imbalance between Yin and Yang, the two polar of clinical, radiological and physiological abnormalities thatopposites present in all aspects of the universe. Internal cannot be explained by, but may coexist with, left atrial orabnormalities may be diagnosed by pulse diagnosis (palpation pulmonary capillary hypertension. Associated with sepsis,of the radial arteries at different positions and depths). multiple trauma, aspiration pneumonitis, multiple bloodThe appropriate organ is then treated by acupuncture at transfusion, pancreatitis, cardiopulmonary bypass and fatspecific points on the skin, often along the meridian named embolism. Onset is usually within 2–3 days of the precipitat-after, and related to, that organ. Yin and Yang, and flow of Qi, ing illness or injury, although direct lung insults usually haveare thus restored. a shorter insult-to-onset time. Acute respiratory distress Modern Western acupuncture involves needle insertion at syndrome (ARDS) is now regarded to be the most severesites chosen for more ‘scientific’ reasons; e.g. around an form of ALI. Both ARDS and ALI have similar diagnosticaffected area, at trigger points found nearby, or more prox- features which include:imally but within the appropriate dermatome. These may be w acute onset.combined with distant or local traditional points, although w bilateral diffuse infiltrates seen on the chest X-ray.conclusive evidence for the existence of acupuncture points w pulmonary wedge pressure £ 18 mmHg or absence ofand meridians has never been shown. The needles may be left clinical evidence of left atrial hypertension.inserted and stimulated manually, electrically or thermally to w arterial hypoxaemia resistant to oxygen therapy aloneincrease intensity of stimulation. Pressure at acupuncture (Pao2/FIo2 < 39.9 kPa [300 mmHg] for definition ofpoints (acupressure) may produce similar but less intense ALI; < 26.6 kPa [200 mmHg] for definition ofstimulation. ARDS), regardless of the level of PEEP.l Possible mechanisms: The definitions of ALI and ARDS are increasingly being w local reflex pathways at spinal level. challenged. w closure of the ‘gate’ in the gate control theory of pain. Other features: w central release of endorphins/enkephalins, and pos- w reduced respiratory compliance, lung volumes and sibly involvement of other neurotransmitters. increased work of breathing. · · w modulation of the ‘memory’ of pain. w V/Q mismatch and increased shunt.Still used widely in China. Increasingly used in the West for w pulmonary vascular resistance may be raised.chronic pain, musculoskeletal disorders, headache and mi- w an air bronchogram may be seen on the chest X-ray.graine, and other disorders in which modern Western medi- w in uncomplicated ALI, plasma oncotic pressure iscine has had little success. Claims that acupuncture may be normal.employed alone to provide analgesia for surgery are now w MODS may occur and is a common cause of death.viewed with scepticism, although it has been used to provide l Pathophysiology: ALI results from damage to either theanalgesia and reduce PONV (e.g. 5 minutes’ stimulation at lung epithelium or endothelium. Two pathways of injurythe point P6 (Pericardium 6: 1–2 inches (2.5–5 cm) proximal exist:to the distal wrist crease, between flexor carpi radialis and w direct effects of an insult on lung cells, e.g. aspiration,palmaris longus tendons). smoke inhalation.Wang SM, Kain ZN, White P (2008). Anesth Analg; 106: w indirect result of an acute systemic inflammatory602–10 and 611–21 response involving both humoral (activation of comple- ment, coagulation and kinin systems; release ofAcute cortical necrosis, see Renal failure mediators including cytokines, oxidants, nitric oxide, etc.) and cellular (neutrophils, macrophages andAcute crisis resource management, see Crisis resource lymphocytes) components. Pulmonary infiltration bymanagement neutrophils leads to interstitial fibrosis, possibly as a
  8. 8. 8 Acute phase response result of damage caused by free radicals. Examples Acute physiology, age, chronic health evaluation, see include sepsis, pancreatitis, fat embolism, etc. APACHE III scoring system Histopathological findings can be divided into three phases: exudative (oedema and haemorrhage), prolifera- Acute physiology and chronic health evaluation, see tive (organisation and repair) and fibrotic. APACHE/APACHE II scoring systems l Treatment is largely supportive: w general support: nutrition, DVT prophylaxis, preven- Acute physiology score (APS). Physiological component tion of infection, etc. of severity of illness scoring systems, such as APACHE II/III w O2 therapy (trying where possible to keep FIo2 below and Simplified APS. Weighted values (e.g. 0 to 4 in APACHE 0.6). CPAP is often helpful as it improves FRC. II) are assigned to each of a range of physiological variables w ventilatory support: IPPV may be necessary if CPAP (e.g. temperature, mean arterial blood pressure, serum creati- is ineffective. PEEP is often required, but airway nine) on the basis of its derangement from an established pressure is often already high because of reduced ‘normal’ range, as measured either upon ICU admission or compliance, increasing the risk of barotrauma and within 24 h of entry. The sum of all assigned weighted values impaired cardiac output. CO2 elimination may demand for the physiological variables that comprise a given scoring increasing minute volumes but this too risks ventila- system constitutes the acute physiological score. The higher tor-associated lung injury. This has led to the devel- the acute physiology score, the sicker the patient. opment of lung protection strategies including See also, Mortality/survival prediction on intensive care unit; low-frequency minute volume ventilation with extra- Simplified acute physiology score corporeal CO2 removal, permissive hypercapnia and the use of smaller than normal tidal volumes. Acute respiratory distress syndrome (ARDS). Previ- Other ventilatory strategies used to minimise ventila- ously termed adult respiratory distress syndrome, despite the tor-associated lung injury in ALI include inverse ratio process also occurring in children. First described in 1967 as ventilation (at I:E ratios of up to 4:1), airway pres- non-cardiogenic pulmonary oedema secondary to condi- sure release ventilation and high frequency ventila- tions not primarily affecting the lungs (e.g. shock, sepsis, tion. Extracorporeal membrane oxygenation has pancreatitis, massive blood transfusion, fat embolism). been used with varying success. Now regarded as the most severe form of acute lung injury w posture of the patient: prone ventilation may improve (ALI). Distinguished from ALI purely on the Pao2/FIo2 ratio oxygenation in some patients. which is < 26.6 kPa (200 mmHg) for ARDS. w fluid restriction is usually instituted to reduce lung Pathophysiology, treatment, etc. is as for ALI. Histo- water, although avoidance of initial fluid overload is logical appearances are similar to respiratory distress syn- thought to be more important. Diuretics have been drome of the newborn, hence its name. Overall mortality of used, with careful monitoring of renal function. ARDS is approximately 50–60% but depends on the under- w vasodilator drugs have been used to decrease pul- lying cause; it is highest following aspiration pneumonitis monary vascular resistance, e.g. prostacyclin. Nitric or sepsis. Early deaths are rare, and patients dying late in the oxide has also been used to produce pulmonary vaso- course of the illness usually die with hypoxaemia not because dilatation, but there is, as yet, little evidence of long- of it. For survivors, residual pulmonary impairment is pos- term benefit. sible but rarely severe. w fears over leakage of colloids into pulmonary interstitial Wheeler AP, Bernard GR (2007). Lancet; 369: 1553–64 spaces, with subsequent exacerbation of oedema, are balanced by possible advantages of colloids in maintain- Acute tubular necrosis, see Renal failure ing oncotic pressure. w corticosteroid therapy is controversial. There appears Acyclovir, see Aciclovir to be no benefit to their prophylactic administration, nor in high-dose, short-term therapy at the onset of ALI/ Addiction, see Alcoholism; Substance abuse ARDS. However, corticosteroids may have a role in non-resolving ARDS. Addison’s disease, see Adrenocortical insufficiency w free radical scavengers, antiprostaglandins and antipro- teases have been investigated. ADEM, Acute demyelinating encephalomyelopathy, see Wheeler AP, Bernard GR (2007). Lancet; 369: 1553–64 Demyelinating diseases Acute phase response. A reaction of the haemopoietic and Adenosine. Nucleoside, of importance in energy homeo- hepatic systems to inflammation or tissue injury, assumed to stasis at the cellular level. Reduces O2 consumption, increases be of benefit to the host. There is a rise in the number/activity coronary blood flow, causes vasodilatation and slows atrio- of certain cells (neutrophils, platelets) and plasma proteins ventricular conduction (possibly via increased potassium (e.g. fibrinogen, complement, C-reactive protein, plasmino- conductance and reduced calcium conductance). Also an gen, haptoglobin) involved in host defence, whilst there is a inhibitory CNS neurotransmitter. reduction in proteins which have transport and binding func- Has become the drug of choice for treatment of SVT tions (e.g. albumin, haemoglobin, transferrin). Initiated by (including that associated with Wolff–Parkinson–White actions of cytokine mediators such as interleukins (IL-1a, syndrome) and diagnosis of other tachyarrhythmias by slow- IL-1b, IL-6 and IL-11), tumour necrosis factors (a and b) and ing atrioventricular conduction. Its short half-life (8–10 s) leukaemia inhibitory factor. and lack of negative inotropism make it an attractive alterna- Serum levels of acute phase proteins (e.g. C-reactive pro- tive to verapamil. Unclassified as an antiarrhythmic drug. tein) can be helpful in diagnosis, monitoring and prognosis of Has also been used as a directly acting vasodilator drug in certain diseases. The rise in fibrinogen levels causes an ele- hypotensive anaesthesia. Increases cardiac output, with vation in ESR. The fall in albumin is due to redistribution and stable heart rate. Its effects are rapidly reversible on stopping decreased hepatic synthesis. the infusion.
  9. 9. Adrenal gland 9l Dosage: Adenylate cyclase, see Adenosine monophosphate, cyclic w SVT: 3 mg by rapid iv injection; if unsuccessful after 1– 2 min this is followed by 6 mg and then 12 mg. ADH, Antidiuretic hormone, see Vasopressin w hypotensive anaesthesia: 50–300 mg/kg/min. ATP has also been used. Adhesion molecules. Molecules normally sited on celll Side effects are usually mild and include flushing, dys- surfaces, involved in embryogenesis, cell growth and differ- pnoea and nausea. Bronchoconstriction may occur in asth- entiation, and wound repair. Also mediate endothelial cell/ matics. Bradycardia is resistant to atropine. Adenosine’s leucocyte adhesion, transendothelial migration and cytotoxic action is prolonged in dipyridamole therapy (because T cell-induced lysis. Four major families exist: integrins, uptake of adenosine is inhibited) and reduced by theo- cadherins, selectins (named after the tissues in which they phylline and other xanthines (because of competitive were discovered: L-selectin (leucocytes), E-selectin (endo- antagonism). Transplanted hearts are particularly sensitive thelial cells), P-selectin (platelets)) and members of the to adenosine’s effects. immunoglobulin superfamily. In general, contact between an adhesion receptor and theAdenosine monophosphate, cyclic (cAMP). Cyclic extracellular milieu results in the transmission of informationadenosine 3’,5’-monophosphate, formed from ATP by the allowing the cell to interact with its environment. Defectiveenzyme adenylate cyclase. Activation of surface receptors interactions involving adhesion molecules are implicated inmay cause a guanine nucleotide regulatory protein (G pro- disease (e.g. certain skin diseases, metastasis of cancer cells).tein) to interact with adenylate cyclase with resultant Many pathogens use adhesion receptors to penetrate tissueincreases in intracellular cAMP levels (Fig. 5). Many sub- cells. Overexpression of intravascular adhesion molecules orstances act on surface receptors in this way, including cat- receptors has been implicated in rheumatoid arthritis andecholamines (b effects), vasopressin, ACTH, histamine, rejection of transplanted organs. Control of vascular integrityglucagon, parathyroid hormone and calcitonin. and defence against invasive pathogens requires regulation of Some substances inhibit adenylate cyclase via an inhibitory adhesive interactions among blood cells and between bloodregulatory protein, e.g. noradrenaline at a2-adrenergic receptors. cells and the vessel walls. Circulating leucocytes bind to the cAMP causes phosphorylation of proteins, particularly selectins of activated endothelial cells, become activated byenzymes, by activating protein kinases. Phosphorylation chemoattractants and migrate through intracellular gaps to thechanges enzyme activity and therefore cell metabolism; thus site of inflammation. Thus adhesion molecules play a part inthe intracellular concentration of cAMP determines cell the inflammatory response in sepsis.activity, and cAMP acts as a ‘second messenger’. cAMP is inactivated by phosphodiesterase to 5’-AMP. Adiabatic change. Volume change of a gas in which there isPhosphodiesterase inhibitors, e.g. aminophylline and no transfer of heat to or from the system. Sudden compressionenoximone, increase cAMP levels. of a gas without removal of resultant heat causes a rise in temperature. This may occur in the gas already present in theAdenosine triphosphate and diphosphate (ATP and valves and pipes of an anaesthetic machine when a cylinderADP). ATP is the most important high-energy phosphate is turned on (hence the danger of explosion if oil or grease iscompound. When hydrolysed to form ADP, it releases large present). Sudden adiabatic expansion of a gas results in cool-amounts of energy which may be utilised in many cellular ing, as in the cryoprobe.processes, e.g. active transport, muscle contraction, etc. Its See also, Isothermal changephosphate bonds are formed using energy from catabolism;aerobic glycolysis generates 38 moles of ATP per mole of Adjustable pressure-limiting valves. Valves which openglucose, and anaerobic glycolysis yields 2 moles of ATP. to allow passage of expired and surplus fresh gas from a Other high-energy phosphate compounds include phos- breathing system, but close to prevent indrawing of air.phorylcreatine (in muscle), ADP itself, and other nucleotides. Ideally the opening pressure should be as low as possible toSee also, Cytochrome oxidase system; Metabolism; Tricar- reduce resistance to expiration, but not so low as to allow theboxylic acid cycle reservoir bag to empty through it. Most contain a thin disc held against its seating by a spring, as in the original Heid- brink valve. Adjusting the tension in the spring, usually by β-Receptor α2-Receptor screwing the valve top, alters the pressure at which the valve opens. The valve must be vertical in order to function correctly. Cell membrane Modern valves, even when screwed fully down, will open Gs Gi at high pressures (60 cmH2O). Most are now encased in a Adenylate hood for scavenging of waste gases. cyclase Phosphodiesterase [Jay A Heidbrink (1875–1957), US anaesthetist] See also, Anaesthetic breathing systems; Non-rebreathing valves ATP cAMP 5-AMP ADP, see Adenosine triphosphate and diphosphate Phosphorylation Protein kinase of enzymes + other proteins Adrenal gland. Situated on the upper pole of the kidney, each gland is composed of an outer cortex and an inner Gs, stimulatory guanine nucleotide regulatory protein medulla. The cortex consists of the outer zona glomerulosa Gi, inhibitory guanine nucleotide regulatory protein (secreting aldosterone), the middle zona fasciculata (secret- ing glucocorticoids) and inner zona reticularis (secreting sex hormones). Hypersecretion may result in hyperaldosteron-Fig. 5 cAMP involvement in transmembrane signalling ism, Cushing’s syndrome and virilisation/feminisation
  10. 10. 10 Adrenaline respectively. Hyposecretion causes adrenocortical insuffi- for general anaesthetics and have also been used for sedation ciency. in ICU. Other a2-receptor agonists (e.g. xylazine, detomidine The adrenal medulla is thought to be derived from a sym- and medetomidine) have been used in veterinary practice as pathetic ganglion in which the postganglionic neurones have anaesthetic agents for many years. lost their axons, and secrete catecholamines into the blood- stream. Hypersecretion results in phaeochromocytoma. b-Adrenergic receptor agonists. Agonists include See also, Sympathetic nervous system adrenaline and isoprenaline which stimulate both b1- and b2-adrenergic receptors. Dopamine and dobutamine act Adrenaline (Epinephrine). Catecholamine, acting as a hor- mainly at b1-receptors. mone and neurotransmitter in the sympathetic nervous Salbutamol and terbutaline predominantly affect system and brainstem pathways. Synthesised and released b2-receptors, and are used clinically to cause bronchodilatation from the adrenal gland medulla and central adrenergic neur- in asthma, and as tocolytic drugs in premature labour. For- ones ( for structure, synthesis and metabolism, see Catechol- oterol and salmeterol are longer acting agents given by inhal- amines). Called epinephrine in the USA because the name ation for chronic asthma. Ritodrine is also used as a tocolytic adrenaline, used in other countries, was too similar to drug. Some b1-receptor effects are seen at high doses, e.g. the US-registered trade name Adrenalin that referred to a tachycardia. They have been used in the treatment of cardiac specific product (both adrenaline (Latin) and epinephrine failure and cardiogenic shock; stimulation of vascular (Greek) referring to the location of the adrenal gland ‘on the b2-receptors causes vasodilatation and reduces afterload. kidney’). Stimulates both a- and b-adrenergic receptors; displays a-Adrenergic receptor antagonists (a-Blockers). Usu- predominantly b-effects at low doses, a- at higher doses. Low ally refer to antagonists which act exclusively at a-adrenergic dose infusion may lower BP by causing vasodilatation in receptors. muscle via b2-receptors, despite increased cardiac output via l Drugs may be: b1-receptors. Higher doses cause a-mediated vasoconstric- w selective: tion and increased systolic BP, although diastolic pressure - a1-receptors, e.g. prazosin, doxazosin, terazosin, indora- may still decrease. min, phenoxybenzamine. Tamsulosin acts specifically at l Clinical uses: a1A-receptors and is used in benign prostatic hypertrophy. w with local anaesthetic agents, as a vasoconstrictor. - a2-receptors: yohimbine. w in anaphylactic reaction, cardiac arrest, bronchos- w non-selective, e.g. phentolamine. pasm. Labetalol and carvedilol (a drug with similar effects) are w as an inotropic drug. antagonists at both a- and b-receptors. Other drugs may also w in glaucoma (reduces aqueous humour production). act at a-receptors as part of a range of effects, e.g. chlorpro- w in croup. mazine, droperidol. Adrenaline may cause cardiac arrhythmias, especially in the Antagonism may be competitive, e.g. phentolamine, or presence of hypercapnia, hypoxia and certain drugs, e.g. non-competitive and therefore longer-lasting, e.g. phenoxy- halothane, cyclopropane and cocaine. During halothane benzamine. anaesthesia, suggested maximal dosage of adrenaline is Used to lower BP and reduce afterload by causing vaso- 10 ml 1:100 000 solution (100 mg) in 10 min, or 30 ml dilatation. Compensatory tachycardia may occur. (300 mg) in 1 h. More dilute solutions should be used if l Side effects: postural hypotension, dizziness, tachycardia possible. Adrenaline should not be used for ring blocks of (less so with the selective a1-antagonists, possibly because digits or for penile nerve blocks, because of possible ischae- the negative feedback of noradrenaline at a2-receptors is mia to distal tissues. unaffected). Tachyphylaxis may occur. l Dosage: w anaphylaxis: 0.1 mg iv (1 ml 1:10 000 solution), b-Adrenergic receptor antagonists (b-Blockers). Com- repeated as required. The recommended initial route in petitive antagonists at b-adrenergic receptors. general medical guidelines is usually im (0.5–1.0 ml l Actions: 1:1000 solution), reflecting the risks of iv administration w reduce heart rate, force of contraction and myocardial without appropriate monitoring. O2 consumption. w cardiac arrest: 1 mg (10 ml 1:10 000) iv. w increase coronary blood flow by increasing diastolic w by infusion: 0.01–0.15 mg/kg/min initially, increasing filling time. as required. w antiarrhythmic action results from b-receptor antagonism w croup: 0.4 ml/kg nebulised up to 5 ml maximum, and possibly a membrane-stabilising effect at high doses. repeated after 30 min if required. w antihypertensive action (not fully understood but may Subcutaneous injection in shocked patients results in un- involve reductions in cardiac output, central sympa- reliable absorption. Adrenaline may be administered via a thetic activity, and renin levels). tracheal tube in 2–3 times the iv dose. w some have partial agonist activity (intrinsic sympatho- See also, Tracheal administration of drugs mimetic activity), e.g. pindolol, acebutolol, celiprolol and oxprenolol. a-Adrenergic receptor agonists. Naturally occurring w practolol, atenolol, metoprolol, betaxolol, bisoprolol, agonists include adrenaline and noradrenaline which nebivolol and acebutolol are relatively cardioselective, stimulate both a1- and a2-adrenergic receptors. but all will block b2-receptors at high doses. Celiprolol Methoxamine and phenylephrine are synthetic a1-receptor has b1-receptor antagonist and b2-receptor agonist prop- agonists, used to cause vasoconstriction, e.g. to correct erties, thus causing peripheral vasodilatation in addition hypotension in spinal anaesthesia. to cardiac effects. Clonidine acts on central a2-receptors. Clonidine and w labetalol and carvedilol have a- and b-receptor blocking other a2-receptor agonists (e.g. dexmedetomidine) have properties. The former is available for iv administration been shown to reduce pain sensation and reduce requirements and is widely used for acute reduction in BP.