12.07.2015 Views

Download Update 11 - Update in Anaesthesia - WFSA

Download Update 11 - Update in Anaesthesia - WFSA

Download Update 11 - Update in Anaesthesia - WFSA

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

<strong>Update</strong> <strong>in</strong> <strong>Anaesthesia</strong> 7Sodium Nitroprusside (SNP) This acts directly onvascular smooth muscle and causes arteriolar and venousdilation. As a consequence blood pressure falls and a reflextachycardia occurs. SNP acts very rapidly and the durationof action is only a few m<strong>in</strong>utes. The drug can producetoxicity by production of cyanide, and there are maximumrecommended doses for both acute and longer term use.GTN, which is discussed elsewhere, can also be used forrapid control of high blood pressure.CARDIOVASCULAR EFFECTS OFANAESTHETICSInhalational agentsAll volatile agents depress myocardial contractility, but thiseffect is most marked with halothane and enflurane. Withthe exception of halothane they all decrease systemicvascular resistance, contribut<strong>in</strong>g further to the fall <strong>in</strong> bloodpressure and result<strong>in</strong>g <strong>in</strong> a reflex tachycardia. Dur<strong>in</strong>ghalothane anaesthesia systemic vascular resistance isunchanged and, due to vagal stimulation, bradycardias andnodal rhythms are common. Unlike other volatile agentshalothane sensitises the heart to the arrhythmogenic effectsof catecholam<strong>in</strong>es, and ventricular ectopics are often seen.High levels of circulat<strong>in</strong>g catecholam<strong>in</strong>es can causeventricular tachycardia or ventricular fibrillation, especially<strong>in</strong> the presence of hypercarbia, which can occur <strong>in</strong> a patientspontaneously breath<strong>in</strong>g halothane. Ether causessympathetic stimulation, catecholam<strong>in</strong>e release and, to acerta<strong>in</strong> degree, vagus nerve blockade. As a result there isan <strong>in</strong>crease <strong>in</strong> cardiac output, heart rate and systemicvascular resistance, so blood pressure is well ma<strong>in</strong>ta<strong>in</strong>ed.Intravenous <strong>in</strong>duction agentsMost <strong>in</strong>duction agents are cardiovascular depressants. Thegreatest effect is seen with propofol, which may cause amarked fall <strong>in</strong> blood pressure, systemic vascular resistanceand heart rate, the latter due to central vagal stimulation.Thiopentone has similar effects, although less pronounced,and there is a reflex tachycardia mediated by thebaroreceptor reflex. This can result <strong>in</strong> <strong>in</strong>creased myocardialoxygen consumption and a consequent <strong>in</strong>crease <strong>in</strong>coronary blood flow. Benzodiazep<strong>in</strong>es such as midazolamand diazepam are associated with cardiovascular stability,and only high doses will cause cardiovascular depression.Etomidate provides the most cardiovascular stability, withonly slight changes <strong>in</strong> haemodynamic variables. Etomidatehas little effect on myocardial oxygen balance. Ketam<strong>in</strong>e,<strong>in</strong> contrast to other <strong>in</strong>duction agents, is a potentcardiovascular stimulant by <strong>in</strong>creas<strong>in</strong>g sympathetic nervousdischarge, although its direct effect on the myocardium isnegatively <strong>in</strong>otropic. On <strong>in</strong>duction there is a marked rise<strong>in</strong> heart rate and blood pressure caused by central nervousstimulation and an <strong>in</strong>crease <strong>in</strong> circulat<strong>in</strong>g catecholam<strong>in</strong>es.ANAESTHESIA AND CHRONIC RENAL FAILUREDr Penny Stewart, Sydney, Australia and Dr Debbie Harris, Frenchay Hospital, UKChronic Renal Failure (CRF) may be caused by primaryrenal disease or by systemic diseases which also affectthe kidney. A decrease <strong>in</strong> nephron function occurs andcan lead to a typical cl<strong>in</strong>ical pattern. CRF only becomesbiochemically evident when less than 40% of the nephronsare function<strong>in</strong>g. Dialysis (either peritoneal or haemodialysis)is generally not required until less than 10% of nephronsare function<strong>in</strong>g. Patients with CRF are more likely to haveassociated atheroma formation and hypertension.Preoperative Assessment and Treatment of MedicalProblems <strong>in</strong> Renal FailureThe follow<strong>in</strong>g factors should be considered when assess<strong>in</strong>ga patient for anaesthesia prior to either an elective oremergency procedure.Fluid balance In CRF sodium and water excretion isrelatively fixed and often reduced. The kidneys can havedifficulty handl<strong>in</strong>g both large fluid loads and dehydration.The degree of hydration should be assessed <strong>in</strong> the usualway us<strong>in</strong>g sk<strong>in</strong> turgor, exam<strong>in</strong>ation of the mucousmembranes, jugular venous pressure, presence ofdependent oedema and presence of pulmonary oedemaon auscultation. Invasive measurement of central venouspressure may occasionally be <strong>in</strong>dicated. Many patientson dialysis regimens will know their normal hydrated weightand their fluid allowance per day.The patient must be normovolaemic prior to surgery. Fluidresuscitation should normally be with normal sal<strong>in</strong>e but ifthere has been blood loss this might also have to bereplaced.

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!