Cardiovascular system

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1 Cardiovascular system

Anaesthesia and cardiac disease

New York Heart Association classification of cardiovascular disease

• I Normal cardiac output. Asymptomatic on heavy exertion

• II Normal cardiac output. Symptomatic on exertion

• III Normal cardiac output. Symptomatic on mild exercise

• IV Cardiac output reduced at rest. Symptomatic at rest

ASSESSMENT OF RISK – Predictors in non-cardiac surgery

Cardiac complications are a major cause of perioperative morbidity and mortality, particularly vascular patients where mortality is 3–4% for open procedures. Perioperative MI accounts for 10–40% of all postoperative deaths. Risk stratification of patients with known, or at risk of, coronary artery disease is based on (1) the patient risk factors; (2) physiological status of the patient; (3) the risk factors of surgery.

Current thought is that if preoperative assessment reveals possible coronary artery disease, then patients booked for elective surgery should be referred to a cardiologist. Angioplasty in the lead up to elective surgery may increase overall 30-day mortality. CABG, however, may improve long-term outcomes in vascular surgical patients.

Previous ischaemia

Previous guidelines recommended waiting 6 months after an MI before non-cardiac surgery. It is now known that risk after an MI is related more to functional status of the ventricles and the amount of ischaemic myocardium. A small MI without residual angina, and good myocardial function, enables non-cardiac surgery 6 weeks post-MI. A large infarct, residual symptoms and LVEF <0.35 results in high risk even at 6 months post-MI.

• High risk: <6 weeks post-MI because myocardial healing is still ongoing

• Intermediate risk: 6 weeks to 3 months (longer if arrhythmias, ventricular dysfunction, or continued medical therapy)

• Low risk: >3 months post-MI with good myocardial function.

Previous cardiac surgery/angioplasty

There is increased risk with non-cardiac surgery if the patient is <3 months post-CABG. Asymptomatic patients >6 months post-CABG are low risk.

Non-cardiac surgery performed within 6 weeks of PCI results in a high risk of stent thrombosis and infarction if the antiplatelet medication is stopped, or of major bleeding if the treatment is maintained throughout the operation.

Important risk studies

• Mahar et al (1978): Patients with IHD who undergo coronary artery bypass grafting (CABG) subsequently have a normal risk of perioperative MI.

• Mangano et al (1990): Postoperative myocardial ischaemia is the most important predictor of adverse outcome. Risk increase ×9.2 (83% of ischaemic events are silent).

Hypertension

Diastolic blood pressure (DBP) is a good indicator of the severity of vascular disease. DBP >110 mmHg is associated with exaggerated swings in BP and an increased risk of perioperative complications. Severe (DBP >115 mmHg) or malignant (DBP >140 mmHg) hypertension should be treated before surgery. LV hypertrophy is associated with reduced ventricular compliance and these patients may benefit from perioperative monitoring of PCWP.

Perioperative hypertension doubles the risk of complications and is associated with increased silent ischaemia.

Investigations

Ambulatory ECG using 24 h Holter monitor. Ischaemic events are a highly significant predictor of adverse postoperative cardiac events. Silent preoperative ischaemia has a positive predictive value of 38% for postoperative cardiac events, whereas its absence precludes perioperative problems in non-vascular surgery in 99% of patients.

Exercise ECG (Bruce protocol). Aim for the target heart rate by stage 4. This is a good predictor of risk in patients with angina. Severe peripheral vascular disease limits exercising and may mask exercise-induced angina (consider the dobutamine stress test in these patients). ST-segment depression ≥0.1 mV during exercise is an independent predictor of perioperative ischaemic events.

ECHO. Ejection fraction, wall motion and valve abnormalities.

Thallium-201 scan. K⁺ analogue injected i.v. and taken up by well-perfused myocardium, showing underperfused areas as cold spots. Cold spots resolving by 4 h are areas of ischaemia; those persisting are infarcted tissue.

Technetium-99m scan. Similar to thallium scan but underperfused areas show as hot spots.

Dipyridamole–thallium scan. Dipyridamole causes coronary vasodilation to assess coronary stenosis. Similar effect with dobutamine, which also increases myocardial work, i.e. pharmacological stress test. Good predictor of postoperative cardiac complications.

Angiography. Definitive investigation. (Right coronary artery supplies sinoatrial node in 60% of patients and atrioventricular node in 50%). Indicated for unstable angina, or when there is a possible indication for coronary revascularization.

General anaesthesia for non-cardiac surgery

Choice of anaesthetic technique or volatile agent has no proven effect on cardiac outcome. Aim to optimize myocardial oxygen balance (Table 1.1).

Table 1.1 Factors affecting oxygen supply and demand

Supply	Demand
Coronary perfusion	Preload (LVEDP)
O₂ content	Afterload (SVR)
Heart rate	Heart rate
	Contractility

Laplace’s law

Wall tension (preload and afterload) determined by Laplace’s law:

Premedication

Continue all cardiac medication until the day of surgery. Heavy premedication reduces anxiety, which may otherwise cause tachycardia, hypertension and myocardial ischaemia. Consider O₂ after morphine premedication to avoid hypoxaemia from respiratory depression; the prevention of tachycardia results in less myocardial ischaemia overall.

β-blockade. Not all studies have shown benefit from perioperative β-blockade. The Peri-Operative Ischemic Evaluation (POISE) trial showed a beneficial effect of high-dose metoprolol on reducing the risk of perioperative MI, but at the risk of increased stroke and overall mortality. AHA 2007 guidelines recommend continuing β-blocker therapy in patients already on this medication, and giving β-blockers only to high risk vascular surgery patients.

Aspirin. Although aspirin increases the risk of bleeding complications, it does not increase the severity level of the bleeding complication. A meta-analysis has shown that aspirin withdrawal was associated with a three-fold higher risk of major cardiac events (Biondi-Zoccai et al 2006).

Monitoring

ECG. Leads II and V₅ together detect 95% of myocardial ischaemic events. Leads II, V₅ and V4R together detect 100% of events. ST segment monitoring may be a more sensitive indicator.

BP (invasive/non-invasive). Invasive BP monitoring enables blood gases/acid–base and K⁺ measurements.

CVP. Use the right atrium (RA) as zero reference point (midaxillary line, 4th costal cartilage). Normal range with spontaneous respiration is 0–6 cmH₂O. The manubriosternal junction is 5–10 cm above the RA when the patient is supine. Ischaemia causes abnormal ‘v’ waves.

Pulmonary artery catheter. Good monitor of LV function but low sensitivity for detection of myocardial ischaemia (ischaemia causes ↑PCWP and ↑PAP). Rao et al (1983) showed increased reinfarction risk if preoperative PCWP was >25 mmHg. Thus, monitoring of PCWP and aggressive treatment with inotropes/vasodilators may reduce the risk of reinfarction. If ejection fraction >0.50 and there is no dyssynergy, CVP is an accurate correlate of PCWP, and PAP monitoring may be unnecessary.

Transoesophageal ECHO (TOE). Developed in the 1950s by Edler and Hertz. Ultrasound waves are formed when a voltage is applied across a substance with piezoelectric properties (usually lead-zirconate-titanate-5, PZT-5). Ultrasound waves are reflected back to the PZT-5 transducer, and converted back into electrical energy. This signal is then processed and displayed on a monitor. TOE requires less penetration than transthoracic ECHO and therefore uses a higher frequency (3.5–7 MHz) to produces higher resolution images.

Useful to assess perioperative:

• Abnormal ventricular filling/function

• Extensive myocardial ischaemia

• Large air embolism

• Severe valvular dysfunction

• Large cardiac masses/thrombi

• Pericardial effusion

• Major lesions of great vessels (e.g. aortic dissection).

Myocardial wall motion abnormalities detected by TOE are a much more sensitive method than ECG in detecting myocardial ischaemia. Post-bypass TOE is a sensitive predictor of outcome (MI, LVF, cardiac death).

Induction

Aimed at limiting hypotensive response to induction agent and hypertensive pressor response to intubation. High-dose opioid is a popular technique.

Anaesthetic

Avoid CVS changes that precipitate ischaemia. Tachycardia and hypertension increase myocardial O₂ consumption and reduce diastolic coronary filling time. Hypotension reduces coronary perfusion pressure.

N₂O is a sympathetic stimulant, but will decrease sympathetic outflow if the SNS is already stimulated, e.g. LVF. In the presence of an opioid, it may cause CVS instability.

Volatiles. Enflurane and halothane both decrease coronary blood flow, but isoflurane, sevoflurane and desflurane increase coronary blood flow and maintain LV function in normotensive patients. Tachycardia with isoflurane increases myocardial work, but this is minimal with balanced anaesthesia. There is some concern that isoflurane may cause coronary steal (Fig 1.1) but it is thought not to do so as long as coronary perfusion pressure is maintained. There is growing evidence that isoflurane has myocardial protective properties, limiting infarct size and improving functional recovery. This mechanism mimics ischaemic pre-conditioning and involves the opening of ATP-dependent K⁺ channels causing vasodilation and preservation of cellular ATP supplies. Desflurane and sevoflurane probably have similar but less marked cardioprotective effects.

Figure 1.1 (A) Myocardial perfusion pressure (P1) reduced by stenosis. Adequate perfusion is achieved through collateral flow. (B) Vasodilator increases run-off, reducing pressure at (P2) and therefore reducing myocardial perfusion pressure distal to the stenosis.

Relaxants. Vecuronium combined with high-dose opioids tends towards bradycardia. Use of pancuronium avoids bradycardia.

Epidural/spinal

This decreases afterload and may improve LV function. General anaesthetic combined with epidural may cause severe hypotension because of vasodilation of vessels that have constricted above the block. In animals, redistribution of blood from epicardial to endocardial vessels reduces MI size. Angina following spinal anaesthesia tends to occur at cessation of the block, probably due to increased pre- and afterload aggravated by volume loading.

Blocks below L₃ have no effect on the SNS. Blocks above T₁₀ block sympathetic afferents to the adrenals and reduce catecholamine release. Blocks to T₁–T₄ interrupt cardioaccelerator fibres, preventing the coronary vasoconstrictive response to surgery, cause coronary vasodilation, decrease coronary perfusion pressure and decrease contractility and heart rate. Central hypovolaemia due to vasodilation causes a vagally mediated bradycardia which responds to fluid challenge.

Pacemakers

There are 200 000 patients with implanted pacemakers in the UK.

Nomenclature

The type of permanent pacemaker is denoted by three or four letters (Fig. 1.2).

Figure 1.2 Pacemaker nomenclature. For example: DDDR = atrial and ventricular sensing and pacing with adaptive rate response; VVI = pacing wire triggers ventricular contraction. Any spontaneous electrical activity is sensed in the ventricle and inhibits pacemaker firing.

Indications for perioperative pacing

• Acute anterior MI

• First-degree heart block combined with bifascicular block or left bundle branch block

• Acute MI with Mobitz type II

• Third-degree heart block

• Sick sinus syndrome

• Faulty permanent pacemaker.

Intraoperative risks

Rate responsive pacemakers sense electrical activity or vibration around the pacing box and cause a tachycardia in response. Thus, shivering may cause a tachycardia. Fasciculations from suxamethonium are too transient to cause a tachycardia, but there is a case report of a pacemaker that stopped firing following administration of suxamethonium.

Pacemakers that sense blood temperature to control rate may trigger a tachycardia as a hypothermic patient is rewarmed. Those that measure respiratory rate by sensing thoracic impedance and adjust heart rate accordingly can also trigger a tachycardia if the ventilator is set at a high respiratory rate.

Risks associated with K⁺ are:

• hypokalaemia – risk of loss of pacing capture

• hyperkalaemia – risk of VT or VF.

Diathermy

Diathermy current risks reprogramming the pacemaker (not AOO, VOO), causing microshock and inducing VF. Bipolar diathermy is the safest. If unipolar, mount the diathermy plate away from the pacemaker and use short bursts of minimum current. Do not use within 15 cm of the pacing box.

Application of a magnet over a non-programmable ventricular-inhibited pacemaker (VVI) reverts it to asynchronous mode (VOO). Application of a magnet over a programmable pacemaker increases the risk of reprogramming, but it will remain in an asynchronous mode until the magnet is removed, when the reprogrammed mode will take over. Do not use any magnets unless the pacemaker reprogrammes during surgery.

Automatic implantable cardioverter defibrillators (AICDs)

There are 4000 patients with implanted pacemakers in the UK, usually for drug-resistant malignant ventricular arrhythmias. This has reduced 1-year mortality from 66% to 9%. AICDs consist of a lead electrode system for sensing, pacing and delivery of shocks for cardioversion/defibrillation and a control unit consisting of a pulse generator, microprocessor and battery. Modern devices also act as DDD pacemakers.

• In general, all AICDs should be deactivated with a programming device before surgery. In modern AICDs, the anti-bradycardia function can be left activated. Effects of magnets are not consistent between devices, but newer AICDs are inhibited by a magnet.

• Electromagnetic interference, e.g. diathermy, can inhibit the AICD or cause shock discharge. If used, place the diathermy plate as far as possible from the generator. Bipolar diathermy generates less current and is therefore preferential.

• External defibrillation pads should be placed prior to surgery, avoiding current pathways through the device. External defibrillation does not damage an AICD. If an AICD discharges, only a mild electric shock will be felt by anyone touching the patient.

Where the precise time since the onset of acute AF is uncertain, use oral anticoagulation for acute AF, as for persistent AF.

Atrial Fibrillation: the Management of Atrial Fibrillation

National Institute for Health and Clinical Excellence, June 2006

Guidance

Figure 1.3 Haemodynamically unstable and acute-onset AF. NICE.

Antithrombotic therapy for acute-onset atrial fibrillation (AF)

For patients with acute AF who are receiving no, or only sub-therapeutic anticoagulation therapy:

• start heparin at initial presentation, unless contraindicated

• continue heparin until a full risk assessment has been made and appropriate antithrombotic therapy started, based on risk stratification.

For patients with a confirmed diagnosis of acute AF (<48 h since onset), use oral anticoagulation if:

• stable sinus rhythm is not restored within the 48-h period following onset

• there are other risk factors for AF recurrence

• it is recommended by the stroke risk stratification algorithm.

Where a patient with acute AF is haemodynamically unstable, begin emergency treatment as soon as possible. Do not delay emergency intervention in order to begin anticoagulation treatment first.

Anaesthetic considerations for heart surgery

Aortic stenosis

Aortic stenosis becomes symptomatic when the normal valve area of 3 cm² is reduced by >25%. Gradient >70 mmHg is severe (= 0.6 cm²); low cardiac output, dependent upon rate. Bradycardia reduces cardiac output and therefore BP. Tachycardia is poorly tolerated because reduced time for LV filling reduces ejection time and diastolic time during which coronary perfusion occurs. Aortic diastolic pressure must be maintained to preserve coronary blood flow. Ischaemia occurs even with normal coronaries. Atrial contraction is important to fill a poorly compliant LV. A fall in SVR is poorly tolerated. Therefore, maintain both pre- and afterload and avoid regional techniques.

Aortic regurgitation

This causes a dilated, overloaded and failing LV. Low aortic diastolic pressure impairs coronary perfusion. Slight tachycardia reduces regurgitant time and keeps LV small (Laplace’s law), thereby improving LV efficiency. A slight reduction in SVR reduces regurgitation but may reduce coronary perfusion pressure.

Mitral stenosis

A value area <1 cm² is severe. There is poor LV filling and a fixed output, dependent upon rate. Low CO is worsened by tachydysrhythmia. Rapid heart rate reduces diastolic time for ventricular filling and thus reduces cardiac output, so bradycardia is beneficial. A high PVP risks pulmonary oedema with overtransfusion, but it is important to maintain adequate filling. A fall in SVR is poorly tolerated. Consider inotropes and pulmonary vasodilators.

Mitral regurgitation

Often well tolerated; PVP remains low. There is slight tachycardia and reduction in SVR which reduce regurgitation. Ischaemia is not usually a problem. General anaesthesia is normally well tolerated, unless pulmonary hypertension has developed, when inotropic support may also be indicated.

Hypertrophic obstructive cardiomyopathy (HOCM)

HOCM is autosomal dominant with variable penetrance. There is variable subaortic obstruction and impaired diastolic function. Try to avoid drugs that depress LV function. Increase pre- and afterload, maintain sinus rhythm and avoid excessive tachy/bradycardia. There is usually good LV function. Ventricular arrhythmias are common. Depression of myocardial contractility reduces outflow obstruction. β-agonists increase outflow obstruction.

Ischaemic heart disease

Rate pressure product (RPP) = heart rate × systolic pressure. Aim to maintain value at below 12 000.

Decrease preload (wall tension) and maintain afterload. A slight decrease in both contractility and rate can be beneficial by reducing work if there is good LV function. Myocardial depression may improve oxygenation unless there is severe IHD or aortic stenosis. If ischaemia occurs, decrease heart rate (β-blockers, calcium-channel blockers), increase ventricular volume (GTN) and increase afterload.

Pulmonary hypertension

Defined as mean pulmonary artery pressure (MPAP) >25 mmHg at rest. Overall, those with severe disease have a 5-year survival of only 27% from time of diagnosis, increasing to 54% with treatment.

Classification of pulmonary artery hypertension

• Idiopathic pulmonary hypertension:

– Collagen vascular disease (e.g. systemic sclerosis)

– Portal hypertension (e.g. pulmonary thromboembolism)

– Congenital heart disease

– HIV infection

– Drugs/toxins

– Persistent pulmonary hypertension of the newborn

– Congenital heart disease.

Causes increased pulmonary vascular resistance (PVR) with increased load on the right heart causing right heart failure. Treatment aims to reduce PVR. Correct reversible causes (e.g. pulmonary thromboembolectomy, congenital heart disease, etc.). Pulmonary vasodilators include epoprostenol (prostacyclin) with its analogues (iloprost and treprostinil), endothelin receptor antagonists (bosentan), phosphodiesterase inhibitors (sildenafil) and inhaled nitric oxide.

Shunts

• Right-to-left shunt (Fallot’s tetralogy, Eisenmenger’s syndrome). Risk from microemboli, LVF and cyanosis. Shunt worsens with ↑ PVR or ↓ SVR. Keep lung inflation pressures low.

• Left-to-right shunt (ASD, VSD, PDA). Shunt worsens with ↓ PVR or ↑ SVR. IPPV increases PVR.

Endocarditis prophylaxis

Antimicrobial Prophylaxis Against Infective Endocarditis in Adults and Children Undergoing Interventional Procedures

National Institute for Health and Clinical Excellence, March 2008 (http://www.nice.org.uk/nicemedia/pdf/CG64PIEQRG.pdf)

Summary

Antibacterial prophylaxis is not recommended for the prevention of infective endocarditis (IE) in patients undergoing procedures of the:

• upper and lower respiratory tract (including ENT procedures and bronchoscopy)

• genito-urinary tract (including urological, gynaecological and obstetric procedures)

• upper and lower gastrointestinal tract

• dental procedures.

While these procedures can cause bacteraemia, there is no clear association with the development of infective endocarditis.

If patients at risk of endocarditis are undergoing a gastrointestinal or genito-urinary tract procedure at a site where infection is suspected, they should receive appropriate antibacterial therapy that includes cover against organisms that cause endocarditis.

Risk factors for the development of infective endocarditis

• acquired valvular heart disease with stenosis or regurgitation

• valve replacement

• structural congenital heart disease, including surgically corrected or palliated structural conditions, but excluding isolated atrial septal defect, fully repaired ventricular septal or fully repaired patent ductus arteriosus, and closure devices that are judged to be endothelialised.

• hypertrophic cardiomyopathy

• previous infective endocarditis

• (atrial septal defect, repaired ventricular septal defect/patent ductus arteriosus not at risk).

Guidelines for the Prevention of Endocarditis

Report of the Working Party of the British Society for Antimicrobial Chemotherapy, 2006

High-risk patients:

• Previous infective endocarditis

• Cardiac valve replacement surgery (mechanical or tissue)

• Surgically constructed shunts or conduits.

Dental procedures

Prophylaxis is only recommended for high-risk patients

Amoxicillin: p.o. – 3 g 1 h preoperatively;

i.v. – 1 g at induction.

If allergic to penicillin

Clindamycin: p.o. 600 mg p.o. 1 h preoperatively;

i.v. – 300 mg immediately preoperatively.

Endocarditis prophylaxis for non-dental procedures

All patients at risk of endocarditis should receive prophylactic antibiotics for invasive genito-urinary, gastrointestinal, respiratory or obstetric/gynaecological procedures as follows:

Amoxicillin 1 g i.v. + gentamicin 1.5 mg.kg⁻¹ i.v. immediately preoperatively.

If allergic to penicillin

Teicoplanin 400 mg i.v. + gentamicin 1.5 mg.kg⁻¹ i.v. immediately preoperatively.

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British Society for Antimicrobial Chemotherapy. Guidelines for the Prevention of Endocarditis. Report of a Working Party, 2006 http://jac.oxfordjournals.org/cgi/reprint/dkl121v1.

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Cardiac surgery

General

There are 20 000 cardiac operations per annum in the UK. Surgical mortality is only 1–2% for low-risk patients. In uncomplicated cases, patients are generally rewarmed and extubated within 3–4 h of the completion of surgery (fast-tracking).

More than 90% of cases are performed using cardiopulmonary bypass (CPB), but off-pump coronary artery bypass grafting (OPCAB) may be performed while the heart is still beating. This avoids costs of CPB circuit, reduces microemboli (may lessen postoperative cognitive dysfunction) and reduces inflammatory response to bypass. However, it results in limited surgical access to more posterior coronary arteries and is associated with increased haemodynamic instability. Analysis of the National Adult Cardiac Surgery Database of 3396 off-pump procedures showed a reduction in risk adjusted mortality from 2.9% in CABG to 2.3% for OPCAB. The complication rate was also reduced from 12% (CABG) to 8% (OPCAB). Other studies have not demonstrated a difference in mortality or morbidity.

Cardiopulmonary bypass

Drug pharmacokinetics

• Haemodilution on bypass decreases plasma drug concentration but is counterbalanced by reduced total protein binding, due to decreased plasma protein concentration.

• Decreased flow into peripheral vascular beds results in decreased drug uptake by peripheral tissues and decreased mobilization of previously stored drugs out of peripheral tissues.

• Decreased liver perfusion and decreased hepatic metabolism.

Therefore, there is little change in most drug concentrations during bypass. Neuromuscular blockers have a small V_D and therefore are greatly diluted on bypass and additional perioperative doses may be needed. Plasma levels of fentanyl rise on rewarming and after separation from CPB due to reperfusion of peripheral compartments and washout of drug bound in lung.

Bypass circuit

A cardiopulmonary bypass circuit is illustrated in Figure 1.4.

Figure 1.4 Membrane oxygenator circuit.

Advantages of membrane over bubble oxygenators

• Less blood trauma and complement activation

• Fewer microemboli

• Ability to regulate O₂ and CO₂ separately

• Less neuroendocrine stress response.

Pump

Most centres now use non-pulsatile flow. However, pulsatile pumps cause less neuroendocrine stress response.

Lower bypass pressure results in less mechanical damage to blood, reduces aortic trauma at the clamp site and allows use of smaller arterial and venous catheters. However, higher pressures (60–90 mmHg) avoid loss of CNS autoregulation (occurs at <50 mmHg) with less postoperative neurological dysfunction.

Pump flow rate is set at 2.4 L/m², pressure at 40–80 mmHg; 99% O₂ ± 1–5% CO₂. Priming volume approx. 2000 mL, usually with crystalloid but blood is used for paediatric bypass. Priming without blood decreases haematocrit to 20–25%, which offsets the increase in viscosity caused by hypothermia.

Cardioplegia solution

This solution, used to arrest and protect the myocardium, contains 15–30 mEq.L⁻¹ K⁺. It may also contain:

• citrate (to bind Ca²⁺)

• GTN (improves distribution)

• glucose and insulin (energy for cells)

• mannitol (decreases cellular swelling)

• bicarbonate (increases intracellular shift of K⁺).

Anaesthesia for cardiac surgery

Preoperative assessment

Assess risk factors: age >60 year, arterial and/or pulmonary hypertension, BMI <20 or >35 kg.m⁻², congestive cardiac failure, peripheral vascular disease, aortic atheroma, diabetes mellitus, renal insufficiency, acute coronary syndromes, chronic pulmonary disease, neurological disease and previous cardiac surgery. Assess for drugs that interfere with coagulation (aspirin, NSAIDs, clopidogrel, glycoprotein IIb/IIIa antagonists, thrombolytics, heparin, warfarin). Assess for drugs affecting the cardiovascular system (β-blockers, ACE inhibitors).

Premedication

Benzodiazepines and opiates. (Anxiety increases endogenous catecholamines and causes coronary vasospasm.) Heavy premedication may cause hypoventilation and hypoxaemia so consider starting oxygen at time of premedication.

Monitoring

ECG. Either CM5 or combinations including lead II (inferolateral wall) or posterior wall (oesophageal lead).

BP. Radial arterial line. Internal mammary artery dissection can dampen ipsilateral arterial line trace.

CVP. Monitoring through multi-lumen line.

Pulmonary artery catheter. Controversial but may improve outcome in selected patients.

Other. Urinary catheter and core temperature (nasopharyngeal, oesophageal, or tympanic thermocouple).

TOE. Detects wall motion abnormalities and is a more sensitive indicator of myocardial ischaemia than ECG or invasive pressure monitoring.

Induction

Aim is to obtund sympathetic response to surgical stimulation in order to avoid tachycardia and hypertension which worsens myocardial ischaemia. Achieved using anaesthesia based on a high-dose opiate technique (50–100 μg.kg⁻¹ fentanyl), which requires postoperative IPPV but improves perioperative cardiovascular stability. Thiopentone, propofol, midazolam and etomidate have all been used as induction agents. Propofol and thiopentone may cause more hypotension on induction, especially in the presence of poor LV function.

Use of thoracic epidural in patients undergoing coronary artery bypass surgery is associated with fewer pulmonary complications but does not decrease the incidence of myocardial infarction or overall mortality.

Intubation

Minimize the pressor response (which worsens ischaemia) by the use of opiates. Use of β-blockers, clonidine or lidocaine also described. Non-depolarizing relaxants reduce chest wall rigidity caused by high-dose opioids.

Maintenance

All volatiles decrease myocardial oxygen demand but also decrease coronary perfusion pressure. Isoflurane/desflurane cause least myocardial depression. There is some evidence that volatile agents have cardioprotective properties, with better preservation of postoperative myocardial function and reduced postoperative myocardial damage. Cessation of pulmonary blood flow during CPB requires maintenance of anaesthesia during this period with propofol infusion or alternatively, volatile agent given directly into the bypass circuit.

Vecuronium avoids CVS side-effects present in other neuromuscular blockers, but mild tachycardia induced by pancuronium may be useful to offset the bradycardia seen with high-dose opioids.

Sternotomy and aortic manipulation cause intense sympathetic stimulation. Further increments of fentanyl may be needed. If there is no CNS disease, a MAP of 35–40 mmHg is adequate when a patient is hypothermic.

Avoid N₂O because of risk of air bubble emboli expanding, especially dangerous with right-to-left shunt. Aim for a haematocrit of 20–30%.

Anticoagulation

Use 3 mg/kg heparin (= 300 U/kg), which accelerates antithrombin III to neutralize clotting factors II, X, XI, XII and XIII. Aim for activated clotting time (ACT) >400. (Celite in test tube at 37°C triggers clotting.) Normal ACT = 120–150 s. Half-life of heparin = 100 min.

Reverse heparin with protamine at 1 mg/100 U heparin. Protamine may increase PVR causing right ventricular failure and also causes hypotension by binding to Ca²⁺.

Acid–base management

• pH-stat approach – arterial blood gases corrected for temperature (pH kept constant)

• Alpha-stat approach – arterial blood gases not corrected for temperature.

pH-stat results in relative hypercarbia and acidaemia which increases cerebral blood flow and may increase the risk of cerebral emboli. Cerebral autoregulation, which keeps blood flow constant at arterial pressures of 50–150 mmHg, is lost during pH-stat and cerebral blood flow becomes pressure-dependent. pH-stat management may be optimal for children undergoing deep hypothermic circulatory arrest, because it increases the rate of brain cooling and results in slower exhaustion of brain O₂ stores, providing better CNS protection.

Alpha-stat management maintains cerebral autoregulation, offers better control of cerebral blood flow and demand, and limits cerebral microemboli load. However, the pressure-dependent characteristics of pH-stat may improve cooling and oxygen delivery to the brain.

CABG patients

Good LV function. The main problem is hyperdynamic circulation. Avoid tachycardia and hypertension. Aim to decrease myocardial work, e.g. with volatiles, β-blockers.

Poor LV function. The main problem is cardiac failure. Minimize use of drugs causing myocardial depression, i.e. use high-dose opioids. Use volatiles sparingly. May require inotrope infusion to wean from bypass which is continued in the immediate postoperative period.

Sequence of events in CABG surgery

Anaesthesia. Invasive monitoring and induction of general anaesthesia.

Pre-bypass. Surgical incision and sternal splitting. Disconnect the ventilator during sternal splitting, allowing lungs to deflate, reducing risk of damage from the sternal saw.

Heparin is administered into a central vein and ACT checked prior to commencing CPB.

Pericardial stretching during cardiac manipulation may impair venous return and lower BP.

Nitrous oxide is discontinued to avoid enlargement of any air emboli (or not used at all).

Establishment of bypass. The aortic cannula is first inserted through a purse string suture into the ascending aorta to allow infusion of volume from the bypass reservoir if the BP drops. The venous cannula is then inserted into the right atrium or superior and inferior venae cavae.

CPB is then initiated. Ventilation is stopped when full bypass is established. The aorta is clamped proximal to the cannula and cardioplegia solution infused into the aortic root where it perfuses the coronary arteries causing asystole (Fig. 1.5).

Figure 1.5 Diagram of aortic root showing arrangement of cannulae and cross-clamp for administration of cardioplegia.

Hypothermia is achieved by cooling the blood through a heat exchanger to reduce myocardial and cerebral oxygen requirements. Core temperature ≈︀ 32°C is adequate for most cases.

Coronary artery surgery. The vein grafts are anastomosed to the diseased coronary arteries, the distal anastomosis being performed first to enable administration of cardioplegia solution distal to the stenosis.

Rewarming is begun once the final distal anastomosis is complete. The aorta is unclamped, which results in washout of cardioplegia solution from the myocardium. The proximal vein graft anastomoses are completed.

Weaning from bypass. Once the heart is rewarmed, it begins to contract. Internal paddles (10 J) are used to defibrillate the heart if VF/VT occurs. Lungs are re-expanded to peak pressure of 30–40 cmH₂O with 100% O₂ and IPPV is started. Flow through the venous cannulae is reduced to allow the heart to refill and spontaneous cardiac output subsequently increases. Once adequate filling and output are established, the venous and then arterial cannulae are clamped.

Post-bypass management. If the patient remains hypotensive, give fluid challenge in 50–100 mL increments from venous reservoir. Further fluid continues to be needed because of continued rewarming of vascular beds causing vasodilation, changing ventricular diastolic compliance and continued bleeding before heparin reversal. If hypotension persists despite adequate filling, inotropes and/or vasoconstrictors may be required.

Once adequate output is established, venous and arterial cannulae are removed and the effects of heparin are reversed with protamine.

Intra-aortic balloon-pump counterpulsation

This is used as a mechanical assist device for the failing myocardium. The intra-aortic balloon is placed in the aortic arch/early descending thoracic aorta via the femoral artery so that the tip lies distal to left subclavian artery, but is not occluding renal arteries (Fig. 1.6).

• Diastolic effects. Expands during diastole, increasing aortic diastolic pressure and therefore coronary perfusion pressure.

• Systolic effects. Sudden decrease in balloon volume prior to systole decreases systemic vascular resistance, afterload and myocardial work, and increases cardiac output, cerebral and renal perfusion (Fig. 1.7).

Figure 1.6 Intra-aortic balloon pump showing inflated and deflated position.

Figure 1.7 Arterial pressure changes using an intra-aortic balloon pump.

Perioperative placement is considered in high-risk patients, e.g. severe LV dysfunction, congestive heart failure, cardiomyopathy, prolonged bypass. The IABP decreases afterload, increases cardiac output and increases coronary and systemic perfusion, facilitating the patient’s weaning from CPB.

Postoperative complications

Cardiac. Avoid postoperative hypertension, common in fit young patients with good LV function, post-aortic valve replacement for aortic stenosis or those with pre-existing hypertension. Worsened by inadequate analgesia/sedation and hypothermia. Often due to neuroendocrine responses to CPB (renin–angiotensin activation).

Low-output syndrome is associated with poor preoperative LV function, intraoperative damage and effects of bypass.

Respiratory. Infection and sputum retention are relatively common. Cardiogenic and non-cardiogenic pulmonary oedema may develop at any time in the postoperative period.

Neurological. 2–6% of patients have neurological damage following CPB. Usually slight (neuropsychiatric) rather than gross. Cause of subtle damage may be unknown but may include micro/macroemboli (particularly common at insertion of aortic cannula and initiation of bypass), air bubbles, effect of non-pulsatile flow, inadequate cerebral perfusion or hyperglycaemia during neuroischaemia. Known risk factors include age, prolonged bypass, severe atherosclerosis and hypertension.

Renal. Risk of prerenal failure and failure from direct tubular damage, e.g. myoglobin, antibiotics.

Haematology. Haemorrhage is a major complication, usually due to platelet dysfunction. Worsened by preoperative aspirin and/or clopidogrel. Antifibrinolytic agents (e.g. aprotinin, tranexamic acid, aminocaproic acid) preserve the adhesive capacity of platelets, which are altered by circulation through the CPB circuit, and may reduce postoperative blood loss. Platelet transfusions and FFP may be needed if bleeding persists. Thromboelastography is useful to identify causes of coagulopathy (inadequate protamine, lack of clotting factors, poor platelet function, fibrinolysis).

Neurological monitoring and protection

Monitoring

Unmodified EEG. Some evidence for correlation with outcome.

Processed EEG. Easier to interpret.

Transcranial Doppler. Research tool. Correlates with neuroinsults.

Jugular bulb O₂ saturation. Desaturation is common but significance is not known.

Regional cerebral blood flow. Research tool.

Cerebral oximetry. Non-invasive and only monitors small regions.

Protection

Physiological. Pulsatile flow, hypothermia, alpha-stat management, euglycaemia, filtration of arterial blood to remove microemboli.

Pharmacological.

Barbiturates: may protect in high doses (>30 mg/kg) but conflicting studies.

Steroids: no evidence for benefit.

Death Following a First Time, Isolated Coronary Artery Bypass Graft

A report of the National Confidential Enquiry into Patient Outcome and Death, 2008

Recommendations

Multidisciplinary case planning

• Each unit undertaking coronary artery bypass grafting should hold regular preoperative MDT meetings to discuss appropriate cases. Core membership should be agreed and a regular audit of attendance should be performed.

Patient investigations

• There must be a system in place to ensure that preoperative investigations are reviewed by a senior clinician and acted upon.

Medical management

• NCEPOD supports the guidance of the American College of Cardiology and the American Heart Association that clopidogrel should be stopped prior to surgery wherever practicable.

Non-elective, urgent, in-hospital cases

• There should be a protocol to ensure a timely and appropriate review of unstable cases that involves both cardiologists and cardiac surgeons.

• A ‘track and trigger’ system should be used to provide early recognition of clinical deterioration and early involvement of consultant staff.

Comorbidities

• Where preoperative comorbidity exists, there should be a clear written management plan, which is followed in order to optimize the physical status of the patient prior to surgery, and identify the need for specific postoperative support to be available.

Perioperative management and postoperative care

• Cardiac recovery areas/critical care units are best suited to managing the majority of patients who recover uneventfully.

• Patients who are developing critical illness and additional organ failure should be managed in an environment with sufficient throughput of such patients to have the resources and experience to provide optimum outcomes.

• Senior clinicians should be readily available throughout the perioperative period in order to ensure that complications are recognized without delay and managed appropriately.

Communication, continuity of care and consent

• Protocols must exist for handover between clinical teams and patient locations to ensure effective communication and continuity of care.

• A consultant should obtain consent for coronary artery bypass grafting.

Multidisciplinary review and audit

• Morbidity and mortality audit meetings should be held in all cardiothoracic units. The majority of units should hold meetings at least monthly. If the numbers of cases performed in a unit are small, alternative arrangements should be made to incorporate these cases in other surgical audit meetings.

• A common system for grading of quality of care of patients should be employed for all patients discussed in morbidity and mortality audit meetings. The peer review scale used by NCEPOD provides such a system.

Free radical scavengers (e.g. superoxide dysmutase) and calcium channel blockers remain experimental.

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Shaaban Ali M., Harmer M., Kirkham F. Cardiopulmonary bypass and brain function. Anaesthesia. 2005;60:365-372.

Major vascular surgery

Abdominal aortic aneurysm

Pathogenesis

Destruction of elastin in the media results in abnormal widening of all three layers of the vessel wall. Genetic predisposition, acquired risk factors (smoking, hypertension, atherosclerosis), defective and decreased elastin. If >6 cm, 50% rupture in 10 years.

Associated common pathology:

• hypertension (50%)

• diabetes (10%)

• chronic renal failure (10%).

Mortality

• elective: 6%

• emergency: 65% if ruptured.

Anaesthetic aims

• maintain cardiovascular stability

• blood replacement

• maintain renal function

• temperature control.

Anaesthetic management

Preoperative. Mostly elderly patients. Full cardiac work-up for elective patients. Assess severity and treat other co-existing diseases. Systolic BP at presentation is the most important predictor of survival.

Fluid resuscitation. There is some evidence that aggressive preoperative fluid resuscitation may increase mortality by accelerating bleeding, increasing the risk of clot dislodgement and causing a dilutional coagulopathy. Bleeding makes surgery more difficult and distended veins (IVC and left renal vein) are at greater risk of rupture. It is suggested that the MAP should be maintained at ≈︀ 65 mmHg until the aorta has been clamped, after which blood, FFP and platelets should be given to restore haemodynamic parameters. All fluids should be warmed.

Preparation. Prepare and drape the patient in the operating theatre. Induction may result in cardiovascular collapse as the tamponading effect of abdominal muscle tone is lost and surgeons must therefore be ready to start immediately.

Adequate analgesia with small doses of i.v. opioids prevents hyperventilation, hypertension, increased endocrine stress response and increased oxygen consumption.

Induction. Ketamine may be of benefit with severe haemorrhagic shock but increases cardiac work, possibly precipitating ischaemia. Induction with combined opioid (e.g. fentanyl) and hypnotic (e.g. midazolam) provides the best CVS stability. Thiopentone and propofol may cause CVS collapse if the patient is haemodynamically unstable. Commence GTN infusion if known IHD or ischaemic ECG changes.

Maintenance of anaesthesia

General anaesthesia. Nitrous oxide–oxygen–relaxant technique and nitrous oxide–oxygen–relaxant–volatile technique alone are associated with depressed ventricular performance and hyperdynamic circulation. Addition of high-dose fentanyl/remifentanil maintains cardiac function and is not associated with hyperdynamic changes. Isoflurane is relatively stable on the cardiovascular system and has been shown to maintain a higher GFR than halothane during aneurysm surgery.

Combined regional and general anaesthesia. Regional anaesthesia combined with a light GA may reduce operative mortality and postoperative morbidity. Epidural followed by heparinization does not increase the risk of epidural haematoma. Regional techniques may improve regional blood flow and maintain GFR although there is no evidence for improved postoperative creatinine clearance. Increases perioperative fluid requirements in elective surgery by 25–50%.

Haemodynamic changes

Mesenteric traction syndrome. Causes flushing, hypotension and tachycardia due to prostacyclin and PGF_1α release. Treat with fluids and vasoconstrictors. Abolish if patient on NSAIDs.

Aortic cross-clamping. Location of clamp determines degree of cardiovascular stress and increase in MAP. Increased afterload increases myocardial wall tension and may worsen LV function. Infrarenal clamping reduces stroke volume by 15–35%, increases SVR by 40% and reduces renal cortical blood flow. Results in increased perfusion proximal to the clamp and anaerobic metabolism distal to the clamp.

Decrease afterload with vasodilators. Nitroglycerine infusion at 0.25–5 μg.kg⁻¹.min⁻¹ reduces myocardial wall tension by reducing pre- and afterload, and may maintain normal myocardial blood flow, decrease arterial blood pressure, lower SVR and reduce myocardial oxygen consumption. Lumbar epidurals attenuate the increased SVR that occurs with cross-clamping.

Declamping. Hypoxic vasodilation, sequestration of blood in pelvic and lower limb capacitance vessels, hypovolaemia and release of vasoactive and myocardial depressant metabolites (lactate, K⁺) cause hypotension. Severity of hypotension is related to cross-clamp time and the speed at which the clamp is released. Fluid loading until PCWP is 3–5 mmHg above preoperative value prior to declamping reduces hypotension. Severe hypotension may necessitate vasoconstrictor/inotrope support and partial reclamping. Epidurals may exaggerate hypotension after declamping but tend to produce greater CVS stability.

Postoperative. Ventilate until warm, well-filled and cardiovascularly stable. Correct any clotting abnormalities. Monitor renal function closely. Good analgesia is important. Postoperative complications are common and include MI (40%), respiratory failure (40%), renal failure (35%), bleeding (15%) and stroke (5%).

Arterial supply to the spinal cord

The major arterial supply to the spinal cord is a single anterior spinal artery lying in the anterior median fissure of the cord and two posterior spinal arteries located just medial to the dorsal roots. The anterior spinal artery is fed from several sources (Figs 1.8, 1.9):

• C₁–T₄: vertebral, thyrocervical and costocervical arteries

• T₄–T₉: intercostal arterial branches

• below T₉: artery of Adamkiewicz which arises from the aorta between T₉ and L₂.

Figure 1.8 Arterial supply to the spinal cord.

Figure 1.9 Cross-section of the spine showing the relationship between the artery of Adamkiewicz and the anterior spinal artery.

(Reproduced from Djurberg & Haddad 1995.)

The anterior spinal artery supplies the anterior two-thirds of the cord and anastomoses with both posterior spinal arteries.

Spinal cord injury

Impaired flow in the artery of Adamkiewicz during cross-clamping results in cord ischaemia and paraplegia. There is a 40% incidence of paraplegia following emergency repair of a dissecting aneurysm compared with 0.1% for elective infrarenal procedures. Motor damage–sensory damage. Poor recovery. Attempts to protect cord function include:

• avoiding glucose-containing solutions

• monitoring of cord function with SSEPs

• maintaining distal aortic pressure with shunts

• 3 mL 1% preservative-free epidural papaverine has been shown to protect the cord during prolonged aortic cross-clamping by dilating anterior spinal arteries

• cross-clamping causes increased CSF pressure, further decreasing cord perfusion. Lumbar drain insertion in an attempt to decrease CSF pressure has shown variable results in reducing cord damage

• steroids, barbiturates and superoxide dismutase

• regional lumbar spinal cord cooling.

Renal function

There is a high risk of renal failure due to hypovolaemia, renal atherosclerosis, changes in renal perfusion with cross-clamping and nephrotoxic drugs.

Optimize fluid and electrolyte balance and consider mannitol, furosemide and renal-dose dopamine. Prophylactic administration of mannitol (25–50 mL 25% solution) prior to cross-clamping may protect against renal cortical ischaemia by several mechanisms:

• osmotic diuresis

• volume expansion, increasing renal blood flow and GFR

• haemodilution

• free radical scavenger activity

• atrial expansion, suppressing renin release

• reducing endothelial cell swelling.

Postoperative

Patients are prone to developing abdominal compartment syndrome (ACS), defined as intra-abdominal pressure >20 mmHg. Risk factors for ACS are anaemia, prolonged ↓ BP, CPR, hypothermia, severe acidosis (base deficit >14 mEq) and massive blood transfusion.

Carotid artery surgery

Patients with severe carotid artery stenosis (>70%) have a better outcome with surgery. Benefits for moderate stenosis (30–69%) are unclear. Surgery for carotid artery obstruction may be carried out if patient is having transient ischaemic attacks:

• 80% TIAs from carotid territory

• 20% TIAs from vertebrobasilar territory.

Vessels distal to a stenosis are maximally dilated and further flow can only come via collaterals from the circle of Willis. Thus, these patients are extremely sensitive to hypotension. If non-diseased areas vasodilate, a ‘reverse steal’ may occur, reducing collateral flow to post-stenotic areas.

Preoperative

A detailed preoperative neurological examination is needed to enable assessment of the postoperative neurological state. Also, examine the cardiovascular system to assess the degree of atherosclerosis. Diabetes and hypertension are common. Stop smoking.

Anaesthetic techniques

Recent GALA trial (Lancet 2008) failed to show a difference in outcome between local and general anaesthetic techniques.

Premedication. Short-acting only to prevent prolonged postoperative somnolence and allow early assessment of neurological function. Short-acting benzodiazepine is suitable.

Monitoring

CVS. Potential for large swings in heart rate and BP due to manipulation of carotid baroreceptors. Consider invasive BP monitoring.

Neurological. The awake patient allows continuous assessment of multiple levels of neurological function, but this is less sensitive if the patient is sedated. Also consider EEG, SSEPs, transcranial Doppler or intracarotid xenon washout curve to measure cerebral blood flow (CBF), and internal carotid artery distal stump pressure >50 mmHg (but poor correlation with regional CBF).

Regional technique (C₂–C₄). Deep and superficial cervical plexus block or cervical extradural anaesthesia. Provides excellent haemodynamic stability resulting in a very low incidence of perioperative MI. However, oxygenation and ventilation are poorly controlled and hypoxaemia/hypercarbia may necessitate intubation during surgery.

General anaesthesia. No specific technique has been shown to be of any advantage. Pre-oxygenate. Induction with thiopentone followed by vecuronium/rocuronium. Avoid pressor response to intubation (topical/i.v. lidocaine, opioids, esmolol, nitroprusside, etc.). Oxygen–air mixture + isoflurane may provide more EEG depression than halothane or enflurane for a given blood flow. Animals pretreated with barbiturates show protection from ischaemia, but there is no evidence suggesting thiopentone protects in humans.

Swings in BP are best treated with changes in volatile concentration, because use of short-acting haemodynamic drugs (nitroprusside, nitroglycerine, adrenaline, etc.) is associated with greater myocardial ischaemia.

Hyperglycaemia during ischaemia may worsen the neurological outcome by increasing anaerobic metabolism. Patients with poorly controlled blood glucose following a stroke have a worse outcome. Therefore, although no outcome studies have proven the risks of hyperglycaemia in carotid artery surgery, maintain tight control of perioperative glucose in diabetic patients.

Postoperative

Avoid postoperative hypertension and hypercapnia, which increase the risk of cerebral oedema and haemorrhage, because maximally vasodilated areas are unable to autoregulate. Hypocapnia may cause cerebral ischaemia.

Wound haematoma may cause airway obstruction. Laryngeal and hypoglossal nerve injury has been documented. Myocardial infarction is the commonest cause of perioperative mortality.

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Hypotensive anaesthesia

First described by Gardner in 1946 who used controlled haemorrhage to induce hypotension. (Introduced clinically by Griffiths & Gillie in 1948.) There was initial concern over high morbidity and mortality, but recent studies suggest that when carefully performed, the technique is reasonably safe. East Grinstead reported a mortality rate of 1 in 4128 cases.

Effects of hypotension

CVS. Reduced diastolic pressure reduces coronary perfusion pressure.

Respiratory. Greatly increased physiological dead space, ↑ V/ (ventilation/perfusion) mismatch and ↓ FRC. Volatile agents may further impair hypoxic pulmonary vasoconstriction. May need F_io₂ >0.3 to maintain arterial saturation.

CNS. Loss of cerebral autoregulation <50 mmHg. Risk of ischaemia in the presence of hypocapnia.

Renal. Poor GFR below 50 mmHg with risk of renal failure.

Techniques of induced hypotension

Premedication

Avoid atropine. Ensure patient is well sedated. Consider droperidol/chlorpromazine.

Induction

Spray cords. Thiopentone, fentanyl and neuromuscular blocker (not pancuronium which causes tachycardia – tubocurare was used because of its hypotensive effects). Maintenance with isoflurane/N₂O and a high F_io₂.

Posture

Head-up tilt reduces arterial and venous pressure in tissues higher than the heart.

IPPV

Positive intrathoracic pressure reduces venous return and thus cardiac output. Reflex vasoconstriction then normally maintains the BP but ganglion blockade or β-blockers may abolish this compensatory reflex. Positive end-expiratory pressure (PEEP) produces a further reduction in venous return and BP. Hyperventilation augments hypotension.

Volatiles

Halothane > enflurane causes peripheral vasodilation and myocardial depression. Isoflurane/sevoflurane/desflurane have little effect on myocardial contractility and hypotension is a result of peripheral vasodilation. Increasing doses cause CNS depression, which limits any reflex tachycardia. Isoflurane/sevoflurane/desflurane have the advantage that their cardiovascular effects can be altered with a change in inspired concentration faster than enflurane or halothane and they have less effect on intracranial pressure.

Sympathetic ganglion blockade

Trimetaphan (3–4 mg.min⁻¹) blocks nicotinic receptors at PNS and SNS ganglia. The SNS block reduces myocardial contractility but the PNS block results in tachycardia which may impair the degree of hypotension. Tachyphylaxis is marked.

Non-depolarizing neuromuscular blockers

Alcuronium and d-tubocurarine induce hypotension through histamine release. Mild ganglionic blockade also contributes to the hypotensive effect.

Alpha-adrenoceptor blockade

Phentolamine (5–10 mg i.v.), phenoxybenzamine, chlorpromazine and droperidol all produce competitive blockade of sympathetic postsynaptic noradrenergic receptors. Phentolamine is short-acting whereas phenoxybenzamine is usually used preoperatively for chronic vascular expansion. Droperidol and chlorpromazine are useful additions to the premedication.

Beta-adrenoceptor blockade

Reduces cardiac output and heart rate. Labetalol (50 mg i.v. over 1 min; max. 200 mg) is short-acting and also has some α-blocking action. Esmolol (100–300 μg.min⁻¹) is a short-acting drug which may be suitable for intraoperative i.v. use. Preoperative oral administration of β-blockers, e.g. propanolol, may prevent wide fluctuations in BP.

Direct-acting vasodilators

The very short half-life of sodium nitroprusside (SNP) enables rapid reduction in BP and equally rapid restoration (2–4 min). It dilates resistance and capacitance vessels. Vasodilation causes raised intracranial pressure and SNP should not be used in neurosurgery until the cranium has been opened. SNP increases aortic flow, increasing shearing pressure; therefore β-blockers may need to be used in addition. Start at 0.3 μg.kg⁻¹.min⁻¹ to limit cyanide toxicity (max. 8 μg.kg⁻¹.min⁻¹). Base deficit >–7 mmol.L⁻¹ is suggestive of CN⁻ toxicity. Sodium thiosulphate reduces CN^– levels by providing sulphydryl groups at the rate-limiting step (Fig. 1.10).

Figure 1.10 Metabolism of nitroprusside.

Glyceryl trinitrate (0.25–5.0 μg.kg⁻¹.min⁻¹) causes a slower reduction and recovery in BP (10–20 min) than SNP, with a greater effect on the systolic than on the diastolic BP. Dilates capacitance vessels with little effect on resistance vessels. Maintains coronary perfusion pressure more effectively than SNP but may raise intracranial pressure even more. Degree of hypotension achievable may be limited. Hydralazine (5–10 mg i.v. slowly) is also suitable for rapid control of BP.

Regional anaesthesia

Spinal and epidural anaesthesia with blocks extending to thoracic levels will produce hypotension by arterial and venous dilatation. Blocks extending to cardioaccelerator fibres (T2–T4) augment the hypotension further by preventing a compensatory tachycardia.

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Related

Clinical Notes for the FRCA