Table Of ContentC
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Cardiovascular system
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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 mor-
tality, particularly vascular patients where mortality is 3–4% for open proce-
dures. 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-car-
diac 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.
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Box 1.1 Classification of cardiac risk factors
for non-cardiac surgery
Major factors (unstable coronary artery disease):
• Congestive heart failure
• Malignant arrhythmias
• MI <6 weeks
• Angina class III/IV
• CABG/PCI <6 weeks
Intermediate factors (stable coronary disease):
• MI >6 weeks but <3 months
• Angina class I/II
• CABG or PCI within 3 months
• Diabetes mellitus
• Age >70 years
• Heart failure/ejection fraction <0.35
Minor factors (risk factors for coronary artery disease):
• Family history of ischaemic heart disease
• Uncontrolled hypertension
• Smoking
• ECG abnormalities (LVH, left bundle branch block)
• CABG or PCI >3 months but <6 years (symptom free and no
therapy).
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).
CArDIoVASCULAr SyStEM 3
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 preopera-
tive 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 vascu-
lar 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 i schaemic 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 postopera-
tive cardiac complications.
Angiography. Definitive investigation. (Right coronary artery supplies sinoa-
trial node in 60% of patients and atrioventricular node in 50%). Indicated for unsta-
ble 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 car-
diac outcome. Aim to optimize myocardial oxygen balance (Table 1.1).
Laplace's law
Wall tension (preload and afterload) determined by Laplace's law:
4 CliniCal notes for the frCa
pressure × internal radius
Wall tension∝
wall thickness
Table 1.1 Factors affecting oxygen supply and demand
Supply Demand
Coronary perfusion Preload (LVEDP)
o content Afterload (SVr)
2
Heart rate Heart rate
Contractility
Premedication
Continue all cardiac medication until the day of surgery. Heavy premedica-
tion reduces anxiety, which may otherwise cause tachycardia, hypertension
and myocardial ischaemia. Consider O after morphine premedication to avoid
2
hypoxaemia from respiratory depression; the prevention of tachycardia results
in less myocardial ischaemia overall.
b-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 recom-
mend 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 V together detect 95% of myocardial ischaemic events.
5
Leads II, V and V4R together detect 100% of events. ST segment monitoring
5
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 cmHO. The
2
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
CArDIoVASCULAr SyStEM 5
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 elec-
trical 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 sensi-
tive 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 O consumption and reduce diastolic coronary filling time.
2
Hypotension reduces coronary perfusion pressure.
NO is a sympathetic stimulant, but will decrease sympathetic outflow if the
2
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 main-
tain 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 grow-
ing evidence that isoflurane has myocardial protective properties, limiting
infarct size and improving functional recovery. This mechanism mimics ischae-
mic 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.
6 CliniCal notes for the frCa
Stenosis
P1 MYOCARDIUM
(A) P1 = perfusing pressure. Stenosis reduces
flow to myocardium but adequate perfusion is
achieved through collateral flow.
Stenosis
P2
P1
MYOCARDIUM
(B) Vasodilator increases run off, reducing
pressure at P2 and therefore reducing perfusion
pressure of myocardium
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
CArDIoVASCULAr SyStEM 7
spinal anaesthesia tends to occur at cessation of the block, probably due to
increased pre- and afterload aggravated by volume loading.
Blocks below L have no effect on the SNS. Blocks above T block sympa-
3 10
thetic afferents to the adrenals and reduce catecholamine release. Blocks to T–T
1 4
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).
First and second letters
e.g. D D D R O = None
A = Atrium
Programmability
V = Ventricle
D = Dual (atrium and ventricle)
Response to sensing
Third letter
I = Inhibited
Chamber-sensed T = Triggered
D = Dual response
Chamber-paced
Fourth letter
O = None
P = Simple
M = Multi-programmable
R = Adaptive rate pacing
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.
8 CliniCal notes for the frCa
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 tachy-
cardia 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), caus-
ing 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 con-
sisting 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.
CArDIoVASCULAr SyStEM 9
• 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 antico-
agulation for acute AF, as for persistent AF.
AtriAl FibrillAtion: the MAnAgeMent oF AtriAl
FibrillAtion
National Institute for Health and Clinical Excellence, June 2006
Guidance
Patients with acute 1 1 Diagnosis to be confirmed by
haemodynamic ECG. Check electrolytes and
instability secondary review chest X-ray. Attempt to
to AF establish aetiology of acute
haemodynamic instability.
Is the situation 2 2 Any emergency intervention
life-threatening? should be performed as soon
as possible, and the initiation
No Yes of anticoagulation should not
delay any emergency
intervention.
Is the AF Emergency
known to be electrical
permanent cardioversion
No
(or not Yes
known)
3 Where urgent pharmacological
Electrical Pharmacological rate-control is indicated,
cardioversion rate-control intravenous treatment should
be with i) beta-blockers or
rate-limiting calcium
antagonists, or ii) amiodarone,
where beta-blockers or calcium
antagonists are contraindicated
or ineffective.
4 4 Where there is a delay in
Pharmacological
organising electrical
cardioversion
cardioversion, intravenous
amiodarone should be used.
In those with known WPW
syndrome, flecainide is an
alternative (atrioventricular
node-blocking agents such as
diltiazem, verapamil or digoxin
should not be used).
Figure 1.3 Haemodynamically unstable and acute-onset AF. NICE.
10 CliniCal notes for the frCa
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 pres-
sure 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, depen-
dent 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 overtrans-
fusion, but it is important to maintain adequate filling. A fall in SVR is poorly
tolerated. Consider inotropes and pulmonary vasodilators.
Description:1 Chapter ANAESTHESIA AND CARDIAC DISEASE New York Heart Association classification of cardiovascular disease • I Normal cardiac output. Asymptomatic on heavy exertion
