Tests should only be performed in the context of the above, and if they are likely to alter management. With surgical emergencies, there is no point in mucking around doing a host of tests that will cause harmful delays.
The report stratifies cardiac risk according to the nature of the surgery, with major risk factors (high risk surgery) being:
The authors also indicate that the following are 'major clinical predictors' of poor outcome:
'Intermediate clinical predictors' are considered to be:
They present a complex flow diagram for pre-operative assessment (Fig 1 of the report). We've paraphrased it as follows:
We would perhaps tend to be a little bit less aggressive in investigating someone with intermediate clinical predictors (for major surgery) if they have excellent effort tolerance. Our views are in keeping with the "overriding theme" of the article that the nature of the heart disease, rather than the non-cardiac surgery, dictates cardiac management. The rest of the report looks in some detail at specific cardiac diseases, specific tests, and "perioperative therapy".
The guidelines can be found at:
One topic of particular interest that is alluded to is that of beta blocker use in the perioperative period. This topic is contentious, to say the least. There is a considerable body of evidence to suggest that fast heart rates are bad, although the reasons for this are far from clear.
The traditional explanation was that ischaemia is produced due to the relative shortening of diastole with fast heart rates. Coronary perfusion is thus compromised, and portions of the heart with impaired blood supply become ischaemic.
This explanation doesn't explain increased rates of perioperative myocardial infarction. We know that myocardial infarction is related to formation and propagation of thrombus on a crack in the surface of an atheromatous lesion. It is not clear why beta blockade should be protective against such events - is it a rate-related phenomenon, or related to something else like mural tensile stress?
Whatever the mechanism, several recent studies suggest that beta blockers are indeed protective. For a review, see that in a recent JAMA (March 20, 2002, Vol 287(11) 1435-1444). Numbers are still small, but the effect is consistent. Much criticism has been levelled at Mangano's original study (mainly because patients in the control group may have received sub-optimal therapy, on account of some having their beta blockers stopped in the peri-operative period). Such criticism cannot be levelled at the study of Poldermans et al, which showed a massive reduction in peri-operative death and infarction rates with the use of bisoprolol. The study was randomised but was not blinded (it is difficult to see how blinding might have been achieved where all one has to do to 'unblind' is to observe the heart rate). The major question related to the Poldermans study is whether the results are generalisable from the population in question, who had dobutamine stress echo evidence of reversible ischaemia. This is a generic problem with all 'evidence-based' studies, unless the evidence is only applied to an identical population. To a certain extent, the onus would appear to be on skeptics to demonstrate populations in which beta blockade is convincingly not beneficial, noting that there is absolutely no evidence that beta blockade is harmful in patients with severe peripheral vascular disease, nor in those with chronic obstructive airways disease or diabetes. In asthmatics, use of beta blockers with intrinsic sympathomimetic activity is probably advisable. In general, the risks of perioperative beta blockade seem small, and the potential benefit, substantial. (One suspects that those who routinely administer peculiar drugs such a dopamine or dobutamine in their high-care or intensive care units may be rendered distinctly dysphoric by the presence of beta blockade).
Other questions remain, notably whether the beneficial effects seen are a class effect, or whether certain beta blockers only are beneficial. Everything at present points to the former.
There are two new ideas in atrial fibrillation (AF). The first is related to pathogenesis - we used to think that the most important factor in the pathogenesis of AF was "multiple re-entrant wavelets" due to disordered conduction within an (often enlarged) atrium. Many people now believe that this concept is very simplistic, and that in a substantial proportion of people with AF, another mechanism is very important. The idea is that ectopic activity within the pulmonary veins near the point where they enter the left atrium is responsible for initiating and sustaining atrial fibrillation in many (and perhaps most) people who suffer from the disorder.
See: Nattel S. Nature 2002 Jan 10;415(6868):219-26 New ideas about atrial fibrillation 50 years on
Also check out an older (but seminal) article: Ha´ssaguerre M et al. N Engl J Med 1998 339(10) 659-666. available online.
The second important idea is that simple rate control may be as good as rhythm control. This concept comes from two big studies that were recently published. The more prominent of these trials is probably the AFFIRM (Atrial Fibrillation Follow-Up Investigation of Rhythm Management) trial, which looked at 4060 North American patients over 65 years of age. The patients were randomised to either rhythm or simply rate control, with warfarinisation being encouraged in both groups. There was no significant difference in death rates in the two groups (and it is thus pointless to comment on the slightly greater number of deaths in the rhythm group). There were more hospitalisations and adverse drug effects in the rhythm control group. In both groups, if warfarin was stopped, then patients tended to have strokes. The main question you have to ask yourself about this study is:
The smaller RACE trial from the Netherlands supported the results of the AFFIRM trial. The reference is: Van Gelder IC, Hagens VE, Bosker HA, Kingma JH, Kamp O, Kingma T, et al. A comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J Med 2002;347(23):1834-40. Stanley Nattel has written an insightful comment on the trials in CMAJ.
Another vital concept is that "atrial fibrillation begets AF". The ion to blame is as usual, calcium. With repetitive, rapid atrial muscle depolarisation, the fibres become loaded with calcium. Unfortunately, the short-term compensatory mechanisms that the cell uses to protect against this calcium loading predispose to the persistence of AF, mainly because of changes in membrane channels, and transmembrane potential! The vital term is "electrical remodel(l)ing".
There's also been a lot of enthusiasm about the "maze procedure" for suppression of AF. This started off as a high-mortality (one is tempted to say, desperation) procedure where the atria were incised and then re-sutured, with the hope that refractory AF would be cured. The procedure has now been refined, but even enthusiasts (such as Cox) admit that the current operative mortality is about 2 to 3%. Carefully directed radiofrequency ablation or atrial 'lesioning' may be the procedure of the future when definitive treatment of AF is desired.
Other topics of note
Other topics that could be considered somewhat important are:
A good internet (Google) search for information on pacemaker classification is simply:
nbg bpeg naspe
(Why?) You will encounter sites such as "studio-delos", which explore the classification in some detail. We've here shamelessly snitched one of their tables:
The above table isn't as formidable as you might expect. It's also rather logical. The primary function of a pacemaker is, well, to pace, so the first position says which chamber is paced. It's usually not a great idea to pace without sensing, hence ... position two! Mode can be quite fancy, but note that in DDD pacing, which is now common, there is a variety of different combinations of which chamber is paced and sensed. Most pacemakers are extensively programmable - this implies that they can communicate, doesn't it? Rate modulation with exercise is a topic on its own, but is rather smart, and now fairly robust. Antitachycardia devices are expensive, fancy, and work surprisingly well, provided you agree that being kicked in the chest occasionally is better than dying!
Okay, perhaps we're fishing to find something blue, to finish our little essay. Perhaps the 'blue' is the attitude of the average anaesthesia candidate to the presence of a clinical component in their higher exam? Here are a few clinical pearls that might help:
Atrial fibrillation (again)!
Note that if the pulse is "irregularly irregular" (that dreadful term) then it's very likely that it is AF, although frequent extrasystoles or a multifocal atrial tachycardia may confuse. Get an ECG. When you encounter AF, you should immediately ask yourself "What is the cause"?
The commonest association of AF is systemic arterial hypertension, although the relationship need not be causal. Other things to think of are:
If you're a musician, then there's a cute trick you can use to distinguish between atrial and ventricular extrasystoles, at the bedside! Tap out the rhythm, and wait for an extrasytole. Continue tapping the rhythm, after the extrasystole. If subsequent beats are in time with your tapping, the extrasystole was a VE; if the beat is not kept, then the atrial pacemaker has been reset, and the extrasystole was almost certainly atrial (Very occasionally, a VE may propagate retrogradely and capture the atrial pacemaker).
Common valve lesions, in a nutshell
Note that you should have a strong clinical suspicion of the lesion you're dealing with, before you lay your stethoscope on the chest. The history is more important than the examination.
Often, the patient has a 'right sided' picture, with evidence of right sided failure (JVP up, oedema, hepatic congestion, even TR). They may rarely even have a 'mitral facies' with high colour in their cheeks! Frequently there will be a left parasternal heave (from the big RV), and a loud pulmonary component of the second heart sound (P2). Duroziez described the typical findings in tight pliable MS as "ffout tat ta rou", the 'ffout' being the presystolic accentuation and loud S1, the tat ta indicating S2 followed closely by an opening snap, and the 'rou' being the rumbling mid diastolic murmur. But remember that if the mitral valve is calcified, then S1 is often soft, and even the mid-diastolic rumble may be elusive, unless the patient is exercised and the apex is auscultated lying on their left side. Very important in MS is that the apex is usually undisplaced , and often tapping in nature. AF is common.
On history there is a spectrum of presentation, from severe pulmonary oedema (in those with low compliance of the left heart and vessels draining into it), to chronic lethargy and tiredness (related in part to lowered cardiac output). Clinically, in contrast to MS, the apex will be diffuse and laterally displaced, owing to the chronic volume overload of the LV. The 'classic' MR murmur is blowing (quite different from harsh aortic murmurs), heard best at the apex, and radiating well to the axilla. It is pansystolic. This site and radiation is related to the usual MR abnormality involving the anterior mitral leaflet. If the PML is involved, then the murmur commonly radiates well to the left parasternal border, and poorly to the axilla. Additional features in substantial MR are the presence of an S3, and sometimes, a left atrial lift . When MR is associated with a billowing mitral valve, the murmur often starts later in systole, after the non-ejection systolic click(s). The murmur of acute MR associated with rupture of a chorda tendinea is much more musical, and is said to have a "cooing dove" like quality!
Another condition in which the LV is volume overloaded, this valve lesion more than any other should be diagnosed when examining the periphery. A clue is the presence of a collapsing pulse (Systolic BP more than twice the diastolic - now that's easy, isn't it)? Although a host of signs and associated labels/eponyms has been attached to AR, most of these features are either unreliable or only found with really overt AR. (Consult your clinical methods books for detailed descriptions of De Musset's sign/ titubation, Quincke's sign, dancing retinopathy, and so on). The best sign that indicates at least moderate plus (and probably severe) AR is Duroziez's sign. This sign is elicited by pressing with your index finger over the femoral pulse, and ausculating proximal to your finger with the bell of the stethoscope. Vary the pressure and listen carefully - in everyone, you will hear a conspicuous systolic 'woosh' as the blood flows forward through the constricted artery, but this isn't what you're looking for! You are listening for a short diastolic 'whew', which is soft, but easily noted by the practiced ear. This signifies reversal of flow as a vast regurgitant jet enters the left ventricle. For some obscure reason, in my hands, it seems to work better at the left femoral than the right!
If you are not already alert to the suspicion of AR, it's easy to miss the rather high pitched early diastolic (decrescendo) murmur of AR on auscultation. Listen with the patient sitting forward, using the diaphragm of the stethoscope applied to the upper central chest, often best heard in the 2nd left interspace or a bit lower down. In severe AR, there may also be a soft mid-diastolic rumble, related to the large regurgitant jet interfering with the anterior mitral leaflet. This can be difficult to distinguish from coexisting MS, but the short duration of the rumble and lack of associated features of MS suggest that the AR is causing the rumble (Austin-Flint murmur). Note that it's common to have a fairly florid systolic murmur (even up to 4/6) with AR, even in the absence of significant aortic stenosis!
Most threatening to the anaesthetist, tight AS may easily be missed in the elderly. Suspect it with any one of (a) angina; (b) heart failure, and (c) syncope (especially). A wide pulse pressure is utterly and totally unreliable in excluding the presence of tight AS, especially in the elderly. You should however be able to suspect, or even diagnose tight AS simply on palpating the carotid pulse - a slow rising pulse correlates well with the presence of tight AS. If you are uncertain, 'calibrate' using your own carotid pulse, which we hope is normal!
Another fine print (but useful) trick is to gently feel the brachial and radial pulses of the same arm, simultaneously. In normal individuals, the pulses should be synchronous, and a palpable delay is a pretty reliable sign of tight AS! (There is some literature to support this contention, mainly an article in the Lancet from about 1991).
Worry if you haven't made the diagnosis of AS before you auscultate. A well-localised, thrusting apex that indicates systolic overload supports the diagnosis. The aortic component of the second heart sound should be soft, and is often inaudible. If heard, there may be paradoxical splitting of S2. There may be an S4. The murmur of significant AS is (of course) ejection systolic, but is often long and late-peaking. Characteristically, the AS murmur is rather harsh , and radiates widely, not only to the neck (its 'classic' site) but all over the precordium. In some patients, the murmur may be heard best at the apex, deceiving the casual listener into believing that some other lesion is present! Tight calcific AS is somewhat different from e.g. rheumatic AS, as the murmur is often rather musical, somewhat reminiscent of the cry of a seagull, at least to the fanciful ear!
This lesion is diagnosed peripherally, not by auscultation. Look for large V waves in the jugular venous pulse ('CV' waves), as well as a pulsatile liver. Do not rely on the occasional finding of a somewhat squeaky murmur heard best in the epigastrium, that varies markedly with respiration!
And oh, occasionally you'll encounter an adult with something strange like Eisenmenger's complex, leaving you feeling really somewhat blue!