The college is particularly fond of aortic stenosis, as is demonstrated by their constant asking of questions on this topic. Specifically, multiple questions have been asked on the topic of severity staging of aortic stenosis:
So, as assessment drives learning, the topic of severity staging for AS - whatever it's actual importance is to critical care practice - has taken on a significant "know it for your exam" level of importance, which merits the entire front half of the valve dysfunction chapter. Beyond the issue of cynical exam cramming, there is also the management of the aortic stenosis patient who is haemodynamically unstable, and knowing what to expect from their circulatory performance in response to stress. An even more interesting matter is what to do when these AS patients have their valve replaced. The consequences of exposing the systemic circulation to a massively overpowered LV are worth discussing.
In summary, for severe aortic stenosis:
- Keep them well filled; avoid venodilators and diuretics
- Slow the rate (50-60), but avoid excessive beta-blockade
- Avoid AF as much as possible
- If there is evidence of heart failure, avoid drugs which impair contractility (eg. beta-blockers and calcium channel blockers)
- Avoid high afterload (it overload the LV) but keep an adequate diastolic pressure to prevent coronary insufficiency
In short, these people need to be wet, slow and with some mid-range blood pressure (not too high, not too low).
A balloon pump might be of some use if the patient is in cardiogenic shock.
Apart from the anaesthesia textbook mentioned below, the other useful reference is Christ et al (2005), which is a discussion of the anaesthetic perioperative management of aortic stenosis patients. By combining anaesthetic agents, blood loss and various cross-clamps and Valsalvas, the perioperative environment is a good model for all the various shock states and physiological bewilderments one might encounter in the ICU, and so this article's topics make it a good surrogate for a proper ICU-centric paper.
Aortic valve area is measured as an index to body surface area, and is represented as cm2/m2.
Mild stenosis is compensated for by LV hypertrophy, as the LV is expected to generate an increasing pressure to drive blood across the narrowing valve.
Moderate stenosis (an aortic valve index below 0.7cm2/m2) results in some degree of LV failure and tends to result in increased myocardial workload and increased oxygen demand. The ventricle loses its contractility and coronary perfusion pressure decreases due to an elevated LVEDP. Even in the absence of coronary artery disease, coronary ischaemia my ensue. Once symptoms of LV failure develop, life expectancy is usually 1-2 years; only 18% survive to 5 years.
Critical stenosis represents an aortic valve index below 0.5cm2/m2. At this stage, pulmonary venous hypertension develops. A left atrial pressure of over 25-30mmHg tends to result in pulmonary oedema. If you manage to survive all this, right ventricular failure will eventually develop.
The LV is hypertrophied, and therefore its compliance is poor. A higher preload is required for normal systolic function. This is a game of balancing one's PEEP with one's fluid overload. A higher FiO2 may need to be tolerated in order to allow an increased intravascular volume.
Diuretics and vasodilators- particularly venodilators- should be avoided. A drop in preload would be disastrous for the cardiac output. These are patients who are very sensitive to propofol-related vasodilation, and may have catastrophic hemodynamic responses to boluses of sedation.
Because it takes some considerable time to eject blood through the narrowed valve, a slow heart rate is important. Let the ventricle take its time. Slow rates are ideal, and the textbook rates are 50-60. It also allows the beefy hypertrophied ventricle time to relax, helping defeat the diastolic failure. If the aortic stenosis co-exists with regurgitation, you may allows a higher heart rate.
However, in many of these patients, cardiac output is really only maintained by the superhuman effort of a hypertrophied LV. If there are features of heart failure (i.e. low blood pressure and pulmonary oedema) the LV is said to be overloaded. In this case, β-blockers can actually make things worse.
It is critically important to maintain sinus rhythm. These patients will not cope well with a loss of diastolic filling which occurs with atrial fibrillation. Remember that every last drop of preload is precious.
Frequently these patients are already hyper-contractile. Increased myocardial contractility is the mechanism of adjustment to extreme valve narrowing. Certainly one would want to avoid anything that impairs this coping mechanism, like beta blockers or calcium channel blockers (see above).
In these people, the afterload is essentially fixed. It is generally said that there is no way to manipulate it by playing with systemic vascular resistance - the stenosis is in the aortic valve, not the peripheral circulation. Thus, lowering the blood pressure artificially is supposed to have little effect on afterload or myocardial oxygen demand.
An increased systemic blood pressure tends to make things worse. If you have systemic hypertension, the LV needs to work against an increased resistance, on top of the usual effect of the stenotic valve. As such, control of hypertension is important. One should avoid high peaks of blood pressure. However, this is not as important as prevention of hypotension. If the diastolic falls too low, the coronary arteries will not get enough filling - and they require a larger than usual amount of diastolic driving pressure to penetrate into that hypertrophied subendocardium. Thus, it is important to keep the diastolic pressure high.
With the caveat that too much or too little blood pressure is bad, one may aim for some sort of moderate middle. If the blood pressure is high, it is reasonable to use afterload-reducing arterial vasodilators. The UNLOAD trial (Khot et al, 2003) found that, using nitroprusside, one can improve the cardiac index of such patients from 1.6 to 2.5 by dropping the MAP from 81 to 69 (i.e. not by much). A similar effect could be expected from an aortic balloon pump (which, apart from improving afterload, would probably also improve diastolic perfusion of the hypertrophied LV).