It’s 05:30, you are almost at the end of another busy night of standing around ramped at hospital, and you are trying to get back to branch to maybe snatch 5 minutes of sleep when your MDT starts beeping: Breathing Problems, Severe Respiratory Distress (Cardiac History). The patient is 72. Even with your brain at half-mast, you realise that there is a good chance that this patient has acute pulmonary oedema (APO) (well, maybe not, it’s actually hard to pick, but for the sake of argument…)
Sure enough the patient is extremely short of breath, ashen grey and diaphoretic with a BP of 220/120 and rales you can hear from the door. So, what are we going to do to help this patient?
First of all we should probably clarify what we mean by ‘pulmonary oedema’… Pulmonary oedema is the leakage of fluid from the pulmonary capillaries into the alveolar space as a result of increased hydrostatic pressure or capillary permeability. There are many things that can cause this leakage, but when ambos talk about APO they are typically referring to acute, sympathetically mediated, cardiogenic pulmonary oedema, and this is what we are discussing today. Around 20% of patients who develop APO will not get out of hospital alive, and this number is higher if the APO is associated with an AMI, so it is worth knowing about this condition and how to optimally treat it in the ambulance.
APO occurs when the left ventricle is unable to cope with it’s preload and afterload. This can be caused by a number of factors such as exacerbation of pre-existing left ventricular failure (LVF), acute myocardial infarction (AMI), cardiomyopathy, valvular dysfunction or dysrhythmias. Ultimately, irrespective of the underlying cause, APO is essentially the mother of all hypertensive crises.
Acute left ventricular dysfunction leads to a vicious cycle that rapidly spirals down to death if it is not broken: LV dysfunction leads to… decreased contractility and cardiac output,which leads to… sympathetic activation and catecholamine production, which leads to… increased afterload and preload, which leads to… increased ventricular wall tension and increased O2 demand, which leads to… myocardial ischaemia, which leads to… LV dysfunction, which leads to… backflow into pulmonary circulation and increased hydrostatic pressure in the pulmonary vascular beds, which leads to… Transudation of fluid into the alveoli and interstitium, which leads to… hypoxia, which leads to myocardial ischaemia and anxiety, which leads to… catecholamine release…
Round and round we go! As this cycle continues there is also shunt physiology occurring increased pulmonary vascular resistance, which leads to right ventricle afterload increases and increased left ventricle failure from diastolic ventricular interaction.
To have any hope of making this patient better we need to break this cycle as soon and as efficiently as we can. To this end there are three main goals we need to achieve:
- Decrease preload
- Decrease afterload
- Increase contractility and improve cardiac output.
Ambulance protocols have typically included three treatment modalities for the patient in APO which are mostly aimed at reducing preload and afterload: Nitrates (mostly sublingual GTN), frusemide and morphine. Inotropes (typically adrenaline) may be used to improve contractility and output in the patient with decreased cardiac output.
Most of these are either of no use, or may actually be doing more harm than good. Fortunately some services are moving with the times and removing some of these treatments and adding effective treatment such as CPAP.
GTN is the mainstay of pharmacological treatment of APO and should be used early and aggressively. GTN, a nitric oxide donor, quickly and reliably vasodilates, causing venous pooling and thus decreased preload. It also dilates arterioles, leading to decreased afterload, although this effect is less pronounced that the venous dilation.
Administration of sublingual GTN is safe and well tolerated by most patients, however if CPAP (discussed below) is available sublingual administration becomes problematic as it requires frequent breaking of the mask seal and therefore loss of positive intrathoracic pressure. I think that there is a sound argument to be made for the inclusion of IV GTN for use by intensive care paramedics. Whilst there may be some issues with the storage of GTN I don’t believe that this is insurmountable.
Frusemide has always been considered a fundamental part of the treatment of APO, however it should have no place in the initial management. The rationale for it’s use was that it causes some vascular dilation and removes excess fluid through diuresis. There are two problems with this rationale. First of all, the vasodilatory properties of frusemide are slight, inconsistent and unpredictable. In fact far from causing vasoldilation frusemide may in fact cause vasoconstriction, the very thing we are fighting so hard to avoid. Administration of frusemide results in an initial sympathetic surge and activation of the renin-angiotensin-aldosterone system which will clearly have the exact opposite effect than we are seeking.
Secondly, many patients (around 40%) with acute pulmonary oedema are not fluid overloaded, they are euvolemic or even hypovolemic, so there is no excess fluid to remove. Certainly there is fluid in the wrong place, but this doesn’t mean that there is too much of it overall. Of course there are a subset of patients in whom fluid overload may be present, and in any case removal of fluid will decrease preload, however this comes at the cost of electrolyte derangement and ongoing hypotension. Frusemide also takes a long time to work due to reduced renal blood flow as a result of the increased systemic vascular resistance, and time is of the essence when attempting to break the vicious cycle of APO.
Such studies as have been done in the prehospital setting have shown a significant increase in mortality in patients treated with frusemide, many of whom required fluid replacement later. Despite these issues, I don’t know that I am ready for frusemide to be removed from the drug bag entirely. There are clearly a subset of patients in whom diuresis may be appropriate (the chronically fluid overloaded or medication non-compliant patients) and it may be indicated in other situations beside pulmonary oedema. However I believe that in the vast majority of cases of acute pulmonary oedema cases we treat it is inappropriate and the paramedic should have the discretion to withhold administration. We need to think of APO not as fluid overload, but as fluid maldistribution.
There are two reasons that morphine has traditionally been used in the treatment of APO. One is the vasodilatory effects and the other is the supposed anxiolytic effect. Unfortunately beneficial haemodynamic effects of morphine have not been demonstrated. Adverse effects have. Any haemodynamic effects associated with the use of morphine are probably mediated by histamine release which can come with further negative effects such as nausea, vomiting, itching and so forth. Morphine may also have a direct myocardial depressant effect, as well as causing respiratory depression which is clearly not going to be useful in a patient with a heart that is already performing poorly and respiratory compromise.
Studies have demonstrated adverse outcomes in patients with APO treated with morphine in the pre-hospital setting, and in-hospital studies have shown increased need for ICU admission and intubation in patients receiving morphine. Of course the use of morphine may be a marker of sicker patients (ie those who will do badly anyway) but there seems to be little justification in continuing use of morphine when better agents for both vasodilation (GTN) and anxiolysis (benzos) are readily available. Fortunately it seems that most protocols are now de-emphasising the use of morphine, although sadly my own still call for it if the patient is anxious.
Some services are now allowing intensive care paramedics to use CPAP in the treatment of APO, typically with devices such as the WhisperFlow or Boussignac system. Patients suffering from APO have stiff, fluid filled alveoli which tend to collapse on expiration. By maintaining patency of these airways the patients work of breathing is decreased as they no longer have to expend energy trying to reopen atelectatic alveoli. Gas exchange is also improved so better oxygenation is able to be achieved. Increased intrathoracic pressure also further reduces preload and afterload which leads to improved cardiac output.
There is and argument from some quarters that CPAP is not very useful as it does not reduce mortality. Even if this were true, CPAP significantly reduces the need for intubation and admission to ICU. Anything that can keep a patient from ICU with all the associated risk and cost seems to be of benefit to me. The same goes for avoiding intubation. Intubating APO patients is fraught with danger and unless adequate equipment such as PEEP valves (or proper ventilators) is available it may even be counterproductive, to say nothing of the risks of barotrauma, volutrauma, ARDS and VAP that comes with being tubed.
Quite aside from what seem to me to be the obvious benefits of reduced intubation/ICU admission, a Cochrane review in 2008 showed a reduction in mortality in patients treated with NIPPV of about 8.5%. This is not insignificant given the large numbers of patients we treat (a NNT of 13 for mortality)
(Warning: Anecdote ahead) Finally I believe there is another benefit to CPAP. Most paramedics realise that we are not life saving machines, but that there is benefit in reducing suffering (eg through the liberal use of analgesia) In my experience, patients with APO who are treated with NIPPV show rapid and dramatic improvement in their air hunger and anxiety. Even if we are not ‘saving lives’ I believe that the relief of suffering we can achieve with optimal treatment is a valid goal as well. CPAP devices are relatively cheap, definitely effective and safe so there seems to me to no compelling reason not to use them.
Acute, sympathetically mediated cardiogenic pulmonary oedema is primarily a issue of hypertension, resulting in inappropriate distribution of fluid into the lungs. It is not typically a problem of fluid overload. Treatment needs to be directed at reduction of preload and afterload, primarily through the use of GTN. NIPPV should be used early in conjunction with nitrates to reduce mortality and morbidity.
Some practical tips: Don’t be in a hurry to move these patients, especially if it is a cold night. Take the time to start getting the BP down and the oxygenation up. Any movement is going to add further workload and patients often deteriorate rapidly when this occurs. Taking the patient out into the cold night will potentially cause vasoconstriction as well.
I see many people trying to use a bag-valve mask to provide a high concentration of oxygen to these patients. I appreciate the thought, however I think that it often causes more harm than good. These patients are already extremely anxious and having a BVM held on their face does nothing to alleviate this. BVM technique can also be a bit tricky. Even if you get a good seal it is very difficult to synchronise ventilations with the patient, and for a BVM to work properly you need to make sure you are opening the duck-bill valve in the head of the device. If you just hold the mask on without ventilating you then further increase work of breathing even if you are providing more O2. I think it is far better to use a non-rebreather to provide a high FiO2 until CPAP can be applied. Concentrate on treating the BP with nitrates, maybe getting a line and organising the logistics of extrication and transport. Obviously if your patient is in extremis you may need to start ventilating though. We obviously need to get the patient to definitive care in a timely fashion but this should never occur at the expense of good patient care.
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