Hypertension in the ED
Over the last year it has been an increasingly common presentation to EDs. It has long been the case that patients would bring themselves to emergency departments with high blood pressure, the commonest cause of which in my experience was anxiety about their high blood pressure. However, we are seeing increasing numbers being referred from other source, like primary care. So, the question is what should we be doing for these patients and why are other clinicians referring their patients with hypertension.
As always NICE has some good guidance but, its more aimed at primary care and the specifics pertinent to acute medics and emergency medics is not all that clear. Hopefully below we can simplify what is the current guidance and make it applicable to emergency departments. Long the attitude has been GTN/labetalol or get out, but this seems to be changing and the big question is why?
First it is probably worth having some understanding of how hypertension is diagnosed:
- If the patient as the lowest of 2 readings higher than 140/90 then they are offered ambulatory blood pressure monitoring or if that is not tolerated home blood pressure monitoring. (both require at least 2 readings a day for 7 days, ideally during their usual day, one in the morning and one in the evening)
- Whilst the patient has their HTN confirmed it is expected that the patient has assessment of their end organs and an assessment of their cardiovascular risk.
- Now if their initial BP reading in the clinic was greater than 180/120, this is classed as severe hypertension it is suggested that they have investigations for target organ damage as soon as possible.
o If there is no evidence of target organ damage, they can still have the confirmation of HTN through ambulatory or home BP monitoring.
- Patients with a BP of 180/120 or higher and signs of retinal haemorrhage/papilloedema or life threatening symptoms (new onset confusion, chest pain, heart failure or AKI) need to be referred for same day specialist assessment.
- Initial HTN management in primary care is to give ACEi to anyone who has Diabetes or are aged under 55 and are not afro-caribean. Calcium channel blockers are for those over 55 without diabetes or are of black African/afro-caribbean orgin.
Now we understand how these patients end up in the emergency department – they have potentially life threating causes of their hypertension (papilloedema) or have evidence of current damage from their HTN (MI, encephalopathy, renal failure). When we are looking for target organ damage, we want to assess the following:
- Haematuria
- Retinal Haemorrhage or Papilledema
- ECG
What we are looking for is evidence of microvascular injury which leads to inflammation and then further autoregulatory dysfunction. You will find when you read around hypertensives emergencies that the language varies. There are multiple terms – malignant and accelerated hypertension being one example – that are interchangeable. There is also a lack of good evidence and research into managing hypertensive emergencies. The combination of the two makes it hard to follow and understand at time, and might go to explain some of the variation in management and assessment between clinicians.
Little on the physiology of hypertension. To start we need to look at what makes up our blood pressure, it’s the product of the cardiac output (in turn made up by the stroke volume and heart rate) and the peripheral vascular resistance.
Most people with hypertension have essential hypertension (ie doesn’t have another cause, only 2-5% of hypertensives will have renal or adrenal disease causing their raised BP). In these people they have a normal cardiac output but a high peripheral vascular resistance. Small arterioles are the vessels that provide this resistance through contraction of the smooth muscle in their lamina, this is calcium mediated (hence calcium channel blockers). Like any muscle, prolonged use will lead to structural changes – usually thickening and so the vessel walls narrow on the lumen causing irreversible changes in peripheral vascular resistance. It is possible that in the initial phase of hypertension, very early on, it maybe increased cardiac output that starts the cascade and PVR is normal due to sympathetic over activity and that the rise in PVR is actually a compensatory mechanism to protect the capillary beds.
Secondary Hypertension is a rare presentation and nice recommends that all adults under 40 with new HTN have investigations looking for causes of their hypertension. This is usually done by an endocrinologist and/or a renal physician rather than an acute medic/emergency department or a cardiologist. However, it is perfectly reasonable to assume that it is likely that these patients could present to our acute services. The diagnosis that is most likely sitting behind their acute presentation with secondary hypertension is a phaeochromocytoma. These patients will adrenaline mediated symptoms – palpitations, sweating, anxiety, tremor and pallor. They are complex and challenging to diagnose and will need input from an endocrinologist. The initial focus will be about ensuring the safety of the patient by controlling their blood pressure.
When thinking about secondary causes, there can be physiological causes of hypertension, such as anxiety and pain. These need to be considered for and managed before moving further into managing a hypertensive crisis. It is not uncommon to see patients who have an initially higher reading, around the 160s/170s, who then continue to check their BP or seek reassurance but end up with further increases in their BP until they arrive in the ED.
Our blood pressure is a complex control system that we first learn about in our early days at medical school, there is clinical relevance to those systems and we talk about them in the context of hypotension in our shock and sepsis areas. They are more relevant (in the context of hypertension) for medicine outside of an emergency hypertension focus. If you want to go and remind yourself about the renin-angiotensin-aldosterone system (RAAS), the role of bradykinins as a vasodilator, nitric oxide and ANP I would encourage you to do so. We will touch on them as we look at the impact of hypertension across the organs we look at for end organ damage.
- Heart
o RAAS leads to systemic vasocontricton, causing Left Ventricular Hypertrophy and reducing myocardial perfusion (remember that perfusion of the heart occurs during diastole, not systole and the perfusion pressure in the left ventricle is the difference between the left ventricle end diastolic pressure and aortic diastolic pressure)
o Increasing hypertrophy leads to increasing O2 demand, whilst compromising blood supply. When put into the context of a hypertensive crisis this leads to myocardial ischaemia (cause the heart is literally working harder to maintain those pressures and continue the flow of blood) and/or LV failure leading to pulmonary oedema.
- Brain
o Usual blood flow in the brain is kept constant, if this mechanism is exceeded there is endovascular damage in the brain. This causes cerebal oedema and microhaemorrhage which presents as hypertensive encephalopathy.
- Kidneys
o Endovascular damage, Fibrinoid Necrosis and renal ischaemia are the consequences of hypertension in the kidneys.
There is little understanding of the exact pathophysiology leading to rapid and severe BP rises. It is thought that humoral vasoconstrictor release leading to endothelial damage plays a role, creating a vascular ischaemic state, from which RAAS is activated though pressure natriuresis (poor renal perfusion pressures). This creates a vicious cycle of sorts, where further vascular injury leads to worsening organ perfusion and so further RAAS activation.
The hyperactivity of the RAAS system makes patients extremely sensitive to administration of ACEi or ARBs and so these are generally avoided in the acute phase. There is also potential for Beta Blockers to have a similar effect (suggesting some sort of catecholeamine involvement in the pathophysiology) but when given in low doses they are typically considered safe.
Clinical Assessment:
What we need to do is rule out the significant problems associated with hypertensive crises. This table explains what the potential condition is and how it would present
Isolated Headache is a controversial symptom when I comes to hypertension in general. It can be a feature in a hypertensive emergency, for example as part of cerebral haemorrhage or as a symptom of a cause like phaeochromocytoma. It appears that as a stand alone symptoms it is not sufficient to diagnose malignant or accelerated hypertension, however it maybe present as a feature of a hypertensive crisis (a BP >180/110 with no other symptoms) that also would need managing urgently if not immediately. https://pubmed.ncbi.nlm.nih.gov/30874912/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829292/
When Investigating an acutely hypertensive patient in the emergency department the two questions we are asking are
1. Is this accelerated/malignant hypertension?
2. Are we sure that this is primary/essential hypertension and that it isn’t a secondary hypertensive episode.
With these question in mind our investigations should be easy to remember:
- Look for evidence of renal failure/compromise with U+Es and Urinalysis, both dip (protein and blood would be concerning as evidence of glomerular damage), and where appropriate Pregnancy test (eclampsia would be a cause of secondary hypertension)
- An ECG would show any new ischaemic changes and also any evidence of Left ventricular hypertrophy.
- Pulmonary oedema will hopefully be seen on a CXR or lung US but not all these patients need a CXR, if they have no dyspnoea and no chest pain the a CXR has limited utility.
- Specfic clinical concerns and questions will need specific investigations – for example thoracic aortic dissection will need a CTA and those with concerns for cerebral encephalopathy or bleed will need a CT head. (in my view just a headache and hypertension doesn’t warrant a CT head).
Approach to managing these patients:
Most hypertensive patients in ED do not have malignant hypertension and so can be discharged and managed as outpatients/in community.
Those with end organ damage will need urgent control of their BP and those without can often have their medication titration started. In both groups we want to avoid rapid, profound reductions in BP as this can lead to organ hypoperfusion and a general target is a BP of 160/90. It is worth saying again that patient do not have to and should not wait in the ED for this target to be met if they are being discharged, they can still be hypertensive and be discharged. Those that are hypertensive >180/120 but have had secondary causes and End organ damage excluded can be referred to as uncomplicated acute severe hypertension. The BP number itself doesn’t constitute the need for a referral to ED, but the need for urgent rule out of end organ damage tends to lead the patients to emergency departments.
The concept of a rapid reduction in BP causing harm is to do with the autoregulation of blood flow. This is where organs receive a consistent, constant flow regardless of the arterial pressure. In high flow, low resistance organs, like the brain and kidney, flow autoregulation is particularly important. Normotensive people autoregulate across a range of mean arterial pressures (50mmHg to 150mmHg). In chronic hypertension, cerebral autoregulation is shifted up, limiting the ability to regulate flow if the MAP falls, and in malignant hypertension, the autoregulation itself is compromised. In these people, lowering the BP to a low or even a ‘normal’ value can cause low flow. (this is also a good opportunity to reflect on the consequences of unwell chronically hypertensive people being left with relatively low BPs) There are reports of multiple problems occurring because of these low flow states – cortical blindness, stroke, MI being an examples from rapid BP reductions with IV meds or short acting, rapidly absorbed meds like sublingual nifedipine.
Our approach to those with uncomplicated, acute severe hypertension should be first to check compliance/adherence to their current hypertensive medication and then arrange ambulatory BPs for the next 7 days with a reassessment. If needing medication for confirmed, new hypertension then the NICE guidance of ACEi or CCB should be followed, and if preexisting hypertension an increase in their current meds should be sufficient. The aim is to achieve the target BP in 6-12 weeks. Oral medication is much less likely to precipitate a rapid, harmful fall in BP.
Hypertensive Emergency
These patients need admission to an area with the ability to regularly monitor their BP and to administer and titrate the IV antihypertensives, typically a level 2 area, like a HOBS or HDU.
Outside severe pre-eclampsia, there is little RCT evidence for the management of hypertensive emergencies and most guidelines are built from non-randomized observational studies and expert opinion. Interestingly RCTs in this area have excluded very high BPs (>220/110) and tend to have a BP target, which is flawed when taking into account the autoregulation theory we have covered. Eg https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9453047/
The aim is to reduce the BP by 20-25% in the first 6-24hrs. We do not want to aim for a specific target, we want to match our target to the initial hypertensive state, to avoid ischaemic injury.
Generally, labetalol (alpha and beta blocker) is the first line agent, particularly in hypertensive encephalopathy, intracranial haemorrhage, and aortic dissection. Esmolol is an alternative short acting betablocker. Betablocker can be used as stand-alone treatment or in conjunction with vasodilators like GTN.
GTN is used as a first choice in those with volume-replete pulmonary oedema and ACS, and in conjunction with a betablocker in those with acute aortic syndrome.
There is some evidence that calcium channel blockers may be more effective than either GTN or labetalol. Nicardipine seems to be the drug of choice if you are reaching for a CCB. It is easier to titrate compared to labetalol, as it has a shorter half-life and as such is less likely to accumulate (outside of liver failure as it is cleared hepatically).
EMcrit has an excellent summary https://emcrit.org/ibcc/htn/
As is this table from the British and Irish Hypertension Society https://www.nature.com/articles/s41371-022-00776-9/tables/2
The theory behind picking a CCB over a betablocker seems to be that most of the pathophysiology behind malignant hypertension is vasoconstriction and by using a beta blocker (admittedly one with some alpha action) you are mostly reducing cardiac output rather than the systemically vascular resistance and are potentially more likely to trigger hypotension or poor organ perfusion due to low flow.
In addition to the vasoconstriction, a lot of patients with malignant hypertension will also have some pressure naturesis, leading to overall volume depletion and dehydration. It makes even more sense to reach for a CCB over a beta blocker.