1st November 2018
A raised blood pressure, as a clinical sign, has always rather perturbed me. At medical school we were always taught – and this has not changed as far as I know – that an underlying cause for high blood pressure will not be found in ninety per cent of patients.
Ninety per cent… In truth, I think it is more than this. I have come across a patient with an absolute, clearly defined cause for their high blood pressure about five times, in total, and I must have seen ten thousand people with high blood pressure. I must admit I am guessing at both figures and may be exaggerating for dramatic effect.
Whatever the exact figures, it is very rare to find a clear, specific cause. The medical profession solved this problem by calling high blood pressure, with no identified cause, “essential hypertension”. The exact definition of essential hypertension is ‘raised blood pressure of no known cause.’ I must admit that essential hypertension certainly sounds more professional than announcing, ‘oh my God, your blood pressure is high, and we do not have the faintest idea why.’ But it means the same thing.
Doctors have never been good at admitting they haven’t a clue about something. Which is why we have a few other impressive sounding conditions that also mean – we haven’t a clue.
Idiopathic pulmonary fibrosis – progressive damage of the lungs – and we don’t know why
Cryptogenic stroke – a stroke caused by something – but we don’t know what
Essential hypertension – high blood pressure – we haven’t a clue why its high.
Can you turn something into a disease, simply by giving it a fancy Latin title? It appears that you can. Does it help you to understand what you are looking at? No, it most certainly does not.
So, why does the blood pressure rise in some people, and not in others. It is an interesting question. You would think that, by now, someone would have an answer, but they don’t. Or at least no answer that explains anything much.
Excess salt consumption has been blamed by some. However, even if you take the more dramatic figures, we are talking no more than 5mmHg. Indeed, the effect of reducing salt intake on people without high blood pressure is about 1mmHg, at most
‘Almost all individual studies of participants with normal blood pressure (BP) show no significant effect of sodium reduction on BP.’ 1
Which would mean that the effect of raising salt intake would be almost zero. So, if it is not salt, what is it? A magic hypertension fairy that visits you at night? Could be, seems as likely as anything else.
When you have a problem that is difficult to solve, I always like to turn it inside out, and see what it looks like from the opposite direction. Presently, we are told that essential hypertension increases the risk of cardiovascular disease.
Looking at this from the other direction, could it be that cardiovascular disease causes high blood pressure. Well, this would still explain why the two things are clearly associated, although the causal pathway may not be a → b. It could well be b → a.
I must admit that I like this idea better, because it makes some sense. If we think of cardiovascular disease as the development of atherosclerotic plaques, leading to thickening and narrowing of the arteries then we can see CVD is going to reduce blood flow to vital organs, such as the brain, the kidneys, the liver, the heart itself.
These organs would then protest, leading to the heart pumping harder to increase the blood flow and keep the oxygen supply up. The only way to increase blood flow through a narrower pipe, is to increase the pressure. Which is what then happens.
Over time, as the heart is forced to pump harder, and harder, the muscle in the left ventricle will get bigger and bigger, causing hypertrophy. Hypertrophy means ‘enlargement.’ So, in people with long term, raised blood pressure, we would expect to see left ventricular hypertrophy (LVH). Which is exactly what we do see.
LVH is often considered to be a cause of essential hypertension. I would argue that LVH is a result of CVD. This is not exactly a new argument, but it does make sense.
Two models strongly support the idea that CVD causes high blood pressure. The first is a rare condition called renal artery stenosis. This is where an artery to one of the kidneys narrows, or starts life narrowed. This causes the kidney to protest at a lack of blood supply and increase the production of renin.
Renin converts angiotensinogen, a protein made in the liver that floats about in the blood, into angiotensin I. Then angiotensin converting enzyme (ACE) turns angiotensin I into angiotensin II. And angiotensin II is a very powerful vasoconstrictor (narrows blood vessels), this raises the blood pressure.
Angiotensin II also stimulates the release of aldosterone, a hormone produced in the kidneys. Aldosterone increases the reabsorption of sodium and water into the blood from the kidneys, simultaneously driving the excretion of potassium (to maintain electrolyte balance). This increases the volume of fluid in the body, which also increases blood pressure.
This whole system is called the Renin angiotensin aldosterone system (RAAS), sometimes shortened to RAS. Activate at your peril. Angiotensin II is, amongst other things, a potent nitric oxide (NO) antagonist. Which, as you might expect, can do very nasty things to endothelial cells and the glycocalyx (glycoprotein layer that protects artery walls).
If you discover that the patient with very high blood pressure has got renal artery stenosis, the artery can be opened, and the blood pressure will – in most cases – rapidly return to normal. Which proves that narrow arteries can, indeed, lead to high blood pressure.
The other model is the situation whereby a number of blood clots build up in the lungs, a condition known as chronic thromboembolic pulmonary hypertension. It is not nice. The arteries are effectively narrowed by blood clots – in order to keep the blood flow up, the heart must pump harder. In this case the right side of the heart because it is this side that pushes the blood through the lungs.
So, you usually end up with Right Ventricular Hypertrophy (RVH). Eventually the heart cannot pump any harder and starts to fail, leading to Right Ventricular Heart Failure (RVF). Shortly after this, you die.
There is an operation that can be done to remove all the blood clots from the lungs. It has a very high mortality rate. Basically, you open up the lungs and pull out a great big complicated blood clot, that looks a bit like a miniature tree. If the operation is not fatal (pulmonary endarterectomy), the blood pressure drops, the LVF improves rapidly, and the outcomes are excellent.
This is another example which demonstrates that a rise in blood pressure is caused by narrowed blood vessels. Again, if you open the blood vessels the pressure drops, the stress on the heart falls, and rapid improvement can take place.
So, if CVD causes high blood pressure, is there any point in trying to lower the blood pressure with drugs. After all, you are doing nothing for the underlying disease.
Well, you would be taking pressure off the heart, so you might be improving left ventricular hypertrophy, and/or left ventricular failure. But, of course, you also lowering the blood flow to important organs, which is not so good. Indeed, it is well recognised that, in the elderly, you can increase the risk of falls by lowering the blood pressure – which can lead to fractured hips, and suchlike.
Also, if you lower the blood pressure too much the kidneys start to struggle, another major problem in the elderly. In fact, I often tell nurses working with me in Intermediate Care that dealing with the elderly can turn into a battle between the heart and the kidneys. Get one under control and the other one goes off.
Then, if you lower the blood pressure you are in danger of triggering the RAAS system into action as the body tries to bring the pressure back up again, and the RAAS system can be quite damaging to the blood vessel themselves. You will definitely disrupt the control of blood electrolytes such as sodium and potassium as aldosterone kicks into action.
I am forever battling to keep sodium levels up and potassium levels down, or vice versa, depending on which anti-hypertensive are being used. All of these are reasons why I do not bother to treat high blood with drugs, until it is far higher than the current medical guidelines would recommend.
What I do recommend to patients is:
- Increase potassium consumption
- Go on a high fat, low carb diet
- Use relaxation techniques: mindfulness, yoga, whatever floats your boat
- Take exercise
- Get out in the sun – this stimulates NO synthesis
- Try L-arginine and L-citrulline – as above
- Increase magnesium consumption
This will often, if not always, do the trick.
If you must take medication, I was a very strong supporter of ACE-inhibitors, in that they blocked angiotensin II, and increased NO synthesis. Both good things. However, some research has come out recently, suggesting they may increase the risk of lung cancer. Not by a great deal, but there you go. Best to take nothing at all, if you possibly can.