COPD stands for Chronic Obstructive Pulmonary Disease. The terms 'COPD' and 'Emphysema' are often mistakenly used interchangeably. COPD is an umbrella-term, covering a spectrum of airway tract diseases from chronic bronchitis to emphysema. The two ends of the spectrum are similar, as both are caused by smoking-related lung damage.

We will quickly explain the difference between chronic bronchitis and emphysema before covering COPD more generally - as most patients have a bit of both. 

Chronic bronchitis is a long-term inflammation of the bronchi (the tubes in the lung) caused by smoking. If you had one or two cigarettes as a teenager at the school disco - thankfully, that's not enough to do too much damage (still, say no kids!). This inflammation of the airways is caused by a repetitive and harmful stimulus (namely, smoke) passing through the lungs for decades. 

Chronic bronchitis comes with a definition - three months of daily, productive coughing (mucus - any colour) for at least two consecutive years. 
Basically, if you're coughing this much in back to back years, it doesn't take a genius to figure out that something's wrong. The constant inflammation of the bronchi produces a thick mucus, which settles deep in the chest and makes you more prone to infection (bacteria love swimming in it). The inflammation leads to a swelling of the bronchi, making it even more difficult to cough up the nasty gunk - and if they're really narrow, you may even struggle to breathe (the chest will be wheezy in this instance). 
This cycle can be hard to break. A lot of long-term, heavy smokers will stop smoking once the diagnosis of lung damage has been made - but the damage is often irreversible. That being said, quitting smoking at any point will increase a COPD patient's life expectancy - even the human chimneys in their eighties!

Emphysema is the term used when the smoking-related lung changes affect the alveoli (the little airbags shaped like a bunch of grapes). The alveoli sit at the very end of the airway tract, and it is here that the gas exchange of oxygen (O2) and carbon dioxide (CO2) takes place. The little airbags spread out widely as we inhale, the edge of the alveolar lining thins and gets even closer to the capillary (blood vessel). At this point, the O2 hops from the alveolus into the blood and the CO2 hops from the blood into the alveolus. Once the exchange is made, we breathe out - the alveoli spring back into their original, tucked-in shape and the CO2 is propelled back up the airway tract to be exhaled. 

With emphysema, the years of smoking damages the elasticity of the alveolar lining - this leaves the alveoli stuck in their expanded form. It decreases the efficiency of the O2 reaching the bloodstream, but even more commonly in COPD - it largely effects the ability of the CO2-filled sacs to propel the gas up the airway tract. 

The result? The body's bloodstream holds onto way too much CO2 - which if severe, can make us feel drowsy to the point of coma, and short of breath. 

Okay, so chronic bronchitis describes damage to the tubes, and emphysema describes damage to the little sacs at the end of the airway tract - simple. Most long-term smokers will have an element of both. If the sacs are really bad, the doctor will probably say you have emphysema. If the sacs aren't too bad, the doctor will just call in COPD.
In reality, COPD is the umbrella-term - so, let's just use that term from now on. 

How much do I have to smoke to get COPD?
Well, that's a tough one. When a doctor takes your medical history, they will ask you how many cigarettes you smoked a day and for how many years. Twenty cigarettes a day for one year is called a 'pack year'. So, if you smoked ten a day for twenty years - we would call that ten pack years. If you smoked twenty a day for ten years - we would also call that ten pack years. 
Unfortunately, we can't give an exact number - but the more pack years, the more likely you are to develop COPD as you age. The disease takes a while to establish itself, so it is quite rare in those under forty. If you are a heavy smoker, or have a history of heavy smoking - even with no symptoms - your doctor should send you for spirometry testing. 

Spirometry is an outpatient test which basically requires you to blow into a load of tubes. Depending on your lung capacity, and how quickly you can expel your capacity - a diagnosis can be made. 

Catching COPD early is very helpful in slowing the rate of disease progression. If found, the doctor will strongly encourage you to quit smoking and likely commence some long-term inhalers (known as preventers). You should use the inhaler(s) everyday to suppress the cycle of airway tract inflammation. 

When you become more breathless than usual, we call this a COPD exacerbation. 
COPD exacerbations can be infective (IECOPD) or non-infective (NIECOPD). Infective exacerbations are caused by a bug of some kind, and if bacterial, you will require antibiotics. Non-infective exacerbations are caused by some other trigger - maybe you passed by a construction site earlier that day. 

Whatever the cause, you will become short of breath, develop a harsh cough with a wheezy, restrictive chest. This is due to a sudden surge of (usually subtle) inflammation in the lining of the airway tract. If the exacerbation is mild, you can be treated by your local GP. Because they don't know the initial trigger - they will cover you with antibiotics (especially if you have a fever). To tackle the airway inflammation (causing the wheeze and shortness of breath), they will start a steroid (usually prednisolone tablets). The steroid tablets will work well in the background to dampen down inflammation. In the meantime, you'll need something to widen out those tubes. The GP will advise you to use your short-acting inhalers (relievers) - usually Ventolin and Atrovent - to dilate the bronchioles. 

If that's not enough, or you feel really crook - you'll end up in the ED. The difference here is that we have oxygen, and other machines that will open up your airways. We can give antibiotics and steroids straight into the veins. We have a special mask called a nebuliser that delivers inhaler medication via a mist. Of course, we can also monitor your bloods, get chest x-rays, look for other causes of your shortness of breath - aren't we just great?

Speaking of the machine to open your airways - what I was referring to is a machine called BiPAP - the big mask strapped to your face like Hannibal Lecter (or Bane, a nicer reference for the more sensitive-folk). BiPAP stands for Bi-level Positive Airway Pressure. A CPAP machine (Continuous Positive Airway Pressure) looks similar to it - people use these at night for sleep apnoea. Let's talk about these machines for a while - for the geeks out there. 

A CPAP mask will blow air into your face at a single pressure. For the snorers out there, the additional pressure keeps the airway open - stopping you from having 'apnoeic' episodes where you temporarily stop breathing.

A BiPAP machine alternates between two pressures, the IPAP and the EPAP, inspiratory and expiratory pressures respectively. When you breathe in, the machine supports the inspiration at a high pressure. When you breathe out, the machine supports the expiration at a slightly lower pressure. The change in pressures mimics normal breathing, increasing the efficiency of your lungs expelling CO2.
We use BiPAP machines in hospital when somebody's blood gas shows a dangerously high level of CO2. Makes sense now, huh? I hope...

COPD patients often retain CO2, and for that reason, when they come into hospital short of breath and requiring oxygen, we can give some...but not too much. 
Too much oxygen? Surely, you can't be serious doctor? 
- I am serious, and don't call me Shirley. Let me explain. 

In hospital, we measure people's oxygen saturation in their blood with a little probe on their finger. Anywhere between 96% and 100% is normal in a healthy patient. We also measure their respiratory rate (how often they breathe in a minute - yes, this is the only reason that the attractive nurse is staring at you).
When you exert yourself, your body produces more CO2 - and it's the increase in CO2 in the blood that tells the brain to instruct the lungs to breathe more. Unfortunately, with COPD patients, their CO2 is always high - their brain becomes tolerant to it. 
Much like the relationship of a lobster and the temperature in a boiling pot of water - if the CO2 is rising further, the COPD patient won't recognise the need to increase the respiratory rate. They rely on a low oxygen level to stimulate their brain - and so, we will always aim for oxygen saturations of 88-92%. 

If we give too much oxygen, the CO2 will continue to climb - making the patient more drowsy and even more short of breath - how do you like those apples?! So, remember, when we turn down the oxygen, we're not being cruel - except Susie. 

When COPD progresses to the end-stage, you may need oxygen at home to keep your saturations even as low as 88%.  Oxygen tanks can only be provided to those who no longer smoke - to prevent lighter-induced explosions...just another reason to quit!