now, before we start, how good do you reckon yourselves to be reading a CXR (that's short for chest x-ray)? most vitally, before reading a CXR, do you order a CXR for every patient that comes into your practice coughing and wheezing?
going in alphabetical order, let us begin with my personal favourite: ASTHMA. patient comes in wheezing (heeeeeeeeeeeeeee), coughing (cough here is NON productive. if there's copious sputum, think of a bacterial infection exacerbating an asthmatic patient or hop onto the next possible diagnosis: bronchitis).
oh, asthma doesn't really come under COPD (chronic obstructive pulmo dis) because it is a REVERSIBLE process. in between attacks, patients will have normal PFTs (pulmonary function tests). i'm throwing asthma in this post anyway because i want you to know how to differentiate between a person with an acute asthma attack and someone with bronchitis from having smoked for 60 years. both people will have difficulty breathing...but for very different reasons and pathogenesis.
see, in asthma, you have an allergic/ immunogenic pathogenesis. the person has either been sensitized to an ag from the environment or over-responses to something in the environment.
two main things: BRONCHOSPASM and airway INFLAMMATION which increases airway secretion ---> obstruction.
asthma attacks are usually triggered by something. such triggers can be intrinsic (non allergic), such as: a viral infection [RSV at kids and rhinovirus at adults], cold air, exercise, stress) or it could be extrinsic (atopic/ allergic), which means there's a specific ag the person is sensitized against. extrinsic triggers also cause other symptoms of allergies: urticaria, runny nose, watery eyes, itching. attacks by extrinsic triggers tend to be seasonal (e.g, at spring-pollen) or at a specific time of the day (occupational exposure-only weekdays, in the mornings).
the expiration phase is prolonged in asthma (air can't go out...hence the wheeze).
at auscultation, there will be diffused, ant and post wheezing. non productive cough (sputum is thick and there's not as much of it as there would be at bronchitis).
goal of treatment in asthma: you want to cause the bronchioles to dilate (first line: B2 agonists...then cholinoblockers-ipratropium, PDE3i-aminophylline, prevention-cromolyn [usually for exercise induced asthma]) and decrease inflammation @ immunosuppression (steroids). inhalers are usually dilators for acute attacks and steroids (+ipratropium) for prevention of future attacks. oral drugs such as monteleukast (leukotriene inhib) can also be prescribed to patients to prevent attacks.
now, after treatment, your patient should feel better, because remember, asthma is REVERSIBLE. however, if you find your patient's wheezes are diminishing, don't get too comfy just yet. it could be a sign of worse things to come, i.e RESPIRATORY FAILURE due to the respiratory apparatus fatiguing.
your patient will be using his accessory resp muscles--> bulging neck muscles, retracted internal intercostal muscles. there will be pulsus paradoxus (BP drops at inspiration...WHY? at asthma, patient takes huge breaths, which increase intrathoracic P, which increases venous return to the right side of the heart, which compromises the fillin gof the LV and therefore the systemic pressure drops. also, if you do an ABG on the patient, you will see an increase of the PCO2 (false increase, as it happens because air can't go out, and not because patient has stopped hyperventilating), no normalization of the PO2 and an acidic pH. all signs of impending respiratory failure. ahhhh!!! what to do? INTUBATE of course. just make sure your patient isn't having an increase PCO2 because of you treating him correctly, thus causing his PO2 to normalize and his peak flow to increase and him generally feeling much bettter before you stick a tube down his throat.
now, that was the easy stuff. onto the bigger thing: COPD! let's classify two main diseases under this heading, namely BRONCHITIS and EMPHYSEMA. now, they both involve chronic obstruction of the bronchioles, but are caused by very different reasons.
bronchitis's mechanism of obstruction is because the airways are filled with thich, viscous secretion. the -itis end should give you a clue about it being an inflammation of the bronchi...and what do inflammed bronchis do? they constrict, get edematous (even more obstruction) and secrete mucous (more gunk to block the already shrinking airways). so cough here, is PRODUCTIVE. to put down bronchitis as a diagnosis, the patient must have frequent, daily sputum for 3 months for 2 consecutive years.
emphysema's mechanism of obstruction is NOT due to hypersecretion, but because of the decrease elastic recoil of the lung tissue (the lung tissue must elastically shrink on itself, to push air inside out). usually, this function is lost because of the fibrosis and scarring that occurs in a constantly inflammed lung (outcome of chronic bronchitis, smoking).
the cough in emphysema is never productive, but the PFTs have an obstructive pattern because:
a) air cannot go out and
b) there's a destruction of the alveolar capillary membrane, which means that there's poorer gas exchange and therefore a decrease of the diffussion of lung carbon monoxide (DCLO). the DCLO is normal at bronchitis, because the process of gas exchange between the alveoli and capillaries isn't affected. it's getting the air exchanged to move in and out that is the problem.
COPD is usually, more often than not a result of SMOKING. there are two non smoking causes of COPD (that i can think of now):
- cystic fibrosis. usually kids/ teens. resembles bronchitis...why?
patient's with CF have problems with their chloride channels and make thick, viscous secretions (mucous plugs) that clog the airways.
how to differentiate? you can confirm a patinet has CF by doing a sweat test. also CF patients are at particular risk for psuedomonas infections (rarely a causative agent for common bronchitis). - congenital defect in alpha-anti-trypsin levels (deficient), that causes proteolytic digestion of the alveoli walls --> enlarged into blebs and then bullae.
the danger here is, you have a huge airpocket, but the walls surrounding it are still the same thin alveoli walls, but the air pressure has increased which can cause spontaneous pneumothorax (a hole forming in the lung, without any trauma due to the rupture of the thin walls of these bullae).
patients with a-a-t deficiencies usually have a family history of relatives with liver cirrhosis (young patients, with no history of hepatitis or alcohol abuse) or non smoking relatives with chronic bronchitis.
now, what will be your number one worry of a patient with COPD?
cor pulmonale!
but wait...how does the heart come to be involved in a problem affecting the lungs? (i hear you ask).
patients who've had COPD for a long time, usually have PHT (pulmonary hypertension).
what happens at PHT? the S2 has an increased in the P2 component. normally the A2 is louder than the P2, because of the greater pressure in the LV. however at PHT, the pressure in the RV is higher (to overcome the increased pressure in the pulmonary circulation), which causes the P2 to become louder.
you may not have the auscultation skills required to pick this up, but let's just say you got this case on an exam...what clues give you a hint about possible PHT?
a) the P2 increases at inspiration (remember the whole right side of heart has increasing pressure at inspiration, because of the increased venous return caused by the increased intrathoracic pressure).
b) patient has a right ventricular heave
c) EKG shows signs of RV hypertrophy.
but so what if the heart sounds volume increase a little bit? how does this lead to cor pulmonale?
first, what is cor pulmonale?
imagine the RV pumping against an increasing pressure in the pulmonary circulation (PHT) and it keeps working at pumping against the very high pressure, until it eventually fails. rings a bell? RHF?!! = cor pulmonale. it's akin to the LHF caused by the LV pumping against a very high systemic pressure.
*breathes* that's a lot to take in, huh?
back to CXRs.
asthmatic patients don't need a CXR, because asthma is reversible, it won't help you in the treatment of the patient and you would have just lost money for a test that didn't help with how you're going to go about treating the patient and the patient usually isn't in the condition to stand for an xray anyway,
COPD patients, do an CXR. why?
- to rule out pneumonia (a bronchitis that morphed into something more serious)
- you can see the increased lung markings (usually at chronic bronchitis)
- you can see the blebs and bullae at emphysema. also flattening of the diaphragm because of the hyperinflation of the lungs and an increase in the AP diameter if you're taking an ant-post film. the heart also appears to look smaller on the XR (although there's no direct pathology) because the borders of the hyperinflated lungs kinda mask it.
don't memorise treatment regimes. understand the goal of the treatment. what is it you set out o fix with the drugs/ instructions you want your patient to take/ follow.
treatment goals in COPD would be:
- decrease inflammationsteroids. they won't be as affective as they were treating asthma, because COPD largely involves inflammation, scaring, as well as fibrosis.
- increase dilation of bronchiolesipratropium will be more helpful here, as its effect is usually felt in 1/2 hour (not so great for someone having an asthma attack, hence why it's used more as a preventive measure, than an immediate treatment).
also beta2 agonists. - treat any infectionpneumococcus, H. influenza, moxerella catarrhalis. rotate use antibiotics (penicillins, tet, sulfa, cephalosporins) to prevent resistance from forming.
- improve gas exchangegive O2 to any hypoxic patient. how would you know who's hypoxic, who's not?
if PO2 at rest is less than 55mmHg, there's obviously not enough oxygenation of tissues. give O2!
if PO2 is 56-59mmHg and higher but patient has signs of end organ damage (ischemia) or erythrocytosis on CBC (here's a gem...COPD patients have a Hct of 50-55 because the body compensates for the hypoxia by increasing reticulocytes and its number of rbc, so don't think polycythemia rubra vera immediately when you see a high Hct...your patient could just be someone who smoked for the last 40 years).
- decrease work of breathing
this is to prevent respiratory fatigue. best drug? PDE3 inhibitors. lousy at asthma treatment, but works like a charm here because they increase the central respiratory drive and improve diaphragm contractility. minimal bronchial dilation (hence it not being first line for asthma). also...lots of side effects (tachycardia, arryhtmias, seizures) and possible drug-drug interactions (erythromycin, cipro, cimetidine, coumadine).
until the next huge mind dump...over and out and back to the books!
