Cough

Cough seems a strange thing to have on the syllabus, but we do see lots of patients presenting with cough. They often want antibiotics...and these aren't often the answer. The references at the bottom of the page have got some excellent management guidelines.

Acute Cough
Viral Cough - self limiting. No anti-tussive therapy needed. Efficacy of OTC medications is not compelling. Home based remedies like honey and lemon or honey and coffee.

Chronic Cough
Lasts >8 weeks. Mostly women, with an average age of 55. Can treat empirically before investigations.

Differentials
Pertussis
Tuberculosis
Pulmonary fibrosis - get honeycomb on the CT. Make sure you treat any concurrent reflux,
Reflux - if asymptomatic don't treat. Otherwise, PPI BD + ranitidine. Next step pro-kinetics like metoclopramide.

Drug Differentials 
Latanoprost - augments cough-reflex sensitivity
ACE inhibitors - may take up to several months to stop. ACE inhibitors upregulate the cough reflex
Nitrofurantoin
Bleomycin, methotrexate and amiodarone may cause pulmonary fibrosis

Investigations
CXR
-  if >40 and has ever smoked and has cough, fatigue, SOB, chest pain, weight or appetetite loss.
- if >40 and persistent or recurrent chest infection, clubbing, specific lymphadenopathy, chest signs consistent with lung cancer, thrombocytosis.
Spirometry
Consider checking for sleep apnoea - CPAP may help

Treatment
Treat cause - first generation antihistamines can help.
If cold related consider brompheniramine and SR pseudoephedrine. Naproxen can also help.

References
http://www.rcemlearning.co.uk/modules/a-constant-cough/
http://www.rcemlearning.co.uk/modules/bloody-cough/
http://www.rcemlearning.co.uk/exams/unusual-cough/
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1692
http://www.doctors.net.uk/ecme/wfrmNewIntro.aspx?moduleid=1388
http://journal.publications.chestnet.org/data/Journals/CHEST/934853/51496.pdf
http://rebelem.com/long-cough-respiratory-illness-last/
https://www.brit-thoracic.org.uk/document-library/clinical-information/cough/cough-guidelines/recommendations-for-the-management-of-cough-in-adults/
https://www.brit-thoracic.org.uk/document-library/clinical-information/cough/cough-guidelines/recommendations-for-the-management-of-cough-in-children/
http://journal.publications.chestnet.org/data/Journals/CHEST/22039/1S.pdf 

CVP

The CVP
This is the pressure recorded from the right atrium or superior vena cava 
It is representative of the filling pressure of the right side of the heart 

Normal is 8- 12 mmHg in a spontaneously breathing non-ventilated patient
recorded at the end of expiration

It is made up of many different waves:
a = atrial contraction (dominant in pulmonary HTN, TS, PS)
c = closing and bulging of the tricuspid valve (cannon in heart block) 
x = atrial relaxation (absent in AF, exaggerated in tamponade)
v = passive filling of atrium (dominant in TR)
y = opening of the tricuspid valve (sharp in severe TR, constrictive pericarditis. Slow in TR)

Raised CVP 
Fluid overload (although there is a poor relationship)
High PEEP settings (PEEP of 10cm H20 = CVP increase 3cm H20) 

Right ventricular failure
Tricuspid stenosis or regurgitation
Pericardial effusion or constrictive pericarditis
Superior vena caval obstruction

References
http://lifeinthefastlane.com/ccc/cvp-measurement/
Oxford Handbook of Critical Care

Cyanosis

This seems like a random curriculum item to me. A quick trawl through the Oxford Handbook of EM suggests I need to think about:
Anaphylaxis
Asthma
COPD
Aspiration
Pulmonary Embolism
Seizure
Toxicology - opioid poisoning, paraquat lung, petrol and paraffin poisoning, anthrax
Respiratory distress - chest wall injury, pneumothorax
Uncommon in cyanide poisoning

LITFL splits it further
Central Causes - low sats, metHb, altitude
Peripheral Causes - cold, reduced cardiac output including congenital heart disease.

References
http://www.rcemlearning.co.uk/exams/he-looks-a-bit-blue-doctor/ 
http://www.rcemlearning.co.uk/modules/papa-smurf-has-a-seizure/ 
http://lifeinthefastlane.com/resources/cyanosis-ddx/

Oxygen Therapy

Administering extra oxygen is easy, but there are some more things we could and should think about. Once 30% or more of the blood in the pulmonary circulation passes through an area of low V/Q, the hypoxia cannot be corrected by simply increasing the oxygen content of the inspired gas.

Hypoxic Drive
Oxygen induced hypercapnea is likely to include:
- Worsened ventilation-perfusion mismatch (due to pulmonary vasoconstriction)
- Decreased binding affinity of haemoglobin for carbon dioxide
- Reduced minute ventilation.
So giving extra oxygen is unlikely to be a problem but we need to be aware of it, and monitor it.

Alveolar Gas Equation 
PAO2 = 95 x FIO2(%) – 1.25 x PaCO2
Under normal circumstances the difference between this and the arterial O2 tension (PaO2) measured by the ABG machine is 2-4 kPa. This difference is known as the A-a gradient. Its calculation can help to distinguish between types of hypoxia.


References
http://learning.bmj.com/learning/module-intro/oxygen-therapy.html?moduleId=10053774&searchTerm=%E2%80%9Coxygen%E2%80%9D&page=1&locale=en_GB

http://www.rcemlearning.co.uk/modules/oxygen-in-human-physiology/

http://www.rcemfoamed.co.uk/portfolio/hypoxic-drive-fact-or-fiction/

http://emcrit.org/wp-content/uploads/2015/06/nejmoa1503326.pdf

http://www.annemergmed.com/article/S0196-0644(15)01500-0/abstract

Hyperkalaemia

Hyperkalaemia is a medical emergency that we should know how to manage. Following a guideline is easy - but sometimes we need to know more than just how to follow the guideline! So..if you have a high potassium consider:

1. Is it really hyperkalaemia?
- Prolonged TK time
- Haemolysis
- Acidosis causing transcellular shift
- The ABG analyser result does correlate well with a true result

2. Stop all likely causes
- Treat pre-renal (and renal) failure
- Stop drugs (amiloride, spironolactone, ACE inhibitors, NSAIDs)

3. Do an ECG
The changes don't appear at a set potassium level, but it does show the cardiac toxicity.
- Symmetrical T wave peaking - T wave looks uncomfortable to sit on
- PR interval prolongation
- Reduced P wave amplitude
- QRS complex widening
- sine wave formation
- Fine ventricular fibrillation and asystole
- Progressive bradycardia.

4. If ECG changes present, protect the heart - give some calcium.
Calcium Chloride - more toxic if extravasated
Calcium chloride contains about three times as much calcium as calcium gluconate (0.68 mmol/ml versus 0.22 mmol/ml) and  has a greater bioavailability than gluconate. If you use calcium gluconate, you are more likely to need to give repeated doses.

Give slowly over 20min + 10ml glucose 5% if on digoxin, as rapid calcium administration may precipitate myocardial digoxin toxicity.

5. Shift Potassium into the cells
- Insulin-Glucose IV infusion
- Nebulised sabutamol

6. Remove potasium from the body
- Consider calcium resonium which takes >2 hours to work.
- Sodium bicarbonate may precipitate pulmonary oedema due to its sodium load, or tetany, and is not very effective. You cannot give calcium salts and sodium bicarbonate via the same intravenous line because this causes precipitation of calcium carbonate. May be more useful in acidotic patients.
- Furosemide can help if you have good urine output.

7. Monitor

8. Look for signs and symptoms
Muscle weakness and paraesthesia may occur in patients with severe hyperkalaemia and may progress to flaccid paralysis. The respiratory muscles are usually spared. Muscle weakness normally starts in the lower limbs and progresses to the trunk and upper limbs, and is more common when serum potassium is more than 8.0 mmol/l

Generalised twitching
Confusion
Pericardial friction rub
Urinary retention

9. Understand normal
How does the body handle the overall balance of potassium?
A normal Western diet contains about 100 mmol of potassium per day. Most potassium is renally excreted.

10. Recheck and Review
Recheck potassium level after 4 hours and as indicated according to the levels obtained.

References
http://learning.bmj.com/learning/module-intro/hyperkalaemia-diagnosis-management.html?moduleId=6055258&searchTerm=%E2%80%9Chyperkalaemia%E2%80%9D&page=1&locale=en_GB
http://learning.bmj.com/learning/module-intro/hyperkalaemia.html?moduleId=10047565&searchTerm=%E2%80%9Chyperkalaemia%E2%80%9D&page=1&locale=en_GB
http://www.aliem.com/2013/mythbuster-calcium-gluconate-raises-serum-calcium-as-calcium-chloride/
http://first10em.com/2016/01/21/hyperkalemia/
http://www.rcemfoamed.co.uk/portfolio/hyperkalaemia/

Hyperventilation

The term "hyperventilation" is one I am not particularly fond of. I think there are three separate causes of hyperventilation:

1. Pathological - eg PE, pneumonia, pain 
2. Iatrogenic - "overbagging"
3. Panic / anxiety/ hysteria

The third is the cause of hyperventilation we are now going to focus on. It seems to me to be an exaggeration of a normal physiological response - a form of control system dysfunction. The respiratory distress is driven by the brain. 

The DSM-IV criteria for a panic attack is quite specific. They define it as a period of intense fear or discomfort developing abruptly, and peaking within ten minutes + 4 of:

a. Chest pain/ discomfort, b. Chills or hot flushes, c. Derealisation or depersonalisation, d. Fear of loosing control, e. Feeling dizzy, f. Feeling of choking, g. Nausea, h. Palpitations, i. Paraesthesias. j. SOB, k. Impending doom, l, Sweating, m. Trembling

Carpopedal Spasm

• Rapid breathing results in excess excretion of carbon dioxide in the lungs 
• This reduces the concentration of CO2 in the blood
• The blood pH becomes alkali
• This causes increased binding of calcium ions to proteins in the blood
• The reduced level of calcium causes "carpopedal spasm"
• This could also lead to tetany 

Investigation

The lactate can be high - is not helpful 

ABG would show a normal PO2 and a marked respiratory alkalosis. The Ca may be low. 

Treatment

Control the breathing. This is really difficult to do, and very frustrating! Telling them to control their breathing or calm down is likely to make matters worse, not better. 

• Give them a cold drink
• Ask them to read a sentence out loud 
• Paper bags are NOT recommended - lots of patients ended up getting a paper bag for asthma
• Long term - CBT may be needed

References

http://www.ncbi.nlm.nih.gov/pubmed/20659878

Methaemoglobin

Pathogenesis
- Oxidisation of the haem of haemoglobin by free radicals or things like hydrogen peroxide and nitric oxide. 
- Shifts O2 dissociation curve to the left. 

Causes
- Hereditary / Congenital: Hb and NADH-MetHb reductase deficiency
- Acquired: 
  *   Medications eg. Amyl nitrite, Benzocaine, Dapsone, Lidocaine, Nitroglycerin, Nitroprusside, Phenacetin, Phenazopyridine, Prilocaine, Quinones, Sulfonamides (eg. sulfamethoxazole). Chloroquine. 
  *   Chemical agents eg. Aniline dye derivatives (shoe dyes, inks) Butyl nitrite, Chlorobenzene, Nitrate-containing foods, Isobutyl nitrite, Naphthalene, Nitrophenol, Nitrous gases, Silver nitrate, and Trinitrotoluene. Sodium nitrite - used in food preservation. 

Signs & Symptoms
- chocolate brown discoloration of the blood. 
- SaO2 readings go crazy 

0-10% - Features unlikely

10-30%- Mild effects 
Blue-grey ‘apparent’ central cyanosis, fatigue, dizziness, headaches

30-50% - Moderate effects – weakness, tachypnoea, tachycardia

50-70% - Severe effects 
stupor, coma, convulsions, respiratory depression, cardiac arrhythmias, acidosis

> 70% - Potentially fatal

Treatment
<20% - nothing
20 - 30% - oxygen therapy 
>30% - methylene blue
            1-2 mg/kg IV over 5 minutes - 1% (10mg/ml solution) 
            repeat up to 7 mg/kg 
SpO2 normally dives as you give the methylene blue. 
Recheck levels after an hour 

Interesting Note
Hydrogen sulfide poisoning is similar to cyanide poisoning and can be treated by inducing metHb. 

References
http://stemlynsblog.org/feeling-blue-at-st-emlyns/
http://www.rcemlearning.co.uk/modules/papa-smurf-has-a-seizure/
http://emergencymedicineireland.com/2011/07/why-methaemoglobinaemia-is-a-good-thing/
http://emergencymedicineireland.com/2011/07/why-methaemoglobinaemia-is-a-bad-thing/