Saturday, 4 April 2015

Pulmonary Oedema

Pulmonary oedema - a sign of heart failure, not synonomous

Causes of Pulmonary Oedema
Left ventricle can't empty, causing raised pressure in the lungs. This means the hydrostatic pressure is greater than the oncotic pressure. Fluid moves into the interstitium and alveoli. Some of it is reabsorbed by the lymphatic system. If this can't happen, the accumulating fluid starts to hinder gas exchange, resulting in hypoxia. 
The hypoxia triggers catecholamine release causing vasoconstriction and further left ventricle emptying problems. 

Cardiac Causes: 
Specifically left heart failure and mitral regurgitation


I nhaled Toxins (Ammonia, Chlorine, Phosgene, Nitrous oxide, heroin)
S IRS / Sepsis / Septic Shock

N eurogenic (seizure, strangulation, trauma)
O verdose (Heroin, methadone, cocaine)
T hyrotoxicosis

T rauma
H eat (Smoke! Remember to also consider carbon monoxide!)
E lectrocution

H igh altitude pulmonary edema
E mbolism (Pulmonary Embolism, Acute Gas Embolism, Amniotic Fluid Embolism)
A spirin toxicity
R eperfusion or Re-expansion (ARDS)
T ransfusion
asthma, post-obstructive/ post intubation, near drowning

Neurogenic - pulmonary oedema after a significant CNS insult, probably as a result of a catecholamine surg. It's under recognised, and may happen after head injuries. Management is still supportive, and treat the underlying CNS insult.

Typically mentioned acute dyspnoea with frothy blood stained sputum. Some of the more recent articles on pulmonary oedema have split the presentation into four categories, and this makes the management and the presentation make a lot more sense.

1. SCAPE  - Sympathetic Crashing Acute Pulmonary (O)Edema)
Often there is no history of CCF, no oedema, no clear ‘trigger’, normal LV function.  This process is largely neuro-hormonal in aetiology and comes on pretty quickly – over hours.

2. Acute-on-chronic (Acute decompensated HF)
Slower onset - over days

3. Acute Causes
These people have a new cause for their oedema - ACS / STEMI, rapid AF / arrhythmia, PE, valve rupture, high output state – sepsis, anaemia. Often a reversible cause.

4. Iatrogenic
Too much IV fluids to treat a chronically low blood pressure!

Clinical Examination
Bibasal inspiratory crepitations or wheeze.
Pale, cold and clammy
Sinus tachycardia or atrial fibrillation
Gallop rhythm may be present.
Murmurs, especially mitral regurgitation and aortic stenosis, may be a precipitating cause.

Assess the JVP, mucus membranes and urine output.
Look for peripheral oedema and hepatomegaly suggesting right heart failure.

Lots of studies suggest the first thing you should do is put CPAP on. BiPAP instead doesn't cause harm - so only use it if there's hypercapnea too. 
Start at 6 cmH20 and rapidly increase to 10cmH20 as tolerated. 

The classic indications for CPAP are: 
RR >20/min
With "official cautions" being right ventricular failure, cardiogenic shock, severe obstructive airways disease, agitated patient. Contraindications are ET indicated, resp arrest, life threatening hypoxia, unconscious patient.

- Nitrates
Help reduce afterload. 
Resources seem to suggest a higher dose than I've ever used - 400mcg/ minute. As a GTN SL spray is 400mcg/dose, my assumption would be whilst you're mixing up the infusion, get SL in! Put a big bolus in initially to get the GTN up into the therapeutic range. Get an ART line in as soon as possible, so you can control the BP well. 
Be really careful using nitrates in patients with aortic stenosis. 

- Morphine
Morphine is associated with increased mortality, although it makes your patients feel better - so don't give it. They have a theoretical physiological advantage as they reduce pre-load, but this is not born out in real life.

- Diuretics
These have caused much controversy in the NICE guidelines. I've never much liked giving a big dose of furosemide as it takes so long to work - and a lot can happen whilst you're waiting, and it causes a lot of harm. Evidence now suggests that as some patients in pulmonary oedema are euvolaemic, they can make the patients worse.
Diuretics reduced preload (prevent NaCl reabsorption --> increased fluid excretion and vasodilate).

- Inotropes
Commence early, and stop early. Dobutamine -  2-3mcg/kg/min and increase as required.

ECG - rarely normal. Often tachycardia, and possibly left ventricular hypertrophy.
 May show precipitating causes - ST segment changes or arrhythmia

CXR -Excludes other causes
cardiogmegaly, interstitial and alveolar oedema and upper lobe diversion.
bat wing or butterfly shadowing - perihilar shadowing
peri-bronchial cuffing
pleural effusions
Kerley lines:
  A lines - course towards hilar. Thickening of the interlobular septa. Only really seen on HRCT
  B lines - 1-2 cm thin lines in the peripheries of the lung. Extend to pleural surface. Perpendicular to the pleural surface. Usually seen at lung bases.
  C lines - short lines that do not reach the pleura
  D lines - B lines seen on lateral CXRs
Differential is diffuse pulmonary haemorrhage - has no dependent gradient, and usually no pleural effusion.

ABG- Type 1 respiratory failure (hypoxaemia)

Take FBC, U&E, LFT, troponin and INR to identify precipitants
Check BNP - produced by stretched cardiomyoctes. No limited identified for acute diagnosis, but BNP is sensitive so can rule out heart failure as a cause of breathlessness - unless the heart failure has happened very very quickly. It can also be raised in sepsis, renal or liver failure, hypoxia, myocardial ischaemia and tachycardia.

Worse outcome if:
Advanced Age
Wide QRS
Precipitated by ischaemia
Previous hospitalisation for heart failure
Marked BNP elevation
Elevated troponin
Hyponatraemia and raised urea and creatinine


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