pulm oedema Flashcards

1
Q

define

A

= a diffuse extravascular accumulation of fluid in the pulmonary tissues and air spaces due to changes in hydrostatic forces in the capillaries or to increased capillary permeability.

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2
Q

causes

A

due to an increase in capillary pressure

  • left heart failure:
  • atrial, e.g. mitral stenosis
  • ventricular, e.g. myocardial infarction, hypertension
  • pulmonary venous obstruction
  • IV fluid overload, e.g. from blood transfusion

due to an increase in capillary permeability

  • pneumonia
  • inhalation of toxins - such as chlorine, mustard gas
  • circulating toxins - such as histamine, septicaemia
  • disseminated intravascular coagulation
  • renal failure
  • radiation pneumonitis
  • Adult Respiratory Distress Syndrome - ARDS

due to a reduction in plasma oncotic pressure

  • any cause of hypoalbuminaemia e.g. nephrotic syndrome, liver cirrhosis

due to lymphatic obstruction

  • tumour
  • parasitic infections

other causes

  • raised intracranial pressure
  • pulmonary emboli
  • pregnancy induced hypertension
  • high altitude
  • heroin overdose
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3
Q

s/s of pulm oedema

A

Possible early symptoms:

  • shortness of breath - principle symptom
  • exercise dyspnoea
  • tachypnoea
  • cough
  • orthopnoea
  • paroxysmal nocturnal dyspnoea

Later symptoms include:

  • a cough with foaming, bright red sputum
  • cyanosis
  • extreme dyspnoea

On examination:

  • breathing may be laboured and wheezing or rapid and panting. There may be a fine rattling sound audible
  • Cheyne stokes respiration may be present in severe cases
  • jugular venous pressure is usually elevated
  • basal crepitations on auscultation may be heard
  • heart sounds - triple or gallop rhythm
  • a pleural effusion may also be present - in patients with chronic heart failure
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4
Q

ix

A
  • chest radiograph
  1. interstitial oedema
  2. bat’s wing appearance
  3. upper lobe diversion (increased blood flow to the superior parts of the lung)
  4. Kerley B lines [thin linear pulmonary opacities caused by fluid or cellular infiltration into the interstitium of the lungs.]
  5. pleural effusion
  6. cardiomegaly may be seen if there is cardiogenic cause
  • ECG - look for signs of myocardial infarction
  • U and E’s, troponin
  • ABG:blood gases - normally low PaCO2 due to hyperventilation; usually a low PaO2
  • consider echo
  • BNP - may be helpful if suspect heart failure
  • lung function tests - not appropriate in an emergency admission:
    • restrictive ventilatory impairment
    • VC is reduced and the FEV1 is reduced in proportion. The forced expiratory ratio is normal or higher than normal.
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5
Q

inital mx of severe pulm oedema

A
  1. Make sure the patient is sitting upright and then:
  2. oxygen - should be given in as high a concentration as practicable (100% if no pre-existing lung disease).
  3. iv access + monitor ECG
  4. rx any arrythmias eg. AF: digoxin - dose 0.75-1.25 mg PO, but can be iv very slowly if urgent.
  5. analgesia - if there is no COAD or liver failure then diamorphine 5mg iv slowly.
  6. furosemide iv- larger doses needed in renal failure
  7. GTN 2 puffs/ 2x0.3 mg tabs SL - dont give if SBP <90mmHg
  8. necessary ix, exam hx
  9. if SBP > 100mmHg: start nitrate inusion es. isosorbide dinitrate
  10. if pt deteriorating
    1. further dose furosemide
    2. consider CPAP
      1. improves ventilation by recruiting more alveoli
      2. drives fluid out of alveolar spaces into vasculature
      3. GET HELP BEFORE INITIATING
    3. consider alternative diagnosis
      1. eg. hypertensive heart failure
      2. aortic dissection
      3. PE
      4. pneumonia

details concerning the treatment of acute left ventricular failure is on next flashcard

Note, it may be difficult to discriminate bronchospasm, pneumonia and pulmonary oedema and, especially in elderly patients, all three may be present. If in doubt then treat all three simultaneously, e.g. salbutamol nebuliser, i.v. frusemide, diamorphine, ampicillin.

~~

nb: Morphine in Pulmonary Oedema  Make pt. more comfortable  Pulm venodilators → ↓ pre-load → optimise position on Starling Curve

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6
Q

principles of treating acute LVF

A

The principles of treating acute heart failure are presented below:

  • lung function optimisation:
    • sit the patient up
    • administer maximal oxygen concentrations
  • intravenous diuretic:
    • 40-80 mg frusemide
  • intravenous opiate analgesia:
    • 5 mg diamorphine over 5 min
  • treatment of arrhythmias:
    • may require DC cardioversion or intravenous anti- arrhythmic therapy
  • vasodilator therapy
  • digoxin:
    • cautious intravenous administration if the above fail
  • venesection:
    • a pint may be removed from a moribund patient who fails to respond to the above
  • inotropes: if SBP <100mmHg
    • dobutamine infusion
    • dopamine infusion
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7
Q

continuing mx in pulm oedema ie. once stable + improving

A
  1. Patient progress is monitored by checking blood pressure, pulse rate, heart sounds, chest sounds and urine output regularly.
  2. Check urea and electrolytes, ECG and weight each day [aim to reduce 0.5kg/day], with regular chest radiography. Restrict fluids.
  3. If the patient is improving then change to oral frusemide/bumetanide
  4. ACEi + β-B if heart failure
    1.  Consider spironolactone
    2.  Consider digoxin ± warfarin (esp. if in AF)
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