Besides history and clinical examination, what investigations may help distinguish between cardiac and non-cardiac causes of pulmonary oedema in the critically ill patient?

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College Answer

1) Measurement of PCWP and CI
2) Serum BNP
3) Echocardiography
4) PICCO

Discussion

Echocardiography is a straightforward answer, as is BNP.

PCWP and cardiac index are indirectly related to this answer- one can cave a patient with a noncardiogenic pulmonary oedama as well as a poor cardiac index; the inference that the oedema has occurred because of the poor cardiac index would be incorrect.

The PICCO is even more obscure. Yes, it gives to you the extravascular lung water, but this only tells you that there is water in the lungs (which you already knew).

However, some authors have asserted that thermodilution measurements of pulmonary permeability can differentiate pulmonary oedema from ARDS.

Causes of Acute Pulmonary Oedema
Cardiogenic Non-cardiogenic

Excessive LV afterload

  • Severe hypertension
  • Aortic stenosis
  • HOCM (LVOTO)

Excessive LV preload

  • Fluid overload
  • Rapid fluid bolus

Excessive left atrial afterload

  • Mitral stenosis
  • Mitral thrombosis
  • Mitral prolapse
  • Atrial myxoma

Poor contractility

  • Cardiomyopathy
  • Drug effect (eg. beta blockers)
  • Metabolic disease (eg. hypothyroidism)
  • Infectious causes (eg. myocarditis)

Ineffective contractility

  • Mitral regurgitation
  • Takotsubo cariomyopathy

Increased capillary permeability

  • ARDS; systemic inflammatory state
  • Reperfusion (eg. following relief of an embolic occlusion)
  • Reperfusion of transplant lung
  • Near drowning (surfactant loss)

Neurogenic pulmonary oedema

  • Intracranial haemorrhage
  • Seizures
  • Electroconvulsive therapy

Drug-induced pulmonary oedema

  • Opiate induced (eg. heroin overdose)
  • Salicylate overdose

Raised pulmonary arterial pressure

  • High altitude pulmonary oedema
  • Massive PE
  • Pulmonary veno-occlusive disease
  • Post pneumonectomy
  • Air embolism

Negative pressure pulmonary oedema

  • Airway obstruction
  • Re-expansion pulmonary oedema, eg. following the drainage of a particularly large pleural effusion
Investigations to Help Discriminate Between Cardiac and Non-Cardiac Causes of Acute Pulmonary Oedema
Investigation Cardiogenic pulmonary oedema Non-cardiogenic pulmonary oedema
History
  • Chest pain
  • Paroxysmal nocturnal dyspnea or orthopnea
  • Worsening exercise tolerance
  • Pneumonia, sepsis, aspiration, high altitude, drug overdose, recent lung transplant, recent pleural effusion drainage, all the obvious stuff.
Examination
  • S3 gallop: suggests an elevated end-diastolic LV pressure; a highly specific finding with low sensitivity.
  • Mitral stenosis or regurgitation murmur
  • Raised JVP
  • Cool extremities
  • Low JVP
  • Warm vasodilated extremities
  • Vigorous strong pulses
ECG findings
  • Ischaemia
  • Heart block
  • Arrhythmia
  • Right ventricular strain, eg. as in PE
Troponin
  • Can confirm cardiac ischaemia
  • May be elevated in renal failure, sepsis, SAH, etc...
Brain natriuretic peptide (BNP)
  • More than 100pg/ml suggests that CCF is contributing to the APO
  • Less than 100pg/ml in ED or 200pg/ml in ICU suggests that the oedema is non-cardiogenic (eg. it may be ARDS)
Chest Xray
  • Cardiac causes of APO usually have more perihilar infltrates. Classical "bat wing" appearance is rare in non-cardic pulmonary oedema
  • Cardiomegaly is a clue
  • One may be able to see engorged pulmonary veins.
  • Non-cardiac APO tends to feature peripheral lung infiltrates. However, all sorts of ARDS look the same on Xray.
  • In massive PE the oedema will be irregular (i.e. limited to areas which are still perfused) whereas the rest of the lung will be oligaemic.
Echocardiography
  • Gold standard for diagnosis of cardiac structural and functional disease, but does not rule out non-cardiac causes. It is possible to have both poor baseline LV function and acute pulmonary oedema of a totally non-cardiogenic cause. 
  • Massive PE and similar things can be found on TTE.
  • A normal TTE all ut excludes cardiac causes of APO.
Swan-Ganz catheter
  • PAWP is valuely related to LA filling pressure, and a PAWP over 18mmHg suggests either cardiogenic APO or volume overload.
  • A normal or increased cardiac output, combined with a normal PAWP, all but excludes cardiogenic causes of APO 

References

References

Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.

Monnet, Xavier, et al. "Assessing pulmonary permeability by transpulmonary thermodilution allows differentiation of hydrostatic pulmonary edema from ALI/ARDS." Intensive care medicine 33.3 (2007): 448-453.

Ware, Lorraine B., and Michael A. Matthay. "Acute pulmonary edema." New England Journal of Medicine 353.26 (2005): 2788-2796.

 

Gluecker, Thomas, et al. "Clinical and radiologic features of pulmonary edema." Radiographics 19.6 (1999): 1507-1531.

 

Karmpaliotis, Dimitri, et al. "Diagnostic and prognostic utility of brain natriuretic Peptide in subjects admitted to the ICU with hypoxic respiratory failure due to noncardiogenic and cardiogenic pulmonary edema." CHEST Journal 131.4 (2007): 964-971.

 

Maisel, Alan S., et al. "Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure." New England Journal of Medicine 347.3 (2002): 161-167.

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