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Acute cardiogenic pulmonary oedema

Pathophysiology

  • increase in pulmonary microvascular pressure results in increased fluid filtration and exhaustion of lymphatic reserve
  • ? stress failure of pulmonary microcirculation due to massive abrupt rise in pulmonary capillary pressure with resultant increase in capillary permeability
  • pulmonary capillary pressure can be estimated from:
  • PCP=LAP + 0.4(PAP-LAP)
  • rise in LAP may result from LV systolic dysfunction with secondary increase in LVEDV (figure 1) or from diastolic dysfunction with decrease in LV compliance (figure 2). Former shifts LV pressure volume loop to right along same diastolic pressure volume relationship while latter shifts loop up. Thus diastolic failure results in an increase in LVEDP without a rise in LVEDV (the combination of pulmonary oedema with a normal heart size should alert one to the possibility of diastolic failure (image). Combined systolic and diastolic failure results in marked increase in LVEDP (figure 3).

Figure 1

Figure 2

Figure 3

  • both rate and extent of myocardial relaxation are major determinants of LV diastolic distensibility. This is a dynamic process which is essential for adequate filling of LV at low diastolic pressure. Involves rapid energy-dependent flux of Ca, largely into sarcoplasmic reticulum, against a huge concentration gradient. This transport system is extremely vulnerable to energy depletion.
  • adequacy of relaxation is not only a function of Ca egress from cytosol but can also be modified by varying affinity of cardiac troponin C for Ca. Wall stretch, a stimulation and alkalosis increase Ca sensitivity and impair dynamic relaxation.
  • acute ischaemia is an important cause of severe impairment in LV diastolic distensibility
  • respiratory work markedly increased due to decrease in respiratory system compliance and increase in airways resistance
  • elevation in closing volume contributes to shunt

Methods of lowering LVEDP

  • Appropriate strategy depends on predominant mechanism. In diastolic failure resolution of ischaemia often central to improvement of LV relaxation. Other options somewhat limited but drugs with lusitropic effects (b agonists, phosphodiesterase inhibitors) and reduction in pressure load will improve LV relaxation

Diastolic failure

  • Improve LV chamber distensibility
  • enhance LV relaxation: decrease ischaemia, BP and LV volume; lusitropic drugs
  • Decrease LV wall stiffness: decrease BP and coronary turgor
  • Reduce central blood volume: venodilation or diuretics

Systolic failure

  • Reduce LVESV: inotropes, decrease LV afterload, LV assist device
  • Improve LV chamber distensibility
  • Reduce central blood volume. Reduction in central blood volume is a time-honoured method for treating cardiac failure. Magnitude of benefit depends, in part, on mechanism of elevated LVEDP. In predominant diastolic failure, with normal chamber volume, LV may already be operating on flat portion of pressure-volume curve and any reduction of central blood volume may simply reduce stroke volume without a significant change in LVEDP. However in the volume overloaded patient with an increased LVEDV a reduction in central blood volume will often dramatically lower LAP.
  • In systolic failure aim is to reverse cause of impaired contractility and to increase stroke volume. This may result in a reduction in LVESV and a fall in diastolic pressure accompanying a leftward pressure-volume shift.
  • Most patients have a combination of both diastolic and systolic failure.

Drugs

Frusemide

  • no studies showing benefit from administration of frusemide in acute cardiogenic pulmonary oedema
  • in normals and patients with LVF following MI it reduces PAOP by early venodilatation. Associated increase in neurohumoral activity (renin-angiotensin system and catecholamines) results in decreased cardiac output, increased peripheral resistance. Diuretic effect delayed until about 15 mins and associated reduction in lung water occurs after about 4 h
  • in patients with chronic heart failure and oedema produces less venodilatation and increase in plasma noradrenaline associated with rise in PAOP, reduction in stroke volume and reduction in cardiac output prior to diuresis
  • patients with acute cardiogenic pulmonary oedema who respond to treatment with frusemide show a concurrent 30% increase in plasma volume suggesting that hypervolaemia and diuresis have little to do with recovery from acute cardiogenic pulmonary oedema
  • in patients with normal renal function maximum effect is achieved with 1 mg/kg IV

Inotropes

  • both b agonists and phosphodiesterase inhibitors may be used to improve contractility and also to improve diastolic relaxation
  • lusitropic effects due to rise in cAMP. This enhances rate of relaxation by reducing affinity of cardiac troponin for Ca and by increasing uptake of Ca by sarcoplasmic reticulum

Digoxin

  • improves systolic function in acute ischaemic heart failure
  • however inhibits Na-K pump. This results in a secondary increse in diastolic intracellular Ca via sarcolemmal Na-Ca exchange and an impairment of diastolic relaxation
  • should not be used in conditions in which diastolic dysfunction predominates (eg myocardial hypertrophy or ischaemia)
  • role, if any, in acute cardiac failure unclear. Inotropic effect in presence of high levels of sympathetic stimulation is negligible. May reduce cardiac output in cardiogenic shock due to its effect on afterload.
  • although it improves symptoms in chronic cardiac failure it has no effect on mortality

CPAP

  • decreases work of breathing, predominantly due to a reduction in resistive component
  • decreases venous return and afterload
  • if LV contractility normal any increase in cardiac output due to decreased afterload will be small due to decreased preload
  • if LV contractility markedly impaired reduction in afterload will tend to overcome concomitant decrease in venous return and cardiac output will rise

Mechanical ventilation

  • Potential advantages over CPAP: more complete reduction in respiratory work, additional afterload reduction, safe administration of sedatives (help to decrease myocardial ischaemia) and maintenance of an airway in the event of cardiac arrest. However mask CPAP is usually only required for a relatively short period of time so probably worthwhile to avoid additional risks of intubation and ventilation

Further reading

Bersten AD, Holt AW. Acute cardiogenic pulmonary edema. Curr Opinion in Crit Care, 1995; 1:410-419

 


© Charles Gomersall July 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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