![]() ![]() Note the ‘descending limb’ of the Starling curve for patients with severe heart failure: the implication is that a reduction in preload might (paradoxically) increase ventricular work (click to enlarge) Figure 10. With increasing severity of heart failure (brown lines), a greater preload is needed for a given level of activity. The horizontal lines show the ventricular work required at rest, then for mild and finally severe exertion. In the normal heart (blue), ventricular work increases as a function of preload. At this point, fluid accumulates in the interstitium of the lung and then the alveoli. ![]() In the acutely failing left ventricle, the relation is shifted downward and to the left so that to maintain any given cardiac output, a higher filling pressure is required.Īs the filling pressure is the same as the pulmonary venous pressure, the rise results in an increase in the rate of transudation from pulmonary capillaries into the lung tissues, and the rate eventually exceeds the rate at which fluid can be removed by the lymphatics. This is the Frank-Starling relation ( figures 9 and 10): as filling pressure rises, so does cardiac output. Left ventricular work (and cardiac output) is determined by left ventricular filling pressure (that is, end-diastolic pressure). There is a net (small) constant transudation of fluid from the pulmonary capillaries which is removed by the lymphatics. Fluid is held in the pulmonary capillaries by the balance between the hydrostatic pressure in the capillary tending to push fluid out and the colloid osmotic pressure (largely generated by plasma proteins) tending to hold fluid in the vascular space. Pathophysiology: Pulmonary oedema is best understood in haemodynamic terms. There is usually a gallop rhythm and widespread crackles and wheezes through the lung fields. On examination there is massive sympathetic nervous system activation, and the patient is thus usually pale and clammy, with a tachycardia and often hypertension. There is usually an acute precipitant that has triggered the episode of illness ( table 4). The breathlessness is often accompanied by wheeze and cough productive of pink frothy sputum. ![]() The experience for the patient is terrifying: she has to sit upright, is barely able to speak and often fears that she will die. Patients present with severe breathlessness which is usually of abrupt onset. Pulmonary oedema: Pulmonary oedema is an acute medical emergency. Common precipitants of acute pulmonary oedema Broadly, patients divide into those with acute pulmonary oedema, where there is fluid in the airspaces in the lung, and those with peripheral oedema, where the problem is fluid retention. Acute heart failure is a problem of fluid distribution. The majority, perhaps as many as two thirds, of patients with heart failure are initially diagnosed during a hospitalisation. Here, we will take acute heart failure to describe patients with sufficiently severe symptoms and signs that they present acutely seeking medical attention (and are often admitted to hospital) whereas chronic heart failure describes the syndrome patients have once acute heart failure has been medically treated. However, even then, the terms can be confusing. The most useful distinction to make is between acute and chronic heart failure. It makes sense, perhaps, to consider the separate heart failure syndromes as the pathophysiology of them is distinct: the differences highlight important differences in therapeutic approach. Over many years, the heart failure syndrome has attracted a number of different terminologies of varying degrees of usefulness. ![]()
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