For many conditions, it is possible to define a typical profile of the haemodynamic abnormalities that characterise the pathological state.

Profiles of some 'classical' conditions are described below.

Cardiogenic shock.
Cardiogenic shock is due to a severe depression of left ventricular contractile performance. The patient is frequently obtunded, oliguria is present, and the extremities are cold and cyanotic. The condition is most commonly caused by myocardial infarction, but it can also complicate conditions such as acute myocarditis and follow prolonged aortic cross-clamping during cardiac surgery.

The typical picture of cardiogenic shock is characterised by:

Haemorrhagic shock.
Haemorrhagic shock usually becomes apparent when about 20% of circulating blood volume (CBV) has been lost (Figure 1) and an uncompensated loss of more than about 40% of CBV is unsurvivable. It should be borne in mind that these values describe the response to graded blood loss over a 30 minute period in an individual with intact cardiovascular reflexes.

Survivability of haemorrhage may be greatly reduced if the cardiovascular reflexes are impaired either by drugs (such as beta blocking or general anaesthetic agents), or by disease. In the absence of cardiovascular reflexes, only about 15-20% of CBV can be removed in a 30 minute period before death occurs.

The typical picture of haemorrhage is characterised by:

Septicaemic shock.
Septicaemic shock ('Hot shock') can complicate infection occurring at almost any site in the body. It is particularly associated with gram negative septic foci in either the gastrointestinal or urogenital tract. The picture can be reproduced in humans by the administration of endotoxin ¹ which probably exerts its effects by stimulating the release of inflammatory mediators such as tumour necrosis factor alpha (TNF-a) or Interleukin - 1 ².

The classical pattern of cardiovascular function in septicaemic shock includes findings of:

Note that, in contrast to cardiogenic and haemorrhagic shock, cardiac output is often well-maintained.

The increased end-diastolic volume is thought to reflect an increase in ventricular compliance ³.

Cardiac tamponade.
Cardiac tamponade may occur acutely after, for example, cardiac surgery or more chronically in the setting of constrictive pericarditis. The pathophysiology of tamponade is complex and possibly for this reason, the presentation of tamponade is frequently atypical ⁴.

The essential hydraulic 'component' of tamponade is the presence of pericardial constraint which may be either circumferential or localised. When constraint occurs, filling of the adjacent cardiac chamber is impaired and secondary effects - particularly the equalisation of diastolic pressures and the exaggeration of ventricular interdependence, start to become apparent.

Equalisation of filling pressures is a classic sign of tamponade. In the early stages of tamponade, RVEDP is elevated and equal to the intrapericardial pressure (IPP), but both remain less than the LVEDP. Under these circumstances, pulsus paradoxus is usually not present ⁵. As the condition becomes more severe, LVEDP equalises with RVEDP and IPP and pulsus paradoxus becomes a more consistent feature of the syndrome. In a recent study which examined the reliability of the various signs of tamponade as it occurred in post cardiac surgical patients, equalisation of filling pressures was found to be the most reliable single sign of circumferential tamponade ⁴.

Diastolic ventricular interdependence is a feature of normal cardiac function, but becomes more important in conditions such as tamponade. It occurs when the filling of one ventricle is determined by the degree of filling of the other - as one fills more completely, so the other fills less. In the diagnosis of post cardiac surgical tamponade, right ventricular diastolic collapse is bettered only by equalisation of filling pressures as a reliable sign of circumferential tamponade ⁴.

Because total intrapericardial volume is constrained, atrial, as well as ventricular volumes are also tightly coupled. Furthermore, because intrapericardial volume is greater during expiration than inspiration (Figure 2), respiration may significantly affect both arterial ('Pulsus Paradoxus') and venous ('Kussmaul's Sign') pressure.

The typical picture of tamponade is characterised by:

Low systemic vascular resistance syndrome.
Cardiopulmonary bypass provokes a complex neuroendocrine response in most patients. Partly as a result, systemic vascular resistance tends to be low in the immediate post-bypass period although it then usually rises ⁶. However, in about 7-8% of cases a persistently low vascular resistance state ⁷ , characterised by abnormally high levels of Interleukin-6 ⁸, develops. This syndrome shares many of the features of septicaemic shock, is often associated with the development of lactic acidosis ⁹ and may be caused by endotoxaemia occurring as a result of gut hypoperfusion during bypass ¹⁰. Low SVR syndrome is associated with the use of adrenaline in the post-operative period ¹¹.

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Last edited on: 13/11/2000