In uncomplicated cases careful interpretation of the CVP is an adequate guide to the filling pressures of both sides of the heart. In many critically ill patients, however, this is not the case and there is a disparity in function between the two ventricles. Most commonly, left ventricular performance is worst, so that the left ventricular function curve is displaced downward and to the right. This situation is encountered in some patients with clinically significant ischaemic heart disease and has also been reported in major trauma, sepsis, peritonitis, hepatic failure, valvular heart disease and after cardiac surgery. High right ventricular filling pressures, with normal or low left atrial pressures, are less common but may occur in right ventricular ischaemia and in situations where the pulmonary vascular resistance (i.e. right ventricular afterload) is raised, such as acute respiratory failure and pulmonary embolism.
If there is a disparity in ventricular function after cardiac surgery, then the left atrium can be cannulated directly. If the thorax is not open, however, some other means of determining left ventricular filling pressure must be devised.
Pulmonary artery pressure
A ‘balloon flotation catheter’ enables prompt and reliableatheterization of the pulmonary artery, without the need for screening, and minimizes the incidence of arrhythmias.
These ‘Swan-Ganz’ catheters can be inserted centrally through the femoral vein or via a vein in the antecubital fossa. Passage of the catheter from the major veins, through the chambers of the heart, into the pulmonary artery and into the wedge position is monitored and guided by the pressure waveforms recorded from the distal lumen. A chest X-ray should always be obtained to check the final position of the catheter. Once in place, the balloon is deflated and the pulmonary artery mean, systolic and end-diastolic pressures (PAEDP) can be recorded. The pulmonary artery occlusion pressure (PAOP-previously known as pulmonary artery wedge pressure PAWP) is measured by reinflating the balloon, thereby propelling the catheter distally until it impacts in a medium-sized pulmonary artery. In this position there is a continuous column of fluid between the distal lumen of the catheter and the left atrium, so that PAOP is usually a reflection of left atrial pressure. The technique is generally safe-the majority of complications are related to user inexperience. Pulmonary artery catheters should preferably be removed within 72 hours, since the incidence of complications then increases progressively.
The only quantitatively accurate methods for measuring cardiac output are invasive. Of these, the thermodilution technique is most commonly used clinically. This uses a modified pulmonary artery catheter with a lumen opening in the right atrium and a thermistor located a few centimetres from its tip. A known volume (usually 10 rnl) of ice-cold 5% dextrose is injected as a bolus into the right atrium. This mixes with, and cools, the blood passing through the heart and the transient fall in temperature is continuously recorded by the thermistor in the pulmonary artery. The cardiac output is computed from the total amount of indicator (i.e. cold) injected, divided by the average concentration, i.e. the amount of cooling, and the time taken to pass the thermistor.
Delays in making the diagnosis and initiating treatment, as well as inadequate resuscitation, contribute to the development of MOF and must be avoided. A patent airway must be maintained and oxygen is given. If necessary, an oropharyngeal airway or an endotracheal tube is inserted. The latter has the advantage of preventing aspiration of gastric contents. Very rarely emergency tracheostomy is indicated. The underlying cause of shock should be corrected, e.g. haemorrhage should be controlled or infection eradicated. In patients with septic shock, every effort must be made to identify the source of infection and isolate the causative organism. As well as a thorough history and clinical examination, X-rays, ultrasonography and CT scanning may be required to locate the origin of the infection. Appropriate samples (urine, sputum, cerebrospinal fluid, pus drained from abscesses) should be sent to the laboratory for microscopy, culture and sensitivities. Several blood cultures should be performed and ‘blind’ antibiotic therapy should be commenced. If an organism is isolated, the therapy can be adjusted appropriately. The choice of antibiotic depends on the source of infection-whether this was acquired in hospital or in the community. Abscesses must be drained and infected indwelling catheters removed.
Whatever the aetiology of the haemodynamic abnormality, tissue blood flow must be restored by achieving and maintaining an adequate cardiac output, as well as ensuring that arterial blood pressure is sufficient to maintain perfusion of vital organs.
Pre-load and volume replacement
Optimizing pre-load is the most efficient way of increasing cardiac output. Volume replacement is obviously essential in hypovolaemic shock but is also required in anaphylactic and septic shock because of vasodilatation, sequestration of blood and loss of circulating volume due to capillary leak.
In mechanical shock, high filling pressures may be required to maintain an adequate stroke volume. Even in cardiogenic shock, careful volume expansion may, on occasions, lead to a useful increase in cardiac output. On the other hand, patients with severe cardiac failure, in whom ventricular filling pressures may be markedly elevated, often benefit from measures to reduce pre-load (and after-load) such as the administration of diuretics and vasodilators.
The circulating volume must be replaced quickly (in minutes not hours) to reduce tissue damage and prevent acute renal failure. Fluid is administered via wide-bore intravenous cannulae to allow large volumes to be given quickly and the effect is continuously monitored. Care must be taken to prevent volume overload, which leads to cardiac dilatation, a reduction in stroke volume, and a rise in left atrial pressure with a risk of pulmonary oedema. Pulmonary oedema is more likely in very ill patients because of a low colloid osmotic pressure (usually due to a low serum albumin) and disruption of the alveolar-capillary membrane (e.g. in ARDS). The development of pulmonary oedema can also be influenced by other unquantifiable factors, such as the hydrostatic and oncotic pressures within the interstitial spaces. Since the pulmonary lymphatics remove excess fluid, pulmonary oedema will only occur when this mechanism is overwhelmed or impaired. Left ventricular filling pressures should therefore not be allowed to rise to more than 15-18 mmHg in the critically ill. In general, however, many more patients are undertransfused rather than overtransfused.