The normal range is 900–1400 dyn/s/cm−5.
What are the complications of insertion?
These include complications from central line insertion (see Central Access: Central Lines)
Cardiac arrhythmias: most commonly atrial and ventricular ectopics. Ventricular tachycardia and ventricular fibrillation as well as heart block also reported
Cardiac valve injury: leading to incompetence of the tricuspid or pulmonary valves
Pulmonary artery rupture: presents as shock and haemoptysis and occurs from injury by the J-wire or following balloon inflation
Pulmonary infarction: if the balloon is kept in the wedged position for too long. Also occurs if there is embolisation of a thrombus formed at the catheter tip or catheter migration
Other complications include the catheter knotting and generalised sepsis from the presence of a foreign body. Therefore, it requires some expertise and an aseptic non-touch sterile technique for insertion.
By which principle is the cardiac output measured?
The cardiac output is measured using the indicator dilution or the thermodilution techniques. Both of these have similar principles. With the indicator dilution technique, indocyanine green is injected into the circulation and samples are taken peripherally from the radial artery. A graph of the concentration of the dye in the peripheral blood over time is plotted. The cardiac output equates to the amount of dye injected divided by the area under the curve.
In the case of the thermodilution method, 10 ml of cold crystalloid is injected peripherally, and the change of temperature detected by a thermistor at the end of the catheter. A graph is also plotted for the change of temperature of the blood passing the thermistor against time. This graph is used to calculate the cardiac output.
Renal replacement therapy
What types of renal replacement therapies are available?
These may be continuous or intermittent therapies
What are the indications for commencing these?
The agreed indications for replacement therapy in acute kidney injury or chronic kidney disease are
Refractory fluid overload
Hyperkalaemia of >6.5 mmol/L
Acidosis of pH <7.1
Urea >30 mmol/L
Creatinine >300 µmol/L
Uraemic complications, e.g. encephalopathy, pericarditis, neuropathy or myopathy
Drug overdose
What are the basic features of haemodialysis and haemofiltration?
Haemodialysis: the principle is that the blood interfaces the dialysis solution across a selectively permeable membrane which permits the passage of molecules of <5 kDa down a diffusion gradient. Unlike haemofiltration, it may be administered as either an intermittent or a continuous regimen
Haemofiltration: this relies on the continuous convection of molecules across a membrane to which they are permeable. The fluid that is removed from the patient is replaced with a buffered physiological solution. Thus it is more effective in removing large volumes of fluid, but is not as effective as dialysis in clearing smaller molecules
When is intermittent haemodialysis used, and what are the basic components of the circuit?
This may be used several times per week in those with chronic kidney disease and much less commonly used in the critically ill patient with acute kidney injury. The essential components of the circuit are
Vascular access: which may be through a central line or a surgical arteriovenous fistula for use in the long term
Extracorporeal circuit: this has an air trap and heparin pump to prevent air emboli and clotting in the circuit, respectively
Dialysis machine: the dialysate solution passes through a dialyser cartridge that houses the diffusion membrane. Blood passes through and permits diffusion across to the dialysate at the membrane interface
The circuit is driven by a roller pump.
Give the most important complications of haemodialysis
Dysequilibrium syndrome: this follows sudden changes in the serum osmolality that occurs when molecules such as urea are filtered out. It can lead to cerebral oedema that usually presents with headaches, nausea and occasionally seizures
Hypotension: following a sudden reduction in the intravascular volume
Immune reactions: may occur when the extracorporeal circuit causes systemic complement cascade activation
Hypoxia: as part of the systemic immune response leading to neutrophil aggregation in the lungs
Sepsis: from the indwelling line
Loss of circuit connection leading to air embolism or haemorrhage
What types of continuous renal replacement therapies are there?
There are a number of continuous renal replacement modalities, depending on whether they rely on dialysis or filtration, and on the pattern of vascular connection
Continuous arteriovenous haemofiltration (CAVH): the flow is driven by the arteriovenous pressure difference
Continuous venovenous haemofiltration (CVVH): flow relies on roller pumps and so does not depend on the unstable arterial pressure of the critically ill patient (NB. good vascular access is required)
Continuous arteriovenous or venovenous haemodialysis (CAVHD/CVVHD): this is useful for slow ultrafiltration and diffusion of solutes, and the solution runs countercurrent to the direction of blood
How does peritoneal dialysis work?
Peritoneal dialysis is a slow form of continuous dialysis that relies on the peritoneum and its capillary network to act as the selectively permeable membrane. As with haemodialysis, solute flows down a diffusion gradient, and fluid flows by osmosis. The dialysate is introduced into the peritoneum by way of a Tenckhoff catheter and dwells within the abdomen for several hours before being drained off.
This technique has been used in the intensive care setting, but has been superseded by other replacement therapies that are faster and more effective in removing urea and other solutes. However, it still has a place in the haemodynamically unstable patient and the ambulating patient with chronic renal failure.
It is particularly useful in the paediatric setting when vascular access can be difficult.
What is the classical infective complication? How is this recognised and treated?
The important infective complication is peritonitis that occurs following introduction of exogenous organisms. It may initially be recognised by the presence of a turbid effluent when the dialysate is drained, with >50 white cells per ml. It is caused by gram-positive organisms in 75% of cases, predominantly Staphylococcus epidermidis and Staphylococcus aureus. Occasionally it is fungal. It may be managed by the addition of broad spectrum antibiotics to the dialysate, such as cefuroxime and gentamicin.
Septic shock and multi-organ dysfunction syndrome (MODS)
What is an endotoxin?
An endotoxin is composed of lipopolysaccharides derived from the cell walls of gram-negative bacteria, and is the most common causative agent of septic shock. It has three components
Lipid A, e.g. the lipid portion, and is the source of much of the molecule’s systemic effects
Core polysaccharide
Oligosaccharide side chains
What is the difference between bacteraemia, sepsis and severe sepsis?
Bacteraemia: the presence of viable bacteria in the circulation
Sepsis: the syndrome associated with the systemic response to infection, e.g. presence of >2 SIRS criteria due to infection. It is characterised by a systemic inflammatory response and diffuse tissue injury
Severe sepsis: this is sepsis with organ dysfunction, hypoperfusion and hypotension (systolic <90 mmHg), e.g. lactic acidosis, decreased urine output and altered GCS
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