VNJ Volume 39 (3) June 2024 | Page 44

Another consideration in using this therapy is the effect on the myocardium . Severe acidaemia can cause decreases in vascular tone and myocardial contractility [ 8 ] . There is insufficient evidence to show that NaHCO 3 will improve this haemodynamic performance , and it could potentially worsen it [ 13 ] . If excessive NaHCO 3 is administered , this could result in decreased ionised hypocalcaemia , due to the increased binding of calcium to albumin and translocation of ionised calcium to the intracellular compartment [ 12 ] , and contribute to cardiotoxicity [ 14 ] . However , it has some benefit in reducing hyperkalaemia by shifting extracellular K + into cells via H + / K + exchange , meaning that it is a practical treatment for patients with metabolic acidosis with hyperkalaemia [ 7 ] . Conversely , it should be used cautiously in patients with oliguria / anuria , due to the high risk of fluid overload . Other potential side effects include increased haemoglobin affinity for oxygen , increased lactate concentration , hypercapnia , increased intracellular acidosis , hypernatraemia , hyperosmolality , hypervolaemia and phlebitis [ 7 ] . Therefore , the possible benefit may not compensate for the potential side effects that could be detrimental to the patient .
Sampling errors in phlebotomy can cause abnormal results in blood gas analysis . It is imperative that there is minimal exposure of the sample to room air , and bubbles in the sample should be removed as they can alter the PCO 2
. Inappropriate dilution of the sample with anticoagulant and analysis more than 15 min after sample collection could give inaccurate results [ 8 ] . The frequency of repeating sampling and analysis will be case dependent ; as a minimum in UO cases , a blood sample should be analysed before and after relief of the obstruction [ 7 ] . When urine can be expelled , the kidneys will be able to excrete H + as normal , rectifying the metabolic acidosis . For a patient with severe acidosis , such as the cat in this case study , frequent monitoring would be indicated ; a central line would be appropriate , to prevent the stress or pain associated with repeated venepuncture . Further details on central lines and their nursing care are outside the scope of this article . In this case , serial blood gas analysis was not done because the decision was made to euthanase the patient . However , had treatment continued , it is the clinic ' s policy to repeat blood gas analysis as part of the hospitalisation of unstable and critical patients .
Unfortunately , this patient had been unable to correct its metabolic acidosis , due to the clamping of the urine collection system and the acidifying fluid ( saline ) IVFT with which it had been transferred . The PCP was unlikely to possess a blood gas analyser ; this is understandable , as this is not routine laboratory equipment for general practice clinics . The PCP may therefore have underestimated the critical importance of acid – base , particularly in cases of UO . Instead , the focus of the PCP lay in correcting hyperkalaemia , another potentially fatal component in UO .
Fluid therapy
Fluid therapy is critical in patients with UO . Patients that present with hypovolaemia will require shock rate fluids , as prescribed by the treating VS [ 15 ] . Typically , a bolus of 10 – 20 ml / kg is given over 15 min [ 16 ] , but 5 – 10 ml / kg would be more appropriate in cats , to prevent fluid overload . The response to the bolus is monitored by the VN by determining haemodynamic changes in vital signs , such as improvements in pulse quality and synchronisation . Feline patients in hypovolaemic shock may present tachycardic , tachypnoeic and hypothermic , with pale pink MMs , weak , thready peripheral pulses and decreased mentation [ 8 , 16 ] . In severe cases , cats can become bradycardic ; in such cases immediate treatment needs to be initiated . The VN ' s role would be to assess the patient ' s response to fluid boluses . This would include monitoring the heart rate , RR , non-invasive blood pressure and body temperature , which can be aided by the use of a multiparameter monitor , if available . In patients that are hyperlactataemic , serial monitoring of blood lactate can indicate the patient ' s response to a fluid bolus , with a decrease in lactate indicating improving perfusion [ 3 ] . It is imperative that the VN communicates changes in any of the patient ' s parameters to the VS , to allow treatment to be tailored to the patient . Once hypovolaemia has been stabilised , the hydration status of the patient should be assessed and appropriate calculation of maintenance fluids used [ 16 ] .
In this case , the patient was bradycardic , with a normal RR and respiratory effort , and normotensive . Had a fluid bolus been administered , the patient ' s heart rate may have normalised . In patients with abnormal RR or respiratory effort , a fluid bolus could correct these abnormalities . However , this treatment should be used with caution in patients that are dyspnoeic due to pulmonary oedema . Abnormal blood pressure or body temperature could be due to poor perfusion ; a fluid bolus would aid in improving perfusion and might restore these parameters to within their normal ranges .
Traditionally , VSs used saline fluid therapy in patients with UO due to the secondary hyperkalaemia that occurs in UO . This is because saline does not contain K + , which was thought to exacerbate the hyperkalaemia [ 12 ] . However , a recent study [ 7 ] discussing the treatment of hyperkalaemia stated that the use of saline , compared with a buffer-containing solution , did not influence the normalisation of K + but did directly worsen metabolic acidosis . Therefore , in cases of UO in which hyperkalaemia coincides with metabolic acidosis , a buffer-containing fluid would be preferable . The presence of a buffer such as sodium lactate in the fluid – as is the case in lactated Ringer ' s solution or Hartmann ' s solution [ 8 ] – is essential in treating metabolic acidosis , as it is metabolised by the liver to generate HCO 3
– and consume H + , and therefore has an alkalinising effect [ 7 ] . The effect of the IVFT on metabolic acidosis can be monitored by repeated blood gas analysis , which can
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