may have a temperature of < 35.5 ° C, a HR < 140 bpm, and an apparently normal RR of 10 – 30 breaths / min [ 5 ] or agonal breathing. Their mentation will be obtunded to stuporous, and they will have pale / grey MMs, a CRT > 2 seconds and a MAP of < 60 mmHg [ 2, 3 ].
A patient with a MAP of < 60 mmHg is in a very serious condition; a MAP this low indicates potential damage to or failure of body systems. A hypotensive hypovolaemic shock patient is at high risk of mortality. Hypotension can lead to organ ischaemia, resulting in organ damage and failure, arrhythmias, acute kidney injury, hypothermia, changes in mentation, coagulopathies and, eventually, the death of the patient [ 6 ]. Thus, it is important that the VN can recognise which compensatory state the patient is in so appropriate treatment can be started promptly, to prevent organ damage and give the patient the best chance of survival.
There are several ways the VN can provide care to these patients. IVFT, oxygen therapy and blood gas analysis( BGA) are the most important when they are presented at the clinic. However, it is also vital for the VN to understand how hypovolaemic shock can cause changes in blood serum lactate due to anaerobic metabolism [ 3, 7 ].
MAP is commonly monitored in general practice using Doppler ultrasonography and oscillometric methods. The VN needs to know where to place the blood pressure cuff on a GDV patient to get the most accurate reading. It is best to apply the cuff to a forelimb in these patients, due to compromised venous return from the hindlimbs caused by the distended stomach compressing the caudal vena cava.
Blood serum lactate
A patient that has presented at the clinic with possible GDV will typically have an increase in blood serum lactate and their cellular respiration will be anaerobic, resulting in metabolic acidosis. GDV in canine patients will lead to hypovolaemic shock, due to their stomach swelling by a significant amount and compressing the vena cava. This will compromise the patient ' s cardiovascular system drastically, resulting in hypoperfusion and hypoxia [ 2 ].
The patient ' s metabolic status will deteriorate further when there is an imbalance between oxygen requirements and oxygen supply, causing cellular aerobic respiration to change to anaerobic respiration. Although oxygen is vital for cellular function, anaerobic respiration provides the patient with short-term energy production without the use of oxygen, in order to provide a short-lived supply of energy to the intracellular and interstitial space. Anaerobic cellular respiration will result in the accumulation of lactic acid in the blood serum, leading to metabolic acidosis and metabolic shock [ 2 ].
Hyperlactataemia is the state when there is an excessive amount of lactate in the blood serum, higher than the species-specific range. The normal blood serum lactate concentration in dogs is in the range of 0.3 – 2.5 mmol / l, whereas for a dog with GDV, blood serum lactate measurements are generally between 13 and 15 mmol / l [ 7, 8 ]. Blood serum lactate concentrations between 13 and 15 mmol / l reflect type A lactic acidosis, resulting from a decreased oxygen supply and an increase in the demand for oxygen, and would suggest that the patient is not yet fluid resuscitated. Type A lactic acidosis, which is caused by ischaemia, is more serious than type B lactic acidosis, which occurs when blood oxygen and MAP are within their normal ranges, and could be due to the inadequate use of oxygen in the body or the presence of certain toxins [ 8 ]. In metabolic acidosis, the patient has a low blood pH, which can lead to cell damage and cell death. Therefore, it is very important to carry out BGA to determine the blood serum lactate concentration, and then start rapid fluid resuscitation to resolve metabolic acidosis [ 7 ].
Intravenous fluid therapy
Administering hypertonic saline( HTS)( 7.2 – 7.5 % sodium chloride) to a patient that is in severe hypovolaemic shock, such as a GDV patient, can be advantageous. It works rapidly by osmotically pulling water into the intravascular space to achieve fluid resuscitation in as little as 30 minutes [ 9 ]. Administration of HTS results in a transfer of large volumes of fluid from the interstitial and intracellular spaces, leading to a prompt increase in fluid in the intravascular space. HTS is beneficial for intravascular volume expansion in large-breed dogs. By contrast, if using isotonic crystalloids, a larger fluid volume will be required for fluid resuscitation of the patient [ 10 ]. For a dog, HTS should be administered at a rate of 4 – 7 ml / kg over 2 – 5 minutes [ 9, 11 ]. However, it is recommended to administer it over 10 minutes to prevent the patient ' s interstitial and intracellular spaces becoming rapidly compromised, causing the onset of dehydration due to a huge pull of volume from these spaces into the intravascular space. If time is a critical factor, then administering the volume over 2 – 5 minutes is still beneficial to the patient as it will resuscitate the loss in the intravascular space. Giving HTS over this short time period will produce the same intravascular volume expansion as giving 2 – 3 litres of isotonic crystalloids at a 60 – 90 ml / kg fluid rate [ 7, 10 ].
Once the patient has received the HTS, another BGA should be carried out to determine whether the hyperlactataemia has resolved so blood serum lactate is within the normal range of < 2.5 mmol / l [ 8 ]. This is a good indication of adequate fluid resuscitation; hyperlactataemia occurs due to poor perfusion, so if the blood serum lactate level returns to normal, HTS administration can be stopped. However, BGA should continue to be monitored every 30 – 60 minutes until the GDV is repaired or sooner, at the veterinary surgeon ' s( VS ' s) discretion.
30 Veterinary Nursing Journal