Shock, lactate and acute fluid therapy Flashcards
Define hypovolaemic , cardiogenic, obstructive and distributive shock and list the common causes in each category
Hypovolaemic shock = loss of >20% of circulating blood volume , dec venous return leads to dec. SV , CO and BP - acute haemorrhage, diarrhoea/vom? dehydration?
Cardiogenic shock = forward heart failure, with dec. SV and/or dec. CO due to primary heart disease
Obstructive shock = physical obstruction of blood flow returning to, or inhibiting ejection from the heart. Splenic torsion, GDV, inc. intrathoracic pressure, heart base tumour
Distributive shock = non-uniform loss of peripheral resistance which results in vasodilation, e.g. septic, anaphylactic, neurogenic
Describe how clinical examination can differ in different types of shock
Distributive shock - normal BV but massive increase in vascular space due to vasodilation which leads to a relative hypovolaemia . vasocontrictors offen indicated to improve , parameters as well as fluids at shock rates - more injected mm
Cariogenic - heart murmur present? Fluid therapy and vasoconstriction contraindicated, diuretics and vasodilators are tx of choice
Obstructive - venous return is reduced
Hypovolaemic -
Outline the monitoring techniques used to differentiate and monitor shock
Describe the intravenous fluids and administration rate options for the treatment of hypovolaemia and jusge the suitability of any particular fluid
Crystalloids -
LRS and 0.9% nacl
- useful, run at shock rate for 15-30 mins then reassess
- 70-90ml/kg hr (DOG)
- 40-60ml/kg/hr (CAT)
Colloids -
-can interfere with clotting factors if give too much
Important to be clear on volume and time frame given over so as to not overload the patient!
Hypertonic saline (HTS)
Give 4-7ml/kg (D) or 2-4ml/kg (C) diluted 1:3 with normal saline and given over 10-15 mins .
-respnose similar to crystalloid dose of 60-90ml/kg
high osmolality, pulls fluid out of interstitial and Intracellular space , rapidly expanding intravascular volume.
Effects can wane in as little as 30 mins as Na rapidly diffuses out of vasculature
Advantages over crystalloid alone include greater and more rapid restoration of arterial BP
Inc. cardiac contractility
Greater cardiac output
Improved o2 delivery and consumption
Improved organ blood flow
Lower intracranial pressure post-resusc
Improved survival in certain studies
Lower total volume of fluids required
Reduction in time taken to resusc
Inexpensive
Contraindications = dehydrated animals, hypernatraemia, heart or lungs dz , ongoing haemorrhage , pulmonary contusions
Dont give rapidly
Dont repeat twice due to hyperNa
Discuss the major contraindications to performing aggressive fluid therapy
Can exacerbate bleeding from the inc. blood pressure , haemabdomen or pulmonary contusions
Ongoing bleeding
Intracranial dz
Pulmonary dz
Volume overload with pulmonary oedema
In which case would go for hypotensive fluid resusc
Describe how lactate protects against intracellular and extracellular acidosis
Hyperlactatemia - increased plasma lactate
Under normal conditions with glycolysis, pyruvate is produced, and then enters the mitochondria to convert to acetylcoA and produced 36 ATP. under normal aerobic conditions only a small amount of pyruvate is converted to lactate.
When there is not enough oxygen, the TCA and acetyl cycles are slowed, so NAD+ falls, NADH builds up and this slows down glycolysis also. To keep glycolysis going smoothly (although a small supply of ATP at 2 moles, it is better than nothing and it is fast!) , pyruvate is converted to lactate (NOT lactic acid). This uses up H+ (so has a protective effect) AND restored NAD+ so that glycolysis can continue. As glycolysis continues in the face of anaerobic conditions, ATP is used and produces H+. This H+ cannot be consumed as normal and builds up, so this is the reason for the acidosis, not the lactate production itself.
It allows cellular energy production to continue when tissue oxygen supply is inadequate for aerobic metabolism.
Lactate production does not cause acidosis. Lactate protects against acidosis.
When it is produced from pyruvate H+ ions are consumed
Pyruvate + NADH + H+ -»»»lactate + NAD+
Lactate extrusion from the cell occurs via monocarboxylate transporter which also extrudes H+ from the cell. (main way protects against IC acidosis)
Lactate can either be converted to glucose or oxidised to C02 and H20 , both of which consume H+.
Lactate production is a protective response to tissue oxygen deficiency to allow cellular energy production to continue and protect against acidosis.
List the major causes of hyperlactataemia
Type A is the most common and occurs with evidence of relative or absolute tissue oxygen deficiency. Either increased oxygen demand or decreased oxygen delivery (usually due to hypoperfusion )
Shock (systemic hypoperfusion) = hypovolaemic, cardiogenic, maldistributive
Local hypoperfusion = gastric necrosis and other causes of splanchnic ischaemia , aortic thromboembolism
Increased oxygen demand such as seizure activity, intense muscle activity - half life of 30-60 minutes so should resolve in this timeframe. If not, then pathological process underlying,
Type B occurs in the absence of clinical evidence of decreased oxygen delivery
Discuss the benefits and limitations of lactate as an indicator of hypoperfusion
Lactate is an indicator of severe hypoperfusion, NOT mild. It does not rise until decompensation is occurring and there is an absolute or relative tissue oxygen deficiency.
Discuss the clinical use of lactate as a prognostic indicator
Global hypoperfusion is the most common pathological cause of hyperlactataemia in dogs and cats. It rises proportionally to the severity of hypoperfusion in dogs and the magnitude of hhyperL seen is proportional to the severity of the insult (but not necc its reversibility)
Failure of lactate to return to normal over 24-48hr is a grave prognostic indicator in most situations.
There are many causes for mild hyperL but large >5 inc in lactate usually only occur due to hypoperfusion or muscle activity such as seizure or excercise.
Useful as a prognostic indicator if the underlying cause has a high mortality, not as useful if eg. haemorrhage, that can be easily corrected.
Shock rates of fluid
Rate is designed to give one blood volume in one hour , should be able to improve perfusion in 15-30 mins even in severe cases, if they dont have ongoing losses
Colloid shock rate
5-10ml/kg over 15 mins (repeat up to TOTAL 15ml/kg cat or 20ml/kg dog
BV of a dog ml/kg = 70-90ml/kg?
BV of a cat ml/kg = 40-60ml/kg?
If giving colloids, give crystalloids as well at rate of 5-10ml/kg/hr
Hypertonic saline will restore BV the quickets
Significant osmotic effect,
Conttraindicated in dehydrated and bleeding, will inc. blood flow and blood loss , and can ‘blow the clots off’ small vessels that have constricted and coagulated
Dont repeat more than twice as hypenatraemia
Whole blood
Inc. o2 delivery , gives volume and colloids and red cell mass.
But transfusion reactions
Dogs dont have alloantibodies, so if no transfusion before its fine
Cats need to type or cross match
Trauma patient
OXYGEN first - stay on it until proved to have normal perfusion and no hypoxia
Then IV
Recheck CV signs every 10 mins so can change the fluid rate as perfusion is restored
Going to give fluids
Colloids at shock rate of 10ml/kg over 15 mins so about 100ml
Give methadone? Pain relief
FAST scan of abdomen to check for free fluid and tap if any seen, try to visualise bladder as well
Set a volume limit when you are setting shock rate fluids
Open fracture?
Dont reduce
Clip and clean
Sterile saline , no antiseptics on open wounds
Cover with sterile dressing (wet to dry?)
Robert jones or modified splint to stabilise until patient is stable
Iv ab’s , not subcut as perfusion deficits
Long bone fractures can bleed excessively especially in closed fractures so keep an eye for ongoing haemorrghage
Fix the most life-threatening problem FIRST , not necc the most severe
Vit K i/v works quicker
Otherwise oral takes 6 hours? #
In this case I would transfuse if PCV dropped below 25 or 18?
PCV normal 45 and TP 65
Takes 4-6 hr to drop after acute haemorrhage
Goals for small volume resusc
GOALS
Normal HR , pink mm, normal CRT
SYS 90-100mmHg
Mean 70-80mmHg
CVP <10cm H20
Normal goals for fluid resusc
Blood volume replacement in trauma case
Replace what has been lost
If practice has stored red cells and FFP
Start crystalloid fluid therapy so that perfusion is restored iin 10-20mins ,
In the meantime grab packed RBCs and give slowly while the plasma is defrosting
Bleeding wont stop until you give clotting factors so need plasma
Once plasma defrosted, stop rbc’s, and run plasma in over an hour or two, then start rbc’s again
If practice has stored whole blood
Start the transfusion while treating for shock with SALINE (calcium in LRS will inactivate the clotting factors)
Although clotting factors degrade in stored blood, in most cases the vit K dependant factors will be present still
Recheck clotting times after transfusion to see if need to top up with fresh whole blood or plasma
