Triage Flashcards

1
Q

What is triage briefly?

A

Triage is prioritising of need – trying to work out which of the patients is likely to die/decompensate first

Sometimes easy, sometimes harder!

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2
Q

The following emergencies come in:

–Dog that has been hit by a car – can walk

–Cat that is mouth-breathing

–Animal found largely unresponsive in lateral recumbency with distended abdomen

  1. What do you think regarding triage?
A

Dog that has been hit by a car: Could decompensate quite fast is does have a head injury, but at the moment it is probably our last priority here?

  • Cat onto oxygen, deal with the dog then? Cats do mouth breathing later in the disease than others. GDV – can stabilise it, can decompress and then do the surgery – but then cat left for a while!
  • Gayle might try and work out why its mouth breathing – CHF, pleural fluid? Might be quicker to quickly stabilise the cat and then go onto the dog
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3
Q

What are some important aspects to success with assessment of the poly-traumatised patient?

A

–Appropriate equipment and trained staff – in the right place!

–Enough staff

–Good initial assessment and rapid response to findings

–Care with identification and action on all abnormal findings

–In the order of ABC

  • Airway
  • Breathing
  • Circulation
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4
Q

What are the 3 first steps to start to success with the emergency patient?

A

•1) Need dedicated area with equipment that may be required for these challenging patients

–Reduces time of successful resuscitation

–Shown to increase survival in paediatric/adult human patients

–Also in dogs and cats

•2) Appropriately trained staff and someone to take charge

–If multiple people available to manage the animal – likely increased success

–Approach patient in a horizontal approach – multiple tasks at once

•Faster and more successful than vertical approach (one task at a time)

–Need to practice and train team with specific jobs - cadavers

•3) Appropriate equipment and pharmacological agents

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5
Q

What should you do and look for when doing an initial assessment of an ECC patient?

A

•Appropriate advice given on the telephone to finder/owner at site of trauma so animal can be appropriately cared for at the scene – massive effect on success

–Need to train reception staff

•Wear gloves and gowns

–Animals at increased risk of infection esp in trauma cases – all at risk of sepsis

•Check your watch!

–Always have an idea of how long things are taking

–Platinum 5 minutes – if something very sick, should be doing ABC within 5 minutes of arrival

•‘Priority of need’

–Rapidly assess level of urgency required to ameliorate global, tissue and cellular consequences of each injury

•Rapid primary survey to assess and discover injuries or results of injuries that are the most life-threatening

–Always includes the airway, breathing, and cardiovascular systems in that order

  • Treat in that order as long as not arrested
  • Severe problems must be addressed in the initial ‘platinum 5 minutes’
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6
Q

What is the purpose of a goal directed primary survey?

A

•Focus of all severely poly-traumatised or critically ill patient protocols is to

–recognise and treat life-threatening problems

–reduce global and local hypoxia and hypercarbia

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7
Q

When would you do a goal directed primary survey?

What should you do/what are you looking for?

A

•The ability to recognise and treat oxygen debt and lactic acidosis correlates with the trauma patient’s recovery

–If we can fix this quickly, will improve likelihood of recovery

•Only after resuscitation is initiated and deemed appropriate is a detailed head to tail to toe (physical exam section and secondary survey) performed

–Only do a head to toe once patient stable!

  • Primary survey should be done the same each time – focus on airway, breathing, circulation and neurological disability
  • If life-threatening problems are noted during the primary survey, the problem is addressed before further assessment is continued
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8
Q

What should all animals with multiple injuries require according to a crash plan?

A

•All animals with multiple injuries require at least a 2 view radiographic study (lateral and VD or DV) of the entire body – DOGOGRAM AND CATOGRAM

–‘Trauma films’ controversial, but have proven beneficial in many severely polytraumatised patients

–Rule out spinal injury and give panoramic view of patient with minimal manipulation compared with specific views

–Specific and special studies are done if indicated and deemed safe

–If not safe, do not underestimate the value of ultrasound

–Can rule out spinal injury but can only do it if its stable

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9
Q

What things can you do as part of ‘A CRASH PLAN’ - secondary survery diagnostics?

A

•All animals with multiple injuries require at least a 2 view radiographic study (lateral and VD or DV) of the entire body – DOGOGRAM AND CATOGRAM

–‘Trauma films’ controversial, but have proven beneficial in many severely polytraumatised patients

–Rule out spinal injury and give panoramic view of patient with minimal manipulation compared with specific views

–Specific and special studies are done if indicated and deemed safe

–If not safe, do not underestimate the value of ultrasound

–Can rule out spinal injury but can only do it if its stable

•Baseline and serial blood samples

–CBC, platelets, total plasma protein, glucose, venous PO2, PCO2, HCO3-,pH, lactate, and all major chemistry analytes including ionised calcium, sodium, potassium and chloride

–Some biochemistry might be important, but blood gas machines will give us a lot of crucial information

•Special noninvasive diagnostic techniques - clipping the thoracic, flank and abdominal hair to detect bruises, and invasive tests including diagnostic peritoneal lavage which is 95% accurate in detecting abdominal haemorrhage or hollow visceral leakage

–Clipping – find holes, bruises etc.

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10
Q

What is the goal of a secondary survey?

A

•Goal of secondary survey - detect all injuries that will lead to life-threatening consequences early enough to prevent serious complications and death

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11
Q

What is the difference between MBSA and full physical exam?

A

Is the patient showing signs consistent with shock?

  • MBSA focussed on cardiorespiratory largely!
  • Pattern of abnormalities in the clinical setting that should be recognised as indicative of decreased tissue perfusion. The following parameters should therefore be assessed and cross-referenced:
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12
Q

When looking for shock - what should you look for with regards to mentation?

What is consistent with shock?

A
  • . Mentation – the brain is an obligate user of oxygen and glucose and has few energy stores. Inadequate delivery of oxygen and glucose to the brain results in loss of the normal mental state in seconds. The following scale may be useful:
  • alert and normally responsive
  • depressed or obtunded
  • stuporous or semicomatose (suggests functional brain disease)
  • comatose (suggests functional brain disease)
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13
Q

When looking for shock - what should you look for with regards to MM colour?

What is consistent with shock?

A
  • Mucous membrane colour - normal colour is salmon pink (cats and horses normally paler than dogs).
  • A pale to white colour is caused by depletion of volume or of haemoglobin. Much darker pink if dealing with sepsis or SIRS
  • A red colour suggests poor perfusion and vasodilatation (blood trapped within the capillary beds) as in sepsis.
  • Cyanosis, which is represented by a blue-purple discolouration, is caused by the presence of >5g/dl deoxygenated haemoglobin. Severe hypoxaemia can occur without cyanosis.
  • Methaemoglobinaemia, associated with paracetamol toxicity in cats, can cause mucous membranes to be pale, cyanotic, and muddy or brown in colour. Sulphaemoglobinaemia can also cause cyanosis. Carbon monoxide toxicity can cause the mucous membranes to be cherry red, although this is a late and unreliable sign.
  • Icterus is indicative of bilirubin, suggesting haemolysis, hepatocellular disease or extrahepatic/intrahepatic biliary tract disease
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14
Q

When looking for shock - what should you look for with regards to CRT?

What is consistent with shock?

A
  • Capillary refill time (CRT) - normally <2 seconds (buccal mucosa refills slightly slower than gingival mucosa). CRT determined by pre-capillary sphincter tone, increases in tone lengthening CRT and decreases in tone shortening CRT
  • Vasoconstriction caused by an increase in sympathetic tone, such as in response to a decrease in circulating blood volume in shock, can cause CRT to be > 2 seconds as can hypovolaemia.
  • Vasodilatation is characteristic of SIRS & sepsis and can result in a shortened CRT.
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15
Q

When looking for shock - what should you look for with regards to pulse evaluation?

What is consistent with shock?

A

–Femoral pulses, is it symmetrical? Move to peripheral pulses

–NO information about blood pressure as pulses are the difference between systolic and diastolic pressure and as such can be an estimate of stroke volume

–Careful palpation of the pulse in patients with compensated hypovolaemia reveals a pulse profile that is taller and narrower than normal reflecting a slightly decreased pulse volume - hyperdynamic or bounding

–More severe hypovolaemia progresses - decompensated hypovolaemic shock

  • global tissue perfusion is severely compromised
  • Increased heart rates (170–220 bpm in dogs)
  • Femoral pulse profile is short and narrow - weak or thready (C) and metatarsal pulses are absent

–Heart rates faster than 220-240 bpm are unlikely sinus tachycardia in response to hypovolaemia - more likely to be a primary tachydysrhythmia.

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16
Q

Describe these pulses and roughly what does each mean?

A
  • A – normal pulse
  • B – compensated shock, a reduction in SV but the body is trying to get it out of the body. Narrow but tall pulse
  • C – decompensated shock, weak, thread pulses
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17
Q

When looking for shock - what should you look for with regards to core extremity temperature difference?

What is consistent with shock?

A

•Normally a temperature difference between central temperature and that of the extremities of less than 8°F or 4°C. Peripheral vasoconstriction causes the temperature in the extremities to approach an ambient level.

–Feel the toes, and note if they are cold. One can measure the extremity temperature in the toe web by placing a thermometer or temperature probe there and compressing the tissue over it. Compare this with the temperature obtained from a central location (usually rectal).

–Be alert for the presence of cold pelvic limbs in cats associated with peripheral cyanosis of the footpads, suggesting a saddle thrombus.

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18
Q

What are some scenarios that will cause hypovolaemia, dehydration and both?

A
  • Terms regarding hydration status are often misused and this is not helpful to us when considering appropriate fluid type and speed of administration
  • Majority of our emergency and critically ill patients are HYPOVOLAEMIC

–They have lost circulation volume and lost fluid from intravascular space

•In longstanding disease animals may be both HYPOVOLAEMIC AND DEHYDRATED

–Dehydration – fluid sucked from cells and interstitial space

  • Dogs left in hot cars and those animals’ with severe burns, DEHYDRATION is likely to be the primary fluid loss (cats with renal failure)
  • We are extremely good at assessing hypovolaemia, but very poor at identifying dehydration
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19
Q

What is dehydration?

How can you assess it?

A
  • Describe a loss of electrolytes and water from the interstitial and intracellular spaces
  • Skin turgor (elasticity) BUT depends on the amount of fluid as well as fat in the skin and subcutaneous tissues – lots of variabilities!

–Does reduce with age as collagen and elastin concentrations change.

–Normally hydrated thin patients, older patients and certain breeds with ‘lots of skin (e.g. Bassett hounds and Sharpei) have decreased skin turgor

–Obese patients have increased skin turgor

–Puppies and kittens have increased total body water, and their skin turgor is normally greater than that of an adult.

•Gently lift the skin over the back just behind the scapula

–let it return to its resting position (normal <2 seconds)

–Slowness of return is correlated to various degrees of dehydration

–Mild – 2-3 seconds (5%)

–Moderate – 3-5 seconds (7%)

–Severe - >5 seconds (12%)

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20
Q

Why should you take care with certain methods of assess dehydration?

How can you overcome these issues?

A
  • Take care in interpreting the skin turgor over the dorsal neck, because the skin in this area normally returns to its resting position more slowly than skin over the back
  • Assess the moistness of the mucous membranes

–That’s okay unless they have increased salivation or they are nauseous – they have moist MM when they shouldn’t – look at cornea and conjunctiva

  • Interpret changes in light of the effects of other conditions, such as nausea, which causes increased salivation, and azotaemia, which causes dry oral mucous membranes
  • Observe the cornea and conjunctivae for moistness suggesting adequate tear production
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21
Q

Distinction between hypovolaemia/ hypovolaemic shock and dehydration – why do we care?

A
  • Will influence order of likely differential diagnoses
  • May change fluid choices

–Certain fluids are contra-indicated in dehydration

–Hypertonic saline not for use in dehydration!

–If hypovolaemic – need to rapidly expand intravascular space. If dehydrated, need to be a slower increase so it has time to diffuse into extracellular spaces and expand this slowly etc.

  • Will change required fluid resuscitation rates
  • Will change DD and treatment choices!
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22
Q

What should we do with regards to pain relief in ECC?

A
  • There is a high likelihood that an emergency or critically ill patient is in pain.
  • Observe the patient’s behaviour and response to stimulation, bearing in mind species and breed differences.
  • Observe for painful responses to manipulation or palpation.
  • Assume that the patient is in pain until proven otherwise especially if you identify a disease or injury that would be painful to you
  • Adequate analgesia also increases the likelihood that a thorough physical examination can be performed – so you can do a better job
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23
Q

What are some things we should consider with active bleeding? e.g. where can it be coming from?

A

•Exsanguinating external bleeding is usually obvious

–examine the entire patient

–palpate with the fingertips in heavily coated patients to identify all wounds and thus likely points of bleeding

  • Substantial bleeding may occur into traumatised soft tissues (e.g. around fracture sites) especially in the smaller patient
  • Nasal haemorrhage usually obvious, but substantial amounts of blood can be swallowed - haematemesis if severe
  • Abdominal organs as highly vascular common source of internal bleeding
  • Bleeding in the thorax may involve multiple sites - lung parenchyma, large or small airways, pericardial sac, pleural cavity
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24
Q

How can you look for active bleeding in a patient?

A
  • If on the outside – simple! If internally and you given fluid bolus, they look brighter and HR comes down etc., then another fluid bolus – they don’t improve too much, then you give another fluid bolus and then they look worse – you have managed to increase BP and they feel better, then you give more and pop the clot and they start bleeding again
  • Signs - Hypoperfusion and the space occupying effects of blood accumulation or excretion of blood in urine or faeces or from the nose.
  • Internal bleeding suspected in patients that respond to initial fluid resuscitation and then deteriorate
25
Q

What are some things that can be evidence of bleeding disorders?

A

•Evidence of bleeding disorders (disease affecting primary or secondary haemostasis) include

–Petechiation

–Haematoma formation in non-traumatised areas

–Re-bleeding or persistent bleeding from venepuncture sites

–Can also commonly occur with sepsis and septic shock

26
Q

What should you look for with an initial neurological assessment?

A

–consciousness

–breathing pattern

–pupil size and responsiveness

–ocular position and movements

–skeletal motor responses

27
Q

How can neurological status relate to hypovolaemia and hypoxaemia?

A
  • In the primary survey need to concentrate on life-threatening conditions
  • Hypovolaemia and hypoxaemia must be recognised and treated

–strongly correlated with increased ICP and increased mortality in human TBI victims

28
Q

What are some things you should look for, for a more detailed part of the secondary survey?

A
  • Once these issues have been addressed then a more complete physical exam can be performed. This should include:
  • Respiratory system
  • Cardiovascular system
  • Head and neck – more neuro
  • Abdomen
  • Genitourinary system – more neuro
  • Musculoskeletal system – more neuro
  • Skin & body surface
  • Lymphatic structures
  • Body temperature
29
Q

What do you see on ultrasound of a pneumothorax?

A
  • Will see thicker parietal pleura
  • Line won’t glide
  • Can allow mapping of extent
  • Choose appropriate position for drain if no radiography
  • Success of treatment
30
Q

What is the key to success with an ECC patient?

A

•During both primary and secondary it is VITAL to repeat your examinations of key systems

–Cardiovascular

–Respiratory

–Neurological

  • Need to quickly identify changes so can act on them
  • Time is the essence to success
  • As is attention to detail!

–Don’t underestimate minor changes

–Especially on physical exam

31
Q

How can SIRS manifest in dogs and cats?

A

•Wide variety of severe clinical insults, manifested by two (dogs) or three (cats) of the following conditions:

32
Q

What is sepsis?

A

•As for SIRS plus infectious agent identified (assumed in veterinary)

SIRS - Wide variety of severe clinical insults, manifested by two (dogs) or three (cats) of the following conditions

33
Q

What is severe sepsis/SIRS?

A

•Sepsis (SIRS) associated with organ dysfunction, hypoperfusion, or hypotension

–Septic peritonitis, pyometras, some GDVs

34
Q

What is refractory (septic) shock/SIRS shock?

A

•Subset of severe sepsis (SIRS) and defined as sepsis (SIRS) induced hypotension despite adequate fluid resuscitation Patients receiving inotropic or vasopressors may no longer be hypotensive yet they would still be considered to have septic (SIRS) shock

35
Q

What is multiple organ dysfunction syndrome?

A
  • Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
  • Results in death a lot! Poor prognosis
36
Q

Define shock

A

•Inadequate cellular energy production

–Most commonly secondary to poor tissue perfusion

  • Low or unevenly distributed blood flow
  • Leads to critical decrease in oxygen delivery (DO2) compared to oxygen consumption in the tissues (VO2)
37
Q

What is hypovolaemic shock?

A

•Hypovolaemic (decreased circulating blood volume)

–Fluid loss from intravascular space

–Trauma

–Haemorrhage

38
Q

What is cardiogenic shock?

A

•Cardiogenic (decreased forward flow from the heart)

–Congestive heart failure

–Cardiac dysrhythmias

–Cardiac tamponade

–Drug overdose (anaesthetic agents, beta-blockers, calcium channel blockers)

–Tricky – If you fluid overload, end up with ascites and/or pulmonary oedema – controlled amounts of fluid are needed

39
Q

What is distributive shock?

A

•Distributive (loss of systemic vascular resistance)

–Sepsis

–Obstruction (saddle thrombosis, heartworm)

–Anaphylaxis

40
Q

What is metabolic shock?

A

•Metabolic (deranged cellular metabolic machinery) – rare, or we are poor at identifying it

–Hypoglycaemia

–Cyanide toxicity

–Mitochondrial dysfunction

–Cytopathic hypoxia of sepsis

41
Q

What is hypoxaemic shock?

A

•Hypoxaemic (decreased oxygen content in arterial blood)

–Anaemia

–Severe pulmonary disease

–Carbon monoxide toxicity

–Methaemoglobinaemia

–Fluids good initially but then often require blood!

42
Q

What is cryptic shock?

A

•Cryptic (normal global circulation but poor microcirculation)

–SIRS

–Sepsis

–Capillary beds shut down, manage with fluids but who knows if there are better things

43
Q

What is the most common manifestation of shock?

A

•Due to reduced oxygen delivery

–One of three mechanisms

–Loss of intravascular volume (hypovolaemic shock)

–Maldistribution of vascular volume (distributive and cryptic shock)

–Failure of the cardiac pump (cardiogenic shock)

44
Q

What is the initial diagnosis of shock?

A

•Reduced perfusion

–CV instability

–Other PE findings

–Point of care testing

–Should then initiate therapy

•Should be

–RAPID

–AGGRESSIVE

–APPROPRIATE MONITORING

–REMOVAL OF UNDERLYING CAUSE(S)

–If want successful outcome

45
Q

What is the clinical presentation of hypovolaemia?

A

–Underlying diseases

•Blood loss

–Internal or external

•Loss of other body fluids

–D++, V++, PU, burns

–The heart

  • Dec CO – reduced venous return triggers compensatory mechanisms
  • Increased sympathetic activity
  • Vasoconstriction
  • Inc contractility
  • Increased HR
  • CO=SVxHR
46
Q

What happens during hypovolaemic shock?

A

–Extreme vasoconstriction and changes in microcirculation

•Mobilisation of fluid from interstitial and extracellular spaces to IV space

–Dec renal circulation

  • Activates RAAS
  • Further upregulates SNS
  • Na and H2O retention due to increased production of aldosterone and ADH

–Since net effect of all these changes increases intravascular volume

•Signs subtle initially

47
Q

What are the initial, mild signs of hypovolaemic shock?

A

–Mild to moderate depression

–Tachycardia with normal to prolonged CRT

–Cool extremities

–Tachypnoea

–Normal blood pressure

–Pulse quality normal

–COMPENSATED SHOCK

48
Q

What are the clinical signs of ongoing compromise of hypovolaemic shock?

A

–Compensatory mechanisms inadequate and fail

–Pale mucous membranes

–Poor peripheral pulse quality

–Depressed mentation

–Fall in blood pressure

–DECOMPENSATED SHOCK

49
Q

What is the hyperdynamic phase of shock?

A
  • Tachycardia
  • Fever
  • Bounding peripheral pulses
  • Hyperaemic mucous membranes secondary to cytokine (NO) mediated peripheral vasodilatation
  • Also referred to as vasodilatory shock
50
Q

What causes progression of shock into septic shock/SIRS?

What are clinical signs?

A

•Due to cytokine effects on the myocardium

–Decreased CO

–Signs of Hypoperfusion

•Clinical signs

–Tachycardia

–Pale/ icteric

–Prolonged CRT

–Significantly reduced mentation

•Hypodynamic shock

–Organ dysfunction and death

51
Q

What is the shock organ in a dog (and cow)?

What does it cause?

A

•Dog

–GI tract (and cow) – shock organ

–End up with: Ileus, diarrhoea and melaena

52
Q

What is the shock organ in a cat?

What does it cause?

A

•Cat

–Rarely see hyperdynamic phase

–Changes in heart rate unpredictable cf dogs/horses- tachy or bradycardia!!

–Pale/icteric MM, weak pulses, cold extremities, hypothermia and generalised weakness/ collapse

–Lung – shock organ – resp dysfunction

53
Q

What happens with a GDV?

What is compromised and what kind of shock do you get?

A
  • Normal (ish) circulating blood volume (usually if present early)!
  • Compression of major vessels because of distended stomach which:

–Decreased venous return

–Reduced CO

–End up with relative hypovolaemia, got blood but not getting blood out of the thorax

  • Complex mix of types of shock
  • Then they often have cryptic shock
  • Hypovolaemic shock – blood loss secondary to rupture of short gastric vessels
54
Q

What kind of shock do you get with septic peritonitis?

A
  • Distributive – tissue hypoxia secondary to SVR (systemic vascular resistance)
  • Hypovolaemic – especially if has severe cavitatory effusions or severe/ prolonged vomiting

–Dump loads of fluid into abdominal cavity

55
Q

What is the diagnosis and monitoring for shock?

A

•Basic tests for all shock patients

–Extent of organ injury

–Aetiology of shock state

  • Lactate
  • Haematology
  • Biochemistry
  • UA
  • (Coagulation panel and blood typing)
56
Q

Once the ECC patient is stabilised, how should we go forward with monitoring?

A
  • Full and repeated MBSA
  • Thoracic and abdominal ultrasonography and radiography
  • Echocardiography
  • ECG
  • BP monitoring
  • Pulse oximetry
57
Q

How can you monitor tissue perfusion and oxygen delivery?

What is it like in a well perfused patient?

A
  • Magnitude of tissue oxygen deficit key predictor in outcome
  • Optimising oxygen delivery and tissue perfusion goal of treatment
  • Well perfused patient:

–CVP – 5-10 cm H2O (2-5 cm H2O – cats)

–Urine production – 1 ml/kg/hr

–MAP – 70-120 mmHg

–N HR, RR, temp, pink MM, CRT <2 secs

58
Q

In BRIEF summary - what is the treatment of shock?

A
  • Early recognition
  • Rapid restoration of CV function
  • Normalise tissue oxygen delivery as soon as possible
  • For all types of shock (except cardiogenic and perhaps cryptic)

–Mainstay

–Large volumes of IV fluids

–Short, large bore catheters

•Ideally central (IO) rather than peripheral vv