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SA ER Med > Midterm > Flashcards

Midterm Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

What’s a general breakdown of Vet emergencies?

A

10% true emergencies

40% non life-threatening ERs

50% Client ERs

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2
Q

Difference between GP and ER

A
  • GP: Ps tx’ed in series
  • ER: Ps tx’ed in parallel
  • GP: Client-patient relationship present, ER absent
  • GP has med hx, ER typically doesn’t
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3
Q

What must you know in ER?

A
  • how to recognize and tx shock
  • CPR
  • Critical Respiratory Resuscitation
  • how to stop hemorrhage
  • how to stop a seizure

and more

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4
Q

What are the greatest sources of stress in regards to emergency medicine

A
  • global terror (anxiety before the case even comes in)
  • personal confidence (“Am I capable of this?”)
  • client confidence (“Is this vet even qualified?”)
  • communication
  • difficult cases
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5
Q

What are the key things to communicate?

A
  • This is what I know
  • this is what I don’t
  • this is what I need to find out
  • this is what I need to do to find out

Project confidence, but be realistic, and don’t set up false hopes

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6
Q

What are the expectations of ER med?

A
  • be prepared
  • have basic procedure skills
  • stay current
  • triage the patient
  • stabilize the patient
  • Treat within your means or transfer to ER/CC
  • communicate w/ client
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7
Q

what are the three types of telephone calls?

A
  • obvious ERs (any problem O considers an ER)
  • obvious non-ERs (try to talk to O, but if they want to be seen, it’s ultimately their choice
  • Everything in-between (refusing to see an animal is bad policy; if you’re not sure if P should be seen, recommend it be evaluated)
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8
Q

What kind of things can you tell the client?

A
  • number for poison control- call ahead
  • directions- have posted near phone
  • bring samples (vomit, diarrhea, etc.)
  • apply pressure to bleeding wounds
  • mouth to snout resp 10-12x/ min
  • don’t remove the penetrating object!
  • don’t pull string from the mouth or anus!!
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9
Q

Important points of intro to ER

A
  • in ER, often no doctor-client-patient relationship
  • cannot dx a condition and/or Rx tx over the phone
  • you can make recommendations for first aid for transport to the hospital
  • remind Os that Ps are seen in order in which they REQUIRE care, not order of arrival. O doesn’t determine order, we do
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10
Q

What is triage?

A
  • the evaluation of patients to DETERMINE URGENCY and to prioritize cases for further care by the veterinary staff
  • to guide allocation of limited resources to selected individuals within a group
    (a way to maximize the # of survivors)
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11
Q

What are the important points of In-hospital triage?

A
  • capsule hx
  • Utilize the ABC’s of ER care (airway, breathing, circulation)
  • Add D and F (dysfunction of CNS; freaked-out client)
  • goal: P stable/unstable?
  • determine urgency of further therapy
  • add to order to be seen
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12
Q

What emergencies require immediate attention?

A
  • respiratory distress
  • signs of hypovolemic shock
  • cardiopulmonary arrest
  • unconscious or altered LOC
  • ongoing seizure activity
  • trauma
  • dystocia
  • burns
  • exposure to toxins
  • severe hypothermia / hyperthermia
  • open fractures
  • dehiscence
  • prolapsed organs
  • excessive bleeding
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13
Q

So… what exactly is shock?

A
  • inadequate O2 delivery to the tissues, which can result in cellular damage and death if untreated
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14
Q

Why is O2 so important?

A

body creates more energy (ATP) with O2 than w/o

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15
Q

What is the main job of tlhe Cardiovascular system?

A

to deliver O2 and nutrients to the tissues

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16
Q

What results in O2 deficiency?

A
  • hypovolemic shock
  • distributive shock
  • cardiogenic shock
  • obstructive shock
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17
Q

What is hypovolemic shock? what can cause it?

A
  • decreased volume

- hemorrhage, dehydration, hypoproteinemia

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18
Q

What is distributive shock?

what can cause it?

A
  • abnormal distribution in small vessels to organs
  • form of hypovolemic shock
  • sepsis, SIRS, hyperthermia, seizures
19
Q

what is cardiogenic shock?

What causes it?

A

pump failure

cardiac dz

20
Q

what causes obstructive shock?

What can cause it?

A

obstruction of flow

GDV, ATE

21
Q

So how does the body detect hypovolemia?

A
  • there are baroreceptors and stretch receptors in the aorta and carotid artery
  • volume receptors kidney and heart
22
Q

At what volume loss does a signficant response to hypovolemia occur? What happens

A

25% (10-15 ml/kg)

a neuro signal is sent to the brain increasing HR, myocardial contractility and vascular tone

23
Q

What happens when the baroreceptors are not stretched?

what does this lead to?

A
  • catecholamine release (epi/norepi)
  • incr. HR and contractility
  • incr. systemic resistance (arterial & venous)
  • all result in incr. CO and
  • RASS incr. water retention -> incr. volume

all of this leads to the compensatory stage of shock

24
Q

Signs of compensatory shock

A
  • (often missed)
  • tachycardia, incr. HR
  • bounding pulses
  • P is alert
  • Rapid CRT
  • normal to incr. BP
  • maybe slight tachypnea
  • MM hyperemic, bright pink/red
25
Q

What happens when the baroreceptors fail to stretch during / in response to compensatory shock?

A
  • now its survival of the fittest
  • signficant incr. HR and peripheral vasoconstriction
  • blood is resdistributed to vital organs (brain, heart, and AWAY from skin, MM, and abd. organs)
  • O2 demand incr., Incr. BG, Incr. ATP

leads to early decompensatory stage

26
Q

Signs of early decompensatory shock

A
  • tachycardia, tachypnea
  • weak pulses, prolonged CRT
  • pale MM
  • obtundation
  • hypotension
  • hypothermia
  • oliguria
27
Q

But the body needs that blood to function. How does it respond to that shunting?

A

GI: microulcers, bacterial translocation (GIT is shock organ of DOGS)

Liver: cholestasis

Heart: myocardial ischemia

Lungs: microvascular shunting (Lung is shock organ in CAT)

Kidney: shunt from cortical nephrons to juxtomedullary nephrons-> oliguria when MAP < 60 mmHg

28
Q

We’re now in early decompensatory shock, but we’re not seeing improvement. what is the body going to do?

A
  • local tissue hypoxia
  • inflammatory response
  • local system overrides-> vasodilation and maldistribution of blood
  • vessels become leaky
  • blood is redirected from core to periphery

this leads to late decompensatory shock

29
Q

Signs of Late Decompensatory shock

A
  • normal to decr. HR
  • hypothermia
  • Poor to absent pulses
  • White MM
  • Absent CRT
  • stupor, coma
  • oliguria, anuria
30
Q

What do we also see with late decompensatory shock

A
  • massive decr. in Intravascular volume
  • complete vascular collapse -> no blood to brain/heart
  • cell membrane swelling and death
  • organ failure
  • death
31
Q

So cats are NOT small dogs. What should we keep in mind?

A
  • we will NOT see the compensatory stage
  • with hypothermia, peripheral vasculature loses responsiveness to catecholamines
  • cats SHOULD BE WARMED PRIOR to aggressive fluid resuscitation
32
Q

What is the kitty triad of shock?

A

When they present with shock they will commonly also be:

  • hypothermic
  • hypotensive
  • bradycardic
33
Q

Okay so now we can recognize hypovolemic shock. Now what?

A

the key to successful tx is rapid recognition and aggressive fluid therapy

34
Q

what are the goals of treatment of shock

A
  • restore O2 delivery to the tissues
  • improve intravascular volume
  • improve vascular tone
  • improve cardiac function and output
35
Q

What immediate intervention do we engage in with treating shock?

A
  • O2 supplementation
  • establish venous access
  • provide analgesia
  • fluid adminstration
  • address the underlying problem
36
Q

Why is O2 supplementation important?

A
  • it must be provided to all shock patients in the initial treatment phase until you determine exactly what is going on with the patient

methods of provision:
- mask, flow-by, nasal, O2 cage/hood

37
Q

Types of venous access

A

IV catheter (large bore, short catheter, multiple catheters in large dogs, can utilize cut down if needed)

IO catheter

38
Q

Importance of analgesia

A
  • pain/anxiety MAGNIFY the effects of shock
  • use pure opioids (hydro or morphine; they’re reversible (?))
  • titrate to effect
  • do NOT use NSAIDS
  • do NOT use Alpha-2 Agonists
39
Q

so why do we give fluids?

A
  • dehydration

- decreased perfusion

40
Q

What does colloid oncotic pressure (COP) do?

A

pulls fluid to higher COP

41
Q

what does hydrostatic pressure (HP) do?

A

pushes fluids out, related to BP

42
Q

importance of membrane permeability

A

fluid can leak through the membrane

43
Q

difference between capillary walls and cell membranes

A

water and small molecules move freely through the capillary wall

water can move freely through cell membrane, but small ions must be pumped through cell wall by active transport (which requires energy)

44
Q

Overview of isotonic crystalloids

A
  • LRS, plasmalyte, 0.9% saline, Normosol-R
  • H20 base, similar to osmolality to blood
  • Na+ compared to intracellular Na+ determines “tonicity”
  • “balanced” by buffers (lactate, acetate, gluconate); similar to blood pH 7.4
  • small MW particles- freely move across capillary membrane results in INTERSTITIAL volume replacement

SA ER Med (1 decks)

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