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FCP Week 5 > Triage and Shock > Flashcards

Triage and Shock Flashcards

1
Q

What is triage (2)

A

Processofquicklyexaminingpatientswho are taken to todecidewhichonesare the mostseriouslyilland must betreatedfirst
Processofexaminingproblemsinordertodecidewhichonesare the mostseriousand must bedealtwith first

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2
Q

What is shock

A

Inadequate cellular energy
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)

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3
Q

Signs of shock (4)

A

Altered mentation
Mucous membranes- pale to white or red
Capillary refill time >2 seconds (could also be shorter in SIRS & sepsis)
Cold extremities
Weak pulse

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4
Q

Why does mentation change in sock

A

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

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5
Q

Descriptions used to describe mentation (4)

A

Alert and normally responsive
depressed or obtunded
stuporous or semi comatose (suggests functional brain disease)
Comatose (suggests functional brain disease)

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6
Q

Normal colour of mucous membrane (and how different in cats/horses)

A

Salmon pink
Cats/horses- normally paler

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7
Q

What does red mucous membranes suggest

A

Poor perfusion and vasodilation (blood trapped within the capillary beds) as in sepsis (or SIRS)

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8
Q

How is CRT different in different locations

A

buccal (lips/cheek) mucosa refills slower than gingival (gums) mucosa

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9
Q

What determines CRT

A

Pre-capillary Sphincter tone
increase in tone-> lengthening CRT (and vice versa)

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10
Q

What does pulse evaluation tell us

A

Estimation of stroke volume
Pulse gives us the difference between diastolic and systolic pressure- no info about blood pressure
Weak pulse= hypovolaemia

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11
Q

What is a hyperdynamic or bounding pulse and when does it occur

A

In early, compensated hypovolaemia
Pulse profile that is taller and narrower than normal reflecting decreased pulse volume, the heart is having to work harder
can also be due to increase CO as a result of increased oxygen demand e.g. after exercise

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12
Q

What happens as severe hypovolaemia progresses

A

Becomes decompensated hypovolaemic shock
Global tissue perfusion severely compromised
Increased heart rate (170-220bpm in dogs)
Femoral pulse is short and narrow- weak or thready and metatarsal pulses are absent- metatarsal lost first

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13
Q

What is SIRS

A

Systemic Inflammatory Response Syndrome
Wide variety of severe clinical insults manifested by 2 (dogs) or three (cats) of altered parameters (see one note for table)
Look at: HR, Temp, Resp. rate/ PaCO2 and WBCC

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14
Q

What is Sepsis

A

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

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15
Q

What is severe sepsis/SIRS

A

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

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16
Q

What is multiple organ dysfunction syndrome (MODS)

A

Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
Last phase, normally just before death

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17
Q

What is refractory (septic) shock/ SIRS shock

A

Subset of severe sepsis (SIRS)
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

18
Q

What is hypovolaemic shock

A

Decreased circulating blood volume
- Fluid loss from intravascular space
- Trauma
- Haemorrhage

19
Q

What is cardiogenic shock

A

Decreased forward flow from the heart
- Congestive heart failure
- cardiac dysrhythmias
- cardiac tamponade (compression of heart)
- Drug overdose (anaesthetic agents, beta-blockers, calcium channel blockers)

20
Q

What is distributive shock

A

Loss of systemic vascular resistance
- sepsis
- obstruction (saddle thrombis, heartworm)
- anaphylaxis

21
Q

What is metabolic shock

A

Deranged cellular metabolic machinery
Hypoglycaemia
Cyanide toxicity
Mitochondrial dysfunction
Cytopathic hypoxia of sepsis

22
Q

What is hypoxaemic shock

A

Decreased oxygen content in arterial blood
- Anaemia
- Severe pulmonary disease
- Carbon monoxide toxicity
- Methaemoglobinaemia

23
Q

What is cryptic shock

A

Normal global circulation/ parameters but poor microcirculation- oxygen and glucose transport from capillaries into cells
- SIRS
- Sepsis

24
Q

What is most common type of shock

A

Combines
Commonly hypovolaemic and distributive (and cryptic)

25
Q

Most common mechanisms causing reduced oxygen delivery

A

Loss of intravascular volume (hypovolaemic shock)
Maldistribution of vascular volume (distributive and cryptic shock)
Failure of the cardiac pump (cardiogenic shock)

26
Q

Examples of underlying diseases taht casue hypovolaemia

A

Blood loss- internal or external
Loss of other body fluids- burns, Diarrhoea. vommiting etc.

26
Q

Examples of underlying diseases taht casue hypovolaemia

A

Blood loss- internal or external
Loss of other body fluids- burns, Diarrhoea. vommiting etc.

27
Q

How does the heart compensate in hypovolaemic shock

A

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

28
Q

Compensatory mechanisms to increase IV volume in hypovolaemic shock (venous and renal)

A

Extreme vasoconstriction and changes in microcirculation- mobilisation of fluid from interstitial and extracellular spaces to IV space
Decreased renal circualtion
-> activates RASS
-> upregulated SNS
-> Na and H2O retention due to increased aldosterone and ADH

29
Q

Signs of compensated shock

A

Mild to moderate depression
Tachycardia with normal to prolonged CRT
Cool extremities
Tachypnoea
Normal blood pressure
Pulse quality normal

30
Q

Signs of decompensated shock

A

Compensatory mechanisms inadequate and fail
Pale mucous membranes
Poor peripheral pulse quality
Depressed mentation
Fall in blood pressure

31
Q

What is oliguria

A

Low urine output

32
Q

Does sepsis lead to hypovolaemic shock

A

no
leads to distributive shock

33
Q

what is the hyperdynamic phase of shock

A

Abnormally increased circulatory volume

34
Q

Signs of hyperdynamic phase of sock

A

tachycardia
fever
bounding peripheral pulses
hyperaemic (increase blood flow) mucous membranes secondary to cytokine (NO) mediated vasodilation
Also referred to as vasodilatory shock

35
Q

Shock organ for dogs

A

GI tract
see ileus, diarrhoea and melaena

36
Q

what is melaena

A

the production of dark sticky faeces containing partly digested blood, as a result of internal bleeding or the swallowing of blood.

37
Q

What is shock organ of cat

A

lungs
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

38
Q

What is shock organ of cow

A

GI- same as dog

39
Q

How can pulse be used to estimate stroke volume

A

Stroke volume is the amount of blood ejected by the heart with each beat. The pulse and stroke volume are related, and changes in pulse can give an estimation of stroke volume.
by measuring the pulse and assessing its strength, it is possible to estimate the stroke volume.
This is often done using a technique called pulse pressure analysis, which involves measuring the difference between the systolic blood pressure (the highest pressure generated by the heart during a contraction) and diastolic blood pressure (the lowest pressure between contractions). The pulse pressure is then used as an indicator of stroke volume.

40
Q

What is cytopathic hypoxia

A

Cytopathic hypoxia is a type of tissue hypoxia that can occur in sepsis,
In sepsis, the body’s immune system releases a variety of chemicals that can damage the lining of blood vessels, leading to a decrease in blood flow to vital organs such as the lungs, liver, and kidneys -> the cells in these organs are unable to use the available oxygen to produce energy due to damage to their internal machinery caused by the immune system chemicals. This leads to cellular dysfunction and can contribute to the development of organ failure in sepsis.

it is thought to involve a combination of factors, including impaired mitochondrial function, altered metabolic pathways, and oxidative stress.
Treatment of sepsis typically involves aggressive management of the underlying infection, supportive care, and interventions to improve tissue oxygenation and prevent organ dysfunction

FCP Week 5 (12 decks)

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