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VTS(ECC) Preparation > Shock, stabilisation & venous access > Flashcards

Shock, stabilisation & venous access Flashcards

1
Q

Define collapse

A

A sudden loss of postural tone sometimes accompanied with L.O.C

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2
Q

What is the basic definition of syncope?

A

Transient loss of consciousness due to global cerebral hypoperfusion caused by an acute drop in systemic BP.

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3
Q

What are the three classifications of syncope? What are some examples of what causes each?

A
  1. Cardiac: bradyarrhythmia (SSS, 2/3 AVB, A Standstill), tachyarrhythmia (AFib, vtach, atach), Structural (Thrombosis, stenosis, AV valve disease, DCM)
  2. Reflex-mediated: neurocardiogenic (stress, fear, pain), situational (excitement, increased activity, coughing, vomiting, defecating), carotid sinus hypersensitivity (baroreceptor dysfunction [fainting collie, genetic mutation], cervical neoplasia)
  3. Orthostatic: drug-induced hypotension, volume depletion
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4
Q

How does to BJ Reflex said to cause syncope?

A

A drop in BP (‘perceived’ hypovolaemia) is sensed by baroreceptors in the carotid sinus, which augments activity of the efferent sympathetic fibers causing increased heart rate, increased contractility and vasoconstriction. This leads to an underfilled ventricle which causes stimulation of the mechanoreceptors in the ventricular wall to send impulses via afferent C-fibers to the medulla oblongata (brain). There is then sudden withdrawal of sympathetic tone and increased vagal tone resulting in paradoxical bradycardia, hypotension, reduced contractility causing syncope.

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5
Q

What is the typical length of a syncopal event and how may it differ from a seizure?

A

Seconds to minutes. Usually patients completely recover whereas seizure patients may be mentally inappropriate and take some time to return to normal.

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6
Q

What monitoring/diagnostics are involved in the work up of the collapsed patient?

A
  • BP
  • ECG
  • Holter study
  • Echocardiogram
  • Neurological exam
  • Biochemistry
  • T4
  • Cardiac enzymes
  • CBC
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7
Q

When does shock occur?

A

When tissue oxygenation consumption (VO2) exceeds tissue oxygen delivery (DO2). Thus there is inadequate oxygenation and anaerobic metabolism.

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8
Q

Activation of the renin-angiotensin-aldosterone system occurs in response to:
a. volume overload
b. decreased baroreceptor firing
c. respiratory distress
d. kidney failure

A

b.

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9
Q

In a giant-breed dog suffering from hypotension and hypovolemic shock, which of the following fluids will provide the fastest physiological response in the patient to increase intravascular volume?
a. Hypertonic saline
b. Lactated Ringer’s solution
c. Synthetic colloid
d. Packed red blood cells

A

a.

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10
Q

This test is used to determine platelet function.
a. Platelet estimate
b. PT
c. aPTT
d. BMBT

A

d.

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11
Q

How is hypoxia defined?
a. When metabolic demand is less than oxygen delivery
b. When metabolic demand exceeds oxygen delivery
c. When partial pressure of oxygen and oxygen saturation are equal
d. When partial pressure of oxygen and oxygen saturation are unequal

A

b.

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12
Q

Which answer best describes cardiogenic shock?
a. A physical obstruction in the circulatory system
b. Decreased intravascular volume
c. Inability of the heart to maintain a normal cardiac output
d. Frequently associated with decreased systemic vascular resistance

A

c.

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13
Q

Which of the following is not a cause of type B hyperlactatemia?
a. Systemic disease
b. Toxicity
c. Inherited disease
d. Poor perfusion

A

d.

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14
Q

Which of the following is not associated with volume overload?
a. Pulmonary edema
b. Chemosis
c. Decreased skin turgor
d. Increase in respiratory rate or effort

A

c.

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15
Q

A patient has a heart rate of 150^bpm and a systolic blood pressure of 90^mmHg. Calculate the patient’s shock index.
a. 60
b. 13^500
c. 0.6
d. 1.6

A

d.

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16
Q

Nasal oxygen flow rates via a cannula should be:
a. 50–150^mL/kg/min
b. 50–150^ml/kg/h
c. always 1–2^L/min
d. 200–500^mL/kg/min

A

a.

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17
Q

Which of the following does not contribute to delivery of oxygen to tissue?
a. Blood pressure
b. Cardiac output
c. Hemoglobin
d. PaO2

A

a.

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18
Q

Solutions of greater than how many milliosmoles should only be given through a central venous catheter?
a. 300^mOSm
b. 450^mOSm
c. 600^mOSm
d. 750^mOSm

A

c.

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19
Q

Which catheter type and length should have the most maximal flow?
a. 18 G × 2”
b. 18 G × 1¼”
c. 20 G × 2”
d. 20 G × 1¼”

A

b.

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20
Q

In which patient would a central venous catheter potentially be contraindicated?
a. A cat with DKA
b. A dog with Evans syndrome
c. A hypoglycemic puppy on 7.5% dextrose
d. A cat receiving IV chemotherapy

A

b.

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21
Q

When Virchow’s triad is applied to IV catheters, which of the following can be a cause of thrombosis?
a. Endothelium damage
b. Hypercoagulation
c. Turbulent flow
d. All of the above

A

d.

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22
Q

Winged or butterfly catheters are contraindicated for which use?
a. Long-term use
b. Blood draws
c. Cortrosyn administration
d. Subcutaneous fluid administration

A

a.

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23
Q

In anticipation of a patient’s needs, when is an IO catheter indicated?
a. Hemodynamically stable seizure patient
b. 1^kg kitten with hypovolemia
c. 45^kg GDV
d. Six-month-old Shepherd for OVH

A

b.

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24
Q

Over-the-needle intravenous catheters should be left in place:
a. no longer than 48 hours
b. no longer than 72 hours
c. as long as there are no complications with the insertion site
d. only if the patient is receiving intravenous fluids

A

c.

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25
Q

Which of the following can occur when pulling the catheter back over the needle after partially advancing it into a vessel?
a. Extravasation
b. Air embolism
c. Catheter embolism
d. Thrombosis

A

c.

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26
Q

A patient requiring simultaneous infusions of several drugs will most likely benefit from:
a. a multilumen catheter
b. a PICC line
c. a butterfly catheter
d. an over-the-needle peripheral catheter

A

a.

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27
Q

The first step to proper intravenous catheter placement is:
a. appropriate contact time with scrub solutions
b. shaving all the way around the limb
c. placement of a tourniquet to occlude the vessel
d. the placer washes their hands with soap and water

A

D

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28
Q

What are the four broad categories of shock?

A
  1. Hypovolaemic
  2. Cardiogenic
  3. Distributive
  4. Obstructive
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29
Q

What is the calculation for O2 content in arterial blood (CaO2)?

A

CaO2 = (1.36 X [Hb] X SaO2) + (0.003 x PaO2)

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30
Q

How can maldistribution of blood flow occur?

A
  • peripheral vasoconstriction
  • catecholamine release
  • release of vasoactive substances
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31
Q

If microcirculatory perfusion failure persists, what are some of the consequences?

A
  • Platelet aggregation
  • Impaired capillary perfusion
  • Decreased blood flow
  • Sludging of blood
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32
Q

When there is endothelial injury due to trauma there is exposure of endothelial tissue factor. What are consequences of this?

A
  • promotion of release of inflammatory mediators
  • stimulates procoagulant response
  • further exacerbation of systemic inflammation
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33
Q

When there is decreased delivery of O2, cyclo-oxygenase stimulates the production of 1) _______. This causes 2) ____________. Lipoxygenase stimulates the production of 3) ______. This causes 4) _________. Neutrophils release lysosomal enzymes and reactive oxygen species which 5) _________. If DO2 remains impaired these cascades perpetuate themselves leading to 6) ___________.

A
  1. Thromboxane
  2. Vasoconstriction, platelet aggregation
  3. leukotrienes
  4. stimulation of systemic inflammatory response through the activation and mobilisation of neutrophils.
  5. cause further cellular damage, oedema formation, impairment of oxygen diffusion from local capillary beds, and excessive endothelial tissue permeability.
  6. SIRS -> MODS -> Death
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34
Q

What is the target objective in shock patients?

A

Optimising DO2

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35
Q

What is the traditional shock rates for dogs and cats

A

Dogs 90ml/kg
Cats 60ml/kg

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36
Q

What is the general rule of delivering shock rates to veterinary patients?

A
  • initial bolus of 20-50% of shock rate
  • reassess perfusion parameters
  • additional fluid resuscitation (incrementally) until resuscitation end-points met.
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37
Q

If a patient is non-responsive to fluid boluses what are the likely causes?

A
  • Haemorrhage
  • cardiogenic shock
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38
Q

Haemorrhage is the most common form of refractory shock. Initially due to splenic contraction PCV 1) _____ and TP 2) _______. After fluid resuscitation, PCV 3) __________ and TP 4) __________.

A
  1. Normal
  2. Low
  3. Low (<30)
  4. Low (<35)
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39
Q

When there is severe haemorrhage non-responsive to fluid resuscitation what should be considered?

A
  1. HTS
  2. Blood products
  3. Colloids
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40
Q

1) ____ is the primary carrier of oxygen. It is approximately 2) ______ of the PCV. Signs of low 3) _____ are 4) ____.

A
  1. Hb
  2. 1/3
  3. Hb
  4. Tachycardia, tachypnoea, bounding/weak pulse, reduced mentation, hypotension, and arrhythmias.
41
Q

What is the definition of anaphylaxis?

A

Acute, severe generalised or systemic reactions that are rapid onset, can be life-threatening or fatal, and occur suddenly after contact with an allergy causing substance.

42
Q

Acute local hypersensitivity reactions are _________. They cause ________.

A
  • restricted to cutaneous abnormalities
  • erythema, urticaria, pruritis, angioedema
43
Q

Acute generalised or systemic reactions are ______. Some symptoms include __________.

A
  • ones that show signs of systemic inflammation.
  • dizziness, hypotension, tachycardia, nausea/vomiting, collapse, dyspnoea, hypoxaemia, altered mentation, stridor.
44
Q

What is the general pathophysiology of Type I hypersensitivity reactions?

A

exposure to antigen > increased IgE antibodies bind to mast cell + basophils > re-exposure to antigen > cross-linking of adjacent IgE > mast cell degranulation > vasoactive mediator release and release of PAF > vasodilation, tachycardia, hypotension, increased vascular permeability, enhanced PLT aggregation, histamine release.

45
Q

What are the systems most commonly affected by anaphylaxis?

A
  • cardiovascular
  • integument
  • respiratory
  • gastrointestinal
  • neurological
46
Q

What is considered first-line treatment in anaphylaxis? What does this medication do?

A
  • epinephrine/adrenaline
  • a1 adrenergic effects: potent vasocinstriction of small arterioles
  • b1 adrenergic effects: increased contractility
  • b2 adrenergic effects: alleviate respiratory signs, decrease histamine release.
  • decreases mediator release from mast cells
47
Q

Glucocorticoids should be used as a first line treatment in anaphylaxis?

A

False, can take hours to take effect. Adrenaline first line treatment.

48
Q

When are antihistamines indicated in anapylaxis?

A

Cutaneous reactions

49
Q

What is the definition of shock?

A

Inadequate delivery of oxygen tissues leading to tissue perfusion and cellular O2 debt.
VO2 exceeds DO2 and there is a measurable change in organ function.

50
Q

Tissues can offset a decrease in DO2 by 1) ________. Normally 2) ______ is extracted from arterial blood but can go up to 3) _______. Despite this ability, ongoing decreased DO2 eventually leads to 4) ________.

A
  1. Increasing O2 extraction from arterial blood.
  2. 25%
  3. 70-80%
  4. Ischaemia and cellular hypoxia
51
Q

What are the consequences of cellular acidosis?

A
  • protein degradation
  • diminished enzyme function
  • disruption of transport mechanisms
  • ion pump failure
52
Q

What occurs in the initial phase of shock?

A

Body attempts to restore tissue perfusion by increasing O2 extraction, activation of SNS. Baroreceptors sense decreased vessel wall distension and chemoreceptors detect hypoxia, hypercapnoea and acidaemia. Catecholamines are released causing periph constriction, tachycardia, increased contractility which results in increased CO and SVR which restores MAP. Activation of RAAS and vasopressin release causes further vasoconstriction. In hypovolaemic patients a drop in hydrostatic pressure shifts fluids from interstitium into circulation to improve circulating volume.

53
Q

What happens during the early decompensatory phase of shock?

A

There is evidence of impaired core perfusion i.e. hyperlactataemia and hypotension. Catecholamines continue to be released and there is exhaustion of compensatory mechanisms resulting in vasodilation and bradycardia. There is also loss of vasomotor tone and therefore poor blood flow to ‘non-essential organs’, reduced CO and reduced venous return.

54
Q

What happens during decompensatory phase of shock?

A

Compensatory mechanisms exhausted. Cardiovascular collapse, death.

55
Q

How does SIRS occur?

A

Happens secondary to widespread tissue ischaemia or reperfusion injury and upregulation of inflammatory cytokines, also infiltration of neutrophils.

56
Q

In relation to SIRS, 1) _______ sticking to endothelium plugs capillaries causing obstruction of 2) _______. Neutrophils release 3) _________ that cause 4) __________.

A

1) Neutrophils
2) microcirculation
3) reactive oxygens, nitrogens and proteolytic enzymes
4) Vasodilation, increased capillary permeabilitity and destruction of the extracellular matrix.

57
Q

In relation to SIRS, the leaking of protein and fluid into the interstitium leads to _____.

A
  • tissue oedema
  • disturbance of metabolite and oxygen exchange
  • cellular swelling and dysfunction
58
Q

Activation of the complement system causes _______

A
  • increased vascular permeability
  • split-product release
  • increased inflammatory mediator release i.e. histamine, cytokines, granulocytes
59
Q

In relation to SIRS, hypoxic cellular injury stimulates _____

A

production of leukotrines and prostaglandins that recruit inflammatory cells, PLT aggregation and activity, and alter vascular permeability and vasomotor tone.

60
Q

When there is decreased intestinal perfusion, then ______

A
  • intestinal barrier dysfunction
  • translocation of bacteria causing infection complications
  • increased inflammatory cascade
61
Q

What are the systemic sequelae of shock

A
  • SIRS
  • Coagulopathy
  • Mitochondrial dysfunction
  • Microcirculatory dysfunction
  • MODS
62
Q

Hypovolaemia occurs after a loss of ______.

A
  • Fluid
  • Plasma
  • Whole blood
63
Q

What is the succinct pathophysiology of hypovolaemic shock?

A

Decreaed blood vol > decreased cardiac output and venous return> decreased wall strech detected by baroreceptors in the carotid sinus and aortic arteries > increased sympathetic tone (inotropy, chronotropy) due to direct cardiac innervation and arteriole constriction from catecholamine release > epi and norepi released from adrenal medulla resulting in further vasoconstriction and clinical signs of shock:
- tachycardia
- pallor
- prolonged CRT
- small pulse wave
- cool peripheries

64
Q

What is a brief summary of the pathophysiology of RAAS in sodium and water retention to improve blood volume?

A

decreased renal perfusion > activation RAAS > ATII causes vasoconstriction to maintain GFR > Aldosterone released to reabsorb Na in collecting tubule; ADH released to stimulate vasoconstriction and water reabsorption > fluid shift from interstitium to intravascular space via starling forces > attempt to restore blood volume.

65
Q

What is the shock index? How is it calculated?

A

Useful tool in identifying patients with shock.
SI = HR/SBP
(>0.9 = shock)

66
Q

How is hypovolaemic shock treated?

A
  • Fluid challenges and fluid resuscitation
  • Blood component therapy
  • Treat underlying problem/stop haemorrhage
67
Q

What are the complications of hypovolaemic shock?

A
  • reperfusion injury: after tissue oxygenation restored
  • dilutional coagulopathy/thrombocytopaenia: after fluid resuscitation and may result in further haemorrhage
  • interstitial oedema: from fluid overload
  • glycocalyx damage: increased vascular permeability, hypercoagulobility, and pro-inflammatory response
68
Q

Why may permissive hypotension be indicated in haemorrhaging patients?

A

Achieving MAP 60 in haemorrhage patients supports cardiovascular system and renal perfusion and avoids dilutional coagulopathy. Once the haemorrhage is controlled can aim to increase BP as required.

69
Q

What is cardiogenic shock?

A

Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume

70
Q

What are the three diagnostic indicators of cardiogenic shock?

A
  1. SBP <90mmHg, MAP <65mmHg
  2. LVEDP >18
  3. Severely reduced cardiac index (<1.8L/min/m2)
71
Q

What is the cardiac output equation?

A

CO = HR X SV

72
Q

What are some clinical signs of cardiogenic shock?

A
  • tachypnoea/dyspnoea
  • tachycardia/bradycardia
  • heart murmur
  • reduced mentation
  • poor pulses
  • cool extremities
  • pale MM
  • Arrhythmias
73
Q

What are the treatment options for cardiogenic shock?

A
  • relieve pericardial effusion etc.
  • diuretics to relieve pulmonary congestion
  • pimobendan (inodilator)
  • oxygen
  • glucagon (positive inotropic effects to increase CO + BP)
  • treat arrhythmias if indicated
74
Q

What is distributive shock?

A

Maldistribution of blood flow due to a marked decrease in SVR and is most commonly in SIRS and sepsis.

75
Q

What is obstructive shock?

A

Physical impedence to blood flow resulting in decreased perfusion i.e. GDV, PTE, pleural space disease

76
Q

What are some other forms of shock except the four main categories?

A

Metabolic and reduced PaO2

77
Q

What are characteristics of well perfused patients?

A
  • Normal heart rate and rhythm
  • Normal respiration rate and effort
  • Normal MM + CRT
  • Normal temperature
  • MAP 70-120mmHg
  • Urine at least 1ml/kg/hr
  • CVP 0-5mmHg
78
Q

What is ischaemia-reperfusion injury (IRI)?

A

Occurs after return of blood flow following a period of reduced to absent blood flow to an organ or tissue.

79
Q

What happens with ischaemia?

A

Reduces the delivery of oxygen resulting in tissue hypoxia leading to cellular dysfunction and necrosis when blood flow re-established.

80
Q

1) _______ are potent mediators for mucosal and microvascular injury in IRI. Activated neutrophils may increase 2) __________ which damage the vascular endothelium. They can also cause a ‘no-reflow’ phenomenon where neutrophils 3) _________.

A
  1. Neutrophils
  2. oxidants and the release of proteolytic enzymes
  3. ‘stick’ to endothelium causing diminished blood flow, cellular swelling, PLT activatation, thrombus formation and further neutrophil recruitment.
81
Q

What are some disorders associated with IRI?

A
  • GDV
  • Arterial thromboembolism
  • ROSC
  • Myocardial infarction
  • Crush and spinal cord injuries
  • TBI
82
Q

What are some medications used to treat IRI? How do they work?

A
  • Lidocaine: tachyarrhythmias, scavenging superoxides and hydroxy radicals, modulates inflammation
  • N-acetylcysteine: inhances cellular antioxidant capabilities, preserves systolic function, reduction myocardial oedema in CPA
  • Ischaemia preconditioning
  • Deferoxamine: chelates free iron
  • Allopurinol: XO inhibitor
  • Cyclosporine: decreases T-cell
83
Q

What are the 3 most common bacteria seen in bite wounds?

A
  1. Pasteurella spp
  2. Staphylococcus spp
  3. Streptococcus spp
84
Q

How is HTS useful in trauma patients?

A
  • increases contractility in cardiovascular collapse
  • may reduce vascular resistance to improve peripheral haemodynamics
  • may decrease pro-inflammatory cytokines and increase inflammatory interleukins limiting SIRS
  • effective in TBI
  • restores intravascular volume with less volume with crystalloids
85
Q

How may TXA help haemorrhaging patients?

A

TXA is a lysine derivative that block lysine sites on plasminogen to prevent tPA and prevent fibrinolysis

86
Q

What are some P.O.C diagnostics for patients suspected of experiencing shock?

A
  • Look for evidence of haemorrhage or coagulopathy
  • VBG/ABG, Biochemsitry, CBC, PCV/TS, Coag profile, blood smear
  • AFAST/TFAST
87
Q

Which fluid type is not suitable for use in shock patients?
a. Hypertonic fluids
b. Hypotonic fluids
c. Isotonic fluids
d. Blood products

A

B.
Free water so will distribute fluid excessively into the cell (intracellular)

88
Q

What is the maximum amount of colloid that dogs and cats can have in a 24h period?

A

Dog: <20ml/kg/day
Cat: <10ml/kg/day

89
Q

When a patient is still hypotensive after restoration of volume there is either ________.

A

vasodilation or decreased contractility (inotropy)

89
Q

When a patient is still hypotensive after restoration of volume there is either ________.

A

vasodilation or decreased contractility (inotropy)

90
Q

What are the resuscitation end points?

A
  • CVP 8-10mmHg
  • Decreasing blood lactate levels
  • O2 uptake >100ml/min/m2
  • Normal HR
  • MAP 80-100
  • CO >2L/min
  • Normalised BE
  • PCWP 10-12mmHg
91
Q

How is MAP calculated? what is MAP a product of?

A

MAP = diastolic + ((sys-dia)/3))
MAP = CO X SVR

92
Q

What is the equation for CO?

A

CO = HR X SV

93
Q

What are the three broad causes of hypotension? How do they occur? How do we approach them?

A
  1. Reduced preload: blood loss <30%, significant fluid loss, venodilation, obstruction. Treatment: IVF resus, treat underlying cause, relieve obstruction.
  2. Reduced cardiac function: primary or secondary myocardial dysfunction, ventricular dilation and reduced contractility. Treatment: positive inotrope, anti-arrhythmic, treat CHF, address underlying cause
  3. Reduced SVR: inappropriate vasodilation resulting in maldistribution of blood flow. Treatment: address underlying cause, provide IVFT, administer vasopressors.
94
Q

How does the chemoreceptor reflex system work (brief)?

A

low tissue oxygen tension either from increased CO2 or decreased pH > increased chemoreceptor signalling > excitement of vasomotor centre to promote sympathetic outflow

95
Q

What are the 3 elements of Virchow’s triad?

A

Mechanisms for venous thrombosis
1. Blood flow abnormal/stasis
2. Hypercoagulable state
3. Endothelial injury/dysfunction

96
Q

Shock patients that remain hypotensive despite fluid resuscitation (adeq vol)….

A

Require vasopressors and inotropes to increas SVR and cardiac output
I.e. epinephrine, norepinephrine, vasopressin, corticosteroids, dopamine, phenylephrine

97
Q

Fluid of choice for resuscitation of TBI

A

0.9% NaCl as least likely to contribute to cerebral oedema

98
Q

Ideal PCWP/PAOP

A

10-12mmHg

  • Over 15-20mmHg may promote pulmonary oedema and impaired DO2

VTS(ECC) Preparation (21 decks)

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