Acute and critical care Flashcards

1
Q

What are the prerequisites for a blood transfusion?

A

2 independent G&S taken by different people at different times

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2
Q

What blood group is given in an emergency?

What may be given in future? Why?

A

O negative

O positive. Save O negative for pregnant women to prevent rhesus disease.

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3
Q

If you have an obese person you need to given fluids to, to what weight do you calculate their fluid requirements?
Equations?

A

Ideal body weight.
Males = 0.9xH(cm)-88
Females = 0.9xH(cm)-92

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4
Q

If you are dealing with major trauma and the patient has massive haemorrhage, what are your fluid options? Which one first?

A

Red blood cells (first), FFP, Fluids (crystalloids)

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5
Q

Given the adult therapeutic dose and time for administration of:

  • Red cells
  • Platelets
  • Cryoprecipitate
  • FFP
A

Red cells = 1 bag over 2-3 hours
Platelets = 1 bag over 30 minutes (max)
Cryoprecipitate = 2 bags stat
FFP = 3 bags, 30 minutes max per bag (1.5hrs)

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6
Q
  1. What does TACO stand for?
  2. What are the signs and symptoms?
  3. Time frame for diagnosis?
  4. Investigation?
  5. Management?
A

1)Transfusion associated circulatory overload
2) Pulmonary oedema so: dyspnoea, wheezing, cough, cyanosis, tachypnoea
Heart overload: chest tightness, rapid increase in blood pressure, distended neck veins
Peripheral oedema
3) Within 24 hours of transfusion
4) CXR
5) Treatment = diuretics, (morphine), nitrates
Prevention = Giving single units, prophylactic diuretics, regular reviewing of patient

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7
Q

What is major trauma?

A

Serious and often multiple injuries where there is a strong possibility of death or disability

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8
Q

What is the Golden hour? Platinum 10 minutes?

A

Getting patients into hospital within 1 hour until their morbidity and mortality declines.
Life saving interventions should be implemented within 10 minutes of admission.

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9
Q

What are the steps of the primary survey of major trauma?

A
CABCDE
Control catastrophic haemorrhage
Airways and C-spine protection
Breathing with ventilation
Circulation with haemorrhage control
Disability - neurological status (eyes, GCS/AVPU), glucose
Exposure/ environment
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10
Q

What are possible mechanisms of injury in major trauma?

A
RTC
Fall from standing height (elderly)
Fall from height (>2 stories = bad)
Assault - head injury, stamping
Penetrating - knife, gun shot
Crush injury - industrial/ building falling
Blast injury - explosion
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11
Q

What are the ways that a blast injury can injure you?

A

Primary - blast wave disrupts gas filled structure
Secondary - impact of airborne debris
Tertiary - transmission of body
Quaternary - All other forces

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12
Q

What is the paramedic trauma handover?

A
ATMIST
Age
Time of injury
Mechanism of injury
Injuries
Signs
Treatments given already
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13
Q

What tool can you use to decide if a person needs a specialist major trauma centre?

A

Yorkshire major trauma triage tool

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14
Q

What to do in each of the CABCDE approach

A

C. 1) Direct, focussed pressure, keep pushing harder

2) Indirect pressure proximally
3) Torniquet - 3 inches above, another above if not sufficient
4) Haemostatic agents (ceelox)

A. Secure the airway - Immobilise the C-spine
Look listen feel for breathing
Suction, chin lift/jaw thrust, Guedel airway
Proceed to RSI/intubation if indicated

B. Give oxygen
Depends on causative issue:
- Tension pneumothorax - thoracocentesis/ thoracotomy + chest drain
- Massive haemothorax - Requires IV access + fluids before draining
- Cardiac tamponade - thoracotomy and drain

C. Stop catastrophic bleeding
Pelvic binder
Splint long bone fractures
Permissive hypotension with fluid replacement (RBC, PLTs, FFP)
Transexamic acid 1g over 10 mins the 1g infusion
Emergent damage control surgery
Interventional radiology
Limit crystalloid

D. Prevent secondary brain injury
Secure airway in GCS less than 8 or control ventilation
Maintain normal - ICP, Glucose, Oxygen, CO2

E. Ensure patient is warm
Pain management

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15
Q

What is the time frame for securing an airway in major trauma upon arrival?

A

45 minutes

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16
Q

Absolute indications for intubation

A
Inability to maintain airway
Inability to maintain adequate oxygenation upon less invasive manoeuvres
Inability to maintain normocapnia
Deteriorating conscious level
Significant facial injuries
Seizures
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17
Q

What are the indications for intubation with burns?

A

Deep facial burns, hypoxia or hypercapnia, full thickness neck burns.
Early intubation before swelling and fluid builds up

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18
Q

Relative indications for intubation

A

Haemorrhagic shock
Agitated patient
Multiple painful injuries
Transfer to another area of hospital/ expected clinical course

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19
Q

Indications for c-spine immobilisation?

A

High force mechanism of injury with a reduced consciousness level

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20
Q

Life threatening injuries on primary survey

A
ATOM FC
Airway obstruction
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Flail chest
Cardiac tamponade
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21
Q

Textbook signs of tension pneumothorax

In reality

A
1.Diminished breath sounds
Hyperesonance
Distended neck veins
Deviated trachea
Hypoxia
Tachycardia
Hypotension
  1. Air hunger/agitation
    Hypoxia
    Hypotension
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22
Q

Immediate management of tension pneumothorax

A

Thoracocentesis in 2nd intercostal space mid-clavicular line

Thoracotomy with large bore chest drain

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23
Q

Define massive haemothorax
Signs
Management

A
  1. Over 1.5L blood into the chest cavity
  2. Reduced air sounds, hyporesonance (contrasts tension)
  3. Obtain IV access because when you drain it they can bleed more into the space causing hypotension
    Thoracotomy (indications >1.5L blood loss or >200ml/hr)
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24
Q

What is an open pneumothorax?

A

Wound to chest wall communicating with the pleural cavity. Needs to be 2/3 aperture of trachea. Air moves inwards but wound closes on way out creating a 1 way valve

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25
Q

Define flail chest

A

Fracture of 2 or more ribs in 2 or more places.

This creates a floating rib section that move paradoxically. This severely impairs ventilation.

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26
Q

Signs of a cardiac tamponade
Pathophysiology
Investigation?
Treatment?

A

Beck’s triad:

1) Hypotension
2) Diminished heart sounds
3) Distended neck veins

Penetrative trauma into the pericardium (cardiac box) which blood collects and compresses the heart causing the triad

USS

Thoracotomy and incision of the pericardium (removing fluid)

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27
Q

Life changing injuries on secondary survey

A
Simple pneumothorax
Aortic injuries
Diaphragmatic injuries
Fractured ribs
Lung contusion
Cardiac contusion
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28
Q

Most accurate signs to show a bleeding patient in hypovolaemic shock
Others?

A

Tachypnoea
Pale
Sweaty

Anxious/ confused
Tachycardiac
Narrow pulse pressure
CRT
Hypotension
Bradycardia - terminal sign
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29
Q

Sites for massive haemorrhage

A

Blood on the floor (external haemorrhage) and four more:

  1. Chest
  2. Abdomen
  3. Long bones
  4. Pelvis
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30
Q

Causes of abdominal bleeding
Signs
Investigation required
Treatment + indications

A

Blunt force trauma/ penetrating

Not always obvious. Peritonism is a late sign so scan

CT abdo required

Laparotomy/ interventional radiology
Peritonism
Radiological evidence of free air
GI haemorrhage
Persistant/ resistant haemodynamic instability
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31
Q

Treatment of pelvic fractures

A

Pelvic binders to push it back together

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32
Q

What is permissive hypotension?

Numbers?

A

Allow lower BP
MAP 50mmHg
Systolic 90mmHg

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33
Q

Why are crystalloids not used in trauma?

A

It doesn’t carry oxygen

High chloride content so causes hyperchloraemic acidosis

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34
Q

Indications for fluid administration in trauma?

A

Systolic pressure <90mmHG
HR >130mmHg
Reduced consciousness level
Obvious massive ongoing blood loss

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35
Q

How are patients volume resuscitated in trauma?

A

1 unit RBC
1 unit platelet
1 unit FFP

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36
Q

What is the sequence of management in massive haemorrhage?

A
Stop catastrophic bleeding
Pelvic binder
Splint long bone fractures
Permissive hypotension
Transexamic acid 1g over 10 mins the 1g infusion
Emergent damage control surgery
Interventional radiology
Limit crystalloid
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37
Q

How is neurology assessed on the primary survey?

A

AVPU
GCS - particularly motor for outcomes
Pupillary response
Sensory level if able

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38
Q

What is the Cushing’s reflex?

A

Altered cardiac functioning from raised ICP (pre-coning and a very bad sign)
Raised ICP = Raised BP = baroreceptor stimulation = bradycardia

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39
Q

Management of head injuries

A

Prevent secondary brain injury
Secure airway in GCS less than 8 or control ventilation
Maintain normal - ICP, Glucose, Oxygen, CO2

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40
Q

What are the respiratory differences in the elderly?

A
Weak respiratory muscles
Kyphotic T spine
Rigid chest wall
Reduced alveolar exchange surface area
Impaired central response to hypoxia
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41
Q

What are the cardiovascular differences in the elderly?

A

Total body water reduces (preload)
Reduced vascular compliance and increased rigidity (afterload)
Myocardium becomes fat and collagen reducing contractility
All the above lead to reduced stroke volume

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42
Q

What drugs can cause falls?

A
Antihypertensives
Opioids
NSAIDs
Sedatives
Steroids
Beta-blockers
Anticoagulants (higher risk of bleeds on fall)
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43
Q

Diagnostic criteria for a UTI in the elderly?

A

New urinary symptoms or fever with:

  • Change in urinary character
  • or haematuria
  • or loin tenderness
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44
Q

What are the types of pelvic fractures?

Which one is made worse by pelvic binders?

A

Lateral compression fracture - worse with pelvic binder
AP compression/ open book fracture
Vertical shear

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45
Q

What angles are required for a c-spine fracture?

How to structure interpretation

A

AP, lateral, odontoid peg (requires opening of mouth)

ABCS
A - alignment of bony structures
B - bones (any fractures)
C - cartilage (any widening of spaces)
S - Soft tissue
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46
Q

Indications for a CT head

A

GCS <13 at presentation
GCS<15 at 2 hours after injury
Suspected open or depressed skull fracture
Any sign of basal skull fracture
Post-traumatic seizure
Focal neurological deficit
More than one episode of vomiting since injury

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47
Q

What radiological method is used to rapidly assess for trauma?
What does it look at?

A

FAST scan (Focused assessment with Sonography in Trauma)

Cardiac region
Left upper quadrant - spleen
Suprapubic region - fluid in peritoneal cavity

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48
Q

What are the three core features of acute liver failure?

Epidemiology?

A

Jaundice, coagulopathy (INR>1.5), hepatic encephalopathy (absence of chronic disease and within 12 weeks for diagnosis)
Rare but serious

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49
Q

How to assess for hepatic encephalopathy

A

Hands outstretched and they start to flap

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50
Q

What are the classifications of acute liver disease?
What causes fit into each?
Worst prognosis?

A

Hyperacute - within 7 days:
- Paracetamol, drugs, viral hepatitis

Acute - 1 to 4 weeks:
- Viral hepatitis, ischaemic hepatitis

Sub-acute - 4-12 weeks (Worst prognosis):

  • Seronegative hepatitis
  • Autoimmune hepatitis
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51
Q

What are the causes of acute liver failure?

How does this change by area of the world?

A

Paracetamol overdose - most common in UK
Viral hepatitis - A, E (commonest worldwide), B
Other drugs

52
Q

What drugs can cause acute liver failure?

General causes

A

Commoner - Paracetamol, isoniazid, NSAIDs, sodium valproate, carbamazepine
Rarer - TCA, phenytoin, allopurinol, amiodarone

Ischaemic hepatitis
Autoimmune hepatitis
Acute fatty liver of pregnancy
Wilson's disease
Budd chiari syndrome
Mushrooms (amanita phalloides)
Post-hepatectomy
53
Q

What is the upper limit of paracetamol dose per day?

Max dose per day in chronic liver disease or weight <50kg?

A

4g

2-3g

54
Q

What investigations need doing in acute liver failure?

Management?

A

Drug concentrations - paracetamol
Immunoglobulins - IgM, IgG
Autoantibodies
Ultrasound - fatty liver

Stop causative drug
Reverse if possible - NAC
IV fluids
Abx and antifungals
Liver transplant
55
Q

Risk factors for paracetamol overdose

A

Staggered overdose
Alcohol excess
Malnutrition
Chronic liver disease

56
Q

What compound is deficient in acute liver failure?

A

Glutathione - it is used up

57
Q

Investigations in a paracetamol overdose?

Management?

A

Paracetamol levels
INR
U/E
Liver function tests

N-acetyl cysteine
IV fluids
Antibiotics and antifungals

58
Q

What is the earliest indicator of hepatitis B?

Management?

A

HBV C IgM

Tenofovir
Daily INR, U/E, LFT
Call transplant team

59
Q

What are the complications of acute liver failure?

A

Encephalopathy - high levels of ammonia

Cardiorespiratory disease - infections, ARDS

60
Q

How is fluid distributed in the body?

A

Rule of thirds
2/3 intracellular
1/3 extracellular - 2/3 interstitial, 1/3 intravascular

61
Q

What fluid is utilised to fluid resus a patient?

Why?

A

Hartmann’s

It is closest to normal physiological values

62
Q

What are daily fluid requirements per kg?

A

Water - 30mls
Na - 1-2 mmols
K - 1 mmol
Energy - 30Kcal

63
Q

What are the types of fluid loss?

Give examples of each?

A

Sensible - measureable

  • Haemorrhage
  • Urine output

Insensible - not measurable

  • Breath
  • Sweat
  • Stool
64
Q

What are the signs of dehydration?

What percentage dehydration does thirst indicate?

A

Restlessness/ irritability
Sunken eyes
Thirsty
Reduced skin turgor

Thirst = 10% dehydration

65
Q

How do fluids need to be monitored?

Why?

A

Minimum 12 hourly U/Es (more frequently really)

IV fluids do not constitute normal blood constituents and therefore, derangement of electrolytes is common

66
Q

How do you calculate fluid requirements?

Example: 56kg woman, on floor for 48 hours and is confused and lethargic

A

100/50/20 per 24 hours or 4/2/1 per hour

Correct deficit = 96mls for every hour she has been on the floor = 4,608ml over 12-24 hours
Maintenance = 96mls/hr whilst NBM

67
Q

Features of shock

A

Tissue hypo-perfusion
Energy deficit
Build up of metabolites

68
Q

Types of shock

A

The fluid - Hypovolaemic, haemorrhagic
The pump - Obstructive (Tension ptx, PE, tamponade), cardiogenic (ischaemic, arrhythmia)
The pipes - Distributive (neurogenic, endocrine), septic, anaphylactic

69
Q

Management of shock

A
Call for help
A,B,C
Give oxygen
Cannulate a vein
ECG, BP, SpO2
Treat underlying cause:
- Hypovolaemic - IV fluids
- Septic/anaphylactic - Abx, fluids, vasopressors (adrenalin)
- Cardiogenic - inotropes (dopamine)
70
Q

75 year old man post-surgery has a urine output of 5mls over 2 hours, BP 120/70, HR 50

What finding is abnormal?
Likely cause?

A

Low urine output
Low BP (most likely has a baseline much higher)
Low HR

Post-surgical bleeding causing shock

71
Q

At what BP would you define hypotension?

What is a better measure and what is the definition using this?

A

<90 systolic or a drop of more than 40mmHg from baseline

Mean arterial pressure (MAP) - <65mmHg

72
Q

Define respiratory failure

What are the types? Pathophysiological cause of each?

A

pO2<8
Type 1 = hypoxia without hypercapnia - V/Q mismatch
Type 2 = hypoxia with hypercapnia - failure of ventilation

73
Q

Patient with asthma presents with hypoxia without hypercapnia, are you concerned?

A

Yes, normal CO2 is considered life threatening

74
Q

How can you support breathing in respiratory failure?

What are the different types and for what are they used?

A

Non-invasive ventilation

ePAP (expiratory) - type 1 RF - oedema, anaesthesia, pneumonia
iPAP (inspiratory) - type 2 RF

ePAP + iPAP = BiPAP
ePAP = cPAP

75
Q

Contraindications to non-invasive ventilation

A

Asthma - air trapping
PTX
Agitation
Airway loss

76
Q

Classification of AKI?

A

Stage 1 - Creatinine 1.5x, Urine output <0.5ml/kg/hr for > 6hrs
Stage 2 - Creatinine 2x, UO <0.5ml/kg/hr for >12hrs
Stage 3 - Creatinine 3x, UO <0.3ml/kg/hr for >24hrs, Anuria > 12hrs

77
Q

Causes of AKI?

A

Prerenal - shock (hypovolaemic, septic, cardiogenic), pressure optimisation (low BP)
Renal - toxins (NSAIDs, Acute interstitial nephritis, contrast, gentamicin)
Postrenal - Obstruction

78
Q

Renal complication of shock? Why?

A

Acute tubular necrosis
Low circulatory pressure or leaky vessels (sepsis) causes avascularisation of the renal tubules and therefore, necrosis occurs

79
Q

What two ions are in excess intravascularly in AKI?

Why?

A

K+, H+

The transporters K-3Na and H-Na don’t function leaving potassium and hydrogen ions in circulation

80
Q
Interpret this ABG:
pH 7.37
PaCO2 7*
PaO2 8.1*
HCO3 32*
BE 3*
A

Type 2 respiratory failure
Respiratory acidosis with renal compensation (chronic)

This is a classic picture of a patient with COPD

81
Q

Algorithm for interpreting an ABG?

A
pO2 - in resp failure?
pCO2 - type 1 vs type 2
pCO2 again - respiratory acidosis/alkalosis
BE/HCO3 - metabolic goes with the pH
pH - acidosis/alkalosis/compensated
82
Q

Define sepsis

What is the scoring system for it?

Scoring used more in practice?

A

Life threatening organ dysfunction caused by a dysregulated host response to infection

SOFA scoring
NEWS

83
Q

Indicators of organ dysfunction

A
  1. Hypotension - BP<90, MAP <65
  2. Renal - oliguria <0.5 mls/kg/hr for 2 hrs, creatinine >177mcmol/L
  3. Hypoperfusion - serum lactate >2
  4. Marrow and clotting - plts <100, INR>1.5, aPPT>60s
  5. Hypoxia - SpO2<90% or needing O2
84
Q

Define septic shock

A

Sepsis + hypotension unresponsive to fluid

85
Q

Management of sepsis

A
BUFALO - within 1 hour of admission
Blood cultures
Urine output
IV fluid 
Abx
Lactate
Oxygen
86
Q

Causes of coma

A

CNS - seizure, infection, SOL, CVA
CVR - Low CO state
Resp - hypoxia, hypercapnia, CO poisoning
MET - uraemia, hepatic encephalopathy, hypoglycaemia, hypo/hypernatraemia, hypothyroidism, hypothermia
Drugs - opiates, benzo’s, TCA

87
Q

How do you assess disability in an ABCDE assessment?

A

AVPU/ GCS
Glucose
Pupillary response

88
Q

What are the features of the GCS?

A

EVM 456

  • Eyes: 4 spontaneous, 3 to speech, 2 to pressure, 1 none
  • Verbal: 5 orientated, 4 confused, 3 inappropriate words, 2 incomprehensible sounds, 1 none
  • Motor: 6 obeys commands, 5 localises, 4 normal flexion to pain, 3 abnormal flexion to pain, 2 extension to pain, 1 none
89
Q

A patient has a CT head with an extradural evident, what do you do?

A
Regular monitor (30 mins) of neurological signs
Call a neurosurgeon
Anaesthetic referral - for intubation/ airway securing
90
Q

Patient with a head injury suddenly develops a fixed dilated pupil, what has happened?

A

Intracranial bleed (EDH,SDH) causing raised ICP.
Raised ICP causes uncal herniation.
This compresses on the oculomotor nerve causing the fixed dilated pupil

91
Q

What factor do you monitor to optimise cerebral perfusion?
Equation?
Target value?
In what circumstance would you consider a lower value?

A

Mean arterial pressure (MAP)
Cerebral perfusion pressure (CPP) = MAP - ICP
MAP = 85mmHg
If there is another massive area of haemorrhage (therefore, undergoing permissive hypotension), you need to weigh up which one is going to be more detrimental

92
Q

Methods to reduce ICP

A

Cerebral dehydration - mannitol or hypertonic saline
Reduction of cerebral blood volume:
- Head up 30 degrees
- Correct hypercapnia (pCO2 4.5-5) and hypoxia (pO2>8.5)

93
Q

What grading system is used to assess their disease burden/ risk in anaesthetics?

A
ASA
1-Normal
2- Mild systemic disease
3- severe systemic disease
4 - above + threat to life
5 - Not expected to survive 24hrs without surgery
6 - brain dead
E - emergency
94
Q

What is pre-optimisation?

What may be done?

A

Optimising the patient physiologically and obtaining sufficient access to allow best outcomes in theatre

Invasive blood pressure monitoring
Urinary catheter
Central venous access - pulmonary arterial flotation catheter
Inotropic support - BP will drop on anaesthesia
Cardiac output monitoring
Maximise oxygen delivery
Surgery school/ fit-4-surgery (lifestyle advice) - elective cases

95
Q

What preoperative measures are usually undertaken?

A

Give oxygen
Give fluids
Give regular medications

96
Q

What drugs need to be omitted pre-op

A

ACEi - 24-72hrs
ARBs - 24-72hrs
Anti-TNFs - 2 weeks
Platelet inhibitors - aspirin, clopidogrel - 7-10 days
DOACs - 4 days (reversal agent available, Praxbind)

97
Q

Why are NSAIDs avoided in anaesthesia?

Which one may be used?

A

Increased risk of intraoperative bleeding

Parecoxib

98
Q

What are patients given intraoperatively?

A
Oxygen
Fluids
Blood/ blood products
Antibiotics
Anaethesia
Analgesia - morphine
Muscle relaxation
99
Q

How is anaesthesia induced?
Maintained?
Why is there a shift in the method of maintenance?

A

Propofol

Inhalation agent - sevaflurane, desflurane
TIVA - total intravenous anaesthesia (propofol throughout)

The inhalation agents are strong greenhouse gases (desflurane)

100
Q

How do anaesthetics work?

A

They increase the action of GABA on the reticular activating system preventing consciousness

101
Q

What muscle relaxants are used?
How do they work?
How can they reversed?

A

Depolarising - suxamethonium - rapid action, short duration (so used in RSI)
Non-depolarising - rocuronium, atracurium

Depolarisation - Interacts with the nicotinic receptors on the post-synaptic membrane of the NMJ causing depolarisation and fasciculations
Non-depolarisation - inhibits the nicotinic receptors of NMJ. Takes a while as it is a competitive inhibitor but takes a while to wear off (20-40 mins)

Sugammadex - encapsulates the drugs and reverses it (within 1.5mins)

102
Q

What are patients given post-operatively?

A

Analgesia - simple, opioids or regional analgesia
Epidural - may be controlled by the patient
Fluids/ blood products
Inotropes/ vasopressors
Anti-emetics/ anticoagulants/ abx

103
Q

Why is patient controlled epidural analgesia safe?

A

Usually knock yourself out before you can press the button enough to give yourself respiratory depression

104
Q

What are the two types on local anaesthetics used?

What type of procedure are each used in?

A

Lidocaine - cuts and lacerations b/c immediate onset and lasts about 15 minutes
Bupivicaine - in regional anaesthesia, spinals and epidurals. 10 minutes onset and lasts 2 hours

105
Q

What type of drugs is usually utilised in epidurals?

A

Opioids (therefore don’t give more b/c you’ll OD them)

106
Q

What are the two types of sedation maintenance?

Give examples of each

A

Inhalational - desflurane, sevoflurane (quick offset is the benefit, greenhouse gas is negative)
Total intravenous anaesthesia (TIVA) - propofol or thiopenthal in the emergency situation

107
Q

What are the types of simple airway?

A

Face mask
Oropharyngeal (guedel)
Nasopharyngeal

108
Q

What are the types of advanced airways?
What is the definition of a definitive airway?
What of the above are in this category?

A

Laryngeal mask
Endotracheal (Definitive)
Tracheostomy (definitive)

A definitive airway is one that is placed below the laryngeal inlet

109
Q

What are the types of non-invasive ventilation?
In what situation is each used?
Why?

A

CPAP: Used in type 1 resp failure. Problem with oxygenation because airway collapse of expiration therefore, positive pressure keeps them open
BiPAP: Used in type 2 resp failure. This is a failure of ventilation so pressure is applied in both inspiratory and expiratory phases

110
Q

What are the two type of invasive ventilation?
What are the two type of control that can be used?
When is each control method used?

A

Endotracheal tube
Tracheostomy

Pressure controlled - pressure increases until target TIME is reached. Used in ITU almost exclusively
Volume controlled - volume increases until target VOLUME is reached. Used in theatres

111
Q

How do anticholinergic medications act on the heart?
Examples?

Beta-agonists?
Examples?

A

Inhibits the vagus nerve preventing parasympathetic action and therefore, increasing heart rate
Atropine, glycopyrrolate

Stimulates the myocardium so increases heart rate and contractility
Dobutamine
Used in ITU mostly for heart failure

112
Q

How do alpha-agonists work?
What are they used for?
Examples?

A

They stimulate alpha receptors found in peripheral blood vessels and therefore, cause vasoconstriction.
Used to treat hypotension
Peripheral - phenylephrine, metaraminol
Central - Noradrenaline

113
Q

What is the function of filtration?

What are the indications?

A

To act like the kidneys, removing metabolites and maintaining fluid, electrolyte balance
Indications: fluid overloads, uraemia, severe metabolic acidosis, hyperkalaemia, poisoning

114
Q

How do NSAIDs work?
What is the results of this?
What are the other places it acts on? Causing?

A

They prevent the conversion of arachidonic acid (derived from phospholipase A2) into prostaglandins by COX. Prostaglandins are involved in peripheral inflammation therefore, NSAIDs reduce this

Stomach acid - peptic ulcers
Renal blood - acute kidney injury
Platelets - blood thinning (why they are rarely used in anaesthetic situations)

115
Q

What are the three anti-emetic receptors and where are they?

Give medications that act on each?

A

5-HT3 found in GI tract, solitary tract nucleus and area postrema - Ondansetron
Dopamine-2 found in GI tract, solitary tract nucleus and area postrema - domperidone
Histamine found in cerebellum (acting on area postrema) and chemoreceptor trigger zones - cyclizine - causes motion sickness

116
Q

Features of hyponatraemia?

Management? (in a fit person without any chronic onset)

A

Drowsiness, agitation, urinary incontinence

3% saline 150ml bolus over 20 mins - not usually done this quick
Usually 0.9% saline over 24 hours

117
Q

Features of Addison’s disease?

Management?

A

Lethargy, nausea, loss of appetite (features of hypothyroidism up to now), weight LOSS.
Postural hypotension.
Hyponatraemia with high urine sodium. High TSH (lacking cortisol which usually inhibits TSH synthesis)

Hydrocortisone and .9% saline

118
Q

Causes of hyponatraemia?
Indicators of each?
Management in each scenario?

A

Hypervolaemic (dilutional):

  • CCF, nephrotic syndrome, cirrhosis of liver
  • Low urine sodium, oedematous
  • Fluid restrict (<1L/24hrs)

Euvolaemic:

  • Hypothyroidism (check TSH), adrenal insufficiency (9am cortisol), drugs, SIADH (High urine osmolarity and sodium)
  • Fluid restriction

Hypovolaemic:

  • Vomiting/ diarrhoea, burns, pancreatitis
  • Diuretics, Addison’s, salt-wasting nephropathy
  • Replacement saline
119
Q

Dose and route of hydrocortisone acutely

A

100mg IM

120
Q

What cortisol level excludes adrenal insufficiency?

A

300/350 mg/L

121
Q

Management of adrenal insufficiency?

A

Measure cortisol and ACTH
IV .9% saline
Hydrocortisone 100mg IM 6 hourly until eating and drinking
Treat precipitant
Resolving: hydrocortisone 20 mg PO TDS
Maintenance: hydrocortisone 5/10 mg and fludrocortisone 0.1/0.2mg/day (for primary)

122
Q

Young adult presents with systolic BP>200 and tachycardia. Initial management?
Diagnosis?

A

Start alpha blocker (phenoxybenzamine) - need to bring down BP
Measure plasma catecholamines and urine metanephrines. ?plasma aldosterone

Pheochromocytoma

123
Q

What do you need to measure if you suspect pheochromocytoma?

What are each of these compounds?

A

Plasma catecholamines - noradrenalin, adrenalin

Urine metanephrines - catecholamine breakdown products

124
Q

Patient is found to have a pituitary mass on CT scan, what should you give immediately and why?

A

IV hydrocortisone to prevent adrenal insufficiency

125
Q

Main causes of hypercalcaemia? How do you differentiate?
Investigations + findings?
Management?

A
Primary hyperparathyroidism (High/ normal PTH as you would expect it to be low with high calcium)
Malignancy (low PTH)

Adjusted calcium
PTH
Phosphate, ALP, renal function
ECG - short QT

.9% 4-6L/24 hours
IV bisphosphonates - zoledronic acid
Glucocorticoids
Calcimimetics - Cinacalcet 
Denosumab