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Year 4 > ACC > Flashcards

ACC Flashcards

1
Q

What information can be used to spot a sick patient

A

Collateral information (notes, concern from other staff, observations/ NEWS)
How the patient looks/ sounds/ smells
What the patient says (sinister symptoms)
The patient’s current observations/ NEWS
Patient’s clinical examination
New investigations (nearside and distant tests)

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2
Q

How do people deteriorate?

A

Airway obstruction
Breathing problem
Circulation problem

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3
Q

What are the causes of airway obstruction

A 
CNS depression
Foreign body (blood, vomit, secretions, food)
Trauma
Blocked tracheostomy
Swelling (infection, oedema)
Laryngospasm
Bronchospasm
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4
Q

How does airway obstruction kill

A 
Cerbral oedemna
Pulmonary oedema
Exhaustion
Hypoxic brain injury
Secondary apnoeas
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5
Q

What are the causes of breathing problems

A

CNS depression causing decreased/ abolished respiratory drive
Poor/diminished respiratory effort from muscle weakness or pain or restrictive abnormalities
Disorders of lung function (pneumonia, pneumothorax, haemothorax, asthma, COPD, PE, ARDS, oedema)

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6
Q

How do breathing problems kill

A 
Hypercapnia and apnoeas
Pulmonary oedema
Exhaustion
Hypoxic brain injury
Secondary cardiac ischaemia
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7
Q

What are the causes of circulation problems

A

Primary cardiac: MI, ischaemia, arrhythmia, cardiac failure, tamponade, rupture, myocarditis, HOCM

Secondary: asphyxia, tension pneumothorax, blood loss, hypoxia, hypothermia, septic shock, hyperthermia, Rhabdomyolysis

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8
Q

How do cardiac problems kill

A

Cardiac arrest

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9
Q

What is the approach to a relatively well patient

A 
Systematic history
Systematic examination 
Review of notes/ previous consultations
Review of investigations
Review of medications
Collateral history
More investigations
More consultations
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10
Q

What is the approach to an acutely unwell patient

A

Collateral information
Focussed history (presenting complaint based
Focused examination
Investigations
Establish working diagnosis and initiate treatment/ management plan

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11
Q

What is the approach to the critically unwell patient

A 
Time plays a key role
Before touching the patient, think: 
- what do I already know
- what can I be told
ABCDE approach with treatment 
Investigations
Establish working diagnosis and initiate treatment/ management
*hopefully returns patient to acutely unwell stage*
Focussed history 
Focussed examination
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12
Q

What does the A to E assessment entail

A

A:

  • Look for signs of airway obstruction
  • Treat the obstruction as an emergency
  • Give oxygen at high concentration (15L by nonrebreath mask)

B:

  • Look, listen and feel for respiratory distress
  • Count the RR
  • Assess quality of breathing
  • Note any deformity
  • Record O2 sats and concentration O2
  • Listen near the face then palpate, percuss and auscultate the chest
  • Trachea position check
  • Initiate treatment

C:

  • Look at and feel the hands
  • Assess peripheral and central cap refill time
  • Assess venous filling (hypovolaemic, uvolaemic, hypervolaemic)
  • Count heart rate and look at it on the cardiac monitor
  • Palpate central and peripheral pulses
  • Measure the blood pressure
  • Listen to the heart
  • Look for signs of poor cardiac output
  • Look for haemorrhage
  • Treat the cause of the cardiovascular collapse (usually large boar cannula and fluid course)

D:

  • Review and treat ABC’s: checking no hypoxia or hypotension
  • Check drug chart for reversible drug induced decreased GCS (poisonings- opiates or benzos)
  • Examine the pupils (looking for haemorrhages
  • Assess GCS or AVPU
  • Check lateralising signs
  • Check capillary glucose
  • Ensure airway protection

E:

  • Examine peripheries
  • Check temperature

Should hopefully have returned to acutely unwell rather than critically so:

  • Take history
  • Review notes
  • Review results
  • Consider which level of care is required
  • Reassess response
  • Document everything
  • Decide upon definitive treatment (instigate any care throughout A to E assessment when discovered, do not wait till the end)
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13
Q

What are the signs of airway obstruction

A

Partial:

  • stridor: sound on inspiration associated with airway narrowing (at rest implies a reduction in airway diameter of >50%)
  • difficulty breathing: gasping or noisy, effortful breathing
  • dysphagia
  • drooling
  • coughing
  • extreme anxiety or agitation

Total:

  • inability to effectively cough, breath or speak
  • no air movement
  • indrawing of spaces between ribs and above the collarbones
  • may be clutching the throat with both hands (universal sign for choking)
  • unconscious
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14
Q

What is hypotension

A

SBP <90mmHg
or MAP <60mmHg
or a decrease greater than 40mmHg or 30% from patient’s baseline MAP
or combination of all above
Can appear as a normal BP in those who are chronically hypertensive

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15
Q

What should be assessed in those who are hypotensive

A 
Heart rate (cause (then treat tachycardia) or response to hypotension)
Volume status (cause (then treat with fluid bolus) or response to hypotension)
Cardiac performance (looking for conditions causing problem, can perform ECG here)
Systemic vascular resistance (usually reduced, in patients with sepsis or anaphylaxis)
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16
Q

How is oxygen prescribed

A

Is prescribed for hypoxaemic patients to increase oxygen tension and decrease the work of breathing necessary to maintain a given PaO2.
The concentration of oxygen required depends on the condition being teated as an inappropriate concentration may have serious or even lethal effects.

It is a treatment for hypoxaemia not breathlessness.

Aim is to achieve normal (94-98% target) or near normal o2 sats for all acutely ill patients apart from those at risk of hypercapnic respiratory failure (88-92% target), or those recieving terminal palliative care.

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17
Q

What are the oxygen flow rates for each breathing apparatus used in hospital

A

Nasal cannulae: 1-6L/min
Hudson mask (simple face mask): 5-10L/min
Non-rebreathe mask: 12-15L/min
Venturi mask and valve: Flow rate depends upon valve chosen
Bag valve mask: 15L/min (+ positive pressure rather than relying on patient’s own respiratory drive)
CPAP: 1-15L/min (+ positive pressure)
Ventilator: 1-15L/min (+ invasive positive pressure
Nasal high flow: 60L/min

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18
Q

What is CPAP

A

A non-invasive ventilatory strategy

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19
Q

What is meant by oxygen creep

A

It is essential that a patient’s escalating oxygen requirement is captured as this is a sign of deterioration which can be innocuous and easily missed.
Patient will need a thorough reassessment to investigate deterioration and it would be beneficial to highlight such patient’s to crictical outreach team

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20
Q

What is CURB-65 score

A

The acronym for each of the risk factors measured in those with pneumonia, where each risk factor scores 1 point, for a maximum score of 5

Confusion of new onset (AMTS of 8 or less)
Urea greater than 7mmol (19mg/dl)
Respiratory rate of 30 breaths per minute or greater
Blood pressure less than 90 systolic or less than 60 diastolic
Age 65 or older

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21
Q

What are the common pneumonia pathogens

A 
S. pneumoniae
S. aureus
Mycoplasma pneumoniae
Haemophilus influenza
Chlamydophila pneumoniae
Respiratory viruses
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22
Q

Who should get a blood gas

A

Critically ill

Unexpected or inappropriate hypoxaemia (SpO2 <94%) or any patient requiring oxygen to achieve this target range

Deteriorating oxygen saturations or increasing breathlessness with previously stable hyperaemia

Deteriorating patient who now requires a significant oxygen concentration to maintain a constant oxygen saturation

Those with risk factors for hypercapnic respiratory failure who develop acute breathlessness, detiorating oxygen saturation or drowsiness or other symptoms of CO2 retention

Those with breathlessness and thought to be at risk of metabolic conditions

Acute breathlessness or critically illness and poor peripheral circulation in whom a reliable oximetry signal cannot be obtained

Any other evidence that would indicate that blood gas results would be useful in the patient’s management

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23
Q

How should blood gas interpretation be approached

A 
How is the patient clinically
Oxygen
pH
CO2
Bicarbonate
Other stuff (electrolytes, Hb and glucose)
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24
Q

What is Shock

A

Clinical syndrome caused by inadequate tissue perfusion and oxygenation leading to abnormal metabolic function

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25
Q

What are the types of shock

A 
Cardiogenic
Neurogenic
Hypovolaemic
Anaphylactic 
Septic
Obstructive
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26
Q

What are the 4 types of hypoxia

A

Hypoxic hypoxia: decreased O2 supply
Anaemic hypoxia: decreased haemoglobin function
Stagnant hypoxia: inadequate circulation
Histotoxic hypoxia: impaired cellular O2 metabolism

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27
Q

What is hypovolaemic chock

A

Caused by losses of blood, plasma or fluid

AKA haemorrhagic chock

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28
Q

How is hypovolaemic shocktreated

A

IV access
IV fluids +/- blood
Treat cause (eg stop bleed)
Monitor response

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29
Q

What is anaphylactic shock

A

Sudden onset generalised immunce condition caussed by exposure to causative substance in a sensitised person

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30
Q

How is anaphylactic shock treated

A

A, B or C issue then IM adrenaline then repeated bolus 5 mins later.
Also give fluid challenge of crystalloid
Give antihistamine and steroid too

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31
Q

What is septic shock

A

Sepsis accompanied by hypotension and perfusion abnormalities despite adequate fluid resuscitation

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32
Q

What is cardiogenic shock

A

`Tissue hypoperfusion that is primarily attributable to damage to the heart.

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33
Q

How is cardiogenic shock classified

A 
PROVED?
Pump (cardiogenic)
Rhythm abnormalities 
Obstructive
Volume (hypovolaemia)
Endocrine causes
Distributive (due to vasodilation)
? is it real (check BP, is arterial line in an artery, is the transducer at the correct height?)
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34
Q

How does cardiogenic shock present

A 
SOB
Dyspnoea on exertion
Diaphoresis
Cough with pink sputum
Chest pain
Air hunger
Hypoxia
Tachycardia
JVP
Rales
Skin pallor/motting
Altered mental status
Decreased urine output
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35
Q

What is the antidote for paracetamol overdose

A

N-Acetyle-cysteine

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36
Q

What is the antidote for benzodiazepines

A

Flumazenil

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37
Q

What is the antidote for hypoglycaemia

A

Glucagon

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38
Q

What is the antidote for hyperkalaemia

A

Dextrose

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39
Q

What is the antidote for local anaesthetic toxicity

A

20% lipid emulsion

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40
Q

What is the antidote for bradycardia

A

Atropine

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41
Q

What is the antidote for carbon monoxide

A

Oxygen

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42
Q

What is the antidote for TCADs arrhythmias

A

Sodium bicarbonate

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43
Q

How is a patient’s admission to ICU decided

A 
Diagnosis
Reversibility 
Comorbidity
Functional status and frailty
Patient's wishes
Parent team opinion
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44
Q

What are the cons of admission to ICU

A 
Critical care neuro-myopathy
Hospital acquired infections
Physical reconditioning and functional impairment 
Cognitive impairment 
Delirium
PTSD, anxiety, depression
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45
Q

What is the fundamental difference between type 1 and type 2 respiratory failure

A

Type 1: decreased PaO2

Type 2: increased PaCO2

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46
Q

What is meant by shunt

A

When there is normal perfusion to an alveolus but ventilation fails to supply the perfused area

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47
Q

What is meant by dead space

A

When there is normal ventilation of an alveolus but perfusion fails to supply the ventilated area

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48
Q

What are vasopressors

A

Drugs that work on alpha-receptors to increase the systemic vascular resistance

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49
Q

What are inotropes

A

Drugs that work on beta-receptors to increase the contractility of the heart

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50
Q

How is cerebral perfusion pressure calculated

A

CPP=MAP-ICP

Cerebral perfusion pressure = Mean arterial pressure - intracranial pressure

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51
Q

What are the key common respiratory pathogens

A

Gram + cocci:

  • Staphylococci
  • Streptococci

Gram - cocci:
-Morazella catarrhalis
Gram + bacilli:
-Clostridium difficile

Gram - bacilli:

  • Pseudomonas aeruginosa
  • E.Coli
  • Klebiella
  • Proteus

Gram - coccobacilli
-Haemophilus

Spiral bacteria:
Helicobacter

Atypical pathogens:

  • Mycoplasma
  • Legionella
  • Chlamydia
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52
Q

Which antibiotics should be used in respiratory tract infection

A

PO:

  • Amoxicillin
  • Doxycycline
  • Co-amoxiclav
  • Clarithromycin
  • Ciprofloxacin
  • Cotrimoxazole

IV:

  • Amoxicillin
  • Clarithromycin
  • Co-amoxiclav
  • Cefuroxime
  • Piperacillin-tazobactam
  • Temocillin
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53
Q

What is the difference between infection and colonisation

A

Infection: presence od micro-organisms causing damage to body tissues, usually occuring in the presence of acute inflammation

Colonisation: presence of bacteria on body sites that are exposed to the environment which do not cause infection or inflammation

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54
Q

What are the guidelines in Leeds for those with hospital acquired pneumonia that are positive for MRSA

A

Oral co-trimoxazole (non-severe HAP)
or
Combination of IV/oral linezolid plus ciprofloxacin (severe HAP)

Therapy is given for 5-7 days depending on the speed of clinical response

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55
Q

What iis involved in MRSA decolonisation

A

Nasal mupirocin plus chlorhexidine body washes for 5 days then a repeat MRSA screen, need three consecutive negative screens taken at least 48h apart to declare patient MRSA free

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56
Q

What framework can be used to investigate patient safety incidents

A

The Yorkshire Contributory Factors Framewwork:

Decision to investigate
Select investigation team
Gather data
Determine incident chronology
Identify care delivery problems
Identify contributory factors
Recommendations and action plan
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57
Q

How is a major trauma defined

A

Patient with an injury severity score of >15

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58
Q

What is the Golden hour

A

A concept used in trauma which depicts the window of opportunity that can potentially allow clinicians to improve the mortality or morbidity of patients through quality treatment in the pre-hospital or emergency depratment environments

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59
Q

What is the mechanism of injury and why is it useful to know

A

The physical circumstances causing the injury event
It does not accurately predict the severity of the injury but it may alter the thresholds for imaging, intervention or hospital admission.
It may give information about the magnitude of energy transfer, which is the key to severity of injury.

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60
Q

What is triaging

A

A continual and dynamic process that sorts patients, to allow optimal care and the best use of resources.
It is particularly useful in mass casualty scenarios but is also used as an everyday tool in the emergency department.
Patients should be frequently reevaluated as their triage category may change

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61
Q

What is involved in triage in trauma

A

Combination of mechanism of injury, anatomical and physiological data.

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62
Q

What is the mneumonic for life threatening thoracic injuries

A

ATOM FC

Airway obstruction
Tension pneumothorax
Open chest wound
Massive haemothorax
Flail chest
Cardiac tamponade
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63
Q

What is the mneumonic for assessing circulatory signs

A 
HEP B
Hands (temp/sweat/cap refill)
End organ perfusion (conscious levels/urine output)
Pulse (rate/quality/regularity)
Blood pressure (hypotension *late sign)
64
Q

What is the Glasgow Coma Scale

A 
Clinical grading system used for head injury
Minor brain injury: GCS 13-15
Moderate: GCS 9-12
Severe: GCS 3-8
A GCS <8 is considered to be coma

Looks at Eye opening, verbal response, Best motor response

E: 4 spontaneous, 3 to speech, 2 to pain, 1 none

V: 5 oriented, 4 confused, 3 inappropriate words, 2 sounds, 1 none

M: 6 obeys commands, 5 localises to pain, 4 normal flexion, 3 abnormal flexion, 2 extension, 1 none

65
Q

How is the log roll performed on a trauma patient

A

To move the patient to allow the posterior of the patient to be examined without their active movement.
Requires 5 people:
-1 to stabilise the neck (controls the process and gives instructions)
-3 to roll the patient (hands placed as: on top of the shoulder and on top of the hip; on top of the upper thigh and between the thighs supporting the upper thigh; between the knees supporting the upper knee and between the ankles supporting the upper ankle)
-1 to examin the back/spine and perform PR if indicated

Ideally patients should be rolled away from injured sides
Helpers are put in height order

66
Q

What are the key spinal cord syndromes

A

Central cord syndrome
Anterior cord syndrome
Brown-sequard syndrome
Complete spinal cord syndrome

67
Q

What do pelvic binders do

A

Usually applied pre-hospital with the aim to stabilise a fractured pelvis to prevent movement and distruption of haematoma in the pelvic cavity, due to the risk of potentially massive blood loss.

68
Q

How is trauma care initiated

A

Primary survey:

  • Life threatening injuries
  • A to E approach
  • Treat as soon as identified
  • Reassess and monitor

Secondary survey:

  • Once patient is stable
  • Look at all other injuries
  • Severe (limb threatening)
  • Minor
  • Occult (high level of suspicion)
  • Definitive care
69
Q

How is radiology used in trauma

A

Full trauma CT (head, neck, chest, abdomen and pelvis) within 30 minutes of arrival at MTC
Ultrasound may be used
Chest xray and pelvic xray role in primary survey

70
Q

How do airways sound and present

A

Open: quiet with air movement
Obstructed: quiet with no air movement
Partially obstructed: noisy

71
Q

How is a massive haemothorax defined

A

> 1500ml blood in the chest

72
Q

What is a flail chest

A

Mobile segment of chest wall due to two or more ribs being broken in two or more places

It is an indicator of very high force and energy transfer

Often lung is crushed underneath, resulting in pulmonary contusion

May present with:

  • respiratory distress
  • visible injury and tenderness
  • reduced air entry
  • hypoxaemia
73
Q

How is flail chest treated

A

Adequate oxygenation and ventilation
Cautious fluid resuscitation
Analgesia

74
Q

What is cardiac tamponade

A

Injury to myocardium, usually sharp
Blood leaks out into the pericardial sac
Heart unable to fill effectively
Cardiac output falls dramatically

Presents as:
Shock
Distended neck veins
Muffled heart sounds

75
Q

How are patients on fluid bolus management categorised

A

Rapid responder: Bleeding stopped or slowing
Transient responder: Bleeding ongoing
Non responder: Bleeding torrential and life threatening

76
Q

What are the types of anaesthesia

A

General: total loss of sensation
Regional: loss of sensation to a region or part of the body
Local: topical, infiltration, numbing the area

77
Q

What is an anaesthetic drug

A

A drug that induces partial or total loss of sensation

78
Q

What are the three types of drugs the create a balanced anaesthesia

A

Amnesic: lack of response and recall to noxious stimuli (unconsciousness)
Analgesic: pain relief
Akinetic: immobilisation/paralysis

79
Q

How is General anaesthetic commenced

A

Amnesic (induction agents)

  • Induce loss of consciousness in one to twp arm-brain circulation times
  • 10 to 20 seconds
80
Q

How are amnesic drugs categorised

A

Induction agents - to start the process

Maintenance agents: to maintain amnesia for the duration of anaesthetic

81
Q

What are the main induction agent drugs

A

Propofol
Thiopentone
Ketamine
Etomidate

82
Q

What are the main amnesia maintenance agent drugs

A

Propofol infusion: total IV anaesthesia
Inhalational agents: inhalational anaesthesia (vapours) started after induction and administrated via vaporisers or breathing circuits

83
Q

What are the key inhalation agents

A

Isoflurane
Sevoflurane
Desflurane
Enflurane

84
Q

What is the definition of MAC

A

Minimum alveolar concentration
1 MAC is concentration of the vapour that prevents the reaction to a standard surgical stimulus (traditionally a set depth and width of skin incision) in 50% of subjects (ie 50% patients pain free, amnesion in 100% patients)

85
Q

What is 1 MAC of nitrous oxide

A

104%

86
Q

What is 1 MAC of sevoflurane

A

2%

87
Q

What is 1 MAC of isoflurane

A

1.15%

88
Q

What is 1 MAC of desflurane

A

6%

89
Q

What is 1 MAC of enflurane

A

1.6%

90
Q

Why is analgesia used in anaeasthetic procedures

A

Required for:

  • Insertion of airway
  • Laryngeal mask airway
  • Intubation
  • Intraoperative pain relief
  • Postoperative pain relief
91
Q

What are the two categories of muscle relaxants and how do the work

A

Depolarising: act similarly to acetylcholine on nicotinic receptors but are very slowly hydrolysed by acetylcholinesterase. They therefore cause muscle contraction, muscle then fatigues and relaxes

Non-depolarising: they block the nicotinic receptors, therefore the muscle relaxes

92
Q

What are the most common anaesthesia issues

A

Intraoperative labile blood pressure: hypotension or hypertension

Postoperative nausea and vomiting

93
Q

What causes labile blood pressure and how is it managed

A

Intraoperative hypotension:

  • due to fluid loss/ blood loss
  • treated with fluids, bloods, inotropic agents

Intraoperative hypertension:

  • due to inadequate anaesthesia
  • treated with increased depth of anaesthesia by giving analgesics or increasing amnesia
94
Q

What are the key vase-active drugs used in hypotension in anaesthetics

A

Common:

  • ephedrine (rise in HR and contractility leading to rise in BP)
  • phenylephrine (Rise in BP by vasoconstriction)
  • metaraminol (Rise in BP by vasoconstriction)

Severe hypotension/ ICU:

  • noradrenaline
  • adrenaline
  • dobutamine
95
Q

What does PONV mean

A

Post Operative Nausea and Vomiting

96
Q

What are the key anti-emetic drugs

A 
5HT3 blockers: ondansetron
Steroids: dexamethasone
Antihistamine: cyclizine
Phenothiazine: prochlorperazine (stemetil)
Anti-dopaminergic: metoclopramide
97
Q

What is the order of usage of anti-emetics

A

Ondansetron -> Dexamethasone -> Cyclizine -> Prochlorperazine

98
Q

How are patients woke up out of general anaesthetic

A

Stop anaestheic vapours ->
Give oxygen ->
Perform throat suction ->
Reverse muscle relaxation (reversal)

99
Q

What are the key anaesthetic reversal drugs

A

Neostigmine (anti-cholinesterase, prevents breakdown of acetylcholine)

Sugammadex (causes water soluble complex formation (1:1 ratio with steroidal muscle relaxants), Rocuronium, Vercuronium, Pancuronium, no effects on nicotinic or muscarinic receptors)

100
Q

How are patients transferred from surgery to post anaesthesia care unit

A

Administer O2 during transfer

Handover the patient:

  • brief history
  • any anticipated problems
  • intraoperative analgesia and PONV prophylaxis

Prescribe:

  • rescue analgesia
  • rescue anti emetics
  • fluids
  • other indicated medications
101
Q

What is a DVT

A

Deep vein thrombosis

The formation of one or more blood clots in a deep vein, typically of the lower extremities

102
Q

What are the two type of DVT

A

Proximal DVT: DVT of the lower extremity affecting the femoral vein, profunda femoris vein, and/or the popliteal vein (up to the calf vein trifurcation)

Distal DVT: DVT of the lower extremity that is confined to the veins beyond the calf vein trifurcation (i.e., below the knee joint)

103
Q

What is VTE

A

Venous thromboembolism

An umbrella term that encompasses DVT and PE

104
Q

What is a recurrent VTE

A

VTE that recurs in a patient after the completion of the first 2 weeks of antithrombotic therapy

105
Q

What is a provoked VTE

A

VTE in an individual with ≥ 1 risk factor for VTE

106
Q

What is an unprovoked VTE

A

aka idiopathic VTE

VTE in an individual without risk factors for VTE

107
Q

What causes DVT

A

Any factor that causes hypercoagulability, endothelial damage and/or venous stasis can cause DVT

108
Q

What are the risk factors for VTE

A

Transient:

  • Surgical
    • Surgery under general anaesthesia
    • Cesarean delivery
  • Immobilisation
    • Acute illness requiring complete bed rest
    • Lower extremity injury with restricted mobility for at least 3 days
    • Long distance travel
  • Estogen-rekated factors
    • Pregnancy
    • Use of OCPs or HRT
  • IV devices
    • Indwelling venous catheter
    • Implanted pacemaker or cardiac defibrillator leads
  • Patient factors
    • Obesity
    • Smoking
    • IV drug use
    • Nonadherence to VTE prophylaxis

Chronic:

  • Patient factors
    • Age >60 y
    • Personal or FH of VTE
  • Prothrombotic chronic illnesses
    • Active cancer
    • Nephrotic syndrome
    • Autoimmune disorders
  • – APLA syndrome
  • – IBD
    • Hereditary thrombophilia
  • – Factor V leiden
  • – Antithrombin III deficiency, protein C deficiency and protein S deficiency
  • – Prothrombin mutation
109
Q

What is the DVT risk factor mneumonic “THROMBOSIS” for

A 
Travel
Hypercoagulable/ HRT
Recreational drugs
Old (>60)
Malignancy
Blood disorders
Obesity/Obstetrics
Surgery/Smoking
Immobilisation
Sickness (CHF/MI, IBD, nephrotic syndrome, vasculitis)
110
Q

What is the Virchow triad

A

Hypercoagulability
Endothelial damage
Venous stasis

111
Q

How does VTE present

A

May be asymptomatic
Localised unilateral symptoms:
- typically affects deep veins of the legs thighs or pelvis
- more common in the left lower extremity
-Swelling, feeling of tightness or heaviness
-warmth, erythema and possible livid discolouration
-Progressive tenderness, dull pain
– Homans sign: calf pain on dorsal flexion of the foot
– Meyer sign: compression of the calf causes pain
– Payr sign: pain when pressure is applied over the medial part of the sole of the foot
-Distention of superficial veins
-Distal oulses are normal
General symptoms: fever
Possible signs of PE: dyspnea, chest pain, dizziness, weakness

112
Q

What is the WELLS score for DVT

A

Used to calculate the pretest probability of DVT of the lower extremities

Criteria:
+1-Active cancer
+1-Previously documented DVT
+1-Paralysis, paresis, or recent (cast) immobilisation of lower extremities
+1-Recently bedridden for ≥ 3 days or underwent major surgery within the past 12 weeks under general/local anaesthesia
+1-Tenderness localised along the deep venous system
+1-Swelling of the entire leg
+1-Calf swelling ≥3cm compared to the contralateral leg
+1-Pitting oedema confined to the symptomatic leg
+1-Distended collateral superficial veins (non varicose)
-2-Alternative diagnosis as likely as or more likely than DVT

0: low
1-2: intermediate
≥ 3: high

113
Q

How is a DVT diagnosed

A

Calculate pretest probability using Wells criteria for DVT

Check D-dimer (first for low PTP): neg <500ng/ml - rule out DVT, pos ≥500ng/ml - possible DVT

Venous ultrasound for intermediate or high PTP, low with positive D-dimer

Negative ultrasound:

  • Intermediate and low PTP: DVT ruled out
  • High PTP: repeat venous US within within a week if no alternate diagnosis

Positive US:
-DVT confirmed, screen for underlying cause if no risk factors for DVT are identified on initial evaluation

Inconclusive US:

  • Consider venography
  • CT venography
  • MR venography
114
Q

What are the differentials in suspected DVT

A 
Superfical thrombophlebitis 
Muscle or soft tissue injury (post traumatic swelling or haemotoma)
Lymphadema
Venous insufficiency 
Ruptured popliteal cyst
Cellulitis
Compartment syndrome
115
Q

How is DVT treated

A

Treat concomitant PE and stabilise the patient as needed
Assess bleeding risk on anticoagulation
Initiate anticoagulation therapy based on extent and aetiology of DVT:
- Expectant management: serial venous US without anticoagulant
- Primary treatment: anticoagulant for 3-6 months (first line is DOAC - apixaban)
- Secondary prevention of recurrent DVT: extended anticoagulation after completion of primary treatment
Treat underlying cause
Supportive care:
-minimise bedrest
-graduated compression stockings
-analgesics for pain relief
-delay any elective surgery for at least 3 months after initiation of anticoagulation therapy

116
Q

What are the potential complications of DVT

A 
PE
Postthrombotic syndrome (chronic venous insufficiency)
Venous gangrene (rare)
117
Q

What is cellulitis

A

Local infection of the deep dermis and subcutaneous tissue

118
Q

How does cellulitis present

A

Skin changes:

  • Erythema (red discolouration)
  • Warm or hot to touch
  • Tense
  • Thickened
  • Oedematous
  • Bullae (fluid filled blisters)
  • A golden yellow crust can be present and indicate a staphylococcus aureus infection (seen in impetigo)
119
Q

What are the common causes of cellulitis

A

Staph aureus
Group A streptococcus (mainly strep pyogenes)
Group C streptococcus (mainly strep dysgalactiae)
MRSA

120
Q

What is the Eron Classification

A

The classification system NICE recommends for the assessment of the severity of cellulitis:
Class 1: non systemic toxicity or comorbidity
Class 2: systemic toxicity or comorbidity
Class 3: significant systemic toxicity or significant comorbidity
Class 4: sepsis or life-threatening

121
Q

How is cellulitis treated

A

Give antibiotics:

Admit the patient for IV antibiotics if they are class 3 or 4 and also consider for frail, very young or immunocompromised patients

Flucloxacillin is very effective against staph infections and also works well against other gram positive cocci.
It is usually first choice in treating cellulitis and can be given oral or IV.

Alternative antibiotics are:

  • Clarithromycin
  • Clindamycin
  • Co-amoxiclav
122
Q

What is the definition of acute coronary syndrome

A

The suspicion or confirmed presence of acute myocardial ischaemia

123
Q

How is ACS classified

A

NSTE-ACS: acute coronary syndrome manifesting without ST elevations on ECG:

    • NSTEMI: positive myocardial injury biomarkers
    • Unstable angina: Absence of detectable myocardial injury biomarkers

STE-ACS: acute coronary syndrome manifesting with ST-elevations on ECG

Subtypes of ACS cannot be differentiated based on clinical presentation alone

124
Q

What is myocardial injury

A

Any damage to myocardial tissue that leads cardiac troponin (cTn) levels to rise above the 99th percentile of the upper reference limit.

125
Q

How does ACS present

A 
Typical :
Acute retrosternal chest pain
Typically dull, squeezing pressure and/or tightness
Commonly radiates to left chest, arm, shoulder, neck, jaw and/or epigastrium
Precipitated by exertion or stress
Often occurs in the morning
SOB
Pallor
Nausea, vomitting
Clammy 
Anxiety
Dizziness, lightheadedness, syncope
Tachycardia
Arrhythmias 
New heart murmur on auscultation
Symptoms of heart failure (orthopneoa, pulmonary oedema) or cardiogenic shock (hypotension, tachycardia, cold extremities)

Atypical:
(seen in elderly, diabetics, women)
Stabbing, sharp chest pain
No or minimal chest pain (silent MI more common in patients withDM as result of polyneuropathy)
Autonimc symptoms of nausea, excessive sweating etc

In inferior wall infarction more common:
Epigastric pain
Bradycardia
Clinical triad in RV infarction: hypotension, elevated JVP, clear lung fields

Classically, STEMI manifests with more severe symptoms than NSTEMI but not always the case

126
Q

How is ACS diagnosed

A

ECG asap when clinically suspected

  • ST elevations present then immediate revascularisation therapy
  • No St elevations then management guided by ECG findings, troponin levels, clinical features and risk factors
  • repeat every 15-30 min in first hour, especially if the first ECG is inconclusive or symptoms recur or change in quality
  • compare with previous ECGs if available
Cardiac troponin levels:
- measure asap and repeat after 1-6 hours
-repeat if symptoms or ECG changes occur
-consider repeat after 72 hours as marker of infarct size
Findings:
-STEMI usually elevated
-NSTEMI elevation above 99th percentile
-Unstable angina usually normal

Consider Echo if unclear diagnosis
-do not let this delay repurfusion therapy
-useful in those with atypical symptoms or if diagnosis is unclear
Indications:
-cardiogenic shock
-Infarct like symptoms but inconclusive ECG findings
-Evaluation for complications of MI
Findings:
-Wall motion abnormalities
-Decreased LV function
-Signs of different conditions that cause chest pain

127
Q

What are the ECG changes in STEMI

A

Significant ST elevation in two contiguous leads
Hyperacute T waves can be present without ST elevations in the very early stages of ischaemia
If inferior myocardial infarction is suspected, investigate for signs of RV involvement

Timeline of ECG changes in STEMI:
Acute stage: myocardial damage ongoing
-hyperacute T waves (peaked T wave)
-ST elevations in two contiguous leads with reciprocal ST depressions
Intermediate stage: myocardial necrosis present
-absence of R wave
-T wave inversions
-pathological Q wave (>0.04 seconds long, amplitude >1/4 of the R wave or >0.1 mV, any Q wave in leads V1-3
Chronic stage: permanent scarring
-persistent, broad and deep Q waves
-often incomplete recovery of R waves
-ermanent T wave inversion is possible
128
Q

How is STEMI managed

A

“time is muscle” - revascularisation should occur asap in those with STEMI, all other interventions can wait

Revascularisation:

Emergency coronary angiography with PCI:

  • indication: preferred method
  • procedure: balloon dilatation with stent implantation
  • first medical contact to PCI time should ideally be <90 mins and not exceed 120 mins

Fibrinolytic therapy in STEMI:

  • indications: where symptoms started <12 hours prior, is PCI cannot be performed within 120 mins and no contraindications present
  • timing: within <30 mins of pt arrival at hospital
  • contraindications: if >24 hours after symptoms onset
  • regimens:
    • tenecteplase
    • alteplase
    • reteplase
    • streptokinase
  • Postfibrinolysis check TIMI coronary grade flow and transfer to a facility with PCI capabilities
  • PCI should be performed even if successful lysis

Coronary artery bypass grafting is not routinely recommended for acute STEMI

Antiplatelet therapy and anticoagulation therapy should be initiated without delaying revascularisation in STEMI

129
Q

What are the ECG changes in NSTEMI or Unstable angina

A 
No ST elevations present
Nonspecific signs of ischaemia:
-ST depression
-Transient ST deviations
-T wave inversions

To identify STEMI or STEMI equivalent ECG findings, repeat ECGs if the initial one is inconclusive or any changes in symptoms occur

130
Q

How is NSTE-ACS managed

A

Depends on patients mortality risk, clinical findings, and the availabiltiy of resources

Anticoagulation therapy

131
Q

What are the options for medical management of MI

A

MONA-BASH

Morphine
Oxygen
Nitroglycerin
Antiplatlet drugs (aspirin and ADP receptor inhibitor eg clopidogrel)
Beta blockers
ACE inhibitors
Statins
Heparin
132
Q

What are the differentials in suspected ACS

A 
Cardio causes:
Myocarditis 
Decompensated congestive heart failure
PE
Cardiac arrhythmia, tachycardia
Aortic dissection
Hypertensive emergencies
Structural heart disease
Myocardial drug toxicity
Cardiac trauma
Takotsubo cardiomyopathy 
Stroke

Noncardio causes:
Renal failure
Critical illness (sepsis)
Hypothyroidism or hyperthyroidism

133
Q

What are potential differntials of ST elevations on ECG

A 
Early depolarisation 
LBBB
Brugada syndrome
Myocarditis
Pericarditis
PE
Hyperkalaemia
Tricyclic antidepressant use
Poor ECG lead placement
134
Q

What is angina

A

Chest pain cuased by myocardial ischaemia (necrosis of myocytes has not yet occurred) due to narrowing (eg thrombus) or spasm (eg prinzmetal angina) of the coronary artery

135
Q

What is stable angina

A

A type of angina that occurs upon exertion, mental stess and/or exposure to cold adn usually subsides within 20 mins of rest or after administration of nitroglycerin (eg GTN spray)

136
Q

What is coronary artery disease

A

Ischaemic heart disease due to narrowing or blockage of the coronary arteries, most commonly due to atherosclerosis, resulting in a mismatch between myocardial oxygen supply and demand

137
Q

What is the epidemiology of Coronary artery disease

A

The leading cause of death worldwide

Lifetime risk of CAD at age 50 is ~50% for men and 40% for women

138
Q

What causes coronary artery disease

A

Atherosclerosis is the most common causes

139
Q

How does angina present

A

Retrosternal chest pain or pressure
Pain may radiate to the left arm, neck, jaw, epigastric region, or back
Pain is not affected by body position or respiration
No chest wall tenderness
May gradually increase in intensity
May present as GI discomfort
May be silent especially in geriatric and diabetic patients
Dysnoea (SOB)
Dizziness
Palpitations
Restlessness
Anxiety
Autonomic symptoms (sweating, nausea, vomiting, syncope)

140
Q

How do symptoms present in stable angina

A

Symptoms are reproducible/ predictable
symptoms often subside within mins with resy or after administration of GTN spray
Common triggers include mental/ physical stress or exposure to cold
ECG is usually normal

141
Q

How is angina treated

A

Goal is to reduce cardiovascular morbidity and mortality, improve ischaemic symptoms and maintain quality of life

All patients receive pharmacotherapy and selevt patient get revascularisation

Pharmacotherapy:
Antiagninal drugs:
-first line: beta blockers (bisoprolol, metoprolol)
-second line: Calcium channel blockers (amlodipine, nifedipine, verapamil, diltiazem), nitrates ( short acting nitrate - nitroglycerin; long acting nitrates - isosorbide denigrate, isosrbide mononitrate), metabolic modulator - ranolazine
-third line: ranolazine if BB, CCB and nitrates are ineffective or not tolerated

Secondary prevention:

  • antiplatelet (aspirin, clopidogrel, or both) - recommended for all pts with CAD
  • ACEIs or ARBs (lisinopril, ramipril or losartan, valsartan)- for pts with HTN, DM, LV ejection fracture <40%, CKD

Revascularisation:
Decided by specialist MDT, complex decision,
indicated in those with high risk anatomic lesions involving multiple or critical vessels; activity limiting symptoms due to significant coronary artery stenosis that persists despite medical treatment or pr has contraindications to pharmacotherapy
Options:
- CABG
- PCI

142
Q

How does costochondritis present clinically

A

Sharp, well localised pain that is repoducible on palpatient of costal cartilage
History of recent exercise, exertion or chest wall trauma

143
Q

How is costochondritis diagnosed

A

Clinical diagnosis by history and exam

Normal chest xray

144
Q

How is costochondritis treated

A

Pain mangement
Rest
Cough suppressants (eg codeine)
Heat or ice packs

145
Q

What is a pulmonary embolism

A

AKA a PE
Luminal obstruction of one or more pulmonary arteries, typically by a blood thrombi that come from deep vein thrombosis and embolize to the lungs

146
Q

What causes PE

A

“PE is FATAL”

Fat
Air
Thrombus
Amniotic fluid
Less common (bacterial, tumor and cement)
147
Q

How does a PE present

A

Acute onset oftern triggered by specific event (eg on rising in the morning, sudden physical strain/ exercise)
Dyspnoea and tachypnoea
Sudden pleuritic chest pain, worse on inspiration
Cough and haemoptysis
Possibly decreased breath sounds, dullness on percussion
Tachycardia, hypotension
Raised JVP and Kussmaul sign (in massive PE)
Low grade fever
Features of DVT- unilateral painful leg swelling
Features of massive PE- syncope and obstructive shock with circulatory collapse due to a saddle thrombus

Features of PE under anaesthesia during surgery are:

  • increased HR
  • drop in BP
  • drop in partial pressure of end-tidal CO2 in capnography
  • drop in PaO2 sats
148
Q

What is the WELLS criteria for PE

A 
Clinical symptoms of DVT +3
PE more likely than other diagnoses +3
Previous PE/DVT +1.5
Tachycardia >100bpm +1.5
Surgery or immobilisation in past 4 weeks +1.5
Haemoptysis +1
Malignancy +1

Total score 0–1: low probability of PE
Total score 2–6: moderate probability of PE
Total score ≥ 7: high probability of PE

Modified Wells score (clinical probability)
Total score ≤ 4: PE unlikely
Total score > 4: PE likely

149
Q

What is the PERC criteria

A 
Pulmonary embolism rule out criteria
Age > 50 years +1
Heart rate > 100/min +1
Oxygen saturation < 95% +1
Hemoptysis +1
Estrogen use +1
Prior history of DVT or PE +1
Recent surgery or trauma in the past 4 weeks +1
Unilateral lower limb edema +1

Clinical pretest probability
Total score 0: pretest probability < 1%; no further testing needed
Total score ≥ 1: PE is not ruled out; further testing needed

150
Q

How is a suspected PE diagnosed

A

Assess for haemodynamic stability
Assess pretest probability for PE using WELLS
Other lab tests:
-If patient stable and low PE probablity assess using PERC
-If perc not met or intermediate probability in stable patient - obtain d-dimer (if above threshold then scan, if below look for other causes of symtptoms as PE is very unlikely)
-If unstabel patient and/or high probability of PE- obtain CTPA or V/Q scan for definitive diagnosis
-Critically ill patients who cannot be safely transported should have a bedside echo

151
Q

What imaging is done in investigating suspected PE

A

CT pulmonary angiography (CTPA)

  • Contrast enhanced imaging of the pulmonary arteries
  • Most difinitive diagnostic test for PE (high sensitivity, specificity and immediate evidence of pulmonary arterial obstruction
  • Findings :
    • visible intraluminal filling defects of pulmonary arteries
    • wedge shaped infarction with pleural effusion is diagnostic of PE

Ventilation/perfusion scintigraphy (V/Q scan)

  • An alternative to CTPA in pts with renal insufficiency and/or contrast allergy
  • Detects area of ventilation/perfusion mismatch via perfusion and ventilation scintigraphy
  • Findings:
    • Perfusion failure in the normally ventilated pulmonary area (mismatch) suggests PE
    • Discordance between V/Q scan and clinical pretest probability necessitates further evaluation

Echocardiography:

  • suspected right heart strain
  • critically ill patients with suspected PE
  • Findings:
    • Incresed RA pressure
    • Dilatation and hypokinesis of RV (McConnell sign)
    • Venous reflux with dilation of inferior vena cava (with corresponding liver congestion seen on abdo US)
    • Tricuspid regurgitation (tricuspid valve insufficiency)
    • Increased pulmonary artery systolic pressure
152
Q

What are ECG findings of PE

A 
May be normal
Arrhythmias: sinus tachycardia, bradycardia, AF
Signs of right heart strain:
-SIQIIITIII-pattern
-New RBBB
-Right axis deviation
P pulmonale
ST elevation or depression
T wave inversion in the anterior precordial leads (V1-V4)
Predictors of adverse outcome:
AF
Sinus Bradycardia
SIQIIITIII-pattern
New RBBB
ST elevation in aVR
T wave inversion in V1-V4
Inferior Q waves in leads II, III, aVF
153
Q

How should a patient with a PE be managed

A

Supportive care:

  • Haemodynamic support (hyptensive, in shock)
    • IV fluids (gentle bolas of normal saline ≤ 500ml)
    • Avoid hypervolaemia in RV strain
    • Vasopressors if no improvement following IV fluids
  • Respiratory support
    • O2 supplementation
    • Those in resp failure - airway managment and/or mechanical ventilation
  • Analgesics for those in pain
    • Consider morphine or oxycodone
    • Avoid NSAIDs in pts having anticoagulant or thrombolytics

Assess bleeding risk
-high risk in recent surgery, haemorrhagic stroke, active bleeding

Empiric parenteral anticoagulation:

  • consider starting in those awaiting definitive diagnosis, low risk of bleeding, and increased probability of PE
  • Stable patient: LMWH
  • Unstable patient or renally insufficient: unfractionated heparin (HMWH)
  • absolute contrindication in pts with high bleeding risk

Thrombolytic therapy:

  • in massive PE causing RHF with hypotension and a low bleeding risk
  • in nonmassive PE if pt deteriorates after initiation of anticoagulant but not yet developed hypotension and has low bleeding risk
  • Thrombolysis preferably with recombinant tissue type plasminogen activator (tPA) eg alteplase
  • Usually systemic infusion via peripheral catheter
  • Agents: tPA (alteplase), streptokinase, urokinase
  • in pts on anticoagulant: stop anticoagulant prior to thrombolysis; check aPTT 2 hours after completion of thrombolysis; resume anticoagulant when aPTT is <2 time the upper normal limit
  • Complication risk of haemorrhage during thrombolytic treatment

Embolectomy:

  • Last resort when thrombolysis is contraindicated or unsuccessful
  • Surgical removal of an embolus by opening up an artery with an incistion or catheter based thrombus removal

Anticoagulation:

  • inital parenteral anticoagulation for 5-10 days but not required if long term anticoag of rivaroxaban or abixaban planned
    • LMWH (enoxaparin) preferred in normal renal function pts and in those with cancer
    • UFH in those with renal failure, inadequate subcut absorption (obesity), or those who may require thrombolysis
  • Long term anticoagulation (up to 3 months)
    • DOAC
    • Warfarin (vitamin K antagonist) if can’t have DOAC
    • LMWH in cancer pts and pregnant women
  • Reassess need for anticoagulant
    • after 3 months then annually
    • indications for extended anticoagulation:
  • – Unprovoked PE with low to moderate risk of bleeding
  • – Pts with cancer with any level of bleeding risk
154
Q

What are the complications of PE

A

High risk of recurrence without anticoagulant treatment
Right ventricular failure and secondary pulmonary arterial hypertension
Sudden cardiac death due to pulseless electrical activity
Atelectasis (loss of lung volume)
Pleural effusion
Pulmonary infarction
Arrhythmias

155
Q

What is pneumonia

A

A respiratory infection characterised by inflammation of the alveolar space and/or the interstitial tissue of the lungs

Year 4 (6 decks)

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