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)
2
Q
How do people deteriorate?
A
Airway obstruction
Breathing problem
Circulation problem
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
4
Q
How does airway obstruction kill
A
Cerbral oedemna Pulmonary oedema Exhaustion Hypoxic brain injury Secondary apnoeas
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)
6
Q
How do breathing problems kill
A
Hypercapnia and apnoeas Pulmonary oedema Exhaustion Hypoxic brain injury Secondary cardiac ischaemia
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
8
Q
How do cardiac problems kill
A
Cardiac arrest
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
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
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
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)
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
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
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)
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.
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
18
Q
What is CPAP
A
A non-invasive ventilatory strategy
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
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
21
Q
What are the common pneumonia pathogens
A
S. pneumoniae S. aureus Mycoplasma pneumoniae Haemophilus influenza Chlamydophila pneumoniae Respiratory viruses
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
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)
24
Q
What is Shock
A
Clinical syndrome caused by inadequate tissue perfusion and oxygenation leading to abnormal metabolic function
25
What are the types of shock
```
Cardiogenic
Neurogenic
Hypovolaemic
Anaphylactic
Septic
Obstructive
```
26
What are the 4 types of hypoxia
Hypoxic hypoxia: decreased O2 supply
Anaemic hypoxia: decreased haemoglobin function
Stagnant hypoxia: inadequate circulation
Histotoxic hypoxia: impaired cellular O2 metabolism
27
What is hypovolaemic chock
Caused by losses of blood, plasma or fluid
| AKA haemorrhagic chock
28
How is hypovolaemic shocktreated
IV access
IV fluids +/- blood
Treat cause (eg stop bleed)
Monitor response
29
What is anaphylactic shock
Sudden onset generalised immunce condition caussed by exposure to causative substance in a sensitised person
30
How is anaphylactic shock treated
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
31
What is septic shock
Sepsis accompanied by hypotension and perfusion abnormalities despite adequate fluid resuscitation
32
What is cardiogenic shock
`Tissue hypoperfusion that is primarily attributable to damage to the heart.
33
How is cardiogenic shock classified
```
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?)
```
34
How does cardiogenic shock present
```
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
```
35
What is the antidote for paracetamol overdose
N-Acetyle-cysteine
36
What is the antidote for benzodiazepines
Flumazenil
37
What is the antidote for hypoglycaemia
Glucagon
38
What is the antidote for hyperkalaemia
Dextrose
39
What is the antidote for local anaesthetic toxicity
20% lipid emulsion
40
What is the antidote for bradycardia
Atropine
41
What is the antidote for carbon monoxide
Oxygen
42
What is the antidote for TCADs arrhythmias
Sodium bicarbonate
43
How is a patient's admission to ICU decided
```
Diagnosis
Reversibility
Comorbidity
Functional status and frailty
Patient's wishes
Parent team opinion
```
44
What are the cons of admission to ICU
```
Critical care neuro-myopathy
Hospital acquired infections
Physical reconditioning and functional impairment
Cognitive impairment
Delirium
PTSD, anxiety, depression
```
45
What is the fundamental difference between type 1 and type 2 respiratory failure
Type 1: decreased PaO2
Type 2: increased PaCO2
46
What is meant by shunt
When there is normal perfusion to an alveolus but ventilation fails to supply the perfused area
47
What is meant by dead space
When there is normal ventilation of an alveolus but perfusion fails to supply the ventilated area
48
What are vasopressors
Drugs that work on alpha-receptors to increase the systemic vascular resistance
49
What are inotropes
Drugs that work on beta-receptors to increase the contractility of the heart
50
How is cerebral perfusion pressure calculated
CPP=MAP-ICP
| Cerebral perfusion pressure = Mean arterial pressure - intracranial pressure
51
What are the key common respiratory pathogens
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
52
Which antibiotics should be used in respiratory tract infection
PO:
- Amoxicillin
- Doxycycline
- Co-amoxiclav
- Clarithromycin
- Ciprofloxacin
- Cotrimoxazole
IV:
- Amoxicillin
- Clarithromycin
- Co-amoxiclav
- Cefuroxime
- Piperacillin-tazobactam
- Temocillin
53
What is the difference between infection and colonisation
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
54
What are the guidelines in Leeds for those with hospital acquired pneumonia that are positive for MRSA
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
55
What iis involved in MRSA decolonisation
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
56
What framework can be used to investigate patient safety incidents
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
```
57
How is a major trauma defined
Patient with an injury severity score of >15
58
What is the Golden hour
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
59
What is the mechanism of injury and why is it useful to know
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.
60
What is triaging
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
61
What is involved in triage in trauma
Combination of mechanism of injury, anatomical and physiological data.
62
What is the mneumonic for life threatening thoracic injuries
ATOM FC
```
Airway obstruction
Tension pneumothorax
Open chest wound
Massive haemothorax
Flail chest
Cardiac tamponade
```
63
What is the mneumonic for assessing circulatory signs
```
HEP B
Hands (temp/sweat/cap refill)
End organ perfusion (conscious levels/urine output)
Pulse (rate/quality/regularity)
Blood pressure (hypotension *late sign)
```
64
What is the Glasgow Coma Scale
```
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
How is the log roll performed on a trauma patient
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
What are the key spinal cord syndromes
Central cord syndrome
Anterior cord syndrome
Brown-sequard syndrome
Complete spinal cord syndrome
67
What do pelvic binders do
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
How is trauma care initiated
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
How is radiology used in trauma
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
How do airways sound and present
Open: quiet with air movement
Obstructed: quiet with no air movement
Partially obstructed: noisy
71
How is a massive haemothorax defined
>1500ml blood in the chest
72
What is a flail chest
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
How is flail chest treated
Adequate oxygenation and ventilation
Cautious fluid resuscitation
Analgesia
74
What is cardiac tamponade
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
How are patients on fluid bolus management categorised
Rapid responder: Bleeding stopped or slowing
Transient responder: Bleeding ongoing
Non responder: Bleeding torrential and life threatening
76
What are the types of anaesthesia
General: total loss of sensation
Regional: loss of sensation to a region or part of the body
Local: topical, infiltration, numbing the area
77
What is an anaesthetic drug
A drug that induces partial or total loss of sensation
78
What are the three types of drugs the create a balanced anaesthesia
Amnesic: lack of response and recall to noxious stimuli (unconsciousness)
Analgesic: pain relief
Akinetic: immobilisation/paralysis
79
How is General anaesthetic commenced
Amnesic (induction agents)
- Induce loss of consciousness in one to twp arm-brain circulation times
- 10 to 20 seconds
80
How are amnesic drugs categorised
Induction agents - to start the process
| Maintenance agents: to maintain amnesia for the duration of anaesthetic
81
What are the main induction agent drugs
Propofol
Thiopentone
Ketamine
Etomidate
82
What are the main amnesia maintenance agent drugs
Propofol infusion: total IV anaesthesia
Inhalational agents: inhalational anaesthesia (vapours) started after induction and administrated via vaporisers or breathing circuits
83
What are the key inhalation agents
Isoflurane
Sevoflurane
Desflurane
Enflurane
84
What is the definition of MAC
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
What is 1 MAC of nitrous oxide
104%
86
What is 1 MAC of sevoflurane
2%
87
What is 1 MAC of isoflurane
1.15%
88
What is 1 MAC of desflurane
6%
89
What is 1 MAC of enflurane
1.6%
90
Why is analgesia used in anaeasthetic procedures
Required for:
- Insertion of airway
- Laryngeal mask airway
- Intubation
- Intraoperative pain relief
- Postoperative pain relief
91
What are the two categories of muscle relaxants and how do the work
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
What are the most common anaesthesia issues
Intraoperative labile blood pressure: hypotension or hypertension
Postoperative nausea and vomiting
93
What causes labile blood pressure and how is it managed
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
What are the key vase-active drugs used in hypotension in anaesthetics
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
What does PONV mean
Post Operative Nausea and Vomiting
96
What are the key anti-emetic drugs
```
5HT3 blockers: ondansetron
Steroids: dexamethasone
Antihistamine: cyclizine
Phenothiazine: prochlorperazine (stemetil)
Anti-dopaminergic: metoclopramide
```
97
What is the order of usage of anti-emetics
Ondansetron -> Dexamethasone -> Cyclizine -> Prochlorperazine
98
How are patients woke up out of general anaesthetic
Stop anaestheic vapours ->
Give oxygen ->
Perform throat suction ->
Reverse muscle relaxation (reversal)
99
What are the key anaesthetic reversal drugs
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
How are patients transferred from surgery to post anaesthesia care unit
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
What is a DVT
Deep vein thrombosis
| The formation of one or more blood clots in a deep vein, typically of the lower extremities
102
What are the two type of DVT
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
What is VTE
Venous thromboembolism
| An umbrella term that encompasses DVT and PE
104
What is a recurrent VTE
VTE that recurs in a patient after the completion of the first 2 weeks of antithrombotic therapy
105
What is a provoked VTE
VTE in an individual with ≥ 1 risk factor for VTE
106
What is an unprovoked VTE
aka idiopathic VTE
| VTE in an individual without risk factors for VTE
107
What causes DVT
Any factor that causes hypercoagulability, endothelial damage and/or venous stasis can cause DVT
108
What are the risk factors for VTE
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
What is the DVT risk factor mneumonic "THROMBOSIS" for
```
Travel
Hypercoagulable/ HRT
Recreational drugs
Old (>60)
Malignancy
Blood disorders
Obesity/Obstetrics
Surgery/Smoking
Immobilisation
Sickness (CHF/MI, IBD, nephrotic syndrome, vasculitis)
```
110
What is the Virchow triad
Hypercoagulability
Endothelial damage
Venous stasis
111
How does VTE present
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
What is the WELLS score for DVT
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
How is a DVT diagnosed
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
What are the differentials in suspected DVT
```
Superfical thrombophlebitis
Muscle or soft tissue injury (post traumatic swelling or haemotoma)
Lymphadema
Venous insufficiency
Ruptured popliteal cyst
Cellulitis
Compartment syndrome
```
115
How is DVT treated
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
What are the potential complications of DVT
```
PE
Postthrombotic syndrome (chronic venous insufficiency)
Venous gangrene (rare)
```
117
What is cellulitis
Local infection of the deep dermis and subcutaneous tissue
118
How does cellulitis present
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
What are the common causes of cellulitis
Staph aureus
Group A streptococcus (mainly strep pyogenes)
Group C streptococcus (mainly strep dysgalactiae)
MRSA
120
What is the Eron Classification
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
How is cellulitis treated
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
What is the definition of acute coronary syndrome
The suspicion or confirmed presence of acute myocardial ischaemia
123
How is ACS classified
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
What is myocardial injury
Any damage to myocardial tissue that leads cardiac troponin (cTn) levels to rise above the 99th percentile of the upper reference limit.
125
How does ACS present
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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
How is ACS diagnosed
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
What are the ECG changes in STEMI
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
How is STEMI managed
"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
What are the ECG changes in NSTEMI or Unstable angina
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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
How is NSTE-ACS managed
Depends on patients mortality risk, clinical findings, and the availabiltiy of resources
Anticoagulation therapy
131
What are the options for medical management of MI
MONA-BASH
```
Morphine
Oxygen
Nitroglycerin
Antiplatlet drugs (aspirin and ADP receptor inhibitor eg clopidogrel)
Beta blockers
ACE inhibitors
Statins
Heparin
```
132
What are the differentials in suspected ACS
```
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
What are potential differntials of ST elevations on ECG
```
Early depolarisation
LBBB
Brugada syndrome
Myocarditis
Pericarditis
PE
Hyperkalaemia
Tricyclic antidepressant use
Poor ECG lead placement
```
134
What is angina
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
What is stable angina
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
What is coronary artery disease
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
What is the epidemiology of Coronary artery disease
The leading cause of death worldwide
| Lifetime risk of CAD at age 50 is ~50% for men and 40% for women
138
What causes coronary artery disease
Atherosclerosis is the most common causes
139
How does angina present
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
How do symptoms present in stable angina
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
How is angina treated
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
How does costochondritis present clinically
Sharp, well localised pain that is repoducible on palpatient of costal cartilage
History of recent exercise, exertion or chest wall trauma
143
How is costochondritis diagnosed
Clinical diagnosis by history and exam
| Normal chest xray
144
How is costochondritis treated
Pain mangement
Rest
Cough suppressants (eg codeine)
Heat or ice packs
145
What is a pulmonary embolism
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
What causes PE
"PE is FATAL"
```
Fat
Air
Thrombus
Amniotic fluid
Less common (bacterial, tumor and cement)
```
147
How does a PE present
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
What is the WELLS criteria for PE
```
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
What is the PERC criteria
```
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
How is a suspected PE diagnosed
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
What imaging is done in investigating suspected PE
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
What are ECG findings of PE
```
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
How should a patient with a PE be managed
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
What are the complications of PE
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
What is pneumonia
A respiratory infection characterised by inflammation of the alveolar space and/or the interstitial tissue of the lungs
