ITU Flashcards

Question

What are the indications for BiPAP?

Answer 1

Type 2 RF, COPD exacerbation, post-surgery in COPD, weaning from invasive ventilation, type 2 RF from neuromuscular/chest wall disease.

Answer 2

Reduces work of breathing, improves V:Q, cheaper, no sedation required, available outside ICU, can be interrupted for breaks.

Answer 3

Requires cooperation and conscious patient, can be uncomfortable (tight mask/ noisy), risk of aspiration, can lead to gastric inflation.

Answer 4

* Uncooperative/unconscious patient * vomiting * inability to protect airway * pneumothorax * trauma/burns to face * too unwell for intubation * pathological leak - basal skull #

Answer 5

Administered O2 at pressure above atmospheric.

Answer 6

Decompression illness, CO poisoning, anaerobic infections (nec fasc), could be used in anaemic Jehovah's Witness patients.

Answer 7

* Increases O2 dissolved in blood (Henry law) * increases O2 bound to Hb * creates a larger gradient for O2 into tissues. * Hyperoxia causes vasoconstriction and high SVR – HTN and reflex brady

Answer 8

TV = 6-8ml/kg, PEEP 5cmH20, RR 12-14, I:E 1:2, peak pressure limit = 30 cmH20.

Answer 9

**Airway** o Complications with intubation – trauma , aspiration, hypoxia o Complications related to tracheostomy o Unable to speak o ET tube can damage lips/ tongue etc – fixation devices can help with this o Damage to larynx – ulceration, adhesions, stenosis , vocal cord damage o Laryngeal oedema – post extubation stridor – steroids/ adrenaline / reintubate o Damage to subglottic area by cuff – better with high vol, low pressure – less ischaemia. Can lead to tracheomalacia or tracheal stenosis **- Breathing** o Baro, volu, atelectotrauma o Pneumothorax, pneumomediastinum, surgical emphysema o Atelectasis – VQmismatch o VAP o O2 toxicity o Weakness of respiratory muscles **- CVS** o Reduced preload and CO – important to optimise intravascular volume o Increase in RV afterload **- CNS** o Increased ICP o PTSD o Effects of sedation – delirium **- GI** o Stress ulcers o Paralytic ileus = prokinetics can be used o Artificial nutrition and problems associated with NGT

Answer 10

By minimizing barotrauma, volutrauma, and atelectotrauma through lung protective ventilation.

Answer 11

o Barotrauma minimised by TV 6-8ml/kg o Maintain low p plateau pressure < 30cmH20 o PEEP = Reduce atelectotrauma / sheer stress – keep alveoli open o Supported by ARDSnet trial idea is less trauma = less inflammation = less long term lung damage but also less likely to trigger SIRS

Answer 12

Airway pressure release ventilation, an open lung method of invasive ventilation used in severe ARDS as a trial to improve oxygenation

Answer 13

Two pressures (P high and P low) and time in each phase (T high and T low), with T high being much longer than T low. high pressure for long time allows recruitment and improved oxygenation short period of pressure release helps CO2 clearance patient breathes spontaneoysly on top

Answer 14

APRV has a long period of high pressure for recruitment and a short low pressure release for CO2 removal , minimizing lung injury.

Answer 15

P high = patient's current p plateau pressure (ideally < 30cmH20), P low = 0 cmH20, T high = 3-8 seconds, T low = 0.3-0.8 seconds, FiO2 100% initially. T low initially start at 0.5s and then adjusted to start next breath at 75% peak expiratory flow rate – to prevent completely reaching 0 pressure, prevents de-recruitment

Answer 16

Release pressure intermittently and spontaneous ventilation.

Answer 17

- Reduce T high – number of release breaths per min would be increased by doing this. - Increase P high – analogous to increasing TV - Reduce sedation to increase spontaneous breathing

Answer 18

* Reduced sedation (haemodynamic, ICU-AW, delirium) * improved weaning * allows ventilation/CO2 removal throughout the cycle * less need for paralysis hence ICU-AW * opens dependant lung units improving VQ * promotes venous return.

Answer 19

- High intrathoracic pressure = impaired venous return and CO - Increased pulmonary vascular resistance and hence and RV afterload and hence LV preload - Impaired coronary perfusion, ischaemia and dysfunction

Answer 20

- LV uncoupling – reduced transmural pressure hence less pressure required for pumping. Less LV work - Reducing preload in overloading patient with HF - Improved oxygenation may result in improved myocardial function - More haemodynamic stability from reduced sedation to allow spontaneous vent.

Answer 21

- Bronchopulmonary fistula - Pneumothorax – without chest drain - Pulmonary artery HTN / RHF - Restrictive lung disease – bronchospasm - Severe CVS instability – hypovolaemia - Recent lung surgery - Raised ICP/ traumatic brain injury – however will improved O2 outweigh the harm of pressure

Answer 22

Higher risk of pneumothorax, CVS instability esp if RHF or PAH, and higher metabolic demand from spontaneous ventilation.

Answer 23

Reduce FiO2 when good PaO2, then reduce P high, increase T high, eventually transition to CPAP with spontaneous breathing.

Answer 24

Increase FiO2, increase P high by 2, increase T high by 0.5s, reduce T low.

Answer 25

Superoxide, hydrogen peroxide, hydroxyl free radicals.

Answer 26

Glutathione and superoxide dismutase. exogenous = vit C

Answer 27

**Lungs =** - oxygen free radicals cause inflammation = tracheobronchitis, impairment of surfactant and atelectasis, ARDS, pulmonary fibrosis. - absorption atelectasis, - Bronchopulmonary dysplasia in neonates - loss of hypoxic vasoconstiction - shunting as there are still poorly ventilated regions of lung - CVS = vasoconstriction - cerebral and coronary. ROS creates a prothombotic state - CNS = headache, dizziness, visual distrubance, seizures and coma - Retina = retinopathy of prematurity

Answer 28

cyanide poisoning cluster headache CO poisoning decompression sickness - the bends anaerobic infections

Answer 29

ROS can cause damage to DNA - mutation damage to RNA - impaired protein production lipid oxidation and membrane dysfunction oxidation to proteins / enzymes

Answer 30

retinopathy bronchopulmonary dysplasia

Answer 31

Bleomycin, which can cause pulmonary fibrosis within 6 months.

Answer 32

regional over GA where possible tolerate sats >85% if known bleomycin lung injury OR 88-92% in those with possible bleomycin lung injury lung protective ventilation

Answer 33

- FiO2 = 100% should not be given for more than 12 hours / day (hyperbaric event less) - FiO2 = 80% should not be given for more than 24 hours / day - < 50% is theoretically safe indefinitely

Answer 34

O2 should be prescribed target saturations for each patient - use ABG to titrate too 15L non rebreathe reserved for emergencies

Answer 35

Phagocytosis by macrophages use oxygen free radicals .

Answer 36

Nasal and carina irritation, coughing, changes to smell and taste.

Answer 37

- PEEP, recruitment manoeuvres, - optimise fluid within lungs - ventilator synchrony - proning, - physiotherapy - increasing MV - increase inspiratory time - overall increases mean alveolar pressures (hence opens lung).

Answer 38

Increase MV ensure adequate expiration time I:E reduce deadspace/rebreathing permissive hypercapnia. alveolar deadspace reduced by improving perfusion = adequate filing and CO, avoiding excess intrathoracic pressure. reduce equiptment deadspace

Answer 39

* Weaning on ITU * ventilation in upper airway obstruction (burns, trauma, tumour) * after major H&N surgery (free flaps/ oral tumour) * for long term ventilation in neuromuscular weakness - C spine injury

Answer 40

* Less sedation required * better mouth hygiene * can speak * less risk of laryngeal injury * improves respiratory muscle strength * protects from secretions * helps recover laryngeal desensitisation. * discharge to tracheostomy ward

Answer 41

* Larynx desensitised - poor cough, aspiration, poor speach * VAP * ICU-AW * delirium.

Answer 42

Immediate: * insertion complications - sedation related, loss of airway, hypoxia (derecruitment) * bleeding, pneumothorax * oesophageal damage, recurrent laryngeal nerve injury. Short term: blockage with secretions, infection of stoma, accidental decannulation, haemorrhage. Long term: tracheomalacia, trachea-oesophageal fistula, psychological/cosmetic.

Answer 43

Compared early tracheostomy insertion vs late; no difference in mortality or ventilator days, but less sedation needed in tracheostomy group.

Answer 44

Personnel: operator, bronchoscopist, seditionist, runner. Pre-procedure: consent, position neck extended, identify landmarks USS , check kit inc. cuff, pre-oxygenate, increase sedation + relaxant Procedure: fibreoptic scope down ET, withdraw ET to subglottic area, sterile prep, insert needle between 2nd/3rd tracheal ring, seldinger (guidewire, remove needle, dilator, insert tracheostomy), inflate cuff, ventilate.

Answer 45

Anatomy related: * aberrant vessels * abnormal tracheal/thyroid anatomy * morbid obesity * inability to extend neck * previous tracheostomy Respiratory: * PEEP >10 cmH20 * FiO2 >0.6 Other: coagulopathy, local infection.

Answer 46

Different sizes, fenestrated for airflow, cuffed/uncuffed, inner tube for safety, presence of subglottic suction, use of passey muir valves.

Answer 47

Hypoxia, respiratory distress, tachypnoea, audible cuff leak, abnormal capnography, tachycardia and hypertension, fresh blood.

Answer 48

- Call for help - 15L non rebreathe O2 via upper airway and tracheostomy site - Get tracheostomy box and algorithm **- Assess breathing** o Feel mouth / tracheostomy site for air flow o Chest movements o Listen – stridor / secretions / air leak o Can attach water circuit and capnography to assess breathing – DO NOT BAG - If not breathing – check pulse = ? CPR otherwise… - Remove passey muir valve / sweedish nose - Remove inner tube - Attempt to pass suction catheter – if this passes, then can ventilate via it - Deflate cuff - Remove tracheostomy - At each stage reassess for improvement - Once tracheostomy removed

Answer 49

**- Cover with gauze and ventilate from mouth** o If recent stoma < 7 days or obese patient or known difficult stoma – o Bag mask, LMA, intubate o Insert tube beyond tracheostomy site **- Can also intubate stoma** o with small tracheostomy or size 6.0mm tube o If not recent stoma >10days old , surgical tracheostomy, known difficult upper airway o Can use an Aintree catheter (airway exchange catheter) loaded onto fibreoptic scope to facilitate this (Aintree catheter than acts as a bouje)

Answer 50

Paediatric size facemask, spare tracheostomy and inner cannula, tracheal dilators.

Answer 51

Responsible for making algorithms and training to provide safer care; found worse outcomes when cared for on wards due to untrained staff, lack of equipment, lack of monitoring.

Answer 52

Date performed, tube size, patient details, percutaneous or surgical, who to call in an emergency.

Answer 53

**- Surgical** o Trachea cut and stoma stitched open o Stoma will be established sooner – around 2 days o Used after H&N surgery or if anatomy is difficult to perform percutaneous **- Percutaneous** o Performed by dilating tissues via seldinger o Takes 7-10 days to be established o Can be performed at bedside in ICU

Answer 54

- Complicated anatomy – tracheal deviation, short neck, concerns about aberrant vessels crossing the site - When tracheostomy is performed as part of operative procedure e.g. ENT surgery - Morbid obesity - Cervical instability

Answer 55

Between 2nd and 3rd tracheal ring.

Answer 56

Horizontal, window, vertical slit (H shape), Bjork flap.

Answer 57

Sutures placed to hold open the stoma site of a tracheostomy.

Answer 58

- Reduced deadspace = reduced work of breathing - Bypass natural humidifcation and filtering = need humidifiers and suctioning of secretions - Removes ability to speak – can use passey muir - Can affect taste and smell - Affects swallow = NGT

Answer 59

Passive: Sweedish node/HME; Active: hot water baths.

Answer 60

Smaller size, no room for inner tube, uncuffed usually, usually surgical.

Answer 61

**- Trachy related** o Blocked tracheostomy with mucus / dried blood o Displacement of tracheostomy and hence obstructed o Cuff deflation / herniated over end of tube o Cuff inflated with passey muir valve **- Respiratory:** o Pneumonia – VAP or Aspiration o Pneumothorax o Atelectasis / V:Q mismatch o Bronchospasm o Clot in airway e.g. obstructing main bronchus o P.E **- Technical** o Low FiO2

Answer 62

Tracheostomies contributed to ITU airway complications significantly common problems included failure to recognize blocked/displaced tubes, lack of emergency equipment, lack of capnography.

Answer 63

Process of reducing ventilatory support until patient is spontaneously breathing and extubated

Answer 64

- Recovered from illness e.g. pneumonia - Awake and cooperative – appropriate sedation holds - Good cough / intact airway reflexes - Minimal vasopressor support - Normal metabolic parameters - PEEP of 5 - PaO2/ FiO2 >20 (150mmHg)

Answer 65

**- Neuromuscular** o Underlying NM disease e.g. myasthenia o Critical illness myopathy o Electrolyte disturbance – hypoK/PO4/Ca/Mg o Respiratory depression – no longer respond to high CO2 – sedatives **- Respiratory** o Increased airway resistance – bronchospasm , thick secretions o Reduced compliance = pneumonia, diaphragmatic splinting - **Increased O2 consumption** o Sepsis **- psych** o delirium

Answer 66

Mucosal inflammation and swelling caused by ET tube and cuff, resulting in oedema, swelling, and stridor after extubation

Answer 67

* Difficult traumatic intubation * High cuff pressure >30cmH20 * Prolonged intubation * Self-extubation

Answer 68

* Adrenaline nebulisers * Steroids * CPAP * Heliox

Answer 69

* Gradually wean support * Allow spontaneous breathing trials

Answer 70

* RR >35 * Sats < 90% * Tachycardia >140 * HTN or hypotension * Sweating/agitation * Respiratory distress * RSBI >105 ## Footnote rapid shallow breathing index = RR/ TV

Answer 71

Reintubate or trial NIV

Answer 72

- Cuff down trial – if subglottic secretion load is minimal , SALT agree - Passey muir valve - Decannulation cap – block off tracheostomy so upper airway used - Decannulate / downsize tracheostomy– if tolerating for 24 hours a day o MDT decision

Answer 73

An extracorporeal circuit that functions as an artificial lung, oxygenating blood and removing CO2

Answer 74

- **Venous venous – VV ECMO** – blood taken from vein and back into vein o IJ or femoral used o No circulatory support required o Used for when gas exchange is the issue e.g. ARDS - **Veno-arterial – VA ECMO** – femoral vein and back into femoral artery o Oxygenation and pumping support o Used for cardiogenic shock - **Arterio venous AV ECMO** o Uses arterial blood at a pressure to pump through an oxygenator and return to venous system

Answer 75

- Blood is taken from patient via drainage cannula and enters extracorporeal circuit - Through centrifugal pump – provides additional circulatory support - Then gas exchange takes place at membrane oxygenator - Finally passes through a heat exchanger - And then Back to patient via return cannula - Circuit must be anti-coagulated

Answer 76

180 to 220 seconds

Answer 77

= Argatroban or bivalirudin or danaparoid or fondaparinux

Answer 78

- Haematological o Clotting / bleeding o Severe thrombocytopenia – consumptive or HIT o Haemolysis o Blood and platelet transfusions often required – associated complications - Other o Air embolism o AKI o Infection o Limb ischaemia

Answer 79

* Irreversible organ damage * End stage malignancy * Multi-organ failure * Coagulopathy * Severe pulmonary HTN relative - high BMI, > 65yrs, intracranial bleed, > 7days on high pressure vent with FiO2>0.8

Answer 80

Significant reduction in mortality in patients with ARDS who went on ECMO versus conventional management

Answer 81

- Potentially reversible severe respiratory failure – PaO2 < 10kpa for >6hours - Severe hypercapnia acidosis pH < 7.2 - Trial of prone position and optimal ventilation with lung protective strategies unsuccessful - Murray Lung injury score of 3 or more There are 6 ecmo centres in the UK

Answer 82

Chronic inflammatory condition of the airways characterised by recurrent episodes of reversible wheeze, cough, and shortness of breath (SoB) - due to bronchial smooth muscle contraction, inflammation and mucus hypersecretion

Answer 83

**- Initial sensitisation event** o IgE production by B lymphocytes upon exposure to allergen o IgE binds mast cells prepared for next exposure **- Subsequent exposure** o IgE binds allergen o Mast cell degranulation – histamine release o Cascade of immune mediators released = leukotrienes, prostaglandins etc o Immune cell migration o Results in  Smooth muscle contraction  Mucus production  Inflammation o Thus airways become narrowed

Answer 84

- Respiratory effects o Narrowed airways affects expiratory phase o Poor emptying of alveoli – intrinsic PEEP and High intrathoracic pressures o Overall poor ventilation and V:Q mismatch and hypoxaemia o Increased work of breathing and eventually respiratory fatigue - CVS effects o Raised intravascular pressure can also reduce venous return

Answer 85

- Triad = SoB, cough, wheeze - Atopy = hayfever, asthma, eczema - Worse at night / diurnal variation

Answer 86

- A to E – sit patient up - Hx o normal treatment and control, previous ICU admissions, usually PEFR, recent / recurrent steroid use - Ix o CXR , PEFR, ABG, ECG **- Specific initial treatment ** o B agonist = salbutamol 5mg nebuliser – 4 hourly or back to back (every 15 mins) o Muscarinic antagonist = ipratropium 0.5mg 4 hourly o Steroid = prednisolone 40-50mg 5 days OR IV hydrocortisone 200mg then 100mg 6 hrly **- Specific other options…** o MgSO4 = 2g over 20 mins o Aminophylline – 5mg/kg loading dose over 20 mins followed by infusion 0.5-1mg/kg/hr o IV salbutamol – 250mg IV bolus o Ketamine – bronchodilator o Sevoflurane = AnaConDa o Nebulised adrenaline o Heliox

Answer 87

- Ventilatory support required: o Persisting hypoxia despite O2 o Worsening CO2 / acidosis o Appear tired / confused / low GCS o Deterioration in PEFR o Cardiorespiratory arrest - Any features of life threatening or near fatal - May be referred for aminophylline infusion and monitoring if HDU not available

Answer 88

Hypokalaemia from salbutamol treatment

Answer 89

- Anatogonises Calcium - Which is needed for smooth muscle contraction - Hence smooth muscle dilation - Also mediates parasympathetic Ach release

Answer 90

- Needs monitoring HDU / ITU – cardiac monitor due to risk of tachyarrhythmias - Check levels 4-6 hours after infusion - If already on theophylline – check levels before starting

Answer 91

NIV intubation

Answer 92

- RSI – ketamine and rocuronium - Lung protective ventilation o TV 4-6ml/kg, low RR 8-12/min , high I:E ratio, very little PEEP <5cmH20, permissive hypercapnia - Treatment of likely cardiovascular collapse - fluids prior to induction and vasopressors ready

Answer 93

- Positive pressure ventilation and high intrathoracic pressures from autoPEEP (dynamic hyperinflation) – reduced venous return = if this happens can try disconnecting from ventilator and allowing gas to escape - Vasodilation via anaesthetic affects and negative ionotropy– reduced SVR and CO – especially significant in dry patient - Development of tension pneumothorax – due to PPV and gas trapping - Hypovolaemia due to reduced oral intake with development of asthma and increased evapourative respiratory losses

Answer 94

- High risk of pneumothorax - Ensure no endobronchial intubation

Answer 95

- Allowing a safe level of high CO2 to protect the lungs from excessive barotrauma/ hyperinflation from ventilation. General rule pH >7.2 - Generally high CO2 is tolerated well – can cause vasodilation and cerebral oedema, pulmonary vasoconstriction and reduced myocardial contractility - Caution in head injury patients as effects ICP - Potentially benefits = right shift in dissociation curve, vasodilation and improved perfusion

Answer 96

- To give time for alveolar emptying through narrowed airway and prevent gas trapping - Paradoxically by reducing auto PEEP and intrathoracic pressures, it can improve blood flow to the lungs and hence reduce deadspace and lower CO2 despite a lower minute volume

Answer 97

79:21 helium:oxygen mixture that reduces work of breathing due to less density and more laminar flow

Answer 98

Frequent life threatening exacerbations and poor response to treatment

Answer 99

- Heavy use of inhalers - 3 or more classes of medications - Previous near fatal - Previous admission in last year - Brittle asthma - Adverse psychological/ behavioural features

Answer 100

- Speeds recovery and shortens hospital stay - Reduces need for B2 agonists - Reduces no. of admissions

Answer 101

- Pulsus paradox is a drop in arterial BP of 10mmHg during inspiration and negative intrathoracic pressure. - In asthma, airway obstruction increases the effort needed for inspiration, leading to a more negative intrathoracic pressure. - Exaggerated pulsus paradox

Answer 102

- After ventilation from very high airway pressures leading to pneumothorax or reduced venous return from dynamic hyperinflation

Answer 103

- Increased airway resistance – infiltration by inflammatory cells, bronchial smooth muscle constriction, mucus plugging - Intrinsic PEEP – rapid respiratory rate, not enough time to fully exhale - Increased lung volumes result in flattening of diaphragm and reduced compliance – worsening ventilation

Answer 104

Chronic airway disease characterised by persistent airway obstruction, heavily linked to smoking

Answer 105

- Spectrum of diseases involving bronchitis and emphysema - Bronchitis o Airway inflammation, cilia dysfunction, hypertrophy and mucus plugging - Emphysema o Loss of elastin and alveolar destruction o Reduced surface area for gas exchange o Collapse of smaller bronchioles

Answer 106

* Breathlessness * Chronic cough * Sputum * Wheeze

Answer 107

FEV1/FVC <0.7 with lack of reversibility with B agonists

Answer 108

* GOLD 1 mild: FEV1 >/= 80% predicted * GOLD 2 moderate: 50-80% * GOLD 3 severe: 30-49% * GOLD 4 very severe: < 30% based on FEV1 , for all categories FEV1/FVC < 0.7

Answer 109

**- Conservative** o Smoking cessation o Pneumococcal and influenza vaccines o Pulmonary rehabilitation = 6 weeks of aerobic training, strength training, education and nutrition advice **- Pharmacological** o SABA or SAMA o 2nd step = LABA + ICS (or LAMA and stop SAMA) o 3rd step = LAMA + LABA + ICS **- Other** o LTOT = mortality benefit

Answer 110

- SABA = salbutamol/ terbutaline - SAMA = ipratropium - LABA = salmeterol , formoterol - LAMA= tiotropium - Combined steroid o fluticasone/ salmeterol = Seretide - Budesonide / formoterol = symbicort

Answer 111

- Infection e.g. H.influenzae, S.pneumonia, Moraxella catarrhalis - Other triggers = cold , physical exertion, atmospheric pollution - Increase in resistive and elastic work of breathing - Airway obstruction can result in intrinsic PEEP - Intrinsic PEEP will need to be overcome by next breath – increased work of breathing - Risk of fatigue and rise in CO2

Answer 112

- Abx , salbutamol nebs, steroids - Sats – 88 -92% via venturi devices - May require NIV or invasive ventilation

Answer 113

- Severe hypercapnia / acidosis / hypoxia - Impaired conscious level - CVS instability - NIV failed

Answer 114

* PaO2 < 7.3kpa * PaO2 < 8kpa with secondary polycythemia/pulmonary HTN - can be used for atleast 15 hours / day - no smoking in household

Answer 115

- GOLD criteria – FEV1 - Frequency of exacerbations - Hospitalisations / ITU - Exercise capacity - MRC dyspnoea scale

Answer 116

- Grade 1 = no trouble with breathlessness except on strenuous exercise - Grade 2 = SoB on walking up hill / fast walking - Grade 3 = SoB when walking and has to stop - Grade 4 = has to stop every 100m or few minutes - Grade 5 = SoB in house e.g. when dressing

Answer 117

- Exacerbation and Type1/2 RF - Pneumothorax - Cachexia - Depression - polycythaemoa - pulmonary HTN and RHF

Answer 118

Acute onset of severe hypoxic respiratory failure characterized by diffuse inflammatory alveolar injury - Caused by increased pulmonary vascular permeability

Answer 119

* Onset within 1 week of known clinical insult * Imaging showing bilateral infiltrates or opacifications * Oedema not due to cardiogenic cause or fluid overload * Hypoxemia defined by PaO2/FiO2 <300mmHg and PEEP > 5 cmH2O

Answer 120

* Mild: < 39.9 kPa (300 mmHg) * Moderate: < 26 kPa (200 mmHg) * Severe: < 13.3 kPa (100 mmHg)

Answer 121

* Pneumonia * Trauma - drowning, contusions, inhalation injury * Pulmonary embolism

Answer 122

* Major trauma / burns * Pancreatitis * TRALI * Fat embolism * Sepsis

Answer 123

* Age * Comorbidity (e.g., malignancy) * Multiple organ failure * Smoking / alcohol * Genetic susceptibility

Answer 124

**- Exudative – acute phase** o Diffuse alveolar damage, loss of BM and leaky alveoli o Exudate forms = hypoxia & resp failure o Infiltrates on CXR o Tissue factor released from damaged cells – microthrombi form within pulmonary capillaries o Reduced surfactant – reduced compliance **- Proliferative phase** o Repair and inflammation **- Fibrotic phase** o Collagen and fibrosis = hypoxia, long term ventilation requirement, high pulmonary pressures

Answer 125

- Idiopathic pulmonary fibrosis - Drug induced fibrosis = methotrexate - Congestive HF

Answer 126

* CXR / CT for infiltrates * ECHO to rule out cardiogenic cause * Blood tests for ABG and coagulation - Bronchoalveolar lavage – neutrophilia

Answer 127

**- Strategies to improve O2** o Trial of HFO / CPAP initially o Invasive ventilation = Increase PEEP (can go up to 15-20cmH20) , restrict fluids, consider furosemide , Lung protective ventilation (6ml/kg) and permissive hypercapnia o NMBA trial – atracurium infusion + BIS monitoring and TOF monitoring - For 48hrs only o Proning – good evidence compared to APRV o APRV – no evidence that one mode is better than another o ECMO **- Supportive care – **analgesia, sedation, nutrition, VTE and gastroprophylaxis - **Other options** – Steroids (GuARDS trial)

Answer 128

**- Improves V/Q** o Front of chest not full of exudate and when proned perfusion to this side will increase due to gravity. o Fluid will slowly drain to front side, need to alternate between prone and non-prone **- Homogenous distribution of TV and hence improved pressures and injury** o when supine there is fluid/stuff at base and so only top of lungs are being used. All the volumes are being squeezed into top of lungs – barotrauma, inflammation, cytokines, worsening of ARDS but also inflammatory response and multiorgan failure. o Proning allows better spread of the fluid /consolidation so alvolei can share the volume now, so less pressure exerted on each one. less barotrauma and inflam damage. **- Increases FRC** Improved drainage of secretions from dorsal lung areas to central airways **Recruitment of dorsal lung units that aren’t damaged by barotrauma**

Answer 129

* Requires good staffing levels * Facial oedema * Airway concerns * Peripheral nerve damage * Ocular injuries * Increased intracranial and abdominal pressures * lines may get pulled during the process

Answer 130

16 hours or more in 24 hours

Answer 131

**- Absolute** o Spinal instability o Open chest post cardiac surgery / trauma o Patient less than 24 hours post cardiac surgery o Central cannulation for veno-arterial ECMO or biventiricular assist device support. (venovenous ecmo is not a contraindication) **- Relative** o Severe facial fractures o TBI or raised ICP o Raised intraocular pressure o Frequent seizures o Morbid obesity o Pregnancy T2/3 o Tracheostomy in last 24 hours

Answer 132

- Adequate staff including anaesthetist to manage airway - Locsipp - Airway equipment in case of tube dislodgement - Pre-oxygenate with 100% O2 - Adequate sedation - NG feed stopped and tube aspirated - Eyes lubricated and taped

Answer 133

To assess severity of ARDS or lung injury - Looks at PEEP, PaO2/FiO2, lung compliance, CXR quadrants involved - Each score 0-4 and then average taken - Helps to consider whether ECMO required - A score of >/= 3 and pH < 7 = critical resp failure = ECMO discussions

Answer 134

- Recruitment – open lung ventilation – reduces shunt and hence improves oxygenation and reduces hypoxic vasocontriction - prevents derecruitment and atlectotrauma - reduces pulmonary oedema

Answer 135

* Increases intrathoracic pressure * Reduces preload / hypotension * Increases deadspace

Answer 136

- Improves chest wall compliance, ventilator synchrony, reduces metabolic demands - However increases risk of pneumonia, delirium risk and ICU acquired weakness

Answer 137

- PROS – improves V/Q and oxygenation by recruitment, allows rest of respiratory muscles - CONS – pneumonia, ICU acquired weakness, paralytic ileus, delirium

Answer 138

* Peak inspiratory pressures (PIP) exerted on bronchi * Plateau pressures exerted on alveoli ## Footnote - In asthma usually PIP high but p plateau is low – may have to accept high PIP - In ARDS both high

Answer 139

Plateau pressure - PEEP ## Footnote should be less than 15cmH20

Answer 140

Mean airway pressure x FiO2 x 100 / PaO2 3 clinical indices used to quantify oxygenation in ARDS higher QI indicates worse lung function

Answer 141

- Open lung ventilation strategy – Peak airway pressures < 30cmH20, PEEP around 15cmH20 (or minimising driving pressure between PEEP and plateau pressures) - Recruitment manoeuvres - Proning - Atracurium infusion to facilitate synchrony and ventilation - APRV - Protocolised ventilator weaning strategies - Use of ventilator care bundles

Answer 142

* Conservative fluids * Steroids * ECMO (Ventilatory- open lung / PEEP, recruitment manouvres, proning , NMBA, APRV)

Answer 143

* High pressure ventilation - lowers CO * Loss of pulmonary capillaries from inflammation and microvascular damade

Answer 144

A nosocomial lung infection occurring 48 hours after endotracheal intubation ## Footnote VAP can be classified as early (by 4 days) and late (5 days or more since intubation)

Answer 145

Microaspiration of respiratory secretions around low pressure high volume ET cuff ## Footnote Microchannels form between cuff and tracheal wall allowing secretions to track into lungs

Answer 146

* Klebsiella pneumonia * Pseudomonas aeruginosa * S.aureus

Answer 147

Colonization with gram negatives ## Footnote Most common organisms include H.influenzae, E.coli, Klebsiella pneumonia, Pseudomonas aeruginosa, and Proteus

Answer 148

Early onset VAP is likely due to antibiotic sensitive organisms while late onset VAP is typically caused by antibiotic resistant organisms like MRSA and ESBL. ## Footnote Early onset organisms include H.influenzae, Klebsiella, Streptococcus; late onset includes MRSA, ESBL, Pseudomonas aeruginosa.

Answer 149

* Fever * Worsening saturations/O2 requirements * Crackles on auscultation * Increased purulent secretions

Answer 150

CXR showing infiltrates/consolidation ## Footnote Bronchoalveolar lavage can also provide positive cultures/gram staining.

Answer 151

Clinical pulmonary infection score (CPIS) It includes temperature, PaO2/FiO2, WCC, micro, tracheal secretions, and CXR infiltrates. o Each scored 0,1,2 o Score of 7 or more = VAP likely

Answer 152

**- ITU related** o Duration of ventilation o Supine position o Enteral feeds – NGT o Sedation / paralysis o Nasal intubation - predisposes to sinusitis and thus a source of infected secretions **- Patient related** o Immunosuppression o Smoking o Raised intra abdo pressure

Answer 153

HDCSPG = happy doctors can stop pneumonia growing  Head of bed elevated 30 degrees  Daily sedation holds/ spontaneous breathing trials  Chlorhexidine oral care - 12 hourly  Subglottic suction - 2 hourly  Pressure in cuff checked 20-30cmH20 - 4 hourly  Gastroprophylaxis = (Stress ulcer prophylaxis – actually increases risk of VAP but usually part of VAP bundle as risk vs benefit of GI bleeding )

Answer 154

VAP bundle other stuff... o Silver coated ET tubes – reduces biofilms o Closed circuit suction system o Hand washing and isolation o Minimise length of intubation where possible o Tapered high vol low pressure cuff to reduce microchannel formation

Answer 155

Healthcare acquired infection not present on admission Defined as occurring after 48hrs of admission or within 3 days of hospital discharge, or within 30 days after operation ## Footnote .

Answer 156

- Immune barriers are breached o skin with IV lines o ET tubes passing through humidification and filtering process o sedation impairs cough - Catheters – UTI - Gut ischaemia from vasopressors/ sepsis – bacterial translocation - Impaired immunity from malnutrition and immunosuppression

Answer 157

* Endotracheal aspirates * Non-directed bronchoalveolar lavage * Direct BAL during bronchoscopy

Answer 158

- Subglottic suction ports - Tapered Inflatable cuff to avoid channelling - Antimicrobial coating to discourage biofilm development

Answer 159

- Avoid routine circuit changes – excessive manipulation is thought to contribute to VAP - Minimising circuit disconnections – e.g. used closed circuit suctioning - Hand hygiene and gloves when manipulating circuit

Answer 160

- Loss of cough reflex - Biofilm development on inner surface of tube - Pooling secretions on top of cuff that can get through microchannels / microfolds

Answer 161

Hypoxaemia PaO2 <8kPa when breathing room air, at rest, at sea level with no significant shunt ## Footnote It is the failure of the respiratory system to achieve adequate gas exchange.

Answer 162

* Type 1: Hypoxaemia (PaO2 <8kPa) * Type 2: Hypercarbia (PaCO2 >6kPa + hypoxemia PaO2 <8kPa)

Answer 163

* Low FiO2 * Poor diffusion (fibrosis, pulmonary edema) * Shunting/V:Q mismatch = Pneumonia/atelectasis , Cardiac (R to L shunt) * Pulmonary embolism

Answer 164

- More of a ventilation problem **- Central:** o Respiratory depression – opioids, sedatives, desensitisation from chronic high CO2 e.g. OSA / COPD o Peripheral nerves – GBS **- Mechanical:** o Muscle issue – fatigue in acute asthma / other type 1 causes , muscular dystrophies o Flail chest

Answer 165

**- O2 therapy – increase FiO2** o Greater the shunt fraction, the less effective this is. o Nasal canula, face mask, Non rebreathe o High flow o CPAP / NIV o Mechanical ventilation o ECMO **- Treat the cause ** o Diuretics and CPAP for pulmonary oedema o Abx for pneumonia o Anticoagulation or thrombolysis for P.E

Answer 166

* Shortness of breath * Haemoptysis * Pleuritic chest pain * Palpitations * Confusion/agitation * Syncope

Answer 167

o Hypoxia o Tachypnoea o Pleural rub o Wheeze

Answer 168

- Previous DVT/PE - Malignancy - Fractured lower limb - Surgery – hip/knee replacement, major abdo/pelvic - Obesity - Age - COCP/ HRT - Pregnancy / post partum - Immobility – critical illness, long distance travel

Answer 169

* Non-massive: stable + normal RH function * Sub-massive: stable but evidence of RV strain * Massive: hemodynamic instability

Answer 170

- CTPA - V/Q scan - ECHO – useful in massive P.E when too unstable for CT

Answer 171

persistent hypotension cardiac arrest

Answer 172

- Underfilled left heart - RV dilation

Answer 173

- Sinus tachycardia – most common - RV strain – ST depression / T inversion in V1-V4 +/- inferior leads - Right axis deviation - RBBB - S1Q3T3 = S wave in V1, Q wave in lead 3 and T wave in lead 3 - P pulmonale – peaked p waves from RA enlargement - PEA - AF / atrial arrhythmia

Answer 174

A breakdown product from the fibrin clot that suggests the presence of a clot when elevated ## Footnote A negative test excludes P.E but can be positive in other conditions.

Answer 175

- LMWH - Long term – apixaban / edoxaban - Massive P.E o Thrombolysis = alteplase 50mg IV bolus + infusion 50mg over 30mins or streptokinase o IVC filter – large clot burden plus bleeding risk o Surgical embolectomy o Percutaneous catheter directed therapy – femoral catheter and then mechanical or USS fragmentation and then aspirate thrombus OR deliver thrombolytic agent directly to clot.

Answer 176

- Absolute o Active bleeding o Previous intracranial haemorrhage o Ischaemic stroke in last 6 months o CNS neoplasm o Recent spinal/ neuro surgery o Close head / facial trauma – 3 weeks o Suspected aortic dissection o Allergy to alteplase - Relative o Severe HTN >180/110 o Major surgery within 4 weeks o Pregnancy within 4 weeks post partum o Acute pancreatitis, oesophageal varices or GI ulcer

Answer 177

- Increase in pulmonary artery pressure  RH afterload increases  RV dilation  tricuspid regurgitation - Eventually RH failure - RV wall stress and reduced coronary perfusion results in sub endocardial ischaemia and a rise in troponins

Answer 178

- Increase in deadspace o CO2 clearance impaired – compensated for by increase in minute ventilation o Thus Type 1 RF - Shunting / VQ mismatch o Loss of surfactant and pulmonary haemorrhage can result from a P.E o Causes atelectasis and shunting

Answer 179

**- Disruption to endothelium ** o Vascular injury, indwelling catheters, surgery **- Blood stasis / turbulent flow ** o Sedation / paralysis – lack of muscle pump in calves o Viscous blood **- Hypercoagulability ** o Pregnancy, drugs, inflammation/infection, smoking

Answer 180

- Hypotension from anaesthetic agents - Worsened venous return with increased pressures – reduced RH cardiac output - Worsening of V:Q mismatch – increased pressures reduces blood flow in lungs

Answer 181

- D dimer is useless as likely high from inflammation - Hypotension and hypoxia anyway from other illness - Asleep patient cant report new symptoms – chest pain

Answer 182

- autoimmune condition - B cells of islets of Langerhans are destroyed - loss of insulin production - This results in impaired ability of cells to uptake glucose resulting in fatty acid metabolism and ketoacidosis if left untreated. - Other metabolic changes o Proteolysis, gluconeogenesis = Hence weight loss and loss of muscle mass o Osmotic diuresis due to hyperglycaemia = dehydration, hyperosmolarity and hypovolaemia o Increase in stress hormones – cortisol, glucagon, catecholamines

Answer 183

- Beta cells of islets of Langerhans = Insulin - Alpha cells of islets of Langerhans = Glucagon - Delta cells of islets of Langerhans = somatostatin

Answer 184

Insulin released when glucose is high - Glucose enters B cell --> glycolysis--> ATP production - ATP binds ATP sensitive K+ channels and closes them - Cell depolarises -->VG Ca channels open--> Exocytosis of insulin vesicles

Answer 185

- Peptide hormone - Proinsulin – alpha and beta chains formed by disulphide bond - Proinsulin cleaved to insulin and C peptide

Answer 186

- Binds tyrosine kinase receptors on target cells - Activation of tyrosine kinase results in cascade and amplification of numerous phosphorylation reactions resulting in changes to gene expression o Increased GLUT 4 – uptake of glucose o Increased glucogenesis and lipogenesis o Decreased glucogenolysis and gluconeogenesis

Answer 187

- Starvation - DKA - Low carb diet - Alcoholic ketoacidosis - Glycogen storage disease

Answer 188

- Liver - Heart - Brain -initially uses glucose but during starvation can adapt to use ketones

Answer 189

- RBC – no mitochondria - Renal medulla cells - Lens of the eye

Answer 190

- Acetone - Acetoacetic acid - B hydroxybutyric acid

Answer 191

* Ketones > 3mM or +2 on dipstick * Glucose > 11mM * pH < 7.3 or bicarbonate > 15mM

Answer 192

- Abdominal pain , N&V - Unwell – low BP, tachycardia, weak / lethargy - Kussmaul breathing, acetone breath - Thirst and polyuria - Low GCS / confusion

Answer 193

Deep breaths caused by acidosis stimulating carotid bodies ## Footnote It is a compensation by increasing CO2 excretion.

Answer 194

- A to E - Fluid resuscitation is key o 1L over 1 hour , 1L over 2 hrs x 2, 1L over 4hr x2, 1L over 6h - Fixed rate insulin infusion o 0.1units / kg/hr o Until DKA resolves - Continue long acting insulin - Hourly BMs and ketones and VBG (K+) o When BMs < 14 mM – run 5% glucose infusion too and consider dropping to 0.05units/kg/hr - Others o VTE prophylaxis o Treat cause e.g. Abx for infection o Catheter o Diabetic specialist nurse review within 24 hours

Answer 195

- 50 units of Actrapid or Humulin S in 50ml with 0.9% saline - 1 unit / ml

Answer 196

- VRII - When patient E+D move back to normal insulin regime

Answer 197

- pH >7.3 - ketones <0.6mM - bicarb >15mM

Answer 198

- Insulin drives K+ into cells via Na/K ATPase – drops K+ - Also osmotic diuresis and vomiting = excretion of K+ - Needs replacing - If K+ >5.5 mM = no potassium replacement - 3.5 -5.5 mM = 40mM in 1L - <3.5 = senior review / ? ITU

Answer 199

* Drop in ketones 0.5mM/h * Drop in glucose 3mM/h * Rise in bicarbonate 3mM/h * Maintain potassium between 4 and 5.5

Answer 200

- Inadequate insulin - Inadequate resuscitation - Sepsis - Hyperchloremic acidosis

Answer 201

Hyperglycaemia causes hyponatraemia due to water following glucose by osmosis, diluting sodium concentration. As DKA is treated, glucose falls and water leaves, resulting in a rise in sodium concentration.

Answer 202

- Electrolyte disturbances – hyper/hypoK +/- arrythmias , hyponatremia - Hypoglycaemia – risk of brain injury / seizures - Hyperchloremic acidosis - Cerebral oedema - VTE - AKI / fluid overload

Answer 203

- Stewart theory of acid and base o strong ion difference o total weak acids e.g. albumin o pCO2 - if chloride is high there lack of balance in strong ions - if chloride conc is high, less room for bicarbonate, hence less buffering capacity

Answer 204

- Anion gap = (Na + K ) – (Cl + HCO3) - Normally 8-16 - In DKA this will be raised due to ketones – buffered by HCO3 which lowers this value in the equation

Answer 205

- Osmolar gap = measured osmolality - calculated osmolarity - Calculated osmolarity = 2(Na+) + glucose + urea - Should be <10mOsm/L - Significant osmolar gap suggests active osmoles from other substances

Answer 206

**- Biochemical findings** o pH < 7.1 o bicarb < 5mM o ketones >6mM o anion gap >16 o hypokalaemia on admission < 3.5mM **- clinical findings** o Sats < 92% o Systolic < 90mmHg o HR >100 or < 60 o GCS< 12 **- Patient factors** o Elderly o Pregnant o < 25yrs o Significant comorbidities – heart / renal failure

Answer 207

- BMs – blood glucose testing - Ketones – ketostick - Urine ketones and glucose - VBG – pH, electrolytes, bicarb

Answer 208

* Call for help, A to E – consider intubation * Hypertonic saline 3% (3-5ml/kg) or mannitol 0.5-1g/kg * Reduce fluids to half the maintenance rate * Neuroprotection * Raise head of bed – 30 degrees * Avoid hypotension * CT head once stable ## Footnote Prompt management is crucial to prevent further complications.

Answer 209

Cerebral oedema.

Answer 210

Hypokalaemia and ARDS.

Answer 211

* Starvation ketosis * Alcoholic ketosis * Hyperosmolar hyperglycaemic state (HHS) * Euglycemic ketoacidosis (associated with SGLT2 inhibitors)

Answer 212

Raised anion gap acidosis and ketonemia (>3mM) in those with diabetes without rise in glucose. It is associated with SGLT2 inhibitors

Answer 213

* Treat with insulin 0.1 units/kg/hr * Give glucose infusion 10% 125ml/hr * Stop SGLT2 inhibitors ## Footnote Management is critical to prevent complications.

Answer 214

Stop SGLT2 inhibitors in any unwell patient in hospital.

Answer 215

* All require HDU/ICU * Greater emphasis on fluid resus - Can treat with oral fluid if not dehydrated to reduce risk of cerebral oedema * If shocked, 10ml/kg then maintenance fluid * Careful monitoring for cerebral oedema= Monitor sodium and neurology * High threshold for intubation ## Footnote These adjustments are made to reduce risks associated with DKA in children.

Answer 216

* Deficit = weight x %dehydration x 10 * Replace deficit over 48hrs * Maintenance = 100:50:20 rule ## Footnote Accurate calculations are essential for effective treatment.

Answer 217

* Younger age * Low socioeconomic background * Drug/alcohol abuse / psych problems * Ethnic minority background * Current illness ## Footnote Awareness of these risk factors can aid in prevention and early intervention.

Answer 218

Catecholamines and cortisol in illness cause hyperglycaemia, requiring more insulin. ## Footnote This can lead to a higher risk of DKA.

Answer 219

* Younger age * Severe DKA * Increased serum urea * Severe hypocapnia * Increase in serum sodium * New onset diabetes * Treatment with bicarbonate ## Footnote Identifying these risk factors is crucial for monitoring and prevention.

Answer 220

* Sudden onset headache * Fall in HR * HTN * Abnormal respiratory pattern * Change in neurology (restless, irritable, drowsy, confused) * Neurological deficit (CN palsy) ## Footnote Recognizing these features can lead to timely intervention.

Answer 221

- Risk of exacerbating cerebral oedema - Hypocapnia resulting from compensation of metabolic acidosis has developed and likely well compensated for and hence cerebral blood flow actually normal despite this. - At intubation -PaCO2 will rise rapidly – vasodilation and hence risk of oedema and rise in ICP - If necessary – avoid changes in CO2 via hyper/hypoventilation

Answer 222

Rare life threatening metabolic syndrome associated with propofol infusions Due to impairment of mitochondrial fatty acid metabolism and impaired ATP production, resulting in cell hypoxia and acidosis.

Answer 223

* Children * Critical illness * Traumatic brain injury * Low carb diet * Parenteral nutrition * Glycogen storage disease * Mitochondrial disease * Drugs (propofol >48hrs, high rate infusion, Steroid use , Catecholamines)

Answer 224

* New onset metabolic acidosis * Rhabdomyolysis * AKI + hyperkalaemia * Cardiac dysfunction - arrhythmias, brady, failure * Hypertriglycerides * Hepatomegaly + high LFTs * Pyrexia

Answer 225

* Raised CK * Raised triglycerides * Metabolic acidosis with raised lactate * Raised urea/creatinine * Hyperkalaemia

Answer 226

* Monitor CK/triglycerides after 48hrs * Stop propofol if CK rising * Start alternative e.g. alfentanil * Give glucose infusion * Supportive care (RRT, CVS support, treat hyperkalaemia, fluids)

Answer 227

* Safe dose <4mg/kg/hr * Use multimodal sedation * Avoid in paediatrics or known mitochondrial/glycogen storage disease * Early enteral feeding with good carb load

Answer 228

HLH is a life-threatening condition of uncontrolled inflammation and cytokine storm characterised by fever, cytopenias, and organ dysfunction.

Answer 229

- 3 F’s = Fever, Falling cell counts , high Ferritin - Can mimic sepsis - Organomegaly – lymphadenopathy, hepato/splenomegaly - Organ dysfunction – ARDS, circulatory shock, pericardial effusions, arrhythmias , AKI, liver failure, seizures, delirium - Cytopenias e.g. thrombocytopenia and low white cells.

Answer 230

* Primary HLH – a genetic condition, usually appearing in infancy, requiring bone marrow transplant. * Secondary (Acquired) HLH – can occur at any age, often influenced by genetic susceptibility but without a single identified genetic defect.

Answer 231

Failure of body to stop inflammation leading to uncontrolled activation of T lymphocytes and macrophages, triggered by multiple factors.

Answer 232

* Infection (e.g. covid, TB, HIV) * Autoimmune diseases (e.g. SLE, RA) * Therapies (e.g. organ transplant) * Other (severe burns, vaccines)

Answer 233

Using HLH 2004 criteria - better for primary HLH or HScore, which includes ferritin, cytopenias, organomegaly, triglycerides, fibrinogen, AST.

Answer 234

- Those to diagnose / monitor HLH – fibrinogen, ferritin, triglycerides, cell counts (FBC), coagulation - Daily H score – response to treatment? - Those to monitor complications – CT scan, ECHO, troponin, BNP , CXR - Those to find cause – bacterial cultures, viral serology, autoimmune pannel (completement, autoantibodies),

Answer 235

Can be high in other conditions; very high ferritin (>10000) is associated with HLH.

Answer 236

- Both involve dysregulated immune response to infection - HLH is a very severe hyperinflammatory subtype of sepsis - HLH typically causes persistent fever whereas sepsis is swinging - HLH may have low or normal CRP, sepsis its high - HLH has low WCC , sepsis is high - Ferritin is a lot higher in HLH

Answer 237

- Aims are to supress inflammation and identify & treat trigger o immunosuppression even in presence of infection First line – methylprednisolone 1g IV / day for 3 days Second line – IL1 inhibitor – anakinra o Also treat infection – Abx, anti virals o Supportive – VTE prophylaxis, gastro prophylaxis

Answer 238

- H score >50% - Severe illness deterioration - Persistent unexplained fever - Presence of HLH markers – 3Fs Mortality is 50% even when treated

Answer 239

- Hypoventilation o Inadequate TV/RR / increased dead space o Leads to high CO2 which causes drop in O2 – alveolar gas equation o Caused by  Respiratory depression = sedation, opioids  Respiratory disease and exhaustion - V:Q mismatch o Pneumonia, ARDS , atelectasis, pulmonary oedema, P.E - Obstructive airway disease o Asthma / copd - Impaired diffusion o Pulmonary oedema, emphysema, fibrosis

Answer 240

- Increase in cardiac output will reduce deadspace but increase shunting and vice versa - Low CO reduces the shunt fraction and can improve PaO2 - However Low CO increases deadspace and increases CO2 which may worsen hypoxaemia

Answer 241

- Increase FiO2 = increases alveolar O2 via alveolar gas equation , however limited use if there is a shunt - Mechanical ventilation o PEEP – maintains FRC above closing capacity – reduces atelectasis and shunting o Support when tiring / hypoventilation - Proning - Sedation and NMBA – synchrony - Recruitment manoeuvres – open atelectatic lung - Chest physiotherapy and sputum management = saline nebs, regular suctioning - Careful fluid balance

Answer 242

* Hypoxaemia - low partial pressure of oxygen (PO2) in the blood * Hypoxia - low partial pressure of oxygen in the tissues

Answer 243

Neurological injury causing irreversible brainstem damage, leading to inability to breathe and irreversible loss of consciousness. But heart is still beating and body is kept alive by ventilator

Answer 244

**- Preconditions are met** o Apnoeic coma GCS 3 – deeply unconscious, apnoeic and mechanically ventilated o Pathology of known aetiology is irreversible e.g. hypoxic brain injury / haemorrhage **- Exclusion of reversible contributions to apnoeic coma state** o Drugs = No NMBA, sedative medications – may need to wait for 4x half life of drug or use reversal agents o Metabolic = temp >36 degrees, normal electrolytes , normoglycaemia , pH 7.35 -7.45 o Physiological = CVS stability – MAP >60mmHg -**Formal Brainstem death testing – above 2 must be present first** o Loss of brain stem reflexes o Apnoea test

Answer 245

- PaCO2 5.3kpa (previously 6kpa) - pH <7.4

Answer 246

2 qualified clinicians, one consultant, one with at least 5 years GMC, no conflict of interest.

Answer 247

Head flexed 30 degrees, visualize tympanic membrane, slowly inject 50ml of ice cold water and watch for eye movement.

Answer 248

- Increase FiO2 to 100% for 10 mins - Reduce the minute volume such that PaCO2 rises - Check ABG - PaCO2 needs to be 5.3 with pH < 7.4 before starting - Disconnect ventilator – provide O2 via tracheal catheter - Start 5 min timer and observe for respiratory effort - Recheck ABG after 5 mins – confirm paO2 >8kpa with pH < 7.3 and rise in PaCO2 > 2.7kpa – this states completion of the test

Answer 249

- < 37 weeks gestation = not valid to test - 37 weeks to 2 months = same as adults however… o Minimum Period of observation for 24hours o Period of 24hours between the 2 apnoea tests o No Ancillary tests required - > 2 months = same as adults

Answer 250

- Difficulty assessing cranial nerves e.g. facial trauma - High cervical cord injury may mask some reflex - inability to complete apnoea test = profound hypoxia / CVS instability - examples o cerebral angiography = no blood flow to brain o EEG = no activity

Answer 251

- 1 doctor needed - Absent pupil and corneal reflex - No response to pain - 5 mins of confirmed asystole – ECG or arterial line - Apnoeic

Answer 252

- Apnoea test now starts at 5.3kpa (previously 6kpa) - Ends with PaCO2 >8kpa with pH < 7.3 and rise in PaCO2 >2.7kpa – this states completion of the test (previously looked for a rise by 0.5kpa) - The time of death is now stated as the completion of the second test (previously the first) - Temperature needs to be minimum of 36 degrees for atleast 24 hours before testing - If unable to examine both eyes and ears then ancillary tests are required.

Answer 253

* Living donor * Donation after brainstem death * Donation after circulatory death

Answer 254

- Absolute o Age >85yrs o Haematological malignancy o Metastatic malignancy o Primary intracerebral lymphoma o Secondary intra cerebral tumours o Melanoma o HIV / TB - Relative o Systemic sepsis o Hep B/C

Answer 255

- Liver, lungs, kidneys, pancreas, heart

Answer 256

- Modified Maastricht criteria - Category 1 = dead on arrival - category 2 = sudden unexpected cardiac arrest with unsuccessful resuscitation - category 3 = planned withdrawal of life sustaining therapy – majority fall into this category - category 4 = sudden cardiac arrest after brain death diagnosis during donor life management but prior to organ recovery

Answer 257

- death of brain stem = autonomic storm **- CVS:** o Sympathetic stimulation to maintain cerebral perfusion – HR, SVR o Can lead to cardiac ischaemia and arrhythmias o Cushings reflex from brain swelling = bradycardia **- Respiratory** o Neurogenic pulmonary oedema = inflammatory response increases capillary permeability. **- Endocrine / haem** o Stress hormones – electrolyte changes and fluid shifts o DIC o Pituitary ischaemia = diabetes insipidus **- Hypothermia** o Disruption in hypothalamic thermoregulation o Heat loss by peripheral vasodilation and reduced BMR

Answer 258

- Dehydration secondary to diabetes insipidus and neurogenic pulmonary oedema - LV impairment with reduced CO following sympathetic storm - Loss of sympathetic tone and adrenoreceptor desensitisation

Answer 259

- Hypernatraemia - Hypokalaemia - Increased serum osmolarity

Answer 260

- Fluid replacement - Vasopressors MAP >70mmHg - Electrolyte replacement - Bear huggers - High dose methylprednisolone can help in retrieval of lungs – pulmonary oedema - Minimise time between death and retrieval - Desmopressin - Continue Abx / enteral feeds - Lung protective ventilation

Answer 261

- Lung protective ventilation – TV 4-6ml/kg and PEEP 5-10cmH20 - Chest physio, suctioning, repositioning - 30-45 degree head up - Maintain cuff inflation of ET tube

Answer 262

- All adults are considered consented for organ donation unless they have a recorded decision not to OR o < 18yrs o Lack mental capacity to opt out o Visiting patients

Answer 263

- Donors after cardiorespiratory death = longer duration of warm ischaemic time

Answer 264

- No need to give anaesthesia - Paralysis is required due to spinal reflexes - Haemodynamic stability – vasopressors / opioids - Intra op drugs required by transplant team = antibiotics, heparin , steroids

Answer 265

- Kidneys – < 2-4 hours - Lungs < 1hr - Pancreas and liver < 30mins

Answer 266

* Non-infectious causes (malabsorption, ischaemic colitis, abx, enteral feeds ) * Infectious causes (C. diff, norovirus)

Answer 267

* Hyper osmotic feed * Flow too high * Migration of NGT into duodenum

Answer 268

stool sample to exclude infection, adjust enteral feed rate, hydration and electrolyte replacement, opioids/loperamide, Flexiseal

Answer 269

* CT head * Lumbar puncture - if ICP not high * Ceftriaxone 2g TDS + aciclovir 10mg/kg TDS

Answer 270

Herpes simplex 1, Varicella zoster, Enterovirus

Answer 271

temporal lobe oedema +/- haemorrhage Hypoattenuation

Answer 272

CMV, Toxoplasmosis, EBV, Cryptococcus, Asperigillus, Neutropenic sepsis

Answer 273

* < 0.5 x10^9 cells /L * Plus source of infection and > 38 degrees

Answer 274

broad spectrum antibiotics like tazocin, consider gentamicin

Answer 275

oncological emergency characterized by breakdown of a large number of tumour cells causing metabolic and electrolyte derangements

Answer 276

Rise in K, PO4, urea, low Ca

Answer 277

AKI, arrhythmia, seizures, arrest

Answer 278

Fluids, replace/correct electrolytes, allopurinol - xanthase oxidase inhibitor - reduces Uric acid production

Answer 279

Life threatening dysregulated immune response to infection that results in organ dysfunction * Organ dysfunction defined as an Increase in SOFA by 2 or more points

Answer 280

Sequential Organ Failure Assessment

Answer 281

* PaO2:FIO2 (respiratory) * GCS (neuro) * MAP and need for Vasopressors/ionotropes (cardio) * Bilirubin (liver) * Platelet count (coag) * Creatinine and urine output (renal) each 4 points - max 24

Answer 282

Quick assessment with resp rate >22, altered mental state, systolic < 100

Answer 283

- Old method of defining sepsis o SIRS - temp >36, HR >90, RR> 20, raised WCC - 2 or more = sepsis o Severe sepsis = SIRS plus one of organ dysfunction, lactate >2 , hypotension o Septic shock - MAP < 70mmHg despite fluid resuscitation - Now o SOFA / qSOFA used o septic shock is defined by = sepsis + MAP < 65 or lactate > 2 despite fluids or requiring vasopressors

Answer 284

Sepsis + MAP < 65 or lactate >2 despite fluids or requiring vasopressors

Answer 285

* Myocardial depression by immune mediators - reduced ejection fraction * Systemic vasodilation by immune mediators * Endothelial dysfunction and capillary leakage leading to hypovolaemia * Last 2 - hypotension and hypoperfusion

Answer 286

* ADSORPTION - delayed gastric emptying and changes to pH, variable fat / muscle due to reduced perfusion * DISTRIBUTION = Changes to plasma proteins , reduced Vd due to poor peripheral perfusion esp lipophilic (anaesthetic drugs) , 3rd space losses increased Vd of hydrophilic , * METABOTISM & EXCRETION = Reduced ADSORPTION, DISTRIBUTION, METABOLISM & EXCRETION changes

Answer 287

* clostridium tetani - spores found in soil / environment can enter wound * Anaerobic bacterium that produces tetanus toxin which is a neurotoxin * Binds presynaptic membrane snare proteins preventing vesicle release of NT of GABA and glycine - inhibitory neurons * Failure of CNS to inhibit motor reflexes * Increased muscle tone and spasm

Answer 288

* muscle rigidity , spasms , autonomic instability * Includes laryngospasm and ventilation difficulties * Autonomic may be hypotension or hyper , Brady or tachy. Also salivation, sweating and pyrexia

Answer 289

Nurse in dark room, low threshold to intubate, supportive management, human tetanus immunoglobulin, metronidazole, benzodiazepines

Answer 290

Prevents ACh release * Flaccid paralysis plus autonomic features (dry mouth, tachy , postural hypotension) 4 Ds = dysphagia, diplopoa, dysarthria, dysphonia

Answer 291

clostridium botulinum gram positive anaerobic

Answer 292

* obesity * diabetes * immunocompromised * IV drug use

Answer 293

Cellulitis is more superficial; necrotising fasciitis affects deep fascia and is more severe + systemic organ dysfunction

Answer 294

A to E, urgent debridement, antibiotics (taz and clindomycin), hyperbaric O2

Answer 295

hypomobility of bowel in absence of obstruction

Answer 296

dilated bowel loops

Answer 297

* patient factors - age , diabetes * Anaesthetic factors - morphine , vasopressors, volume overload * Surgical - emergency op, long op , intestinal resection

Answer 298

* Reduce handling intra op * Correct electrolyte abnormalities * Careful fluid balance * Avoid systemic opioids * Early physio and mobilisation

Answer 299

Supportive management, optimise physiology, mobilise, nutrition pro kinetics (metoclopramide, erythromycin, neostigmine)

Answer 300

When intra-abdominal pressure is >20mmHg and there is new abdominal organ dysfunction

Answer 301

* Intra abdo HTN > 12 mmHG * Normal IAP is 5-7mmHg

Answer 302

Directly with a needle into bowel or indirectly using a pressure transducer in an abdominal viscus - usually bladder using a Foley catheter

Answer 303

* Grade 1 = 12-15 mmHg * Grade 2 = 16-20 mmHg * Grade 3 = 21-25 mmHg * Grade 4 = >25 mmHg

Answer 304

* Respiratory: diaphragm splinting + increased pressures, * CVS: compression of vessels - reduced preload, increased afterload * Renal: reduced GFR * CNS: increased ICP due to reduced venous drainage * Bowel: ischaemia , oedema, bacterial translocation * Liver: ischaemia and dysfunction. pressure on biliary tree and stasis

Answer 305

* medical - NgT, enema , flatus tubes * Optimise sedation and analgesia * Prevent coughing / ventilator dysynchrony * Surgical decompression - open abdomen (laparotomy ) and cover in sterile bag or vacuum dressing

Answer 306

* reduced wall compliance - burns , prone, high BMI, * Increased Intra abdo contents - ascites , ileus , pneumoperitoneum * Fluid shifts - sepsis , pancreatitis * IPPv

Answer 307

State of circulatory failure such that the delivery of O2 does not meet the demand.

Answer 308

o Cardiogenic – ventricular dysfunction e.g. arrhythmias, valves, cardiomyopathy o Hypovolaemic – blood loss/ dehydration o Distributive – anaphylaxis and sepsis and neurogenic o Obstructive – physical obstruction – P.E / tamponade / tension pneumothorax

Answer 309

High CO, low SVR, low/normal preload.

Answer 310

Low CO, high SVR, high preload (raised JVP).

Answer 311

* Respiratory: hypoxia, tachypnoea, pulmonary oedema * CVS: chest pain, cool peripheries, raised JVP, ankle swelling * Neuro: tiredness, confusion

Answer 312

* Morphine * Oxygen * Nitrates * 300mg Aspirin

Answer 313

Within 2 hours.

Answer 314

- MONA = morphine, oxygen, nitrates, 300mg aspirin - PCI o UK target within 2 hours from presentation to performance - Supportive o may need intubating / CPAP if pulmonary oedema, arterial line. o Careful fluids – pulmonary oedema/ failing heart o Careful vasopressors – increases afterload – already high circulating catecholamines o Ionotropes – adrenaline, dobutamine, milrinone, levosimendan (calcium sensitiser) o Intra aortic balloon pump / ventricular assist device

Answer 315

Medical emergency when a seizure continues for >5 minutes or more than 1 without recovery in between.

Answer 316

* Epilepsy * Drug related- Alcohol withdrawal, Ketamine, pethidine/tramadol, cocaine * Intracranial issues (head injury, cerebrovascular disease, infection, neoplasm) * Metabolic issues (hypoglycaemia, hyponatraemia, hypoxia) * Other (eclampsia)

Answer 317

* Non-epileptic seizure * Vasovagal syncope * Stroke

Answer 318

* A to E o 15 L non -rebreathe / support airway o IV access and bloods inc toxocolgy and anti-epileptic levels o BMs and temp - Specific o Lorazepam 0.1mg/kg (4mg) IV  Alteratives rectal diazepam 10mg-20mg , buccal midazolam 10mg o Antiepileptics  Phenytoin 20mg/ kg IV  Valproate 40mg/kg IV  Keppra 60mg/Kg IV over 15mins o Still continue …  GA + intubation – propofol or thiopentone  OR phenobarbital - Other o Pabrinex and glucose – if alcohol hx o EEG monitoring – have seizures stopped? o CT head / CSF analysis

Answer 319

* Propofol * Thiopentone * Volatiles * Midazolam

Answer 320

* Airway & respiratory: Apnoea, hypoxia, pulmonary oedema, aspiration pneumonia * CVS: Arrhythmias, hyper/hypotension * Neuro: Cerebral oedema, intracranial haemorrhage, cerebral hypoxia/ischaemia * Metabolic: Lactic acidosis, hyperkalaemia, rhabdomyolysis, DIC

Answer 321

* Buccal midazolam 10mg * PR diazepam up to 20mg * IV lorazepam 0.1mg/kg up to 4mg

Answer 322

* Alcohol withdrawal seizures - pabrinex * Eclampsia - MgSO4 * Hypoglycaemia or other metabolic disturbance (e.g., hypoNa) * Tumours - dexamethasone

Answer 323

VG Sodium channel blocker; binds and blocks Na into neurons preventing propagation of action potentials.

Answer 324

* Bradycardia = AV block * Negative inotropic effect from propylene glycol solvent.

Answer 325

* Bradycardia * Heart block * Hypotension * Nystagmus * Diplopia * Confusion * Ataxia * Hyperglycaemia * Slurred speech

Answer 326

* Hirsutism * Acne * Gum hyperplasia * Peripheral neuropathy teratogen

Answer 327

KDIGO * Stage 1: 1.5 to 1.9 x baseline creatinine, < 0.5ml/kg/hr * Stage 2: 2-2.9 x baseline creatinine, < 0.5ml/kg/hr for >12 hr * Stage 3: >3x baseline creatinine, < 0.3ml/kg/hr for 24 hrs OR anuria for 12 hours OR initiation of RRT

Answer 328

* Pre-renal: dehydration, sepsis, low CO/HF, renal artery stenosis, abdominal compartment syndrome * Renal: acute tubular necrosis (rhabdo, NSAIDs,ACEi) , glomerulonephritis, vasculitis * Post-renal: obstruction by stone, tumour, large prostate

Answer 329

- NSAIDs - ACEi - Aminoglycosides – gentamicin - Contrast media

Answer 330

* Dehydration * Critical illness * CKD * Multiple comorbidities (diabetes, HF, HTN, chronic liver disease) * Pancreatitis * Trauma * Age

Answer 331

Based on creatinine clearance; methods include CKD-EPI, MDRD, Cockcroft-Gault.

Answer 332

No, but it is a good estimate and has a non-linear relationship with GFR. - Most accurate would be inulin clearance o However not practical – requires constant inulin infusion and 24 hour urine collection

Answer 333

More unreliable; changes with diet, upper GI bleed, catabolic state.

Answer 334

* UEs (urea, creatinine, electrolytes, GFR) * Urine output * Other bloods, urine dip, immunological tests, imaging (USS/CK KUB) * Renal biopsy

Answer 335

* Identify and manage cause (e.g., unblock catheter) * Fluids (accurate fluid balance) * Stop nephrotoxins, metformin, adjust meds to renal dose * May need ionotropes/vasopressors * Loop diuretic can help sometimes * Manage complications (e.g., hyperkalaemia) * RRT if needed

Answer 336

* Electrolyte disturbances and arrhythmias * Reduced clearance of drugs and toxic effects * Build up of toxins (uraemia, acidosis) * Death or long-term CKD

Answer 337

* Acidosis (metabolic acidosis unresponsive to treatment) * Electrolytes (hyperkalaemia refractory to treatment >6.5) * Intoxication (salicylates) * Overload (refractory to treatment) * Uraemia (with toxic symptoms)

Answer 338

* Peritoneal dialysis * Intermittent haemodialysis * Continuous RRT (e.g., continuous veno-venous haemofiltration, continuous veno-venous haemodialysis) * transplant

Answer 339

- Filtration = o blood passes across a filter under pressure. forces water through a membrane together with dissolved solutes (convection) to form ultrafiltrate (removed fluid) o removes large volume of fluid and then replacement fluid is added back to blood with appropriate electrolytes and buffered with lactate - Dialysis = o Blood passes across a filter in contact with dialysate on the other side in countercurrent direction. o Solute passes across semipermeable membrane via diffusion – amount depends on concentration gradients, molecular weight and flow o Solutes with low Vd, low protein binding and that are small are most readily dialysed.

Answer 340

- Previously catheter inserted into artery and return to vein - Arterial pressure was used to drive through machine - However newer pumps now generate high flow rates allowing venous system to be used. - The arterial method had a number of complications – hypotension resulted in failure of dialysis hence reliant on CVS function and there was risk of damage to vessels

Answer 341

* IJV * Subclavian * Femoral

Answer 342

- Dialysate is infused into peritoneal cavity - Peritoneal membrane is used as a filter - Diffusion occurs across this semi permeable membrane - The fluid is then removed after some time - The dialysate fluid is hyperosmolar so water is drawn into peritoneum – how much depends on the osmotic pressure of dialysate

Answer 343

* Advantages: can occur at home, no anticoagulation needed * Disadvantages: infection risk, diaphragmatic splinting, intensive 4-6x/day at home

Answer 344

- Continous venovenous haemofiltration (CVVH) o More haemodynamically stable than intermittent techniques so good for critically ill o Requires anti-coagulation of the filter – clotting is common in the machine and results in interruptions o Better for severe volume overload as more fluid can be removed - Intermittent haemodialysis o Blood removed from venous cannula or AV fistula o Rapid correction and thus less complicated by filter clotting o However risk of haemodynamic instability and more technically demanding o Risk of cerebral oedema o Better for more stable patients with chronic kidney disease

Answer 345

* Tubing: not too long to hinder flow, material reduces clotting activation * Filter: size of pore and material selected to reduce clotting and inflammation * Pump: low pressure

Answer 346

Unfractionated heparin or sodium citrate due to the highly thrombogenic nature of the extracorporeal circuit. blood flow is also slower and more turbulent

Answer 347

* Unfractionated heparin: cheap, easy to monitor with APTT, risk of haemorrhage and HIT * Sodium citrate: only affects filter, less risk of haemorrhage, but requires other VTE prophylaxis and has risks of citrate toxicity.

Answer 348

combined with Ca

Answer 349

 Hypocalcaemia – binds Ca  HypoMg – binds Ca-citrate complex  Acidosis – accumulation of citrate  Alkalosis – citrate metabolised to bicarb

Answer 350

- Usually around 35 ml/kg/hr

Answer 351

- Access related = infection, bleeding, pneumothorax - CVS = hypotension and haemodynamic instability – especially on initiation - Anti coag related = HIT, clotting of filter , bleeding - Other = air embolus, hypothermia , raised lactate (used as a buffer for replacement fluid – but can rise in liver dysfunction

Answer 352

* Not enough anticoagulation * Kinking of lines * Reduced flows

Answer 353

- Some drugs are filtered, and others aren’t - E.g. metronidazole and tazocin are moderately filtered so can increase dose from renal dose - E.g. gentamicin and vanc are highly filtered – significant dose increase and monitor levels

Answer 354

* Tall tented T waves * Prolonged PR * Wide QRS * Flat P waves * Sine wave * VT

Answer 355

- PRE RENAL = o Hypovolaemia = dehydration from starvation, 3rd space fluid losses, bleeding o Lower CO and vasodilation from anaesthetic agents o Pneumoperitoneum - RENAL = o use of nephrotoxic drugs – aminoglycosides o acute tubular injury from SIRS response - POST RENAL = o urinary retention from drugs e.g. anticholinergics

Answer 356

Bacterial infection of the ascitic fluid within the peritoneum that does not result from another intra-abdominal source, exclusively seen in cirrhotic patients with ascites.

Answer 357

Neutrophils >250 cells/mm3 on ascitic tap.

Answer 358

* Alcoholic liver disease * Non-alcoholic steatohepatitis (NASH) * Hepatitis C infection * Less common: drug, autoimmune hepatitis, Wilson's disease, Budd-Chiari syndrome

Answer 359

* A to E: haemorrhage management, blood/coagulation, lethal triad * Terlipressin: portal vasodilation reduces portal pressure and variceal bleeding * Endoscopic treatment: injection of adrenaline, banding of varices * Balloon tamponade with Sengstaken Blakemore tube if necessary

Answer 360

* Oesophageal rupture * Rebleed

Answer 361

Acute kidney injury seen in those with advanced liver disease, characterized by cirrhosis with ascites, elevated creatinine, and absence of shock or nephrotoxins or intrinsic renal disease

Answer 362

* Cirrhosis with ascites * Creatinine >133 * Absence of shock, nephrotoxins, intrinsic renal disease * No improvement in renal function with fluids/stopping diuretics

Answer 363

* - Drugs = paracetamol, halothane - Toxins = mushrooms - Vascular = hepatic vein thrombosis (budd chiari syndrome), ischaemic hepatitis - Viral = hep A-E, EBV, CMV - Metabolic – alpha 1 antitrypsin deficiency, acute fatty liver of pregnancy - Autoimmune hepatitis

Answer 364

* Grade 1: alterations to behaviour, mild confusion, slurred speech, sleep disturbance * Grade 2: lethargy, moderate confusion * Grade 3: somnolent but rousable * Grade 4: coma, unresponsive to painful stimulus

Answer 365

- Airway + breathing o May need intubation especially if severely encephalopathic o Minimal PEEP to help with cerebral venous drainage and minimise ICP o PEEP also impairs hepatic drainage - CVS o Arterial line and consider CO monitoring o Liver failure causes low SVR and CO o May need fluids, vasopressors / ionotropes - Neurological o Neuroprotection – PaO2 >8kpa, CO2 4.5-5, 30 degree head up, MAP >65mmHg, adequate sedation, glucose 4-11mM , treat fever o Treat high ICP with hypertonic saline - Renal o Likely to have AKI too – consider RRT - Haematological o Liver produces clotting factors – likely severe coagulopathy o Blood products and ROTEM

Answer 366

* Adverse reaction to halothane * Type 1: Mild transient postoperative rise in serum liver enzymes. secondary to free radicals on metabolism * Type 2: Autoimmune reaction with high mortality (50%). secondary to TFAA hepatocyte complex. centrolobular necrosis and fulminant liver failure ## Footnote Halothane is metabolised to trifluoracetic acid (TFAA) which binds hepatocytes and activates the immune system.

Answer 367

* Epigastric upper abdominal pain * Vomiting

Answer 368

GETSMASHED: * Gall stones * Ethanol * Trauma / tumour * Scorpion * Mumps * Autoimmune * Steroids * Hyperlipidaemia / hypercalcaemia * ERCP * Drugs: azathioprine, valproate, sulfasalazine

Answer 369

Using Atlanta criteria: 2 or more of the following: * Clinical features: severe, acute, persistent epigastric pain radiating to back * Biochemical: raised amylase/lipase x 3 upper limit * Imaging: CT contrast evidence

Answer 370

* Mild: no organ failure or local complications * Moderate: <48 hours of organ failure or local complications * Severe: persistent organ failure >48 hours

Answer 371

- Glasgow pancreatic score - BISAP score for mortality - CT severity index – collections of fluid on CT and inflammation/necrosis

Answer 372

* PaO2 <8kpa * Age >55 * Neutrophil >15 x 10^9 * Ca <2mM * Renal: urea >16mM * Enzymes: raised LDH/AST * Albumin <32 * Sugar: glucose >10 pancreas mneumonic ## Footnote Score of 3 or more indicates severe pancreatitis, consider critical care.

Answer 373

- Local o Necrosis and infection o Pancreatic fistula o Pseudoaneurysm of splenic / gastroduodenal artery and risk of bleed o Risk of splenic / portal vein thrombosis o Pancreatic pseudocyst – can become infected, can lead to gastric outlet obstruction - Systemic o VTE o ARDS o Septic shock /MoF - Chronic pancreatitis o Exocrine insuffiency o Endocrine insufficiency – diabetes

Answer 374

- Supportive - Fluids – resuscitation and maintenance - NBM - start enteral feeds at 48hrs (in mild cases ,24hrs) ( avoid TPN unless enteral is impossible ) - Analgesia - Antiemetics - Routine use of Abx not recommended unless infection confirmed ERCP - gallstones

Answer 375

* Normalize lactate * Urine output >0.5ml/kg/hr

Answer 376

- Avoid excessive fluids – pulmonary oedema - Good analgesia to promote deep breathing and prevent basal atelectasis - Avoid IPPV where possible

Answer 377

- A to E / resuscitation - Hx – how much, what, intention, preparations – slow release - Examination – pin point pupils / dilated , hypothermia, hyperthermia, rigidity (serotonin syn) - Ix – bloods / ABG/ BM / Tox screen / CK , ECG / continuous cardiac monitoring - Mx o Within 1 hour – activated charcoal / gastric levage o Use toxbase – national poisons information service (NPIS) o Specific antidotes ## Footnote Use toxbase for guidance and specific antidotes.

Answer 378

- Hypothermia = TCA, barbiturates - Hyperthermia = amphetamine, ectasy, cocaine, MAOi

Answer 379

* Corrosive substances * Airway not protected (must be intubated or fully awake)

Answer 380

50g for adults, 1g/kg for children

Answer 381

An up-to-date, evidence-based resource for managing poisoning, available 24 hours a day. ## Footnote Accessed online via TOXBASE database or via telephone.

Answer 382

o Naloxone for opioids o Flumazenil for benzos o NAC for paracetamol o Glucagon / high dose insulin for B blockers o Physostigmine for anticholinergics o Ethanol and fomepizole for ethylene glycol/ methanol o Digibind for digoxin

Answer 383

* CVS: tachycardia, hypotension, wide QRS, long QT, ventricular arrhythmias * Neurological: mydriasis, hyperreflexia, low GCS, seizures, respiratory depression

Answer 384

- Sinus tachycardia - Long QRS - Long QT - Torsades de pointes - Ventricular arrhythmias - Prolonged PR and heart block

Answer 385

If QRS >100ms, pH <7.2, or other cardiac arrhythmia 8.4% sodium bicarb - Often worth correcting acidosis before intubation if safe to do so as use of anaesthetic agents causes myocardial depression (acidosis also depresses myocardium) ## Footnote Aim for pH 7.45-7.55.

Answer 386

* Low GCS to protect airway * Control of ventilation in respiratory depression * Refractory seizures ## Footnote – in respiratory depression and hypoventilation o Hypoventilation would worsen acidosis and TCA toxicity – less protein binding

Answer 387

* Fluids * Sodium bicarbonate * MgSO4 * Alpha agonist (e.g., adrenaline infusion) * IV glucagon

Answer 388

- Alkalinisation of blood o Increases protein binding of TCA to reduce free portion o Reverses affects of acidosis – myocardial depression - High sodium load o Opposes the blockage of Na channels in myocardium by TCA

Answer 389

use benzo dont use - - Phenytoin – Na channel blocker - TCAs also exert their toxic effects through Na channel blockage

Answer 390

A life-threatening condition caused by excessive serotonin in the CNS, often triggered by drug overdose with serotonergic drugs. - E.g. tramadol, SSRIs, TCAs, ectasy, cocaine, fentanyl

Answer 391

* Change in mental state: headache, confusion, agitation, coma, seizures * Autonomic hyperactivity: hyperthermia, sweating, shivering, tachycardia, nausea, diarrhea * Neuromuscular: myoclonus, hyperreflexia, tremor

Answer 392

* Neuroleptic malignant syndrome * Malignant hyperthermia * Sepsis

Answer 393

* Supportive care: cooling, fluids, intubation, paralysis, sedation * diazepam * Specific: cyproheptadine

Answer 394

* RUQ pain * Nausea and vomiting * Severe cases: jaundice, encephalopathy, bleeding (coagulopathy)

Answer 395

* Jaundice / raised bilirubin * High INR / PT * Raised LFTs

Answer 396

* CYP450 inducers: carbamazepine, rifampicin, phenytoin, alcohol * Malnourished patients with lower glutathione levels ## Footnote These patients have a separate nonogram with a lower threshold for treatment.

Answer 397

* Under 4 hours * Staggered dosing

Answer 398

Mostly via phase 2 (conjugation with sulfate and glucuronide). Phase 1 produces NAPQI in zone 3, which is then conjugated with glutathione. In overdose, phase 2 is saturated, glutathione is saturated, and NAPQI builds up, leading to centrolobular necrosis.

Answer 399

Replaces glutathione stores and detoxifies NAPQI.

Answer 400

- SNAP regime – latest, simpler and less anaphylactoid o 100mg/kg over 2 hours o 200mg /kg over 10 hours - Previously 3 bag regime over 21 hrs

Answer 401

Post-resuscitation pH <7.3 OR all 3 of the following: * PT >100s * Creatinine >300umol/L * Grade 3 or 4 encephalopathy

Answer 402

* Respiratory alkalosis - direct effects on medulla resp centre = hyperventilation * Metabolic acidosis * Increased metabolic rate: pyrexia, sweating * CNS effects: tinnitus, dizziness, reduced consciousness * Other: bleeding, hypokalemia

Answer 403

* Sodium bicarbonate: alkalinization of urine and blood * Haemodialysis ## Footnote Alkalinization prevents salicylates from crossing the BBB. trapped in tubules

Answer 404

* Respiratory depression * Low GCS * Miosis

Answer 405

* A to E – intubation/ventilation * Naloxone 400ug and repeat every 2-3 min until GCS improves, may need infusion.

Answer 406

Synthetic opioid receptor antagonist with highest affinity for u receptor, but also kappa and delta.

Answer 407

* Severe hypotension * Bradycardia * Possible bronchospasm, coma, hypoglycemia

Answer 408

* Gastric lavage/activated charcoal within 1 hour Manage bradycardia... * with isoprenaline/adrenaline * Use glucagon/high dose insulin * Temporary pacing

Answer 409

* Increase in vagal tone leading to AV block and bradycardia (beneficial for AF) * Inhibition of Na/K ATPase improves intracellular calcium and contractility in heart failure

Answer 410

* Bradycardia * Visual disturbances * Nausea and vomiting * Agitation

Answer 411

Narrow therapeutic window; increased risk in renal failure and hypokalemia.

Answer 412

* Activated charcoal/gastric lavage * Supportive care: correct electrolytes * Potassium chloride * Digibind for severe cases

Answer 413

Anti-freeze

Answer 414

Paint remover / household items

Answer 415

Both are metabolized by alcohol dehydrogenase; treatment involves blocking this enzyme with ethanol or fomepizole.

Answer 416

Nerve gas – sarin

Answer 417

* Inhibition of acetylcholinesterase leading to high levels of Ach * Flaccid paralysis * Muscarinic effects: bradycardia, bronchospasm, miosis, secretions, gut contractions * CNS effects: agitation, seizures

Answer 418

* Atropine to block Ach receptors * Pralidoxime to reactivate acetylcholinesterase * Supportive care including intubation/ventilation * Remove clothes/wash

Answer 419

Higher affinity to hemoglobin reduces binding sites for oxygen, leading to anemia and a leftward shift in the oxygen dissociation curve.

Answer 420

* Headache * Nausea and vomiting * Confusion * Can lead to convulsions, cardiac ischemia, arrhythmias

Answer 421

* A to E – oxygen saturation unreliable * Administer 100% oxygen or hyperbaric 100% oxygen if levels >30%

Answer 422

Acute change in consciousness and awareness that fluctuates over time, with multiple precipitating factors and is reversible.

Answer 423

* Altered state of consciousness * Reduced focus/attention * Change in cognition: memory, disorientation, language * Onset over hours/days * Fluctuates over the course of the day * Disturbance to sleep * Hallucinations/delusions

Answer 424

* Hypoactive: inattention, withdrawn, sleepy * Hyperactive: combative, confused, aggressive, paranoid * Mixed: most common

Answer 425

* CAM ICU (Confusion Assessment Method - ICU) * Intensive Care Delirium Screening Checklist (ICDSC)

Answer 426

- 4 criteria 1. Acute onset or fluctuating course 2. Inattention – 10 letters read and ask patient to squeeze hand when letter A is heard – more than 2 errors scores a point 3. Altered consciousness – RASS score other than 0 4. Disorientated thinking – questions asked and more than 1 mistake will score E.g. will a stone float on water - Positive CAM ICU if 1 and 2 present and EITHER 3 or 4

Answer 427

- 8 points assessed including consciousness, attention, disorientation, sleep/wake disturbance, fluctuation, hallucination etc - If 4 or above = delirium

Answer 428

- Predisposing factors – non modifiable o Age o Pre-existing cognitive impairment / dementia o pre-existing HTN o increased ASA grade o nicotine or alcohol use o increased functional dependence o sensory impairment – poor vision - precipitating factors o acute illness – trauma, sepsis, pain, cerebral ischaemia o medication – benzos, opioids, anticholinergic , steroids o environmental – lack of daylight, noisy ward o other – constipation, urinary retention

Answer 429

- regular screening to help identify - more evidence for the non pharmacological interventions o daylight exposure / night day differentiation o ear plugs at night o reduce noise o family members o reorientation – remind them of where they are, time of day (clocks) o mobilisation o maintain sensory inputs – hearing aids/ glases - pharmacological o avoid benzos/ ketamine where possible o dexamedetomidine has been shown to reduce incidence of delirium as a preventative o melatonin

Answer 430

Day/night differentiation, Ear plugs, Family involvement, Mobilisation - treat cause o laxatives, analgesia, correct electrolytes ## Footnote These interventions help create a supportive environment for patients.

Answer 431

Haloperidol, Quetiapine ## Footnote Monitoring QTc and treating underlying causes are also important.

Answer 432

- short term o harm to themselves e.g. accidental extubation, line removal - medium term o prolonged ICU admission o increased ventilation requirement, morbidity and mortality - long term o long term cognitive impairment o PTSD , depression, anxiety

Answer 433

Dementia, Psychosis, Serotonin syndrome, Confusion ## Footnote Confusion differs as consciousness remains normal.

Answer 434

Opioid-sparing analgesia, Avoiding benzodiazepines, Using dexmedetomidine, Monitoring depth of anaesthesia ## Footnote BIS monitoring helps minimize excessive anaesthesia.

Answer 435

- Hyperglycaemia or hypo - Dehydration - Electrolyte imbalance - Hyponatraemia - Acidosis - Hypoxia , hypercarbia - Hypotension - Pain

Answer 436

When patient is a risk of harming themselves or others, Significant patient distress

Answer 437

- Clinically detectable weakness in critically ill patients where there is no other plausible cause other than critical illness - Symmetrical peripheral weakness that is facial sparing and not pre-existing - Common cause of morbidity in critically ill patients

Answer 438

Critical illness polyneuropathy (CIP), Critical illness myopathy (CIM), Critical illness neuromyopathy (CINM) ## Footnote CIP affects nerves, CIM affects muscles, and both can co-exist.

Answer 439

o Multifactorial o Non demyelinating axonopathy due to  Microvascular ischaemia due to systemic hypotension / inadequate perfusion pressure  Endothelial dysfunction  Mitochondrial dysfunction ## Footnote .

Answer 440

o Muscle denervation o Reduced muscle membrane excitability o Altered sarcoplasmic reticulum function – reduced Ca release o Decreased contractile protein function o Muscle mitochondrial dysfunction o Disuse muscle atrophy / being bed bound

Answer 441

- Weakness after onset of critical illness - Usually following number of days of MoF, high dose steroids, NMBA - Generalised weakness – proximal and distal, symmetrical - Flaccid and Muscle wasting - Spares cranial nerves - Autonomic and sensory preserved - Difficulty weaning / ventilator dependency

Answer 442

- Patient factors o Female, age - Illness related o Severe sepsis, MoF, prolonged duration , prolonged mechanical ventilation - Drug related o Steroids, vasopressors, NMBA, parenteral nutrition - Other o Hyperglycaemia, electrolyte imbalance, high lactate

Answer 443

- Nerve conduction studies o Reduced compound motor action potentials o Sensory AP reduced in critical illness polyneuropathy only o Nerve conduction velocity = normal = myelin in tact - Electromyography o Motor unit potentials amplitude  Spontaneous fibrillation, high amplitude in CIP  Spontaneous fibrillation, low amplitude in CIM - Electrophysiology studies – stimulation of nerves and muscles - Rule out other cause – CT / LP

Answer 444

- Early physiotherapy and mobilisation - Weaning early from ventilator / sedation breaks / trials of spontaneous breathing - Optimisation of nutrition – high protein - Close management of blood glucose - Minimise periods of NMBA ## Footnote These strategies aim to maintain muscle function.

Answer 445

- Central o Stroke o Cervical spinal cord pathology - Peripheral o Guillian barre o Inflammatory myositis - Systemic o Electrolyte disturbance – hypoK ## Footnote T

Answer 446

Risk of hyperkalaemia, Contraindicated in critically ill patients for more than 1 week ## Footnote ICU-AW increases extra junctional nACh receptors.

Answer 447

- Short term o Increases need for ventilation / difficult wean / may need tracheostomy o Increased risk of VAP , VTE o Increased ICU stay and M&M - Long term o Most recover , 30% have long-term disability

Answer 448

mannitol levetiracetam

Answer 449

- Pyrexia will increase cerebral metabolic rate and O2 demand and hence promote secondary brain injury - Reduction in cerebral oedema associated with reperfusion - Supresses reactive oxygen species / free radicals during reperfusion Supresses destructive neuroexcitotoxic cascade e.g. glutamate release, receptor activation, intracellular calcium overload and death

Answer 450

major cardiac = common complications post op such as myoocardial oedema and hypovolaemia. may need ionotropic/ vasopressor support. rare but serious complication - tamponade vascular = most patients have significant cormorbidities, complications post op e.g. major haemorrhage, aneurysmal rupture, coagulopathies. AKI and RRT requirement is common. neurosurgery - risk of complications, ICP monitoring. maintain CPP. risk of seizures, SIADH, bleeding. emergency laparotomy - if they require ongoing CVS support / respiratory support, persistent acidosis. faecal soiling of peritoneum. high NELA

Answer 451

* patient comorbidities * type of surgery - serious complicatio that need monitoring * Scoring tools can guide * intraoperative events e.g. anaphylaxis / sux apnoea / major haemorrhage

Answer 452

acute physiology age and chronic health evaluation system score used to predict mortality can help decide on ITU admission

Answer 453

ileus bowel obstruction retroperitoneal haematoma - AAA / trauma large volume fluid resusitation peritonitis pancreatitis and fluid collections sepsis / severe burns - capillary leak + oedema

Answer 454

early - bleeding, arrhythmias, pneumothorax, VAE late - infection, microshock (subclavian high risk of pneumothorax) (femoral high risk of infection

Answer 455

mastoid process and sternal notch identified = half way feel carotid - insert lateral to this also in apex of 2 heads of SCM insert needle down towards ipsilateral nipple

Answer 456

preparation - trained assistant, prepare airway equiptment - check cuff, emergency drugs, AABGI pre oxygenate - FiO2 =100% increase sedation position - head extended remove dressing insert bouje remove insert tracheostomy over inflate cuff check misting/ chest/ CO2 (ensure enteral feeds have been stopped 6 hours before and aspirate NGT)

ITU Flashcards

(486 cards)