General ICM Flashcards

Question

What are the 4 diagnostic criterion for delirium according to the DSM IV?

Answer 1

a) disturbance in consciousness b) change in cognition c) acute d) caused by the direct physiological consequences of a general medical condition, or drug/withdrawal induced

Answer 2

a) clouding of consciousness b) disturbance of cognition c) psychomotor disturbances - unpredicatble shifts from hypo to hyper activity - increased reaction time - increased or decreased speech - enhanced startle reaction d) sleep/wake disturbance e) acute f) underlying illness is responsible

Answer 3

Neurotransmitter imbalance, with reduced acetylcholine and increased dopamine resulting in neuronal excitability There may also be cerebral microvascular dysfunction following exposure to inflammatory mediators, or global failure of oxidative metabolism resulting in cerebral insufficiency

Answer 4

Very | 70-80% of mechanically ventilated patients are affected

Answer 5

1. Hyeractive - confused, agitated, combative, aggressive, paranoid - 1% 2. Hypoactive delirium - inattentive, stuporous, withdrawn, often mistaken for depression - 35% 3. Mixed - 64%

Answer 6

1. Patient factors - age, comorbidities, baseline cognitive impairment, psychiatric history, alcohol or substance abuse 2. Illness related - high APACHE II score, sepsis, hypoxaemia, metabolic derrangement, surgery esp CPB 3. Iatrogenic - disturbed sleep/wake cycle, sedatives esp benzos, anticholinergic medication

Answer 7

1. Increased risk of short-term complications e.g. accidental extubation/line removal 2. Medium term complications - increased LOS, increased duration MV, increased mortality (independent risk-factor for a 3-fold increase in mortality at 90 days) 3. Long-term complications - risk of PTSD, risk of long-term cognitive impairments

Answer 8

The 2 most widely used bedside scoring systems are 1. Confusion assessment method (CAM) - ICU 2. Intensive Care Delirium Screening Checklist (ICDSC)

Answer 9

1. Is the patient different from their baseline mental status? or has the patient had any fluctuaiton in mental status in the past 24 hours? 2. Test of inattention - hand squeezing on the letter A >2 = positive 3. Is the RASS score anything other than 0 4. Disorganised thinking - e.g. will a stone float on water Feature 1 plus 2 and either 3 or 4 present = CAM-ICU positive

Answer 10

The ABCDE bundle (Vasilevskis et al 2010) Awake and Breathing (daily sedation breaks and SBTs) Choice of sedation - minimise medications that can provoke delirium e.g. benzos Delirium monitoring Early mobilisation Plus, sleep hygiene, removal of invasive lines when no longer needed

Answer 11

1. Antipsychotics are the drug of choice for those posing risk to themselves e.g. haloperidol, olanzipine 2. Use of dexmedetomadine as a sedation agent

Answer 12

1. DahLIA trial (JAMA 2016) - double blind MC RCT. Showed a statistically significant reduction in median ventilator-free hours at day 7 and a significant decrease in antipsychotic use. Non-significant decrease in ICU LOS. 2. Midex-Prodex trial (JAMA 2012) - DB MC parallel design that showed the non-inferiority of dexdor when compared to midaz or propofol. Duration of sedaiton was significantly shorter with dexdor. There was a non-significant decrease in ICU LOS.

Answer 13

Primary respiratory impairment following submersion or immersion in a liquid medium, whatever the outcome. The term near drowning is no longer used.

Answer 14

According to the findings at the scene 1. No evidence of aspiration 2. Evidence of aspiration but with adequate ventilation 3. Evidence of aspiration with inadequate ventilation. 4. Absent ventilation and drowning

Answer 15

1. The diving reflex. Stimulated by cold water to the face. Mediated via CN V1. Results in apnoea, bradycardia and vasoconstriction 2. A massive cathecholamine surge during the diving reflex causing profound vasoconstriction, arrhythmias, pumonary oedem. 3. Progressive hypoxaemia and hypothermia leading to bradycardia, pulmonary hypertension and cardiac failure

Answer 16

Hypoxic brain injury - starts within 5 minutes - hypothermia not usually protective because its onset is unlikely to occur before the hypoxia starts

Answer 17

Hypothermia No clinically significant differences in volume status, electrolytes or lung function in those who drown in fresh compared with salt water

Answer 18

Aspiration of contaminated fluid results in infection in up to 50% Aerobic gram positive organisms (strep/staph) may be aspirated from the oropharynx Aerobic Gram-negative organisms (e.g. Pseudomonas, Aeromonas, Burkholderia pseudomallei, Leptospira) may contaminate fresh water Fungal infections including delayed CNS infections due to Aspergillus and Pseudallescheria boydii are a risk, esp in immunocompromised patients.

Answer 19

Immersion or submersion results in panic, breath-holding, laryngospam, aspiration and swallowing of water. These lead to hypoxia, which eventually results in relaxation of laryngeal muscles. Hypercapnia and acidosis result in respiratory stimulation which result in aspiration. This results in direct alveolar toxicity - resulting in pulmonary oedema, surfactant washout and dysfunction resulting in atelectasis and bronchospasm.These all result in V/Q mismatch (shunt), reduced compliance and ARDS.

Answer 20

1. Age - 0-4 year olds may drown in the bath tub, or swimming pools e.g where fencing is inadequate. Adolescence when risk taking behaviour may occur. 2. Male gender 3. Intoxication 4. Occupation/hobbies - scuba diving, farming, fishing 5. Medical conditions - IHD, cardiomyopathies, arrhythmias, epilepsy, diabetes, depression 6. Conditions increasing the risk of drowning - currents, rip tides, waves, cold water.

Answer 21

1. Remove from the water 2. Consider whether spinal precautions are needed 3. 5 rescue breaths 4. Start chest compressions if there's no response 5. Compression only CPR is not appropriate in drowning 6. Consider the effects of hypothermia

Answer 22

1. ATLS approach - secure airway is needed, treat any life-threatening injuries 2. Optimize oxygenation - lung protective ventilation, bronchoscopy may help to remove the aspirated debris 3. Optimize cardiac output - fluid resus as likely to be hypovolaemic, may need vasopressors/inotropes 4. Neuroprotective measures 5. Temperature control

Answer 23

A retrospective review published in Resuscitation 2016 (Burke et al) revealed 247 patients who received ECLS following drowning between 1986 and 2015. Cardiac arrest with ROSC prior to ECLS occurred in 34.8%, ECLS was initiated during cardiac arrest in 31.2% and 34% did not arrest prior to ECLS. Overall survival was 51.4%, with al increase in survival across all 3 categories. Veno-venous ECLS was associated with a better survival that veno-arterial ECLS in patients with cardiopulmonary failure. The presence of AKI and need for CPR during ECLS were associated with increased mortality.

Answer 24

1. Submersion > 5-10 minutes 2. Resuscitation not attempted for > 10 minutes after resuce 3. > 25 minutes of resuscitation 4. GCS < 5 or unreactive pupils on arrival to hospital 5. Pulseless and apnoeic on arrival to hospital 6. pH < 7.10 on initial blood gas

Answer 25

1. Preload 2. Afterload and SVR 3. Myocardial contractility

Answer 26

Ventricular end-diastolic volume (EDV), which is governed by the volume and pressure of blood returning to the heart. Haemorrhage, sepsis, anaphylaxis and raised intra-thoracic pressure are all common causes of inadequate preload.

Answer 27

Valve stenosis, hypertension, high SVR, low intrathoracic pressures and ventricular dilatation

Answer 28

1. Systolic dysfunction | 2. Diastolic dysfunction

Answer 29

- Inadequate systolic ejection which is a result of reduced contractility (e.g. ischaemia, cardiomyopathy) or increased impedence (e.g. hypertension, aortic stenosis). Increasing EDV will maintain SV provided myocardial reserve is adequate, otherwise SV and CO will fall and inotropes will be required.

Answer 30

Characterised by reduced ventricular compliance with impaired diastolic filling (i.e. stiff ventricle). It may be caused by mechanical factors e.g. restrictive cardiomyopathy, or impaired relaxation due to myocardial ischaemia or severe sepsis. - The resulting increase in end-diastolic pressure and associate venous congestion can cause characteristic 'flash' pulmonary oedema

Answer 31

Endomyocardial ischaemia caused by small vessel arteriopathy

Answer 32

Hypertension - blood flow from the epicardium to endomyocardium is impeded by ventricular wall hypertrophy and the resulting ischaemia impairs ventricular relaxation

Answer 33

- No treatment aimed at organ donation should be started prior to the decision to withdraw being made. - Maintenance of life-sustaining treatment can be considered in the best interests of patients who wanted to be donors if this facilitates donation and doesn't cause harm or distress. - Agents can be used to maintain arterial pressure - It's not appropriate to initiate treatment against the wishes of the family

Answer 34

- Withdrawal of life-sustaining treatment one retrieval team and family are ready. - Following cessation of cardio-resp function there is a 5 minute window to confirm monitored asystole prior to certification - The relatives have 5 minutes to spend with the patient prior to transfer to the OT - For lung donation reintubation is required and lungs are recruited with a single breath and CPAP maintained with 100% O2. Ventilation is reinstated once the chest has been opened and the aorta clamped.

Answer 35

Starts when the SBP falls below 50mmHg of sats < 100%. Stand-down times from the onset of FWI vary by organ and by receiving centre. Approx times are: - Liver 30 mins - Pancreas 30 mins - Lungs 60 mins from FWI to reinflation - Kidney 120 mins

Answer 36

There are 2 principle types of DCD - controlled and uncontrolled 1 - uncontrolled - dead on arrival 2 - uncontrolled - unsuccessful resus 3 - controlled - cardiac arrest following planned withdrawal 4 - either - cardiac arrest in a patient who is drain dead 5 - uncontrolled - cardiac arrest in hospital inpatient

Answer 37

Absolute: vCJD HIV disease Unlikley to be accepted: - Active invasive cancer in the past 3 years excl non-melanoma skin cancer and primary brain tumour - Primary intracerebral lymphoma - All secondary intracerebral tumours - Haematological malignancy - Melanoma - Untreated systemic infection - Active and untreated TB - West Nile virus - History of Ebola infection There is no upper or lower age limit

Answer 38

1. Coma 2. Vegative state 3. Minimally conscious state

Answer 39

- A state of absent wakefulness and absent awareness - Unrousable unresponsiveness lasting > 6 hours - Can't be awakened - Fails to respond to pain, light and sound - Lacks normal sleep-wake cycle and - Does not initiate voluntary actions

Answer 40

- Wakefulness with absent awareness - Severe cortical damage with preservation of some brainstem activity - Preserved capacity for spontaneous or stimulus-induced arousal, evidenced by sleep-wake cycles and a range of reflexive and spontaneous behaviours - Complete absence of environmental awareness or awareness of self

Answer 41

- Wakefulness with minimal awareness - A state of severely altered consciousness in which minimal but clearly discernible behavioural evidence of self or environmental awareness is demonstrated. - Inconsistent by reproducible responses above the level of spontaneous or reflexive behaviour.

Answer 42

1. TBI 2. Vascular event - ICH, SAH, CVA 3. Toxic/metabolic - alcohol, drugs/poisons, anaesthetics, benzos, hypoglycaemia, hyper or hypo-osmolar states 4. Infection - encephalitis, abscess, vasculitis, sepsis 5. Hypoxia 6. Systemic illness - liver failure, renal failure, endocrine

Answer 43

ABCDE approach Intubation to protect the airway if GCS < 9 Indentify cause - BM, u+es, LFTs, ammonia, FBC, TFTs, ABG, culture, CT/MRI, consider LP Maintain normal physiology - o2, BP, correct hypoglycaemia, correct hypo/hyperthermia, correct electrolyte abnormlities Review meds EEG Detailed neurological assessment ICP management if needed

Answer 44

- Should start 72 hours after ROSC - Exclude confounders - If M1-2 and no pupil or corneal reflexes or bilateral absent SSEPs ->poor outcome very likely (FPR < 5%, 95% CI) - If these criteria aren't met them two or more of the following also suggest likely poor outcome - status myoclonus < 48 hours after ROSC; High NSE level, Unreactive birst-suppression or status on EEG, diffuse anoxic brain injury on CT.

Answer 45

1. Absence of EEG reactivity to external stimuli 2. Presence of burst suppression 3. Status epilepticus

Answer 46

Results from brain stem pathology that disrupts voluntary control of movement Wakefulness and Awareness are both still preserved Able to communicate by blinking

Answer 47

A life-threatening organ dysfunction caused by a disregulated host response to infection (SEPSIS-3 definition, published in JAMA 2016)

Answer 48

A subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality that with sepsis alone - Identified clinically by vasopressor requirement, or lactate > 2 - The combination is associated with an in-hospital mortality of > 40%

Answer 49

Used as a quick bed-side guide to diagnosing those with poor outcomes due to sepsis, if they have 2 or more of the following 1. RR > 21 2. SBP < 100 3. GCS < 15

Answer 50

1. Vasoldilatation (iNOS causes endothelial NO production) 2. Loss of endothelial integrity due to inflammatory mediator-related disruption of the tight junctions 3. Reduced cardiac contractility 4. Activation of the coagulation cascade and fibrinolysis due to IL-1,6 and TNF-a 5. Mitochondrial dysfucntion - results in reduced O2 utilisation

Answer 51

Peptides secreted by Gram +ve bacteria

Answer 52

Located within the Gram -ve bacterial cell walls

Answer 53

- Measure lactate, Obtain cultures, administer broad-spectrum antibotics - 30mls/kg IV fluid for hypotension/ lactate > 4 - if hypotension persists then vasopressors to maintain MAP > 65 and reassess fluid status e.g. CVP, ScvO2, ECHO, SLR, LiDCO

Answer 54

A complete and irreversible loss of brain and brainstem function as a result of neurological injury. The heart is still beating but respuratory function is dependent on a ventilator. The Academy of the Medical Royal Colleges Uk outlines 3 essential components -1. Fulfilment of essential preconditions -2. Exclusion of potentially reversible causes of coma -3. Formal demonstration of coma and apnoea.

Answer 55

1. Pt should be deeply unconscious, apneoic and mechanically ventilated 2. Irreversible brain damage of known aetiology

Answer 56

Ensure that coma is not secondary to reversible factors such as CNS depressant drugs, biochemical/metabolic abnormalities or hypothermia.

Answer 57

1. A period of observation 2-3 times the elimination half-life of the drug in question 2. Administration of specific antagonists 3. Plasma analysis 4. Confirmatory test to confirm absence of cerebral flow/perfusion

Answer 58

1. Circulatory - ensure MAP > 60 2. Respiratory - ensure normal pH, PCO2< 6, PO2 > 10 3. Metabolic - ensure temp > 34 4. Biochemical - ensure Na 115-160, K > 2, Mg 0.5-3, Po4 > 0.5, gluc 3-20

Answer 59

1. Midazolam - brainstem testing should not take place if levels > 10 micrograms/litre 2. Thiopentone - brainstem testing should not be done if levels > 5 mg/l

Answer 60

2 competent clinicians who have held GMC registration for > 5 years, one of whom must be a consultant

Answer 61

1. It assesses the integrity of the sensory and motor pathways of the cranial nerves reflexes 2. An apnoea test.

Answer 62

1. Pupillary reflex (afferent II, efferent III) - check for direct and consensual reflexes 2. Corneal reflex (afferent V, efferent VII) - the cornea os brushed lightly with a swab 3. Response to painful stimuli (Afferent V, efferent VII) - a painful stimulus is applied to the supraorbital ridge 4. Vestibulo-ocular reflex (afferent VIII, Efferent III, IV, VI)- visualise the TM prior to beginning the test. Instil 50mls ice cold saline into each external auditory meatus in tuen, looking for eye movements/nystagmus 5. Gag reflex (afferent IX, efferent, X) - the pharynx is stimulated with a spatula/similar 6. Cough reflex (afferent X, efferent X) - a bronchial catheter is passed down the ET tube to stimulate the carina

Answer 63

1. Increase FiO2 to 1.0 2. Perform ABG to confirm measured PaCO2 and SaO2 correlate with monitored values 3. decrease the MV until ETCO2 > 6. Check PaCO2 > 6 and pH < 7.4 on ABD 4. Maintain apnoeic oxygenation by either instilling 5L O2 per minute via suction catheter of by using CPAP 5. Five minute observation to look for the presence of spontaneous resp activity 6. Perform final ABG to confirm an increase in PaCO2 of > 0.5kPa Following the test the ventilator should be recorrected and any acid-base abnormality corrected prior to carrying out the second set of tests. There is no defined time period between the 2 sets.

Answer 64

The time at which the first set of tests was completed

Answer 65

1. Inability to exclude the influence of sedatives 2. High cervical cord injury 3. severe maxillofacial injury

Answer 66

1. Measure brain electrical activity - EEG - little value in hypothermia or drug intoxication as these factors suppress neuronal activity - SSEPS - peripheral stimulus to median nerve looking for response at the contralateral primary sensory cortex 2. Flow studies - cerebral angiography - reveals absence of intracerebral filling beyond the entry of the carotid and vertebral arteries into the skull - transcranial doppler - useful only if a reliable waveform is found - complete absence of flow may not be reliable if inadequate windows exist

Answer 67

1. Neutropenia and sepsis 2. Resp failure - infection, pulmonary oedema/haemorrhage/infiltration by underlying disease 3. Tumour lysis syndrome 4. Graft vs host disease 5. Complications of chemotherapy and stem cell transplant 6. CNS dysfunction and seizures - hyperviscosity syndrome/intracerebral bleed or thrombosis, underlying malignancy, electrolyte imbalance 7. GI dysfunction including neutropenic enterocolitis (typhlitis) 8. Acute renal failure - nephrotoxic drugs/sepsis/underlying disease

Answer 68

Neutrophil count < 0.5 x 10(9)/l

Answer 69

Neutropenia and clinical signs of infection OR temp > 37.9

Answer 70

1. Reverse barrier nursing 2. Positive pressure side room isolation 3. Avoid invasive procedures where possible 4. Avoid rectal exam/rectal temp probe insertion 5. Meticulous oral hygiene

Answer 71

ABCDE aproach 1. History and exam - including pets/exposure/hobbies/travel/occupation/invasive lines. Examine for infection ensuring you check oropharynx, skin and perirectal areas. 2. Follow surviving sepsis guidelines - cultures, antibiotics, lactate, bloods, fluid and vasopressors as needed 3. Imaging - CXR and any abdo imaging as necessary

Answer 72

1. IV anti-pseudomonal B-lactam e.g. piperacillin-tazobactam or meropenem 2. Additional antibiotics (e.g. aminoglycoside) if Gram-negative or resistant organisms suspectd, or if hypotensive or potential respiratory infection For those anaphylactic to penicillin alternatives include ciprofloxacin and clindamycin, or vancomycin and aztreonam

Answer 73

Metabolic derangement that occurs when large volume tumour cells are lysed, usually following chemotherapy. Typically a/w acute leukaemia and high-grade lymphomas Metabolic derangement include hyperkalaemia, metabolic acidosis and renal failure, severe hypocalcaemia and hyperphosphataemia can occur and increased serum and urinary urate levels are seen

Answer 74

ABCDE approach 1. Aggressive fluid resuscitation 2. Treat hyperkalaemia 3. Rasburicase (a recombinant urate oxidase enzyme which reduces plasma uric acid concentration)

Answer 75

Early (< 100days) -infection, haemorrhage, acute GvHD, interstitial pneumonitis, aplastic anaemia secondary to graft failure Late complications -chronic GvHD, chronic pulmonary disease, infections, autoimmune disorders

Answer 76

An immune-mediated disease following allogenic haematopoietic cell transplant (and transplant of solid organs containing lymphoid tissue) that results from a complex interaction between donor and recipient adaptive immunity (APCs of the recipient interact with the mature T-cells of the donor). It can occur even when the donor is perfectly matched

Answer 77

Typically with enteritis, hepatitis and dermatitis | Diagnosis can be histological (skin, liver, rectal) or by using a clinical diagnosis and staging system

Answer 78

Diverse syndrome with varying clinical features resembling autoimmune disease e.g. sclerodermia, primary biliary cirrhosis, bronchiolitis obliterans and chronic immunodeficiency.

Answer 79

1. High dose steroids 2. Immunosuppressant e.g. ciclosporin 3. Parenteral nutrition may be required to facilitate gut rest

Answer 80

Neutropenic enterocolitis Life-threatening complication of chemotherapy Symptoms include nausea, abdo pain and distension, fever and chills Poor prognosis and successful treatment depends on an early diagnosis achieved with a high index of suspicion and use of CT imaging. Elective right hemicolectomy may be required to prevent recurrence.

Answer 81

1. Replace normal fluid and electrolyte losses 2. Maintain BP, cardiac output and tissue perfusion to satisfy metabolic needs, aid temperature regulation and facilitate waste removal 3. Replenish substantial defects or ongoing losses 4. Avoid excessive tissue oedema

Answer 82

- Osmotic pressure exerted by small diffusible ions e.g. Na - Osmotic pressure reflects ion concentration gradients between compartments created by cellular ion pumps, e.g. Na and Cl that are mainly extracellular and K and PO4 that are intracellular e. g. saline increased extracellular Na and Cl, raising ECF osmotic pressure and attracting water out of the intracellular compartments in to the ECF

Answer 83

1. Plasma oncotic pressure - which is the ability of large plasma proteins to bind and retain water in the circulation. POP is normally ~ 3.4kPa with 75% of the effect due to albumin, 20% Hb and 5% globulins. 1g albumin 'binds' about 18mls water, thus intravascular albumin binds ~ 2.25L of plasma water 2. Vascular permeability - normal albumin leakage across capillary membranes is limited to 4-5% per hour by its high MW and negative charge. Thus all of the normal intravascular albumin leaks into the ISF each day. It returns via the lymph and thoracic ducts at the same rate. Inflammation increases vascular permeability and albumin leakage by up to 300%. Acute illness also decreases production of albumin by 15g/day. Low albumin reduces intravascular volume, and increases in ISF albumin causes oedema 3. Circulatory hydrostatic pressure - increases leakage of intravascular water, whilst plasma oncotic pressure draws water into and maintains plasma volume

Answer 84

1.5-2.5L /day

Answer 85

~70-100mmol | 1-1.5mmol/kg/day

Answer 86

40-70mmol/day | 0.5-1mmol/kg/day

Answer 87

620-740 mosmol/dau

Answer 88

60% of body weight ~42L in a 70kg man ~25L = IC and 15-17L = EC The ECF comprises ISF 11-13L and intravascular plasma 3-4L

Answer 89

``` Haemolytic uraemic sydrome It's a triad of 1. Microangiopathic haemolytic anaemia 2. Thrombocytopenia 3. Renal failure ```

Answer 90

There are 2 causes - epidemic and atypical. The epidemic form is a/w a prodromal illness and bloody diarrhoea following infection with verotoxin-producing enterococci (E.coli 0157) or Shigella Atypical is much rarer and has a poorer prognosis. It may occur following -step pneumoniae, CMV or HIV infection -bone marrow transplant/solid organ transplantation -drug exposure e.g. quinine, heroin, ciclosporin -malignancy -pregnancy

Answer 91

Following ingestion of the toxin bloody diarrhoea occurs as a result of haemorrhagic colitis. AKI develops as a result of direct injury to the renal vascular endothelium secondary to toxin production. This leads to excessive platelet aggregation, platelet microvascular thrombin and ultimately AKI. Subsequent HTN and fluid overload are common -In atypical HUS there is often dysregulation of the complement system

Answer 92

1. Bloods - FBC and film: looking for reticulocytes, evidence of haemolysis and thrombocytopenia - Direct Comb's test: differentiate between immune and non-immune mediated - Lactate dehydrogenase (LDH, raised in haemolysis) - U+Es (AKI) - LFTs: including split bilirubin - Clotting- incl fibrinogen and d dimers - HIV and hepatitis serology - Full renal screen: autoimmune and vasculitis screen 2. Stool MC+S 3. Urinalysis 4. Consider renal imaging to rule out other causes of AKI

Answer 93

``` ABCDE aproach Specific: 1. O2 2. Fluid and electrolyte balance 3. CV support/BP control 4. Renal and haematology input early 5. Treat the cause - cipro for e.coli and shigella 6. Plasma exchange - PEx is often used as HUS can be difficult to distinguish from thrombotic thrombocytopenia purpura initially, recommended in atypical HUS. In epidemic HUS PEx, IVIg, steroids and anti platelets have not proved beneficial ```

Answer 94

Mortality rate is 3-5% 70-85% with epidemic HUS recover normal renal function Atypical HUS has poorer prognosis with an initial mortality of ~25%, and up to 50% progressing to ESRD.

Answer 95

They are considered a spectrum of the same disease process TTP is a malignant condition with a mortality of >90% if untreated It's a clinical diagnosis characterised by: 1. Thrombocytopenia 2. MAHA (microangiopathic haemolytic anaemia) 3. Fluctuating neurological signs (due to endothelial injury in the cerebral circulation) 4. Renal impairment 5. Fever Clotting is usually normal - DIC is a late, ominous sign.

Answer 96

The hallmark in TTP is deficiency of von Willebrand factor-cleaving protease, which may be genetic or acquired. vWF is a large glycoprotein present in the plasma whose functions include binding factor VIII, and activating and binding platelets in response to endothelial injury. It is produced in the endothelium as ultra-large multimers that are inactivated when cleaved by the vWF-CP. In TTP, these multimers are not cleaved and there is uncontrolled platelet activation. Fibrin is deposited and thrombus propogated creating ischaemia distally, and red cells are shredded as they pass the fibrin/platelet mesh (i.e MAHA)

Answer 97

Specific interventions are recommended by the British Committee for Standards in Haematology 1. PEx using Octaplas, this should continue daily for at least 2 days after platelet counts recover. This removes the autoantibodies from the circulation and replaces their plasma with plasma containing normal levels of vWF-CP 2. Adjuvant high-dose pulsed methylprednisolone can be considered. Has been shown to improve outcome but not RCT of PEx and steroids vs Pex alone 3. Rituximab - used in life-threatening TTP and in patients with refractory or relapsing disease 4. Low dose aspirin when plts > 50 5. Supportive measures - RBC and folate supplementation during active haemolysis, plt transfusions are contraindicated unless life-threatening haemorrhage, routine thromboprophylaxis once plts > 50.

Answer 98

135-145 mmol/l

Answer 99

Small intestine

Answer 100

1. Renin-angiotensin-aldosterone system 2. ADH 3. Thirst 4. B-adrenoreceptor stimulation at the PCT

Answer 101

70% PCT 20% thick ascending loop of Henle 5% DCT 3% collecting duct

Answer 102

Typically classified according to the tonicity of the extracellular fluid/plasma osmolality and the patients volume status - specifically hyper-, eu- and hypovolaemia

Answer 103

Low sodium level in the presence of hypoosmolality Hyponatraemia occurring without hypoosmolality is referred to as pseudohyponatraemia (occurs secondary to elevated levels of lipids or proteins)

Answer 104

TBW and total body sodium are low, but there is a disproportionate loss of sodium compared to water. e.g. increased ADH secretion in hypovolvaemic states (vomiting, diarrhoea, xs sweating). Urinary sodium differentiates renal vs extra-renal losses: urinary sodium < 20 suggests an extra renal cause

Answer 105

The most common category of low sodium in hospital patients. Causes include: SIADH, glucocorticoid deficiency, hypothyroidism, low solute intake (e.g. beer potomania), psychogenic polydipsia.

Answer 106

Essentially due to dilutional hyponatraemia. Oedema is seen as a result of impairment of the kidneys ability to excrete water maximally. There is paradoxical increase in total body sodium, but a simultaneous and proportionally larger increase in total body water. Causes include: Nephrotic syndrome, CCF, cirrhotic liver disease

Answer 107

Result from changes in the osmotic gradient that develops between the intracellular and extracellular fluid compartments producing tissue oedema. The effects of this tissue swelling are clinically most pronounced in the brain, where the non-compliant skull combined with lack of adaptive mechanisms means raised ICP can be rapidly devastating. This is particularly important in patients with severe hyponatraemia that has occurred over hours, when convulsions, coma and death secondary to cerebral herniation can result.

Answer 108

Due to shifts of water out of cells due to osmotic gradient e.g. due to: Hyperglycaemia Mannitol

Answer 109

Pseudohyponatraemia - increase in the non-water component of plasma results in a falsely low reading e.g. hyperlipidaemia, hyperproteinaemia

Answer 110

Vomiting, diarrhoea, sweating, burns, pancreatitis

Answer 111

Low solute intake | Polydipsia

Answer 112

Hypothyroidism Adrenal insufficiency SIADH

Answer 113

CCF Nephrotic syndrome Cirrhosis

Answer 114

Renal failure

Answer 115

ABCDE approach 3% hypertonic saline until symptoms subside The aim is to address the cerebral oedema but not to normalise sodium. Increasing the Na by 4-6 mmol/l or a level of about 120 is normally sufficient to reverse the most severe manifestations of acute hyponatraemia. It is possible to calculate the expected change in sodium concentration on the basis of the volume of and rate at which the hypertonic saline is infused Admit to critical care and monitor sodium levels 1-2 hourly. The rate of increase shouldn't exceed 8-10 mmol/l in a 24hour period.

Answer 116

Rare neurological disorder characterised by symmetrical midline demyelination of the central pons. Extrapontine lesions can occur in the basal ganglia, internal capsule, lateral geniculate body and cortex. Symptoms include motor dysfunction, respiratory paralysis, mental state changes and coma. Osmotic demyelination is the major risk associated with excessively rapid sodium correction.

Answer 117

``` Malnourished Alcoholics Burns victims Hypokalaemia Na change > 12 mmol/24 hours. ```

Answer 118

Failure to suppress ADH production in lowered osmolality states This results in disproportionate water retention compared with sodium.

Answer 119

Drugs: hypoglycaemic agents, antipsychotics, antidepressants, chemo esp vincristine and cyclophosphamide Malignancy: Lung (esp small cell), brain, neck, duodemun, pancreas CNS disorders: Infection, trauma, ischaemia, haemorrhage Pulmonary disorders: Pneumonia, acute respiratory failure Pain: Can mediate an increase in ADH secretion post-op

Answer 120

1. Fluid restrict aiming for slow rise in Na of 1-1.5 mmol/l/day 2. If symptomatic - hypertonic saline 1.8% 3. Demeclocycline 600-1200mg/day to inhibit the renal response to ADH (i.e it induces nephrogenic DI) 4. ADH receptor antagonists are available e.g. conivaptan

Answer 121

Clinically detectable weakness in critically ill patients in whom there is no plausible aetiology other than critical weakness The underlying pathology may be myopathy, neuropathy or a mixture of both. The clinical presentations of each are indistinguishable

Answer 122

1. Severe sepsis and MOF 2. Prolonged MV 3. Excessive sedation 4. Muscle immobilisation 5. Use of corticosteroids 6. Neuromuscular blockade 7. Hyperglycaemia

Answer 123

Symmetrical, flaccid tetraparesis with sparing of the facial muscles Motor weakness can be assessed using the MRC sumscore. Three muscles in both upper and both lower limbs are assessed and each graded from 0-5. A sum-scors of < 48 suggests polyneuromyopathy.

Answer 124

``` Arm abduction Flexion at elbow Wrist extension Hip flexion Extension at the knee Foot dorsiflexion ```

Answer 125

1. Guillain-Barre syndrome 2. Myasthenia gravis 3. Lambert-Eaton syndrome 4. Motor neurone disease 5. Spinal cord injury 6. Rhabdomyolysis 7. Drug-induced weakness 8. Myopathy/myositis 9. Infective causes, including botulism

Answer 126

1. Lab tests: infl markers, ESR, electrolytes, CK, auto-antibodies, B12 level; LP 2. Imaging - MRI brainstem and spine 3. Neurophysiological investigations - Nerve conduction studies. CIM: normal; CIPN decreased compound muscle action potential and sensory action potentials with noraml conduction velocity. Electromyography: pts need to be fully compliant. Typical patterns of myopathic EMGs are motor unit potentials with small amplitudes and short duration. 4. Muscle biopsy - only indicated where there is diagnositic uncertainty. Excludes other diagnoses. Allows subclassification into the 3 morphological subtypes 1. unspecific and uncomplicated CIM; 2 thick filament myopathy; 3 acute necrotising myopathy

Answer 127

MDT supportive approach Focus on prevention and avoidance of risk factors Early mobilisation, sedation weaning protocols, daily physical and occupaitonal therapy Optimise nutrition, correct electrolytes Minimise steroids and neuromuscular blockade Strict glycaemic control is the only strategy that has been shown to reduce the incidence of critical illness polyneuropathy - although this is in conflict with the conclusions drawn from the NICE-SUGAR trial.

Answer 128

A cytopathic retrovirus that preferentially infects CD4-receptor positive (CD4+) T helper cells This results in reduced immune surveillance and increased susceptibility to opportunistic infections and malignancy

Answer 129

Acquired immunodeficiency syndrome (now call HIV-related disease) is defined as a CD4 count < 200cells/mm3 in a person infected with HIV, or the presence of an AIDS defining illness

Answer 130

According to the CDC: Group 1 - acute seroconversion illness - occurs soon after infection, although most patients are asymptomatic. There is a high viral load, but there is a 3 months period where anti-HIV IgG antibodies are not detectable in the blood Group 2- Asymptomatic infection - most people with HIV remain asymptomatic, the virus reproduces at a slow rate. Approx 10% will develop AIDS within the first 3 years, the remainder progress with a median of 10 years Group 3- persistent generalised lymphadenopthy Group 4 - Symptomatic HIV infection. Untreated patients with AIDS typically survive 3 years.

Answer 131

1. Resp failure - Pneumocystis jirovecii penumonia (PCP); exacerbations of chronic lung disease; bacterial pneumonia 2. TB 3. Cardiovascular disease - IHD is common - which may be attributable to HAART; endocarditis and myocarditis esp in IVDUs 4. Liver failure - often due to coninfection with hep b or c. NrTIs and NNRTIs may cause hepatotoxicity 5. Gastro - CMV colitis and cryptosporidial diarrhoea; GI bleeding secondary to ulcer,lymphoma or kaposis sarcoma; AIDs cholangiopathy; pancretitis 6. Renal failure - HIV-associated nephropathy; diabetes and hypertension are common 7. Neuro - meningoencephalitis, SOL incl toxoplasmosis, aspergillomas, abscesses or lymphoma; progressive multifocal leucoencephalopathy

Answer 132

A poor prognosis is a/w - high apache 2 score - organ failure - AIDS - defining illness - sepsis

Answer 133

Pneumocystis pneumonia is caused by the yeast-like fungus Pneumocystis jirovecci It has a slow and indolent course Presents with SOB, fever and dry cough CXR may reveal diffuse granular opacities resembling ARDS, penumoatoceles or pneumothoraces Definitive diagnosis is based on presence of organism in samples of induced suptum or from BAL or lung biopsy

Answer 134

IV co-trimoxazole for 2-3 weeks +/- IV pentamidine Second line is primaquine +clindamycin; atovaquone; trimethoprim +dapsone Steroids given within 48-72 hours of diagnosis reduce the risk of respiratory failure, meachanical ventilation and death and are indicated if: PaO2 < 9; A:a > 5

Answer 135

Normally involves 3 antiretrovirals (ARV) - most commonly 2 NRTIs plus a protease inhibitor

Answer 136

ARV drig e.g. Lamivudine and zidovudine Act as a false nucleotide and functions as a competitive inhibitor s/es lactic acidosis, hepatic steatosis, rhabo

Answer 137

ARV drug e.g. nevirapine binds to reverse trascriptase and inhibits enzyme activity s/es - hepatotoxicity

Answer 138

ARV drug e.g. saquinavir Prevents processing of viral proteins s/e/ SJS, dyslipidaemias

Answer 139

ARV drug e.g. enfurviratide Blocks fusion of HIV virus with host cell membranes s/e/ GI side-effects

Answer 140

Continue pre-admission HAART Input from ID/HIV pharmacist 1. Drug delivery - only zidovudine has an IV preparation. Others are tablets/capslues that can be crushed and used NG 2. Absorption may be affects by pathology. NG feed has to be interrupted to give certain ARVs. Gastric alkalinsation is CI'd with some ARVs 3. Dosing - changes in hepatic insufficiency and renal impairment 4. Interactions - benzos should be used with causiton with NNRTIs. NRTIs interact with numerous agents incl benzos, amiodarone, PPIs and H2RAs 5. Toxicity - can result in severe and life-threatening side-effects incl SJS, heoatic necrosis, pancreatitis and lactic acidosis 6. Immune reconstitution inflammatory syndorme (IRIS)

Answer 141

1. AIDS-defining illness 2. CD4 < 200cells/mm3 3. Anticipated prolonged stay 4. Deterioration despite optimal ICU management

Answer 142

If knowledge of HIV status will make a difference to the treatment of a patient without capacity then it should be done

Answer 143

There is a risk of precipitating IRIS on initiation HAART Immune function begins to recover and then responds to the previously acquired opportunistic infection with an overwhelming inflammatory response Treatment should be initiated against the offending organism. Supportive care is used and steroids are given in severe cases.

Answer 144

``` Candidiasis of the esophagus, bronchi, trachea, or lungs (but NOT the mouth) Cervical cancer Coccidioidomycosis Cryptococcosis, Cryptosporidiosis, Cytomegalovirus disease (other than liver, spleen, or nodes) Cytomegalovirus retinitis (with loss of vision) Encephalopathy, HIV related Herpes simplex: chronic ulcer Histoplasmosis Kaposi sarcoma Lymphoma, Burkitt's (or equivalent term) Lymphoma Mycobacterium avium Mycobacterium tuberculosis Mycobacterium, other species Pneumocystis jiroveci pneumonia Pneumonia, recurrent Progressive multifocal leukoencephalopathy Salmonella septicemia Toxoplasmosis of brain Wasting syndrome due to HIV ```

Answer 145

2012 Berlin definition: -ARDS is an acute diffused, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight and loss of aerated lung tissue with hypoxaemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space and decreased lung compliance.

Answer 146

PaO2/FiO2 200-300mmHg (26.7-40kPa) + PEEP > 5

Answer 147

PaO2/FiO2 ratio 100-200mmHg (13.3-26.7kPa) + PEEP > 5

Answer 148

PaO2/FiO2 ratio <100mmHg (< 13.3kPa)

Answer 149

- Development within one week of insult/worsening resp symptoms - i.e. acute - Bilateral opacities on CXR not explained by effusions, collapse or nodules - Respiratory failure not explained by LVF or fluid overload - Oxygenation criteria - Patient has to be ventilated for a diagnosis of ARDS to be considered

Answer 150

Direct - pneumonia, pulmonary contusion, aspiration pneumonitis, inhalational injury, pulmonary vasculitis, submersion.drowning Indirect - sepsis, burns, major trauma, TRALI, severe acute pancreatitis, cardiopulmonary bypass

Answer 151

1. Exudative phase (days 2-4): inflammatory insult to epithelium, leakage of protein-rich fluid and inflammatory cells into alveoli and intersititium; destruction of the pulmonary vascular bed; dysregulation of coag and fibrinolysis leading to microthrombus formation; results in V/Q mismatch, leading to hypoxic hypoxia and a reduction in lung compliance, causing increased WoB. 2. Proliferative stage (days 4-7): proliferation of type II pneumocytes and fibroblasts, with alveolar fibrin deposition; organisation of exudate leading to scar formation 3. Fibrotic stage (days 7-14): fibrosis of lung tissue and global damage to underlying lung structure.

Answer 152

Patient presents with increasing respiratory distress, hypoxia and tachycardia Presentation will vary according to the underlying aetiology Patients often have a level of multi-organ failure which is their usual cause of death

Answer 153

Blood tests incl infl markers, serum amylase/cultures, ABG CXR or CT chest ECHO - if there are no known risk factors for ARDS

Answer 154

ARDSnet protocol 1. Low tidal volumes - 5-7 ml/kg IBW with a high RR (< 35) to minimise volutrauma 2. Aim sats 88-95% - consider increasing I:E ratio or using inverse ratios if oxygenation a problem 3. Use PEEP to minimise atelectrauma - aim to find the optimum PEEP, there is evidence for mortality benefit to using high PEEP in severe ARDS 4. Maintain plateau pressures (< 30) to minimise barotrauma

Answer 155

1. Volutrauma (overdistension of healthy aveoli) 2. Barotrauma (high pressure injury to aveoli) 3. Atelectrauma (shearing forces due to repeated collapse and expansion alveoli) 4. Biotrauma (release of inflammatory mediators in response to high-volume ventilation)

Answer 156

Severity scoring for patients with ARDS

Answer 157

0 1 2 3 4 PaO2/FiO2 ratio >40 <13 PEEP <5 >15 Compliance (ml/cmH2O) >80 <19 CXR (quads infiltrated) 0 4

Answer 158

more than or equal to 3

Answer 159

Inflates in diastole (after aortic valve closure, corresponds to dichrotic notch) and deflates in early systole (immediately prior to the aortic valve opening - just prior to to the upstroke) Inflation causes volume displacement in both directions - leading to a potential increase in coronary blood flow and systemic blood flow

Answer 160

Balloon inflates in diastole - increasing diastolic pressure and deflates in systole decreasing LV afterload Increased myocardial o2 supply Decreases myocardial oxygen demand Renal perfusion should increase

Answer 161

``` Acute MI Cardiogenic shock Acute MR and VSD Refractory unstable angina Weaning from bypass Refractory LVF Refractory ventricular arrythmias Sepsis ```

Answer 162

``` Absolute: - aortic regurg - aortic dissection - chronic end-stage heart disease with no - chance of recovery - aortic stents Relative: -uncontrolled sepsis -AAA -tachyarrythmias -severe PVD -major arterial reconstructive surgery ```

Answer 163

``` Limb ischaemia Thromboembolism Compartment syndrome Aortic dissection Local vascular injury - false aneurysm, bleeding, haematoma Infection Balloon rupture +/- gas embolism Thrombocytopenia and haemolysis Malposition causing cerebral or renal compromise Cardiac tamponade ```

Answer 164

Blood is pumped from the venous to the arterial circulation | Facilitates gas exchange and provides haemodynamic support

Answer 165

Blood is removed from and returned to the venous circulation Facilitates gas exchange Doesn't provide any haemodynamic support

Answer 166

Extracorporeal CO2 removal

Answer 167

1. Cannulae 2. Tubing (heparin bonded) - systemic heprain is used but is not essential in the bleeding patient 3. Pump - blood movement is facilitated by an external pump with a centrifugal or roller mechanism of action 4. Membrane oxygenator and heat exchanger 5. Gas blender

Answer 168

``` Irreversible organ damage Multi-organ failure Those who are not candidates for transplant Advanced malignancy Chronic severe pulmonary hypertension ```

Answer 169

1. Age > 75 2. Polytrauma with multiple bleeding sites 3. CRP > 60 mins 4. MOF 5. CNS injury

Answer 170

Severe aortic regurgitation | Aortic dissection

Answer 171

Unsupportable cardiac failure Severe pulmonary hypertension Cardiac arrest

Answer 172

1. Cannulation - pneumothorax, vascular disruption, infection, emboli, bleeding 2. Systemic anticoagulation - haemorrhage incl intracranial and GI bleeding 3. Equipment - exsanguination from circuit disruption, oxygenator failure, pump failure

Answer 173

``` 9gNaCl/L h20 Na 154 mmol/L Cl 154 mmolL Osmolarity 300mosmol/L pH 5-6.5 ```

Answer 174

``` Contains Na 131 mmol/L Cl 111 mmol/L K 5 mmol/L Ca 2 mmol/L HCO3 as lactate 29 mmol/L Osmolarity: 278 mosm/L pH 6.8 ```

Answer 175

1.8g NaCl and 40g glucose/L Na 31 mmol/L Cl 31 mmol/L Osmolarity 271 mosm/kg H2O

Answer 176

50g glucose /L 205 calories/L Osmolarity 278mosm/L

Answer 177

The ability to make your own decisions

Answer 178

The mental capacity act 2005 - it protects vulnerable adults and empowers them to make their own decisions - applicable to those over 16

Answer 179

1. A person is assumed to have capacity until proven otherwise 2. A person is not to be treated as unable to make a decision unless all practicable steps to help him/her to do so have been taken without success 3. A person is not to be treated as unable to make a decision merely because they make an unwise decision. 4. An act done, or decision made, under this Act for or on behalf of a person who lacks capacity must be done, or made, in his/her best interests 5. Before the act is done, or the decision is made, regard must be had to whether the purpose for which it is needed can be as effectively achieved in a way that is least restrictive of the persons rights and freedom of action.

Answer 180

Stage 1: Is there a disorder or disability of the brain or mind? Stage 2: Can the patient -understand the information given to them -retain this information long enough to make a decision -weight the information in the decision making process -communicate their decision

Answer 181

Apply the principles of best interest. This involves: 1. Ascertain the patients past and present wishes, including advanced decisions/directives 2. Ascertaining the beliefs and values of the patient that may influence their decision 3. Discussion with the next of kin or an IMCA (a doctor is not obliged to adhere to the opinion of an IMCA but should document clearly why not)

Answer 182

The Mental Capacity Act was amended in 2009 to include deprivation of liberty. Article 5 of the human rights act 1998 requires that no one should be deprived of their liberty except in certain, pre-defined, circumstances. There must also be an appropriate, legally based, procedure in place to protect the individuals rights

Answer 183

1. To protect vulnerable adults who lack capacity against arbitrary detention that is not in their best interests 2. Gives the person a right to challenge their confinement

Answer 184

Anyone who lacks the capacity to consent to detention imputable to the state (ie in a public sector facility) that is determined by an independent review to be in their best interests e.g. pts with delirium, those requiring restraint, long stays and those with red flags (trying to leave/family conflicts etc)

Answer 185

As determined by the Cheshire West case in 2014 1. The patient lacks the capacity to consent to their care/treatment arrangements 2. The patient is under continuous supervision and control 3. The patient is not free to leave (wants to but is being prevented from)

Answer 186

Any DOL resulting from the administration of life-saving treatment falls outside of article 5 as long as it is unavoidable as a result of circumstances beyond the control of the authorities and necessary to avert a real risk of serious injury or damage and is kept to a minimum for that purpose.

Answer 187

- Those who have previously consented to the accommodation e.g. as part of pre-op assessment - Pts who are deeply unconscious - Pts who are expected to regain capacity within 7 days - Pts who are expected to die

Answer 188

Justifiable where a person lacks capacity to consent to this: 1. If it is in their best interests to protect them from harm 2. It is a proportional response compared to the harm faced by the person 3. If there is no less restrictive alternative

Answer 189

Application is made to the trust (if urgent) or the local authority (if not urgent). Urgent authorisations can only be made where a standard authorisation has been applied for but is not yet granted An independent assessment is then carried out - usually by a psychiatrist It's not transferable between institutions.

Answer 190

``` To prevent pain To relieve anxiety To relieve dyspnoea To permit mechanical ventilation To facilitate nursing care To decrease oxygen consumption To treat delirium ```

Answer 191

Severe anxiety and agitation Acute cardiopulmonary instability (hypertension, tachycardia, tachypnoea) Ventilator dysynchrony Hypoxaemia Inadvertent removal of devices and catheters Unplanned extubations

Answer 192

Drug-induced coma Undetected intrathoracic or intracranial catastrophes Unnecessary investigations (e.g. CT brain) Cardiovascular instability (hypotension, bradycardia) Drug accumulation Prolonged mechanical ventilation Prolonged ICU length of stay

Answer 193

there are 3 scoring systems: 1. Ramsay sedation scaler 2. Riker Sedation-Agitation Scale 3. Richmond Agitation-sedation scale +4 Combative: Overtly combative, violent, immediate danger to staff +3 Very agitated: Pulls or removes tubes or catheters; aggressive +2 Agitated: Frequent non-purposeful movement, fights ventilator +1 Restless: Anxious, but movements not aggressive or vigorous 0 Alert and calm -1 Drowsy: Not fully alert, but has sustained awakening (eye-opening/eye contact) to voice (>10 s) -2 Light sedation: Briefly awakens with eye-contact to voice (<10 s) -3 Moderate sedation: Movement or eye-opening to voice, (but no eye-contact -4 Deep sedation: No response to voice , but movement or eye-opening to physical stimulation -5 Unrousable: No response to voice or physical stimulation

Answer 194

Fewer days on mechanical ventilation Fewer days on ICU Fewer diagnostic studies to investigate alterations in mental status More patient days spent awake and able to follow commands Enhanced physician/patient communication and improved physical examination Allows focused downward titration of infusion rates over time Facilitates spontaneous breathing trials

Answer 195

Abrupt awakening and agitation Risk of self-extubation Cardiopulmonary instability and stress response

Answer 196

``` Sleep deficit Nosocomial infection Hypoxia Substance withdrawal Congestive cardiac failure Metabolic disturbance Electrolyte imbalance Dehydration Hyperthermia Prolonged immobility ```

Answer 197

``` Sedatives Midazolam Fentanyl Morphine Propofol Anticholinergics Steroids ```

Answer 198

``` Advanced age Dementia Depression Hypertension Smoking Alcoholism ```

Answer 199

1. Likely site of infection 2. Likely causative organism 3. Likelihood of resistance - recent abx, LOS in hospital/ICU, institution, recent travel, occupation, results from screening swabs, local resistance 4. Severity of infection 5. Risk of side effects 6. Potential drug interactions 7. Pharmacokinetic consideration eg cross BBB

Answer 200

They may be 1. Bacteriostatic - limit bacterial growth allowing the immune system to get rid of the bacteria 2. Bactericidal- cause cell death

Answer 201

Bactericidal - penicillins, cephalosporins, aminoglycosides, glycopeptides, quinolone, nitroimidazoles, rifampicin, nitrofurantoin Bacteriostatic-macrolides, tetracyclines, lincosamides, sulphonamides, trimethoprim

Answer 202

1. Inhibition of cell wall synthesis- prevent cross linking within the call walls 2. Inhibition of DNA synthesis or function 3. Inhibition of tetrahydrofolate synthesis 4. Inhibition of protein synthesis

Answer 203

Refers to agents whose activity depends on the amount of time the serum concentration is above the minimum inhibitory concentration These include beta-lactams, erythromycin, clindamycin, linezolid, vancomycin They are therefore doses regularly to keep the serum levels above MIC as long as possible

Answer 204

Refers to agents whose activity correlated with peak serum concentration. Eg aminoglycosides and quinolones. Higher doses are used with lower frequency of administration. However this may impact toxicity. Eg gent toxicity correlates to tissue accumulation (ie trough levels) rather than peak serum concentration and works best at 10-12 times MIC

Answer 205

``` Actinomyces Bacillus Clostridia Diphtheria Listeria ```

Answer 206

Type A: Involves the ascending aorta | Type B: Involves the descending aorta only, distal to the origin of the left subclavian artery

Answer 207

Type I: Originates in the ascending aorta and propogates at least to the aortic arch Type II: Involves the ascending aorta only Type III: Originates in the descending aorta and has 2 subtypes - type IIIa: limited to the thoracic arch - type IIIb: extends below the diaphragm

Answer 208

``` Hypertension Advanced age Male gender Smoking Family history Pregnancy Trauma (deceleration injury) Congential disorders e.g. Marfans, Ehlers-Danlos, aortic corarctation, Turners, congential aortic stenosis, bicuspid valve ```

Answer 209

1. Pain - type A = sudden onset, severe anterior chest pain with extension into the back. Type B - back pain 2. Differential or absent pulses in the extremities 3. Aortic regurg (early diastolic murmur best heard between the scapulae in expiration) 4. Syncope - resulting from impairment of cerebral blood flow, stroke and other neuro manifestations may also be present.

Answer 210

CVS - acute aortic regurg, MI or ischaemia, cardiac tamponade, HTN, hypotension or shock (secondary to tamponade, dissection or coronaries, acute AR, blood loss, intra-abdo catastrophe), limb ischaemia. Neuro - Ischaemic stroke, acute paraplegia secondary to spinal cord hypoperfusion Pulmonary - pleural effusions - usually left Renal - AKI Haematological - major transfusion requirment, coagulopathy GI - mesenteric ischaemia

Answer 211

Widened mediastinum Cardiomegaly secondary to effusion Blunting of the costophrenic angles as a result of haemothorax Possibly be able to see separation of calcified intima at the aortic knuckle

Answer 212

May be able to see intimal flap | Aortic regurg

Answer 213

true and false lumens may be identified

Answer 214

CT MRUI Aortography - used to be gold standardbut now rarely performed

Answer 215

ABCDE approach 1. Initial investigation and management - o2, large bore cannulae, bloods, BP monitoring, catheter, 12-lead ECG, analgesia 2. Manage hypotension - judicious volume resuscitation aiming BO 100-120mmHg; search for underlying aeitology 3. Manage hypertension - it's important to reduce shear force around the origin of the dissection by avoiding tachycardia, therefore adequate beta-blocker should be establish prior to vasodilator (GTN or sodium nitroprusside) 4. Imaging and ongoing care, transfer to regional cardiothoracic centre as appropriate.

Answer 216

Type A are surgical emergencies and are usually surigcally fixed via and median sternotomy Complicated type B will usually require a left lateral thoracotomy Uncomplicated type B are normally managed with beta-blockers and anti-hypertensives. There is a developing role for endovascular intervention for some type B dissections.

Answer 217

``` Any healthcare event that is: Unexpected Unintended Undesired Associated with actual or potential harm ```

Answer 218

Pts are: 1. undergoing highly invasive treatments with concomitant complications 2. Receiving frequent parenteral drugs/fluids 3. Undergoing invasive interventions 4. Lacking capacity 5. Lacking physiological reserve 6. More likely to be sedated and unable to communicate concerns

Answer 219

1. prescribing 2. transcription 3. preparation 4. dispensing 5. administration - the majority occur here

Answer 220

Medications errors are any mistakes in the prescription/preparation/administration of a drug. Doesn't necessarily result in harm. Adverse drug events are medication errors where harm occurs

Answer 221

Patient factors - severity of illness, extremes of age, prolonged hospitalisation, sedation, lack of capacity, altered pharmocodynamics Environmental and human factors - high turnover of patients and staff, difficult work conditions, high stress, emergency admissions, knowledge and performance deficits, communication problems, inadequate information technology Medication specific - number of medications (risk of interactions), types of medications - use of infusions and boluses, pump programming, use of estimated weight

Answer 222

1. Eliminate environmental and situational risk factors - avoid excessive working hours, minimise interruptions, trainee supervision 2. Optimise the medication process - computer systems, IV infusion devices, medication standardisation 3. Prevention of oversights - adequate staffing, pharmacist involvement, education and quality assurance

Answer 223

Serious incidents that are wholly preventable, as guidance or safety recommendations that provide strong systemic protective barriers are available at a national level and should have been implemented by all healthcare providers

Answer 224

Surgical - wrong site, retained foreign object post-procedure Medication - mis-selection of a strong potassium-containing solution, insulin ODs due to abbreviations or wrong device, wrong route of administration of medication, mis-selection of high strength midazolam for conscious sedation General - misplaced NGT, transfusion of ABO-incompatible blood products

Answer 225

1. Nothing should be introduced down an NGT until its position is confirmed 2. 1st line testing - pH 1-5.5 is the safe range. 3. 2nd line: CXR. Documentation should include who authorised the CXR, who confirmed the position, confimration that the x-ray was the most current one for the correct patient, the rationale for confirmation of the position 4. Checking the external markings for displacement remains vital.

Answer 226

1. two person checking drugs/blood 2. barcode scanners 3. checklists 4. debriefs 5. standardisation of processes 6. team training in communication and awareness of human factors 7. mandatory learning modules and competency based training for staff. 8. growing culture of open communication to enable learning from mistakes

Answer 227

Immediate steps should be taken to ensure patient safety systems and procedures are reviewed 1. Patient safety is paramount - ensure they're stable and treat any complications 2. Inform the consultant responsible for care asap. 3. Inform the patient/family/carer asap 4. complete an incident report 5. never events must be highlighted to the commissioner within 2 working days as per the serious incidents framework 6. they must be investigated in line with the serious incidents framework (e.g. root cause analysis)

Answer 228

Evidence of tissue hypoperfusion secondary to primary cardiac failure after correction of preload

Answer 229

SBP < 90 Hr > 60 oliguria with or without evidence of organ congestion

Answer 230

- Impaired LV systolic function leads to decreased CO and SV. Results in hypotension, decreased coronary perfusion and ischaemia. Decreased systemic perfusion results in compensatory vasoconstriction and fluid retention. These lead to progressive myocardial dysfunction. - Impaired LV diastolic function results in increased LVEDP, pulmonary congestion, hypoxemia, ischaemia and also results in progressive myocardial dysfuction.

Answer 231

The most common cause is acute decompensation of established cardiac failure, which can be triggered by non-compliance with meds, ishaemia, arrythmia, hypertensive crisis, brain injury, sepsis, drug abuse or volume overload. Can also present de novo in a patient with previously normal cardiac function. 1. Arrythmias 2. Valvular pathology - acute or decompensation of a chronic state 3. Viral myocarditis - e.g. coxsackie and adenovirus 4. Tamponade - trauma/dissection/pericarditis 5. High output cardiac failure - thyroid storm/severe anaemia 6. Decompensation of chronic cardiac failure

Answer 232

- Hypertensive heart disease i.e. diastolic heart failure - Dilated cardiomyopathy - alcohol, toxins e.g. heavy metals, drugs e.g. doxorubicin, MDMA, cocaine, peripartum - Restrictive cardiomyopathy - infiltrative e.g. sarcoid, amyloid, haemochromatosis, CT disorders, and radiation. - Congenital - hypertrophic cardiomyopathy

Answer 233

CV - cool peripheries with prolonged crt, tachy or brady, arrythmias, BP may be high due to high SVR or low is decompensated, myocardial ischaemia, signs of RHF incl peripheral oedema, raised JVP and hepatomegaly with RUQ tenderness Resp - tachypnoea with pulm oedema, hypoxia Neuro - low GCS, confused/altered mental state Renal - oliguria

Answer 234

ABCDE approach 1. O2, may need NIV or I+V 2. IV access - bloods for FBC/U+E/LFTs/cardiac enzymes/BNP/clotting/viral serology if indicated 3. ECG/CXR/ECHO 4. Cautious fluid bolus ideally with cardiac output monitoring 5. Low threshold for inotropic support and consider vasodilators to reduce preload and afterload and reduce myocardial work. May need a vasopressor. 6. Mechanical support e.g. IABP, ventricular assist device as a bridge to recovery or transplant

Answer 235

1. Adrenaline - low dose: b1 and b2 (tachycardiac, positive inotropy, vasodilation); high dose: a1 effects (vasoconstriction) 2. Dobutamine - predominantely b1 effects, some b2

Answer 236

1. Milrinone/enoxiomone - phosphodiesterase 3 inhibitor (increases cyclic AMP). Reduces PVR and SVR, positive inotropy and lusitropy. Useful in diastolic heart failure. 2. GTN - nitric oxide donor - predominantly causes venodilatation.

Answer 237

- Sensitises troponin C to calcium (positive inotropy) - Opens ATP-dependent potassium channels (increased coronary perfusion, reduced preload, reduced afterload) - Overall effect: increased contractility without increasing myocardial oxygen consumption - Evidence that it improves short and long term survival in patients with cardiac failure

Answer 238

1. Reduce hr - ensure adequate preload, beta-blockade if diastolic dysfunction, sedation 2. Reduce afterload - vasodilators, diuretics if volume overloaded, sedation

Answer 239

1. Increase myocardial perfusion - vasodilators, inotropes | 2. Increase oxygen carrying capacity - increase fio2, consider blood transfusion

Answer 240

Inserted via femoral artery, and lies within the descending aorta just distal to the origin of the left SCV. Balloon is inflated with helium during diastole to augment DBP, which improves coronary perfusion. Balloon is deflated in systole to reduce afterload. The overall effect is improved myocardial oxygen delivery and reduce myocardial oxygen demand.

Answer 241

- Inflate in the middle of the T wave (dicrotic notch) | - Deflate at the peak of the R wave (just before the systolic upstroke)

Answer 242

Absolute: - aortic regurg - aortic dissection/aneurysm - severe PVD Relative: - arterial turtuosity - LVOT obstruction - Sepsis - CI to anti-coagulation

Answer 243

Vascular - bleeding - haematoma - pensudoaneurysm - dissection - perforation Balloon-related - mesenteric/renal ischaemia - left upper limb/cerebral ischaemia - helium embolus - haemolysis - thrombocytopenia

Answer 244

A surgically placed mechanical device that can support the left (LVAD) or right (RVAD) or both ventricles (BiVAD). BiVAD implantation is uncommon as RV failure often results from pulmonary hypertension secondary to LV failure and will improve with LVAD insertion They reduce myocardial work, allowing the ventricles to rest whilst ensuring forward flow and organ perfusion They can be used as a bridge to recovery instead of VA ECMO in acute heart failure or as a bridge to transplantation in chronic cardiac failure

Answer 245

1. Bleeding 2. Tamponade 3. Haemodynamic distrubance - if the pt is hypovolaemic the IV septum is entrained towards the inflow cannula 4. RV failure 5. Fluid overload - may occur as fluid is mobilised as a result of the higher CO. 6. Infection 7. Intra-cardiac thrombosis

Answer 246

A potentially life-threatening metabolic complication of diabetes defined by a triad of ketonaemia, hyperglycaemia and acidaemia.

Answer 247

Usually occurs as a result of relative insulin deficiency which, when combined with increases in glucagon, catecholoamines and cortisol stimulates lipolysis, free fatty acid production and ketogensis. Accumulation of ketoacids (3-B-hydroxybutyrate, acetone, and acetoacetate) then results in a metabolic acidosis. Hyperglycaemia results from increased hepatic gluconeogenesis and glycolysis in addition to reduced glucose uptake peripherally due to insulin deficiency

Answer 248

1. Osmotic diuresis secondary to hyperglycaemia 2. Vomiting 3. Reduced oral intake secondary to reduced consciousness

Answer 249

``` Thirst Polyuria N+V Abdo pain Dehydration Ketotic breath Kussmaul breathing Confusion Coma ```

Answer 250

As stated by the Joint British Diabetes Societies 1. Cap blood glucose > 11 2. Ketonaemia > 3mmol/l or urinary ketones > 2+ 3. Venous bicarb < 15 or pH < 7.3

Answer 251

1. Bloods ketones > 6 2. Bicarb < 5 3. pH < 7.1 4. hypokalaemia on admission < 3.5 5. GCS < 12 6. SpO2 < 92% 7. SBP < 90 8. hr < 60 or > 100 9. Anion gap > 16

Answer 252

(Na + K) - (Cl + HCO3)

Answer 253

``` Most hospitals have clear guidelines ABCDE approach Main principles: 1. Fluid and electrolyte replacement 2. Insulin therapy 3. Treatment of underlying cause 4. Other supportive treatment - thromboprophylaxis, stress ulcer prophylaxis ```

Answer 254

- 0.9% saline is fluid of choice (still debated) - aim to restore circulating volume, clear ketones and correct electrolyte imbalances - if SBP < 90 then 500mls bolus - normally 1L in the first hour then one over 2 and then a further over 4 - rate needs to be modified in the young and elderly and those with renal and heart failure (increased risk of cerebral oedema) - normally 3-5 mmol/kg of potassium debt. Each bag of saline should have potassium replacement when K < 5.5.

Answer 255

- Suppresses ketogenesis, decreased blood sugar and corrects electrolyte disturbances - fixed insulin infusion should be started at 0.1unuts/kg/hr - continue long acting insulin - aim to decrease ketones by 0.5mmol/l/hr; increase bicarb by 3/hr/decrease BVM by 3/hr/maintain K 4-5.5 - increase infusion if targets not met - add in 10% glucose once blood glucose falls to allow insulin to continue

Answer 256

Cerebral oedema

Answer 257

Increased cerebral oedema in paeds - necessitates judicious use of fluid 1. 10ml/kg bolus only if shocked 2. fluid requirement = deficit + maintenance - volume used in resuscitation. Tis volume is given over 48 hours. 3. insulin therapy is delayed by 1 hour

Answer 258

Severe hyperglycaemia and fluid depletion with no or mild ketosis. It's usually seen in elderly patients with uncontrolled type 2 diabetes and often other significant co-morbidities.

Answer 259

15-30 % (higher than DKA)

Answer 260

1. Hypovolaemia - estimated between 100-220ml/kg 2. Marked hyperglycaemia (>30) without significant hyperketonaemia (<3) and no significant acidosis. 3. serum hyperosmolarity (> 320) Symptoms are vague and include anorexia, malaise, weakness, severe dehydration, renal impairment and coma. Tends to develop over days and consequently metabolic derangement and dehydration may be very severe.

Answer 261

ABCDE 1. Treat underlying cause 2. Normalise osmolality 3. Replace fluid and electrolyte losses - normally with 0.9% saline +/- K 4. Reduce Na by <10mmol/24 hours 5. Reduce glucose by < 5mmol/hr - only stsrt low dose insulin (0.005 units/kg/hr) once glucose stops falling with fluids alone. Otherwise risks precipitous drop in glucose. 6. Prevent complication - thrombotic events in particular.

Answer 262

1. Osmolality > 350 2. Na > 160 3. pH < 7.1 4. K < 3.5 or K > 6 5. GCS < 12 6. SpO2 < 92% 7. SBP < 90 8. Hr < 60 > 100 9. U/o < 0.5mlk/kg/hr 10. Cr > 200 11. Hypothermia 12. MI, stroke or other serious comorbidity

Answer 263

2NA + glucose + urea

Answer 264

A fluid containing large molecules that exert an oncotic pressure at the capillary membrane

Answer 265

Natural - bloods and its constituents, albumin | Synthetic - gelatins, hydroxyethyl starch

Answer 266

- Modified bovine collagen suspensions. - Ave molecular weight 35kDa - Long shelf-life - Rapidly excreted by the kidneys - effect lasts about 1.5 hours - May cause anaphylaxis

Answer 267

- Corn/potato starch suspensions - Large ethylated, polymerised amylopectin molecules - Available in several different molecular weights - Longer plasma half-life than other synthetic colloids (>6 hours) - The higher MW solutions impair factor VIII and vWF causing coagulopathy. Increased incidence of renal failure and mortality in critically ill

Answer 268

A globular single polypeptide with a MW 69kDA Highly negatively charged and is repelled by the negatively charged glycocalyx of the endothelium which extends its intravascular half life to 5-10 days when given as a volume expander (assuming intact capillary endothelium)

Answer 269

A solution containing protein derived from plasma, serum and normal placentas. Available in 2 concentrations in the UK: isotonic 4.5% and concentrated 20%. Its made from thousands of pooled donations and therefore carried a theoretical risk of new variant CJD

Answer 270

In the liver Rate of 0.2g/kg/day Under the influence of the neuroendocrine systems and the plasma oncotic pressure Accounts for about 50% of the plasma proteins It's a negative acute phase protein, with its production being suppressed in physiological stress

Answer 271

1. Transport molecule - cations, hormones e.g. T4, steroids, unconjugated bilirubin, bile salts, acidic drugs e.g. NSAIDS, warfarin 2. Maintenance of oncotic pressure - it accounts for ~80% of colloid oncotic pressure in healthy people 3. Acid-base balance (acts as a buffer)

Answer 272

1. Fluid resuscitation 2. Prophylaxis and management of HRS 3. Facilitate large volume paracentesis in cirrhosis 4. As a replacement fluid in plasmaphoresis

Answer 273

NEJM 2004 Double-blind multi-centre Australian RCT Compared 4% HAS to 0.9% saline for fluid resus in ICU patients Equivalent mortality in the 2 groups Non-significant trend favouring 0.9% saline in trauma and albumin in sepsis. Sub-group analysis showed increased mortality in pts with TBI who received albumin

Answer 274

NEJM 2014 Non-blinded multi-centre Italian RCT Compared 20% HAS (to maintain albumin > 30) with crystalloid in adults with severe sepsis and septic shock No difference in mortality between the 2 groups

Answer 275

1. Worsens TBI 28 day mortality and long-term outcomes when used as a resus fluid 2. More expensive 3. May worsen third space loss in patients with endothelial dysfunction (protein molecules leak into the interstitial space, drawing water with them) 4. There is a theoretical risk of new variant CJD transmission

Answer 276

Efficacy of volume substitution and insulin therapy in severe sepsis, NEJM 2008. German multi-centre RCT focussing on the safety and efficacy of HES versus Hartmanns in pts with severe sepsis/septic shock -It was stopped early for safety reasons -HES increases risk of AKI and need for RRT - However high doses were used and may not reflect usual practice -They also looked at intensive glycaemic control which found an increased rate of adverse events associated with hypos

Answer 277

NEJM 2012 Scandinavian double-blinded multi-centre RCT Compared HES with Ringers lactate No difference in 28 day mortality but a significant increase in 90-day mortality and use of RRT in the intervention group Pts in the HES group were more likely to receive blood products, with a trend towards more bleeding.

Answer 278

NEJM 2012 Double-blind multicentred Antipodean RCT Compared 6% HES with 0.9% saline for fluid resus in critically ill pts No difference in 90-day mortality Use of RRT was greater and received more blood products in the HES group.

Answer 279

A progressive inflammatory condition affecting peripheral and central airways, lung parenchyma and pulmonary vasculature Defined as "a common, preventable and treatable disease characterised by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by exposure to noxious particles and gases"

Answer 280

- Smoking - air pollution - occupational exposure - alpha1- antitrypsin deficiency

Answer 281

1. Symptoms - exertional breathlessness, chronic cough, regular sputum production and frequent winter bronchitis or wheeze 2. Spirometry - demonstrable airway obstruction with a post-bronchodilator FEV1/FVC < 0.7

Answer 282

Grade 1: Strenuous exercise 2: SOB when hurrying on the level or walking up a slight hill 3: Walks slower than most on the flat, stops after 15mins of walking. 4: Stops after 100yrds or a few minutes 5: Too SOB to leave the house or breathless on dressing/undressing

Answer 283

1: Mild - FEV1>80% predicted 2: Moderate - FEV1 50-79% predicted 3. Severe - 30-49% predicted 4: Very severe - < 30% predicted

Answer 284

1. Airflow limitation and gas trapping 2. Gas exchange abnormalities 3. Mucous hypersecretion 4. Pulmonary hypertension 5. Exacerbations 6. Systemic features - muscle wasting and cachexia

Answer 285

Peripheral airway limitation traps gas during expiration, resulting in hyperinflation Static hyperinflation reduced inspiratory capacity and is commonly a/w dynamic hyperinflation during exercise leading to increased SOB and limitation of exercise capacity

Answer 286

Worsens as disease progresses Reduced ventilatory drive and increased dead space lead to reduced ventilation, which leads to CO2 retention Abnormalities in alveolar ventilaiton and reduced pulmonary capillary bed further worsen V/Q abnormalities

Answer 287

Results in a chronic cough and is due to chronic airway irritation by cigarette smoke and other noxious agents. Leads to increased number of goblet cells and enlarged submucosal glands

Answer 288

Hypoxic vasoconstriction of the small pulmonary arteries results in structural changes including intimal and smooth muscle hyperplasia, causing pulmonary hypertension. This usually occurs late in the course.

Answer 289

1. Persistent or worsening hypoxaemia and/or resp acidosis (pH < 7.25) despite supplemental oxygen and NIV 2. Need for ventilation 3. Need for vasopressors/inotropes 4. Changes in mental state/consciousness 5. Severe dyspnoea responding poorly to initial treatment

Answer 290

ABCDE approach 1. Investigations: bloods, sputum, ABG, CXR, consider TTE 2. Pharmacological therapies: B2-agonists, anti-cholinergics, steroids, antibiotics, oral mucolytics, aminophylline isn't recommended due to its side effect profile 3. Resp support: target sats 88-92%, controlled oxygen delivery, NIV, I+V 4. Prevent further exacerbaitons - optimise bronchodilators and mucolytics, pneumococcal and flu vaccines, assess need for LTOT

Answer 291

1. Persistent or worsening resp acidosis despite optimal medical therapy 2. Severe acidosis (pH < 7.25) - these pts have a higher risk of treatment failure and should be managed on ICU 3. As ceiling of treatment for pts who are not candidates for invasive ventilation.

Answer 292

1. Smoking cessation | 2. LTOT - confers a survival benefit and improves pulmonary haemodynamics.

Answer 293

1. Stable, chronic COPD and a resting PaO2 < 7.3 | 2. Resting PaO2 < 8 and evidence of peripheral oedema, polycythaemia (hct > 55%) or pulmonary hypertension

Answer 294

1. Imminent resp arrest 2. Severe respiratory distress 3. Failure of or contra-indications to NIV 4. Persisting pH < 7.15 or deterioration despite NIV 5. GCS < 8

Answer 295

1. Reduced resp rate or I:E ratio - produces prolonged exp time, reducing the risk of breath-stacking; reduced minute volume will consequently lead to hypercapnia, acidosis, increased PVR and potential haemodynamic instability 2. Application of extrinsic PEEP - keeps small airways open during expiration, if values are kept below iPEEP there should be no significant increase in alveolar pressure and no worsening of CV effects 3. Treatment of bronchospasm to optimise gas flow

Answer 296

1. Decreased venous return and consequent hypotension 2. Increased PVR and right heart strain 3. Pulmonary barotrauma, volutrauma, hypercapnia and acidosis.

Answer 297

Hepatic - cirrhosis, Budd-Chiari, Portal vein thormosis Nephrogenic Cardiogenic - CCF, constrictive pericarditis Malignant - Gynae/GI/peritnoeal carcinomatosis Infectious - SBP, TB, fungal infections, parasites, chalamydia Miscellaneous - pancreatitis, chylous ascites, protein losing enteropathy, SLE, sarcoidosis, ovarian disease

Answer 298

``` Simple - not infected or a/w development of hepatorenal syndrome. Sub-class 1 (detetable by US only to 3 - marked abdo distension) Refractory - ascites that cannot be mobilised or early recurrence that cannot be prevented by medical therapy - diuretic resistant and diuretic intractable (can't effectively diurese due to complications a/w the diuretic) ```

Answer 299

Diagnostic - aetiology/presence of infection | Therapeutic - to relieve the pain of peritoneal stretch or resp compromise due to diaphragmatic splinting

Answer 300

Absolute: DIC, pt refusal Relative: pregnancy, bowel obstruction, infection of the abdominal wall. Normally ok if plts > 20.

Answer 301

2-4 cm medial and cephalad of the ASIS. Left lower quadrant may be better than the right.

Answer 302

SAAG serum albumin - ascitic albumin If > 11 then= acites is a/w the presence of portal hypertension

Answer 303

Cirrhosis Cardiac failure Hepatic malignancy

Answer 304

``` Prolonged ventilation Aids weaning Tracheal toilet Reduce sedation Prevent aspiration Upper airway obstruction ```

Answer 305

Abnormal/difficult anatomy - short neck, obesity, congential abnormalities Unstable C-spine (difficult not to move neck with the force required) Unstable patients - FiO2 < 60 and PEEP < 10 should be ok Coagulopathy

Answer 306

Bleeding Barotrauma Lobar collapse (loss of recruitment during the procedure) Damage to the posterior tracheal wall resulting in tracheo-oeophageal fistula (rare) Nerve damage - rare

Answer 307

``` Bone mineralisation Neuronal function Coagulation Co-factor for many enzymes and proteins Essential in endocrine, exocrine and neurocrine functions Second messengers in signal transduction Mediates muscle contraction ```

Answer 308

1. free ions 2. ions bound to plasma proteins - primarily albumin, reduced by metabolic acidosis, increased in resp alkalosis 3. diffusible complexes

Answer 309

- It ensures tight plasma control of ionised calcium by 1. Release of calcium from bones (increased osteoclast activity) 2. Increased reabsorption from distal convoluted tubule 3. Reduced phosphate reabsorption, leading to increased ionised calcium levels (less phosphate available to complex with calcium) 4. Vitamin D3 conversion to 1,25-dihydroxy-vitamin D3, which causes GI calcium absorption.

Answer 310

It's released from C-cells of the thyroid in response to hypercalcaemia and opposes the action of PTH 1. Inhibits calcium absorption from the GIT 2. Inhibits osteoclast activity 3. Stimulates osteoblast activity 4. Inhibits tubular reabsorption leading to increased excretion - but it does also inhibit reabsorption of phosphate in the DCT.

Answer 311

Serium calcium > 2.6mmol/l

Answer 312

Groans - constipation, vomiting, anorexia, nausea, pancreatitis, peptic ulcer. Bones - bony pain (osteolysis, fractures) Moans - psychosis, hallucinations, confusion Stones - kidney stones Cardiac arrhythmias with ECG abnormalities incl short QTc and broad T waves, prolonged PR interval, Cardiac arrest due to AV block may occur if calcium > 3.75

Answer 313

Malignancy - bony mets, myeloma, ectopic PTH and 1,25-(OH)D Endocrine - primary hyperparathyroidism, hyperthyroidism, familial hypocalcuric hypercalcaemia, tertiary hyperparathyroidism Granulomatous disease - sarcoid, TB Drugs - thiazides, lithium, aminophylline, vit D Misc - rhabdo, milk-alkali syndrome, renal failure

Answer 314

ABCDE approach Treat underlying cause 1. IV hydration with 0.9% saline - this forces diuresis 2. Bisphosphonate therapy - pamidronate 60-90mg over 2-4 hours 3. Diuretics - furosemide, although this promotes bony uptake of calcium 4. stop any contributing meds 5. Calcitonin, mobilisation, RRT

Answer 315

Ca < 1.9mmol/l

Answer 316

Endocrine - primary hypoparathyroidism, congenital deficiency (DiGeorge syndrome), psuedohypoparathyroidism, vit D deficiency Malnutiriotn - decreased intake, intestinal malabsorption, rickets, osteomalacia Drugs - furosemide, calcitonin, bisphosphonates, phenytoin, aminoglycosides, amphotericin B Misc - acute hyperphosphataemia, tumour lysis syndrome, rhabdomyolysis, acute renal failure, acute pancreatitits

Answer 317

QTC prolongation, which may progress to polymorphic VT

Answer 318

Oral or parenteral calcium supplementation | Calcium chloride contains 6.8mmol calcium vs 2.2mmol in calcium gluconate

Answer 319

Mental status changes Neuromuscular excitability - tetany, Chvostek sign (contracture of the facial muscles produced by tapping on the facial nerve), Trousseaus sign (carpopedal spasm with contraction of fingers elicited by BP cuff inflation) Seizures

Answer 320

RIFLE (risk injury failure loss end-stage renal disease) KIDGO (kidney disease:improving global outcomes) AKIN (acute kidney injury network)

Answer 321

The development of AKI within 48 hours of a contrast load

Answer 322

1. direct nephrotoxicity of reactive oxygen species 2. imbalance of vasoconstriction vs vasodilatation 3. increased oxygen consumption 4. contrast-induced diuresis 5. increased viscosity of urine

Answer 323

1. >75 yrs 2. Underlying renal impairment - eGFER < 60 - pre-renal: hypovolaemia, hypoxaemia - renal: diabetes, hypertension, renl artery stenosis - post-renal: renal calculi, other obstruction 3. Nephrotoxic drugs 4. IV contrast > oral contrast; risk proportional to the load.

Answer 324

1. Cr 1.5-2 fold increase in baseline. > 26.5 increase. urine output < 0.5ml/kg/hr for 6-12 hours 2. 2-3 fold increase in baseline creatinine. u/o < 0.5ml/kg/hr for > 12 hours 3. > 3 fold increase in baseline Cr, Cr > 354, need for RRT. U/o < 0.3 ml/kg/hr for > 24 hours or anuric for >12 hours.

Answer 325

1. Avoid contrast in high risk patients - consider other imaging modalities. If contrast is necessary - use the lowest possible dose, avoid repeat dosing. 2. Stop other nephrotoxics 3. IV hydration 4. IV sodium bicarb - it's postulated that alkalinisation of renal tubular fluid reduces production of ROSin addition to volume expansion. 4. RRT - removes contrast but there's no evidence that it works prophylactically. 5. NAC - given for 2 days prior to contrast - no definitive evidence for any benefit.

Answer 326

A rise in serum creatinine > 44 or an increase in cr by 25% from baseline within 48 hours of contrast (KDIGO)

Answer 327

ABCDE approach The London AKI network have producerd a STOP-AKI acronym S - sepsis and hypoperfusion - treat sepsis, ensure euvolaemia, optimise cardiac output T - toxins - remove nephrotoxics O - Obstruction - rule this out with renal trast US +/-0 catheterisation P - primary renal - screen for intrinsic renal disease, urine dip +/- immunological/viral screen

Answer 328

1. Metabolic acidosis 2. Hyperkalaemia 3. Symptomatic uraemia 4. Fluid overload unresponsive to medical therapy 5. treatment of overdose with dialysable toxins e.g lithium and salicylates

Answer 329

Continuous veno-venous haemofiltration - utilises the principle of v=convection - there is bulk flow of solute and water down a hydrostatic pressure gradient, across a semi-permeable membrane - rate of fluid removal is proportional to blood flow rate, hydrostatic pressure gradient and membrane surface area.

Answer 330

Continuous veno-venous haemodialysis - utilises the principle of diffusion (not widely used in the UK) - There is a countercurrent of flow of blood and dialysate, with diffusion of solutes down a concentration gradient, across a SPM - The higher the dialysate and blood flow rates the better maintained the concentration gradient and the more effective the solute removal.

Answer 331

Combines convective and diffusive clearance of solutes

Answer 332

Slow continuous ultrafiltration Ultrafiltration only - i.e. solely fluid removal

Answer 333

Sustained low-efficiency daily dialysis Can be performed for 8-10 hours per day, usually overnight benefits from being intermittent but with less haemodynamic and osmotic disturbance that intermittent haemodialysis

Answer 334

Generally it's initially started at 35ml/kg/hr - The RENAL trial (NEJM 2009) showed no mortaloty benefit when doses in excess of 25 were used - the IVOIRE study (ICM 2013) failed to show any benefit with ultra-high flow rates (70)

Answer 335

By 30% or less in the first 24 hours | Otherwise you risk disequilibrium syndrome

Answer 336

- If you replace fluid pre-filter you reduce the bloods viscosity and reduce the risk of clotting inside the filter, however it also reduces solute clearance - if you replace it post then this is better for solute clearance, however my compromise the lifespan of the filter. Typically a compromise is made e.g. pre:post ratio 30:70.

Answer 337

Advantages - goo regional anticoagulation, decreased risk of bleeding, premixed solutions with established protocols to follow. Disadvantages - large sodium load with trisodium citrate, metabolic alkalosis (citrate metabolised to lactate in the liver), special dialysate required, contra-indicated in liver failure (citrate is acidic, so causes a metabolic acidosis in liver failure)

Answer 338

1. Burn -> SIRS -> activation of inflammatory cascade (can lead to ARDS)-> increased vascular permeability -> generalised oedema 2. Inhalational injury -> ARDS or airway obstruction 3. Hypermetabolic state -> increased protein catabolism, increased gluconeogenesis, decreased protein synthesis -> decreased wound healing, immunosuppression, increased infective complications.

Answer 339

1. Burn area | 2. Burn depth

Answer 340

1. Lund-Browder charts - age specific 2. Rule of nines (head =9%, back =18%, arm = 9%, leg = 18%, perineum = 1%) 3. Patients palm and adducted fingers also estimate 1%

Answer 341

1. Superficial - involves the epidermis only, erythematous, painful and dry with no blistering 2. Partial thickness - erythematous, painful and oedematous with blistering 3. Full-thickness - painless and white

Answer 342

ATLS approach 1. Airway 2. IV access and fluid resuscitation 3. Analgesia - opioid +/- ketamine 4. Avoid hypothermia 5. Early surgical management - urgent escharotomy. Debridement of deep burns allows controls of the SIRS response and reduces metabolic rate - improves M+M.

Answer 343

1. Features suggestive of potential inhalational injury - facial burns, carbonaceous sputum, singeing of nasal hair, oropharyngeal oedema, stridor, hoarse voice 2. Other features e.g. neck burns, resp failure, reduced conscious level, to facilitate intervention/humanitarian

Answer 344

Parkland formula calculates the volume required for the first 24 hours = 4mls x kg x %BSA Half is given in the first 8 hours and the other half over 16.

Answer 345

Caused by prolonged smoke exposure in a confined space particular in the presence of neurological impairment. It includes: 1. Upper thermal injury - may cause significant airway oedema - consider early intubation with an uncut tube 2. Chemical irritation throughout the respiratory tract - caused by direct injury to the respiratory epithelium and capillary endothelium by acidic or alkaline compounds released from burning material - results in severe tracheobronchitits, impaired mucociliary clearance and loss of surfactant causing atelectasis - early inflammatory and capillary leak followed later by exudate formation produce an ARDS-type picture

Answer 346

1. Early bronchoscopy - confirms diagnosis and assesses severity 2. BAL/aggressive pulmonary toilet 3. Triple nebuliser therapy - bronchodilators, heparin (to reduces fibrin deposition), NAC (mucolytic) 4. Lung protective ventilation

Answer 347

A term used to describe the combination of hypovolaemic, distributive and cardiogenic shock seen in patients with major burns, which is refractory to massive fluid resuscitation

Answer 348

Regular microbiological surveillance should be carried out Three criteria from the American burn association should be present in addition to a documented infection before sepsis can be diagnosed 1. Temp < 36.5 or >39 2. Resp rate > 25, or MV > 12 3. Hr > 110 4. Glucose >12.8 in a non-diabetic pt 5. Intolerance of enteral feed for > 24 hours 6. Plt count < 100 (> 3 days after resuscitation phase)

Answer 349

CO has an affinity for Hb 250 times that of oxygen. There is impaired oxygen delivery to the tissues due to reduced oxygen carrying capacity and reduced dissociation once bound - left shift in the oxygen dissociation curve Additionally there is inhibition of cytochrome oxidase, resulting in impaired oxygen utilisation at the mitochondrial level

Answer 350

``` N+V Headache Hypotension Confusion, coma, seizures Cherry-red skin discolouration in rarely seen ```

Answer 351

HbCO level on ABG

Answer 352

100% oxygen, which reduces the half-life of CO from 4 hours to 1 I+V if HbCO > 25% Hyperbaric oxygen at 3atm reduces half-life to 15-20 mins, which might be indicated in pregnancy if > 15%, if > 40% or pt is in a coma

Answer 353

Cyanide inhibits mitochondrial cytochrome oxidase, blocking oxidative phosphorlylation and resulting in anaerobic metabolism.

Answer 354

``` SOB hypotension Dizzy Vomiting Psychomotor agitation LOC Unexplained metabolic acidosis and high central venous saturation ```

Answer 355

``` Supportive therapy aimed at maximising oxygen delivery Antidotes: 1. Hydroxycobalamin 2. Dicobalt edetate 3. Sodium thiosulphate ```

Answer 356

Poor correlation between HbCO level, symptoms and long-term outcome HbCO > 60% is likely to be fatal

Answer 357

Good for patients with moderate symptoms and rapid treatment Poor in those who suffer cardiac arrest Those who survive are at risk of neurological sequelae including delayed manifestations such as movement disorders and neuropsychiatric disturbance.

Answer 358

1. age < 5 or > 60 2. Presence of significant co-morbidities e.g. DM, pregnancy, cardioresp disease, immunosuppression, cirrhosis. 3. Site - hands, face, perineum, any flexure, circumferential full or partial thickness. 4. Inhalational injury 5. Mechanism - chemical injruy, ionising radiation, high pressure steam, high tension electrical injury, cold injury, hydrofluoric acid, suspicious of NAI 6. Dermal or full thickness burns > 5% in under 16s or > 10% over 16.

Answer 359

Generalised oedema Abdo/limb compartment syndrome Pulmonary oedema Need for prolonged ventilation

Answer 360

Airway obstruction | ARDS

Answer 361

Arrythmias Ischaemia Cardiac failure Vasoplegia

Answer 362

Pain | Opioid tolerance

Answer 363

AKI - secondary to under resuscitation, abdo compartment syndrome or rhabdo

Answer 364

Increased nutritional requirements due to hypermetabilism - may last up to 2 years increased protein catabolism Stress ulceration

Answer 365

An abnormal communication between the bronchial tree and pleural space, which causes an air leak from the lunk It manifests as a persistent air leak or a failure to re-inflate the lung despite chest tube drainage for 24 hours.

Answer 366

The Robert David Cerfolio classification 1. Continuous - the leak is present throughout the respiratory cycle. Seen in those receiving mechanical ventilation or who have a BPF 2. Inspiratory 3. Expiratory 4. Forced expiration

Answer 367

1. Most commonly post pulmonary resection with increased risk in right sided procedures, uncontrolled pleural/pulmonary infection, pre-op steroids, radiation, diabetes, malignancy, mechanical ventilation for > 24 hours 2. Other causes includer - trauma - ARDS - infection - necrotising lung disease - iatrogenic - persistent spontaneous pneumothorax - complication of mechanical ventilation

Answer 368

1. Dyspnoea 2. hypotension 3. SC emphysema 4. Cough with expectoration of purulent material 5. Shifting of the trachea and mediastinum 6. persistent air leak in a MV patient 7. persistent bubbling of ICD

Answer 369

1. CXR - increase in intrapleural space, new air/fluid level, tension pnuemothorax 2. Bronchoscopy - can confirm and localise by visualisation of continuous return of bubbles on bronchial washing 3. CT chest - imaging modality of choice 4. Others - vetilation scintigraphy

Answer 370

A BPF is a direct communication between the central bronchial tree and the pleural cavity A pneumothorax is a peripheral communication between a ruptured bleb or alveolar duct and the pleural cavity

Answer 371

Continuous air leak leading to delayed healing - Inability to apply PEEP - Loss of effective tidal volume secondary to inability to maintain adequate alveolar ventilation - failure of lung re-expansion - inappropriate cycling of the ventilator - delayed weaning from the ventilator

Answer 372

Initial management - treat tension pneumothorax, major bronchial stump dihiscence will need immediate re-suturing, pulmonary flooding will need affected side down posture General - large chest drain, suction to drain, treat infection Ventilated pts - minimise PEEP, TV, insp time and resp rate, encourage spont vent, extubate if able

Answer 373

Independent lung ventilation using DLT and 2 ventilators Bronchoscopic repair if < 8mm Surgery - thoracoplasty, stump stapling, pleural abrasion and decortication ECMO

Answer 374

1. Difficulty weaning 2. Hypoxia/hypercarbia 3. Inability to apply PEEP 4. Prolonged use of sedatives 5. Need for further surgery 6. Potential need for DLT/2 ventilators 7. High M+M

Answer 375

May be classified according to 1. Heart rate - i.e. brady or tachy 2. Origin of arrhythmia - i.e SVT or VT 3. Regular vs irregular

Answer 376

1. Hypovolaemia 2. Sepsis 3. Metabolic disturbances e.g. hypokalaemia, hypomagnesaemia 4. Hypoxia 5. Ischaemia 6. Thyrptoxicosis 7. PE

Answer 377

ABCDE approach 1. DCCV if there are adverse signes e.g. SBP < 90, pulmonary oedema, reduced GCS/syncope, chest pain 2. Treat underlygin cause e.g. electrolyte disturbances, sepsis 3. Rate control vs cardioversion Rate control with beta blocker or CCH e.g. diltiazem/verapamil e.g. if AF > 48 hours Chemical cardioversion with amiodarone or electrical - may be unsuccessful if underlying cause is not treated.

Answer 378

A type of SVT that is caused by the presence of a re-entry circuit within the right atrium The atrial rate approaches 300 bpm and the AV node blocks the rapid flutter waves producing a lower ventricular rate e.g. 2:1 (rate ~150) or 3:1 (rate ~ 100)

Answer 379

It's normally unresponsive to vagal manoeuvres Adenosine may reveal the underlying rhythm but will not cardiovert it Rate control to increase the AV block, or chemical or electrical cardioversion may be required

Answer 380

AVNRT is a type of SVT and is the commonest cause of palpitations in patients with a structurally normal heart It's paroxysmal often provoked by alcohol or caffeine The resultant tachycardia is regular and ranges between 140-280 bpm There are typically 2 functional pathways located aorund the AVN: a slow, posterior, pathway and a fast, anterior, pathway. One allows antegrade conduction and the other retrograde.

Answer 381

1. Slow-fast AVNRT (80-90%) - slow anterograde and fast retrograde conduction. P waves often hidden within corresponding QRS complexes or seen as a pseudo-R wave just after the QRS in V1 or V2 2. Fast-slow (~10%) - fast anterograde and slow retrograde conduction. QRS-P-T complexes are seen (P waves within the ST segment) 3. Slow-slow (< 5%) - slow anterograde and slow retrograde conduction via fibres in the left atrium. P wave seen in mid-diastole, often just before the QRS complex meaning may be mistaken for sinus tachycardia.

Answer 382

1. Vagal maneouvres 2. Adenosine may cardiovert rhythm 3. Beta-blockers 4. Flecainide or amiodarone are second line.

Answer 383

AVRT is an SVT caused by a re-entrant circuit that is anatomically distinct from the AVN and can cause pre-excitation of the ventricles. This can degenerate into tachycardia because there is no AVN to delay conduction. The commonest cause of AVRT is WPW syndrome.

Answer 384

It's caused by aberrant conduction via the Bundle of Kent, a congenital accessory pathway. Impulses may be conducted in a antereograde or retrograde fashion, but more commonly are bidirectional.

Answer 385

The ECG changes (which may only be present intermittently) include: 1. Delta waves 2. PR < 120 ms 3. QRS-T wave discordance (i.e the T wave deflection is in the opposite direction to the QRS) 4. Presence of tall R waves and T wave inversion in the precordial leads mimicking either RV or LV hypertrophy

Answer 386

Type A or type B Type A = positive delta wave in precordial leads, dominant S wave in V1 (left-sided pathway) Type B = negative delta wave in V1 (right sided pathway)

Answer 387

AVRT is often triggered by premature beats and the features of pre-excitation are lost. Conduction through the AVN may be either: 1. Orthodromic (~95%) - antegrade with retrograde conduction through the accessory pathway resulting in narrow complexes, rate 200-300, no visible p waves, pattern mimics AVRNT 2. Antidromic - retrograde, with antegrade conduction through the accessory pathway resulting in broad complexes, rate 200-300

Answer 388

1. Vagal manoeuvres 2. Adenosine may cardiovert the rhythm 3. CCBs are first line if adenosine unsuccessful 4. DCCV is necessary in the presence of adverse signs

Answer 389

The accessory pathway allows for rapid conduction directly to the ventricles, bypassingthe AVN. The complexes are broad and the rate is well over 200bpm treatment with AVN blocking drugs e.g. adenosine, beta-blockers and CCBs may increase conduction via the accessory pathway and cause degeneration into VT or VF. Procainamide or DCCV are preferred.

Answer 390

A broad complex tachycardia is more likely to be VT if there is: 1. AV dissociation (P waves superimposed on T waves or between QRS complexes) 2. Extreme axis deviation (lead 1 is positive, lead aVF is negative) 3. QRS > 160ms 4. Fusion beats (hybrid of sinus + ventricular complexes 5. Capture beats (normal conduction or an atrial impulse through the AVN) 6. Concordance across the precordial leads 7. Notching seen near the top of the S wave - Josephson's sign

Answer 391

1. Congenital - Romano-Ward syndrome (AD|) - Jervell-Lange-Neilson (AR, a/w/ congenital deafness) 2. Electrolyte disturbance - hypokalaemia, hypomagnesaemia, hypocalcaemia 3. Drugs - antiarrhymics e.g. sotolol, amiodarone - antibiotics e.g. erythromycin, fluconazele - psych drugs e.g. TCAs, SSRIs, phenothiazines 4. Myocardial ischaemia 5. SAH 6. Hypothermia

Answer 392

Commonly by using the Vaughn Williams classification Class 1: sodium channel blockers, reduce the rise of phase 0. - Type 1a - prolong the absolute refractory period e.g. procainamide - Type 1b - shorten ARP e.g. lignocaine, phenytoin - Type 1c - ARP unchanged e.g. flecainide Class 2: beta blockers; reduce AVN conduction, prolong phase 4, reduce contractility Class 3: potassium channel blockers; prolong phase 3, increase duration of phase 4, reduce contractility e.g. amiodarone, sotolol Class 4: calcium channel blockers; reduce SA and AV node automaticity e.g. verapamil.

Answer 393

0 - depolarisation (fast Na+influx). Rapide increase in membrane potential from -90 to +20 1 - Repolariation (K+ efflux) 2 - Plataeu phase (K+ efflux balanced by calcium influx through slow L-type ca2+ channels) 3 - Repolarisation (L-type ca channels close) 4- RMP restored by Na/K ATPase (Na efflux/K influx)

Answer 394

It's an endogenous nucleoside with rapid onset and ultra-short duration of action It acts on A1 receptors.causing transient AVN block and is used in the diagnosis and treatment of SVT. It may cause severe bronchospasm and should be avoided in asthmatics.

Answer 395

Flucuates between 35.5 and 37.5

Answer 396

Core body temp < 35 degrees. Mild - 32-35 Moderate - 28-32 severe - < 28

Answer 397

``` Radiation (40%) Convection (30%) Evaporation (15%) Conduction (5%) Respiration (10%) ```

Answer 398

1. Increased heat loss - trauma: exposure, open body cavities, wet, neurogenic shock - surgery - anaesthesia - immersion - burns 2. decreased thermogenesis - hypothyroidism, hypoadrenalism, elderly, malnutrition 3. Impaired thermoregulation - Drugs impairing thermoregulatory mechanisms e.g. anaesthetic agents - Drugs impairing behaviour - hypothalamic impairment that may occur as a result of any CNS pathology 4. Altered hypothalamic set point e.g. sepsis, burns

Answer 399

1. Extremes of age 2. Low socio-economic status 3. Trauma 4. Surgery

Answer 400

1. initial catecholamine surge causes hypertension and tachycardia with increased CO 2. Widespread peripheral vasoconstriction 3. decreasing temperature is subsequently accompanied by bradycardia 4. Below 33 the ECG may show J waves (positive deflection at the J point) roughly proportional to the degree of hypothermia 5. Bradyarrythmias esp AF are common 6. Below 28 the heart become susceptible to developing VT/VF 7. Asystole occurs at core temps < 20

Answer 401

Depression of the normal ventilatory responses, with progressive bradypnoea Cough reflex is lost and the pt develops profound bronchorrhoea Apnoea occurs < 24 degrees

Answer 402

CNS depressant effect - reduced GCS, confusion and lethargy Tendon reflexes are diminished and lost < 28 degrees Coma ensues and pupils are fixed and dilated below 30 The EEG is isoelectric at temps < 20

Answer 403

- The initial profound vasoconstriction results in cold diuresis in response to the apparent increase in central intravascular volume - the ensuing hypovolaemia becomes clinically apparent as the patient is rewarmed. - Hypothermia impairs ADH secretion and increases resistance to its action, worsening the polyuria

Answer 404

Gastric motility is impaired | Hepatic blood flow is reduced, slowing drug metabolism

Answer 405

- The BMR reduces by 7% for every 1 degree drop in core temp - there is reduced oxygen consumption, co2 production, and glucose and fat metabolism - there is metabolic acidosis with accompanying hyperkalaemia, hypermagnesaemia and hyperglycaemia - shivering occurs - which increases BMR by a factor of 5-at a maximal at 35 degrees and decreases as temp drops further. It ceases completely when hepatic glycogen stores are exhausted and muscles stiffen (< 32) - hypothermia causes pancreatitis and increases insulin resistance

Answer 406

1. There is thrombocytopenia due to sequestration, bone marrow depression and consumption 2. A progressive coagulopathy develops, eventually resulting in DIC (enzymes in the coag-cascade are temp sensitive) 3. Blood viscosity increases as temperature drops 4. WCC drops and immunity is impaired

Answer 407

ABCDE approach 1. Resus - pulse check may be difficult, echo may help For hypothermia-associated cardiac arrest defib is unlikely to be successful in VF - give up to three shocks and then try again after temp > 30; avoid ALS drugs until temp > 30 - double dose intervals at core temps 30-35. You are not dead until you're warm and dead (temp > 32) 2. Manage the hypothermia 3. Treat any underlying cause 4. Manager complications of hypothermia

Answer 408

In acute hypothermia rewarming can occur quite rapidly at 2-3 degrees per hour 1. Passive rewarming - remove wet clothes, dry pt, increase ambient temp, blankets, hat, encourage mobilisation if possible 2. Active external rewarming - forced air blankets, radiant heaters 3. Active internal warming - warm IV fluids, warm inspired gases, peritoneal or intravesical lavage with warm water, central venous heat exchange catheters, extracorporeal methods

Answer 409

1. Afterdrop - vasodilatation and release of cold blood from peripheries into the core may cause a second drop in temperature, not usually clinically significant. 2. Acidosis and hyperkalaemia - consequence of reperfusion 3. Shock (multifactorial). Hypovolaemia as a result of vasoconstriction and subsequent cold diuresis, cardiogenic shock due to myocardial depression, distributive shock due to vasodilatation on rewarming.

Answer 410

In 2002, 2 RCTs in the NEJM of TH after OOHCA demonstrated significant improval in neurological outcomes. As a result the International liaison Committee on Resuscitation (ILCOR) recommended that all unconscious patients who have suffered an OOHCA where the rhythm was shockable should receive 24 hours of TH to 32-34 degrees. The UK resus council extrapolated this to include all cardiac arrests regardless of underlying rhythm. - however, in 2013 the TTM trial (NEJM) compared targeted temp management to either 33 or 36 degrees. There was no difference in neuro outcome or all-cause mortality between the 2 groups. Interestingly, there was no difference in the incidence of adverse events.

Answer 411

1. OOHCA 2. Perinatal hypoxia 3. Deep hypothermic arrest for aortic root surgery It's not used following TBI - increases mortality.