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34 Cards in this Set
- Front
- Back
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ARDS defn
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- has radiological and clinical criteria
- radiological changes of bilateral infilltrates on CXR consistent with APO - acute onset - no evidence of left heart failure - hypoxaemia - PaO2/FiO2 <200 ARDS, <300 ALI high mortality! ~50% in ICU if ARDS |
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Causes of ARDS
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Direct
- pneumonia - aspiration - drowning - PE - pulmonary contusion - inhalational injury - reperfusion injury - ventilation strategy (barotrauma, volutrauma) Indirect: - sepsis - blood transfusion (TRALI) - pancreatitis - trauma - burns - drugs |
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Pathophysiology with ARDS
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3 stages
- acute phase: leakage of protein rich fluid into alveoli, PMN mediate tissue injury, and can cause systemic injury - subacute stage: interstitial fibrosis, microvascular thrombus formation - chronic stage: widespread pulmonary fibrosis and loss of normal lung structure |
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Ventilation strategy
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- aim is to maintain gas exchange
- use low TV (6mls/jg) on predicted ideal body weight - use pressures <30cmH20 (large volumes and pressures just damage healthy lung units and release inflammatory cytokines) - PEEP useful as prevents atelectotrauma - permissive hypercapnoea (accepted consequence of protective lung ventilation, too pH >7.2. Gave HCO3 in ARDSnet trial) - decrease FiO2 - other: no benefit from recruitment moves or mode of ventilation used eg VCV or PCV - all from ARDSnet study |
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Other strategies
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- FACTT study recommends restrictive fluid strategy
- no mortality benefit with steroids - volatiles potentially protective - Prone ventilation improves V/Q mismatch, improved clearance of secretions but no mortality benefit - nitric oxide causes vasodilation to ventilated units but no mortality benefit - ECMO - some evidence to support, benefit via avoiding further damage to lung units - ICU care: stress ulcer prophylaxis, DVT prophylaxis, antibiotic cover for VAL, sugar control and early enteric feeding |
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DKA
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- due to lack of insulin
- results in increase in blood glucose - glucose from hepatic prodn from GNG, and glycogenolysis - leads to dehydration from osmotic diuresis - dehydration activates SNS activity, RAAS system, thirst - lipolysis leads to large amounts of acetyl CoA. Too many substrates for citric acid cycle, exceeds capacity leading to producton of ketones -> metabolic acidosis - metabolic acidosis --> respiratory compensation via tachyopnoea and renal compensation to increase HCO3 reabsorption - K abnormality as acidosis causes extracellular movement of K, loss of K in osmotic diuresis and exchanged for Na for volume compensation via aldosterone |
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Albumin
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- prepared from pooled human plasma. Pasteurized to inactivate pathogen, reduces infection risk
- available as 4% in N saline (reduced Cl) or 20% with even less Cl - remains intravascular for 4/24, 40% intravascular, 60% extravascular - no difference between crystalloids and colloids for volume replacement - used for treatment ovarian hyperstimulation - expensive to produce (not to hospitals) - in glass bottle so cant be compressed eg with level 1 |
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SAFE study
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- 2004 NEJM
- saline vs 4% albumin for treatment of septic and hypovolumic patients in ICU - no improvement in morbidity or mortality - increased mortality in head injured patients |
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CHEST
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- NEJM 2012
- randomised multicentre trial - comparison between N saline and HES for fluid resuscitation - showed no difference in mortality at 3/12 - increased risk of RRT, RIFLE-I, hepatic impairment and adverse events vs N saline |
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O2 flux
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= oxygen delivery to the tissues
= (CO (dL/min) x Hb (g/dL) x 1.34 x SpO2) + (COx PaO2x 0.003) |
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Factors affecting oxygen delivery to tissues
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- CO (= SV x HR, further divide into preload, afterload and contractility and rhythm and rate)
- Hb concentration - FiO2 and PaO2 - gas exchange - regional blood flow (pH, SNS tone, electrolytes) - obstruction to flow eg pneumoperitoneum |
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Hyponatraemia
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Hypovolumic
- GIT loss - renal loss of Na eg Addisons - CSWS Euvolumia - drugs eg thiazide - SIADH - hypothyroid - iatrogenic eg glycine hypervolumic - SIADH - CCF - ARF - nephrotic syndrome |
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Tests for hyponatraemia
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urine sodium
plasma osmolality urine osmolality - short synacthen test/serum cortisol - fluid state |
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Fluid rate for correction of hyponatraemia
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- 0.6 x weight (kg) x2 = mls of 3% saline which will raise serum Na by 1mmol/L/hr
- if chronic hyponat (present >48/24) want to correct at 0.5mmolhr and no faster than 12mmol/day to avoid cerebral pontine myelinosis - use 3% saline if symptomatic or severe hyponat (<120mmol/L) |
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shock
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- occurs due to inadequate tissue perfusion or substrate delivery to meet the metabolic demands of the tissues
- results in tissue ischaemia and metabolic acidosis due to change from aerobic to anaerobic metabolism - leads to SIRS |
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consequences of shock
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- anaerobic metabolism -> metabolic acidosis
- cell dysfunction and death - endothelial dysfunction and increased vascular permeability - activations of SIRS |
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Systemic inflammatory response
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- WCC <4 or >12
- tachycardia >90 - RR > 20 - temp <36 or >38 require 2 or more - occurs due to release of inflammatory mediators (from sepsis or from ischaemic cells) |
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Types of shock
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- distributive eg sepsis, neurogenic, anaphylaxis
- hypovolumic - obstructive eg PE, tension PTx, tamponade, PE - cardiogenic eg AMI |
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Hypoxia
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- hypoxic
- stagnant eg low CO - anaemic eg low Hb - Histotoxic eg cyanide poisoning |
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Draw normal, fixed upper airway, variable intrathroacic and variable extrathoracic obstruction
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- fixed decreased both insp and exp
- intrathoracic is decreased on expiration - extrathoracic decreased on inspiration |
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mixed venous SpO2
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- normal 70-80%
- sampled from pulmonary artery as represents true venous admixture - reflects balance of O2 delivery and O2 use - affected by CO, PaO2, Hb concentration and tissue usage of O2 |
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problems with mixed venous O2
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- falsely elevated if admixture with arterial blood, histotoxic hypoxia (eg cyanide poisoning), sepsis
- requires PAC (and all inherent risks) - expense - accuracy (requires frequent recalibration) - reflects global changes not individual organ ischaemia |
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brain death
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- occurs when ICP is > than CPP such that no intracerebral flow occurs
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pre-conditions for brain death
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- MAP >60mmHg
- no sedation or paralysis -absence of severe electrolyte, metabolic abnormality or endocrine disturbance eg Na, PO4, Mg, liver, renal, glucose - normothermia - access to one eye and ear - ability to perform apnoea testing (ie not in severe respiratory failure, cervical cord injury) - minimum of 4/24 with GCS 3, unreactive pupils, absent cough reflex - 2 medical practitioners with ability to perform testing independently on 2 separate occasions |
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tests for braindeath
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- no response to noxious stimuli in CN distribution, trunk and 4 limbs
- absent pupillary light reflex - no corneal reflex - no vestibular ocular reflex with instillation of cold water into ear without nystagmus - absence of gag - apnoea testing with 5 mins of apnoea after pre-O2 and nil respiratory effort despite PaCO2>60mmHg - imaging demonstrating absence of cerebral blood flow on 4 vessel CT if unable to meet pre-conditions or doubt |
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unsuitability for organ donation
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- HIV or CJD
- metastatic or non-curable malignant disease or previous high risk cancer eg melanoma - no restrictions on age, Hepatitis, current organ failure |
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Hypothermia after cardiac arrest
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- NEJM 2002
- prospective RCT - included those with OOH VF/VT arrest - both groups sedated with midaz and fent but hypothermic group cooled to 32-34 degrees for 24.24 then passively rewarmed - significant improvement in neurology (NNT 6) and mortality (NNT 7) in hypothermia group - trend towards increased sepsis in hypothermia group |
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NICE sugar
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- NEJM 2009
- large prospective RCT - compared tight (4.5-6mmol/L) vs liberal (BSL <10mmol/L) in ICU patients - showed reduced mortality in liberal group, with much less hypoglycaemic episodes |
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changes to cardiac arrest algorithm
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- start with CPR rather than 2 ventilation
- charge defib whilst performing CPR to minimise interuptions to CPR - fist pump for VT only if defib not available and monitored - decreased emphasis on early ETT as interupts CPR |
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post resus care
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- avoid hypoxaemia titrate O2 to SpO2 94-98%
- PCI in those appropriate - SBp >100mmHg - BSL <10mmol, avoid hypoglycaemia - aggressive seizure control - emphasis on identifying cause of arrest - cool all those with OOH VF/VT/asystolic arrest to 32-34 for 24/24 then passive rewarming |
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Resuscitation drugs
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non-shockable rhythm
- 1mg adrenaline straight away and then every alternate cycle shockable - 1mg adrenaline after 2nd shock with recommencement of CPR and then alternate loops - 5mg/kg of amiodarone after 3rd shock |
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4Hs and 4Ts
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1/ hypoxaemia
2/ hypovolumia 3/ hypokalaemia/hyperkalaemia and metabolic disorders 4/ hypothermia 1/ tamponade 2/ tension PTx 3/ thrombosis 4/ toxins |
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RFTs
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FEV1/FVC 70% is normal
60-70% mild obstruction 50-60% moderate <50% is severe bronchodilator response of >10% is significant restrictive picture generally >80% |
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DCR
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- biphasic use 200J (unless stated by manufacturer)
- synch for all except VT/VF to avoid R on T - synch delivers shock on R |
