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What are the functions of an intensive care unit?
- Specialised monitoring
- High degree of expertise
- High nurse:patient ratio
- Organ support
- All used for patients with a critically ill or unstable condition
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What does the APACHE II scoring system predict?
The likelihood of mortality or morbidy of ICU patients
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What observations are used in the APACHE II scoring?
- Obs: Temp, MAP, HR, RR, PaO2
- Bio: pH, Sodium, Potasisum Creatinine
- Bloods: Haematocrit, WBC
- GCS
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What is the signifance of the following in a clinical setting:
- Heart rate
- RR
- SBP
- GCS
- O2
- Temp
- Tachycardia is related to a poor outcome
- Tachypnoea occurs in sepsis/PE and other acute disease
- Lowers in sepsis and blood loss
- Disease affects cellular function
- Lung/airway/CV pathology
- Disease affects metabolism or sepsis/drug
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Describe some other important investigations used in ICU, apart from general observations
- Urine output: Normal suggests adequate perfusion. Hypovolaemia, renal disease.
- Bioch: Lactate, glucose, [acid/base] = metabolism/perfusion
- Pain: Actual/potential tissue damage
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What does the SOFA score predict?
Determines the rate and extent of a patient's organ function and failure
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What factors are used in the SOFA score?
- Pa02: <400 = 1, <100 = 4
- GCS: <14, <12, <9, <6
- Bilirubin: >1.9, >12
- Platelets: <150, <20
- Creatinine: >145 (2), >382 (5)
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Outline the pathogenesis of sepsis
- Microorganism invades blood stream
- Endo/exotoxins cause mediator release, including NO
- Profound vasodilation = renal failure+ albumin enters ECM
- Pulmonary oedema + tissue hypoxia
- Multiple organ dysfunction syndrome
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What are the adverse effects of mechanical ventilation?
- Infection
- Barotrauma
- O2 toxicity
- Together may cause ARDS
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- Define sepsis
- Define severe sepsis
- Define septic shock
- SIRS criteria + confirmed or presumed infection
- Sepsis with 1 or more organ dysfunctions
- Severe sepsis and hypotension unaffected by IV fluids
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How are septic patients managed?
- 1. High flow O2
- 2. Take 2 blood cultures
- 3. Investigations; CSF, urine culture, CXR etc
- 4. Antibiotics, within 1st hour. 1+ active against likely pathogen
- 5. 250 ml IV crystalloids + consider fluid challenge
- 6. Vasopressors if severe hypotension
- 7. Lactate and Hb measured; hypoperfusion/hypovolaemia
- - Check urine output constantly
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What is the significance of AKI in ICU?
- ~10% of patients in hospital are at risk of AKI
- Directly related to mortality, even at risk stage
- Increases likelihood of organ failure
- 20% of patients in ICU require RRT
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What are the classical reasons for renal failure?
- Pre-renal: Hypovolaemia, stenosis
- Renal: Vasculitis, glomerulonephritis, drugs
- Post-renal: Obstruction, e.g prostate, stone
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What are the multi-factorial reasons for AKI?
- Theory that many factors cause AKI at once
- Many sepsis related: poor CO + PR = renal ischaemia
- Toxin mediated (including rhabdomylysis/drugs)
- Obstruction
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What are the RIFLE criteria used for?
- Assessing measurements (RIF) and outcomes (LE) of AKI (after resuscitation + IV fluids)
- R: Risk; Creatinine x 1.5, urine <5ml/kg/hr for 6 hrs
- I: Injury; Creatinine x 2, urine <5ml/kg/hr for 12 hrs
- F: Failure; Creatinine x 3, urine <3ml/kg/h x 24 hr
- L: Loss; Persistent ARF= complete function loss >4 weeks
- E: End stage renal disease
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What are the indications for dialysis?
- When urine production lowers and urea/creat rises
- Renal function related disease; hyperkalaemia, acidosis, uraemia
- Survivable injury/decent prognosis (age, ESRD etc.)
- Opportunity to stop RRT in future
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What is the difference between haemofiltration and dialysis?
- Dialysis: Withdrawal of desirable ions using concentration gradients across a semi-permeable membrane.
- Haemofiltration: Similar, but positive hydrostatic pressure also used to remove larger solutes. More expensive
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If urine output decreases, and urea increaes, how should the patient be managed?
- ABCDE to check for hypoxia/hypotension/sepsis
- Ensure perfusion (peripheral temp or capillary refill)
- Exclude obstruction, e.g. flush catheter/bladder with saline
- Next give IV fluids to ensure perfusion/BP
- Renal replacement therapy if no difference
- NOTE: Diuretics should NOT be used
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What are the clinical findings of ALI?
- Hypoxaemia
- Pulmonary oedema: bilateral infiltrates
- Decreased compliance
- No evidence of left atrial hypertension
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What are the main causes of ALI?
- Pulmonary: Pneumonia, aspiration, injalation, fatty emboli
- Extra-pulmonary: Sepsis, trauma
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What are the acute pathological mechanisms of ALI?
- Early phase: Exudative
- Type 1 pneumocytes swell and detach from BM after damage
- Thrombi in capillaries = V/Q mismatch
- Respiratory membrane dysfunction = proteinacious leak
- Type 2 pneumocyte damage = reduced surfactant = alveolar collapse
- Neutrophil infiltration and cytokine release = damage/thrombi
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How does ALI resolve?
- Late phase: Fibroproliferative
- Myofibroblast infiltration + exudate = granulation
- Type 2 pneumocytes become type 1
- Neutrophil apoptosis
- Either recovery or 'honeycombing' (end stage fibrotic lung disease)
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What co-morbidities are common in ALI?
- Chronic liver disease
- Sepsis
- Chronic alcoholism
- Chronic respiratory disease
- Low serum pH
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Define ARDS
- Acute respiratory distress syndrome
- A more severe result of ALI
- A Pa/Fi ratio less than 26kPa and persistence, with an associated cause
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What does the Murray score measure and estimate?
- Measures alveolar consolidation, Pa02/Fi02 ratio and lung volume
- Used to estimate the severity of ARDS
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Outline the clinical presentation of ARDS
- Within 1-2 days of insult
- Progressive, severe dyspnoea and dry cough
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What are the clinical findings of ARDS?
- Diminished air entry into lung base
- Coarse crackles
- May be unexpectedly normal
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What are the systemic effects associated with ARDS?
- Pulmonary manifestation of systemic response
- Hypotension/vasodilation
- AKI
- Pulmonary hypertension/Right heart failure (thrombi)
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What investigations are appropriate in ARDS?
- General Obs: Patient's well being
- Bronchoalveolar lavage: Neutrophils/macrophages
- Transbronchial/open lung biopsy
- Radiology
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Outline the treatment of ARDS
- High 02 to maintain tissue xygenation
- Fluids used to prevent shock, but may cause late damage via oedema
- Support other failing organs
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What are the clinical features of respiratory failure?
- RR <8 or >30 (slow = exhaustion)
- Pale/sweaty/clammy
- Exhaustion/accessory muscle use
- Confusion/convulsion 2nd to hypoxia
- Prolonged expiratory phase, maybe with wheeze
- Low GCS 2nd to hypercapnia
- Tachycardia or late bradycardia
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How does O2 therapy administration differ in COPD
- T1RF: High flow 02 used and steadily decreased
- T2RF: Low flow 02 used and steadily increased, with GCS, RR and ABGs monitored
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Define Fi02
- The percentage of O2 inspired that participates in gas exchange in the alveoli
- Differs from Pa02 as it is unaffected by V/Q
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When are fixed performance masks used?
- When Fi02 must be a known, acceptable amount
- E.g. in COPD where 02 delivery is essential but must be monitored
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What are the indications for respiratory support?
- Unresponsive hypoxaemia
- Exhaustion
- Severe hypercapnia
- Time needed to investigate/treat underlying condition
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How can CPAP reduce gas exchange?
- In unilateral or lobar diseases, CPAP forces blood out from the ventilated to the 'dead space'
- In fully compliant lungs, CPAP can increase pulmonary vascular resistance
- Flattening diaphragm may increase expiratory muscle use
- In pneumothorax, GI bleeds etc. positive pressure a bad thing
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Define and outline some 'rescue therapies'
- A procedure which aids the treatment of respiratory failure but doesn't rely on gas exchange
- NO: Vasodilation improves oxygenation (no effect on outcome)
- Extra-corporeal: Blood removed from body and CO2 removed.
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What are the causes of unilateral effusions found on a CXR?
- Pneumonia
- Empyema
- Trauma
- Malignancy
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What are the causes of bilateral effusions found on a CXR?
Heart or renal failure
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What are the findings of ARDS on a CXR?
- Diffuse alveolar shaddowing/patchy opacity
- Progressive changes
- Effusions are not a major feature
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What are the findings of heart failure or fluid overload in a CXR?
- Interstitial thickening occurs across the lung, highlighting the lobules
- Underlying lung is normal, with effusions
- Cardiomegaly
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What are the problems with diagnostic imaging in ICU?
- Suboptimal positioning and exposure, which varies between images
- Magnification of mediastinal contours
- Reduced kilovoltage of portable units = underexposure and motion blur
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Describe some commonly used IV fluids
- Crystalloids: Different ionic concentrations in solute. Associated with oedema
- Colloids: Larger molecules e.g. albumin; preserve osmotic pressure (helpful in oedema)
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Outline the process and purpose of a fluid challenge
- An end point is selected (e.g. normal HR, GCS, perfusion)
- 250ml given rapidly; response monitored
- Patient reassessed, especially SV
- No response = further challenge and continued treatment
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What is the mechanism of action of catecholamines?
- B1 effect: Inotropy via calcium release, chronotropy via calcium channel opening = Increase CO and ischaemia
- B2 effect: Vasodilation via calcium uptake into sarco. ret. = smooth muscle relaxation and greater muscle 02
- A1 effect: Vasoconstriction via G proteins = increase PR
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What are the effects of Dobutamine?
- B1 and B2 receptor effect (3:1 ratio of strength)
- Strong inotrope, weak chronotrope
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What are the effects of noradrenaline?
- Alpha agonist, slight B activity
- Vasoconstriction, weak inotropy/chronotropy
- Reliable increase in BP and cardiac blood flow
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What are the effects of adrenaline?
- Mainly Beta agonist in lower doses
- Increase pulmonary pressure and peripheral ischaemia
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What are the effects of PDE inhibitors?
- Used if catecholamines ineffective/resistant
- Increase cAMP = calcium entry = inotropy (not via beta receptors)
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What are the effects of vasopressin?
- Used in refractory septic shock
- V1a receptor = inotropy and noradrenaline sensitivity
- V2 receptor = increased ion/water uptake in kidneys
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Describe the CV monitoring of a septic patient
- Goal to monitor BP and CO
- Tissue oxygenation measured (not ABG)
- If low value despite normal ABG, CO insufficient
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What does MEWS predict?
- "Modified Early Warning Score"
- Guide used to quickly determine the degree of illness
- Four readings: SBP, HR, RR, temp and GCS
- The more the patient's diverse from the norm, the greater the score
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Apart from OBs, what other investigations are important in acute medicine? What do they indicate?
- Urine output: Hypovolaemia, renal disease, overhydration, drugs. Normal = adequate perfusion
- Biochem: lactate, glucose, acid/base. Metabolic function and perfusion
- Pain: Associated with actual or potential tissue damage
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What are the problems with the measurements used in the RIFLE criteria?
- Several conditions can cause a drop in urine production unrelated to renal failure
- Creatinine can also be affected by other conditions (e.g. diabetes, muscle mass)
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