Critical Care Flashcards
How can local anaesthetics be classified?
Amides - lidocaine, bupivacaine, prilocaine
Esters - cocaine, procaine
What are the possible complications of local anaesthetics?
Neurological - personal & glossitis paraesthesia, light-headedness, drowsiness, seizures, tinnitus, tremors, confusion, coma
Cardiovascular - bradycardia, hypotension, VF, asystole
How would you manage a patient with lidocaine toxicity?
ALS approach
Primarily supportive
Seizure control with diazepam / midazlolam (phenytoin ineffective).
Cardiac monitoring
Which local anaesthetic is used in haematoma blocks?
Plain prilocaine, no adrenaline.
- undergoes faster hepatic metabolism and has lower direct neurotoxicity
- can cause methaemoglobinaemia
What are the safe maximum doses of local anaesthetic?
Lidocaine: 3mg/kg (7mg/kg with adrenaline)
Bupivacaine: 2mg/kg (3mg/kg with adrenaline)
What are the potential complications of spinal anaesthetics?
Hypotension & urinary retention
- During insertion: direct neural injury, bleeding, haematoma, headaches
- Due to catheter: block, dislodgement, infection, chronic fibrosis
- During removal: haematoma, cord compression & paralysis. Anti-coags should be stopped prior to removal.
What is a burn injury?
Jackson’s burn model describes burns as ‘tri-zone injuries’
- central area of coagulative necrosis
- surrounded by static area of inflammation and ischaemia
- further encircled by an area of hyperaemia
How would you classify burn injuries?
Depth: superficial, partial thickness, full thickeness
Cause: flash/flame, contact (hot/cold), friction, chemical, electrical, radiation
How do you assess burn size?
- Patient’s palm ~1% TBSA
- Wallace’s rule of nines: adult, head 9%, arm 9%, ant leg 9%, post leg 9%, ant trunk 18%, post trunk 18%, perineum 1%
- Lund & Browder Chart: most accurate, adjusted for age
What fluid regime would you use to treat a burn injury?
Parkland formula = %TBSA x weight (kg) x 4ml in 24 hrs, first 50% given in first 8 hours post burn injury.
Required for adults with TBSA >15% or children with TBSA >10%
Which burns injuries should be referred to a burns unit?
- full thickness TBSA >5%
- partial thickness TBSA >10% in pts <10 or >50yrs
- face, eyes, ears, hands, feet, genitalia & perineum
- joints
- inhalation, chemical and electrical
- circumferential
Prognosis of burns patients?
Bull Chart estimates chance of survival based on age and %TBSA.
If patients age + %TBSA >100 survival is poor ~20%
How is a CVP line used to measure left atrial pressure?
Line inserted into SVC / right atrium to record right atrial pressure
- assumed to be equal to left atrial pressure
- if sides are asynchronous the assumption is no longer valid
How does cardiopulmonary bypass work?
- right atrium cannula insertion
- gravitational drainage of venous blood into reservoir
- blood heparinisation
- membrane oxygenator add O2 and removes CO2
- heat exchanger controls blood temperature
- oxygenated blood is passed through a bubble trap and microemboli filter
- blood is returned to aortic circulation
What are the clinical indications for cardiopulmonary bypass?
- Cardiothoracic surgery e.g. aortic surgery, CABG, valve repair / replacement, lung transplant, pulmonary thrombectomy
- Neurosurgery e.g. basilar artery aneurysm repair
- Supportive (critically ill pts) e.g. drug overdose, hypothermia
What are the complications of cardiopulmonary bypass?
- immediate: air embolism, coagulopathy, hypothermia, inflammatory response, thrombocytopenia
- early: ARDS, arrhythmia, AKI
- late: coma, focal neurological deficit, mesenteric ischaemia, pancreatitis, seizures
What is the difference between primary and secondary brain injury?
Primary: occurs at time of injury e.g. direct brain cortex injury
Secondary: occurs after the injury, may be due to:
- Hypoxia
- Hypotension
- Hypercarbia
- High ICP
What is the Monro-Kellie doctrine?
Describes the intracranial pressure-volumes relationship as governed by: brain tissue, blood & CSF within a closed rigid box of fixe volume.
Change in 1 component must result in a compensatory change in another component in order to prevent a rise in ICP
What are the causes of increased intracranial pressure?
- Medical: electrolyte imbalance, infection, stroke
- Surgical: haemorrhage / haematoma, oedema (contusions & DAI), tumour
What is the cerebral perfusion pressure?
CPP = MAP - ICP
It is the pressure gradient which drives cerebral blood flow, O2 delivery and metabolite clearance.
What are the key constituents of TPN?
- carbohydrates >50%
- fat >30%
- amino acids
- water
- electrolytes
- trace elements
- vitamins
Define acute and chronic renal failure
- Acute: sudden, usually reversible impairment of functioning nephrons, resulting in reversible (usually) kidney function impairment
- Chronic: progressive, permanent loss of functioning nephrons, resulting in irreversible kidney function impairment. CRF = advanced stage 4/5 CKD
How is renal failure classified?
Pre-renal
- hypovolaemia (inadequate fluids, haemorrhage, burns, D&V)
- decreased cardiac output (HF, PE)
- hypotension (sepsis, anaphylaxis)
- vascular (renal artery or vein obstruction)
Intrinsic renal
- Drugs (gentamicin, NSAIDs)
- Glomerular (glomerulonephritis, antibody-mediated)
- Interstitial (pyelonephritis, sarcoid, lupus)
Post-renal (calculus, carcinoma for all)
- Ureteric
- Cystic
- Prostatic (BPH)
- Urethral (blocked catheter, stricture)
What are the types of renal replacement therapy?
- haemodialysis (works by diffusion)
- haemofiltration (works by convection)
- haemodiafiltration (combination of above)
- peritoneal dialysis
What are the indications for renal replacement therapy?
- severe U&Es derangement e.g. refractive hyperkalaemia >6 or urea >35
- severe acidosis e.g. ph <7
- severe fluid overload e.g. resistant pulmonary oedema
- uraemia complications e.g. encephalopathy & pericarditis
- ESRF
- cr clearance <10ml/min
- removal of toxic drugs e.g. aspirin overdose
What is the composition of Hartmann’s, Normal saline and dextrose-saline?
Hartmann’s: Na 131, Cl 111, Lactate 29 (metabolised to bicarb), K 5, Ca 2
Normal: Saline: Na 150, Cl 150
Dextrose-Saline: Na 30, Cl 30
What are the fluid requirements of an average 70kg male of 24 hrs?
Maintenance: 2.5L water, 120-140 mmol Na, 70 mmol K
Insensible Losses: 600mls (skin), 400mls (lungs), 100mls (faeces)
What are the normal reference ranges for PaO2 & PaCO2?
At sea-level:
PaO2 10-14 kPa
PaCO2 4.5-6 kPa
How can you classify the causes of hypoxaemia?
- Hypoxic (respiratory failure)
- Anaemic (reduction or alteration of Hb)
- Histotoxic (impaired mitochondrial respiration e.g. CN poisoning)
- Stagnant (poor tissue perfusion e.g. CF, vascular obstruction
What is acute lung injury and ARDS?
ALI and ARDS represent a spectrum of disease characterised by:
- non-cardiogenic pulmonary oedema (diffuse pulmonary infiltrates on CXR)
- progressive hypoxaemia
- reduced lung compliance
What are some causes of ALI & ARDS
FAT HIPS
- Fat embolus
- Aspiration pneumonia
- Trauma & burns
- Heart bypass
- dIc
- Pancreatitis
- Sepsis
How would you diagnosis ALI & ARDS?
Acute onset with diffuse pulmonary infiltrated on CXR. Pulmonary artery wedge pressure <18mmHg
- PaO2 / FiO2 < 40 kPa - ALI
- PaO2 / FiO2 < 26.6 kPa - ARDS
What pathological changes occur in ALI & ARDS and what are the treatment principles?
- inflammation / exudation due to cytokines, proteases, free-radicals. Interstitial alveolar oedema occurs & hyaline membranes formed. Supportive management and treat cause. PEEP & inverse & prone ventilation.
- proliferation within 1-2 weeks of type II pneumocystis & fibroblasts. Granulation tissue narrows alveoli & vessels. Inhaled NO may help vasodilation and improve V?Q mismatch.
- Fibrosis occurs over 2-4 weeks, steroids may be useful.
What modes of ventilation are there?
- IPPV: ventilator driven
- PEEP: ventilator driven which ‘splints’ alveoli open and prevents collapse, helpful in ARDS.
- CPAP: Patient driven and ‘splints’ alveoli open
- SIMV (synchronised intermittent mandatory ventilation), ventilator kicks-in if inhalation missed whilst IPPV weaning
- PSV (pressure support ventilation) patient ventilates spontaneously with added ventilator pressure support to ensure adequate tidal volume whilst IPPV weaning
What are the complications of O2 therapy?
- reduced hypoxic ventilatory drive (COPD)
- pulmonary toxicity & fibrosis (free radical generation
- absorption atelectasis (O2 flushes out N2 resulting in decreased alveolar ‘splintage’
- retinopathy of prematurity (retrolenticular fibroplasia)
- fire
What are the causes of acute pancreatitis?
I GET SMASHED
- Idiopathic
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune
- Scorpion venom
- Hyper-calcaemia/lipidaemia
- ERCP
- Drugs e.g. azathioprine / furosemide
How would you manage a patient with acute pancreatitis?
ALS approach - fluid resuscitation priority
Full history and thorough clinical examination
Prognostic blood tests and ABG
USS - assessment of gallstones
CT - between 3-10 days to delineate severity
What are the modified glasgow criteria?
PANCREAS
- PaO2 <8 kPa
- Age >55
- Neutrophils >15 x 10^9/L
- Corrected Ca <2 mmol/L
- Renal (Urea) >16 mmol/L
- Enzymes (LDH) >600 U/L
- Albumin <32 g/L
- Sugar (glucose) >10 mmol/L
What are the complications of acute pancreatitis?
- Local: abscess, ascites, haemorrhage, necrosis, phlegmon, pseudocyst
- Gastro: paralytic ileus
- Haem: DIC
- Hepatobiliary: CBD stricture, jaundice, portal vein thrombosis
- Metabolic: hypo-albuminaemia/calcaemia/magnesaemia, hypoxaemia, hyperglycaemia
- Renal: ARF
- Respiratory: ARDS, pleural effusion
- Other: chronicity, mortality ~10%
What is SIRS?
2 or more of
- temp <36 or >38
- RR >20 or PaCO2 <4.3
- HR >90
- WCC <4 or >12 or >10% neutrophils
What causes SIRS?
Progression of inflammation throughout the body: non-infective / infective
- cardiovascular: major haemorrhage / infective endocarditis
- GI: pancreatitis / bowel anastomosis leak
- GU: ATN / UTI
- Resp: Aspiration pneumonia / LRTI
- Soft tissues: embolus -> ischaemia / nec fasciitis
- General: Burns & trauma / sepsis
What is MODS and MOFS?
Multiple organ dysfunction syndrome - reversible
Multiple organ failure syndrome - irreversible
When would you consider patient admission to an ICU?
- homeostatic failure: electrolytes / thermoregulation
- high risk of MODS: pancreatitis
- high risk procedure: AAA repair
- intensive monitoring required: cardiovascular/neurological
- mechanical support required: ventilation
- pre-optimisation: pre-operative
- severe condition: head injury / septicaemia
What important conditions must be confirmed prior to diagnosing brainstem death?
- patient comatose / ventilated
- coma cause known
- irreversible brain damage
- reversible causes or coma excluded (alcohol, drugs, endocrine and metabolic disturbance, hypothermia, recent circulatory arrest)
How would you diagnose brainstem death?
Must be performed by 2 doctors (1 thats a consultant), both registered >5 yrs & not part of transplant team. The following must be tested and ABSENT - pupillary light response - occulovestibular reflex - corneal reflex - occulocephalic reflex - gag reflex - motor response to pain - ventilatory effort following apnoea testing (PaCO2 rises to 6.65 kPa)
