Causes And Lists - 22-33 Flashcards
Define COPD
Progressive inflammatory condition of the peripheral and central airways, lung parenchyma and pulmonary vasculature
GOLD definition:
A common, preventable and treatable disease
Characterised by persistent respiratory symptoms
Airflow limitation
Due to airway and alveolar abnormalities cause by exposure to noxious particles and gases
Grade the severity of COPD
Symptoms (dyspnoea), Spirometry and clinical features
MRC - grade 1-5 1 - Not breathless except on excercise 2 - Short of breath hurrying 3.- Stops after 15 minutes 4 - 100yds 5 - Breathless Undressing
Spiro
GOLD 1-4
FEV1
Mild - >80%
Mod 50-79%
Severe - 30-49%
Very - <30%
Clinical
Hypoxamiea, hypercapnia, pulmonary hypertension, failure, polycyth
How is COPD diagnosed
Symptoms and spirometry
Symptoms: Smokers over 35 Exertional breathlessness Chronic cough Sputum production, Frequent bronchitis and wheeze
Spirometry
Airway obstruction with post bronchodilator FEV1/FVC < 0.7
When to admit to ITU with COPD
Persistent worsening hypoxaemia Worsening acidosis < 7.25 Needs MV Vasopressors intropes Change in mental state Not responding to tx
Pathophysiology of COPD
Airflow limitation and gas trapping on expiration - hyperinflation
Gas exchange abnormalities - reduced ventilation drive and increased dead space. CO2 retention
Mucous hypersecretion - increase goblet cells and submucosal glands
Pulmonary hypertension from hypoxia and HPV
Exacerbation - bacterial/viral/environmental
Systemic - hyperinflation alters cardiac function, muscle wasting, cachexia
When to use NIV in COPD
BTS guidance
Worsening acidosis PaCO2 >6.5. pH<7.35
Severe acidosis pH<7.25 (these have a high risk of failure)
As a ceiling a tx for pts not for I&V
Drugs in COPD
B2 agonist - salbutamol
Anticholinergics - ipratropiunm
Steroids - improve FEV1
ABx where needed
Mucolytics - carbocysteins
Aminophyline - side effects!
(Mg)
Key interventions to help with COPD
STOP SMOKING
LTOT
Indications for LTOT
Chronic stable COPD with PaO2 <7.3
OR
Rest PaO2 < 8 AND polycythaemia, pulmonary hypertension or oedema
When to intubate
BTS -
Imminent respiratory arrest Severe resp distress Failure of NIV OR can’t have NIV pH<7.15 GCS < 8
Effects of intrinsic PEEP
Limited exp flow - breath stacking, intrinsic PEEP rises.
Decreases venous return and hypotension
Increased PVR and right straing
Pulmonary barotrauma, volutrauma, hypercapnoea
Ventilation in COPD
Reduce RR, and I:E ratio
(Hypercapnea may increase PVR and therefore instability)
Keep ePEEP lower than iPEEP
Treat bronchospasm
What is colloid
Fluid containing large molecules
Exert an ONCOTIC pressure at
Capillary membrane
(Molecules suspended in crystalloids)
Types of colloids
Natural and synth
Natural -
Blood. Blood constiuents. Albumin.
Synth
Gelatins and staraches
Describe albumin
Globular single polypeptide
MW = 69 kDa
Negative charge and repelled by negative endothelium
Used as volume expander
Comes from plasma, serum and placenta at 4.5% and 20%
From pooled donations
RISK OF CJD
How is albumin made
0.2g/kg/day under Neuro endocrine influence
And plasma onc pressure
Made in liver
Reduced production in illness
Functions of Albumin
Transport molecule - Cations - calcium, Na, K
Hormones T4
Bilirubin and bile salt
Drugs - warfarin, barbiturates
Maintain oncotic pressure
Acid-base - buffer
When might we use albumin
Fluid resus - surviving sepsis, once large crystalloid given
Treatment and prophylaxis of HRS
Large volume paracentesis in cirrhosis
Plasmapheresis replacement fluid
Problems with albumin
DO NOT USE IN TBI - worsens outcomes
More expensive than crystaloid
May worsen third space in endothelial dysfunction
RIsh of CJD
Research on albumin
98 - Cochrane - initially said HAS associated with mortality especially burns
SAFE - 4% HAS vs saline in ICU - similar mortality. Worse in TBI
ALBIOS - no survival advantage with HAS in sepsis
What is a patient safety incident
Any healthcare event that is :
Unexpected
Unintended
Undesired
Associated with actual/potential harm
What is a medication errors and an adverse drug event
Med Error: any mistake in the prescription, transcriptions, preparation or administration of a drug.
May not cause harm.
ADE - medication error where harm occurs
Why do medication errors happen
Patient factors, environmental and med specific.
Patient - prolonged hospital stay, lack of capacity, ICU alters pharmacokinetics
Environment - turnover of patients and staff, stress, distractions, wide variation in knowledge
Meds - large number of them, use of pumps, boliuses, programming, weights
What is a Never Event
Serious incident
Wholly preventable
As guidance and safety recommendation exist that already provide strong protective barriers at national level
And should have been implemented
Examples of Never Events
Surgical - Wrong site, wrong implant, retained FB
Meds - Potassium, wrong route of admin, insulin OD, methotrexate OD in cancer, wrong conc of midaz
MH - collapsible shower, rail curtains
General - fall from a window, trapped in bed rails, transfusion issues, NG/OG
PH for NG tube
1-5.5
Must be a clear distinction between 5 and 6
Never event - what to do
1 -treat complications to patient and ensure safety
2 - tell consultant and CD.
3 -tell patient and family - candour
4 - Incident report
Never events to the Strategic Exec within 2 days
5 - Investigate, RCA, tell the relevant commissioning body
Diagnostic criteria for DKA
Capillary glucose > 11
Ketones > 3mmol or 2+ on dipstick
Venous HCO3< 15 +/- pH <7.3
When to admit DKA to ITU
Ketones > 6 Bicarb < 5 pH < 7.1 Hypokalaemia <3.5 GCS<12 Sats< 92% BP < 90 Tachy or Brady Anion Gap >16
Define DKA
A life threatening metabolic complication of Diabetes, defined by the triad of
Acidaemia
Ketonaemia
Hyperglycaemia
Causes of DKA
Stress - surgery, pregnancy Infection Myocardial infarction Non-compliance New diagnosis
Pathophys of DKA
Lack of insulin
Glucagon increases
Catecholamine and cortisol rises —> lipolysis, fatty acids and ketonegenesis
Ketones accumulate (met acidosis)
Fluid depletion due to osmotic dieuresis through high glucose
Vomiting
Reduced intake
High sugar due to - increased gluconeogensis and glycolysis
Fluid regime for DKA
500mls if hypotenisve
1 litre saline over 1 hours 1 litre over 2 hours +KCl 1 litre over 2 hours +KCL 1 over 4 1 over 4 1 over 6
1, 2, 2, 4, ,4 ,6
Insulin in DKA
FRII
0.1 unit/kg/hour
DO NOT BOLUS
Goals of Tx for DKA
Decrease ketones by 0.5mmol/l/hour
Increase HCO by 3
Decrease glucose by 3
Potassium 4 to 5.5
Add dextrose 10% when BM < 14
What is HHS
Hyperglycaemia >30
Hypovolaemia and
Hyperosmolar state >320
With or without ketones and acidaemia
Goals of HHS
Treat the underlying cause
Normalise the osmolality (2xNa) + Ur+ glucose
Replace fluid and electrolytes
Aim to keep K 4 to 5.5
Na reduced by <10 over 1 days
Glucose down by 5 per hour
Insulin ONLY once glucose isn’t falling with fluid alone
Rate of 0.05 units/kg/hour
Complications of DKA/HHS
Cerebral oedema
VTE
MI
Pressure areas
When should HHS come to ITU
Osm > 350 Na >160 PH <7.1 K high or low GCS < 12 SpO2 < 92 Urine <0.5 Cr >200 Hypothermia MI or CVA
Define death and BSD
Death - simulataneous irreversible loss of capacity to breath and be concours
BSD - irreversible loss of brain stem function as a result of neurological injury. Heart beats but breathing depends on a vent
Diagnostic criteria for BSD (AoMRC)
Fulfil the precondition - (unconscious, apneoic and MV)
Brain damage of known aetiology
Exclude reversible causes
Demonstrate coma and apnoea
Exclusion/reversible criteria for BSD
Not on drugs that may affect - midaz/thio (blood test or wait 3 half lives)
(Give antagonists)
Circulatory - MAP >60
Ph normal
PCO2 <6
Po2 >10
Temp> 34!
Na 115 - 160
K >2
Mg 0.5 to 3
Sugar - 3:20
Who does BSD
2 clinicians
1
Consultant
1 with 5 years GMC reg
BSD tests of CNS
Pupillary 2 to 3
Cornea 5 to 7
Pain 5 to 7
Vestibule - 8 to 3, 4, 6 (nystagmus)
Gag 9 to 10
Cough 10 to 10
When can’t you do BSD
Can’t exclude effects of drugs
High C-spine injury
Max fax injury
Tests when you can’t do BSD
Brain activity - EEG, SSEP
Flow - Cerebral 4 vessel angio
TCD
