Chronic stable COPD with PaO2 <7.3 OR Rest PaO2 < 8 AND polycythaemia, pulmonary hypertension or oedema

Causes And Lists - 22-33 Flashcards by Peter Turton

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

How well did you know this?

Not at all

Perfectly

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 well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Drugs in COPD

B2 agonist - salbutamol
Anticholinergics - ipratropiunm

Steroids - improve FEV1

ABx where needed

Mucolytics - carbocysteins

Aminophyline - side effects!

(Mg)

How well did you know this?

Not at all

Perfectly

Key interventions to help with COPD

STOP SMOKING

LTOT

How well did you know this?

Not at all

Perfectly

Indications for LTOT

Chronic stable COPD with PaO2 <7.3

Rest PaO2 < 8 AND polycythaemia, pulmonary hypertension or oedema

How well did you know this?

Not at all

Perfectly

When to intubate

BTS -

Imminent respiratory arrest
Severe resp distress
Failure of NIV OR can’t have NIV
pH<7.15
GCS < 8

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Ventilation in COPD

Reduce RR, and I:E ratio

(Hypercapnea may increase PVR and therefore instability)

Keep ePEEP lower than iPEEP

Treat bronchospasm

How well did you know this?

Not at all

Perfectly

What is colloid

Fluid containing large molecules

Exert an ONCOTIC pressure at

Capillary membrane

(Molecules suspended in crystalloids)

How well did you know this?

Not at all

Perfectly

Types of colloids

Natural and synth

Natural -
Blood. Blood constiuents. Albumin.

Synth
Gelatins and staraches

How well did you know this?

Not at all

Perfectly

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 well did you know this?

Not at all

Perfectly

How is albumin made

0.2g/kg/day under Neuro endocrine influence

And plasma onc pressure

Made in liver

Reduced production in illness

How well did you know this?

Not at all

Perfectly

Functions of Albumin

Transport molecule - Cations - calcium, Na, K
Hormones T4
Bilirubin and bile salt
Drugs - warfarin, barbiturates

Maintain oncotic pressure

Acid-base - buffer

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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