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Pete FFICM SOE/OSCE > Gen - Causes And Lists - 22-33 > Flashcards

Gen - Causes And Lists - 22-33 Flashcards

1
Q

Define COPD

A

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

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2
Q

Grade the severity of COPD

A

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

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3
Q

How is COPD diagnosed

A

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

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4
Q

When to admit to ITU with COPD

A 
Persistent worsening hypoxaemia 
Worsening acidosis < 7.25
Needs MV
Vasopressors intropes
Change in mental state
Not responding to tx
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5
Q

Pathophysiology of COPD

A

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

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6
Q

When to use NIV in COPD

A

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

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7
Q

Drugs in COPD

A

B2 agonist - salbutamol
Anticholinergics - ipratropiunm

Steroids - improve FEV1

ABx where needed

Mucolytics - carbocysteins

Aminophyline - side effects!

(Mg)

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8
Q

Key interventions to help with COPD

A

STOP SMOKING

LTOT

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9
Q

Indications for LTOT

A

Chronic stable COPD with PaO2 <7.3

OR

Rest PaO2 < 8 AND polycythaemia, pulmonary hypertension or oedema

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10
Q

When to intubate

A

BTS -

Imminent respiratory arrest
Severe resp distress
Failure of NIV OR can’t have NIV
pH<7.15
GCS < 8
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11
Q

Effects of intrinsic PEEP

A

Limited exp flow - breath stacking, intrinsic PEEP rises.

Decreases venous return and hypotension
Increased PVR and right straing
Pulmonary barotrauma, volutrauma, hypercapnoea

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12
Q

Ventilation in COPD

A

Reduce RR, and I:E ratio

(Hypercapnea may increase PVR and therefore instability)

Keep ePEEP lower than iPEEP

Treat bronchospasm

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13
Q

What is colloid

A

Fluid containing large molecules

Exert an ONCOTIC pressure at

Capillary membrane

(Molecules suspended in crystalloids)

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14
Q

Types of colloids

A

Natural and synth

Natural -
Blood. Blood constiuents. Albumin.

Synth
Gelatins and staraches

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15
Q

Describe albumin

A

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

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16
Q

How is albumin made

A

0.2g/kg/day under Neuro endocrine influence

And plasma onc pressure

Made in liver

Reduced production in illness

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17
Q

Functions of Albumin

A

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

Maintain oncotic pressure

Acid-base - buffer

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18
Q

When might we use albumin

A

Fluid resus - surviving sepsis, once large crystalloid given

Treatment and prophylaxis of HRS

Large volume paracentesis in cirrhosis

Plasmapheresis replacement fluid

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19
Q

Problems with albumin

A

DO NOT USE IN TBI - worsens outcomes

More expensive than crystaloid

May worsen third space in endothelial dysfunction

RIsh of CJD

20
Q

Research on albumin

A

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

21
Q

What is a patient safety incident

A

Any healthcare event that is :

Unexpected

Unintended

Undesired

Associated with actual/potential harm

22
Q

What is a medication errors and an adverse drug event

A

Med Error: any mistake in the prescription, transcriptions, preparation or administration of a drug.

May not cause harm.

ADE - medication error where harm occurs

23
Q

Why do medication errors happen

A

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

24
Q

What is a Never Event

A

Serious incident

Wholly preventable

As guidance and safety recommendation exist that already provide strong protective barriers at national level

And should have been implemented

25
Q

Examples of Never Events

A

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

26
Q

PH for NG tube

A

1-5.5

Must be a clear distinction between 5 and 6

27
Q

Never event - what to do

A

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

28
Q

Diagnostic criteria for DKA

A

Capillary glucose > 11

Ketones > 3mmol or 2+ on dipstick

Venous HCO3< 15 +/- pH <7.3

29
Q

When to admit DKA to ITU

A 
Ketones > 6
Bicarb < 5
pH < 7.1
Hypokalaemia <3.5
GCS<12
Sats< 92%
BP < 90
Tachy or Brady
Anion Gap >16
30
Q

Define DKA

A

A life threatening metabolic complication of Diabetes, defined by the triad of

Acidaemia
Ketonaemia
Hyperglycaemia

31
Q

Causes of DKA

A 
Stress - surgery, pregnancy
Infection
Myocardial infarction
Non-compliance
New diagnosis
32
Q

Pathophys of DKA

A

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

33
Q

Fluid regime for DKA

A

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

34
Q

Insulin in DKA

A

FRII

0.1 unit/kg/hour

DO NOT BOLUS

35
Q

Goals of Tx for DKA

A

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

36
Q

What is HHS

A

Hyperglycaemia >30
Hypovolaemia and
Hyperosmolar state >320

With or without ketones and acidaemia

37
Q

Goals of HHS

A

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

38
Q

Complications of DKA/HHS

A

Cerebral oedema
VTE
MI
Pressure areas

39
Q

When should HHS come to ITU

A 
Osm > 350
Na >160
PH <7.1
K high or low
GCS < 12
SpO2 < 92
Urine <0.5
Cr >200
Hypothermia
MI or CVA
40
Q

Define death and BSD

A

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

41
Q

Diagnostic criteria for BSD (AoMRC)

A

Fulfil the precondition - (unconscious, apneoic and MV)
Brain damage of known aetiology

Exclude reversible causes

Demonstrate coma and apnoea

42
Q

Exclusion/reversible criteria for BSD

A

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

43
Q

Who does BSD

A

2 clinicians

1
Consultant
1 with 5 years GMC reg

44
Q

BSD tests of CNS

A

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

45
Q

When can’t you do BSD

A

Can’t exclude effects of drugs
High C-spine injury
Max fax injury

46
Q

Tests when you can’t do BSD

A

Brain activity - EEG, SSEP

Flow - Cerebral 4 vessel angio
TCD

Pete FFICM SOE/OSCE (199 decks)

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