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respiratory emergencies Flashcards

1
Q

summarise the anatomy of the lung

A

upper airway - nasopharynx, oropharynx, laryngopharynx
lower - trachea - dividees into L and R main bronchi then bronchioles then alveoli
capillary comes into contact with alveolus - deoxygenated blood from teh R side of the heart has a high partial pressure of CO2 - moves from capillary to low partial pressure in alveoli
air has a high PP of oxygen - diffuse into low pp ox deoxygenated blood - gas exchange

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2
Q

summarise the nervous innervation of the lungs

A

o At medulla – ventral and dorsal resp gps – collection nerves innervate resp system leave spinal cord at C3-5 – send fibres to C3-5 phrenic nerve innervate diaphragm
At thoracic vertebrae nerves branch out that innervate the intercostals

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3
Q

what is resp failure

A

Defined as PO2 <8kPa

• Two types – Differentiated by PCO2 (normal range 4.6-6kPa)

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4
Q

type 1 resp failure

A

– PCO2 Normal or Low

- Arises due to a ventilation, perfusion mismatch - not getting oxygen into the body

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5
Q

type 2 resp failure

A 
PCO2 High (>6kPa)
- Arises due to alveolar hypoventilation (cant get the CO2 out) +/- Ventilation mismatch
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6
Q

how do you assess the acutely unwell pt

A

call for help
Airway – Patent?, Stridor? Obstructed? – IF yes 2222
Breathing – Speech(full sentences? - if not they have oxygen deficit and are breathless), RR, Sats, ABG, auscultation, CXR
Circulation – HR, BP, CRT (check perfusion), ECG
Disability – GCS, Glucose, Pupils, Neuro-exam (stroke/central problem can suppress the resp drive)
Exposure/Everything else – Abdomen, Signs of overload,
Re-assess!!!!

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7
Q

what is asthma

A

chronic inflammatory disease characterised by reversible airway obstruction

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8
Q

describe the changes in the airways in asthma

A

– airway lumen narrower, thicker mucus – hypersecretion due to goblet cell hyperplasia
thicker SM - hyperresponsive = bronchoconstriction = obstruction

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9
Q

airways in an acute asthma attackm

A

more mucus, bronchoconstriction = mucus plugging

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10
Q

what is a moderate asthma attack

A

PEF at 50-75% of best or predicted

• No signs of severe asthma

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11
Q

what is a severe asthma attack

A

PEF at 33-50% of best or predicted
• respiratory rate ≥25/min
• heart rate ≥110/min
• Inability to complete sentences in one breath

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12
Q

what are the signs of life threatening asthma

A

acronym CHEST

Cyanosis - SpO2 <92%, PaO2 <8 kPa – blue fingers, lips, tongue
• Hypotension (cardiopulmonary compromise with tachycardia)
• Exhaustion – Poor inspiratory effort,
Confusion, Normal PCO2 (should be blowing CO2 off, if CO2 normal = poor ventilation)
• Silent chest
• Tachy-/Brady- Arrhythmias

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13
Q

management of life threatening severe asthma - ABCDE assessment
Are there any signs of Severe or life threatening
Asthma?
YES

A

call for help -> ITU/HDU
Oxygen – Aim Sats 98%
Bronchodilators: Salbutamol +/- Ipratropium,
IV Magnesium
Steroids: PO Prednisolone/IV Hydrocortisone
reassess

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14
Q

management of life threatening severe asthma - ABCDE assessment
Are there any signs of Severe or life threatening
Asthma?
NO

A

Oxygen – Aim Sats 98%
Bronchodilators: Salbutamol +/- Ipratropium,
IV Magnesium
Steroids: PO Prednisolone/IV Hydrocortisone
RE-ASSESS
if improve:
Continue Bronchodilators, Steroids (5-7 days),
Wean O2
Serial PEF – Discharge if PEF ≥ 75%
TAME asthma (Technique, Avoid triggers,
Monitor PEF so know when attacks coming, Educate with specialist)
if the don’t improve - treat as severe

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15
Q

when do you involve ITU for asthma

A

acute severe or life-threatening asthma, who is not
responding to treatment
Requiring ventilatory support

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16
Q

how can ITU/HDU help in acute asthma

A

high flow ox - 60L/min (4x what available on the ward)
help with ventilation:
• Non-invasive – mask
• Invasive – intubate them

17
Q

initial treatment of infective exacerbation of COPD

A

Oxygen, bronchodilators, steroids, AB, paracetamol

18
Q

what do you need if you have decompensated t2 resp failure with acidosis

A

ventilation support

19
Q

what is COPD

A

Minimally reversible airflow obstruction characterised by an FEV1/FVC ratio
of <0.7

20
Q

how do you assess the severity of COPD

A

Mild FEV1 >80% predicted
• Moderate FEV1 50-80% Predicted
• Severe – FEV1 30-50% Predicted
• Very severe – FEV1 <30% Predicted

21
Q

what does the management of COPD depend on

A

symptoms,

exacerbation and severity of obstruction

22
Q

management of COPD: ABCDE assessment

Are there any signs of Decompensated T2RF? YES

A

Call for help -> ITU/HDU for possible NIV
Oxygen – Aim Sats 98%
Bronchodilators: Salbutamol +/- Ipratropium,
Steroids: PO Prednisolone/IV Hydrocortisone
RE-ASSESS
ventilatory support

23
Q

management of COPD: ABCDE assessment

Are there any signs of Decompensated T2RF? NO

A

Oxygen – Aim Sats 94-98% or 88-92% if T2RF
Via Venturi Mask
Bronchodilators: Salbutamol +/- Ipratropium,
Steroids: PO Prednisolone/IV Hydrocortisone
Antibiotics: If needed
RE-ASSESS
if improve:
Continue Bronchodilators, Steroids (5-7 days),
Wean O2
Complete Course of antibiotics
Chest Physio – If sputum+++
Inhaler technique & Smoking Cessation advice
Pulmonary Rehabilitation
if decompensate: as before

24
Q

summarise non-invasive ventilation

A

Bi-level Continuous Positive
Airway pressure (BiPAP)
provides you with 2 pressures
Inspiratory Positive Airway
pressure (IPAP) – Breathe In - higher number and forces air into the lungs
Expiratory positive airway
pressure (EPAP) – Breathe Out - lower number, pressure in lungs at end of expiration, to make sure airways stay open and don’t collapse

25
Q

what is a PE

A

Venous Thrombi that pass into the pulmonary circulation causing
occlusion. Normally arise from DVTs
poor perfusion = poor gas exchange

26
Q

RF for DVT/PE

A
  • Immobilisation - stasis of blood = clot
  • Malignancy - hypercoag state
  • Recent Surgery
  • HRT/COCP - oestrogen = procoag
  • Thrombophilias - hypercoag state
27
Q

how do you diagnose a PE

A

Gold Standard – CT Pulmonary Angiogram - see bv and where clots are - high sensitivity and specificity
Ventilation/Perfusion Scan (V/Q Scan) – will demonstrate perfusion
defects and a V/Q Mismatch
Use scoring tools to help your diagnosis i.e. Wells score and Geneva
score

28
Q

how does PE effect the heart

A

puts strain on the R heart - because increased pressure in the pulmonary system
pt can go into cardiopulmonary compromise

29
Q

signs of R heart strain on ECG

A

deep S waves in lead 1
deep Q waves in lead 2
T wave inversion in lead 3

30
Q

management of an acute PE - haemodynamically STABLE

A

Call for help
Oxygen, Fluids
Admit for urgent thrombolysis – Local or systemic
Or Percutaneous Embolectomy

31
Q

management of an acute PE - haemodynamically UNSTABLE

A 
Risk Stratification
-Hestia Score
- Pulmonary Embolism Severity Index (PESI)
- Simplified Pulmonary Embolism Severity Index (sPESI)
LOW RISK: 
Discharge with high dose LMWH (cancer)
DOAC and Warfarin for Three Months and
Outpatient follow up for monitoring
If unprovoked, investigate cause
MODERATE TO HIGH RISK 
Admit to Hospital and commence LMWH
Give Oxygen if hypoxic
32
Q

what does a raised JVP indicate

A

fluid overload

33
Q

what is acute pulmonary oedema

A

an accumulation of fluid within the lung parenchyma, resulting in
impaired gaseous exchange

34
Q

causes of acute pul oedema

A

Cardiogenic – Heart Failure, Arrhythmia, Myocardial Infarction
• Renal – Acute, severe Kidney failure
• Acute respiratory distress syndrome (ARDS) – Caused by lung injury, i.e.
infection (Cov-Sars-2)

35
Q

management of acute cardiogenic pul oedema

A 
ABCDE assessment 
position uprighy 
Give Oxygen if hypoxic
High Dose IV Diuretics - Furosemide Bolus
Treat Cause - Beta Blockers for arrhythmia
Re-Assess
IF IMPROVE
Regular Diuretics (get fluid out of the lungs)
Fluid Restriction
Daily Weights – lose 1kg a day (1 Litre)
IF DONT IMPROVE 
Consider Nitrate Infusion (i.e. GTN) if
systolic BP >100 mmHg
Consider Continuous Positive Airway
Pressure (CPAP)
-Recruits alveoli
-Drives fluid out of alveolar spaces
36
Q

why give nitrates in PE

A

reduce resistance of pul vasculature = reduce strain on heart

37
Q

signs on XR of tension pneumothorax

A

tracheal deviation awayu
mediastinal shift away (Cause lung top collapse and shove mediastinum away)
loss of lung markings on affected side - indicating presence of air

38
Q

what is a tension pneumothorax

A

Life threatening condition defined as air trapped in the pleural cavity
under a positive pressure, causing cardiopulmonary compromise

39
Q

treatment of tension pneumothorax

A

emergency needle decompression - 2nd ICS MCL if cardiopul compromise because will go into cardiac arrest
high flow oxygen
chest drain to help pneumothorax resolve

DPD (38 decks)

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