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5. ACUTE CARE > Key Principles > Flashcards

Key Principles Flashcards

1
Q

ABG pH

A

7.35-7.45

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2
Q

ABG PaCO₂

A
  1. 6-6.0 kPa

5. 0-6.4 on a VBG

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3
Q

ABG PaO₂

A

10.5-13.5 kPa

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4
Q

HCO₃

A

22-28 mmol/L

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5
Q

Base excess

A

+1 to -2

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6
Q

ABG lactate

A

0.5-2.2 mmol/L (below 2)

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7
Q

What are the two types of airway obstruction

A

Complete obstruction: absent airflow (feel over mouth), accessory muscle use, intercostal recession on inspiration, paradoxical abdominal movement (abdo draws in as chest inflates) + absent breath sounds on chest auscultation.

Causes: aspiration, laryngeal oedema (e.g. allergy, burns), bronchospasm & pharyngeal obstruction by tongue (reduced tone causes tongue to fall back)

Partial obstruction: ↓ airflow despite ↑ respiratory effort, breathing often noisy: stridor suggests laryngeal obstruction, snoring suggests nasopharyngeal obstruction.

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8
Q

What are the 2 main causes of airway obstruction (broadly speaking)?

A

Airway / swallow dysfunction:

  1. Neurological (coma / anaesthesia, MND / MS, brainstem stroke / haemorrhage, congenital / genetic, muscular weakness / poor cough)
  2. Direct (injury, malignancy, burns, infection)
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9
Q

List 7 causes of airway obstruction

A
  1. Foreign body (acute onset, may be unilateral, stridor)
  2. Secretions/blood/vomit (may have gurgling sounds)
  3. Soft tissue swelling: anaphylaxis (rash, shock, angioedema) or infection (e.g. quinsy).
  4. Mass in surrounding tissues (e.g. tumour).
  5. Laryngospasm
  6. ↓ conscious (opioid OD, head injury, coma/anaesthesia, brainstem stroke).
  7. Muscle weakness / ↓cough (MND/MS)

Conscious level / GCS forms part of airway assessment, as reduced conscious level (GCS <8) > aspiration risk

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10
Q

How to manage an airway obstruction?

A

Airway maintenance whilst awaiting senior input:

  1. Head tilt & chin lift manoeuvre
  2. Jaw thrust if noisy breathing persists
  3. Airway adjunct if still compromised

Oropharyngeal (Guedel) airway only if unconscious (otherwise may gag / aspirate)

Nasopharyngeal airway better tolerated if patient partially conscious

Pharyngeal obstruction by tongue (e.g. coma) can usually be prevented by chin lift manoeuvres or Guedel airway. Most foreign bodies & vomit / blood can be removed by suction. Occasionally, endotracheal intubation or even emergency cricothyroidectomy may be required

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11
Q

ABC: how to assess breathing?

10 things

A
  1. RR <8 or >20 most useful early sign.
  2. SaO₂ (& FiO₂): 94-98% (or 88-92% in COPD). Should be >90% in all critically ill patients. ABG can provide information about ventilation as well as oxygenation (e.g. if sats normal but PaCO₂ high due to poor ventilation).
  3. Central cyanosis: hypoxia can have CNS, respiratory, cardiac & haematological causes
  4. Breath sounds: rattling suggests secretions
  5. Expose chest: respiratory distress, sweating, accessory muscles, abdominal breathing.
  6. Chest expansion (unequal may indicate pathology e.g. pulmonary fibrosis, consolidation, tension pneumothorax)
  7. Examine depth & pattern of breathing:
    Cheyne-Stokes respiration, Kussmaul’s respiration
  8. Feel trachea for mediastinal shift
  9. Percuss
  10. Auscultate: bronchial breathing (e.g. pneumonia), reduced breath sounds (pneumothorax, pleural fluid, consolidation), unilateral crackles (consolidation), bibasilar crackles (pulmonary oedema, bronchitis)

Note: Respiratory acidosis or hypoxaemia despite high flow oxygen therapy requires urgent intervention (treatments depend on cause e.g. COPD)

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12
Q

What is Cheyne-Stokes respiration?

A

Cyclical apnoeas: then varying depth of inspiration / rate of breathing): raised ICP, pulmonary oedema, opioid toxicity, hyponatraemia, carbon monoxide poisoning

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13
Q

What is Kussmaul’s respiration?

A

deep, sighing: metabolic acidosis / DKA

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14
Q

What could cause abnormal RR?

A

↓ - nb resp acidosis: sedation, opioid toxicity, benzodiazepines, brain injury, raised ICP, sleep apnoea / oxygen sensitivity, muscular fatigue, exhaustion in airway obstruction (e.g. COPD).

↑ - nb resp alkalosis: airway obstruction, asthma, pneumonia, PE, pneumothorax, respiratory failure, anxiety

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15
Q

What should be considered when assessing patients saturations?

A

94-98% (or 88-92% in COPD).

Should be >90% in all critically ill patients.

Hypoxaemia: PE, aspiration, COPD, asthma, pulmonary oedema.

ABG can provide information about ventilation as well as oxygenation (e.g. if sats normal but PaCO₂ high due to poor ventilation).

Respiratory acidosis or hypoxaemia despite high flow oxygen therapy requires urgent intervention (treatments depend on cause e.g. COPD)

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16
Q

What chest examination findings are there with consolidation?

Chest wall movement
Percussion
Breath sounds
Added sounds

A

Chest wall movement ↓ ipsilateral
Percussion ↓ dull
Breath sounds: bronchial
Added sounds: coarse crackles

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17
Q

What chest examination findings are there with collapse / atelectasis?

Chest wall movement
Percussion
Breath sounds
Added sounds

A

Chest wall movement ↓↓ ipsilateral
Percussion ↓ dull
Breath sounds: absent or bronchial

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18
Q

What chest examination findings are there with pneumothorax?

Chest wall movement
Percussion
Breath sounds
Added sounds

A

Chest wall movement ↓ ipsilateral
Percussion: normal or hyperresonant
Breath sounds: absent or reduced

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19
Q

What chest examination findings are there with effusion?

Chest wall movement
Percussion
Breath sounds
Added sounds

A

Chest wall movement: ↓ ipsilateral
Percussion: ↓↓ stony dull
Breath sounds: reduced
Added sounds: may have pleural rub

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20
Q

What chest examination findings are there with asthma / COPD?

Chest wall movement
Percussion
Breath sounds
Added sounds

A

Chest wall movement: ↓ bilateral, hyperinflation, accessory muscles
Percussion: normal or hyper-resonant
Breath sounds: vesicular with prolonged expiration
Added sounds: expiratory wheeze

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21
Q

ABC: how to manage patients with breathing issues?

A

ABG if abnormal obs / exam.
Portable CXR if lung pathology suspected.
SOB - should be sat up if possible (aids inspiration).

15L O₂ via non-rebreathe mask if critically unwell (if COPD: sats 88-92% and consider Venturi mask: 24% [4L] or 28% [4L]).

Consider NIV in acute COPD exacerbations after appropriate review. Acute COPD exacerbation: O₂, steroids, nebulisers (+/- antibiotics).

Acute severe asthma: nebulisers.
Treat pneumonia/pneumothorax/PE as identified.

Reassess after any intervention.

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22
Q

Outline GCS

A

Eyes /4
Verbal / 5
Motor / 6

Eyes: open spontaneously, open to command/speech/shout, open to pain, no opening

Verbal: orientated, confused but answer questions, inappropriate responses / words discernable, incomprehensible sounds/speech, no verbal response

Motor: obeys movement commands, purposeful movement to painful stimulus, withdraws from pain, abnormal (spastic) flexion / decorticate posture, extensor (rigid) response / decerebrate posture, no motor response

Lowest score = 3, Highest score 15

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23
Q

How is brain injury classified by GCS?

A

13-15: minor injury
8-12: moderate injury
3-8: severe injury

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24
Q

How to access circulation in ABC?

A
  1. Obs (temp, HR, BP): enough info to identify SIRS: if so perform sepsis 6 immediately! (oxygen, IV Abx & IV fluids
    blood cultures, serial lactates, measure urine output).
  2. Peripheral perfusion: limb temperature, cyanosis
  3. CR (>2s suggests shock / dehydration)
  4. JVP: raised in fluid overload, sunken in dehydration
  5. Central & peripheral pulses: rate, rhythm, volume & equality. Thready & fast pulses indicate poor CO, bounding suggest sepsis or fluid overload. Irregular pulse may be AF.
  6. Ankle / sacral oedema
  7. Auscultate: new murmur suggests endocarditis, pericardial rub / muffled heart sounds (e.g. pericarditis), third HS may indicate HF
  8. Fluid output: oliguria may suggest hypovolaemia, poor cardiac output, acute kidney injury (AKI) or dehydration - suspect retention or obstruction if patient otherwise stable. Output may be high in fluid overload
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25
Q

Discuss how to assess obs when assessing circulation in ABC

A

Temp (36-37.9): pyrexia most commonly infection, beware febrile neutropenia! Septic patients may have high or low temperature. Consider warming (e.g. Bair Hugger) in hypothermia & seek senior help.

HR: tachycardia e.g. hypovolaemia, arrhythmia, infection, hypoglycaemia, thyrotoxicosis, anxiety, pain, iatrogenic causes (e.g. salbutamol). Bradycardia e.g. ACS, IHD, electrolyte imbalance & iatrogenic e.g. beta-blockers.

BP: target is patients normal or systolic >100. HTN: if childbearing age woman consider pre-eclampsia; may suggest fluid overload, endocrine abnormalities (Conn’s, Cushing’s), hypertensive emergency (systolic >180 or diastolic >100): confusion, drowsiness, breathlessness, chest pain, visual disturbances > immediate senior help. Hypotension causes: hypovolaemia, sepsis, iatrogenic (opioids, antihypertensives, diuretics).

Extremes of HR or BP with worrying features (e.g. shock, new HF, syncope, myocardial ischaemia) suggests patient may be peri-arrest: seek immediate senior help + alert crash team as appropriate.

Enough information to identify SIRS: if so perform sepsis 6 immediately!
Administer: oxygen, IV Abx & IV fluids
Take: blood cultures, serial lactates, measure urine output

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26
Q

How are blood volume and BP related?

A

BP initially maintained by compensatory mechanisms e.g. increased peripheral resistance. CO must fall by >20% before BP falls (equivalent to 1L rapid blood loss).

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27
Q

How should you manage circulatory issues in the ABC assessment? (investigations)

A

Cannula: at least one wide-bore cannula (14G or 16G) + bloods: FBC, U&Es + LFTs for all patients. For sepsis: CRP, lactate, blood cultures. For haemorrhage / surgical emergency: coagulation & cross-match. For ACS: cardiac enzymes. For arrhythmia: Ca, Mg, phosphate, TFTs, coagulation. For PE: D-dimer (depending on Well’s score).
For overdose: toxicology screen. For electrolyte imbalance: Ca, Mg, phosphate. For ruptured ectopic: coagulation, cross-match, β-HCG levels. For anaphylaxis: consider serial mast cell tryptase levels.

ECG if appropriate (e.g. chest pain, arrhythmia, murmur, suspected electrolyte imbalance) + consider continuous ECG monitoring.

Bladder scan if suspected retention or obstruction.

Urine pregnancy test in any fertile woman with shock/abdominal pain/gynaecological symptoms.

Cultures / swabs e.g. sputum, urine, line swabs if suspected sepsis. Fluid output / catheterisation: commence balance chart if not already in place & plan to catheterise if appropriate.

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28
Q

How should you manage circulatory issues in the ABC assessment? (fluids)

A

Hypovolaemia: fluid challenge

  1. Lay supine & raise legs if appropriate
  2. Give 500ml bolus Hartmann’s / 0.9% NaCl (warmed if available) over 15 minutes (if HF give 250ml as above, check chest for crackles after each bolus due to risk of fluid overload & pulmonary oedema)
  3. Repeat up to 4 times (2000ml / 1000ml): monitoring response

Stop + seek help if negative response. Seek senior help if not responding adequately to repeated boluses.

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29
Q

What are the main causes of circulatory issues in the ABC assessment and how should you manage these?

A

Metabolic acidosis + raised lactate (>2) indicates tissue hypoxia. Hypovolaemia should be considered primary cause of shock (i.e. resuscitate with IV fluids if hypotensive, tachycardic & cool peripheries) unless obvious HF

ACS: manage with pain relief, nitrates, aspirin & oxygen as per guidelines and seek senior input.

Sepsis: sepsis 6 as per guidelines and seek senior input.

Haemorrhage: restore intravascular volume with blood products & slow bleeding – seek urgent senior input.

Fluid overload: manage with diuretics & seek senior input.

AF: manage with rate/rhythm control or cardioversion, seek senior input.

30
Q

How to assess disability in ABCDE?

A

Assessment of Consciousness:

  1. Repeat AVPU
  2. Pupils: size, symmetry, reaction to light (pinpoint in opioid overdose, dilated in TCA overdose or intracerebral pathology)
  3. GCS if appropriate
  4. Check drugs chart for opioids, sedatives, anxiolytics & antihypertensives
  5. Measure blood glucose
  6. Check if diabetic: ketones if BM >15mmols as may be in DKA
31
Q

What is the initial part of the ABCDE assessment (first thing you should do)?

A

AVPU
Do they look unwell / pale / difficulty breathing, any obvious signs of bleeding, adjuncts around the bed (IV lines, monitoring equipment)
If can answer questions (how are you / pain): suggests orientated & airway patent ✓

32
Q

How should you manage any issues in the D stage of the ABCDE assessment?

A

Capillary blood glucose, urine dip/ketostick for DKA

CT head if suspected intracranial pathology after discussion with senior.

Concerns about consciousness level always warrant senior input: re-assess & maintain the airway.

If opioid overdose, use naloxone as per hospital policy + seek senior advice. If hypoglycaemia, administer glucose as per guidelines & seek senior advice. In DKA, manage with fluids & insulin according to local guidelines & seek senior advice. Reassess after any intervention.

33
Q

How should you manage any issues in the D stage of the ABCDE assessment?

A

Capillary blood glucose, urine dip/ketostick for DKA

CT head if suspected intracranial pathology after discussion with senior.

Concerns about consciousness level always warrant senior input: re-assess & maintain the airway.

If opioid overdose, use naloxone as per hospital policy + seek senior advice. If hypoglycaemia, administer glucose as per guidelines & seek senior advice. In DKA, manage with fluids & insulin according to local guidelines & seek senior advice. Reassess after any intervention.

34
Q

What should you check in the exposure part of ABCDE?

A

Ask about pain

• Rashes (ADR, meningococcal sepsis), signs of infection, bruising (coagulation disorders)
• Calves: red, swelling, tenderness (DVT)
• Lines: phlebitis or infection – replace concerning lines and consider tip culture
• Catheter output: pus or blood: infection or injury?
• Surgical wounds: signs of bleeding or infection,
? concealed internal bleeding e.g. into peritoneum, pelvis, thoracic cavity
• Drains: low/high output, pus or blood – all worrying

35
Q

How to manage potential issues identified in exposure assessment?

A

If bleeding identified: estimate total loss + rate of loss. Severe haemorrhage or shock (hypotension, tachycardia), seek immediate expert help + be aware of the major haemorrhage protocol in local hospital. In any post-op bleeding: advice from surgical registrar ( + severe bleed managed as emergency), manage with blood products as appropriate

Swabs / samples of any potential infection source, including line tip cultures if appropriate.

  • Infection: any pt with suspected infection should have sepsis screen, manage as per guidelines using sepsis 6, consult local guidelines and/or microbiology advice to guide appropriate treatment
  • DVT: if suspected calculate Well’s score + manage appropriately – seek senior advice
36
Q

What sounds indicate what types of airway obstruction?

A

Inspiratory stridor: laryngeal obstruction
Snoring: partial nasopharyngeal occlusion by tongue (+/- palate)
Crowing: laryngeal spasm
Expiratory wheeze: airway obstruction

37
Q

What can cause oropharyngeal obstruction?

A

Oropharyngeal obstruction often caused by tongue (falls backwards when normal muscle tone reduced i.e. drowsy, unconscious, sedated). Also caused by solid particulate matter (food, coins, teeth, vomit), laryngeal oedema (e.g. allergy, burns, inflammation), tumours & laryngeal spasm (e.g. due to foreign bodies, blood, secretions, inhaled toxic gas).

38
Q

What causes tracheobronchial obstruction?

A

Tracheobronchial obstruction is caused by aspiration of particulate matter, bronchospasm, tumours or pulmonary oedema.

39
Q

What are simple measures to manage an upper airway obstruction?

A

• Heimlich manoeuvre: following aspiration of object that completely occludes larynx or trachea – unable to speak/breathe & rapidly cyanosed – attempted if sharp blow to back fails to dislodge objected

Airway clearance:
o Sweeping index finger around oral cavity
o Head tilt - chin lift
o Jaw thrust: method of choice if suspected spinal injury

40
Q

What is a Guedel Airway?

A

Oropharyngeal Airway: OPA

Rigid airway that lifts tongue + epiglottis away from posterior pharyngeal wall & serves as bite block to reduce damage during jaw clenching.

Key Risks: may vomit if have gag reflex. If too large: can close glottis + ∴ close airway. Improper sizing can cause bleeding in the airway.

Correct size: FIRST INCISORS > ANGLE OF JAW

INSERT UPSIDE DOWN & rotate 180° into the functional position (take care not to damage teeth, or increase obstruction by pushing tongue backwards!)

Not for conscious patients as can cause gag reflex, vomiting & laryngeal spasm! Remove when consciousness returns.

41
Q

What is a nasopharyngeal airway?

A

The Soft Nasopharyngeal Airway (SNPA)

Firm but compressible tubes in different sizes + diameters – extend beyond base of tongue after insertion > creates airway & facilitates nasopharyngeal secretion removal.

Topical nasal anaesthesia + lubrication (e.g. lidocaine / lignocaine gel) reduces insertion discomfort, however, traumatic epistaxis not uncommon.

Correct size: lateral edge nostril > tragus

Key Risks: infective (e.g. sinusitis) + erosive complications with continuous use). Contraindicated in coagulopathy, nasal obstruction & basilar skull fracture.

42
Q

What is mask ventilation?

A

Allows ventilatory support + supplementary oxygen delivery in non-intubated patients (increased oropharyngeal pressure delivered during ventilation- in addition to jaw thrust).

Anaesthetic facemasks available in many shapes / sizes (for tight fit). Firm downward pressure on mask with thumb + forefinger maintains seal while mandible simultaneously lifted with 3 remaining fingers + head extended (optimises airway during ventilation). Two-handed technique with assistant to squeeze bag may be necessary.

43
Q

What is a laryngeal mask airway?

A

Useful if intubation fails or is difficult. Sits over the laryngeal inlet & allows temporary positive pressure ventilation in sedated or unconscious patients. Their use is limited in ICU due to potential aspiration, laryngospasm, gastric inflation or poor ventilation.

44
Q

What is a combitube?

A

Oesophageal-tracheal double lumen airway for pre-hospital emergencies for use by those without specialist airway skills. Blindly inserted into oropharynx up to the indicated markings + following inflation of the appropriate cuffs – may aid ventilation.

If patent airway / adequate ventilation cannot be achieved – endotracheal intubation performed . Occasionally, emergency cricothyroidectomy or surgical tracheostomy is required to establish airway.

45
Q

When may acute oxygen therapy be indicated?

A
  1. Cardiac + respiratory arrest
  2. Hypoxaemia (PaO₂ <8kPa, SaO₂ <90%)

Arterial hypoxaemia requires: treatment of cause (e.g. pneumonia), supplemental oxygen and reduction of V/Q mismatch by ensuring optimal ventilation, sputum clearance, bronchodilation & alveolar recruitment.

  1. Hypotension (systolic BP <100mmHg)
  2. Low cardiac output
  3. Metabolic acidosis (bicarbonate < 18mmol/l)
  4. Respiratory distress (RR > 24/min)
46
Q

How is oxygen prescribed?

A

Target saturations must be indicated (except palliative terminal care). Prescribe: dose, delivery, duration and target sats: in emergency often started without prescription but must be documented retrospectively.

47
Q

What are the aims of oxygen therapy? (i.e. target sats)

A

Depends on risk of hypercapnic respiratory failure (HCRF)

  1. Low risk (normal patient): age <70: aim 94-98%, if age >70: aim 92-98%
  2. If at risk (e.g. neuromuscular disease, COPD): target should be 88-92% pending ABG analysis (higher SaO₂ has fewer benefits but can cause hypoventilation, hypercapnia and respiratory acidosis)
48
Q

What is moderate dose oxygen therapy? When is it used?

A

40-60%: delivered via nasal cannulae (2-6L/min) or simple facemasks (5-10L/min).

Aim for SaO₂ 92-98% and reservoir mask is substituted if target saturations not achieved. If at risk of HCRF, manage with low-dose (controlled) supplemental oxygen.

49
Q

What is low dose oxygen therapy? When is it used?

A

Low-dose (controlled) supplemental oxygen (24-28%): fixed performance Venturi mask (mask with adjustable valves of different colour for diff oxygen concentrations).

When stable: replace Venturi mask with nasal cannulae: 1-2L/min.

Indicated if risk of HCRF (COPD, neuromuscular disease, chest wall disorders, morbid obesity, CF). Long-term smokers >50 years old with exertional dyspnoea without other cause are treated as COPD.

50
Q

What is high dose oxygen therapy? When is it used?

A

High dose (>60%): delivered via non-rebreathe reservoir mask at 10-15L/min.

Indicated for critical illnesses e.g. cardiac / respiratory arrest, shock, major trauma, sepsis, CO poisoning.

Once stability restored, dose is reduced whilst maintaining 92-98%. Seriously ill at risk of HCRF are initially treated with high dose O2 pending ABG analysis.

51
Q

How can excretion of carbon dioxide be improved?

A

CPAP: via lung recruitment

NIV: increase in minute ventilation

Drugs: respiratory analeptics (doxapram) and antagonists (naloxone, flumazenil)

Formal mechanical ventilation

All breathless patients: measure sats regularly + record with o2 dose in the obs chart.

52
Q

How is suspected hypercapnic respiratory failure managed?

A

Low dose oxygen therapy: target sats 88-92% whilst awaiting ABG results – if PaCO2 normal – SaO2 is adjusted to 92-98% (except in patients with previous HCRF) and ABG rechecked at 1 hour.

Patients with previous HCRF are issued with alert card + Venturi mask to warn future emergency staff of potential risk. If air compressor not available nebulisers can be driven with oxygen but only for 6 minutes. If both hypercapnic (>6kPa) and acidotic (<7.35) consider NIV, especially if acidosis >30min despite medical treatment.

53
Q

In general, how are patients with acute respiratory failure managed and monitored?

When can oxygen be stopped?

A

Unstable patients: continuous SaO₂ monitoring in high dependency areas. Observe SaO₂ for 5 mins after starting / changing o2 dose and adjust to achieve target.

If possible: ABG before + within 1 hour of starting O₂ (especially if risk of HCRF), then at intervals to assess response.

STOP therapy when clinically stable on low dose oxygen (1-2L/min) and within target SaO₂ on 2 consecutive occasions. Monitor SaO₂ for 5 mins after stopping & recheck at 1 hour (if still within target than oxygen has been safely discontinued).

54
Q

What is NIV?

A

Non-invasive Ventilation (NIV)

or NIPPV / NPV - mechanical ventilation without intubation, positive pressure ventilation which assists inspiration

55
Q

What are different types of NIV?

A

BiPAP: Bilevel positive airway pressure = provides 2 pressure levels IPAP (~30) + EPAP(~5).

Note: Inspiratory positive airway pressure (IPAP): controls peak inspiratory pressure during inspiration. Expiratory positive airway pressure (EPAP): controls the end expiratory pressure.

Positive end-expiratory pressure (PEEP): ventilation method where airway pressure maintained above atmospheric at the end of exhalation (keeps alveoli open to ↓ shunting of blood & ↑ gas exchange).

Auto-PEEP: common in patients with obstructive lung disease: incomplete expiration causes progressive air trapping (hyperinflation). Auto-PEEP refers to the accumulation of air which increase alveolar pressure at the end of expiration. EPAP offsets intrinsic PEEP.

Pressure support (PS): patient determines breath timing and frequency (respiratory effort triggers the ventilator on/off – assisted spontaneous breathing). Pressure can be adjusted to support inspiration and most have back-up breath rate of 6-8/min in patients who make no respiratory effort.

Pressure controlled ventilation: pre-set number of mandatory breaths delivered in absence of patient effort but triggering can also occur (triggered breaths delay the next mandatory breath). Delivered breaths are identical to the mandatory breaths.

56
Q

What is CPAP?

A

Continuous positive airway pressure (CPAP)

(IPAP = EPAP): positive airway pressure during spontaneous breaths. Does NOT assist inspiration (not ventilation/no mechanical breaths)

57
Q

What are the aims of NIPPV?

A

Reduce WOB, relieve symptoms, improve / stabilise gas exchange, improve alveolar ventilation (alveolar recruitment), optimise patient comfort, achieve patient-ventilator synchrony, avoid endotracheal intubation (ETI) / laryngeal mask / tracheostomy, minimise risk to patient.

58
Q

Benefits and limitations of NIPPV?

A

✔︎ Avoids complications associated with mechanical ventilation (MV) e.g. pulmonary infection, pressure induced damage & with endotracheal tubes (ETT) e.g. mini-aspiration, upper airway trauma ✔︎ Allows rest periods ✔︎ Preserves cough ✔ Allows oral nutrition, & speech (decision making) ✔︎ Earlier mobilisation ✔︎ Time to decide if MV is appropriate

✘Lack of airway protection ✘No endotracheal suction ✘Correction of blood gases is less complete than with MV ✘ Mask discomfort, eye damage ✘Prolonged use difficult: nasal bridge ulceration ✘Gastric dilation and vomiting (may need NG tube) ✘Limits ventilatory capacity ✘Increases nursing time ✘Needs patient reassurance ✘Intolerance and distress
✘Impedes sputum clearance

59
Q

What are complications of NIPPV?

A

Complications: hypotension, gastric distension & aspiration, pneumothorax, pressure necrosis (nose bridge, ears), eye irritation, adverse haemodynamic effects reported but rare

60
Q

When is NIPPV indicated?

A

Signs or symptoms of acute respiratory distress

RR >24/min / accessory muscle use / abdominal paradox

mod-severe dyspnoea (increased over usual)

PaCO₂ > 7kPa and pH <7.35

PaO₂-FiO₂ ratio <26kPa (200mmHg) i.e. ARDS

61
Q

When is NIPPV used?

A
  1. Acute hypercapnic respiratory failure: COPD with respiratory acidosis, or 2°ry to chest wall deformity / neuromuscular weakness
  2. Pulmonary oedema
  3. Obstructive sleep apnoea
  4. Assist weaning from MV
  5. Post-op respiratory failure.

Less common indications: pneumonia (caution), immunocompromised patients with respiratory failure + CF. Also used when ETI considered inappropriate (e.g. end-stage respiratory failure).

62
Q

What are contraindications to NIPPV?

A 
✘Respiratory arrest 
✘Inability to use mask due to trauma / surgery ✘Excessive secretions 
✘Haemodynamic instability or life-threatening arrhythmia ✘High risk of aspiration 
✘Impaired mental status 
✘Uncooperative or agitated patient
✘Severe hypoxaemia 
✘Focal consolidation on CXR 
✘Undrained pneumothorax
63
Q

How is NIPPV initiated?

A
  1. Bed at 45° angle, choose correct mask size
  2. Initiate at 5cm H₂O CPAP and IPAP of 0-5cm H₂O
  3. Hold mask gently on patients face until comfortable + in full synchrony with the ventilator. Secure mask with head straps, but avoid a tight fit
  4. Slowly increase IPAP to 10-20cm H₂O

Evaluate that respiratory support is adequate: reduced dyspnoea, reduced RR, Good VT, comfort for the patient

O₂ may be given through NPPV to give sats > 90%. A backup rate may be provided if concerned about apnoeic. In patients with hypoxaemia, increase CPAP in increments of 2-3cm water until FiO₂ is <0.6. Set the ventilator alarms and backup apnoea parameters. Encourage the patient. Monitor with oximetry, ABG.

Monitoring:
• Clinical assessment: chest wall movement, synchrony of respiratory effort, accessory muscle recruitment, patient comfort
• Simple observations: HR, RR, pulse oximetry (SaO₂ > 85%), mental state
• If at risk of hypercapnia, aim for sats of 88-92% - document target range in notes, ob chart & prescribe in JAC. (↑O₂ can cause ↑CO₂ for complex reasons, more complicated than textbook ‘loss of hypoxic drive’)
• ABG: at one hour +/- 4-6 hours

Adjustments to settings
Level of ventilatory support is difference between IPAP + EPAP
To increase PaO₂: ↑ EPAP. If PaCO₂ remains elevated: ↑IPAP or ↓EPAP

Review and stepping up/down:
• Early specialist referral, optimisation of medication, home nebulisers/oxygen, education, support + pulmonary rehabilitation, long term domiciliary NIV

64
Q

Most important obs

A

RESPIRATORY RATE is most important & first to change. Next most important: new confusion.

65
Q

Why is the new NEWS chart different

A

Adult NEWS 2 cannot be modified by specialty & is optimised for identification of sepsis, alternative oxygen targets in underlying lung disease, and the onset of delirium.

66
Q

What is low score group (MEWS)?

Mgmt?

A

Patient causing concern OR total mews ≥4 or mews ≥2 in any one parameter

Complete mews log, ↑ frequency of obs (at least hourly) + inform nurse in charge. Nurse in charge activates medical response or requests repeat in 30mins.

67
Q

What is medium score group (MEWS)?

Mgmt?

A

Mews ≥4 or remain concerned

Inform nurse in charge, activate medical response, voicemail 6286, junior doctor reviews within 30mins

68
Q

What is high score group (MEWS)?

Mgmt?

A

Pt continues to cause concern, fails to improve within 2 hours or reactivates within 24 hours

Immediate response: emergency call to team with critical care competencies + diagnostic skills. Must be reviewed by consultant or SpR. Consider need for critical care outreach (9191), MHDU, ICU (2110).

Calling 2222 acceptable if serious situation, not necessarily cardiac arrest…

Consider: fluid balance, blood tests, investigations e.g. ECG, CXR, other imaging. Timely senior review.

  • Assessment, monitoring plan, management plan
  • Involve senior help early

Only SpR or consultant can make decision to stop early warning score parameters.

69
Q

CPAP vs BiPAP

A

CPAP: not a form of ventilation

Improves FRC, recruits + prevents collapse of lower airways (alveolar recruitment) + improves oxygenation (by improving VQ mismatch)

Indications: atelectasis, acute pulmonary oedema, acute lung injury (ALI), obstructive sleep apnoea (OSA)

BiPAP: assists in airflow in + out of lungs
IPAP increases tidal volume / ventilation + therefore CO₂ clearance. EPAP prevents rebreathing + works like CPAP (as above).

Improvement in gas exchange occurs due to an increase in increase in alveolar ventilation – externally applied expiratory pressure (i.e. PEEP) decreases the work of breathing by partially overcoming the auto-PEEP.

Indications: ↑CO2 respiratory failure (acute type II): acute COPD exacerbation & obesity hypoventilation syndrome.

70
Q

What is optiflow?

A

Optiflow: High flow nasal spec oxygen, humidified, better oxygen delivery, wash out of dead space, delivery of low level CPAP

71
Q

What is non invasive negative pressure ventilation?

A

Resurgence of non-invasive negative pressure ventilation: lower pressure surrounding chest wall during inspiration + reversing to atmospheric level during expiration.

More normal physiology, can talk/cough/eat/drink, can help secretion clearance

72
Q

What is bad about volume ventilators?

A

Volume ventilators are generally poorly tolerated due to high inspiratory pressures > discomfort + mouth leaks, usually used in difficult to wean patients e.g. morbidly obese, thoracic deformity.

5. ACUTE CARE (5 decks)

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