Respiratory Flashcards

1
Q

Pulmonary Embolism

2021.2 Station

Female presents with acute SOB 10 post c-section

Give differential diagnosis

Discuss assessment

Becomes hypoxic and hypotensive
- outline management

Key points:
don’t intubate
start vasopressors early
excessive fluid resuscitation can worsen RV function

PE ECG:
- tachycardia
- T wave inversion
- S1, Q3, T3 pattern
- partial or complete RBBB
- ST elevation in inferior leads (especially III, aVF)
- ST elevation in aVR

PE Echo:
- RV dilatation (RV >LV)
- McConnels sign - RV akinesis with sparing at the apex
- Flat interventricular septum/ D-shaped septum

A

DIFFERENTIAL DIAGNOSES:
- PE
- Peripartum cardiomyopathy
- Anaemia
- Community acquired pneumoniae
- Post partum pre-eclampsia with pulmonary oedema

PULMONARY EMBOLISM:

Patients at HIGH RISK of death:
- RV dysfunction + troponin rise
- Persistent hypotension/shock

These patients need IV thrombolysis if low risk of bleeding

ABSOLUTE CONTRAINDICATIONS TO THROMBOLYSIS:
- Previous ICH
- ischemic stroke within 3 months
- Major trauma, surgery, or head injury in previous 3 weeks
- Bleeding disorders
- Active bleeding

RELATIVE CNTRAINDICATIONS:
- Oral anticoagulation
- Pregnancy or first post-partum week
- Non-compressible puncture sites
- Traumatic resuscitation
- Refractory hypertension (systolic BP >180 mmHg)
- Active peptic ulcer

ALTEPLASE

65 kg or more: 10 mg intravenously as an initial dose, followed by 90 mg by intravenous infusion over 2 hours

(maximum 1.5 mg/kg total dose in patients less than 65 kg)

HIGH RISK OF BLEEDING
high risk of bleeding (eg advanced age): 10 mg intravenously as an initial dose, followed by 40 mg by intravenous infusion over 1 hour. A further dose of alteplase may be given based on clinical response

Patients at INTERMEDIATE RISK with RV dysfunction + raised trop but NO hypotension

These patients can be treated with anticoagulation alone

Other options include:
- catheter-directed thrombolysis
- aspiration thrombectomy
- surgical thrombectomy

PATIENT DETERIORATES - becomes hypoxic and hypotensive. Outline your management.

  • Sit up right
  • Oxygenate: 100% oxygen 15L NRBM and HFNP 15L
  • Cautious fluid resuscitation: 500ml 0.9% NS IV bolus (too much fluid can worsen RV function and reduce CO further)
  • Vasopressors:
  • Noradrenaline infusion 0.0.5/kg/min (positive inotropy but can worsen tissue perfusion with excessing vasoconstriction)
  • Dobutamine 2-20mcg/kg/min (positive inotropy but can potentiate hypotension with peripheral vasodilation without adequate dose of noradrenaline infusion)

Or adrenaline 0.2-1mcg/kg/min

Avoid intubation and positive pressure ventilation - HFNP is preferred

Can’t give IV thrombolysis because it is contraindicated in this case (as she had c-section 10 days earlier)

Will need to do discuss with respiratory to alternative management
- catheter directed thrombolysis
- mechanical thrombectomy

Arterial line placement

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2
Q

ASTHMA

A

Escalate oxygen therapy - High flow nasal prongs, flow rate 2ml/kg, FiO2 100%

Continuous nebulised salbutamol 2x 5mg undiluted vials
add nebulised ipratropium 500mcg every 20min (3 doses)

IV access - blood gass

Methylprednisone 1mg/kg IV

Magnesium 2g (40mg/kg) IV over 20min

Aminophylline 10mg/kg IV over 1hr

Salbutamol 5mcg/kg/min for 1hr

Request portable chest xray

b)

dynamic hyperinflation ‘gas trapping’ decreases the venous return causing hypotention - Disconnect the ETT from the ventilator circuit and compress the chest - this allows the trapped gas to be released - then ventilate with RR 5-8/min with tidal volume of 5-7ml/kg

tension pneumothorax - needle decompression and then chest tube placement

hypovolemia - fluid bolus 20ml/kg 0.9% NS push dose metaraminol 0.5mg aliquots

Anaphylaxis to induction agents/sedation - adrenaline 10mcg/kg IM repeat after 5min

Excess sedation - especially propofol and fentanyl - reduce sedation infusion rate, consider changing sedation or add a adrenaline infusion

Sepsis - vasopressors + antibiotics

Adrenal insuficiency - hydrocortisone 100mg IV

c)
Use the largest tube possible.
Use lowest FiO2 to achieve SpO2 of 90-92%
Use a small tidal volume, 5-7ml/kg
Use a slow respiratory rate, 8 breaths per minute
Use a long expiratory time, with I:E ratio 1:4
Increase inspiratory flow rate to maximum 60-80L/min
Reset the pressure limits (i.e. ignore high peak airway pressures). .
Use heavy sedation.
Use neuromuscular blockade.
Use minimal PEEP 0cmH2O
Keep the Pplat below 25cmH2o to prevent dynamic hyperinflation.

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3
Q

Status asthmaticus

22yo asthmatic went into respiratory. Intubated in the field by paramedics. Patient arrives in ED. Placed on the ventilator. He is difficult to ventilate. He is hypoxic and hypotensive.

HR 130
BP 85.40
SaO2 80% on 100% oxygen
ETCO2 70mmHg

He has only received 100mcg fentanyl and 100mg suxamethonium when he was intubated in the field.

A

MANAGEMENT:

Disconnect from the ventilator
Compress chest to release trapped gasses
Bag valve tube ventilation slowly RR 6, low TV 6-7ml/kg

TENSION PNEUMOTHORAX:
- unilateral hemithorax inflation,
- distended neck veins
- tracheal deviation to contralateral side
Rx: finger thoracostomy and ICC insertion

DISLODGEMENT:
Oesophageal intubation - insuflate air and listen for gas bubbles over the stomach
eTCO2 trace
Right main bronchus intubation - auscultate chest - no breath sounds heard in left hemithorax
- chest xray (ETT should be 3cm above carina)

OBSTRUCTION:
pass suction catheter
use tube exchange catheter to change tube

CUFF RUPTURE:
check cuff pressure (should be 20-30cm H2O)

BRONCHOSPASM:
- continuous nebulized salbutamol 15mg over 60min
- nebulized ipratropium bromide 500mcg Q20min for 3 doses

ANAPHYLAXIS:
- rash, swelling, hypotension
- 10-20mcg IV bolus of adrenaline until adrenaline infusion commenced

PATIENT/VENTILATOR DYSYNCHRONY:

deepen sedation and paralyse:
Propofol (bronchodilator effect) induction Bolus 1 – 2.0mg/kg -> maintenance 4 – 12mg/kg/hr

I would use an adrenaline infusion alongside the propofol infusion. 0.05mcg/kg/min. The adrenaline may aid in bronchodilation and will counteract the hypotension that the propofol may cause at high doses required

Ketamine (bronchodilator effect)
Induction dose 1-2 mg/kg IV
Maintenance dose 30-90 mcg/kg/min

PARALYSE:
Rocuronium 1.2mg/kg IV
makes ventilating easier

SET VENTILATOR SETTINGS:
Aim to prevent gas trapping and dynamic hyperinflation which lead to tension pneumothorax and obstructive shock.

Low Tidal Volumes: 5-7ml/kg
Low RR: 8
Long expiratory time I:E ratio 1:4
(hence need large ETT to accomodate the high inspiratory flow rates 80L/min)
PEEP 0-5cmH2O
FiO2 100% titrate down aiming for SaO2 >88%
Adjust peak pressure alarm to accept higher airway pressures 35cmH2O - to stop it from alarming constantly

PERMISSIVE HYPERCAPNOEA:
Allowing for high CO2 in order to prevent life threatening barotrauma
Monitor the plateau pressure with an end-expiratory hold maneuver. Plateua pressures should be <35cmH2O

accept pH pH7.2, PCO2 80

ASTHMA TREATMENT:
Salbutamol nebulised 15mg/hr
Ipratropium nebulised 3x 500mcg Q20min
Hydrocortisone 200mg (5mg/kg) IV
Magnesium 2g (40mg/kg) IV over 20min
Salbutamol infusion 10mcg/kg loading followed by 5mcg/kg/min infusion
Aminophylline 10mg/kg IV over 1hr
Adrenaline infusion 1mcg/kg/min

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4
Q

End Stage COPD

2022.1 CBD station

discuss with the examiner, the management of a
patient with end stage COPD.

1) outline how to determine limits of care in this patient
2) describe how you would communicate this to the family

A

1)
Disease progression
- oxygen dependent
- multiple exacerbations and hospital admission

Reversibility of respiratory failure

How have they responded to initial therapies - NIV, steroids, bronchodilators, magnesium

Response to previous intubation and mechanical ventilation

Likelyhood of successful extubation and return home

Co-morbidities

Premorbid level of functioning/Quality of life
- activity of daily living
- functional decline

Patients values and wishes

2)
SETTING THE SCENE:
- Private, quiet space
- Patients family and social supports
- Allow enough time
- No interruptions

Introduce
My name is…
I am the emergency doctor caring for your mother
Thank you for coming into the hospital
Is it okay if we discuss your mothers condition in more detail?
Do you have a support person or other family members who you wish to be here?

GAUGE PERCEPTION
- Assess their understanding about the current clinical situation and prognosis

“what is your understanding of your mothers illness”

  • establish baseline level of function
    “what is her day to day life like”

INVITATION TO RECEIVE INFORMATION:

“would you like me to tell you all the details of your mother’s condition?

KNOWLEDGE OF THE CONDITION
- provide the bad news
- check for patient understanding

“I feel badly to have to tell you this, but….
“I’m afraid the news is not good….

EMPATHY & EXPLORATION
- offer tissues
- acknowledge feelings
- give time to respond
- remind patient you won’t abandon them

“I imagine this is very hard for you to hear”
“We will do whatever we can to help you”

Patient Goals of Care:

  • have you had any discussions about advanced care directives or end of life care?

We are not withdrawing treatment
Comfort oriented approach

Incomplete recovery
Prolonged death
Uncomfortable investigations and further complications from proposed medical interventions
Allowed natural death

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5
Q

Massive Haemoptysis
- most common cause of death is asphyxia not blood loss
- bronchial artery bleed >90%
- TB, bronchiectasis and fungal infection are the most common causes

DIFFERENTIAL DIAGNOSIS:

Haematological:
- anticoagulation therapy
- haemophilia

Infection:
- TB
- bronchiectasis
- necrotizing pneumoniae
- schistosomiasis
- fungal - aspergillus

Vascular:
- aortobronchial fistula (aortic aneurysm erosion)
- AV malformation

Vasculitis:
- SLE with pneumonitis
- Wegeners granulomatosis
- goodpastures syndrome

Malignancy:
- bronchial carinoma

Cardiac:
- Massive PE
- LV failure/Mitral stenosis

Iatrogenic:
- lung biopsy
- paracentesis
- ICC placement

Trauma:
- lung contusion
- penetrating lung injury

A

MANAGEMENT:

attach continuous cardiac monitoring and pulse oximetry

PPE and eye protection for all staff involved in resuscitation

Sit up right - patient needs to cough and expel blood

Oxygenate - HFNP 60L/min FiO2 100% (won’t tolerate face mask)

2x large bore yankauer or decanto suction catheters

2x large bore IV access - VBG, FBC, Coags, Group and Screen, Calcium, fibrinogen

Reverse coagulopathy
Tranexamic acid 1g IV, 500mg nebulized

Early CXR to locate side of bleeding if unilateral

INTUBATION:

Indications for intubation for massive hemoptysis

1) Tiring of respiratory effort/inability to clear secretions with coughing
2) Signs of respiratory distress including frank hypoxemia and/or dyspnea
3) Too unstable to allow safe transport to CT scan or interventional radiology

Difficult airway – call for help from anaesthetist

RSI with ketamine and suxamethonium

Use standard laryngoscope – video laryngoscope camera will be covered in blood

Use the largest size ETT possible >8.0 – blood will occlude small ETT’s, need to be able to perform fibre optic bronchoscopy

DuCanto suction-assisted laryngoscopy airway decontamination (SALAD) approach to managing massive hemoptysis

Mainstem bronchus intubation for massive unilateral hemoptysis

Consider selective lung intubation if severe haemoptysis and unilateral bleeding

Foley catheter occlusion

  • ETT into affected side main bronchus
  • Foley catheter through ETT and inflate in bronchus
  • Withdraw ETT to normal position to ventilate normal lung

VENTILATOR SETTINGS:
- need to adjust tidal volume following mainstem intubation

adjusted tidal volume =
(normal tidal volume -100mls)/2 (+100mls)

Post intubation – lateral decubitus position with bleeding lung down to prevent soiling of non-bleeding lung

CRICOTHYROTOMY:
Indications for cricothyrotomy in massive hemoptysis
If the ability to suction is overwhelmed by the volume of blood in the airway, intubation will not be possible. A supraglottic airway, followed by front of neck access/cricothyrotomy should be performed immediately.

CONSIDER ACTIVATION OF MTP:
- prevent hypother, acidosis and coagulopathy

LOCALISING SOURCE OF BLEEDING:

Portable CXR - locate side of bleeding

CT chest with contrast in arterial phase
- diagnostic accuracy and ability to identify the source decreases with the accumulation of blood
- CT scan with the patient in lateral decubitus position and the bleeding lung downward to avoid contamination of the contralateral lung

DEFINATIVE MANAGEMENT:

Bronchoscopy (diagnostic and therapeutic)
- extract clots
- place bronchial blockers
- endobronchial TXA and adrenaline
- balloon tamponade

Interventional radiology - Bronchial artery embolization - if CT angio shows blush amenable to emblization, if available

Surgery – lobectomy or pneumonectomy

  • cardithoracic surgeon available
  • ongoing bleeding not amenable to IR
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6
Q

PNEUMOTHORAX

EM Rapid bombs - ep 132 re-expansion pulmonary oedema

Primary pneumothorax is spontaneous or because of penetrating trauma

b) secondary pneumothorax is due to underlying lung disease

Airway disease

  • COPD (ruptured bullae)
  • Asthma
  • Cystic fibrosis (8%–20% will develop one in lifetime)

Interstitial lung disease:

  • Sarcoidosis
  • Pulmonary fibrosis
  • Tuberous sclerosis

Infection

  • HIV with Pneumocystis jerovecii pneumoniae
  • Tuberculosis
  • Bacterial pneumonia, necrotizing
  • Lung abscess

Connective tissue disease

  • Marfan’s syndrome
  • Ehlers-Danlos syndrome
  • Scleroderma
  • Rheumatoid arthritis

Cancer
- Primary lung or metastatic disease

Catamenial pneumothorax (endometriosis on the pleura)

A

SIZE:

American College of Chest Physicians:

erect PA film measure apex - cupula >3cm = Large

The British Thoracic Society:

Interpleural distance at the level of the hilum
2cm = 50% pneumothorax
<2cm = small
>2cm = large

IMAGING:

Erect CXR - inspiratory PA view
Can miss 80% of pneumothorax on supine CXR

POCUS:
“More sensitive than CXR and rapidly available at the bedside”

Absence of lung sliding.
Absence of Comet tails
Presence of the “lung point” or “transition point”
Absence of seashore sign in M mode (presence of barcode sign)

Can quantify size with POCUS

MANAGEMENT:

small, asymptomatic primary pneumothorax. ie. no underlying lung disease
- discharge home with repeat CXR in 72hrs
- have to be able to access urgent medical care if required

small symptomatic:
high flow oxygen 10L hudson mask and repeat CXR in 6-12hrs

OR

needle aspiration
(just as safe and as effective and ICC but shorter length of stay and reduced hospital admissions)

post aspiration CXR and a period of observation before discharge home

Large primary pneumothorax should have needle aspiration

If needle aspiration fails, will need small bore ICC and admission

All secondary pneumothorax require admission
small secondary can try needle aspiration first

Give all patients high flow oxygen 10L hudson mask - four-fold increase in rate of resolution

Suction should not be routinely employed as there is a risk of Re-expansion pulmonary oedema (RPO)

Surgical - VATS pleurodesis
- recurrent pneumothorax

DISCHARGE ADVICE:

Follow up – GP/Respiratory physician 2weeks for review and repeat CXR

High risk activity advice
- No flying until full resolution/clearance by respiratory physician

  • No diving at any point (unless surgical fixation and normal CT with clearance by respiratory physician)

Return advice - worsening pain or dyspnoea

Smoking cessation - Rx NRT, smokers quit line

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7
Q

Pneumoniae

2021.1 RMO Interaction

discuss with a junior doctor the assessment and management of a 42 year old female who has presented with a cough and pleuritic chest pain.

INVESTIGATIONS:
VBG - respiratory acidosis with respiratory failure, metabolic acidosis from sepsis

FBC - leukocytosis, thrombocytopenia
UEC - raised urea, renal impairment
LFT’s - derranged in legionella

blood cultures are not useful and the management of mild CAP and should be reserved for more severe cases where the aetiology is unknown

CXR:
- cavitating (S. aureus)
- patchy infiltrates (Haemophilus influenza)
- pleural effusion (moraxella catarrhalis)

Further investigations if the patient is to be admitted

sputum culture

pneumococcal urinary antigens is a useful test - can be done reasonably quickly and is sensitive and specific for pneumococcus

legionella urinary antigens

viral swab for respiratory viruses

influenza, mycoplasma, legionella and chlamydia serology are often requested by the inpatient teams but don’t alter our management in ED

OUTPATIENT MANAGEMENT: eTG

amoxycillin 1g TDS 7days
doxycycline 100mg bd

Moderate severity:

Benzylpenicillin 1.2g QID
Doxycycline 100mg bd

Moxifloxacin 400mg daily if penicillin allergic

Severe:

Ceftriaxone 2g daily
Azithromycin 500mg IV

Vancomycin 25mg/kg IV for MRSA
Pipperacillin-Tazobactam 4.5g for pseudomonas

A

PATHOGENS:

Strep pneumoniae
Atypicals - chlamydia, mycoplasma, legionella
Influenza can develop into S. aureus pneumoniae

CLINICAL PREDICTION RULE

CURB65 - Validated for predicting mortality in community acquired pneumoniae. Can help make decisions about disposition.

Confusion
Urea >7
RR >30
SBP <90
Age >65

The risk of death at 30 days increases as the score increases:

0 - 0.7%

1 - 3.2%

2 - 13.0%

3 - 17.0%

4 - 41.5%

5 - 57.0%

Disposition recommendations based on score:
0-1: Treat as an outpatient

2-3: Consider a short stay in hospital or watch very closely as an outpatient

4-5: Requires hospitalisation, consider ICU admission

SMART-COP (predicts likelyhood of requiring respiratory and inotropic support.

Systolic BP < 90 mmHg (2 points)

Multilobe infiltrate (1 point)

Albumin < 35g/L

RR (age adjusted < 50yrs > 25/min, > 50 yrs> 30/min) (1 point)

Tachycardia > 125 bmp (1 point)

Confusion (acute onset) (1 point)

Oxygenation (age adjusted: SpO2 < 93%, PaO2 < 70 mmHg, PF <333 mmHg) (2 points)

pH < 7.35 (2 points)

Scoring:

0 - 2 points: Low risk ( < 2% 30 day mortality)

3 - 4 points: Moderate risk (5- 13% 30 day mortality)

5 - 6 points: High risk (11 - 18% 30 day mortality)

7 or more points: Very high risk (33% 30 day mortality)

In the Australian Community-Acquired Pneumonia Study (ACAPS) cohort, the accuracy for predicting patients who required IRVS (a SMART-COP score of 3 or more points) was a sensitivity of 92%, specificity of 62%.

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8
Q

Pleural Effusion

Most common causes:
- pneumoniae
- CCF
- malignancy

DIFFERENTIAL DIAGNOSES:

Haemothorax

Chylothorax - damage to thoracic duct

Pseudochylothorax

Transudate (increase in pulmonary vascular pressure and low colloid oncotic pressure)

  • CCF
  • nephrotic syndrome
  • liver cirrhosis
  • PE
  • hypothryroid myxoedema
  • Ovarian hyperstimulation syndrome
  • Meig’s syndrome (ovarian carcinoma)

Exudate: (inflammation leading to leaky capillaries)

  • Malignancy
  • Bacterial pneumoniae with parapneumonic effusion
  • Autoimmune - SLE, rheumatoid arthritis
  • pulmonary infarction
  • Uraemia
  • Pancreatitis
  • Post cardiac surgery
  • Dresslers syndrome
  • Drug related: amiodarone, methotrexate
A

EXAMINATION:
- assymetrical chest expansion
- lack of breath sounds
- reduced vocal fremitus
- stony dull percussion

POCUS:
- can identify septations better than CT

CXR:
can detect >200ml on AP
can detect >50ml on lateral - loss of hemidiaphragms

Light’s criteria state that the pleural fluid is an exudate if one or more of the following criteria are met (sensitivity 98%, specificity 83% for exudate):

Pleural fluid protein : serum protein > 0.5

Pleural fluid LDH : serum LDH > 0.6

Pleural fluid LDH > 2/3 upper limit of normal serum LDH

Additional criteria used to confirm exudate if results equivocal:

Serum albumin – pleural fluid albumin

The British Thoracic Society (BTS) guidelines recommend against aspirating bilateral pleural effusions strongly suggestive of a transudate unless there are atypical features or they fail to respond to therapy.

RE-EXPANSION PULMONARY OEDEMA:

age < 30 years
> 3 L pleural fluid
Use of suction
Rapid drainage ie >1.5l/hr

“Acute drainage of larger volumes is associated with reexpansion pulmonary edema”

MANAGEMENT:
Admit patients with new unilateral pleural effusions for further investigation

diagnostic thoracentesis
- gram statin, microscopy + culture
- cytology
- biochemistry (LDH and protein)

CT chest to look for underlying malignancy

+/- cardiothoracics for invasive diagnostic or therapeutic procedures.
- percutaneous pleural biopsy,
- video assisted thoroscopy
- medical or surgical pleurodesis

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