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AIP > Shortness of Breath > Flashcards

Shortness of Breath Flashcards

1
Q

What are the important aspects of history in an acute asthma attack?

A
  • Baseline severity
  • Exacerbation history
  • Previous ICU admissions
  • Normal PEFR
  • Inhaler technique
  • Home oxygen/nebs
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2
Q

What investigations should be done for a suspected asthma attack?

A
  • Peak flow
  • ABG
  • CXR to exclude pneumothorax
  • Bloods - regular potassium monitoring
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3
Q

What will an acute asthma attack abg show?

A

Will show hyperventilation

If it shows hypoxia/hypercapnia then patient is tiring

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4
Q

What are the features of a life-threatening asthma attack?

A 
33, 92, CHEST
PEFR <33% predicted
<92% saturations
Cyanosis
Hypotension
Exhaustion
Silent chest
Tachycardia
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5
Q

What are the features of severe, moderate and mild asthma attacks?

A
  • Severe <50% predicted PEFR, cannot complete full sentences, resp rate >25, HR >110
  • Moderate <75% PEFR
  • Mild >75% PEFR
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6
Q

What is the management for an acute asthma exacerbation?

A

O SHIT ME
Oxygen - oxygen driven nebs
Salbutamol 2.5-5mg nebulised - back to back initially
Hydrocortisone 100mg IV
Ipratropium - 500mcg NEB
Theophyline - amniophylline infusion - usually in ICU
Magnesium sulphate 2g IV over 20 mins - one off dose
Escalate care - intubation and ventilation

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7
Q

What is the management for an acute exacerbation of COPD?

A 
O SHIT
Oxygen - venturi controlled 88-92%
Salbutamol 5mg NEB
Hydrocortisone 100mg IV
Ipratropium 500mcg NEB
Theophylline - usually in ICU

Antibiotics should be prescribed if signs of infection
Chest physio
Consider BiPAP if can’t maintain oxygenation without depressing respiratory drive

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8
Q

What are the intensive care indications for Acute asthma/COPD?

A

If they require ventilator support
Worsening hypoxia/hypercapnia/acidosis
Exhaustion
Drowsiness/confusion

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9
Q

What are the investigations for suspected pulmonary embolism?

A 
To confirm/exclude diagnosis:
-D-Dimer if low PE wells score
-CTPA
To investigate severity:
-ECG may show RV strain (T-wave inversion in inferior leads), S1Q3T3
-CXR may show wedge infarcts, effusion
-ECHO - for right heart strain/overload
Look for cause e.g. anti-phospholipid, malignancy, thrombophilia
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10
Q

How do you manage a PE?

A

Calculate the PE wells score
If high risk or D-dimer positive - Start treatment dose LMWH 1.5mg/kg OD for 5 days
Most patients are then started on DOACs or Warfarin for 6 months anticoagulation
In patients with massive PE (SBP <90) then throbolyse with alteplase
In patients with sub-massive PE (e.g. saddle PE) - unfractionated heparin infusion for 72 hours so thrombolysis can be considered

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11
Q

What investigations should you do for acute pulmonary oedema?

A

Bloods - ABG, FBC, LFT, U+E, BNP, Trops if ACS suspected
CXR
ECG
echo
serial weights with catheter for accurate UO

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12
Q

What is the immediate managament for acute pulmonary oedema?

A 
PODMAN
Position - sit up
Oxygen - high flow
Diuretics - IV furosemide
Morphine - causes venodilation and reduces preload
Anti-emetic - metoclopramide 10mg IV
Nitrates - in severe pulmonary oedema
CPAP if still hypoxic
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13
Q

What is the long term management of heart failure?

A 
Treat cause where possible
-ACE inhibitor
-Beta blocker
-Diuretic - if pulmonary/peripheral oedema
can add aldosterone antagonists e.g. spironolactone
Non-pharmocological:
-Cardiac resync deice
-Implantable cardioverter defibrillator
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14
Q

When in the day are asthma symptoms usually worst?

A

Usually at night or early in the morning

Cold can make them worse

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15
Q

How is asthma diagnosed?

A

In high likelihood of asthma: Asked to keep a peak flow diary, diurnal variation will be greater than 20% and will improve with treatment
In intermediate likelihood of asthma: reversibility testing with spirometry

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16
Q

What 3 questions should be asked at an annual asthma review?

A

Has your asthma affected your sleeping?
Have you had your asthma symptoms during the day?
Has your asthma affected your daily activities?

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17
Q

What are the steps of treating asthma in the community?

A

1) SABA e.g. salbutamol
2) Add steroid e.g. beclomethasone, this is indicated by using SABA more than 3 times a week or having night symptoms
3) LABA e.g. salmeterol added
4) refer at this point, can add leukotriene receptor antagonists e.g. montelukast
Alternatively xanthine derivative such as theophylline

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18
Q

What are the two main patterns of wheezing in children?

A

There is Trasient acute wheezing (viral induced wheeze) and usually resolves by age 5
Chronic recurrent wheezing is usually due to asthma

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19
Q

How does asthma management in the community differ in children?

A

1) SABA
2) Leukotriene receptor antagonists
3) add inhaled steroid
4) increase steroid dose and consider theophyline

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20
Q

What should prompt hospital admission in chest infections in the community?

A

CURB-65 score >1 or SpO2 <94%

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21
Q

What are the components of the CURB-65 score? What scores equate to what severity?

A 
Confusion
Urea >7
Resp rate >30
Systolic BP <90
Age >65
Score >2 moderate, >3 severe, >4 ITU
22
Q

What is the commonest causative organism for community aquired pneumonia?

A

Strep pneumoniae followed by haemophilus influenzae

23
Q

What antibiotics should be used to treat CAP?

A

In community give amoxicillin 500mg TDS for 5 days
In moderate CAP give oral amoxicillin 500mg TDS and clarithromycin 500mg BD for 7-10 days
If severe then IV 1.2g Co-amoxiclav TDS and IV 500mg BD clarithromycin changing to oral when there is improvement, 7-10 days in total

24
Q

What is the definition of HAP?

A

Must develop >48 hours after hospital admission

25
Q

What are the common causative organisms for HAP?

A

Commonly staph aureus and pseudomonas

26
Q

What investigations should be requested for a pneumonia?

A 
Gain IV access
Take bloods
FBC shows raised WCC
U and E and LFT for baseline and curb65
LFT can be raised in legionella
ESR/CRP may be elevated
ABG in patients with o2 <94%
Blood cultures
Sputum cultures
Urine antigen testing for pneumococcal and legionella
CXR
ECG to rule out other causes
27
Q

What are some potential causes of acute heart failure?

A

ACS
Acute mechanical disruption e.g. septal rupture or valve regurge
Arrhythmia
Acute outflow obstruction e.g. massive PE, tension pneumothorax, tamponade

28
Q

How can pulmonary oedema be sub divided?

A 
Cardiac and non cardiac
Non cardiac:
-ARDS
-Hypoalbuminaemia
-Iatrogenic fluid overload
-Smoke inhalation
29
Q

What are the signs a patient will present with in acute pulmonary oedema?

A 
SOB
Pink frothy sputum
Widespread crackles
Raised JVP
Decreased sats
gallop rhythm
30
Q

What is the acute management of a patient with acute heart failure and severe pulmonary oedema?

A

A-E
Sit patient up and start high flow oxygen if decreased sats
Take ABG
Attach to cardiac monitor, blood pressure and spO2 monitoring
Get IV access
Give diamorphine 2.5-5mg IV slowly and metoclopramide 10mg IV
Give furosemide 20-40mg by slow IV injection
If SBP >90 give GTN spray

31
Q

What investigations should be done for acute heart failure?

A 
ABG if breathless
FBC for anaemia
U and E, troponins, INR, BNP
ECG - look for ACS
CXR to look for oedema
echo for structual defects
32
Q

What is the management fo acute heart failure after the initial stage?

A

Daily weights - aim for reduction of 0.5kg/day, regular obs
Repeat cxr
Switch IV furosemide to oral
If on large doses of loop diuretics consider thiazide in addition e.g. bendoflumethiazide
ACE i should be added if LVEF <40%
Consider beta blocker
Consider K+ sparing spironolactone if hypokalaemic
Consider if patient suitable for biventricular pacing

33
Q

What are the 3 different types of AF?

A
  • Paroxysmal AF is self-terminating within 7 days, this can be recurrent
  • Persistent AF lasts >7 days and is not self-terminating, termination can be with cardioversion to sinus rhythm. This can degenerate into permanent AF
  • Permanent AF lasts >1 year and has not been terminated by cardioversion
34
Q

What is the first line treatment for atrial flutter?

A

Catheter ablation

If this fails can be rate controlled with beta blockers (Bisoprolol) or calcium channel blockers (verapamil)

35
Q

What are the causes of SVT?

A

AVNRT - commonest
AVRT
atrial tachycardia

36
Q

Which group of patients is adenosine contraindicated in?

A

Asthmatics as it causes bronchospasm

37
Q

What us wolff-parkinson-white?

A

This is an accessory pathway from the atria to ventricles that causes an antegrade AVRT
This must be treated promptly as it can degenerate into VF as all electrical activity is bypassing the AV node

38
Q

What are the ECG findings of WPW?

A

Short PR interval

Wide QRS with a slurred upstroke (delta wave)

39
Q

What are the two conditions that make up COPD?

A

Chronic bronchitis is clinical and is a chronic productive cough for three months of the year for the last 2 years
Emphysema is permanent enlargement of the airways distal to the terminal bronchioles

40
Q

What are the symptoms suggestive of COPD?

A

Exertional dyspnoea, chronic cough, regular sputum production, frequent chest infections, and wheeze
There should be exclusion of red flag symptoms such as weight loss, haemoptysis, ankle swelling, and PND

41
Q

How can dyspnoea be quantified in COPD?

A

The mrc dyspnoea scale
1
Not troubled by breathlessness except on strenuous exercise
2
Short of breath when hurrying or walking up a slight incline
3
Walk slowly on flat because of breathlessness
4
Stops for breath after a few minutes/100m on flat
5
Too breathless to leave the house/ breathless on dressing and undressing

42
Q

What are the signs of COPD?

A

Cachexia, hyper-inflated chest, pursed lip breathing, use of accessory muscles, paradoxical movement of lower ribs, reduced cricosternal distance
Wheeze, prolonged expiratory phase

43
Q

What are the spirometry results in COPD?

A

FEV1/FVC is less than 0.7 and FEV1 <80% predicted

44
Q

What are the main types of non small cell lung cancers?

A

Squamous cell carcinomas, generally more centrel, obstructive, local spread and show keratin formation
Adenocarcinomas are more peripheral, common in non smokers and invade the pleura and mediastinal nodes
Large cell carcinomas
Carcinoid tumours

45
Q

What are the parts that make up the TNM staging of lung cancers?

A

T involves the size and location of the tumour
N involves which nodes are infiltrated
M is whether there is metastatsis or not

46
Q

What are small cell lung cancers, how do they present?

A

These are derived from APUD endocrine cells and lead to undifferentiated, highly malignant tumours
Present with haemopysis, persistent cough, weight loss, dyspnoea etc.

47
Q

What is the treatment of lung cancer?

A

Can have surgery which is typically lobectomy
Radical radiotherapy can be used when surgery not possible
Will have hilar and mediastinal lymph node sampling for staging
Chemotherapy can be used in conjunction with surgery
In NSCLC usually gemcitabine
In SCLC usually cisplatin or carboplatin
If NSCLC have EGFR mutation then can use biological agents such as gefitanib

48
Q

What is the difference between adjuvant and neoadjuvant chemo?

A

Adjuvant is aiming to cure

neo adjuvant is aiming to shrink the tumour prior to survery or other curative options

49
Q

What kind of spirometry defect will interstitial lung disease show?

A

It causes loss of elasticity so causes a restrictive defect

50
Q

What medications can be used to slow the progression of idiopathic pulmonary fibrosis?

A

Acetylcysteine can be used

51
Q

How can most idiopathic interstitial pneumonias be treated?

A

With corticosteroids

52
Q

What sort of pneumonia is associated with target lesions (erythema multiforme)?

A

Mycoplasma pneumonia

AIP (19 decks)

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