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CardioResp Flashcards

1
Q

What is the 5-year survival rate for lung cancer?

A

13%

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2
Q

What are the risk factors for lung cancer?

A 
Smoking
Airflow obstruction
Increasing age
Family history
Carcinogens eg asbestos
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3
Q

What is the performance scale for lung cancer used for?

A

To indicate patient’s level of fitness, used when deciding treatment options

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4
Q

What staging is used for lung cancer?

A

TNM

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5
Q

What is the use of PET scanning in lung cancer?

A

Helps detect small mets not seen on staging CT

Used if patient is surgical candidate and initial CT suggests low stage

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6
Q

What are the 2 main histological types of lung cancer?

A

Small cell lung cancer

Non-small cell lung cancer

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7
Q

What are the different types of non-small cell lung cancer?

A

Squamous cell
Adenocarcinoma
Large cell carcinoma
Bronchoalveolar cancer

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8
Q

In what stages of lung cancer is surgery considered?

A

I and II (providing patient is fit for surgery)

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9
Q

What is the prognosis for small cell lung cancer?

A

Poor
Median survival if untreated is 4-12 weeks
Rapid growth
Almost always too extensive for surgery

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10
Q

What is the prognosis for non-small cell lung cancer?

A

Depends on stage

Stages I and II following resection 5y survival up to 70%

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11
Q

What proportion of lung cancer cases are in smokers or ex-smokers?

A

85%

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12
Q

What are the components of COPD?

A

Emphysema

Chronic bronchitis

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13
Q

What is emphysema?

A

Alveolar wall destruction causing irreversible enlargement of air spaces, distal to the terminal bronchioles

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14
Q

What are the causes of COPD?

A

Smoking
Alpha 1 antitrypsin deficiency
Industrial exposure eg soot

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15
Q

What is the most effective way of preventing COPD progression?

A

Smoking cessation

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16
Q

What are the aims of long term oxygen therapy in COPD?

A

Preventing renal and cardiac damage caused by long periods of hypoxia

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17
Q

How long does oxygen therapy need to be given for per day in order to provide survival benefit?

A

At least 16 hours per day

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18
Q

At what oxygen level is LTOT offered for COPD?

A

pO2 consistently below 7.3

Or below 8kPa with for pulmonale

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19
Q

What are the conditions for patients having LTOT?

A

Must be non-smokers

Must not retain high levels of CO2

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20
Q

What are the disadvantages of LTOT?

A

Loss of independence

Reduced activity

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21
Q

Why are pulmonary rehabilitation classes beneficial for COPD?

A

Prevent muscles weakening
Prevent increasing breathlessness
Increase livelihood
Prevent social isolation

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22
Q

What do pulmonary rehabilitation classes consist of?

A

Supervised exercise
Unsupervised home exercise
Nutritional advice
Disease education

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23
Q

What are the signs of an infective exacerbation of COPD?

A

Change in sputum colour or volume
Fever
Raised WCC and/or CRP

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24
Q

What nebs are given in a COPD exacerbation?

A

Salbutamol

Ipratropium

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25
Q

What steroids are used in COPD exacerbation?

A

Prednisolone 30mg stat

Once daily for 7 days

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26
Q

When are antibiotics indicated for COPD exacerbation?

A

Raised CRP/WCC

Purulent sputum

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27
Q

When is NIV considered for COPD exacerbation?

A

Type 2 resp failure

pH 7.25 - 7.35

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28
Q

When should you consider ITU referral for exacerbation of COPD?

A

pH less than 7.25

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29
Q

What does ABPA stand for?

A

Allergic Bronchopulmomary Aspergillosis

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30
Q

What are the modifiable risk factors for cardiovascular disease?

A

Smoking
Diabetes
Hypertension
Hyperlipidaemia

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31
Q

What is S1?

A

Closure of AV valves (mitral and tricuspid)

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32
Q

What is S2?

A

Closure of outflow valves (aortic and pulmonary)

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33
Q

In terms of heart sounds, when is systole?

A

After S1, before S2 starts

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34
Q

When is a 3rd heart sound normal?

A

Below age 30

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35
Q

What are the causes of S3 and S4 being heard?

A

Heart failure
MI
Cardiomyopathy
Hypertension

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36
Q

What is a murmur?

A

Sound produced by turbulent flow of blood through heart, especially over abnormal valves

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37
Q

What murmurs are louder on inspiration? Why?

A

Right-sided

Inspiration increases venous return to the right side of the heart

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38
Q

What is a thrill?

A

Palpable murmur

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39
Q

What are the causes of mitral stenosis?

A

Rheumatic fever
Old age
Calcification

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40
Q

What is the major association with mitral stenosis?

A

Atrial fibrillation - 60-70% of mitral stenosis patients

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41
Q

What is the murmur of mitral stenosis?

A

Mid-diastolic murmur ‘rumbling’

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42
Q

Where is mitral stenosis best heard?

A

With the bell
In apex
Patient lying on left side

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43
Q

How may mitral stenosis lead to right axis deviation on ECG?

A

High LA pressure due to stenosis AV valve on left (mitral)
Pulmonary venous HTN, leading to pulmonary arterial HTN
Right ventricular hypertrophy

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44
Q

How can mitral stenosis lead to right heart failure?

A

High LA pressure causing pulmonary HTN

Right ventricular hypertrophy leading to tricuspid regurgitation, and right heart failure

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45
Q

What is the murmur of mitral regurgitation?

A

Pansystolic - no gap between S1 and S2

Radiates to axilla

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46
Q

What are the causes of mitral regurgitation?

A 
Prolapsing mitral valve
Rheumatic mitral regurg
Papillary muscle rupture post-MI
Cardiomyopathy
Connective tissue disorders
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47
Q

What are the ECG signs of mitral regurgitation?

A

Bifid P waves

Left ventricular hypertrophy

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48
Q

What are the symptoms of aortic stenosis?

A

Exercise-induced syncope, angina and SOB

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49
Q

What is the murmur of aortic stenosis?

A

Ejection systolic

Radiates to carotids

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50
Q

What are the other signs of aortic stenosis on examination?

A

Slow-rising pulse

Low volume pulse

Forceful apex beat

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51
Q

Describe what you hear in aortic stenosis

A

Murmur loudest straight after S1

Audible gap before S2

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52
Q

What are the causes of aortic regurgitation?

A

Rheumatic fever
Bicuspid valve
Infective endocarditis

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53
Q

What does the pulse feel like in aortic regurgitation?

A

Collapsing - wide pulse pressure

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54
Q

What is the murmur of aortic regurgitation?

A

High-pitched early diastolic murmur
Best heard left sternal edge 4th IC space
Patient leaning forward with breath held in expiration

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55
Q

What are the 3 main causes of heart failure?

A

Ischaemic heart disease
Non-ischaemic dilated cardiomyopathy
Hypertension

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56
Q

What is the equation for cardiac output?

A

Cardiac output = stroke volume x heart rate

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57
Q

What is the end diastolic volume?

A

Volume of blood in a ventricle at the end of diastole

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58
Q

What is Starling’s law?

A

More blood entering the heart during diastole, the more blood is ejected during systolic contraction

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59
Q

What is the ejection fraction?

A

Fraction of blood pumped out of ventricles with each heart beat

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60
Q

Define pneumonia

A

LRTI with new consolidation on X-Ray

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61
Q

What is the most common organism causing community acquired pneumonia?

A

Streptococcus pneumoniae

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62
Q

What are the symptoms of an LRTI?

A 
Usually cough (new or changed in character)
Sputum production
Breathlessness
Wheeze
Chest pain
Fever
Sore throat
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63
Q

What clinical finding makes CAP likely?

A

Lung crackles

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64
Q

How may CAP present in elderly patients?

A

Confusion

Less likely to have fever

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65
Q

What is PUO?

A

Pyrexia of unknown origin

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66
Q

What 5 factors predict risk of death from pneumonia?

A 
Respiratory rate
Blood pressure
Confusion
Blood urea
Age over 65 years
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67
Q

What respiratory rate indicates severe pneumonia?

A

Over 30 per minute

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68
Q

How do you assess confusion in pneumonia?

A

Abbreviated mental test

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69
Q

What CURB-65 score indicates severe pneumonia?

A

3 or more

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70
Q

What do you do if a patient has a CURB-65 score of 2?

A

Use clinical judgement to decide if short inpatient stay required, or hospital supervised outpatient care

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71
Q

What potential complications of pneumonia may be seen on CXR?

A

Parapneumonic pleural effusion
Empyema
Lung abscess

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72
Q

What are the side effects of beta blockers?

A 
GI disturbances
Bradycardia
Fatigue
Cold peripheries
Heart failure
Hypotension
Dizziness
Sexual dysfunction
Peripheral vasoconstriction
Bronchospasm
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73
Q

Give three examples of beta blockers

A

Bisoprolol
Atenolol
Propranolol

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74
Q

What are the indications for beta blockers?

A

Hypertension
Angina
Following MI
Cardiac dysrhythmias e.g. AF

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75
Q

What are the contraindications to beta blockers?

A

Asthma
Marked bradycardia
Heart block
Hypotension

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76
Q

What are the three main processes responsible for asthma symptoms?

A

Bronchospasm
Smooth muscle hypertrophy
Mucus plugging

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77
Q

How do you calculate ejection fraction?

A

Stroke volume divided by end-diastolic volume

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78
Q

What is a normal ejection fraction?

A

Over 50%

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79
Q

What is REFHF?

A

Reduced ejection fraction heart failure

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80
Q

What is PEFHF?

A

Preserved ejection fraction heart failure

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81
Q

Give some differentials for bilateral leg swelling

A 
Drug reaction
Heart failure
Abdominal mass
Obesity
Renal failure
Liver failure
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82
Q

Give some differentials for unilateral leg swelling

A

DVT
Trauma
Cellulitis (infective)

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83
Q

What blood results would indicate hepatic congestion?

A

Hyperbilirubinaemia
Elevated transaminases
Hypoalbuminaemia

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84
Q

What is the most common cause of REFHF?

A

Ischaemia heart disease

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85
Q

What is the most common risk factor for PEFHF?

A

Hypertension

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86
Q

What are the risk factors for PEFHF?

A 
Diabetes
Hypertension
Obesity
Age
Renal impairment
Lung disease
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87
Q

What type of heart failure do arrhythmias commonly cause?

A

Right or left or congestive

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88
Q

What type of heart failure does obesity commonly cause?

A

Left PEFHF

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89
Q

Where do you feel for the character of the pulse?

A

Carotid ie blood leaving the heart

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90
Q

What does a collapsing pulse indicate?

A

Aortic regurgitation

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91
Q

What does a slow-rising pulse indicate?

A

Aortic stenosis

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92
Q

How should you determine the rate in AF?

A

Listen at the apex

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93
Q

What do you look for in the hands in CVS exam?

A 
Clubbing
Splinter haemorrhages
Tar staining
Koilonychia
Peripheral cyanosis

Do capillary refill!

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94
Q

What is a thrill?

A

Palpable murmur

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95
Q

What are the 4 main risk factors for IHD?

A

Smoking
Diabetes
Hypertension
Hypercholesterolaemia

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96
Q

Give a quick way of doing a systems review

A

Bowels OK?
Problems with water works?
Breathing problems?

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97
Q

Describe the typical pain caused by an MI

A

Dull, Central crushing pressure

Radiating to shoulder, arms or jaw

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98
Q

What is pleuritic chest pain?

A

Sharp
Worse on inspiration
Associated with shortness of breath

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99
Q

What is pericardial pain like?

A

Sharp

Improved by leaning forward

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100
Q

What is the pain of aortic dissection like?

A

Instant
Tearing
Inter scapular
May be retrosternal

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101
Q

What is musculoskeletal chest pain like?

A

Tender areas

Pain reproduced by movement

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102
Q

What is a Stoke-Adams attack?

A

Collapse without warning plus loss of consciousness for a few seconds
Usually due to third degree heart block

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103
Q

What features of syncope suggest a cardiac cause?

A

Chest pain, palpitations or shortness of breath before the event

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104
Q

What features of syncope suggest a CNS cause?

A

Aura
Headache
Dysarthria
Limb weakness

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105
Q

How does the recovery from a syncopal episode help diagnosis?

A

Cardiac - quick recovery

Seizure - prolonged drowsiness

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106
Q

What are the causes of slow palpitations?

A

Sick sinus syndrome
AV block
Occasional extrasystoles with compensatory pauses

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107
Q

What are the causes of increased stroke volume?

A

Valvular lesions

High-output states e.g. Anaemia, pregnancy, thyrotoxicosis

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108
Q

What are the causes of regular, rapid palpitations?

A

Sinus tachy
Atrial flutter
Atrial tachy
SVT re-entry tachy

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109
Q

What are the ECG signs of aortic stenosis?

A

P-mitrale

Left ventricular hypertrophy

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110
Q

What are the common bacterial causes of infective endocarditis?

A

Strep Viridans
Staph aureus or epidermis is
Enterococcus

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111
Q

What are the empirical antibiotics used for infective endocarditis?

A

Benzylpenicillin and gentamicin

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112
Q

What is the normal speed for ECG paper?

A

25mm/s

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113
Q

What does the T wave represent?

A

Ventricular depolarisation

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114
Q

What is the normal PR interval?

A

120-200ms

3-5 small squares

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115
Q

What is the normal QRS complex?

A

Less than 120ms

Ie 3 small squares

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116
Q

When is T wave inversion OK?

A

aVR

Isolated in lead III

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117
Q

How do you calculate rate from an ECG?

A

300 divided by RR interval (in large squares)

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118
Q

Which leads do you use to calculate the heart axis?

A

I and aVF

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119
Q

How do you check correct limb lead placement on an ECG?

A

Look at aVR - everything should be negative

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120
Q

What does atrial flutter look like on ECG?

A

Sawtooth P waves

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121
Q

What is the underlying rate in atrial flutter? Why is this not the true heart rate?

A

300

Too fast for AV node to conduct - there is either a 2:1, 3:1 or 4:1 block

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122
Q

What rates may be atrial flutter?

A

300
150
100
75

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123
Q

What is p-mitrale?

A

Left atrial enlargement

Bifid p waves

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124
Q

What is p-pulmonale?

A

Right atrial enlargement

Tall p waves

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125
Q

What does biatrial enlargement look like on ECG?

A

Tall and bifid p waves

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126
Q

When is 1st degree heart block significant?

A

PR >300ms
Another conducting disease is present eg BBB
IE with aortic valve involvement

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127
Q

What is Mobitz I?

A

Wenckebach
Progressive lengthening of PR interval until 1 QRS is dropped
P waves occur at constant rate

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128
Q

What is Mobitz II?

A

Intermittent failure of AV node to conduct atrial depolarisations to ventricles

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129
Q

What does complete heart block look like on ECG?

A

No relationship between p waves and QRS

Rate is slow, usually 30-50

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130
Q

What are the causes of complete heart block?

A

Coronary artery disease
Fibrosis of AV node or bundle of His
Drugs eg digoxin toxicity, diltiazem

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131
Q

What does a short PR interval indicate?

A

An accessory pathway

The impulse is not going through the AV node (where it would be delayed before reaching the ventricles)

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132
Q

What does right ventricular hypertrophy look like on ECG?

A

R wave > 5 mm in right ventricular leads

Plus right axis deviation

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133
Q

How can lead V1 be used to assess bundle branch block?

A

Major deflection up - Right BBB

Major deflection down - Left BBB

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134
Q

What are the principles of AF treatment?

A

Reduce thromboembolic risk
Control ventricular rate
Alleviate symptoms

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135
Q

How do you estimate stroke risk in AF?

A

CHADSVASc

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136
Q

What factors predispose to AF?

A 
Hypertension
Heart failure
IHD
Valvular heart disease
Thyroid disease
Excess alcohol
Drug misuse
Acutely unwell/periop
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137
Q

Define paroxysmal AF

A

Duration less than 7 days

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138
Q

Define persistent AF

A

Duration greater than 7 days

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139
Q

Define permanent AF

A

Duration greater than 7 days and resistant to therapy

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140
Q

What is the prevalence of AF?

A

1% general population

10% population over age 80

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141
Q

What is the rate in AF?

A

Can be fast or slow, depends on ventricular response

Irregularly irregular rhythm

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142
Q

Where do clots tend to form in AF?

A

Left atrial appendage

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143
Q

What is used for rate control in AF?

A

Beta blockers
Calcium channel blockers
Digoxin

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144
Q

Why is digoxin only used in sedentary patients?

A

It doesn’t allow the heart rate to rise physiologically

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145
Q

When is cardio version used in AF?

A

If acute AF is causing cardiovascular compromise

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146
Q

How can you reduce the frequency of episode of paroxysmal AF?

A 
Beta blockers
Class Ic (flecainide or propafenone)
Class III (amiodarone)
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147
Q

What is consolidation?

A

Replacement of alveolar air by fluid, cells, pus or other material

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148
Q

What is air bronchogram?

A

Air-filled bronchus surrounded by fluid-filled or solid alveoli

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149
Q

What is the clinical equivalent of air bronchogram?

A

Bronchial breathing

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150
Q

In what conditions do you get air bronchogram?

A

Consolidation eg pneumonia
Collapse
Pulmonary oedema

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151
Q

In acute asthma, what monitoring should be done?

A

Continuous pulse of, ECG and blood pressure

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152
Q

What is the medical management of acute asthma?

A 
Nebulised salbutamol 5mg (every 15-30min)
Oral prednisolone 40mg
Nebulised Ipratropium 0.5mg (4-6hrly)
IV magnesium sulfate
IV aminophylline (senior)
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153
Q

What are the main inflammatory cells involved in asthma?

A

Eosinophils and mast cells

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154
Q

What are the main inflammatory cells involved in COPD?

A

Neutrophils

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155
Q

What is the most effective bronchodilator in COPD?

A

Anticholinergics eg Ipratropium bromide

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156
Q

When is steroid treatment beneficial in COPD?

A

Acute exacerbation a

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157
Q

What is step 1 for asthma treatment?

A

Inhaled short acting beta 2 agonist PRN

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158
Q

What is step 2 of asthma management?

A

Add inhaled steroid 200-800mcg/day

Often start at 400mcg

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159
Q

What is step 3 of asthma management?

A
  1. Add long acting beta 2 agonist

2. Increase steroid dose up to 800mcg as appropriate

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160
Q

What is step 4 of asthma management?

A

Consider trial of…
A) increase steroid up to 2000mcg/day
B) add a 4th drug e.g. Leukotriene receptor antagonist, theophylline or beta 2 agonist tablet

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161
Q

When is step 5 of asthma management appropriate?

A

Continuous or frequent use of oral steroids

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162
Q

What is step 5 of asthma management?

A

Daily steroid tablet at lowest dose providing adequate control
Maintain high dose (2000mcg/day) inhaled steroid
Refer to specialist care

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163
Q

What are the common precipitating factors for asthma?

A 
Allergens
Viral infections
Occupational factors eg solder fumes, flour
Drugs eg beta blockers and NSAIDs
Others eg cold air, exercise, emotion
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164
Q

Define type 2 respiratory failure

A

PaO2 6.5kPa

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165
Q

What is the mechanism behind type 2 respiratory failure?

A

Ventilatory failure

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166
Q

What are the pulmonary causes of type 2 respiratory failure?

A 
COPD
Asthma
Fibrosis
OSA
Pneumonia
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167
Q

What may cause a decreased respiratory drive?

A

CNS trauma
Sedative drugs
Trauma

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168
Q

What neuromuscular problems can cause type 2 resp failure?

A

Cervical cord lesions
Guillain-Barre
Myasthenia gravis
Diaphragm paralysis

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169
Q

What is the underlying reason for type I respiratory failure?

A

V/Q mismatch

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170
Q

What are the causes of type I resp failure?

A

PE
Pulmonary oedema
Pneumonia
Acute severe asthma

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171
Q

When is CPAP used in type I resp failure?

A

When pO2 remains less than 8kPa despite 60% O2

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172
Q

What is the difference between CPAP and NIV?

A

CPAP is constant pressure and so not a form of ventilators support
NIV has 2 pressures (one inspiratory and one expiratory) and is a form of ventilatory support

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173
Q

What are the clinical features of hypoxia?

A

Cyanosis
Confusion
Restlessness and agitation
Shortness of breath

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174
Q

What are the clinical features of hypercapnia?

A 
Drowsiness
Tremor
Headache
Confusion
Peripheral vasodilatation
Papilloedema
Tachycardia
Bounding pulse
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175
Q

What are the risk factors for PE?

A 
Surgery
Obs: late pregnancy, C-section
Lower limb fracture
Varicose veins
Malignancy
Reduced mobility
Previous proven VTE
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176
Q

When is D dimer increased?

A 
Thrombosis
Inflammation
Post-op
Infection
Malignancy
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177
Q

What are the symptoms of PE?

A

Pleuritic chest pain
Shortness of breath
Haemoptysis

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178
Q

What are the ECG signs of PE?

A 
Sinus tachy
RV strain pattern in V1-3
Right axis deviation
RBBB
AF
Deep S wave in I
Q waves in III
Inverted T waves in III
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179
Q

What are the clinical signs of PE?

A 
Pyrexia
Cyanosis
Tachypnoea
Tachycardia
Hypotension
Raised JVP
Pleural rub
Pleural effusion
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180
Q

How do you manage a PE?

A 
ABCDE approach
Oxygen if hypoxia
Fluid rests if hypotensive
Morphine 5-10mg + metoclopramide 10mg
Thrombolysis if massive PE
HEPARIN: dalteparin 17,000units
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181
Q

When is thrombolysis considered for PE?

A

Hypotensive
Imminent cardiac arrest
Signs of R heart strain on CT/echo
Check for contraindications

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182
Q

What are the absolute contraindications to thrombolysis?

A

Hemorrhagic stroke/ischaemic stroke

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183
Q

What are the relative contraindications to thrombolysis?

A

Warfarin
Pregnancy
Advanced liver disease
Infective endocarditis

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184
Q

What are the complications of thrombolysis?

A 
Bleeding
Hypotension
Intracranial haemorrhage
Stroke
Reperfusion arrhythmias
Systemic embolisation/thrombus
Allergic reaction
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185
Q

What are the causes of pneumothorax?

A 
Spontaneous
Chronic lung disease
Infection
Traumatic
Carcinoma
Connective tissue disorders
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186
Q

What does a pneumothorax look like on CXR?

A

Area with no lung markings lateral to the edge of the collapsed lung

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187
Q

What are the symptoms of pneumothorax?

A

Asymptomatic
Sudden onset sob
Pleuritic chest pain
Sudden deterioration of chronic disease

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188
Q

What are the signs of pneumothorax?

A

Reduced expansion
Hyper-resonance to percussion
Diminished breath sounds
Deviation of trachea in tension pneumothorax

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189
Q

When should you aspirate a pneumothorax?

A

If SOB, and rim of air>2cm on CXR

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190
Q

How should you manage a secondary pneumothorax?

A

Chest drain if: SOB, >50y, rim of air >2cm on CXR

IF criteria not met, aspirate and admit for 24h

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191
Q

Why is tension pneumothorax a medical emergency?

A

Pushes the mediastinum into the opposite hemithorax which compresses the great veins
Leads to Cardiorespiratory arrest if the air is not removed quickly

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192
Q

How do you manage a tension pneumothorax?

A

Don’t delay with a CXR
Wide bore needle & syringe into 2nd IC space, midclavicular line
Remove plunger to allow trapped air to bubble through syringe, using saline as a water seal

Alternatively, large bore cannula in same location

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193
Q

What are Light’s criteria?

A

Used if protein in pleural effusion is 25-35g/L
It is an exudate if any 1 of the following are true:
Pleural fluid : serum protein ratio>0.5
Pleural fluid : serum LDH ratio>0.6
Pleural fluid LDH >2/3 upper limit of normal

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194
Q

What are the causes of an exudative pleural effusion?

A

Infection
Inflammation
Malignancy

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195
Q

What are the underlying causes of a transudative pleural effusion?

A

Raised venous pressure

Hypoproteinaemia

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196
Q

What are the causes of raised venous pressure?

A

Cardiac failure
Constrictive pericarditis
Fluid overload

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197
Q

What are the causes of Hypoproteinaemia?

A

Cirrhosis
Nephrotic syndrome
Malabsorption

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198
Q

What are the clinical signs of pleural effusion?

A 
Decreased expansion
Stony dull percussion
Reduced breath sounds
Bronchial breathing above effusion
Tracheal deviation
Signs of associated disease
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199
Q

What are the symptoms of pleural effusion?

A

May be none

May be SOB and have pleuritic chest pain

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200
Q

When is a chest drain indicated in pleural effusion?

A

If symptomatic

Don’t insert drain until the diagnosis is well-established

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201
Q

What are the signs of pleural effusion on CXR?

A

Blunting of costophrenic angles

Meniscus sign

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202
Q

Where should a pleural effusion be aspirated?

A

One or two IC spaces below the top of the effusion

Just above the upper rib border

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203
Q

What are the criteria for scoring pneumonia severity?

A

Confusion
Urea > 7mmol/L
Resp rate > 30
BP

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204
Q

What does clear and colourless sputum indicate?

A

Chronic bronchitis

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205
Q

What does yellow-green sputum indicate?

A

Pulmonary infection

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206
Q

What does red sputum indicate?

A

Haemoptysis

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207
Q

What does black sputum indicate?

A

Smoke or coal dust

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208
Q

What does frothy white-pink sputum indicate?

A

Pulmonary oedema

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209
Q

What are the three most common causative organisms in CAP?

A

Strep pneumoniae
Haemophilus influenzae
Mycoplasma pneumoniae

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210
Q

What are the three most common organisms causing hospital-acquired pneumonia?

A

Gram negative bacilli
Staph aureus
Pseudomonas
Klebsiella

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211
Q

What antibiotics are used to treat CAP?

A

Amoxicillin
Clarithromycin
Doxycycline

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212
Q

What are the symptoms of pneumonia?

A 
Fever
Rigors
Malaise
Anorexia
Dyspnoea
Cough
Purulent sputum
Haemoptysis
Pleuritic chest pain
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213
Q

What are the signs of pneumonia?

A 
Pyrexia
Cyanosis
Confusion
Tachypnoea
Tachycardia
Hypotension
Pleural rub
Consolidation: decreased expansion, dullness to percussion, increased tactile vocal fremitus, bronchial breathing
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214
Q

What are the clinical signs of consolidation?

A

Reduced chest expansion
Dullness to percussion
Increased tactile vocal fremitus
Bronchial breathing

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215
Q

What are the potential complications of pneumonia?

A 
Pleural effusion
Empyema
Lung abscess
Resp failure
Septicaemia
Brain abscess
Pericarditis
Myocarditis
Cholestatic jaundice
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216
Q

What is the prevalence of angina?

A

In over 55s:
Men 12%
Women 5%

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217
Q

Describe angina

A

Heavy/crushing central chest pain
Pain on exertion
Relieved by rest of GTN spray

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218
Q

What is CCS class I angina?

A

Angina only during strenuous or prolonged physical activity

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219
Q

What is CCS class 4 angina?

A

Inability to perform any activity without angina - angina at rest

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220
Q

What are the non-modifiable risk factors for ischaemic heart disease?

A

Age
Male
Family history
Personal history of IHD

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221
Q

What is primary prevention?

A

Control or reversal of risk factors to prevent disease occurring

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222
Q

What factors exacerbate angina?

A

Cold
Exertion
Large meals
Stress

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223
Q

Why can angina cause breathlessness?

A

Ischaemic may lead to LV systolic impairment
Causes increased pressure in pulmonary vasculature
Leads to SOB

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224
Q

What is stable angina?

A

Pain brought on by exertion and relieved by rest or GTN spray, within 10 minutes

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225
Q

What things would make you worry a patient’s angina was unstable?

A

Increase in severity or duration of symptoms

Reduction of threshold for symptoms

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226
Q

What functional tests are used for angina?

A

Exercise ECG
Perfusion scanning
Stress ECHO
Perfusion MRI

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227
Q

What symptomatic therapies are used for angina?

A

Nitrates
Calcium channel blockers
Potassium channel blockers

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228
Q

Give an example of a calcium channel blocker used for angina

A

Amlodipine

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229
Q

How do beta blockers work in angina?

A

Reduce sympathetic stimulation of myocardium and reduce work load

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230
Q

How does aspirin work?

A

Anti platelet

Reduces platelet function to prevent progression of atherosclerotic plaques

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231
Q

When is PCI used in angina?

A

For pain uncontrolled by medical therapy

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232
Q

Describe PCI

A

Balloon used to force open narrowed coronary artery lumen
Squeezes the fatty plaque to one side
A stent is inserted to keep the plaque in position and maintain the lumen

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233
Q

What vessel is used for CABG?

A

Long saphenous vein or

Internal mammary artery

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234
Q

What is the incidence of STEMI?

A

5 people per 1000 in the UK per year

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235
Q

Who is at increased risk of silent MI?

A

Elderly
Heart transplant patients
Diabetics

236
Q

What comprises acute coronary syndrome?

A

Unstable angina
NSTEMI
STEMI

237
Q

What is the pathogenesis of acute coronary syndrome?

A

Plaque becomes unstable
Fissures and exposes underlying plaque to flowing blood
Stimulates platelet aggregation and clotting cascade
Clot forms and acutely obstructs the artery
Sudden reduction in blood flow to myocardium

238
Q

What is the pathogenesis of MI?

A

When the ischaemia from a clot concluding a coronary artery is not reversed within 10 minutes, myocardial necrosis results (MI)

239
Q

Why does unstable angina require admission?

A

It is potentially pre-myocardial infarction

240
Q

What are the diagnostic criteria for MI?

A

Clinical history suggestive of ACS

Evidence of cardiac myocyte death - increase in serum troponin I or T

241
Q

Why do you do a CXR in ACS?

A

To excuse pulmonary oedema or aortic dissection

242
Q

What are the ECG findings during an MI?

A

Immediate: hyper acute T waves
ST elevation
T wave inversion
Pathological Q waves

243
Q

What leads does an anterior MI present in?

A

V1-4 (ST elevation)

244
Q

What vessel is affected if there is ST elevation in leads V1-4?

A

Left anterior descending

245
Q

What part of the myocardium is affected if there is ST elevation in leads V3 and 4?

A

Septal LV (LAD)

246
Q

What vessel is affected when the lateral LV is infarcted?

A

Left circumflex

247
Q

What leads would show a posterior MI?

248
Q

What leads show an infarction in the right ventricle? What artery is occluded?

249
Q

How do you differentiate between NSTEMI and unstable angina?

A

Cardiac bio markers raised in MI but not in unstable angina

Ie troponin I/T and CK

250
Q

What immediate medications are given for an NSTEMI?

A

Aspirin 300mg
Clopidogrel
LMWH
IV nitrates and opiates

251
Q

What secondary prevention is given for NSTEMI?

A

Statin
Beta blocker
ACE inhibitor

252
Q

Why is a STEMI more serious than an NSTEMI?

A

More likely to present with complications due to larger area of myocardium involved

253
Q

What is the mortality of STEMI?

A

4.4% for patients reaching hospital

30% of patients die before reaching hospital

254
Q

What is the immediate management of ACS?

A

Opiates (morphine 5mg + metoclopramide 10mg)
Nitrates
Aspirin 300mg
Oxygen via reservoir mask

255
Q

What oxygen therapy is unsuitable for COPD patients and why?

A

Reservoir mask
Simple face mask
High FiCO2 which is bad for patients who already retain CO2

256
Q

Define pulmonary hypertension

A

Mean systolic pressure in pulmonary artery >25mmHg at rest or >30mmHg during exercise

257
Q

What is the most common cause of primary pulmonary hypertension?

A

Pulmonary embolism

258
Q

What causes secondary pulmonary hypertension?

A

Gradual changes in pulmonary circulation as a result of chronic diseases of the lung or heart

Eg COPD or congestive cardiac failure

259
Q

Define cor pulmonale

A

When chronic hypoxic lung disease causes pulmonary hypertension and right heart failure

260
Q

What are the signs of cor pulmonale?

A 
Central cyanosis
Ankle oedema
Raised JVP
Atrial gallop rhythm
Loud pulmonary second sound
Tricuspid regurgitation
261
Q

What does a loud P2 indicate?

A

High pressure in the pulmonary artery causing forceful closure of the pulmonary valve

262
Q

Why may patients with cor pulmonale complain of chest pain?

A

Due to right ventricular hypertrophy which increased myocardial oxygen demand

263
Q

Why may cor pulmonale patients experience syncope?

A

Inability to increase cardiac output during exercise

264
Q

What are the signs of right ventricular hypertrophy?

A

Parasternal heave

265
Q

What are the signs of right heart failure?

A

Additional S3 - mid-diastolic gallop

S4 heart sound - pre-systolic gallop caused by a poorly compliant hypertrophied RV

266
Q

What are the clinical signs of tricuspid regurgitation?

A

Left para sternal pan systolic murmur
Visible S waves in JVP
Pulsatile hepatorenal you

267
Q

What is the only non-invasive test that can measure pulmonary arterial pressure?

268
Q

How do you take a history of syncope?

A 
FAINTS:
Frequency
Associated symptoms
Initiating events
Nature of recovery
Timing
Speed of onset
269
Q

Give a cause of cardiac syncope

A

LV outflow obstruction e.g. Aortic stenosis

270
Q

What is neurocardiogenic syncope?

A

A stimulus causes an abnormal autonomic reflex leading to hypotension, tachycardia or both
= Vasovagal

271
Q

Describe cardiac syncope

A

Sudden onset, rapid recovery
May be brought on by exercise
Associated with chest pain and palpitations

272
Q

What is the underlying pathophysiology of bradycardia?

A

Conditions reducing the automaticity or causing infiltration or fibrosis of the conduction tissues

273
Q

What is sinus node disease also called?

A

Sinus mode dysfunction

Sick sinus syndrome

274
Q

What arrhythmias can result from sick sinus syndrome?

A 
Sinus pauses
Sinus tachy or Brady
Atrial tachycardia
Chronotropic incompetence
Atrial fibrillation
275
Q

What is chronotropic incompetence?

A

Heart rate is normal at rest, but fails to rise in response to exercise or physiological stress

276
Q

What ECG factors indicate severity in complete heart block?

A

Slower ventricular escape rate
Broader QRS

Both mean the rhythm is more unstable

277
Q

What is Virchow’s triad?

A

Abnormality of vessel wall
Abnormality of blood components
Abnormality of blood flow

278
Q

What is the mechanism of action of warfarin?

A

Competitively antagonises reduction of oxidised Vit K

So vit K dependent clotting factors cannot be synthesised

279
Q

How can warfarin be reversed and why?

A

Vitamin K

Because warfarin is a competitive inhibitor, so can be displaced

280
Q

What are the vitamin K dependent clotting factors?

A

2, 7, 9 and 10

281
Q

Why does warfarin have a slow onset of action?

A

It takes time for the clotting factors already in the system to be removed

282
Q

Why does warfarin have to be stopped 3 days prior to any surgery?

A

It has a slow offset of action, as there has to be time for new clotting factors to be synthesised

283
Q

How is warfarin metabolised?

A

CYP450 system

284
Q

How is warfarin monitored?

A

INR

International normalised ratio - time taken for clotting compared to average for specific age and gender

285
Q

What is the target INR for warfarin therapy in AF?

286
Q

What is the target INR for warfarin therapy in mechanical prosthetic heart valves?

287
Q

What are the side-effects of warfarin?

A

Haemorrhage: GI, epistaxis, intracranial, excess bruising

Pregnancy - teratogenic

288
Q

How is warfarin reversed?

A

Vitamin K

Fast reversal: fresh frozen plasma (in emergency)

289
Q

What is the mechanism of action of heparin?

A

Acts on anti-thrombin III to inhibit thrombin and factor Xa

290
Q

How does unfractionated heparin work?

A

Binds to Anti-thrombin III

Inhibits thrombin AND factor Xa

291
Q

How does low molecular weight heparin work?

A

Inhibits only factor Xa (no inhibition of thrombin)

292
Q

Why is heparin never administered IM?

A

Would cause bleeding into the muscle

293
Q

Why is heparin administered IV or subcutaneously?

A

Poor GI absorption

294
Q

How is the dose and effect of heparin monitored?

A

APTT - activated partial thromboplastin time

295
Q

Why are LMWHs used for prophylaxis of VTE?

A

They are as effective as unfractionated, but have a lower risk of heparin-induced thrombocytopenia

296
Q

How is heparin used in treatment of VTE?

A

Initial management before warfarin to cover whilst warfarin loading is achieved

297
Q

Why is heparin preferred to warfarin during surgery?

A

Heparin has a quicker offset of action, so can be stopped quickly if severe haemorrhage occurs

298
Q

What are the side effects of heparin?

A

Haemorrhage eg intracranial, injection sites, GI, epistaxis

Heparin-induced thrombocytopenia

299
Q

How is heparin reversed?

A

Protamine sulfate

Causes dissociation of the heparin-AT III complex and binds irreversibly to heparin

300
Q

How does aspirin work?

A

It is a COX inhibitor and inhibits production of thromboxane A2 to prevent platelet aggregation

301
Q

What is the function of thromboxane A2?

A

Released from activated platelets to promote further platelet aggregation/vasoconstriction

302
Q

How does furosemide work in heart failure?

A

Reduces ECV to reduce oedema

Venodilatory effect to reduce after load on the heart

303
Q

What is the mechanism of action of furosemide?

A

Inhibits NKCC2 channel in thick ascending limb of loop of henle

304
Q

Why are thiazides used to prevent renal calculi?

A

They promote calcium reabsorption to limit calcium loss

305
Q

Give an example of a potassium sparing diuretic

306
Q

How does amiloride work?

A

Acts on ENaC in late DCT/CD
Prevents Na+ reabsorption
No effect on K+ reabsorption

307
Q

How does Spironolactone work?

A

Inhibits action of aldosterone on mineralocorticoid receptors
Reduces expression of Na+/K+-ATPase and ENaC

308
Q

What are the side effects of Spironolactone?

A

Hyperkalaemia

Gynaecomastia

309
Q

What are the indications for Spironolactone?

A

Heart failure
Hypertension
Liver failure
Conn’s syndrome

310
Q

What are the side effects of thiazides?

A

Gout

Erectile dysfunction

311
Q

Which diuretics interact with digoxin to cause hypokalaemia?

A

Thiazides

Loop diuretics

312
Q

Define diuretic resistance

A

Patient unable to meet their clinically required de congestive targets despite large doses of loop diuretics

313
Q

What drugs are potentially nephrotoxic?

A 
ACE inhibitors
Amino glycosides eg gentamicin
Penicillins
Ciclosporin A
Metformin
NSAIDs
314
Q

In a 40 year old Caucasian lady, what is the first step of anti-hypertensive therapy?

A

ACE inhibitor

315
Q

What is step 2 of anti-hypertensive therapy?

A

ACE inhibitor + calcium channel blocker
Or
ACE inhibitor + thiazides

316
Q

What is step 3 of anti-hypertensive therapy?

A

ACE inhibitor + calcium channel blocker + thiazide diuretic

317
Q

In a 40 year old Afro Caribbean lady, what is the first anti-hypertensive agent you would use?

A

Calcium channel blocker

Or thiazide diuretic

318
Q

What is the mechanism of action of losartan?

A

Angiotensin receptor blocker

Inhibits vasoconstriction and aldosterone stimulation

319
Q

Give 2 examples of dihydropyridines. What is their mechanism of action?

A

Nifedipine
Amlodipine
L-type calcium channel blockers mainly acting on peripheral vascular smooth muscle

320
Q

What are the side effects of dihydropyridines?

A

Sympathetic activation - tachycardia, palpitations, flushing, sweating, throbbing headache
Oedema
Gingival hyperplasia

321
Q

What is the mechanism of action of ramipril?

A

ACE inhibitor, preventing formation of angiotensin II

322
Q

What are the side effects of ramipril?

A

Dry cough
Angioedema
Renal failure
Hyperkalaemia

323
Q

What is the mechanism of action of verapamil?

A

Calcium channel blocker
Class IV anti-arrhythmic
Peripheral vasodilation, decreased cardiac preload and myocardial contractile th

324
Q

What are the side effects of verapamil?

A

Constipation
Risk of bradycardia
Can worsen heart failure due to decreased contractility

325
Q

What is the mechanism of action of doxasozin?

A

Alpha receptor blocker

Reduces contractile effects of noradrenaline on vascular smooth muscle to reduce TPR

326
Q

What are the side effects of doxasozin?

A 
Postural hypotension
Dizziness
Headache
Fatigue
Oedema
327
Q

How do calcium channel blockers affect the pacemaker potential?

A

Reduce calcium ion influx in upstroke of action potential

Blocking these channels means it takes longer to depolarise/reach peak

328
Q

How do beta agonists affect the cardiac pacemaker potential?

A

Increase slope of funny current

329
Q

How does adenosine affect the pacemaker potential?

A

Muscarinic agonist

Decreases slope of funny current to slow HR

330
Q

How do class I anti-arrhythmic agents work?

A

Sodium channel blockers
Bind to Na+ channels and inhibit AP propagation in myocytes
Affect phase 0 of depolarisation

331
Q

What are class II anti-arrhythmic agents?

A

Beta blockers

332
Q

What are the effects of beta blockers on the heart?

A

Negative chronotropic and inotropic

333
Q

What drug is used to treat WPW syndrome?

A

Flecainide

334
Q

Give an example of Class Ib anti-arrhythmics and its mechanism of action

A

Lidocaine
Used for acute VT and VF
Affects fast-beating/ischaemic tissue, as it is fast-binding/offset

335
Q

What are class III anti-arrhythmic agents?

A

Potassium channel blockers

336
Q

How does amiodarone work?

A 
Potassium channel blocker
Increases refractory period
Slows speed of AV conduction
Increases threshold for AP firing
Effective for most arrhythmias
337
Q

What is sotalol?

A

Potassium channel blocker

338
Q

What are class IV anti-arrhythmic agents?

A

Calcium channel blockers

Eg verapamil and diltiazem

339
Q

How does adenosine work?

A

Binds to A1 receptors in AVnode
Activates K+ currents in AV and SA nodes to hyper polarise cardiac tissue and decrease heart rate

Causes transient temporary heart block

340
Q

What is adenosine used to treat?

341
Q

How does digoxin work?

A

Enhances vagus nerve activity

Slows AV conduction and heart rate

342
Q

How does atropine work?

A

Selective muscarinic antagonist

Blocks bagel activity to speed AV conduction and heart rate

343
Q

What are the potential complications of pneumonia?

A 
Pleural effusion
Empyema
Lung abscess
Respiratory failure
Septicaemia
Brain abscess
Pericarditis
Myocarditis
Cholestatic jaundice
344
Q

Define COPD

A

Fixed airflow obstruction
Minimal or no reversibility with bronchodilators
Slowly progressive and irreversible deterioration in lung function, causing worsening symptoms

345
Q

What are the signs of COPD?

A 
Increased respiratory rate
Barrel chest
Pursed lip breathing
Quiet breath sounds and wheeze
Signs of cor pulmonale and CO2 retention
346
Q

Define mild COPD

A

FEV1 > 80% predicted

347
Q

Define moderate COPD

A

FEV1 50-80% predicted

348
Q

Define severe COPD

A

FEV1 30-49% predicted

349
Q

Define very severe COPD

350
Q

What is stage 1 on the MRC dyspnoea scale?

A

Only short of breath with strenuous exercise

351
Q

What is stage 3 on the MRC dyspnoea scale?

A

Walks slower than contemporaries or has to stop for breath on level ground

352
Q

What is stage 4 on the MRC dyspnoea scale?

A

Stops after 100 m or a few minutes

353
Q

What is stage 5 on the MRC dyspnoea scale?

A

Too breathless to leave the house or breathless when dressing

354
Q

What is the BODE grading for COPD?

A

BMI
Obstruction (FEV1)
Dyspnoea
Exercise capacity (6min walk distance)

355
Q

When are inhaled steroids indicated for COPD?

356
Q

How do steroids work in COPD?

A

Reduce frequency of exacerbations but don’t slow decline in lung function

357
Q

Name a mucolytic agent used in COPD

A

Carbocisteine

358
Q

How do you ensure you’ve got the correct diagnosis in COPD?

A

Use pulmonary function tests and chest x Ray to assess severity

Ensure there are no other causes for the symptoms

359
Q

What is the outcome of exacerbations in COPD?

A

Many don’t regain the lung function they had before the exacerbation
Frequent exacerbations cause a more rapid decline in lung function

360
Q

Define an acute exacerbation of COPD

A

Acute increase in symptoms beyond normal daily variation

361
Q

What are the common bacterial causes of COPD exacerbation?

A

H.influenzae
S.pneumoniae
Moraxella catarrhalis

362
Q

What are the common viral causes of COPD exacerbation?

A

Rhinovirus
Influenza
Coronavirus
Adenovirus

363
Q

What are the differential diagnoses to COPD exacerbation?

A

PE
Pneumothorax
Pulmonary oedema

364
Q

What are the symptoms of COPD exacerbation?

A

Increased cough/sputum production/purulence
Increased shortness of breath and wheeze
Chest tightness
Fluid retention

365
Q

How do you assess severity of an acute exacerbation of COPD?

A 
Resp rate
Sats
Air entry
Tachycardia
Peripheral perfusion and BP
Conscious level
Mental state
366
Q

What initial investigations would you order in a suspected acute exacerbation of COPD?

A

Blood gas
CXR
ECG
Blood: WCC, CRP, UEs, FBC etc

367
Q

What O2 therapy would you give in an acute exacerbation of COPD?

A

24-35% via a Venturi

Aiming for sats of 88-92%

368
Q

What nebs would you give in an acute exacerbation of COPD?

A

Salbutamol 2.5 - 5 mg

Ipratropium 500micrograms

369
Q

When do you use NIV in COPD exacerbation?

370
Q

When are antibiotics indicated in COPD exacerbation?

A

Purulent sputum
Pyrexia
Raised CRP
New changes on CXR

371
Q

When are oral steroids indicated for COPD exacerbation?

A

All exacerbations requiring admission, or if they are significantly more breathless than usual

372
Q

What steroids would you prescribe in COPD exacerbation?

A

Prednisolone 30mg per day for 1-2 weeks

373
Q

What are the side effects of aminophylline?

A

Tachycardia

Nausea

374
Q

What are the complications of COPD?

A 
Polycythaemia
Respiratory failure
Lung carcinoma
Cor pulmonale
Pneumothorax
Malnutrition
Depression
375
Q

What are the signs of COPD on chest X-Ray?

A 
Hyperinflation
Flat hemidiaphragms
Large central pulmonary arteries
Decreased peripheral vascular markings
Bullae
376
Q

What may the ECG show in COPD?

A

Right atrial and ventricular hypertrophy due to cor pulmonale

377
Q

What are the indications for surgery in COPD?

A

Recurrent pneumothorax
Isolated bulbous disease
Lung volume reduction surgery

378
Q

What conservative measures help in COPD?

A 
Smoking cessation
Exercise
Treat poor nutrition/obesity
Influenza and pneumococcal vaccination
Pulmonary rehabilitation
Palliative care
379
Q

What is symbicort made up of?

A

Budesonide and formoterol

380
Q

What are the majority of deaths in COPD patients due to?

A

Heart failure

381
Q

What are the clinical signs of cor pulmonale?

A 
Cyanosis
Tachycardia
Raised JVP
RV heave
Loud S2
Pansystolic murmur of tricuspid regurgitation
Hepatomegaly
Oedema
382
Q

What are the symptoms of cor pulmonale?

A

Dyspnoea
Fatigue
Syncope

383
Q

How does COPD cause cor pulmonale?

A

High pressure in pulmonary arterial system means RV has to work harder to push blood into pulmonary system
RV hypertrophied and eventually fails

384
Q

Which other lung diseases cause cor pulmonale?

A

Bronchiectasis
Pulmonary fibrosis
Severe chronic asthma
Lung resection

385
Q

What are the symptoms of pulmonary hypertension?

A 
Shortness of breath
Dizziness and fainting
Leg swelling
Fatigue
Non-productive cough
Angina
386
Q

How does pulmonary venous hypertension present?

A

Orthopnoea

Paroxysmal nocturnal dyspnoea

387
Q

What are the clinical signs of pulmonary hypertension?

A

Split S2
Loud S2 due to pulmonary valve closure
Right ventricular (para sternal) heave
Signs of systemic congestion due to right heart failure

388
Q

Describe the pathogenesis of pulmonary hypertension due to chronic lung disease

A

Hypoxic pulmonary vasoconstriction (initially a protective response aiming to direct blood away from damaged areas of lung not containing O2)
Widespread and prolonged damage means vasoconstriction occurs across a large portion of the pulmonary vascular bed

389
Q

What are the general clinical features of interstitial lung disease?

A 
Shortness of breath on exertion
Non-productive paroxysmal cough
Abnormal breath sounds
Abnormal CXR / HR CT
Restrictive spirometry
Low DLCO
390
Q

What are the pathological features of interstitial lung disease?

A

Fibrosis and remodelling of the interstitium
Chronic inflammation
Hyperplasia of type II epithelial cells/pneumocytes

391
Q

Why is gas transfer reduced in interstitial lung disease?

A

Scarring and thickening of tissue around alveoli makes it difficult for oxygen to diffuse into the blood

392
Q

What are the categories of causes of interstitial lung disease?

A

Occupational
Environmental
Systemic
Drugs

393
Q

What are the types of interstitial lung disease with no known cause?

A

Idiopathic pulmonary fibrosis (=usual interstitial pneumonia)
COP - cryptogenic organising pneumonia
LIP - lymphocytic interstitial pneumonia

394
Q

What are the general symptoms of interstitial lung disease?

A 
Dry cough
Exertional dyspnoea
Malaise
Weight loss
Arthralgia
395
Q

What are the classical clinical findings in interstitial lung disease?

A

Clubbing
Cyanosis
Reduced chest expansion
Fine inspiratory crepitations (like pulling Velcro)
May have features of pulmonary hypertension

396
Q

What is the commonest form of interstitial lung disease?

A

Idiopathic pulmonary fibrosis

397
Q

What are the complications of IPF?

A

Respiratory failure

Increased risk of lung cancer

398
Q

What is the management of IPF?

A 
Oxygen
Pulmonary rehabilitation
Opiates
Palliative care
Clinical trials? Lung transplant?
399
Q

What is the prognosis for IPF?

A

50% 5 years survival

400
Q

What is extrinsic allergic alveolitis?

A

= hypersensitivity pneumonitis

Hypersensitivity reaction to allergens inhaled

401
Q

What are the different types of extrinsic allergic alveolitis?

A

Acute

Chronic

402
Q

What are the symptoms of acute extrinsic allergic alveolitis?

A 
Fever
Rigors
Myalgia
Dry cough
Dyspnoea
Inspiratory crackles
403
Q

What is the management of acute EAA?

A

Remove allergen
Give 35-60% O2
Oral prednisolone 40mg/24hr

404
Q

What are the features of chronic EAA?

A

Increased SOB especially on exertion
Weight loss
Type I respiratory failure
Cor pulmonale

405
Q

What are the histological features of sarcoidosis?

A

Non-caseating granulomas

406
Q

Define bronchiectasis

A

Abnormal dilation of the bronchi

407
Q

What are the common pathogens in mild bronchiectasis?

A

H.influenzae
S.pneumoniae
M.catarrhalis
S.aureus

408
Q

What organism is commonly involved in moderate bronchiectasis?

A

Pseudomonas aeruginosa

409
Q

What is the most common cause of bronchiectasis?

A

Idiopathic

410
Q

What proportion of cases of bronchiectasis are caused by airways inflammation?

A

25%

Eg COPD, ABPA, RA

411
Q

Why do bacteria colonise the lungs in bronchiectasis?

A

Bronchial dilation and epithelial damage disrupts mucociliary clearance

412
Q

Why do patients develop purulent phlegm in bronchiectasis?

A

Chronic bacterial infection leads to neutrophil if inflammatory response
Causes increased mucus production and purulent phlegm

413
Q

Why do patients with severe bronchiectasis get airway obstruction?

A

Inflammation of bronchi also spreads to small airways

414
Q

What are the classic clinical features of bronchiectasis?

A

Cough

Daily sputum production

415
Q

What are the additional symptoms of bronchiectasis?

A 
Minor haemoptysis
Malodorous breath
Malaise
Fatigue
Shortness of breath on exertion
Wheeze
MSK-type chest pain
416
Q

What are the clinical signs of bronchiectasis?

A

Finger clubbing
Focal creps, usually bi basal
Signs of airway obstruction in severe disease

417
Q

What does CT scanning show in bronchiectasis?

A

Bronchial dilatation - to a width greater than that of the accompanying vessel
Bronchial wall thickening

418
Q

What further investigations (after CT diagnosis) are required in bronchiectasis?

A

Pulmonary function testing
Sputum culture
Specific tests for potential causes eg IgG levels

419
Q

What are the management principles for bronchiectasis?

A

Identify and treat the cause
Improve QoL by minimising sputum production and reducing exacerbation frequency
Maintain/improve pulmonary function

420
Q

How is pulmonary function maintained in bronchiectasis?

A

Minimise active chronic infection
Reduce frequency and severity of exacerbations
Regular bronchodilator use

421
Q

How can sputum production and frequency of exacerbations be reduced in bronchiectasis?

A

Self-administered lung clearance techniques
Prolonged ABx course to effectively treat exacerbation
Oral/nebulised prophylactic ABx for severe disease
Long-term azithromycin

422
Q

What are the effects of long-term azithromycin in bronchiectasis?

A

Anti-inflammatory effects

Very effective in reducing sputum production and exacerbation frequency

423
Q

What percentage of patients die from their bronchiectasis?

424
Q

What is the incidence of cystic fibrosis?

A

1 in 2000-3000 newborns

425
Q

What is the genetic defect in cystic fibrosis?

A

Autosomal recessive in CFTR gene

426
Q

What does the CFTR gene code for?

A

Transmembrane chloride channel,found in respiratory epithelium, expiring glands and sweat ducts

427
Q

What happens when the CFTR gene is not working properly?

A

Chloride ion flow across membranes is impaired
Means sodium and water don’t move out of the cell
Mucus is inadequately hydrated, forming thick sticky mucus

428
Q

What are the clinical features of cystic fibrosis?

A

Chronic phlegm production and recurrent infective exacerbations

429
Q

What characteristics of cystic fibrosis are different to non-CF bronchiectasis?

A

Usually starts in early childhood
Worse in lung apices
Almost always results in fatal respiratory failure due to severe airways obstruction

430
Q

What are the signs of cystic fibrosis?

A 
Clubbing
Low BMI
Extensive crepitations in both lungs
Obvious signs of airways obstruction
Poor respiratory function
431
Q

What are the extra-pulmonary complications of cystic fibrosis?

A

Pancreatic insufficiency
Chronic sinusitis
Infertility
Abnormal LFTs

432
Q

What is the diagnostic test for cystic fibrosis?

A

Measure sweat chloride concentration - increased in CF

433
Q

What are the main principles for cystic fibrosis management?

A

Regular Physio supported by chest clearance devices
Frequent antibiotics for bronchial infections
Regular use of inhaled beta agonists

434
Q

What prophylactic therapy is used in cystic fibrosis?

A

Flucloxacillin and azithromycin

435
Q

What is the median age of death in cystic fibrosis?

436
Q

What is the medical management of anaphylaxis?

A

High-flow O2
0.5mg adrenaline IM - every 5mins until CVS stable
200mg hydrocortisone IV
10mg chlorpheniramine IV

Salbutamol and adrenaline nebs as required for bronchospasm and laryngeal oedema respectively

437
Q

What are the features of anaphylaxis?

A 
Pruritis
Urticaria
Angioedema
Hoarseness
Stridor
Wheeze
438
Q

What medications are given for an acute asthma attack?

A

5mg salbutamol nebs
40mg prednisolone PO
Ipratropium bromide 500ug neb if severe

IV aminophylline if life-threatening

439
Q

How do you manage an exacerbation of COPD?

A

O2 via Venturi
Nebs: salbutamol and Ipratropium
Prednisolone 30mg stat and OD for 7 days

ABx if raised WCC/CRP or purulent sputum
Consider IV aminophylline

440
Q

When is NIV indicated in exacerbation of COPD?

A

If type 2 respiratory failure and pH 7.25-7.35

441
Q

Define massive haemoptysis

A

> 240ml in 24hrs

>100ml/day for consecutive days

442
Q

How do you manage massive haemoptysis?

A

Lie patient on side of suspected lesion
Oral tranexamic acid for 5 days
Stop NSAIDs, aspirin and anticoagulants
Consider vit K

443
Q

Name a long-acting anti muscarinic agent

A

Tiotropium

444
Q

What are the ADRs of antimuscarinics?

A

Dry mouth
Constipation
Cough
Headache

445
Q

Name 2 xanthines

A

Aminophylline

Theophylline

446
Q

How do xanthines work?

A

Block phosphodiesterases to decrease cAMP breakdown and cause bronchodilation
Also have positive chronotropic and inotropic effects, and a diuretic action

447
Q

What are the side effects of aminophylline?

A 
Headache
GI upset
Reflux
Palpitations
Dizziness
448
Q

What is the therapeutic window of theophylline?

449
Q

What are the toxic effects of aminophylline?

A

Serious arrhythmias
Seizures
Nausea and vomiting
Hypotension

450
Q

Give 3 examples of inhaled glucocorticoids

A

Beclomethasone
Budesonide
Fluticasone

451
Q

What are the side effects of inhaled steroids?

A

Cough
Oral thrush
Unpleasant taste
Hoarse voice

452
Q

Give some side effects of systemic steroid use

A 
Hyperglycaemia
Psychosis
Insomnia
Indigestion
Mood swings
Diabetes
Osteoporosis
Muscle wasting
Skin thinning
Cushingoid appearance
453
Q

Give 2 examples of long-acting beta agonists

A

Formoterol

Salmeterol

454
Q

What are the side effects of beta agonists?

A 
Tremor
Headache
GI upset
Palpitations
Tachycardia
Hypokalaemia
455
Q

Give 2 examples of short-acting beta agonists

A

Salbutamol

Terbutaline

456
Q

What questions do you need to ask about a cough?

A 
Dry vs productive
Triggers and relieving factors
Associated with eating/dyspepsia
Positional
Nasal secretions
Fever
457
Q

What questions do you need to ask about shortness of breath?

A 
Exercise tolerance
Triggers/relieving factors
Diurnal variation
Orthopnoea
PND
458
Q

What are the presenting complaints for respiratory?

A 
Shortness of breath
Chest pain
Wheeze
Cough
Sputum
Haemoptysis
459
Q

What social history do you need to include in a respiratory history?

A 
Smoking
Occupation
Pets
Recent foreign travel
Immobility
Activities of daily living
Alcohol
460
Q

Why can RBBB cause either LAD or RAD?

A

The LBB contains anterior and posterior fascicles which can both conduct action potentials

461
Q

What do ventricular escape rhythms look like?

A

Broad QRS because the impulse has to travel further, ie not via the usual fast conducting system

462
Q

What does a regular rhythm in AF mean?

A

There is an escape rhythm, due to complete heart block (none of the atrial depolarisations are being conducted through to the ventricles)

463
Q

What causes ST elevation?

A

Acute MI

Pericarditis

464
Q

What causes ST depression?

465
Q

Which is a better indicator of coronary artery disease: horizontal ST depression or down-sloping?

A

Down-sloping: 90% have CAD

Horizontal: 82% have CAD

466
Q

What is the normal length of the QRS complex?

467
Q

How do you calculate QTc?

A

QT(ms) / square root of RR (s)

468
Q

What do delta waves signify?

A

There is an extra circuit conducting electrical signals from the atria to the ventricles

469
Q

How can AF lead to sudden death?

A

Superconductor, so an extra circuit conducts signals from the atria to the ventricles
Eg WPW

470
Q

What are torsades de pointes?

A

A form of polymorphic VT

The depolarisation is twisting on its electrical axis

471
Q

What are the causes of a regular tachycardia with broad QRS complexes?

A

VT
SVT with aberrancy or BBB
WPW antidromic

472
Q

What are the causes of an irregular tachycardia with broad QRS complexes?

A

VF
Polymorphic VT
Torsades
Pre-excited AF

473
Q

What are the causes of an irregular tachycardia with narrow QRS complexes?

474
Q

How do you treat tachycardia?

A

Carotid sinus massage

Valsalva manoeuvre

475
Q

What are the hallmarks of ventricular tachycardia?

A
  1. VA dissociation
  2. Capture beat
  3. Fusion beat
476
Q

What are capture beats?

A

A narrower beat than the broad-complex VT that’s going on elsewhere

477
Q

What are fusion beats?

A

Not as broad/narrow as others. Happen when VT is colliding with the sinus beat

478
Q

What are the ECG features of Wolff-Parkinson White syndrome?

A

Delta waves

Short PR interval

479
Q

What are the non-cardiac causes of bradycardia?

A 
Sleep
Athletic training
Beta blockers
Amiodarone
Hypothyroidism
Hypothermia
Deranged potassium/calcium/magnesium/sodium
OSA
480
Q

What are the cardiac causes of bradycardia?

A

Sinus node disease (sick sinus syndrome)
Heart block
Atrial fibrillation
Chronotropic incompetence

481
Q

How is Mobitz II treated?

A

Permanent pacemaker if symptomatic

482
Q

What does complete heart block look like on ECG?

A

Regular p waves
Regular QRS
But no association between the two

483
Q

What are the symptoms of bradycardia?

A 
Palpitations
Light headedness
Dizziness
Collapse
Syncope
484
Q

What is the management of bradycardia causing acute cardiac instability?

A

Transcutaneous pacing (pads)
Transvenous temporary pacing
IV drug infusion eg atropine

485
Q

What is automaticity?

A

All cells in the heart are able to regularly produce an action potential
Some are more inclined to do so than others (eg SA node)

486
Q

What does a narrow complex tachycardia indicate?

A

Supra ventricular tachycardia (SVT)

487
Q

What is the most common form of SVT?

A

AVNRT - atrioventricular nodal re-entry tachycardia

488
Q

What symptoms can tachycardia cause?

A 
Palpitations
Shortness of breath
Fatigue
Ischaemic chest pain
Low BP
489
Q

What are the vagal manoeuvres used to treat tachycardia?

A

Valsalva manoeuvre

Carotid sinus massage

490
Q

What medication is used to treat tachycardia?

A

Beta blockers

Calcium channel blockers

491
Q

What drugs are used to treat tachycardia in WPW?

A

Flecainide

Amiodarone

492
Q

Why is ventricular tachycardia more malignant than SVT?

A

It can cause VF which can lead to cardiac arrest and death

493
Q

What does VT look like on ECG?

A

Regular broad complex tachycardia
VA dissociation
Capture and fusion beats

494
Q

What are the causes of torsades de pointes?

A 
Long QT syndrome
Hypokalaemia
Hypomagnaesemia
Amiodarone
Erythromycin
Methadone
495
Q

How is VT classified?

A

Pulsed vs pulse less
Sustained (>30s)
Mono- or polymorphic (QRS appearance consistent or changing?)

496
Q

What are the symptoms of VT?

A

Palpitations
Syncope
Symptoms of heart failure in sustained VT

497
Q

What is AV dissociation?

A

Regular P waves and regular QRS complexes, but at different rates

498
Q

When is emergency synchronised DCCV indicated in VT?

A

Any patient whose condition is compromised eg hypotension or ischaemia

499
Q

What drugs are used to treat VT?

A

Amiodarone

Beta blockers

500
Q

How do ICDs work?

A

Don’t reduce the frequency of ventricular arrhythmia, but restore sinus rhythm if arrhythmia occurs

501
Q

What is the myocardium doing in ventricular fibrillation?

A

There is no coordinated electrical or mechanical activity, so there is no cardiac output

502
Q

Why is VF so dangerous?

A

There is no cardiac output and it always results in cardiac arrest

503
Q

What are the components of CHADS-VASc?

A 
Coronary failure
Hypertension
Age > 75 (2 points)
Diabetes
Previous Stroke or TIA
Vascular disease
Age 65-74
Sex female
504
Q

What is used to control rate in AF?

A

Beta blockers
Calcium channel blockers
Digoxin

505
Q

Who is digoxin prescribed for and why?

A

Sedentary patients

Doesn’t allow the heart rate to rise physiologically

506
Q

Why are the conditions for DCCV in AF strict?

A

Risk of inducing stroke

507
Q

What drugs can be used to reduce the frequency of paroxysmal AF?

A

Beta blockers
Class Ic drugs eg flecainide
Class III drugs eg amiodarone

508
Q

What is decubitus angina?

A

Angina precipitated by lying flat

509
Q

Define angina

A

Central chest tightness or heaviness

Brought on by exertion and relieved by rest

510
Q

What symptoms are associated with angina?

A

Shortness of breath
Nausea
Sweatiness
Fatigue

511
Q

What is the medical management of angina?

A

Aspirin
Beta blockers
Nitrates
Long-acting calcium antagonists eg amlodipine 10mg OD

K+ channel activator if still not controlled eg nicorandil

512
Q

What nitrate prophylaxis may be prescribed in angina?

A

Isosorbide mononitrate 20-40mg BD

513
Q

How effective is aspirin in angina?

A

Decreases mortality by 34%

514
Q

Define an acute MI

A 
Increase then decrease in cardiac biomarkers plus either...
A) symptoms of ischaemia
B) ECG changes of new ischaemia
C) development of pathological Q waves
D) loss of myocardium on imaging
515
Q

What is the initial management of ACS?

A 
Airway Breathing Circulation
IV access
12-lead ECG
Give:
Oxygen
Nitrates
Aspirin
Morphine + anti-emetic
516
Q

When does cardiac troponin peak during an MI?

517
Q

What is the target level for cholesterol?

A

Total cholesterol

518
Q

When is treatment indicated for hypercholesterolaemia?

A

High CVS risk (smoker, HTN, gender)
Not responsive to conservative measures
Familial hypercholesterolaemia
Coronary, carotid or peripheral artery disease

519
Q

What is the 1st line lipid-lowering therapy?

520
Q

How do statins work?

A

HMG-CoA reductive inhibitors - this enzyme is responsible for cholesterol synthesis

521
Q

Why are statins taken at night?

A

Most cholesterol synthesis occurs overnight, so they have greater effect

522
Q

What are the side effects of statins?

A 
Indigestion
Headache
Diarrhoea
Insomnia
Liver injury
Myalgia, myosotis, myopathy
Rhabdomyolysis
523
Q

What are the contraindications to statins?

A

Severe liver or renal disease
Myopathy
Pregnancy or breast-feeding

524
Q

What are the second line lipid-lowering agents?

525
Q

How do fibrates work?

A

Increase lipoprotein lipase activity by activating PPAR

Increases lipid metabolism and lowers LDL and triglycerides

526
Q

What are the side effects of fibrates?

A

Indigestion
Myosotis
Rash
Anaemia

527
Q

How does ezetimibe work?

A

Brush border lipase inhibitor

Inhibits uptake of dietary cholesterol from the gut at the brush border epithelium, so reducing plasma LDL levels

528
Q

How does colestyramine work?

A

Bile acid sequestrant - combines with bile acids in intestines to cause them to be excreted in faeces
Increases oxidation of cholesterol to form bile acids, increasing the activity of HMG-CoA reductase to reduce circulating LDL

529
Q

What are the side effects of colestyramine?

A

Itching
Diarrhoea
Abdominal pain
Constipation

530
Q

How does heart failure present?

A 
Shortness of breath
Fatigue and weakness
Nocturia
Cough
Epi gastric discomfort
Anorexia
531
Q

What are the causes of shortness of breath in heart failure?

A

Pulmonary oedema
Impaired skeletal muscle function
Depressed respiratory muscle function
Reduced lung function

532
Q

What different types of dyspnoea can heart failure present with?

A

Exertional shortness of breath
Orthopnoea
Paroxysmal nocturnal dyspnoea

533
Q

Explain the process of orthopnoea in heart failure

A

Central blood volume increases when the patient is lying flat, which the failing heart can’t cope with, leading to pulmonary oedema

534
Q

What is NYHA Class I?

A

Asymptomatic during normal activity

535
Q

What is NYHA Class II?

A

Mild symptoms during normal activity

536
Q

What is NYHA Class III?

A

Marked limitation to normal activity, comfortable only at rest

537
Q

What is NYHA Class IV?

A

Symptoms at rest

538
Q

Why may patients get a cough with pink, frothy sputum in heart failure?

A

Pulmonary oedema

539
Q

Why may patients get a dry, nocturnal cough in heart failure?

A

Bronchial oedema/cardiac asthma

540
Q

What does the pulse feel like in heart failure?

A

Rapid, weak and thready

541
Q

What does palpation of the chest reveal in heart failure?

A

LV enlargement causing a downward and laterally displaced apex beat
Diffuse apex beat indicates severe LV dysfunction

542
Q

What does the heart sound like in heart failure?

A

Gallop rhythm - 3rd heart sound and tachycardia

543
Q

What valvular lesion can heart failure cause?

A 
Mitral regurgitation (functional)
Due to LV dysfunction
544
Q

What are the signs of heart failure on chest X-Ray?

A 
Alveolar oedema
Kerry B lines
Cardiomegaly
Dilated prominent upper lobe vessels
Pleural Effusion
545
Q

What is the conservative management of heart failure?

A 
Low level exercise
Low salt diet
Smoking cessation
Education
Vaccination
546
Q

What are the main drugs used in heart failure?

A

Diuretics - furosemide
ACE inhibitors
Beta blockers
Spironolactone

547
Q

What dose of furosemide should you start at in heart failure?

A

40mg

Titrate up as needed

548
Q

Why are beta blockers used in heart failure?

A

Catecholamine levels are high in heart failure (sympathetic activation)

549
Q

How can the patient help decide how effective diuretics are in heart failure?

A

Monitor their own weight and degree of breathlessness

550
Q

How does weight help decide diuretic dose in heart failure?

A

Weight gain - increase dose

Weight loss - decrease dose

551
Q

How do nitrates work in heat failure?

A

Veno- and arteriolar dilators so reduce load on the heart

552
Q

How does digoxin work?

A

Cardiac glycoside
Inhibits sodium-potassium pump in sarcolemma cell membranes to reduce calcium transport out of the cell
Digoxin thus increases intracellular calcium and is positively inotropic
At AV node: increased calcium prolongs refractory period to decrease AV node conduction and is negative chronotropic

553
Q

What are the signs of digoxin toxicity?

A

Bradycardia, AV block or sinus arrest
Nausea and vomiting
Xanthopsia

554
Q

When are bi ventricular devices indicated for heart failure?

A

Class III or IV

Ejection fraction

555
Q

What 4 processes can lead to pulmonary oedema?

A

Increased afterload (raised LA pressure)
Increased preload (too much fluid)
Decreased oncotic pressure
Leaky vessels

556
Q

What is the most common cause of increased LA pressure?

A

LV diastolic failure

557
Q

What are the causes of raised LA pressure?

A 
LV diastolic or systolic failure
Hypertension
Aortic stenosis
Mitral regurgitation
Mitral stenosis
Aortic regurgitation
Atrial fibrillation
VT
Left atrial myxoma
558
Q

How does malignant hypertension present?

A

One of…
A) pulmonary oedema
B) papilloedema
C) stroke

559
Q

What are the causes of malignant hypertension?

A

Phaeochromocytoma
Conn’s syndrome
Cushing’s syndrome

560
Q

Why are beta blockers useful in angina?

A

Slowing the heart rate makes diastole longer, giving more time for the coronary arteries to be perfused and hence reducing the ischaemia

561
Q

How do IABPs work?

A
  1. Suddenly deflates at the beginning of systole to decrease the afterload and increase cardiac output
  2. Beginning of diastole: inflates and increases coronary perfusion
562
Q

How do you treat acute pulmonary oedema?

A 
O2 60-100%
Furosemide 80mg IV
Morphine 5-10mg IV
Metoclopramide 10mg IV
Nitrates: GTN or buccal
CPAP
563
Q

How does CPAP work in acute pulmonary oedema?

A

Increases pressure in alveoli to force water out

Works quickly and is safe

564
Q

How do morphine and metoclopramide work in pulmonary oedema?

A

Anxiolytics - decrease the sympathetic drive

565
Q

When should you NOT give nitrates?

A

Severe aortic stenosis - further decreases the blood pressure and can kill!

566
Q

What is the typical presentation of acute pulmonary oedema?

A 
Pale
Increased resp rate
Sat up
Tachycardic
Hypertensive
Sats 95%
Clammy, distressed and sweaty
567
Q

Why is preload increased in heart failure?

A

Sodium and water retention leading to increased ECV

568
Q

Describe the ‘vicious cycle’ of the physiological response to heart failure

A

Decreased cardiac output leads to activation of RAAS and the sympathetic nervous system
This causes sodium and water retention, and vasoconstriction, further increasing the work load of the heart causing it to fail even more

569
Q

What are the causes of right heart failure?

A

Chronic lung disease
PE or pulmonary hypertension
Tricuspid or pulmonary valve disease

570
Q

What are the signs of right heart failure?

A 
Increased JVP
Cardiomegaly
Hepatic enlargement
Ascites
Dependent pitting oedema
571
Q

What are the signs of left heart failure?

A 
Displaced apex beat
Gallop rhythm
Mitral regurgitation features
Basal lung crackles
Pitting oedema
572
Q

What is the leading cause of sudden cardiac death in young people?

A

Hypertrophic cardiomyopathy

573
Q

What is the inheritance of hypertrophic cardiomyopathy?

A

Autosomal dominant

574
Q

What are the poor prognostic factors for hypertrophic cardiomyopathy?

A

Younger than 14y or syncope at presentation

Family history of HCM or sudden cardiac death

575
Q

What is dilated cardiomyopathy associated with?

A 
Alcohol
Hypertension
Haemochromatosis
Viral infection
Autoimmune
Peri or post-party's
Thyrotoxicosis
Congenital
576
Q

What are the causes of pericarditis?

A

Viruses, bacteria, fungi
MI
Drugs eg penicillin, isoniazid
Uraemia, RA, SLE

577
Q

How does pericarditis present?

A

Central chest pain worse on inspiration or lying flat
Relieved by sitting forward
Pericardial friction rub

578
Q

What does the ECG look like in pericarditis?

A

Concave/saddle-shaped ST elevation

579
Q

How do you treat pericarditis?

A

Analgesia and treat cause

580
Q

Define pericardial effusion

A

Fluid accumulation in the pericardial sac

581
Q

Define constrictive pericarditis

A

When the heart is encased in a rigid pericardium, preventing it from contracting properly

582
Q

What is the purpose of pericardiocentesis?

A

Diagnostic or therapeutic

583
Q

Define cardiac tamponade

A

Accumulation of pericardial fluid causing raised intrapericardial pressure leading to poor ventricular filling and a fall in cardiac output

584
Q

What are the causes of cardiac tamponade?

A 
Anything causing pericarditis
Aortic dissection
Haemodialysis
Warfarin
Cardiac catheterisation
Post-cardiac biopsy
585
Q

What is Beck’s triad?

A

Signs of cardiac tamponade:

  1. Falling BP
  2. Rising JVP
  3. Muffled heart sounds
586
Q

What does echo show in cardiac tamponade?

A

Echo-free zone around the heart of > 2cm or > 1cm if acute

Phase 2 (21 decks)

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