CardioResp Flashcards
1
Q
6 key cardiology symptoms
A
Plapitations Chest Pain SOB Orthopnea Ankle swelling/ oedema Syncope/ dizziness
2
Q
Describe the NYHA Heart Failure Classification system
A
1-4 1 = no limitation 2= mild PA limitation (mild HF) 3= marked PA limitation (moderate HF) 4= symptoms at rest (severe HF)
3
Q
Final part of cardiology history?
A
System view e.g. just Bowel and water works Anything i missed? What have you been told so far? ICE
4
Q
Cause of third heart sound? describe sound
A
a-stiff-wall
lub dub dee
5
Q
Cause of forth heart sound? describe
A
Slosh-ing-in
Dilation
Low pitched
6
Q
Causes of third and forth heart sound
A
Both caused by HF MI Cardiomyopathy Hypertension
7
Q
Grading of murmurs describe
A
1-6 (last three with a thrill) 1- barely audible 2 soft 3 heard easily 4 loud with thrill 5 very loud with thrill, may be heard with streph partially off 6 same as 5
8
Q
Causes of mitral stenosis
A
Rheumatic fever (chorea) in 50% Age and calcification
9
Q
Signs of mitral stenosis
A
Pulmonary oedema signs
AF (highly associated due to atrial changes)
RHF late
Malar flush
10
Q
How does ausculation change with mitral stenosis progression
A
Earlier the murmur/ mitral ‘snap’ with more severe disease due to Left atrium hypertrophy
Followed by low rumbling - bell at apex with patient lying on left side
11
Q
Chest Xray mitral stenosis
A
Pulmonary hypertension- upper lobe diversion, bat winging, loss of menisci
LAH
12
Q
ECG mitral stenosis
A
RVH - lead to right axis deviation and tall R in V1/2
AF
Bifid P wave - LAH causing left atrial delay
13
Q
Mitral Regurg causes:
A
More common than MS Rheumatic heart disease Papillary muscle necrosis (MI) Cardiomyopathy CT disorders - Ehlers Danlos - Marfans - Osteogenesis Imperfecta Endocarditis
14
Q
Mitral regurg signs
A
Malar flush
Displaced apex beat (volume overload)
Palpable thrill
Pansystolic murmur radiating to axilla “burr” - not gap before S2 unlike AS
15
Q
Mitral regurg xray and ECG
A
Cardiomegaly (grows more to maintain BP desite loss of blood the wrong way, V and A) Left displacement (S in V1 and tall R in V5/6) Bifid P wave
16
Q
AS causes
A
<65 bicuspid valve
>65 Calcification age related
Rheumatic heart disease
17
Q
AS symptoms
A
Syncope on exercise
Angina
SOB
Poor prognosis without surgery
18
Q
Signs of AS
A
Collapsing pulse Slow rising character Low volume - small PulseP Forceful apex beat Eject systolic mkurmur to cartids lub-whoosshhh (pause) dub
19
Q
CXR and ECG of AS
A
Enlarged aorta (post stonotic dilatation) LV straign pattern - depressed ST with inverted T in all ventricular facing leads
20
Q
AR causes
A
Bifid aortic valve
Rheumatic valve disease (commonest)
infective endocarditis
Marfan’s (CT causes regurg)
21
Q
AR signs and ECG
A
Loudest at 4th intercostal space left sternal edge, sitting forward and breathing out.
High pitched early diastolic murmur. (think other MR is high pitched too “burrr”) lub taaarr
Collapsing pulse (wide pulse pressure)
Pistol shot femorals - femoral artery
low volume pulse
Quincke’s sign - capillary pulsation in the nail beds
De Musset’s sign - head nodding with each heart beat
(all three to do with PULSITATION / wide PP)
Displaced apex beat (LVH)
ECG - LVH - LAD,
22
Q
Angles of limb leads
A
I 0 II 60 aVf 90 III 120 aVr -150 avL -30
23
Q
Placement of chest leads
A
V1: Fourth intercostal space, right of the sternum.
• V2: Fourth intercostal space, left of the sternum.
• V3: Directly between leads V2 and V4.
• V4: Fifth intercostal space at midclavicular line.
• V5: Level with V4 at left anterior axillary line.
• V6: Level with V5 at left midaxillary line.
24
Q
Why is the rhythm of atrial flutter normally around 150, 100 or 75bpm?
A
Depends on ratio of A:V dependent on how many beats AVN is conducting (degree of block)
25
VT ECG appearence
Wide QRS
Concordance pos or neg
Fusion or capture beats (normal or semi normal beats)
No relation to P waves
No delta wave (would make it WPW)
No BBB (would make it SVT with abberancy or BBB)
120-180 bpm
26
VF ECG
Chaotic irregular deflections of varying amplitude
No identifiable P waves, QRS complexes, or T waves
Rate 150 to 500 per minute
Amplitude decreases with duration (coarse VF -> fine VF)
concordance - all limb leads show either positive or negative
Capture or fusion beats
capture beats - occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
27
Treatment of Broad complex tachycardias
Haemodynamically unstable - DC shocks followed by amioderone
IF stable and regular
- asssume VT and give amioderone and K/ Mg if needed
- If known history of SVT and BBB consider adenosine (as it's likely to be that).
If irregular:
- AF with BBB (treat same as AF)
- Pre excited AF (amioderone)
- Polymorphic VT (e.g. Torsade de pointes - varying axis, long QT syndrome) high dose BB for torsade/ May need to correct hypokalaemia and give Mg sulfate
28
4 causes of wide complex reg tachy:
1) SVT abberancy
2) WPW
3) SVT with BBB
4) VT
29
When and why do you never give adenosine? When could you give it?
1) VT - blocking AVN wont help
2) Pre-excited SVT (e.g. AF) - narrow complex or broad as may be abberant/ BBB as it may force it down accessory pathway, (think pre-exciting must refer to the possibility of an accessory pathway).
3) SVT - impossible to tell if there is an accessory pathway however... consider if regular and there is a history of SVT and BBB (as you know it is not pre-excited)
("pre-exitiation refers to contraction of ventricles viva an accessory pathway"- by definition isn't this broad complex so wouldn't adenosine help block pathway? i.e. can't force down accessory pathway by blocking AVN as it is already going down?)
30
No P waves in narrow complex tachy?
AVNRT - simulatieous contaction? think Somani diagram
31
Causes of narrow complex tachycardia?
```
AFib
Aflut
AT
JET:
-AVNRT
-AVRT
All causes of SVT
```
32
Treatment of NC tachy?
AF/ flutter - normally
multifocal AT (ectopics) - most common in COPD, correct hypoxia and hypercapnia. If normal AT normally due to digoxin toxicity.
```
SVT - haemodynamically stable
1- Vagal
2 - adenosine
3 - Verapamil
4 - atenolol or sotalol
5 - DC cardioversioon
```
If unstable
-DC cardioversion
33
Main causes of LAD and RAD
LAD:
- LVH
- Ischaemia of LBB
RAD
- RVH
34
Causes of werid P waves
Left atrial enlargement e.g. MS or HYT
Bifid P wave (P mitrale) - enlarged
Tall P wave (P pulmonale):
Right atrial dysfunction e.g. pulmonary hyt, COPD, congenital HD (TOF, Pulmonary stenosis)
35
Names of 2nd degree HB
```
Mobitz I (Wenckebach) - prolongs progresively
Mobitz II - failure of AVN to conduct all
```
36
Causes and presentation of 3rd degree HB
Total failure, bradycardia (30-50)
Stokes-Adams attack (sudden collapse/ syncope due to the brady)
MI
AVN fibrosis or bundle of hiss
Drugs - digoxin, diltiazem (especially with BB)
37
ECG signs of LVH
Englarged S wave in V1 (35mm or 3.5 squares)
Englarged R wave in V5/6 35mm
Possible T wave inversion in V5/6 at late stage
Sokolow-Lyon Voltage criteria
Note no axis deviation really?
38
ECG sings of RVH
Right axis deviation
Dominant R wave in V1 (> 7mm tall or R/S ratio > 1).
Dominant S wave in V5 or V6 (> 7mm deep or R/S ratio < 1).
QRS duration < 120ms (i.e. changes not due to RBBB).
39
Desribe ECG BBB
Normal QRS duration is 0.12s (3 small squares)
o Widened in Bundle Branch Block (BBB)
o If the major deflection in V1 is up then it is Right
BBB, if down then Left BBB
o Remember WiLLiaM and MaRRoW
o LBBB: W in V1 and a M in V6
o RBBB: M in lead V1 and a W in lead V6
40
What does ST deepression up sloping mean?
ST depression that is Upsloping is rate related, not ischaemia
41
Changes in ECG post MI?
Hyperacute T waves first
ST elevation
Pathological Q waves (at least 1/4 of QRS height) hours-days
T wave inverison
42
Describe the territories of MI
```
v1-2: septal
v3-4: anterior
v5-6: lateral
avL-I: high lateral
avR, II, III: Inferior
```
v1-v3 depression: posterior
43
Describe ECG changes in PE
```
Tachycardia most common
S in I = large
Q in III = large
T in III = large
SIQIIITIII
```
P HYT can cause RAD
44
ECG changes of hyperkalaemia
Broad Bizarre QRS
Hyperacute T wave
Low flat P wave
Slurring into ST segment
45
Causes of HF in order of likelihood
70% IHD
30% Non ischaemic cardiomyopathy (genetic, alcohol, drugs)
5% hypertension
```
also:
Valve disease
Pulmonary pathology
Hyperdynamic circulation (increased volume) - anaemia, thyrotoxicosis, Paget's
Pericarditis/ Pericardial effusion
Alcohol and drugs
CHD
Arrhythmias including AF and heart block
```
46
Pathophysiological changes in HF and subsequent mechanisms to maintain CO broadly. Early and late mechanisms.
```
Ventricular dilation
Myocyte enlargement
Neurohumeral: Increased ANP
Increased symp activation
Increased peripheral vasocnstriction
Increased fluid retention
```
Early
- Normally Low CO counteracted by increase in VP and starlings curve
- Mild HF, Low CO counteracted by increase in VP and HR, decreased ejection fraction.
Late
- CO maintained by large increases in VP and sinus tachy, not in exercise. Increase in VP causes signs and symptoms
Severe HF - decreased CO at rest even with VP and HR.
47
How do the physiological response to HF increase the damage?
Chronic activation of RAAS and adrenergic systems causing vasoconstriction and Na and water retention increase afterload and preload and increase cardiac work leading to further myocyte damage
48
Signs and symptoms of LHF
```
Symptoms:
o Fatigue (common)
o Exertional dyspnoea
o Orthopnoea / PND
• Physical signs are few and not prominent until a late
stage or if LV failure is acute:
o Displaced Apex Beat
Cardiomegaly
o Gallop Rhythm on Auscultation
3rd heart sound heard
o Features of Mitral Regurgitation
Dilatation of the mitral annulus
o Crackles at Lung Bases
Pulmonary oedema
o Dependent Pitting Oedema
Activation of RAA
```
49
Causes of RHF
1. Chronic Lung Disease (Cor pulmonale)
2. PE or Pulmonary Hypertension
3. Tricuspid / Pulmonary Valve Disease
Also:
o Left-to-Right shunts e.g. ASD / VSD
o Isolated Right Ventricular Cardiomyopathy
50
Symptoms and signs of RHF
```
• Symptoms:
o Fatigue
o Dyspnoea
o Anorexia / Nausea
• Physical signs are usually more prominent than the
symptoms:
o ↑ Jugular Venous Distension
± V waves of tricuspid regurgitation
o Cardiomegaly
Dilatation of the right ventricle produces
cardiomegaly ...and may give rise to functional
tricuspid regurgitation
o Hepatic Enlargement
Tender and smooth
o Ascites
Development of free abdominal fluid
o Dependent Pitting Oedema
```
51
Diagnosis and staging of HF
Diagnosis of Heart Failure should not be solely based
on history and examination
• Evidence of cardiac dysfunction must be
demonstrated
• Investigations include
o Bloods
o CXR
o Echocardiogram
• The underlying cause must be established in all
patients
NYHA Heart Failure Classification
Symptoms
Class I - No limitation of physical activity
Class II - Slight limitation of physical activity
(symptomatically mild heart failure)
Class III - Marked limitation of physical activity
(symptomatically moderate heart failure)
Class IV - Symptoms at rest
(symptomatically severe heart failure)
52
Management of HF
General Management
• Low level exercise
• Low salt diet
• Stop smoking
• Education
• Vaccination
Medical Management
1. Diuretics
o Step 1: Furosemide (loop diuretic) 40mg and
titrate up if needed.
o Step 2: Change to Bumetanide (loop diuretic)
if Furosemide not working.
o Step 3: Add a Thiazide for complete diuresis
...must watch U&E’s
2. Ace Inhibitor (ACEi)
o Trials have shown ACEi in heart failure
improves symptoms and prognosis.
o Replace with an Angiotensin II receptor
antagonist if patient gets a dry cough.
3. β-Blockers
o Used in chronic stable heart failure.
o Should be initiated in confirmed heart failure
due to left ventricular systolic dysfunction after
diuretics and ACE-I therapy.
4. Spironolactone (aldosterone antagonist)
o 30% reduction in all-cause mortality when
added to conventional treatment in patients
with moderate to severe HF.
5. Inotropic agents
o Dopamine & Dobutamine. - IV Inotropes are frequently used to support myocardial function in
patients with acute left ventricular failure with hypotension.
o Digoxin. - Patients who are hospitalized or present with severe heart failure in spite
of therapy with vasodilators, beta-blockers, diuretics (and also patients
with rapid AF), may benefit from digoxin.
6. Nitrates
o Reduce preload and afterload.
o Short and long acting nitrates (e.g. Glyceryl Tri-
Nitrate (GTN) and Isosorbide Mononitrate (ISMN)).
o With chronic use, tolerance develops, hence
administered at 0800 and 1400 hours BD.
7. Anticoagulation
o Can be considered as HF is associated with a
4x increase in stroke risk.
Non Pharmacological Management
• Revascularization
• Biventricular pacemaker or Implantable Cardioverter
Defibrillator (ICD)
• Cardiac Transplantation
• LVAD (Left Ventricular Assist Device) and Artificial
Heart
53
Management of a STEMI
```
Airway, Breathing, Circulation
• IV access
• 12-lead ECG
• Give:
• Oxygen
• Nitrates (GTN spray 2 puffs sublingually)
• Aspirin (300mg)
• Diamorphine (2.5-10mg IV, plus antiemetic)
Investigations
• Bloods:
o FBC, U&E, LFTs, glucose, lipids, CK, troponin I
• Portable CXR
```
54
Indications for thrombolysis in ACS
```
o < 12 hours onset pain
+ any 1 of the following:
o ST elevation >1mm in 2+ consecutive limb
leads
o ST elevation >2mm in 2+ consecutive chest
leads
o Posterior infarct
o New onset LBBB
```
55
Thrombolysis containdications
```
Haemorrhagic stroke or Ischaemic stroke < 6 months
CNS neoplasia
Recent trauma or surgery
GI bleed < 1 month
Bleeding disorder
Aortic Dissection
```
Relative
Warfarin
Pregnancy
Advanced Liver Disease
Infective Endocarditis
56
Indications for primary PCI
```
(<90mins
from pain onset)
• Indication:
o Same as thrombolysis indications.
o If does not fulfil thrombolysis criteria or
thrombolysis contraindicated.
o If symptomatic post-thrombolysis or develops
cardiogenic shock.
```
57
Complications of STEMI
```
S - Sudden death or from VF
P - Pump failure / Pericarditis
- First 48hours
Following transmural MI
Worse lying plat
Pericardial rub
Pericardial effusion
R - Rupture papillary muscles or septum
E - Embolism
A - Aneurysm / Arrhythmias
D - Dressler’s syndrome
```
58
What is Dressler's syndrome?
```
2-6 weeks after MI
Autoimmune reaction against proteins in recovering myocardium
Fever
Pleuritic pain
Pericardial effusion
Raised ESR
Treat with NSAIDs
```
59
Discharge management for STEMI
```
Aspirin
• Clopidogrel
• ACE inhibitor
• β-blocker
• Statin
• Address modifiable risk factors
• 1 month off work
• Need to inform DVLA – no driving for 4 weeks.
```
60
Management of NSTEMI.
```
Close monitoring with ECG
Aspirin 300mg
Nitrates - GTN or sublingual
morphine for chest pain
O2 if sats <90?% of SOB
Clopidogrel 300mg and continued for 12months
```
PCI or thrombolysis if indicated.
Fondaparinex or enoxaparin, oral BB or enoxaparin if waiting for angiotraphy
Long term same as stemi (probably):
```
Aspirin
• Clopidogrel
• ACE inhibitor
• β-blocker
• Statin
• Address modifiable risk factors
```
61
When would PCI be considered in NSTEMI
96hr of first admission if 6 month mortality above 3% or if clinically unstable
Very high Trop I
Symptoms dispite maximal medical therapy
<6 months since last PCI
Heart failure/ poor LV function
Haemodynamically unstable
Based on GRACE score
62
Signs and symptoms of Acute LVF
Acute breathlessness
o Cough & frothy pink sputum
o Orthopnoea, paroxysmal nocturnal dyspnoea
o Collapse, arrest, cardiogenic shock
Distressed, pale and sweaty
o Tachycardic
o Fine crepitations bilaterally
o Gallop rhythm: 3rd heart sound
63
Cause of Acute LVF
Myocardial ischaemia
o Hypertension
o Aortic stenosis or aortic incompetence
o Mitral incompetence
64
Management of Acute LVF
```
• Airway, Breathing, Circulation
• Sit upright
• 100 % O2 via non-rebreather mask
• IV access and monitor ECG
• Morphine 2.5-5mg IV (with antiemetic)
Other:
• If SBP >100mmHg – Nitrate (GTN) IV infusion
• Furosemide 40-80mg IV
• CPAP
```
65
Investigations of acute LVF
```
ECG: Arrhythmia, tachycardia, MI, LVH
• Bloods: FBC, U&E, CK, Troponin I
• CXR
• ABG
• Echo
```
66
Radiological signs of heart failure
```
ABCDE
Airspace shadowing
Kerley B lines (septal lines)
Cardiomegaly
Diversion of blood to upper lobes
Effusions
```
67
3 ways tachhy arrythmias are produced
```
Accelerated automaticity
o An area of myocardial cells depolarises faster
than the SA node
2. Triggered activity
o Myocardial damage
3. Re-entry
o Propagating action potential
keeps meeting excitable myocardium.
o There must be 2 pathways around
an area of conduction block.
```
68
VT Precipitating factors
```
Metabolic (low K or Mg)
• IHD
• Cocaine
• Cardiomyopathy
• MI
```
69
SVT Precipitating factors
* IHD
* Thyrotoxicosis
* Caffeine
* Alcohol
* Amoking
70
AF Precipitating factors
```
Same as SVT & also:
• Mitral valve disease
• Hypertension
• Lung disease
• Post op
• Pericardial disease
• Cardiomyopathy
```
71
Normal bug in infective endocarditis
Usually bacterial
o Streptococcus viridians
Upper respiratory tract commensals
• Others
o Staphylococcus aureus – Skin infections,
abscesses, central lines, IV drug abusers...
• And more...
72
Pathophysiology of infecive endocarditis
1 Endothelial damage/ damaged valve
Platelets andfibrin deposition (Sterile fibrin-platelet vegetation)
3 Bacteraemia
4 Adherence and colonisation of bacteria
5 Fibrin aggregates protect the bacteria vegetation from host defence mechanisms
• Consequences
o Disruption of the valve cusps, commonly
leading to mitral or aortic regurgitation.
o Vegetations embolise.
o Deposition of immune complexes.
73
Clinical presentation of infective endocarditis
```
HEART MURMUR + FEVER
• Four processes causing the clinical picture:
o Systemic infection
o Valvular / Cardiac damage
o Embolisation
o Immune vasculitis
1. Systemic infection
o Malaise
o Pyrexia
o Myalgia
o Weight loss
o Fatigue
2. Valvular / Cardiac damage
o Changing Murmur
Aortic regurgitation
Mitral regurgitation
o Heart failure
o Conduction Abnormalities
3. Embolisation
o Cerebral
o Pulmonary
o Coronary
o Renal (haematuria)
4. Immune Vasculitis
o Roth spots (Retinal infarcts with surrounding
haemorrhage)
o Oslers nodes
o Janeway lesions
o Clubbing
o Splinter haemorrhages
o Glomerulonephritis
```
74
Diagnosis of infective endocarditis
A. Positive blood culture for Infective Endocarditis:
o Typical organism in 2 separate cultures.
OR
o Persistently positive cultures (3 sets, at different
times, from different places, at peak temperature).
B. Evidence of Endocardial involvement:
o Positive echocardiogram (Vegetation, abscess,
prosthetic valve damage).
OR
o New valvular regurgitation.
1. Predisposition
2. Fever >38°C
3. Vascular / Immunological signs
4. Positive blood culture (But does not meet Major criteria)
5. Positive echocardiogram (But does not meet Major criteria)
```
2 Major
OR
1 Major, 3 Minor
OR
5 Minor
```
75
Investigation infective endocarditis
Bloods - full work up - emboli damage
| Urinalysis
76
Treatment infective endocarditis
Airway, Breathing, Circulation – Stabilise the patient
• Always involve a microbiologist and a cardiologist
• Depends on organism
• Empirical treatment is:
o BENZYLPENECILLIN & GENTAMICIN
• Treatment can often be at least 4 weeks IV antibiotics
77
Prevention of infective endocarditis/ prevention
Who’s at Risk?
o Structural congenital heart disease
o Acquired valve disease
o Prosthetic valves
o Previous endocarditis
• Explain to patient:
o Benefits and risks of antibiotic prophylaxis, and
why antibiotic prophylaxis is no longer
routinely recommended.
Importance of maintaining good oral health.
o Symptoms of infective endocarditis and when
to seek expert advice.
o Risks of undergoing invasive procedures,
including body piercing or tattooing.
78
Explain the anatomy of heart layers
```
Myocardium
Visceral pericardium
Pericardial space (with 15-50ml of pericardial fluid)
Parietal pericardium
Fibrous layer
```
Visceral pericardium: An inner serous membrane
made of a single layer of mesothelial cells.
• Pericardial fluid drains via the thoracic duct and right
lymphatic duct into the right pleural space.
79
Presentation of acute pericarditis
```
Acute pericarditis is an inflammation of the pericardium
characterized by:
o Chest pain
o Pericardial friction rub
o Serial ECG changes
```
Substernal or left precordial pleuritic chest pain with radiation to the trapezius ridge, which is relieved by sitting up and bending forward and worsened by lying down
dry cough, fever, fatigue, and anxiety
```
Pericardial pain: 5 features
o like pleurisy:
1. Sharp
2. Worse on inspiration
o like angina:
3. Central chest pain
4. Radiating to left shoulder
o specific:
5. Eased sitting forward
• +/- Dyspnoea, especially with tamponade
• +/- Fever
```
80
Pathophysiology of pericarditis
```
xPericardium is acutely inflamed.
• Infiltration of polymorphonuclear (PMN) leukocytes
and pericardial vascularisation.
o May develop constrictive pericarditis
Exudates & adhesions encase the heart
within a non expansile pericardium.
o May develop a pericardial effusion
Serous or haemorrhagic.
May lead to cardiac tamponade.
```
81
Causes of pericarditis
```
Viral (most common)
o Particularly Coxsackie Viruses
o Treatment is symptomatic, with observation for
the development of pericardial tamponade.
• Idiopathic
• Tuberculosis
• Bacterial
o Causes purulent pericarditis.
o Requires antibiotics for at least 4 weeks and
drainage of pericardial fluid.
o Develops from:
Direct pulmonary extension
Haematogenous spread
Myocardial abscess
Endocarditis
Penetrating injury to chest wall (trauma or surgery)
Subdiaphragmatic suppurative lesion
• Cardiovascular disease
o Myocardial infarction
o Dresslers Syndrome
• Neoplasm
o Lung tumours
o Metastatic disease
• Renal failure
o Before dialysis, pericarditis developed in 35-
50% of patients with uremia and chronic renal
failure.
o Often died within a few weeks.
o Requires intensive dialysis.
• Inflammatory
o Rheumatoid Arthritis
o Sarcoidosis
o Systemic Lupus Erythematosus (SLE) etc...
```
82
Examination of pericarditis
• Tachycardia + Tachypnoea + Fever
• Pericardial friction rub
o Auscultate with diaphragm over the left lower
sternal edge
• If constrictive pericarditis:
o Right heart failure
↑JVP, severe ascites, hepatomegaly, Kussmaul’s
sign (JVP ↑ with inspiration)
o Hypotension, Pulsus Paradoxus (↓ in palpable pulse
and ↓ in systolic BP on inspiration)
• Loud high-pitched S3 (pericardial knock)
83
Investigations pericarditis
```
Bloods: FBC, U&E, LFT, CRP, CK, Troponin I
• Further investigations:
o Virology screen
o Blood cultures
o Antistreptolysin titre
o Rheumatoid factor
o Antinuclear antibodies (ANA)
o Anti-DNA antibodies
o Tuberculin testing
o Sputum for acid-fast bacilli
```
Echocardiography (ECHO)
o If pericardial effusion or tamponade is
suspected.
o If there is a pericardial effusion, you may see
right ventricle compression as this is
compromised first.
• CT / MRI
84
ECG changes in pericarditis
Classic acute pericarditis evolves through 4 stages:
o Stage 1: Saddle shaped ST elevation (Diffuse
concave upward ST elevation, except aVR and V1 (usually
depressed).
o Stage 2: Occurs several days later. ST
segment returns to baseline, followed by T
wave flattening.
o Stage 3: T wave inversion.
o Stage 4: ECG returns to the pre-pericarditis
baseline weeks to months after onset.
• All 4 stages are only present in 50% of patients.
• T wave inversion may persist indefinitely with the
chronic inflammation observed with Tuberculosis,
Uremia, or Neoplasm.
85
Pericardial effusion/ Cardiac tamponade definition
• Pericardial effusion
o Pericardial effusion is an abnormal
accumulation of fluid in the pericardial cavity.
• Cardiac Tamponade
o Pericardial effusion causing haemodynamically
significant cardiac compression.
Pericardial pressure increases inhibiting
venous return to the heart.
This results in reduced cardiac output,
hypotension and shock.
86
PEricardial effusion/ Cardiac tamponade aetiology and grouping
```
• ‘Acute’
o Trauma
o Iatrogenic (cardiac surgery / catheterisation /
anticoagulation)
o Aortic dissection
o Spontaneous bleed (uraemia / thrombocytopenia)
o Cardiac rupture post-MI
• ‘Subacute’
o Malignancy
o Idiopathic pericarditis
o Uraemia
o Infection (including TB)
o Radiation
```
87
Presentation of pericardial effusion/ tamponade
```
• Depends on speed at which fluid accumulates!
• Commonly
o Cardiac arrest
o Hypotension
o Confusion
o Shock
• Slowly developing tamponade
o SOB
o Cough, hiccups, dysphagia
Signs
• Beck’s triad:
o ↑ JVP
o ↓ BP
o Muffled heart sounds
• Tachycardia
• Kussmaul’s sign (JVP ↑ with inspiration)
• Pulsus paradoxus (↓ in palpable pulse and ↓ in systolic BP on
inspiration)
```
88
Treatment of PEricardial effusion/ Cardiac tamponade
ABC
IV acess
ECG
Bloods
Get senior help
• Pericardiocentesis
o Needle inserted at level of Xiphisternum, aim
for tip of left scapula, aspirating continuously.
o Blind – complication risk 5-50%, only if
emergency.
o USS guided – relatively safe.
o Send the pericardial fluid for microbiology and
cytology.
• A drain may be left in temporarily to allow sufficient
release of fluid
89
Side effects if beta blockers
GI disturbances; bradycardia; fatigue;
cold peripheries; heart failure; hypotension; dizziness;
sexual dysfunction; peripheral vasoconstriction;
bronchospasm.
90
CI to beta blockers
asthma; marked bradycardia;
heart block; uncontrolled heart failure; PVD - peripheral vasc disease;
Prinzmetal's angina; hypotension; cardiogenic shock.
91
Types of CCBs and functions/ indications
Non-dihydropyridines
o Verapamil & Diltiazem
Negatively inotrophic / chronotrophic but DO NOT
USE IN HEART FAILURE
• Dihydropyridines
o Amlodipine, Felodipine, Nifedipine
Dilates peripheral arteries, ↓ after-load, dilates
coronary vessels, act on vessels > myocardium
Indications:
o Verapamil: fast AF, SVT, hypertension.
o Dihydropyridines: hypertension; to prevent
angina.
92
Side effects of CCBS
o Verapamil & Diltiazem: constipation; N&V;
flushing, headache, dizziness; fatigue.
o Dihydropyridines: abdominal pain; nausea;
palpitations, flushing, oedema; headache;
dizziness; sleep disturbances; fatigue.
93
Contraindications of CCBs
Verapamil & Diltiazem: HF, 2nd or 3rd degree
heart block, cardiogenic shock.
o Dihydropyridines: Unstable angina, significant
AS.
94
Nitrates contraindications
• Contraindications: hypersensitivity to nitrates;
hypotensive conditions; hypovolaemia; hypertrophic
obstructive cardiomyopathy; AS; MS; cardiac
tamponade; constrictive pericarditis; marked anaemia.
95
Nitrates side effects
postural hypotension; tachycardia;
throbbing headache; dizziness.
o TOLERANCE
96
ACE MoA
Action: Inhibits conversion of angiotensin 1 into
angiotensin 2, therefore inhibiting angiotensin 2 having
its effects:
o Increasing sympathetic activity.
o Fluid retention by kidney – via Increase in
aldosterone and direct action.
o Arteriolar vasoconstriction.
o Stimulating ADH secretion causing increased
fluid retention.
ACE inhibitors also cause:
o Reversal of left ventricular hypertrophy.
o Reversal of endothelial dysfunction.
97
Side effects ACE
renal impairment; persistent dry cough;
angioedema; rash; hypotension; pancreatitis;
hyperkalaemia; GI effects.
98
Containdications to ACEi
hypersensitivity to ACEi
(angioedema); renal artery stenosis; pregnancy; aortic
stenosis; toxicity.
May adversely affect fetal and neonatal BP control and renal
function; possible skull defects and oligohydramnios; toxicity.
99
Treatment of pericarditis
• If a cause is found, this should be treated!
• Bed rest and oral NSAIDs
o High-dose aspirin, indometacin or ibuprofen.
o But NOT post-MI: NSAID associated with
myocardial rupture.
o Corticosteroids have been used when the
disease does not subside rapidly.
• Further Treatment:
o Pericardial window
o Pericardiectomy
100
Causes of reversible cardiac arrest
Hypoxia
Hypovolaemia
Hypokalaemia
Hypothermia
Tension Pneumothorax
Tamponade
Thromboembolism/ PE
Toxicity
101
MoA Loops
Blocks Na+/K+/Cl- co-transporter in the apical
membrane of the thick ascending limb of loop of
Henle.
102
Indication Loops
hypertension; water overload: pulmonary
oedema in LVF, chronic HF, nephrotic syndrome, renal
failure.
103
Side effects Loops
hypokalaemia; metabolic alkalosis;
sodium & magnesium depletion; hypovolaemia &
hypotension; deafness; nausea; allergies.
104
Thiazide action
Inhibits Na+ reabsorption at the beginning of
the distal convoluted tubule. Blocks Na+/Cl- symporter
that is associated with the luminal membrane.
105
Indications Thiazide
hypertension; severe resistant oedema;
| HF.
106
Side effects Thiazide
postural hypotension; hypokalaemia;
hypomagnesaemia; hyponatraemia; hypercalcaemia;
metabolic alkalosis; hyperuricaemia; impotence;
hyperglycaemia.
107
Thiazide contraindications
refractory hypokalaemia;
hyponatraemia; hypercalcaemia; symptomatic
hyperuricaemia; Addison's disease.
108
K sparing e.gs and action
Act on collecting tubules. Spironolactone is
an aldosterone antagonist. Other potassium sparing
diuretics act by directly inhibiting sodium channels e.g.
Amiloride.
109
Inidcations of spiroono
co-use with K+ losing diuretics; CCF;
| cirrhosis; oedema.
110
Side effects of spirono
GI disturbances; impotence;
gynaecomastia; menstrual irregularities; lethargy;
headache; confusion; hyperkalaemia; hyponatraemia;
hepatotoxicity.
111
MoA statin
Blocking liver enzyme hydroxy-methylglutarylcoenzyme
A reductase (HMG-CoA reductase),
thereby inhibiting liver synthesis of cholesterol.
o This leads to upregulation of expression of LDL
receptors on liver cells causing ↑ absorption of
LDL from the circulation.
112
Side effects statin (when augmented?)
myositis; rhabdomyolysis; headache;
| altered LFTs; paraesthesia; GI effects.
113
Contraindications statin
active liver disease; pregnancy;
| breast-feeding.
114
Main therapeutic diff between statin and fibrates
Lower triglycerides more than LDL.
115
MoA aspirin
Suppresses production of prostaglandins and
thromboxane by irreversibly inactivating the
cyclooxygenase (COX1) enzyme.
• Irreversibly blocks the formation of thromboxane A2 in
platelets, inhibiting platelet aggregation.
116
MoA Clopidogrel
Inhibits ADP-induced aggregation through an active
| metabolite.
117
Dipyridamole MoA and indication
Phosphodiesterase inhibitors – more cAMP, inhibits thromboxane a2 production. less aggregation. Positive inotrope and vasodilatory (flushes, headache), prevention of stroke - history of recurrent cerebrovasc disease
118
Action of UFH
Binds to Antithrombin III (ATIII).
o ATIII is an endogenous inhibitor of coagulation.
o Increases ATIII ability to inhibit factors IXa, Xa,
XIa, XIIa (serine proteases) and thrombin
(unfractionated).
119
Action of LMWH
Inhibits factor Xa but not thrombin.
120
Intrinsic and extrinsic clotting
```
Intrinsic
XII
XI
IX (VIII)
X
II
I
```
```
Extrinsic
VII
X
II
I
```
121
Reversibility of heparins
Only UFH fully reversible with protamine
122
Differences in duration of action, effect on thrombin, side effects, monitoring between LMWH and UFH
```
Mode &
duration of
action:
• Does not affect
thrombin
• Given 1-2
times / day
• Inactivates thrombin
• Short acting,
continuous infusion
Side effects: • Bleeding
• Bleeding
• Heparin induced
thrombocytopenia
```
```
Monitoring: • No
• Yes
• Daily platelets
Reversal: • No
• Yes
• Protamine
```
123
Warfarin MoA
Action: Inhibits vitamin K dependent clotting factors
(II, VII, IX, X, protein C & S). Does this through
inhibiting the reductase enzyme responsible for the
regeneration of the active form of vitamin K.
124
How to handle warfarin overdose
INR <6: Decrease / omit Warfarin
INR 6-8: Stop Warfarin. Restart
when INR<5
INR >8: If no bleeding stop
Warfarin & give 0.5-
2.5mg vitamin K if risk of
bleeding.
• Major bleed: Stop Warfarin. Give prothrombin
complex concentrate (Beriplex) contains factors II, VII,
IX, X or FFP. Give 5mg vitamin K. Get HELP!
125
HPC regarding dyspnoea
MRC score, Exercise Tolerance,
triggers, relieving factors, diurnal variation,
orthopnoea, PND
126
HPC regarding wheeze
triggers, relieving factors, diurnal
| variation (asthma worse at night), associated cough
127
HPC regarding Cough
dry or productive, triggers, relieving
factors, diurnal variation, association with eating
or dyspepsia (GORD), positional, nasal secretions (rhinitis),
associated fever
128
HPC regarding haemoptysis
quantity and frequency, fever /
night sweats, appetite, weight loss
^=Cancer Qs
129
Give MRC dyspnoea scale
1 - breathless only on strenuous exercise
2 Breathless hurrying or walking up slight hill
3 Breathless walking flat >100m or slower than used to be
4 - breathless walking <100m flat
5 - breathless putting clothes on/ too breathless to leave the house
130
Drug history to remember
Adherence
```
What drug
• Dose
• Frequency
• Route
Over the counter/herbal
```
131
Family history to specifically ask for
```
• Respiratory Disease
• Cardiac disease
• Cancer
• Thrombophilia (if DVT / PE)
• Cystic Fibrosis (if young and chest
infections)
```
132
Social history resp
Smoking – current (pack years), ex (pack years,
when stopped), never
• Occupational History – specifically asbestos
• Pets – specifically cats, birds (budgies, parrots,
pigeons) – also friends / neighbours
• Recent Foreign Travel
• Immobility – flights / long car or bus journeys
• Activities of daily living – self care, cooking, cleaning,
shopping, type of accommodation, helpers / carers
• Alcohol
• Performance Status (Cancer)
133
WHO performance status
0 Normal - Fully active without restriction
1 Restricted in physically strenuous activity but ambulatory and
able to carry out light work e.g., light house work, office work
2 Ambulatory and capable of all self-care but unable to carry
out any work activities. Up and about more than 50% of waking
hours
3 Capable of only limited self-care, confined to bed or chair
more than 50% of waking hours
4 Completely disabled. Cannot self-care. Totally confined to
bed or chair
5 Dead
134
Resp systems review
```
Bowels ok? Appetite / weight loss
• Any problems with your water works?
• Joint pains? Rashes?
• Neuro / Cardio
Summarise and also ask:
Is there anything you feel that I have missed?
What have you been told so far?
```
135
Resp exam face
Eyes for Horner’s syndrome
• Mouth – central cyanosis
• Swelling - SVCO
136
Resp exam neck
Trachea
• JVP
• Lymph Nodes
137
What to do if you hear crackles
Cough and repeat
138
What is bronchial breathing
abdnormal far from main airway
high pitched
Insp and Exp equal (vesicular inspiration is longer)
Definite gap between each phase (Unlike vesicluar)
Heard in consolidation/ collapse with patent bronchus
139
Radiological features of lobar collapse CXR
elevation of the ipsilateral hemidiaphragm
crowding of the ipsilateral ribs
shift of the mediastinum towards the side of atelectasis
crowding of pulmonary vessels or air bronchograms
140
Causes of lobar collapse
```
luminal
aspirated foreign material
mucous plugging
mural
bronchogenic carcinoma
extrinsic
compression by adjacent mass
```
141
Atelectasis vs lobar collapse
Lobar collapse refers to the collapse of an entire lobe of the lung. As such it is a subtype of atelectasis (although collapse is not entirely synonymous is atelectasis), which is a more generic term for 'incomplete expansion'. Individual lobes of the lung may collapse due to obstruction of the supplying bronchus.
142
What does stridor sound like and mean?
High-pitched wheeze caused by disrupted airflow
Larynx or tracheal.
insp, exp, biphasic
(Seems to be higher pitch that wheeze and less breath soundy) - would it fit clinical picture?
143
What does stertor
```
Originates in the pharynx
Snoring or gasping
low-pitched non-musical
Inspiratory only
e.g. OSA, CNS stuff, post-ictal seizure
```
144
How to complete resp exam?
```
Look at legs
• State that you would like to see Observation chart
• PEFR if appropriate
• Cover patient / help them get dressed
• Thank the patient
```
145
System for CXR
Name and age of patient
• Date CXR taken
• Type of CXR (e.g. PA or AP, erect or mobile)
• Quality of film – rotation, penetration vertebrae are just visible behind the heart The left hemidiaphragm should be visible to the edge of the spine, adequate
inspiration 5th to 7th anterior ribs in the mid-clavicular line
• Systematic approach e.g. ABC = Airways / lungs,
Bones (all), Cardiac
• Don’t forget the trachea, apices, behind the heart,
beneath the diaphragm and soft tissues (including
breast shadows)
• Say what you can definitely see (e.g. “loss of right
costophrenic angle which may be in keeping with a
pleural effusion” as opposed to “a right pleural
effusion”)
146
Types of shadowing
Shadowing can be complete (whiteout of whole lung
field), dense / consolidation (affecting one or more
zones), diffuse, alveolar (cotton wool like
appearance)
147
Difference in largeairway obstruction vs small airway obstruction on flow volume loop
Sinks later in small airway - first bit normal as this is large airways
148
Explain 4 causes of low PaO2
V/Q mismatch
Hypoventilation
Diffusion capacity
Shunt - whereby blood does not get ventilated e.g. AV malformation or physiologically via coronary arteries into left ventricle
149
Causes of V/Q mismatch
Low in chronic bronchitis, asthma, hepatopulmonary syndrome, and acute pulmonary edema.
High in PE (less perfusion) or some emphysema - remodeling (more ventilation per available perfusion area)
150
Causes of respiratory acidosis
Hypoventilation e.g. neuromuscular diseases
| • “Alveolar hypoventilation” e.g. COPD
151
How is a the A-a gradient calculated? what is the use?
PAO2 (pressure of O2 in alveoli) - PaO2
PA02 is calculated using the alveolar gas equation i think?
Under 2kPa is normal.
Indicates problem in diffusion
152
Pathophysiology of anaphylaxis
Sensitised individual exposed to specific antigen
• Commonly from insects bites/ stings, food, medications
• Immunological response:
– IgE → antigen → mast cell & basophils ‡ →
histamine ↑ → body response
153
Symptoms and signs of anaphylaxis
Pruritus, urticaria & angioedema,
hoarseness, progressing to stridor & bronchial
obstruction, wheeze & chest tightness from
bronchospasm
154
Treatment of anaphylaxis including acute comps
• DO NOT DELAY! GET HELP
• Remove trigger, maintain airway, 100% O2
• Intramuscular adrenaline 0.5 mg
(Repeat every 5 mins as needed to support CVS)
• IV hydrocortisone 200mg
• IV chlorpheniramine 10 mg
• If hypotensive: lie flat and fluid resuscitate
• Treat bronchospasm: NEB salbutamol
• Laryngeal oedema: NEB adrenaline
155
Classification of asthma
```
Mild:
• No features of severe asthma
• PEFR >75%
Moderate:
• No features of severe asthma
• PEFR 50-75%
Severe (if any one of the following):
• PEFR 33 – 50% of best or predicted
• Cannot complete sentences in 1 breath
• Respiratory Rate > 25/min
• Heart Rate >110/min
Life threatening (if any one of the following):
• PEFR < 33% of best or predicted
• Sats <92% or ABG pO2 < 8kPa
• Cyanosis, poor respiratory effort, near or fully silent
chest
• Exhaustion, confusion, hypotension or arrhythmias
• Normal pCO2
Near Fatal:
• Raised pCO2
```
156
Acute asthma management
Acute Asthma Management:
• ABCDE
• Aim for SpO2 94-98% with oxygen as needed, ABG if
sats <92%
• 5mg nebulised Salbutamol (can repeat after 15 mins)
• 40mg oral Prednisolone STAT (100mg IV Hydrocortisone if
PO not possible)
If severe:
• Nebulised Ipratropium Bromide 500 micrograms (0.5mg) (ever 6hr)
• Consider back to back Salbutamol (monitor ECG)
If no improvement consider single doseof MgSO4 1.2-2g IV over 20min
```
If life threatening or near fatal:
• Urgent ITU or anaesthetist assessment
• Urgent portable CXR
• IV Aminophylline
• Consider IV Salbutamol if nebulised route ineffective
```
```
If improvement
-Continue nebs (all that have been started every 4-6hr
Pred 40mg PO OD for 5-7 days
Monitor PEFR and sats
Follow up in clinic
```
157
Types of COPD exacerbations and how to tell the difference
```
Infective
o Change in sputum volume / colour
o Fever
o Raised WCC +/- CRP
• Non-infective
```
158
Management acute COPD
ABCDE approach
Oxygen:
- via a fixed performance face mask due to risk of
CO2 retention
- aim for SaO2 88-92% being guided by ABGs
• NEBs – Salbutamol and Ipratropium
• Steroids – Prednisolone 30mg STAT and OD for 7
days
• Antibiotics if raised CRP / WCC or purulent sputum
• CXR
• Consider IV aminophylline if no response
If still no response
• Consider NIV if Type 2 respiratory failure and pH 7.25-7.35 or RR <30 or PCo2 rising
• If pH <7.25 consider ITU referral
If NIV unavailable e.g. agitation, confusion, tachycardia, nausea consider doxapram only short term
159
Dianosis of pneumonia
Consolidation on CXR with fever +/- purulent sputum +/ raised
WCC and / or CRP (signs of infection)
160
Management of pneumonia
ABCDE
• If any features of sepsis – immediately treat using
sepsis pathway – NO DELAY in initiating IV
antibiotics and fluids
• Otherwise treat with antibiotics as per CURB-65
score, local pneumonia guidelines and awareness of
any patient drug allergies
ABG if low sats
CURB 1 - amox or clarithro or doxy
CURB 2 - hospital, blood ciltures (if febrile) sputum cultures (if not abx yet)and urine pneumococcal antigen, Viral throat swab or myoplasma PCR/serology? pleural fluid aspiration
Amox + clarithro OR doxy
3: itu referral. Urine legionella antigen. Co amox or cefuroxime AND clarithro
Add fluclox and or rifampicin if staph suspected, vanc for MRSA
Fluroquinolone for Legionella
CHECK WITH GUIDELINES
161
CURB criteria
CURB-65 Score
C Confusion, MMT 2 or more points worse - abbreviate MT <=8
U Urea > 7.0
R > 30 / min
B < 90 mm Hg systolic or < 60 mm Hg diastolic
65 Age above 65 years
162
What is massive haemoptysis?
>240mls in 24 hours
OR
• >100mls / day over consecutive days
(chronic inflammatory conditions e.g. bronchiectasis, TB and lung abcess or neoplasia)
163
Management of massive haemoptysis
ABCDE
• Lie patient on side of suspected lesion (if known)
• Oral Tranexamic Acid for 5 days or IV
• Stop NSAID’s / aspirin / anticoagulants
• Antibiotics if any evidence of respiratory tract
infection
• Consider Vitamin K
• CT aortogram – interventional radiologist may be
able to undertake bronchial artery embolisation
164
Tension pneumothorax symptoms and sings
Asymptomatic, sudden inset dyspnoea/ pleuritic chest pain - sudden deterioration in asthma/' COPD, hypoxia in mechanically ventillated patients
```
hypotension
Reduced expansion
Hyper resonance to percussion
Diminished breath sounds
o tachycardia
o deviation of the trachea away from the side of
the pneumothorax
o Mediastinal shift away from pneumothorax
```
165
Management of Tension pneumothorax
Management of Tension Pneumothorax - dont do CXR if suspect:
- Large bore intravenous cannula 14-16g into 2nd ICS MCL
- Chest drain into the affected side
If not suspected do CXR, monitor sats.
ABG in hypoxic patients with lung disease
Due to trauma/ mechanical ventilation requires chest drain
Surgerical advice if bilateral pneumothoraces
All in all most aspirate pneumoathorax then add central line - 4-6th ICS- ant to mid AL (safe triangle)
As per BTS guidelines:
Primary – If symptomatic and rim of air >2cm on
CXR give O2 and aspirate. If unsuccessful
consider re-aspiration or intercostal drain. Remove
drain after full re-expansion / cessation of air leak.
Secondary – as above but lower threshold for ICD
If persistent air leak >5 days (bronchopleural
fistula) refer to thoracic surgeons
Discharge advice – No flying or diving until
resolved
166
Causes of pneumothorax
Spontaneous, Chronic lung disease (fibrosis, asthma, COPD), infection - pneumonia, TB, abscess,
Trauma including iatrogenic, percutanous liver biopsy
Carcinoma
Marfan's syndrome
```
Pneumothorax Risk Factors
- Pre-existing lung disease
- Height
- Smoking/ Cannabis
- Diving
- Trauma/ Chest procedure
- Association with other conditions e.g. Marfan’s
syndrome
```
167
Complications of pneumonia
Plural effusion, empyema, pneumothorax, lobar collapse, lung abscess, resp failure, sepsis, pericarditis/ myocarditis, cholestatic jaundice, AKI
168
Symptoms of PE
```
– Chest pain (pleuritic)
– SOB
– Haemoptysis
– Low cardiac output followed by collapse (if
Massive PE)
```
169
Risk factors PE
```
• Surgery
– Abdominal/pelvic; Knee/ hip replacement
Post-operative spell on ITU
• Obstetric
– Late pregnancy; Caesarian section
• Lower Limb
– Fracture; Varicose veins
• Malignancy
– Abdominal/ Pelvic/ Advanced/ Metastatic
• Reduced Mobility
• Previous proven VTE
```
170
Describe Wells score
clinically suspected DVT — 3.0 points
alternative diagnosis is less likely than PE — 3.0 points
tachycardia (heart rate > 100) — 1.5 points
immobilization (≥ 3d)/surgery in previous four weeks — 1.5 points
history of DVT or PE — 1.5 points
hemoptysis — 1.0 points
malignancy (with treatment within six months) or palliative — 1.0 points
Score > 4 — PE likely. Consider diagnostic imaging.
Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.
171
Management of PE
ABCDE
• Oxygen if hypoxic
• Fluid resuscitation (if hypotensive)
• Thrombolysis should be considered if a massive PE
is confirmed on Echo or CT scan
– consider without imaging if there is
substantial clinical suspicion and cardiac
arrest is imminent e.g. hypotension
– check for contraindications
• Should be fully anticoagulated - with DOAC may not need LMWH overlap
Massive PE
• hypotension/ imminent cardiac arrest
• signs of right heart strain on CT / Echo
• Consider thrombolysis with IV alteplase
172
Thrombolysis complications
```
Bleeding
• Hypotension
• Intracranial haemorrhage / stroke
• Reperfusion arrhythmias
• Systemic embolisation of thrombus
• Allergic reaction
```
173
Pathophysiology of asthma
Airway epithelial damage – shedding and
subepithelial fibrosis, basement membrane
thickening
• An inflammatory reaction characterised by
eosinophils, T-lymphocytes (Th2) and mast cells.
Inflammatory mediators released include histamine,
leukotrienes, and prostaglandins
• Cytokines amplify inflammatory response
• Increased numbers of mucus secreting goblet cells
and smooth muscle hyperplasia and hypertrophy
• Mucus plugging in fatal and severe asthma
174
Wheeze differentials
```
• Acute Asthma Exacerbation
• Bronchitis – viral or bacterial
Other causes of wheeze less likely:
• Pulmonary oedema
• PE
• Vocal cord dysfunction
• Gastro-oesophageal reflux
• Foreign body
• Allergy
• Hyperventilation / psychosocial
• Cardiac disease
• Vasculitides – Churg-Strauss syndrome, polyarteritis
nodosa, Granulomatosis with Polyangiitis
(Wegener’s granulomatosis)
• Carcinoid syndrome with hepatic metastases –
release of HIAA
```
175
Criteria for safe asthma discharge after exacerbation
PEFR >75%
• Stop regular nebulisers for 24 hours prior to
discharge
• Inpatient asthma nurse review to reassess inhaler
technique and adherence
• Provide PEFR meter and written asthma action plan
• At least 5 days oral prednisolone
• GP follow up within 2 working days
• Respiratory Clinic follow up within 4 weeks
• For severe or worse, consider psychosocial factors
176
Is eosinophilia signifcant in asthma?
More effective steroids
177
DDX eosinophillia
```
Airways inflammation (asthma or COPD)
• Hayfever / allergies
• Allergic Bronchopulmonary Aspergillosis
• Drugs
• Churg-Strauss / vasculitis
• Eosinophilic Pneumonia
• Parasites
• Lymphoma
• SLE
• Hypereosinophilic syndrome
```
178
Asthma trigger factors
Smoking
• Upper respiratory tract infections – mainly viral
• Allergens – pollen, house dust mite, pets
• Exercise – also cold air
• Occupational irritants
• Pollution
• Drugs – aspirin, beta blockers (including eye drops)
• Food and drink – dairy produce, alcohol, orange
juice
• Stress
• Severe asthma – consider inhaled heroin,
pre-menstrual, psychosocial aspects
179
Management of chronic asthma
BTS guidelines
1 - low-dose inhaled corticosteroid in combination with a short-acting beta agonist (Up to 3 x per week)
2- Add LABA (combination)
3 - Remove LABA if it didnt help, increase to medium dose ICS
4: Trail: High dose ICS, LTRA, SR thophylline, slow release BA tablet or tiotropium. Refer
5: Oral pred, Refer
180
COPD definition
COPD is characterised by airflow obstruction. The
airflow obstruction is usually progressive, not fully
reversible and does not change markedly over several
months. The disease is predominantly caused by
smoking.
181
Pathophysiology COPD
Mucous gland hyperplasia
• Loss of cilial function
• Emphysema – alveolar wall destruction causing
irreversible enlargement of air spaces distal to the
terminal bronchiole
• Chronic inflammation (macrophages and
neutrophils) and fibrosis of small airways
182
Causes oF COPD
Smoking
• Inherited α-1-antitrypsin deficiency
• Industrial exposure, e.g. soot
183
COPD outpatient management
```
• ‘COPD Care Bundle’
• SMOKING CESSATION
• Pulmonary Rehabilitation
• Bronchodilators
• Antimuscarinics
• Steroids
• Mucolytics
• Diet
• LTOT if appropriate
• LUNG VOLUME REDUCTION if appropriate
MDT!
```
184
Bleeding risk on Warfarin/ management
```
Situation Management
Major bleeding Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*
INR > 8.0
Minor bleeding Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0
INR > 8.0
No bleeding Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
INR 5.0-8.0
Minor bleeding Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0
INR 5.0-8.0
No bleeding Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose
```
Minor bleed e.g. epistaxis
185
Describe rationale and criteria fir LTOT
Extended periods of hypoxia cause renal and
cardiac damage – can be prevented by LTOT
• Continuous oxygen therapy for most of the day – at
least 16 hours/day for a survival benefit
• LTOT offered if pO2 consistently below 7.3 kPa, or
below 8 kPa with cor pulmonale
• Patients must be non-smokers and not retain high
levels of CO2
• O2 needs should be balanced with loss of
independence and reduced activity which may occur
186
Describe pulmonary rehab for COPD
Many COPD patients with COPD avoid exercise and
physical activity because of breathlessness
• This may lead to a vicious cycle of increasing social
isolation and inactivity leading to worsening of
symptoms
• Pulmonary Rehabilitation aims to break this cycle –
an MDT 6-12 week programme of supervised
exercise, unsupervised home exercise, nutritional
advice, and disease education
COPD Exacerbations
187
CXR consolidation DDX
* Pneumonia
* TB (usually upper lobe)
* Lung cancer
* Lobar collapse (blockage of bronchi)
* Haemorrhage
188
Pneumonia follow up
```
• HIV test
• Immunoglobulins
• Pneumococcal IgG serotypes
• Haemophilus influenzae b IgG
• Follow up in clinic in 6 weeks with a repeat CXR to
ensure resolution
```
189
Causes of non-resolving pneumonia
CHAOS
• Complication – empyema, lung abscess
• Host – immunocompromised
• Antibiotic – inadequate dose, poor oral absorption
• Organism – resistant or unexpected organism not
covered by empirical antibiotics
• Second diagnosis – PE, cancer, organising
pneumonia (bronchiolitis obliterans assoc eith RA/ dermatomyositis/ amioderone)
190
TB features
Often fever and nocturnal sweats (typically
drenching)
• Weight loss (weeks – months)
• Malaise
• Respiratory TB: cough ± purulent sputum/
haemoptysis, may also present with pleural effusion
• Non-Respiratory TB: Skin (erythema nodosum);
Lymphadenopathy; Bone/joint; Abdominal; CNS
(meningitis); Genitourinary; Miliary (disseminated);
Cardiac (pericardial effusion)
191
DDX haemoptysis
```
Infection:
• Pneumonia
• Tuberculosis
• Bronchiectasis / CF
• Cavitating lung lesion (often fungal)
Malignancy:
• Lung cancer
• Metastases
Haemorrhage:
• Bronchial artery erosion - aneurysm or TB
• Vasculitis
• Coagulopathy
Others:
• PE
```
192
TB RFs
Past history of TB
• Known history of TB contact
• Born in a country with high TB incidence
• Foreign travel to country with high incidence of TB
• Evidence of immunosuppression–e.g. IVDU, HIV,
solid organ transplant recipients, renal failure/
dialysis, malnutrition/ low BMI, DM, alcoholism
193
Management principles for resp TB
• ABCDE approach & aim to culture whenever
possible
• Admit to a side room& start infection control
measures (e.g. masks & negative pressure room)
• If productive cough: x3 sputum samples for
AAFB&TB culture (ideally early morning samples)
• (If no productive cough & pulmonary TB suspected
consider bronchoscopy)
• Routine bloods (especially LFTs) & include HIV test
and vitamin D levels
• Consider CT chest if pulmonary TB suspected but
clinical features/ CXR not typical
• Must perform MRI brain/spine if military TB is
suspected followed by LP ideally
• If diagnosis between pneumonia and TB not clear:
start antibiotics for pneumonia (as per CURB-65)
whilst investigating possibility of TB.
• If patient critically unwell and high likelihood of TB
(no time to wait for sputum results) then start anti-TB
therapy AFTER sputum samples sent.
• Notify case to TB nurse specialists (support patient
in investigation, during treatment, public health
issues and initiate contact tracing)
• TB culture can take 6-8 weeks. So, treatment is
often started before a culture confirmed diagnosis
can be made. In some cases, positive culture is not
obtained and treatment depends on a strong clinical
suspicion.
194
Anti TB therapy practicalities
• Standard regimen is with 4 antibiotics for the first two
months (Rifampicin, Isoniazid, Pyrazinamide,
Ethambutol) followed by 4 months on two antibiotics
(Rifampicin, Isoniazid)
• Treatment for a minimum of 6 months in total (can
vary – see NICE/ BTS guidelines)
• Patient’s weight is important: dose of anti-TB
antibiotics is weight dependent
• Check baseline LFT’s and monitor closely
• Check visual acuity before giving Ethambutol
• Compliance is crucial and Directly Observed
Therapy (DOT) sometimes used for patients
• Provide leaflets on treatment & ensure patient is
aware of common and serious side effects (see
below)
• Pyridoxine also given (while on Isoniazid) as
prophylaxis against peripheral neuropathy
• Corticosteroids sometimes used, mainly seen in
those with TB meningitis
195
side effects of anti tb
Rifampicin – Hepatitis, rashes, febrile reaction,
orange/red secretions (N.B. contact lenses),
many drug interactions including warfarin and
OCP
• Isoniazid – Hepatitis, rashes, peripheral
neuropathy, psychosis
• Pyrazinamide – Hepatitis, rashes, vomiting,
arthralgia
• Ethambutol – Retrobulbar neuritis
196
Define bronchiectasis
Chronic dilatation of one or more bronchi. The
bronchi exhibit poor mucus clearance and there is
predisposition to recurrent or chronic bacterial
infection
• Gold standard diagnostic test = High Resolution CT
197
Bronchiectasis causes
Post infective – whooping cough, TB
• Immune deficiency – Hypogammaglobulinaemia
• Genetic / Mucociliary clearance defects – Cystic
fibrosis, primary ciliary dyskinesia, Young’s
syndrome (triad of bronchiectasis, sinusitis, and
reduced fertility), Kartagener syndrome (triad of
bronchiectasis, sinusitits, and situs inversus)
• Obstruction – foreign body, tumour, extrinsic lymph
node
• Toxic insult – gastric aspiration (particularly post lung
transplant), inhalation of toxic chemicals/gases
• Allergic bronchopulmonary aspergillosis
• Secondary immune deficiency – HIV, malignancy
• Rheumatoid arthritis
• Associations – inflammatory bowel disease; yellow
nail syndrome
198
Bronchiectasis common organisms
```
• Haemophilus influenzae
• Pseudomonas aeruginosa
• Moraxella catarrhalis
• Stenotrophomonas maltophilia
• Fungi – aspergillus, candida
• Non-tuberculous mycobacteria
• Less common - Staphylococcus aureus (think about
CF)
```
199
Typical and atypical causes of CAP
Typical – Staph aureus, Haemophilus influenzae, Staph aureus
Atypical – Legionella, Chlamydia spp, Mycoplasma e.g. tuberculosis
Viral – Influenza, Respiratory syncytial virus (RSV)
Immunosuppressed – Candida albicans, aspergillus pneumocystis jirovecii, Viruses, CMV, HSV, VZV), pseudomans auruginosa
200
Bronchiectasis management
Treat underlying cause
• Physiotherapy – mucus clearance
• Antibiotics according to sputum cultures /
sensitivities for acute exacerbations and often
chronic suppressive therapy
• Supportive – flu vaccine, bronchodilators if required
• Pulmonary Rehab – MRC Dyspnoea Score >3
Postural drainage
Surgical options if severe
201
What is CF:
CF is an autosomal recessive disease leading to mutations in
the Cystic Fibrosis Transmembrane Conductance Regulator
(CFTR). This can lead to a multisystem disease (most
commonly affecting the respiratory and gastrointestinal
systems) characterised by thickened secretions.
202
CF diagnosis
One or more of the characteristic phenotypic features -
• Or a history of CF in a sibling
• Or a positive newborn screening test result
And
• An increased sweat chloride concentration
(> 60 mmol/l) – SWEAT TEST
• Or identification of two CF mutations – genotyping
• Or demonstration of abnormal nasal epithelial ion
transport (nasal potential difference)
203
CF Presentations
1. Meconium ileus
• In 15-20% of newborn CF infants the bowel is
blocked by the sticky secretions. There are signs of
intestinal obstruction soon after birth with bilious
vomiting, abdominal distension and delay in passing
meconium.
2. Intestinal malabsorption
• Over 90% of CF individuals have intestinal
malabsorption. In most this is evident in infancy. The
main cause is a severe deficiency of pancreatic
enzymes.
3. Recurrent Chest infections
4. Newborn screening
204
Features of CF
Chronic sinusitis, nasal polyps, LRTI, bronchiectasis, abnormal sweat secretion,, liver disease, gall stones, potal hypertension, pancreatic insufficiency, DM, finger clubbing, steatorrhea, male infertilkity, osteoporosis, arthropathy/itis
205
Common CF complications
1. Respiratory Infections
- Needs aggressive therapy with physio and antibiotics
- Patients often receive prophylactic antibiotics to maintain
health
2. Low Body Weight
- needs careful monitoring
- may be consequence of pancreatic insufficiency (lack of
pancreatic enzymes), therefore in those patients give
pancreatic enzyme replacement therapy
- high calorie intake and often extra supplements
- may need NG or PEG feeding
3. Distal Intestinal Obstruction Syndrome (DIOS)
- DIOS vs. constipation – faecal obstruction in ileocaecum
versus whole bowel
- Due to intestinal contents in the distal ileum and proximal
colon (thick, dehydrated faeces)
- Most often due to insufficient prescription of pancreatic
enzymes or non-compliance, also salt deficiency / hot
weather
- Often presents with palpable right iliac fossa mass
(faecal)
- Diagnosis: Symptoms, palpable Right Iliac Fossa Mass,
AXR demonstrating faecal loading at junction of small
and large bowel
4. CF Related Diabetes
206
CF lifestyle advice
• No smoking
• Avoid other CF patients
• Avoid friends / relatives with colds / infections
• Avoid jacuzzis (pseudomonas)
• Clean and dry nebulisers thoroughly
• Avoid stables, compost or rotting vegetation – risk of
aspergillus fumigatus inhalation
• Annual influenza immunisation
• Sodium chloride tablets in hot weather / vigorous
exercise
207
Types of pneumothorax
1. Spontaneous
i. Primary (no lung disease)
ii. Secondary (lung disease)
2. Traumatic
3. TENSION: emergency
4. Iatrogenic (e.g. post central line or pacemaker insertion)
208
Approach to Pleural effusion
History & Examination is cornerstone
•CXR
•ECG
•Bloods: FBC, U&E’s, LFT’s, CRP, Bone profile, LDH,
clotting
•ECHO (if suspect heart failure)
•Staging CT (with contrast) if suspect exudative cause
209
Treatment CF
```
Abx
Azithromycin prophylactic possible
Salbutamol nebs
Lung transplant
Croeon+ fat sol vitamins
Airway clearance technique e.g. chest physio
```
210
Pleural effusion diagnosis
Pleural Effusion Diagnosis:
Ultrasound guided pleural aspiration
- Biochemistry (protein, pH, LDH)
- Cytology
- Microbiology (including AAFB)
N.B. Never insert a chest drain unless the diagnosis is well
established (e.g. known metastatic lung cancer) otherwise
draining all fluid off may hinder the opportunity to obtain
pleural biopsies. Only indication for urgent chest drain
insertion for a new effusion would be an underlying
empyema (pH of pleural fluid <7.2 or visible pus on
aspirate).
Consider Thoracoscopy or CT Pleural Biopsy
211
Management of Pleural effusion
```
Do not drain unless pH of aspirate <7.2 or visible empyema on aspirate as was hinder opportunity for pleural biopsy
Treat cause (transudates)
```
212
Causes of transudates
```
Common:
Heart failure
Cirrhosis
Hypoalbuminaemia (nephrotic syndrome or
peritoneal dialysis)
Less common:
Hypothyroidism, mitral stenosis, pulmonary
embolism
Rare:
Constrictive pericarditis, superior VC obstruction
```
213
Causes of exudates
Common:
Malignancy
Infections – parapneumonic, TB, HIV (kaposi’s)
Less common:
Inflammatory (rheumatoid arthritis, pancreatitis,
benign asbestos effusion, Dressler’s, pulmonary
infarction/pulmonary embolus), Lymphatic
disorders, Connective tissue disease
Rare:
Yellow nail syndrome, fungal infections, drugs
214
What is lights criteria?
If pleural fluid protein level between 25 and 35 g/
L (i.e.
borderline) use
Light’s criteria
– exudate if one or more of the following:
–
Pleural fluid/Serum protein >0.5
–
Pleural fluid/Serum LDH >0.6
–
Pleural fluid LDH > 2/3 of the upper limit of normal
215
What is ILD? what does this include?/ method
```
Umbrella term describing a number of conditions tha
t affect
the lung parenchyma in a diffuse manner including:
•
Usual Interstitial Pneumonia (UIP)
•
Non-specific Interstitial Pneumonia (NSIP)
•
Extrinsic Allergic Alveolitis
•
Sarcoidosis
•
Several other conditions
```
Look at organic e.g. birds, pets, farmers lung (extrinsic allergic pneumonitis)
Look at inorganic e.g. asbestos, welding, soot, silicon (rocks or sand)
Look at drugs e.g. nitro, amioderone, MTX
Look at CT disroders/ rheum
If not idiopathic (CT may fit into this too)
216
What is UIP?
```
Commonest type of Pulmonary Fibrosis
Usually Idiopathic
Classical Findings:
•
clubbing, reduced chest expansion
•
Auscultation – fine inspiratory crepitations (like
pulling Velcro slowly) – usually best heard basal /
axillary areas
•
Cardiovascular – may be features of pulmonary
hypertension
```
Commenest type of idiopathic I think? Diagnosis of exclusion/ histological but often made form history and CT by MDT
217
Investigations in ILD
```
- Important to take a comprehensive occupational /
environmental history
- Typically restrictive lung diseases on PFT’s
- For new diagnoses of ILD should obtain a comprehe
nsive
array of investigations including:
ANA
ENA
Rh F
ANCA
Anti-GBM
ACE
Ig G to serum precipitins
(HIV
```
218
What is extrinsic allergic alveolitis and how is it treated?
Also known as Hypersensitivity Pneumonitis
• Inhalation of organic antigen to which the indivi
dual has
been sensitised
Clinical Presentation:
–ACUTE – short period from exposure, 4-8 hrs. Usually
reversible: spontaneously settle 1-3 days. Can recu
r.
–CHRONIC – chronic exposure (months – years). Less
reversible.
The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects
219
What is Sarcoidosis?
• Multisystem inflammatory condition of unknown cau
se
• Non-caseating granulomas (Histology important)
• Immunological response
• Commonly involves Resp system BUT can affect nearl
y
all organs
• 50% get spontaneous remission, others get progres
sive
disease
Some evidence for mycophenylate/ ciclosporin
220
Investigations in sarcoidosis?
• PFTs: (obstructive until) fibrosis
• CXR: 4 stages
• Bloods: renal function, ACE (high in sarcoid), Calcium (high due to increased Vit D)
• Urinary Calcium
• Cardiac involvement: ECG, 24 tape, ECHO, cardiac MR (conduction abnormalities or arrhythmias)
I
• CT/MRI head: headaches – Neuro sarcoid (many things e.g. cranial nerves)
221
ILD treatment principles
```
Depends on underlying pathology
• Occupational exposure – remove
• Drug associated – avoid
• Stop smoking
• Nintedinab Pirfenidone
• Transplantation
• Treatment of infections (atypical)
• Oxygen
• MDT
• Palliative care
```
222
Xray/ Ct changes in IPF
Honeycombing
Diffuse thickening, bases and peripheral
Traction bronchiectasis
223
Lung cancer presentation
Asymptomatic, incidental finding
• Any respiratory symptom/systemic deterioration
• Superior Vena Caval Obstruction
• Horner’s syndrome
• Metastatic disease – liver, adrenals (Addison’s),
bone, pleural, CNS
• Paraneoplastic – clubbing, hypercalcaemia,
anaemia, SIADH, Cushing’s syndrome, Lambert-
Eaton myasthenic syndrome, thrombo-embolic
disease
224
Lung cancer RFs
* Large number of smoking pack years
* Airflow obstruction
* Increasing age
* Family history of lung cancer
* Exposure to other carcinogens, e.g. asbestos
225
Diagnostic tests LC
MDT approach vital (Physicians, Oncologists, Surgeons,
Radiologists, Pathologists, Palliative Care Team, Specialist
Nurses, Primary Care)
• Bloods – FBC, U&E, Calcium, LFT’s, INR
• CXR
• Staging CT – Spiral CT Thorax and Upper Abdo –
helps to stratify TNM stage
Histology options
• US guided neck node FNA for cytology if
lymphadenopathy
• Bronchoscopy – endobronchial, transbronchial,
endobronchial ultrasound (if mediastinal
lymphadenopathy)
• CT Biopsy
• Thoracoscopy if pleural effusion present
PET Scan
• MDT Decision if patient is a surgical candidate
and initial CT suggestive of low stage
• Helps to detect small metastases not seen on
staging CT
226
histological classificiation of LC
Classified primarily into two groups which account for about
95% of cases
1. Small cell (oat cell) lung cancer (SCLC)
2. Non-small cell lung cancer (NSCLC)
- includes squamous cell, adenocarcinoma, and large cell
carcinoma, bronchoalveolar cancer
Others -, bronchial gland ca, carcinoid tumour
227
Lung cancer treatment summary
• Curative surgery for stages I & II – assuming fit for
surgery
• Surgery & adjuvant chemotherapy clinical trial for
stage IIIa – assuming fit for surgery & chemo
• Chemotherapy – consider in patients with stage
III/IV disease and WHO PS 0-2
• Radiotherapy – curative (CHART = continuous
hyperfractionated accelerated radiotherapy) for
people not fit for surgery OR palliative
• Palliative Care
• Do nothing / watch & wait
228
Prognosis of lung cancer
NSCLC 5 year
All NSCLC – 10-13%
• Stage 1 following surgical resection – 60-70%
• Stage II following surgical resection – 30-55%
• Stage III – 7%
• Stage IV – 1%
Rapid growth rate and almost always too
extensive for surgery at time of diagnosis
• Mainstay of treatment is chemotherapy
• Also palliative radiotherapy
• Untreated – median survival is 4-12 weeks
• Combination chemotherapy – median survival 6-
15 months
229
OSA definition
upper airway narrowing,
provoked by sleep, causing sufficient sleep
fragmentation to result in significant daytime
symptoms, usually excessive sleepiness
230
RFs OSA
OSA are male, and
tend to have a combination of upper body obesity
(collar size >17 in), and a relatively undersized or
set back mandible
231
Pathophysiology OSA
Upper airway patency depends on dilator muscle
activity. All muscles relax during sleep (including
pharyngeal dilators).
Some narrowing of the upper airway is normal
Excessive narrowing can be due to either an
already small pharyngeal size during awake state
which undergoes a normal degree of muscle
relaxation during sleep causing critical narrowing
OR excessive narrowing occurring with relaxation
during sleep
232
Causes of small pharyngeal size
Fatty infiltration of pharyngeal tissues and external
pressure from increased neck fat and/or muscle
bulk
Large tonsils
Craniofacial abnormalities
Extra submucosal tissue, e.g. myxoedema
233
Clinical effects of OSAexcessive narrowing of the airway during sleep
Severe OSA leads to repetitive upper airway
collapse, with arousal required to re-activate the
pharyngeal dilators. There may be associated
hypoxia and hypercapnia which are corrected
during the inter-apnoeic hyperventilatory period.
Recurrent arousals lead to highly fragmented and
unrefreshing sleep – snoring and apnoea attacks
often witnessed by partner
Excessive daytime sleepiness results (Epworth
Sleepiness Scale score >9)
With every arousal there is a rise in BP, often over
50 mmHg. It is not clear if this damages the CVS.
There is also a rise in daytime BP.
Nocturia
Less common - Nocturnal sweating, reduced
libido, oesophageal reflux
234
Describe the Epworth Sleepiness Scale
```
Points for following:0=would never doze, 1=slight chance,
2=moderate chance, 3=high chance
Sitting & reading
Watching TV
Sitting in a public place, e.g. theatre
Passenger in a car for an hour
Lying down to rest in the afternoon
Sitting & talking
Sitting quietly after lunch without alcohol
In a car, while stopped in traffic
```
235
Diagnosis of OSA
Overnight oximetry alone
Limited sleep study – oximetry, snoring, body
movement, heart rate, oronasal flow,
chest/abdominal movements, leg movements –
usual study of choice
Full polysomnography – limited study plus EEG,
EMG
236
Management OSA
Treatment is given based on symptoms/quality of
life – NOT on severity seen on sleep study
Also consider livelihood, e.g. driving as occupation
SIMPLE APPROACHES:
Weight loss, sleep decubitus rather than supine,
avoid/reduce evening alcohol intake
FOR SNORERS & MILD OSA:
Mandibular advancement devices, consider
pharyngeal surgery as last resort
FOR SIGNIFICANT OSA:
Nasal CPAP, consider gastroplasty/bypass, and
rarely tracheostomy
FOR SEVERE OSA & CO2 RETENTION:
May require a period of NIV prior to CPAP if
acidotic, but compensated CO2 may reverse with
CPAP alone
237
OSA Driving advice
Tell all patients with OSA to NOT drive while
sleepy; stop and have a nap. On diagnosis the
patient should notify the DVLA
The doctor can advise drivers to stop altogether
(e.g. HGV drivers)
238
CPAP moA
Usually given via nasal mask, but can use
mouth/nose masks
Upper airways splinted open with approximately
10cm H2O pressure – this prevents airways
collapse, sleep fragmentation, and ultimately
daytime somnelence
Also opens collapsed alveoli and improves V/Q
matching
239
CPAP vs BIPAP
xCPAP supplies constant positive pressure during
inspiration and expiration and is therefore not a
form of ventilatory support. It can be used to treat
OSA and helps oxygenation in some patients with
acute respiratory failure, e.g. pulmonary oedema
Non-invasive ventilation (NIV) does provide
ventilatory support with two levels of positive
pressure (bilevel) – pressure support provided
between selected inspiratory and expiratory
positive pressures (IPAP & EPAP). They can also
be set up with back up rates so the machine
operates when the respiratory rate drops below a
fixed level.
240
Aortic dissection most likely person
Afro-carribean males aged 50-70
HYT
CT disorder
241
Aortic dissection classification
The dissection may spread either proximally or distally with subsequent disruption to the arterial branches that are encountered.
In the Stanford classification system the disease is classified into lesions with a proximal origin (Type A) and those that commence distal to the left subclavian (Type B).
Proximal (Type A) lesions are usually treated surgically, type B lesions are usually managed non operatively.
242
Diagnosis of aortic dissection
Diagnosis may be suggested by a chest x-ray showing a widened mediastinum. Confirmation of the diagnosis is usually made by use of CT angiography
243
Complications of aortic dissection/ other symptoms
CHF - pericarditis/ tamponade from a bleed, syncope, stroke, ioschemia peripheral neuropathy, cardiac arrest. MI in 1-2% duer to involvement of coronary arteries. Pleural effusion due to inflam reaction
Pain
Aortic insufficiency - aortic rejurg,
244
What is Boerhaave syndrome?
Spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting.
The rupture is usually distally sited and on the left side.
Patients usually give a history of sudden onset of severe chest pain that may complicate severe vomiting.
Severe sepsis occurs secondary to mediastinitis.
Diagnosis is CT contrast swallow.
Treatment is with thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin.
Delays beyond 24 hours are associated with a very high mortality rate.
The Mackler triad for Boerhaave syndrome: vomiting, thoracic pain, subcutaneous emphysema. It commonly presents in middle aged men with a background of alcohol abuse.
245
INR targets for Warfarin
venous thromboembolism: target INR = 2.5, if recurrent 3.5
atrial fibrillation, target INR = 2.5
mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.
246
E.g.s of xanthines and mOS
Aminophylline, Theophylline
Block phosphodiesterases resulting in
decreased cAMP breakdown causing
bronchodilation
247
Side effects of xanthines
```
Common Side
Effects
Headache, GI upset, reflux,
palpitations, dizziness
Therapeutic
Window
Plasma level 10-20 mg/L. Toxic effects
are serious arrhythmias, seizures,
N&V, hypotension
```
248
Common side effects of inhaled corticosteroids
Cough, oral thrush, unpleasant taste,
| hoarseness
249
ABPA symptom
```
Normally diagnosed with asthma
Wheeze (episodic)
Coughing
SOB
Exercise intolerance (common with CF)
```
Bronchiectasis like symptoms:
- Thick sputum
- pleuritic chest pain and fever (mimicking recurrent infection)
250
ABPA treatmetn
Manage underlying asthma or CF.
Steroids mainstay treatment to prevent fibrosis
Oral anti fungal to clear A from airways
251
ECG hypokalaemia
```
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
```
