Cardiology - Heart Failure and CM Flashcards
(359 cards)
1
Q
What is heart failure
A
A syndrome characterised by fatigue, breathlessness and fluid retention
Caused by impaired cardiac function leading to circulatory insufficiency
2
Q
What does dx of heart failure rely on
A
Clinical judgement based on several factors e..g symptoms and signs, severity, underlying cardiac abnormality, co-morbidities
3
Q
Classification of heart failure based on LVEF
A
HF w/ reduced LVEF (HFrEF) - <40%
HF w/ mid-range LVEF (HFmrEF) - 40-49%
HF w/ preserved LVEF (HFpEF) - >50%
4
Q
LVEF
A
LV ejection fraction
5
Q
Calculating Ejection fraction
A
End diastolic volume - end systolic volume / end-diastolic volume
6
Q
How can we measure EF
A
Echo
MRI
Myocardial perfusion scan
7
Q
What is a lower ejection fraction associated with
A
Higher risk of mortality
8
Q
What is a lower ejection fraction associated with
A
Higher risk of mortality
9
Q
What does EF look at
A
How much blood is pumped out of the heart vs the volume in ventricles before
10
Q
Normal EF
A
55%
11
Q
What are causes of systolic heart failure
A
IHD
DCM
Myocarditis
12
Q
Causes of diastolic heart failure
A
HCM/ HOCM
Restrictive CM
Cardiac tamponade
13
Q
Main causes of high-output cardiac failure
A
Anaemia and pregnancy
14
Q
Pathophysiology of heart failure
A
Initial event causing myocardial damage –> increase in wall stress –> activates multiple neuroendocrine systems causing further damage to myocardium
15
Q
Epidemiology of heart failure
A
CAD is leading cause of HF in UK
Incidence increases w/ age - age at first px is 76 yrs, M > F
16
Q
Prognosis of HF
A
Usually poor - 3yrs survival from dx, 40% die within 1 yr
17
Q
Presentation of HF
A
SOB Fatigue Orthopnoea PND Swollen ankles Palpitations
18
Q
NYHA clinical classification of HF
A
Class I - no limitations on activity
Class II - symptoms brought on by ordinary physical activity (mild HF)
Class III - Marked limitation of physical activity (moderate HF)
Class IV - pts have symptoms at rest (severe HF)
19
Q
Ix in HF
A
Standard bloods Other bloods Urinalysis BNP & N-terminal pro BNP ECG Echo CXR Cardiac imaging
20
Q
Standard bloods for HF ix
A
FBC
Renal function
21
Q
Extra bloods for HF ix
A
LFT
TFT
Glucose
Cholesterol
22
Q
Urinalysis for HF ix
A
Looking for protein and glucose
23
Q
What happens if BNP is normal in suspected HF
A
Normal BNP generally rules out HF
24
Q
When does BNP increase
A
In ventricular stretch/ LVEDP (preload)
25
CXR in a/c HF
Cardiomegaly - cardiothoracic ratio > 0.5
Pulmonary oedema
Bilateral blunting of costophrenic angles
26
Mx of a/c pulmonary oedema
Oxygen
Diuretics
Nitrates
Morphine
Weight pt daily and take daily U&Es
27
Key imaging method for pts w/ suspected heart failure
Echo
| Provides info on structure and function of cardiac chambers, valves and pericardium
28
When can you not do an echo
If the 'window' is poor
29
What do stress echos look for
Reversible ischaemia
30
What does a cardiac MR provide info about
Extent of fibrosis and perfusion abnormalities
31
When is a cardiac MR particularly useful
When echo images are poor due to obesity or COPD
32
What is usually required for cardiac MR
Specialist referral
33
Ddx of HF
```
Chest diseases
Venous insufficiency in LL
Drug-induced ankle swelling/ fluid retention
Angina
Hypoalumineamia
Intrinsic renal/ hepatic failure
Severe thyroid disease
Bilateral renal artery stenosis
```
34
General measures for managing HF
```
Pt education
Wt control
Reducing salt and fluid
Smoking cessation
Mx of co-morbidities
```
35
Poor prognostic factors in HF
```
Low EF (<30%) - most important
Low systolic BP
Coronary disease
Raised creatine/ eGFR
Hyponatremia
DM
Anaemia
Arrhythmia
AF
```
36
Aims of therapy in HF
Improve life expectancy
| Improve QoL
37
Aims of treatment of a/c HF
Improve haemodynamic & symptomatic profile
| Prevent myocardial & renal damage
38
A/c HF mx
PODMAN
```
Positioning - sit up (high Fowler's position)
Oxygen
Diuretics (loop)
Morphine
Antiemetics
Nitrates (IV)
```
May also give IV dobutamine and non-invasive ventilation (CPAP, BiPAP)
39
Diuretics therapy for HF
Rapid relief of congestive symptoms and fluid retention w/ loop diuretics e.g. furosemide, bumetanide
May be titrated according to need after adding new meds
40
Which HF symptoms do loop diuretics improve
Breathlessness
| Exercise performance
41
Drugs for c/c HFrEF
ACEi/ ARB
BB - reduce HR
Aldosterone receptor blockers (spironolactone, eplerenone)
Sacubitril/ valsartan
42
When would you use sacubitril/valsartan in c/c HF
Replaces ACEi/ ARB when EF <35%
43
Other potential treatments for c/c HF
Ivabradine (similar to BB)
Digoxin (esp w/ AF)
Amiodarone (pts w/ arrhythmias)
Anticoags
44
Why does ACE cough develop
ACE inactivates bradykinin
| ACE inhibition therefore leads to increase in bradykinin levels ---> cough and angiodema
45
Mx of pts w/ HF due to LV systolic dysfunction
ACEi (titrated up to correct dose)
| Treatment should be initiated before BB introduced
46
MOA of sacubutril/ valsartan
Neprilysin inhibits naturietic peptides and sacubutril is a neprilysin inhibitor (prevents breakdown)
Also inhibits angiotensin pathway
47
Treating HF and AF
Anticoag - consider for those w/ hx of thromboembolism, LV aneurysm or intracellular cardiac thrombus
Amiodarone - effective against most ventricular arrhythmias
48
Side effects of amiodarone
Thyroid dysfunction
Pulmonary fibrosis
Liver damage
Neuropathy
49
Surgery and devices for c/c HF
```
Coronary revascularisation
Transplantation
LVAD
CRT - biventricular pacing
Ablation for AF
ICD
Valve repairs if indicated
```
50
LVAD
LV Assist Device
51
Revascularisation for HF
PCI/ CABG may relieve ischaemic symptoms and improve mortality in heart failure pts w/ multi-vessel disease and stable angina
52
CRT for HF
~30% of HF pts have dyssynchronous ventricular contraction (LBBB)
53
When should CRT be considered in HF pts
LVSD (EF < 35%) on medical therapy and a QRS duration > 120msec
54
Heart transplant for HF
Limited availability of donor organs
Few UK centres
c/c immunotherapy required
55
Mechanical support for HF pts
Implanted mechanical pumps can provide circulatory support for short/medium term
56
When should mechanical support be considered for HF pts
Specialists consider this in pts w/ severe refractory symptoms, or refractory symptoms or refractory cardiogenic shock
57
What is HFpEF associated with
Older age and HTN/ LV hypertrophy, obesity, DM
58
Mutation seen in Marfan syndrome
FBN1 gene --> less functional fibrillin-1 produced
59
Inheritance pattern for Marfan syndrome
Autosomal dominant
60
Mutations seen in Long QT syndrome
KCNQ1, KCNH2 and SCN5A genes
61
Inheritance pattern for long QT syndrome
Autosomal dominant
62
Fabry disease
Results from build up of fat, globotriaosylceramide
63
What mutations cause Fabry disease
GLA --> absence of alpha-galactosidase A --> globotriaosylceramide isn’t broken down
64
Inheritance pattern of Fabry disease
X-linked
65
Mutations causing familiaal hypercholesterolaemia
Mutations in APO8, LDLR, LDLRAP1 or PCSK9
66
Most common cause of familial hypercholesterolaemia
Changes in LDLR --> less LDL receptors made --> less LDLs removed from blood stream
67
Inheritance pattern of familial hypercholesteolaemia
Autosomal dominant pattern
68
Genetic variation affecting mx of pts w/ CVD
Some pts treated w/ statins have bad ADRs e.g. myopathy associated w/ simva and a variant of gene SLCO1B1
Some pts treated w/ clopi don't benefit as variants of cytochrome P450 can alter conversion of inactive prodrug to its active metabolite
69
Cardiomyopathy
Disorder in which heart muscle is structurally and functionally abnormal (in absence of other heart condns severe enough to cause the heart muscle abnormality)
70
Commonest types of cardiomyopathies
Hypertrophic
Dilated
Arrhythmogenic
71
What type of impairment is seen in HCM
Diastolic
72
What type of impairment is seen in DCM
Systolic
73
Commonest CM
HCM
74
HCM
Unexplained LV hypertrophy - Pattern is usually asymmetric septal hypertrophy
Most common inherited cardiac disease (autosomal dominant)
Commonest cause of sudden death in young (<35yrs) and in athletes
75
What % of HCM pts have Fhx
50%
76
Usual px of HCM
HCM can px at any age - birth to >90
| Most cases are asymtpmatic
77
What % of HCM pts have an obstructive form
25%
78
What is HCM a disease of
Sarcomere
Mutated peptides incorporated into sarcomere --> impaired contractile function --> increased myocyte stress --> compensatory hypertrophy and increased fibrosis
79
Which proteins in the sarcomere are affected by HCM
Myosin binding protein c
| B myosin heavy chain
80
Hypertrophy vs hyperplasia
Hypertrophy is increase in muscle cell SIZE
| Hyperplasia is increase inn cell no.
81
Examination findings in HCM
May be normal
Double apical impulse
S4
Features of systolic outflow obstruction
82
Features of systolic outflow obstruction
Jerky pulse
| Systolic murmur - obstruction --> murmur at LSE (dynamic - changes depending on preload and afterload), MI
83
Jerky pulse
Brisk carotid upstroke which suddenly stops
84
ECG in HCM
Typically, v abnormal showing LVH w/ strain pattern
85
Imaging tests of choice in suspected HCM
Echo or MRI
86
Mx of HCM
```
General measure
Treat symptoms
Manage AF risk
Assess risk of sudden death
Family screening
```
87
General measures for HCM
Avoid competitive sports
Reassure pt w/out high-risk features
Overall prognosis is good
88
Treating symptoms of HCM
BB (or verapamil)
- Decreased HR --> increased diastolic filling time
- Decreased force of contraction ---> decreased myocardial oxygen demand
Myomectomy (or septal ablation) if still symptomatic
89
Myomectomy
Surgeon removes small amount of thickened septal wall to widen outflow tracts from LV to aorta
90
Family screening for HCM
Screen by ECG and echo (and genetic testing if mutation known)
91
What is DCM characterised by
Enlargement of one or both ventricles w/ impaired contractile function
92
What does DCM commonly cause
Systolic HF
93
Pathophysiology of DCM
Myocyte injury --> decreased contractility --> decreased SV
| This leads to increased ventricular filling pressure, LV dilatation, decreased CO
94
Types of DCM
```
Idiopathic
Familial
Infl
Toxic
Metabolic
Tachycardia induced
Neuromuscular
```
95
Infl DCM
Infectious - post viral
| Non-infectious - CTD, peripartum mypoathy, sarcoidosis
96
When does peripartum myopathy occur
Between 6th to 9th month of pregnancy
97
Toxic DCM
Alcohol - may be reversible by stoping alcohol intake
| Chemotherapy
98
Metabolic DCM
Caused by hypothyroidism
99
Tachycardia-induced DCM
May recover fully w/ treatment of arrhythmia
100
Neuromuscular DCM
Muscular or myotonic dystrophy
101
Px of DCM
Usually presents w/ signs of CCF
102
What should you ask a DCM pt when they px
Fhx
Alcohol
Exposure to chemotherapeutic drugs
103
Ix for DCM
```
Bloods
ECG
CXR
Echo/ MRI
Angiography
```
104
Bloods for DCM
U&E's
Ca
P
TFTs
105
ECG for DCM
No spp features
| Finding incl non-spp ST/T wave changes, conduction defects (incl BBB)
106
CXR findings for DCM
Cardiomegaly
107
Eco/ MRI findings for DCM
Enlargement of all 4 chambers w/ decreased systolic function
108
Angiography for DCM
To exclude IHD
109
Arrhythmogenic CM
An inherited heart muscle disorder characterised by replacement of RV myocardium by fibrofatty tissue
110
What is arrhythmogenic CM a disease of
Desmosome
111
Px of arrhythmogenic CM
Presents in young-middle age
| May be asymptomatic or present w/ palpitation, syncope or SCD
112
SCD
Sudden cardiac death
113
CCF
Congestive cardiac failure
114
ECG for arrythmogenic CM
Usually abnormal, showing T wave inversion nd localised prolongation of QRS interval in R precordial leads (V1 - V3)
115
Typical arrhythmia seen in arrhythmogenic CM
LBBB morphology VT
116
Dx of arrhythmogenic CM
Combi of ECG, imaging, Fhx, biopsy
117
ICD for arrhythmogenic CM pts
Pts who have survived cardiac aresst
Pts who've had haemodynamically unstable ventricular arrhythmias
Pts who have severe cardiac impairment
118
What do desmosomes do
Bind muscle cells together
119
Restrictive CM
Rare
Due to myocardial fibrosis or infiltration (usually amyloid)
Poor prognosis
120
Pathophsyiology of restrictive CM
Rigid myocardium leads to increased diastolic ventricular pressure --> venous congestion
As well as decreased ventricular filling --> decreased CO
121
Myocarditis
Infl of heart muscle
122
Which groups can the causes of myocarditis be divided into
Infection
Immune mediated
Toxic
123
Infection as a cause of myocarditis
Viral (commonest) - coxsackie (enterovirus), adenovirus, others e.g. Chaga disease
124
What is the commonest infection causing myocarditis worldwide
Trypanosoma cruzi
| Endemic in Central and South America
125
Immune-mediated myocarditis
Incl giant cell myocarditis, sarcoidosis
126
Toxic causes of myocarditis
Drugs (anthracycline)
Alcohol
Radiation
127
Which drugs can induce swelling
CCB
128
Which drugs can induce fluid retention
NSAIDs
129
Px of myocarditis
Classically presents w/ febrile illness w/ resp/ GI symptoms followed by any cardiac symptoms (fatigue, SOB, chest pain, palpitations, HF)
130
Spectrum of disease for myocarditis
Asymptomatic to cardiogenic shock
131
Cardiogenic shock
Life-threatening condn where heart suddenly cannot pump blood to meet body's needs
132
Px of myocarditis on young pts vs older pts
A/c flulike px is commoner in younger pts
| Older pts are more likely to px w/ DCM and HF
133
Ix for myocarditis
Bloods
ECG
Imaging
Endomycoardial biopsy
134
Blood results for myocarditis
Increased troponin
135
ECG changes in myocarditis
Non-spp ST/ T wave changes
May mimic MI
Arrhythmias
136
Imaging of choice for myocarditis
CMR
137
Endomyocardial biopsy
Gold standard test for myocarditis
Not performed as is invasive and hit & miss
Generally reserved for sickest pts
138
Layers of pericardium
Parietal pericardium
| Visceral pericardium
139
Functions of pericardium
Anchors heart to thorax
Barrier to infection
Limits a/c dilatation of heart
140
Is the pericardium essential
No
| Congenital absence or surgical removal aren't associated w/ adverse effects
141
What can go wrong w/ the pericardium
```
Infl (pericarditsi)
Fluid accumulation (effusion --> tamponade)
Fibrosis (constriction)
```
142
How can the causes of a/c pericarditis be split up
Infectious
| Non-infectious
143
Infectious causes of a/c pericarditis
```
Idiopathic/ viral - Coxsackie B, influenza, mumps, rubella (80% of cases)
Other infections (bacterial, TB, fungal)
```
144
Non-infectious causes of a/c pericarditis
```
Post MI (Dressler syndrome)
Uraemia
Malignancy from mediastinal tumours
CTD (SLE, RhA)
Radiation induced
Drug induced
```
145
Examples of mediastinal tumours
Lung
Breasts
Lymphoma
146
Clinical features of a/c pericarditis
Severe, sharp retrosternal/ left sided chest pain
Low grade fever is common
Sometimes tamponade can occur
Pericardial rub - evanescent
147
Pain in pericarditis
May radiate to back and trapezius ridges
Pleuritic
Positional (worse lying down, better leaning forward)
148
Pericardial rub
High pitches, scratchy sound heard at LSE
149
Ix for pericarditis
Bloods
ECG
CXR
Echo
150
Bloods for pericarditis
```
Increased infl markers and WCC
Normal troponin (unless concomitant myocarditis)
```
151
CXR in pericarditis
Look at heart size - cardiomegaly suggests effusion, lung lesions?
152
Echo for pericarditis
Assessing for pericardial effusion
153
ECG in a/c pericarditis
Concave ST elevation - widespread (no pattern)
| PR segment depression
154
ECG in MI vs pericarditis
MI - ST elevation - dome shaped and regional
| Pericarditis - concave and widespread
155
Mx of pericarditis
In most pts, idiopathic/ viral pericarditis is self-limiting w/out significant complications
Should be advised to restrict activity
156
Drugs for pericarditis
Anti-infl drugs - high dose ibuprofen/ aspirin for 1-2/52 AND colchicine for 3/12
Low dose steroids can be used if necessary
157
When would you give low dose steroids for pericarditis
NSAIDs & colchicine have either failed, are contraindicated or there's an autoimmune cause e.g. SLE
158
How can the causes of pericardial effusions be split up
Infl
Non-infl
Haemopericardium
159
Infl causes of pericardial effusion
Any cause of pericarditis e.g staph, strep, pneumo
160
Non-infl causes of pericarditis
Increased capillary permeability (e.g hypothyroidism)
Increased capillary hydrostatic pressure (HF)
Reduced plasma oncotic pressure (nephrotic syndrome, cirrhosis)
161
Haemopericardium
Bleeding into pericardial sac
162
Haemopericardium as a cause of pericarditis
Rupture of free wall post MI
Trauma
Cardiac procedure related (e.g. following angioplasty)
Dissecting aortic aneurysm
163
Commonest causes of pericardial tamponade
Malignancy
| Post-idiopathic/ viral pericarditis
164
What can pericarditis cause
Heart failure
165
In which condn is electrical alternans seen
In large pericardial effusion
166
Electrical alternans
Seen in V1
Height of QRS complex varies from beat to beat due to electrical axis constantly hanging as the heart swings from side to side in pericardial effusion
One large wave then a small one and it continues
167
Pathophysiology of cardiac tamponade
Impaired diastolic filling of ventricles leading to elevated venous pressure and impaired SV --> decreased CO
168
Symptoms of cardiac tamponade
Medical emergency
Anxiety
SOB
Chest pain
169
Signs seen in cardiac tamponade
Tamponade quadrad
Tachycardia
Hypotension
Elevated JVP
Pulsus paradoxus
170
Pulsus paradoxus
Abnormally large decrease in SV, systolic bp and pulse during inspiration
171
Pulsus alternans
Alternations of one strong beat and one weak beat, without change in cycle length
172
Treatment of pericardial effusion
Draining fluid in heart using a large needle between paraxiphoid area and apical area - pericardiocentesis
173
Constrictive pericarditis cause
Rare
| Most commonly idiopathic (but can be due to any cause of pericarditis)
174
Pathophysiology of constrictive pericarditis
Thickened fibrosed pericardium forms a rigid shell around heart --> inhibits normal filling of chambers
175
Clinical features of constrictive pericarditis
```
Decreased output (fatigue, hypotension, tachycardia)
Increased systemic venous pressure
```
176
Symptoms of constrictive pericarditis
Increased JVP, hepatomegaly, ascites, peripheral oedema (systemic venous congestion)
177
Treatment of constrictive pericarditis
Surgical removal of pericardium
178
How does LV rupture usually present
W/ a/c heart failure and signs of cardiac tamponade
179
What is pulsus alternans a sign of
LV failure
180
Syncope definition
```
Rapid onset
Transient LOC due to global cerebral hypo perfusion
Short duration (9 secs to 1/2 mins)
```
181
Usual cause of syncope
Usually benign w/ vasovagal syncope by far being commonest cause
182
What is syncope characterised by
Rapid onset
Short duration
Spontanoeus, complete recovery
183
Causes of syncope by %
60% reflex
15% orthostatic
15% cardiac
10% unknown
184
Types of reflex syncope
Situational
Vasovagal
Carotid sinus syndrome
185
Common triggers of vasovagal syncope
Pain
Fear
Prolonged standing
Having blood taken
186
Symptoms of vasovagal syncope
Dizziness or light-headedness
Blurred or tunnel vision
Sweating
Turning pale
187
Situational syncope
Form of reflex syncope caused by spp triggers e.g. defecations, coughing, laughing, swallowing
188
Micturition syncope
Fainting occurring shortly after or during urination
189
Who does situational syncope usually occur in
Men
190
Situational syncope in younger men
Usually benign
| May be precipitated by alcohol
191
What is situational syncope in older pts often associated w/
Comorbidities and postural hypotension
192
Triggers of situational syncope
Genito-urinary
Resp
GI
193
Carotid sinus reflex
Dilatation at the base of the internal carotid artery that contains baroreceptor which monitor BP
194
Carotid sinus massage
Simple, bedside test to test the carotid sinus reflex
195
Normal response to carotid sinus syndrome
Slight drop in HR and/or BP
196
When do we see an exaggerated response to carotid sinus massage
Carotid sinus hypertrophy
197
Carotid sinus syndrome
Syncope w/out warning and exaggerated CSM response w/ reproduction of syncope
198
When can pacing help w/ carotid sinus syndrome
If CSM mainly causes decreased HR
199
Who does carotid sinus syndrome usually occur in
Older pts (particularly men)
200
Triggers
Head turning
Shaving
Tight collar
201
Orthostatic hypotension explanation
Standing from a supine position causes 10-15% of our blood volume to be redistributed to the abdomen and LL thereby reducing venous return and CO
W/out, compensatory mechanisms there would be a fall in BP ---> syncope
202
What may orthostatic hypotension cause
Syncope
Dizziness on standing
Falls
203
Orthostatic hypotension definition
Decreased SBP of >20 mmHg (or >DBP of 10 mmHg) < 3 mins of standing OR
Decreased SBP <90 mmHg on standing
204
Who gets OH
Those with autonomic failure, hypovolaemia or taking certain drugs
205
Primary autonomic failure causing OH
Parkinsons
206
Secondary autonomic failure causing OH
Aging/ DM
207
Hypovoleamia causing OH
```
Antihypertensives
Anti-anginals
Anti-BPH
Anti-depressants
Anti-psychotics
Anti-Parkinsonian
Alcohol
```
208
Why are elderly pts most susceptible to the hypotensive effects of drugs
Reduced baroreceptor sensitivity
Decreased cerebral blood flow
Renal Na wasting
Impaired thirst mechanisms
209
When are OH symptoms worse
```
On standing
In the morning
After meals
After exercise
In hot environments
```
210
When are OH symptoms better
When lying down or sitting
| OH doesn't occur when pt is supine
211
Mx of reflex syncope and OH - everyone
Reassurance
Education
Lifestyle changes - increase water, decrease salt
Stop/ reduce BP lowering drugs (if possible)
212
Mx of reflex syncope and OH - if still symptomatic
Counter pressure manœuvres
213
Mx of reflex syncope and OH - in selected pts
Increase BP - fludrocortisone, midodrine
| Pacing - selected pts w/ reflex syncope only to increase HR
214
When should pacing be considered for reflex syncope pts
Recurrent syncope despite medical therapy
Bradycardia and systolic pauses
Will only benefit pts whose main problem is bradycardia and not low BP
215
Why does pacing help w/ reflex syncope
Newer pacemakers can detect when the ventricle is underfilled (happens before the bradycardia has been triggered) and increase HR to try and maintain BP
216
What causes cardiac syncope
Arrhythmia
| Structural
217
Arrhythmias causing cardiac syncope
Brady - sinus node disease, AV block
| Tachycardia - VT, SVT
218
Structural causes of cardiac syncope
Cardiac - AS, ACS, CM
| Vascular - PE, aortic dissection
219
Syncope red flags - symptoms
Exertion
Supine
No warning
220
Syncope red flags - PMH
Structural heart diseases
CAD
Heart failure
221
Syncope red flags - Fhx
SCD
222
Syncope red flags - other symptoms
```
Chest pain
Palpitations
SOB
Abdo pain
Headaches
```
223
Syncope red flags - examination
Low BP
Slow HR
Undiagnosed systolic murmur
224
Key points in syncope hx
6 P's
Before - Provoking factors, posture, prodrome, PMH (DH, FH)
During - passer-by account
After - post-event
225
Key points in syncope exam
Arrhythmia
Lying and standing BP
Carotid sinus hypersensitivity
Systolic murmur - AS, HCM
226
High risk feature on ECG of syncope pts
```
Arrhythmia
A/c MI
Channelopathy - Brugada, LQT1
Structural heart disease - LVH, LBBB
Conduction disease
```
227
Ix in syncope
ECG
Echo - if structural heart disease is suspected
Cardiac rhythm monitoring
Tilt test
228
Cardiac rhythm monitoring
Holter
| Loop recorder
229
Cardiac rhythm monitoring - Holter
Symptoms happening frequently, and arrhythmic cause suspected
230
Cardiac rhythm monitoring - Loop recorder
Symptoms happening infrequently by arrhythmic cause suspected
231
When is the tilt test done
Syncope of unknown cause where reflex syncope is suspected
232
Implanatable Loop Recorder
Useful in dx of recurrent syncope of unknown origin
233
What does implantable loop recorder dx
Arrhythmic syncope if it records an arrhythmia when pts has syncope
Suggests arrhythmic syncope when high risk arrhythmias are detected in an asymptomatic pt
234
Tilt table test
Provokes reflex syncope in a lab setting
Used to confirm dx of reflex syncope in a pt w/ syncope of unknown cause (where reflex syncope is suspected but not been proven)
235
What is a +ve tilt table test
Decrease in SBP
| Decrease in HR
236
Hypersensitivity
Exaggerated or inappropriate immune response against a foreign or self-antigen
237
Hypersensitivity classification
Allergic
Cytotoxic
Immune Compex
Delayed
238
Most common hypersensitivity
Allergic/ atopic hypersensitivity
| Up to 40% of people in developed countries suffer from Type 1 HS
239
What is allergic HS mediated by
IgE
Th2 cells
Mast cells
Eosinophils
240
Associated diseases w/ allergic HS
Allergic rhinitis
Asthma
Atopic dermatitis
Anaphylaxis
241
Key phases in Type I HS
Sensitisation
Activation
Effectors
242
Sensitisation in Type I HS
IgE produced by B cells in response to allergen
| IgE binds to FcR on mast cell & basophils
243
Activation in Type 1 HS
Re-exposure to allergen (reaction doesn't happen 1st time)
| Allergen cross-link IgE ---> immediate degranulation
244
Effectors in Type I HS
Tissue damage - vascular permeability, mucus secretion, immune cell infiltration
245
Mediators secreted during Type I HS reaction
Histamine
Prostaglandins and leukotrienes
IL-4
IL5
246
Outcomes of mediator secretion in Type I HS reaction
```
Vascular leak
Broncho-constriction
Interstinal hyper motility
Infl
Tissue remodelling
```
247
Typical allergens causing asthma
Pollens
Dust mites
Animal dander
248
Asthma allergens route of entry
Inhalation
249
Main symptoms of asthma
Wheezing, dyspnoea, tachypnoea
250
Allergic rhinitis
Hay fever
251
Typical allergens causing allergic rhinitis
Pollen spores
Animal dander
House dust mite faeces
252
Main symptoms of allergic rhinitis
Runny nose
Redness
Itching of eyes
253
Atopic dermatitis
Eczema
254
Typical allergens for atopic dermatitis
Dust mites
Pet fur
Pollen
Moulds
255
Main symptoms of eczema
Itchy, dry, cracked, sore and red skin
256
Allergic gastroenteropathy
Food allergies
257
Main symptoms of allergic gastroenteropathy
Vomiting
| Diarrhoea
258
Main symptoms. of anaphylaxis
Shock
Hypotension
Wheezing
259
How long does early phase of asthma last
15-30 mins
260
How long does late phase of asthma last
6 - 9 hrs
261
C/c infl in asthma
Goblet cell/ smooth muscle hyperplasia
Collagen deposition
Non-spp bronchial hyperactivity
262
Systemic atopy
Food allergy
| Anaphylaxis shock
263
Urticaria
Hives
264
Potentially fatal consequences of an anaphylaxis
Laryngeal oedema
Bronchial constriction
Peripheral oedema
2' mediators cause prolonged effects later - late phase reactions
265
Clinical tests for allergies
Skin prick tests
Blood test
Test diet or food challenge
266
Skin prick test for allergies
Intradermal injection of antigen
| 30 min readout for wheal/ flare
267
Blood test for allergies
Determine serum IgE levels (total or against spp antigens)
268
Test diet for allergies
Pt placed on diet free from common allergen various foods added over time
269
CNS symptoms of anaphylaxis
```
Lightheadedness
LOC
Confusion
Headache
Anxiety
```
270
Treatment of Type 1 HS
Allergen avoidance
Desensitisation
Drugs
271
Desensitisation for Type I HS
Repeated injection of small but increasing doses of purified allergenic over several months ---> modification of Th2 response (IgG, allergen binding and less IgE)
272
Drugs given for Type I HS
Antihistamines
Corticosteroids
Adrenaline (Epipen and Anapen)
273
Which allergic condns have genetic components
Hayfever, asthma, and atopic dermatitis
30% chance of allergy w/ one allergic parent and 50% w/ 2 parents
274
Hygiene hypothesis sand risks of allergy
Limiting market -life infection impeded natural immune system development and causes predisposition to allergic disease
275
Type II hypersensitivity
Cytotoxic HS
| Directed against cell surface on extracellular matrix antigens
276
What do most common Type II reactions involve
RBCs
277
How are cytotoxic HS reactions activated
Via IgM or IgG
278
What does the complement pathway create
Membrane attack complex
| Creates holes in membrane, cells become leaky and die
279
Associated diseases of cytotoxic HS reactions
Autoimmune haemolytic anaemia
Myasthenia gravis
Goodpastures disease
280
Incompatible blood tranfusions as a Type II HS reaction
Incompatible donor cells are lysed as they enter the blood stream
Intravascular haemolysis via complement
Leads to renal failure and death
281
How is blood typing done
Haemoaggluitination
282
How do we prevent incompatible blood transfusions
Cross-matching pt serum w/ donor RBC
283
Haemolytic disease of newborn
Occurs in pregnancy - when Rh-ve mother is exposed from Rh+ve foetus it causes sensitisation
Subsequent pregnancies cause mother to create anti-Rh antibodies causing Rh+ve foetus and lysis of their blood cells
284
Drug induced haemolytic anaemia
Drugs (or their metabolites) can provoke HS reactions against RBCs and platelets
Drug binds to surface protein on RBC ---> Antibody binds to drug and activates complement --> complement causes haemolysis
285
When do we see autoimmunity
IgG directed against self Ag on tissues
286
Autoantigen against autoimmune haemolytic anaemia
Rh blood group antigens
287
Autoantigen against Goodpasture's syndrome
Collagen type IV (basement membrane)
288
Pathogenesis of Goodpasture's syndrome
Necrosis of glomeruli --> nephritis, lung haemorrhage
289
Autoantigen against Myasthenia graves
Ach receptor
290
Pathogenesis of Myasthenia gravis
Blocked transmission at neuronal synapses --> muscle weakness
291
Glomerulonephritis
Group of kidney disease caused by infl in glomeruli
292
Type III HS
Immune complex-mediated HS
| Similar to Type II HS but Abs directed against soluble Ags
293
How are immune complexes normally removed from the body
RBC binding and phagocytosis by liver/ spleen
294
How do Type III HS reactions cause damage
Deposition and build up of complexes in tissues or walls of small blood vessels
295
Examples of infections that can form immune complexes
```
Hepatitis
Endocarditis
Malaria
Leprosy
Haemorhagic fever
```
296
Examples of Type II HS reactions
```
Rheumatoid disorders (SLE, Henoch-schonlein, 1' Sjorgens)
Arthus reaction
Inhaled antigens (e.g. Farmers lung)
```
297
Rheumatoid disorders as Type III HS reaction
Continued production of auto-Abs --> immune complex formation and deposition in tissues → cutaneous vasculitis
298
Arthus reaction as Type III HS reaction
Formation of Ag/IgG complexes after intradermal Ag injections (e.g. vaccines, sting) into sensitised individuals
Deposition in dermal blood vessels --> local vasculitis
299
Farmer's lung as a Type III HS reaction
Repeated exposure to high Ag quantities (e.g. fungi in mouldy hay) induce IgG --> immune complex formation in lung
300
Type IV HS
Delayed
301
What are delayed HS reactions mediated by
Ag-spp T cels (mostly Th1)
302
What happens in Type IV HS reactions
Ag internalised by dendritic cell ---> migration to lymph node and activation of T cells/ memory cell formation (priming phase)
Re-exposure: recruitment of memory T cells causes tissue damage
303
How long does the reaction take in Type IV HS
2-3 days
304
Type IV HS - contact HS
Small antigens (haptens) penetrate skin and combine with tissue protein and mediate immune reactions
305
Principal APCs in the skin
Langerhans cells
306
What can cause localised eczematous skin reactions
```
Contact with:
o Nickel salts in jewellery
o Drugs
o Components in hair dye
o Chromates
o Chemicals in leather/ rubber
o Poison ivy
```
307
What is the Mantoux test used for
Dx of latent TB
308
What is the clinically most important form of DTH
Granulomatous Type IV HS
| Ag persistence causing c/c T cell and macrophage activation ---> granuloma formation
309
When does granulomatous DTH develop
After 21-28 days
310
What does DTH cause
Caesation and tissue necrosis inside granuloma
311
When are granulomas seen
TB
Leprosy
Infection w/ parasites - Leishmaniasis, Schistosomiasis
312
Signs of L side HF
Bibasal lung crackles
LV heave (due to hypertrophy)
Dilated LV
Displaced apex beat
313
Cor pulmonale
R HF due to pulmonary HTN
314
Which drug can cause pitting oedema
CCB
315
Signs of R HF
```
Pitting oedema in peripheries
RV heave
Raised JVP
Ascites
Scrotal oedema
```
316
Why do we see fluid retention in symptoms of HF
RAAS
317
How can AF cause HF
Can cause atrial failure which leads to ventricular failure
318
When is S3 heard
HF
319
Categories of disease causing HF
```
Reduced ventricular contraction
Ventricular outflow obstruction
Ventricular inflow obstruction
Venticular volume overload
Arrhythmia
Diastolic dysfunction
```
320
Reduced ventricular contraction causing HF
IHD
| Myocarditis
321
Ventricular outflow obstruction
AS
| HTN
322
Ventricular inflow obstruction causing HF
MS
323
Ventricular volume overload causing HF
AR
| MR
324
Arrhythmia causing HF
AF
325
Diastolic dysfunction causing HF
HCM
RCM
Cardiac tamponade
326
Why might oromorph be given for c/c HF
Vasodilation
327
Rhabdomyolysis caused by statin
Blood in urine but -ve for RBC
328
Cardiorenal syndrome
Heart and renal failure together
329
Which drugs can cause angiodema
ACEi
330
Pathophysiologic difference between HFrEF and HFpEF
Reduced - cardiomyocytes dysfunction
| Preserved - due to endothelial dysfunction
331
Why do HF pts experience SOB
Increased filling pressure
| Low CO
332
What is v suggestive fo SOB being caused by HF
Orthopnea and PND
333
Measuring cardiothoracic ratio on Xray
Draw midline and mark largest bulge on R and L
| Choose the highest number and divide by sternal diameter of thorax
334
Dx algorithm for HF
IF pt has risk factors, symptoms& signs and an abnormal ECG --> measure NT-pro BNP --> if elevated do an Echo
335
Does furosemide have an effect on mortality
Yes, increases mortality as is a disease-modifying drug
336
Drug therapy for systolic heart failure
Diuretics - furosemide 40mg od, Spiro 25mg od
Ramipril 2.5mg note
Bisoprolol 2mg od
337
Class I therapies in HFrEF
```
Quadruple therapy:
ACEi/ Entrestro
BB
Spiro - MRA
Dapagliflozin
```
Add loop diuretic if signs of congestion
338
When is CRT suggested for HF pt
After drug therapies failed and if pts has broad QRS
339
When is an ICD suggested for HF pts
If pt has narrow QRS w/ LVH
340
Why might c/c HF pts lose wt
Impaired absorption due to GI congestion
341
Why might we see skeletal muscle atrophy in c/c HF
Immobility
342
CXR for HF
```
Alveolar oedema (batwing opacity)
Kerly B lines
Cardiomegaly
Dilated upper lobe vessels
Pleural effusion
```
343
Cardiac MR in HF
Ventricular volumes
| Mass and evidence of remodelling
344
Physiologic changes seen in a/c Left HF
Pulmonary oedema
345
Physiologic changes seen in c/c Left HF
Reflex pulmonary vasoconstriction to protect from oedema, increased resistance and pulmonary HTN
346
Physiologic changes seen in Right HF
Reduced RV output
| Increased RA and systemic venous pressure
347
What should me be done is PODMAN isn't effective for a/c HF
Give inotropic agents e..g IV dobutamine
| Insert intra aortic balloon pump
348
When should a HF pt have ventilation
Non-invasive - if cardiogenic pulmonary oedema w/ severe dyspnoea
Invasive - resp failure or reduced consciousness
349
Bilateral oedema ddx
```
Congestive heart failure
Hepatic failure
Renal failure
Neohrotic syndrome
Malnutrition
Immobility
Drugs (NSAIDs or CCBs)
```
350
Unilateral oedema ddx
DVT
Cellulitis
Ruptured Baker's cyst
Lymphatic obstruction
351
Mx of bilateral oedema
Diuretics - monitor renal function
If oedema is resistant, diuretic and thiazide
Spiro or amiloride (K sparing diuretics)
352
When is ivabradien indicated for hF failures
NYHA classification ois II to IV w/ systolic dysfunction AND sinus rhythm of 75+bpm
BB contraindicates/ not tolerated
LVEF of 35% or less
353
How do ACEi improve mortality and morbidity in hF
Reduce afterload to improve EF
Reduce preload to decrease pulmonary congestion
Improves oxygen supply
Prevents cardiac remodelling
354
What is the best time to give statins
Nocte
| Except atorva which can be taken any time
355
Interaction between ACEi and ARBs
Hyperkalaemia
Hypotension
Renal impairment
356
How doe BBs improve mortality and morbidity in HF pts
Reduces HR --> increasing filling time --> increase EF
| Reduces cardiac remodelling
357
MOA of aldosterone antagonists
Antagonises effects of aldosterone so more Na and water can be excreted, preventing fluid retention
358
Interactions of aldosterone antagonists
ACEi and aldosterone antagonists = hyperkalaemia (Monitor K+ levels)
359
In which condn do we see a displaced apex beat
LV dilatation - HF
