cardiology 2 Flashcards
1
Q
DVLA and heart failure for HGVs?
A
Symptomatic heart failure will lead to revocation of a Group 2 licence, regardless of whether the symptoms lead to incapacity. If a patient on treatment becomes asymptomatic, then they may be relicensed only if their LVEF is >= 40%.
2
Q
What will lead to persistent ST elevation following recent MI with no chest pain?
A
Persistent ST elevation following recent MI, no chest pain - left ventricular aneurysm
3
Q
Indications for Surgery in infective endocarditis?
A
severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy
4
Q
What is the mechanism of action of fondaparinux?
A
Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa. It is given subcutaneously.
5
Q
what causes cannon waves in the JVP?
A
Cannon a waves result from atrial contraction against a closed tricuspid valve and therefore can be seen in VT when atrial and ventricular contraction is not co-ordinated. They can also be seen in complete/3rd degree heart block and atrial flutter for the same reason.
6
Q
Treatment of PAHTN?
A
If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers
If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists
non-selective: bosentan
selective antagonist of endothelin receptor A: ambrisentan
phosphodiesterase inhibitors: sildenafil
7
Q
What is Brugada syndrome?
A
Brugada syndrome is a form of inherited cardiovascular disease with may present with sudden cardiac death. It is inherited in an autosomal dominant fashion and has an estimated prevalence of 1:5,000-10,000. Brugada syndrome is more common in Asians.
8
Q
Pathophysiology of Brigade Syndrome?
A
around 20-40% of cases are caused by a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
9
Q
What ECG changes would you expect to see IN Brugada syndrome?
A
convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
partial right bundle branch block
the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome
10
Q
Management of Brugada syndrome?
A
ICD
11
Q
How do loop diuretics work?
A
Furosemide and bumetanide are loop diuretics that act by inhibiting the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle, reducing the absorption of NaCl.
12
Q
why do patients with poor renal function need higher doses of loop diuretics?
A
As loop diuretics work on the apical membrane they must first be filtered into the tubules by the glomerulus before they can have an effect. Therefore patients with poor renal function may require escalating doses to ensure a sufficient concentration is achieved within the tubules.
13
Q
Adverse effects of loop diuretics?
A
hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
ototoxicity
hypocalcaemia
renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout
14
Q
Causes of long QTc syndrome?
A
congenital
Jervell-Lange-Nielsen syndrome
Romano-Ward syndrome
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants
antipsychotics
chloroquine
terfenadine
erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
myocarditis
hypothermia
subarachnoid haemorrhage
15
Q
what is Torsades de pointes?
A
Torsades de pointes (‘twisting of the points’) is a form of polymorphic ventricular tachycardia associated with a long QT interval. It may deteriorate into ventricular fibrillation and hence lead to sudden death.
16
Q
management of torsades?
A
IV magnesium
17
Q
What is long QT syndrome?
A
Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles.
The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel.
Long QT syndrome - usually due to loss-of-function/blockage of K+ channels
.
18
Q
Normal QTc?
A
A normal corrected QT interval is less than 430 ms in males and 450 ms in females.
19
Q
Features of LQT syndrome?
A
Long QT1 - usually associated with exertional syncope, often swimming
Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
Long QT3 - events often occur at night or at rest
sudden cardiac death
20
Q
Management of long QT syndrome?
A
avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)
beta-blockers***
implantable cardioverter defibrillators in high risk cases
***note sotalol may exacerbate long QT syndrome
21
Q
How do drugs cause long QT?
A
the usual mechanism by which drugs prolong the QT interval is blockage of potassium channels.
22
Q
ECG findings in HOCM ?
A
left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen
23
Q
Echo Findings in HOCM?
A
mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
24
Q
Features of HOCM?
A
often asymptomatic
exertional dyspnoea
angina
syncope
typically following exercise
due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat
systolic murmurs
ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting
pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
25
Pathophysiology of HOCM?
the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output
characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy
26
How do endothelin receptor antagonists work in Pulmonary artery hypertension ?
Endothelin receptor antagonists decrease pulmonary vascular resistance in patients with primary pulmonary hypertension
27
Prosthetic heart valves - antithrombotic therapy
bioprosthetic: aspirin
mechanical: warfarin + aspirin
28
Half life of amioderone?
Amiodarone has a long half-life - it is highly lipophilic and widely absorbed by tissue, which reduces its bioavailability in serum. Therefore, a prolonged loading regime is required to achieve stable therapeutic levels
approximately 20-100 days
29
Adverse effects of amiodarone?
thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
'slate-grey' appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
30
JVP in TR?
JVP: giant v waves in tricuspid regurgitation
31
Different types of stents used in PCI?
bare-metal stent (BMS)
drug-eluting stents (DES): stent coated with paclitaxel or rapamycin which inhibit local tissue growth. Whilst this reduces restenosis rates the stent thrombosis rates are increased as the process of stent endothelisation is slowed
patients with drug-eluting stents require a longer duration of clopidogrel therapy
32
PCI
Percutaneous coronary intervention (PCI) is a technique used to restore myocardial perfusion in patients with ischaemic heart disease, both in patients with stable angina and acute coronary syndromes. Stents are implanted in around 95% of patients - it is now rare for just balloon angioplasty to be performed
33
what happens following stent insertion in PCI?
Following stent insertion migration and proliferation of smooth muscle cells and fibroblasts occur to the treated segment. The stent struts eventually become covered by endothelium. Until this happens there is an increased risk of platelet aggregation leading to thrombosis.
34
Periprocedural complications in PCI?
minor bleeding/haematoma at the site of vascular access
retroperitoneal haematoma
may occur if the puncture site occurs proximal to the inguinal ligament
may be asymptomatic or present with flank pain/hypotension
femoral pseudoaneurysm
pulsatile mass, femoral bruit and compromised distal pulses
cholesterol embolisation
occurs due to embolisation of cholesterol released from atherosclerotic plaques
purpura, livedo reticularis
renal impairment
blue toes
35
Long term complications in PCI?
restenosis
due to excessive tissue proliferation around the stent
occurs in around 5-20% of patients, most commonly in the first 3-6 months
usually presents with the recurrence of angina symptoms
risk factors include diabetes, renal impairment and stents in venous bypass grafts
stent thrombosis
due to platelet aggregation as above
occurs in 1-2% of patients, most commonly in the first month
usually presents with acute myocardial infarction
36
Physiological changes during exercise ?
BP - systolic increases, diastolic decreases
leads to increased pulse pressure
in healthy young people the increase in MABP is only slight
Cardiac output
increase in cardiac output may be 3-5 fold
results from venous constriction, vasodilation and increased myocardial contractibility, as well as from the maintenance of right atrial pressure by an increase in venous return
heart rate up to 3-fold increase
stroke volume up to 1.5-fold increase
Systemic vascular resistance falls in exercise due to vasodilatation in active skeletal muscles.
37
Inherited long QT syndrome, sensorineural deafness - what syndrome?
Jervell and Lange-Nielsen syndrome
38
What is the mechanism of action of bivalirudin?
Direct thrombin inhibitor
Generally given intravenously
Dabigatran is a type of direct thrombin inhibitor that is taken orally. It is often grouped alongside the direct oral anticoagulants (DOACs).
39
Signs of tricuspid regurgitation?
pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave
40
Causes of Tricuspid regurgitation?
right ventricular infarction
pulmonary hypertension e.g. COPD
rheumatic heart disease
infective endocarditis (especially intravenous drug users)
Ebstein's anomaly
carcinoid syndrome
41
What is HOCM characterised by on Biopsy ?
Hypertrophic obstructive cardiomyopathy - characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy
41
mechanism of action of warfarin?
inhibits epoxide reductase preventing the reduction of vitamin K to its active hydroquinone form
this in turn acts as a cofactor in the carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.
42
Side effects of Warfarin?
haemorrhage
teratogenic, although can be used in breastfeeding mothers
skin necrosis
when warfarin is first started biosynthesis of protein C is reduced
this results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration
thrombosis may occur in venules leading to skin necrosis
purple toes
43
What should INR be before dental procedure?
Dentistry in warfarinised patients - check INR 72 hours before procedure, proceed if INR < 4.0
44
Which part of the jugular venous waveform is associated with the fall in atrial pressure during ventricular systole?
x descent = fall in atrial pressure during ventricular systole
45
what type of drug is atropine?
Atropine is an antagonist of the muscarinic acetylcholine receptor - anticholinergic drug
46
what is atropine used for?
symptomatic bradycardia
IV atropine is the first-line treatment for bradycardia with adverse signs
treatment of organophosphate poisoning
47
Physiological effects of atropine?
tachycardia
mydriasis
atropine may trigger acute angle-closure glaucoma in susceptible patients
48
Features of severe AS?
narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
left ventricular hypertrophy or failure
49
Management of aortic stenosis?
if asymptomatic then observe the patient is a general rule
if symptomatic then valve replacement
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
options for aortic valve replacement (AVR) include:
surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined
transcatheter AVR (TAVR) is used for patients with a high operative risk
balloon valvuloplasty
may be used in children with no aortic valve calcification
in adults limited to patients with critical aortic stenosis who are not fit for valve replacement
50
Mechanism of action of Nicroandil?
Nicorandil is a vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
51
Adverse effects and contraindications of Nicorandil?
Adverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Contraindications
left ventricular failure
52
what is syndrome X
Features
angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography
Management
nitrates may be beneficial
53
what are the causes of mitral stenosis?
Rheumatic fever
Rarer causes that may be seen in the exam include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis
54
Features of mitral stenosis?
Dyspnoea --> ↑ left atrial pressure → pulmonary venous hypertension
Haemoptysis - due to pulmonary pressures and vascular congestion
mid-late diastolic murmur (best heard in expiration)
loud S1
opening snap
indicates mitral valve leaflets are still mobile
low volume pulse
malar flush
atrial fibrillation
secondary to ↑ left atrial pressure → left atrial enlargement
55
what are the features of severe MS?
Features of severe MS
length of murmur increases
opening snap becomes closer to S2
56
what is seen on XR in mitral stenosis?
left atrial enlargement may be seen
57
What does echo show in mitral stenosis?
the normal cross-sectional area of the mitral valve is 4-6 sq cm. A 'tight' mitral stenosis implies a cross-sectional area of < 1 sq cm
58
How is mitral stenosis managed?
patients with associated atrial fibrillation require anticoagulation
currently warfarin is still recommended for patients with moderate/severe MS
there is an emerging consensus that direct-acting anticoagulants (DOACs) may be suitable for patients with mild MS who develop atrial fibrillation
asymptomatic patients
monitored with regular echocardiograms
percutaneous/surgical management is generally not recommended
symptomatic patients
percutaneous mitral balloon valvotomy
mitral valve surgery (commissurotomy, or valve replacement)
59
ECG changes assoicated with hypothermia?
bradycardia
'J' wave (Osborne waves) - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
## Footnote
Hypothermia features: Jesus, Its Bloody Freezing
J wave
Irregular pattern (long QT interval, atrial and ventricular arrhythmias)
Bradycardia
First degree and higher heart blocks
60
What is a contraindication to becoming pregnant with VSD?
Pulmonary hypertension
61
62
Causes of VSD?
congenital VSDs are often association with chromosomal disorders
Down's syndrome
Edward's syndrome
Patau syndrome
cri-du-chat syndrome
congenital infections
acquired causes
post-myocardial infarction
63
Post natal presentation of VSD?
failure to thrive
features of heart failure
hepatomegaly
tachypnoea
tachycardia
pallor
classically a pan-systolic murmur which is louder in smaller defects
64
Management of VSD?
small VSDs that are asymptomatic often close spontaneously and simply require monitoring
moderate to large VSDs usually result in a degree of heart failure in the first few months
nutritional support
medication for heart failure e.g. diuretics
surgical closure of the defect
65
VSD complications?
Aortic regurgitation
Infective endocarditis
Eisenmenger's complex
Right heart failure
Pulmonary HTN
## Footnote
aortic regurgitation is due to a poorly supported right coronary cusp resulting in cusp prolapse
pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality
66
What is Eisenmenger's syndrome?
due to prolonged pulmonary hypertension from the left-to-right shunt
results in right ventricular hypertrophy and increased right ventricular pressure. This eventually exceeds the left ventricular pressure resulting in a reversal of blood flow
this in turn results in cyanosis and clubbing
67
Features of cardiac tamponade?
Classical features - Beck's triad:
hypotension
raised JVP
muffled heart sounds
## Footnote
Other features:
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul's sign - much debate about this
ECG: electrical alternans
68
How to differentiate bewteen cardiac tamponade and constictive pericarditis?
69
What is the primary pharmacological effect of drugs that prolong the QT interval?
They lengthen cardiac re-polarisation mostly by blocking specific cardiac potassium channels
## Footnote
This effect is critical in understanding how certain drugs can lead to arrhythmias.
70
Besides excessive lengthening of the QT interval, list other predisposing factors to drug-induced torsade de pointes.
* Bradycardia
* Electrolyte imbalance
* Female sex
* Genetic polymorphisms in various ion channel constituents
## Footnote
These factors can further increase the risk of developing torsade de pointes.
71
Features suggesting VT rather than SVT with aberrant conduction
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms
72
73
What is the Stanford classification type A?
Type A - ascending aorta, 2/3 of cases
## Footnote
Type A involves a dissection that affects the ascending aorta.
74
What is the Stanford classification type B?
Type B - descending aorta, distal to left subclavian origin, 1/3 of cases
## Footnote
Type B involves a dissection that occurs in the descending aorta.
75
What is the DeBakey classification type I?
Type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
## Footnote
Type I indicates a dissection that starts in the ascending aorta and can extend to the arch.
76
What is the DeBakey classification type II?
Type II - originates in and is confined to the ascending aorta
## Footnote
Type II is limited to the ascending aorta without extending distally.
77
What is the DeBakey classification type III?
Type III - originates in descending aorta, rarely extends proximally but will extend distally
## Footnote
Type III starts in the descending aorta and typically does not go back up towards the heart.
78
What initial investigation is commonly used for aortic dissection?
Chest x-ray - widened mediastinum
## Footnote
A widened mediastinum on a chest x-ray can be a sign of aortic dissection.
79
What is the investigation of choice for stable patients with suspected aortic dissection?
CT angiography of the chest, abdomen and pelvis
## Footnote
CT angiography is preferred for its ability to visualize the dissection and assess its extent.
80
What is a key finding in diagnosing aortic dissection?
A false lumen
## Footnote
The presence of a false lumen on imaging is crucial for confirming aortic dissection.
81
Why is Transoesophageal echocardiography (TOE) used?
More suitable for unstable patients who are too risky to take to CT scanner
## Footnote
TOE provides critical information while minimizing the need for patient transport.
82
What is the management approach for Type A aortic dissection?
Surgical management, blood pressure control to a target systolic of 100-120 mmHg
## Footnote
Immediate surgery is often necessary for Type A dissections.
83
What is the management approach for Type B aortic dissection?
Conservative management, bed rest, reduce blood pressure IV labetalol
## Footnote
Type B dissections are often managed non-operatively to prevent progression.
84
What are complications associated with backward tears in aortic dissection?
* Aortic incompetence/regurgitation
* Myocardial infarction (MI)
## Footnote
Backward tears can lead to significant cardiac complications.
85
What are the complications of a forward tear in aortic dissection?
* Unequal arm pulses and BP
* Stroke
* Renal failure
## Footnote
Forward tears can cause various systemic issues due to compromised blood flow.
86
Management of eclampsia?
Magnesium sulphate is used to both prevent seizures in patients with severe pre-eclampsia and treat seizures once they develop
in eclampsia an IV bolus of 4g over 5-10 minutes should be given followed by an infusion of 1g / hour
87
What should be monitored when giving magnesium in eclampsia?
urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment
respiratory depression can occur: calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression
88
What is an atrial myxoma?
Atrial myxoma is the most common primary cardiac tumour.
Overview
75% occur in left atrium, most commonly attached to the fossa ovalis
more common in females
89
Features of an atrial myxoma?
systemic: dyspnoea, fatigue, weight loss, pyrexia of unknown origin, clubbing
emboli
atrial fibrillation
mid-diastolic murmur, 'tumour plop'
echo: pedunculated heterogeneous mass typically attached to the fossa ovalis region of the interatrial septum
90
What are examples of Adenosine diphosphate (ADP) receptor inhibitors?
Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine
91
Mechanism of action of Adenosine diphosphate (ADP) receptor inhibitors
Adenosine diphosphate (ADP) is one of the main platelet activation factors, mediated by G-coupled receptors P2Y1 and P2Y12.
The main target of ADP receptor inhibition is the P2Y12 receptor, as it is the one which leads to sustained platelet aggregation and stabilisation of the platelet plaque.
92
side effects of ticagrelor?
ticagrelor may cause dyspnoea
due to the impaired clearance of adenosine
93
Druh Interactions with Adenosine diphosphate (ADP) receptor inhibitors
* A drug interaction exists between clopidogrel and proton pump inhibitors, particularly omeprazole and esomeprazole, leading to reducing antiplatelet effects.
* Patients with prior stroke or transient ischaemic attack, high risk of bleeding, and prasugrel hypersensitivity are absolute contraindications to prasugrel use.
* Ticagrelor is contraindicated in patients with a high risk of bleeding, those with a history of intracranial haemorrhage, and those with severe hepatic dysfunction. It is also to be used with caution in those with acute asthma or COPD, as ticagrelor-treated patients experience higher rates of dyspnoea.1
94
What is the most common cause of infective endocarditis?
Staphylococcus aureus
## Footnote
Particularly common in acute presentation and in intravenous drug users (IVDUs)
95
Which organism was historically the most common cause of infective endocarditis?
Streptococcus viridans
## Footnote
This is no longer the case, except in developing countries.
96
Which are the two most notable viridans streptococci?
* Streptococcus mitis
* Streptococcus sanguinis
## Footnote
They are both commonly found in the mouth and dental plaque.
97
What is the link between viridans streptococci and endocarditis?
Poor dental hygiene or following a dental procedure
## Footnote
Endocarditis caused by these organisms is associated with these factors.
98
Which coagulase-negative Staphylococci commonly cause endocarditis in patients following prosthetic valve surgery?
Staphylococcus epidermidis
after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)
## Footnote
Usually results from perioperative contamination.
99
What organism is associated with colorectal cancer?
Streptococcus bovis
## Footnote
The subtype Streptococcus gallolyticus is most linked with colorectal cancer.
100
Which conditions can lead to non-infective endocarditis?
* Systemic lupus erythematosus (Libman-Sacks)
* Malignancy (marantic endocarditis)
## Footnote
These conditions are not caused by infectious agents.
101
Culture negative causes of IE?
prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
102
what is the mechanism of action of amiodarone?
Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
103
Monitoriong whilst on amiodarone?
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months
104
Adverse effects of amiodarone?
thyroid dysfunction: both hypothyroidism and hyper-thyroidism
corneal deposits
pulmonary fibrosis/pneumonitis
liver fibrosis/hepatitis
peripheral neuropathy, myopathy
photosensitivity
'slate-grey' appearance
thrombophlebitis and injection site reactions
bradycardia
lengths QT interval
105
What is Eisenmenger's associated with?
ventricular septal defect
atrial septal defect
patent ductus arteriosus
106
What are the features of Eisenmenger's syndrome?
original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism
107
What kind of murmur would be heard is ASD?
Ejection systolic murmur heard loudest on inspiration
108
What treatment is contraindicated in WPW ?
Verapamil, a non-dihydropyridine calcium channel blocker, can be dangerous in patients with WPW as it blocks conduction through the AV node while having no effect on conduction through the accessory pathway. This can result in preferential conduction down the accessory pathway, potentially precipitating ventricular fibrillation in patients with atrial fibrillation and WPW.
109
ECG features of WPW?
short PR interval
wide QRS complexes with a slurred upstroke - 'delta wave'
left axis deviation if right-sided accessory pathway
in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation
right axis deviation if left-sided accessory pathway
## Footnote
Differentiating between type A and type B
type A (left-sided pathway): dominant R wave in V1
type B (right-sided pathway): no dominant R wave in V1
110
What is Takayasu's arteritis?
Takayasu's arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in younger females (e.g. 10-40 years) and Asian people.
111
Features of Takayasu's arteritis?
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit and tenderness
absent or weak peripheral pulses
upper and lower limb claudication on exertion
aortic regurgitation (around 20%)
112
What is the management of Takayasu's arteritis?
Steroids
113
What is Long QT syndrome usually due to?
Long QT syndrome - usually due to loss-of-function/blockage of K+ channels
114
What are the variants of long QT syndrome?
Long QT1 - usually associated with exertional syncope, often swimming
Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli
Long QT3 - events often occur at night or at rest
115
Causes of regular and irregular cannon waves?
Caused by the right atrium contracting against a closed tricuspid valve. May be subdivided into regular or intermittent
Regular cannon waves
ventricular tachycardia (with 1:1 ventricular-atrial conduction)
atrio-ventricular nodal re-entry tachycardia (AVNRT)
Irregular cannon waves
complete heart block
116
What is the main mechanism causing hypokalaemia in thiazide diuretics?
Thiazides/thiazide-like drugs (e.g. indapamide) - inhibits sodium reabsorption by blocking the Na+-Clˆ’ symporter at the beginning of the distal convoluted tubule
Increased delivery of sodium to the collecting ducts causes the sodium-potassium exchanger to release more potassium into the urine. Another cause is activation of the renin-angiotensin-aldosterone system secondary to hypovolaemia
117
What is Dipyridamole?
Dipyridamole is an antiplatelet mainly used in combination with aspirin after an ischaemic stroke or transient ischaemic attack.
118
What is the mechanism of action of Dipyridamole?
inhibits phosphodiesterase, elevating platelet cAMP levels which in turn reduce intracellular calcium levels
other actions include reducing cellular uptake of adenosine and inhibition of thromboxane synthase
119
what murmur is heard in aortic regurgitation?
Aortic regurgitation - early diastolic murmur, high-pitched and 'blowing' in character
120
What drug is contraindciation in VT?
Verapamil should NOT be used in VT.
121
when should statin be held in derranged LFTs?
Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
122
Anticoagulation post valve replacement +/- CABG?
mechanical : warfarin
bioprosthetic: aspirin
bioprosthetic + CAD/CABG - aspirin
mechanical + CAD/CABG - warfarin and aspirin
123
Managemnt of angina?
aspirin and statin
GTN to abort attacks
BB or CCB first line (If CCB used as monotherapy. verapamil should be used, if used with BB then longer acting CCB should be used - amlodipine, MR nifedipine)
If poor response - increase to the maximum dose
Can add in:
long acting nitrate
Ivabradine
Niorandil
Ranolazine
124
125
What is pulsus paradoxus?
Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
## Footnote
Commonly associated with severe asthma and cardiac tamponade
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What condition is indicated by a slow-rising or plateau pulse?
Aortic stenosis
## Footnote
This type of pulse is characterized by a gradual rise and fall.
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What does a collapsing pulse indicate?
Aortic regurgitation, patent ductus arteriosus, hyperkinetic states (anemia, thyrotoxic, fever, exercise/pregnancy)
## Footnote
This pulse type is marked by a rapid rise and fall.
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What is pulsus alternans?
Regular alternation of the force of the arterial pulse
## Footnote
Often observed in severe left ventricular failure (LVF).
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What characterizes a bisferiens pulse?
'Double pulse' - two systolic peaks
## Footnote
Typically seen in mixed aortic valve disease.
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What does a 'jerky' pulse indicate?
Hypertrophic obstructive cardiomyopathy
## Footnote
HOCM may occasionally be associated with a bisferiens pulse.
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When is BNP released?
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.
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What are the effects of BNP?
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
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Features of tetralogy of Fallot?
ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta
Causes a right to left shunt
Ejection systolic mumur
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What should be given to pregnant ladies at high risk of developing pre-eclampisa ?
Aspirin 75-150mg daily from 12 weeks gestation until birth
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what are the features of cholesterol embolisation?
eosinophilia
purpura
renal failure
livedo reticularis
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How do you manage respiratory depression following IV magnesium treatment in eclampsia?
calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression
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Factors that may potentiate warfarin?
liver disease
P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
cranberry juice
drugs which displace warfarin from plasma albumin, e.g. NSAIDs
inhibit platelet function: NSAIDs
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Features of HOCM?
often asymptomatic
excertional dyspnoea
angina
syncope
Sudden death due to ventricular arrhythmias
Jerky pulse
Large a wave
double apex beat
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what murmurs may be heard in HOCM?
ejection systolic murmur: due to left ventricular outflow tract obstruction. Increases with Valsalva manoeuvre and decreases on squatting
pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
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What are the echo findings in HOCM?
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
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ECG changes in HOCM?
left ventricular hypertrophy
non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen
deep Q waves
atrial fibrillation may occasionally be seen
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Managemnt of HOCM?
Management
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
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Drugs to avoid in HOCM?
nitrates
ACE-inhibitors
inotropes
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causes of ST depression?
secondary to abnormal QRS (LVH, LBBB, RBBB)
ischaemia
digoxin
hypokalaemia
syndrome X
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what is commonly associated with Seborrhoeic dermatitis?
otitis externa and blepharitis may develop
