Cardiology Gap Flashcards
1
Q
Features suggesting VT rather than SVT with aberrant conduction
A
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
2
Q
The strongest risk factor for developing infective endocarditis is—
A
- a previous episode of endocarditis.
3
Q
Brugada Syndrome is caused by which genetic change?
A
a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
4
Q
ECG in Brugada
A
convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
partial right bundle branch block
5
Q
Third Heart Sound found in
A
S3 caused by diastolic filling of the ventricle
- considered normal if < 30 years old (may persist in women up to 50 years old)
- heard in left ventricular failure (e.g. dilated cardiomyopathy)
- constrictive pericarditis (called a pericardial knock)
- mitral regurgitation
DCM has three letters - S3
D- Dilated Cardiomyopathy/LVF
C- Constrictive Pericarditis
M- Mitral Regurgitation
HOCM has four letters - S4
6
Q
Fourth Heart Sound
A
- Aortic stenosis
- HOCM
- Hypertension
7
Q
HTN in pregnancy Rx
A
- Oral labetalol is now first-line following the 2010 NICE guidelines
- Oral nifedipine (e.g. if asthmatic)
- Hydralazine
8
Q
Thiazide Diuretics Causes
A
Hypotension (Postural)
Hypokalaemia
Hyponatraemia
Hypercalcaemia
Hypocalciuria
Hyperglycemia (Impaired glucose tolerance)
9
Q
angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography
is the hallmark of–
A
Cardiac Syndrome X
10
Q
Angina Rx stepwise
A
Step 1: start with BB or CCB
Step 2: increase to maximum tolerated dose
Step 3: if still poor response > add BB/CCB
(if CCB used in combination with a BB then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)
if a patient is on monotherapy and cannot tolerate the addition of CCB or BB then consider one of the following drugs:
- a long-acting nitrate
- Ivabradine
- Nicorandil
- Ranolazine
Step 4: if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG
11
Q
Sydrome X
A
Angina-like chest pain on exertion
ST depression on exercise stress test
but normal coronary arteries on angiography
12
Q
Rate limiting CCB
A
Verapamil
Diltiazem
13
Q
Poor prognostic factors for IE
A
- Staphylococcus aureus infection
- Prosthetic valve (especially ‘early’, acquired during surgery)
- Culture negative endocarditis
- Low complement levels
14
Q
IE Rx:
Native
Prosthetic Valve
Strep B
Staph
A
- pRosthetiG (all prosthetic valves require Rifampicin and Gent)
- streB (all strep IEs require Benpen)
- steF (all staph IEs require Fluclox)
- Vallergic (all pen allergic patients receive vanc)
- All Prosthetic valves: have to give Rifamipcin + Low dose Gent (+ other agent either Flucloxacillin or Vanc)
- Pen allergy: Switch Penicillin to Vancomycin + low dose Gent (except in native valve staph where you give Vancomycin + Rifampicin)
15
Q
Define Anginal Chest Pain
A
- constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain
16
Q
Choice of prosthetic Heart Valves
A
- Comparatively young (expected lifespan >15-20 years) = Mechanical (with longterm anticoagulation)
- Old (less lifespan) = Bioprosthetic (short term anticoagulation)
17
Q
Anticoagulation for Prosthetic Valves
A
Bioprosthetic: Aspirin
Mechanical: Warfarin
18
Q
Target INR for Prosthetic Valves
A
Aortic: 3.0
Mitral: 3.5
AM 3:35
19
Q
Why shouldn’t you prescribe BB with Verapamil
A
for the risk of Complete Heart Block
20
Q
Endocrine causes of Secondary HTN
A
Primary hyperaldosteronism
Phaeochromocytoma
Cushing’s syndrome
Liddle’s syndrome
Congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
Acromegaly
21
Q
Drug Causes of Secondary HTN
A
Steroids
Monoamine oxidase inhibitors
The combined oral contraceptive pill
NSAIDs
Leflunomide
22
Q
Poor prognostic indicator for HOCM
A
Syncope
Family history of sudden death
Young age at presentation
Non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
Abnormal blood pressure changes on exercise
An increased septal wall thickness of > 3 cm
23
Q
Association of Aortic Dissection
A
Hypertension: the most important risk factor
trauma
bicuspid aortic valve
Collagens: Marfan’s syndrome, Ehlers-Danlos syndrome
Turner’s and Noonan’s syndrome
Pregnancy
Syphilis
24
Q
Classification of Aortic Dissection
A
Stanford classification:
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification:
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally
25
Features of severe MS
length of murmur increases
opening snap becomes closer to S2
26
Which feature in the murmur indicates mitral valve leaflets are still mobile
opening snap
indicates mitral valve leaflets are still mobile
27
Indications for a temporary pacemaker
- Symptomatic/haemodynamically unstable bradycardia, not responding to atropine
- post-**ANTERIOR** MI: type 2 or complete heart block
(Note: post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable)
- trifascicular block prior to surgery
28
The effect of Adenosine is enhanced by
Dipyridamole (antiplatelet agent)
**DE-AR Adinosine**
Dipyradimole Elevate
Aminophylline Reduce
29
The effects of adenosine is blocked by
Theophyllines
**DE-AR Adinosine**
Dipyradimole Elevate
Aminophylline Reduce
30
Adenosine M/A
Rule of A
**A**gonist of **A1** Receptor
of the **AV** Node
causes transient **AV **Block
inhibits **A**denylyl cyclase thus reducing c**A**MP
(and causing hyperpolarization by increasing outward potassium flux)
+
**DE-AR Adinosine**
Dipyradimole Elevate
Aminophylline Reduce
31
Mechanism, Adverse Effect and Contraindication of Nicorandil
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.
**Adverse effects**
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
**Contraindications**
left ventricular failure
32
causes of infective endocarditis
**Staphylococcus aureus** - most common- in acute presentation and IVDUs
Streptococcus viridans( Streptococcus mitis and Streptococcus sanguinis) - historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries
technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are
they are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure
coagulase-negative Staphylococci such as Staphylococcus epidermidis
commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.
after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)
Streptococcus bovis
associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer
non-infective
systemic lupus erythematosus (Libman-Sacks)
malignancy: marantic endocarditis
Culture negative causes:
prior antibiotic therapy
Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
33
Investigations for stable angina:
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography
**Examples of non-invasive functional imaging:**
myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
stress echocardiography or
first-pass contrast-enhanced magnetic resonance (MR) perfusion or
MR imaging for stress-induced wall motion abnormalities
34
Verapamil should not be prescribed concurrently with
B Blockers (risk of CHB)
35
remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
verapamil (risk of complete heart block)
36
Why beta-blockers should not be prescribed concurrently with verapamil
risk of complete heart block
37
Rate Limiting CCBs
Verapamil
Diltiazem
38
Rx of Angina
- all patients should receive aspirin and a statin in the absence of any contraindication
- sublingual glyceryl trinitrate to abort angina attacks
+
**1. beta-blocker/calcium channel blocker**
( if only CCB, use rate-limiting one such as verapamil or diltiazem)
**2. Maximize dose**
**3. Add BB/CCB**
(if CCB used with a BB, then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine, felodipine)
+
Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
**4. If on monotherapy and cannot tolerate the other one, then consider one of the following drugs:
- a long-acting nitrate
- Ivabradine
- Nicorandil
- Ranolazine**
**5. if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG**
39
First cardiac enzyme to rise
Myoglobin
40
Which cardiac marker is useful to look for reinfarction
CK-MB
41
Which Cardiac Markers bind with which protein?
**TIC - TAC**
T Troponin T binds with T: Tropomyosin
I Troponin I binds with A: Actin
T Troponin C binds with C: Calcium ions
42
Arrhythmogenic right ventricular cardiomyopathy
ECG Finding
Echo Finding
Clincial finding
**the right ventricular myocardium is replaced by fatty and fibrofatty tissue**
Presents with palpitations, syncope, sudden cardiac death
ECG abnormalities in V1-3, typically T wave inversion. **An epsilon wave** is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall
Rx:
Sotalol
catheter ablation
Implantable cardioverter-defibrillator
43
All Murmurs
**Ejection systolic:**
**louder on expiration:**:
- aortic stenosis
- hypertrophic obstructive cardiomyopathy
**louder on inspiration:**
- pulmonary stenosis
- atrial septal defect
also: tetralogy of Fallot
**Holosystolic (pansystolic):**
- mitral/tricuspid regurgitation (high-pitched and 'blowing' in character)
- tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect ('harsh' in character)
Late systolic
mitral valve prolapse
coarctation of aorta
Early diastolic
aortic regurgitation (high-pitched and 'blowing' in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)
Mid-late diastolic
mitral stenosis ('rumbling' in character)
Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)
Continuous machine-like murmur
patent ductus arteriosus
RILE
Right-sided murmur → heard best on Inspiration
Left-sided murmur → heard best on Expiration
44
Ejection Systolic Murmur
:
AHPAT
Louder on expiration:
- aortic stenosis
- hypertrophic obstructive cardiomyopathy
louder on inspiration:
- pulmonary stenosis
- atrial septal defect
also: tetralogy of Fallot
45
Late systolic Murmur
mitral valve prolapse
coarctation of aorta
46
Early diastolic
aortic regurgitation (high-pitched and 'blowing' in character)
Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)
47
The examination findings of a pansystolic murmur, loudest in the mitral area and crackles on chest auscultation after MI
The examination findings of a pansystolic murmur, loudest in the mitral area and crackles on chest auscultation suggest a diagnosis of acute mitral regurgitation and pulmonary oedema, which is most likely to be caused by a rupture of the papillary muscle. This typically occurs 1-7 days post-infarction.
48
Prinzmetal Angina
Prinzmetal (vasospastic) angina is a rare form of angina in which pain is experienced at rest rather than during activity. It is caused by narrowing or occlusion of proximal coronary arteries due to spasm and cannot be diagnosed by coronary angiography. Beta blockers should not be used in
this form of angina because they may worsen the coronary spasm. ****Patients with this condition may be treated effectively with a dihydropyridine derivative CCB such as amlodipine, Felodipine ****
49
Adverse effects of amiodarone use
বালডা সবজায়গায় সমস্যা করে
1. Eyes: corneal deposits, photosensitivity
2. Thyroid:- thyroid dysfunction: both hypothyroidism and hyper-thyroidism
3. Heart: bradycardia, lengths QT interval
4. Lungs: pulmonary fibrosis/pneumonitis
5. Liver: liver fibrosis/hepatitis
6. Limbs; peripheral neuropathy, myopathy
7. Appearance; 'slate-grey' appearance
Even
thrombophlebitis and injection site reactionsl
50
Monitoring of patients taking amiodarone
Monitoring of patients taking amiodarone
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months
51
what type of drug is 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)
52
Thiazide Diuretics
Thiazide diuretics
Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by **blocking the thiazide-sensitive Na+-Clˆ’ symporter.** Potassium is lost as a result of more sodium reaching the collecting ducts. Thiazide diuretics have a role in the treatment of mild heart failure although loop diuretics are better for reducing overload. The main use of bendroflumethiazide was in the management of hypertension but recent NICE guidelines now recommend other thiazide-like diuretics such as indapamide and chlortalidone.
Common adverse effects:
dehydration
postural hypotension
hypokalaemia
due to increased delivery of sodium to the distal part of the distal convoluted tubule → increased sodium reabsorption in exchange for potassium and hydrogen ions
hyponatraemia
hypercalcaemia
the flip side of this is hypocalciuria, which may be useful in reducing the incidence of renal stones
gout
impaired glucose tolerance
impotence
Rare adverse effects:
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
53
M/A of Loop Diuretics
Loop diuretics
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. There are two variants of NKCC; loop diuretics act on NKCC2, which is more prevalent in the kidneys.
54
Adverse Effects of Loop Diuretics
Adverse effects
hypotension
hyponatraemia
hypokalaemia, hypomagnesaemia
hypochloraemic alkalosis
ototoxicity
hypocalcaemia
renal impairment (from dehydration + direct toxic effect)
hyperglycaemia (less common than with thiazides)
gout
55
Indications for a temporary pacemaker
Indications for a temporary pacemaker
- symptomatic/haemodynamically unstable bradycardia, not responding to atropine
- post-ANTERIOR MI: type 2 or complete heart block
post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable
- trifascicular block prior to surgery
56
The key diagnostic tests used to identify patients likely to benefit from cardiac resynchronization therapy is -----
transthoracic echocardiogram and ECG.
57
Indication of Biventricular Pacing
Heart Failure EF < 35%
Wide QRS >120
58
HOCM genetics-
mutation in
**Autosomal Dominant**
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
59
HOCM is associated with
Neuro
Cardio
Friedreich's ataxia
Wolff-Parkinson White
60
Echo Findings of HOCM
Echo findings - mnemonic - **MR SAM ASH**
mitral regurgitation (MR)-
systolic anterior motion (SAM) of the anterior mitral valve leaflet- (SAM+MR causes Pansystolic Murmur)
asymmetric hypertrophy (ASH)-
61
Murmurs of HOCM
systolic murmurs
1. ejection systolic murmur: due to left ventricular outflow tract obstruction. **Increases with Valsalva manoeuvre and decreases on squatting**
2. pansystolic murmur: due to systolic anterior motion of the mitral valve → mitral regurgitation
62
Drugs to avoid in HOCM
nitrates
**ACE-inhibitors**
inotropes
63
Rx for HOCM
ABCDE
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
64
Poor Prognostic feature of HOCM
syncope
family history of sudden death
young age at presentation
non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
abnormal blood pressure changes on exercise
An increased septal wall thickness is also associated with a poor prognosis.
65
Drugs for HD Stable VT
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide
66
Which drug should not be used in VT
Verapamil
( due to the risk of causing significant hypotension, ventricular fibrillation and cardiac arrest. H)
67
What if drug therapy fails in VT
EPS
ICD
68
Indication of ICD in VT
Significantly reduced EF
69
Drugs causing Prolonged QT
Long QT drugs: ABCDE + Hypo
A: anArrhythmic: ie Amiodrone
B: anBiotics: Macrolides, Quinolone
C: pCychotics: Haloperidol
D: antDepressant: SSRI, TCA
E: antEmetics: Ondansetron
Hypo ( hypokalemia, hypomagnesaemia, hypocalcemia)
70
First Line investigations for Palpitation
12-lead ECG
Thyroid function tests
Urea and electrolytes
Full blood count
**
Then
Holter
Then
External loop recorder
Implantable loop recorder****
71
ECG changes of Pericarditis
'saddle-shaped' ST elevation
**PR depression: most specific ECG marker for pericarditis**
72
Drugs for Pericarditis
NSAIDs
+
Colchicine
73
'Stress'-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
Transient, apical ballooning of the myocardium
Treatment is supportive
Takotsubo
74
What happens in Takotsubo
Transient, apical ballooning of the myocardium
Treatment is supportive
75
Types of Cardiomyopathy
1. Primary
a. Genetic: HOCM, Arrhythmogenic right ventricular dysplasia
b. Mixed: Dilated, Restrictive
c. Acquired: Peripartum, Takotsubo
2. Secondary:
Infective, Infiltrative, Storage, Toxicity
(Please check passmed)
76
Dilated cardiomyopathy Classic causes include:
ABCD
ABCD
Alcohol
Beriberi (Wet)
Coxsackie B virus
Doxorubicin
77
Restrictive Cardiomyopathy causes
SLASHER
SLASHER
Sarcoidosis
Lofflers
Amyloid
Scleroderma
Haemochromatosis
Eendocardial fibroelastosis
Post-Radiation fibrosis
78
What happpens in Arrythmogenic Rt ventricular Dysplasia
**Right ventricular myocardium is replaced by fatty and fibrofatty tissue**
Around 50% of patients have a mutation of one of the several genes which encode components of desmosome
ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
79
ECG Abnormalities seen in What happpens in Arrythmogenic Rt ventricular Dysplasia
**ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex**
- T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
- Epsilon wave (most specific finding, seen in 50% of patients)
- Localised QRS widening in V1-3 (> 110ms)
80
Epsilon wave seen in
Arrythmogenic Rt Ventricular Dysplasia
81
Inv in Cardiomyopathy
Echo
cMRI
82
Restrictive myocarditis causes systolic/diastolic dysfn
causes predominately diastolic dysfunction
83
Features suggesting restrictive cardiomyopathy rather than constrictive pericarditis
prominent apical pulse
absence of pericardial calcification on CXR
the heart may be enlarged
ECG abnormalities e.g. bundle branch block, Q waves
84
PARTS OF JVP
A WAVE
C WAVE
V WAVE
X DESCENT
Y DESCENT
85
DETAILS OF JVP
**'a' wave = atrial contraction:**
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation
**Cannon 'a' waves:
caused by atrial contractions against a closed tricuspid valve. therefore can be seen in VT when atrial and ventricular contraction is not co-ordinated.
are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing**
**'c' wave**
closure of tricuspid valve
not normally visible
**'v' wave**
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation
'x' descent = fall in atrial pressure during ventricular systole
'y' descent = opening of tricuspid valve
86
Auscult of Coarc of Aorta
mid systolic murmur, maximal over the back
apical click from the aortic valve
87
Association of Coarc of Aorta
TBBN
Turner's syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
88
Brugada Genetics
AD
More in Asianas
a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
89
ECG in Brugada
**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
90
Inv of Choice for Suspected Brugada
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
91
Rx for Brugada
ICD
92
Causes of Culture Neg IE
Prior antibiotic therapy
**Coxiella burnetii
Bartonella
Brucella
HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)**
93
Organisms for IE
**Staphylococcus aureus- most common cause of infective endocarditis-** particularly common in acute presentation and IVDUs
Streptococcus viridans- common in developing countries
(Streptococcus mitis and Streptococcus sanguinis)- poor dental hygiene or following a dental procedure
coagulase-negative Staphylococci such as Staphylococcus epidermidis- commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination.
**Streptococcus bovis- associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer**
94
Diagnostic Criteria of IE
Infective endocarditis diagnosed if-
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria
95
Poor prognostic factors of IE
Staphylococcus aureus infection
prosthetic valve (especially 'early', acquired during surgery)
culture negative endocarditis
**low complement levels**
96
Prophylaxis for IE
not routinely recommended. But:
- any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing
- if a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
97
Most common organism of IE after dental procedure
Viridans
(Mitis and Galactolytoicus)
98
Organism of IE post valve surgery
Epidermidis/
Coagulase Neg
99
What should you monitor when MgS04 is given?
urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment
100
Types of CCBs
rate-limiting CCBs/Non-dihydropyridine:
Verapamil
Diltiazem
dihydropyridine CCBs:
amlodipine, nifedipine)
101
4 As of Rheumatic fever
organism
blood tests
histology
The 4 As of rheumatic fever:
* caused by group-A-strep
* high ASO-titre
* presence of Aschoff bodies and Anitschkow cells
102
Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of ----------
Pulmonary arterial hypertension (PAH) may be defined as a resting mean pulmonary artery pressure of >= 20 mmHg. E
103
Features of Pulmonary HTN
Features
progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
104
Clinical signs in PH
**right ventricular heave:** indicating right ventricular hypertrophy or dilatation
**loud P2: **early in the disease reflects increased pulmonary artery pressure and may be accompanied by a palpable P2 in severe cases. With advanced PAH there may be right ventricular failure leading to a soft S2
**raised JVP with prominent 'a' waves: **reflects increased resistance to right atrial emptying due to elevated right ventricular end-diastolic pressure
**tricuspid regurgitation**
105
How to decide management plan for PH?
**acute vasodilator testing** is central to deciding on the appropriate management strategy. Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide.
106
What plays a key role in pathogenesis of PAH?
Endothelin
107
Management of PAH
**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
a. non-selective: bosentan
b. selective antagonist of endothelin receptor A: ambrisentan
- phosphodiesterase inhibitors: sildenafil
Patients with progressive symptoms should be considered for a heart-lung transplant.
108
Amiodarone half life
109
Amiodarone mechanism of action
Amiodarone is a class III antiarrhythmic agent.***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)**
110
Which class is amiodarone
class 3
111
Adverse effects of Amiodarone use
Adverse effects of amiodarone use
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
112
Features of severe aortic stenosis
Narrow pulse pressure
Slow rising pulse
Delayed ESM
Soft/absent S2
S4
Thrill
Duration of murmur
Left ventricular hypertrophy or failure
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Management for 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
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Causes of aortic stenosis
**- Degenerative calcification (most common cause in older patients > 65 years)
- Bicuspid aortic valve (most common cause in younger patients < 65 years)**
- William's syndrome (supravalvular aortic stenosis)
- Post-rheumatic disease
- Subvalvular: HOCM
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Commonest cause of Aortic Stenosis in Older patients
Degenerative Calcification
116
Causes of AS in younger patients
Bicuspid aortic valve
117
First cardiac marker to rise
Myoglobin
118
Role of troponin in cardiac muscle
Component of thin filament
to remember: **troponIN = thIN**
119
Chronic Heart Failure Management
120
MRAs
Spironolactone
Eplerenone
Finerenone
121
ACEI causes
ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli
122
Adenosine M/A
A1 agonist
123
Amiodarone M/A
Amiodarone is a class III antiarrhythmic agent
The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential.
Amio
Da
Rone
hence class 3
124
Monitoring for Amiodarone
Monitoring: 'TLC Every 6'
T: TFTs (Thyroid function tests)
L: LFTs (Liver function tests)
C: CXR (Chest X-ray, before treatment)
E: Every 6 months (TFT and LFT monitoring)
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Amiodarone adverse effects
Adverse Effects: 'B-PLANT G'
B: Bradycardia
P: Pulmonary fibrosis/pneumonitis
L: Liver fibrosis/hepatitis
A: Appearance changes (Slate-grey skin, Photosensitivity)
N: Neuropathy (Peripheral neuropathy, myopathy)
T: Thyroid dysfunction (Hypo- and Hyperthyroidism)
G: Gray corneal deposits
126
How does ARBs work?
- block effects of angiotensin II at the AT1 receptor
127
Classification of dissection
Stanford classification
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases
DeBakey classification
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally
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Inv of choice for dissection
CT angiography of the chest, abdomen and pelvis is the investigation of choice
129
Inv of choice for dissection HD unstable
TOE
130
Indications for Aortic valve surgery in AR
symptomatic patients with severe AR
asymptomatic patients with severe AR who have LV systolic dysfunction
131
Murmur of AR
- early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
- mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
132
Most common Causes of AS
- degenerative calcification (most common cause in older patients > 65 years)
- bicuspid aortic valve (most common cause in younger patients < 65 years)
133
When is surgery indicated in AS
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
134
ARVD ECG
**- T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
- Epsilon wave (most specific finding, seen in 50% of patients)**
Localised QRS widening in V1-3 (> 110ms)
Prolonged S wave upstroke of 55ms in V1-3
Ventricular ectopy of LBBB morphology, with frequent PVCs > 1000 per 24 hours
Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)
135
M/A Atropine
Atropine is an antagonist of the muscarinic acetylcholine receptor
136
Types of ASD
Two types of ASDs are recognised, ostium secundum and ostium primum. Ostium secundum are the most common
137
ECG findings of Osteum Secondum
Ostium secundum (70% of ASDs)
Two R= RBBB, RAD
ECG: RBBB with RAD
138
ECG findings of Osteum Primum
****
ECG: RBBB with LAD, prolonged PR interval
139
Rhythm control agents for AF
AF => Atrial fibrillation
(A)miodarone
(F)lecainide (if no structural disease)
140
M/A of 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
141
Bicaspid aortic valve is associated with
- left dominant coronary circulation (the posterior descending artery arises from the circumflex instead of the right coronary artery)
- Turner's syndrome
- around 5% of patients also have coarctation of the aorta
142
INR Target for people on warfarin
(Note Warfarin is second-line after DOACs):
- venous thromboembolism: target INR = 2.5, if recurrent 3.5
- atrial fibrillation, target INR = 2.5
143
M/A 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.
144
What to do with Warfarin, when a dental proedure needs to be done
Dentistry in warfarinised patients - check INR 72 hours before procedure, proceed if INR < 4.0
145
Most Specific ECG marker for Pericarditis
PR Depression
146
deteriorating renal function post angioplasty + Rash = ?
deteriorating renal function post angioplasty = contrast induced nephropathy
(however, usually starts quite earlier than a week)
deteriorating renal function post angioplasty+Rash = Cholesterol embolisation
147
RX OF PAH
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
148
# 1.
Association of WPW
Associations- THEMS
- Thyrotoxicosis
- HOCM
- Ebsteins anomaly
- Mitral valve prolapse
- Secondum ASD
149
Glycoprotein 2a/3b receptor antagonists
Examples include;
abciximab
eptifibatide
tirofiban
