Cardiology 3 Flashcards
What cause of IE carries good prognosis?
Infective endocarditis - streptococcal infection carries a good prognosis
What are poor prognostic factors in IE?
Staphylococcus aureus infection (see below)
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels
Mortality according to organism in IE?
staphylococci - 30%
bowel organisms - 15%
streptococci - 5%
Antibiotics for IE?
Indications for surgery in IE?
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
mechanism of action of statins?
Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis.
What is the most common cause of acyanotic heart defects?
Ventricular septal defects (VSD)
VSD accounts for 30% of cases.
List the common causes of acyanotic heart defects.
- Ventricular septal defect (VSD)
- Atrial septal defect (ASD)
- Patent ductus arteriosus (PDA)
- Coarctation of the aorta
- Aortic valve stenosis
What are the most common causes of cyanotic heart defects?
- Tetralogy of Fallot
- Transposition of the great arteries (TGA)
- Tricuspid atresia
Which cyanotic heart defect is more common at birth?
Transposition of the great arteries (TGA)
Patients with Tetralogy of Fallot generally present at around 1-2 months.
Aetiology 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
How does VSD present post natally?
failure to thrive
features of heart failure
hepatomegaly
tachypnoea
tachycardia
pallor
classically a pan-systolic murmur which is louder in smaller defects
How is VSD managed?
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
Complications of VSD?
AR - due to poorly supported right coronary cusp resulting in cusp prolapse
IE
Eisenmenger’s
Right heart faillure
Pulmonary HTN
Mechanism of action of Ambrisentan?
Endothelin receptor A antagnoist
What is the most common cause of IE following valve surgery?
Staphylococcus epidermidis if < 2 months post valve surgery
after 2 months the spectrum of organisms which cause endocarditis return to normal
What is the mechanism of hypokalaemia when using thiazides?
Mechanism of hypokalaemia due to thiazides: increased delivery of sodium to the distal part of the distal convoluted tubule
What is the strongly associated with risk of sudden death in the first six months after myocardial infarction?
The most important factor predicting outcomes post-STEMI is the presence of new systolic heart failure. It suggests that a large amount of myocardial damage. Those with systolic heart failure post MI can be up to 10x more likely to die than those that do not have an MI.
what is Ebstein’s anomaly?
Ebstein’s anomaly is a congenital heart defect characterised by low insertion of the tricuspid valve resulting in a large atrium and small ventricle. It is sometimes referred to as ‘atrialisation’ of the right ventricle.
Ebstein’s anomaly may be caused by exposure to lithium in-utero.
What is Ebstein’s anomaly associated with?
patent foramen ovale (PFO) or atrial septal defect (ASD) is seen in at least 80% of patients, resulting in a shunt between the right and left atria
Wolff-Parkinson White syndrome
Clinical features of Ebstein’s anomaly?
cyanosis
prominent ‘a’ wave in the distended jugular venous pulse,
hepatomegaly
tricuspid regurgitation
pansystolic murmur, worse on inspiration
right bundle branch block → widely split S1 and S2
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
management of atrial flutter?
is similar to that of atrial fibrillation although medication may be less effective
atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
What is Catecholaminergic polymorphic ventricular tachycardia?
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a form of inherited cardiac disease associated with sudden cardiac death. It is inherited in an autosomal dominant fashion and has a prevalence of around 1:10,000.
Pathophysiology
the most common cause is a defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum
Features of Catecholaminergic polymorphic ventricular tachycardia?
Features
exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
sudden cardiac death
symptoms generally develop before the age of 20 years
Management of Catecholaminergic polymorphic ventricular tachycardia?
beta-blockers
implantable cardioverter-defibrillator
What is syndrome x and what are the features and managament?
a microvascular angina
Features
angina-like chest pain on exertion
ST depression on exercise stress test (down sloaping)
but normal coronary arteries on angiography
Management
nitrates may be beneficial
What is associated with aortic dissection?
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
Features of aortic dissection?
Chest/back pain
(typically severe and sharp, tearing in nature)
pulse deficit
Aortic regurgitation
HTN
other features may result from the involvement of specific arteries. For example:
coronary arteries → angina
spinal arteries → paraplegia
distal aorta → limb ischaemia
the majority of patients have no or non-specific ECG changes. In a minority of patients, ST-segment elevation may be seen in the inferior leads
Classification of aortic 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
classically chest pain is more common in type A dissection and upper back pain is more common in type B dissection. However, there is considerable overlap and both chest and back pain are present in many patients
Mechanism of action of Dipyridamole?
Mechanism of action
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
what is S1 and S2?
S1
closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis
S2
closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal
what causes 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) and mitral regurgitation
what causes s4?
may be heard in aortic stenosis, HOCM, hypertension
caused by atrial contraction against a stiff ventricle
therefore coincides with the P wave on ECG
in HOCM a double apical impulse may be felt as a result of a palpable S4
How long should patients be anticoagulated after cardioversion?
Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence
What murmur would you hear in ASD?
ejection systolic murmur louder on inspiration
Angina management?
Aspirin and statin
BB or CCB
Increase to the max tolerated dose
If ongoing angina - can add:
a long-acting nitrate
ivabradine
nicorandil
ranolazine
if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used
if used in combination with a beta-blocker then use a longer-acting dihydropyridine calcium channel blocker (e.g. amlodipine, modified-release nifedipine)
remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block)
What clotting factirsd are affected by warfarin?
1972 (10, 9, 7, 2)
Causes of a loud S2?
hypertension: systemic (loud A2) or pulmonary (loud P2)
hyperdynamic states
atrial septal defect without pulmonary hypertension
Causes of a sof S2?
Aortic stenosis
causes of a fixed split S2?
atrial septal defect
Causes of a widely split s2?
deep inspiration
RBBB
pulmonary stenosis
severe mitral regurgitation
causes of reversed split s@
Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)
LBBB
severe aortic stenosis
right ventricular pacing
WPW type B (causes early P2)
patent ductus arteriosus
What is likely to be found on ausculatation of the heart in LBBB?
Reversed split s2
What are the stages of HTN?
Lifestyle advice in HTN?
a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg
caffeine intake should be reduced
the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight
First line treatment for HTN?
patients < 55-years-old or a background of type 2 diabetes mellitus: ACE inhibitor or a Angiotensin receptor blocker (ACE-i or ARB): (A)
angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
patients >= 55-years-old or of black African or African-Caribbean origin: Calcium channel blocker (C)
ACE inhibitors have reduced efficacy in patients of black African or African-Caribbean origin are therefore not used first-line
Step 2 treatment in HTN?
if already taking an ACE-i or ARB add a Calcium channel blocker or a thiazide-like Diuretic
if already taking a Calcium channel blocker add an ACE-i or ARB or a thiazide-like Diuretic
for patients of black African or African-Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
Step 3 and 4 HTN management?
Step 3 treatment
add a third drug to make, i.e.:
if already taking an (A + C) then add a D
if already (A + D) then add a C
(A + C + D)
Step 4 treatment
NICE define step 4 as resistant hypertension and suggest either adding a 4th drug (as below) or seeking specialist advice
first, check for:
confirm elevated clinic BP with ABPM or HBPM
assess for postural hypotension.
discuss adherence
if potassium < 4.5 mmol/l add low-dose spironolactone
if potassium > 4.5 mmol/l add an alpha- or beta-blocker
Blood pressure targets?
Management of SVT?
Acute management
vagal manoeuvres:
Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
carotid sinus massage
intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
contraindicated in asthmatics - verapamil is a preferable option
electrical cardioversion
Management of STEMI
Aspirin
P2Y12 receptor antagonist (clopi or ticagrelor)
Unfractionated herparin in those who are going to have PCI (alternative =LMWH)
PCI
Thrombolysis is PCI is not available
An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation
if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis
for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation
Causes of restrictive cardiomyopathy?
amyloidosis (e.g. secondary to myeloma) - most common cause in UK
haemochromatosis
post-radiation fibrosis
Loffler’s syndrome: endomyocardial fibrosis with a prominent eosinophilic infiltrate
endocardial fibroelastosis: thick fibroelastic tissue forms in the endocardium; most commonly seen in young children
sarcoidosis
scleroderma
Pathophysiology of restrictive cardiomyopathy?
primarily characterized by decreased compliance of the ventricular endomyocardium
causes predominately diastolic dysfunction
Features of restrictive cardiomyopathy?
Features
similar to constrictive pericarditis
low-voltage ECG
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
Investigations for restrictive caridomyopathy?
echo
cardiac MRI
What causes pulses alterans?
Pulsus alternans is a physical finding characterised by alternating strong and weak pulses despite a regular heart rhythm. It is highly specific for severe left ventricular systolic dysfunction, particularly in the setting of acute decompensated heart failure.
Pulsus alternans occurs due to beat-to-beat variation in stroke volume, reflecting the heart’s inability to maintain consistent contractile force when severely compromised
Its presence indicates significant cardiac decompensation and correlates with elevated left ventricular filling pressures, making it the most specific finding for this clinical scenario.
What is Woff-Parkinson White?
Wolff-Parkinson White (WPW) syndrome is caused by a congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT). As the accessory pathway does not slow conduction AF can degenerate rapidly to VF.
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
Differentiating between type A and type B WPW?
type A (left-sided pathway): dominant R wave in V1
type B (right-sided pathway): no dominant R wave in V1
What is associated with WPW?
HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD
Management of WPW?
definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol, amiodarone, flecainide
sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation
In patients with accessory pathways, such as those with Wolff-Parkinson-White syndrome, AV nodal blocking drugs should be avoided in atrial fibrillation. This is because blocking the AV node may enhance the rate of conduction through the accessory pathway, causing atrial fibrillation to degenerate into ventricular fibrillation (VF).
What is Ivabradine and what is its mechanism of action?
Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.
Adverse effects of Ivabradine?
visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block
Mechanism of action of ACEi?
inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys
renoprotective mechanism
angiotensin II constricts the efferent glomerular arterioles
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
this is particularly important in diabetic nephropathy
ACE inhibitors are activated by phase 1 metabolism in the live
Side effects of ACEi?
cough
occurs in around 15% of patients and may occur up to a year after starting treatment
thought to be due to increased bradykinin levels
angioedema: may occur up to a year after starting treatment
hyperkalaemia
first-dose hypotension: more common in patients taking diuretics
Cautions and contraindications of ACEi?
pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
Monitoring of ACEi?
urea and electrolytes should be checked before treatment is initiated and after increasing the dose
a rise in the creatinine and potassium may be expected after starting ACE inhibitors
acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.
significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis
Adenosine mechanism of action?
causes transient heart block in the AV node
agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux
adenosine has a very short half-life of about 8-10 seconds
Adenosine is most commonly used to terminate supraventricular tachycardias. The effects of adenosine are enhanced by dipyridamole (antiplatelet agent) and blocked by theophyllines. It should be avoided in asthmatics due to possible bronchospasm.
Adverse effects of adenosine?
chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
what are examples of adenosine diphosphate receptor inhibitors?
Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine
Mechanism of action of 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.
Interactions of 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
Examples of ARBs and mechanism of action?
Examples
candesartan
losartan
irbesartan
Like ACE inhibitors they should be used with caution in patients with renovascular disease. Side-effects include hypotension and hyperkalaemia.
Mechanism
block effects of angiotensin II at the AT1 receptor
Interactions of clopidogrel?
concurrent use of proton pump inhibitors (PPIs) may make clopidogrel less effective
PPIs such as lansoprazole should be OK
What drug group is clopidogrel?
Clopidogrel belongs to a class of drugs known as thienopyridines which have a similar mechanism of action. Other examples include:
prasugrel
ticagrelor
ticlopidine
What is the mechanism of action of clopidogrel?
antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets
When do the coronary arteries fill?
during diastole
What are the actions of BNP?
vasodilator: can decrease cardiac afterload
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
What is the most common primary cardiac tumour?
Atrial myxoma
75% occur in the keft atrium - most commonly attaches to the fossa ovalis
Features of 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
What is anginal pain defined as?
NICE define anginal pain as the following:
1. constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
2. precipitated by physical exertion
3. 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 pai
How should stable angina be investigated?
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE recommend the following (e.g. symptoms consistent with typical/atypical angina OR ECG changes):
1st line: CT coronary angiography
2nd line: non-invasive functional imaging (looking for reversible myocardial ischaemia)
3rd line: invasive coronary angiography
Whar are 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
what on examination indicated that in MS the mitral valve leaflets are still mobile?
Opening snap
What is nicorandil and what is the mechanism of action ?
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.
Contraindications to Nicorandil?
left ventricular failure
Adverse effects of Nicorandil?
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
What is the most common cause of death following MI?
The most common cause of death in patients following a myocardial infarction is ventricular fibrillation.
Causes of myocarditis?
viral: coxsackie B, HIV
bacteria: diphtheria, clostridia
spirochaetes: Lyme disease
protozoa: Chagas’ disease, toxoplasmosis
autoimmune
drugs: doxorubicin
Presentation of myocarditis?
usually young patient with an acute history
chest pain
dyspnoea
arrhythmias
Investigations for myocarditis?
bloods
↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP
ECG
tachycardia
arrhythmias
ST/T wave changes including ST-segment elevation and T wave inversion
Managment of myocarditis?
treatment of underlying cause e.g. antibiotics if bacterial cause
supportive treatment e.g. of heart failure or arrhythmias
Complications of myocarditis?
heart failure
arrhythmia, possibly leading to sudden death
dilated cardiomyopathy: usually a late complication
What is the pulmonary embolism rule0out criteria?
all the criteria must be absent to have negative PERC result, i.e. rule-out PE
this should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn’t the diagnosis
this low probability is defined as < 15%, although it is clearly difficult to quantify such judgements
a negative PERC reduces the probability of PE to < 2%
if your suspicion of PE is greater than this then you should move straight to the 2-level PE Wells score, without doing a PERC
What is included in the PE wells score?
ECG findings in PE?
the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen
What medications can be used for medical cardioversion in AF?
Atrial fibrillation - cardioversion: amiodarone + flecainide
others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone
Less effective agents
beta-blockers (including sotalol)
calcium channel blockers
digoxin
disopyramide
procainamide
Features of VT rather than SVT with abarrent 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
Can warfarin be used in breast feeding?
yes
What does Bisferiens pulse indicate?
mixed aortic valve disease
In Bisferiens pulse you would see two systolic peaks to their pulse
What is heard in the heart sounds in CHB?
Variable intensity of S1
variation in PR interval seen in CHB causes variation in S1 intensity.
What is patent ductus arteriosus?
a form of congenital heart defect
generally classed as ‘acyanotic’. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis
connection between the pulmonary trunk and descending aorta
usually, the ductus arteriosus closes with the first breaths due to increased pulmonary flow which enhances prostaglandins clearance
more common in premature babies, born at high altitude or maternal rubella infection in the first trimester
Features of PDA?
left subclavicular thrill
continuous ‘machinery’ murmur
large volume, bounding, collapsing pulse
wide pulse pressure
heaving apex beat
Management of PDA in pre-term infants?
most centres now recommend initial expectant supportive care rather than early pharmacologic therapy as spontaneous closure often occurs
if hemodynamically significant ΡDA remains or the infant remains ventilator dependent after one week of age then pharmacological closure is generally recommended:
ibuprofen, indomethacin or paracetamol
inhibits prostaglandin synthesis
given to the infant, not to the mother in the antenatal period
closes the connection in the majority of cases
indomethacin use is declining due to increased side-effect profile compared to other drugs
Management of PDA in term infants?
indications for closure
moderate or large ΡDA
prior episode of endocarditis
small audible PDΑ
technique: transcatheter ΡDA closure rather than pharmacological therapy (ibuprofen/indomethacin) which is not effective in term infants
Modfied Dukes criteia?
Infective endocarditis diagnosed if
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria
Pathological criteria
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content)
Major criteria
Positive blood cultures
two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococcus viridans and the HACEK group, or
persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or
positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci, or
positive molecular assays for specific gene targets
Evidence of endocardial involvement
positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or
new valvular regurgitation
Minor criteria
predisposing heart condition or intravenous drug use
microbiological evidence does not meet major criteria
fever > 38ºC
vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
Management of HOCM?
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
What drugs should be avoided in HOCM?
nitrates
ACE-inhibitors
inotropes
What causes a cough in patients taking ACEi?
The persistent dry cough experienced by the patient after starting treatment with lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, is a well-known side effect due to the accumulation of bradykinin. ACE inhibitors block the conversion of angiotensin I to angiotensin II, which results in vasodilation and reduced blood pressure. However, ACE also degrades bradykinin, a potent vasodilator peptide. When ACE is inhibited by lisinopril, bradykinin accumulates and can cause a persistent dry cough.
occurs in around 15% of patients and may occur up to a year after starting treatment
thought to be due to increased bradykinin levels
