Cardiology Flashcards
What does the P wave represent on ECG
What does the PR interval represent electrically and physiologically and how long is this?
Atrial depolarisation
The atria contracts during the PR interval, the PR interval is the time taken for electrical activity to spread from the SA node to the AV node
This is from the start of the P wave to the start of the QRS complex
120-220ms, 3-5 small squares
What does the QRS complex on the ECG represent?
How long does this take?
ventricular depolarisation
120ms 3 small squares
What does the ST segment on the ECG represent?
end of the S wave to the start of the T wave
ventricular contraction
What does the T wave represent?
Venticular repolarisation
what is the QT interval and how long should this be?
start of the Q wave to the end of the T wave
400-440ms prolonged is more than 450
What causes the first heart sound (S1)
- what would cause this to be loud
- what would cause this to be soft
- Closure of mitral and tricuspid valves
- Soft if long PR or mitral regurgitation
- Loud in mitral stenosis
- Variable intensity in complete heart block
What causes the second heart sound S2?
caused by the closure of the aortic valve (A2) closely followed by that of the pulmonary valve
(P2)
What would cause a loud S2?
Causes of a loud S2
• Hypertension: systemic (loud A2) or pulmonary (loud P2)
• Hyperdynamic states
• Atrial septal defect without pulmonary hypertension
What would cause a soft S2?
Causes of a soft S2
• Aortic stenosis
What would cause a fixed split S2?
What would cause a widely split s2?
Causes of fixed split S2
• Atrial septal defect
Causes of a widely split S2 • Deep inspiration • RBBB • Pulmonary stenosis • Severe mitral regurgitation
what would Cause a reversed (paradoxical) split S2 (P2 occurs before A2)?
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 S3? what is this caused by?
- 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, constrictive pericarditis
- Gallop rhythm (S3) is an early sign of LVF
What is S4? what is this caused by?
- may be heard in aortic stenosis, HOCM, hypertension
- caused by atrial contraction against a stiff ventricle
- in HOCM a double apical impulse may be felt as a result of a palpable S4
what is pulsus parodoxus?
-when is this seen?
Pulsus parodoxus
• Greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or
absent pulse in inspiration
• Severe asthma, cardiac tamponade
when is a slow rising pulse seen?
Slow-rising/plateau
• Aortic stenosis
when is a collapsing pulse seen?
Collapsing
• Aortic regurgitation
• Patent ductus arteriosus
• Hyperkinetic (anemia, thyrotoxic, fever, exercise/pregnancy)
what is pulsus alterans? when is this seen?
Pulsus alternans
• Regular alternation of the force of the arterial pulse
• Severe LVF
what is a bisferiens pulse? when is this seen?
Bisferiens pulse
• ‘Double pulse’ - two systolic peaks
• Mixed aortic valve disease
*HOCM may occasionally be associated with a bisferiens pulse
when is a jerky pulse felt?
‘Jerky’ pulse
• Hypertrophic obstructive cardiomyopathy
What does the ‘a’ wave in JVP represent?
- when is this large?
- what are cannon ‘a’ waves? when is this seen?
‘a’ wave = atrial contraction
• Large if high 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
• Are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm,
single chamber ventricular pacing
what causes the ‘c’ wave in jvp?
-is this normally visible?
- Closure of tricuspid valve
* Not normally visible
when are giant ‘v’ waves seen in JVP?
• Giant v waves in tricuspid regurgitation
what is the ‘x’ descent in JVP?
Fall in atrial pressure during ventricular systole
what is the ‘y’ descent in JVP?
Opening of tricuspid valve
what happens to blood pressure during exercise?
Blood pressure
• Systolic ↑, diastolic ↓
• Leads to ↑ pulse pressure
• In healthy young people the ↑ in MABP is only slight
what happens to cardiac output in exercise?
- what does this result from?
- what happens to heart rate and stroke volume?
• ↑ in cardiac output may be 3-5 fold
• Results from venous constriction, vasodilation and ↑ myocardial contractibility, as well as from
the maintenance of right atrial pressure by an ↑ in venous return
• Heart rate up to 3-fold ↑
• Stroke volume up to 1.5-fold ↑
how is the left ventricular ejection fraction worked out?
how is stroke volume worked out?
Left ventricular ejection fraction = (stroke volume / end diastolic LV volume) * 100%
Stroke volume = end diastolic LV volume - end systolic LV volume
what are normal ECG variants seen in an athlete?
In an athlete: • Sinus bradycardia • Junctional rhythm • First degree heart block • Wenckebach phenomenon
what are ECG changes seen in hypothermia?
- Bradycardia
- ‘J’ wave - small hump at the end of the QRS complex
- First degree heart block
- Long QT interval
- Atrial and ventricular arrhythmias
what are the ECG changes seen in digoxin toxicity?
- Down-sloping ST depression (‘reverse tick’)
- Flattened/inverted T waves
- Short QT interval
- Arrhythmias e.g. AV block, bradycardia
what are causes of ST depression on the ECG?
- Normal if upward sloping
- Ischemia
- Digoxin
- Hypokalemia
- Syndrome X
what is seen on the ECG in LBBB?
what are the causes?
W in V1 and M in V6 Causes: • Ischemic heart disease • Hypertension • Cardiomyopathy • Idiopathic fibrosis
what is first degree heart block? what causes this?
PR interval is lengthened beyond 0.20 seconds (>5small squares)
Also named: 1st degree heart block
Causes: • Idiopathic • Ischemic heart disease • Digoxin toxicity • Hypokalemia* • Rheumatic fever • Aortic root pathology e.g. Abscess secondary to endocarditis • Lyme disease • Sarcoidosis • Myotonic dystrophy
what causes LAD?
left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people
what are causes of RAD?
- Right ventricular hypertrophy
- Left posterior hemiblock
- Chronic lung disease
- Pulmonary embolism
- Ostium SECUNDUM ASD
• Wolff-parkinson-white syndrome* - left-
sided accessory pathway
- Normal in infant < 1 years old
- Minor RAD in tall people
Who does isolated systolic hypertension affect?
Isolated systolic hypertension (ISH) is common in the elderly, affecting around 10% of
people older than 70 years old.
How can you group secondary causes of hypertension?
Renal disease - 80% Endocrine disorders Others o Pregnancy o Coarctation of the aorta o The combined oral contraceptive pill o Steroids o Maoi
What are the renal causes of secondary hypertension?
o Glomerulonephritis
o Pyelonephritis
o Adult polycystic kidney disease
o Renal artery stenosis
what are the endocrine disorders that can causes secondary hypertension?
o Cushing’s syndrome
o Primary hyperaldosteronism including Conn’s syndrome
o Liddle’s syndrome
o Congenital adrenal hyperplasia (11-β hydroxylase deficiency)
o Pheochromocytoma
o Acromegaly
what are direct renin inhibitors?
- how does this work?
- what have trials looked into?
- adverse effects?
- what does this have a role in?
• e.g. Aliskiren (branded as Rasilez)
• By inhibiting renin blocks the conversion of angiotensinogen to angiotensin I
• No trials have looked at mortality data yet. Trials have only investigated fall in blood pressure.
Initial trials suggest aliskiren ↓ blood pressure to a similar extent as angiotensin converting
enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
• Adverse effects were uncommon in trials although diarrhea was occasionally seen
• Only current role would seem to be in patients who are intolerant of more established
antihypertensive drugs
what are three centrally acting antihypertensives?
• Methyldopa: used in the management of hypertension during pregnancy
• Moxonidine: used in the management of essential hypertension when conventional
antihypertensives have failed to control blood pressure
• Clonidine: the antihypertensive effect is mediated through stimulating α-2 adrenoceptors in the
vasomotor center.
what is the blood pressure target in DM?
what drugs are used first line?
which drugs should be avoided?
Hypertension and DM is an added cardiovascular risk factor for diabetics and should therefore by
actively looked for and treated. It is also a risk factor for the development of diabetic nephropathy.
Selected points
• The blood pressure target for diabetics is 140/80 mmHg. If there is end-organ damage the target
is 130/80 mmHg
• ACE inhibitors are first-line*. Otherwise managed according to standard NICE hypertension
guidelines
• BNF advises to avoid the routine use of beta-blockers in uncomplicated hypertension, particularly when given in combination with thiazides, as they may cause insulin resistance,
impair insulin secretion and alter the autonomic response to hypoglycemia
*increase insulin sensitivity and can therefore theoretically cause hypoglycemia - rarely clinically
relevant
what are the clinical features of pericarditis?
- Chest pain: may be pleuritic. Is often relieved by sitting forwards
- Other symptoms include non-productive cough, dyspnea and flu-like symptoms
- Pericardial rub
- Tachypnea
- Tachycardia
what are the causes of pericarditis?
- Viral infections (Coxsackie)
- TB
- Uremia (causes ‘fibrinous’ pericarditis)
- Trauma
- Post MI, Dressler’s syndrome
- Connective tissue disease
- Hypothyroidism
what ECG changes are seen in pericarditis?
ECG changes
• Widespread ‘saddle-shaped’ ST elevation
• PR depression
what are the causes of myocarditis?
Causes • Viral: coxsackie, HIV • Bacteria: diphtheria, clostridia • Spirochetes: Lyme disease • Protozoa: Chagas' disease, toxoplasmosis • Autoimmune • Drugs
what is the clinical presentation of myocarditis?
- Usually young patient with acute history
* Chest pain, SOB
what are risk factors for endocarditis? which is the strongest one?
the strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. Other factors include:
• Previously normal valves (50%, typically acute presentation)
• Rheumatic valve disease (30%)
• Prosthetic valves
• Congenital heart defects
• Intravenous drug users (IVDUS, e.g. Typically causing tricuspid lesion)
what are the causes for endocarditis?
- most common
- seen in prosthetic valves
- seen in IVDUs
- seen in colorectal ca
- which is a complication of colonic resection?
- culture -ve causes?
Causes
• Streptococcus viridans (prev. Most common cause)→ has good prognosis, poor dental hygiene
• Staphylococcus epidermidis (especially prosthetic valves)
• Staphylococcus aureus (especially acute presentation, IVDUS most common cause)
• Streptococcus bovis is associated with colorectal cancer
• Bacteroides fragilis endocarditis is very rare complication of colonic resection, bacteria reaches
heart via venous return, this is why it affects right > left side → Treat with Metronidazole
• Non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic
endocarditis
Culture negative causes (BP-CHB)
• Brucella
• Prior antibiotic therapy
• Coxiella burnetii
• HACEK: Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
• Bartonella
Following prosthetic valve surgery Staphylococcus epidermidis is the most common organism in the
first 2 months and is usually the result of perioperative contamination. After 2 months the spectrum of
organisms which cause endocarditis return to normal, except with a slight ↑ in Staph aureus infections
what are 4 poor prognostic factors in endocarditis?
- Staph aureus infection (see below)
- Prosthetic valve (especially ‘early’, acquired during surgery)
- Culture negative endocarditis
- Low complement levels
what is the mortalitis according to organism in endocarditis
- staphylococci
- bowel organism
- streptococci
Mortality according to organism
• Staphylococci - 30%
• Bowel organisms - 15%
• Streptococci - 5%
how is endocarditis diagnosed?
- Pathological criteria positive, or
- 2 major criteria, or
- 1 major and 3 minor criteria, or
- 5 minor criteria
what are pathological criteria in the diagnosis of endocarditis?
Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
(valve tissue, vegetations, embolic fragments or intracardiac abscess content)
what are the major criteria in the diagnosis of endocarditis?
- Positive blood cultures
• Two positive blood cultures showing typical organisms consistent with infective endocarditis,
such as Streptococcus viridans and the HACEK group.
• Persistent bacteremia 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.
• Positive serology for Coxiella burnetii, Bartonella species or Chlamydia psittaci.
• 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
what are the minor criteria in the diagnosis of endocarditis?
• Predisposing heart disease
• Microbiological evidence does not meet major criteria
• Fever > 38oc
• Vascular phenomena: major emboli, splenomegaly, clubbing, splinter hemorrhages, petechiae
or purpura
• Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots (boat shaped
hemorrhages in retina)
• Elevated CRP or ESR
what is the current management for endocarditis?
- inital blind therapy with and without prosthetic valve
- in staphyloccal endocarditis
- in streptococcal endocarditis
• Initial blind therapy - flucloxacillin + gentamicin (benzylpenicillin + gentamicin if symptoms
less severe)
• Initial blind therapy if prosthetic valve is present or patient is penicillin allergic - vancomycin
+ rifampicin + gentamicin
• Endocarditis caused by staphylococci - flucloxacillin (vancomycin + rifampicin if penicillin
allergic or MRSA)
• Endocarditis caused by streptococci → benzylpenicillin + gentamicin (vancomycin +
gentamicin if penicillin allergic)
what are the 7 indications for surgery in endocarditis?
Indications for surgery
• Severe valvular incompetence (both native and prosthetic)
• Early prosthetic valve endocarditis
• 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
• HACK group, brucella, coxilla, pseudo- aeruginosa and vancomycin resistant enterococci
when should patients be given antibiotic prophylaxis for endocarditis?
• 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
What did SAVE, SOLVD, CONSENSUS trials show with regards to heart failure?
ACE inhibitors improve mortality in heart failure
what did RALES trial show with regards to heart failure?
Spironalactone improves mortality in heart failure
what did CIBIS trial show with regards to heart failure?
β-blockers improve mortality in heart failure
what did the VHEFT-1 trial show with regards to heart failure?
Hydralazine with nitrates improve mortality in heart failure
what is the management of heart failure?
- what vaccines should be given?
- does digoxin have a role?
• All patients should be given an ACE inhibitor unless contradictions exist
• Once an ACE inhibitor has been introduced a β-blocker should be started regardless of whether
the patient is still symptomatic
• Offer annual influenza vaccine
• Offer pneumococcal vaccine
Digoxin has also not been proven to ↓ mortality in patients with heart failure. It may however improve
symptoms due to its inotropic properties. Digoxin is strongly indicated if there is coexistent atrial
fibrillation
what is used to classify severity of heart failure?
(NYHA) The New York Heart Association (NYHA) classification is widely used to classify the
severity of heart failure:
describe the stages of heart failure with NYHA
NYHA Class I
• No symptoms
• No limitation: ordinary physical exercise does not cause undue fatigue, dyspnea or palpitations
NYHA Class II
• Mild symptoms
• Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue,
palpitations or dyspnea
NYHA Class III
• Moderate symptoms
• Marked limitation of physical activity: comfortable at rest but less than ordinary activity results
in symptoms
NYHA Class IV
• Severe symptoms
• Unable to carry out any physical activity without discomfort: symptoms of heart failure are
present even at rest with ↑ discomfort with any physical activity
describe the treatment of acute pulmonary oedema
• High-flow oxygen
• Furosemide 0.5-1 mg/kg IV
• Morphine 2-4 mg IV
• Sublingual nitroglycerine (GTN).
• Steps then are dictated by the systolic BP after initial treatment:
o If the BP is >100 mmHg, start IV nitroglycerine 10-20 μg/min
o BP of 70-100 mmHg, with no shock start IV dobutamine 2-20 μg/min
o If the BP is 70-100 mmHg with shock, start IV dopamine 5-15 μg/min
o If the BP is < 70 mmHg with shock, start IV noradrenaline 0.5-30 μg/min.
what amount of heart failure is diastolic? what is the mortality?
- 1/3 of heart failure is diastolic (normal Left Ventricular Systolic Function-LVSF)
- Mortality in Diastolic HF is 5-8% (lower than Systolic HF: 10-15%)
what is the diagnosis of diastolic heart failure?
Diagnosis:
• Echo is the golden diagnostic tool
• CXR and ECG cannot differentiate Diastolic vs. Systolic HF.
what is the management of diastolic heart failure?
Management:
• Initially, reduction of pulmonary venous pressure (PVP) and congestion, using diuretics
• ARBs are superior to ACE inhibitors
describe the features of cardiac tamponade
- JVP
- HR and BP
- heart sounds
- pulse
- ECG
- Raised JVP, with an absent Y descent - this is due to the limited right ventricular filling
- Tachycardia
- Hypotension
- Muffled heart sounds
- Pulsus paradoxus (which occurs also in Asthma)
- Kussmaul’s sign (much debate about this) (more in constrictive pericarditis)
- ECG: electrical alternans (QRS complex amplitude alternates)
what is kussmauls sign?
Kussmaul’s sign is a paradoxical rise in jugular venous pressure (JVP) on inspiration, or a failure in the appropriate fall of the JVP with inspiration.
describe the differences between constrictive pericarditis and cardiac tamponade
- JVP
- pulses paradoxus
- Kussmauls sign
- CXR
JVP
- Absent Y descent in cardiac tamponade
- X + Y present in constrictive pericarditis
Pulses paradoxus present in cardiac tamponade
Kussmauls sign seen more in constrictive pericarditis
Pericardial calcification on CXR in constrictive pericarditis
DVLA rules in driving with:
- elective angioplasty
- ACS
- angina
- pacemaker insertion
- ICD
- successful catheter ablation
- Aortic aneurysm
- heart transplant
• Angioplasty (elective) - 1 week off driving
• CABG - 4 weeks off driving
• Acute coronary syndrome- 4 weeks off driving, 1 week if successfully treated by angioplasty
• Angina - driving must cease if symptoms occur at rest/at the wheel
• Pacemaker insertion - 1 week off driving
• Implantable cardioverter-defibrillator: if implanted for sustained ventricular arrhythmia: cease
driving for 6 months. If implanted prophylatically then cease driving for 1 month
• Successful catheter ablation - 2 days off driving
• Aortic aneurysm > 6cm - notify DVLA. Licensing will be permitted subject to annual review.
An aortic diameter of 6.5 cm or more disqualifies patients from driving
• Heart transplant: DVLA do not need to be notified
name 3 examples of nuclear imaging of the heart
• Thallium
• ‘MIBI’ or (SPECT) scans: Cardiac Single Photon Emission Computed Tomography uses
Technetium (99mTc) sestamibi, a coordination complex of the radioisotope technetium-99m
with the ligand methoxyisobutylisonitrile (MIBI).
• Positron Emission Tomography (PET) scans: Fluordeoxyglucose (FDG) is used.
what is the role of SPECT scanning of the heart?
The primary role of SPECT is to assess myocardial perfusion and myocardial viability. Two sets of
images are usually acquired. First the myocardium at rest followed by images of the myocardium
during stress (either exercise or following adenosine / dipyridamole). By comparing the rest with stress
images any areas of ischemia can be classified as reversible or fixed (e.g. following a myocardial
infarction). Cardiac PET is predominately a research tool at the current time
what is MUGA and what is this used for in scanning the heart?
MUGA
• Multi Gated Acquisition Scan, also known as radionuclide angiography
• Radionuclide (technetium-99m) is injected intravenously
• The patient is placed under a gamma camera
• May be performed as a stress test
• Can accurately measure left ventricular ejection fraction. Typically used before and after
cardiotoxic drugs are used
what is cardiac CT used for?
Cardiac Computed Tomography (CT): useful for assessing suspected IHD, using two main methods:
• Calcium score: there is known to be a correlation between the amount of atherosclerotic plaque
calcium and the risk of future ischemic events. Cardiac CT can quantify the amount of calcium
producing a ‘calcium score’
• Contrast enhanced CT: allows visualization of the coronary artery lumen
If these two techniques are combined cardiac CT has a very high negative predictive value for ischemic
heart disease.
what is cardiac MRI used for?
Cardiac MRI: (commonly termed CMR) has become the gold standard for providing structural images
of the heart. It is particularly useful when assessing congenital heart disease, determining right and
left ventricular mass and differentiating forms of cardiomyopathy. Myocardial perfusion can also be
assessed following the administration of gadolinium. Currently CMR provides limited data on the
extent of coronary artery disease.
when is exercise ECG not used and what is used instead?
Exercise ECG: USELESS in patients with: • Conduction abnormalities • resting (ECG) abnormalities like ST segment depression of >1mm • WPW • Digoxin • Ventricular paced rhythm In such patients myocardial perfusion imaging is the preferred modality for evaluation of CAD.
in patients with chest pain
- what warrants emergency admission
- what warrants same day assessment
- what if the chest pain has been ongoing more than 72 hours
• Current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency
admission
• Chest pain 12-72 hours ago: refer to hospital the same-day for assessment
• Chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement
before deciding upon further action
describe 3 features that NICE describe as anginal chest pain
- what is typical angina
- what is atypical angina
- what is non-anginal chest pain
NICE define anginal pain as the following:
o Constricting discomfort in the front of the chest, neck, shoulders, jaw or arms
o Precipitated by physical exertion
o 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
if patients have typical angina - who of these need further investigation?
If patients have typical anginal symptoms and a risk of CAD is greater than 90% then no further
diagnostic testing is required. It should be noted that all men over the age of 70 years who have typical
anginal symptoms fall into this category.
For patients with an estimated risk of 10-90% further investigations are needed
what investigation is used for patients who have typical angina and a risk of 61-90
61-90% Coronary angiography
what investigation is used for patients who have typical angina and a risk of 30-60%
Functional imaging, for example:
• Myocardial perfusion scan with SPECT
• Stress echocardiography
• First-pass contrast-enhanced magnetic resonance (MR) perfusion
• MR imaging for stress-induced wall motion abnormalities.
what investigation is used for patients who have typical angina and a risk of 10-29%
10-29% CT calcium scoring
management of angina
- in stable angina with good exercise tolerance
- if pain is worsening
NICE 2011 Guidelines:
• In good exercise tolerance, consider medical therapy before angiography (β-
blocker is the most important)
• If pain is worsening, no need for exercise test, directly do angiography (Cath)
describe the medical management of angina
- what should all patients recieve
- what is the preferred initial treatment
• All patients should receive aspirin and a statin in the absence of any contraindication
• Sublingual glyceryl trinitrate to abort angina attacks
• β-blocker is the preferred initial treatment. For patients unable to take a β-blocker there is no
clear guidelines on the best alternative. Options include a rate-limiting calcium-channel blocker
(verapamil or diltiazem); a long-acting dihydropyridine calcium-channel blocker (e.g. modified-
release nifedipine); a nitrate; or a potassium-channel activator
• If there is a poor response to initial treatment then the β-blocker should be ↑ to the maximum
tolerated dose (e.g. atenolol 100mg od)
• Again, there are no clear guidelines on the next step treatment. CKS advise adding a long-acting
dihydropyridine (e.g. nifedipine, amlodepine, felodipine) although other options include
isosorbide mononitrate and nicorandil
what is the treatment of prinzmetal angina
Prinzmetal angina - treatment = dihydropyridine calcium channel blocker
what to do with patients who develop nitrate tolerance?
Nitrate tolerance
• Many patients who take nitrates develop tolerance and experience ↓ efficacy
• BNF advises that patients who develop tolerance should take the second dose of isosorbide
mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for
4 hours and maintains effectiveness
• This effect is not seen in patients who take modified release isosorbide mononitrate
what is ivabradine?
- how does it work?
- adverse effects?
Ivabradine (Procoralan) • A new class of anti-anginal drug which works by reducing the heart rate
• Acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity
• Adverse effects: visual effects, particular luminous phenomena, are common. Bradycardia, due
to the mechanism of action, may also be seen
• There is no evidence currently of superiority over existing treatments of stable angina
when should fondaparinux not be used in ACS, what is used instead?
Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patient’s creatinine is > 265 μmol/l unfractionated heparin should be given.
if a patient is using clopidogrel what should omeprazole be switched to?
lansoprazole
when should tirofiban be used in ACS
Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to
patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month
mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital
admission.
when should coronary angiography be considered in ACS
Coronary angiography should be considered within 96 hours of first admission to hospital to patients
who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in
patients who are clinically unstable.
how does aspirin work?
Aspirin Antiplatelet - inhibits the production of thromboxane A2
how does clopidogrel/ticagrelor work?
Clopidogrel Antiplatelet - inhibits ADP binding to its platelet receptor
how does enoxaparin/fondaparinux work?
Enoxaparin Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa
how does bivalirudin work?
Bivalirudin Reversible direct thrombin inhibitor
what are poor prognostic factors for ACS?
Poor prognostic factors: • Age • Development (or history) of heart failure, Killip class* • Peripheral vascular disease • ↓ systolic blood pressure • Initial serum creatinine concentration • Elevated initial cardiac markers • Cardiac arrest on admission • ST segment deviation
describe Killip classification
I No clinical signs heart failure 6%
II Lung crackles, S3 17%
III Frank pulmonary edema 38%
IV Cardiogenic shock 81%
describe the arterial supply of the heart
left aortic sinus → left coronary artery (LCA)
right aortic sinus → right coronary artery (RCA)
LCA → LAD + circumflex
RCA → posterior descending
RCA supplies SA node in 60%, AV node in 90%
describe the venous drainage of the heart
Venous drainage of the heart: coronary sinus drains into the right atrium
describe the ECG leads affected in:
anteroseptal inferior anterolateral lateral posterior
Myocardial infarction and the associated vessels.
Anteroseptal: V1-V4: Left anterior descending
Inferior: II, III, aVF: Right coronary
Anterolateral: V4-6, I, aVL: Left anterior descending or left circumflex
Lateral: I, aVL +/- V5-6: Left circumflex
Posterior: Tall R waves V1-2: Usually left circumflex, also right coronary
Post MI, what drugs should be offered
- ACE inhibitor
- β-blocker
- Aspirin
- Statin
when should an aldosterone antagonist be used post MI
Aldosterone antagonists:
patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy
How long is DAPT given for post ACS
Most patients who’ve had an acute coronary syndrome are now given dual antiplatelet therapy (DAPT). Clopidogrel was previously the second antiplatelet of choice. Now ticagrelor and prasugrel (also ADP-receptor inhibitors) are more widely used. The NICE Clinical Knowledge Summaries now recommend:
post acute coronary syndrome (medically managed): add ticagrelor to aspirin, stop ticagrelor after 12 months post percutaneous coronary intervention: add prasugrel or ticagrelor to aspirin, stop the second antiplatelet after 12 months this 12 month period may be altered for people at a high-risk of bleeding or those who at high-risk of further ischaemic events
what are contraindications to thrombolysis?
- Active internal bleeding
- Recent hemorrhage, trauma or surgery (including dental extraction)
- Coagulation and bleeding disorders
- Intracranial neoplasm
- Stroke < 2 months
- Aortic dissection
- Recent head injury
- Pregnancy
- Severe hypertension
when does dresslers syndrome usually occur?
This usually occurs 1 to 8 weeks after MI.
what is the presentation of dresslers syndrome?
Presentation:
• Malaise, fever, pericardial pain
• Elevated erythrocyte count
• Sometimes may also have pleuritis and pneumonitis.
what is dresslers syndrome caused by?
It has been postulated that the syndrome results from release of cardiac antigens which then stimulate
antibody production. The immune complexes are then deposited in the pericardium, pleura and lung.
There may be accompanying pleural and pericardial effusion and therefore echocardiography should be
done.
what is the treatment for dresslers syndrome?
Treatment involves aspirin and analgesics. Corticosteroids and non-steroidal anti-inflammatory agents are best avoided in the first 4 weeks after MI as they delay myocardial healing. Aspirin in large doses is
effective. Recurrences can occur, and in such cases colchicine is helpful.
Thrombolysis for STEMI
- what drugs are used?
- what is done 90mins following thrombolysis
tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase
tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile
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
list 5 complications from coronary angiography
• Vascular complications: the most common complication overall is hemorrhage from access
(right femoral artery mostly then right radial artery), much less common is rupture of coronary
artery during revascularization or rupture of any artery from access to target artery
• Contrast Induced Nephropathy (CIN), higher incidence in diabetic patients and patients known
to have renal dysfunction (prevented by good hydration)
• Cholesterol embolisation
• Arrhythmias (include arrest, ventricular and supraventricular) especially in primary intervention
(in case of acute MI)
• Reaction to contrast
describe 2 complications of stenting
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 ↑ risk of platelet aggregation leading to thrombosis.
Two main complications may occur due to stenting:
• 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
• Restenosis: due to excessive tissue proliferation around 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
what are the two types of stent
Types of stent
• Bare-metal stent (BMS)
• Drug-eluting stents (DES): stent coated with paclitaxel or rapamycin which inhibit local tissue
growth. Whilst this ↓ restenosis rates the stent thrombosis rates are ↑ as the process of stent
endothelisation is slowed
what is the most important factor following stent insertion to prevent stent thrombosis
Following insertion the most important factor in preventing stent thrombosis is antiplatelet therapy.
Aspirin should be continued indefinitely. The length of clopidogrel treatment depends on the type of
stent, reason for insertion and consultant preference.
what is the risk of restenosis in T2DM patients with BMS
BMS in T2DM: restenosis risk in 6 months is 40-50%
what is the mode of action of clopidogrel?
Clopidogrel is a pro-drug whose action may be related
to adenosine diphosphate (ADP) receptor on platelet
cell membranes. The specific subtype of ADP receptor
that clopidogrel irreversibly inhibits is P2Y12 and is
important in platelet aggregation and the cross-linking
of platelets by fibrin. The blockade of this receptor
inhibits platelet aggregation by blocking activation of
the glycoprotein IIb/IIIa pathway. The IIb/IIIa
complex functions as a receptor mainly for fibrinogen
and vitronectin but also for fibronectin and von
Willebrand factor. Activation of this receptor complex
is the “final common pathway” for platelet
aggregation, and is important in the cross-linking of
platelets by fibrin.
Platelet inhibition can be demonstrated two hours after
a single dose of oral clopidogrel, but the onset of
action is slow, so that a loading-dose of 300-600 mg is
usually administered.
what is cholesterol embolism?
-who is this seen more commonly in?
Cholesterol embolisation is a well-documented
complication of coronary angiography
Cholesterol emboli may break off causing renal
disease
• Seen more commonly in arteriopaths, abdominal
aortic aneurysms
describe the features of cholesterol embolism
• Eosinophilia
• Purpura
• Renal failure
• Livedo reticularis (is a common cutaneous finding
consisting of a mottled reticulated vascular pattern
that appears like a lace-like purplish discoloration
of the lower extremities, caused by swelling of
(venules) in the skin, which makes them more
visible)
what are the causes for SVT?
Episodes are characterized by the sudden onset of a narrow complex
tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include
atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.
describe the acute management of SVT
• Vagal maneuvers: e.g. Valsalva maneuver
• Adenosine 6mg then 12mg then 12mg - contraindicated in asthmatics - verapamil is a preferable
option (if no control) then
• Electrical cardioversion
what is used to prevent episodes of SVT?
Prevention of episodes
• β-blockers (Sotalal)
• Flecainide.
• Radio-frequency ablation
when is premature ventricular contraction significant?
usually insignificant except
• Occurring frequently ( ≥6 beats/min )
• Bigeminal rhythm
• Short runs of ventricular tachycardia (V. Tach)
• R-on-T phenomenon
• Associated with serious organic heart disease
• Left ventricular decompensation (Decompensated Heart Failure)
what are the different types of atrial fibrillation?
AF may by classified as either first detected episode, paroxysmal, persistent or permanent.
first detected episode (irrespective of whether it is symptomatic or self-terminating) recurrent episodes, when a patient has 2 or more episodes of AF. If episodes of AF terminate spontaneously then the term paroxysmal AF is used. Such episodes last less than 7 days (typically < 24 hours). If the arrhythmia is not self-terminating then the term persistent AF is used. Such episodes usually last greater than 7 days in permanent AF there is continuous atrial fibrillation which cannot be cardioverted or if attempts to do so are deemed inappropriate. Treatment goals are therefore rate control and anticoagulation if appropriate
which drugs are used to rate control AF?
A beta-blocker or a rate-limiting calcium channel blocker (e.g. diltiazem) is used first-line to control the rate in AF.
If one drug does not control the rate adequately NICE recommend combination therapy with any 2 of the following:
a betablocker diltiazem digoxin (preferred choice if co-existant heart failure)
(a common contraindication for beta-blockers is asthma
what agents are used to cardiovert AF?
Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation
• Amiodarone
• Flecainide (if no structural heart disease)
• Others (less commonly used in UK): quinidine, dofetilide, ibutilide, propafenone
Less effective agents
• β-blockers (including sotalol)
• Calcium channel blockers
• Digoxin
• Disopyramide
• Procainamide
which agents can be used to maintain sinus rhythm in atrial fibrillation patients?
• Sotalol • Amiodarone • Flecainide • Others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone, quinidine
what factors may favour rate control in AF?
Older than 65 years
History of ischaemic heart disease
what factors may favour rhythm control in AF?
- Younger than 65 years
- Symptomatic
- First presentation
- Lone AF or 2nd° AF (e.g. alcohol)
- Congestive heart failure
describe the management of AF less than 48hours onset
If atrial fibrillation (AF) is of less than 48 hours onset patients should be heparinised and a
transthoracic echocardiogram performed to exclude a thrombus. Following this, patient may be
cardioverted, either:
• Electrical - ‘DC cardioversion’
• Pharmacology - amiodarone if structural heart disease, flecainide in those without structural
heart disease
Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further
anticoagulation is unnecessary
describe the management of AF of more than 48hours onset
If AF is of greater than 48 hours then patients should have therapeutic anticoagulation for at least 3
weeks. If there is a high risk of cardioversion failure (e.g. previous failure or AF recurrence) then it is
recommended to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion. If there
was very acute history on presentation and the patient was in significant heart failure then DC
cardioversion would be appropriate, as per Advanced Life Support guidelines.
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 is holiday heart syndrome, what is the treatment
Supraventricular arrhythmias (including AF) secondary to acute alcohol intake are well characterized and have been termed 'holiday heart syndrome'. No specific treatment is required
when should catheter ablation be considered for AF?
NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication
what are the complications of catheter ablation for AF?
notable complications include
cardiac tamponade stroke pulmonary valve stenosis
what is the success rate for catheter ablation in AF?
success rate
around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously longer term, after 3 years, around 55% of patients who've had a single procedure remain in sinus rhythm. Of patient who've undergone multiple procedures around 80% are in sinus rhythm
describe the scoring system used in stroke prevention for AF patients
C Congestive heart failure 1 H Hypertension (or treated hypertension) 1 A2 Age >= 75 years 2 Age 65-74 years 1 D Diabetes 1 S2 Prior Stroke or TIA 2 V Vascular disease (including ischaemic heart disease and peripheral arterial disease) 1 S Sex (female) 1
0 No treatment
1 Males: Consider anticoagulation
Females: No treatment (this is because their score of 1 is only reached due to their gender)
2 or more Offer anticoagulation
Remember that if a CHA2DS2-VASc score suggests no need for anticoagulation it is important to ensure a transthoracic echocardiogram has been done to exclude valvular heart disease, which in combination with AF is an absolute indication for anticoagulation
what risk assessment can be used in anticoagulation for AF
H Hypertension, uncontrolled, systolic BP > 160 mmHg 1
A Abnormal renal function (dialysis or creatinine > 200) Or Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal
1 for any renal abnormalities 1 for any liver abnormalities
S Stroke, history of 1
B Bleeding, history of bleeding or tendency to bleed 1
L Labile INRs (unstable/high INRs, time in therapeutic range < 60%) 1
E Elderly (> 65 years) 1
D Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs)
Or
Alcohol Use (>8 drinks/week) 1 for drugs 1 for alcohol
There are no formal rules on how we act on the HAS-BLED score although a score of >= 3 indicates a ‘high risk’ of bleeding, defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease >2 g/L, and/or transfusion.
what are the two types of VT
There are two main types of VT:
• Monomorphic VT: most commonly caused by myocardial infarction
• Polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by
prolongation of the QT interval. The causes of a long QT interval are listed later.
With patients with VT when would immediate cardioversion be indicated?
If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure or rate > 150 beats/min) then immediate cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks
what features would suggest VT rather than SVT with aberrant conduction?
- A V 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>160ms
what drug therapy is used for VT?
- Amiodarone: ideally administered through a central line
- Lidocaine: use with caution in severe left ventricular impairment
- Procainamide
what drug shouldnt be used in VT?
VERAPAMIL SHOULD NOT BE USED IN VT
Verapamil should never be given to a patient with a broad complex tachycardia as it may precipitate
ventricular fibrillation in patients with ventricular tachycardia. Adenosine is sometimes given in this
situation as a ‘trial’ if there is a strong suspicion the underlying rhythm is a supraventricular tachycardia
with aberrant conduction
what should be used in VT with digoxin toxicity?
V Tach in Digoxin Toxicity:
Treat with lidocaine and phenytoin
Avoid Amiodarone and Procainamide (↑ Toxicity)
D/C shock when all measures fail (but usually unsuccessful)
What is used for management of VT when drug therapy fails?
if drug therapy fails Electrophysiological study (EPS) Implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
what is torsades de pointes?
Torsades De Pointes (‘twisting of the points’) is a rare arrhythmia associated with a long QT interval. It may deteriorate into ventricular fibrillation and hence lead to sudden death
what are the risk factors for torsades de pointes?
Risk factors: •♀ • ↓HR • CHF • Digoxin • Prolonged QT and Subclinical long QT syndrome • Severe alkalosis • Recent conversion from AF
what are 11 causes of prolonged QT
Causes of long QT interval • Congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome • Antiarrhythmics: amiodarone, sotalol, class I-a antiarrhythmic drugs • Tricyclic antidepressants • Antipsychotics • Chloroquine • Terfenadine • Erythromycin • Electrolyte: Hypocalcemia, Hypokalemia, Hypomagnesemia • Myocarditis • Hypothermia • Subarachnoid hemorrhage
what is the management of torsades de pointes?
Management • IV magnesium sulphate • Correct K+ if hypo • Override pacing (set pacemaker to be faster than patient rate then decrease the rate) • D/C shock
what is multifocal atrial tachycardia?
-who is this common in?
Multifocal Atrial Tachycardia (MAT) may be defined as irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease (e.g COPD)
what is the management of multifocal atrial tachycardia?
Management
• Correction of hypoxia and electrolyte disturbances
• Rate-limiting calcium channel blockers are often used first-line
• Cardioversion and digoxin are not useful in the management of MAT
In patients with tachycardia what are the adverse signs which would indicate an unstable patient?
-what treatment should be given
• Systolic BP < 90 mmHg • ↓ conscious level • Chest pain • Heart failure If any of the above adverse signs are present then synchronised DC shocks should be given
what treatment is given to patients who have had synchronised DC shocks for VT and has a regular broad complex tachycardia?
Regular • Assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block) • Loading dose of amiodarone followed by 24 hour infusion
what treatment is given to patients who have had synchronised DC shocks for VT and have an irregular broad complex tachycardia?
Irregular
• AF with bundle branch block - treat as
for narrow complex tachycardia
• Polymorphic VT (e.g. torsade de pointes) - IV magnesium
what treatment is given to patients who have had synchronised DC shocks for VT and have a regular narrow complex tachycardia?
Regular
• Vagal manoeuvres followed by IV adenosine
• If above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. β- blockers)
what treatment is given to patients who have had synchronised DC shocks for VT and have an irregular narrow complex tachycardia?
Irregular
• Probable atrial fibrillation
• If onset < 48 hr: consider electrical or chemical cardioversion
• >48 HR: Rate control (e.g. β-blocker or digoxin) and anticoagulation
In patients with bradycardia, what factors would indicate haemodynamic compromise?
-what is the treatment for this?
Adverse signs
The following factors indicate hemodynamic compromise and hence the need for treatment:
• Heart rate < 40 bpm
• Systolic blood pressure < 100 mmHg
• Heart failure
• Ventricular arrhythmias requiring suppression
Atropine is the first line treatment in this situation. If this fails to work, or there is the potential risk of asystole then transvenous pacing is indicated
what would indicate a potential risk of asystole in patients with bradycardia?
The following indicate a potential risk of asystole and hence the need for treatment with transvenous pacing: • Complete ♥ block • Recent asystole • Mobitz type II ♥ block • Symptomatic 2nd degree • Ventricular pause > 3 seconds
what to do if there is a delay for patients who need transvenous pacing
If there is a delay in the provision of transvenous pacing the following interventions may be used:
• Atropine, up to maximum of 3mg
• Transcutaneous pacing
• Adrenaline infusion titrated to response
what are the features of complete heart block?
- clinically
- pulse/HR
- JVP
- on auscultation
- Syncope
- Heart failure
- Regular bradycardia (30-50 bpm)
- Wide pulse pressure
- JVP: cannon waves in neck
- Variable intensity of S1.
what is trifasicular block?
Trifasicular Block: The PR interval is grossly prolonged (1st degree block) and there is an RSR complex in V1 (RBBB) and a left anterior hemi-block (LAHB is diagnosed when QRS in lead II is negative). The combination of RBBB, LAHB and long PR interval has been called trifasicular block.
what do bifasicular block and trifasiscular block refer to? when would this indicate a permenent pacemaker?
Bifascicular and trifascicular block refer to conduction disturbances below the atrioventricular (AV) node in which two or more of the fascicles of the left bundle branch and the right bundle branch are involved. It has been suggested that unexplained syncope in the presence of bifascicular or trifascicular block is an indication for a permanent pacemaker.
what are the indications for a temporary pacemaker?
• Symptomatic/hemodynamically unstable bradycardia, not responding to atropine
• Post-ANTERIOR MI: type 2 or complete heart block*
• Trifascicular block prior to surgery
*post-Inferior MI complete heart block is common and can be managed conservatively if asymptomatic and hemodynamically stable
what are the indications for an ICD
• Long QT syndrome
• Hypertrophic obstructive cardiomyopathy (HOCM)
• Previous cardiac arrest due to VT/VF
• Previous myocardial infarction with non-sustained VT on 24 hr monitoring, inducible VT on
electrophysiology testing and ejection fraction < 35%
• Brugada syndrome
what is long QT syndrome
-what can this lead to?
is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in α subunit of the slow delayed rectifier potassium channel. A normal corrected QT is less than 440 ms in ♂s and 450 ms in ♀s.
what drugs can causes long QT?
- Amiodarone
- Sotalol*
- Class I-a antiarrhythmic
- Tricyclic antidepressants • Chloroquine
- Terfenadine
- Macrolide (erythromycin) • Quinolones
what are the congenital causes of long QT?
- Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
- Romano-Ward syndrome (no deafness)
what electrolyte causes exist for long QT
-what other causes are there?
o Hypocalcemia
o Hypokalemia
o Hypomagnesemia
- Acute MI
- Myocarditis
- Hypothermia
- Subarachnoid hemorrhage
How may long QT syndrome be picked up? What are the associations for: -Long QT1 -Long QT2 -Long QT3 -Long QT4
• May be picked up on routine ECG or following family screening
• Long QT1 - usually associated with exertional syncope, often swimming
• Long QT2 - often associated with syncope occuring following emotional stress, exercise or
auditory stimuli
• Long QT3 - events often occur at night or at rest (associated with brady, so pacemaker may be
beneficial)
• Long QT4 – associated with Parox. AF
• Sudden cardiac death
what is the management for long QT
- Avoid drugs which prolong QT and other precipitants if appropriate (e.g. Strenuous exercise)
- 1st line pharmacological therapy is Mg+ IV (bolus then infusion)
- β-blockers (sotalol may exacerbate)
- Implantable cardioverter defibrillators in high risk cases (if β-blockers fail)
- Left stellate sympathectomy (if β-blockers fail or when there is multiple ICD shocks)
what is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC):
- what may this present with?
- common?
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) is a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death. It is generally regarded as the second most common cause of sudden cardiac death in the young after hypertrophic cardiomyopathy.
how is arrythmogenic right ventricular cardiomyopathy inherited? what does this cause?
Pathophysiology
• Inherited in an autosomal dominant pattern with variable expression
• The right ventricular myocardium is replaced by fibrofatty tissue
what is the presentation of arrythmogenic right ventricular cardiomyopathy?
Presentation
• Palpitations
• Syncope
• Sudden cardiac death
what ECG abnormalities are seen in arrythmogenic right ventricular cardiomyopathy?
- 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
- Magnetic resonance imaging is useful to show fibrofatty tissue
what is the management for arrythmogenic right ventricular cardiomyopathy?
- Drugs: sotalol is the most widely used antiarrhythmic
- Catheter ablation to prevent ventricular tachycardia
- Implantable cardioverter-defibrillator
what is naxos disease?
Naxos disease
• An autosomal recessive variant of ARVC
• A triad of ARVC, palmoplantar keratosis, and woolly hair
what is Wolff-Parkinson White (WPW)?
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
what are the possible ECG changes in WPW?
Possible ECG features include:
• Short PR interval
• Wide QRS complexes with a slurred upstroke - ‘delta wave’
• Left axis deviation if right-sided accessory pathway
• Right axis deviation if left-sided accessory pathway
in the majority of cases, or in a question without Specification, Wolff-Parkinson-White syndrome is associated with left axis deviation
how to differentiate between WPW type A and type B
Differentiating between type A and type B
• Type A (left-sided pathway): dominant R wave in V1, seen in the above ECG.
• Type B (right-sided pathway): no dominant R wave in V1
what 5 conditions are associated with WPW?
- HOCM
- Mitral valve prolapse
- Ebstein’s anomaly
- Thyrotoxicosis
- Secundum ASD
what is the management of WPW
- Definitive treatment: radiofrequency ablation of the accessory pathway
- Medical therapy: sotalol, amiodarone, flecainide
- For cardioversion: Flecainide is superior to Amiodarone
what drugs should be avoided in WPW
sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may ↑ the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation.
Adenosine should be avoided as blocking the AV node can paradoxically ↑ ventricular rate resulting in fall in cardiac output.
Verapamil and digoxin should also be avoided in patients with Wolff-Parkinson White as they may precipitate VT or VF.
what is cetecholaminergic polymorphic VT?
- acquired or inherited?
- what can this cause?
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.
what is the pathophysiology of catecholaminergic VT?
Pathophysiology
• The most common cause is a defect in the ryanodine receptor (RYR2) which is found in the myocardial sarcoplasmic reticulum
what are the clinical features of catecholaminergic VT?
- Exercise or emotion induced polymorphic ventricular tachycardia resulting in syncope
- Sudden cardiac death
- Symptoms generally develop before the age of 20 years
what is the management of catecholaminergic VT?
Management
• β-blockers
• Implantable cardioverter-defibrillator
what is brugada syndrome?
- acquire/inherited
- prevalence
- demographic
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.
what is the pathophysiology of brugada syndrome?`
Pathophysiology
• A large number of variants exist
• Around 20-40% of cases are caused by a mutation in the SCN5a gene which encodes the myocardial sodium ion
channel protein
what ECG changes are seen in brugada syndrome?
• Convex ST elevation V1-V3
• Partial right bundle branch block
• Changes may be more apparent following
flecainide
what drug can be used to unmask brugada syndrome?
Ajmaline (class Ia antiarrhythmic) is used to unmaks hidden Brugada
what is the management of brugada syndrome?
Management
• Implantable cardioverter-defibrillator
• Quinidine is useful in VF storm (indicated
by fast repeated ICD shocks)
what is HOCM?
- what is this a disorder of?
- acquired/inherited
- prevalence
- what does this cause?
Hypertrophic Obstructive Cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500. Mutations to various proteins including β-myosin, α-tropomyosin and troponin T have been identified. Septal hypertrophy causes left ventricular outflow obstruction. It is an important cause of sudden death in apparently healthy individuals.
what are the features of HOCM?
Features
• Often asymptomatic
• Dyspnea, angina, syncope
• Sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
• Jerky pulse, large ‘a’ waves, double apex beat
• Ejection systolic murmur: ↑ with valsalva manoeuvre and ↓ on squatting
what 2 conditions are assoc. with HOCM
- Friedreich’s ataxia
* Wolff-Parkinson White
what can be seen on the ECG in HOCM?
- Left ventricular hypertrophy (L VH)
- Atrial enlargement (abnormal P morphology)
- Progressive T wave inversion
- ST-T abnormalities
- Deep Q waves
- Axis deviation
- Prolonged PR or sinus bradycardia
- BBB (bundle brach block)
- Ectopic atrial rhythm
- Atrial fibrillation may occasionally be seen
what is seen on echo in HOCM?
Echo (Mr. Sam Ash):
• Mitral regurgitation (MR)
• Systolic anterior motion (SAM) of the anterior mitral valve leaflet
• Asymmetric hypertrophy (ASH)
what are poor prognostic factors in HOCM?
- Syncope
- Family history of sudden death
- Y oung age at presentation
- Non-sustained ventricular tachycardia on 24 or 48-hour holter monitorin
- Abnormal blood pressure changes on exercise
- ↑ Septal wall thickness, > 3cm
what is the management of HOCM?
- Amiodarone
- β-blockers or verapamil for symptoms
- Cardioverter defibrillator
- Dual chamber pacemaker
- Endocarditis prophylaxis
what drugs to avoid in HOCM
- Nitrates
- ACE-inhibitors
- Inotropes
- Digoxin is contraindicated if there is significant LVOT gradient
dilated cardiomyopathy:
- prevalence
- what is the annual mortality and HF
- what happens in this? what chambers are affected?
- what are the features?
- Prevelance is 1% in adult – it ↑ to 10% at age of 80 yrs
- Annual mortality of cardiomyopathies and HF is 20%
- Dilated heart leading to systolic (+/- diastolic) dysfunction
- All 4 chambers affected but LV more than RV
- Features include arrhythmias, emboli, mitral regurgitation
- Absence of congenital, valvular or ischemic heart disease
what are different causes of dilated cardiomyopathy?
- Alcohol: may improve with thiamine (best prognosis after removing the cause)
- Peripartum
- Hypertension
Other causes
• Inherited
• Infections e.g. Coxsackie A and B, HIV, diphtheria, parasitic
• Endocrine e.g. Hyperthyroidism
• Infiltrative* e.g. Hemochromatosis, sarcoidosis
• Neuromuscular e.g. Duchenne muscular dystrophy
• Nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency
• Drugs e.g. Doxorubicin
what proportion of patients with DCM are thought to have a genetic disposition? how are the majority of defects inherited?
• Around a third of patients with DCM are thought to have a genetic predisposition
• A large number of heterogeneous defects have been identified
• The majority of defects are inherited in an autosomal dominant fashion although other patterns
of inheritance are seen
how to differentiate restrictive cardiomyopathy with constrictive pericarditis?
Restrictive cardiomyopathy vs Constrictive pericarditis, in restrictive:
• Prominent apical pulse
• Absence of pericardial calcification on CXR
• Heart may be enlarged
• ECG abnormalities e.g. Bundle branch block, Q waves
What are different causes of restrictive cardiomyopathy?
Causes • Amyloidosis (e.g. Secondary to myeloma) - most common cause in UK • Hemochromatosis • Loffler's syndrome • Sarcoidosis • Scleroderma
what are the features of constrictive pericarditis?
dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul's sign is positiveAtrial myxoma
what is this?
where does this arise?
who is this more common in?
most common primary cardiac tumour
• 75% occur in left atrium
• More common in ♀s
what are the features of atrial myxoma?
Features • Systemic: weight loss, fever, clubbing • Emboli • Atrial fibrillation • Mid-diastolic murmur, 'tumour plop'
what are 8 features of severe AS?
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
how does LVSD affect AS murmur?
Left ventricular systolic dysfunction will result in a ↓ flow-rate across the aortic valve and hence
a quieter murmur and low gradient on Echo
what are the causes of AS?
Causes of AS
• Degenerative calcification (most common cause in elderly patients)
• Bicuspid aortic valve (most common cause in younger patients)
• William’s syndrome (supravalvular aortic stenosis)
• Post-rheumatic disease
• Subvalvular: HOCM
what is the management of AS?
Management
• If asymptomatic then observe the patient is general rule
• If symptomatic then valve replacement
• If asymptomatic but valvular gradient > 50 mmHg and with features such as left ventricular
systolic dysfunction then consider surgery
• Balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve
replacement
what are the features of aortic regurgitation?
Features
• Early diastolic murmur
• Collapsing pulse
• Wide pulse pressure
• Mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral
valve cusps caused by the regurgitation streams
what are the causes due to valve disease of AR?
- Rheumatic fever
- Infective endocarditis
- Connective tissue diseases e.g. RA/SLE
- Bicuspid aortic valve
what are the causes due to aortic root disease of AR?
- Aortic dissection
- Spondylarthropathies (e.g. Ankylosing spondylitis)
- Hypertension
- Syphilis
- Marfan’s, Ehler-Danlos syndrome
how common is mitral valve prolapse?
Mitral Valve Prolapse is common, occurring in around 5-10 % of the population. It is usually idiopathic but may be associated with a wide variety of cardiovascular disease and other condition
what are 8 associations of mitral valve prolapse?
- Congenital heart disease: PDA, ASD
- Cardiomyopathy
- Turner’s syndrome
- Marfan’s syndrome, Fragile X
- Osteogenesis imperfecta
- Pseudoxanthoma elasticum
- Wolff-Parkinson White syndrome
- Long-QT syndrome
what are the features of mitral valve prolapse?
- Patients may complain of atypical chest pain or palpitations
- Mid-systolic click (occurs later if patient squatting)
- Late systolic murmur (longer if patient standing)
- Complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death
what is the management of mitral valve prolapse?
- Patients > 75 years who are in AF or with LVSF impairment, should be referred to surgical assessment as early as possible
- TOE (transesophageal echo)can tell if the valve is for repair or replacement, can be done intra- operatily
- Follow up is crucial as 15% of MVP patients develop the most serious complication after 15 years period of being prolapsed (TIA, Ischemic Stokes)
- Mild to moderate MVP with normal LVSF → β blockers + echo follow up every 2-3 years
what is the cause for mitral stenosis?
Mitral Stenosis: it is said that the causes of mitral stenosis are rheumatic fever, rheumatic fever and rheumatic fever. Rarer causes that may be seen in the MRCP include mucopolysaccharidoses, carcinoid and endocardial fibroelastosis
describe features of mitral stenosis
Features • Mid-diastolic murmur (best heard in expiration) • Loud S1, opening snap • Low volume pulse • Malar flush • Atrial fibrillation
Features of severe MS
• Length of murmur ↑
• Opening snap becomes closer to S
what is seen on echo for mitral stenosis?
Echocardiography
• The normal cross sectional area of the mitral valve is 4-6 cm2. A ‘tight’ mitral stenosis implies a cross sectional area of < 1 cm2.
when would percutaneous balloon valvotomy to treat severe mitral stenosis be contraindicated?
Percutaneous Balloon Valvotomy: used to treat severe M.S. it is contraindicated in:
• Moderate to severe mitral regurgitation
• Left atrial thrombus
• Heavily calcified mitral valve
• Concomitant coronary artery or other valve disease requiring surgery
what are the signs of tricuspid regurgitation?
Signs • Pan-systolic murmur • Giant v waves in JVP • Pulsatile hepatomegaly • Left parasternal heave
what are the causes of tricuspid regurgitation
Causes • Right ventricular dilation • Pulmonary hypertension e.g. COPD • Rheumatic heart disease • Infective endocarditis (especially intravenous drug users) • Ebstein's anomaly • Carcinoid syndrome
biological heart valves:
- origin
- disadvantages
Usually bovine or porcine in origin
Major disadvantage is structural deterioration and calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve
Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term
mechanical heart valve:
- what type is most common?
- disadvantage
The most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays
Mechanical valves have a low failure rate
Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed. Aspirin is normally given in addition unless there is a contraindication.
Target INR
• Aortic: 3.0
• Mitral: 3.5
what is prosthetic valve thrombosis?
Prosthetic Valve Thrombosis (PVT): This complication occurs in 0.03 to 5.5% annually with equal frequency in bioprosthesis and mechanical valves. It is more common in mitral prosthesis and with subtherapeutic anticoagulation, this resulting in shock.
what is the diagnosis for prosthetic valve thrombosis?
Diagnosis:
• The best diagnostic modality is transoesophageal echocardiography
• Transthoracic echocardiography is the initial choice in sick patients, and if adequate
visualisation is not obtained TEE can be done.
what is the management of prosthetic valve thrombosis?
Mangement:
• Thrombolytic therapy should be given for patients in pulmonary edema or hypotension.
• In stable patients, surgery is a better option for left-sided PVT, while right-sided PVT should be
treated with thrombolytic agents.
• Serial echocardiography should be performed, and if the response is inadequate repeat
thrombolytic therapy can be given.
what is type A aortic dissection
what is the management
Ascending aorta (2/3 of cases)
Surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention, by IV Labetalol
what is type B aortic dissection
what is the management
Descending aorta, distal to left subclavian origin
• Conservative management
• Bed rest
• ↓ blood pressure IV labetalol to prevent
progression
what are 7 associated conditions with aortic dissection?
Associations • Hypertension • Trauma • Bicuspid aortic valve • Collagens: marfan's syndrome, ehlers-danlos syndrome • Turner's and noonan's syndrome • Pregnancy • Syphilis
what are the complications in a backward tear aortic dissection?
Complications of backward tear
• Aortic incompetence/regurgitation
• MI: inferior pattern often seen due to right coronary involvement
what are complications of a forward tear aortic dissection?
Complications of forward tear
• Unequal arm pulses and BP
• Stroke
• Renal failure
what is primary pulmonary hypertension/idiopathic pulmonary arterial hypertension
Primary pulmonary hypertension (PPH, now IPAH)
• Pulmonary arterial pressure > 25 mmHg at rest, > 30mmHg with exercise
• PPH is diagnosed when no underlying cause can be found
• Around 10% of cases are familial: autosomal dominant
• Endothelin thought to play a key role in pathogenesis
• Associated with HIV, cocaine and anorexigens (e.g. Fenfluramine)
what are secondary causes of pulmonary hypertension?
Secondary causes of pulmonary hypertension include COPD, congenital heart disease
(Eisenmenger’s syndrome), recurrent pulmonary embolism, HIV and sarcoidosis.
what are the features of IPAH?
Features
• More common in ♀s, typically presents at 20-40 years old
• Progressive SOB
• Cyanosis
• Right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation
what is the management of IPAH?
Management • Diuretics if right heart failure • Anticoagulation • Vasodilator therapy: calcium channel blocker, IV prostaglandins, bosentan: endothelin-1 receptor antagonist • Heart-lung transplant
what is pulmonary arterial hypertension?
Pulmonary Arterial Hypertension (PAH) may be defined as a sustained elevation in mean pulmonary arterial pressure of greater than 25 mmHg at rest or 30 mmHg after exercise
what are the features of pulmonary arterial hypertension?
Features
• Exertional dyspnea is the most frequent symptom
• Chest pain and syncope may also occur
• Loud P2
• Left parasternal heave (due to right ventricular hypertrophy)
what are the 5 groups of pulmonary arterial hypertension?
Group 1: Pulmonary arterial hypertension (PAH)
• Idiopathic
• Familial
• Associated conditions: collagen vascular disease, congenital heart disease with systemic to
pulmonary shunts, HIV, drugs and toxins, sickle cell disease
• Persistent pulmonary hypertension of the newborn
Group 2: Pulmonary hypertension with left heart disease
left-sided atrial, ventricular or valvular disease such as left ventricular systolic and diastolic dysfunction, mitral stenosis and mitral regurgitation
Group 3: Pulmonary hypertension secondary to lung disease/hypoxia
• COPD
• Interstitial lung disease • Sleep apnoea
• High altitude
Group 4: Pulmonary hypertension due to thromboembolic disease Sickle cell, Polycythemia ..etc
Group 5: Miscellaneous conditions
Lymphangiomatosis e.g. secondary to carcinomatosis or sarcoidosis
what is the single most important investigation for pulmonary artery hypertension?
Whilst echocardiography may strongly point towards a diagnosis of pulmonary hypertension all patients need to have right heart pressures measured. Cardiac catheterisation is therefore the single most important investigation.
what is done to determine management of pulmonary artery hypertension
Management should first involve treating any underlying conditions, for example with anticoagulants or oxygen.
Following this, it has now been shown that 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
If there is a positive response to acute vasodilator testing • Oral calcium channel blockers
If there is a negative response to acute vasodilator testing
• Prostacyclin analogues: treprostinil, ilioprost
• Endothelin receptor antagonists: bosentan
• Phosphodiesterase inhibitors: sildenafil
what are the most common causes for cyanotic and acyanotic congenital heart diseases?
- Cyanotic: TGA most common at birth, Fallot’s most common overall
- Acyanotic: VSD most common cause
Acyanotic - most common causes
• Ventricular septal defects (VSD) - most common, accounts for 30%
• Atrial septal defect (ASD)
• Patent ductus arteriosus (PDA)
• Coarctation of the aorta
• Aortic valve stenosis
VSDs are more common than ASDs. However, in adult patients ASDs are the more common new
diagnosis as they generally presents later
Cyanotic - most common causes • Tetralogy of Fallot • Transposition of the great arteries (TGA) • Tricuspid atresia • Pulmonary valve stenosis
what is Patent Ductus Arteriosus (PDA) caused by?
-who is this more common in?
• acyanotic congenital heart defect • connection between the pulmonary trunk and descending aorta • more common in premature babies, born at high altitude or maternal rubella infection in the first trimester
what are the features of patent ductus arteriosus?
Features • Left subclavicular thrill • Continuous 'machinery' murmur • Large volume, collapsing pulse • Wide pulse pressure • Heaving apex beat
what is the management of patent ductus arteriosus?
Management
• Indomethacin closes the connection in the majority of cases
• If associated with another congenital heart defect amenable to surgery then prostaglandin E1 is
useful to keep the duct open until after surgical repair
VSD:
- common?
- how many will close spontaneously?
Ventricular Septal Defects (VSD) are the most common cause of congenital heart disease. They close spontaneously in around 50% of cases. Non-congenital causes include post myocardial infarction
what are the features of a VSD?
Features
• Classically a pan-systolic murmur which is louder in smaller defects
what are the complications of a VSD?
Complications
• Aortic regurgitation
aortic regurgitation is due to a poorly supported right coronary cusp resulting in cusp prolapsed. AF is associated with ASD
- Infective endocarditis
- Eisenmenger’s complex
- Right heart failure
Atrial septal defects:
- mortality
- how many types exist?
Atrial Septal Defects (ASDs) are the most likely congenital heart defect to be found in adulthood. They carry a significant mortality, with 50% of patients being dead at 50 years. Two types of ASDs are recognised, ostium secundum and ostium primum. Ostium secundum are the most common
what are the features of atrial septal defects?
Features
• Ejection systolic murmur, fixed splitting of S2
• Embolism may pass from venous system to left side of heart causing a stroke
what is seen on ECG with ostium secundum?
-is this common?
Ostium secundum (70% of ASDs)
• Associated with Holt-Oram syndrome (tri-phalangeal thumbs)
• ECG: RBBB with RAD (secondum).
what is seen on ECG with ostium primum?
-what is this assoc with?
Ostium primum
• Present earlier than ostium secundum defects
• Associated with abnormal A V valves
• ECG: RBBB with LAD, prolonged PR interval
what can a patent foramen ovale allow?
- how common is this?
- what is another assoc.?
Patent foramen ovale (PFO) is present in around 20% of the population. It may allow embolus (e.g. from DVT) to pass from right side of the heart to the left side leading to a stroke - ‘a paradoxical embolus’. It’s the most common cause of stroke following DVT.
There also appears to be an association between migraine and PFO. Some studies have reported improvement in migraine symptoms following closure of the PFO
DO TOE (Transesophageal echocardiography
what is coarctation of the aorta?
- more common in males or females?
- what is the treatment?
Coarctation of the Aorta describes a congenital narrowing of the descending aorta, it is more common in ♂s (despite association with Turner’s syndrome). Surgical repair is the treatment, but even with repair sometimes recurrence happen.
what are the features of coarctation of the aorta?
Features
• Infancy: heart failure
• Adult: hypertension
• Radio-femoral delay
• Mid or late systolic murmur, maximal over back
• Apical click from the aortic valve
• Notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
what are 5 association with coarctation of the aorta?
Associations • Turner's syndrome • Bicuspid aortic valve • Berry aneurysms • Neurofibromatosis • Accelerated Coronary Artesry Disease (CAD)
what is eisenmenger’s syndrome?
Eisenmenger’s Syndrome is characterized by the reversal of the left-right shunt due to pulmonary hypertension. The original murmur may disappear once Eisenmenger’s syndrome develops.
what is eisenmenger’s syndrome assoc. with?
Associated with
• VSD • ASD • PDA
what are the features of eisenmenger’s syndrome?
Features • Original murmur may disappear • Cyanosis • Clubbing • Right ventricular failure • Hemoptysis, embolism
what is the management of eisenmengers syndrome?
Management
• Heart-lung transplantation is required
Bicuspid Aortic Valve
- how common is this?
- what develops as a result?
- what is this assoc with?
Overview
• Occurs in 1-2% of the population
• Usually asymptomatic in childhood
• The majority eventually develop aortic stenosis or regurgitation
• Associated with a left dominant coronary circulation (the posterior descending artery arises
from the circumflex instead of the right coronary artery) and turner’s syndrome
• Around 5% of patients also have coarctation of the aorta
what complications arise from bicuspid aortic valve?
Complications
• Aortic stenosis/regurgitation.
• Higher risk for aortic dissection and aneurysm formation of the ascending aorta
what is the tetralogy of fallot?
- is this common?
- when is this picked up?
- what are the four features?
Tetralogy of Fallot (TOF) is the most common cause of cyanotic congenital heart disease*. It typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old
The four characteristic features are:
• Ventricular septal defect (VSD)
• Right ventricular hypertrophy
• Right ventricular outflow tract (RVOT) obstruction, pulmonary stenosis
• Overriding aorta
what determines the degree of cyanosis in tetralogy of fallot?
The severity of RVOT obstruction determines the degree of cyanosis and severity
what other features other than the four characteristic features are seen in tetralogy of fallot?
Other features
• Cyanosis
• Causes a right-to-left shunt
• Ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
• A right-sided aortic arch is seen in 25% of patients
• Chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy
what is the management of tetralogy of fallot?
Management
• Surgical repair is often undertaken in two parts
• Cyanotic episodes may be helped by β-blockers to ↓ infundibular spasm
what are the ECG features of dextrocardia?
-what is the life expectancy?
Classical ECG features:
• Inverted P in lead I
• Shift of the P axis (usually about +120 degrees) and reversed R wave progression.
• Reverse placement of the praecordial leads on the right chest at sites corresponding to the left
chest positions corrects this trend.
Typically patients have a normal life expectancy if no cardiac anomalies are present.
what are the 5 different treatment option for superior vena cava obstruction?
Treatment depends on the cause and pace of the progression of symptoms.
• Although SVCO is an emergency in the presence of airway compromise, where possible it is
important to get tissue for a histological diagnosis, as some tumours are better treated with chemotherapy than radiotherapy. In this case, if feasible, a bronchoscopy would probably provide tissue for a diagnosis.
• For most tumours, radiotherapy is a good treatment and relieves symptoms in 90% of patients within 2 weeks.
• Patients should be sat up and given oxygen to provide initial relief.
• In severe cases high-dose steroids can be helpful.
• For patients with recurrent SVCO, insertion of expandable wire stents under radiological
guidance provides relief in a high proportion of patients.
how does cardiac amyloidosis most commonly present?
Cardiac amyloidosis most commonly presents as restrictive cardiomyopathy, associated with AL Amyloidosis
Presentation:
• Typical presentation of right heart failure: o Jugular venous distension
o Peripheral oedema
o Orthopnoea and paroxysmal nocturnal dyspnea are typically absent
• In more advanced stages systolic dysfunction also occurs
what is the diagnosis of cardiac amyloidosis?
Diagnosis:
• Combination of low-voltage ECG and thickened ventricular walls is one of the characteristic features of cardiac amyloidosis.
• Echocardiographic abnormalities include dilatation of atria, thickened interatrial septum, diastolic dysfunction and small-volume ventricles. The most distinctive feature of cardiac amyloidosis is a sparkling, granular appearance of myocardium, but this is a relatively insensitive feature occurring only in about 25% of cases.
Which of these: have to wait 10-14 days, have to wait 4-6weeks, should not fly, have to wait 7-10 days, and have to wait 5 days to go on a aeroplane
- Unstable angina, uncontrolled hypertension, uncontrolled cardiac arrhythmia, decompensated heart failure, severe symptomatic valvular disease
- Uncomplicated myocardial infarction
- Complicated myocardial infarction
- Coronary artery bypass graft (CABG)
- Percutaneous coronary intervention (PCI)
- Unstable angina, uncontrolled hypertension, uncontrolled cardiac arrhythmia, decompensated heart failure, severe symptomatic valvular disease: SHOULD NOT FLY
- Uncomplicated myocardial infarction: may fly after 7-10 days
- Complicated myocardial infarction: after 4-6 weeks
- Coronary artery bypass graft (CABG): after 10-14 days
- Percutaneous coronary intervention (PCI): after 5 days
what are cardiac causes of clubbing
- Cyanotic congenital heart disease (Fallot’s, TGA)
- Bacterial endocarditis
- Atrial myxoma
what is ebsteins abnormality?
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.
Associations
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
Ebstein’s anomaly may be caused by exposure to lithium in-utero
