Cardiology Flashcards
Pulsus paradoxus
greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration
severe asthma, cardiac tamponade
Slow-rising/plateau pulse
aortic stenosis
Collapsing pulse
aortic regurgitation
patent ductus arteriosus
hyperkinetic states (anaemia, thyrotoxic, fever, exercise/pregnancy)
Pulsus alternans
regular alternation of the force of the arterial pulse
severe LVF
Bisferiens pulse
‘double pulse’ - two systolic peaks
mixed aortic valve disease
Jerky’ pulse
Hypertrophic obstructive cardiomyopathy- may also be associated with bisferiens pulse
ECG signs: Digoxin toxicity
ECG features
down-sloping ST depression ('reverse tick', 'scooped out')
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardiaEjection systolic murmur
louder on expiration aortic stenosis hypertrophic obstructive cardiomyopathy louder on inspiration pulmonary stenosis atrial septal defect also: tetralogy of Fallot
Holo/pan systolic murmur
mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
tricuspid regurgitation becomes louder during inspiration, unlike mitral stenosis
during inspiration, the venous blood flow into the right atrium and ventricle are increased → increases the stroke volume of the right ventricle during systole
ventricular septal defect (‘harsh’ in character)
Late systolic
mitral valve prolapse
coarctation of aorta
Early diastolic murmur
aortic regurgitation (high-pitched and 'blowing' in character) Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character)
Mid-late diastolic murmur
mitral stenosis ('rumbling' in character)
Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)Continuous machine-like murmur
patent ductus arteriosus
Causes of prolonged QT
Congenital
Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
Romano-Ward syndrome (no deafness
Causes of prolonged QT
drugs
amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine** erythromycin haloperidol ondanestron
Causes of prolonged QT
other
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia acute myocardial infarction myocarditis hypothermia subarachnoid haemorrhage
heart sounds
S1
closure of mitral and tricuspid valves
soft if long PR or mitral regurgitation
loud in mitral stenosis
heart sounds
s2
closure of aortic and pulmonary valves
soft in aortic stenosis
splitting during inspiration is normal
heart sounds s3
aused 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
heart sounds 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
Causes of left axis deviation (LAD)
ECG
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
Causes of Right axis deviation (RAD)
right ventricular hypertrophy left posterior hemiblock lateral myocardial infarction chronic lung disease → cor pulmonale pulmonary embolism ostium secundum ASD Wolff-Parkinson-White syndrome* - left-sided accessory pathway normal in infant < 1 years old minor RAD in tall people
Adenosine
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.
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
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 is an a wave?
large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
absent if in atrial fibrillation
What are 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 are ‘c’ waves?
closure of tricuspid valve
not normally visible
what are ‘v’ waves?
due to passive filling of blood into the atrium against a closed tricuspid valve
giant v waves in tricuspid regurgitation
What is ‘X’ descent?
fall in atrial pressure during ventricular systole
What is ‘Y’ descent?
opening of tricuspid valve
Pathophysiology of Hypertrophic obstructive cardiomyopathy
the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C
results in predominantly diastolic dysfunction
left ventricle hypertrophy → decreased compliance → decreased cardiac output
characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes (‘disarray’) and fibrosis on biopsy
Features of hypertrophic obstructive cardiomyopathy
often asymptomatic
exertional dyspnoea
angina
syncope
typically following exercise
due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat
ejection systolic murmur
increases with Valsalva manoeuvre and decreases on squatting
hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation
Conditions associated with hypertrophic obstructive cardiomyopathy
Freidreich’s ataxia
Wolf-Parkinson’s White
ECHO findings in hypertrophic obstructive cardiomyopathy
mnemonic - MR SAM ASH
mitral regurgitation (MR)
systolic anterior motion (SAM) of the anterior mitral valve leaflet
asymmetric hypertrophy (ASH)
Mitral stenosis features
mid-late diastolic murmur (best heard in expiration) loud S1, opening snap low volume pulse malar flush atrial fibrillation
Features of severe mitral stenosis
lengthening of murmur
opening snap becomes closer to S2
CXR findings of mitral stenosis
left atrial enlargement may be seen
Third heart sounds (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
Fourth heart sounds (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
Anteroseptal MI
Leads and arteries
V1-V4
Left anterior descending
Inferior MI
Leads and arteries
II, III, aVF,
Right coronary artery
Anterolateral MI
Leads and arteries
V4-6, I, aVL,
Left anterior descending or left circumflex
Lateral MI
Leads and arteries
I, aVL, V5-6
Left circumflex
Posterior MI
Leads and arteries
Tall R Waves in V1-2
Left circumflex and right coronary
Causes of left axis deviation
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
causes of right axis deviation
right ventricular hypertrophy left posterior hemiblock lateral myocardial infarction chronic lung disease → cor pulmonale pulmonary embolism ostium secundum ASD Wolff-Parkinson-White syndrome* - left-sided accessory pathway normal in infant < 1 years old minor RAD in tall people
What is BNP
produced mainly by left ventricle in response to strain
effects of BNP
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
What reduces BNP?
ACE-i
ARBs
diuretics
Patients at risk of infective endocarditis
- previously normal mitral valve
- rheumativ heart disease
- congenital defects
- IVDU
- recent piercings
Causes of infective endocarditis
- used to be staph epidermidis
- up to 2 months post valve replacement- strep viridans
- 2+ post valve replacement/ generally most common - staph aureus
- SLE
Culture negative causes of infective endocarditis
prior antibiotic therapy Coxiella burnetii Bartonella Brucella HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
Causes of constrictive pericarditis
- TB
- any cause of pericarditis
Features of constrictive pericarditis
dyspnoea
right heart failrue - raised JVP, ascites, oedema, hepatomegaly.
JVP - prominent X & Y descent
pericardial knock - loud S3
Kussmaul positive (paradoxical rise in JVP on inspiration
CXR findings - constrictive pericarditis
calcified pericardium
Features of cardiac tamponade
JVP - absent Y descent
pulsus paradoxus
Kussmaul - rare
Mechanism of action of Amiodarone
class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
Amiodarone monitoring
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months
Adverse reactions to amiodarone
thyroid dysfunction: both hypothyroidism and hyper-thyroidism corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia lengths QT interval
Causes of prolonged PR interval
idiopathic ischaemic heart disease digoxin toxicity hypokalaemia* rheumatic fever aortic root pathology e.g. abscess secondary to endocarditis Lyme disease sarcoidosis myotonic dystrophy
History of cardiac tamponade
a 60-year-old man with a history of lung cancer presents with dyspnoea. On examination he is tachycardic, hypotensive, has a raised JVP with an absent Y descent and has pulsus paradoxus
History of constrictive pericardititis
a 60-year-old man with a history of tuberculosis presents with dyspnoea and fatigue. On examination the JVP is elevated, there is a loud S3 and Kussmaul’s sign is positive. Hepatomegaly is also noted
Causes of constrictive pericarditis
TB
any other cause of pericarditis
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 positive
Mechanism of action of thiazide diuretics
inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. Potassium is lost as a result of more sodium reaching the collecting ducts.
Common adverse effects of thiazide diuretics
dehydration postural hypotension hyponatraemia, hypokalaemia, hypercalcaemia* gout impaired glucose tolerance impotence
Rare adverse effects of thiazide diuretics
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
What is Takayasu’s arteritis
Takayasu’s arteritis is a large vessel vasculitis. It typically causes occlusion of the aorta and questions commonly refer to an absent limb pulse. It is more common in females and Asian people
Associated with renal artery stenosis
Managed with steroids
Features of Takayasu’s arteritis
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit
intermittent claudication
aortic regurgitation (around 20%)
Causes of PR prolongation
idiopathic ischaemic heart disease digoxin toxicity hypokalaemia* rheumatic fever aortic root pathology e.g. abscess secondary to endocarditis Lyme disease sarcoidosis myotonic dystrophy
History of left ventrivcular wall rupture
a patient develops acute heart failure 10 days following a myocardial infarction. On examination he has a raised JVP, pulsus paradoxus and diminished heart sounds
History of post MI VSD
a patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination
Causes of LBBB
ischaemic heart disease hypertension aortic stenosis cardiomyopathy rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
Causes of dilated cardiomyopathy
idiopathic: the most common cause
myocarditis: e.g. Coxsackie B, HIV, diphtheria, Chagas disease
ischaemic heart disease
peripartum
hypertension
iatrogenic: e.g. doxorubicin
substance abuse: e.g. alcohol, cocaine
inherited: Duchenne’s
infiltrative e.g. haemochromatosis, sarcoidosis
+ these causes may also lead to restrictive cardiomyopathy
nutritional e.g. wet beriberi (thiamine deficiency)
Pathophysiology of Dilated Cardiomyopathy
dilated heart leading to predominately systolic dysfunction all 4 chambers are dilated, but the left ventricle more so than right ventricle eccentric hypertrophy (sarcomeres added in series) is seen
Features of Dilated Cardiomyopathy
classic findings of heart failure
systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
S3
‘balloon’ appearance of the heart on the chest x-ray
Risk factors for Mitral Regurgiation
Female sex Lower body mass Age Renal dysfunction Prior myocardial infarction Prior mitral stenosis or valve prolapse Collagen disorders e.g. Marfan's Syndrome and Ehlers-Danlos syndrome
Causes of Mitral Regurgitation
Following coronary artery disease or post-MI Mitral valve prolapse Infective endocarditis Rheumatic fever. Congenital
Symptoms of Mitral Regurgitation
Symptoms tend to be due to failure of the left ventricle, arrhythmias or pulmonary hypertension.
Signs of Mitral Regurgitation
The murmur heard on auscultation of the chest is typically a pansystolic murmur described as “blowing”. It is heard best at the apex and radiating into the axilla. S1 may be quiet as a result of incomplete closure of the valve. Severe MR may cause a widely split S2
Investigations of Mitral Regurgitation
ECG may show a broad P wave, indicative of atrial enlargement
Cardiomegaly may be seen on chest x-ray, with an enlarged left atrium and ventricle
Echocardiography is crucial to diagnosis and to assess severity
Treatment options of Mitral Regurgitation
Medical management in acute cases involves nitrates, diuretics, positive inotropes and an intra-aortic balloon pump to increase cardiac output
If patients are in heart failure, ACE inhibitors may be considered along with beta-blockers and spironolactone
In acute, severe regurgitation, surgery is indicated
The evidence for repair over replacement is strong in degenerative regurgitation, and is demonstrated through lower mortality and higher survival rates
When this is not possible, valve replacement with either an artificial valve or a pig valve is considered
Other processes during PCI
Primary coronary intervention for patients with STEMI
thrombus aspiration, but not mechanical thrombus extraction, should be considered
complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock
Drug therapy during PCI
Primary coronary intervention for patients with STEMI
patients undergoing PCI with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus
patients undergoing PCI with femoral access:
bivalirudin with bailout GPI
Antiplatelet therapy during PCI
Primary coronary intervention for patients with STEMI
this is termed ‘dual antiplatelet therapy’, i.e. aspirin + another drug
if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel
Fibrinolysis for patients with STEMI
Fibrinolysis used to be the only form of coronary reperfusion therapy available. However, it is used much less commonly now given the widespread availability of PCI.
Patients undergoing fibrinolysis should also be given an antithrombin drug.
An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
Management of unstable angina/NSTEMI
antithrombin treatment
fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately
if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given
What does GRACE stand for?
Global Registry of Acute Coronary Events age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels
Which patients with NSTEMI/unstable angina should have coronary angiography (with follow-on PCI if necessary)?
immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk
coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission
Primary coronary intervention for patients with NSTEMI/unstable angina
Further drug therapy
unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not
further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI
if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
if taking an oral anticoagulant: clopidogrel
Conservative management for patients with NSTEMI/unstable angina
Further drug therapy
further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug)
if the patient is not at a high risk of bleeding: ticagrelor
if the patient is at a high risk of bleeding: clopidogrelECG P wave changes
increased P Wave amplitude
cor pulmonale
ECG P wave changes
Broad, notched (bifid) P waves
often most pronounced in lead II
a sign of left atrial enlargement, classically due to mitral stenosis
Tricuspid stenosis JVP
Large A waves
Causes of RBBB
normal variant - more common with increasing age
right ventricular hypertrophy
chronically increased right ventricular pressure - e.g. cor pulmonale
pulmonary embolism
myocardial infarction
atrial septal defect (ostium secundum)
cardiomyopathy or myocarditis
Thrombolysis
Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. They in primarily used in patients who present with a ST elevation myocardial infarction. Other indications include acute ischaemic stroke and pulmonary embolism, although strict inclusion criteria apply.
Examples
alteplase
tenecteplase
streptokinase
Contra-indications to thrombolysis
active internal bleeding recent haemorrhage, trauma or surgery (including dental extraction) coagulation and bleeding disorders intracranial neoplasm stroke < 3 months aortic dissection recent head injury severe hypertension
Features of patent ductus arteriosus
left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat
Management of patent ductus arteriosus
indomethacin or ibuprofen
given to the neonate
inhibits prostaglandin synthesis
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 repa
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 Aortic regurgitation
early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
collapsing pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)
mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
Valvular Causes of aortic regurgitation
rheumatic fever
infective endocarditis
connective tissue diseases e.g. RA/SLE
bicuspid aortic valve
Aortic causes of aortic regurgitation
aortic dissection spondylarthropathies (e.g. ankylosing spondylitis) hypertension syphilis Marfan's, Ehler-Danlos syndrome
Stage 1 hypertension
Clinic BP >= 140/90 mmHg and subsequent ABPM daytime average or HBPM average BP >= 135/85 mmHg
Stage 2 hypertension
Clinic BP >= 160/100 mmHg and subsequent ABPM daytime average or HBPM average BP >= 150/95 mmHg
Stage 3 Hy[erension
Clinic systolic BP >= 180 mmHg, or clinic diastolic BP >= 110 mmHg
Step 1 Hypertension
Management
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 Hypertension
Management
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
(A + C) or (A + D) or (C + A) or (C + D)
Step 3 Hypertension
Management
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 Hypertension management
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
New hypertension drugs
Direct renin inhibitors
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 reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists
adverse effects were uncommon in trials although diarrhoea was occasionally seen
only current role would seem to be in patients who are intolerant of more established antihypertensive drugs
Ischaemia of the papillary muscle
History
a patient is noted to have a new early-to-mid systolic murmur 10 days after being admitted for a myocardial infarction
Post-myocardial infarction ventricular septal defect
History
a patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination
What is bivalirudin?
Bivalirudin is a reversible direct thrombin inhibitor used as an anticoagulant in the management of acute coronary syndrome.
Nitrate side effects
hypotension
tachycardia
headaches
flushing
Mechanism of action - nitrates
nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand
Nitrate tolerance
many patients who take nitrates develop tolerance and experience reduced efficacy
the 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
Mechanism of action of ACE-i
inhibit the conversion angiotensin I to angiotensin II
ACE inhibitors are activated by phase 1 metabolism in the liver
Side effects of ACE-i
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 ACE-i
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
Interactions with ACE-i
patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
significantly increases the risk of hypotension
Monitoring ACE-i
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
Arrythmogenic right ventricular cardiomyopathy
What is it?
Arrhythmogenic right ventricular cardiomyopathy (ARVC, also known as arrhythmogenic right ventricular dysplasia or ARVD) 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.
Pathophysiology of arrhythmogenic right cardiomyopathy
inherited in an autosomal dominant pattern with variable expression
the right ventricular myocardium is replaced by fatty and fibrofatty tissue
around 50% of patients have a mutation of one of the several genes which encode components of desmosome
Presentation of arrhythmogenic right ventricular cardiomyopathy
palpitations
syncope
sudden cardiac death
Investigation of arrhythmogenic 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
Management of arrhythmogenic right ventricular cardiomyopathy
drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator
What is Naxos disease
an autosomal recessive variant of ARVC
a triad of ARVC, palmoplantar keratosis, and woolly hair
What is Buerger’s disease?
(also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.
Features of Buerger’s disease
extremity ischaemia intermittent claudication ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon
Contraindications to beta blockers
uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia
Side Effects of beta blockers
bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction
Uses of adenosine
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.
Mechanism of action of adenosine
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
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 is nicorandil?
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.
Side effects of nicorandil
flushing
headache
kin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration
Cntra indicated in LVF
ECG changes 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
Anti-platelets
ACS
1st line
Aspirin (lifelong) & ticagrelor (12 months)
Anti-platelets
ACS
2nd Line
If aspirin contraindicated, clopidogrel (lifelong
Anti-platelets
PCI
1st Line
Aspirin (lifelong) & prasurgrel or ticagrelor (12 months)
Anti-platelets
PCI
2nd Line
If aspirin contraindicated, clopidogrel (lifelong)
Anti-platelets
TIA
1st Line
Clopidogrel (lifelong)
Anti-platelets
TIA
1st Line
Aspirin (lifelong) & dipyridamole (lifelong)
Anti-platelets
Ischaemic stroke
1st line
Clopidogrel (lifelong)
Anti-platelets
Ischaemic stroke
2nd Line
Aspirin (lifelong) & dipyridamole (lifelong)
Anti-platelets
Peripheral arterial disease
1st Line
Clopidogrel (lifelong)
Anti-platelets
Peripheral arterial disease
2nd Line
Asprin (lifelong)
Poor prognostic factors in infective endocarditits
Staphylococcus aureus infection (see below)
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels
DVLA rules
Hypertension
can drive unless treatment causes unacceptable side effects, no need to notify DVLA
if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more
DVLA rules
elective angioplasty
1 week off driving
DVLA rules
CABG
4 weeks off driving
DVLA rules
ACS
4 weeks off driving
1 week if successfully treated by angioplasty
DVLA rules
Angina
driving must cease if symptoms occur at rest/at the wheel
DVLA rules
Pacemaker insertion
1 week off driving
DVLA rules
ICD insertion
if implanted for sustained ventricular arrhythmia: cease driving for 6 months
if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers
DVLA rules
successful catheter ablation for an arrhythmia
2 days off driving
DVLA rules
aortic aneurysm >6cm or more
notify DVLA. Licensing will be permitted subject to annual review.
an aortic diameter of 6.5 cm or more disqualifies patients from driving
DVLA
heart transplant
do not drive for 6 weeks, no need to notify DVLA
Ranson criteria
Acute pancreatitis
Waterlow score
Assesses the risk of a patient developing a pressure sore
Alcohol screening tool
FAST
CAGE
Audit
CHA2DS2-VASc
Used to determine the need to anticoagulate a patient in atrial fibrillation
ABCD2
Prognostic score for risk stratifying patients who’ve had a suspected TIA
What is Brugada syndrome
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.
Pathophysiology of Brugada
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
ECG changes in Brugada
convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
partial right bundle branch block
the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome
Managment of Brugada
implantable cardioverter-defibrillator
What is BNP
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain.
Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics.
Effects of Dyspnoea
vasodilator
diuretic and natriuretic
suppresses both sympathetic tone and the renin-angiotensin-aldosterone system
Pathogenesis of Rheumatic Fever
Streptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells
B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated
there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry
the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries
this response leads to the clinical features of rheumatic fever
Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
Major criteria for Rheumatic Fever
treptococcus pyogenes infection → activation of the innate immune system leading to antigen presentation to T cells
B and T cells produce IgG and IgM antibodies and CD4+ T cells are activated
there is then a cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry
the cell wall of Streptococcus pyogenes includes M protein, a virulence factor that is highly antigenic. It is thought that the antibodies against M protein cross-react with myosin and the smooth muscle of arteries
this response leads to the clinical features of rheumatic fever
Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever
congenital heart conditions - acyanotic
ventricular septal defects (VSD) - most common, accounts for 30% atrial septal defect (ASD) patent ductus arteriosus (PDA) coarctation of the aorta aortic valve stenosis
congenital heart conditions - cyanotic
tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia
features of cardiac tamponade
Hypotension
Raised JVP
Muffled heart sounds
other features of cardiac tamponade
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans
features of Patent ductus arteriosus
left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat collapsing pulse
management of patent ductus arteriosus
indomethacin or ibuprofen
given to the neonate
inhibits prostaglandin synthesis
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
Hypercalcaemia features
‘bones, stones, groans and psychic moans’
corneal calcification
shortened QT interval on ECG
hypertension
Mitral/tricuspid regurgitation murmur
Holosystolic murmur, high-pitched and ‘blowing’ in character
ECG changes: arrhythmogenic right ventricular cardiomyopathy
inverted T waves
JVP in SVC obstruction
a non-pulsatile raised JVP
JVP in complete heart block
cannon A wave pulse
Mechanism of action- hydralazine
increases cGMP leading to smooth muscle relaxation
Contra-indicated in SLE, IHD, CVD
Adverse effects of hydralazine
tachycardia palpitations flushing fluid retention headache drug-induced lupus
Pulse in patent ductus arteriosus (also aortic regurg)
Collapsing pulse
pulse in aortic stenosis
slow rising pulse
What is the most appropriate long-term antiplatelet choice for percutaneous coronary intervention (no drug allergies)?
Aspirin (lifelong) & prasugral or ticagrelor (12 months), no other antiplatelets
ACS anti-platelets: Indications for Clopidogrel (lifelong), no other anti-platelets)
peripheral arterial disease (no drug allergies)
ischaemic stroke (no drug allergies)
TIA (no drug allergies)
ACS anti-platelets: which conditions managed with:
Aspirin (lifelong) & dipyridamole (lifelong), no other antiplatelets
TIA (cannot take clopidogrel) ischaemic stroke (cannot take clopidogrel)
Management of prosthetic valve endocarditis caused by staphylococci?
Flucloxacillin + rifampicin + low-dose gentamicin
Management of native valve endocarditis caused by staphylococci
Flucloxacillin
Adverse effects of adenosine
chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)
Hypertrophic obstructive cardiomyopathy is associated with which genetic condition
Freidreich’s ataxia
blood pressure target (> 80 years, clinic reading) is:
150/90
What is Buerger’s disease
Buerger’s disease (also known as thromboangiitis obliterans) is a small and medium vessel vasculitis that is strongly associated with smoking.
Features extremity ischaemia intermittent claudication ischaemic ulcers superficial thrombophlebitis Raynaud's phenomenon
Initial blind therapy of infective endocarditis (prosthetic valve)
Vancomycin + rifampicin + low-dose gentamicin
Patent ductus arteriosus -murmur
Continuous ‘machinery’ murmur
Opening snap
Mitral stenosis
Split S2
mitral regurgitation
JVP pulse: absent Y descent
cardiac tamponade
NSTEMI identified, aspirin given, 6-month mortality intermediate/high(>3%) -
PCI within 72hrs
What is ivabradine
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
Genetics of hypertrophic obstructive cardiomyopathy
Usually due to a mutation in the gene encoding beta-myosin heavy chain protein
Side effects of ARBs
Hyperkalaemia
Hypotension
ECG changes: Hypokalaemia
ST depression
a long QT interval
a prolonged PR interval
U waves
ECG Changes Brugarda syndrome
Elevated ST
inverted T wave
mechanism of action: isosorbide mononitrate
Increases cGMP leading to smooth muscle relaxation
Stereotypical history: aortic regurgitation
a 50-year-old man with Marfan syndrome presents with palpitations and dyspnoea. On examination he has a collapsing pulse, the blood pressure is 160/60 mmHg and a high-pitched diastolic murmur is heard
Stereotypical history mitral regurgitaion
a 70-year-old woman is found to have a pan-systolic murmur after presenting with dyspnoea. A soft S1 and split S2 is also noted
Causes of pulsus paradoxus
severe asthma, cardiac tamponade
Mechanism of action of thienopyridines (clopidogrel, prasugrel, ticagrelor, ticlopidine)
antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets
indications of ticagrelor
Everyone who has a MI - NSTEMI or STEMI
Contraindications for bisoprolol
Concurrent verapamil - can cause complete heart block
Use nicorandil instead
Mechanism of action: dipyrimadole
Dipyridamole increases the levels adenosine and inhibits the phosphodiesterase enzymes that normally break down cAMP. Exogenous use of adenosine (e.g. treatment of supraventricular tachycardia) is contraindicated in patients on dipyridamole for this reason.
Mechanism of action: nicorandil
relaxes coronary vascular smooth muscle by stimulating guanylyl cyclase and increasing cyclic GMP (cGMP) levels (as shown first in our laboratory) as well as by a second mechanism resulting in activation of K+ channels and hyperpolarization
Ebstein’s abnormality
tricuspid regurgitation → pansystolic murmur, worse on inspiration
associated with benzos and lithium in pregnancy
Indications for surgery in infective endocarditis
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
what reduces the impact of adenosine
Aminophylline
Dipyramidole enhances the impact of adenosine
Causes of ST depression
secondary to abnormal QRS (LVH, LBBB, RBBB) ischaemia digoxin hypokalaemia syndrome X
What is syndrome X
Microvascular angina
Relieved by rest or nitroglycerin
Normal coronary arteriograms
the cause of ischemia seems to be reflex intramyocardial coronary constriction and reduced coronary flow reserve. Other patients have microvascular dysfunction within the myocardium: The abnormal vessels do not dilate in response to exercise or other cardiovascular stressors; sensitivity to cardiac pain may also be increased.
Treatment of pulmonary hypertension: vasodilator negative
much more common than a positive response, can be treated with prostacyclin analogues, endothelin receptor antagonists or phosphodiesterase inhibitors. Patients often require combination therapy.
Bosentan is the correct answer and is an endothelin receptor antagonist.
Treprostinil and iloprost are prostacyclin analogue
Congential heart disease
cyanotic: TGA most common at birth, Fallot’s most common overall
acyanotic: VSD most common cause
Overview of cholesterol embolism
cholesterol emboli may break off causing renal disease
the majority of cases are secondary to vascular surgery or angiography. Other causes include severe atherosclerosis, particularly in large arteries such as the aorta
Features of cholesterol embolism
eosinophilia
purpura
renal failure
livedo reticularis
Pulmonary arterial hypertension
esting mean pulmonary artery pressure of >= 25 mmHg. Endothelin thought to play a key role in pathogenesis of PAH. It is more common in females and typically presents between the ages of 30-50 years. Pulmonary hypertension may of course develop secondary to chronic lung diseases such as COPD. 10% Autosomal dominant inheritance
Features of pulmonary arterial hypertension
progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation
negative response to acute vasodilator testing (majority of patients)
pulmonary artery hypertension
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil
positive response to cute vasodilator testing (a minority of patients)
pulmonary arterial hypertension
oral calcium channel blockers
Most important investigation in pulmonary artery hypertension
cardiac catheterisation to measure right heart pressures
ECG features of Wolf-Parkinson White
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*
Types of Wolf Parkinson White
type A (left-sided pathway): dominant R wave in V1 type B (right-sided pathway): no dominant R wave in V
Management of Wolf Parkinson White
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
Conditions associated with Wolf Parkinson White
HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD
Mechanism of action: amiodarone
blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)
Why should you check U+Es before giving amiodarone
to detect underlying hypokalaemia- dramatically increases the risk of arrhythmias
Conditions 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
DeBakey Classification of aortic dissection
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
Stanford classification of aortic dissection
type A - ascending aorta, 2/3 of cases
type B - descending aorta, distal to left subclavian origin, 1/3 of cases
Features of aortic dissection
chest pain: typically severe, radiates through to the back and ‘tearing’ in nature
pulse deficit
weak or absent carotid, brachial, or femoral pulse
variation (>20 mmHg) in systolic blood pressure between the arms
aortic regurgitation
hypertension
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
Warfarin guidelines in dentistry
check INR 72 hours before procedure, proceed if INR < 4.0
ECG changes 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
Normal ECG variation in young athletes
sinus bradycardia
junctional rhythm
first degree heart block
Wenckebach phenomenon
Poor prognostic factors in infective endocarditis
Staphylococcus aureus infection
prosthetic valve (especially ‘early’, acquired during surgery)
culture negative endocarditis
low complement levels
Definitive investigation for Streptococcus gallolyticus
Colonoscopy.
Streptococcus gallolyticus is the subtype of Streptococcus bovis most linked with colorectal cancer
Drug causes of prolonged QT
amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram) methadone chloroquine terfenadine** erythromycin haloperidol ondanestron
Management of broad complex tachycardia
amiodarone: ideally administered through a central line
lidocaine: use with caution in severe left ventricular impairment
procainamide
Verapamil should NOT be used in VT.
ECG changes in Hypercalcaemia
shortening of the QT interval. Other findings include prolonged PR, widened QRS and ST elevation
Hypercalcaemia causes certain calcium ion channels to be opened for shorter amounts of time which in turn reduce phase 2 (the plateau phase) of the cardiomyocyte. This shortens the QT interval.
Causes of aortic stenosis
younger patients < 65 years: bicuspid aortic valve
older patients > 65 years: calcification
Clinical features (symptomatic disease) in aortic stenosis
chest pain
dyspnoea
syncope
murmur
an ejection systolic murmur (ESM) is classically seen in aortic stenosis
classically radiates to the carotids
this is decreased following the Valsalva manoeuvre
Features of aortic stenosis
narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill duration of murmur left ventricular hypertrophy or failure
Causes of aortic stenosis
degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM
Management of aortic stenosis
if asymptomatic then observe the patient is 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
cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined
balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement
Indications for warfarin
venous thromboembolism: target INR = 2.5, if recurrent 3.5
atrial fibrillation, target INR = 2.5
mechanical heart valves, target INR depends on the valve type and location. Mitral valves generally require a higher INR than aortic valves.
Factors that potentiate warfarin
liver disease
P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
cranberry juice
drugs which displace warfarin from plasma albumin, e.g. NSAIDs
inhibit platelet function: NSAIDs
Side effects of Warfarin
haemorrhage
teratogenic, although can be used in breastfeeding mothers
skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration. Thrombosis may occur in venules leading to skin necrosis
purple toes
