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
