Cardiology 3/8/20 Flashcards
anatomical groups of ECG leads which leads are lateral?
precordial: V5 and V6 (low lateral) limb: I and aVL (high lateral)
anatomical groups of ECG leads which leads are inferior?
II, III and aVF
PR interval should be between…
120-200ms (3-5 small squares)
- long PR interval = 1st degree AV block
QRS complex should be…
- ≤120ms duration (<3 small squares)
RA enlargement shown on ECG by…
tall (>2.5mm), pointed P waves (P pulmonale)
- typically in chronic lung disease (eg. COPD)
LA enlargement shown on ECG by…
bifid/notched P wave (M shape - P mitrale) in limb leads
- mitral regurg/stenosis
causes of short PR interval
Wolff-Parkinson-White syndrome (delta wave)
causes of prolonged PR interval (1st degree heart block)
- idiopathic
- ischaemic heart disease
- hypokalaemia (hyperkalaemia rarely can cause prolonged PR)
- digoxin toxicity
- infection
> rheumatic fever
> endocarditis
> Lyme disease
normal cardiac axis
-30 to +90 degrees (shown by both leads I and II being positive)
left axis deviation
-30 to -90 degrees (shown by leads I and aVF/III LEAVING)
right axis deviation
+90 to +180 degrees (shown by lead I and aVF/III RETURNING)
north west axis
-90 to -180 degrees (lead I negative and aVF negative - very rare)
tachycardia with broad QRS can be…?
- atrial (supraventricular) tachycardia with BBB
- ventricular tachycardia
- in atrial tachycardia with BBB, each QRS complex is preceded by a P wave at a constant distance
- in ventricular tachycardia, atria and ventricles are beating independently of one another so QRS complexes are not preceded by P waves at a constant distance
acute inferior MI
- ST elevation in the inferior leads II, III and aVF
- reciprocal ST depression in the anterior leads
acute anterior MI
- ST elevation in the anterior leads V1 - 6, I and aVL (V3/V4 more pronounced)
- reciprocal ST depression in the inferior leads II, III, aVF
- hyperacute (tall) t waves
old MI shown by…
- pathological Q waves in anatomical distribution (eg. II, III and aVF for an inferior lesion)
broad QRS caused by:
- ventricular origin (eg VT)
- BBB
- hyperkalaemia
- pacemaker
causes of ST depression
- myocardial ischaemia
- digoxin toxicity
- hypokalaemia
- ventricular hypertrophy
QT interval should be….
- <440 for men
- <460 for women
ECG signs of LBBB
- broad QRS
- WiLLiaM (W in QRS of V1/2, M in V6)
- left axis deviation
ECG signs of RBBB
- broad QRS
- MaRRoW (M in QRS of V1/2, W in V6)
- wide S wave in lead I
first degree heart block
lengthened PR interval (>200ms)
second degree heart block
type 1 (Mobitz I)
- progressive prolongation of the PR interval until a dropped beat occurs
type 2 (Mobitz II)
- PR interval is constant but the P wave is often not followed by a QRS complex (intermittent dropped beats)
third (complete) degree heart block
- no association between the P waves and QRS complexes
- can be fatal and usually symptomatic
electrolyte responsible for cardiac myocyte depolarisation
Na+
electrolyte responsible for cardiac myocyte repolarisation
K+ (Ca2+ causes partial plateau)
causes of LVH
- hypertension
- valvular disease (AS)
- hypertrophic cardiomyopathy
- athletes
- congenital HD
causes of RVH
- pulmonary hypertension
- valvular disease (pul. regurg)
- lung disease
- congenital HD
features of arrhythmogenic right ventricular cardiomyopathy (ARVC)
autosomal dominant inheritance
- RV myocardium replaced by fibrofatty tissue
- palpitations
- syncope
- sudden cardiac death
- ECG changes
- enlarged hypokinetic RV with a thin wall may be seen on echo
ECG abnormalities of arrhythmogenic right ventricular cardiomyopathy (ARVC)
in V1-3:
- T wave inversion
- epsilon wave (in 50%) - ε = M shaped terminal notch in QRS complex
management of arrhythmogenic right ventricular cardiomyopathy (ARVC)
- sotalol
- catheter ablation to prevent ventricular tachycardia
- implantable cardioverter-defibrillator
ECG change with severe hypothermia
- J waves (Osborne waves)
- atrial or ventricular arrhythmias
- bradycardia
features of Brugada syndrome
autosomal dominant inheritance
- more common in asian populations
- around 30% have a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein
- sudden cardiac death
- ECG changes
ECG changes of Brugada syndrome
- ST elevation followed by a negative T wave in > 1 of V1-V3
- right bundle branch block
- ECG changes may be more apparent following the administration of flecainide or ajmaline (the investigation of choice in suspected cases of Brugada syndrome)
management of Brugada syndrome
implantable cardioverter-defibrillator
features of hypertrophic obstructive cardiomyopathy
autosomal dominant inheritance
- common cause of sudden death (leading cause of sudden cardiac death in young athletes - Muamba)
- echo findings include:
> mitral regurgitation (MR)
> asymmetric septal hypertrophy
> systolic anterior motion (SAM) of the anterior mitral valve
features of dilated cardiomyopathy
genetic predisposition, worsened by environmental factors
- most common cardiomyopathy
- classic findings of heart failure
- systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
- balloon appearance of the heart on the chest x-ray
causes of dilated cardiomyopathy
genetic predisposition combined with:
- alcohol
- IHD
- coxsackie B virus
- wet beri beri
- doxorubicin
MOST COMMONLY it is idiopathic
features of restrictive cardiomyopathy
autosomal dominant
- least common cardiomyopathy
- rigid heart walls prevent efficient pumping of blood
- may be asymptomatic
- heart failure symptoms
causes of restrictive cardiomyopathy
genetic predisposition combined with:
- amyloidosis/sarcoidosis/haemochromatosis
- post-radiotherapy
- Loeffler’s endocarditis
management of restrictive cardiomyopathy
treat symptoms of heart failure
features of peripartum cardiomyopathy
develops between last month of pregnancy and 5 months post-partum
- more common in
> older women
> greater parity
> multiple gestations
- symptoms of heart failure
features of Takotsubo cardiomyopathy
- stress-induced cardiomyopathy e.g. patient just found out family member dies then develops chest pain and features of heart failure
- transient, apical ballooning of the LV
- treatment is supportive
which artery and which leads - LAD
V1-V4 (anterior)
which artery and which leads - right coronary
II, III, aVF (inferior)
which artery and which leads - circumflex
I, V5-V6 (lateral)
immediate management of acute coronary syndrome (STEMI/NSTEMI/unstable angina)
no longer MONA
- morphine only in severe pain
- nitrates
- aspirin 300mg
- ticagrelor (or clopidogrel)
- unfractionated heparin (especially prior to PCI)
- PCI if eligible ASAP
- monitor O2 sats, only offer O2 to:
> those with sats <94% who are not at risk of hypercapnic resp failure (aim for 94-98%)
> those with COPD who are at risk of hypercapnic resp failure (aim for 88-92%) further management and secondary prevention once stable
secondary prevention of ACS (STEMI/NSTEMI/unstable angina)
- ACE inhibitor (indefinitely)
- dual antiplatelet therapy (aspirin plus a second antiplatelet) for up to 12 months
- beta-blocker (indefinitely if reduced left ventricular ejection fraction)
- statin
ECG findings of hypokalaemia
- ST depression
- prominent U wave
- shallow T wave
- prolonged PR
ECG finding of hyperkalaemia
- tall, tented T waves
- loss of P wave
- broad QRS complex
- ST elevation
ECG features of digoxin
- down-sloping, ‘scooped out’ ST depression
- flattened/inverted T waves
ECG changes in PE
- classic ECG changes seen in PE are:
(‘S1Q3T3’)
> large S wave in lead I
> large Q wave in lead III
> inverted T wave in lead III
- only seen in 20% patients
- also commonly:
> RBBB
> right axis deviation
causes of RBBB
- increasing age
- right heart overload (ventricular hypertrophy/cor pulmonale/PE/atrial septal defect/RV strain)
- myocardial infarction
- cardiomyopathy or myocarditis
causes of LBBB
- ischaemic heart disease
- hypertension
- aortic stenosis
- cardiomyopathy
rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
ECG features of multifocal atrial tachycardia
- at least 3 different P wave morphologies
- rate = 100-180bpm
- irregular rhythm
CHA2DS2VASc
C = CHF
H = hypertension
A = age
> 75+ = 2
> 65-74 = 1
D = diabetes
S = prior stroke or TIA (2 points)
V = vascular disease (eg. IHD/PAD)
S = sex (female = 1 point)
0 = no treatment (check transthoracic echo for valvular disease)
1 = consider anticoagulation in males, no treatment in females
>1 = offer anticoagulation
HASBLED2
score to assess bleeding risk
H = hypertension (uncontrolled - sys >160)
A = abnormal:
> renal function = dialysis or creatinine > 200
> liver function = cirrhosis or bilirubin > 2x normal or ALT/AST/ALP > 3x normal
S = previous stroke
B = history of major bleed/tendency to bleed
L = labile/high INRs
E = elderly (>65 yrs)
D = drugs, drink
> medication predisposing to bleeding = 1 point
> drinks > 8 alcoholic drinks/week = 1 point
3+ points = high risk of bleed so anticoag should be avoided where possible
true abdo aortic aneurysm (AAA)
involves all 3 layers of arterial wall
- most common in elderly men
false abdo aortic aneurysm (AAA)
only involves 1 layer of arterial wall
indications for surgical management of AAA
- symptomatic aneurysms (80% annual mortality if untreated)
- increasing size above 5.5cm if asymptomatic
- rupture (100% mortality without surgery)
S3 heart sound (gallop)
- caused by diastolic filling of the ventricle
- considered normal if < 30 years old and athletes
- heard in:
> left ventricular failure (e.g. dilated cardiomyopathy)
> constrictive pericarditis (called a pericardial knock)
> mitral regurgitation
S4 heart sound
- 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
split S2 vs S3
- S3 is a low-pitched sound (better heard with bell)
- split S2 is high pitched (better with diaphragm)
- S3 sound is heard best at the cardiac apex
- split S2 is best heard at the left upper sternal border
cause of waterhammer/collapsing pulse
aortic regurgitation
indications for digoxin use
- atrial fibrillation (rate control)
- has use for symptom relief in heart failure
effects of digoxin
- reduced conduction through AV node, leads to reduced ventricular rate AF and AFlutter
- increases strength of cardiac contaction (+ inotropic)
- slows heart rate via vagus nerve stimulation
features of digoxin toxicity
not defined by plasma concentration
- arrhythmias (e.g. AV block, bradycardia)
- generally unwell (lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision)
- gynaecomastia
causes of digoxin toxicity
narrow therapeutic range so digoxin toxicity more likely to occur in:
- hypokalaemia (classically)
- iatrogenic
> amiodarone
> verapamil
> diltiazem
> spironolactone
> PPI (increases digoxin effect, while antacids decrease effect)
- elderly
- renal failure
- myocardial ischaemia
management of digoxin toxicity
- digibind
- correct arrhythmias
- monitor potassium
- remove cause if poss (eg. medication)
features of aortic dissection
- chest pain: typically severe, radiates through to the back and ‘tearing’ in nature
- aortic regurgitation
- hypertension
- other features may result from the involvement of specific arteries, eg. coronary arteries → angina, spinal arteries → paraplegia, distal aorta → limb ischaemia
management of aortic dissection
Type A (ascending aorta, 2/3rds cases)
- BP control
- surgical management
Type B (descending aorta)
- beta blocker (IV labetalol)
- bed rest
complications of aortic dissection
- cardiac tamponade
- MI
- renal failure
- unequal arm pulses and BP
- mediastinal bleed
left anterior fascicular block
- left axis deviation
- qR complexes in lateral leads I and aVL
- rS complexes in inferior leads II, III, aVF
- QRS may be broad
left posterior fascicular block
- right axis deviation
- qR complexes in inferior leads II, III, aVF
- rS complexes in lateral leads I and aVL
- QRS may be broad
rate or rhythm control in AF
factors favouring rate control:
- >65 years
- history of ischaemic heart disease
factors favouring rhythm control:
- <65 years
- symptomatic
- first presentation
- lone AF or AF secondary to a corrected precipitant (e.g. alcohol)
- congestive heart failure
features of cardiac tamponade
life-threatening compression on heart (while pericardial effusion is less threatening)
Beck’s triad:
- hypotension
- raised JVP
- muffled heart sounds
also can have:
- dyspnoea
- tachycardia
- electrical alternans (differing QRS heights due to rocking of heart in pericardium)
cardiac tamponade vs constrictive pericarditis
- JVP
> tamonade = X only (TAMPaX)
> CP = X+Y (Coldplay X&Y)
- pulsus paradoxus
> T = present
> CP = absent
- Kussmaul’s sign (paradoxical rise in JVP on inspiration)
> T = rare
> CP = present
- pericardial calcification on CXR
> T = absent
> CP = present
management of cardiac tamponade
- urgent pericardiocentesis
features of acute pericarditis
- chest pain: may be pleuritic, often relieved by sitting forwards
- non-productive cough
- dyspnoea/tachypnoea
- tachycardia
- pericardial rub
- ECG changes
ECG changes of acute pericarditis
- changes in pericarditis are often global unlike by territories seen in ischaemic events
- ‘saddle-shaped’ ST elevation
- PR depression: most specific ECG marker for pericarditis anyone suspected of acute pericarditis should have an echocardiogram
management of acute pericarditis
- treat underlying cause
- NSAIDs/colchicine for pain relief
- supportive
- corticosteroids if resistant and non-infective
- reduce exercise for recurrent pericarditis, can add IVIg/azathioprine, then consider pericardiectomy if still unresponsive for pericardial effusion, pericardiocentesis may be required
causes of cardiac tamponade
- pericarditis
- TB
- iatrogenic (invasive procedure-related, post-cardiac surgery)
- trauma
- malignancy
- connective tissue disease eg. SLE
causes of pericarditis
- viral infections (Coxsackie)
- tuberculosis
- uraemia (causes ‘fibrinous’ pericarditis)
- trauma
- post-myocardial infarction, Dressler’s syndrome
- connective tissue disease
- hypothyroidism
- malignancy
adverse effects of amiodarone
amiodarone is a class III antiarrhythmic
- thyroid dysfunction
- pulmonary fibrosis
- liver fibrosis
- photosensitivity
- peripheral neuropathy
- lengthened QT interval (proarrhythmic)
- thrombophlebitis (so should be given at central veins ideally)
- drug interactions (p450 inhibitor)
VT
V fib
AF
AFlutter
Torsades de points
STEMI anterolateral
ischaemia
bilateral PE
consequences of long cQT interval
ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death
drug causes of prolonged QT interval
- amiodarone, sotalol
- tricyclic antidepressants, SSRIs (especially citalopram)
- methadone
- erythromycin
- haloperidol
- ondanestron
non-drug causes of prolonged QT interval
- congenital
- electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
- myocardial infarction
- myocarditis
indications for surgery in infective endocarditis
- haemodynamic instability
- severe heart failure
- severe sepsis despite antibiotics
- valvular obstruction
- infected prosthetic valve
- persistent bacteraemia
- repeated emboli
- aortic root abscess
