Sudden cardiac death conditions Flashcards
WPW ECG features
Short PR (less tan 0.12 seconds)
long QRS (over 0.12 seconds)
discordance of ST segment and T waves.
WPW mechanism
Pre excitation of the ventricles due to accessory pathyway/bundle of kent. These are formed during cardiac development and can be in multiple positions.
delta waves
produced by pre-excitation.
Left sided AP produces positive delta wave in all precordial leads and R/S>1 in V1.
Right sided AP produces negative delta waves in V1-2.
Arrhythmogenic right ventricular cardiomyopathy pathophysiology
genetic defect effecting the desmosomes proteins which hold the cardiac myocytes together. Cardiac myocytes can detach and cause infarction and fatty deposits replace them, these will disrupt the cardiac conduction system. These changes can cause ventricular arrythmias, heart blocks and heart failure.
ARVC Clinical presentation
palpitations
dizziness
syncope
SOB
chest pain
fatigue
oedema
ascites
cough
sudden death
ARVC ECG criteria
T wave inversion in inferior leads without RBBB
Epsilon waves (blip/wiggle) in V1
QRS broadening in V1/2
ARVC Treatment and management
medicines to control rhythms (beta blocker)
medications to prevent abnormal rhythms
diuretics for oedema
medicines to reduce workload
Always transfer for investigation, pre alert depends on other clinical presentations and stability.
Brugada syndrome pathophysiology
due to a genetic mutation of the cardiac sodium ion channels there is alteration to the cardiac conduction system. Mechanism is unclear but repolarisation theory and depolarisation theory have been proposed.
Brugada syndrome clincal presentation
dizziness
syncope
laboured breathing DURING SLEEP OR REST
irregular heart beat
arrythmias DURING SLEEP OR REST
tachycardia
seizures
Brugada syndrome ECG changes
Brugada sign (only diagnostic criteria) = Coved ST segment >2mm followed by negative T waves in V1-3
Type 2 - saddle back shaped ST segment >2mm
Type 3 - Saddle back or coved ST under 2mm
Brugada syndrome treatment
medication to treat and prevent arrythmias
ICD implantation
lifestyle changes to reduce arrythmias (reduce alcohol, certain medications)
Hypertrophic cardiomyopathy
Genetic heart disease where heart muscle becomes thick due to mutation of sarcomere genes. Thickening of the myocardium reduces volume capacity of the effected chamber and effects ability of the chamber to empty.
HCM clinical presentations
SOB
Chest pain
Dizziness
syncope
Palpitations
Sudden cardiac death
HCM ECG changes
Left ventricular hypertrophy with precordial voltage changes
ST segment and T wave abnormalities (non specific)
Narrow Q waves mimicking prior MI
HCM treatment
medication to manage heart rhythm and symptoms
Septal myectomy to thin the thickened muscle
ICD to prevent sudden cardiac death
lifestyle modifications to reduce risk of death
Long QT syndrome pathophysiology
Genetic disorder with various genotypes. Mainly effecting cardiac ion channels especially passive channels responsible for efflux of positive ions. This causes prolonged action potential and delayed repolarisation which can interrupt the cardiac cycle.
Long QT syndrome clinical presentation
normally asymptomatic
can be bradycardic, hearing loss, skeletal defects
triggered by cold water, emotion, auditory stimuli.
Long QT syndrome ECG changes
Schwartz scoring system assessing
QT duration, QT duration after exercise, presence of torsade’s de pointes, T wave alternations and bradycardia.
Long QT syndrome treatment and management
Beta blockers to prevent arrythmias by stabilising action potential.
ICD to prevent sudden cardiac death
lifestyle changes such as avoiding triggers (swimming, exercise, stress, some medications)
surgery called sympathectomy
Myocarditis
inflammation of the heart muscle due to infection/genetic cause leading to necrosis of cardiomyocytes effecting the hearts ability to pump blood and causing abnormal heart rhythms.
myocarditis clinical presentation
asymptomatic in mild cases
chest pain
discomfort
SOB
fatigue
abnormal heart rhythms
heart failure
sudden cardiac death.
Myocarditis ECG changes
Sinus tachycardia ( response to inflammation and potential heart dysfunction)
Non-specific ST and T wave changes mimicking MI
PR segment depression seen where myocarditis accompanies pericarditis
low voltage QRS complex
arrythmias
heart blocks
T wave inversions
Myocarditis treatment
Beta blockers, ACE inhibitors and aldosterone receptor antagonists to reduce heart rate and prevent arrythmias.
Corticosteroids for some viral infections
ECMO during heart recovery and rest in severe cases.
