Diagnosis and Treatment of Arrhythmia Flashcards

1
Q

What is the definition of syncope?

What are the characteristics?

A
  • Syncope is defined as TLOC (transient loss of consciousness) due to cerebral hypoperfusion.
  • Characterised by:
    • Rapid onset
    • Short duration
    • Spontaneous complete recovery - reperfusion following falling to the ground (supine position increases venous return).
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2
Q

What are the causes of syncope?

A
  • Vasovagal / vasodepressor / neurally mediated
  • Cardiac
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3
Q

Describe vasovagal syncope.

A
  • Fainting: caused by incorrect nerve control of your peripheral circulation.
  • Vasovagal syncope isa temporary loss of consciousness caused by a neurological reflex that produces either sudden dilation of the blood vessels in the legs, or a bradycardia, or both.
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4
Q

Describe cardiac syncope.

A
  • Arrhythmia / heart failure.
  • Very fast ventricular tachycardia - incorrect filling during diastole causing decreased cardiac output.
  • Heart failure - has to be very bad to cause syncope, may arise from extensive use of medication causing hypotension.
  • The presence of infection may further compromise cardiac output, causing syncope in a patient with heart failure.
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5
Q

Which questions would you ask in Hx to rule out dangerous causes of syncope?

A
  • Was the syncope associated with tachycardic palpitations?
    • May be an underlying sinister fast heart rhythm.
  • Associated with exertion?
    • Asymmetric septal hypertrophy (also called hypertrophic cardiomyopathy).
  • Is there FHx of sudden cardiac death?
    • May be due to channelopathy.
      • Brugada syndrome - a genetic disorder in which the electrical activity within the heart is abnormal; associated with mutations in the gene encoding the cardiac sodium channel.
  • Is there complete heart block at an early age?
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6
Q

What are the usual investigations for cardiac syncope?

A
  • ECG
  • 24 hour tape
  • Echocardiogram
  • Exercise tolerance test
  • Cardiac MRI
  • CT coronary angiogram
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7
Q

Describe the use of echocardiogram.

A
  • 2D real-time imaging of the heart with an ultrasound probe, allowing you to look for:
    • Left ventricular hypertrophy (cardiomyopathy)
    • Measure the septum thickness
    • Check valvular function
    • Look for left ventricular function
  • Can help to detect:
    • Damage from a heart attack
    • Heart failure
    • Congenital heart disease - birth defects
    • Endocarditis - an infection of the heart valves
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8
Q

Describe the use of an exercise tolerance test.

A
  • The patient is on treadmill and simultaneously connected to an ECG.
  • In women who are perimenopausal (menopause transition) the test is wrong as many times as it is right (positive predictive value 50%), therefore is not worth doing.
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9
Q

Describe the use of CT coronary angiography.

Give an example of a problem it could identify.

A
  • May identify coronary anomalies that underlie syncope.
    • A coronary artery may come off the wrong cusp, going right around the aorta. During systole, the aorta compresses the coronary artery, compromising blood to the left coronary artery.
    • This can cause chest pain and syncope.
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10
Q

Describe the history of a patient with low risk syncope.

A
  • Associated with prodrome typical reflex syncope: light-headedness, feeling of warmth, sweating, nausea and vomitting.
  • After sudden unexpected sight, sound, smell or pain.
  • After prolonged standing or in crowded, hot places.
  • During a meal or post-prandial.
  • Triggered by: cough, micturition or defecation.
  • With head rotation OR pressure on the carotid sinus (tumour, shaving, tight collars).
  • Standing from supine/sitting position.
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11
Q

Describe the history of a patient with high risk syncope.

A
  • New onset of chest discomfort, breathlessness, abdominal pain or headache.
  • Syncope during exertion when supine.
  • SUDDEN ONSET palpitation immediately followed by syncope.
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12
Q

What syncopal symptoms are associated with minor risk, only if associated with structural heart disease or abnormal ECG?

A
  • No warning of symptoms or short (10s) prodrone.
  • FHx of sudden cardiac death at a young age.
  • Syncope in sitting position.
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13
Q

Describe a low-risk past medical history in a patient with syncope.

A
  • Long history (years) or recurrent syncope with low-risk features with the SAME CHARACTERISTICS of the current episode.
  • Absence of structural heart disease.
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14
Q

Describe a high-risk past medical history in a patient with syncope.

A

Severe structural or coronary artery disease: heart failure, low left ventricular ejection fraction (e.g. 30%, when should be >50%) or previous MI.

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15
Q

Explain what findings on physical examination of a patient with syncope would dennote high risk.

A
  • Unexplained systolic BP in A&E of <90mmHg (hypotension and syncope is bad, usually caused in the elderly by sepsis and medication).
  • Suggestion of GI bleed on rectal examination (PR bleed).
  • Persistent bradycardia (<40BPM) in awake state and in absence of physical training.
  • Undiagnosed systolic murmur - indicated aortic stenosis, or in a younger person may be a mitral murmur, presenting as a systolic murmur that is associated with hypertrophic cardiomyopathy.
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16
Q

What ECG findings associated with a Hx of syncope are high risk (major) findings?

A
  • ECG changes consistent with acute ischaemia.
  • Mobitz II second- and third- degree AV block.
  • Slow AF (<40bpm).
  • Persistent sinus bradycardia (<40BPM), or repetitive SA block or sinus pauses >3 seconds in awake state and in absence of physical training.
  • Bundle branch block, intraventricular conduction disturbance, ventricular hypertrophy or Q waves consistent with ischaemic heart disease or cardiomyopathy.
  • Sustained and non-sustained VT.
  • Dysfunction of an implantable cardiac device.
  • Type 1 Brugada pattern.
  • ST elevation with type 1 morphology in leads V1-V3 (Brugada pattern).
  • QT interval >460ms in repeated 12-lead ECGs indicating LQTS (long QT syndrome).
17
Q

List the avoidance techniques for patients with vasovagal syncope.

A
  • Attention to fluid balance - these syncopal patients do not tolerate dehydration.
  • Educating a patient that frequently experiences pre-syncopal prodrome (light-headedness) in physical counterpressure manoeuvres, that act to increase venous return.
    • Crossing your legs
    • Clenching the muscles in your lower body
    • Squeezing your hands into a fist - increases vasopressor outflow, increasing venous return.
    • Tensing arm muscles.
    • Lying down with feet in the air.
    • Squatting.
  • Fludrocortisone - corticosteroid that has a very high mineralocorticoid activity and increases sodium resorption and therefore boosts BP.
    • Clinical trial data hasn’t shown much better effects than placebo.
  • Syncope is best managed in holistic syncope service.
18
Q

Which factors affect the risk of sudden death in HCM patients?

A
  • FHx of sudden cardiac death during exercise.
  • Syncope
  • Non-sustained ventricular tachycardia
    • 4 ectopic beats in a row = VT
    • Thick, bulky heart does not fill properly during diastole
19
Q

Describe how symptoms can be managed in HCM.

A
  • REFER TO HCM SPECIALIST!
  • Drugs are used for symptom management
    • Anti-cardiac output drugs e.g. beta blockers and calcium antagonist to reduce cardiac output.
  • Septal ablation - cath lab - inject alcohol down the septal arteries to destroy the tissue.
  • Surgical myectomy - open the heart, pass through the aorta and remove several grams of ventricular tissue.
20
Q

Describe the use of ICDs in patients with HCM.

A
  • ICD (implantable cardioverter defibrillator) may be implanted, and is used for survival instead of symptom management.
  • Those with a FHx of sudden cardiac death, syncope upon exertion and with a very thick septum are indicated for an ICD.
  • ICDs are used for primary and secondary prevention:
    • Primary - the patient has had a cardiac arrest or an aborted sudden cardiac death with HCM, and so they are at an increased risk of developing dangerous arrhythmias.
    • Secondary - ICDs are offered to patients with a history of dangeous sustained ventricular arrhythmias.
21
Q

What are the adverse factors of installing ICDs?

A
  • ICDs only last ~5 years before needing to be changed.
    • Putting an ICD in a younger person commits them to a lifelong time of repeated surgical intervention - this must be discussed as part of ‘personalised medicine’.
  • ICDs can occasionally become infected an give the patient endocarditis.
  • Reserve ICD implantation for high-risk patients only.
22
Q

Describe the adaptations of the heart which can be caused by exercise.

A
  • Athletic adaptation:
    • Ejection fraction measures below normal ~40-45% found during an echo at rest.
    • Atrial stretch; atria grow to cope with the increased cardiac output.
    • Left ventricular hypertrophy can be associated with athletic heart.
  • It is difficult in the early stages of syncope presenting to determine if the patient has early dilated cardiomyopathy or just physiological adaptations of the heart to exercise.
23
Q

Describe pacemaker nomenclature.

A
  • First letter is the chamber being paced.
  • Second letter is the chamber being sensed.
  • Third letter is the response to the intrinsic ‘beat’.
  • Fourth letter is for special features:
    • ‘R’ = rate-responsive, meaning that it allows you some fluctuation in your heart rate.
  • Note: the more intrinsic heart activity there is, the better. Becoming pace-dependent is not so good.
24
Q

Describe atrial fibrillation.

A
  • AF is a common abnormal heart rhythm that happens when electrical impulses fire off from different places in the atria in a disorganised way.
  • This causes the atria to twitch and is felt as an irregular pulse.
  • AF is a major cause of stroke due to vegetations forming from stagnant blood in the atria, forming thrombi that can enter the brain via the internal carotid.
25
Q

Describe atrial flutter.

A
  • The electrical impulses from the SA node form a smaller circuit in the atria, instead of travelling to the AV node.
  • These impulses circulate very fast around the atria, causing ~300bpm instead of the usual 60-90bpm.
  • The ventricles cannot pump that fast, causing the atria and ventricles to contract at different speeds, putting the heart under strain.
  • Thrombi can form in the atria and cause a stroke.
26
Q

What is second-degree heart block?

A
  • Second-degree AV heart block happens when one or more (but not all) of the atrial impulses fail to conduct to the ventricles due to impaired conduction.
  • There are 2 types of second-degree heart block:
    • Mobitz II - the heart skips beats in a regular pattern; the body can usually cope well with this, so patients do not usually have symptoms.
    • Mobitz II - the heart skips beats in an irregular pattern; the body cannot compensate for this and this type of heart block can lead to presyncope, dizziness and syncope.
  • Causes of second-degree heart block:
    • Underlying heart condition
      • Coronary heart disease
      • Cardiomyopathy
      • Congenital heart disease
27
Q

What is third-degree heart block?

A
  • Referred to as ‘complete heart block’ - the most serious type of AV heart block.
  • It occurs when the SA node electrical impulse does not pass to the AV node.
  • A back-up system will take over (myocytes can intrinsically generate their own electrical rhythm), but the ventricles will beat too slowly to meet the oxygen demands of the body.
  • Causes of complete heart block:
    • Most people with complete heart block have an underlying heart condition:
      • Coronary artery disease
      • Cardiomyopathy
      • Congenital heart disease
28
Q

What are the symptoms of complete heart block?

A
  • Dizziness
  • Syncope
  • Tiredness
  • Breathlessness
  • Oedema
29
Q

What are the different types of heart block?

A
  • Atrioventricular heart block
    • First degree
    • Second degree
    • Third degree
  • Bundle branch block
    • Left
    • Right
  • Tachybrady syndrome
30
Q

Describe the difference between first- second- and third- degree AV block.

A
  • First-degree
    • Usually does not cause any symptoms or need treatment.
      • The PR interval is lengthened beyond 0.2 seconds.
  • Second-degree
    • Some, but not all of the SA node electrical impulses fail to conduct to the ventricles.
  • Third-degree
    • Complete heart block.
31
Q

Describe bundle branch blocks.

A
  • A defect of the bundle branches of fascicles in the electrical conduction system of the heart.
  • Left BBB - usually caused by an underlying condition, such as:
    • Congenital heart disease
    • Cardiomyopathy
    • Left ventricular hypertrophic cardiomyopathy
    • Ageing of the electrical pathway in the heart
  • Right BBB - can be caused by congenital heart disease, or some lung conditions.
    • It can also happen naturally in people with a normal heart and no heart problems.
32
Q

Describe tachybrady syndrome.

A
  • If the SA node does not work properly, it can cause the heartbeat to become too fast or too slow, or switch between fast and slow rhythms.
    • e.g. atrial flutter alternating with a slow heart rhythm.
33
Q

Describe the use of ILRs.

A
  • ILRs (Implantable Look Recorders) are used if the patient has symptoms such as palpitations, dizzy spells or blackouts that may not happen very often, a small USB-sized stick is implanted and records the heart’s electrical activity.
  • Battery lasts up to 3 years, and so is useful if an ECG has not been able to determine the cause of symptoms.
  • Collects arrhythmic data.
34
Q

Describe the action of ICDs.

A
  • ICDs are used to detect ventricular tachycardia or ventricular fibrillation.
  • ICDs deliver shocks or ATP (anti-tachycardic pacing) when the heart is in VT - 30 joule shock is delivered, and keeps delivering a cycle of ATP, followed by a shock until the patient is successfully cardio-converted back to a normal sinus rhythm.
  • CPR can be delivered to the patient during the ICD shock.
35
Q

Describe the use of CRTs.

A
  • Cardiac resynchronisation therapy is offered if the patient has a broad QRS complex secondary to heart disease or an MI damaging the left ventricle.
  • One way to resynchronise the QRS complex to make the heart ejection more physiologically normal is to PACE BOTH VENTRICLES.
    • Simultaneous pacing of both ventricles results in a more efficient ventricular contraction, thus improving the ventricle ejection.
36
Q

Describe the role of CRT in heart failure.

A
  • When the heart becomes enlarged in heart failure, its electrical circuits can become stretched, leading to communication breakdown between different parts of the heart.
    • This disrupts the normal coordinated cotraction of the heart, making it inefficient.
  • A CRT-P (also called a biventricular pacemaker) can be implanted that it sends small electrical impulses to both ventricles to help them to contract at the same time.