The cardiovascular system - Arrhythmias, syncope and arrest Flashcards

Question

What is an alternative treatment to long-term anti-arrhythmic drugs to maintain sinus rhythm?

Answer 1

Catheter ablation

Answer 2

It involves passing a small catheter via a transferral venous approach to eventually reach the left atrium Several mechanisms (e.g., radio-frequency ablation or cyroablation) may then be used to damage left atrial tissue and prevent electrical transmission This is predominately focused around area where AF is 'triggered' such as the pulmonary vein

Answer 3

1. Perform a clinical assessment (ABCDE) and determine haemodynamic stability - Haemodynamic stability: emergency DC cardioversion - Haemodynamic stability: rate or rhythm control strategies 2. In patients who are stable, the key determinant to further management is precise time of onset. This is because cardioversion is associated with an increased risk of embolic events - Onset > 48 hours: increased risk of thromboembolism. Patients need adequate anticoagulation (minimum 3 weeks) to reduce thromboembolic risk prior to cardioversion - Onset < 48 hours: low risk of thromboembolism. Patients' can be considered for immediate electrical or pharmacological cardioversion

Answer 4

If unstable then immediate help emergency cardioversion If stable check anticoagulation status. If therapeutic then immediate or delayed cardioversion If no anticoagulation status then initiate anticoagulation. If onset <48 hours then do early cardioversion. If onset > 48 hours then do elective cardioversion (min. 3 weeks)

Answer 5

This is because cardioversion is associated with an increased risk of embolic events. Therefore time of onset determines whether anticoagulation is required. If onset <48 hours then low risk of thromboembolism so you can then do early cardioversion If onset > 48 hours then high risk of thromboembolism so anticoagulation for a minimum of 3 weeks is required. Therefore you'll do an elective cardioversion (min. 3 weeks)

Answer 6

CHA2DS2-VASc score

Answer 7

a) C- Congestive heart failure +1 H - Hypertension +1 A - Age 75 years or older +2 D - Diabetes +2 S - Stroke, TIA or thromboembolism previously +1 b) Va - vascular disease (previous MI, PAD, or aortic plaque)+1 A- Age 65-74 years +1 Sc - Sex category (female) +1 b) Anticoagulation should be considered in men with a score of 1 and greater Anticoagulation should be considered in females with a score of 2 or greater c) DOAD

Answer 8

Vitamin k antagonist e.g., warfarin

Answer 9

ORBIT score

Answer 10

a) O - older age > 74 +1 R - reduced haemoglobin +2 B - bleeding history (GI bleeding, intracranial bleeding, haemorrhagic stroke) +2 I - insufficient kidney function +1 T - treatment with antiplatelets +1 B) Score of 4-7 is considered high risk, 3 is medium risk and 0-2 is low risk

Answer 11

- Patients with infrequent paroxysmal may be treated with a 'pill-in-pocket' regimen - Patients can self-administrate of flecainide or sotalol at the onset of AF to induce pharmacological cardioversion

Answer 12

a) - Heart failure - Tachycardia-induced myopathy - Ischaemia - Sudden cardiac arrest b) - Thromboembolic events: stroke, TIA, mesenteric ischemia, limb ischaemia - Bleeding events

Answer 13

- Hypertension - Diabetes mellitus - Obesity - Obstructive sleep apnea (OSA) - Smoking - Alcohol

Answer 14

- Blood pressure control - Weight reduction - Lipid control - Blood sugar level control - treat/manage obstructive sleep apnea - Smoking cessation - Alcohol reduction

Answer 15

- Sinus tachycardia - AF - Atrial flutter - Focal atrial tachycardia - Atrioventricular re-entrant tachycardia (AVRT) - Atrioventricular nodal re-entrant tachycardia (AVNRT)

Answer 16

- Ventricular tachycardia - Ventricular fibrillation - "SVT" with aberration - Pre-excited tachycardia - Pacemaker associated tachycardia

Answer 17

QRS complex shorter than 120 ms (three small squares on the ECG)

Answer 18

1. Patients should be assesses using the ABCDE approach 2. If haemodynamically unstable (shock, syncope, acute pulmonary oedema or myocardial ischaemia) then emergency DC cardioversion required 3. Haemodynamically stable and regular rhythm (SVT) - vagal manoeuvres (carotid sinus massage or valsalva manoeuvre) - If that fails then administer adenosine (initially 6mg iV bolus, if this fails 12mg followed by a further 18mg) - asthma, COPD and heart failure and some of the contraindications for using adenosine so verapamil 2.5-5mg instead 4. Haemodynamically stable and irregular - most likely AF - onset <48 hrs usually managed with rhythm control - onset >48 hrs usually managed with rate control

Answer 19

a) Asthma, COPD, decompensated heart failure b) verapamil 2.5-5mg

Answer 20

a) An increase in the heart rate to more than 100 bpm in adults. Normal sinus rhythm is observed b) - Majority of patients (90%) are female - Peak incidence of 38 years old c) Common causes: - Physiological: exercise, pain, anxiety, pregnancy - Drugs: adrenalines, salbutamol, antihistamines, tricyclic antidepressants - Pulmonary embolism Other causes - Cardiac: heart failure, ischaemic heart disease, cardiomyopathies - Metabolic - hyperthyroidism, anaemia - Infection - Substances - cocaine, amphetamines, cannabis, caffeine - Psychological - anxiety d) Increased automaticity because of sympathetic activation and/or parasympathetic inhibition e) May present with palpitations, breathlessness, and light-headedness f) - Rate of more than 100 bpm - Normal visible p waves often buried in preceding t waves ('camel hump' appearance) g) - Treat underlying cause for remove offending agent - Pharmacological therapy: beta-blockers or ivabradine may be used in symptomatic patients with chronic sinus tachycardia - Surgical: radiofrequency ablation of SA node is performed if patient is resistant to medical therapy. The treatment modality for sinus tachycardia are exceedingly rare h)

Answer 21

a) An increase in the heart rate to more than 100 bpm in adults. Normal sinus rhythm is observed b) - Majority of patients (90%) are female - Peak incidence of 38 years old c) Common causes: - Physiological: exercise, pain, anxiety, pregnancy - Drugs: adrenalines, salbutamol, antihistamines, tricyclic antidepressants - Pulmonary embolism Other causes - Cardiac: heart failure, ischaemic heart disease, cardiomyopathies - Metabolic - hyperthyroidism, anaemia - Infection - Substances - cocaine, amphetamines, cannabis, caffeine - Psychological - anxiety d) Increased automaticity because of sympathetic activation and/or parasympathetic inhibition e) May present with palpitations, breathlessness, and light-headedness f) - Rate of more than 100 bpm - Normal visible p waves often buried in preceding t waves ('camel hump' appearance) g) - Treat underlying cause for remove offending agent - Pharmacological therapy: beta-blockers or ivabradine may be used in symptomatic patients with chronic sinus tachycardia - Surgical: radiofrequency ablation of SA node is performed if patient is resistant to medical therapy. The treatment modality for sinus tachycardia are exceedingly rare

Answer 22

a) Atrial tachyarrhythmia which is characterised by a regular, rapid atrial rate b) - Less common than AF - More common in males - Incidence increase with age c) Common causes - Right atrial dilatation: pulmonary embolus, mitral and/or tricuspid pathologies, congestive heart failure - Ischaemic heart disease - Idiopathic - Normal variant: tall males - Patients with a history of endurance sports (causing atrial enlargement) Other causes - Drugs: flecainaide, propefoneone - Metabolic disturbances: hyperthyroidism, alcohol - Iatrogenic: previous catheter ablation, cardiac surgery d) Macro re-entrant circuit within the right atrium, most commonly around the tricuspid annulus in an anti-clockwise fashion. This results in a rapid regular atrial activity at a rate of around 300 bpm e) - Breathlessness - Palpitations - Syncope - Severe dysponea f) - Narrow complex tachycardia with a classic atrial rate of 300bpm - Regular 'sawtooth' pattern of future waves - Fixed conduction ratios (2:1, 3:1 etc) g) - Adenosine unmasks flutter waves - Management is similar to AF so first-line is beta-blockers - Radiofrequency ablation highly recommended in patients with chronic atrial flutter

Answer 23

a) A type of paroxysmal supraventricular tachycardia (SVT) caused by an aberrant circuit within the AV node b) - Most common cause of paroxysmal SVT - Female predominance c) Idiopathic d) - In AVRNT, a re-entrant circuit occurs within the AV node - It most commonly involving dual pathways of different conduction velocities (i.e., a slow and fast pathway) - Typically, a conduction via the slow pathway will be anterograde (forward direction) and retrograde (backward direction) - In AVNRT every time it goes around the circuit an electrical signal is fired down into the ventricle (slow pathway), which depolarises normally, and backwards up into the atrium (fast pathway) which depolarise with an inverted p wave - This leads to depolarisation of ventricle and atrium at the same time - This is known as the slow-fast type and is the most common cause of AVRNT observed in clinical practice e) - Sudden onset of rapid palpitations - Dizziness - Breathlessness - Syncope occasionally occurs f) - Regular narrow complex tachycardia - P waves may not visible as they buried in QRS complexes g) - Some AVNRTs can be terminated by vagal manoeuvres - IV adenosine or rate-limiting calcium channel blockers may be used if vagal manoeuvre fails - In emergencies, when patients present with haemodynamic compromise, DC cardioversion is advised - Catheter ablation - indicated in patients with recurrent episodes; associated with a less than 1% risk of heart block

Answer 24

a) - A form of paroxysmal SVT caused by anatomically defined re-entrant circuit involving one or more accessory pathways b) - Wolff-Parkinson-White (WPW) syndrome often leads to AVRT - 60-70% of patients with WPW have no evidence of heart disease c) - Congenital - Associated with hypertrophic cardiomyopathy and Epstein's anomaly d) - Accessory pathways (e.g., Bundle of Kent in WPW) are fibres of abnormal myocytes extending across the atrioventricular groove forming an aberrant connection between the atria and ventricles - This results in an anatomical re-entrant circuit comprising the normal AV conduction system and the accessory pathway - Therefore a beat arises in atrium and conducted into ventricles but then goes back up through accessory pathway into the atrium and depolarises it e) - Palpitations - Chest pain - Syncope f) - 'Delta' wave (slurring of the QRS uspstroke) - Short PR interval (<0.2 s) g) - In the acute setting vagal manoeuvre, IV adenosine and procainamide or rarely DC cardioversion may be used to terminate the tachyarrythmia - Flecainide and amiodarone may also be useful in the acute setting - Catheter ablation of the accessory pathway is the definitive therapy

Answer 25

In AVRT retrograde p wave is usually more distinct from the QRS complex than in AVRNT (this is because of sequential depolarisation of the atrium and ventricle)

Answer 26

Accessory pathways do not have that time delay property that AV nodes so there is rapid conduction of accessory pathways

Answer 27

Catheter ablation of the accessory pathway

Answer 28

Orthodromic - most common type that involves anterograde conduction via the AV node (down AV node) and retrograde conduction via the accessory pathway (back up the accessory pathway) -> narrow QRS complex Antidromic - anterograde conduction occurs via the accessory pathway and retrograde conduction through the AV node -> broad QRS complex

Answer 29

a) VT refers to tachyarrhthmias that originate from the ventricles producing three or more successive broad QRS complexes at a rate of more than 100 beats per minute b) Peak incidence in middle-aged patients c) Common causes - Ischaemic heart disease: scarring post MI - Structural heart disease: cardiomyopathies, valvular heart disease - Electrolyte disturbances: hyper-/hypokalaemia, hyper-hypomagneasaemia Other causes - Drugs and substances - digoxin toxicity, cocaine - Channelopathies - long QY syndrome, Brugarda syndrome - Idiopathic d) 1. Re-entrant circuit (most common) - usually due to post-MI scarring 2. Trigger activity 3. Increase automaticity

Answer 30

a) Haemodynamically stable patients - Palpitations - Dizziness/light-headedness - Syncope Haemodynamically unstable patients (severely hypotensive and tachycardia) - Low cardiac output symptoms: severe dyspnoea, dizziness, syncope - Eventually leading to cariogenic shock and cardiac arrest b) - JVP may be elevated, - Intermittent cannon A waves may be seen

Answer 31

- Broad QRS complexes (>0.12s) - Slurred initiation of QRS - Positive/negative concordance - Basically regular - Extreme axis - Not a typical bundle branch block - AV dissociation - Fusion beat (a P wave happens to get conducted through the AV node to start depolarisation of the ventricles via the conduction tissue at the same time as a beat of VT, giving a combination of the two, which is narrower than a normal VT complex) - Capture beat (a P wave is conducted through the AV node time exactly so that it depolarises the ventricle normally)

Answer 32

a) A scar at back of the heart will cause all depolarisation to be towards the chest leads V1 to V6, which will be positive in polarity - hence "positive concordance" A scar on the anterior surface will cause depolarisation away from all the chest leads - hence "negative concordance" b) Not essential to diagnose VT - but if it is present, it make VT more likely

Answer 33

a) 1. Immediate resuscitation (100-230 chest compressions with 2 rescue breaths) - if no pulse 2. Emergency DC cardioversion - synchronised shock recommended if there is a pulse 3. After seeking expert help, amiodarone (300mg IV over 10-20 minutes, followed by 900mg over 24 hours) should be administrated 4. ICD implantation b) Management deepends on underlying cause: 1. IV amiodarone (non-idiopathic VT)  300 mg IV over 20-60 minutes followed by 900 mg over 24 hours 2. Elective synchronised DC cardioversion may be indicated if resistant to medical therapy c) Non-idiopathic VT - consider ICD or catheter ablation (patients with structural heart disease) Idiopathic VT - pharmacological therapy (beta-blockers, rate-limiting calcium channel blockers) may be considered

Answer 34

a) A form of polymorphic VT associated with a prolonged QT interval. Torsos de pointes is French for "twisting of the point" b) Female predominance (females have a longer baseline QT interval) c) - Congenital long QT syndrome - Acquired QT syndrome e.g., electrolyte imbalance - Drugs e.g., clarithomycin and fluoxetine d) Derangeemnt of cardiac ions, particularly sodium, potassium and calcium increase the duration of action potential, resulting in early after-depolarisation e) - Usually asymptomatic - Commonly presents with self-limiting episodes of palpitations, light-headedness or syncope f) - Broad QRS comps - Peaks of the QRS twist around the isoelectric line (corkscrew appearance) - Irregular intervals - Tachycardia with ventricular rate of 160 to 250 bpm - Prolonged QTc g) - Treat underlying cause - IV magnesium sulphate (given as a slow infusion) - 2mg magnesium sulphate over 10 mins IV if no adverse effects - If resistant to medical therapy, consider temporary pacing - If patient is haemodynamically unstable, non-synchronised electrical cardioversion may be indicated

Answer 35

a) - An autosomal sodium channelopathy associated with sudden cardiac deaths - Defective sodium channels impair influx of sodium ions resulting in shorter action potentials b) - Most prevalent in Asia - High male predominance (8:1) c) - Syncope and cardiac arrest in otherwise normal asymptomatic panic d) 'brugarda' sign -> downscoping coved ST elevation followed by an inverted T wave - only presents in leads V1 and V2 d) - ICD implantation is the only definite treatment

Answer 36

a) A rapid, uncoordinated and life-threatening arrhythmia resulting in more myocardial contraction, eventually leading to cardiac death b) Has a bimodal distribution peaking at under 6 months and 45-75 years c) Common causes - Ischaemic heart disease - Electrolyte abnormalities (particularly hypokalaemia) - Idiopathic Other causes - Long QT syndrome - Structural heart disease - Systemic - PE, sepsis d) - Multiple wavelets – continuous micro re-entrant circuits are formed within the ventricles - Very rapid (up to 500 bpm) irregular electrical activity results in unsynchronised ventricular contractions - Cardiac output will be significantly reduced and ultimately the patient will go into cardiogenic shock e) - Chaotic waveforms with varying amplitude - Unidentifiable P waves, QRS complexes or T waves f) i) Immediate management - adavancec cardiac life support - most important shockable rhythm - IV amiodarone (1st line) or procainamide (2nd line) can be sued as a last resort if all measures have failed ii) Long-term management - ICD insertion - Amiodarone may be used when ICDs are contraindicated

Answer 37

Atrial flutter should always be suspected in tachycardias with a fixed atrioventricular conduction ratio (2:1). Atrial flutter classically produces an atrial rate of approximately 300 bpm and a ventricular rate of 150 bpm So if heart rate is exactly 150 bpm - think atrial flutter

Answer 38

a) Block the AV node b) i) Adenosine blocks the AV node, and you can see the the atrial activity underlying, but does not terminate the tachycardia e.g., AF, atrial flutter ii) Adenosine terminates tachycardia e.g., AVNRT, AVRT iii) Adenosine has no effect on tachycardia e.g., VT

Answer 39

Only the SA and AV nodes are well supplied by parasympathetic nerves. The rest of the cardiac conduction system (bundle of His, left and right bundle branch and purkinje fibres ) is supplied by sympathetic nerves

Answer 40

Fastest: SA node Second fastest: AV junction Slowest: Purkinje network

Answer 41

Heart rate < 60 bpm

Answer 42

Physiological - Sleep - High level athletic conditioning Pathological - Congenital - Acquired e.g., degenerative, ischaemic heart disease, drugs, electrolyte/metabolic, infection, (e.g., endocarditis), iatrogenic (ablation, cardiac surgery), infiltrative diseases (e.g., sarcoid, amyloid), neuromuscular disease (e.g., myotonic dystrophy)

Answer 43

- Fatigue - Difficult concentrating - Exercise intolerance - Falls - Syncope - Breathlessness - Dizziness

Answer 44

a) A group of arrhythmias due to a syndrome of SA node dysfunction that encompasses sinus bradycardia, sinus pause and sinoatrial block b) Common causes - Idiopathic fibrosis of the SA node (because of ageing) - Myocardial ischaemia Other causes - Infiltrative conditions: sarcoidosis, amyloidosis - Drugs: beta-blockers, digoxin, calcium channel blockers, amiodarone - Metabolic: hypothyroidism, hyperkalaemia c) Degenerative and ischaemic changes in the SA node, nerve supply, and the surrounding atrial tissue can result in abnormalities of impulse formation, conduction or both c) - Chronic frequent episodes of intermittent bradycardia and tachycardia - Fatigue - Palpitations - Dizziness - Syncope d) - Treat underlying cause of present - IV atropine may be useful in patients with severe symptoms - Dual chamber pacemaker implantation recommended for patients with symptomatic chronic disease

Answer 45

a) Delayed atrioventricular conduction resulting in a constant prolong PR interval (>0.2s) on ECG b) Commonly affects patients over age of 65 c) Common causes - Idiopathic degeneration (fibrosis) of the conduction system - Physiologcal: ncreased vagal tone (e..g, athletes, during sleep) - Myocardial ischaemia (RCA supplies the AV node e.g., inferior MI) - Drugs (beta-blockers, calcium channel blockers, digoxin) d) Usually, asymptomatic e) - Prolonged PR interval - Sinus rhythm f) Benign condition, treatment is not usually required g) Normal, although some patient will progress to higher degrees of AV block over time

Answer 46

a) Atrioventricular conduction deficit resulting in progressive prolongation of the PR interval until one p wave is not followed by a QRS complex b) - Occurs in 45% of post-inferior MI - More common than Mobitz type II c) Common causes - Idiopathic fibrosis of conduction system - Drugs (beta-blockers, calcium channel blockers, digoxin, procainamide) - Increased vagal tone – athletics, children, during sleep Other causes - Iatrogenic – transcatheter aortic valve implantation (TAVI) - Post-Inferior MI d) - Caused by progressive induction block, more commonly within the AV node itself (70%) and sometimes distally in the conduction system (30%) e) - Progressive prolongation of the PR interval until QRS is not followed - Narrow QRS complex - PR interval longest before the dropped beat (QRS and shortest after f) - Treatment not usually required unless symptomatic - IV atropine ma be used in emergency situations of severe Brady cardia - Permanent pacemaker implantation is indicated in patients with non-resolving symptomatic block

Answer 47

a) An atrioventricular conduction deficit resulting in intermittent dropped beats without changes in the PR interval, until one p wave is not followed by a QRS b) Common causes - Idiopathic fibrosis of the conduction system - Anterior MI Other causes - Drugs (beta-blockers, calcium channel blockers, digoxin) - Infiltrative disease (sarcoidosis, amyloidosis, hemachromatosis) c) In contrast Mobitz type I, the conduction block in kibitz type II tends to occur infra-nodally, in the His bundles (20%) or Purkinje fibres (80%) d) - Dizziness - Syncope - May present with haemodynamic instability and sudden cardiac death in some cases e) - Constant PR interval and then a p wave is not followed by QRS - QRS complex may be broad if the AV block occurs at the Purkinje fibres - May be associated with a fixed ration 2:1, 3:1 etc f) i) Treat haemodynamic compromise with: 1. IV atropine 2. IV adrenaline 3. IV isoprenaline infusion 4. If all measures fail, and permanent pacing is not immediately consider temporary external pacing ii) Permanent pacemaker implantation is indicated for all patients (even as asymptomatic patients) g) - Commonly progress to third degree heart block

Answer 48

a) Refers to complete failure of the AV conduction system resulting in a loss of communication between the atria and ventricles, causing them to beat independently of one another b) Common causes - Idiopathic degeneration of the conduction system (ageing) - Anterior and inferior MI - due to interruption of the blood supply to the AV node - Drugs (beta-blockers, calcium channel blockers, digoxin, anticholinesterase inhibitors e.g., Donepezil) Other causes - Congenital: maternal SLE - Iatrogenic: cardiac surgery, cardiac catheterisation c) - Complete failure of the AV conduction system results in complete AV block - Latent pacemaker cells in the His-purkinje fibres system will resume the role of the AV node as a physiological compensatory mechanism to ensure ventricular contractions and maintain cardiac output. d) - Symptoms of low cardiac output: dizziness, breathlessness, fatigue - Stokes-Adams attacks 9episode of syncope characterised by a sudden unexpected collapse, accompanied by a transient loss of consciousness - Palpitations e) - Rate tends to be less than 50bpm - Constant P-P and R-R intervals but apparent AV dissociation - QRS complexes may be narrow (junctional escape rhythm) or wide (subjuntional escape rhythm) f) i) 1. Emergency iV atropine 2. IV isoprenaline infusion ii) - Correct reversible causses - Permanent pacemaker implantation is indicated for all patients

Answer 49

1. Assess with ABCDE approach 2. Give oxygen if appropriate and obtain IV access 3. Monitor ECG, BP, SpO2, record 12-lead ECG 4. Identify and treat reversible causes e.g., electrolyte abnormalities 5. If evidence of life threatening signs (shock, syncope, MI, HF) - atropine mcg IV and if no satisfactory response interim measures: atropine 500 mcg IV repeat to maximum 3 mg, isoprenaline 5 mcg min-1 IV, adrenaline 2-10 mcg min-1 IV, alternative drugs or transcutaneous pacing. If that fails the seek expert help and arrange transvenous pacing 6. If no evidence of life threatening signs and risk of a aystole (recent asystole, mobitz II AV block, complete heart block with broad QRS, ventricular pass > 3 s) then carry out interim response. If no risk of asystole, then observe 6. Alternatives include: Aminophyline, dopamine, glucagon (if beta-blockers or calcium channel blocker overdoes), glycopyrrolate can be used instead of atropine

Answer 50

Devices that we implant for either diagnosis or treatment of cardiac arrhythmias and unexplained syncope

Answer 51

a) Loop reorder b) - Permanent pacemaker - Implantable cardioverter defibrillator (ICD) - Cardiac resynchronisation therapy (CRT)

Answer 52

a) Delivers overdrive pacing and/or DC shocks to restore sinus rhythm b) Used to treat ventricular tachyarrhythmias and primary and secondary prevention of sudden cardiac deaths c) Single chamber (RV), dual chamber (RA and rv)

Answer 53

Primary prevention of sudden cardiac death from ventricular arrhythmias - Severe LV impairment - Inherited cardiac conditions Secondary prevention of sudden cardiac death from ventricular arrhythmias - Survivor of VF/VT - Cardiac arrest - Sustained VT with haemodynamic compromise - Sustained VT and severe LF impairments

Answer 54

1. The first thing the ICD looks at is the heart 2. If this is above a certain threshold (e.g., 200 bpm) then the ICD will deliver a shock 3. If the heart rate is not quite as high but still fast (e.g., above 180bpm) the ICD will look at other parameters including: - how did the arrhythmia start? (was it gradual or sudden) - Is it regular or irregular? - is the QRS narrow or broad?

Answer 55

In conventional ICDs the leads can become damaged and may not be straightforward to removed They are overcome by subcutaneous ICD - which are easier to remove

Answer 56

ICD deactivation involves turning off shock therapies. This is best done by pacing physiologists. But in an emergency a doughnut magnet can be strapped over the ICD

Answer 57

An electronic device that regulates the heart rate. It consists of a generator (battery and circuit) and pacing leads (insulated electrodes)

Answer 58

1. To detect the patient's own intrinsic impulses - "Sense" 2. To depolarise the heart if there isn't any impulses - "Capture"

Answer 59

1. Temporary pacing 2. Permanent pacemaker

Answer 60

1. Transvenous 2. Transcutaneous

Answer 61

a) Prevent bradycardia b) Sinus node disease and AV node disease (conduction block) c) - Single chamber (RA or RV) - Dual chamber (RA and RV)

Answer 62

a) Ventricle (V) b) Ventricle (V) c) Inhibited (I) = VVI pacemaker

Answer 63

a) Atrium and ventricle (D) b) Atrium and ventricle (D) c) Inhibited or triggered (D) = DDD pacemaker

Answer 64

Traditional pacemakers can become infected and leads can fail overtime This is overcome by headless pacemakers

Answer 65

1. To detect the patient's own intrinsic impulses "Sense" 2. Tod polarise the heart if there isn't any impulses "Capture"

Answer 66

The pacemaker senses the patient's own natural heartbeat and withholds the heartbeat 2. It then sets a timer and if that timer expires without it seeing any electrical activity in that chambers of the heart, then it will stimulate that chamber of the heart to depolarise (capture) 3. There will be a pacing spike followed by a broad QRS

Answer 67

Pacing spikes preceding the p wave

Answer 68

a) - Pacing spikes preceding the QRS complexes. - Broad QRS complexes with an rS' in V1 and notched R wave in V6 (In right ventricular pacing the QRS morphology is similar to left bundle branch block ) (William marrow -W complex in V1 and M shaped complex in V6) b) - Pacing spikes preceding QRS complexes - Broad QRS complexes with an rSr' pattern in V1 (In left ventricular pacing the QRS morphology is similar to right bundle branch block ) (wiliam marrow -M complex in V1 and normal/slurred S in V6)

Answer 69

May be features of atrial pacing - pacing spikes preceding p wave May be features of ventricular pacing - pacing spikes preceding QRS complex May eb features of atrial and ventricular pacing

Answer 70

a) Co-ordinates and synchronise atrial RV and LV contractions b) Heart failure c) - CRT pacemaker - CRT ICDs for patients at high risk of ventricular arrhythmias

Answer 71

The abrupt cessation of activity of the heart, with subsequent loss of cardiac output and haemodynamic collapse

Answer 72

Shockable - VF - Pulseless VT Non-shockable - Pulseless electrical activity - Systole

Answer 73

- Patients lose consciousness within 10-15 seconds secondary to cerebral hypoxia - Rarely symptoms prior to arrest

Answer 74

- CPR - Early defibrillation (if shockable rhythm - VF/ pulseless VT) - Maintain oxygenation

Answer 75

Two questions: what is the cause? Is it reversible? - if yes treat reversible cause History - of the event, PMH, Family Tests - ECG, Echo, Monitoring, imaging (angio/CT/MRI)

Answer 76

4 H's - Hypoxia - Hypovolaemia - Hypothermia - Hyper/hypokalaemia & hypocalcaemia 4 T's - Tension pneumothorax - Tamponade - Toxins - Thrombo-embouls