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39 Cards in this Set
- Front
- Back
Heart beat. What are the following
- P - QRS - T - PR - QT |
- P: atrial depolarisation
- QRS: ventricular depolarisation - T: ventricular repolarisation - PR: atrial activation to the start of ventricular activation - QT: to the end of T: ventricular depolarisation |
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What are the steps involved in the depolarisation of a heart cell?
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There are voltage gated sodium and calcium channels. The calcium channels are also time dependent (slow depolarising)
Late repolarisation makes resistant to depolarisation (absolute refractory period) |
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Persistent bradycardia (eg. "sick sinus syndrome")
- What causes it? - What is the treatment? |
Caused by damage to impulse formation or conduction (either pacemaker cells: AV node or SA node or Bundle of His or Purkinje system)
Treat by: 1. prefer a pace maker 2. atropine (short acting) 3. isoprenaline (infusion) |
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What is Torsades des pointes?
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Type of VT
Has a long QT interval Almost always due to medications |
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What drugs prolong QT interval?
What else prolongs QT interval? |
- genetics, electrolyte disurbances, heart disease
- amiodarone, sotalol - antipsychotics: amisulpride, droperidol, haloperidol and pimozide - TCAs - anti-infectives: clarithromycin, erythromycin, moxifloxacin, quinine, chloroquine, fluconazole, voriconazole, pentamidine - cisapride, dolasetron, methadone, tacrolimus, vardenafil |
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Sinus tachycardia - cause and treatment?
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Usually a physiological response to precipitants such as pain, hypovolaemia, pyrexia, anxiety, but may be due to sympathomimetic drugs or thyrotoxicosis. If there is no obvious cause, drug treatment is not necessary unless symptoms are troublesome, in which case beta-blockers or controlled release verapamil can be used.
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AF
(a) complications (b) symptoms (c) cause (d) result (e) epidemiology (f) diagnosis |
(a) stroke, HF
(b) often asymptomatic, may have palpitations, fainting, dyspnoea (c) generally a re-entry problem, where there is circular impulse propagation in the atria (d) the atria do not contract in a coordinated or useful fashion; the ventricles beat irregularly (e) 10% of people over 80 y/o have AF (f) ECG, echocardiogram, TFTs |
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Rate versus Rhythm contol: when to use which?
Rate control of AF - what goal? - which drugs? - what goal? |
Both are first line. Rhythm might be attempted for a once-off AF, or where there is symptomatic AF. However, if there is persistent or permanent AF, use rate control first because its just as effective with less side effects.
Rate control: Aim: <90bpm at rest, <180 at exercise to prevent HF and control symptoms. Use: 1. BB 2. Verapamil/diltiazem 3. Digoxin (less effective, may be used if there is also HF) 4. Combinations (not BB and verapamil) 5. Amiodarone - specialist territory |
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How do you do rythm converstion?
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1. Anticoagulate
2. Short term control of ventricular rate is usually done with a beta-blocker or verapamil (rather than digoxin) to avoid post-conversion digoxin arrhythmias. 3. It's called DC Cardioversion rather than DC defibrillation (because they are not in VF) - use IV analgesia and sedation because painful and frightening |
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DC cardioversion doesn't work or is CI, use chemical cardioversion. Which drugs are used?
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Flecainide, disopyramide, sotalol and amiodarone can be used. Amiodarone is considered to be the safest agent in heart failure.
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Atrial flutter
(A) what is it (b) management |
Different from AF in that there IS a regular heart beat. It's just very fast. It's different from sinus tacchycardia, in that the beat arises from an ectopic source in the atrial muscle. Rythm can be 250-450bpm.
DDX: AF, but does not respond well to digoxin Tm: Adenosine, verapamil or a beta-blocker may be effective. Also, treat the cause. |
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Cardiac arrest: VF
- treatment? |
CPR, intubate with CPAP at 100% oxygen
Defibrillate @ 200J and increase; attempt 3x at maximum Joules Give adrenaline 1mg IV - give intratracheal if no venous access Then give amiodarone, sotalol or lignocaine with adrenaline (alternate) & DC CARDIOVERSION Stabilise with amiodarone/sotalol or (second line) atenolol/metoprolol - The dosage is ?? symptom relief may not = VF relief |
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Cardiac arrest: Asystole
- treatment? |
Very poor prognosis
CPR, CPAP, adrenaline |
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When do you use
- pacemakers - Implantable cardioverter defibrillators |
- bradycardia, some tachyarrhythmias (overdrive pacing)
- VTs, VF episode, HF |
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Anti-arrythmics
- drugs not in classes - class 1 drugs - class 2 drugs - class 3 drugs - class 4 drugs |
- digoxin and adenoside
Class 1: blocks Na channels (membrane stabilising) 1a: intermediate & also blocker K channels, prolongs QT interval (quinidine, procainamide, disopyramide) 1b: fast (only at fast heart rate - less potent) (phenyoin, lignocaine, mexiletine) 1c: slow (very potent) (Flecainide, propafenone) **1a,c for SVTs **1b for SVTs and VTs Class 2: Beta blockers *SVTs and VTs Class 3: K channel blockers (prevent depolarisation) *Sotalol, Amiodarone, Bretylium *Increase repolarisation, prolongs QT interval and refractory period * SVTs and VTs Class 4: Ca channel blockers *Useful for SVTs |
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How does digoxin work?
How does potassium interact with digoxin? How do you treat digoxin OD? |
Digoxin
1. Inhibitos Na-K-ATPase: increases Ca2+ release from SR: positive chronotropic effect; also increases extracellular K+ (worrisom in OD) 2. Increases vagal tone (negative chronotropic effect) - at high concentrations increases SNS --> arrythmia - Potassium decreases binding of digoxin to Na-K-ATPase - Low K+ can lead to toxicity in therapeutic range - High digoxin increases extracellular K Give IV atropine and/or Magnesium. Monitor vitals. Give Digoxin antibodies in severe cases. Adenosine - temporarily blocks AV nodal conduction |
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Digoxin
- Indications - Precautions (remember its MOA and when it might not work) - Preg/BF |
Digoxin
Indications: SVT, AF, atrial flutter, HF & fetal arrythmias Precautions: - heart block, - VF/VT/cor pulmonale/constrictive pericarditis, HOCM - When there is increased SNS: hyperthyroidism, fever (~ineffective) - Hypothyroidism: only small doses needed - Increased risk of digoxin toxicity with: low Mg, low K, high Ca, acdiosis, hypoxia - Renal impairment: 70% renally cleared - Elderly - Cat A but unpredictable dose requirement - BF: safe to use |
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Digoxin
- products |
62.5mcg - Lanoxin PG, Sigmaxin PG,
250mcg tab - Lanoxin, Sigmaxin Oral liquid: 50mcg/ml.60ml Injection: 25 & 250mcy/ml.2ml |
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Digoxin
- half life & time to SS - loading dose (when do you need this) - normal dose - TG algorith for calculating initial maintenance dose? |
- 24-36 hours & ss in ~5 days
- 250-500mcg q4-6h, max 1.5mg d (not needed for HF) - 125-250mcg d. elderly/mod RI: 62.5-125, severe RI: 62.5mcg - CrCl x2 +50 (then round up if >70kg or down if <70kg to nearest 62.5mcg) |
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Digoxin concentration monitoring:
1. dose range in HF 2. dose range in AF 3. signs of toxicity 4. when do you take bloods? |
1. 0.6-1nmol/L (0.5-0.8 micromol/L) - higher levels may increase mortality
2. 0.6-2.6 nmol or 0.5-2 micromol per Litre 3. anorexia --> nausea --> vomiting (3 microgram) 4. Trough levels: before next dose or at least 6hr after last dose |
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Digoxin SEs
(common and infrequent) |
Common
- anorexia, n/v, diarrhoea - blurred vision, visual disturbance - confusion, drowsiness, dizziness, nightmares, depression infrequent: - psychosis - VT, VF, heart block |
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Digoxin
- what monitoring? - what if patient reverts to sinus rhythm? - what if another antiarrythmic is used with digoxin? |
- check RF and electrolytes, signs of toxicity
- stop digoxin - it has no preventative role - once stable, try to reduce and stop digoxin |
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Counselling points - digoxin
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LABEL FIVE
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Digoxin DIs
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1. pro-arythmic
2. bradycardia, heart block 3. Electrolyte disturbance (low K, low Mg, high Ca), especially potassium loss, increase risk of arrythmia and QT prolongation 4. Decreases absorption - acarbose, bile acid binding resins (give dig 2 hr before), sucralfate, sulfasalazine, cytotoxics (damage gut can reduce BA OF TABLETS ONLY by almost 50%), St John's Wort, rifampicin (no effect on IV digoxin) 5. Increase absorption - macrolides: clarithro and erythro (rare, monitor conc) & tetracycline (use decimates metabolising bacteria, significant in ~10% of patients) 6. Increases concentration (unknown mechanism: probably excretion inhibition) - amiodarone (starts within 4/52), verapamil (up to 80%, within 2/52), diltiazem, nifedipine, quinine, itraconazole Drugs decreasing renal excretion: trimethoprim, cyclosporin, NSAIDs, ACEIs (only a problem if it decreases RF), spirinolactone (decreases excretion & may also affect some digoxin assays) |
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Amiodarone
- MOA - Indications |
MOA
1. Class III antiarrythmic (inhibits K channel, decreasing repolarisation): slows nodes, conduction, muscle contraction 2. weak BB 3. structural analogue of thyroid hormone Serious arrythmias, resistant to other treatments |
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AMIODARONE precautions
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- CI in iodine allergy
- CI in heart block - OK in HF (least inotropic antiarrythmic) - caution in lung disease, thyroid disease, liver disease and electrolyte disturbance - Preg Cat C. avoid for 3/12 before and during preg (fetal thyroid problems and bradycardia) - DO NOT BREASTFEED |
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Amiodarone products
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100mg.30, 200mg.30 tabs - Aratac, Cordarone X, Amiodarone, Cardinorm, Rithmik
Injectable - Cordarone X |
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Amiodarone
- Adverse Effects |
Common
- N/v (especially at loading doses), constipation, anorexia, taste disturbance - hyper/hypo thyroidism - photosensitivity - blue-grey skin tone - transient elevation in LFTs - fever, headache, dizziness, fatigue, neurotoxicity (tremor, paresthesia), vivid dreams, nightmares - pulmonary toxicity (acute potentially reversible toxicity @ any time & chronic fibrotic, irreversible) Infrequent - bradycardia - arrythmias Rare - hepatotoxicity - torsades des pointes - heart failure |
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Amiodarone
- dose - serum levels - why is concentration monitoring rarely done? - half life? |
maintenance: 100-400mg d
loading: 200-400mg tds for 7/7, then 200-400mg bd for 7/7 Also given IV for acute tachycardias 1.6-4 micromol or 1-2.5mg/L Toxicity can occur within therapeutic range. Effects of dose changes take 1-3/12+ Half life: 30-100 days |
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Advice for administration of amiodarone IV?
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Incompatible with NaCl
Use glucose Use non-PVC giving set |
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What moniroring of amiodarone requried?
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Baseline:
LFTs ECG Chest X-ray TFTs U&E, Cr ** Repeat 6/12 Annual eye exam (stop if eye problems develop) Thyroid probs may develop up to 3/12 after stopping Liver problems up to 1 year after stopping. |
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Amiodarone - patient counselling.
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SEs
- report SOB/dry cough - report toxicity signs: worsening heart problems, n,v, problems with vision - Label 8: sunscreen, sun protection Also - Label 5 & 18 |
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Amiodarone DIs
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1. bradycardia/heart block
2. pro-arrythmic & prolongs QT interval 3. drugs affecting electrolytes (--> pro-arrythmic) 4. inhibits CYP1A2, 2C9, 2D6, 3A4 (all except 2C19!!!) - increases metoprolol, digoxin, phenytoin (also decreased by phenytoin), warfarin (reduce by about 25%), simavastatin, cyclosporin Absorption inhibited by cholestyramine |
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Mexiletine - how does it work?
What is it for? |
It is an orally active lignocaine analogue. Lignocaine is a class 1b antiarrythmic (inhibits sodium channels, only at high heart rates)
1. Prevention of serious VAs 2. neuropathic pain - specialists |
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Isoprenaline
- how does it work? - what is it for? |
- Beta agonist
- heart block, shock, bradycardia with haemodynamic compromise |
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Sotalol
- MOA - Indications |
- Beta blocker & a Class III anti-arrythmic (inhibits K channels, prolonging refractory period)
- atrial and ventricular arrythmias |
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Sotalol
- A/Es |
- palpitations, hypotension, bradycardia, dyspnoea, fatigue, dizziness, headache
- n/v/d, dyspepsia - impotence Infrequent: prolong QT, Torsades, heart block |
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Sotalol
- products - dose |
- 80mg, 160mg.60 tabs (Solavert, Sotacor, Cardol)
- injectable (Sotacor) Dose: 40-160mg bd (max 320mg bd) |
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Sotalol drug interactions
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1. QT intervals, pro-arrythmics, drugs disturbing electrolyte concentratiosn
2. DIs as for BBs: (a) hypotension, decreased HR (b) ergot alkaloids - increased risk of peripheral vasoconstriction (c) isoprenaline, beta agonist (d) clonidine - enhanced bradycardia and hypotension of paradoxical effect; withdraw over 7 days before withdrawing clonidine to prevent rebound hypertension |