Cardio Flashcards
Summary of stable angina?
Typically symptomatic when >70% coronary stenosis
<20 mins, subsides after rest/GTN
Exertion
Stress test: ST depression/elevation, T wave inversion
Angio: coronary a stenosis
Treatment of stable angina?
GTN
1st: Ca channel blocker or β blocker
2nd: add other
3rd: long acting nitrate, ivabradine, nicorandil or ranolazine
ACEi/ARB, aspirin/clopi, statin
CABG/PCI
Summary of unstable angina?
Sx at rest
ECG: ST depression, T wave inversion
Serial trop
300mg aspirin Nitrates Morphine O2 if <94% Fondaparinux if no immediate PCI PCI: immediate if unstable, within 72 hrs if GRACE score >3%, give heparin Aspirin + prasugrel or ticagrelor if high risk bleeding Aspirin + clopi if low risk bleeding
if GRACE score <3% - conservative management, give aspirin + ticagrelor if not high risk of bleeding, or aspiring + clopidogrel if high risk
What does GRACE score take into account?
age heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine) cardiac arrest on presentation ECG findings troponin levels
Summary of vasospastic angina?
Coronary artery vasospasms
Triggers: cold weather, stress, hyperventilation, smoking, cocaine use, alcohol, allergic reactions, drugs that tighten BVs
Can occur any time
ECG - Transient ST elevation
Tx: Ca channel blockers Nitrates Aspirin can aggravate ischaemic attack β blockers can ↑vasospasm.
Complications of MI?
DARTH VADER
Death Arrthymia Rupture Tamponade Heart Failure
Valve disease Aneurysm Dressler syndrome Embolism Recurrence regurgitation
Investigations for MI?
Trop
CKMB
STEMI: ST↑, new onset LBBB, reciprocal ST depression
NSTEMI: ST depression, loss of R wave, T wave inversion
Management of MI?
Aspirin 300mg Morphine, metoclopramide O2 <94% GTN, IV nitrates Dual anti-plt Statins Cardiac rehab
STEMI
Thrombolysis: Tenecteplase, alteplase
If presents within 12 hrs > PCI within 120 mins. Heparin with bailout glycoprotein IIb/IIa
NSTEMI
Fondaparinux if not having angiography
PCI if unstable, >3% GRACE score. Heparin
Inferior leads?
II, III, aVF
RCA
Anteroseptal leads?
V1-V4
LAD
Anterolateral leads?
V4-6, I, aVL
LAD or L circumflex
Lateral leads?
I, aVL +/- V5-6
L circumflex
Posterior leads?
Changes in V1-V3
Reciprocal changes of STEMI are typically seen: horizontal ST depression tall, broad R waves upright T waves dominant R wave in V2
Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)
Usually L circumflex, also R coronary
Causes of bradycardia?
Intrinsic causes: congenital abnormalities, fibrosis, post MI, IE, infections, iatrogenic, amyloid, sarcoid, SLE, hypothyroidism.
Extrinsic: toxins, drugs (digoxin, β blockers, CCBs), hyperkalaemia, hypothyroid, adrenal insuff, hypoxia, hypothermia, Cushing’s triad, AN.
Management of bradycardia?
Unstable
Atropine 500mcg, repeat every 3 mins, up to max 3mcg
Adrenaline, dopamine, isopremaline
Transcut/transvenous pacing
Causes of heart block?
Infiltrative/ dilated cardiomyopathies eg myocarditis, amyloidosis, sarcoidosis, lymphoma. Muscular dystrophy Lyme disease/ acute rheumatic fever. Myocardial ischaemia Congenital heart disease + congenital 3rd degree AV block. Hyperkalaemia High vagal tone Cardiac surgery/ trauma Meds: BB, CCB, digoxin CO, cyanide Lev’s disease
Summary of 1st degree heart block?
PR interval > 0.2 seconds, every P wave followed by normal QRS
Signal delayed, continues to ventricles
Usually asymptomatic
R away from P = first degree
No Tx, if Sx can get pacemaker fo transact pacing
Summary of T1 2nd degree heart block?
Morbitz 1/Wenckebach
Usually asymptomatic
Light-headedness, dizziness, syncope
Longer, longer, longer, drop = Wenkebach
PR interval lengthens each beat until blocked (dropped beat/no QRS)
Constant PP interval
Following omission, PR interval reset + cycle repeats
Narrow irregular QRS
No treatment if asymptomatic
If Sx can get pacemaker of transscut pacing
Summary of T2 2nd degree heart block?
Morbitz II
Block commonly bundle of His
Intermittent dropped beats, no progressive lengthening of PR interval
Often regular conduction intervals eg 2:1
Fatigue, dyspnoea, chest pain, syncope
PR interval is constant but the P wave is often not followed by a QRS complex
Prolonged PR interval >200ms
Regular QRS complexes with occasional dropped QRS
PR interval constant
Pacemaker
Transcut pacing
Some P’s don’t get through, then Mobitz II
Summary of 3rd degree AV block?
Signal blocked every time, no association between atrial + ventricle activity.
Ventricles contract at lower rates than atria, ventricular pacemaker cells set rate
Syncope, confusion, dyspnoea, severe chest pain, risk of dying
No association between P + QRS
Regular PP + RR intervals
ICU, CCU
Epinephrine
Pacing
If Ps and Qs don’t agree, then you have third degree
Summary of LBBB?
Electrical signal for contraction of L ventricle completely blocked/delayed along 1 bundle branch.
Retrograde depolarisation from R>L via purkinje fibres
Asymptomatic
Reversed splitting on auscultation
New LBBB is always pathological. Causes of LBBB include:
> myocardial infarction - diagnosing a myocardial infarction for patients with existing LBBB is difficult, Sgarbossa criteria can help with this
> hypertension
> aortic stenosis
> cardiomyopathy
> rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
WilliaM
- W in V1
- M in V6
QRS complex > 120Ms
Neg V1, pos V6
V1: QS or ‘little r’ rS, no R wave, deep S wave W shape
V6: large, notched R wave, M shape
Summary of RBBB?
Electrical signal for contraction of R ventricle completely blocked/delayed along 1 bundle branch.
Asymptomatic
Wide splitting on auscultation
Causes of RBBB > normal variant - more common with increasing age > right ventricular hypertrophy > chronically increased right ventricular pressure - e.g. cor pulmonale > pulmonary embolism > myocardial infarction > atrial septal defect (ostium secundum) > cardiomyopathy or myocarditis
in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
QRS complex > 120Ms
T wave inversion
QRS double peaked.
M shape in V1 tall R waves, W-shape in V6 from wide slurred S shape
ST depression + T wave inversion in leads V1-V3.
Summary of sick sinus syndrome?
a disease in which the SAN becomes damaged and is no longer able to generate normal heartbeats at the normal rate.
Abnormal heart rhythms caused by malfunction of SAN
Brady, tachy, tachy-brady, long pauses
Sarcoidosis, amyloidosis, haemochromatosis, chagas disease, cardiomyopathies
Meds: CCB, BB, digoxin
Complications:
Sinus arrest
AT, AF
VTE
ECG
Tilt table testing
Holter monitor
Exercise/ atropine stress test: inadequate ↑HR
Management
Pacemaker
Treat tachy with meds > BB
Management of narrow-complex tachycardia?
Regular
> vagal manoeuvres, carotid sinus massage, Valsalva manoeuvre
> followed by IV adenosine 6mg, then 12mg, then 18mg. CI in asthmatics
> if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. beta-blockers)
> electrical cardioversion
> probable SVT
Irregular
> probable atrial fibrillation
> if onset < 48 hr consider electrical or chemical cardioversion
> rate control: beta-blockers are usually first-line unless there is a contraindication, then diltiazem
> if HF - digoxin or Amiodarone
Management of broad-complex tachycardia?
Regular
> assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)
> loading dose of Amiodarone 300mg over 20-60 mins, then followed by 900mg 24 hour infusion
> if SVT with BBB - treat for regular narrow complex tachy
Irregular
> seek expert help.
> Possibilities include:
atrial fibrillation with bundle branch block - the most likely cause in a stable patient - treat as narrow complex
> atrial fibrillation with ventricular pre-excitation > give Amiodarone
> torsade de pointes
Summary of sinus tachycardia?
Narrow complex QRS, regular ventricular rhythm. P before every QRS. Rhythm originates in SAN.
Causes = Physical deconditioning, hypoxia, PE, hypovolaemia, hyperthyroid, anaemia, caffeine, alcohol, nicotine, cocaine, amphetamines, aminophylline, atropine, clozapine, catecholamines.
Inappropriate: persistent ↑HR, unrelated to/out of proportion to cause
What is focal atrial tachy?
SVT, atrial focus outside SAN. Mostly idiopathic HTN, heart disease, cardiomyopathy MI, infection, alcohol poisoning Congenital heart disease Catecholamine excess Drug toxicity: cocaine, digoxin, theophylline
ECG:
Morphology of P waves depends on site origin but remains constant
Regular rhythm
Management: Vagal manoeuvres If persists: IV adenosine, CCB (verapamil, diltiazem), BB blockers Catheter ablation Pacemaker
What is multifocal atrial tachy?
Multifocal origin of pacemaker activity
Causes = COPD, theophylline, isoproterenol, ↓K, Mg, hypoxia, hypercapnia, acidosis, RA enlargement
Typically in seriously ill patients with respiratory failure. Tends to resolve following Tx of underlying disorder.
ECG: HR > 100bpm Irregularly irregular P waves 3+ varying morphologies Narrow QRS SVT
Management: Beta blockers CCB eg verapamil IV Mg Correct reversible causes
What is junctional tachycardia?
Abnormal automaticity or myocytes in AVN or proximal bundle of His
a form of supraventricular tachycardia
Narrow complex
Regular
P wave inverted in lead 2, can be hidden within QRS or immediately before QRS
Short PR interval
Prevention
BB eg metoprolol
CCB > verapamil
Catheter ablation
Acute management
vagal manoeuvres:
> Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
> carotid sinus massage
intravenous adenosine
rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
contraindicated in asthmatics - verapamil is a preferable option
> electrical cardioversion
Summary of atrial fibrillation?
first detected, recurrent, paroxysmal, persistent, permanent (cannot be cardioverted or deemed inappropriate)
Palpitations, dyspnoea, chest pain
Irregularly irregular pulse
Rate/rhythm control
- rate control except in coexistent HF, first onset AF or where obvious reversible cause
Rate - BB or rate-limiting CCB (diltiazem). Can have combination of 2 of BB, diltiazem or digoxin if mono therapy doesn’t control rate
Rhythm - short duration of Sx (<48 hours) or anticoagulation prior
Summary of CHA2DS2-VASc score?
C - congestive HF - 1
H - hypertension (or treated HTN) - 1
A2 - age >75 = 2, age 65-74 = 1
D - diabetes - 1
S2 - prior stroke, TIA to thromboembolism = 2
V - vascular disease (including IHD, and PAD) = 1
S - sex (female) = 1
0 - no treatment
1 - males - consider anticoagulation, females- no Tx
2 - offer anticoagulation
Choice of anticoagulation - warfarin and NOACs
Summary of atrial flutter?
a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.
ECG findings
> ‘sawtooth’ appearance
> as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
> flutter waves may be visible following carotid sinus massage or adenosine
Management
> is similar to that of atrial fibrillation although medication may be less effective
> atrial flutter is more sensitive to cardioversion however so lower energy levels may be used
> radiofrequency ablation of the tricuspid valve isthmus is curative for most patients
What is AV re-entrant tachycardia?
Accessory pathway between atria + ventricles.
Allows signal to move backwards. More than 1 ventricular contraction can be stimulated from 1 impulse from SAN.
Orthodromic: through AVN, ventricles contract, up through accessory pathway, atria contract, back down AVN etc.
Antidromic: signal down through accessory pathway, ventricles contract, up through AVN atria contract, back down accessory.
Features: Palpitations Chest discomfort SOB Light-headed Syncope
Orthodromic: regular, narrow QRS tachy, p waves retrograde (after QRS)
Antidromic: regular, wide QRS tachy. P waves often not visible, delta waves, short PR interval.
Acute termination: vagal manoeuvre, carotid sinus massage, adenosine, electrical cardioversion.
Chronic prevention: amiodarone, procainamide, sotalol, flecainide, radiofrequency catheter ablation.
What is WPW syndrome?
Congenital accessory pathway (Bundle of Kent) conducts signal between A+V. Ventricles start to contract a bit early, pre-excitation.
As accessory pathway does not slow conduction AF can degenerate rapidly to VF
Signal takes longer through AVN, combines with single from BoK to contract ventricle.
Set up re-entry loop, BoK propagate signals both ways. Come down AVN, go back up BoK, causing atria contraction + AVRT.
Tachyarrhythmias Palpitations Chest discomfort SOB Light headed Syncope Find physical activity exhausting
Short PR interval
Delta wave: slurred upstroke of QRS
Widening of QRS complex due to ventricular pe-excitation
AF or flutter, very high >200-250
Differentiating between type A and type B** type A (left-sided pathway): dominant R wave in V1 type B (right-sided pathway): no dominant R wave in V1 (in exams mostly type B with LAD)
Associations of WPW HOCM mitral valve prolapse Ebstein's anomaly thyrotoxicosis secundum ASD
Management
definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol***, amiodarone, flecainide
*** sotalol avoided if coexistent AF > can deteriorate to VF
Summary of atrioventricular nodal re-entry tachycardia (AVNRT)?
Supraventricular tachycardia
Accessory pathway within AVN. 2 pathways, form loop
Slow-fast: typical, signal depolarisation down both pathways, reaches end of β path (fast) 1st. signal splits, travels. To ventricles (contraction), + travels up α path, meets slow signal, cancel each other out. Both go into refractory. α refractory shorter, ready 1st, signal from α exits to ventricles. Also travels up β, by time all way round, α out of refractory, re-entrant loop.
Fast slow: atypical, anterograde conduction via fast pathway, retrograde via slow.
RF: F>M, stress, alcohol, caffeine hyperthyroid, exercise, electrolyte disturbance
ECG
SVT 140-280bpm
Absent p waves, signal getting through atria + ventricles almost same time
p waves immediately before/ after QRS complex. P waves inverted/ retrograde
R waves (small secondary R waves)
Narrow QRS complexes
Management:
Adenosine
Ca channel blockers eg verapamil, diltiazem
Slow AVN: vagal manoeuvre (carotid sinus massage/ valsalva manoeuvre) > activates vagus nerve, blocks AVN temporarily.
Electrical cardioversion
Prevention
Beta blockers eg metoprolol
Radiofrequency catheter ablation: ablation of slow alpha pathway
Summary of VT?
broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential to precipitate ventricular fibrillation and hence requires urgent treatment.
monomorphic VT: most commonly caused by myocardial infarction
polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval
Non re-entrant/focal
Abnormal automaticity of specific area of ventricle. Ventricular pacemaker cells fire at high rate, preventing SAN firing.
Re-entrant VT
More common
Cardiomyocytes altered when stressed by stimuli eg drugs, changing conduction speed + refractory period
Non-sustained: at least 3 beats, resolve spontaneously in <30s.
Sustained: >30s, or requiring termination earlier due to haemodynamic instability.
Adverse signs (SBP < 90, chest pain, HF) then immediate cardioversion. If not, then antiarrhytmics. if these fail, then electrical cardioversion may be needed.
Drug therapy
> amiodarone: ideally administered through a central line
> lidocaine: use with caution in severe left ventricular impairment
> procainamide
If drug therapy fails
> electrophysiological study (EPS)
> implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
Electrical cardioversion: pulse delivered to heart on R wave, if delivered on T wave could induce VF
Causes of long QT interval?
Congenital:
> Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel)
> Romano-Ward syndrome (no deafness)
Drugs: > amiodarone, sotalol, class 1a antiarrhythmic drugs > tricyclic antidepressants, fluoxetine > chloroquine > terfenadine > erythromycin
electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage
