Cardio Flashcards
Normal axis
-30 - +90 degrees
PR interval
From atrial depolarisation to ventricular depolarisation *120-200ms
Prolonged = AV block
Shortened = atrial impulse to ventricles quicker i.e. accessory pathway associated with delta wave (slurred QRS upstroke) in Wolff Parkinson White
QRS
Width, height, shape. Normal = 80-120ms.
Narrow = <120ms, impulse down His and Purkinje
Broad = >120ms, abnormal depolarisation, e.g. ectopic
Height: small = <5mm in limb and <10mm in chest, tall = ventricular hypertrophy
Delta = WPW
Pathological Q: >2mm or >40ms
R and S: normally have R wave progression (small in V1 and large in V6) transition S>R to R>S is normally in V3 or V4
ST segment
End of S to start of T: elevation significant if >1mm in 2 or more limb leads or >2mm in 2 or more chest leads, depression significant if >0.5mm in 2 contiguous leads
T wave
Ventricular repolarisation:
tall if >5mm in limb AND >10mm in chest associated hyperacute STEMI and hyperkalaemia
Inverted: *normal in V1 and lead III, associated ischaemia, PE, BBB
U wave
A small deflection after T wave, 0.5mm, best seen in V2 and V3
Seen in electrolyte disturbances, hypothermia, antiarrhythmics e.g. digoxin, more pronounced with slower
Sinus bradycardia Definition Causes Symptoms Treatment
<60bpm where every P wave is followed by a QRS
Physiological: athletes, young due to *high resting vagal tone (vagal activity is continuous)
Pathological: acute MI, drugs (BB, dig, amiodarone), hypothyroid, hypothermia, sick sinus, raised ICP
Syncope, fatigue, dizziness, ischaemic chest pain, palpitations depending on cause
Treatment is Rate < 40 or symptomatic - IV atropine -
Temporary pacing wire
Sick sinus syndrome
Dysfunction of SA node with impairment of ability to generate impulse
Normally idiopathic fibrosis of node, also associated with ischaemia and digoxin toxicity (fibrosis may be amyloid or sarcoid)
Causing - Sinus bradycardia, sinoatrial block (Pause length of 2 or more PP intervals), sinoatrial arrest
Treatment - Pacing
Heart block
Causes
Types
Managment
MI/ischaemia (inferior), infection (Lyme disease), immunological (SLE), myocarditis, endocarditis, degeneration of HIS-PURKINJE, drugs (digoxin, BB, CCB)
Delay of atrial impulse to ventricles
1st = PR > 0.2s, PR constant, every P followed by QRS
Intermittent failure of conduction from atria to ventricles. Some P are not followed by QRS
Mobitz type I (Wenckebach) failure at level of AV node. PR interval progressively lengthens and is then blocked.
Mobitz type II intermittent failure of P wave conduction. Fixed PR interval, dropped QRS waves (2:1 block or 3:1 block)
Unstable - Atropine & Trans cutaneous pacing
Stable - Usually a organic cause & Dual chamber pacing
Sinus tachy
Causes
Ix
Treatment
Every P followed by QRS, rate 100 - 270
Physiological: exertion, anxiety, pain
Pathological: fever, anaemia, hypovolaemia
Endocrine: thyrotoxicosis, phaeo
Pharmacological: sympathomimetic, adrenaline, alcohol, caffeine, salbutamol
Ix - 12 lead ECG, cardiac enzymes, FBC (anaemia), TFT
Treatment
Acute: Hemodynamically stable - Vagal manoeuvres
BB or non-dihydropyridine CCB (diltiazem, verapamil)
Atrial SVT
Causes
ECG findings
Types
Typically from ectopic source in atrial muscle
150-250 bpm (slower than flutter)
Abnormal p-wave morphology
Atrial rate 150-250
Variable ventricular rate but regular
Benign (80-140bpm elderly)
Incessant ectopic (rare)
Multifocal (COPD, varying p-wave morphology)
Atrial tachycardia with block (digoxin toxicity) basically a fast heart block
AVNRT SVT Common? Symptoms ECG Treatment
- Most common cause of paroxysmal narrow complex tachycardia
- Late teens or early 20s
Sudden onset palpitations ± CP, SOB ± syncope
*Neck pulsation
Regular rhythm, narrow QRS, rate 130-250
Retrograde atrial conduction: inverted P waves in II, III, AVF (inferior)
Atrial and ventricular depolarisation together - P waves buried in QRS
Haemodynamically unstable - DC cardioversion
First line: Vagal maneuvers may stop as transiently block AV node
Second line: *Adenosine
Prophylaxis - Drugs affecting AV node: digoxin, diltiazem, verapamil, fleicanide or a B blocker
Curative: radiofrequency ablation
AF Risk factors Causes Precipitants Symptoms
Age, HTN, heart failure, CAD, valvular disease, DM, CKD
CAD, HTN, valvular disease, hyperthyroidism, alcohol
Alcohol, caffeine
SOB, palp, syncope, chest discomfort, stroke/TIA
Chronic AF Management
Rate control
First line: standard BB or rate limiting CCB (diltiazem, verapamil)
Dual therapy add digoxin or two of above (**ONLY DILTIAZEM)
Rhythm control
Cardiovesion with flecanide (Treat with amiodarone for 4w preceding CV)
B Blocker/ AV node ablation
Acute AF treatment
If hemodynamically unstable:
DC cardioversion is preferred + continue thrombophylaxis for 4 weeks
If pharmacological cardioversion - Amiodarone IV
Offer heparin immediately then introduce warfarin
CHADsVasc
HAS BLED
Targert INR
CHF (1), HTN >140/90 (1), >75 (2), DM (1), prior stroke/TIA (2), vasc dis: MI, PVD (1), 65-75 (1), female (1)
Consider male > 1 or anyone > 2, warfarin or NOAC
HASBLED - HTN (>160), abnormal liver or renal 1/2, stroke, bleeding Hx or predisp e.g. anaemia, labile INR, elderly >65, drugs (alcohol, NSAIDs, antipt) 1/2
INR 2-3 (non valvular) (n.b. Prosthetic valves, post MI = 2.5-3.5)
Atrial flutter managment
Rhythm control: cardioversion or medications
DC cardioversion (if >48hours ensure adequate anticoag)
Or IV amiodarone, sotalol, fleicanide
Recurrence: *radiofrequency catheter ablation (90-95% success)
Broad Complex tachycardia types
Ventricular tachycardia
Regular: Monomorphic ventricular tachycardia, right ventricular outflow tract tachycardia, fascicular tachycardia
Irregular: Torsades de Points, polymorphic ventricular tachycardia
Supraventricular with aberrant conduction or ventricular-pre excitation
Aberrant conduction - usually manifests as LBBB or RBBB (Suspect if has prev BBB)
WPW
AF with atrioventricular re-entrance
Nb always treat as VT are more likely and more dangerous
VT ecg changes
ECG normally monomorphic QRS complex (unless disturbed by capture or fusion beats)
Needs 3 in a row
Bizarre QRS morphology as impulse does not follow normal intraventricular conduction
If starts in left vent gives RBBB, if starts in right vent gives LBBB
Ventricular rate 120-300
VT management
Unstable
Stable
Support ABC, O2 and venous access
Monitor ECG, BP, sats
Identify and treat reversible cause e.g. electrolyte abnormalities potassium
Unstable (chest pain, reduced consciousness, heart failure) *reduced CO
Synchronised DC shock (up to 3 attempts)
Amiodarone 300mg IV over 10-20 minutes and repeat shock then 900mg over 24 hours if refractory
If regular/stable (VT) - Amiodarone as above.
VT is usually due to damage so requires maintenance anti-arrhythmics (BB/CCB) or consider ICD implantable cardioversion defibrillator
Nb If stable but irregular = TdP
Torsades de points
Risk
Treatment
Causes
Type of polymorphic ventricular tachycardia in which cardiac axis rotates over a sequence of 5-20 points. QRS amplitude varies similarly giving twisting appearance.
In sinus may be seen as prolonged QTc.
May deteriorate to Ventricular fibrillation
IV magnesium sulphate (2g magnesium for other broad irregular i.e. polymorphic)
Drugs: anti-arrhythmics class III (amiodarone), antibacterials (erythromycin, trimethoprim), TCAs *Electrolyte: hypokalaemia/hypomagnaesaemia
VF
Causes
ECG changes
Treatment
Antiarrhythmic drugs, AF, hypoxia, ischaemia, fast VT, previous heart disease
*Shockable: VF and pulseless VT
Non-shockable: asystole and PEA (pulseless electrical activity)
Chaotic (varying amplitudes)
No identifiable P, QRS, T
Rate 150-500
Amplitude decreases with duration: coarse to fine.
Defibrillation
BB and ICD (implantable cardioverter defibrillators)
Brugada syndrome
Brugada sign
Autosomal dominant gentic condition affecting sodium channels causing sudden death <45yrs
Coved ST segment elevation >2mm in >1 of V1-V3 followed by -ve T (Brugada sign)
+ Documented VF or PVT
ICD implantable cardioverter defibrillator
PE ECG changes
*Sinus tachycardia - main finding
S1Q3T3 - deep S, deep Q wave in 3, deep T wave in 3 - only 10%
Assoc RBBB
R heart strain = T wave inversion in V1-V4
Amiodarone Indications Pharmacology Side effects CIs
For tachyarrhythmias (AF, AFl, SVT) when other drugs or electrical cardioversion don’t work
Blockade Na/K/Ca channels, antagonist alpha and beta adrenergic receptors which reduces automaticity.
Hypotension during IV infusion.
Chronic use lungs (pneumonitis), prolonged QT (AV block), liver (hepatitis), skin (grey discolouration), hypothyroid (Iodine rich)
Severe hypotension, heart block, thyroid disease
Adenosine
Indications
Pharmacology
Side effects
First line diagnostic and therapeutic in SVT (inc junc)
Adenosine receptor agonist on cell surface.
Very short duration - half life 10s
Blocks SA and AV node - causes bradycardia and asystole - doom feeling
May induce bronchospasm in asthma or COPD
CCB Indiactions Pharmacology Side effects CIs
Verapamil (most cardio-selective) + diltiazem (non-dihydropyridine) + amlodipine (dihydropyridine)
Rate control in SVT inc AF +AFl
Decrease Ca entry to vascular and cardiac cells induces relaxation + vasodilation in arterial smooth muscle + myocardial contraction in heart. Reducing rate, contractility and afterload decreases oxygen.
Ankle swelling, flushing, headache - dihydropyridine e.g. amlodipine
Verapamil - constipation, bradycardia, heart block
Diltiazem (mixed)
Don’t prescribe with BB - both negatively inotropic and chronitropic so may cause HF, bradycardia + asystole
B Blockers Indications Pharmacology Side effects CIs
First line in IHD reduce angina CHF improve prognosis AF reduce rate and maintain sinus rhythm SVT to restore sinus rhythm
B1 in heart, B2 in smooth muscle blood vessels and airways
Via B1 reduce force and speed of conduction in heart - reduces cardiac work and oxygen demand and increase myocardial perfusion via prolonging AV refractory.
Lower BP by reducing renin secretion
Fatigue, cold extremities, headache, impotence
Asthma - B2 blockade causes bronchospasm, usually safe in COPD
Choose a B1 selective (ABM, atenolol, bisoprolol, metoprolol), rather than non-specific (propanolol)
Preload
Volume of blood in the ventricles at the end of diastole
Afterload
Resistance LV must overcome to circulate blood
