Cardiology Flashcards
LVH criteria (Sokolov-Lyon)
Voltage: S wave depth in V1 + tallest R wave height in V5 or V6 > 35 mm
+ Non-voltage: Increased R wave peak time (>50ms in V5 or V6) + ST segment depression and TWI in left-sided leads (LV strain pattern)
Drugs associated with QT prolongation (5 categories)
Non-pharmacological causes of long-QT
- Age, Female gender
- Congenital QT prolongation
- Left ventricular failure
- Recent cardioversion
- Metabolic abnormalities
- Hypomagnesemia
- Hypokalemia
- Hypocalcemia
- Hepatic dysfunction
Echo findings suggestive of cardiac tamponade
- Presence of pericardial effusion (>2cm)
- Right atrial diastolic collapse
- Right ventricular diastolic collapse
- Right atrial early systolic collapse
- Dilated IVC with no respiratory collapse
- Diastolic flow reversal in the hepatic veins
13yo syncope playing sport
Hypertrophic cardiomyopathy
i. Left ventricular hypertrophy (no delayed R wave peak time, however)
ii. Non-specific global ST-segment depression (?c/w LVH/LMCA but age 15)
iii. aVR, V1, V2 ST segment elevation (?c/w LMCA but age 13)
iv. P-wave abnormalities (large P-waves globally/retrograde P-wave V2)
v. PR interval normal (i.e. no short PR)
vi. Sinus rhythm (i.e. no arrhythmia)
vii. Non-specific T-wave changes especially laterally (?c/w LVH)
Causes of ST elevation that aren’t myocardial ischaemia
- Pericarditis
- Benign early repolarization
- Left bundle branch block
- Left ventricular hypertrophy
- Ventricular aneurysm
- Brugada syndrome
- Ventricular paced rhythm
- Raised intracranial pressure
Special cases for acute BP management, preferred agents and targets
ECG: 83M 2/52 lethargy, anorexia, dehydration BG AF
Likely digoxin toxicity (downsloping STD V2) Ddx incl. hyperK, ischaemia, TCA/beta blocker/CaCB toxicity
- Underlying atrial activity likely fibrillation (seen best in inferior leads)
- Regular ventricular response at 65/min
- Regular QRS in context of AF suggests complete block of A-V conduction
- Wide QRS complexes consistent with ventricular escape (or “accelerated idioventricular”)
- Rightward axis, tall left “rabbit ear” in V1
Calcium treatment in suspected digoxin toxicity?
In theory (and in limited case reports) calcium can exacerbate digoxin toxicity (“stone heart”) and it is widely said to be contra-indicated
However frequently these patients will be hyperkalaemic and if delay to getting digoxin level, empiric Tx with calcium probably acceptable
ECG: 45M 20min chest pain
Proximal LAD occlusion -> Treat as STEMI – lysis or urgent PC
Hyper acute t wave antero-septal (de Winter)
Up sloping ST segment V3-V6
ST elevation I, aVL
ST depression III, aVF
Fibrinolytic regimes for STEMI
Alteplase
>65 kg: 15 mg intravenous bolus, followed by 50 mg by intravenous infusion over 30 minutes, then 35 mg over the next 60 minutes
<=65 kg: 15 mg intravenous bolus, followed by 0.75 mg/kg by intravenous infusion over 30 minutes, then 0.5 mg/kg over the next 60 minutes
OR
Tenectaplase
<60 kg: 30 mg (6000 units) intravenous bolus
60 to 69 kg: 35 mg (7000 units) intravenous bolus
70 to 79 kg: 40 mg (8000 units) intravenous bolus
80 to 89 kg: 45 mg (9000 units) intravenous bolus
>=90 kg: 50 mg (10 000 units) intravenous bolus
ECG: 23F syncope
Long QT
ECG: 41M brief syncope, no relevant history
Brugada Syndrome, Type I
ST elevation >=2mm followed by negative T wave in V1-2 or coved ST elevation >2mm in V1-2; in association with syncope, this is diagnostic of Brugada syndrome
DDx incl:
* Atypical RBBB
* Myocardial ischaemia/infarction
* Benign Early Repolarisation
* PE
* Myo/pericarditis
* Athletes
* Pectus excavatum
* RV outflow obstruction or other RV abnormality
Exacerbating factors for Brugada syndrome
Fever
Ischaemia
Multiple Drugs
- Sodium channel blockers eg: Flecainide, Propafenone
- Calcium channel blockers
- Alpha agonists
- Beta Blockers
- Nitrates
- Cholinergic stimulation
- Cocaine
- Alcohol
Hypokalaemia
Hyperkalaemia
Hypothermia
Post DC cardioversion
Diagnostic criteria for Brugada syndrome
Coved ST-segments (Brugada sign; type I)
PLUS one or more of:
- Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT)
- Family history of sudden cardiac death at <45 years old
- Coved-type ECGs in family members
- Inducibility of VT with programmed electrical stimulation
- Syncope
- Nocturnal agonal respiration
Contraindications to fibrinolysis in STEMI
Absolute contraindications
* Any prior ICH
* Known structural cerebral vascular lesion (eg, arteriovenous malformation)
* Known malignant intracranial neoplasm (primary or metastatic)
* Ischemic stroke within 3 mo
* Suspected aortic dissection
* Active bleeding or bleeding diathesis (excluding menses)
* Significant closed-head or facial trauma within 3 mo
* Intracranial or intraspinal surgery within 2 mo
* For streptokinase, prior treatment within the previous 6 mo
Relative contraindications
* History of chronic, severe, poorly controlled hypertension
* Significant hypertension on presentation (SBP >180 mm Hg or DBP >110 mm Hg)
* History of prior ischemic stroke >3 mo
* Dementia
* Known intracranial pathology not covered in absolute contraindications
* Traumatic or prolonged (>10 min) CPR
* Major surgery (<3 wk)
* Recent (within 2 to 4 wk) internal bleeding
* Noncompressible vascular punctures
* Pregnancy
* Active peptic ulcer
* Oral anticoagulant therapy
What constitutes failure of thrombolysis, suggesting the need for rescue PCI?
- Failure of ST elevation to reduce by (50% - 75%) at 90 minutes post lysis
- Persistent pain
- The absence of chest pain following thrombolytic therapy does not imply reperfusion;
however persistent ischaemic chest pain indicates failure (de Belder 2001). Cardiogenic
shock may occur because of the already infarcted myocardium.
Features on history favouring syncope over seizure?
Features Favouring Syncope:
● Rapid Neurological Recovery / no post ictal period
● No neurological symptoms
● Postural symptoms
● Pre-syncope symptoms
● An absence of seizure like movements
ECG: 62M chest pain - which coronary artery is culprit?
STE aVR + widespread anterolateral STD
Causes:
- Left main coronary artery (LMCA) stenosis
- Proximal left anterior descending artery (LAD) stenosis
- Severe triple vessel disease
(- Hypoxia or hypotension, for example following resuscitation from cardiac arrest)
Clinical outcomes of anterior MI (LAD infarct) vs inferior MI
Anterior MI has higher incidence of:
- In-hospital mortality (11.9 vs 2.8%)
- Total mortality (27 vs 11%)
- Heart failure (41 vs 15%)
- Significant ventricular ectopic activity (70 vs 59%)
- Lower ejection fraction on admission (38 vs 55%)
Presumed due to the larger area of MI size. Poorest prognosis of all infarct locations.
ECG: 67M chest pain. Primary ECG feature?
De Winter T waves
- Upsloping ST depression (> 1mm at J point) in the precordial leads V2-6, plus leads I and II
- Peaked anterior T waves, with the ascending limb of the T wave commencing below the isoelectric baseline
- ST elevation in aVR > 0.5mm
- The de Winter pattern is seen in ~2% of acute LAD occlusions and is often under-recognised by clinicians
- Key diagnostic features include ST depression and peaked T waves in the precordial leads
ECG: 65F chest pain. Which coronary artery likely cuprit?
Inferior STEMI - RCA occlusion
- Marked ST elevation in II, III and aVF with early Q-wave formation.
- Reciprocal changes in aVL.
- ST elevation in lead III > II with reciprocal change present in lead I and ST elevation in V1-2 suggests RCA occlusion with associated RV infarction: This patient should have right-sided leads to confirm this.
ECG: 65F chest pain. Which coronary artery likely culprit?
Inferior STEMI - Left circumflex artery occlusion
- ST elevation in II, III and aVF.
- Q-wave formation in III and aVF.
- Reciprocal ST depression and T wave inversion in aVL
- ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST segment) suggests a left circumflex artery occlusion
Circumflex occlusion is suggested by:
- ST elevation in lead II = lead III
- Absence of reciprocal ST depression in lead I
- Signs of lateral infarction: ST elevation in the lateral leads I and aVL or V5-6
ECG: 19M chest pain following blunt chest trauma.
High Lateral STEMI - mechanical occlusion of first diagonal artery. (Interesting!)
- ST elevation is present in the high lateral leads (I and aVL).
- There is also subtle ST elevation with hyperacute T waves in V5-6.
- There is reciprocal ST depression in the inferior leads (III and aVF) with associated ST depression in V1-3 (which could represent anterior ischaemia or reciprocal change).
- This pattern is consistent with an acute infarction localised to the superior portion of the lateral wall of the left ventricle (high lateral STEMI).
- The culprit vessel in this case was an occluded first diagonal branch of the LAD.
ECG: 65F chest pain. Which coronary artery likely culprit?
Hyperacute Anterolateral STEMI - prox LAD occlusion.
- Early STE with hyperacute t waves in anteroseptal leads (V1-4)
- Subtle STE in high lateral leads (I and aVL)
- Reciprocal STD in inferior leads (III and aVF) makes lateral STE more obvious
- STE in procordial leads + high lateral leads = prox LAD
ECG: 61M chest pain. ECG features?
Posterior STEMI.
Posterior MR suggested by presence of:
- Largely horizontal STD V1-3
- Tall, broad R waves (>30ms) V2-3
- Dominant R wave (R>S) in V2
- Upright T waves in V2-3
Duke Criteria for infective endocarditis
BE FIVE PM
Major criteria
1. Blood-culture positive
A. Typical micro-organism (S. aureus,, S viridans, S bovis, HACEK groun, enterococci) in 2 separate BCs, OR
B. Persistent positive BCs, typical organisms >=2 positive cultures taken >12 hours apart or >3 if organisms common skin contaminant
C. Single positive BC for coxiella burnetii or phase I IgG Ab titre >1:800
- Evidence of endocardial involvement
A. Positive echocardiogram (vegetation, abscess, or valve dehiscence)
B. New valvular regurgitation (increase or change in pre-existing murmur)
Minor critera
1. Fever >38 degC
2. Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth’s spots, RF+)
3. Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, Janeway lesions)
4. (Echocardiography minor criteria eliminated)
5. Predisposition - heart condition or IVDU
6. Microbiologic evidence (positive BC but not meeting major criteria or serological evidence of active infection with organisms consistent with IE)
Clinical criteria:
- 2 major OR
- 1 major + minor OR
- 5 minor
Possible IE:
- 1 major + 1 minor
- 3 minor
Infective endocarditis causative organisms
IVDU
- Staph aureus ~2/3
- Strep 25% (usually S. viridans)
- Candida
- Gram negatives ~10%
Non-IVDU
- Staph aureus 30-40%
- Staph lugdenesis
- Associated with high risk valve destruction
- Strep bovis (a.k.a. gallolyticus) 20%, esp. elderly
- Sanguis, mutans, mitis
- Q fevers in animal workers
- HACEK ~5%
- Haemophillus parainfluenzae
- Aggregatibacter actinomycetemcomitans
- Cardiobacterium hominis
- Eikenella corrodens
- Kingella kingae
Antibiotic treatment for infective endocarditis
Native valve IE:
Benzylpencillin 1.8g q4hrly
+
Flucloxacillin 2g q4hrly
+
Gentamicin 7mg/kg (septic) or 4-5mg/kg (not septic or renal dysfunction)
SWITCH fluclox to vancomycin 25-30mg/kg loading if MRSA suspected
Prosthetic valve and cardiac implantable device-associated:
Flucoxacillin 2g q4hrly
+ Vancomycin 25-30mg/kg loading
+ Gentamicin as above
If non-severe penicillin hypersensitivity replace fluxocavillin with cefazolin 2g q8hrly (up to q6hrly if septic)
OR
As per Dunn:
Vanc + gent + ceftriaxone
ECG features of VT (not morphology criteria)
- Wide complex
- Regular
- Rate 140-200 (not specific)
- Presence of fusion or capture beats
- Concordance is precordial leads from V1-6 (either positive OR negative)
DDx incl.
SVT aberrancy, SVT with WPW, PPM -mediated tachycardia, Na-channel toxicity (e.g. tricyclics)
AF spontaneous reversion rates
<1 hour - 25%
<6 hours - 40%
<24 hours - 50%
<48 hours - 65%
>1 week - rare
Factors decreasing likelihood of spontaneous AF reversion
*age > 65 years of age
*presence of heart failure
*late presentation
-90% revert with treatment if new onset and < 48 hours duration
-50% revert if new onset and > 48 hours duration
*previous episodes of AF
*recurrence whilst on appropriate anti-arrhythmic therapy
*structural cardiac lesions
*left atrial size
*secondary AF
AF reversion strategy options, pros and cons
IV options for rate control of AF
Metoprolol
- First line in most cases, safe in pregnancy and lactation
- 1-2mg aliquots to 5-15mg
Verapamil
- 1mg aliquots to 5-10mg
- Rapid but temporary rate contol
- Negative inotropy with greated relative effect at rapid HR
- Use with caution in elderly
Digoxin
- Rate-control often ineffective with significant sympathetic stimulation/secondary AF e.g. shock, sepsis, hypoxia
- Use predominantly for sedentary patients
- 500mcg IV (or PO) then 250mch 4-6 hourly to total 1500mcg loading
- Maintenance 62.5-250mcg/day
Magnesium
- 10mmol (2.5g) IV over 20 mins
- Additional modest reduction in ventricular rate whe used with digoxin or sotalol
- Moderately increases reversion rate to sinus rhythm
(Diltiazem IV not readily available in Aus; 20mg IV over 2 mins with second dose after 10-15 mins, as required; theoretically less risk of hypotension)
Causes/RFs of AF
- IHD 40%
*valvular heart disease
- especially involving the mitral valve
- hypertension
- obesity
* obstructive sleep apnoea
* genetic predisposition
- RR 3.5 for 1st degree relative with AF
- RR 1.6 for 2nd degree relative
* electrolyte disturbances
-hypokalaemia
-hypomagnesaemia
* thyrotoxicosis
-low TSH in 5%
-clinical hyperthyroidism in 1%
* cardiomyopathy
- sick sinus syndrome
* acute alcohol intoxication
- also known as holiday heart
- high spontaneous reversion rate
- lone fibrillators
- no cause found
- 5% of total
- 10% of those now appear to have a genetic endothelial defect that may be responsible
* channelopathies
- Brugada
- long and short QTc syndromes
Components of CHA2DS2Va score
Chronic heart failure +1
Hypertension +1
Age - 65-74 +1, >75 +2
Diabetes +1
Stroke/TIA/arterial TE, in past +2
Vascular disease +1
Score = 1, consider anticoagulation
Score >1, anticoagulation recommended
Superior to CHA2DS2VaSc which included female gender as +1
ECG: 50F 2/24 chest pain
LBBB – left axis deviation, QRS broad approx. 160ms
STEMI equivalent Sgarbossa criteria
- Concordant ST elevation (I, avL)
- Excessively discordant ST elevation >5mm (V2 V3)
Hyperacute tall T waves anterior leads (V2-V4)
ECG: 30M palpitation and chest pain
AF with RVR in context of WPW
- Rhythm irregularly irregular – atrial fibrillation
- Ventricular rate variable – approx. 200-250/min – very fast
- Left ward axis of broad complexes
- 2 types QRS complex – narrow and broad (mostly) – represent different pathways of activation of ventricles – narrow through AV node, broad through accessory pathway
- Delta wave seen best in V4
Historical features suggestive of VT
- Age > 35 (positive predictive value of 85%)
- Structural heart disease
- Ischaemic heart disease
- Previous MI
- Congestive heart failure
- Cardiomyopathy
- Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)
ECG: 18F collapse BG anorexia nervosa. ECG abnormalities?
Long QT
Sinus bradycardia
LVH - voltage criteria + LV-strain pattern
U waves
ECG: 45M 2/24 central chest pain. Main pathology and complication
Inferolateral STEMI with monomorphic VT
Inferolateral STEMI:
STE inferolateral leads II, III, aVF, V4-6
STE III>II suggestive of RV involvement
Q wave III
Reciprocal STD I aVL
Monomorphic VT:
Wide-complex tachycardia, regular, rate ~200/min
Fusion beat, capture beat
QRS concordance
AV dissociation
Jones Criteria for acute rheumatic fever
Carditis (including subclinical evidence of rheumatic valvulitis on echo)
Polyarthritis (or aseptic monoarthritis or polyarthralgia in high risk groups)
Sydenham chorea
Erythema marginatum
Subcutaneous nodules
Arrhythmogenic Right Ventricular Dysplasia (ARVD) ECG criteria
- T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
- Epsilon wave (most specific finding, seen in 50% of patients); sensitivity can be increased with Fontaine Leads (bipolar precordial leads with RA, LA and LL overlying RV)
- Localised QRS widening in V1-3 (> 110ms)
- Prolonged S wave upstroke of 55ms in V1-3
- Ventricular ectopy of LBBB morphology, with frequent PVCs > 1000 per 24 hours
- Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)
Epsilon wave
- Small deflection (“blip” or “wiggle”) buried in the end of the QRS complex
- On Standard 12-lead ECG (S-ECG), best seen in ST segment of V1 and V2, they are usually present in leads V1 through V4
- Caused by post-excitation of myocytes in the right ventricle
- Characteristic finding in patients with arrhythmogenic right ventricular dysplasia (ARVD)
Enhanced detection with Fontaine leads FI-III
Right ventricular outflow tract (RVOT) tachycardia ECG features
- LBBB morphology
- Inferior axis
- rS complex in V1 and R complex in V6
- Precordial transition usually ≥ V3, with the exception of septal origin, which occurs at ≤ V3
Largely idiopathic, can be caused by ARVD
Management options for reduction of risk of recurrent TdP post-successful cardioversion?
- Chemical overdrive pacing - Isoprenaline 5-30mcg/min, aim HR >100 BPM
- Synchronised transcutaneous pacing , aim HR 100 BPM
- Seek and treat electrolyte disturbance - aim Mg >1.0, K+ 4.5-5.0
- Calcium
- Avoid suspected precipitants
- Atropine if organophosphates suspected cause
Two treatments for APO + mechanisms
- NIV with CPAP - Commence at 8-10mmH20
- preload reduction through impeding SVC/IVC emptying into R heart; effect of improving gas-exchange at the alveolar-capillary membrane
- End-point: SBP <140 mmHg, decreased WOB, normoxia - GTN infusion - Commence at 25mcg/min (1.5mg/hr; 3mL/hr of 500mcg/mL)
- Vasodilation and preload reduction w/ mild benefit on myocardial work and oxygen demand through afterload and vasodilatory effects
- End-point: SBP <140mmHg
LAFB ECG criteria
- Left axis deviation (usually -45 to -90 degrees)
- qR complexes in leads I, aVL
- rS complexes in leads II, III, aVF
- Prolonged R wave peak time in aVL > 45ms
Brugada algorithm to differentiate VT from SVT with aberrancy
Step 1. Absence of RS complex in all precordial load? Yes -> VT
Step 2. R to S interval >100ms (in one precordial lead)? Yes -> VT
Step 3. AV dissociation? Yes -> VT
Step 4. Morphology criteria for VT present both in precordial leads V1-2 and V6?
- RBBB-like morphology: V1-2 has smooth monophasic R wave with notched downslope of the R wave (taller LEFT rabbit ear) and qR complex in V1; V6 QS complex w/ S>R (R:S ratio <1)
- LBBB-like morphology: V1-2 has initial R wave >30-40ms duration, notching or slurring S wave (Josephson sign) and RS interval >60-70ms; V6 QS waves and qR complexes
ECG features suggestive of VT
- Absence of typical RBBB or LBBB morphology
- Extreme axis deviation - negative QRS in both I and aVF
- Very broad complexes >160ms
- AV dissociation
- Capture beats
- Fusion beats
- Positive or negative concordance through precordial leads
- RSR’ complexes with taller left rabbit ear (in contrast to typical RBBB morphology)
- Brugada sign - Distance from onset of R wave to nadir of S wave >1000ms in V1-6
- Josephson sign - Notching/slurring near the nadir of the S wave
DDD Pacing - Definition, advantage, disadvantage
- Dual sensing of both atrium and ventricle
- Dual pacing of both atrium and ventricle
- If both SA and AV node functioning, pacemaker will just sense
- If either not functioning, pacemaker will take over
Advantages:
- AV synchronicity maintaned
- Use in AF and high grade AV blocks
- Heart rate responsive
- Possible decreased thrombotic events
Disadvtanges:
- Pacemaker mediated endless-loop tachycardia possible
- Pacemaker syndrome if incorrectly set-up
- May not be able to assess ST segments
Differential for tachyarrhythmia with PPM in situ
- Pacemaker-mediated tachycardia (PMT)
A re-entry tachycardia is created by the pacemaker forming an anterograde pathway and the AV acting as a retrograde pathway. the retrograde p wave is sensed as native atrial activity and further ventricular pacing is propogated causing inappropriate tachycardia
- May be treated with applying a magnet, vagal manoeuvres, adenosine or verapamil - Sensor-induced tachycardia
The sensor may misfire from ‘noise’ such as vibrations, loud noises, hyperventilation, surgical electrocautery etc. - Lead displacement dysrhythmia
A dislodged pacemaker lead may be irritating the myocardium
AAI pacing - Definition, advantages and disadvantages
- Atrial pacing and sensing
- If no electrical impulse sensed then PPM will pace at pre-programmed rate
- If electrical impulse sensed, pacing inhibited
Advantages:
- Single lead
- AV synchrony maintained
- Able to assess ST changes
Disadvantages:
- Unable to use in AF
- Ventricular vradycardia may occur in presence of high-grave AV block
- Instability of single atrial lead
- Higher risk in thin atrial atrial wall
VVI pacing - Definition, advantages and disadvantages
- Ventricular pacing and sensing
- If no electrical impulse sensed then PPM will pace at pre-programmed rate
- If no electrical impulse then pacing inhibited
- Asynchronous pacing
Advantages:
- Requires single lead
- Useful in presence of AF and high-grade AV block
Disadvantages:
- AV synchronicity lost
- Unable to assess ST changes
- Loss of atrial kick
- Risk of PPM syndrome
Sgarbossa criteria
- Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)
- Concordant ST depression > 1 mm in V1-V3 (score 3)
- Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)
*Smith-modified: “Proportionally excessive discordant STE in >=1 lead, >=25% depth of preceding S wave
Factors favouring rate vs rhythm control in AF/flutter
Drug treatment of SVT with failure to respond to vagal manoeuvres and adenosine
Verapamil
- 5mg slow aliquots up to 15mg
- 5mg 80% reversion
- 10mg 95% reversion
Potentially more effective than adenosine in patients with caffeine ingestion in preceding 4 hours
SE hypotension but can be mitigated with pre-treatment of 5mL CaGluconate 10%
What is Beck’s Triad?
Clinical triad for acute cardiac tamponade
1. Muffled heart sounds
2. Hypotension
3. Raised CVP
Causes of pericardial effusion
ECG: 74F chest pain, PPM in situ for slow AF - findings and management
Pacemaker-mediate tachycardia (PMT)
- Paced rhythm at ~130 BPM
- Pacing spikes after every QRS
- Retrograde p-waves (I, V1-2,V5-6)
Apply magnet to pacemaker
- When applied converts to asynchronous pacing which turns off the sensing mode and allows the PPM to pace the atria and ventricles asynchronously
