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.