Cardiology quickfire 2 Flashcards
LAFB vs LPFB vs bifasicular block
LAFB:
- QRS <120ms
- Left axis deviation
- qR pattern in Lead I and aVL
- rS pattern in leads II, III and aVF
LPFB:
- QRS <120ms
- Right axis deviation
- rS pattern in leads I and aVL
- qR pattern in leads II, III and aVF
Bifascicular block
- RBBB + LAFB = RBBB pattern + QRS >120ms + left axis deviation
OR
- RBBB + LPFB = RBBB pattern + QRS >120ms + Right axis deviation
(note: RBBB in isolation does not produce axis deviation)
Trifascicular block:
- Bifascicular block + complete heart block
Endocarditis
- indications for urgent surgical referral
- Prolonging PR interval, which indicates aortic root abscess
- Fever persisting for >1 week, which indicates intra-cardiac abscess
- Recurrent septic emboli despite antibiotics
- Heart failure secondary to MR/AR
- Septal perforation
- Large vegetations >15mm require surgical opinion but not necessarily urgent surgery
Familial hypercholesterolaemia
a) 3 core features
b) Inheritance
c) Management
a) - LDL cholesterol >5 (often >10 in homozygous)
- Tendon xanthomata
- Coronary artery disease at young age (if homozygous, likely CAD in 20-30s)
b) Autosomal dominant
- Low-density lipoprotein receptor (LDLR) gene mutation in 90%
c) Statins +/- etezimibe +/- colestyramine
- Ezetimibe inhibits the intestinal absorption of cholesterol
- N.B. Fibrates have no effect on LDL-C. They are used to reduce serum triglycerides only
H2FPEF score
H - heavy (BMI >30)
H - hypertensive (2+ anti-HTNs)
F - fibrillation (AF)
P - pulmonary HTN (PA >35 mmHg)
E - elderly (age >60)
F - mitral Filling pressure (E/e >9)
Aortic dissection
a) Stanford Classification
b) De Bakey classification
c) Management
d) If cardiac tamponade present
a) - Group A - involve Ascending aorta (De Bakey 1 and 2)
- Group B - do not involve ascending aorta (De Bakey 3)
b) De Bakey:
1 = ascending aorta to the arch (highest mortality - 1% per hour)
2 = ascending aorta but not as far as the arch
3A = descending aorta not beyond the diaphragm
3B = descending aorta beyond the diaphragm
c) - Cardiothoracics needed urgently
- Labetalol* for BP control to prevent progression of dissection
*Contraindications: severe asthma/COPD, heart block, bradycardia, hypotension
d) - Suggests bleeding from an ascending aortic dissection into pericardial sac causing haemopericardium
- Presents as muffled heart sounds and dilated neck veins
- Pericardiocentesis can increase the intra-aortic pressure and worsen the dissection, so must only be attempted if severe hypotension due to tamponade
Normal heart pressures
a) Left ventricle
b) Right ventricle
c) Left atrium (how is this assessed?)
d) Right atrium (CVP)
e) Pulmonary artery
a) LV: 100-140 systolic, 3-12 diastolic
b) RV: 15-30 systolic, 3-8 diastolic
c) LA: 2-15
(measured via pulmonary capillary wedge pressure) - raised in mitral stenosis or pulmonary hypertension
d) RA (CVP): 3-8
e) Pulmonary artery: 15-25
VSD
a) Saturations in RV vs RA
b) Pressures in heart
a) Elevated RV sats >80% (due to shunting of oxygenated bloods from LV to RV), and reduced LV sats
b) Elevated RV pressure >30 (due to shunting of oxygenated bloods from LV to RV
AVRT
a) What is an accessory pathway? (example)
b) Orthodromic vs Antidromic conduction in AVRT, and treatment for each
c) Pre-excitation explained
d) ECG findings in WPW
a) - Conducting tissue connecting the atria and ventricles (usually separated by non-conducting tissue, relying on AV node conduction)
- Example: Bundle of Kent in WPW
b) Orthdromic (95%):
- Anterograde depolarisation from Atria –> AVN –> Bundle of His/Purkinje
- Then retrograde depolarisation via Accessory pathway. Once it reaches AVN, cycle starts again
- As uses normal conducting pathway to depolarise, it is a narrow complex tachycardia (mistaken for sinus tachy/AVNRT)
- Rx: adenosine*, DC cardioversion if unstable
*Avoid any AV nodal blockers if AF or flutter present
Antidromic (5%):
- Anterograde depolarisation via Accessory Pathway, which results in cell-cell depolarisation of ventricles slowly (hence wide QRS)
- Then retrograde depolarisation up Bundle of His and to the AV node. Once it goes back to the accessory pathway, the cycle begins again
- As depolarisation does not use normal conduction pathway, causes a wide complex tachycardia (mistaken for VT)
- Rx: (as for broad-complex tachycardia) amiodarone, DC cardioversion if unstable
c) Conduction to ventricles via accessory pathway before conduction via AVN, causing a delta wave
d) Pre-excitation:
- Short PR, with Delta wave and prolonged QRS (due to slurred delta wave)
WPW with orthodromic AVRT:
- No delta waves
- Narrow QRS <120 ms
- May result in narrow complex tachycardia
WPW with Antidromic AVRT:
- Short PR interval with Delta waves
- Broad QRS >120 ms
- May result in broad complex tachycardia
WPW with AF:
- Variable QRS morphology - some narrow (orthdromic conduction) and some broad (antidromic conduction)
- Rate up to 300bpm
- Delta waves may be visible
AVNRT
a) What is an AVNRT?
b) 2 basic types
c) Which pathway does radio-ablation usually affect?
d) Why is adenosine useful?
e) ECG findings
a) - 2 pathways form within the AV node, connecting the atria and ventricles - a fast and slow pathway
- The fast pathway has a fast conduction but long refractory period, while the slow pathway has a slow conduction but short refractory period
retrogradely up the fast pathway and then cycles back round the slow pathway ad infinitum
Slow-fast (90%):
- Anterograde conduction via the slow pathway
- Retrograde (re-entrant) conduction via the fast pathway
Fast-slow (10%):
- Anterograde conduction via the fast pathway
- Retrograde (re-entrant) conduction via the slow pathway
c) Slow pathway (if fast pathway destroyed, may result in heart block)
d) Temporarily blocks AV node conduction, which can break the re-entry circuit
e) - Narrow complex tachycardia, Rate 140 - 280 bpm
- P waves often not visible (as atrial contraction occurs simultaneously with ventricular contraction)
- If p waves visible, may be inverted in inferior leads (due to retrograde conduction)
Cardioversion for AF
a) Anticoagulation
b) Shock delivery
c) Success and relapse rates
a) - If presenting within 48h, or in an emergency give LMWH then cardiovert
- Otherwise, effective anticoagulation (INR >2) needed for 4 weeks (if not, TOE performed to exclude a clot in left atrial appendage)
- After successful cardioversion, anticoagulation must be continued for 4 weeks*
- If slow AF, pacing wire fitted pre-cardioversion
- Control any hyperthyroidism, heart failure and hypokalaemia before cardioversion
*If high risk for stroke (e.g. previous Stroke/TIA), would be considered for lifelong anticoagulation even after successful cardioversion
b) - 100J (1x), then 200J (1x), then 360J (up to 2x)
- Synchronise* with R wave to prevent R-on-T and Torsades
*Only cardioversion for VF/VT arrest should be unsynchronised
c) 90% success, but 50% relapse at 1 month and 90% at one year
Heart block in ACS
a) Most common arteries affected and relative prognosis
a) Proximal RCA:
- Inferior MI
- High grade AV block (Mobitz II or 3rd degree) in 25%
Distal RCA:
- Inferior MI
- More likely to cause 1st degree HB or Mobitz type 1
Proximal LAD:
- Anteroseptal MI
- If heart block is present, indicates massive infarct affecting both bundle branches, with very poor prognosis
Circumflex:
- Lateral infarct
- 10% patients have AV nodal supply from CxA but this is much less common than RCA and LAD as cause of heart block
ARVC
a) ECG finding
a) Epsilon potentials:
- Notch after the QRS in V1 and V2, indicating delayed RV depolarisation
Valsalva manoeuvre
a) How modified valsalva works in SVT
b) Contraindications
a) - Blowing into syringe for 15 secs causes rise in intra-thoracic pressure and decreased venous return.
- When this is stopped, there is an abrupt increase in venous return and cardiac output, causing a reflex bradycardia which may terminate the SVT
- This can be enhanced by putting legs in the air
b) - Haemodynamically unstable
- AF, atrial flutter
- MI in last 3 months
- Aortic stenosis
- Glaucoma
- Retinopathy
- Pregnancy 3rd trimester
ASD
a) Ostium primum vs secundum
b) vs. PFO
c) When can PFOs cause issues?
d) How are PFOs investigated?
e) Other ASD
f) When do ASDs tend to present?
g) Indications for closure
a) ASDs are congenital heart diseases from a failure of atrial septal closure:
- Ostium secundum occurs when the mid-portion of the septum (secundum) fails to close - this is the most common. It commonly causes RBBB, and MVP
- Ostium primum occurs when the lower portion of the atrial septum (primum) fails to close. This commonly causes LBBB, and cleft mitral valve
b) - PFO is not a congenital heart disease, as it is the failure of foramen ovale closure AFTER birth
- Occurs in around 25% people, most are asymptomatic. There are no signs/murmurs on examination for PFO
c) - Usually kept closed by increased left heart pressure
- Increased right heart pressure can cause it to open (e.g. scuba-diving), resulting in cyanotic heart disease
- Paradoxical embolus
d) Agitated saline (bubble) ECHO:
- After administration of IV saline, bubbles seen in right atrium (normal)
- Valsalva performed –> leads to opening PFO and bubbles seen in left atrium (abnormal)
e) Sinus venosus - associated with arrhythmias and anomalous pulmonary veins
f) In adulthood. 50% mortality by age 50
g) Systemic SpO2 <92%
- Shunt ratio > 1.5 : 1
- Note: ASDs don’t usually cause an issue in pregnancy
Hypertensive emergency.
a) Define
b) Aim of treatment
c) Treatment types
a) >180/120 (or signs of end organ damage)
b) - Reduce MAP by 25% in first 24h
(more than this risks organ hypoperfusion)
- Or aim for diastolic BP reduction of one-third
c) - Bed rest + oral treatment preferred
- If required (e.g. severe end organ damage), IV treatment can be used but requires monitoring:
1. Labetalol 2mg/min (up to max dose 200mg)
2. GTN
3. Hydralazine
4. Sodium nitroprusside
