passmed Flashcards
long QT - what is normal
QT interval in females = <450ms and in males <430ms
causes of long QT syndrome
Inherited mutations - Jervell Lange Nielsen, Romano Ward
Acquired causes:
-Electrolyte imbalance - HYPOKALAEMIA, HYPOCALCAEMIA, HYOPMAGNAESAEMIA
-Meds - tramadol, amiodarone, TCAs, SSRIs, erythmocyin, methadone, chloroquine, terfenadine etc
-CNS lesions: SAH + ischaemic stroke
-Malnutrition
-Hypothermia
what can long QT syndrome lead to
VT / TdP –> collapse/sudden death
cholesterol of 5.1 + QRISK score of 11%
what is the mx
statins - atorvastatin 20mg 1st line for primary prevention
- INCREASE DOSE IF NON-HDL has not REDUCED by >40%
- atorvastatin 80mg for secondary prevention
- simvastatin for those who can’t tolerate it
- save dietary measures for those with qrisk <10%
statins MoA and adverse effects (3)
HMG CoA reductase INHIBITOR , rate-limiting enzyme, in hepatic CHOLELSTEROL synthesis
Adverse effects:
-MYOPATHY - myalgia, myositis, rhabdomyolysis + asympt raised CK
-LIVER IMPARIMENT - check LFTs at baseline, 3m, 12m
-STATINS - can incr risk of ICH in pts who hv had previous stroke - effect not seen in primary prevention
statins CI (2)
Macrolides = stop statins till pt course complete
pregnancy
difference between primary and secondary preventio
primary - measures to prevent onset of illness before disease process begins eg QRISK >10% OR most T1DM pts OR CKD eGFR<60 —> ATORVASTATIN 20mg
secondary - measures that lead to early dx and prompt tx of disease eg known IHD OR CVD OR PAD –> ATORVASTATIN 80mg OD
ECG changes for thrombolysis or PCI
ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR
ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR
New Left bundle branch block
how do loop diuretics work
furosemide and bumetanide are loop diuretics that act by INHIBITING NA-K-Cl cotransporter in the thick ascending LoH, reducing the absorption of NaCl
Loop diurtics adverse effeects
LOW BP, Na+, K+, Mg+, Cl
LOW Ca2+ –> excess PTH secretion –> more calcium released from bone –> weakens structure
RENAL IMPAIRMENT (from dehydration + direct toxic effect)
HIGH GLUCOSE (less common than with thiazides)
GOUT
posterior MIs ECG findings
cause reciprocal changes in V1-3 (anterior leads) as these leads are directly opposite posterior surface
- ST depression
- tall broad R waves
- upright T waves
- dominant R wave in V2
complete heart block following an MI, where is the lesion
commonly RCA lesion
-AVN is supplied by a branch of the RCA, posterior interventricular artery
aortic stenosis mx
- observe pt is general rule
- if symptomatic then valve replacement
- if asymptomatic but valvular gradient >40mmHg and features eg LV systolic dysfunction then consider surgery
- as CVD can coexist, often do angiogram before surgery so procedures can be combined with PCI
- BALLOON VALVULOPLASTY limited to pts with critical aortic stenosis
acute pericardits acute mx
NSAIDs + colchicine used 1st line - for pts with acute idiopathic or viral pericarditis
thiazides affect on calcium levels - in blood + urine
BLOOD - HYPERCALCAEMIA
URINE - HYPOCALCIURIA
MX for bradycardia + signs of shock
require 500micrograms of IV atropine (repeated up to max 3mg)
- bradycardia only req tx when HR is less than 60 + SYMPTOMATIC/signs of haemodynamic compromise
- if this fails then consider TCPacing
- NB. amiodarone is a RF for dev severe bradycardai
cardiac tamponade becks triad
HYPOTENSION
RAISED JVP
MUFFLED HEART SOUNDS
cardiac tamponade : JVP, Pulsus Paradoxus, Kussmauls sign
JVP - absent Y descent - TAMpaX
PP - present
K..Sign - Rare
Constrictive pericarditis: JVP, Pulsus paradoxus, Kussmauls, Char Feat
JVP - X+Y present
PP - absent
Kussmauls- present - JVP rises on inspiration
Char feat - pericardiac calcification on CXR
trifascicular block
RBBB + left anterior or posterior hemiblock + 1st-degree heart block = trifasicular block
bifascicular block
combination of RBBB with left anterior or posterior hemiblock
e.g. RBBB with left axis deviation
how to reduce the risk of sudden cardiac death in HOCM
ICD
can LBBB be normal in athletes
NO NEVER NORMAL - means underlying ischaemic or structural heart disease
what are cannon a waves and when do they occur
due to atria and ventricles contracting together –> RA contracts against closed tricuspid valve , column of blood shoots up the SVC into the jugular vein
-COMPLETE HEART BLOCK
what JVP waveform is seen in TR
Large V waves
-ventricular contraction causing blood to surge through an incompetent TV through RV into Jugular vein
what is Kussmaul sign + what is it caused by
paradoxical rise in JVP on inspiration
-caused by conditions that impari ventricular filling
eg CONSTRICTIVE PERICARDITIS
what JVP waveform is seen with tricuspid stenosis
Slow Y descent
what happens to JVP in SVCO
raised JVP with ABSENT PULSATION
what is dresslers syndrome
PERICARDITIS after MI (can cause pericardial effusion)
2-10 weeks later due to production of AUTOANTIBODIES after MI
DIFFERENT to simple post-MI pericarditis 2-4 DAYS after MI
