Cardio Summary Flashcards
define VT
a broad complex tachycardia, originates from a ventricular ectopic focus, hence activity is independent of the atria and does not depend on AVN conduction.
most common cause of monomorphic VT?
MI
what are the ECG features of monomorphic VT?
regular rhythm, fast HR-broad complex tachycardia
capture beats-result of normal conduction via AVN producing ventricular contraction which results in a narrow complex
fusion beats-intermediate between VT beat and a capture beat
AV dissociation-lots of Rs (ventricular depolarisation from ectopic focus), not many Ps
indications for immediate synchronised DC cardioversion for VT treatment?
pt is haemodynamically unstable-systolic BP less than 90, evidence of heart failure, chest pain.
what is given and how as drug treatment for VT WITHOUT adverse signs?
IV amiodarone 300mg over a few mins, (class III antiarrhythmic) followed by 900mg IV over 24hrs, given through a central line
or
IV lidocaine 50-100mg over 3-5mins which can be rpt after 5 mins. (use with caution in severe LV impairment).
temporary overdrive pacing may be useful in resistant VT
if fail, consider DCCV or pacing
if non sustained VT (less than 30s) can treat with a beta blocker.
LT=ICD
congenital causes of long QT?
romano-ward syndrome
jervell-lange-nielsen syndrome (includes deafness and is due to abnormal K+ channel)
indications for treating a patient with stage 1 HTN?
this is a pt who on ambulatory/HBPM averages at 135/85 or more
start treatment if pt under 80yrs AND any 1 of following:
10 year CVS risk score of 20% or more
target organ damage
renal impairment
DM
established CVD
a 35 year old afro caribbean pt has been found to have an average BP on ambulatory monitoring of 139/85, how should they be managed?
stage 1 HTN: 1st line drug tment=Ca2+ blocker e.g. amlodipine as afro-caribbean, but ONLY if pt had either 1 of: CVD, CKD, DM or evidence of end organ damage e.g. HTN retinopathy, HF, or 10 year CVD risk of 20% or more.
if BP fails to be controlled with this, next step would be to add an ACEI/AngIIRB.
as pt under 40yrs, consider referral to a specialist to investigate for secondary causes e.g.
vasc-renal artery stenosis, aorta coarctation
metabolic and endocrine-conn’s syndrome, CAH, cushing’s syndrome
neoplasia-pheochromocytoma-palpitations, headache and HTN
drugs-steroids
other-PKD
when should adenosine NOT be given to terminate an SVT?
adenosine contraindicated in patients with: asthma COPD decompensated HF long QT 2nd or 3rd degree HB sick sinus syndrome (unless pacemaker fitted) severe hypotension
in asthma patients, verapamil is the preferred option
causes of RBBB?
normal variant RV hypertrophy chronically increased RV pressure e.g. cor pulmonale PE MI ASD cardiomyopathy or myocarditis
pharmacological treatment of acute SVT?
adenosine IV 6mg, then 12mg, then 12mg
for LT treatment at home pt may have a beta blocker or sotalol (class III), or flecainide or diltiazem or verapamil.
this follows vagal stimulation e.g. valsalva, carotid massage, immersing face in ice cold water, with ECG monitoring.
failure to terminate may suggest atrial flutter or focal atrial tachycardia.
drugs shown to improve mortality in chronic heart failure?
ACEIs beta blockers spironolactone angII RBs nitrates combined with hydralazine
what is an alternative treatment to CRT or digoxin for patients with chronic HF who are not managed adequately on an ACEI, beta blocker and spironolactone?
can give ivabradine=lowers the HR by selective and specific inhibition of If funny Na+ channel current in pacemaker cells in the SAN.
what estimating RISK criteria are available for patients with ACS?
TIMI and GRACE scoring
GRACE-estimates admission to 6 mnth mortality for ACS patients, more validated for distinguishing between low and high risk patients.
most specific ECG marker of pericarditis?
PR depression
causes of pericarditis?
often viral-coxsackie post MI-dressler's synrome trauma TB CTD e.g. SLE uraemia hypothyroidism
initial drug treatment of haemodynamically stable patient with an irregular broad complex tachycardia?
?polymorphic VT, torsades-QT interval prolongation, pre-excited AF, AF with aberrant conduction
IV magnesium sulfate 2g
for torsades, other than magnesium may also consider a beta blocker or pacing.
lifestyle advice for managing HTN?
low salt diet, aiming for less than 6g/day and ideally less than 3 lower caffeine intake healthy balance diet exercise lose weight smoking cessation reduce alcohol intake
drug treatment for stable angina?
-consider antiplatelet (aspirin 75mg daily) and statin (atorvastatin 80mg) in absence of any contraindication for secondary prevention of CVD.
SL GTN for angina attacks
beta blocker or Ca2+ channel blocker 1st line depending on pt choice, comorbidities and CIs, if Ca2+ as monotherapy use rate limiting e.g. diltiazem or verapamil. if in comb with beta blocker then long acting dihydropyridine e.g. nifedipine
increase to max tolerated dose if inadequate control, if still inadequate swap to other or add it on
if cannot tolerate, then consider adding LA nitrate or ivabradine-ADR include luminous phenomena or nicorandil or ranolazine
3rd anti anginal only if pt not controlled and is awaiting PCI or CABG assessment or these have been deemed inappropriate
biggest RF for infective endocarditis?
previous episode of endocarditis
non-infective causes of endocarditis?
SLE (libman-sacks)
malignancy-marantic endocarditis
when is rate control the preferred 1st line drug treatment for acute AF e.g. beta blocker or rate limiting Ca2+ blocker e.g. verapamil or diltiazem?
if onset is more than 48hrs or is uncertain
would NOT be 1st line if new onset AF, heart failure secondary to AF, AF with a reversible cause, or rhythm control indicated clinically e.g. with flecainide.
preferred treatment for rapid control of ventricular rate in atrial flutter?
IV beta blocker or verapamil
note anticoagulant treatment follows same assessment criteria as for AF
treatment for recurrent atrial flutter?
catheter ablation
treatment of bradycardia post MI?
IV atropine, 500 micrograms every 3-5mins, max=3mg per course
treatment of pre-excited AF?
electrical cardioversion, as risk of sudden death.
