Cardio Flashcards
what is brady+tachy-cardia
Brady <60bpm, tachy >100bpm
what causes acute bradycardia
drug induced = B blocker, CCB
sinus/AV nodal disease
electrolyte abnormalities = hyperK
hypothyroidism
how does bradycardia present
syncope
dizzy, tired
according to ALS, what is the management of bradycardia
DR ABCDE approach - ECG monitoring, treat reversible cause (stop specific drug)
if due to B-blocker/CCB overdose = give glucagon
if heamodynamic instability = IV atropine 500mcg (repeat upto 6 times till 3mg)
if not working, use isoprenaline, adrenaline
definitive treatment = permanent pacemaker
(use transcutaneous pacemaker as an interim)
what is MOA of atropine
blocks vagus nerve activity, so SA firing rate increases
if bradycardia due to B blocker/CCB overdose, what is done
give glucagon (or glycopyrrolate)
how is tachycardia classified
narrow QRS complex <120ms:
irregular rhythm - atrial fib
regular rhythm (SVT) - atrial flutter, AVNRT, WPW (AVRT)
borad complex >120ms:
irregular rhythm - vent fib
regular rhythm - vent tachy (polymorphic VT = torsades)
how is narrow complex tachy managed according to ALS
DR ABCDE approach
determine if broad or narrow QRS complex
determine if regular or irregular rhythm
if haemodynamic instability - shock, syncope, pulmonary oedema, MI = synchronised DC shock
if haemodynamically stable:
irregular (likely AFib) - same management if atrial flutter:
if within 48hr rhythm control (LMWH then flecinaide - if structural heart disease, give amiodarone instead)
if 48+hr rate control + anticoagulant (B-blocker, verapamil - if HF give digoxin)
regular (likely SVT)
1 - vagal manoeuvre (carotid sinus massage, vasalva)
2 - IV adenosine 6mg bolus (repeat twice with 12mg then 18mg boluses) - in asthmatics, use verapamil instead as adenosine causes bronchospasm
when to anticoagulant for Afib
if Afib onset 48+hr
anticoagulant with rate control (B-blocker, verapamil/diltiazem)
how are SVT treated
if haemodynamic instability, shock, pulmonary oedema, syncope, MI = synchronised DC shock
if haemodynamically stable:
vagal manœuvres - carotidien sinus massage, vasalva
IV adenosine 6mg, then 12mg and 18mg boluses
what is an irregular broad complex tachy
ventricular fibrillation - always a pulseless rhythm
QRS complexes are polymorphic + irregular
what is VF
arrhythmia occurring in heart ventricles, creates fibrillation waves
always pulseless + broad complex tachy
on ECG - polymorphic QRS, no identifiable P wave, HR 150-500bpm
according to ALS, how is VF managed
DR ABCDE
shockable rhythm - administer unsynchronised DC
continue chest compressions
after 3rd shock, administer 1mg adrenaline (1:10,000) + 300mg amiodarone
continue giving adrenaline after every alternate shock 3-5min
what are ECG features of VT
tachycardia >100bpm
regular rhythm
no P waves
monomorphic broad QRS >120ms
how is VT managed
if pulseless VT = unsynchronised DC shock
continue CPR and recheck
IV adrenaline (1:10,000) + 300mg amiodarone after 3rd shock
administer adrenaline after every alternate shock
if VT with adverse features (shock, syncope, pulmonary oedema, MI)
synchronised DC shock (max 3x)
IV amiodarone - 300mg over 10min, then 900mg over 24hr
if VT with no adverse features
IV amiodarone - 300mg over 30min, then 900mg over 24hr
what is torsades
polymorphic VT caused by prolonged QT interval
ECG shows QRS complex twisting around isoelectric line
QT interval >450ms (prolonged ventricular repolarisation, disposing to ventricular arrhythmia)
what causes torsades
prolonged QT interval >450ms
drugs:
anti-arrhythmic - amiodarone, quinidine
antibiotics - gentamicin/erhythromicin, fluconazole
TCA, SSRI, antipsychotic - haloperidol
MI, AV block, renal/liver failure, hypothyroidism
romano-ward syndrome (genetic - Na/K channel mutation)
how is torsades managed
if adverse features = synchronised DC shock, then IV amiodarone
if no adverse features = IV MgSO4 (2g over 10min)
stop drugs
treat electrolyte abnormalities - hypoK, hypoMg
what is WPW
AVRT - congenital accessory pathway connecting atria to ventricles, bypassing AV node
causes re-entery circuits, leading to SVT
affects men more than women
what are clinical + ECG features of WPW
clinical: usually aymptomatic
syncope, palpitations, dizzy
ECG: delta waves (slurred upstroke to QRS)
if re-entrant circuit developed, narrow QRS complex <120s
how is WPW diagnosed
ECG - 24hr if paroxysmal symptoms
bloods including TFT
echo to check ventricular function
how is WPW acutely managed
if adverse features (BP <90/60) = synchronised DC shock
if no adverse features = vagal manoeuvre, IV adenosine 6mg (then 12mg then 18mg boluses)
how is WPW managed long-term
definitive = radio frequency ablation of accessory pathway
medical - amiodarone, sotalol (contraindicated in structural heart disease)
what is AF
atrial fibrillation - most common sustained cardiac arrhythmia
atrial fibrillation = unco-ordinated atrial contraction of 300-600bpm
but only some of the impulses are conducted to ventricles, due to AV node delay
so there is irregular ventricular response
what are causes of AF
cardiac:
IHD (most common cause in UK), HTN
rheumatic heart disease of mitral valve (most common in developing countries)
peri/myocarditis
non-cardiac:
hyperthyroidism, alcohol abuse
pneumonia, PE, sepsis
electrolyte disturbance - hypoK, hypoMg
dehydration
how is AF classified
acute = <48hr
paroxysmal = intermittent for <7 days
persistent = lasts 7+ days, amended by cardioversion
permanent = lasts 7+ days, not resolved by cardioversion
fast AF = when ventricular rate >100bpm
what are clinical signs of AF
symptoms - palpitation, chest pain, dyspnoea, dizzy
sign - irregularly irregular pulse + absent P waves
single waveform on JVP as ‘a’ wave lost
apical to radial deficit
what is fast AF
when ventricular rate 100+ bpm
how is AF managed
if haemodynamically unstable (BP <90/60, in shock/syncope, MI/chest pain, pulmonary oedema) = synchronised DC
if no adverse features:
TREAT REVERSIBLE CAUSE - replace K/Mg, IV fluids
1) rate control with B blocker or CCB
if AF perisists:
onset within 48hr, rhythm control = electrical cardio version or pharmacological = felcanide (or amiodarone if old sedentary patients
onset 48+hr, rate control + anticoagulant = B-blocker (or verapamil/diltiazem if asthma)
when is rate control not offered first-line for AF
new-onset AF within 48hr
if reversible cause
heart failure caused by AF
what is given for rate control in AF
B blocker (bisoprolol - contraindicated in asthma/COPD or hypotension)
nonDHP CCB (verapamil, diltiazem - contraindicated in HF) - rate limiting CCB
give digoxin if HF + AF (used in conjunction with B blocker if refractory fast AF)
avoid for younger patients
when is B blocker contraindicated for AF
asthma, COPD
hypotension
use bisoprolol mainly - sotalol not used as it has rhythm control action
why may a TOE echo be done for AF
to rule out thrombus in left atrial appendage
why is anticoagulation done for AF
AF complication = risk of embolic stroke
calculate CHADVASC2 score, anticoagulant if score:
1+ male or 2+ female
offer DOAC - apixaban, rivaroxiban
doesn’t require monitoring, less bleeding risks compared to warfarin
warfarin given if valvular AF
how is bleeding risk assessed in AF
HAS-BLED or ORBIT scores
when is atrial ablation done
if TOE finds thrombus in left atrium (atrial appendage)
what is atrial flutter
type of SVT (narrow complex tachycardia with regularly irregular rhythm)
caused by aberrant macro-circuit in right atrium
atria contract at 300bpm, ventricles contract at 150bpm = 2:1 conduction block
what are ECG features of atrial flutter
regularly irregular rhythm - ventricular rate depends on AV block (150bpm = 2:1, 100bpm = 3:1)
narrow QRS complex <120ms
sawtooth P waves at 300bpm
how is atrial flutter managed
similar to AFib
if haemodynamically unstable = synchronised DC shock
shock BP <90/60 (organ hypo perfusion), syncope (brain hypo perfusion), chest pain (MI), pulmonary oedema (HF)
if haemodynamically stable = rate control pt with B blocker or CCB
if not responding to rate control, then cardiovert pt (electrical > pharmacological)
what disease causes sudden cardiac death in southeast asian male
brugada syndrome - genetic condition causing Na channelopathies
presents with palpitations - tachyarrhythmia (VF/VT)
FH of sudden cardiac death <45yr (investigate with genetic testing)
RF: fever, excess alcohol, dehydration, hypoK/Mg
drugs - flecanide, verapamil, amitriptyline
manage definitively with ICD
what is HF + causes
when heart unable to pump enough blood (so unable to maintain CO) to meet body’s metabolic demands
low-output (CO is too low) - classified as systolic or diastolic dysfunction
high-output (CO is normal but increased body demands): anaemia, AV malformation, pregnancy, Paget disease, thyrotoxicosis, thiamine deficiency (wet Beri-beri)
what is systolic + diastolic HF
systolic HF (reduced EF) = IHD, dilated cardiomyopathy, myocarditis
diastolic HF (preserved EF) = HOCM, restrictive cardiomyopathy, constrictive pericarditis, cardiac tamponade
what are the signs of cardiac tamponade
beck triad = hypotension, raised JVP, muffled heart sounds
how do R + L sided HF differ
L-sided = pulmonary congestion
SOB on exertion, othropnea/PND, nocturnal cough (pink frothy sputum)
tachypnoea, bibasal fine crackles (+ pulses alterans)
R-sided = venous congestion
peripheral oedema (ankle swelling, weight gain), abdo distension
raised JVP, pitting/sacral oedema, hepatomegaly, ascites, bilateral pleural effusion (coarse crackles)
how is HF classified
NYHA classification - 4 stages
1 - no limitation in physical activity
2 - slight limitation in physical activity, comfortable at rest
3 - marked limitation, comfortable at rest
4 - uncomfortable at rest, can’t do any activity
how is HF investigated + when to order TTE/TOE
ECG
bloods = NT-pro-BNP
if BNP 400-2000, order TTE echo in 6wks + specialist assessment
if BNP >2000, order TTE in 2wks + specialist assessment
CXR:
alveolar oedema - batwing shadow
Kelley B lines - interstitial oedema
cardiomegaly - CTR >0.5
upper lobe diversion
pleural effusion - bilateral transudate
how is reduced + preserved EF determined
depending on EF seen on echo
if EF <40%, HFrEF = reduced ejection fraction
if EF 40+ % with raised BNP = HF with preserved EF
how is HF managed
conservative = stop smoking, restrict salt/fluid intake, cardiac rehab
medical = ACEi/ARB + B-blocker
+ mineralocorticoid antagonist (spironolactone) if symptoms persist
if sinus rhythm with HR>75bpm but reduced EF = ivabradine
if HF + AF = digoxin
give loop diuretic (furosemide) for symptom relief
definitive/surgical = ICD for cardiac resynchronisation
what to give if ACEi/ARB not tolerated
hydralazine + nitrate
how is pulmonary oedema in HF acutely managed
sit pt upright
O2 therapy for sats >94%
IV furosemide 40mg + monitor fluid balance with catheter
what are the diagnostic criteria for HTN
BP >140/90 in clinical setting
BP >135/85 on ABPM/HBPM
is HTN mostly essential/primary OR 2ndary
mostly 90% primary
2ndary causes = ROPED
renal disease (renal artery stenosis)
obesity
pregnancy, pre-eclampsia
endocrine - hyperaldosteronism
drugs - alcohol, NSAID, steroid, COCP, E2
how does HTN present
usually asymptomatic
unless malignant HTN (>180/120 + papilloedema/retinal haemorrhage)
what is malignant HTN
BP >180/120 with retinal haemorrhage or papilloedema
how is malignant HTN managed
if BP >180/120 + retinal haemorrhage/papilloedema
1 - same day fundoscopy
2 - IV labetalol, GTN, sodium nitropusside, phentolamine (alpha blocker)
how often is HTN measured
every 5yr to screen for HTN
annually if borderline or T2DM
what investigations are done if end-organ damage is suspected
ECG = LV hypertrophy
dipstick (haem/proteinuria, ACR) = renal disease
bloods = HbA1c, lipid profile
fundoscopy = hypertensive retinopathy
what are lab findings for conn syndrome + renal disease
conn syndrome = hyperNA + hypoK
renal disease = protein/haematuria, low eGFR
how is HTN managed
measure QRISK score - risk of stroke/MI in next 10yr
conservative - lifestyle advice, stop smoking
consider medical management if 80yr+ or stage 2 HTN (BP >160/100 clinic or >155/95 ABPM)
1) ACEi/ARB if <55yr/diabetic or CCB if 55yr+/black
2) ACEi + CCB or ACEi + diuretic or CCB + diuretic
3) ACEi + CCB + thiazide-like diuretic (indapamide)
4) depending on K level (if low <4.5, spironolactone - if normal, alpha blocker)
what are different stages of HTN
stage 1: >140/90 in clinic, >135/85 ABPM
stage 2: >160/100 in clinic, >155/95 ABPM
stage 3 : >180/120
(malignant HTN if this BP + retinal haemorrhage or papilloedema)
is stage 3 HTN = malignant HTN
NO
malignant HTN = stage 3 HTN (BP >180/120)
with retinal haemorrhage or papilloedema
