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302 review > Cardio > Flashcards

Cardio Flashcards

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1
Q

what is brady+tachy-cardia

A

Brady <60bpm, tachy >100bpm

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2
Q

what causes acute bradycardia

A

drug induced = B blocker, CCB
sinus/AV nodal disease
electrolyte abnormalities = hyperK
hypothyroidism

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3
Q

how does bradycardia present

A

syncope
dizzy, tired

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4
Q

according to ALS, what is the management of bradycardia

A

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)

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5
Q

what is MOA of atropine

A

blocks vagus nerve activity, so SA firing rate increases

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6
Q

if bradycardia due to B blocker/CCB overdose, what is done

A

give glucagon (or glycopyrrolate)

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7
Q

how is tachycardia classified

A

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)

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8
Q

how is narrow complex tachy managed according to ALS

A

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

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9
Q

when to anticoagulant for Afib

A

if Afib onset 48+hr
anticoagulant with rate control (B-blocker, verapamil/diltiazem)

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10
Q

how are SVT treated

A

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

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11
Q

what is an irregular broad complex tachy

A

ventricular fibrillation - always a pulseless rhythm
QRS complexes are polymorphic + irregular

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12
Q

what is VF

A

arrhythmia occurring in heart ventricles, creates fibrillation waves

always pulseless + broad complex tachy

on ECG - polymorphic QRS, no identifiable P wave, HR 150-500bpm

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13
Q

according to ALS, how is VF managed

A

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

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14
Q

what are ECG features of VT

A

tachycardia >100bpm
regular rhythm

no P waves
monomorphic broad QRS >120ms

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15
Q

how is VT managed

A

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

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16
Q

what is torsades

A

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)

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17
Q

what causes torsades

A

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)

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18
Q

how is torsades managed

A

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

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19
Q

what is WPW

A

AVRT - congenital accessory pathway connecting atria to ventricles, bypassing AV node

causes re-entery circuits, leading to SVT

affects men more than women

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20
Q

what are clinical + ECG features of WPW

A

clinical: usually aymptomatic
syncope, palpitations, dizzy

ECG: delta waves (slurred upstroke to QRS)
if re-entrant circuit developed, narrow QRS complex <120s

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21
Q

how is WPW diagnosed

A

ECG - 24hr if paroxysmal symptoms
bloods including TFT
echo to check ventricular function

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22
Q

how is WPW acutely managed

A

if adverse features (BP <90/60) = synchronised DC shock

if no adverse features = vagal manoeuvre, IV adenosine 6mg (then 12mg then 18mg boluses)

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23
Q

how is WPW managed long-term

A

definitive = radio frequency ablation of accessory pathway

medical - amiodarone, sotalol (contraindicated in structural heart disease)

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24
Q

what is AF

A

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

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25
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
26
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
27
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
28
what is fast AF
when ventricular rate 100+ bpm
29
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)
30
when is rate control not offered first-line for AF
new-onset AF within 48hr if reversible cause heart failure caused by AF
31
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
32
when is B blocker contraindicated for AF
asthma, COPD hypotension use bisoprolol mainly - sotalol not used as it has rhythm control action
33
why may a TOE echo be done for AF
to rule out thrombus in left atrial appendage
34
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
35
how is bleeding risk assessed in AF
HAS-BLED or ORBIT scores
36
when is atrial ablation done
if TOE finds thrombus in left atrium (atrial appendage)
37
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
38
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
39
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)
40
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
41
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)
42
what is systolic + diastolic HF
systolic HF (reduced EF) = IHD, dilated cardiomyopathy, myocarditis diastolic HF (preserved EF) = HOCM, restrictive cardiomyopathy, constrictive pericarditis, cardiac tamponade
43
what are the signs of cardiac tamponade
beck triad = hypotension, raised JVP, muffled heart sounds
44
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)
45
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
46
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
47
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
48
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
49
what to give if ACEi/ARB not tolerated
hydralazine + nitrate
50
how is pulmonary oedema in HF acutely managed
sit pt upright O2 therapy for sats >94% IV furosemide 40mg + monitor fluid balance with catheter
51
what are the diagnostic criteria for HTN
BP >140/90 in clinical setting BP >135/85 on ABPM/HBPM
52
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
53
how does HTN present
usually asymptomatic unless malignant HTN (>180/120 + papilloedema/retinal haemorrhage)
54
what is malignant HTN
BP >180/120 with retinal haemorrhage or papilloedema
55
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)
56
how often is HTN measured
every 5yr to screen for HTN annually if borderline or T2DM
57
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
58
what are lab findings for conn syndrome + renal disease
conn syndrome = hyperNA + hypoK renal disease = protein/haematuria, low eGFR
59
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)
60
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)
61
is stage 3 HTN = malignant HTN
NO malignant HTN = stage 3 HTN (BP >180/120) with retinal haemorrhage or papilloedema

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