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302 review > Cardio > Flashcards

Cardio Flashcards

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
Q

what are causes of AF

A

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
Q

how is AF classified

A

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
Q

what are clinical signs of AF

A

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
Q

what is fast AF

A

when ventricular rate 100+ bpm

29
Q

how is AF managed

A

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
Q

when is rate control not offered first-line for AF

A

new-onset AF within 48hr
if reversible cause
heart failure caused by AF

31
Q

what is given for rate control in AF

A

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
Q

when is B blocker contraindicated for AF

A

asthma, COPD
hypotension

use bisoprolol mainly - sotalol not used as it has rhythm control action

33
Q

why may a TOE echo be done for AF

A

to rule out thrombus in left atrial appendage

34
Q

why is anticoagulation done for AF

A

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
Q

how is bleeding risk assessed in AF

A

HAS-BLED or ORBIT scores

36
Q

when is atrial ablation done

A

if TOE finds thrombus in left atrium (atrial appendage)

37
Q

what is atrial flutter

A

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
Q

what are ECG features of atrial flutter

A

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
Q

how is atrial flutter managed

A

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
Q

what disease causes sudden cardiac death in southeast asian male

A

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
Q

what is HF + causes

A

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
Q

what is systolic + diastolic HF

A

systolic HF (reduced EF) = IHD, dilated cardiomyopathy, myocarditis

diastolic HF (preserved EF) = HOCM, restrictive cardiomyopathy, constrictive pericarditis, cardiac tamponade

43
Q

what are the signs of cardiac tamponade

A

beck triad = hypotension, raised JVP, muffled heart sounds

44
Q

how do R + L sided HF differ

A

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
Q

how is HF classified

A

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
Q

how is HF investigated + when to order TTE/TOE

A

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
Q

how is reduced + preserved EF determined

A

depending on EF seen on echo
if EF <40%, HFrEF = reduced ejection fraction
if EF 40+ % with raised BNP = HF with preserved EF

48
Q

how is HF managed

A

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
Q

what to give if ACEi/ARB not tolerated

A

hydralazine + nitrate

50
Q

how is pulmonary oedema in HF acutely managed

A

sit pt upright
O2 therapy for sats >94%
IV furosemide 40mg + monitor fluid balance with catheter

51
Q

what are the diagnostic criteria for HTN

A

BP >140/90 in clinical setting
BP >135/85 on ABPM/HBPM

52
Q

is HTN mostly essential/primary OR 2ndary

A

mostly 90% primary

2ndary causes = ROPED
renal disease (renal artery stenosis)
obesity
pregnancy, pre-eclampsia
endocrine - hyperaldosteronism
drugs - alcohol, NSAID, steroid, COCP, E2

53
Q

how does HTN present

A

usually asymptomatic
unless malignant HTN (>180/120 + papilloedema/retinal haemorrhage)

54
Q

what is malignant HTN

A

BP >180/120 with retinal haemorrhage or papilloedema

55
Q

how is malignant HTN managed

A

if BP >180/120 + retinal haemorrhage/papilloedema

1 - same day fundoscopy
2 - IV labetalol, GTN, sodium nitropusside, phentolamine (alpha blocker)

56
Q

how often is HTN measured

A

every 5yr to screen for HTN
annually if borderline or T2DM

57
Q

what investigations are done if end-organ damage is suspected

A

ECG = LV hypertrophy
dipstick (haem/proteinuria, ACR) = renal disease
bloods = HbA1c, lipid profile
fundoscopy = hypertensive retinopathy

58
Q

what are lab findings for conn syndrome + renal disease

A

conn syndrome = hyperNA + hypoK
renal disease = protein/haematuria, low eGFR

59
Q

how is HTN managed

A

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
Q

what are different stages of HTN

A

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
Q

is stage 3 HTN = malignant HTN

A

NO
malignant HTN = stage 3 HTN (BP >180/120)
with retinal haemorrhage or papilloedema

302 review (14 decks)

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