Cardio 7.5 Flashcards
MoA of loop diuretics?
Inhibit the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of loop of Henle, reducing the absorption of NaCl
(2 variants of NKCC - they act on NKCC2, more prevalent in the kidneys)
Indications for loop diuretics?
Adverse effects?
- heart failure: acute IV, chronic PO
- resistant HTN, esp in pts with renal impairment
- hypotension
- hyponatraemia
- hypokalaemia
- hypochloraemic alkalosis
- hypocalcaemia
- ototoxicity
- renal impairment (dehydration + direct toxic effect)
- gout
- hyperglycaemia (less common than with thiazides)
Associations with aortic dissection?
- trauma
- HTN
- bicuspid aortic valve
- pregnancy
- syphilis
- collagens: Marfans, Ehlers-Danlos
- Turners & Noonans syndromes
Features of aortic dissection?
Stanford classifcation?
DeBakey classification?
- chest pain: severe, radiates through to back & ‘tearing’ in nature
- aortic regurgitation
- HTN
- involvement from specific arteries e.g. coronary -> angina, spinal -> paraplegia, distal aorta -> limb ischaemia
Stanford:
type A = ascending, 2/3
type B = descending distal to left subclavian, 1/3
DeBakey:
type I - originates in ascending aorta, propagates to at least the aortic arch & possibly beyond it distally
type II - originates in & is confined to ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally
Causes of a paroxysmal SVT?
- sudden onset narrow complex tachycardia - typically an AVNRT: AV normal re-entry tachycardia
- other causes include AVRT & junctional tachycardias
Acute Rx of SVT?
- vagal manoeuvres
- IV adenosine 6 -> 12 -> 12mg (C/I in Asthma - consider verapamil instead)
- electrical cardioversion
Prevention of SVT?
- beta-blockers
- radio-frequency ablation
Causes of LQTS/Torsades de Pointes
- Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
- TCAs, antipsychotics
- amiodarone, sotalol, class 1a antiarrhythmics
- chloroquine
- terfenadine
- erythromycin
- hypothermia
- myocarditis
- SAH
- hypocalcaemia, hypokalaemia, hypomagnesaemia
Rx of Torsades de pointes/LQTS?
IV magnesium sulphate
Causes of LBBB?
- IHD
- HTN
- aortic stenosis
- cardiomyopathy
- rare: idiopathic fibrosis, digoxin toxicity, hyperkalaemia
Non-pulsatile JVP
superior vena cava obstruction
Kussmaul’s sign: paradoxical rise in JVP during inspiration
constrictive pericarditis
What does A wave show in the JVP waveform?
Absent in?
Large if?
Atrial contraction
- absent in AF
- large if atrial person: TS, PS, pulm HTN
Cannon ‘a’ waves
- caused by atrial contractions against a closed tricuspid valve
- e.g. complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing
What does ‘c’ wave show in JVP?
Closure of tricuspid valve
- not normally visible
What does ‘V’ wave show in JVP?
- due to passive filling of blood into the atrium against a closed tricuspid valve
- giant v waves in tricuspid regurgitation
What does ‘X’ descent show in JVP?
Fall in atrial pressure during ventricular systole
What does ‘Y’ descent show in JVP?
Opening of the tricuspid valve
Drug Rx of Angina:
- what should everyone receive in the absence of C/I?
- what should be used to abort angina attacks?
- what is 1st line?
- 2nd line?
- if monothoerapy inadequate & can’t tolerate dual Rx?
- if on dual Rx and still Sx?
- aspirin + statin
- GTN sublingual prn
Nb always increase to max tolerated dose before stepping up treatment - 1st line = beta-blocker or rate-limiting calcium-channel blocker e.g. verapamil/diltiazem
- 2nd line, combo required of beta-blocker + long-acting dihydropyridine calcium-channel blocker e.g. MR nifedipine
- increase to max tolerated dose
If monoRx inadequate or can’t tolerate dual then consider adding one of:
- long-acting nitrate
- ivabradine
- nicorandil or
- ranolazine
If Sx on dual Rx then:
- only add a 3rd drug whilst a pt is waiting assessment for PCI or CABG
Nitrates in angina - tolerance
- many pts develop tolerance & experience reduced efficacy
- take 2nd dose of ISMN after 8h instead of 12 in pts who develop tolerance, as it allows blood-nitrate levels to fall for 4h & maintains effectiveness
- not seen in pts who take MR ISMN
Ivabradine (used in angina)
- what is the MoA?
- what are the adverse effects?
- acts on If (funny) ion current which is highly expressed in the SAN, reducing cardiac pacemaker activity therefore reduces the heart rate
- visual effects esp luminous phenomena are common
- headache
- bradycardia due to oA
5 ECG features of hypokalaemia?
- they begin when K+ falls below 2.7
- prolonged PR interval
- long QT
- ST depression
- small/absent/inverted T waves
- U waves
What is pre-eclampsia?
When is it seen?
Pregnancy-induced hypertension + proteinuria (>0.3g/24h) +/- oedema
- after 20 weeks gestation
What does pre-eclampsia predispose to?
- fetal: prematurity, IUGR
- eclampsia
- haemorrhage: placental abruption, intra-abdo, intra-cerebral
- cardiac failure
- multi-organ failure
What are moderate & high RFs for pre-eclampsia?
Moderate:
- 1st pregnancy
- age 40+
- pregnancy interval > 10years
- BMI 35+ at 1st visit
- FHx pre-eclampsia
- multiple pregnancy
High RFs:
- hypertensive disease in previous pregnancy
- CKD
- T1DM/T2DM
- chronic HTN
- AI disease e.g. SLE, antiphospholipid syndrome
LQTS = whatare the features ass with each type?
LQT1 - exertional syncope, often swimming
LQT2 - syncope following emotional stress, exercise or auditory stimuli
LQT3 - events often occur at night or at rest
Otherwise: may be picked up on routine ech or family screening; ass with sudden cardiac death
Management of LQTS?
- avoid drugs/precipitants e.g. strenuous exercise
- beta-blockers (NOT sotalol)
- implantable cardioverter defibrillator in high risk cases
MoA of statins?
inhibit HMG-CoA reductase - the rate-limiting enzyme in hepatic cholesterol synthesis
- therefore decreases intrinsic cholesterol synthesis
Statin-induced myopathy is more commnon with which statins?
What are the RFs for myopathy with statins?
More common with LIPOphilic statins e.g. simvastatin/atorvastatin, than relatively hydrophilic ones e.g. rosuvastatin, pravastatin, fluvastatin
- inc age, female sex, low BMI, multisystem disease e.g. DM
Adverse effects of statins?
when to discontinue?
- Myopathy: myalgia, myositis, rhabdomyolysis & aSx raised CK
- Liver impairment - check LFTs at baseline, 3m & 12m
- discontinue if serum transaminase conc rise and persist at 3X ULN - May increase risk of ICH in pts who’ve prev had a stroke therefore avoid if Hx of intracerebral hameorrhage - not seen in 1ry prevention
Who should receive a statin?
1ry atorvastatin 20mg ON
- anyone with 10yr qrisk 10%+
- assess all T2DM with qrisk
- all T1DM Dx at least 10 yrs OR aged 40 OR established nephropathy
2ry atorvastatin 80mg ON
- all with established CVD: stroke, TIA, IHD, PVD
Types of Ventricular tachycardia?
Rx of VT?
VT = broad-complex tachycardia from a ventricular ectopic focus. Has potential to precipitate VF
- Monomorphic VT - most commonly caused by MI
- Polymorphic VT - subtype of which is Torsades (precipitated by prolonged QT)
Adverse signs e.g. chest pain, heart failure, shock -> Immediate cardioversion
No adverse signs -> drug therapy
If drug therapy fails -> electrical cardioversion may be needed with synchronised DC shocks
e.g. EPS: electrophsyiological study or ICD (esp if significantly impaired LV function)
Drugs:
Amiodarone through central line
Lidocaine (caution in severe LV impairment)
Procainamide
Verapamil is contra-indicated - may precipitate VF
Which 4 drugs improve mortality in heart failure?
- ACE-I
- beta-blockers
- spironolactone
- hydralazine with nitrates
Heart failure drug Rx: Cons? 1st line? 2nd line? If Sx persist? What are the criteria for ivabradine?
Cons: rmr annual flu jab & one-off pneumococcal
Diuretics for fluid overload/Sx Rx
1st: ACE-I + beta-blocker (bisoprolol/carvedilol/nebivolol)
2nd: aldosterone antagonist OR A2RB OR hydralazine+nitrate
If Sx persis then consider cardiac resynchronisation therapy or digoxin or ivabradine
Ivabradine: must be on suitable Rx, HR > 75 and LV EF < 35%
Digoxin may improve Sx due to inotropic properties and is strongly indicated if coexistent AF. But doesn’t improve mortality
MoA of Sacubitril (neprilysin inhibitor) in heart failure?
It has een shown to reduce mortality, hospitalisations & improve Sx combined with an A2RB (vs enalapril) in heart failure Rx with reduced EF
Prevents degradation of natriuretic peptides e.g. ANP, BNP
Upregulation of RAAS system in heart failure
RAAS & sympathetic activation & vasopressin
- -> sodum & water retention
- -> increased ventricular preload & afterload & elevated wall stress –> BNP production –> promotes natriuresis & vasodilation
- -> atrial stress –> ANP
- -> ANP & BNP are inactivated by a membrane-bound endopeptidase Neprilysin (found in tissues but v high conc in kidneys)
- Exogenous natriuretic peptides e.g. Nesiritide recombinant human BNP showed promise & relieved dsome dyspnoea but without improving outcomes
- Inhibit natriuretic peptide breakdown: e.g. Sacubitril a neprilysin inhibitor - reduces mortality, hospitalisations & improves Sx when given with Valsartan vs enalapril in Rx of heart failure with reduced EF
Commonest clinical signs with PE?
Tachypnoea RR > 16 96%
Crackles 58%
Tachycardia HR > 100 44%
Fever temp > 37.8 43%
Suspected PE: Hx, Ex & CXR…
2-level PE Wells score?
3 signs & Sx of DVT: minimum of UL leg swelling & pain wilth palpation of deep veins
3 alternative Dx less likely than PE
1.5 HR > 100
1.5 immobilisation >3days or surgery in past 4wks
1.5 prev DVT/PE
1 haemoptysis
1 malignancy on Rx or Rx in last 6m or palliative
> 4 points PE likely -> CTPA
<5 points PE unlikely -> D-dimer
V/Q scan if allergy to contrast media or renal impairment
ECG in PE?
- sinus tachycardia commonest
- RBBB & R axis deviation associated
- S1Q3T3: large S in lead I, large Q in lead III, inverted T in lead III
CTPA in PE?
V/Q scan in PE?
What is the gold standard?
CTPA:
- peripheral emboli affecting subsegmental arteries may be missed
V/Q scan:
- if normal virtually excludes PE but not v specific - other causes inc old PEs, AV malformations, vasculitis, prev RT. COPD gives matched defects
Gold standard = pulmonary angiography
- significant complication rate vs other Ix
Arterial supply of the heart: left aortic sinus? right aortic sinus? left coronary artery? right coronary artery?
Venous drainage??
L aortic sinus -> LCA R aortic sinus -> RCA LCA -> LAD & circumflex RCA -> posterior descending RCA supplies SAN in 60% & AVN in 90%
What is HOCM?
Commonest gene defects?
- autosomal dominant disorder of muscle tissue caused by defects in genes encoding contractile proteins
- most common defects involve mutation in gene encoding beta-myosin heavy chain protein or myosin protein C
- septal hypertrophy causes LV outflow obstruction
- prevalence 1/500
Features & associations of HOCM?
- often aSx
- dyspnoea, angina, syncope
- sudden death (ventricular arrhythmia), arrhythmias, heart failure
- JERKY pulse, large ‘A’ waves, double apex beat
- ESM: increases with valsalva manoeuvre & decreases on squatting
Ass:
- Friedreichs ataxia
- WPW syndrome
Echo features in HOCM?
ECG?
Echo:
MR: mitral regurgitation
SAM: systolic anterior motion of anterior mitral valve leaflet
ASH: asymmetric hypertrophy
ECG:
- LV hypertrophy
- progressive T wave inversion
- deep Q waves
- AF sometimes seen
Which cardiac ion channel is most likely affected in Torsades de points?
Potassium channel:
- they lengthen cardiac re-polarisation mostly by blocking specific cardiac K channels
- the potent blocking of them & excessive lengthening of cardiac re-polarisation -> membrane oscillations (early after-depolarisation) due to Ca2+/Na re-entry
- Early after-depolarisation, when propagated, may trigger torsade de pointes
DVLA notification/off driving?
- HTN
- angioplasty
- CABG
- ACS
- angina
- pacemaker insertion
- ICD
- successful catheter ablation
- aortic aneurysm 6cm+
- heart Tx
- heart failure
HTN -> no need to notify unless unacceptable side-effects, group 2 can’t drive if BP consistently > 180/100
elective angioplasty -> 1 week off
CABG -> 4 weeks off
ACS -> 4 weeks off; 1 week if successful angio
angina -> cannot drive if Sx at rest/wheel
pacemaker insertion -> 1 week off
ICD -> off driving 1month if prophylactic; off driving 6months if for sustained ventricular arrhythmia; no more driving if group 2 driver
successful catheter ablation for arrhythmia -> 2 days off
aortic aneurysm 6cm+ -> notify dvla, needs annual R/v, if 6.5cm+ no more driving
heart Tx -> dvla don’t need to be notified
heart failure -> group 1 don’t need to notify unless incapacitating Sx, but Sx heart failure means no group 2 license regardless of Sx - if becomes aSx can regain license only if EF>40%
Clinical features of Sx aortic stenosis?
Features of Severe aortic stenosis?
- chest pain
- dyspnoea
- syncope
Severe:
- narrow pulse pressure
- slow rising pulse
- delayed ESM
- soft/absent S2
- S4
- thrill
- long murmur
- LV hypertrophy or failure
Causes of aortic stenosis?
Rx?
- degenerative calcification commonest > 65yrs
- bicuspid aortic valve commonest < 65yrs
- WIlliam’s syndrome: supravalvular
- HOCM: subvalvular
- post-rheumatic disease
aSx -> observe
aSx with valvular gradient > 40mmHg & features of LV systolic dysfunction -> consider surgery
Sx -> valve replacement
Balloon valvuloplasty limited to pts with critical aortic stenosis who aren’t fit for valve replacement
Causes of a prolonged PR interval (1st degree heart block)?
- idiopathic
- IHD
- hypokalaemia
- digoxin toxicity
- rheumatic fever
- aortic root pathology e.g. abscess 2ry to endocarditis
- Lyme disease
- sarcoidosis
- myotonic dystrophy
- athletes
Cause of short PR interval?
WPW syndrome
Features of acute pericarditis?
- chest pan: may be pleuritic, often relieved sitting forwards
- non-productive cough, dyspnoea, flu-like Sx
- tachypnoea, tachycardia
- pericardial rub
ECG changes in acute pericarditis - most specific?
Most specific = PR depression
can also see widespread saddle-shaped ST elevation
Causes of acute pericarditis?
- viral e.g. Coxsackie
- TB
- trauma
- uraemia (Fibrinous)
- post-MI, Dressler’s syndrome
- CT disease
- hypothyroidism
- malignancy
2ry prevention of MI:
Cons?
Medical?
Cons:
- mediterranean diet. Don’t recommend omega-3 or oily fish. Switch butter/cheese to plant-based oils
- exercise: 20-30mins/day
- sexual activity can resume 4wks after uncomplicated MI (sex doesn’t increase likelihood of MI; can use sildenafil from 6months, as long as not on nitrates/nicorandil)
Med:
- dual antiplatelet therapy - 12months clopidogrel after NSTEMI, aspirin+clopidogrel 12months if STEMI
- ACE-I
- beta-blocker
- statin
2ry prevention of MI - when to give aldosterone antagonists?
Acute MI + Sx/signs of heart failure & LV systolic dysfunction -> start aldosterone antagonist licensed for post-MI Rx e.g. Eplerenone within 3-14days of MI, preferable after ACE-I Rx
Xanthomata: palmar? eruptive? tendon/tuberous/xanthelasma? Rx?
Palmar xanthoma:
- remnant hyperlipidaemia
- may less commonly be seen in familial hypercholesterolaemia
Eruptive:
- due to high triglyceride levels, present as multiple red/yellow vesicles on extensor surfaces
- familial hypertriglyceridaemia
- lipoprotein lipase deficiency
Tendon xanthoma, tuberous xanthoma, xanthelasma:
- familial hypercholesterolaemia
- remnant hyperlipidaemia
Rx options:
- surgical excision
- topical trichloroacetic acid
- laser therapy
- electrodesiccation
MoA of Atropine?
Use?
Physiological effects?
- antagonist of muscarinic acetylcholine receptor
- Rx of organophosphate poisoning
- mydriasis + tachycardia
Which type of valves/people are affected with infective endocarditis? (biggest RF is prev episode)
- previously normal valves 50%, acute
- rheumatic heart disease 30%
- prosthetic valves
- congenital heart defects
- IVDUs (typically tricuspid)
Culture negative causes of infective endocarditis?
- prior Abx therapy
- Coxiella burnetii
- Bartonella
- Brucella
- HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella
Commonest cause of infective endocarditis?
- in developing countries?
- in IVDUs/acute presentation?
- indwelling lines/prosthetic valve surgery (after 2m the spectrum returns to normal)
- colorectal cancer?
- non-infective?
- malignancy?
Commonest cause = staph aureus
- in developing countries = streptococcus viridans e.g. mitis/sanguinis = common in mouth/poor dental
- in IVDUs/acute presentation = staph aureus
- indwelling lines/prosthetic valve surgery (after 2m the spectrum returns to normal) = coag-negative staph e.g. staph epidermidis
- colorectal cancer = strep bovis
- non-infective = SLE (Libman-Sacks)
- malignancy = marantic endocarditis
ECG features in hypothermia?
- bradycardia
- J wave: small hump at end of QRS
- 1st degree block/ prolonged PR interval
- long QT interval
- atrial & ventricular arrhythmias
Features of aortic regurgitation?
What is the Austin-Flint murmur?
- early diastolic murmur
- collapsing pulse
- wide pulse pressure
- mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams
Causes of aortic regurgitation:
valve disease?
aortic root disease?
Valve:
- rheumatic fever
- infective endocarditis
- CT disease e.g. RA/SLE
- bicuspid aortic valve
Aortic:
- aortic dissection
- spondylarthropathies e.g. ank spond
- hypertension
- syphilis
- Marfan’s, Ehler-Danlos
CHA2DS2VaSc score for AF anticoagulation?
Congestive heart failure 1 Hypertension 1 Age 75+ 2 Age 65-74 1 Diabetes 1 Stroke/TIA 2 Vascular disease: IHD/PVD 1 Sex female 1
If score 1 in males then consider anticoag
If 2+ in females, offer anticoag
HASBLED bleeding risk assessment?
Hypertension uncontrolled sBP > 160 = 1 Abnormal renal function: dialysis/Cr>200 = 1 Abnormal liver function (cirrhosis, bilirubin >2xULN, ALT/AST/ALP>3xULN) = 1 Stroke history = 1 Bleeding history/tendency = 1 Labile INRs (unstable/high, time in therapeutic range<60%) = 1 Elderly >65yrs = 1 Drugs that predispose to bleeding = 1 Alcohol use (>8drinks/wk) = 1
Score 3+ indicates high risk bleeding
- intracranial haemorrhage, hospitalisation, Hb decrease >2, transfusion
What is pulsus paradoxus?
When is it seen?
- > 10mmHg fall in sBP during inspiration -> faint/absent pulse in inspiration
- severe asthma, cardiac tamponade
When can a collapsing pulse be seen?
- aortic regurgitation
- patent ductus arteriosus
- hyperkinetic: anaemia, thyrotoxic, fever, exercise, pregnancy
What is pulsus alternans?
when is it seen?
Regular alternation of the force of the arterial pulse
- severe LVF
What is bisferiens pulse?
when is it seen?
‘double pulse’ - 2 systolic peaks
- mixed aortic valve disease
When is a jerky pulse seen?
HOCM
Which women are at high risk of developing pre-eclampsia?
What should they take?
Aspirin 75mg OD from 12 weeks
- hypertensive disease during previous pregnancies
- CKD
- autoimmune disorders e.g. SLE/antiphospholipid syndrome
- T1DM/T2DM
What happens to BP in normal pregnancy?
How to define hypertension in pregnancy?
- BP normally falls in 1st trimester (esp diastolic), & continues to fall until 20-24wks
- then it usually increases to pre=pregnancy levels by term
sBP > 140 or dBP > 90
or an increase above booking readings of >30 sBP or >15 dBP
ECG features with digoxin?
- down-sloping ST depression (reverse tick)
- flattened/inverted T waves
- short QT interval
- arrthymias e.g. AV block, bradycardia
Clopidogrel is a thienopyridine - what is the mechanism of action & other examples?
- antagonist of the P2Y12 ADP receptor, inhibiting platelet activation
- prasugrel, ticagrelor, ticlopidine
When is clopidogrel indicated?
What makes clopidogrel less effective?
1st line after ischaemic stroke, pts with peripheral arterial disease, and used for 12months with aspirin after ACS
- PPIs may make clopidogrel less effective
- lansoprazole should be ok
N.b. 12months dual anti platelets after placement of a drug-eluting stent v important - delay any elective surgery
HTN Rx?
BP targets?
- <55yrs ACE-I
55+ or Afro-C calcium-channel blocker - ACE-I + Calcium channel blocker
- add a thiazide-like diuretic e.g. CHLORTHALIDONE/INDAPAMIDE
If clinic BP >140/90 after step 3 = resistant hypertension -> step 4 or expert advice
- consider further diuretic Rx
K < 4.5 add spironolactone 25
K > 4.5 add higher-dose thiazide-like diuretic Rx
If further diuretic not tolerate or C/I or ineffective, consider alpha/beta-blocker
Specialist referral if failure to respond to step 4 measures
Age<80yrs:
clinic 140>90 abpm 135/85
Age>80yrs:
clinic 150/90 abpm 145/85
Cons measures &
when to treat HTN?
LOW SALT <6g/day ideally 3g/day
- reduce caffeine, stop smoking, less etoh, exercise, lose weight, balanced diet etc
stage 1 HTN: treat if <80yrs AND target organ damage/established CVD/renal disease/ DM /10yr Qrisk 20%+
stage 2 HTN: offer drug Rx regardless of age
if <40yrs consider specialst referral to exclude 2ry causes
Lifestyle advice for hypertension?
Classification of hypertension:
stage 1?
stage 2?
severe?
- clinic 140/90 or abpm/home 135/85
- clinic 160/100 or abpm/home 150/95
severe: clinic sBP>180 or dBP>110
How do direct renin inhibitors work in hypertension?
e.g. Aliskiren/Rasilez
- inhibits renin, blocking conversion of angiotensinogen -> angiotensin I
- initial trials suggest reduces BP similar to ACE-I/A2RB
- diarrhoea seen
-
What is Eisenmenger’s syndrome?
What is it associated with?
What are 5 features?
What is the Rx?
- reversal of left-to-right shunt in a congenital heart defect due to pulmonary hypertension
Ass with: VSD, ASD, PDA
- original murmur may disappear
- cyanosis
- clubbing
- RV failure e.g. raised JVP, loud P2, large a waves
- haemoptysis, embolism
Rx = heart-lung Tx
What is Wellens’ syndrome?
ECG manifestation of critical proximal left anterior descending artery stenosis in pts with unstable angina
- symmetrical, often deep >2mm T wave inversions in the anterior precordial leads
Coronary territories: anteroseptal inferior anterolateral lateral posterior
anteroseptal V1-4 LAD
inferior II, III, aVF R coronary
anterolateral V4-6, I, aVL LAD/left circumflex
lateral I, aVL +/- V5,6 Left circumflex
posterior tall R waves V1-2, usually left circumflex, also right coronary
Poor prognostic factors in infective endocarditis?
- staph aureus
- prosthetic valve, esp if early/acquired during surgery
- culture negative endocarditis
- low complement levels
Mortality:
staph 30%
bowel organisms 15%
strep 5%
5 indications for surgery in infective endocarditis?
- severe valvular incompetence
- aortic abscess (often indicated by prolonged PR interval)
- infections resistant to Abx/fungal infections
- cardiac failure refractory to standard medical Rx
- recurrent emboli after Abx Rx
Infective endocarditis suggested Abx therapy when BLIND for:
native valve?
native valve if pen allergic/MRSA/severe sepsis?
if prosthetic valve?
Native: amoxicillin +/- gentamicin
or vancomycin + gentamicin
Prosthetic: vancomycin + rifampicin + gentamicin
Infective endocarditis suggested Abx therapy when staphylococcus native valve endocarditis?
Flucloxacillin
or
vancomycin + rifampicin
Infective endocarditis suggested Abx therapy when staphylococcus prosthetic valve endocarditis?
flucloxacillin + rifampicin + gentamicin
or
vancomycin + rifampicin + gentamicin
Infective endocarditis suggested Abx therapy when caused by fully-sensitive streptococci e.g. viridins?
Benzylpenicillin
or
vancomycin + gentamicin
Infective endocarditis suggested Abx therapy when caused by less sensitive streptococci e.g. viridins?
benzylpenicillin + gentamicin
or
vancomycin + gentamicin
When does rheumatic fever develop? how to Dx?
How to get evidence of recent strep infection?
- develops following an immunological reaction to recent (2-6wks ago) strep pyogenes infection
Dx = evidence of recent strep infection +
2 major or
1 major + 2minor criteria
Evidence:
- raised/rising streptococci Ab
- positive throat swab
- positive rapid group A streptococcal Ag test
Major/minor criteria for rheumatic fever?
Major = JONES
Minor = FAPR
Commonest valve affected?
Joint involvement: polyarthritis O = heart = myo/carditis/valvulitis (regurg murmur) Nodules subcutaneous Erythema marginatum Sydenham's chorea
Fever
Arthralgia (as long as arthritis not a major criteria)
Prolonged PR interval
Raised ESR/CRP
Cardiac histology of rheumatic fever?
- Aschoff bodies: granuloma with giant cells
2. Anitschkow cells: enlarged macrophages with ovoid, wavy, rod-like nucleus
Aschoff bodies (granuloma with giant cells) & Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus) on histology?
rheumatic heart disease
Councilman bodies on histology?
hepatitis C
yellow fever
Mallory bodies on histology?
alcoholism (hepatocytes)
Call-Exner bodies on histology?
granulosa cell tumour
Schiller-Duval bodies on histology?
yolk-sac tumour
Causes of ST elevation on ecg?
MI pericarditis/myocarditis normal variant - high tae-off LV aneurysm Prinzmetal's angina (coronary artery spasm) Takotsubo cardiomyopathy rare: SAH
What are the 2 main things the management of bradycardia depends on?
- identifying adverse signs that may indicate haemodynamic compromise
- identifying potential risk of asystole
What are adverse signs that indicate haemodynamic compromise & hence need for Rx with bradycardia?
1st line Rx?
If it fails or potential risk of asystole?
- shock: hypotension sbP <90, pallor, sweating, cold, clammy extremities, confusion, impaired consciousness
- syncope
- myocardial ischaemia
- heart failure
ATROPINE
TRANSVENOUS PACING
4 factors that indicate a potential risk of asystole with bradycardia and hence need for Rx with transvenous pacing?
What 3 interventions can be used if there is a delay in transvenous pacing?
- recent systole
- ventricular pause > 3seconds
- Mobitz type II AV block
- complete heart block with broad complex QRS
- Atropine max 3mg
- transcutaneous pacing
- isoprenaline/adrenaline infusion titrated to response
NSTEMI Rx?
What should be given if not high risk of bleeding?
What should be given to pts who have an intermediate/higher risk of adverse cardiovascular events i.e. 6month mortality>3%, OR will be having angiography within 96h of hospital admission
- Aspirin 300mg STAT
- Clopidogrel 300mg 12 months
- Nitrates/Morphine to relieve chest pain if required
- O2 if required
- ANTITHROMBIN Rx if not high risk of bleeding e.g. Fondaparinux -> if having angio in next 24h or Cr>265 then give unfractionated heparin
IV GLYCOPROTEIN IIb/IIIa receptor antagonists e.g. EPTIFIBATIDE/TIROFIBAN
With NSTEMI Rx:
What should be given to pts who have an intermediate/higher risk of adverse cardiovascular events i.e. 6month mortality>3%, OR will be having angiography within 96h of hospital admission
IV GLYCOPROTEIN IIb/IIIa receptor antagonists e.g. EPTIFIBATIDE/TIROFIBAN
Mechanism of action of e.g. EPTIFIBATIDE/TIROFIBAN
IV GLYCOPROTEIN IIb/IIIa receptor antagonists
- given with NSTEMI if having angio within 96h of hospital admission or higher risk of adverse cardiovascular events
When to consider coronary angiography in NSTEMI?
Within 96h of first admission to hospital in pts who have a predicted 6month mortality >3%
- also asap in pts who are clinically unstable
MoA of aspirin?
antiplatelet - inhibits production of thromboxane A2
MoA of clopidogrel?
antiplatelet - inhibits ADP binding to its platelet receptor
MoA of enoxaparin & fondaparinux?
activates antithrombin III -> potentiates inhibition of coagulation factors Xa
MoA of bivalirudin?
reversible direct thrombin inhibitor
MoA of abciximab/eptifibatide/tirofiban?
glycoprotein IIb/IIIa receptor antagonists
Management if major bleeding when on warfarin?
stop warfarin
IV vitamin K 5mg
prothrombin complex conc - FFP if not available
Management if minor bleeding when on warfarin, with INR>8?
stop warfarin
IV vitamin K 1-3mg
repeat dose vitamin K if INR still too high after 24h
restart warfarin when INR<5.0
Management if no bleeding when on warfarin, with INR>8?
stop warfarin
give vitamin K 1-5mg PO (using IV prep orally)
repeat dose vitamin K if INR still too high after 24h
restart when INR<5
Management if minor bleeding when on warfarin, with INR 5-8?
stop warfarin
IV vitamin K 1-3mg
restart when INR<5
Management if no bleeding when on warfarin, with INR 5-8?
withhold 1-2doses of warfarin
reduce subsequent maintenance dose
What causes S1 1st heart sound?
when is it soft?
when is it loud?
- closure of mitral & tricuspid valves
- soft if long PR or mitral regurgitation
- loud in mitral stenosis
What causes S2 2nd heart sound?
when is it soft?
when does it split?
- closure of aortic & pulmonary valves
- soft in aortic stenosis
- splitting during inspiration is normal
What leads to S3 3rd heart sound?
What are the causes?
- diastolic filling of the ventricle
- normal if <30yrs
- LV failure e.g. dilated cardiomyopathy
- constrictive pericarditis (pericardial knock)
- mitral regurgitation
What leads to S4 4th heart sound?
What are the causes?
- caused by atrial contraction against a stiff ventricle
- aortic stenosis
- HOCM
- hypertension
- in HOCM a double apical impulse may be felt as a result of a palpable S4
PE Rx?
Massive PE/compromise Rx?
PE -> LMWH/fondaparinux
Massive PE -> unfractionated heparin when considering thrombolysis
- warfarin within 24h for 3 months at least - extended time if unprovoked
- lmwh 6months if active cancer
- cont lmwh/fondaparinux at least 5 days or until INR>2 for 24h
Pt with recurrent VTE disease despite maximal Rx or e.g. whilst on maximal Rx dose - what should be considered?
IVC filter
- if recurrent proximal DVT/PE despite adequate anticoag Rx ONLY after considering alternative rx e.g.:
- switching to LMWH
- increasing target INR to 3-4 for long term high-intensity oral anticoagulant Rx
What is most common underlying mechanism causing prolongation of QT segment?
- blockage/loss of function of K+ channels (overload of myocardial cells with K+ during ventricular repolarisation)
What is WPW syndrome?
What are the associations?
- congenital accessory conducting pathway between atria & ventricles leading to a AV re-entry tachycardia
- as the accessory pathway doesn’t slow conduction, AF can degenerate rapidly to VF
- HOCM
- mitral valve prolapse
- Ebstein’s anomaly
- thyrotoxicosis
- secundum ASD
Possible ECG features of WPW syndrome?
- short PR interval
- wide QRS complexes with a slurred upstroke - ‘delta wave’
- LAD if right-sided (commonest)
- RAD if left-sided accessory pathway
Type A = left-sided pathway: dominant R wave in V1
Type B: no dominant R wave in V1
Type C: delta waves are upright in leads V1-2 but negative in leads V5-6
Management of WPW syndrome?
Definitive = radiofrequency ablation of the accessory pathway
medical:
- sotalol (AVOID IF AF - prolonging the refractory period at the AVN may increase the rate of transmission through the accessory pathway -> VT -> VF)
- amiodarone
- flecainide
Major disadvantage of biological/bioprosthetic valves?
What sort of anticoagulation is needed?
- structural deterioration & calcification over time (i.e. higher failure rate)
- most older pts receive a bioprosthetic valve
- long-term anticoag usually not needed
- warfarin 3months depending on pt factors
- low-dose aspirin long-term
Major advantage & disadvantage of mechanical heart valves?
- low failure rate
- increased risk of thrombosis
- target INR aortic valve 3.0
- target INR mitral valve 3.5
- only given Aspirin as well if an additional indication e.g. IHD
What are the features of Takayasu’s arteritis?
Association?
Rx?
- large vessel vasculitis
- typically causes occlusion of the aorta, more common in females & Asians
- systemic features of vasculitis e.g. malaise, headache
- unequal BP in ULs, absent limb pulse
- carotid bruit
- intermittent claudication
- aortic regurgitation 20% eg early diastolic murmur
Ass with renal artery stenosis
Rx = steroids
What are the most important parameters to monitor whilst giving a pt is receiving IV magnesium?
reflexes & resp rate
What is eclampsia? When is magnesium given? how is it given? what should be monitored? how long to continue Rx?
= development of seizures in ass with pre-eclampsia
(after 20wks gestation, pregnancy-induced hypertension, proteinuria)
- Nb fluid restriction is important too
- magnesium sulphate to prevent & Rx seizures
- give when a decision to deliver has been made
- IV 4g bolus over 5-10mins then infusion of 1g/hr
- monitor urine output, reflexes, RR & O2 sats during Rx
- Rx should continue for 24h after last seizure or delivery (40% of seizures occur postpartum)
Features of cardiac tamponade?
Sx = dyspnoea Ex = - tachycardia, hypotension - pulsus paradoxus - raised JVP with absent Y descent (limited RV filling) - muffled heart sounds ECG = electrical alternans
Differences between cardiac tamponade & constrictive pericarditis? JVP pulsus paradoxus Kussmaul's sign characteristic CXR
cardiac tamponade:
- JVP absent Y descent
- pulsus paradoxus +
- Kussmaul’s rare
Constrictive pericarditis:
- JVP X + Y present
- NO pp
- Kussmaul’s sign +
- CXR pericardial calcification
Poor prognostic factors in HOCM?
- genetic mutation in trop T
- young age at presentation
- syncope
- FHx of sudden death
- non-sustained ventricular tachycardia on 24/48h Holter monitoring
- abnormal BP change (low) on exercise
- increased septal wall thickness/ventricular wall thickness>30mm
Adverse signs with a tachycardia that makes a person unstable i.e. peri-arrest?
Rx?
- shock: sBP<90, pallor, sweating, sold, clammy, confused, impaired GCS
- syncope
- myocardial ischaemia
- heart failure
- > electrical cardioversion i.e. DC SHOCK
- > then Rx depends if it is narrow/broad and if rhythm is regular/irregular
Regular broad-complex tachycardia Rx?
- assume ventricular tachycardia (unless previously confirmed SVT with bbb)
- > AMIODARONE loading dose then 24h infusion
Irregular broad-complex tachycardia Rx?
AF with BBB -> treat as narrow complex tachycardia
Polymorphic VT -> IV MAGNESIUM
Regular narrow complex tachycardia Rx?
vagal manoeuvres -> IV adenosine
- if unsuccessful consider Dx of A flutter & rate control
Irregular narrow complex tachycardia Rx?
probable AF
- if onset <48h consider electrical/chemical cardioversion
- rate control e.g. beta-blocker/digoxin & anticoagulation
Features of atrial myxoma?
- site
- systemic
- ecg
- murmur
- echo
- 75% left atrium, more common in females
- dyspnoea, fatigue, weight loss, fever, clubbing, emboli
- AF
- mid-diastolic murmur, ‘tumour plop’
- echo: pedunculated heterogeneous mass typically attached to fossa ovals region of the intertribal septum
What is a well-documented complication of coronary angiography? seen more commonly in arteriopaths, AAAs
What are the features?
Cholesterol embolisation - emboli may break off causing renal disease
- purpura
- livedo reticularis
- eosinophilia
- renal failure
Chest pain referral
- current or in the last 12h with abnormal ecg?
- 12-72h ago
- > 72h ago
current -> emergency admission
12-72h ago -> same-day assessment hospital referral
>72h ago -> full assessment with ecg & troponin
How do NICE define anginal pain?
- constricting discomfort in the front of the chest, or in neck/shoulders/jaw/arms
- precipitated by physical exertion
- relieved by rest/GTN in about 5mins
all 3 = typical angina
2 = atypical angina
1/none = non-anginal chest pain
For patients in whom stable angina cannot be excluded by clinical assessment alone NICE what Ix are recommended by NICE?
What are the options for non-invasive functional imaging?
(e.g. Sx consistent with typical/atypical angina OR ECG changes)
1st line = CT coronary angiography
2nd line = non-invasive functional imaging looking for reversible myocardial ischaemia
3rd line = invasive coronary angiography
Non-invasive:
- myocardial perfusion scintigraphy (MPS) with SPECT
- stress echo
- first-pass contrast-enhanced magnetic resonance MR perfusion
- MR imaging for stress-induced wall motion abnormalities
How does amiodarone work?
What factors limit it’s use?
- class III antiarrythmic used in Rx of atrial, nodal, ventricular tachycardias
- main MoA = blocking K+ channels which inhibits repolarisation -> prolongs action potential
- also has some class I effect
- long half-life 20-100days
- ideally give into central veins (thrombophlebitis)
- pro arrhythmic effect (lengthening of QT interval)
- drug interactions (e.g. decreases metabolism of warfarin)
- numerous adverse effects
Monitoring of patients on amiodarone?
Adverse effects of amiodarone use?
- TFTs, LFTs, U&Es, CXR prior to Rx
- TFT & LFT every 6months
- thyroid dysfunction
- corneal deposits
- pulmonary fibrosis/pneumonitis
- liver fibrosis/hepatitis
- peripheral neuropathy, myopathy
- photosensitivity
- slate-grey appearance
- thrombophlebitis & injection site reactions
- bradycardia
ACE-I:
MoA?
uses?
- inhibit conversion of angiotensin I to angiotensin II
- 1st line HTN in <55yrs, less effective in Afro-C
- heart failure
- diabetic nephropathy
- role in 2ry prevention of IHD
ACE-I:
side-effects?
cautions & C/I?
- cough 15%, upto a year after starting (inc bradykinin)
- angioedema, upto a year after starting
- hyperkalaemia
- 1st dose hypotension, more common in those taking diuretics
Cautions/C/I:
- pregnancy & breastfeeding - AVOID
- renovascular disease - significant impairment if unDx BL renal artery stenosis
- aortic stenosis - may result in hypotension
- high-dose diuretic Rx (>80mg furosemide/day) significantly increases risk of hypotension
- hereditary idiopathic angioedema
What 2 main problems does IHD lead to i.e. the gradual buildup of fatty plaques within coronary artery walls?
What are un/modifiable RFs?
- Gradual narrowing
- less blood -> less O2 reaching myocardium at times of increased demand
- > angina - Risk of sudden plaque rupture
- fatty plaques which have built up in the endothelium may rupture -> sudden occlusion of the artery -> can result in no blood/O2 reaching an area of myocardium
Modifiable:
- smoking, T2DM, HTN, hypercholesterolaemia, obesity
Unmodifiable:
- increasing age, male sex, FHx
Pathophysiology of IHD?
what triggers endothelial dysfunction?
what changes does this lead to of the endothelium?
what infiltrates the endothelium?
how are monocytes/macrophages involved?
how is the fibrous capsule of the fatty plaque formed?
- endothelial dysfunction triggered by e.g. smoking, HTN, hyperglycaemia
- > pro-inflammatory, pro-oxidant, proliferative changes to endothelium & reduced NO bioavialability
- > fatty infiltration of sub endothelial space by LDL particles
- > monocytes migrate from blood -> differentiate into macrophages
- > which phagocytose oxidised LDL -> slowly turning into large ‘foam cells’ -> these macrophages die which can further propagate the inflammatory process
- > smooth muscle proliferation & migration from the tunica media -> intimate -> results in formation of a fibrous capsule covering the fatty plaque
2 complications of atherosclerosis i.e. plaque formation?
- Plaque forms a physical blockage in the coronary artery lumen -> can cause reduced blood flow & O2 to the myocardium - esp at times of increased demand -> angina
- plaque may rupture -> potentially causing a complete occlusion of the coronary artery -> may result in a MI
Why is deep & widespread ST depression on an ecg ass with v high mortality?
it signifies severe ischaemia usually of LAD or left main stem
STEMI Rx?
- morphine, nitrates +/- O2
- aspirin
- clopidogrel
- re-open/revascularise: 1ry PCI - balloon angioplasty & stent via catheter
Revascularisation in an NSTEMI?
- risk stratification e.g. GRACE to decide further Rx
- if high-risk or unstable, then coronary angio performed during admission
- lower risk can have it at a later date
2ry prevention following ACS?
- dual antiplatelet therapy (DAT)
- ACE-I
- beta-blocker
- statin
PCI Rx in a STEMI?
- 1ry PCI tio pts who present within 12h of onset of Sx, IF it can be delivered within 120mins
- otherwise fibrinolysis if >120mins
- if ecg 90mins after fibrinolysis fails to show resolution of ST elevation then they would need transfer for PCI
Anaphylaxis drug Rx: adrenaline/hydrocortisone/chlorphenamine?? <6m 6m-6yrs 6-12yrs >12yrs
<6m: adrenaline 150mcg hydrocortisone 25mg chlorphenamine 250mcg/kg
6m-6yrs: adrenaline 150mcg hydrocortisone 50mg chlorphenamine 2.5mg
6-12yrs: adrenaline 300mcg hydrocortisone 100mg chlorphenamine 5mg
> 12yrs: adrenaline 500mcg hydrocortisone 200mg chlorphenamine 10mg
Serum levels than can be taken to establish true anaphylaxis?
Serum tryptase
- elevated upto 12h post acute episode
MoA of A2RBs?
Uses?
Side-effects?
- block effects of angiotensin II at the At1 receptor
- can be used where ACE-I not tolerated, evidence base that they reduce progression of renal disease in diabetic nephropathy, & losartan reduces CVD & IHD mortality in HTN
- caution in renovascular disease
- hypotension & hyperkalaemia
Antiplatelet Rx 1st & 2nd line for NSTEMI?
lifelong aspirin & clopidogrel/ticagrelor for 12months
lifelong clopidogrel if aspirin C/I
Antiplatelet Rx 1st & 2nd line for STEMI?
Lifelong aspirin + clopidogrel/ticagrelor: 1m if no/bare stent, 12m if drug-eluting stent
- lifelong clopidogrel if aspirin C/I
Antiplatelet Rx 1st & 2nd line for TIA/Stroke?
Lifelong clopidogrel
- if C/I then lifelong aspirin + lifelong dypiradamole
Antiplatelet Rx 1st & 2nd line for peripheral arterial disease?
Lifelong clopidogrel
- is C/I then 2nd line is lifelong aspirin
Complications of aortic dissection?
Backward tear:
- aortic incompetence/regurgitation
- MI - inferior pattern often seen due to R coronary involvement
Forward tear:
- unequal arm pulses & BP
- stroke
- renal failure
What is arrhythmogenic right ventricular cardiomyopathy?
Pathophysiology?
Presentation?
- inherited CVD which may present with syncope/sudden cardiac death - 2nd commonest cause of sudden cardiac death
- autosomal dominant with variable expression
- RV myocardium replaced by fatty & fibrous tissue
- 50% have mutation of 1 of several genes which encode components of DESMOSOME
- palpitations
- syncope
- sudden cardiac death
Ix of ARVDysplasia/Cardiomyopathy?
- ecg
- echo
- MRI
ECG - abnormalities in V1-3, typically T wave inversion
- epsilon wave 50% (terminal notch in QRS complex)
Echo - subtle early on, may show enlarged hyPOkinetic RV with a THIN free wall
- MRI useful to show fibrofatty tissue
What is Naxos disease?
autosomal recessive variant of ARVC/D - traid of:
- ARVC
- palmoplantar keratosis
- woolly hair
what is 1st degree heart block?
PR interval >0.2 seconds
what is 2nd degree heart block Mobitz type I?
wenckeback phenomenon
progressive prolongation of PR interval until a dropped beat
what is 2nd degree heart block Mobitz type II?
regular PR interval but often P wave is not followed by a QRS interval
what is 3rd degree/complete heart block?
no association between p waves & qrs complexes
Features of ASDs?
- most likley congenital heart defect to be found in adulthood
- 50% mortality at 50yrs
- ESM, fixed splitting of S2
- embolism may pass from venous system to left side of heart causing a stroke
Difference between ostium secundum & ostium primum ASDs?
secundum 70%
- ass with Holt-Oram syndrome (tri-phalangeal thumbs)
- ECG: RBBB with RAD
Primum
- presents EARLIER than secundum defects
- ass with abnormal AV valves
- ECG: RBBB with LAD, prolonged PR interval
What is atrial flutter?
ecg?
Rx?
- SVT characterised by a succession of rapid atrial depolarisation waves
- sawtooth
- underlying atrial rate is often ~300/min therefore the ventricular/HR is dependent on the degree of AV block (e.g. 2:1 block is 150bpm)
- flutter waves may be visible following carotid sinus massage/adenosine
Rx similar to AF but may be less effective
- more sensitive to cardioversion so lower energy levels may be used
- radiofrequency ablation of tricuspid valve isthmus curative for most pts
What is paroxysmal AF?
recurrent episodes of AF that terminate spontaneously
- last <7d, usually <24h
What is persistent AF?
recurrent episodes of AF that is not self-terminating - usually last >7days
What is permanent AF?
continuous AF that cannot be cardioverted or if attempts to do so are inappropriate
- Rx goals therefore rate control & anticoag as appropriate
What is first detected episode of AF?
first detected episode (irrespective of whether it is symptomatic or self-terminating)
Sx & signs of AF
Ix?
- palpitations, dyspnoea, chest pain
- irreg irreg pulse
ECG: ventricular ectopics, sinus arrhythmia etc can also give irreg pulse
Rate-control AF medical strategies?
beta-blocker or
rate-limiting calcium channel blocker e.g. diltiazem is 1st line
If monotherapy isn’t adequate, combo therapy with 2 of:
- beta blocker
- diltiazem
- digoxin
When to consider rhythm control in AF i.e. cardiovert?
- 1st onset AF
- coexistent heart failure
- obvious reversible cause
If onset of AF < 48h offer rate/RHYTHM control
(if >48h, start rate control)
AF onset <48h how to manage?
If AF <48 h then HEPARINISE & risk stratify for long-term anticoag
Rx = Cardioversion
- electrical DC
- pharm - AMIODARONE if structural heart disease, if not, then FLECAINIDE/amiodarone
- after electrical cardioversion if AF confirmed <48h then further anticoagulation is unnecessary
AF onset >48h how to manage cardioversion:
i.e. how long should pts be anticoagulated first?
when can the be cardioverted immediately?
what to do if high risk of cardioversion failure?
duration of anticoagulation after electrical cardioversion?
- should be anticoagulated for at least 3 weeks before cardioversion
- OR can offer a TOE to exclude a left atrial appendage LAA thrombus - if excluded then can heparinse & cardiovert immediately (electrically)
If high risk of cardioversion failure e.g. previous failure/recurrence, then at least 4 weeks AMIODARONE/SOTALOL before electrical cardioversion
- after electrical cardioversion, anticoagulate at least 4 weeks -> then decide further individual basis
Agents with proven efficacy in the pharmacological cardioversion of atrial fibrillation?
amiodarone
flecainide
others less common: quinidine, dofetilide, ibutilide, propafenone
Agents used to control rate in patients with atrial fibrillation?
beta-blockers
calcium-channel blockers - rate-limiting
digoxin (not first line but preferred if coexistent heart failure)
Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation?
sotalol
amiodarone
flecainide
Factors favouring rate control in AF?
> 65yrs
Hx of IHD
Factors favouring rhythm control in AF?
<65yrs Symptomatic 1st presentation Lone AF or AF 2ry to a precipitant e.g. etoh Congestive heart failure
Patients with AF who develop a stroke/TIA…. what should be given and when for anticoag?
(Warfarin) is antocoag of choice - aspirin/dypiradmole only if needed for other comorbidities
- in acute stroke & haemorrhage excluded, can start anticoag AFTER 2 wks - LONGER if imaging shows a v large cerebral infarction
Causes of a raised BNP (hormone produced mainly by LV myocardium in response to strain)?
heart failure
myocardial ischaemia
valvular disease
CKD (reduced excretion)
(ACE-I, A2RBs & diuretics reduce BNP levels)
What are the 3 effects of BNP?
- vasodilator
- diuretic & natriuretic
- suppresses both sympathetic tone & RAAS
Clinical uses of BNP? Dx Rx Prognosis Screening
Dx: pts with acute dyspnoea - if low <100 then heart failure unlikely therefore helpful to rule it out
Rx: effective Rx in chronic heart failure lowers BNP levels (i.e. monitoring is helpful)
Prognosis: initial evidence suggests BNP is useful marker of prognosis in chronic heart failure
Screening: for cardiac dysfunction - NOT recomended for population screening
Side-effects of beta-blockers?
Contra-indications?
Indications?
- bronchospasm, cold peripheries
- fatigue, sleep disturbances
C/I in:
- uncontrolled heart failure
- asthma
- sick sinus syndrome
- concurrent verapamil -> severe bradycardia -> block
Indications:
- angina, post-MI, heart failure, AF, (HTN)
- migraine prophylaxis, thyrotoxicosis, anxiety
Bicuspid aortic valve - what is it ass with?
what are the complications?
- usually aSx in childhood, occurs in 1-2% population
Ass: - Left dominant coronary circulation (posterior descending artery arises from Circumflex instead of RCA)
- Turner’s syndrome
- 5% also have coarctation of aorta
Comp:
- aortic stenosis/regurgitation
- high risk aortic dissection & aneurysm of ascending aorta
In a broad complex tachycardia, what features are suggestive of VT rather than SVT with aberrant conduction??
FAQ PILL
Fusion/capture beats AV disocciation QRS>160ms Positive QRS concordance in chest leads IHD Hx LAD, marked Lack of response to adenosine/carotid sinus massage
What is Brugada syndrome?
Pathophysiology?
ECG changes?
Rx?
inherited CVD which may present with sudden cardiac death - autosomal dominant, more common in Asians
- large number of variants
- 20-40% caused by mutation in the SCN5A gene which encodes myocardial sodium ion channel protein
ECG:
- convex ST elevation >2mm in >1 of V1-3 followed by a negative T wave
- partial RBBB
- changes may be more apparent following fleainide
Rx = implantable cardioverted-defibrillator
What is Buerger’s disease?
What are the features?
= thromboangitis obliterans
- small & medium vessel vasculitis stongly ass with smoking
- extremity ischaemia: intermittent claudication, ischaemic ulcers
- superficial thrombophlebitis
- Raynaud’s phenomenon
Cardiac enzymes - which is the first to rise?
Which is useful to look for re-infarction as it returns to normal after 2-3days (trop T remains elevated upto 10days)
When does Trop T peak?
Myoglobin first to rise
CK-MB useful to look for re-infarction
Trop T peaks at 12-24h
Normal oxygen sat of blood in LA/LV/Aorta?
And in RA/RV/PA?
What is abnormal in ASD?
in VSD?
in PDA?
in VSD with Eisenmenger’s?
in PDA with Eisenmenger’s?
in ASD with Eisenmenger’s?
100% in left circulation
70% in right-sided circulation
ASD: pulmonary circ is 85%
VSD: RA normal 70%, RV & PA is 85%
PDA: PA 85%
VSD + E: RA, RV & PA normal 70% but LV & aorta 85%
PDA+E: aorta 85%
ASD+E: left side all 85%
Ways of classifying cardiomyopathies?
1ry - predominately involve the heart
2ry - pathological myocardial involvement as part of a generalised systemic disorder
Genetic (HOCM, ARVD)
Mixed (e.g. genetic predisposition triggered by 2ry process)
Aquired (peripartum, Takotsubo)
Causes of 2ry cardiomyopathy? (involves dilated/restrictive) infective infiltrative storage toxicity inflammtory/granulomatous endocrine neuromuscular nutritional deficiencies autoimmune
infective - Coxsackie B, Chagas disease
infiltrative - amyloid
storage - haemochromatosis
toxicity - doxorubicin, etoh
inflammtory/granulomatous - sarcoid
endocrine - DM, thyrotoxicosis, acromegaly
neuromuscular - Friedreich’s ataxia, Duchenne-Becker, muscular dystrophy, myotonic
nutritional deficiencies - Beri-Beri (thiamine)
autoimmune - SLE
Acquired peripartum cardiomyopathy - when does it develop? RFs?
- last month of pregnancy & 5months post-partum
- more common in older women, greater parity & multiple gestations
Acquired Takotsubo cardiomyopathy - cause? Sx?
Rx?
What is seen?
- stress induced eg bereavement
- chest pain & features of heart failure
- supportive Rx
- transient, apical ballooning of myocardium
Classic causes of dilated cardiomyopathy? ABCD
Alcohol
Beri beri (wet)
Coxsackie B virus
Doxorubicin
Classic causes of restrictive cardiomyopathy?
Amyloid (commonest in UK)
post-RT
Loefller’s endocarditic (fibrosis in eosinophilic myocarditis)
- also haemochromatosis, sarcoid, scleroderma
Echo findings in HOCM?
mr sam ash
MR
Systolic Anterior Motion of the anterior mitral valve
Asymmetic Septal Hypertrophy
ECG abnormalities in ARVD?
- usually T1-3 abnormal
- T wave inversion
- epsilon wave in 50% - terminal notch in QRS complex
What is CPVT: catecholaminergic polymorphic ventricular tachycardia?
pathophysiology?
- inherited cardiac disease ass with sudden cardiac death
- autosomal dominant, 1:10,000 prevalence
- commonest cause is a defect in the RYR2: ryanodine receptor, found in myocardial sarcoplasmic reticulum
Features & Rx of CPVT: catecholaminergic polymorphic ventricular tachycardia ?
- exercise/emotion induced polymorphic ventricular tachycardia -> syncope
- sudden cardiac death
- Sx generally develop before age 20
Rx = beta-blockers, ICD
3 examples of centrally active antihypertensives?
Methyldopa - used in HTN Rx in pregnancy
Moxonidine - used in essential HTN Rx when conventional drugs failed to control BP
Clonidine - antihypertensive effect mediated throug alpha-2 stimulation in vasomotor centre
What are the 2 types of Cardiac CT, sueful for assessing suspected IHD?
Calcium score: known to be a correlation between amount of atherosclerotic plaque calcium and the risk of future ischaemic events
Contrast-enhanced CT: allows visualisation of coronary artery lumen
If combined, they have a v high NPV for IHD
What is now the gold standard for providing structural images of the heart?
When is it useful?
CMR: Cardiac MRI
- useful when assessing congenital heart disease, determining RV & LV mass, and differentiating forms of cardiomyopathy
- can also assess myocardia perfusion with gadolinium
- limited data on extent of coronary artery disease
Examples of nuclear cardiac imaging radiotracers extracted by normal myocardium?
- thallium
- technetium (99mTc) sestamibi - complex used in MIBI & cardiac SPECT scans
- FDG: fluorodeoxyglucose - used in PET scans (1rily research atm)
Nuclear cardiac SPECT imaging - what is the role?
- to assess myocardial perfusion & myocardial viability
- 2 sets of images acquired, at rest then at stress e.g. exercise of adenosine/dypridamole
- comparing the two helps to identify areas of ischaemia that are reversible or fixed
What is cardiac MUGA scanning? what is it for?
Multi-Gated Acquisition Scan = radionuclide angiography
- IV radionuclide technetium-99m injected
- pt placed under a gamma camera
- can be performed as a stress test
- can accurately measure LV ejection fraction
- typically used before & after cardiotoxic drugs are used
What are the 3 indications for a temporary pacemaker?
- symptomatic/haemodynamically unstable bradycardia, NOT responding to atropine
- post-ANTERIOR MI: type 2 or complete heart block (post-inferior MI complete block is common and can be managed conservatively is aSx & haem stable) - obserev for 7 days before considering permanent pacing
- Trifascicular block prior to surgery
MoA of Nicorandil?
K+ channel activator
A transient uncommon complication of a coronary angiogram 2ry to irritation of the myocardium by the catheter?
Ventricular tachycardia
- pull back catheter immediately to restore normal sinus rhythm
What is a patent foramen ovale?
Rx in pts who’va had a stroke?
persistent patency of a congenital opening/foramen ovale in the interatrial septum, which normally closes after birth
- present in 20%
- may allow embolus to pass from R->L side causing a stroke i.e. paradoxical embolus - consider if stroke in <50yrs
- get decompression Sx related to diving, cold sensation in limb, limb pain
- atrial septal aneurysm is a RF for PFO & when combined, increases risk of CVA. other RFs are congenital heart conditions, FHx or PMHx migraine
- ass between migraine & PFO (closure can improve migraine Sx)
- Rx if stroke is controversial, inc: antiplatelet, anticoagulant, PFO closure
What is coarctation of the aorta?
What are the associations?
What are the features?
- congenital narrowing of descending aorta, commoner in Males
- Ass inc: Turner’s, bicuspid aortic valve, berry aneurysms, neurofibromatosis
Features:
- infancy heart failure
- adult hypertension
- radio-femoral delay
- apical click in aortic valve
- mid-systolic murmur, maximal over the back
- notching of the inferior border of ribs (collateral vessels) is NOT seen in young childers
MoA of warfarin?
Side-effects?
oral anticoagulant that inhibits reduction of vitamin K to its active hydroquinone form -> acts as a cofactpr in carboxylation of clotting factord II, VII, IX, X & protein C (i.e. vit K anatagonist)
- bleeding
- teratogenic (but can be used if breast-feeding)
- skin necrosis (temporary procoagulant state when initiated because protein C synthesis is reduced which can lead to thrombosis & skin necrosis)
- purple toes
Factors that potentiate wafarin?
- liver disease
- p450 enzyme inhibitors e.g. amiodarone, ciprofloxacin
- cranberry juuice
- drugs which displace warfarin from plasma albumin e.g. NSAIDs
- drugs which inhibit platelet functino e.g. NSAIDs
Indications for warfarin & INR targets?
AF target 2.5 VTE target 2.5 recurrent VTE target 3.5 aortic mechanical valve 3.0 mitral mechanical valve 3.5
What is pulmonary arterial hypertension?
Presentation?
resting mean PA pressure 25+mmHg
- more common in females, typically presents age 30-50
- 10% inherited autosomal dominant
- pulm HTN can develop 2ry to chronic lung disease e.g. COPD but PAH is Dx in absence of this - HIV, cocaine, anorexigens etc inc the risk
Features (Sx & signs) of pulmonary arterial HTN?
- progressive exertional dyspnoea classically
- exertional syncope, exertional chest pain, peripheral oedema
- cyanosis
- raised JVP with prominent a waves
- RV heave
- loud P2
- tricuspid regurgitation
Rx of 1ry pulmonary arterial hypertension?
what test do you do first?
Rx if +ve response?
Rx if -ve response?
- > Rx underlying conditions e.g. with anticoagulants/oxygen
- > ACUTE VASODILATOR testing helps decide appropriate Rx strategy - it aims to decide which pts show a significant fall in PA pressure after vasodilators e.g. IV epoprostenol/INH nitric oxide
+ve respone (minority)
= PO calcium channel blockers
- ve response (majority):
- prostacycline analogues: treprostinil, iloprost
- endothelin receptor antagonists: bosentan
- phosphodiesterase inhibitors: sildenafil
Pts with progressive Sx should be considered for a heart-lung Tx
What is the mainstay Rx for 1ry pulmonary arterial HTN?
Prostacyclins
Commonest cause of death as a complication of MI?
VF -> cardiac arrest
- ALS protocol with defib
Complication post-MI if a large part of the ventricular myocardium is damaged in the infarction and the ejection fraction is severely affected? Rx?
Cardiogenic shock (can also be due to a mechanical complication e.g. LV free wall rupture) - inotropic suppor &/or intra-aortic balloon pump
Complication post-MI if pt survives the acute phase of a large part of ventricular myocardium damage what can develop?
Chronic heart failure
- loop diuretic
- drugs that improve mortality
Bradyarrhythmia that is more common after an inferior MI?
AV block
Common 10% complication in the first 48h after a transmural MI?
Pericarditis
- may have effusion on echo
Complication 2-6wks post-MI of fever, pleurisy, pericardial effusion & rasied ESR?
mechanism?
Rx?
Dressler’s syndrome (inc pericarditis)
- autoimmune reaction against antigenic proteins formed as the myocardium recovers
- Rx nsaids
Complication post-MI where ischaemic damage sustained may weaken the myocardium ass with persistent ST elevation & LV failure - what is the cause?
LV aneurysm
- thrombus can form within -> inc the risk of stroke
- therefore, pts are anti coagulated
Complication 1-2wks post-MI seen in 3%, presenting with features of acute heart failure 2ry to cardiac tamponade e.g. raised JVP, pulses paradoxus, diminished heart sounds?
Rx?
LV free wall rupture
- urgent pericardiocentesis & thoracotomy
Complication-post MI seen in 1st week of 1-2% with features of acute heart failure ass with a pan-systolic murmur?
VSD/rupture of the inter ventricular septum
- Dx echo (& exclude acute MR)
- urgent surgical correction
Complication post-MI - more common with infer-posterior infarction with an early-to-mid diastolic murmur?
cause?
Rx?
Acute MR
- may be due to ischaemia of rupture of the papillary muscle
- Rx vasodilator therapy but often require emergency surgical repair
Causes of a loud S2?
HTN (systemic loud A2 or pumonary loud P2)
hyper dynamic states
ASD without pulmonary hypertension
Cause of a soft S2?
aortic stenosis
Cause of a fixed split S2?
ASD
Causes of a widely split S2?
deep inspiration
RBBB
pulmonary stenosis
severe MR
Causes of a reversed (paradoxical) split S2 (P2 before A2)?
LBBB severe aortic stenosis RV pacing WPW type B (causes early P2) PDA
What is the best predictor of mortality post-STEMI before discharge?
Above average exercise capacity
Indications for ETT: exercise tolerance testing ECG?
What is the max predicted & target HR?
- risk stratifying pts after MI
- assessing exercise otlerance
- risk stratifying pts with HOCM
- assessing pts with suspected angina
Sensitivity 80% specificity 70% for IHD
Max predicted HR = 220 - Age
Target HR = at least 85% max predicted to allow reasonable interpretation of a test as low-risk or negative
C/I to ExerciseTT/ecg?
When to stop?
- MI < 7days ago
- unstable angina
- uncontrolled HTN sBP>180 or hypotension sBP < 90
- aortic stenosis
- LBBB
Stop if:
- ‘severe’, ‘limiting’ chest pain
- > 3mm ST depression
- > 2mm ST elevation, stop also if rapid + pain
- sBP > 230
- sBP falling >20
- attainment of max pred HR
- HR falling >20% of starting rate
- arrhythmia develops
In the absence of C/I, what Rx should all be given in a STEMI?
aspirin clopidogrel/ticagrelor (improved outcome but slightly higher risk bleeding)/prasogrel = P2Y12-R antagonist unfractionated heparin (lmwh if C/I)
Thrombolysis in STEMI
- if no access to 1ry PCI
- tPA: tissue plasminogen activator has mortality benefits over streptokinase
- tenecteplase is easier to administer and not inferior to alteplase with a similar adverse effect profile
When to do an ECG after thrombolysis of a STEMI to assess whether there has been a >50% resolution in the ST elevation ?
90mins
- if no adequate resolution -> rescue PCI
- if adequate then PCI still beneficial
Rx of hyperglycaemia in ACS?
- dose-adjusted IV insulin infusion with regular monitoring of levels to BG <11.0
- intensive insulin Rx NOT recommended routinely (DIGAMI)
How to Dx infective endocarditis by modified Duke criteria?
- path criteria +
or 2major
or 1major 3minor
or 5minor
What are pathological criteria for infective endocarditis?
- positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
- i.e. valve tissue, vegetations, embolic fragments or intracardiac abscess content
What are the major criteria in Dx infective endocarditis? (culture & endocardial)
Positive blood cultures:
- 2 +ve BC of typical organise e.g. strep viridans/HACEK group
- persistent bacteraemia from 2 +ve bCs >12h apart OR 3 +ve BCs where pathogen is less specific e.g. staph aureus/epidermidis
- +ve serology for Coxiella burnetii/Bartonella/Chlamydia psittaci
- +ve molecular assays for specific gene targets
Evidence of endocardial involvement:
- new valvular regurgitation
- +ve echo: oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves
Minor criteria for Dx of infective endocarditis?
- predisposing heart condition / IVDU
- microbio evidence that doesn’t meet major criteria
- fever >38
- vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae, purpura
- immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
Features suggestive of restrictive cardiomyopathy rather than constrictive pericarditis?
- prominent apical pulse
- heart may be enlarged on CXR
- absence of pericardial calcification on CXR
- ECG abnormalities e.g. BBB, Q waves
Signs on exam of tricuspid regurgitation?
- giant V waves in JVP
- left parasternal heave
- pan-systolic murmur
- pulsatile hepatomegaly
Causes of tricuspid regurgitation?
- RV dilatation
- pulm HTN e.g. copd
- rheumatic heart disease
- infective endocarditis esp IVDU
- Ebstein’s anomaly
- carcinoid syndrome
What is multifocal atrial tachycardia?
What is the management?
MAT: irregular cardiac rhythm caused by at least 3 different sites in the atria - can show morphologically at distinctive P waves
- more common in elderly with chronic lung disease e.g. COPD
Rx
- correct hypoxia & electrolyte disturbances
- rate-limiting calcium-channel blocker e.g. verapamil often 1st line
- cardioversion & digoxin NOT useful
What is the Valsalva manoeuvre?
What are the stages?
= forced expiration against a closed glottis -> increased intrathoracic pressure
- increased intracthoracic pressure
- increase in venous & RA pressure reduces venous return
- thus reduced preload & fall in cardiac output (Frank-Starling)
- when the pressure is released -> further slight fall in cardiac output due to increased aortic volume
- return of normal cardiac output
What is a dilated cardiomyopathy?
Features>
Where a dilated heart leads to systolic +/- diastolic dysfunction
- all 4 chambers affected but LV > RV
- in the absence of congenital, valvular or ischaemic heart disease
Features inc: arrhythmias, emboli & mitral regurgitation
Causes of dilated cardiomyopathy?
- ETOH (may improve with thiamine)
- postpartum
- HTN
Also:
- inherited (often people have a genetic predisposition, majority autosomal dominant)
- infections e.g. Coxsackie B, HIV, diphtheria, parasitic
- endocrine ege hyperthyroid
- infiltrative eg haemochromatosis, sarcoid
- neuromuscular eg Duchenne
- nutritional eg Kwashiorkor, pellagra, thiamineselenium deficiency
- drugs eg Doxorubicin
MoA of thiazide diuretics?
- inhibit sodium reabsorption at the DCT by blocking Na/Cl symporter -> more Na reaching the collecting ducts means potassium is lost
Common & rare adverse effects of thiazide diuretics?
- dehydration
- postural hypotension
- hyponatraemia, hypokalaemia, hypercalcaemia
- gout
- impaired glucose tolerance
- impotence
Rare:
- thrombocytopenia, agranulocytosis, photosensitivity rash, pancreatitis
What finding on auscultation would most strongly indicate dyspnoea 2ry to isolated LV failure?
S3 gallop rhythm - one of the most specific & early signs
ECG:
- convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
- partial RBBB
- changes may be more apparent following flecainide
What is the Dx?
Brugada syndrome
Prinzmetal angina (coronary artery spasm) treatment?
dihydropyridine calcium channel blocker
What is PCI: percutaneous coronary intervention?
What happens after stent insertion?
What are the types of stent?
- technique to restore myocardial perfusion in IHD in both stable angina & ACS
- stents implanted in 95%
- migration & proliferation of smooth muscle cells & fibroblasts occur to the treated segment
- stent struts eventually become covered by endothelium (until thi shappens there is an increased risk of platelet aggregation leading to thrombosis)
BMS: bare-metal stent
DES: drug-eluting stent, coated with paclitaxel/rapamycin, which inhibit local tissue growth (reducing restenosis rates) but the stent thrombosis rates are increased as the process of stent endothelisation is slowed
- > Aspirin lifelong
- > length of clopidogrel Rx depends on type of stent, reason for insertion & consultant preference
2 main complications of PCI?
Stent thrombosis - due to platelet aggregation
- 1-2%, most commonly in the 1st month
- usually presents with acute MI
Restenosis - due to XS tissue proliferation around stent
- 5-20%, most commonly in first 3-6months
- usually presents with recurrence of angina Sx
- RFs inc DM, renal impairment & stents in venous bypass grafts
Paroxysmal AF successfully treated with DC cardioversion 1 week ago, now on warfarin. A post-cardioversion Echo shows no structural abnormalities. How long to continue warfarin?
4 weeks (at least) after successful cardioversion - if structural abnormalities or AF likely to recur, then longer recommended
MoA of hydralazine?
C/I?
- increases cGMP leading to smooth muscle relaxation to a greater extent in arterioles than veins
(‘older’ antihypertensive)
C/I in SLE & IHD
Adverse effects of hydralazine?
- tachycardia, palpitations, flushing
- headache, fluid retention
- drug-induced lupus
What is the single most important risk factor for stent thrombosis after PCI?
Premature withdrawal anti platelet therapy
Managing 2ry prevention of stable CVD with an indication for an anticoagulant?
anticoagulant mono therapy without anti platelet (generally, if there is a bleeding risk)
Managing post-ACS/PCI with an indication for an anticoagulant?
- stronger indication for antiplatelet Rx
- DAT + anticoagulant for 4wks-6months after the event, then 1 anti platelet + 1 anticoagulant to complete 12months
- but varies
VTE when on anti platelets?
Calculate HASBLED - if intermediate/high-risk bleeding then consider withholding anti platelets for duration of anticoagulant Rx
The use of beta-blockers in treating hypertension has declined sharply in the past five years. Why has this occurred?
Less likely to prevent stroke & potential impairment of glucose tolerance
4 ECG changes that are considered normal variants in an athlete?
sinus bradycardia
junctional rhythm
1st degree heart block
Wenckebach phenomenon
What is malignant hypertension?
What are the features?
- severe HTN >200/130
- occurs in both essential & 2ry types
- fibrinoid necrosis of BVs -> retinal haemorrhages, exudates, proteinurial haematuria due to renal damage (benign nephrosclerosis)
- can lead to cerebral oedema -> encephalopathy
Classically: severe headaches, nausea/vomiting, visual disturbance
Also: chest pain & dyspnoea
- papilloedema
- severe: encephalopathy e.g. seizures
Management of malignant hypertension?
- reduce diastolic no lower than 100mmHg within 12-25h
- bed rest
Most Pts oral therapy e.g. Atenolol
If severe/encephalopathic: IV sodium nitroprusside/labetalol
A 28F comes in with palpitations, no PMHx
HR 160 irregular
BP 123/65 mmHg
SpO2 97% (RA)
Chest clear
ECG: irregular broad complex monomorphic tachycardia with a stable axis
What is the most appropriate Rx?
IRREGULAR broad complex tachycardia (without features to suggest VT) therefore most likely to be SVT/AF with LBBB/aberrant conduction e.g. WPW
therefore most appropriate Rx = Amiodarone
(haemodynamically stable)
(diltiazem, bisoprolol, adenosine would enhance the aberrant pathway -> VF)
What class of drugs can cause a hypertensive crisis (that may be used e,g, in an emergency setting, that may interact with vasopressors used to treat hypotension)?
monoamine oxidase inhibitors e.g. phenelzine
Fillip class system for risk stratification post-MI with 30day mortality risk?
I no clinical signs of heart failure 6%
II lung crackles, S3 17%
III frank pulmonary oedema 38%
IV cardiogenic shock 81%
Poor prognostic factors in ACS?
age development/Hx of heart failure peripheral vascular disease reduced sBP Fillip class initial serum creatinine conc elevated initial cardiac markers cardiac arrest on admission ST segment deviation
HOCM Rx?
abcde
Amiodarone Beta-blockers or verapamil for Sx Cardioverter defibrillator Dual chamber pacemaker Endocarditis prophylaxis
Drugs to avoid in HOCM?
ACE-I
Nitrates
Inotropes
- drugs that reduce preload decrease chamber size and worsen Sx & signs
- vasodilators increase outflow tract gradient and cause a reflex tachycardia that further worsens ventricular diastolic function
- inotropic drugs worsen outflow tract obstruction, don’t relieve the high end-diastolic pressure, and may induce arrhythmias
What is the single most important test to confirm the Dx of pulmonary hypertension?
Cardiac catheterisation
- to measure right heart pressures
Features of mitral valve prolapse?
- atypical chest pain or palpitations
- mid-systolic click (later if pt squatting)
- late systolic murmur (longer if pt standing)
- complications: MR, arrhythmias inc long QT, embolism, sudden death
Associations of mitral valve prolapse?
- 5-10% population, usually idiopathic
- congenital: PDA, ASD, cardiomyopathy, Turner’s, Marfan’s, Fragile X, osteogenesis imperfecta, pseudoxanthoma elasticum, WPW, LQTS, Ehlers-Danlos, PCKD
What is the aim of endothelia receptor antagonist therapy in pulmonary arterial hypertension?
To reduce pulmonary vascular resistance -> reduce strain on the right ventricle (i.e. RV systolic pressure)
What are the key Ix tests used to identify patients likely to benefit from cardiac resynchronisation therapy in heart failure?
What features make them good candidates for CRT/biventricular pacing?
- TTE: LV EF <35%, asynchronous contraction of LV & RV
- ECG: LBBB/QRS>120ms
- biventricular pacing improves quality of life & exercise tolerance by ensuring the ventricles contract at the same time due to asynchronous stimulation (LBBB causing asynchronous activation) via the conduction system
What are the 4 features of cholesterol embolisation?
- purpura
- livedo reticularis
- eosinophilia
- renal failure
MoA of Dypyradimole?
- antiplatelet
- inhibits phosphodiesterase -> elevating platelet cAMP -> reduces intracellular calcium levels
- also reduces cellular uptake of adenosine (i.e. increases the effects) & inhibits thromboxane synthase
Causes of LAD: left axis deviation?
left anterior hemlock LBBB WPW syndrome - R-sided accessory pathway hyperkalaemia congenital: ostium primum ASD, tricuspid atresia minor LAD in obese people
Causes of RAD: right axis deviation?
RV hypertrophy left posterior hemiblock chronic lung disease -> for pulmonate PE ostium secundum ASD WPW syndrome Left sided accessory pathway normal in infant < 1yr old minor RAD in tall people
Causes of myocarditis?
- Coxsackie, HIV
- diphtheria, clostridia
- Lyme disease
- Chagas’ disease, toxoplasmosis
- autoimmune
- doxorubicin
- usually young pt with acute Hx: chest pain, SOB
VSD: ventricular septal defect
- features?
- classically pan systolic murmur which is louder in smaller defects
- commonest cause of congenital heart disease, that close spontaneously in 50%
- congenital ass with chromosomal disorders e.g. Downs, Edwards, Patau
non-congenital eg post-MI
Complications of VSD?
- aortic regurgitation (due to a poorly supported right coronary cusp -> cusp prolapse)
- infective endocarditis
- Eisenmenger’s complex
- right heart failure
- pulmonary hypertension (pregnancy contraindicated in pulm HTN)
Features of severe pre-eclampsia?
- HTN > 170/110 & proteinuria ++/+++
- headache, visual disturbance, papilloedema
- RUQ/epigastric pain
- hyperreflexia
- platelet count <100, abnormal liver enzymes or HELLP syndrome
What are the physiological changes in exercise:
BP?
cardiac output?
- systolic increases, diastolic decreases -> increased pulse pressure
- in healthy young people the increase in MABP is only slight
- increase in cardiac output can be 3-5X
- HR increase unto 3x
- stroke volume increase unto 1.5X
- due to venous constriction, vasodilation & increased myocardial contractibility, as well as from the maintenance of right atrial pressure by an increase in venous return
Causes of mitral stenosis?
RHEUMATIC FEVER
rarer: mucopolysaccharidoses, carcinoid, endocardial fibroelastosis
Features of mitral stenosis?
Features if severe?
- low volume pulse, atrial fibrillation
- loud S1, opening snap
- mid-late diastolic murmur (best heard in expiration)
- length of murmur increases
- opening snap becomes closer to S2
CXR & Echo in mitral stenosis?
CXR: left atrial enlargement
Echo: ‘tight’ mitral stenosis implies a X-sectional area of <1cm squared (normal is 4-6)
What is the intervention of choice in severe mitral stenosis?
percutaneous mitral commissurotomy
- only if unsuccessful/contra-indicated is surgical valve replacement indicated
Contra-indications of percutaneous mitral commissurotomy/valvotomy?
- mitral valve area >1.5
- left atrial thrombus on echo
- > mild MR
- severe valve calcification
- severe concomitant aortic valve disease
- severe combined mixed tricuspid valve disease
- concomitant coronary artery disease req bypass surgery
Indications for an implantable cardiac defibrillator?
- LQTS
- HOCM
- previous cardiac arrest due to VT/VF
- previous MI with non-sustained VT on 24h monitoring, inducing VT on electrophysiology testing & EF <35%
- Brugada syndrome
Causes of palpitations?
What are the 1st line Ix?
- stress, arrhythmias, inc awareness of normal heart beat/extrasystoles
- 12lead ecg
- FBC, U&Es, TFTs
NYHA heart failure classification?
I no Sx, no limitation
II mild Sx, slight limitation eg ordinary activity results in Sx
III moderate Sx, marked limitation of activity
IV severe Sx, often at rest limiting any activity
What Ix can accurately measure LV EF?
Typically done before and after cardiotoxic drugs a usedre
MUGA scan - radionuclide angiography
What is the first cardiac enzyme to rise after an MI?
myoglobin
50y.o. man in ED with palpitations, no chest pain, long Hx of etoh abuse, looks malnourished.
ECG: irregular tachycardia 165bpm with a QRS duration 155ms
K+ 2.1
No signs of chock/heart failure/syncope
Next step in management?
IV magnesium 2g
(irregular tachycardia with broad QRS complex can be either polymorphic VT/pre-excited AF/AF with BBB.
- etoh, hypokalaemia make torsades most likely)
What are the 2ry causes of hypertension?
1ry hyperaldosteronism = commonest
Renal:
- glomerulonephritis, pyelonephritis, APKD, renal artery stenosis
Endocrine:
- phaeochromocytoma, Cushing’s, Liddle’s, CAH/11-beta hydroxylase deficiency, acromegaly
Drug:
- steroids, MAO-Is, COCP, NSAIDs, leflunomide
Other:
- pregnancy, coarctation of aorta
Gold standard Ix for aortic dissection?
CT aortic angiogram
Causes of an ejection systolic murmur?
aortic stenosis pulmonary stenosis HOCM ASD Fallot's
Causes of a pansystolic murmur?
MR/TR (high pitched & blowing)
VSD (‘harsh’)
Causes of a late systolic murmur?
mitral valve prolapse
coarctation of aorta
Causes of a early diastolic murmur?
aortic regurg (high pitched & blowing) Graham-Steel murmur of pulmonary regurg also high pitched & blowing
Causes of a mid-late diastolic murmur?
mitral stenosis (rumbling) Austin-Flint murmur (severe AR, also rumbling)
Cause of a continuous machine-like murmur?
PDA
Causes of ST depression on ecg?
- 2ry to abnormal QRS: LVH, LBBB, RBBB
- ischaemia
- digoxin
- hypokalaemia
- syndrome X
Commonest cause of drug-induced angioedema?
ACE-I
Common side effect of ticagrelor?
Dyspnoea/breathlessness 15%
- triggered by adenosine (as ticagrelor inhibits its clearance)
Nicotinic acid is used in treatment of hyperlipidaemia, although its use is limited by side-effects
- what are the adverse effects
- what are the uses in hyperlipidaemia?
- lowers cholesterol & tirglyceride conc
- raises HDL levels
- flushing
- impaired glucose tolerance
- myositis
Which non-invasive Ix provides the most accurate assessment of whether a pt has coronary artery disease?
Contrast enhanced cardiac CT
What does troponin T bind to?
Tropomyosin which regulates actin - it associates with actin in muscle fibres and regulates muscle contraction by regulating the binding of myosin
24y.o. female develops transient slurred speech following a flight from Aus -> UK.
CT head & ECG normal
What test is most likely to reveal the underlying cause?
TOEcho - paradoxical embolus from a PFO
ECG - abnormalities in V1-3, typically T wave inversion
- epsilon wave 50% (terminal notch in QRS complex)
What is the Dx?
Arrhythmogenic RV cardiomyopathy
What is currently the most common causes of viral myocarditis??
parvovirus b19
HHV-6
Pre-test probability calculation for coronary artery disease for low-risk but cardiac sounding chest pain, what to do if it is:
<30%
30-60%
>60%?
<30% CT calcium scoring
30-60% myocardial perfusion scintigraphy
>60% invasive coronary angiography
What is the treatment of choice to permanently restore sinus rhythm in atrial flutter?
Radiofrequency ablation of tricuspid valve isthmus
How long is it best to monitor a patient for after successful treatment for anaphylaxis?
8 hours
- biphasic reactions (Sx recurrence after apparent resolution) occur in 1-20% of anaphylaxis episodes, and typically ~8h after the 1st reaction, although can occur upto 72h later
What are the features of complete heart block?
- syncope, heart failure
- regular bradycardia 30-50bpm
- wide pulse pressure
- JVP cannon A waves
- variable intensity of S1
How to measure pulmonary capillary wedge pressure PCWP?
What chamber does it roughly equate to?
- balloon tipped Swan-Ganz catheter inserted into pulmonary artery
- pressure is similar to left atrium 6-12mmHg normal
- helps determine whether pulmonary oedema is cardiogenic or not
Which organisms contribute to the highest rate of mortality in infective endocarditis?
staphylococci mortality 30%
Venous drainage of the heart: where does the coronary sinus drain into?
right atrium
What is the Ix for choice for pregnant patients with a suspected DVT?
compression duplex US
What is the Ix for choice for pregnant patients with a suspected PE?
(ECG & CXR for all)
- compression duplex US if there are also Sx/signs of a DVT - if confirms DVT, further Ix not necessary
- decision of V/Q or CTPA is after d/w pt & radiologist
Risk of CTPA & V/Q scan in pregnancy?
CTPA: increases lifetime risk of maternal breast cancer (pregnancy makes breast tissue particularly sensitive)
V/Q scan: slightly increased risk of childhood cancer vs ctpa
MoA of adenosine?
- causes transient heart block in the AV node
- agonist of the A1 receptor -> inhibits adenylyl cyclase -> reducing cAMP -> hyperpolarisation by increased outward K efflus
- v short half life of 8-10seconds
What enhances the effects of adenosine?
What reduces the effects of adenosine?
Enhanced by Dipyradimole
Blocked by theophyllines
What are the adverse effects of adenosine?
- chest pain
- bronchospasm
- can enhance conduction down accessory pathways -> increased ventricular rate e.g. WPW
Most important factor predicting outcome post-STEMI is i.e. strongest ass with sudden death?
Presents of new systolic heart failure
i.e. low LV ejection fraction
large amount of myocardial damage
What is Ebstein’s anomaly?
congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle
Best Ix when you suspect a paradoxical embolisation e.g. from a PDA or ASD?
TOE
