Clinical cardiology + vascular Flashcards
Inotropes
Increase cardiac contractility in order to increase cardiac output (CO) e.g. in cardiac arrest, cardiogenic shock.
Adrenaline
- beta-1 = increases contractility and HR
- 0.05mcg/kg/min.
- At higher doses alpha-1 activity predominates -> vasoconstriction -> end-organ ischaemia
Dobutamine
- in doses of 5- 10mcg/kg/min
- higher doses have more vasopressor effect
Isoprenaline
Milrinone
- Purely inotropic
- Phosphodiesterase inhibitor
- Does not cause tachycardia
Vasopressors
Induce vasoconstriction in order to increase PVR
- e.g. sepsis, hypovolaemia
- Increases the heart’s oxygen demand so risk of angina/ischaemia
Noradrenaline
- alpha-1 = vasoconstriction
- Can combine with dobutamine, milrinone etc.
- Risk of reflex bradycardia and peripheral ischaemia
- 0.05mcg/kg/min
Vasopressin
- VR1 = vasoconstriction.
Phenylephrine
Mean arterial pressure
Aim 65 mmHg
If older, more likely to have atherosclerosis and HTN with chronic adaptation so aim higher e.g. 75-85 mmHg
Too low = hypoperfusion
Too high = ischaemic injury
HFrEF - management
1st line
- Symptomatic
- Loop diuretic
- Prognostic
- ACEi/ARB
- Aldosterone antagnist
- SGLT2 inhibitor
- Other
- Lifestyle advice
- Pneumococcal + influenza vaccines
2nd line with LVEF < 35%
- Switch to sacubitril/valsartan
- If QRS > 120ms, CRT-P/D
- If HR > 75 but sinus, ivabradine
- African-American, hydralazine
3rd line:
- LVAD
- Heart transplant
- Palliative support
Cardiac resynchronisation therapy (CRT)
Indications:
- Heart failure with broad QRS
- Evidence of dyssynchronous activity of the
ventricles
- May signify a level of BBB
- Dyssynchrony impairs the ventricular function
Technique:
- RA + RV + LV leads
- Paces almost all the time for maximum LV function
- Set at a higher than normal rate + patient beta-
blocked
CRT-P
- Biventricular pacemaker to synchronise the ventricles
CRT-D
- Biventricular pacemaker with added defibrillation activity
NYHA functional classification
Class I
- No limitation in physical activity
- No symptoms with ordinary physical activity
Class II
- Slight limitation in physical activity
- Symptomatic with ordinary physical activity
- Asymptomatic at rest
Class III
- Marked limitation in physical activity
- Asymptomatic at rest
- Symptomatic with less than ordinary physical activity
Class IV
- Symptomatic at rest
- Unable to complete personal care without severe symptoms
HFpEF - management
Control BP, heart rate, arrhythmias
Symptomatic support with loop diuretics
ACEi/ARB/ARNI
MRA
SGLT2 inhibitor
Pulsus alternans
When an arterial pulse alternates between strong and weak beats
L-sided = heart failure, AS, cardiomyopathy
R-sided = PE, pulmonary HTN
Acute heart failure aetiology
ACS
Hypertensive crisis
Arrhythmia
PE
Infection/inflammation
Tamponade
Mechanical
- Free wall rupture
- Acute MR
- Chest trauma
- Infective endocarditis
- Aortic dissection
Acute heart failure - the four presentations and management
- Acute decompensation/congestion
- Onset over days
- IV loop diuretics +/- metolozone - Acute pulmonary oedema
- IV loop diuretics
- High-flow oxygen +/- CPAP - Isolated RV failure
- More gentle diuresis + I/O monitoring possible - Cardiogenic shock
- Inotropes
- If not responding, consider vasopressors and acute RRT
HFrEF - causes
Defined as LVEF < 40%
MI
Dilated cardiomyopathy
Myocarditis
Valvular heart disease
HFpEF - causes
Clinical heart failures with LVEF > 40%
HTN
LVH
HOCM
Amyloidosis/sarcoidosis
Valvular heart disease
Hypertrophic cardiomyopathy - causes
HOCM
Friederich’s ataxia
Fabry disease
Dilated cardiomyopathy - causes
Alcohol
Myocardial damage e.g. post-MI or post-myocarditis
Pregnancy
Chagas disease
TB
Infiltrative disease e.g. amyloidosis
Thiamine deficiency
Genetic
Restrictive cardiomyopathy
Genetic
Amyloid
Sarcoid
Scleroderma
Hereditary haemochromatosis
Takotsubo cardiomyopathy
Stress-induced, ?SNS overdrive
ECG changes + trop rise with normal angiogram
Echo - apical hypokinesis
CT angio - no lesions
Mx - diuretics, ACEi, beta-blockers
Peripartum cardiomyopathy
Defined as new clinical heart failure occurring towards the ends of, or up to 5 months after, pregnancy.
Usually presents as reduced LVEF with no other cause found
Stable - vaginal delivery
Unstable - emergency C-section
Variable recovery, up to 70% within 6 months
Pacemarker-induced cardiomyopathy
Defined as a reduction in LVEF > 10% following PPM placement
Develops in 1/8 of people receiving a PPM for complete heart block with normal LVEF.
More common with isolated R-sided pacing due to dyssynchronous contraction
Mx - upgrade to CRT
Clubbing - aetiology
Lung:
- Cancer - esp. NSCLC, mesothelioma
- ILD
- Complicated TB
- Suppurative lung disease e.g. abscess, empyema, bronchiectasis, cystic fibrosis
- Sarcoidosis
Heart:
- Congenital cyanotic heart disease
- Subacute infective endocarditis
- Atrial myxoma
GI:
- Malabsorption
- IBD
- Cirrhosis incl. PBC
Other:
- Grave’s disease
Aortic stenosis - causes and presentation
Occurs in 2% of over-65s
Causes
- Age-related calcification
- Rheumatic fever
- Paget’s disease of the bone
- Bicuspid aortic valve (1-2% of live births)
Signs:
- Slow-rising pulse
- Narrow pulse pressure
- Ejection systolic murmur with radiation
- +/- clinical heart failure
Aortic stenosis - management
Medical
- Beta-blockers
- Diuresis
Surgical
- TAVI
- Surgical valve replacement
Uses metallic valve if age < 65 or biologic if > 65
- Metallic valves must be anticoagulated with warfarin but have a longer life-time
Aortic stenosis surgical criteria
Symptomatic low-flow AS
Asymptomatic severe
- Vmax (peak aortic jet velocity) more than 5 m/s
- Aortic valve area less than 0.6 cm2
- LVEF (left ventricular ejection fraction) less than 60% y
- BNP/NT-proBNP level more than twice the upper limit of normal
- symptoms unmasked on exercise testing.
Mitral regurgitation - causes and presentation
Causes:
- Acute - MI, trauma, endocarditis
- Chronic - age-related, rheumatic fever
Signs:
- Irregularly irregular pulse
- Systolic thrill at apex
- Pansystolic murmur with radiation to axilla
Mitral regurgitation - management
Medical - anticoagulation if concurrent AF
Surgical = valve repair
- LVEF < 60%
- ESDI more than 2.2 cm/m2
- Increase of systolic pulmonary artery pressure to more than 60 mgHg on exercise testing
33% survival at 8 years without surgery
Death usually due to heart failure but can be sudden secondary to arrhythmia
Infective endocarditis - causes
Native valve
- Staph. aureus
- viridans Strep. - post-dental
- Enterococcal
(HACEK, Strep. bovis)
Prosthetic valve
- Staph. epidermidis
- Staph. aureus
- viridans Strep.
(Pseudomonas, HACEK, fungal)
Duke’s criteria
Major
- Positive blood cultures - at least 2 taken more than 12hr apart
- Imaging evidence on TOE
Minor
- Predisposing condition
- Fevers > 38
- Embolic phenomena e.g. Janeway lesions, septic emboli
- Immunological phenomena e.g. Osler’s nodes, Roth spots
- Microbiological findings
Definitive diagnosis requires:
2 major
1 major + 3 minor
5 minor
Infective endocarditis - management
Native valve:
- Min 2-6 weeks of therapy
e.g. vancomycin + gentamicin
Prosthetic valve:
- May require lifelong suppressive therapy
e.g. vancomycin + gentamicin + rifampicin
Surgery
- High mortality and morbidity
- May be required if there is acute severe valve dysfunction or aortic root abscess
Postural hypotension - causes
Neurogenic
- T2DM
- Parkinson’s
- SCLC
- MGUS
Cardiac
- Arrhythmias
- Aortic stenosis
Endocrine
- Dehydration
- Adrenal insufficiency
Medications:
- Diuretics - esp. thiazides
- Alpha-blockers
- Antihypertensives
- Insulin
- Levodopa
Postural hypotension - diagnosis and management
Diagnosis:
- SBP drop by 20 mmHg
- SBP drop to <90 mmHg
- DBP drop by 10 mmHg with symptoms
Management:
- Fludrocortisone - MRA
- Midodrine - alpha-1 agonist
Aortic root dilatation
A form of juxta-cardiac AAA which can cause aortic regurgitation and can acutely dissect
Aetiology:
- Age-related
- CTDs e.g. Marfans, vasculitis
- HTN
S1 abnormalities
Quiet = low CO
- Reduced LV function
- Rheumatic MR
- Long PR interval (1st degree HB)
Loud = high CO
- Large stroke volume
- Mitral stenosis
- Short PR interval
S2 abnormalities
Physiological splitting
- AV closes slightly before PV because left contracts before right
- Increases with inspiration, decreases with expiration
Wide splitting
- Delayed RV emptying e.g. RBBB, pulmonary HTN
Reverse splitting
- Delayed LV emptying e.g. LBBB, LV outflow obstruction
Quiet S2
- Aortic stenosis
Loud S2
- Systemic or pulmonary HTN
S3
Occurs just after S2
‘Lub-dub-ta’
Normal if pregnant, febrile, <30 y.o.
Otherwise HF, MR.
When combined with tachycardia is called a gallop rhythm
S4
The sound of blood being forced into a stiff non-compliant ventricle
Just before S1
ECG parameters
Rate
- R waves x 6
- 300 / no. large squares in R-R interval
Rhythm
Axis
- aVF and I
- normal = both positive
- left = I +ve, aVF -ve
- right = I -ve, aVF +ve
Morphology
- QRS < 120ms aka 3 small
- PR 120-220ms aka 3-5 small
- QT < 450ms
Prolonged PR interval
aka 1st degree heart block
PR > 5 sq or 200ms
AVN fibrosis
Medication e.g. digoxin, amiodarone, CCBs
Hypo or hyperkalaemia
Bundle-branch and fascicular blocks
LBBB
- Always pathological e.g. posterior STEMI
- WiLLiaM
- May have TWI in lateral leads
RBBB
- May be benign
- MaRRoW
Bifascicular block
- RBBB + axis deviation (usually LAD)
- LAD = L anterior fascicle
- RAD = L posterior fascicle
((((Trifascicular block
- RBBB + axis deviation + 1st degree heart block - OLD, TRUE WOULD BE COMPLETE HEART BLOCK))))
Posterior STEMI ECG
Usually occurs alongside inferior ± lateral infarction
Obstruction of LCX is most common
ST depression V1-V4
Dominant R in V1-V2
ST elevation in V7-V9
New LBBB
Anterior STEMI ECG
Poorest prognosis
Obstruction of LAD
ST elevation V1-V4
ST depression II, aVF
Preceding hyperacute T waves
Inferior STEMI ECG
Obstruction of RCA (80%) or LCX (20%) depending on dominance
ST elevation II, III, aVF
ST depression aVL
Preceding hyperacute T waves
Later develop deep Q waves
Supplies nodal arteries so risk of new significant heart block
Lateral STEMI ECG
Usually occurs in conjunction with anterior infarction due to involvement of the main LAD
Obstruction of small branches of LAD or LCX
ST elevation V5-V6, I, aVL
ST depression II, aVF
Occlusion myocardial infarction (OMI)
Defined as ECG patterns which do not fully meet the criteria for STEMI but nevertheless suggest coronary occlusion requiring urgent PCI
- Elevation in 2 contiguous inferior leads + depression in aVL
- New RBBB + LAFB
- T waves out of proportion to R waves
- ST depression maximal in V1-V4 with progression to V5-V6
- Multilead ST depression + ST elevation in aVR
Spontaneous coronary artery dissection (SCAD)
A rare cause of MI most commonly presenting in young healthy women
Causes:
- Connective tissue disorders
- Hormonal changes associated with pregnancy
- No association with atherosclerosis or trauma
Presentation very similar to NSTEMI/STEMI
- Chest pain
- Elevated troponin
- ST changes
Coronary angiogram is key for investigation and treatment
T wave morphologies
Normal:
- Mostly upright
- Possible TWI in aVR and V1
- Amplitude <5mm in limb, <10mm in precordial
Peaked
- Tall, narrow, symmetrical peaked
Hyperacute
- Broad
- Asymmetrically peaked
T wave inversion (TWI)
Can be normal to have TWI in I and aVR.
More widespread TWI is normal in childhood due to right-sided predominance
Other causes:
- BBB - left = I/aVL/V5-6, right = V1-V3
- Hypertrophy
- HTN
- Heart strain/PE
- Ischaemia/infarction - dynamic during, fixed afterwards
- HOCM
Biphasic T waves
In which the T wave has two phases, one going up and the other down
- MI = up - down
- Hypokalaemia = down - up
Wellen syndrome
A pattern of inverted or biphasic T waves in V2-3 which, when accompanied with chest pain, is high suggestive of critical stenosis of the LAD
Type 1 (25%)
- Biphasic T wave - up then down
Type 2 (75%)
- Deep, symmetrical TWI
Wolff-Parkinson-White synrome
Presence of an accessory conducting pathway (the Bundle of Kent) which allows some electricity to bypass the AVN
- Short PR interval
- Delta wave
Causes two types of SVT
- Orthodromic
- Narrow QRS
- Treat as SVT
- Antidromic
- Delta wave + broad QRS
- Treat with procainamide, cardioversion.
Management:
- Medical
- e.g. flecainide, sotalol, amiodarone
- Pathway ablation
- If symptomatic, FHx of sudden death, or high-
risk professions
Palpitations
An increased awareness of the heartbeat - usually because it is strong, fast, or irregular
Causes
- Substances - caffeine, alcohol, tobacco, salbutamol
- Ectopic beats
- Narrow complex tachycardia
- Panic attack
- Thyrotoxicosis
High-risk features:
- Previous MI
- Previous cardiac surgery
- Associated syncope or cardiac chest pain
- FHx of sudden death
Premature ventricular complexes (PVCs)
Ventricular ectopics which are significant because they can lead to VT/VF by setting up circuits
- Associated with sudden cardiac death post-MI
- More = worse prognosis
- In healthy patients can be substance-induced (e.g. caffeine), thyrotoxicosis, iatrogenic (e.g. digoxin)
Treatment:
- Correct electrolytes - K+ > 4.0, Mg > 1.0
- Improve respiratory state
- Avoid triggers
Antiarrhythmics (Vaughan-Williams classification)
Class I
- Block fast sodium channels which cause phase 0 (aka rapid depolarisation)
- Slows upstroke, no effect on duration/refractoriness
- IA and IC bind both activated and inactivated states so are useful during tachyarrhythmia
- IB bind during the inactivated state and are most useful when there is myocardial ischaemia
- IA = procainamide, IB = lidocaine, IC = flecainide.
Class II
- Beta-blockers - esp. action at beta-1-adrenoceptors
- Beta-1 = increased SAN firing, increased
conduction velocity
- e.g. atenolol, bisoprolol etc.
Class III
- Mechanism variable but lead to prolongation of the cardiac action potential, mainly by inhibition of repolarizing K+ currents and increasing QTc
- Esp. potent in suppressing arrhythmias caused by reentrant signs
- e.g. amiodarone, sotalol
Class IV
- Calcium channel blockers
- Suppress ectopic pacemaker action, decrease conduction velocity, prolong repolarisation at the AVN
- e.g. diltiazem, verapamil
Class V
- Increase vagal tone at SAN/AVN
- e.g. digoxin
Pacemakers - implantation
Technique:
- Implanted in subclavian region on opposite side to dominant hand
- Done under local anaesthetic
- Up to three leads - right atrial, right ventricular, left ventricular
Complications:
- Site infection
- Pneumothorax - if leads placed via subclavian vein
Dual chamber pacing
Right atrial + right ventricular leads
- On-demand pacing
Lead selection:
- Atrial fibrillation = RV only
- Paroxysmal AF = RA + RV
- Young sick sinus = RA only. Older = RA + RV
Pacing cycle:
- Intrinsic P wave sensed in RA = A SENSED
- If no ventricular contraction in a given time, ventricle is paced = V PACED
- After this there is no atrial activity so the atria are paced = A PACED
- If ventricular activity is sensed, the RV leads are inhibited = V SENSED
Implantable cardioverter defibrillator (ICD)
Indications
- Primary prevention - high risk of severe ventricular arrhythmia
- Inherited e.g. HOCM, Brugada, long QT
- Prev. surgical repair of congenital heart
disease
- Previous MI with LVEF < 35% and symptomatic
heart failure
- Secondary prevention - known severe ventricular arrhythmia without treatable cause
- Spontaneous sustained VT with syncope or
instability
- Spontaneous sustained VT with LVEF < 35%
and NHYA III symptoms or better
Technique:
- Similar implantation to PPM
- Ventricular leads contain additional defibrillation coil
Brugada syndrome
Aetiology:
- Autosomal dominant channelopathy
- 25% have FHx
- Usually mutation of SCN5 which encodes cardiac voltage-gated sodium channels
Presentation:
- Asymptomatic
- Syncope
- VT/VF
- Sudden death
ECG when in arrhythmia:
- Type 1
- coved ST elevation >2mm in more than one of
V1-V3, followed by TWI.
- Type 2
- Saddle ST elevation >2mm V1-V3
- Type 3
- Either of the above but ST elevation < 2mm
Increased risk of arrhythmia with alcohol, fever, periods of high vagal tone like sleep, rest, or after a meal
Definitive management = ICD
HOCM - ECG
LVH with giant QRS in lateral leads and deep dagger Q waves
± arrythymias e.g. AF, SVT, VT, VF
HOCM - echo
Mnemonic - MR SAM ASH
Mitral regurgitation (MR)
Systolic anterior motion (SAM) of the anterior mitral valve leaflet
Asymmetric hypertrophy (ASH)
Evidence of LVOTO - left ventricular outflow tract obstruction
- Septal hypertrophy + narrowing of LVOT causes abberrant blood flow which displaces mitral valve leaflets anteriorly.
- Mitral valve also anatomically more susceptible to this displacement
- Loss of leaflet coaptation -> LVOTO, MR
LVOTO may need to be elicited e.g. Valsalva, exercise, strain.
HOCM - clinical
Aetiology:
- Unexplained LVH
- 1/500 people
- Often FHx but not always
- 40% due to mutations in beta-myosin heavy
chain
Signs:
- Either ESM (due to LVOTO) or pansystolic (MR)
Investigations:
- Ambulatory ECG
- ECHO - gold-standard
- cMRI if echo suboptimal
- add late gadolinium enhancement (LGE) to
detect secondary myocardial fibrosis
- Genetic testing
Management:
- General:
- Mild-to-moderate exercise
- Pregnancy safe if condition is stable
- Lifestyle changes
- Obstructive symptoms:
- 1st line - beta-blockers
- 2nd line - add diltiazem
- 3rd line - surgical e.g. septal ablation,
myomectomy
- ICD
- Known to have had ventricular arrhythmias
- FHx of sudden death
- Episodes of syncope
- Massive LVH
- LVEF < 50%
- Children with runs of SVT
- End-stage:
- Consider heart transplant if having ventricular
arrhythmias or NYHA III+ symptoms
- LVAD if unavailable
- CRT if develop LBBB
Atrial fibrillation - types
First detected episode
Paroxysmal AF
- At least 2 recurrent self-terminating episodes lasting < 7 days
Persistent AF
- AF which is not self-terminating and has persisted for > 7 days
Permanent AF
- AF which cannot be cardioverted
Atrial fibrillation - investigation and management
Investigations:
- Ambulatory ECG
- TTE - AF + valve pathology is absolute indication for anticoagulation
Rhythm control
- If first episode, co-existent HF, reversible cause
- Electrical cardioversion - synchronised
- Must either have been in AF for < 48h,
anticoagulated for 21-28 days, or no evidence
of clot on TOE
- Will need to stay on anticoagulation for at least
28 days afterwards
- Chemical cardioversion
- Flecainide - no structural disease, pill in pocket
if well with AF and no CKD (dose = 200mg)
- Amiodarone - if IP, more unwell, structural
disease
(- AF ablation)
Rate control
- Beta-blocker e.g. bisoprolol
- Rate-limited CCB e.g. diltiazem, verapamil
- Combination therapy - 2/3rds dose of BB +
CCB/digoxin
- Digoxin used mainly if limited exercise and unable
to tolerate other medications
Digoxin ECGs
Digoxin effect
- normal when taking digoxin
- ‘Reverse tick’ - downsloping ST depression
- Flattened, inverted, or biphasic T waves
- Short QT
Digoxin toxicity
- Frequent PVCs e.g. bigeminy, trigeminy
- Sinus bradycardia
- Slow AF
- AV block
- VT
Digoxin toxicity
Precipitants:
- Overdose
- Renal failure
- Concurrent infection
- Hypokalaemia
Features:
- GI - nausea/vomiting, anorexia, diarrhoea
- Visual - blurred vision, yellow/green, haloes
- CVS - palpitations, pre-/syncope, SOB
- CNS - confusion, fatigue, delirium
ECG - can be a number of arrhythmias
- Frequent PVCs e.g. bigeminy, trigeminy
- Sinus bradycardia
- Slow AF
- AV block
- VT
Diagnosis = digoxin levels
Management = Digibind, correct electrolytes
Tachyarrhythmia - emergency management
Unstable features? e.g. syncope, hypotension, MI, heart failure, shock
- DCCV
Narrow complex regular
- Likely AVNRT or AVRT e.g. SVT
- 1st line - vagal manoeuvres
- 2nd line - IV adenosine 6mg - 12mg - 18mg or
verapamil if asthmatic
- 3rd line - cardioversion
Narrow complex irregular
- Most likely fast AF
Broad complex regular
- Likely VT unless known BBB
- Loading amiodarone (300mg IV over 30 mins)
then maintenance infusion (900mg over 24h)
- oral loading (10-15g total needed to load, 200mg
TDS for 7 days then BD for 7 then OD as long as
needed)
- NB avoid amiodarone if known long QT
Broad complex irregular
- Seek expert advice
- Most commonly AF + BBB but possibility of
torsades de pointes
- Do not give amiodarone until confirmed
VT - ECG appearance
Monomorphic
- Uniform complexes
- Originates from a single complex in the ventricles
Polymorphic
- Complexes of variable amplitude
- Sign of more unstable electrical activity
VT - classification of duration
Salvo
- 3-5 beats
Non-sustained
- VT lasting more than 6 beats but less than 30s
Sustained
- VT lasting >30s or with haemodynamic instability
Atrial fibrillation with rapid ventricular response (RVR)
aka fast AF
Triggers - PIRATES
Pulmonary embolism
Ischaemia
Respiratory disease
Atrial enlargement or myxoma
Thyrotoxicosis
Ethanol
Sepsis/sleep apnea
Unstable - cardioversion
Stable
- Optimise electrolytes
- K+ > 4.0, Mg = 1.0
- Rate control
- Beta-blockers
- Digoxin loading
- Oral - 500mcg, then after 6hr 500mcg,
maintenance at 125mcg
- IV - 500-1000mcg split over 2 doses and 6hr
- Rhythm control
- Consider anticoagulation
Tachy-brady syndrome
Alternating bradycardia and paroxysmal tachycardia
- Usually supraventricular
- After tachy may have delayed sinus recovery
causing a sinus pause or exit block
- If prolonged can cause syncope
Causes
- Idiopathic fibrosis (most common, sick sinus syndrome)
- Ischaemia
- Infiltration
- Cardiomyopathy
- Congenital
- Autonomic dysfunction
- Hypothyroidism
- Hyperkalaemia
- Medications e.g. digoxin, BB, CCBs
Management
- Treat reversible causes
- PPM insertion
Heart block
Most commonly due to age-related fibrosis but can be secondary to many cardiac conditions e.g. ischaemia, infiltration, SLE, lyme disease
Types:
- 1st degree
- PR > 200ms
- 2nd degree
- Type I
- Progressive PR lengthening until dropped
complex
- Usually due to reversible conduction block
at the level of the AV node - increased
fatiguability
- Type II
- Intermittent dropped beats
- Due to failure of the Purkinje fibres, often
irreversible damage
- 3rd degree/complete
- Dissociation between P and QRS
Management:
- Unstable
- Atropine 500mcg IV - up to 3mg total
- Transcutaneous pacing
- Aim for transvenous pacing + PPM insertion as
soon as possible
- Stable
- 1st degree/2nd degree type 1
- nothing if asymptomatic, else atropine
- 2nd degree type 2 + complete
- Monitoring, temporary pacing, aim for PPM
CHA2DS2-VASc
C - Congestive heart failure (1)
H - Hypertension (or treated hypertension) (1)
A2 - Age >= 75 years (2)
- Age 65-74 years (1)
D - Diabetes (1)
S2 - Prior Stroke, TIA or thromboembolism (2)
VA -Vascular disease (including ischaemic heart disease and peripheral arterial disease), (1)
S - Sex (female) (1)
Orbit score
Replacement for HAS-BLED
- Haemoglobin (males < 130, female < 120) or haematocrit (males < 4-0%, female < 36%) = (2)
- Age > 74 = (1)
- Bleeding hx (GI, intracranial, stroke) = (2)
- Renal impairment (eGFR < 60) = (1)
- Treatment with antiplatelets = (1)
Low risk - 0-2
Medium risk - 3
High risk - 4-7
Chest pain - causes
Cardiovascular
- ACS and angina
- Myo/pericarditis
- Aortic dissection
Respiratory
- Pneumothorax
- Pulmonary embolism
- Pneumonia
Gastrointestinal
- Oesophageal spasm
- GORD
- Peptic ulcer
- Pancreatitis
Other
- MSK
- Radiculopathy
- Anxiety
- Shingles
Myocarditis
Myocarditis is an inflammatory cardiac disorder which can lead to acute heart failure
- Fulminant = hours-to-days
- Non-fulminant = days-to-weeks
Causes:
- Viral - coxsackie B, adenoviruses
- Eosinophilic - Chagas, parasites hypersensitivity
- Granulomatous - TB, sarcoid
- Drug-induced - vaccines, chemo, ETOH
Features:
- Sharp stabbing chest pain
- Fever
- New heart failure - SOB, orthopnea, dizziness
- Palpitations
- Recent infectious prodrome - coryza, diarrhoea
Investigations:
- Bloods incl. viral serology, serial trops
- Imaging e.g. cMRI
- Myocardial biopsy is gold-standard
Management:
- Symptomatic relief from acute heart failure
- Colchicine for pain, up to 2-3 months after resolution
Long QTc
QTc = An estimate of QT at a standardised heart rate of 60bpm
Long if :
Men > 440ms
Women > 460ms
Aetiology:
- Hypokalaemia
- Hypomagnesaemia
- Hypocalacaemia
- Hypothermia
- Raised ICP
- Medications
- Ischaemia
- Congenital
T wave alternans
Beat-to-beat variation in T wave amplitude or polarity
Associated with long QT
Often secondary to ischaemia, increases risk of re-entrant arrhythmias
Aortic dissection
Classification:
- Type A
- 2/3
- ascending aorta
- Type B
- 1/3
- descending aorta
Aetiology:
- HTN
- Trauma
- CTDs
- Bicuspid aortic valve, Turner’s, Noonan’s syndrome
Features:
- Severe, ‘tearing’ pain radiating to back
- > 20mmHg discrepancy in BP
- New AR
- Angina, paraplegia, limb ischaemia
Imaging:
- CT angiograhpy - look for false lumen
- TOE - in unstable patients
Management:
- Type A - surgical repair
- Type B - strict BP control (SBP 100-120)
Abnormal JVP x 9
Heart failure: elevated
PE: elevated
Pericardial effusion: elevated, prominent y descent
Pericardial constriction: elevated w kussmauls sign (inc on insp)
SVCO: elevated w loss o pulsation
Afib: absent a waves
Tricuspid stenosis: giant a waves
Tricuspid regurg: giant V waves
Complete heart block: cannon waves
Ventricular septal defects (VSDs)
Most common congenital abnormality in children and second most common in adults
Predominantly create pathology through formation of a shunt, with risk of Eisenmenger syndrome
Features:
- Pansystolic murmur
- Heard best at L sternal edge
- CHF
- Fluid overload, raised JVP etc.
- Eisenmenger
- Cyanosis
- Syncope
- Dyspnea
- Clubbing
Management:
- Small = observation
- Isolated medium/large = percutaneous closure
- Large, complex or haemodynamic compromise = surgical closure
Right heart catheterisation
Insertion of Swan-Ganz catheter into the right side of the heart via a large peripheral vein
RA
< 5 mmHg
RV
- 15-30 / 3-8
Pulmonary artery
- Systolic = RV
- 15-25 / 4-12
PCWP
- Indirect estimate of LA pressure
- Helps to quantify LVF and mitral stenosis
- < 12mmHg
LV
- 100-140 / 3-12
Combination of PA + PCWP, via thermodilution technique, is used to measure pulmonary vascular resistance and therefore diagnose pulmonary HTN
AF ablation
Indications:
- AF which has failed first-line medical treatment
Must take anticoagulation for 4-6 weeks prior
- Do not stop prior to the procedure
Stop beta-blockers, CCBs, and antihypertensives pre-procedure
Perform wide circumferential ablation around the pulmonary veins
Secondary prevention of MI
Non-pharmacological:
- Stop smoking
- Weight loss
Pharmacological:
- ACEI (NNT = 22)
- Statin (NNT = 33)
- Aspirin (NNT = 42)
- Beta-blocker (NNT = 143)
Pericarditis
Inflammation of the pericardium
- Can lead to involvement of the epicardium - ECG changes - or effusion - risk of tamponade
Causes:
- Infection (oft. viral)
- Uraemia
- Autoimmune
- Malignancy (esp. lung)
Features:
- Sharp stabbing central chest pain
- Better leaning forwards
- Worse coughing, lying back, moving
- May radiate to neck and arm
- Pericardial rub
- SOB
Investigations:
- ECG - saddle-shaped ST elevation
- Raised troponin
- Echo - diagnostic
Management:
- Treat underlying cause
- NSAIDS, colchicine
Complications:
- Myocarditis
- Tamponade
Cardiac tamponade
Features:
- Beck’s triad:
- Hypotension
- Raised JVP
- Muffled heart sounds
- Tachycardia
- Pulsus paradoxus
- SOB with normal lung fields
Investigations:
- CXR = large globular heart
- Echo = diagnostic
Management:
- Emergency pericardiocentesis
Constrictive pericarditis
Chronic inflammation leads the pericardium to become dense and fibrous
Aetiology:
- TB
- Trauma
- Purulent pericarditis
Features:
- Peripheral oedema
- Dyspnea
- Ascites
- Hepatomegaly
Investigations:
- CXR - normal sized heart
- Echo - restricted mitral filling, pericardial thickening
Management:
- Surgical excision
Stable angina
Aetiology:
- Coronary atherosclerosis
- Tachycardia
- Anaemia
- Aortic stenosis
- LVH
- Coronary artery spasm
Features:
- Cardiac chest pain occurring on exertion
- Relieved with GTN
- Also fatigue, nausea, belching
Classification of severity:
- Class I - only with prolonged strenuous activity
- Class II - on climbing stairs or walking into wind
- Class III - on climbing 1 flight of stairs or going 50-100m on the flat
- Class IV - on any physical activity
Investigations:
- Stress testing - with ECG, echo, etc.
- Coronary angiography
Management:
- Lifestyle advice + secondary prevention meds
- Medical:
- GTN for breakthrough
- CCBs e.g. diltiazem, verapamil or beta-
blocker
- Consider ivabradine, nicorandil etc.
- If not managed with 4 agents, PCI/CABG
Lown-Ganong-Levine syndrome (LGL)
Presence of an accessory pathway connecting the atria to the bundle of His, leading to bypass of the AVN
- vs WPW where it connects to the ventricular
myocardium
ECG - short PR, no delta waves
Management:
- Beta-blockers
- Pathway ablation
Cardiac enzymes
Myoglobin:
- Released within 1hr of myocardial cell damage, elevated for 1-2 days afterwards
Troponins:
- Released within 4-6 hours of myocardial cell damage and remain elevated for up to 2 weeks
- TnI and Tnt are most sensitive
Creatinine kinase:
- Released c. 24h after myocardial cell damage and remain elevated for 3-4 days
Thrombolysis contraindications
Relative:
- Prolonged traumatic CPR
- Recent surgery
- Bleeding disorders
- Pregnancy
- On anticoagulation and/or INR > 1.8
Absolute:
- BP > 180/110
- Head trauma within 2/52
- Known intracranial malignancy
- Active bleeding
- Stroke < 2/12 ago
- Suspected aortic dissection
HTN - pharmaceuticals
ACEi
- Decrease circulating ATII -> decreased aldosterone -> decreased Na+ reabsorption
- Also increase bradykinin levels
- Dry cough
- Angioedema
ARBs:
- Blockade of AR2
- Useful in those who don’t tolerate ACEi
Thiazides:
- Inhibit the Na/Cl symporter in the DCT -> decreased Na+ reabsorption
- Takes 12 weeks to come into effect
- Early reduction in blood volume
- Slower vasodilation
CCBs:
- Predominantly blockade of L-type voltage-gated calcium channels
- Affects vascular tone + heart contractility
- Only amlodipine can be used in CHF patients
Misc pharmaceuticals
Ivabradine
- Inhibition of If within the SAN - hyperpolarization-activated cyclic-nucleotide gated K+ channel
Hydralazine
- Direct-acting smooth muscle relaxant working primarily in resistance arterioles
- Inhibits inositol triphosphate-induced Ca2+
release from the sarcoplasmic reticulum
Nicorandil
- Nitrate + activates ATP-sensitive K+ channels -> induces hyperpolarization
Clopidogrel:
- Inhibitor of a P2YR, inhbiting ADP-mediated platelet aggregation
- Prodrug requiring activation by CYP2C19 which is active in only 2/3rds the population
Coronary artery vasospasm (CAVS)
Presents on a spectrum from stable angina to ACS with potential to cause ischaemia
Most likely to occur at night due to increased activity of the PNS although SNS is also implicated in it’s pathophysiology
Investigations:
- Coronary angiography with provocative testing
- Need ECG changes, >50% luminal narrowing,
and symptoms
Driving + PPMs
Pacemaker:
- Cannot drive car for 1 week
- Cannot drive group 2 vehicles for 6 weeks
ICD
- Car
- Primary prevention = 1 month
- Secondary prevention = 6 months
- Cannot drive for 6 months after any shock
- Cannot drive group 2
Driving + ACS
Group 1
- Cannot drive for 1 week if had successful angioplasty
- Cannot drive for 4 weeks if either angioplasty was unsuccessful or didn’t happen.
Group 2
- Cannot drive for 6 weeks
Types of myocardial infarction
Type 1 - coronary artery-based
Type 2 - increased demand/reduced supply states with normal coronaries
Type 3 - sudden cardiac death from MI
Type 4 - due to PCI or stent thrombosis
Type 5 - due to cardiac surgery
Type 2 MI
Myocardial infarction secondary to ischaemia due to either increased oxygen demand or decreased supply
- e.g. vasospasm, hypovolaemia, sepsis, PE
Diagnosis:
- Elevated by changing troponin
- Clinical features inconsistent with type 1 MI
- Clinical conditions known to increase oxygen demand and/or decrease supply
Management:
- Treat underlying insult
- Screen for coronary artery lesions
Post-CABG complications (10)
Specific:
- Atrial fibrillation
- Pulmonary HTN
- Pericardial effusion
- Pleural effusion (40%)
- Stroke
- Renal injury
- Haemodynamic instability
General:
- Sternal wound infections
- Graft failure
- Pneumonia
- VTE phenomena
Congenital heart disease - radiological findings
L-> R shunt
- Enlarged heart
- Prominant pulmonary vasculature
- Fluid in lung fields
Aortic stenosis
- Prominent LV
- Aortic dilatation
Pulmonary stenosis
- Post-stenotic pulmonary artery dilatation
Coarctation of the aorta
- Prominent LV
- Rib notching
Tetralogy of Fallot
- Boot-shaped heart - apex above L hemidraphram + concave L heart border
- Small pulmonary arteries
- Oligaemic lung fields
Transposition of the Great Arteries
- Egg-on-side appearance
Total anomalous pulmonary venous drainage
- Small heart
- Pulmonary congestion - can be white-out
Ebstein’s anomaly
- Massively enlarged heart
- Pulmonary oligaemia
Heart disease in congenital conditions
Friedrich ataxia - HOCM
Marfans - aortic dissection/aneurysm/regurg
Glycogen storage disease - type 2 cardiomyopathy
Noonan’s - pulmonary stenosis
William’s - supravalvular aortic stenosis, pulm sten
Romano-ward syndrome - long QT
Tuberous sclerosis - rhabdomyoma
Turners - bicuspid aortic valve
Teratogens affecting the heart
Alcohol - ASD, TOF
Rubella - PDA, coarctation, TOF
Phenytoin - pulm stenosis
Lithium - ebstein anomaly
Heart transplantation - rejection
Fever
Prolonging PR interval + reducing QRS voltages
Increasing heart size on CXR
Acute mesenteric ischaemia
Aetiology:
- Embolic (50%)
- Arrhythmia
- Valve pathology
- Post-MI mural thrombus
- Aortic aneurysm
- Thrombotic (25%)
- Atherosclerosis
- Shock (20%)
- Mesenteric venous thrombosis (<10%)
- Dissection
- Vasculitis
Investigations:
- Blood gas
- Routine bloods
- CT angiography
Management:
- Urgent surgery
- Angioplasty/embolectomy
- Bowel resection if necrotic
- Usually requires relook laparotomy in 24-48hr
Carotid artery stenosis
Plaque mostly found at the bifurcation of the CCA or within the proximal ICA
Can present with TIA/amaurosis fugax but then rapidly progresses to full stroke
Investigation:
- Duplex USS
Management:
- Lifestyle modification
- Medications e.g. statin, clopidogrel
- Surgery:
- If >50% stenosis on one side with sx or >70%
and asymptomatic
- Balance risk of future stroke with risk of stroke
due to intervention
Leriche syndrome
aka aortoilliac occlusive disease
Due to severe atherosclerosis of the distal aorta or proximal common iliac
Classic triad:
- Thigh/buttock claudication
- Absent femoral pulses
- Male impotence
ABPI
Used in the investigation of potential peripheral vascular disease
> 1.3 = arterial calcification
0.9 - 1.3 = normal
0.6 - 0.9 = mild PVD
0.3 - 0.6 = moderate-severe PVD
< 0. 3 = severe to critical PVD
Peripheral vascular disease
Most commonly due to atherosclerosis of the peripheral arteries, with acute presentations due to thrombus formation
Intermittent claudication:
- Leg pain on exertion which is relieved by rest
- Investigations = ABPI
- Management:
- Lifestyle modification
- Supervised exercise training
- Statins, clopidogrel
- Revascularisation procedures
Critical (chronic) limb ischaemia
- Presence of claudication pain at rest, due to critical compromise of blood flow
Acute limb ischaemia
- A sudden decrease in limb blood flow which threatens viability, usually due to acute thrombus formation
- Features = 6 Ps
- Investigation = angiography
- Management:
- Medical - analgesia + unfractionated heparin
- IR - stenting, balloon
- Surgical - embolectomy, endarterectomy
- Limb amputation
- A key complication is compartment syndrome following limb reperfusion injury
Thrombophlebitis
Aetiology:
- Trauma e.g. IV line insertion
- Lupus
- Cancer - migratory, due to hypercoagulable state
- Berger’s syndrome
Features:
- Low-grade fever
- Local redness or swelling along course of vein
- Symptoms worse when limb lowered
Management:
- Elevation + compression
- NSAIDs
- Abx if concurrent infection present
Varicose veins
Common in older life.
Can also occur in pregnancy, usually resolving upon delivery
Investigations:
- ABPI - to rule-out arterial pathology prior to compression stockins
- Duplex USS - prior to surgical referral
Management:
- Weight loss
- Leg elevation
- Compression stockings (incl. in pregnancy)
- Refer to vascular if symptomatic
- Pain, itchiness, heaviness, swelling, chronic
venous insufficiency
- Endothermal ablation, foam sclerotherapy,
ligation + stripping
Phlegmasia
Uncommon condition resulting from acute, massive venous thromboembolism
- Mostly veins of the leg (iliofemoral), rarely arm
- Linked to hypercoagulable state - esp.
malignancy
Features:
- Phlegmasia alba dolens
- Initial phase
- Progresses over hours to days
- Severe pain + limb pallor + edema
- Phlegmasia cerulea dolens
- Second phase
- Severe pain + cyanosis -> bullae and necrosis
Management:
- Limb elevation
- Analgesia + fluids
- Thrombolysis
- Thrombectomy
Lymphoedema
Aetiology:
- Post-surgical esp. for cancer
- Radiotherapy
- Infection - filariasis
- Psoriasis
- DVT/varicose veins
Investigation:
- Rarely required
- MRI or lymphoscintogram
Management:
- Exercise
- Limb elevation
- Limb massage
- Skin/nail care
- Liposuction or lipovascular anastomosis done in a minority of cases at speciality centres
AAA screening
For men 65+ or women 70+ with risk-factors
< 3.0 - discharge
3.0 - 4.4 - repeat in 12 months
4.5 - 5.4 - repeat in 3 months
> 5.5 or growing > 1.0 in 1 year - vascular referral
Symptomatic - urgent vascular referral
Long QT syndrome
A syndrome of channelopathies leading to prolonged QT with risk of arrhythmia and sudden death
Often present in unstable monomorphic VT
Aetiology:
- LQT1
- Most common
- KCNQ1 on Chr 11
- Slow delayed rectifier K+ channel
- LQT2
- KCNH2 on Chr 7
- Rapid delayed rectifier K+ channel
- LQT3
- SCN5A on Chr 3
- Slow Na+ channel
Management:
- Medical
- Beta-blockade
- ICD
- Mainly for LQT2/3 as higher risk of sudden
death
S1
Produced by closure of the mitral and tricuspid valves
- Mitral closes just before tricuspid
- Wide splitting is always pathological
Associated with the ECG R-wave
Quiet S1 - rigid valve or delayed LV systole
- Mitral regurgitation
- Long PR interval
- Obesity
- 1st degree heart block
- LBBB
Loud S1 - long diastole, high volume
- Mitral stenosis
- Hyperdynamic states
- Tachycardia
- Low BMI
- Atrial myxoma
Widely split S1
- RBBB
- Ebstein’s anomaly
- Ventricular tachycardia
Variable intensity S1 - due to variable PR interval
- Complete heart block
S2
Produced by closure of the aortic and pulmonary valves
- Some splitting is typical - aortic closes before
pulmonary due to high systemic pressures
- Splitting increases in inspiration
Loud
- HTN
Quiet/absent
- Severe aortic stenosis
Widely split
- Pathology which delays the end of right ventricular systole or slows exit of blood from the RV
e.g. RBBB, Pulmonary stenosis, VSD, Mitral
regurgitation
Fixed splitting
- aka no change with inspiration - because ASD allows equalisation of pressures between both side
e.g. ASD
Reversed splitting
- Closure of PV prior to AV
- Delayed LV systole - LBBB
- Slowed LV outflow - AS
- Additional supply of blood delaying closure -
PDA
Cholesterol embolism
An uncommon complication of angiography
Features:
- Recent arterial instrumentation
- Marked eosinophilia
- AKI
- Livedo retricularis
- Acrocyanosis
- Limb ischaemia and other embolic phenomena
Management:
- Supportive
- No good evidence for thrombolysis, anticoagulation, or re-intervention
Arrhthymogenic right ventricular cardiomyopathy
aka right ventricular dysplasia
2nd most common cause of sudden death in the young
Features:
- Palpitations
- Syncope
- Cardiac arrest
- Progressive RV failure
ECG:
- TWI in V1-3 without RBBB
- Epsilon potential - small deflection at end of QRS complex due to RV conduction delay
Echo:
- Dilated, hypokinetic RV with prominent apical trabeculae and dilated outflow tract
Histology:
- Fatty infiltration of RV myocytes with subsequent fibrosis
Eisenmenger syndrome
A complication of congenital heart disease in which large anatomical shunts are present
e.g. VSD, ToF, large ASDs
Pathophysiology:
- Initial L -> R shunting
- Elevated RV and pulmonary pressures
- Eventual pulmonary arterial hypertension and
elevated venous resistance
- Then R -> L shunting
Features:
- Cyanosis
- Hypoxaemia despite maximal oxygen therapy (due to mixing)
- Other cardiac stress - oedema, chest pain, syncoep, SOBOE
Management:
- Only curative treatment is a heart transplant
- Vasodilators e.g. endothelin antagonists
Heyde syndrome
Triad of aortic stenosis, GI bleeding, and acquired von Willebrand syndrome
Pathophysiology:
- Shear stresses + increased velocity across stenotic aortic valve cause unfolding and activation of vWF
- Uses up vWF and so less is available for normal clot formation, in particular predisposing to GI bleeding
Management:
- Aortic valve replacement
Restrictive cardiomyopathy
A rare (5%) cause of cardiomyopathy, presenting in a similar way to constrictive pericarditis
Aetiology:
- Idiopathic
- Infiltrative disease - esp amyloidosis
- Radiation therapy
- Hypereosinophilia
Features:
- Right heart failure - raised JVP, peripheral oedema, hepatomegaly, cachexia
- SOB, PND, orthopnea
Investigations:
- ECG
- non-specific repolarisation disturbances,
small complexes
- Bloods
- Echo
- small ventricles, LVH, speckling
- Cardiac biopsy
- +ve Congo Red staining for amyloid
Management:
- Supportive - diuretics
- AF control
Atrial myxoma
A cardiac tumour formed from the atrial muscle
- Most common cardiac tumour
- Mostly on L side
- Benign
- F > M
Features arise from embolisation, intra-atrial obstruction of cardiac output, and constitutional symptoms of malignancy
Features:
- Symptoms
- Fever
- Weight loss
- SOB
- Syncope
- Signs
- Transient mitral stenosis
- Early diastolic ‘plop’
- Distal embolisation
- Finger clubbing
Investigations:
- Bloods
- Raised WCC, low PLT, variable Hb
- Imaging:
- CXR - enlarged heart
- Echocardiogram
Management:
- Urgent surgical resection as high risk of growth and embolisation
