Cardio paces Flashcards
Classifying AF
Paroxysmal - recurrent episodes lasting longer than 30s but less than 7 days, self terminating
Persistent - lasting longer than 7 days or <7 days but requiring pharmacological/electrical cardioversion
Permanent- fails to terminate using cardioversion or is terminated but relapses within 24 hrs or long standing AF where cardioversion is not indicated or has not been attempted
Pathophysiology of AF
Rapidly firing foci cause propagating wavelets which lead to re-entrant circuits in the abnormal atrial myocardium. The AVN receives more electrical impulses than it can conduct whichleads to irregular ventricular rhythm
Investigations for AF
Bloods inc. FBC, all electrolytes and TFTS
ECG
echo
CXR
Clinical signs of aortic stenosis
Slow rising, low volume pulse
Narrow pulse pressure
Thrill in the aortic area
Crescendo/decrescendo ejection systolic murmur loudest in the aortic area during expiration and radiated to the carotids
Anaemia (chronic disease, angiodysplasia/Heyde syndrome)
Clinical findings of severe aortic stenosis
Soft and delayed A2
Delayed ejection systolic murmur
Fourth heart sound
High pitch
Evidence of cardiac failure
Differential diagnosis for systolic murmur
Aortic stenosis
Aortic sclerosis (shorter, softer, no radiation)
Mitral regurgitation ( pansystolic)
HOCM (young)
Pulmonary stenosis ( rare, young, >on inspiration)
VSD (post MI, high mortality)
Aetiology of aortic stenosis
-Degenerative and calcific (80% 70s and above)
- Bicupsid (presents younger 40s-60s)
- Rheumatic fever
Echo findings of severe aortic stenosis
- Peak gradient across the valve of > 64 or a mean gradient of > 40
- valve area <1
- Dimensionless index (ratio of LVOT velocity to aortic valve)
ECG findings of aortic stenosis
Left ventricular hypertrophy
LBBB
10% of patients who have a TAVI go on to have a pacemaker so important to know about re-existing conduction abnormalities
When to consider TAVI
75 or over unless technically not suitable ( bad PVD, bad coronary artery disease)
Or <75 and not suitable for surgery (chest radiation, previous sternotomy, chronic liver disease, pulmonary hypertension, LVSD)
Work up for valve replacement
Routine bloods
Lung function tests
Angiogram
For TAVI: TAVI CT
Complications of TAVI
Conduction abnormality requiring PPM
Damage to vasculature
Stroke
MI
Signs of prosthetic valve
- Midline sternotomy scar without evidence of vein harvesting scar
- AF
- Infective endocarditis signs
- Bruising suggesting warfarin use
- Audible and palpable prosthetic click
- PPM ( 10% of pts with aortic valve replacement require PPM due to damage to AVN)
- Metallic aortic valve will have a soft systolic murmur (AR or loud AS would be abnormal)
Pros and cons of metallic vs. tissue valve
Metallic: more durable, life long Warfarin
Tissue: no warfarin, less durable (10-15 yrs)
Complications of valve replacement
Thromboembolism
Bleeding on warfarin
Haemolysis
Infective endocarditis
- <2 months post op staph epidermis is from the skin
- late infections are strep viridans by haematogenous spread
AF particularly if MVR
What INR range for metallic valve
Does depend on valve type
Mitral ball socket valve requires higher INR: 3-4
Bileaflet mitral: 2.5-3.5
Bileaflet aortic: 2-3
Clinical signs of tricuspid regurgitation
Raised JVP with giant CV waves
Thrill left sternal edge
Pansystolic murmur loudest at the lower left sternal edge loudest on inspiration
Causes of tricuspid regurgitation
Congenital: Ebstein’s anomaly (tricuspid valve dysplasia with a more apical position to the valve
Acquired: IE, functional due to right ventricular dilatation ( most common), rheumatic fever or carcinoid syndrome (would be associated with nodular hepatomegaly and telangiectasia)
How does tricuspid regurgitation present?
Pulsation sensation in the neck
Signs of right heart failure eg. Peripheral oedema and ascites
Investigations for tricuspid regurgitation
CXR: prominent right heart border due to enlarged right atrium
ECG: p-pulmonale, RVH
Echo
Treatment of tricuspid regurgitation
Diuretics, b blocker, ACEi
Valve repair or annuloplasty
Clinical signs of mitral regurgitation
AF, low volume pulse
Displaced apex beat
Thrill at apex
Pansystolic/ mid to late systolic murmur loudest at the apex radiating to the axilla loudest in expiration
May have raised JVP but this is normally related to co-existing TR
Causes of mitral regurgitation
Congenital
Dilated left ventricle
Calcification
Fibrosis
BE
Rheumatic
Connective tissue disorder
Post - MI
Amyloidosis
Investigating MR
ECG: p- mitrale, AF, prev. infarction
CXR: cardiomegaly, enlargement of the left atrium and pulmonary oedema
Echo
Treatment for MR
If mild to mod- monitor with 2 yearly Echo.
Need to intervene early
Intervention guided by severity, symptoms, pulmonary hypertension and left ventricular function.
Mitral clip
Valve repair
Valve replacement
Signs of mitral valve prolapse
Young, tall patient
Associated with connective tissue disease (Marfans) and HOCM
Late systolic murmur with early systolic ejection click
Murmur accentuated by standing from a squatting position or straining
Evidence of severe mitral regurgitation
AF
Thrusting displaced apex beat
Palpable thrill
Pansystolic murmur
Echo findings both direct and indirect (LV impairment)
Aetiology of Marfans
Caused by mutations in the fibrillin-1 gene:
75% of mutations are autosomal dominant
25% of cases are spontaneous mutations and are associated with older paternal age
Pathophysiology of Marfans
Mutation in the FBN1 gene result in the production of abnormal fibrillin protein. This causes mechanical instability and loss of elasticity of connective tissues.
This results in aortic dilatation.
Investigating Marfans
Echo
CT or USS abdo
CXR for pneumothoracices
Slit lamp eye examination to assess for subluxed/dislocated lens or raised IOP
Fibrillin- 1 blood test
Management of Marfans
Surveillance of aortic roof size with annual echo
Surgical management of aortic root dilatation
B blockers and angiotensin receptor blocker to slow aortic root dilatation
Genetic counselling
Clinical signs of pulmonary stenosis
Raised JVP with giant A waves
Right parasternal heave
Thrill in the pulmonary area
Ejection systolic murmur loudest in the pulmonary area on inspiration
Radiates to infraclavicular region
Widely split second heart sound
Functional tricuspid regurgitation
Associated syndromes with pulmonary stenosis
- Tetralogy of Fallot ( PS, VSD, overriding aorta, and RVH)
- Noonans
- Carcinoid tumour ( the secreted mediators cause right- sided heart valve fibrosis causes tricuspid regurgitation and/or pulmonary stenosis)
Signs of noonans disease
Pulmonary stenosis
HOCM
Septal defects
Short stature
Learning difficulties
Pectus excavatum
Proptosis
Ptosis
Strabismus
Characteristic facial features
Clinical signs of Marfans
Tall with long extremities
Arachnodactyly ( can encircle their wrist with their thumb and little finger)
Hyperextendible joints
High arched palate
Pectus carinatum or excavatum
Scoliosis
Aortic regurgitation
Mitral valve prolapse
Coarctation
Inguinal hernia
Signs of ehlers danlos
Fragile skin
Hyperextensible skin
Joint hypermobility
Mitral valve prolapse
Evidence of surgery from aneurysmal rupture or bowel perforation
It is autosomal dominant
Conditions associated with a VSD
Edwards
Patau
Down’s
Turner
Holt Oram
Fetal alcohol syndrome
Tetralogy of Fallot ( right ventricular hypertrophy, overriding aorta, VSD, pulmonary stenosis)
Pathophysiology of VSD
Left to right shunt
Elevated right heart pressures and consequent pulmonary hypertension
Clinical presentation of VSD
Failure to thrive/ poor feeding
Poor exercise tolerance
Ejection systolic or Pansystolic murmur localised to left sternal edge
Hyper dynamic apex beat
Parasternal heave
Investigating a VSD
ECG
- left ventricular hypertrophy
- biventricular hypertrophy
- pulmonary hypertension
CXR
- cardiomegaly
- enlarged pulmonary artery
ECHO
Management of VSD
High calorie diet
Digoxin
Failure treated with diuretics and ACEi
Surgery
When is surgery indicated for VSD
Significant left to right shunt
Other defects requiring cardiac surgery
Pulmonary hypertension
Endocarditis
Acute VSD post MI
Pathophysiology of Eisenmenger
Severe irreversible pulmonary hypertension leads to reversal of the left- to- right shunt
Resulting in cyanosis
Signs of Eisenmenger syndrome
Clubbing
Central cyanosis
Decreased murmur intensity
Loud S2
Palpable P2
Widely split second heart sound
Right ventricular heave
Graham steel murmur ( due to pulmonary regurgitation)
Causes of Eisenmenger
VSD
ASD
PDA
Complications of Eisenmenger
Right ventricular failure
Massive haemoptysis
Cerebral embolism
IE
Causes of VSD
Congenital
Acquired
- traumatic, post- operative or post- MI
What is a Blalock- Tausig shunt?
It partially corrects the Fallot’s abnormality by anastomosing the subclavian artery to the pulmonary artery
There will be an absent/weak radial pulse and a left thoracotomy scar
Associations with TOF
DiGeorge syndrome
Down’s syndrome
Fetal alcohol syndrome
Maternal diabetes
Maternal phenylketonuria
Presentation of TOF
Ultrasound detection
Cyanosis
Feeding difficulties
Failure to thrive
Exertions dyspnoea
Clubbing
Clinical signs tetralogy of Fallot
Loud second heart sound
Crescendo- decresendo murmur
Aortic ejection click
Systolic thrill at the left sternal border
Management of tetralogy of Fallot
Timing of surgery depends on degree of cyanosis and symptoms at birth.
Prostaglandin infusion to keep ductus arteriorsus patent.
Primary surgical repair within the first year of life.
Complications of TOF (following surgery)
Pulmonary regurgitation requiring valve replacement
Endocarditis
Coagulopathy
Polycythaemia
Paradoxical embolism
Arrhythmias
Complications of mitral valve prolapse
Thromboembolic events
IE
CVA
Causes of mitral valve prolapse
Myxomatous
Marfans, ehlers danlos, osteogenesis imperfecta, PKD
Causes of restrictive cardiomyopathy
Myocardial
- idiopathic
- scleroderma
- amyloid
- Haemachromatosis
- glycogen storage disorders
- Gauchers
Endomyocardial
- endomyocardial fibrosis
- hyper- eosinophilic syndromes ( inc. lofflers)
- carcinoid
- malignancy or radiotherapy
- toxin related
Pathophysiology of restrictive cardiomyopathy
Increased stiffness of the myocardium causes ventricular pressures to rise precipitously with small increases in volume. The atria dilate in response and may develop AF. Infiltration of the conducting tissues leads to conduction abnormalities.
Investigating restrictive cardiomyopathy
Bloods
ECG
Cardiac catheterisation (increased right heart pressures)
Echo- small ventricular chamber size, thickened left ventricular wall, restricted diastole
Cardiac MRI
Cardiac biopsy
Managing restrictive cardiomyopathy
Management of heart failure and AF
Management of underlying cause
Transplantation
Clinical signs of mitral stenosis
Malar flush
AF
Tapping apex (palpable first heart sound)
Left parasternal heave if pulmonary hypertension present
Opening snap of S1, then mid diastolic murmur
Tricuspid regurgitation, right ventricular heave and loud p2 if pulmonary hypertension
Embolic complications
Causes of mitral stenosis
- Congenital
- Acquired
- Rheumatic
- Senile degeneration
- endocarditis
Investigating mitral stenosis
ECG: p- mitrale and AF
CXR: enlarged left atrium, calcified valve, pulmonary oedema
TTE: valve area <2cm2 for diagnosis, <1cm2 is severe
Management of mitral stenosis
- Medical
- if AF rate control and anti coagulation
- diuretics - Surgery
- indicated if symptomatic + severe lesion, if asymptomatic surgery considered if raised pulmonary pressure (>50)
- valvotomy or replacement
How is rheumatic fever diagnosed?
- Evidence of recent group A strep infection
- positive throat swab, positive antigen test, raised antibody titre, recent episode of scarlet fever - Plus either 2 major criteria or 1 major and 2 minor
- Major criteria
- chorea
- erythema marginatum
- subcutaneous nodules
- polyarthritis
- carditis - Minor criteria
- raised ESR/WCC, arthralgia, previous rheumatic fever, pyrexia, prolonged PR
How does rhuematic fever affect valves?
Causes endocarditis. Most common affects the mitral valve and more commonly causes regurgitation rather than stenosis.
How is rheumatic fever treated?
High dose aspirin
Penicillin
And then prophylactic PenV
How does IE present?
Malaise, tiredness, infective symptoms
Fever
Arthropathy
Heart failure
Splinter haemorrhages
Oslers nodes (painful), Janeway’s lesions (painless)
Clubbing
Roth’s spots on fundoscopy
Signs of arterial embolisation
Vasculitic rash
What are Duke’s criteria
2 major or 1 major + 3 minor or 5 minor
Major criteria:
- 2 x blood cultures positive for typical organism
- Positive echo finding
Minor criteria:
- predisposing heart condition or IVDU
- fever
- vascular phenomena (arterial emboli, pulmonary infarcts, ICH, janeway haemorrhages)
- immunological phenomena (glomerulonephritis, oslers nodes, roths spots, rheumatoid factor)
- micro evidence but not sufficient to be major criteria
Clinical signs of aortic regurgitation
Collapsing pulse secondary to wide pulse pressure
Corrigans sign (visible neck pulsations)
Quincke’s sign (nail bed capillary pulsation)
De Mussets (head nodding)
Hyper dynamic apex and displaced laterally
Aortic thrill
Early diastolic murmur loudest sat forward in expiration at lower left sternal edge
May also be Austin- Flint murmur (mid-diastolic) due to regurgitant flow impeding mitral opening
Causes of aortic regurgitation
Congenital
- biscuspid valve or perimembranous VSD
Acquired
- endocarditis, rhuematic fever, aortic dissection, Marfans, hypertension, ankylosing spondylitis
Investigations for aortic regurgitation
ECG: lateral T wave inversion
CXR: cardiomegaly, widened mediastinum, pulmonary oedema
Echo
Cardiac catheterisation
Management of aortic regurgitation
ACEi or ARB to reduce after load
Regular review
Valve replacement if symptomatic and/or wife pulse pressure, ECG changes on ETT, or significant LV enlargement or reduced ejection fraction
Indications for aortic valve replacement (stenosis)
Symptomatic patient with PPD >50mmHg
Moderate to severe AS undergoing CABG
VT
Valve area <0.6cm2
Clinical features of Marfans
Tall
Increased arm span to height ratio
Arachnodactyly
Collapsing pulse
Long narrow face
Blue scera
High arched palate, crowded teeth
Pectus excavatum/carinatum
Aortic regurgitation or mitral valve prolapse
Differentials for Marfans
Homocysteinuria
Men 2b (Marfanoid body habitus, mucosal neuromas, medullary thyroid cancer, phaeochromocytoma
Ehlers danlos
Clinical signs of HOCM
Jerky pulse
Double apical impulse (atrial and ventricular contraction)
Thrill at the lower left sternal edge
ESM at lower left sternal edge radiating through the precordium accentuated by straining (Valsalva) or standing from squatting
May be associated with Friedreich’s ataxia or myotonic dystrophy
Investigating HOCM
ECG: LVH with strain (t wave inversion across precordial leads)
CXR: normal
TTE: assymetrical septal hypertrophy, systolic anterior motion of the anterior mitral leaflet across the LVOT due to misalignement of septal papillary muscles
Cardiac MRI
Genetic testing: sarcomeric protein mutations
Management of HOCM
Avoid strenuous exercise, dehydration and vasodilators
If symptomatic and LVOT gradient > 30mmHg:
- b blocker
- Pacemaker
- alcohol septal ablation
- surgical myomectomy
If rhythm disturbance or high risk SCD:
- ICD
Refractory:
Transplant
Genetic counselling (autosomal dominant)
Poor prognostic factors for HOCM
Young age at diagnosis
Syncope
FHx of sudden death
Septal thickness > 3cm
Investigating pulmonary stenosis
ECG: p- pulmonale, RVH, RBBB
CXR: oligaemic lung fields and large right atrium
TTE: assess severity, RV function and associated cardiac lesions
Management of pulmonary stenosis
Pulmonary valvotomy if gradient >70mmHg or RV failure
Percutaneous pulmonary valve implantation
Surgical repair/replacement
How does carcinoid syndrome affect the heart?
Gut primary with liver metastasis secrete 5HT into the blood stream. Secretory mediators cause right sided heart valve fibrosis resulting in TR and PS.
Treat with ocreotide and surgical resection
What is a third heart sound?
heard in early diastole, during the rapid filling phase of the ventricle after the opening of the atrioventricular valve. It is a dull, low-pitched sound, best heard in the tricuspid area.
Normal in the young.
Causes include congestive cardiac failure and severe mitral or tricuspid regurgitation
What is a fourth heart sound?
occurs in late diastole and coincides with the contraction of the atria. It is generated by the left (or right) atrium contracting against a stiffened ventricle.
Due to ventricular hypertrophy or myocardial ischaemia
What is the pathology in a pda?
Connection between the proximal left pulmonary artery and the descending aorta. Should close at birth.
Management of PDA
Percutaneous device closure
Clinical findings of PDA
Continuous machinery like murmur
Radiates to left scapula
Loudest in pulmonary area on expiration
Indications for PDA closure
Left ventricular volume overload
Pulmonary hypertension
What are the indications for aortic root surgery in patients with Marfans?
Dilation > 50mm at aortic root
Or > 45mm in a patient that has a family history of aortic dissection or if rate >3mm/year
Clinical signs of constrictive pericarditis
Raised JVP
- rapid dominant y-descent due to high RA pressures and an early rise in RV diastolic pressure due to poor pericardial compliance
- Kussmaul’s sign - paradoxical increase in JVP on inspiration
Pericardial knock - high pitched snap (audible early S3 due to rapid ventricular filling into a stiff pericardial sac)
Ascites, hepatomegaly, peripheral oedema
Cause: TB, sternotomy scar, radiotherapy tattoos, RA, SLE
Investigations for constrictive pericarditis
CXR: pericardial calcification
Echo: high acoustic signal from pericardium, septal bounce, reduced mitral flow velocity during insp.
Catheterisation: dip and plateau of the diastolic wave form, equalisation of LV and RV diastolic pressures
CT: thickened pericardium
Pathophysiology of constrictive pericarditis
Thickened, fibrous capsule reduces ventricular filling and ‘insulates’ the heart from intrathoracic pressure changes during respiration leading to ventricular interdependence (ie. Filling of one ventricular reduces the size and filling of the other)
Causes of constrictive pericarditis
TB
Post CABG
Radiotherapy
Connective tissue disease: RA, SLE
Management of constrictive pericarditis
Diuretics, fluid restriction
Pericardial stripping
