Cardiology Flashcards
Causes of aortic stenosis
- Age-related calcification
- Congenital bicuspid valve (younger patient)
- Connective tissue disease
- Accelerated calcification e.g. CKD
Pathophysiology of aortic stenosis
Pathological narrowing of the aortic valve, causing left ventricular outflow obstruction.
This leads to LV hypertrophy as a result of chronic increased afterload.
What signs may be seen in aortic stenosis?
Inspection: if replaced, may have midline sternotomy scar
Palpation:
- Pulsus parvus et tardus (weak and slow rising pulse)
- May have LV heave due to LVH
Auscultation:
- Ejection systolic murmur radiating to carotids
- May have quiet or absent S2 if severe
DDx in aortic stenosis
- Aortic sclerosis
- HOCM (ESM at LLSE and apex - louder on valsalva)
- ASD (ESM at pulm. region)
- VSD (pan systolic at LLSE)
- Mitral regurgitation
- Tricuspid regurgitation
What is the difference between aortic stenosis and aortic sclerosis?
Aortic sclerosis: Thickening of the valve without narrowing
- Normal pulse volume
- No radiation of murmur to carotids
Aortic stenosis: Thickening of the valve with narrowing, causing left outflow obstruction
Investigations if suspecting aortic stenosis
- 12-lead ECG: May see LVH
- Echo with doppler: Assess valvular pressure gradient and valve area
Management of aortic stenosis
Symptomatic management with caution:
- Reduction in preload e.g. with AHTs or beta blockers, can increase the pressure gradient across the valve
Symptomatic or severe: Aortic valve procedure
- 1st line: surgical valve replacement (low-intermediate surgical risk)
- 2nd line: Trans-catheter Aortic Valve Implantation (if non-bicuspid and high surgical risk)
How can pacemakers be classified?
Number of chambers paced:
- Single chamber (RA or RV)
- Dual chamber (RA + RV)
- Biventricular (RA + RV + LV)
Duration:
- Permanent pacemaker
- Temporary pacemaker
- Temp-perm (insertion of a PPM until arrhythmia resolved or long-term solution achieved)
Indications for permanent pacemaker
Symptomatic sinus node disease
- Sinus bradycardia
- Sinus pauses
High-degree AV block
- Mobitz II
- CHB
Complications of pacemakers
Insertion-related:
- Pocket haematoma
- Pocket infection
- Pneumothorax
- Lead dislodgement
- Cardiac perforation or tamponade (rare)
Delayed:
- Delayed infection
- Lead fracture
- Thrombosis or stenosis of the veins through which the leads travel
- Inappropriate pacing i.e. incorrectly sensing/pacing electrical activity
How does ICD work?
Dual chamber: RA and RV
Senses high-risk ventricular arrhythmias (VT/VF) and delivers a defibrillation shock
ICD indications
Prevention of VT/VF arrest
PRIMARY PREVENTION:
- HOCM (sustained VT/cardiac arrest)
- LQTS
- Brugada (most patients)
SECONDARY PREVENTION:
- Previous VT/VF arrest
- Sustained VT
Cardiac resynchronisation therapy - principles and indication
CRT is a biventricular pacemaker with 3 leads in the RA, RV and LV
Aims to restore synchronised contractions of the left and right ventricles to improve cardiac output
Generally indicated in:
LVEF <35% and broad QRS and refractory symptoms
Causes of heart failure
Vascular causes:
- Ischaemic heart disease
- Chronic hypertension
Structural causes
- Valve pathology e.g. aortic stenosis causing LVOO
- dilated Cardiomyopathy
Infection e.g. IE
Right heart failure
- Most commonly caused by left heart failure
- Right sided valve disease (tricuspid or pulmonary)
- Lung pathology
- Pulmonary vascular disease
Iatrogenic e.g. cardiotoxic medications (chemo)
Signs of severe AS
Severe aortic stenosis:
- Quiet or absent S2
- Weak and slow rising pulse
- Evidence of left ventricular failure
Management of heart failure
HFpEF: Symptomatic only (diuretics)
HFrEF:
Pharmacological: ABS
- ACE inhibitor
- Beta blocker
- Consider spironolactone
- Dapagliflozin
If refractory to medical treatment and LVEF <35% - consider cardiac resynchronisation therapy
Smoking cessation
Vaccinations
Investigations in suspected heart failure
Bedside:
- ECG
- Urine dip if suspecting IE
Blood tests:
- FBC, U+Es, LFTs (hepatic congestion)
- NT-proBNP
- Lipid profile, HbA1c
Imaging
- CXR
- Echocardiogram: assess LVEF
Features of mitral regurgitation
- Pan systolic murmur radiating to axilla, louder on expiration
- May have displaced, thrusting apex beat
Check for complications:
- AF
- Pulmonary HTN (P2 + raised JVP)
Mitral regurgitation DDx:
- Mitral valve prolapse
- Tricuspid regurgitation
- VSD
Complications of mitral regurgitation:
- Atrial fibrillation
- Left ventricular dilatation
- Cardiac failure
- Pulmonary HTN
Investigations for mitral regurgitation:
Bedside:
- ECG
- Urine dip (protein/blood)
Bloods:
- FBC
- If suspecting endocarditis: WCC, CRP, 3x blood cultures
- NT-proBNP
- consider troponin
Imaging:
- Echocardiogram (valve function, LV function, vegetations)
- CXR (Cardiomegaly/pulm oedema)
Causes of mitral regurgitation
Valvular disease:
- Degenerative
- Infective (endocarditis, rheumatic fever)
Non-structural:
- Functional MR in LV dilatation
- Myocardial infarction - papillary muscle rupture
- Connective tissue disorder
Management of mitral regurgitation
1) Patient education: e.g. smoking cessation
2) Pharmacological:
- management of HF
- management of AF
3) Surgical
- Mitral valve repair or replacement
- Transcatheter mitral valve replacement (Mitraclip) if high anaesthetic risk
Indications for surgery in mitral regurgitation
Symptomatic
OR
Asymptomatic with
- LVEF < 60%
- LV dilatation
OR
Acute mitral regurgitation e.g. papillary muscle rupture in myocardial infarction
Signs of severe AS
Quiet or absent S2
Narrow pulse pressure
Weak and slow rising pulse
A metallic S1 is…
mitral valve replacement
A metallic S2 is…
aortic valve replacement
A right venticular heave indicates…
Pulmonary HTN (loud P2)
or
Pulmonary stenosis (no loud P2)
Pulmonary stenosis DDx
- Pulmonary hypertension (should have loud P2)
- ASD (ESM at pulm area with split S2)
A lateral thoracotomy scar could be…
- Descending aorta surgery
- Mitral valvotomy (older patients)
- Lung surgery
What does inspiration do to venous return/preload?
INspiration INcreases venous return
Target INR for metallic mitral valve
3-4
(think Mitral is More than aortic)
Target INR for metallic aortic valve
2.5 - 3.5
Pulmonary HTN in congenital heart disease - management
- Assess for any shunts which may require treatment
- Otherwise may develop Eisenmenger’s (shunt reversal) whch can lead to central cyanosis
Causes of pulmonary valve disease
- Infection: maternal Rubella
- Syndrome: Downs, Turner’s, Noonan
Features of Tetralogy of Fallot
PROVE:
- Pulmonary stenosis
- Right ventricular hypertrophy
- Over-riding aorta
- Ventricular septal defect
- Eisenmenger’s syndrome may develop (cyanosis)
Causes of tricuspid regurgitation
- Pulmonary hypertension
- Infection e.g. endocarditis
- Congenital heart disease e.g. Ebstein’s anomaly
Why does endocarditis tend to affect the tricuspid valve in IVDU?
The particulate that injectable recreation drugs are ‘cut’ with deposit mostly on the tricuspid valve, as the substances flow through the heart. This predisposes the tricuspid valve to vegetations.
Causes of atrial fibrillation
“SMITHA”
- Sepsis
- Mitral valve disease (typically stenosis)
- IHD
- Thyrotoxicosis
- HTN
- Alcohol
Options for rate control in AF
BCD
- Beta blockers
- Calcium channel blockers
- Digoxin
Importance of valvular pathology and AF
This is an absolute indication for anticoagulation
Echo criteria for severe AS
- Mean pressure gradient across valve of >40 mmHg
- Aortic valve area < 1cm2
Features of severe mitral regurgitation
Displaced apex beat
Pulmonary hypertension - JVP
Left ventricular failure
Marfan’s syndrome complications
Cardiac - aortic root dilation, aortic dissection, AR, MVP
Resp - spontaneous pneumothorax
Eyes - lens dislocation
MSK - Scoliosis, pectus excavatum, pes planus
Pan systolic murmur DDx
Mitral regurgitation
Tricuspid regurgitation
VSD (pan-systolic/ejection systolic character at LLSE)
Patent ductus arteriosus examination
Inspection: Can be young patient
‘Differential cyanosis’: pink fingers and blue toes
Pulse: collapsing pulse may be present
Palpation: may have right ventricular heave, palpaple P2
Auscultation:
- Continuous, machine-like murmur
“rolling thunder” in P area
- radiating to back (loudest over left scapula)
- louder in expiration
Complications of PDA
- Pulmonary hypertension
- Right ventricular dilation → functional tricuspid regurgitation
- Left ventricular dilatation
- Endarteritis - infection of the PDA
Management of PDA
Mild: conservative management
Severe: percutaneous device closure
Mitral valve prolapse causes
Primary: degenerative
Secondary:
- infection
- connective tissue disorders (Marfans, Ehlers Danlos)
- PKD
Mitral valve prolapse complications
- Left heart failure
- Infective endocarditis
- Thromboembolic events
- Atrial fibrillation
Mitral valve prolapse examination
- Systolic click
- Late systolic murmur in (M) area radiating to axilla
- Check for signs of Marfan’s/EDS
Mitral valve prolapse management
- Serial monitoring with echocardiography
- If decompensated: mitral valve repair
(valve replacement if anatomy not amenable to repair)
Eisenmenger Syndrome complications
- Hypoxaemia → cyanosis
- Right ventricular failure
- Thromboembolic events
- Infective endocarditis
Eisenmenger syndrome pathophysiology
Left→Right shunt reverses as RV pressure > LV pressure, and becomes Right→Left shunt
Most common causes: VSD, ASD, PDA
Eisenmenger Syndrome examination
Inspection: Young patient, clubbing, central cyanosis, may have raised JVP
Palpation: RV heave
Auscultation: Fixed split S2 with loud pulmonary component
Pulmonary hypertension causes
Primary: excess endothelin release
Secondary:
1) Respiratory disease e.g. COPD leading to cor pulmonale
2) Cardio pathology e.g. VSD, ASD, PDA
3) Systemic disease e.g. systemic sclerosis
Pulmonary hypertension investigations
Echo
- pulmonary arterial pressure >25mmHg
- Look for any shunts
- can get functional TR from RV dilatation
Cardiac catheterisation is diagnostic
Pulmonary hypertension management
Medications include:
- Calcium channel blockers
- Bosentan
- Iloprost
- Sildenafil
Advise against pregnancy in women (increased mortality)
Complications of prosthetic valves
During intervention:
- Bleeding
- Infection
- Damage to surrounding structure e.g. PTX
- AVN dysfunction in aortic valve intervention -> conduction delay
Post-intervention:
- Infective endocarditis
- Prosthesis failure (paravalvular leaks, displacement)
- Thromboembolism
- Bleeding related to anticoagulation
- Haemolysis across valve
Diastolic murmur DDx
Aortic regurgitation
Mitral stenosis
Pulmonary regurgitation (rare)
Causes of aortic regurgitation
Acute AR = emergency
- Aortic dissection
- Infective endocarditis
- Prosthetic valve failure e.g. displacement
Chronic AR
- Degenerative valve disease
- Congenital bicuspid valve
- Connective tissue disorder e.g. Marfan’s, ankylosing spondylitis
Management of aortic regurgitation
Patient education e.g. smoking cessation
Medical management
- Cause: e.g. antibiotics in IE
- Decompensated HF management
- AVOID BETA BLOCKERS
Severe or symptomatic AR:
- Refer for surgical valve replacement ( or TAVI)
Acute AR
- If in cardiogenic shock may need ICU support
- Do not give beta blockers
Murmur in HOCM
Ejection systolic murmur
Apex and lower left sternal border
No radiation to carotids
Loudest on valsalva
Quieter on hand grip
Valsalva causes decreased venous return
- reduced expansion of the left ventricle
- septal hypertrophy causes more obstruction -> more pronounced murmur
HOCM causes
Primary: genetic mutations (autosomal dominant)
Secondary:
- Amyloidosis
- Friedrich’s ataxia
- Myotonic dystrophy
HOCM examination
Inspection:
- Young patient
- Cardiac device?
- Myotonic dystrophy/Friedrich’s ataxia
Palpation:
- Jerky/thrusting apex beat
Auscultation:
- Ejection systolic murmur loudest at apex and left lower sternal edge
- Louder on valsalva
- Quieter on hand grip
HOCM investigations
- Full history incl. FH
- ECG - LVH, LBBB, VT
- Echo, cMRI
- Holter to assess for VT
Calculate the HOCM-SCD score
Consider ICD
Genetic testing
HOCM management
- Patient education
- Avoid strenuous exercise and caffeine
- Inform DVLA for group 2 license only
Medications: BB or CCB
(AVOID ACEi, nitrates)
Surgical:
- Septal ablation
- Septal myectomy
Consider ICD if high risk for life-threatening arrhythmia
Complications of HOCM
- Left outflow tract obstruction -> cardiac decompensation
- Life threatening arrhythmia
- Sudden death
HOCM inheritance
Autosomal dominant (if inherited)
Otherwise - de novo mutations
VSD causes
Primary - congenital
Secondary - rupture in myocardial infarction
Can be associated with Down’s and DiGeorge syndrome
VSD - examination
May be a young patient
Pansystolic murmur, loudest at LLSE
No radiation
Complications of VSD/ASD
RVH
Functional TR
Pulm. HTN
Eisenmenger’s syndrome
Endocarditis
YOUNG STROKE
VSD/ASD management
Small - monitor
Large - surgical closure
ASD examination
Soft ejection systolic murmur at pulmonary area with fixed widely split S2
Septal defects (ASD or VSD) - investigations
ECG/Holter
Echo
Bubble echo or cmri may be required
CXR
Bloods incl. infection markers
Causes of PDA
Primary: congenital
Secondary: Neonatal rubella
Mitral stenosis causes
Primary: congenital
Secondary:
- Rheumatic fever >90%
- Degenerative calcification
- Infective endocarditis
Mitral stenosis examination
Inspection: malar flush
Palpation: check for AF
May have palpable P2
Auscultation: mid-diastolic murmur with opening snap
- louder on expiration
- radiates to axilla
Mitral stenosis ix
ECG
Bloods incl. infection markers
Echo
Features of severe Mitral stenosis
Symptomatic
Pulmonary HTN
AF
Echo:
Valve gradient >10mmHg
Mitral valve area <1cm2 on echo
Mitral stenosis management
Asymptomatic: observe, W&W
- Conservative mx of AF and HF
Symptomatic or severe: Percutaneous balloon mitral valvuloplasty or surgical MVR
Atrial fibrillation - rate control indications and options
Rate control is first line in all patients EXCEPT for:
- New onset AF
- Heart failure
- Reversible cause
Options: BCD
- Beta-blocker
- CCB (avoid in HF)
- Digoxin (sedentary patients)
Rhythm control options in AF
1) Pharmacological: Amiodarone or fleicanide
2) DCCV (elective, or emergency if unstable)
- Ideally anticoagulate for 4 weeks before
3) Ablation if above unsuccessful
- EP study first to identify correct areas to target
