Cardiology (2) Flashcards
Define deep vein thrombosis
Development of a blood clot in a major deep vein in the leg, thigh, pelvis, or abdomen, which may result in impaired venous blood flow and consequent leg swelling and pain.
Summarise the aetiology of deep vein thrombosis
- Process starts with damage to the endothelium
- Immediate vasoconstriction of blood vessel which limits amount of blood flow
- Platelets adhere to damaged vessel wall and activated by collagen and tissue factor
- Platelet plug formed - primary haemostasis
- Coagulation cascade - secondary haemostasis
What are the risk factors for DVT?
Virchow’s Triad:
- Stasis of blood - turbulence or inactivity of skeletal muscle pump
- Bed rest eg post-op
- Long haul flights
- Long car journey
- Pregnancy - Hyperoagulation state
- Genetic
- OCP
- Surgery
- Cancer - Endothelial damage
- Infection
- Chronic inflammation
- Toxins eg tobacco smoke
- Trauma
Obesity, dehydration, polycythaemia, thrombophilia
Summarise the epidemiology of DVT
Common - 1 in 1000 adults yearly
Increases with age
Slight female predominance in under 35s
What are the presenting symptoms of DVT?
Inflammed leg/unilateral leg swelling Painful leg Red or warm leg Most common in lower limbs below the knee Dilated/distended superficial veins
Very large DVT - phlegmasia cerulea dolens due to ischaemia (blue, painful LEG)
What are the signs on physical examination of DVT?
Local erythema, warmth and swelling Measure the leg circumference Varicosities (swollen/tortuous vessels) Skin colour changes Homan's Sign - forced passive dorsiflexion of the ankle causes deep calf pain
What are the appropriate investigations for DVT?
Wells’ score:
>2 - DVT is likely therefore proceed to imaging
<2 - DVT less likely so confirm with D-dimer
Scoring points:
- active cancer
- calf swelling where affected calf circumference >3cm greater than other leg
- prominent superficial veins
- recent immobility
D-dimer if Wells Score less than 2 - if normal, DVT is excluded. If elevated proceed to imaging
Doppler Ultrasound - GOLD STANDARD – inability to fully compress lumen of vein using ultrasound transducer, reduced or absent spontaneous flow, lack of respiratory variation, intraluminal echoes, colour flow patency abnormalities;
Venography - dye injected into veins, X-ray taken which identifies blockages
D-dimer - measures fibrin break-down product levels - if high suggests clot
If PE suspected: ECG, CXR, ABG
What is the management of DVT?
Prevention:
Compression stocking
Frequent calf exercises during periods of immobility/mobilisation
Prophylactic heparin
Low dose aspirin - prevent formation of clots
ANTI-COAGULATION:
Rivaroxaban
Heparin whilst waiting for warfarin to increase INR to the target range of 2-3
Don’t extend above the knee - observe and anticoagulate for 3 months
Extend beyond knee - anticoagulate for 6 months
Recurrent DVTs require long-term warfarin
Give thrombolytic enzymes to break down clot
Thrombectomy to surgically remove the clot
IVC Filter - if anticoagulation is contraindicated
What are the potential complications of DVT?
Thromboembolism leading to PE or stroke
Venous infarction (phlegmasia cerulea dolens)
Thrombophlebitis (results from recurrent DVT)
Chronic venous insufficiency
What is the prognosis of DVT?
Depends on extent of DVT:
- Below-knee DVTs have a GOOD prognosis
- Proximal DVTs have a greater risk of embolization
If patient dies from DVT, usually due to a PE
Recurrent VTE likely if: Male sex Proximal DVT Ultrasound evidence of residual clot Elevated D-dimer 1 month after stopping a 3-6 month course of oral anticoagulation Unprovoked DVT
Define dyslipidaemia and the ranges for total cholesterol, LDL and HDL
Dyslipidaemia is:
Serum Total Cholesterol, LDL-C, triglycerides concentrations above the 90th percentile
HDL-C concentrations below the 10th percentile for the general population.
Total cholesterol >5.2mmol/L
LDL >3.3mmol/L
HDL <1.55mmol/L
What is defined as hypertryglyceridaemia?
Fasting plasma triglyceride level ≥2.3 mmol/L
Explain the aetiology of dyslipidaemia
Primary:
Single or multiple gene mutations, resulting in a disturbance of LDL and triglyceride production or clearance
Mainly in children and young adults
Familial hypercholesterolaemia - AUTOSOMAL CODOMINANT (LDL >4.9mmol/L in adults and >4.1mmol/L in children)
Secondary: Sedentary lifestyle Excessive consumption of saturated fats and trans-fatty acids Chronic renal insufficiency Diabetes mellitus Abdominal obesity Hypothyroidism Alcohol dependency
Summarise the epidemiology of dyslipidaemia
12% of adult population in US have dyslipidaemia
Prevalence is 80-88% in those with coronary heart disease
Strong correlation between BMI and hyperlipidaemia
More common in industrialised countries than developing countries
What are the presenting symptoms of dyslipidaemia?
Presence of risk factors Consumption of saturated fats and trans-fatty acids Abdominal obesity Angina pain Claudication pain
What are the signs on physical examination of dysplipidaemia?
Xanthelasma
Tendinous xanthoma
Corneal arcus
Obesity
What is the management of dyslipidaemia?
Lifestyle: Exercise Weight loss Stop smoking Decreased saturated fats consumption
Pharmacological:
Statins - 10-20mg atorvastatin if no previous CVS event (increase to 40-80mg if needed)
- Decrease LDL and triglycerides, increase HDL
- Side effects: muscle pain, myopathy, increase diabetes risk, increase AST and ALT
2nd line = selective cholesterol absorption inhibitors eg ezetimibe
- Decrease LDL by preventing cholesterol absorption
- Side effects: diarrhoea
Fibrates (side effects = myopathy, increase AST and ALT)
Bile acid sequestrants (side effects = diarrhoea)
Niacin (side effects = facial flushing therefore taken with 300mg aspirin 30 mins before)
LDL apheresis - blood passed through apparatus which removed LDL and remaining then returned to circulation
Liver transplantation
What are the possible complications of dyslipidaemia?
Ischaemic heart disease Peripheral vascular disease Acute coronary syndrome Stroke Erectile dysfunction
What is the prognosis of dyslipidaemia?
Statins significantly reduce adverse events
Cholesterol reduction is useful as coronary heart disease risk-reduction strategy
Once plasma lipid levels have achieved goals and are stable they can be monitored along with liver function tests every 6 months
Define gangrene
A complication of necrosis characterised by the decay of body tissues. The two major categories are infectious gangrene (wet gangrene) and ischaemic gangrene (dry gangrene). It may result from ischaemia due to arterial or venous compromise, infection, or trauma (or a combination of these processes).
Summarise the aetiology of gangrene
Tissue ischaemia and infarction
Physical trauma
Thermal injury
Infectious gangrene:
Necrotising fasciitis - mainly group A beta-haemolytic Streptococcus species
Gas gangrene: caused by Clostridium perfringens
Ischaemic gangrene: Atherosclerosis Diabetes-associated microangiopathy Hypercoagulable states Vasospasm associated with Raynaud's phenomenom and cocaine Venous obstruction
What are the risk factors of gangrene?
Diabetes mellitus Renal disease Drug and alcohol abuse Malignancy Leg ulcers Immunosuppression Steroid use Puncture/surgical wounds
Ischaemic gangrene: Atherosclerosis Smoking Hypercoagulable states Prolonged application of torniquets
Infectious gangrene:
Trauma or abdominal surgery
Contaminated wounds
Malnutrition
Summarise the epidemiology of gangrene
Relatively common
Occurs equally in men and women
Type I necrotising fasciitis more common in diabetics and those with peripheral vascular disease
Gas gangrene often predisposed by severe penetrating trauma and crush injuries associated with interruption of blood supply
What are the presenting symptoms of gangrene?
Pain - sudden onset in infectious gangrene, long history of claudication pain in ischaemic gangrene
Swelling and redness of the area
Low grade fever and chills for infectious gangrene
Discolouration of affected area
Usually extremities or areas subject to high pressures affected
What are the signs on physical examination of gangrene?
Oedema and erythema of affected region
Skin discolouration
Crepitus - gentle palpation of gas gangrene causes abnormal popping or crackling sound
Diminished pedal pulses and ankle-brachial index in ischaemic gangrene
Painful area = erythematous region around gangrenous tissue
Gangrenous tissue = BLACK because of haemoglobin break down products
Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes
Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection)
What are the appropriate investigations for gangrene?
Bloods:
FBC - leukocytosis if infectious gangrene
U&Es
Glucose
CRP - elevated if infectious gangrene
Blood culture - positive for infective organism
Metabolic panel - metabolic acidosis, liver derangement, liver failure
Imaging:
X-ray - may show gas if gas gangrene
CT/MRI - reveal abscess formation or evidence of enhancement, oedema, or thickening in the fascia
Doppler ultrasound - presence and severity of arterial or venous obstruction
Wound Swab, Pus/Fluid Aspirate - MC&S
Define heart block - 1st, 2nd and 3rd degree
Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles.
1st degree heart block - signals from the atria are delayed in passing to the ventricles, resulting in a prolonged PR interval >200ms due to prolonged conduction through AV node
2nd degree heart block Mobitz I - signals from the atria and progressively more and more delayed until eventually a signal is unable to pass into the ventricles, resulting in progressively lengthening PR intervals followed by a dropped beat. The cycle then begins again
2nd degree heart block Mobitz II - signals from the atria are delayed in passing to the ventricles, resulting in some intermittent, random dropped beats - intermittent failure of conduction through the AV node
3rd degree/complete heart block - signals from the atria are not transmitted to the ventricles and are completely blocked. Ventricular contraction is only due to ventricular escape beats. NO RELATIONSHIP BETWEEN ATRIAL AND VENTRICULAR CONTRACTION.
Summarise the aetiology of heart block
Fibrosis or damage eg calcification to conduction system of the heart
Most common = Ischaemic Heart Disease or MI
Myocarditis
Cardiomyopathies
Infection (e.g. rheumatic fever, infective endocarditis)
Metabolic (e.g. hyperkalaemia)
Infiltration of conducting system (e.g. sarcoidosis)
Coronary Artery Disease
AV-nodal blocking agents - beta-blockers, calcium-channel blockers, digitalis, adenosine
Anti-arrhythmic medications eg sodium channel blockers
Post-catheter ablation
Post-surgery
Summarise the epidemiology of heart block
Majority of the 250,000 pacemakers implanted annually are for heart block
What are the presenting symptoms of heart block?
Type 1 usually asymptomatic
Type 2 Mobitz I usually asymptomatic, sometimes lightheaded, dizzy, syncope
Type 2 Mobitz II: Chest pain Fatigue Syncope Dyspnoea
Type 3: Severe chest pain Syncope Confusion Dyspnoea Increased risk of sudden death
Palpations, nausea and vomiting
What are Stokes-Adams attacks?
Syncope caused by ventricular asystole which is a symptom of Type 2 Mobitz I and Type 3
What are the signs on physical examination of heart block?
Often NORMAL
Heart rate <40bpm
Hypoxaemia
Complete Heart Block:
Slow large volume pulse
JVP may show cannon a waves
Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously. Reflect the contraction of the right atrium against a closed tricuspid valve.
Mobitz Type II and 3rd Degree Heart Block:
Signs of reduced cardiac output (e.g. hypotension, heart failure)
What are the appropriate investigations for heart block?
Bloods:
Troponin - may be elevated if due to ischaemia
Cardiac enzymes
Potassium - electrolyte imbalances can be reversible causes of heart block
Calcium - electrolyte imbalances can be reversible causes of heart block
pH - pH imbalances can be reversible causes of heart block
Digoxin level
TFTs
12 lead ECG:
1st degree - prolonged PR interval >200ms
2nd degree Mobitz I - progressively prolonged PR intervals followed by a dropped beat (p wave with missing QRS complex). Cycle then continues
2nd degree Mobitz II - intermittent dropped beats shown by random missing QRS complexes. May be
a regular pattern of P waves not followed by a QRS (e.g. two P waves per QRS, indicating 2:1 block)
3rd degree - no relationship between P waves and QRS complexes. Regular P and R waves.
CXR: Cardiac enlargement, pulmonary oedema.
Echocardiogram: Wall motion abnormalities, aortic valve disease, vegetations.
What is the management of heart block?
Asymptomatic - monitoring
Acute:
Medication to increase heart rate eg atropine
Transcutaneous temporary pacing using electrodes on the skin
Chronic:
Permanent pacing with implanted device - monitor rhythm and send impulse to ventricle if detects delay
Permanent pacing = type 3, type 2 Mobitz II and SYMPTOMATIC Mobitz I
What are the possible complications of heart block?
Asystole
Cardiac arrest
Heart failure
Complications of inserted pacemaker - bleeding, infection, vascular trauma, pneumothorax, cardiac tamponade
What is the prognosis of heart block?
Mobitz type II and third degree heart block usually indicate serious underlying cardiac disease.
Prognosis is related to the degree of AV block, the severity of associated symptoms and the underlying condition.
Permanent pacing improves survival in patients with third degree heart block
Define hypertension
Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on three separate occasions.
Summarise the aetiology of hypertension
Primary/essential hypertension - 90% of cases
- NO CLEAR CAUSE
Secondary hypertension - 10% of cases
- Low renal blood flow
- Vasculitis
- Fibromuscular dysplasia (young women, thickens artery walls)
- Tumour secreting excess aldosterone
- Obstructive sleep apnoea
Renal: Renal artery stenosis, chronic glomerulonephritis, pyelonephritis, polycystic kidney disease, chronic renal failure
Endocrine: Diabetes mellitus, Hyperthyroidism, Cushing’s syndrome, Conn’s syndrome, Hyperparathyroidism, Phaeochromocytoma, Congenital adrenal hyperplasia, Acromegaly
Cardiovascular: Coarctation of the aorta, Increased intravascular volume, atherosclerosis, aortic dissection
Drugs: Sympathomimetics, Corticosteroids, COCP
Pregnancy: Pre-eclampsia
What are the risk factors for hypertension?
Increasing age High salt diet Obesity Sedentary lifestyle Family history Smoking Alcohol
Summarise the epidemiology of hypertension
Very common - 10-20% of the Western world population
What are the presenting symptoms of hypertension?
Primary hypertension is ASYMPTOMATIC
Secondary hypertension has symptoms associated with underlying cause
Emergency hypertensive crisis: Confusion Drowsiness Chest pain Breathlessness
Accelerated or Malignant Hypertension - Scotomas (visual field loss), Blurred vision, Headache, Seizures, Nausea and vomiting, Acute heart failure
What is a hypertensive crisis and what are the two types?
A rapid increase in blood pressure.
Systolic > 180mmHg, diastolic > 120mmHg
Urgency hypertensive crisis - no end organ damage
Emergency hypertensive crisis - end organ damage present
What are the signs on physical examination of hypertension?
Loud second heart sound, fourth heart sound.
Examine for causes:
- Radiofemoral delay (aortic coarctation)
- Renal artery bruit (renal artery
stenosis)
Examine for end-organ damage:
Fundoscopy for retinopathy.
Keith–Wagner classification of retinopathy:
(I) ‘silver wiring’;
(II) as above, plus arteriovenous nipping;
(III) as above, plus flame haemorrhages and cotton wool exudates;
(IV) as above, plus papilloedema
What are the appropriate investigations for hypertension?
Bloods:
Hb - Anaemia suggests chronic renal failure as underlying cause, polycythaemia suggests phaeochromocytoma
Lipid profile - high LDL or triglycerides, low LDL
U&Es - check for underlying renal dysfunction
Glucose
Fasting metabolic panel and GFR
Urine dip - if blood and protein present, may be glomerulonephritis as underlying cause. Proteinuria shows end organ damage
ECG: May show signs of left ventricular hypertrophy or ischaemia
Ambulatory blood pressure monitoring: Excludes white coat hypertension
Other investigations may be performed if a secondary cause of the hypertension is suspected (e.g. renal angiogram)
What is the management of hypertension?
Conservative: Diet Exercise Stress reduction Stop smoking and alcohol consumption Decrease sodium intake
Medical - treatment recommended if systolic > 160 mm Hg and/or diastolic > 100 mm Hg, or if evidence of end-organ damage.
1st line = ACE Inhibitors (or Angiotensin Receptor Blockers if not tolerated due to cough) IF:
- < 55 years
- Diabetic
- Heart failure
- Left ventricular dysfunction
CCBs - first line if:
> 55 years OR Afro-Caribbean.
NOTE: thiazide diuretics if CCBs not tolerated.
Beta-Blockers - Not preferred initial therapy
CAUTION: combining with thiazide diuretics may increase risk of developing diabetes and risk of heart failure
Alpha-Blockers: 4th line - May be used in patients with prostate disease
- ACEi or ARB (<55) OR CCB (>55 OR Afro-Carribean)
- ACEi/ARB and CCB OR ACEi/ARB and thiazide-diuretic
- ACEi/ARB AND CCB AND thiazide
- Spironolactone/alpha blocker/beta blocker
What is the management for hypertensive crisis?
Urgency:
Oral medication eg ACEi
Emergency:
I.V. beta blockers, CCBs
GRADUALLY REDUCE BP OVER 1-2 DAYS TO PREVENT CEREBRAL INFARCTION
What are the target blood pressures with antihypertensives?
Non-Diabetic: < 140/90 mm Hg
Diabetes without proteinuria: < 130/80 mm Hg
Diabetes WITH proteinuria: < 125/75 mm Hg
What are the possible complications of hypertension?
Aneurysm Heart failure Coronary artery disease Cerebrovascular accidents (MI, stroke) Peripheral vascular disease Emboli Hypertensive retinopathy Renal failure Hypertensive encephalopathy Posterior reversible encephalopathy syndrome (PRES) Malignant hypertension
What is the prognosis of hypertension?
Good prognosis if well controlled
Uncontrolled hypertension is associated with increased mortality
Treatment reduces incidence of renal damage, stroke and heart failure
Define infective endocarditis
Infection of intracardiac endocardial structures (mainly heart valves). It involves the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects, or the mural endocardium.
Explain the aetiology of infective endocarditis
MOST COMMON = VIRIDANS STREPTOCOCCI
- Small vegetations
- No valve destruction
- Found in mouth
Staph aureus
- Most common in IV drug users
- Large vegetations
- Destroys valves
- Often affects tricuspid
Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis
Staphylococci (35%) - S. aureus and S. epidermidis (nosocomial, infected IV catheter or during valve surgery)
Enterococci (20%) - usually E. faecalis (if colorectal cancer, UC)
Other: Haemophilus, Actinobacillus, Cardiobacterium, Coxiella (immunocompromised, pregnant), Histoplasma (fungal)
What are the risk factors of infective endocarditis?
Abnormal valves (e.g. congenital, calcification)
Rheumatic heart disease
Prosthetic heart valves
Turbulent blood flow (e.g. patent ductus arteriosus)
Recent dental work/poor dental hygiene (source of S. viridans)
IV drug use
Summarise the epidemiology of infective endocarditis?
Men are 2.5 more likely than women
Half of patients are over 60y/o
What are the presenting symptoms of infective endocarditis?
Fever with sweats/chills/rigors Malaise Arthralgia Myalgia Confusion Skin lesions Ask about recent dental surgery or IV drug use
What are the signs on physical examination of infective endocarditis?
Pyrexia
Tachycardia
Signs of anaemia
Clubbing
New murmur (Frequency of heart murmurs: Mitral > Aortic > Tricuspid > Pulmonary)
Splenomegaly
Roth spots on retina
Petechiae on pharyngeal and conjunctival mucosa
Janeway lesions (painless macules on the palms which blanch on pressure)
Osler’s nodes (tender nodules on finger/toe pads)
Splinter haemorrhages
What are the appropriate investigations for infective endocarditis?
Bloods:
FBC - normocytic anaemia, leukocytosis, high neutrophils
ESR/CRP - high
U&Es - elevated urea if affecting kidneys due to immune complex deposition
Blood cultures - bacteraemia from causative organism. MC&S
Often rheumatoid factor positive
Urine culture - RBC casts, WBC casts, proteinuria, pyuria
Echo - can see valvular, mobile vegetations
What is the management of infective endocarditis?
Antibiotics for 4-6 weeks
On clinical suspicion = EMPIRICAL TREATMENT Benzylpenicillin
Gentamicin
Streptococci - benzylpenicillin or gentamicin
Staphylococci: Flucloxacillin/vancomycin, gentamicin
Enterococci: Ampicillin, Gentamicin
Culture Negative: Vancomycin, Gentamicin
SURGERY - urgent valve replacement needed if there is a poor response to antibiotics
What are the possible complications of infective endocarditis?
Valve incompetence Intracardiac fistulae or abscesses Aneurysm Heart failure Renal failure Glomerulonephritis Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
What is the prognosis of infective endocarditis?
Biggest predictor of prognosis = congestive heart failure
Mortality increases with age
FATAL if untreated
15-30% mortality even WITH treatment
Define vasovagal syncope
Loss of consciousness due to a transient drop in blood flow to the brain caused by excessive vagal discharge.
Explain the aetiology of vasovagal syncope
Vasovagal syncope is a very common cause of fainting
Can be precipitated by:
Emotions - fear, severe pain, blood phobia
Orthostatic stress - prolonged standing, hot weather, dehydration
Summarise the epidemiology of vasovagal syncope
Vasovagal is the most common cause of syncope
Peaks in frequency in young adults and then again in older adults
More frequent in women
All causes of syncope affects 40% of people
What are the presenting symptoms of vasovagal syncope?
Loss of consciousness lasting short time
Provocative factors - painful or emotionally upsetting experiences, excessive dehydration, vigorous exercise, standing for too long
Vagal symptoms of prodrome: pallor, diaphoresis (feel sweaty, cold, clammy), diminished hearing or vision, palpitations
No family history of sudden death
Normally quick recovery
What are the signs on vasovagal syncope?
No signs
What are the appropriate investigations for vasovagal syncope?
ECG - rule out cardiac arrythmia as cause of syncope
Echo - rules out outflow obstruction - hypertrophic cardiomyopathy, aortic stenosis, poor ventricular function
Lying/standing blood pressure - check for orthostatic hypotension
Bloods: Hb - rule out anaemia as cause Glucose - rule out hypoglycaemia D-dimer - rule out PE Cardiac enzymes - rule out MI U&Es - rule out dehydration
Define mitral regurgitation
Retrograde flow of blood from left ventricle to left atrium during systole.
Summarise the aetiology of mitral regurgitation
MITRAL VALVE PROLAPSE
Infective endocarditis
Ischaemic papillary muscle dysfunction
Rheumatic fever
Damage to papillary muscles post-MI or cardiomyopathy
Left sided heart failure
Myxomatous degeneration (weakened connective tissue)
Chordal rupture and floppy mitral valve associated with connective tissue disease (e.g. Ehlers-Danlos syndrome, Marfan’s syndrome)
Summarise the epidemiology of mitral valve regurgitation
~5% of individuals
Mitral valve prolapse more common in young females
What are the presenting symptoms of mitral valve regurgitation?
Dyspnoea on exertion
Decreased exercise tolerance
Lower extremity oedema
Acute MR - may present with symptoms of left ventricular failure
Chronic MR - may be asymptomatic or present with:
Exertional dyspnoea
Palpitations if in AF
Fatigue
Mitral Valve Prolapse - asymptomatic or atypical chest pain or palpitations
What are the signs on physical examination of mitral regurgitation?
Pan-systolic murmur which radiates to the axilla and loudest at apex beat, soft S1
Mitral valve prolapse - mid-systolic click followed by late systolic murmur. Click later and murmur shorter when squatting due to increased venous return.
Pulse may be irregularly irregular (if in AF)
Laterally displaced apex beat with thrusting (due to left ventricular dilation)
Signs of left ventricular failure in acute mitral regurgitation
What are the appropriate investigations for mitral regurgitation?
Transthoracic echo - shows presence and severity of MR; other structural and flow abnormalities
ECG - NORMAL but may show prior ischaemia as cause or underlying arrhythmia or p mitrale indicating left ventircular hypertrophy
CXR:
ACUTE mitral regurgitation may produce signs of left ventricular failure
CHRONIC mitral regurgitation shows:
Left atrial enlargement
Cardiomegaly (due to LV dilation)
Mitral valve calcification (if rheumatic heart disease is the cause)
Define mitral stenosis
Narrowing of the mitral valve orifice, usually caused by rheumatic valvulitis producing fusion of the valve commissures and thickening of the valve leaflets. This causes obstruction of blood flow from the left atrium to the left ventricle.
Summarise the aetiology of mitral stenosis
Rheumatic fever - 95% of cases
Rare causes: Congenital deformity of the valve Carcinoid syndrome Use of ergot and/or serotogenic drugs such as fenfluramine SLE Mitral annular calcification due to ageing Amyloidosis Rheumatoid arthritis Endocarditis Atrial myxoma
Summarise the epidemiology of mitral stenosis
Mostly women develop mitral stenosis
Incidence is declining due to rheumatic fever becoming more rare
What are the presenting symptoms of mitral stenosis?
May be asymptomatic
History of rheumatic fever
Fatigue
Symptoms due to left atrial pressure increase causing pulmonary congestion:
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Peripheral oedema
Palpitations (related to AF)
Rare symptoms:
Cough
Haemoptysis
Hoarseness caused by compression of left recurrent laryngeal nerve by an enlarged left atrium
What are the signs on physical examination of mitral stenosis?
Opening snap on auscultation due to stiffened valve
Low-pitched rumbling MID-DIASTOLIC MURMUR loudest on left lateral decubitus position
Diastolic murmur radiates to carotids
Malar flush
Neck vein distension due to pulmonary hypertension
Irregularly irregular pulse if in AF
Apex beat not displaced and tapping
Parasternal heave (due to right ventricular hypertrophy secondary to pulmonary hypertension)
Evidence of pulmonary oedema on lung auscultation (if decompensated)
What are the appropriate investigations of mitral stenosis?
ECG: may show atrial fibrillation; left atrial enlargement; right ventricular hypertrophy
CXR:
Double right heart border indicating an enlarged left atrium
Cardiac enlargement
Prominent pulmonary artery
Kerley B lines
Pulmonary congestion
Mitral valve calcification (occurs in rheumatic cases)
Transthoracic echo: DEFINITIVE TEST. Shows hockey stick-shaped mitral deformity
Cardiac Catheterisation: Measures severity of heart failure
Define myocarditis
Inflammation of the heart muscle (myocardium) in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease
Summarise the aetiology of myocarditis
Usually IDIOPATHIC
Viruses: Coxsackie B, EBV, CMV, Adenovirus, Influenza
Bacteria: Post-streptococcal, Tuberculosis, Diphtheria
Fungal: Candidiasis
Protozoal: Trypanosoma cruzi (Chagas disease)
Helminths: Trichinosis
Non-infective:
Systemic: SLE, sarcoidosis, polymyositis
Hypersensitivity myocarditis: sulphonamides
Drugs: Chemotherapy agents (e.g. doxorubicin, streptomycin)
Others: Cocaine, heavy metals, radiation
Summarise the epidemiology of myocarditis
Coxsackie B virus is most common in Europe and USA
Chagas disease is most common in South America
Slightly more common in men
What are the presenting symptoms of myocarditis?
Viral prodrome: fever, malaise, fatigue, myalgias, respiratory symptoms, gastroenteritis 2-3 weeks before presentation Positional sharp chest pain Dyspnoea Orthopnoea Palpitations
What are the signs on physical examination of myocarditis?
Fever
Arrhythmia
Peripheral oedema IF progresses to heart failure
Sinus tachycardia
Pericardial friction rub
Elevated neck veins due to congestive heart failure
S3 gallop
What are the appropriate investigations of myocarditis?
ECG - saddle shaped ST elevation if pericarditis, sinus tachycardia, T wave inversion
CXR - may show cardiomegaly and bilateral pulmonary infiltrates if progresses to congestive heart failure
Echo - shows inflammed heart muscle
Bloods:
Troponine and creatine kinase - elevated due to muscle damage
Serum BNP - raised if heart failure
FBC - raised WCC if infective cause
ESR/CRP - raised
Tests to identify cause e.g. viral/bacterial serology, ANA, TFT
Define tricuspid regurgitation
Backflow of blood from the right ventricle to the right atrium during systole.
Summarise the aetiology of tricuspid regurgitation
Pulmonary hypertension - causes increase R ventricular pressure which dilates valve
Rheumatic heart disease causing fibrosis
Damaged papillary muscles post-MI
Congenital eg Ebstein anomaly
Infective Endocarditis
Other: carcinoid syndrome, trauma, cirrhosis, iatrogenic
Summarise the epidemiology of tricuspid regurgitation
Infective endocarditis is the most common cause
What are the presenting symptoms of tricuspid regurgitation?
Fatigue Dyspnoea Palpitations Leg and ankle swelling Headaches Nausea Anorexia Epigastric pain made worse by exercise Jaundice
What are the signs on physical examination of tricuspid regurgitation?
Pan-systolic murmur which is louder in inspiration and best heard at lower left sternal border Distended neck veins Peripheral oedema Hepatosplenomegaly Irregularly irregular pulse if in AF Parasternal heave
What are the appropriate investigations for tricuspid regurgitation?
ECG: may show P pulmonale due to right atrial hypertrophy, AF
Bloods: FBC Cardiac enzymes Blood cultures LFTs - tricuspid regurgitation leading to chronic congestion can cause liver disease and ascites
CXR: Right-sided enlargement of cardiac shadow
Echocardiography - Extent of regurgitation can be estimated using Doppler ultrasound, may show valve prolapse and right ventricular dilation, assess left and right heart ejection fraction/dilation
Right Heart Catheterisation - assessing pulmonary artery pressure
Define Wolff-Parkinson-White Syndrome
Occurs when an accessory pathway, usually the Bundle of Kent, allows conduction to be passed from the atria to the ipsilateral ventricle, resulting in ventricular pre-excitation. It leads to supraventricular tachycardias.
What is the difference between Wolff-Parkinson-White pattern and Wolff-Parkinson-White Syndrome?
Pattern = ECG changes but ASYMPTOMATIC patient Syndrome = ECG changes and symptomatic patient due to development of supraventricular tachycardias
Summarise the aetiology of Wolff-Parkinson-White syndrome?
Wolff-Parkinson-White syndrome occurs due to a congenital accessory pathway - usually Bundle of Kent
Associations: Congenital cardiac defects Ebstein's anomaly (congenital malformation of the heart characterised by displacement of septal and posterior tricuspid leaflets) Mitral valve prolapse Cardiomyopathies (e.g. HOCM) Coarctation of the aorta Atrial septal defects
Summarise the epidemiology of Wolff-Parkinson-White Syndrome
0.1% of patients have Wolff-Parkinson-White Syndrome 50% are asymptomatic More common in males Highest incidence in 30s-40s Most common ventricular pre-excitation syndromes Found in ALL AGES More common in the YOUNG Prevalence decreases with age
What are the presenting symptoms of Wolff-Parkinson-White syndrome?
If only WPW pattern, patients are ASYMPTOMATIC
Symptoms of supraventricular tachycardia: May occur in childhood Palpitations Dizziness SOB Light-headedness Syncope
What are the signs of Wolff-Parkinson-White syndrome on physical examination?
Tachycardia
Irregularly irregular pulse if AF
Paroxysmal SVT may be followed by a period of polyuria, due to atrial dilatation and release of ANP
Sudden death - if SVT deteriorates into VF
Clinical features of associated cardiac defects (e.g. mitral valve prolapse, cardiomyopathy)
What are the appropriate investigations for Wolff-Parkinson-White Syndrome?
12 lead ECG:
- Short PR interval <120ms
- Delta wave upstroke QRS
- Broad QRS complex >110ms
- Tachycardia
Bloods - check for other causes of arrhythmia · Echocardiogram - check for structural heart defects eg HOCM
Define venous ulcers
Large, shallow, painful ulcers with slopping edges often superior to the medial malleoli due to venous insufficiency due to incompetent valves leading to venous stasis and ulceration
Summarise the aetiology of venous ulcers
Caused by venous insufficiency
Incompetent valves cause stasis of blood, leading to increased venous pressure and ulceration
Risk factors: Obesity Pregnancy Standing for prolonged time Increases age Female Immobility Recurrent DVT Varicose veins Previous injury or surgery to the leg
What are the presenting symptoms of venous ulcers?
Shallow, sloping edged, large ulcer on lower third of leg, often superior to medial malleolus
Irregular margin, overlying yellow fibrous excudate
Relatively painless
Varicose veins
Swelling of leg
Ulcer relieved on elevating leg
Other symptoms in the history: Varicose veins DVT Phlebitis Fracture, trauma or surgery Family history Swelling Itching Aching
What are the signs on physical examination of venous ulcers?
Large, shallow, sloped edged ulcer superior to medial malleolus with yellow fibrous overlying exudate
Varicose veins
Stasis eczema
Lipodermatosclerosis (inverted champagne bottle sign if SEVERE)
Haemosiderin deposition (dark colour)
What are the appropriate investigations for venous ulcers?
Duplex USS - look for obstruction in venous supply of legs
ABPI – should be normal. Allows you to exclude arterial ulcer caused by peripheral vascular disease. If ABPI < 0.8 - do NOT apply a pressure bandage as this could worsen the ulcer
Measure surface area of ulcer - allows monitoring of progression
Swabs for microbiology - if signs of infection
Biopsy - if possibility of Marjolin’s ulcer
What is the management of venous ulcers?
Exclude diabetes, neuropathy and peripheral vascular disease to ensure this is a venous ulcer
Graduated compression stocking to reduce venous stasis
Debridement and cleaning
Elevation of leg
Antibiotics - if infected
Topical steroids - may help with surrounding dermatitis
What are the possible complications of venous ulcers?
Recurrence
Infections
Summarise the prognosis of venous ulcers
GOOD
Results are better if patients are mobile with few comorbidities
