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Infective Endocarditis
This is inflammation of the endocardium that lines surface of the heart valves – usually due to bacterial infection:

Causes:
i) Staphylococcus aureus – this is the most common cause of IE which is usually seen in IV drug abusers
- It is a high virulence organism that destroys valves, most commonly the tricuspid valve
- Risk factors for this bacterium include skin breaches (dermatitis, IV lines), kidney failure and diabetes

ii) Viridans Streptococci – this is a group of low-virulence bacteria that affects previously damaged valves.
- It is associated with poor dentition with sequelae of dental procedures
- It causes small vegetations that do not completely destroy the valve and so causes a subacute endocarditis
- The damaged endocardium develops small thrombotic vegetations of platelets and bacteria

iii) Staphylococcus epidermidis – this is associated with endocarditis of prosthetic valves

iv) Streptococcus bovis – associated with endocarditis in patients with colorectal carcinoma

v) HACEK organisms – These are Gram negative bacteria which give negative blood cultures
- H= haemophilus A= Actinobacillus C= Cardiobacterium E= Eikenella K= Kingella

Endocarditis can also arise due to other infectious and non-infection causes:
- Fungi: Candida and Aspergillus --> seen in IV drug users and immunocompromised patients

- Non - bacterial thrombotic endocarditis --> this is due to sterile vegetations that arise in (1)
association with a hypercoagulable state or an underlying adenocarcinoma
- Vegetations usually occur on the mitral valve and lead to mitral regurgitation

- Libman-Sacks endocarditis --> this is when you get vegetations associated with SLE.
- Vegetations occur on both sides of the mitral valve and lead to mitral regurgitation.
Splinter
Symptoms:
Hemorrhages
- Septic symptoms --> fever, anaemia, clubbing, weight loss

- Cardiac symptoms --> A new murmur, usually pan-systolic (due to mitral/tricuspid regurgitation)
(2)
- Immune complex deposition --> Roth-spots (retinal haemorrhage with pale centres)
+ Splinter haemorrhages + Osler Nodes (tender lesions on fingers and toes)

- Emboli --> these can cause abscesses in organ e.g., skin – called Janeway lesions (on palms) Osler Nodes
Diagnosis- The is done using the modified Duke criteria, which use major and minor criteria:
Major - 2 Positive blood cultures – 3 cultures are usually taken from different sites at time of fever
- Involvement of the endocardium, which is shown by an echocardiogram

Minor - Predisposition (e.g., mitral valve prolapse) - IV Drug use

- Fever > 38oC - Osler nodes/Roth Spots
- Presence of vascular signs e.g., splinter haemorrhages, Janeway Lesions

Treatment:
Most causes are treated with antibiotics – which depends on the type of organism causing the disease.
- Initial empirical therapy --> Amoxicillin + low dose gentamicin

- If staphylococci cultured --> Flucloxacillin + Gentamicin If penicillin allergic à Vancomycin

- If Streptococci cultured --> Benzylpenicillin + gentamicin

Some severe cases may require valve replacement surgery:

- If there is cardiac failure despite treatment - Severe valve incompetence
- Abscess formation around the aorta - Recurrent embolic events

(1) Splarka, Public domain, via Wikimedia Commons

(2) Roberto J. Galindo, CC BY-SA 4.0 <https://creativecommons.org/licenses/by-sa/4.0>, via Wikimedia Commons
Diseases of heart muscle
• Acute myocarditis (Inflammatory cardiomyopathy)
This describes acute inflammation of the myocardium, which is most commonly due to a viral infection.
Most common virus: Coxsackie A and B
Most common parasite: Trypanosoma Cruzi (Chagas Disease) which is the most common cause worldwide
Common drugs: Alcohol, Clozapine, doxorubicin

Symptoms: Patients may have signs of a recent viral infection --> fever, joint pain, fatigue
- Disease mirrors acute coronary syndrome --> acute chest pain, palpitations with shortness of breath

Diagnosis: ECG shows diffuse T wave inversions and saddle-shaped ST elevations

- Raised inflammatory markers CRP/ESR with raised troponin and BNP
- Heart MRI shows inflammation of the heart muscle

Management: Treat underlying cause e.g., if parasitic or bacterial then give antibiotics
- Symptomatic treatment of heart failure and antiarrhythmics
- Half recover in a month whereas many go on to develop dilated cardiomyopathy and severe heart failure.

• Dilated Cardiomyopathy (DCM)

This is dilation of all 4 chambers of the heart – most common form of cardiomyopathy
- This gives systolic dysfunction giving biventricular heart failure and valve incompetence

Causes: Usually idiopathic

- Acute myocarditis (usually due to Coxsackie A/B) - Hypertension
- Haemochromatosis - Vitamin B1 deficiency
- Ischaemic heart disease - Drugs - Doxorubicin

Symptoms: Gives symptoms of heart failure – fatigue, oedema, ascites, S3 gallop heart sounds
- Gives a systolic murmur due to mitral and tricuspid regurgitations
Tests: CXR shows “Balloon” appearance of the heart Management: Heart transplant

• Hypertrophic Obstructive Cardiomyopathy (HOCM)

This is massive hypertrophy of the left ventricle, which is the leading cause of sudden cardiac
death in the young.
- Usually due to a genetic mutation in sarcomere proteins (B-myosin heavy chain most common)
- It is inherited in an autosomal dominant fashion, but associated with Friedrich’s ataxia and WPW
- Hypertrophy means ventricle cannot fill in diastole reducing cardiac output.
- Also, the hypertrophied interventricular septum leads to functional aortic stenosis.

Symptoms: Can be asymptomatic and lead to sudden cardiac death due to ventricular fibrillation
- Mirrors aortic stenosis in young patients --> exertional dyspnoea, angina + syncope following exercise
- Gives ejection systolic murmur with jerky pulse

Tests - Biopsy --> shows hypertrophy of the muscle fibres

- Echo --> MR SAM ASH (Mitral Regurg. + Systolic anterior motion of mitral valve + asymmetric hypertrophy)
- ECG --> shows left ventricle hypertrophy with deep Q waves

Management – If asymptomatic, conservative management

- Next step is medical --> amiodarone (to stop arrythmias) + Beta-blockers
- If unresponsive surgical --> Pacemaker and Implantable cardioverter-defibrillator

• Restrictive Cardiomyopathy
This is decreased compliance of the ventricular endocardium that restricts filling during diastole. This gives it
similar symptoms to constrictive pericarditis.
Causes: Amyloidosis – build-up of amyloid plaques in organs
Haemochromatosis – inherited condition in which iron levels rise over many years
Endomyocardial fibrosis – fibrosis of the endocardium
Loffler’s syndrome - endomyocardial fibrosis with eosinophilic infiltrate and eosinophilia.
Signs: Presents as right heart failure --> Increased JVP, hepatomegaly, oedema, ascites
- Classic finding is low-voltage ECG with diminished QRS amplitude

Tests: Echocardiogram + MRI Management – Treat the underlying cause

Pericardium Conditions
The heart is covered in two layers of pericardium:
- The fibrous pericardium on the outside which is attached to the central tendon of the diaphragm
- The serous pericardium split into an inner visceral layer and outer pericardial layer.
- Between these layers, there is a small pericardial space which contains about 15-50mL of pericardial fluid.
- The pericardium has sensation from the phrenic nerve and so causes referred shoulder pain (C3/4/5).

• Acute pericarditis
This refers to acute inflammation of the pericardium, which surrounds the cardiac muscle.

Causes:
- Infection – TB is one of the most common causes worldwide. Viral infections (Coxsackie)
- Autoimmune – SLE, Rheumatoid arthritis etc.
- Metabolic – anorexia, hypothyroidism, uraemia (causes “fibrinous” pericarditis)
- Cardiac – post-MI, Dressler’s syndrome

Symptoms: Central chest pain worse on inspiration

- Pain is worse on lying flat, but relief when sitting forward
- Shortness of breath, with a non-productive cough
- Low grade fever
- May be able to hear a pericardial rub

Tests – ECG shows global saddle shape concave ST segment elevation and PR segment depression
- CXR – this is needed to rule out other causes of acute chest pain
- Cardiac Troponin- needed to rule out a myocardial infarction
- Echocardiogram – needed to visualise the heart function

Management – NSAID or colchicine with gastric protection for 1-2 weeks

• Constrictive pericarditis
This is a condition which occurs when the heart is encased in a very rigid pericardium. The rigid pericardium
prevents the ventricles from filling leading to a reduced ejection fraction, mimicking right sided heart failure.
Causes - Any cause of pericarditis

Symptoms: Signs of right heart failure – raised JVP, oedema, hepatomegaly, ascites
- Shortness of breath
- Kussmaul sign positive --> rise in the JVP on inspiration

Tests – CXR shows pericardial calcification + Echocardiogram may show reduced ejection fraction
Management – Pericardial stripping, a surgical procedure which peels away the pericardium from the heart

• Cardiac tamponade
This is a condition in which fluid collects within the pericardial sac and which compresses the ventricles
impeding cardiac output.
- If the fluid increases over time, the pericardial sac can hold up to 2l, whereas if the increase in rapid, then as
little as 300ml can result in cardiac tamponade.
Causes - Pericarditis, myocardial rupture, aortic dissection, malignancy

Symptoms:
- Classic Beck’s triad --> Low BP + Quiet heart sounds + Jugular venous distension
- Signs of cardiogenic shock --> shortness of breath, weakness, light headedness, tachycardia
- Pulsus paradox (an abnormally large drop in BP during inspiration)

Tests - CXR shows enlarged, globular heart

- Echocardiogram is the diagnostic investigation and shows an echo-free zone around the heart
- ECG – low voltage QRS complexes which maybe alternating (electrical alternans)

Management – Pericardiocentesis to drain the fluid in the pericardial sac.

Central Vascular Conditions

• Hypertension (HTN)
This is one of the most common medical conditions which is defined as a BP pressure >140/90mmHg
- Hypertension is usually asymptomatic and only gives symptoms if the blood pressure becomes very high.
- It is divided into primary or secondary types based on aetiology.

o Primary – This is the most common type which occurs due to an unknown aetiology
- It is a chronic condition which will develop around middle age and is known essential hypertension
- Risk factors include age, race (higher in Afro-Caribbean’s) obesity, salt diet

o Secondary – This is HTN which occurs secondary to an identifiable aetiology.

It is important to remember that these causes are usually much rarer (5% of cases). Key indicators include
young age, BP >180mmHg unresponsive to medication and electrolyte imbalance.

Examples include:
i) Renal artery stenosis - decreased blood flow to glomerulus leads to increased renin secretion
- This raises Angiotensin II causes water reabsorption leading to hypertension

ii) Fibromuscular dysplasia (young females) – this is a developmental defect of blood vessel walls causing
irregular thickening of arteries, especially renal artery

iii) Genetic diseases e.g., Liddle syndrome – this is a mutation in the renal ENaC channels which causes
high Na+ reabsorption from the DCT leading to increased water reabsorption and severe HTN

Diagnosis:
i) If raised one - off blood pressure >140/90 --> first do ambulatory or home blood pressure monitoring
- ABPM = ambulatory blood pressure monitoring
- Takes 2 BP measurements per hour during the day and gives an average value of 14 measurements

- HBPM = home blood pressure monitoring

- BP is recorded twice daily, in the morning in evening for ideally 7 days and take the average value

ii) Once you have both clinic and ABPM/HBPM, stage the hypertension using the thresholds
Stage Clinic BP ABPM/HBPM
Stage 1 >= 140/90 mmHg >= 135/85 mmHg
Stage 2 >= 160/100 mmHg >= 150/95 mmHg
Stage 3 Systolic BP >= 180 mmHg or Diastolic BP >= 110 mmHg

Management: The treatment depends on the stage of hypertension

- If Stage 1 --> treat only if Age < 80 years AND evidence of organ damage, diabetes or Qrisk > 10%
- If Stage 2 --> All patients with stage 2 should be started on antihypertensive medication
- If Stage 3 --> Urgent fundoscopy to check for papilledema/retinal haemorrhage and an urgent specialist referral

The medication for hypertension follows a stepwise approach:

Step 1: If < 55 --> Start with ACE-inhibitor (e.g., Ramipril)
If > 55 or Afro-Caribbean --> Start with dihydropyridine (Amlodipine)

Step 2: If BP still high, dual therapy of ACE-i + Ca2+ channel blocker

Step 3: If BP still not controlled, add thiazide-like diuretic (e.g., Indapamide)

Step 4: Seek specialist advice as they will need additional medication or investigation

N.B. All diabetic patients should start with an ACE-i first regardless of age
- Normal blood pressure target in diabetic is <140/80mmHg
- If there is any evidence of end-organ damage it is <130/80mmHg (1)

Blood Pressure Targets: Age < 80 years Age > 80 years

Clinic BP 140/90mmHg 135/85mmHg
ABPM/HBPM 150/90mmHg 145/85mmHg

(1) © NICE 2019. Hypertension in adults: diagnosis and management. Available from: www.nice.org.uk/guidance/ng136.
• Aortic Aneurysms
An aneurysm is a dilation >50% of the original diameter of the aorta, which is either true and false type:
- True aneurysm --> abnormal dilation of the vessel which involves all 3 layers of the arterial wall
- False aneurysm --> this involves blood collecting in the tunica adventitia which communicates with the lumen.

Causes – Cardiovascular risk factors --> hypertension, smoking, diabetes, hyperlipidaemia

- Congenital connective tissue disorders --> Ehlers Danlos syndrome and Marfan Syndrome
- Tertiary syphilis --> this causes endarteritis of vasa vasorum which leads to atrophy of vessel wall.

o Thoracic Aortic Aneurysm - This is a dilation of the thoracic aorta >50% of the original diameter:
Symptoms – Acute chest pain which radiates to the back between the shoulder blades
- Major complication is dilation of the aortic valve root, causing aortic valve regurgitation

Management: Surgery or stenting (endovascular aneurysm repair – EVAR)

o Abdominal Aortic Aneurysm - This is dilation of the abdominal aorta > 3cm
Symptoms - These are usually asymptomatic until the diameter increase to > 5.5cm
- If large, can give central abdominal pain radiating to back, renal colicky pain and irritation of leg nerves
- If ruptured, gives hypotension with bleeding in the flanks (this will most likely be fatal)

Management – Screening program is abdominal ultrasound at age 65

- If asymptomatic or aortic diameter <5.5cm --> monitor with ultrasound every 3 months
- If symptomatic, diameter >5.5cm or expanding >1cm/year --> endovascular repair or open surgery

• Aortic dissection
This is a tear in the tunica intima with blood flowing through a false lumen.
- Type A – these must involve the ascending aortic arch at some point
- Type B – this describes dissections which have no involvement of the
ascending aorta, which are less common
Causes: Same as aortic aneurysm risk factors

Symptoms:
- Sharp, tearing chest pain that radiates to the back between the scapulae
- Hypertension

Complications – These can occur when the tear extends either backwards (towards heart) or distally
- If backward tear --> can lead to aortic regurgitation + inferior MI due to right coronary involvement
- Can cause pericardial tamponade (most common cause of death

- If forward tear --> Unequal arm pulses (radio-radial delay) and difference in BP between the arms
- Obstruction of Renal arteries (renal) giving renal failure

Diagnosis – CT angiography is the investigation of choice.

Management: Type A --> Surgical repair needed (BP should be controlled to between 100-120mmHg)
Type B --> Can be managed without surgery. Aim to reduce BP with IV labetalol

• SVC Obstruction
This is an emergency which is caused by pressure on the SVC. This reduces the filling of the heart reducing the
cardiac output. It is considered an oncological emergency as it is associated with cancer.
Causes - Malignancy --> non-small cell lung cancers + Lymphoma
- Vascular --> Aortic aneurysms, SVC Thrombosis

Symptoms:
-Breathlessness - Blurry vision
- Engorged blood vessels of the face - Periorbital oedema
- Headache - Pulseless distended JVP

Management:
- In the acute setting dexamethasone is used. May need endovascular stenting
- If palliative --> may give dose of chemoradiotherapy to reduce shrink the compressing tumour
 Peripheral Vascular Conditions
a) Venous Conditions
As the blood pressure is much lower in veins, there is a tendency for blood to pool in the venous system
- This can lead to problems like venous insufficiency which predisposes to clot formation

• Varicose Veins
This is a condition where the superficial veins become tortuous and enlarged.
- Usually occurs due to valve insufficiency of the leg vein valves, resulting in venous hypertension and dilation
Risk factors: Obesity, family history, pregnancy, oral contraceptive pill
Symptoms: Most are asymptomatic and only give cosmetic deformity (e.g., twisted superficial dilated veins)
- Can occur with aching heavy legs with cramps and itching.
- However, can lead to oedema and eventual ulcer formation with associated symptoms (e.g.

Management – Only should be referred if pain, ulceration or a severe impact on quality of life (not cosmetic)
- Non-surgical management --> avoid prolonged standing, lose weight, compression stockings
- Surgical management:
--> Radiofrequency ablation: catheter inserted into vein heated to 120oC burns endothelium closing vein
--> Endovenous laser ablation: a similar method but uses a laser instead

• Venous Ulcer
This is an ulcer which occurs due to venous hypertension, secondary to chronic venous insufficiency.
- The ulcers form due to capillary fibrin cuff or WBC sequestration
Location Above the ankle, around the malleoli (1)
Painful No
Temperature Warm
Appearance - Irregular margin with brown pigmentation (hemosiderin deposit)
- Oedema around the ulcer and eczema
- Lipodermatosclerosis (inflammation of fat under epidermis)

Tests – Doppler ultrasound with ABPI Management – 4-layer compression banding

- Duplex ultrasound looks at flow in vein - If it fails to heal, skin grafting might be required

• Deep Vein Thrombosis (DVT)

This is the formation of a clot which occurs usually in the femoral, popliteal or iliac veins in the leg
- It occurs due to the stasis of blood which brings pro-coagulants in contact with each other
- It is a major risk factor of causing pulmonary embolism which can be fatal
Symptoms: Tender calves, usually after period of immobilisation. Heavy legs, swelling and redness with oedema

Diagnosis: Calculate a two-level DVT Wells score, which awards points for various risk factors
e.g., +1 point for --> active cancer, previous DVT, leg swollen, localised tenderness over calf (+ other factors)

- If 2 points or more --> do a proximal leg vein ultrasound scan within 4 hours
- If < 2 points --> do a D-dimer test. Only if positive, do proximal leg vein ultrasound within 4 hours

- If the scan cannot be done within 4 hours, then do a D-dimer test and give therapeutic anticoagulation dose
- Ensure the proximal leg vein ultrasound scan done within 24 hours

Management:
- Anticoagulation with a DOAC (e.g., apixaban) is the definitive management
- This is continued for at least 3 months or up to 6 for an unprovoked DVT

When anyone presents with a DVT, it is important to think about various risk factors. 2 of the most important
are malignancy and thrombophilia. Hence in patients with unprovoked DVT, you should investigate for causes:
- Consider a Chest X-ray + Blood test + urinalysis
- If > 40 --> consider abdominal-pelvic CT scan (+ mammogram for women) to look for underlying cancer

• Post-thrombotic syndrome
A condition that can occur as a long-term complication of deep vein thrombosis, due to venous hypertension
Symptoms: Pain in the calves with heaviness and itches, varicose veins and oedema
Management: Aim to reduce venous pooling with compression stockings and keeping the leg elevated
b) Arterial Conditions
• Peripheral Arterial Disease (PAD)
This is a condition which is caused by reduced blood flow to the peripheral limbs, most commonly the legs
- It usually occurs over time due to atherosclerosis leading to increasing ischaemia over time
- However, you can get an acute event which is due to an embolus suddenly obstructing blood flow to the lower
limbs. This is associated with pro-embolic conditions such as atrial fibrillation.
Risk factors: Smoking, Diabetes, Hypertension, Hyperlipidaemia, Atrial Fibrillation

Symptoms:
Peripheral arterial disease represents a spectrum of symptoms from asymptomatic to critical, which can be
graded using the Fontaine stages.
- Stage I --> asymptomatic

- Stage 2a --> intermittent claudication after walking >200m

- This is an aching or burning in the leg muscles following walking
- It is relieved within minutes of stopping and not present at rest
- Stage 2b --> intermittent claudication after walking <200m

- Stage 3 --> this is pain at rest which is often worse at night when the patient’s legs are elevated
- Here, patients will report hanging their legs out of bed so that gravity can aide blood flow to legs

- Stage 4 --> This is critical limb ischaemia with ulcer and gangrene formation
- At this stage, you will normally see the 6P’s of limb ischaemia
- Pallor, Pulseless Painful, Paralysis, Paraesthesia, Perishingly cold

Diagnosis:
- Ankle brachial pressure index (ABPI): ABPI Result Effect
- This compares the blood pressure in the ankle against the arm 1 Normal
- In PAD, the BP is reduced in the lower limb due to atherosclerosis. 0.6-0.9 Claudication
- However, it is possible to get a false positive. Conditions like diabetes
0.3-0.6 Rest pain
lead to calcification of the arteries of the lower limb, which will
increase the blood pressure. <0.3 Impending Ulcer
- This can lead to ABPI >1.3 despite the presence of PAF

- Lower Limb Doppler ultrasound (shows flow within leg arteries)

- Angiography – this is used to visualise the extent of blockage in the arteries. This is done using CT or MRI

Management:
- Conservative --> advise patient to stop smoking and do regular exercise training
- Medical --> optimise hyperlipidaemia, hypertension and diabetes
- Clopidogrel + Atorvastatin 80mg

- Surgical --> if severe, may require stenting or bypass surgery to revascularize the lower limb
- If critical, amputation may be required

• Arterial Ulcer
This is an ulcer which occurs due to chronic limb ischaemia and tissue hypoxia
Location On the toes and lateral surface of the ankle (2)
Painful Yes
Temperature Cold with no palpable pulses
Appearance - Reticular margin with a “punched-out” appearance
- Gangrene may be present

Management:
- As this is a complication of peripheral arterial disease, it should be managed in the same way as PAD
- These patients will likely require surgical management as their PAD will be very severe

(1) Nini00, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons

(2) Jonathan Moore, CC BY 3.0 <https://creativecommons.org/licenses/by/3.0>, via Wikimedia Commons
Pulmonary Circulation Disorders

• Pulmonary hypertension
This is a condition which is caused by a resting mean pulmonary artery pressure >25mmHg.
- The main problem is that raised pulmonary pressure caused increased stress on the right side of the heart and
can lead to right sided heart failure, a complication known as cor pulmonale
- Primary hypertension occurs due to atherosclerosis of pulmonary trunk, smooth muscle hypertrophy and
fibrosis, leading to the development of plexiform lesions.
- Endothelin-1 is a potent pulmonary vasoconstrictor produced in increased amounts in pulmonary hypertension.
It also induces the proliferation of pulmonary vascular smooth muscle.

Causes:
i) Primary – this is typically seen in young adult females, aged 30-50 years
- Due to an idiopathic cause, but there are some autosomal dominant forms due to inactivation mutations of
BMPR2 leading to increased proliferation of vascular smooth muscle

ii) Secondary – due to hypoxemia (e.g. COPD)/ increased circulating volume (heart disease) or PE

Symptoms – Leads to progressive exertional shortness of breath, chest pain and syncope
- Eventual Cor pulmonale - cardiac complication of pulmonary hypertension that involves right ventricular
failure and hence gives jugular venous distension, oedema and hepatomegaly.

Management – Acute vasodilator testing is used to decide on the appropriate management strategy
- If positive response to vasodilator testing: - If negative response:
--> Give oral Ca2+ channel blockers --> PDE 5 inhibitor – Sildenafil
--> Endothelin antagonist – Bosentan
--> Prostacyclin analogues - Iloprost
• Pulmonary Embolus
This is an embolus which becomes lodged in the pulmonary circulation, impairing gas transfer
Causes: Most common source is from a deep vein thrombosis (DVT) in the femoral, iliac or popliteal veins.

There are many risk factors which predispose people – which can be assessed using the Well’s score:
i) Immobility --> especially abdominal or hip/knee surgery + bed rest + long haul flights
ii)Thrombophilia --> antiphospholipid syndrome + Factor V Leiden (most common inherited thrombophilia)
iii) Malignancy --> in people with no known risk factors it is important to check for underlying cancer
iv) Oestrogen --> Combined contraceptive pill/hormone replacement therapy/Pregnancy

Symptoms:
Small emboli are usually clinically silent as the lung has a dual blood supply (pulmonary + bronchial arteries)
- However, large emboli can give rise to pulmonary infarction causing a myriad of symptoms:
- Pleuritic chest pain, shortness of breath and haemoptysis
- Tachycardia + Tachypnoea - Pleural rub (which disappears when you hold your breath)
- Pea-body sign --> clinical sign that involves extreme calf pain upon dorsiflexion of the foot.

Tests – Pulse oximeter --> Low SpO2

- ABG --> shows type I respiratory: Failure: ¯PaO2 and ¯PaCO2.
- CXR --> this will usually be normal
- ECG --> pathognomonic pattern S1-Q3-T3. Deep S waves in lead I, and inverted T waves in lead III
- CTPA is gold standard --> shows vascular filling defect in lung. (1)
- V/Q lung scan can also be used --> shows mismatch between ventilation and
perfusion, used when CTPA is not tolerated, usually due to poor kidney function
Diagnosis - Necessary to first calculate 2-level Well’s score
- If >4 immediate CTPA
- If < 4, do D-dimer test --> if this is raised then then immediate CTPA
N.B. If there is a delay in getting the CTPA, then give therapeutic dose of
anticoagulation until the scan is performed
Management:
- If hemodynamically unstable --> thrombolysis with alteplase
- If stable --> anticoagulation with a DOAC (e.g., apixaban) for 3 months or 6 months ( if unprovoked)
(1) Image: by R.W.Koster, CC BY-SA 3.0 <https://creativecommons.org/licenses/by-sa/3.0>, via Wikimedia Commons