

�� Cardiac Tamponade
�� Introduction:
Cardiac tamponade is a life-threatening condition caused by the accumulation of uid in the pericardial space, leading to increased intrapericardial pressure and compromised heart function.
�� Pathophysiology:
● De nition:
Cardiac tamponade occurs when pericardial uid accumulates under pressure, compressing the heart chambers (particularly the right ventricle), limiting diastolic lling, and reducing cardiac output.
● Causes:
○ Trauma: Penetrating injuries (e.g., stab wounds), blunt chest trauma.
○ Medical Causes: Pericarditis, myocardial infarction (post-MI), malignancy, uremia, connective tissue diseases (e.g., systemic lupus erythematosus), post-cardiac surgery, aortic dissection.
● Mechanism:
As the pericardial uid volume increases, intrapericardial pressure rises, leading to impaired ventricular lling during diastole. This decreases stroke volume and cardiac output, resulting in hypotension and shock if untreated.

�� Clinical Presentation:
�� Classic Triad (Beck's Triad):
● Hypotension: Due to decreased stroke volume and cardiac output.
● Distended neck veins: Jugular venous distension (JVD) due to impaired venous return to the right atrium.
● Muffled heart sounds: Resulting from uid insulating the heart.
�� Additional Signs:
● Pulsus paradoxus: A fall in systolic blood pressure >10 mmHg during inspiration.
● Tachycardia: Compensatory mechanism due to reduced cardiac output.
● Chest pain: Sharp, pleuritic, worsens with breathing or lying at.
● Dyspnoea: Due to reduced cardiac output and subsequent pulmonary congestion
● Signs of shock: Cool, clammy extremities, altered mental status in severe cases.
�� Investigations:
�� Electrocardiogram (ECG):
● Findings: Low voltage QRS complexes and electrical alternans (alternating amplitude of QRS complexes)
● Common Confusions: Low voltage complexes might also be seen in obesity, COPD, and hypothyroidism Electrical alternans is more speci c to large pericardial effusion/tamponade
�� Chest X-ray:
● Findings: Enlarged cardiac silhouette (“water bottle” appearance) if tamponade is due to a large effusion.
● Common Confusions: Cardiomegaly can also be due to heart failure or other causes of uid overload.
�� Echocardiography (ECHO):
● Findings: Most de nitive investigation showing pericardial effusion, diastolic collapse of right atrium and right ventricle, and swinging motion of the heart.
● Reference: Considered the gold standard for diagnosing tamponade.
● Common Confusions: Ensure differentiation between pericardial effusion (without haemodynamic compromise) and tamponade (with haemodynamic compromise).

�� Hemodynamic Monitoring:
● Findings: Right heart catheterisation shows equalisation of diastolic pressures in all four cardiac chambers
● Common Confusions: Hemodynamic parameters may overlap with other causes of shock; context and clinical signs are key
��
Differential Diagnosis for Cardiac Tamponade:
Constrictive Pericarditis:
● Clinical Features: Presents with signs of right-sided heart failure, including elevated JVP, peripheral oedema, ascites, and Kussmaul’s sign (paradoxical rise in JVP on inspiration).
● Differentiation: Unlike cardiac tamponade, constrictive pericarditis does not present with pulsus paradoxus. Pericardial knock is heard in constrictive pericarditis, while muffled heart sounds are characteristic of tamponade. Echocardiography shows thickened pericardium rather than a large pericardial effusion.
�� MCQ Tip: Look for Kussmaul’s sign, pericardial knock, and equal diastolic pressures across all chambers without pulsus paradoxus
Tension Pneumothorax:
● Clinical Features: Acute onset of chest pain, dyspnoea, hypotension, distended neck veins, and absent breath sounds on the affected side. Tracheal deviation away from the side of the pneumothorax.
● Differentiation: Tension pneumothorax presents with respiratory distress, tracheal deviation, and absent breath sounds on one side. Cardiac tamponade presents with muffled heart sounds and pulsus paradoxus, and lung elds are clear.
�� MCQ Tip: Look for tracheal deviation, hyperresonance on percussion, and absent breath sounds on the affected side Immediate needle decompression is required

Acute Right Ventricular Myocardial Infarction (RVMI):
● Clinical Features: Presents with chest pain, hypotension, elevated JVP, and clear lung elds. ECG shows ST elevation in right-sided leads (V4R-V6R).
● Differentiation: RVMI has clear lung elds and hypotension but does not show pulsus paradoxus or muffled heart sounds. Look for ST elevation in right-sided leads on ECG.
�� MCQ Tip: Suspect RVMI in patients with inferior MI and hypotension, clear lungs, and elevated JVP. Manage with uids and avoid nitrates.
Pulmonary Embolism (PE):
● Clinical Features: Presents with sudden onset dyspnoea, pleuritic chest pain, tachycardia, and hypotension. May have haemoptysis or evidence of deep vein thrombosis (DVT).
● Differentiation: PE may cause hypotension and distended neck veins, but usually presents with respiratory symptoms such as pleuritic chest pain and tachypnoea. Pulsus paradoxus and muffled heart sounds are not seen in PE Diagnosed with CT pulmonary angiography
�� MCQ Tip: Look for sudden onset dyspnoea, pleuritic chest pain, and risk factors for DVT/PE D-dimer may be elevated; con rm with CT pulmonary angiography
Severe Aortic Stenosis:
● Clinical Features: Presents with exertional chest pain, dyspnoea, syncope, and a harsh systolic murmur radiating to the carotids.
● Differentiation: Aortic stenosis does not present with pulsus paradoxus or muffled heart sounds. The systolic murmur and a slow-rising, low-volume pulse (pulsus parvus et tardus) are key features.

�� MCQ Tip: Look for syncope, chest pain, and a systolic murmur radiating to the carotids. Pulsus paradoxus and jugular venous distension are not typical
Dilated Cardiomyopathy:
● Clinical Features: Presents with signs of heart failure (dyspnoea, orthopnoea, and paroxysmal nocturnal dyspnoea) and a displaced apex beat.
● Differentiation: Unlike tamponade, dilated cardiomyopathy does not cause pulsus paradoxus or muffled heart sounds. Echocardiography shows a dilated left ventricle with reduced ejection fraction, not a pericardial effusion.
�� MCQ Tip: Consider in a patient with a history of heart failure symptoms, a displaced apex beat, and signs of dilated cardiomyopathy on echocardiogram
Restrictive Cardiomyopathy:
● Clinical Features: Presents with dyspnoea, fatigue, and signs of right-sided heart failure (elevated JVP, hepatomegaly, ascites, peripheral oedema).
● Differentiation: Restrictive cardiomyopathy does not typically present with pulsus paradoxus or muffled heart sounds. Echocardiography shows normal or small ventricles with reduced diastolic lling and biatrial enlargement.

�� MCQ Tip: Look for a history of right-sided heart failure symptoms and normal ventricular size on echocardiogram. No pericardial effusion is present.
Pericardial Effusion (Without Tamponade):
● Clinical Features: Similar to tamponade but without haemodynamic compromise; may present with chest discomfort, dyspnoea, or a “water bottle” appearance on chest X-ray.
● Differentiation: Unlike tamponade, there are no signs of shock or pulsus paradoxus Echocardiography shows pericardial effusion without diastolic collapse of the heart chambers.
�� MCQ Tip: Look for effusion without haemodynamic compromise; echocardiography shows uid but no chamber collapse.
Aortic Dissection (Complicated by Tamponade):
● Clinical Features: Sudden-onset severe chest pain radiating to the back, hypotension, and pulse de cits May present with signs of tamponade if the dissection ruptures into the pericardium.
● Differentiation: Aortic dissection typically presents with severe chest or back pain and may have signs of tamponade if complicated by pericardial rupture. Imaging (CT aortogram) is diagnostic.
�� MCQ Tip: Consider in a patient with sudden-onset chest pain, pulse de cits, and risk factors for dissection (e.g., hypertension, Marfan syndrome).
Tension Haemothorax:

● Clinical Features: Presents with hypotension, reduced breath sounds on one side, and dullness to percussion on the affected side.
● Differentiation: Unlike tamponade, tension haemothorax presents with decreased breath sounds and dullness on percussion. It does not cause pulsus paradoxus or muffled heart sounds.
�� MCQ Tip: Look for signs of haemothorax (dullness to percussion, decreased breath sounds) on the affected side. Manage with chest tube insertion.
�� Management:
● Immediate Management:
○ Urgent Pericardiocentesis: The de nitive treatment to relieve pressure on the heart by aspirating pericardial uid
■ Performed under ultrasound guidance for safety.
○ Fluid Resuscitation: Temporary measure to increase preload and maintain cardiac output.
○ Inotropic Support: Consider in cases of shock while preparing for pericardiocentesis.
● De nitive Management:
○ Pericardiotomy or Pericardial Window: May be required in recurrent or loculated effusions.
○ Surgical Repair: If tamponade is due to trauma or cardiac rupture
● Avoid in Management:
○ Diuretics or Vasodilators: These can reduce preload and worsen cardiac output in tamponade
○ Delay in Pericardiocentesis: Immediate intervention is crucial to prevent circulatory collapse ⚠
Complications:
● Cardiogenic Shock: Due to prolonged low cardiac output.
● Pulseless Electrical Activity (PEA): Cardiac arrest where electrical activity is present but no effective cardiac output.
● Death: If not promptly diagnosed and treated

�� Example Question Review:
Scenario:
A 45-year-old man presents to the ED with a stab wound to the chest. Examination reveals hypotension (BP 63 mmHg), tachycardia (121 bpm), muffled heart sounds, and distended neck veins.
● Correct Answer: C. Cardiac tamponade
● Key Takeaways:
○ Recognise Beck's Triad: Hypotension, JVD, and muffled heart sounds.
○ Understand the Urgency: Rapid diagnosis and intervention (pericardiocentesis) are critical.
○ Differentiate from Similar Conditions: Use clinical signs and context to distinguish between differentials.

Key points
● Recognise Beck's Triad: Hypotension, JVD, and muffled heart sounds are classic signs of cardiac tamponade.
● Understand the Urgency: Cardiac tamponade is a medical emergency; rapid diagnosis and intervention (pericardiocentesis) are critical.
● Differentiate from Similar Conditions:
○ Pericardial effusion: May not present with haemodynamic compromise
○ Tension pneumothorax: Look for tracheal deviation and absent breath sounds on one side
○ Myocardial infarction: Typically presents with chest pain and ECG changes, not necessarily with Beck's triad
● Know the Diagnostic Tools:
○ Echocardiography: Gold standard for diagnosis.
○ ECG Findings: Low voltage QRS and electrical alternans are clues but not de nitive.
● Be Prepared for Confusing Scenarios:
○ Cardiac tamponade may present subtly in patients with chronic conditions (e g , malignancy, renal failure) or post-cardiac procedures. Context is key.
● Avoid Diuretics/Vasodilators: Inappropriately managing uid balance can worsen outcomes.
Note:
At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management you need to apply this knowledge in clinical scenarios, and that comes with experience.
To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you efficiently cover the entire MLA content map, ensuring focused and effective learning.

Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success.
Discover what others say about us:
● What past PLAB 1 Candidates say about MedRevisions
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�� Subclavian Artery
�� Introduction:
The subclavian artery is a major artery of the upper chest, primarily supplying blood to the head, neck, shoulder, and arms Understanding its anatomy, pathology, and clinical signi cance is crucial for diagnosing conditions that involve arterial ow abnormalities, such as vascular stenosis or occlusion.
�� Anatomy of the Subclavian Artery:

● Origin:
○ Left side: Arises from the aortic arch
○ Right side: Arises from the brachiocephalic trunk
● Divisions:
○ First Part: Extends from its origin to the medial border of the scalenus anterior muscle.
○ Second Part: Lies posterior to the scalenus anterior muscle.
○ Third Part: Extends from the lateral border of the scalenus anterior muscle to the outer border of the rst rib, where it becomes the axillary artery.
● Branches:
○ Vertebral artery: Supplies the posterior portion of the brain.
○ Internal thoracic artery: Supplies the anterior chest wall and breasts.
○ Thyrocervical trunk: Supplies the neck and upper back.
○ Costocervical trunk: Supplies the upper ribs and neck muscles
○ Dorsal scapular artery (variable): Supplies muscles of the upper back
��
Subclavian Steal Syndrome:
● De nition: Subclavian steal syndrome is characterised by stenosis or occlusion of the subclavian artery proximal to the origin of the vertebral artery. This condition causes a "steal" phenomenon, where blood ow is reversed in the vertebral artery to supply the affected arm, leading to symptoms of cerebral hypoperfusion.
● Pathophysiology:
○ Stenosis or occlusion of the subclavian artery occurs proximal to the origin of the vertebral artery.
○ When the arm is exercised or exerted, the increased demand for blood ow cannot be met due to the proximal blockage.
○ Blood is "stolen" or drawn from the vertebral artery (which normally supplies the brain) to compensate, resulting in reduced blood ow to the posterior circulation of the brain.
�� Clinical Presentation:
● Symptoms related to arm exertion:
○ Arm claudication: Pain, cramping, or fatigue in the affected arm during use.
○ Coolness or pallor of the affected limb
○ Decreased pulse or blood pressure in the affected limb
● Neurological symptoms:
○ Dizziness, vertigo, or light-headedness.
○ Visual disturbances, such as blurred vision or diplopia.
○ Ataxia or coordination problems
○ Syncope or fainting spells.

❓ Common Confusions in MCQs:
● Differentiating Subclavian Steal Syndrome from Other Vascular Conditions:
○ Confusion: Often confused with conditions like ischemic stroke or vertebrobasilar insufficiency.
○ Clari cation: Key features include:
■ Neurological symptoms during or after arm exertion.
■ Arm claudication symptoms, such as pain or weakness
■ Discrepancy in blood pressure between arms.
■ Presence of a subclavian bruit on auscultation.
● Differentiating from Cardiac Causes:
○ Confusion: Mimics cardiac conditions like myocardial ischemia or thoracic aortic dissection.
○ Clari cation: Involves neurological symptoms triggered by arm exertion and a blood pressure differential between arms.
● Investigation Choice:
○ Confusion: Choosing the correct diagnostic test.
○ Clari cation: Duplex ultrasound is the rst-line diagnostic tool, with CT angiography (CTA) or MR angiography (MRA) providing more detailed images Transcranial Doppler ultrasound may con rm reversed vertebral artery blood ow.
�� Diagnosis and Investigations:
● History and Physical Examination:
○ Focus on symptoms exacerbated by arm exertion.
○ Look for diminished or absent pulses, a bruit over the subclavian artery, and a signi cant difference in blood pressure between arms (usually >15 mmHg).
● Diagnostic Tests:
○ Duplex Ultrasound: First-line investigation to assess blood ow in subclavian and vertebral arteries.
○ CT Angiography (CTA) or MR Angiography (MRA): Provides detailed imaging of the arterial anatomy.
○ Transcranial Doppler Ultrasound: Detects reversal of ow in the vertebral artery
�� Management of Subclavian Steal Syndrome:
● Asymptomatic Patients:
○ Observation and Regular Follow-Up.

○ Control of Cardiovascular Risk Factors: Such as hypertension, diabetes, and hyperlipidemia.
● Symptomatic Patients:
○ Percutaneous Transluminal Angioplasty (PTA) and Stenting: Preferred rst-line intervention.
○ Surgical Bypass or Endarterectomy: Considered if PTA and stenting are not feasible or fail.
● Medical Management:
○ Antiplatelet Therapy: (e g , aspirin) to reduce the risk of embolic events
○ Statins: To control lipid levels and reduce cardiovascular risk.
�� Key points
● Understand the Anatomy and Pathophysiology: Focus on how the subclavian artery's position relative to the vertebral artery creates a "steal" phenomenon
● Identify Symptoms of Subclavian Steal Syndrome: Look for arm claudication, dizziness, vertigo, and blood pressure discrepancies between arms
● Choose the Correct Diagnostic Approach: Duplex ultrasound, CTA, or MRA is often required for con rmation
● Management Strategies: Be familiar with both interventional and conservative management options based on symptom severity.

Note:
At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management you need to apply this knowledge in clinical scenarios, and that comes with experience
To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you efficiently cover the entire MLA content map, ensuring focused and effective learning.
Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success.
Discover what others say about us:
● What past PLAB 1 Candidates say about MedRevisions
● Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was
● 5000+ UKMLA and PLAB 1 Exam style questions
● Unlimited timed mocks
● Spaced repetition learning tool
● And much more
�� Pulmonary Arterial Hypertension (PAH)
�� Introduction:
Pulmonary arterial hypertension (PAH) is a type of pulmonary hypertension characterised by elevated pressure in the pulmonary arteries. It is de ned by:
● Mean Pulmonary Artery Pressure (mPAP): >20 mmHg at rest, measured by right heart catheterisation.
● Pulmonary Vascular Resistance (PVR): ≥3 Wood units
● Pulmonary Capillary Wedge Pressure (PCWP): ≤15 mmHg
PAH is a progressive condition leading to right ventricular failure and, if untreated, death.
�� Epidemiology:
● Prevalence: 15-50 cases per million people.
● Gender: More common in females (female-to-male ratio: 2:1)

�� Classi cation:
PAH Subtypes:
● Idiopathic PAH: No identi able cause.
● Heritable PAH: Linked to genetic mutations (e.g., BMPR2).
● Drug and Toxin-Induced PAH: Associated with anorexigens, methamphetamines, chemotherapy agents.
● PAH with Associated Conditions: Connective tissue diseases, HIV infection, portal hypertension, congenital heart diseases, schistosomiasis.
⚙ Pathophysiology:
1. Vasoconstriction: Increased levels of vasoconstrictors such as endothelin-1 and decreased levels of vasodilators like nitric oxide (NO) and prostacyclin lead to narrowing of pulmonary arteries
2 Vascular remodelling: Hypertrophy and hyperplasia of endothelial and smooth muscle cells contribute to the thickening of pulmonary artery walls.
3. In ammation: In ammatory cells in ltrate the vascular wall, contributing to its remodelling.
4. Thrombosis: In situ thrombosis within the small pulmonary arteries due to endothelial dysfunction �� Clinical Features:
● Symptoms:
○ Progressive dyspnoea: Most common presenting symptom.
○ Fatigue and weakness.
○ Chest pain or discomfort.
○ Syncope or near-syncope: Due to decreased cardiac output
○ Palpitations.
○ Peripheral oedema: Due to right heart failure.
● Signs:
○ Loud P2 component of the second heart sound (pulmonary valve closure)
○ Right ventricular heave.
○ Elevated jugular venous pressure (JVP).
○ Peripheral oedema and ascites in advanced cases.
○ Hepatomegaly due to right heart failure

�� Diagnosis:
● Initial Investigations:
○ Electrocardiogram (ECG): May show right axis deviation, right atrial enlargement, and right ventricular hypertrophy.
○ Transthoracic echocardiography (TTE): Used to estimate pulmonary artery pressures, assess right ventricular size and function, and identify any underlying heart or valvular disease.
○ Chest X-ray: May show enlarged pulmonary arteries and right atrial or ventricular enlargement.
○ Blood tests: To assess for underlying causes, such as autoimmune diseases or HIV
● De nitive Investigation:
○ Right heart catheterisation: Gold standard for diagnosis; con rms elevated mPAP (>20 mmHg) and PVR (≥3 Wood units) with normal PCWP (≤15 mmHg).
● Further Investigations:
○ Pulmonary function tests (PFTs): To rule out parenchymal lung disease.
○ Ventilation-perfusion (V/Q) scan: To exclude chronic thromboembolic pulmonary hypertension (CTEPH).
○ Cardiac MRI: For detailed assessment of right ventricular function.
○ Screening for genetic mutations: In cases of heritable PAH.
�� Management:
Goals: Reduce symptoms, improve quality of life, and slow disease progression.

● Supportive Therapy:
○ Oxygen therapy: To maintain adequate oxygen saturation (>90%).
○ Diuretics: To manage right heart failure and uid overload
○ Anticoagulation: Recommended in patients with idiopathic PAH to prevent thromboembolic events
● Targeted PAH Therapy:
○ Endothelin Receptor Antagonists (ERAs): Such as bosentan and ambrisentan, block the vasoconstrictor effects of endothelin-1, reducing pulmonary vascular resistance They are rst-line therapy in PAH management
○ Phosphodiesterase Type 5 (PDE-5) Inhibitors: Such as sildena l and tadala l, increase levels of cGMP by inhibiting its breakdown, leading to vasodilation of the pulmonary arteries They are used in conjunction with other therapies or as monotherapy in certain cases.
○ Prostanoids: Such as epoprostenol, iloprost, and treprostinil, promote vasodilation and inhibit platelet aggregation. They are used in more advanced PAH or in patients who have not responded to other therapies.
○ Soluble Guanylate Cyclase (sGC) Stimulators: Such as riociguat, enhance the effect of nitric oxide and lead to vasodilation. Used in cases of chronic thromboembolic pulmonary hypertension or when PDE-5 inhibitors are not tolerated.
○ Calcium Channel Blockers (CCBs): Used in a small subset of patients who show a positive response to vasoreactivity testing during right heart catheterisation. Nifedipine, amlodipine, and diltiazem are commonly used.
● Advanced Therapies:
○ Lung Transplantation: Considered in end-stage disease or when medical therapy fails.
❓ Common Confusions in MCQs:
● Differentiating Between PAH and Other Types of Pulmonary Hypertension:
○ Confusion: Students may confuse PAH with other types of pulmonary hypertension, such as those due to left heart disease or chronic lung diseases
○ Clari cation: PAH is speci cally associated with normal PCWP (≤15 mmHg) and elevated PVR (≥3 Wood units) Other types of pulmonary hypertension will show elevated PCWP or evidence of underlying heart or lung diseases
● Choosing the Correct Initial Therapy:
○ Confusion: Uncertainty over which drug to initiate as rst-line therapy.
○ Clari cation: Endothelin Receptor Antagonists (ERAs) are the rst-line therapy in PAH. Other agents, such as PDE-5 inhibitors or prostanoids, are reserved for speci c scenarios or when there is inadequate response to initial therapy.
● Understanding Diagnostic Tools:
○ Confusion: Confusing diagnostic tools such as right heart catheterisation with less speci c investigations like echocardiography.
○ Clari cation: Right heart catheterisation is the gold standard for con rming the diagnosis of PAH. Echocardiography is useful for initial assessment but cannot de nitively diagnose PAH.

��
Key points
● Recognise PAH Symptoms: Progressive dyspnoea, syncope, and right heart failure signs.
● Understand Diagnostic Pathway: Right heart catheterisation is the gold standard
● Know First-Line Therapy: Endothelin receptor antagonists (e.g., bosentan) are preferred for managing PAH
Note:
At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management you need to apply this knowledge in clinical scenarios, and that comes with experience

To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you efficiently cover the entire MLA content map, ensuring focused and effective learning.
Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success.
Discover what others say about us:
● What past PLAB 1 Candidates say about MedRevisions
● Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was
● 5000+ UKMLA and PLAB 1 Exam style questions
● Unlimited timed mocks
● Spaced repetition learning tool
● And much more
Coarctation of the Aorta (CoA)
Coarctation of the aorta (CoA) is a congenital condition characterised by a narrowing of the aorta, usually distal to the origin of the left subclavian artery, at the level of the ductus arteriosus This narrowing increases resistance to blood ow, leading to:
● Hypertension in the upper extremities
● Reduced blood ow to the lower extremities.
��
Epidemiology:
● Prevalence: CoA accounts for 5-8% of all congenital heart defects.
● Gender: More common in males.
● Association: 50-80% of CoA cases have a bicuspid aortic valve.
⚙
Pathophysiology:
● Postductal (Adult Type):
○ Most common in adults
○ Narrowing is distal to the ductus arteriosus
○ Results in differential blood pressure between upper and lower limbs.
● Preductal (Infantile Type):
○ Rare in adults.
○ Narrowing is proximal to the ductus arteriosus
○ Often associated with other congenital defects.

The narrowing of the aorta increases afterload on the left ventricle, causing hypertension in the upper body and diminished perfusion to the lower extremities. Over time, this can result in collateral circulation development, left ventricular hypertrophy, and heart failure if untreated.
��
Clinical Features:
● Hypertension:
○ Often the only sign in adults; refractory or resistant hypertension is a common nding.
○ Blood pressure discrepancy between the upper and lower limbs: higher in the arms than in the legs.
● Murmur:
○ Systolic murmur heard best over the left infraclavicular area and the back (inter-scapular region) It may also be heard over the left intercostal area
○ The murmur may radiate to the back due to turbulence created by the narrowed segment of the aorta.
● Symptoms:
○ Headaches, nosebleeds, and fatigue due to upper body hypertension
○ Leg pain (claudication), cold lower extremities, and weak or delayed femoral pulses due to decreased blood ow to the lower body
○ Radio-femoral delay (difference in the timing of pulses between the radial and femoral arteries)
�� Diagnosis:

● Physical Examination:
○ Measure blood pressure in both arms and legs to detect discrepancies
○ Assess for radio-femoral delay.
○ Auscultate for systolic murmur over the left infraclavicular area and back.
● Imaging:
○ Transthoracic Echocardiography (TTE): Often the rst imaging test; can show the narrowed segment of the aorta and assess the function of the heart and aortic valve.
○ Transesophageal Echocardiography (TEE): Provides a more detailed view if TTE is inconclusive.
○ Chest X-ray: May show rib notching due to collateral vessels and the "3 sign" created by pre- and post-stenotic dilation of the aorta.
○ Magnetic Resonance Imaging (MRI) or Computed Tomography (CT) Angiography: Gold standard for diagnosing CoA, particularly useful for planning surgery or stenting.
● Cardiac Catheterisation:
○ Provides direct pressure measurements across the coarctation and may be used in interventional management.
�� Management:
● Medical Management:
○ Hypertension Control: Beta-blockers or ACE inhibitors are commonly used to manage hypertension.
○ Monitoring: Regular follow-up with blood pressure monitoring and imaging
● Interventional Management:
○ Surgical Repair: Resection of the narrowed segment with end-to-end anastomosis or use of a graft; indicated in severe cases or those with complications.
○ Balloon Angioplasty and Stenting: Minimally invasive option, especially in older children and adults.
● Follow-up and Long-Term Management:
○ Regular monitoring for hypertension, aortic aneurysm, or re-coarctation
○ Lifelong follow-up is essential due to the risk of late complications, such as aortic aneurysm, dissection, or persistent hypertension
❓ Common Confusions in MCQs:

● Identifying Symptoms:
○ Confusion: Differentiating between various congenital heart defects that present with murmurs and hypertension.
○ Clari cation: CoA is associated with:
■ Hypertension (particularly in the upper limbs).
■ Radio-femoral delay and weak femoral pulses
■ Systolic murmur in the left infraclavicular area or back.
■ Associated Bicuspid Aortic Valve.
● Understanding Diagnostic Investigations:
○ Confusion: Choosing the correct diagnostic test
○ Clari cation:
■ Start with Transthoracic Echocardiography (TTE) to assess the anatomy.
■ Use CT or MRI Angiography to con rm the diagnosis and plan the intervention.
● Management Choices:
○ Confusion: When to choose medical versus surgical or interventional management.
○ Clari cation:
■ Medical Management focuses on hypertension control
■ Surgical Repair or Stenting is required for signi cant coarctation, especially if symptomatic or if there are complications like heart failure
Key points
● Recognise Key Signs of CoA: Hypertension in the upper limbs, radio-femoral delay, systolic murmur over the left infraclavicular area or back.
● Understand the Diagnostic Approach: Initial TTE, con rmed by CT or MRI angiography.
● Know When to Manage Surgically: Indications for surgery or stenting include severe cases or complications like heart failure or persistent hypertension.

Note:
At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management you need to apply this knowledge in clinical scenarios, and that comes with experience.
To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement. Plus, our Study Essential Mode helps you efficiently cover the entire MLA content map, ensuring focused and effective learning.
Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success
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�� Patent Foramen Ovale (PFO)
�� Introduction
Patent Foramen Ovale (PFO) is a congenital cardiac anomaly where the foramen ovale, a normal fetal structure, fails to close after birth. While typically asymptomatic and discovered incidentally, it can have clinical signi cance in cases of unexplained strokes, transient ischemic attacks (TIA), or migraines with aura.
��
Anatomy and Physiology:
● Foramen Ovale:
○ A normal opening between the right and left atria in fetal life, allowing oxygenated blood from the placenta to bypass the non-functioning fetal lungs.

● Closure After Birth:
○ Normally closes soon after birth due to increased left atrial pressure. If this closure does not occur, it remains "patent," resulting in a PFO.
⚙ Pathophysiology:
● Right-to-Left Shunt:
○ A PFO can allow a small amount of blood to bypass the lungs, usually minor and asymptomatic but can become signi cant under certain conditions (e.g., increased right atrial pressure during Valsalva manoeuvre, coughing, or sneezing).
● Paradoxical Embolism:
○ The most signi cant complication of a PFO, where a thrombus crosses from the venous to the arterial system, potentially causing a stroke or systemic embolisation.
�� Clinical Features:
● Asymptomatic in Most Cases: PFO is often asymptomatic and detected incidentally during echocardiography performed for other reasons.
● Possible Symptoms and Complications:
○ Cryptogenic Stroke or TIA: Unexplained stroke or TIA, especially in younger patients without traditional risk factors, may prompt investigation for PFO.
○ Migraine with Aura: There is some evidence to suggest an association between PFO and migraines with aura, although the exact mechanism remains unclear.
○ Platypnoea-Orthodeoxia Syndrome: Rarely, PFO can present with platypnoea (dyspnoea that worsens in the upright position) and orthodeoxia (oxygen desaturation on sitting upright).
�� Diagnostic Approach:
● Initial Investigation: Transthoracic Echocardiography (TTE):
○ TTE is often the rst investigation performed, especially in patients presenting with stroke or TIA. It can suggest the presence of a PFO but is not the gold standard.
○ Limitations: TTE may not be sensitive enough to detect a PFO, particularly if the shunt is small or intermittent.
● Gold Standard: Transesophageal Echocardiography (TEE):

○ Indication: TEE is the investigation of choice for con rming the diagnosis of a PFO, particularly when TTE is inconclusive
○ Why TEE? TEE provides a more detailed view of the atrial septum and allows for the use of contrast ("bubble study") to detect shunting across the PFO
○ Procedure: During a "bubble study," agitated saline is injected into a peripheral vein. The appearance of bubbles in the left atrium shortly after injection, particularly during a Valsalva manoeuvre, con rms the presence of a right-to-left shunt
● Other Diagnostic Tools:
○ Electrocardiogram (ECG): Not diagnostic for PFO; may show signs of other cardiac abnormalities but not speci c for PFO
○ Cardiac Troponins: Useful for diagnosing myocardial ischemia, not PFO.
○ Holter Monitoring: Used for detecting arrhythmias; not indicated in diagnosing PFO.
○ Stress Test: Used for diagnosing coronary artery disease, not PFO
�� Management:
● Asymptomatic Patients:
○ No Treatment Required: Most PFOs are asymptomatic and do not require any intervention
○ Observation and Reassurance: Patients are typically reassured, and no treatment is required unless there are associated symptoms or complications
● Symptomatic Patients:
○ Cryptogenic Stroke or TIA:
■ Antiplatelet Therapy: First-line treatment with aspirin or another antiplatelet agent is often recommended.
■ Anticoagulation: Considered in patients with evidence of a hypercoagulable state or venous thromboembolism.
■ PFO Closure: Considered in selected cases, especially in younger patients with cryptogenic stroke, where no other cause of stroke is identi ed. The decision is made on an individual basis, often involving a multidisciplinary team.
● Recurrent Stroke Despite Medical Therapy:
○ Percutaneous PFO Closure: May be considered for patients with recurrent strokes despite optimal medical therapy. This procedure involves inserting a closure device via a catheter to seal the PFO.

❓Common Confusions in MCQs:
● Diagnosis of PFO:
○ Confusion: Using ECG, Holter monitoring, or stress tests for diagnosis.
○ Clari cation: TEE is the gold standard for diagnosing PFO
● Management Options:
○ Confusion: Whether to use anticoagulants, antiplatelet agents, or PFO closure.
○ Clari cation: Antiplatelet therapy is the rst line for stroke prevention; anticoagulation is considered for speci c cases, and PFO closure is for selected patients with recurrent cryptogenic stroke.
● Understanding Symptoms:
○ Confusion: Misinterpreting symptoms such as stroke, TIA, or migraines with aura as unrelated to PFO.
○ Clari cation: Be aware that PFO can cause paradoxical embolism leading to stroke or TIA, and may be associated with migraines with aura �� Key points:
● Diagnostic Tool of Choice: TEE is the gold standard for diagnosing PFO.
● Management: Recognize when PFO may require closure, particularly in recurrent cryptogenic stroke.
● Awareness of Symptoms and Complications: Understand the potential complications, such as paradoxical embolism, and possible associations with migraines with aura.

Note:
At MedRevisions, we have dedicated years to helping candidates excel in the PLAB 1 exam, and we’re now applying our decade-long expertise to the UKMLA. With the PLAB exam now aligned with the MLA content map since August 2024, both exams are administered by the GMC UK. While our notes provide a strong foundation, true success comes from practice. It’s not enough to know the investigations and management you need to apply this knowledge in clinical scenarios, and that comes with experience.
To support your learning, we’ve linked exam-style questions directly to our notes for immediate reinforcement Plus, our Study Essential Mode helps you efficiently cover the entire MLA content map, ensuring focused and effective learning.
Whether you’re in medical school or preparing for your exams, our materials will enhance your clinical decision-making and general medical knowledge. Join the thousands of candidates who have trusted MedRevisions to guide their journey to success.
Discover what others say about us:
● What past PLAB 1 Candidates say about MedRevisions
● Was MedRevisions enough to pass the August 2024 PLAB exam (exam based on the MLA content map): Find out what this doctor’s experience was
● 5000+ UKMLA and PLAB 1 Exam style questions
● Unlimited timed mocks
● Spaced repetition learning tool
● And much more
�� Mitral Valve Stenosis (MVS)
�� Introduction:
Mitral valve stenosis (MVS) is a valvular heart disease characterised by the narrowing of the mitral valve ori ce, obstructing blood ow from the left atrium to the left ventricle during diastole The most common cause is rheumatic fever, leading to progressive valve brosis and calci cation.

�� Epidemiology:
● Cause: Most cases in developed countries are due to rheumatic fever
● Gender: More common in women than men (female-to-male ratio: 3:1)
⚙ Pathophysiology:
● Rheumatic Heart Disease: In ammatory scarring and fusion of valve lea ets and chordae tendineae.
● Haemodynamic Changes:
○ Narrowed valve impedes blood ow, elevating left atrial pressure.
○ Results in left atrial enlargement, pulmonary congestion, increased pulmonary artery pressure, and right heart failure.
● Atrial Fibrillation (AF): Dilated left atrium predisposes to AF, increasing the risk of thromboembolism (e.g., stroke).
�� Clinical Features:
● Symptoms:
○ Dyspnoea on exertion: Due to increased left atrial pressure and pulmonary congestion.
○ Orthopnoea and paroxysmal nocturnal dyspnoea (PND): Due to uid redistribution while lying down.
○ Fatigue: Due to reduced cardiac output
○ Palpitations: Often due to atrial brillation.
○ Haemoptysis: Due to rupture of bronchial veins from increased pulmonary venous pressure.
○ Chest pain: Less common, may be due to pulmonary hypertension.
● Signs:
○ Mid-diastolic murmur: Low-pitched, rumbling murmur best heard at the apex with the bell of the stethoscope, especially in the left lateral decubitus position.
○ Opening snap: High-pitched sound heard shortly after S2, due to abrupt tensing of the mitral valve lea ets.
○ Loud S1: Due to the thickened, stiff mitral valve lea ets closing forcefully
○ Signs of right heart failure: Elevated jugular venous pressure (JVP), peripheral oedema, ascites
○ Malar ush: Due to reduced cardiac output and pulmonary hypertension.

�� Diagnosis:
● Clinical Examination:
○ Auscultation: Detects the characteristic mid-diastolic rumbling murmur and opening snap.
○ Chest X-ray:
■ Straightening of the left heart border: Due to left atrial enlargement.
■ Double shadow sign: Due to left atrial enlargement
■ Pulmonary congestion: Shows upper lobe venous diversion, interstitial oedema, or Kerley B lines
● Electrocardiogram (ECG):
○ Atrial Fibrillation (AF): Common due to left atrial enlargement.
○ P-mitrale: Broad, notched P waves seen in lead II due to left atrial enlargement
● Echocardiography:
○ Transthoracic echocardiogram (TTE): Diagnostic tool of choice. Con rms the diagnosis by measuring the mitral valve area, determining the severity of stenosis, and assessing for associated complications like atrial brillation or thrombus
○ Transesophageal echocardiography (TEE): Used in cases where TTE is inconclusive or to assess for thrombus before any interventional procedure
● Additional Tests:
○ Cardiac catheterisation: Performed when non-invasive tests are inconclusive or before planned surgery.
Management:
● General Measures:
○ Lifestyle modi cation: Avoiding excessive salt intake, regular exercise, and smoking cessation.
○ Infective Endocarditis Prophylaxis: Only for those with a history of infective endocarditis or undergoing high-risk procedures.
● Medical Therapy:
○ Rate control for AF: Beta-blockers (e g , bisoprolol), calcium channel blockers (e g , verapamil, diltiazem), or digoxin to control ventricular rate in atrial brillation.
○ Anticoagulation: Essential in patients with AF or a history of thromboembolism to prevent stroke (usually with warfarin or direct oral anticoagulants (DOACs), although warfarin is preferred in rheumatic heart disease).
○ Diuretics: Used to relieve symptoms of pulmonary congestion and right-sided heart failure.

● Interventional Therapy:
○ Percutaneous Balloon Mitral Valvuloplasty (PBMV): First-line treatment for symptomatic patients with moderate to severe mitral stenosis without signi cant mitral regurgitation or left atrial thrombus.
○ Surgical Mitral Valve Replacement (MVR): Indicated in patients who are unsuitable for PBMV, have associated severe mitral regurgitation, or require other cardiac surgery.
❓ Common Confusions in PLAB 1 MCQs:
● Differentiating Mitral Stenosis from Other Valvular Diseases:
○ Confusion: Students may confuse the murmur of mitral stenosis with other valvular lesions such as mitral regurgitation or aortic stenosis.
○ Clari cation: Mitral stenosis typically presents with a mid-diastolic rumbling murmur best heard at the apex. Mitral regurgitation is associated with a pansystolic murmur, and aortic stenosis with an ejection systolic murmur best heard at the right second intercostal space
● Interpreting Radiological Findings:
○ Confusion: Misinterpretation of chest X-ray ndings, such as straightening of the left heart border.
○ Clari cation: The straightening of the left heart border on chest X-ray is indicative of left atrial enlargement, which is a hallmark of mitral stenosis.
● Management Confusion:
○ Confusion: When to choose medical versus interventional therapy.
○ Clari cation: PBMV is the rst-line treatment for suitable patients with symptomatic moderate to severe mitral stenosis. Medical therapy, such as rate control and anticoagulation, is important in managing AF and preventing complications but does not address the valve stenosis itself.

�� Key points
● Recognise Mitral Stenosis Features: Symptoms like breathlessness, palpitations, and speci c auscultatory ndings.
● Understand Radiological Signs: Left atrial enlargement may appear as straightening of the left heart border on chest X-ray.
● Know First-Line Treatment: PBMV is the preferred treatment for suitable symptomatic patients.
