Which one of the following conditions is associated with Kawasaki's syndrome?
In which of the following conditions is a constant PR interval observed?
A patient with native aortic valve disease presents with right hemiparesis. What is the most appropriate management to prevent further stroke?
Which of the following procedures is contraindicated in Wolff-Parkinson-White syndrome?
A 34-year-old man presents with dyspnea and increasing peripheral edema, following a "flu-like" illness with intermittent sharp left-sided chest pain. On examination, his jugular venous pressure is elevated at 8 cm, heart sounds are soft, and the blood pressure is 104/76 mm Hg, with a 20 mm Hg decrease in systolic arterial pressure during slow inspiration. Which of the following is the most likely diagnosis?
In non-rheumatic atrial fibrillation, which of the following statements is true?
Which of the following is a characteristic EKG finding of ventricular premature beats?
The investigation of choice for DVT is -
Which of the following statements is false regarding restrictive cardiomyopathy?
What is the characteristic feature of pain experienced in intermittent claudication?
Explanation: ***Coronary artery aneurysm*** - **Coronary artery aneurysms** are a major and potentially life-threatening complication, occurring in 15-25% of untreated children with Kawasaki disease [1]. - This is due to the disease's predilection for causing **vasculitis** in medium-sized arteries, particularly the coronary arteries [1]. *Acute rheumatic fever* - Acute rheumatic fever is an **inflammatory disease** that can develop after an infection with Group A Streptococcus (strep throat or scarlet fever) [2]. - It primarily affects the **heart, joints, brain, and skin**, but its pathophysiology and clinical presentation are distinct from Kawasaki disease [2]. *Pulmonary embolus* - A **pulmonary embolus** is a block in one of the pulmonary arteries in your lungs, usually caused by blood clots that travel to the lungs from the legs or, rarely, other parts of the body. - It is not a characteristic feature or complication of **Kawasaki disease**. *Systemic lupus erythematosus* - **Systemic lupus erythematosus (SLE)** is a chronic autoimmune disease that can affect almost any part of the body, leading to a wide range of symptoms. - While it can cause vasculitis, its epidemiology, clinical presentation, and specific organ involvement are distinctly different from **Kawasaki disease**.
Explanation: ***First degree AV block*** - In **first-degree AV block**, every P wave is followed by a QRS complex, but the **PR interval** is consistently prolonged (usually > 0.20 seconds) [1]. - This simply indicates a **delayed conduction** through the AV node, not a missed beat or a variable PR interval [1]. *Third degree AV block* - Characterized by **complete AV dissociation**, where P waves and QRS complexes occur independently with no relationship between them. - The **PR interval is not constant** or even definable, as there is no consistent conduction from atria to ventricles. *Second degree AV block - Mobitz type I* - Also known as **Wenckebach phenomenon**, it shows a **progressive prolongation of the PR interval** until a QRS complex is dropped [1]. - Therefore, a constant PR interval is not observed; instead, it gradually lengthens over a few beats [1]. *Second degree AV block - Mobitz type II* - Involves **intermittent dropped QRS complexes** without prior PR interval prolongation [1]. - While the PR intervals of the conducted beats are constant, the **overall pattern is not one of a continuously constant PR interval** due to the dropped beats [1].
Explanation: Start dual antiplatelet therapy - For patients with **native aortic valve disease** and cerebral ischemia, **dual antiplatelet therapy** is recommended to prevent future embolic events due to the increased risk of thrombus formation on the diseased valve surface [1]. - This approach aims to reduce platelet aggregation and subsequent clot formation, which is the primary mechanism of stroke in this context [1]. *Initiate intravenous anticoagulation* - **Intravenous anticoagulation** is generally reserved for acute ischemic stroke in the setting of atrial fibrillation [1] or in very specific circumstances where there is a high suspicion of a cardioembolic source not amenable to antiplatelets, but it carries a higher risk of hemorrhagic transformation in acute stroke. - In valvular heart disease, long-term anticoagulation is typically with warfarin for mechanical valves, and not usually initiated acutely for native valve disease with stroke. *Start warfarin therapy* - **Warfarin** is indicated for long-term anticoagulation in patients with **mechanical prosthetic heart valves** or in specific cases of native valve disease with atrial fibrillation, but it is not the primary choice for acute stroke prevention in native aortic valve disease without other indications. - Starting warfarin acutely requires careful monitoring and takes several days to achieve therapeutic levels, making it unsuitable for immediate stroke prevention. *Administer one dose of low molecular weight heparin* - A **single dose of low molecular weight heparin (LMWH)** is insufficient for effective long-term stroke prevention in the context of native aortic valve disease. - LMWH may be used in specific situations like bridging before warfarin or for VTE prophylaxis, but not as a primary strategy for preventing recurrent cardioembolic stroke from native valve disease.
Explanation: ### Procainamide - While **procainamide** can be used in Wolff-Parkinson-White (WPW) syndrome for certain **pre-excited arrhythmias**, it is generally **contraindicated** if there is an **atrial fibrillation with rapid ventricular response** because it can paradoxically shorten the refractory period of the accessory pathway. - Shortening the refractory period of the accessory pathway can lead to a **faster conduction** of atrial impulses to the ventricles, potentially causing **ventricular fibrillation** and sudden cardiac death. ### Treadmill test - A **treadmill test** is a common diagnostic tool used to evaluate the presence of **ischemic heart disease** or to assess exercise-induced arrhythmias, and is not contraindicated in WPW [2]. - It can help in risk stratification in patients with WPW by assessing the **response of the accessory pathway** to exercise [2]. ### Electrophysiological studies - **Electrophysiological studies (EPS)** are not only safe but also the **gold standard** for diagnosing and risk stratifying Wolff-Parkinson-White syndrome [1]. - EPS pinpoint the location and characteristics of the **accessory pathway**, and are often performed as a precursor to **catheter ablation** [2]. ### Oral beta blocker - Beta-blockers are generally **contraindicated** in patients with **WPW syndrome** who experience **atrial fibrillation with rapid conduction** over the accessory pathway [3]. - Similar to other AV nodal blocking agents, beta-blockers can block the normal conduction pathway, leading to an **increased reliance on the accessory pathway** and potentially dangerous ventricular rates [3].
Explanation: ***cardiac tamponade*** - The combination of **elevated JVP**, **soft heart sounds**, and **pulsus paradoxus** (20 mmHg decrease in systolic BP during inspiration) constitutes **Beck's triad**, highly suggestive of cardiac tamponade [1]. - The history of a preceding **"flu-like" illness** could indicate a viral pericarditis, which can progress to pericardial effusion and tamponade [1]. *pulmonary hypertension* - While it can cause **dyspnea** and **peripheral edema**, it does not typically present with **pulsus paradoxus** or acutely develop after a flu-like illness with sharp chest pain in this manner. - Heart sounds would generally include a **loud P2** and may have a right-sided S3, not necessarily soft heart sounds. *ventricular septal defect* - A VSD is a **congenital heart defect** usually discovered earlier in life, although smaller defects can present in adulthood. - Its typical presentation involves a **pansystolic murmu**r and, if large, signs of heart failure, but not the acute constellation of symptoms suggesting tamponade. *coarctation of the aorta* - This condition is characterized by **differences in blood pressure** and pulses between the upper and lower extremities. - It would not typically cause **global heart sound softening** or the presence of **pulsus paradoxus**.
Explanation: ***Paroxysmal atrial fibrillation is associated with a similar risk of stroke as persistent atrial fibrillation*** - Both paroxysmal (intermittent) and persistent atrial fibrillation carry a **comparable risk of stroke** because the mechanisms of thrombus formation (stasis in the left atrial appendage) are the same, regardless of the arrhythmia's duration [1]. - This understanding is crucial for determining the need for **anticoagulation**, which is based on stroke risk factors, not on whether the AF is paroxysmal or persistent [1]. *Excess alcohol intake is an unlikely cause* - **Excessive alcohol intake** is a well-established risk factor and a common trigger for atrial fibrillation, often termed "holiday heart syndrome." - Alcohol can induce AF through various mechanisms, including **autonomic nervous system activation** and direct myocardial toxicity. *Cardioversion may be performed without anticoagulation if a transthoracic echocardiogram is normal* - A **transthoracic echocardiogram (TTE)** is not sufficient to rule out left atrial appendage (LAA) thrombi, as the LAA is often not well visualized by TTE [1]. - For cardioversion without prior anticoagulation, a **transesophageal echocardiogram (TEE)** is required to exclude thrombus formation in the left atrium, especially the LAA. *The risk of stroke is less than in atrial fibrillation due to rheumatic valve disease* - **Rheumatic mitral valve disease** is a significant cause of highly thrombogenic atrial fibrillation, carrying a very high risk of stroke compared to non-rheumatic AF [2]. - The presence of severe mitral stenosis or prosthetic mechanical valves generally indicates a need for **lifelong anticoagulation** due to an exceptionally high stroke risk [2].
Explanation: Focusing on the characteristics of ventricular premature beats (VPBs), the EKG typically demonstrates broad, bizarre QRS complexes with no preceding P wave [1]. ***Wide QRS complex*** - A **ventricular premature beat (VPB)** originates in the ventricles, bypassing the normal His-Purkinje system [1]. - This abnormal conduction pathway through ventricular muscle causes a **delayed and wide QRS complex** (typically > 0.12 seconds) on EKG [1]. *Narrow QRS complex* - A **narrow QRS complex** (typically < 0.12 seconds) indicates that ventricular depolarization occurred through the normal His-Purkinje system. - This is characteristic of beats originating above the ventricles, such as **supraventricular premature beats** or normal sinus beats. *Fusion beat* - A **fusion beat** occurs when a beat from the sinoatrial node (or another supraventricular source) and a ventricular beat simultaneously activate the ventricles [1]. - This results in a QRS complex that is a **hybrid** of a normal QRS and a wide, aberrant QRS, but it's not the primary characteristic of a VPB itself. *AV dissociation* - **AV dissociation** refers to the atria and ventricles beating independently [1]. - While it can be seen in various arrhythmias, including some ventricular tachycardias, it is **not a characteristic finding of an isolated ventricular premature beat**.
Explanation: ***Doppler*** - **Duplex ultrasonography** (Doppler ultrasound) is the gold standard for diagnosing DVT due to its **non-invasiveness**, high sensitivity, and specificity in visualizing blood flow and vessel compressibility [1]. - It effectively identifies thrombi in the **proximal deep veins**, which are most likely to embolize [1]. *Plethysmography* - This method measures changes in limb volume and blood flow; while useful for DVT screening, it has **lower sensitivity and specificity** compared to Doppler ultrasound, particularly for calf vein thrombosis. - It is **less commonly used as a primary diagnostic tool** due to its limitations in precisely locating and characterizing thrombi. *Venography* - Previously considered the gold standard, **contrast venography** is an invasive procedure involving injecting contrast dye into the veins to visualize thrombi. - Its use is limited by its **invasiveness**, potential for **allergic reactions**, radiation exposure, and risk of inducing phlebitis, making it secondary to Doppler [1]. *X-ray* - A plain X-ray is **not suitable for diagnosing DVT** as it cannot directly visualize blood clots within veins [2]. - It may be used to **rule out other causes of limb pain** or swelling, such as fractures or soft tissue injuries, but provides no information about venous thrombosis.
Explanation: Filling pressure is decreased. - In restrictive cardiomyopathy, the ventricles become stiff and noncompliant, impairing filling. - This leads to increased filling pressures (e.g., elevated left and right atrial pressures) as the heart attempts to fill adequately. Left ventricular hypertrophy is present. - Left ventricular hypertrophy is common in restrictive cardiomyopathy, particularly in conditions like amyloidosis and sarcoidosis, where infiltrative processes thicken the ventricular walls. - While the chambers are not dilated, the walls can be abnormally thick due to underlying pathology. In the early phase, systolic function is impaired. - In the early stages of restrictive cardiomyopathy, systolic function is typically preserved. The primary defect is diastolic dysfunction—impaired ventricular filling. - Systolic dysfunction may develop in later stages as the underlying disease progresses or due to severe volume overload. Heart failure is predominantly right-sided. - Right-sided heart failure symptoms (e.g., peripheral edema, ascites, jugular venous distension) are often prominent in restrictive cardiomyopathy. - Due to the rigid and non-compliant ventricles inhibiting filling, both ventricles are affected, but systemic venous congestion often dominates the clinical picture.
Explanation: **Brought on by walking and relieved by rest.** - **Intermittent claudication** is classically described as muscle pain or cramping in the lower extremities that is **triggered by exercise** (e.g., walking) and consistently **relieved by rest** within a few minutes [1]. - This pattern occurs due to an imbalance between the oxygen supply (limited by **atherosclerotic** narrowing of arteries) and the metabolic demand of the exercising muscles [1]. *Can occur after a few steps.* - While the pain can indeed occur after a few steps in severe cases, this statement alone does not fully define the **characteristic pattern** of intermittent claudication, which crucially includes relief with rest. - The distance at which pain occurs (claudication distance) varies with the severity of the **peripheral artery disease** [1]. *Relieved by standing still.* - For intermittent claudication, it is the cessation of muscle activity (rest), not just standing still, that provides relief. For example, a patient may stand still and still experience pain if the muscle demand has not sufficiently decreased. - Pain relief by standing still is more characteristic of **neurogenic claudication**, such as that caused by **spinal stenosis**, where positional changes can alleviate nerve compression.
Coronary Artery Disease and Angina
Practice Questions
Acute Coronary Syndromes
Practice Questions
Heart Failure
Practice Questions
Cardiac Arrhythmias
Practice Questions
Valvular Heart Diseases
Practice Questions
Cardiomyopathies
Practice Questions
Pericardial Diseases
Practice Questions
Congenital Heart Disease in Adults
Practice Questions
Hypertension and Hypertensive Emergencies
Practice Questions
Pulmonary Hypertension
Practice Questions
Non-invasive Cardiac Diagnostics
Practice Questions
Preventive Cardiology
Practice Questions
Get full access to all questions, explanations, and performance tracking.
Start For Free