Pericardial friction rub is a common finding in pericarditis and is often described as a sound similar to squeaking leather. This patient exhibits symptoms that are consistent with acute pericarditis, including flu-like illness with muscle pain and fatigue, chest pain that worsens when lying down and improves when sitting up or leaning forward, and the presence of a pleural rub. The gradual onset of symptoms rules out conditions like pulmonary embolism or acute myocardial ischemia. It is important to note that while the pericardial rub is often considered part of the classic triad of clinical features, it is only present in about one-third of patients. Additionally, the rub may come and go, so repeated examinations may increase the chances of detecting this sign.

Further Reading:

Pericarditis is an inflammation of the pericardium, which is the protective sac around the heart. It can be acute, lasting less than 6 weeks, and may present with chest pain, cough, dyspnea, flu-like symptoms, and a pericardial rub. The most common causes of pericarditis include viral infections, tuberculosis, bacterial infections, uremia, trauma, and autoimmune diseases. However, in many cases, the cause remains unknown. Diagnosis is based on clinical features, such as chest pain, pericardial friction rub, and electrocardiographic changes. Treatment involves symptom relief with nonsteroidal anti-inflammatory drugs (NSAIDs), and patients should avoid strenuous activity until symptoms improve. Complicated cases may require treatment for the underlying cause, and large pericardial effusions may need urgent drainage. In cases of purulent effusions, antibiotic therapy is necessary, and steroid therapy may be considered for pericarditis related to autoimmune disorders or if NSAIDs alone are ineffective.

The timing of the initial rise, peak, and return to normality of various cardiac enzymes can serve as a helpful guide. Creatine kinase, the main cardiac isoenzyme, typically experiences an initial rise within 4-8 hours, reaches its peak at 18 hours, and returns to normal within 2-3 days. Myoglobin, which lacks specificity due to its association with skeletal muscle damage, shows an initial rise within 1-4 hours, peaks at 6-7 hours, and returns to normal within 24 hours. Troponin I, known for its sensitivity and specificity, exhibits an initial rise within 3-12 hours, reaches its peak at 24 hours, and returns to normal within 3-10 days. HFABP, or heart fatty acid binding protein, experiences an initial rise within 1.5 hours, peaks at 5-10 hours, and returns to normal within 24 hours. Lastly, LDH, predominantly found in cardiac muscle, shows an initial rise at 10 hours, peaks at 24-48 hours, and returns to normal within 14 days.

Orthostatic hypotension is a condition where patients feel lightheaded and may experience tunnel vision when they stand up from a lying down position. These symptoms are often worse in the morning. The patient’s history of recurrent episodes after being in a supine position for a long time strongly suggests orthostatic hypotension. There are no signs of epilepsy, such as deja-vu or jambs vu prodrome, tongue biting, loss of bladder or bowel control, or postictal confusion. The normal ECG and consistent timing of symptoms make postural orthostatic tachycardia syndrome (PAF) less likely. There are no neurological deficits to suggest a transient ischemic attack (TIA). The prodromal symptoms, such as tunnel vision and lightheadedness, align more with orthostatic hypotension rather than vasovagal syncope, which typically occurs after long periods of standing and is characterized by feeling hot and sweaty. Although carotid sinus syndrome could be considered as a differential diagnosis, as the patient’s head turning on getting out of bed may trigger symptoms, it is not one of the options.

Further Reading:

Blackouts, also known as syncope, are defined as a spontaneous transient loss of consciousness with complete recovery. They are most commonly caused by transient inadequate cerebral blood flow, although epileptic seizures can also result in blackouts. There are several different causes of blackouts, including neurally-mediated reflex syncope (such as vasovagal syncope or fainting), orthostatic hypotension (a drop in blood pressure upon standing), cardiovascular abnormalities, and epilepsy.

When evaluating a patient with blackouts, several key investigations should be performed. These include an electrocardiogram (ECG), heart auscultation, neurological examination, vital signs assessment, lying and standing blood pressure measurements, and blood tests such as a full blood count and glucose level. Additional investigations may be necessary depending on the suspected cause, such as ultrasound or CT scans for aortic dissection or other abdominal and thoracic pathology, chest X-ray for heart failure or pneumothorax, and CT pulmonary angiography for pulmonary embolism.

During the assessment, it is important to screen for red flags and signs of any underlying serious life-threatening condition. Red flags for blackouts include ECG abnormalities, clinical signs of heart failure, a heart murmur, blackouts occurring during exertion, a family history of sudden cardiac death at a young age, an inherited cardiac condition, new or unexplained breathlessness, and blackouts in individuals over the age of 65 without a prodrome. These red flags indicate the need for urgent assessment by an appropriate specialist.

There are several serious conditions that may be suggested by certain features. For example, myocardial infarction or ischemia may be indicated by a history of coronary artery disease, preceding chest pain, and ECG signs such as ST elevation or arrhythmia. Pulmonary embolism may be suggested by dizziness, acute shortness of breath, pleuritic chest pain, and risk factors for venous thromboembolism. Aortic dissection may be indicated by chest and back pain, abnormal ECG findings, and signs of cardiac tamponade include low systolic blood pressure, elevated jugular venous pressure, and muffled heart sounds. Other conditions that may cause blackouts include severe hypoglycemia, Addisonian crisis, and electrolyte abnormalities.

Hypothermia can cause various changes in an electrocardiogram (ECG). These changes include a slower heart rate (bradycardia), the presence of Osborn Waves (also known as J waves), a prolonged PR interval, a widened QRS complex, and a prolonged QT interval. Additionally, the ECG may show artifacts caused by shivering, as well as the presence of ventricular ectopics. In severe cases, hypothermia can lead to cardiac arrest, which may manifest as ventricular tachycardia (VT), ventricular fibrillation (VF), or asystole.

Further Reading:

Hypothermia is defined as a core temperature below 35ºC and can be graded as mild, moderate, severe, or profound based on the core temperature. When the core temperature drops, the basal metabolic rate decreases and cell signaling between neurons decreases, leading to reduced tissue perfusion. This can result in decreased myocardial contractility, vasoconstriction, ventilation-perfusion mismatch, and increased blood viscosity. Symptoms of hypothermia progress as the core temperature drops, starting with compensatory increases in heart rate and shivering, and eventually leading to bradyarrhythmias, prolonged PR, QRS, and QT intervals, and cardiac arrest.

In the management of hypothermic cardiac arrest, ALS should be initiated with some modifications. The pulse check during CPR should be prolonged to 1 minute due to difficulty in obtaining a pulse. Rewarming the patient is important, and mechanical ventilation may be necessary due to stiffness of the chest wall. Drug metabolism is slowed in hypothermic patients, so dosing of drugs should be adjusted or withheld. Electrolyte disturbances are common in hypothermic patients and should be corrected.

Frostbite refers to a freezing injury to human tissue and occurs when tissue temperature drops below 0ºC. It can be classified as superficial or deep, with superficial frostbite affecting the skin and subcutaneous tissues, and deep frostbite affecting bones, joints, and tendons. Frostbite can be classified from 1st to 4th degree based on the severity of the injury. Risk factors for frostbite include environmental factors such as cold weather exposure and medical factors such as peripheral vascular disease and diabetes.

Signs and symptoms of frostbite include skin changes, cold sensation or firmness to the affected area, stinging, burning, or numbness, clumsiness of the affected extremity, and excessive sweating, hyperemia, and tissue gangrene. Frostbite is diagnosed clinically and imaging may be used in some cases to assess perfusion or visualize occluded vessels. Management involves moving the patient to a warm environment, removing wet clothing, and rapidly rewarming the affected tissue. Analgesia should be given as reperfusion is painful, and blisters should be de-roofed and aloe vera applied. Compartment syndrome is a risk and should be monitored for. Severe cases may require surgical debridement of amputation.

Lown-Ganong-Levine (LGL) syndrome is a condition that affects the electrical conducting system of the heart. It is classified as a pre-excitation syndrome, similar to the more well-known Wolff-Parkinson-White (WPW) syndrome. However, unlike WPW syndrome, LGL syndrome does not involve an accessory pathway for conduction. Instead, it is believed that there may be accessory fibers present that bypass all or part of the atrioventricular node.

When looking at an electrocardiogram (ECG) of a patient with LGL syndrome in sinus rhythm, there are several characteristic features to observe. The PR interval, which represents the time it takes for the electrical signal to travel from the atria to the ventricles, is typically shortened and measures less than 120 milliseconds. The QRS duration, which represents the time it takes for the ventricles to contract, is normal. The P wave, which represents the electrical activity of the atria, may be normal or inverted. However, what distinguishes LGL syndrome from other pre-excitation syndromes is the absence of a delta wave, which is a slurring of the initial rise in the QRS complex.

It is important to note that LGL syndrome predisposes individuals to paroxysmal supraventricular tachycardia (SVT), a rapid heart rhythm that originates above the ventricles. However, it does not increase the risk of developing atrial fibrillation or flutter, which are other types of abnormal heart rhythms.

This patient is likely experiencing an acute coronary syndrome, possibly a non-ST-elevation myocardial infarction (NSTEMI) or unstable angina. The troponin test will help confirm the diagnosis. The patient’s ECG showed ST depression in the inferior leads, but this normalized after treatment with GTN and morphine, ruling out a ST-elevation myocardial infarction (STEMI).

Immediate pain relief should be provided. GTN (sublingual or buccal) can be used, but intravenous opioids like morphine should be considered, especially if a heart attack is suspected.

Aspirin should be given to all patients with unstable angina or NSTEMI as soon as possible and continued indefinitely, unless there are contraindications like bleeding risk or aspirin hypersensitivity. A loading dose of 300 mg should be administered right after presentation.

Fondaparinux should be given to patients without a high bleeding risk, unless coronary angiography is planned within 24 hours of admission. Unfractionated heparin can be an alternative to fondaparinux for patients who will undergo coronary angiography within 24 hours. For patients with significant renal impairment, unfractionated heparin can also be considered, with dose adjustment based on clotting function monitoring.

Routine administration of oxygen is no longer recommended, but oxygen saturation should be monitored using pulse oximetry as soon as possible, preferably before hospital admission. Supplemental oxygen should only be offered to individuals with oxygen saturation (SpO2) below 94% who are not at risk of hypercapnic respiratory failure, aiming for a SpO2 of 94-98%. For individuals with chronic obstructive pulmonary disease at risk of hypercapnic respiratory failure, a target SpO2 of 88-92% should be achieved until blood gas analysis is available.

Bivalirudin, a specific and reversible direct thrombin inhibitor (DTI), is recommended by NICE as a possible treatment for adults with STEMI undergoing percutaneous coronary intervention.

For more information, refer to the NICE guidelines on the assessment and diagnosis of chest pain of recent onset.

Adenosine is given through a rapid IV bolus, followed by a flush of saline solution. In adults, the starting dose is 6 mg, and if needed, an additional dose of 12 mg is given. If necessary, another dose of either 12 mg or 18 mg can be administered at intervals of 1-2 minutes until the desired effect is observed.

It is important to note that the latest ALS guidelines recommend an 18 mg dose for the third administration, while the BNF/NICE guidelines suggest a 12 mg dose.

However, patients who have undergone a heart transplant are particularly sensitive to the effects of adenosine. Therefore, their initial dose should be reduced to 3 mg, followed by 6 mg, and then 12 mg.

Amiodarone is recommended to be administered after the third shock in a shockable cardiac arrest (Vf/pVT) while performing chest compressions. The prescribed dose is 300 mg, which should be given as an intravenous bolus. To ensure proper administration, the medication should be diluted in 20 mL of 5% dextrose solution.

In cases where VF/pVT continues after five defibrillation attempts, an additional dose of 150 mg of Amiodarone should be administered. It is important to note that Amiodarone is not suitable for treating PEA or asystole, and its use is specifically indicated for shockable cardiac arrest situations.

To manage aortic dissection, it is important to lower the systolic blood pressure to a range of 100-120 mmHg. This helps decrease the strain on the damaged artery and minimizes the chances of the dissection spreading further. In this patient, symptoms such as tearing chest pain and a widened mediastinum on the chest X-ray are consistent with aortic dissection.

Further Reading:

Aortic dissection is a life-threatening condition in which blood flows through a tear in the innermost layer of the aorta, creating a false lumen. Prompt treatment is necessary as the mortality rate increases by 1-2% per hour. There are different classifications of aortic dissection, with the majority of cases being proximal. Risk factors for aortic dissection include hypertension, atherosclerosis, connective tissue disorders, family history, and certain medical procedures.

The presentation of aortic dissection typically includes sudden onset sharp chest pain, often described as tearing or ripping. Back pain and abdominal pain are also common, and the pain may radiate to the neck and arms. The clinical picture can vary depending on which aortic branches are affected, and complications such as organ ischemia, limb ischemia, stroke, myocardial infarction, and cardiac tamponade may occur. Common signs and symptoms include a blood pressure differential between limbs, pulse deficit, and a diastolic murmur.

Various investigations can be done to diagnose aortic dissection, including ECG, CXR, and CT with arterial contrast enhancement (CTA). CT is the investigation of choice due to its accuracy in diagnosis and classification. Other imaging techniques such as transoesophageal echocardiography (TOE), magnetic resonance imaging/angiography (MRI/MRA), and digital subtraction angiography (DSA) are less commonly used.

Management of aortic dissection involves pain relief, resuscitation measures, blood pressure control, and referral to a vascular or cardiothoracic team. Opioid analgesia should be given for pain relief, and resuscitation measures such as high flow oxygen and large bore IV access should be performed. Blood pressure control is crucial, and medications such as labetalol may be used to reduce systolic blood pressure. Hypotension carries a poor prognosis and may require careful fluid resuscitation. Treatment options depend on the type of dissection, with type A dissections typically requiring urgent surgery and type B dissections managed by thoracic endovascular aortic repair (TEVAR) and blood pressure control optimization.

In order to gain a comprehensive understanding of AF management, it is crucial to familiarize oneself with the terminology used to describe its various subtypes. These terms help categorize different episodes of AF based on their characteristics and outcomes.

Acute AF refers to any episode that occurs within the previous 48 hours. It can manifest with or without symptoms and may or may not recur. On the other hand, paroxysmal AF describes episodes that spontaneously end within 7 days, typically within 48 hours. While these episodes are often recurrent, they can progress into a sustained form of AF.

Recurrent AF is defined as experiencing two or more episodes of AF. If the episodes self-terminate, they are classified as paroxysmal AF. However, if the episodes do not self-terminate, they are categorized as persistent AF. Persistent AF lasts longer than 7 days or has occurred after a previous cardioversion. To terminate persistent AF, electrical or pharmacological intervention is required. In some cases, persistent AF can progress into permanent AF.

Permanent AF, also known as Accepted AF, refers to episodes that cannot be successfully terminated, have relapsed after termination, or where cardioversion is not pursued. This subtype signifies a more chronic and ongoing form of AF.

By understanding and utilizing these terms, healthcare professionals can effectively communicate and manage the different subtypes of AF.