The classic ECG features of atrial fibrillation include an irregularly irregular rhythm, the absence of p-waves, an irregular ventricular rate, and the presence of fibrillation waves. This irregular rhythm occurs because the atrial impulses are filtered out by the AV node.

In addition, Ashman beats may be observed in atrial fibrillation. These beats are characterized by wide complex QRS complexes, often with a morphology resembling right bundle branch block. They occur after a short R-R interval that is preceded by a prolonged R-R interval. Fortunately, Ashman beats are generally considered harmless.

The disorganized electrical activity in atrial fibrillation typically originates at the root of the pulmonary veins.

The second heart sound (S2) is created by vibrations produced when the aortic and pulmonary valves close. It marks the end of systole. It is normal to hear a split in the sound during inspiration.

A loud S2 can be associated with certain conditions such as systemic hypertension (resulting in a loud A2), pulmonary hypertension (resulting in a loud P2), hyperdynamic states (like tachycardia, fever, or thyrotoxicosis), and atrial septal defect (which causes a loud P2).

On the other hand, a soft S2 can be linked to decreased aortic diastolic pressure (as seen in aortic regurgitation), poorly mobile cusps (such as calcification of the aortic valve), aortic root dilatation, and pulmonary stenosis (which causes a soft P2).

A widely split S2 can occur during deep inspiration, right bundle branch block, prolonged right ventricular systole (seen in conditions like pulmonary stenosis or pulmonary embolism), and severe mitral regurgitation. However, in the case of atrial septal defect, the splitting is fixed and does not vary with respiration.

Reversed splitting of S2, where P2 occurs before A2 (paradoxical splitting), can occur during deep expiration, left bundle branch block, prolonged left ventricular systole (as seen in hypertrophic cardiomyopathy), severe aortic stenosis, and right ventricular pacing.

Aortic sclerosis is a condition that occurs when the aortic valve undergoes senile degeneration. Unlike aortic stenosis, it does not result in any obstruction of the left ventricular outflow tract. To differentiate between aortic stenosis and aortic sclerosis, the following can be used:

Feature: Aortic stenosis
– Symptoms: Can be asymptomatic, but may cause angina, breathlessness, and syncope if severe.
– Pulse: Slow rising, low volume pulse.
– Apex beat: Sustained, heaving apex beat.
– Thrill: Palpable thrill in the aortic area can be felt.
– Murmur: Ejection systolic murmur loudest in the aortic area.
– Radiation: Radiates to carotids.

Feature: Aortic sclerosis
– Symptoms: Always asymptomatic.
– Pulse: Normal pulse character.
– Apex beat: Normal apex beat.
– Thrill: No thrill.
– Murmur: Ejection systolic murmur loudest in the aortic area.
– Radiation: No radiation.

Adrenaline should be administered promptly once access to the circulatory system has been established in cases of non-shockable cardiac arrests such as PEA or asystole. The recommended dose is 1 mg, which can be given either as 10 mL of a 1:10,000 solution or as 1 mL of a 1:1000 solution through the intravenous (IV) or intraosseous (IO) routes.

In cases of shockable cardiac arrests like ventricular fibrillation (Vf) or pulseless ventricular tachycardia (pVT), adrenaline should be administered after the third shock has been delivered and chest compressions have been resumed. The same dose of 1 mg can be given using the same concentration options as mentioned earlier.

Subsequently, adrenaline should be administered every 3-5 minutes, alternating with chest compressions, without interrupting the compressions. The alpha-adrenergic effects of adrenaline cause constriction of blood vessels throughout the body, leading to increased pressures in the coronary and cerebral circulation.

The beta-adrenergic effects of adrenaline have positive effects on the heart, increasing its contractility (inotropic) and heart rate (chronotropic), which may also enhance blood flow to the coronary and cerebral arteries. However, it is important to note that these benefits may be counteracted by increased oxygen consumption by the heart, the potential for abnormal heart rhythms, temporary decrease in oxygen levels due to abnormal blood flow in the lungs, impaired microcirculation, and increased dysfunction of the heart after the cardiac arrest.

While there is no evidence supporting the long-term benefits of adrenaline use in cardiac arrest cases, some studies have shown improved short-term survival rates, which justifies its continued use.

The ECG shows the following findings:
– There is ST depression in leads V1-V4 and aVR.
– There is ST elevation in leads V5-V6, II, III, and aVF.
– There is a positive R wave in leads V1 and V2, which indicates a reverse Q wave.
These ECG changes indicate that there is an acute inferoposterior myocardial infarction.

Distinguishing between unstable angina and other acute coronary syndromes can be determined by normal troponin results. Unstable angina is characterized by new onset angina or a sudden worsening of previously stable angina, often occurring at rest. This condition typically requires hospital admission. On the other hand, stable angina is predictable and occurs during physical exertion or emotional stress, lasting for a short duration of no more than 10 minutes and relieved within minutes of rest or sublingual nitrates.

To diagnose unstable angina, it is crucial to consider the nature of the chest pain and negative cardiac enzyme testing. The presence or absence of chest pain at rest and the response to rest and treatment with GTN are the most useful descriptors in distinguishing between stable and unstable angina. It is important to note that patients with unstable angina may not exhibit any changes on an electrocardiogram (ECG).

If troponin results are abnormal, it indicates a myocardial infarction rather than unstable angina.

Further Reading:

Acute Coronary Syndromes (ACS) is a term used to describe a group of conditions that involve the sudden reduction or blockage of blood flow to the heart. This can lead to a heart attack or unstable angina. ACS includes ST segment elevation myocardial infarction (STEMI), non-ST segment elevation myocardial infarction (NSTEMI), and unstable angina (UA).

The development of ACS is usually seen in patients who already have underlying coronary heart disease. This disease is characterized by the buildup of fatty plaques in the walls of the coronary arteries, which can gradually narrow the arteries and reduce blood flow to the heart. This can cause chest pain, known as angina, during physical exertion. In some cases, the fatty plaques can rupture, leading to a complete blockage of the artery and a heart attack.

There are both non modifiable and modifiable risk factors for ACS. non modifiable risk factors include increasing age, male gender, and family history. Modifiable risk factors include smoking, diabetes mellitus, hypertension, hypercholesterolemia, and obesity.

The symptoms of ACS typically include chest pain, which is often described as a heavy or constricting sensation in the central or left side of the chest. The pain may also radiate to the jaw or left arm. Other symptoms can include shortness of breath, sweating, and nausea/vomiting. However, it’s important to note that some patients, especially diabetics or the elderly, may not experience chest pain.

The diagnosis of ACS is typically made based on the patient’s history, electrocardiogram (ECG), and blood tests for cardiac enzymes, specifically troponin. The ECG can show changes consistent with a heart attack, such as ST segment elevation or depression, T wave inversion, or the presence of a new left bundle branch block. Elevated troponin levels confirm the diagnosis of a heart attack.

The management of ACS depends on the specific condition and the patient’s risk factors. For STEMI, immediate coronary reperfusion therapy, either through primary percutaneous coronary intervention (PCI) or fibrinolysis, is recommended. In addition to aspirin, a second antiplatelet agent is usually given. For NSTEMI or unstable angina, the treatment approach may involve reperfusion therapy or medical management, depending on the patient’s risk of future cardiovascular events.

An abnormal QTc, which is the measurement of the time it takes for the heart to recharge between beats, is generally considered to be greater than 450 ms in males. However, some sources may use a cutoff of greater than 440 ms as abnormal in males. To further categorize the QTc, a measurement of 430ms or less is considered normal, 431-450 ms is borderline, and 450 ms or more is considered abnormal in males. Females typically have a longer QTc, so the categories for them are often quoted as less than 450 ms being normal, 451-470 ms being borderline, and greater than 470ms being abnormal.

Further Reading:

Long QT syndrome (LQTS) is a condition characterized by a prolonged QT interval on an electrocardiogram (ECG), which represents abnormal repolarization of the heart. LQTS can be either acquired or congenital. Congenital LQTS is typically caused by gene abnormalities that affect ion channels responsible for potassium or sodium flow in the heart. There are 15 identified genes associated with congenital LQTS, with three genes accounting for the majority of cases. Acquired LQTS can be caused by various factors such as certain medications, electrolyte imbalances, hypothermia, hypothyroidism, and bradycardia from other causes.

The normal QTc values, which represent the corrected QT interval for heart rate, are typically less than 450 ms for men and less than 460ms for women. Prolonged QTc intervals are considered to be greater than these values. It is important to be aware of drugs that can cause QT prolongation, as this can lead to potentially fatal arrhythmias. Some commonly used drugs that can cause QT prolongation include antimicrobials, antiarrhythmics, antipsychotics, antidepressants, antiemetics, and others.

Management of long QT syndrome involves addressing any underlying causes and using beta blockers. In some cases, an implantable cardiac defibrillator (ICD) may be recommended for patients who have experienced recurrent arrhythmic syncope, documented torsades de pointes, previous ventricular tachyarrhythmias or torsades de pointes, previous cardiac arrest, or persistent syncope. Permanent pacing may be used in patients with bradycardia or atrioventricular nodal block and prolonged QT. Mexiletine is a treatment option for those with LQT3. Cervicothoracic sympathetic denervation may be considered in patients with recurrent syncope despite beta-blockade or in those who are not ideal candidates for an ICD. The specific treatment options for LQTS depend on the type and severity of the condition.

Prinzmetal angina is a rare form of angina that typically occurs during periods of rest, specifically between midnight and early morning. The attacks can be severe and happen in clusters. This condition is caused by spasms in the coronary arteries, even though patients may have normal arteries. The main treatment options for controlling these spasms are calcium-channel blockers and nitrates. The spasms often follow a cyclical pattern and may disappear after a few months, only to reappear later on.

Unstable angina may present similarly to Prinzmetal angina, but it does not exclusively occur at night and the exercise tolerance test results are typically abnormal.

Decubitus angina, on the other hand, is angina that occurs when lying down. It is often a result of cardiac failure caused by increased intravascular volume, which puts extra strain on the heart.

Takotsubo cardiomyopathy, also known as acute stress cardiomyopathy, can present in a manner similar to an acute myocardial infarction. The cause of this condition is unknown, but it tends to occur in individuals who have recently experienced significant emotional or physical stress. The term Takotsubo refers to the shape the left ventricle takes on, resembling an octopus pot with a narrow neck and round bottom. ECGs often show characteristic changes, such as ST-elevation, but subsequent angiograms reveal normal coronary arteries. The diagnosis is confirmed when the angiogram shows the distinctive octopus pot shape of the left ventricle.

There is no indication of a psychogenic cause in this particular case.

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.

Wolff-Parkinson-White (WPW) syndrome is a condition that affects the electrical system of the heart. It occurs when there is an abnormal pathway, known as the bundle of Kent, between the atria and the ventricles. This pathway can cause premature contractions of the ventricles, leading to a type of rapid heartbeat called atrioventricular re-entrant tachycardia (AVRT).

In a normal heart rhythm, the electrical signals travel through the bundle of Kent and stimulate the ventricles. However, in WPW syndrome, these signals can cause the ventricles to contract prematurely. This can be seen on an electrocardiogram (ECG) as a shortened PR interval, a slurring of the initial rise in the QRS complex (known as a delta wave), and a widening of the QRS complex.

There are two distinct types of WPW syndrome that can be identified on an ECG. Type A is characterized by predominantly positive delta waves and QRS complexes in the praecordial leads, with a dominant R wave in V1. This can sometimes be mistaken for right bundle branch block (RBBB). Type B, on the other hand, shows predominantly negative delta waves and QRS complexes in leads V1 and V2, and positive in the other praecordial leads, resembling left bundle branch block (LBBB).

Overall, WPW syndrome is a condition that affects the electrical conduction system of the heart, leading to abnormal heart rhythms. It can be identified on an ECG by specific features such as shortened PR interval, delta waves, and widened QRS complex.