Sample ECGs and Quizzes – Oxford Medical Education (2023)

Presentation:

Diagnose:

This EKG shows atrial fibrillation (AF) with a rapid ventricular response. With this history, the underlying diagnosis would be consistent with Holiday Heart Syndrome.

Presentation:

Diagnose:

This is atrial flutter. The atria contract at 300 beats per minute, resulting in a "seesaw" baseline. Pulses are delivered with 2:1, 3:1, or 4:1 block resulting in ventricular rates of 150, 100, and 75 beats per minute, respectively.

Presentation:

Diagnose:

This is polymorphic atrial tachycardia. It occurs in respiratory diseases and reflects an abnormal focus of atrial stimulation. The morphology of the p waves is therefore variable, but all p waves are transmitted through the bundle of His and therefore the QRS complexes are all the same.

We will not go through the EKG as the most important information is contained in the medical history.

This is pulseless electrical activity (PEA). It is the most extreme example of why you should look at the patient in conjunction with the EKG! There are no specific ECG changes in PEA—the important thing is to recognize that this patient is in cardiac arrest and start chest compressionsExtended Life Support (ALS)immediately.

However, the EKG can help you identify the underlying pathology. In this case, there are low-voltage QRS complexes, which may simply be due to a large physical habit or indicate pathology that "disrupts" the signal between the heart and the lead. This may be pericardial fluid or pneumothorax. This is worth considering, given that both tamponade and tension pneumothorax are reversible causes of PEA.

Presentation:

Diagnose:

This is a normal EKG. There are many variations of the normal state and it is worth looking at as many EKGs as possible to familiarize yourself with the most common variations. It is important to remember that a very ill patient may have a normal ECG. So always use all the information available to you and don't just rely on the EKG.

Presentation:

Diagnose:

This is ventricular tachycardia (VT). In this case, the patient is in cardiac arrest due to the lack of a central pulse. He should be treated according to ALS guidelines, starting chest compressions immediately. This is a shocking rate and should be treated with the ALS algorithm with DC cardioversion and adrenaline.

If the patient were conscious, the ALS algorithm would not be needed and treatment would depend on symptoms. In case of acute symptoms, urgent DC cardioversion is indicated. If there were no absorption symptoms (eg, shortness of breath, chest pain, shock, confusion, syncope), it could initially be treated with medication.

Presentation:

Diagnose:

History suggests sinus tachycardia secondary to stress. However, the sinus rhythm rarely exceeds 120 BPM, and in this case P waves are not visible. It is therefore a crossed supraventricular tachycardia (SVT): a narrow complex tachycardia originating from the AV node. Treatment involves vagal maneuvers followed by adenosine.

Atrial flutter would be a reasonable differential as the rate is normal and close to 150. However, there is no baseline variation and no evidence of a sawtooth, making this less likely than SVT.

Presentation:

Diagnose:

The EKG initially shows a low-grade STEMI, which then progresses to ventricular fibrillation (VF). The breaths described are struggling breaths—this does not represent normal respiratory effort, and CPR should be started immediately for cardiac arrest.

Remember: Always start CPR on a collapse with irregular breathing and no central pulse.

Presentation:

Diagnose:

This is sinus bradycardia. In a young, healthy person, this value may be normal. However, in the context of an elderly person with collapse, this should be further investigated. A medication review, blood tests including thyroid function, repeat EKGs, chest x-rays, echocardiograms, and 24-hour films would be reasonable first-line investigations.

Presentation:

Diagnose:

This patient has ST elevation in the anterior and lateral leads. So it is an anterolateral ST-elevation myocardial infarction (STEMI). This dramatic ST elevation is also known as "tombstone" ST elevation, both because of its resemblance to a tombstone and because of the poor prognosis without early intervention.

This patient should be urgently evaluated for STEMI and treated, ideally with primary angioplasty (primary coronary intervention: PCI). Early treatment also includes aspirin, clopidogrel, heparin, nitrites, morphine, and controlled oxygen.

Presentation:

Diagnose:

This is the classic sinusoidal ECG pattern of severe hyperkalemia. Ventricular fibrillation (VF) can develop quickly. There are three main EKG changes in hyperkalemia:

1. In the early stages, you may only see stage or peak T wave levels.

2. Later changes include shortening of the p-wave height and prolongation of the PR interval as conduction through the atrial myocardium slows.

3. This is later accompanied by widening of the QRS and fusion of the QRS complex and the T wave. This pattern eventually degrades to the sine wave pattern shown above.

This is a medical emergency. Treatment is with 10 mL of 10% calcium gluconate to protect the heart, followed by 10 units of rapid-acting insulin (with 50 mL of 50% dextrose) to transport potassium into the intracellular space. Inhaled salbutamol has a similar effect when an IV line is not available. bicarbonate 50 ml i.v. can also be administered. Eventually, the total level of potassium in the body must be reduced - in this case, emergency hemodialysis or hemofiltration is indicated.

Presentation:

Diagnose:

On first examination it looks like an inferior lateral NSTEMI. There is (we assume there is a new) T-wave inversion in consecutive leads matching an anatomic region (inferior lateral) and most importantly, persistent ischemic chest pain caused by GTN is not relieved. However, note ST elevation in aVR. Therefore, this probably indicates a critical closure of the left main trunk. This ECG should therefore be discussed with the cardiologist in anticipation of urgent PCI.

Presentation:

Diagnose:

This picture of a shortened PR interval and a blurred QRS upward motion - also known as a "delta wave" - ​​is characteristic of Wolff-Parkinson-White (WPW) syndrome. These changes represent transmission via an accessory pathway. The history of collapse in this case is worrisome as these episodes may be due to recurrent tachycardias, which can be fatal. Other features not seen here that may be present in WPW include a dominant R wave in V1 and a T wave inversion in the anterior chest leads.

Another example to illustrate the delta wave is shown below:

Presentation:

Diagnose:

No, it's definitely not normal. This ECG is characteristic of Brugada syndrome (type 1). There is ST elevation > 2 mm in leads V1–V3, T waves are inverted, and the ST segment has a characteristic “bulging” shape. This condition carries a high risk of sudden death from ventricular fibrillation (VF). Treatment is with an implantable cardioverter defibrillator (ICD).

Presentation:

Diagnose:

It is an acute posterior myocardial infarction. What we see in the front cables is the equivalent of an "inverted" ST lift. Imagine turning the EKG paper over and looking at it from behind, or seeing the EKG in a mirror held at the bottom end. You would see ST elevation (deep ST depression reversed) and T wave inversion (upright T waves that look upside down) and this represents what is happening in the back area of ​​the heart. Another clue is the bradycardia seen in this case: the vessels that supply the back of the heart also supply the 'pacemaker' area of ​​the SA node.

Presentation:

Diagnose:

The diagnosis is pericarditis. Pericarditis often occurs in young people after a history of viral disease. This shows the characteristic, widespread, saddle-shaped ST elevation and PR depression.

Presentation:

Diagnose:

This EKG shows ST elevation at the bottom of the heart. This patient should be urgently evaluated for STEMI and treated, ideally with primary angioplasty. Early treatment also includes aspirin, clopidogrel, heparin, nitrites, morphine, and controlled oxygen.

Presentation:

Diagnose:

Based on the history, physical examination, and ECG findings, pulmonary embolism (PE) is the most likely diagnosis. In the case of PE, the ECG finding constellation "S1Q3T3" is traditionally described. It is associated with a deep S wave in lead I, a pathologic Q wave in lead III, and an inverted T wave in V3 (and other anterior leads). But while it may be a classic, it is extremely rare in clinical practice! The most frequently observed ECG abnormality in PE is sinus tachycardia. There may also be an RSB or RV stretching pattern with T wave inversion in V1 to V4.

Presentation:

Diagnose:

This patient is hypothermic. The positive excursion after the QRS but before the T wave is an Osbourne J wave. These can also be seen in subarachnoid hemorrhage (SAH) and hypercalcemia. Typically, a hypothermic patient has bradycardia and their EKG shows J waves. In this case, treatment would be with gentle rewarming unless there is an immediate threat to life due to a cardiac arrhythmia.

Presentation:

Diagnose:

This EKG shows changes consistent with hypokalemia. This was probably caused by the new loop diuretic. Also note that furosemide is not a first-line drug for high blood pressure.

Classically, hypokalemia results in T wave flattening with ST depression. In severe cases, a U wave may occur. This is a positive excursion that follows the T wave but precedes the P wave. These are seen in hypokalemia, but also in hypercalcemia and thyrotoxicosis.

Presentation:

Diagnose:

The diagnosis is a tricyclic overdose of antidepressants. This leads to widening of the QRS complex and prolongation of the QT interval due to blockade of sodium channels.

• A, B, C, D, E (venting may be required)
  • blood values, including paracetamol levels. ABG (probable metabolic acidosis)
• Activated charcoal if within 8 hours of ingestion
• Sodium bicarbonate (50 ml 8.4%)
  • Indicate if there is an arrhythmia or QRS > 110
• More options:
  • For ventricular tachycardia: lignocaine (avoid beta-blockers, amiodarone, and calcium channel blockers)
  • For seizures: benzodiazepines

Presentation:

Diagnose:

This is a difficult case and shows trajectories of polymorphic VT or torsades de pointes (literally translated as twisting of the points). It can have a variety of causes, including medications (especially psychotropics) and an electrolyte imbalance. In principle, any cause of a long QT interval can cause polymorphic tachycardia.

Treatment initially consists of magnesium 2 g IV, regardless of serum magnesium concentration, before treating another cause of long QT.

Presentation:

Diagnose:

This patient has a prolonged QT interval and the cause should be sought. In this case, drugs are likely to be the cause: both clarithromycin and the antihistamine diphenhydramine can prolong the QT interval.

The normal QT length varies with heart rate and there is a formula that can be used to correct it. ECG devices automatically give you this "corrected QT" (QTc). Normal QTc is generally less than 480 ms. As a rule of thumb, if the end of the QT interval is more than halfway to the next QRS interval, consider a long QT interval.