ECG Master Course - Read and Understand Any ECG Strip

Third-degree heart block causes complete AV dissociation with independent atrial and ventricular rhythms and bradycardia. P waves and QRS complexes beat independently, and pacing—temporary or permanent—restores atrial before ventricular contraction.

Identify and interpret second-degree AV block Mobitz type II on ECG, noting random dropped QRS complexes, and recognize the key causes and the role of pacemakers as treatment.

Identify second-degree AV block Mobitz type I by its progressive PR interval prolongation followed by a dropped QRS, a hallmark pattern you’ll see in exams.

Identify first-degree heart block as a mild AV node obstruction that prolongs the PR interval, with causes like fibrosis, inflammation, electrolyte imbalances, vagal tone, or post-surgery, usually asymptomatic.

Identify how hypercalcemia shortens the QT interval with widespread prolongation. Cover causes, symptoms, and treatments, including hyperparathyroidism, dehydration, and IV fluids, diuretics, calcitonin, calcimimetics, denosumab, prednisone.

Learn to read and manage hyperkalemia on ecg, from tall tent-shaped t waves in mild cases to qrs widening in severe cases, with causes, symptoms, and calcium gluconate first.

Identify how temperature below 35°C triggers hypothermia and ECG changes below 32°C. Note Osborn waves, generalized P wave and QRS prolongation, shivering artifacts, and gradual rewarming.

Define pericarditis as inflammation of the heart's covering and recognize stage-based ecg patterns—concave st elevation, pr depression, and t-wave changes. Treat with aspirin, ibuprofen, and colchicine.

Explain how digoxin inhibits Na+/K+ ATPase to raise intracellular calcium and enhance contractility, increase vagal tone reducing AV conduction, and recognize toxicity signs including yellow-green vision changes and treatment.

Identify Wellens syndrome by noticing biphasic or deeply inverted T waves in V2 and V3, indicating left anterior descending coronary artery stenosis and risk of anterior myocardial infarction.

Identify polymorphic vt on ecg caused by a calcium release mutation affecting ryanodine receptors, inherited across families, with varying qrs shapes and risk of ventricular fibrillation.

Pericardial effusion accumulates fluid between the heart and its covering, compressing the heart and lowering ECG voltage, and requires pericardiocentesis.

Explore congenital long QT syndrome and torsades de pointes risk, with T wave variations such as biphasic or peaked, Romano-ward, Andersen-tawil, Timothy, and Jervell/Nilsen syndromes, plus propranolol, nadolol, and Mexiletine.

Explore Brugada syndrome, a sodium channel mutation with autosomal dominant risk of sudden cardiac death, its three ECG types, symptoms like dizziness and syncope, and pacing as the main treatment.

Arrhythmogenic right ventricular dysplasia involves fibrofatty replacement of the right ventricle. Desmosomal protein mutations cause it, with epsilon wave, T wave inversion, QRS widening, and ventricular tachycardia.

Explore how preload, cardiac output, and afterload shape shocks. Identify cardiac shocks from infections or myocardial infarction, hypovolemic shock from low blood volume, and fistula-related high output heart failure.

Understand aortic dissection anatomy, true and false lumens, Stanford A/B classification, imaging clues, and management options from beta blockers to surgery.

Identify scarlet fever caused by group A streptococci, with sandpaper rash on the body and strawberry tongue, and learn rapid strep testing and penicillin treatment.

Evaluate loss of consciousness by category: gradual from metabolic disturbances with glucose, oxygen, and CBC; sudden recovery suggests cardiac origin with echo and EKG, noting aortic stenosis as common.

Define hypertensive urgency and crisis as blood pressure above 180/120, with end organ damage indicating crisis. Identify first-line treatments, stop current medications, including labetalol, clevidipine, fenoldopam, nicardipine, and nitroprusside.

Identify rheumatic fever as an autoimmune reaction to group A streptococci after pharyngeal infection, diagnosed by Jones criteria and treated with penicillin for five to ten years.

Learn how hypertension is treated by lowering blood volume with loop and thiazide diuretics, and dilating vessels with calcium channel blockers, ACE inhibitors, ARBs, beta blockers, and alpha blockers.

Learn to read systolic and diastolic blood pressure, classify stages from elevated to hypertensive crisis, and apply lifestyle changes and medications such as ACE inhibitors, ARBs, and diuretics.

Learn how to lower cholesterol by adjusting diet, increasing exercise, and lifestyle changes, and understand medications like statins, bile acid resins, pcsk inhibitors, fibrates, and niacin.

Treat hypertension by reducing heart contraction and dilating vessels using calcium channel blockers such as verapamil, diltiazem, nifedipine, and amlodipine. Target cerebral hemorrhage with nimodipine; dihydropyridines treat Raynaud phenomenon.

Explore how nitrate medications deliver nitric oxide to relax vascular smooth muscle, reduce preload and afterload, and relieve acute angina and acute coronary syndrome.

Ace inhibitors, such as lisinopril, block angiotensin-converting enzyme, raise bradykinin to lower blood pressure, protect the kidney in hypertension and diabetes, and may cause dry cough or angioedema.

Learn how angiotensin II receptor blockers lower blood pressure by blocking receptors, compared with ACE inhibitors. Review key safety notes including creatinine changes, hyperkalemia, teratogenicity, and use in diabetes.

Explore adenosine’s 10–15 second half-life and its rapid AV node conduction reduction via potassium expulsion and hyperpolarization. Use it to diagnose or treat supraventricular tachycardias and for chemical stress tests.

Distinguish primary versus secondary hypertension and treat with diuretics, ACE inhibitors or ARBs, calcium channel blockers, and beta blockers. Note special considerations for heart failure, diabetes, asthma, and pregnancy.

Ranolazine serves as a last-resort angina treatment, reducing myocardial oxygen demand by inhibiting inward sodium currents and the sodium–calcium exchanger, with QT prolongation and side effects like constipation.

Explore opioid receptors delta, kappa, and mu, and how agonism reduces pain mediator release (substance P, serotonin, glutamate) via potassium channel opening and calcium channel closing.

Explore how NSAIDs block cyclooxygenase-1 and -2 to inhibit prostaglandin synthesis, affecting gastric protection, PDA dependence, and renal perfusion.

Explore how acetaminophen inhibits central nervous system cyclooxygenase for antipyretic and mild analgesic effects, its use for fever in children, and overdose management with glutathione, napqi, and NAC.

Explore how aspirin irreversibly inhibits cyclooxygenase, blocking thromboxane A2 at low doses and delivering anti-inflammatory effects at higher doses, with safety considerations including gastric ulcers and renal ischemia.

Identify key red blood cell morphologies—acanthocytes, teardrop cells, bite cells, basophilic stippling, echinocytes, elliptocytes, target cells, spherocytes, sickle cells, schistocytes, and sideroblasts—and their disease associations.

Explore the four hypersensitivity types, from type one anaphylaxis driven by IgE and histamine to type four delayed T cell mediated responses, with examples like contact dermatitis and transplant rejection.

Explore antidotes for acetaminophen, organophosphates, anticholinergic toxicity, arsenic, mercury, benzodiazepines, beta blockers, cyanide, digoxin, heparin, iron, lead, ethylene glycol, methylene blue, naloxone, and warfarin reversal.

Explains how chromosomal karyotypes relate to disease, listing mutations across chromosomes 3 to 22 and the X, with examples like down syndrome and Fragile X syndrome.