ECG basics

Last updated: June 19, 2025

ECG basics

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Cardio

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Behcet's disease
Kawasaki disease
Hypertension
Hypertensive emergency
Renal artery stenosis
Coarctation of the aorta
Cushing syndrome
Conn syndrome
Pheochromocytoma
Polycystic kidney disease
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Persistent truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Tetralogy of Fallot
Hypoplastic left heart syndrome
Patent ductus arteriosus
Ventricular septal defect
Atrial septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Pulmonary hypertension
Aortic aneurysms and dissections: Clinical
Raynaud phenomenon
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

Flashcards

ECG basics

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Questions

USMLE® Step 1 style questions USMLE

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A 55-year-old man is brought to the emergency department with severe midsternal chest pain. The patient reports 2 episodes of non-bloody emesis and diaphoresis since the start of the chest pain half an hour ago. Blood pressure is 110/75 and pulse is 89/min. Physical examination is unremarkable. An electrocardiogram (ECG) is performed based on which a provisional diagnosis of inferior wall myocardial infarction is made. Which of the following patterns of ECG changes are most likely seen in this patient?  

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An electrocardiogram is also known as an ECG; the Dutch and German version of the word, elektrokardiogram, is shortened to EKG. It is a tool used to visualize, or “gram,” the electricity, or “electro,” that flows through the heart, or “cardio.” Specifically, a 12-lead ECG tracing shows how the depolarization wave, which is a wave of positive charge, moves during each heartbeat, by providing the perspectives of different sets of electrodes. This particular set of electrodes is called lead II; one electrode is placed on the right arm and the other on the left leg. Essentially, when the wave’s moving toward the left leg electrode, you get a positive deflection. This big, positive deflection corresponds to the wave moving down the septum.

To understand the basics, let’s start with an example of how we can look at the heart with only one pair of electrodes: a positive and a negative one. These electrodes detect the charge on the outside of the cell. Remember, at rest, cells are negatively charged relative to the slightly positive outside environment; let’s make these cells red. When they depolarize, the cells become positively charged, and leave a slightly negative charge in the outside environment; let’s make these cells green. Now, if we freeze this “wave of depolarization” as it’s moving through the cells, half of the cells are negative, or depolarized, and half are positive and resting; therefore, there’s a difference of charge across this set of cells. You can think of the charge difference as being a dipole, because there are two electrical poles. We can draw this dipole out as an arrow, or vector, pointing towards the positive charge. Remember, the electrodes detect charge on the outside of the cell, so this points toward where the positive charge is, outside.

Now, if there’s a dipole vector pointing toward the positive electrode, then the ECG tracing shows it as a positive deflection; the bigger the dipole is, the bigger the deflection is. If we unpause this, then everything becomes depolarized. Since there’s no difference in charge, there’s no dipole, and thus no deflection. Moments later, a wave of repolarization goes through, and the cells become negative once again. Pausing halfway through again, now the vector dipole goes in the opposite direction, and faces the negative electrode; this means that there will be a negative ECG tracing. Again, the bigger the dipole is, the bigger the negative deflection is. Even though it’d be nice if the depolarization wave lined up perfectly with the electrodes, usually that’s not the case. So, we simply look at the vector component that is parallel to that electrode. For example, let’s say that the depolarization happened this way, at an angle; then, we’d simply break the vector into two parts. The one we care about is the one that’s going towards the positive electrode, which causes a deflection, even though it’s a slightly smaller deflection than previously. In other words, the size of the deflection on the ECG tracing always corresponds to the magnitude, or size, of the dipole in the direction of the electrode. The perpendicular component isn’t pointing at the electrodes, so it doesn’t cause any deflection. In fact, if there’s a depolarization wave that goes straight up, perpendicular to the positive and negative electrodes, there would be no deflection!

In a standard ECG, there are 10 electrodes: four limb electrodes, with one each on the left arm, right arm, left leg, and right leg; and six precordial electrodes, V1 through V6, that wrap around the chest. The right leg electrode is usually used as a neutral lead. The heart is a three-dimensional organ, so V1 through V6 line up in the transverse, or horizontal, plane of the heart. Each electrode is set up to detect any wave of positive charge coming towards it. These are collectively called the chest leads.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2017)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "Screening for Cardiovascular Disease Risk With Electrocardiography" JAMA (2018)
  6. "Screening for Coronary Heart Disease With Electrocardiography: U.S. Preventive Services Task Force Recommendation Statement" Annals of Internal Medicine (2012)
  7. "Activation of the Interventricular Septum" Circulation Research (1955)