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Advanced cardiac life support (ACLS): Clinical (To be retired)
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Pericardial disease: Clinical (To be retired)
Infective endocarditis: Clinical (To be retired)
Valvular heart disease: Clinical (To be retired)
Cardiomyopathies: Clinical (To be retired)
Hypertension: Clinical (To be retired)
Hypercholesterolemia: Clinical (To be retired)
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Sympathomimetics: Direct agonists
Muscarinic antagonists
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
Loop diuretics
Antiplatelet medications
Development of the cardiovascular system
Fetal circulation
Human development days 1-4
Human development days 4-7
Human development week 2
Human development week 3
Ectoderm
Mesoderm
Endoderm
Development of the placenta
Development of the fetal membranes
Development of twins
Hedgehog signaling pathway
Development of the digestive system and body cavities
Development of the umbilical cord
Introduction to the cardiovascular system
Introduction to the lymphatic 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
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 work
Cardiac cycle
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
Electrical conduction in the heart
Cardiac conduction velocity
ECG basics
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG rate and 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
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
Heart failure
Cor pulmonale
Cardiac tumors
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Endocarditis
Myocarditis
Rheumatic heart disease
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
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
Cholinergic receptors
Adrenergic receptors
Premature atrial contraction
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The heart has two upper chambers, which are called the atria, and a premature atrial contraction, or PAC, is when the atria contract earlier than normal in the cardiac cycle.
So normally, the sinoatrial, or SA, node sends an electrical signal called a depolarization that propagates out through the walls of the heart and causes both upper chambers to contract. Then, that signal moves to the atrioventricular, or AV, node, where it’s delayed for a split second. Then, the signal travels down into the ventricles, or lower chambers, where it moves down the bundle of His into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing them to contract as well. This trip is called a depolarization wave, and in a healthy heart, it makes sure that the upper chambers contract before the lower chambers contract. On an electrocardiogram, or ECG, which measures the electrical activity of the heart via electrodes that are placed on the skin, the atrial depolarization and its contraction are seen as a P-wave, the ventricular contraction is seen as a QRS complex, and the ventricular repolarization and its relaxation are seen as a T-wave.
If an atrial cell outside of the SA node initiates a depolarization, that’s called an atrial ectopic focus. Now, this could be initiated by a cell that’s part of the conduction system, or it could just be initiated by another cardiac muscle cell. This typically happens when atrial cells are irritated and stressed by electrolyte imbalances, drugs like cocaine or methamphetamines, ischemic damage like a heart attack, or anything that increases sympathetic activity, like anxiety. Another type of atrial ectopic focus is a reentrant loop, which is when there’s some tissue that doesn’t depolarize properly, which could happen in scar tissue after a heart attack. As a result of this damage, the depolarization wave ends up circling around and around that tissue. A reentrant loop basically starts sending out depolarization waves to the rest of the heart tissue each time the wave goes around.
Premature atrial contraction is when the atria contract too early because of depolarization from an ectopic focus. While the sinoatrial node typically regulates the heartbeat during normal sinus rhythm, premature atrial contractions occur when another region of the atria depolarizes before the sinoatrial node and thus triggers a premature heartbeat. The ECG will show an early and abnormal P-wave, as well as one of three patterns, depending on when the PAC occurs: normal ventricular conduction, aberrant ventricular conduction, or a conduction block.
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