Atrioventricular nodal reentrant tachycardia (AVNRT)

62,812views

test

00:00 / 00:00

Atrioventricular nodal reentrant tachycardia (AVNRT)

FINAL

FINAL

ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
Adrenergic antagonists: Beta blockers
Acyanotic 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
Cardiac tamponade
Endocarditis
Myocarditis
Rheumatic heart disease
Heart failure
Cor pulmonale
Long QT syndrome and Torsade de pointes
Ventricular tachycardia
Premature ventricular contraction
Ventricular fibrillation
Atrial flutter
Premature atrial contraction
Atrial fibrillation
Atrioventricular nodal reentrant tachycardia (AVNRT)
Deep vein thrombosis
Hypotension
Orthostatic hypotension
Polycystic kidney disease
Pheochromocytoma
Cushing syndrome
Renal artery stenosis
Hypertension
Aneurysms
Aortic dissection
Peripheral artery disease
Angina pectoris
Unstable angina
Prinzmetal angina
Myocardial infarction
Stable angina
Arterial disease
ECG normal sinus rhythm
ECG cardiac hypertrophy and enlargement
ECG cardiac infarction and ischemia
ECG basics
ECG intervals
ECG axis
ECG QRS transition
ECG rate and rhythm
Electrical conduction in the heart
Cardiac conduction velocity
Normal heart sounds
Abnormal heart sounds
Cardiovascular changes during postural change
Cardiovascular changes during hemorrhage
Cardiac preload
Cardiac contractility
Cardiac afterload
Measuring cardiac output (Fick principle)
Thrombocytopenia: Clinical
Heparin-induced thrombocytopenia
Immune thrombocytopenia
Gout
Chronic kidney disease: Clinical
Traumatic brain injury: Pathology review
Traumatic brain injury: Clinical
Concussion and traumatic brain injury
Blood groups and transfusions
Blood products and transfusion: Clinical
HIV (AIDS)
Hodgkin lymphoma
Acromegaly
Musculoskeletal injuries: Nursing process (ADPIE)
Hemophilia: Nursing process (ADPIE)
Diabetes insipidus
Diabetes mellitus
Diabetes mellitus: Clinical
Diabetes mellitus: Pathology review
Diabetes mellitus (DM): Nursing process (ADPIE)
Diabetes insipidus: Nursing process (ADPIE)
Managing diabetes during the holidays: Information for patients and families
Hypoglycemics: Insulin secretagogues
Insulins
Epistaxis: Nursing process (ADPIE)
Appendicitis
Appendicitis: Clinical
Appendicitis: Pathology review
Appendicitis: Nursing process (ADPIE)
Hypothyroidism medications
Hyperosmolar hyperglycemic state (HHS): Nursing process (ADPIE)
Sympathomimetics: Direct agonists
Cushing syndrome and Cushing disease: Pathology review
Cushing syndrome: Clinical
Metabolic and respiratory alkalosis: Clinical
Metabolic and respiratory acidosis: Clinical
Conjunctivitis: Nursing process (ADPIE)
Stroke: Clinical
Stroke: Nursing process (ADPIE)
Peptic ulcer
Peptic ulcer disease (PUD): Nursing process (ADPIE)
Peptic ulcers and stomach cancer: Clinical
Gallbladder histology
Gallbladder disorders: Clinical
Acute cholecystitis
Oral cancer
Hepatitis A and Hepatitis E virus
Viral hepatitis: Clinical
Hepatitis medications
Seizures: Pathology review
Seizures: Clinical
Epilepsy
Febrile seizure
Seizure disorder: Nursing process (ADPIE)
Non-urothelial bladder cancers
Inflammatory bowel disease: Clinical
Inflammatory bowel disease: Pathology review
Anticoagulants: Heparin
Postoperative evaluation: Clinical
Trigeminal neuralgia
Trigeminal neuralgia: Nursing process (ADPIE)
Hypoparathyroidism
Pancreatitis: Pathology review
Pancreatitis: Clinical
Acute pancreatitis
Pancreatitis: Nursing process (ADPIE)
Chronic pancreatitis
Sickle cell disease (NORD)
Sickle cell disease: Clinical
Sickle cell disease: Nursing process (ADPIE)
Class IV antiarrhythmics: Calcium channel blockers and others
Hypertension: Clinical
Pulmonary hypertension
Hypertension: Nursing process (ADPIE)
Osteoarthritis
Joint pain: Clinical
Hyperthyroidism: Pathology review
Hyperthyroidism: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Hyperthyroidism
Hyperthyroidism medications
Hyperthyroidism: Nursing process (ADPIE)

Assessments

Flashcards

0 / 11 complete

USMLE® Step 1 questions

0 / 2 complete

High Yield Notes

6 pages

Flashcards

Atrioventricular nodal reentrant tachycardia (AVNRT)

0 of 11 complete

Questions

USMLE® Step 1 style questions USMLE

0 of 2 complete

A 34-year-old male presents to the emergency department with palpitations. He states he drank his morning coffee, went out for a jog, but he suddenly became lightheaded and noted a fluttering sensation in his chest. He had a similar episode in the past, which self-resolved without intervention. Past medical history is noncontributory, and he does not take any medications. Temperature is 37.0°C (98.6°F), pulse is 175/min, respirations are 14/min, and blood pressure is 124/72 mmHg. Physical exam is otherwise unremarkable, and initial electrocardiogram is demonstrated below:  


Image reproduced from Wikimedia Commons  

Based on this patient's clinical presentation, which of the following is the most likely diagnosis?  

Transcript

Watch video only

The atria are the heart’s upper chambers; the ventricles are the lower chambers. Reentrant tachycardias are fast heart rates caused by electrical signals that loop back on themselves.

Normally, an electrical signal starts at the sinoatrial or SA node in the right atrium and propagates out through both atria, including bachmann’s bundle in the left atrium, and then contracts both atria. It’s then delayed just a little bit as it goes through the atrioventricular, or AV node, before it passes through the Bundle of His and on to the Purkinje fibers of the left and right ventricles, causing them to contract as well.

Usually, the only place where a signal can go from the atria to the ventricles is at the AV node, and once that signal gets to the purkinje fibers, it stops and the heart tissue waits for another signal from the SA node. With an atrioventricular reentrant tachycardia, or AVRT, the electrical signal actually uses a separate accessory pathway to get back up from the ventricles to the atria, which causes the atria to contract before the SA node sends out another signal. The signal then moves back down the AV node to the ventricles and purkinje fibers, contracts the ventricles, and goes back up that accessory pathway. This cycle repeats, which is why AVRT can result in rates as high as 200-300 bpm. This type of tachycardia is known as a supraventricular tachycardia because the signal causing the fast rate originates above the ventricles. The most common type of AVRT is Wolff-Parkinson-White syndrome, where the accessory pathway is called the Bundle of Kent. This type of reentry is known as an anatomical reentrant circuit because the accessory pathway is a fixed, anatomically-defined pathway.

Another type of reentrant circuit is atrioventricular nodal reentrant tachycardia, or AVNRT. AVNRT, just like AVRT, is a type of supraventricular tachycardia; however, with AVNRT it’s in or near the AV node, which similarly contracts the ventricle and the atria every time it goes around.

Specifically, there are two separate electrical pathways that make up this loop. One of these pathways has heart tissue that has slow electrical conduction; it’s called the alpha pathway. The other has fast conduction; it’s called the beta pathway. Additionally, the alpha pathway has a short refractory period, which is the time it takes to conduct another signal. The beta pathway, on the other hand, has a long refractory period. Once you have all these things, you’ve got yourself a recipe for AVNRT.

So, let’s say a signal comes down from the SA node in the right atrium, the signal goes down the fast pathway, and reaches the other end before the slow pathway. Next, it splits to travel down to the ventricles, as well as up the alpha pathway, where it meets the slow signal and they both cancel each other out.

At this point, both enter into their refractory period. Because the alpha pathway is shorter, it comes out of refractory sooner and is ready for another signal, while the beta pathway’s still in refractory. So, if another signal comes by, it’ll start down the slow pathway, but since the fast is still in refractory, it’ll be blocked.

At some point while the signal’s going down the alpha side, that beta side will come out of refractory, and then it’ll be ready to go. So, now as the signal exits the alpha pathway to the ventricles and enters the refractory period, it also travels up the beta pathway, and by the time it reaches the alpha pathway again, that pathway’s out of refractory!

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "Differentiation of Slow-Slow Form of AVNRT from AVRT through a Posteroseptal Accessory Pathway by Retrograde P-Wave Amplitude" Pacing and Clinical Electrophysiology (2016)
  5. "Atrioventricular Reciprocating Tachycardia/Atrioventricular Reentrant Tachycardia (AVRT)" StatPearls Publishing (2020 Jan)