Supraventricular arrhythmias: Pathology review

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Supraventricular arrhythmias: Pathology review

ETP Cardiovascular System

ETP Cardiovascular System

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
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Pressures in the cardiovascular system
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Measuring cardiac output (Fick principle)
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Cardiac contractility
Frank-Starling relationship
Cardiac preload
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Law of Laplace
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Altering cardiac and vascular function curves
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Pressure-volume loops
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Action potentials in myocytes
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Cardiac excitation-contraction coupling
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Wolff-Parkinson-White syndrome
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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
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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
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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
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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
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Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
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Questions

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A 73-year-old female presents to the emergency department with shortness of breath. She is concerned her “COPD is flaring up.” Past medical history is notable for hypertension, chronic obstructive pulmonary disease, and type II diabetes mellitus. She has been smoking one pack of cigarettes per day for twenty years. Temperature is 37.0°C (98.6°F), pulse is 136/min, respirations are 22/min, blood pressure is 104/72 mmHg, and oxygen saturation is 92% on room air. The patient is currently speaking in three to four word sentences and demonstrates increased work of breathing. There are bilateral rales throughout the lung fields, and the electrocardiogram from triage is shown below:  


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

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Melissa is a 21 year old college student who is having the time of her life at a party. It’s late, and unfortunately she has class the next morning, so she drinks a ton of coffee to sober up. On her way out, Melissa collapses to the floor, but wakes up after a couple of seconds. On her way to the emergency room, she tells the paramedics that she’s “aware of her heartbeat”. Then comes Taylor, a 32 year old female who is brought to the emergency room by her partner because she suddenly collapsed for a couple of minutes while cooking dinner. Taylor is now awake, and she tells you that right before collapsing she was feeling dizzy and like her heart was racing, but now she’s fine. They are both placed on different monitors. Melissa’s heart rate is 200 beats per minute and regular, and this is Melissa’s ECG. On the other hand, Taylor’s heart rate is 80 beats per minute and regular, so everything seems fine. However, her ECG shows this.

All right, so both Melissa and Taylor experienced palpitations and syncope, and their ECGs reveal they both have some form of arrhythmia. The best way to approach arrhythmias is to first: know what a normal ECG looks like, and second: have a good classification system to narrow down the diagnosis.

First, let’s review the normal electrical conduction pathway in the heart, and how it looks like on an ECG. An ECG tracing specifically shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node and is then conducted through the atrium, creating the P wave on ECG. From the atrium, electrical activity goes to the atrioventricular, or AV node, after which it goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles. On an ECG, this will create the QRS complex, which represents the depolarization of the ventricles; and finally the T wave, which represents the repolarization of the ventricles. To help identify an irregular rhythm you can look at the morphology of the waveform and make sure that there is a P wave before every QRS complex, and a QRS complex after every P wave.

Now let’s take a look at the heart rate. The resting heart beats at a rate between 60 to 100 times per minute, and each of those beats starts off with depolarization of the sinoatrial node, and so we call it a normal sinus rhythm. For your exams, you should be able to figure out the heart rate on an ECG. To do that, you can count the number of boxes between R waves. Each small box represents 0.04 seconds, and each big box is five small boxes, so each big box is 0.2 seconds. One quick way to estimate the heart rate on an ECG, is to remember that the heart rate is 300, 150, 100, 75, 60, 50 depending on whether there’s 1, 2, 3, 4, 5, or 6 boxes between R waves. It's also important to know that there is normally a delay in conduction at the AV node and the Bundle of His, which gives some time for ventricular filling before the ventricle contracts. On the ECG, this is represented by the PR interval, which should be less than 5 small boxes, or 200 milliseconds.

Now, any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical activity is called an arrhythmia. Arrhythmias can be completely asymptomatic, and be picked up incidentally on an ECG. Arrhythmias can also present with palpitations, which is an awareness of one’s heartbeat. Additionally, they may alter cardiac output, causing individuals to present with signs of hypotension and decreased brain perfusion, like dizziness, altered mental status, or syncope. If an arrhythmia is really fast, the heart now demands more oxygen, and if oxygen supply is not met, then the myocardium suffers from ischemia, which presents as angina. In people with underlying heart disease, the sudden onset of an arrhythmia can precipitate acute heart failure. Finally, some arrhythmias may even cause sudden cardiac death.

Now, arrhythmias can be classified into those originating from above the ventricles, so supraventricular arrhythmias, and those originating in the ventricles, so ventricular arrhythmias. In general, what's important to remember is that supraventricular arrhythmias have a narrow QRS complex because there’s a rapid excitation of the ventricles, which means the arrhythmia is originating above or within the bundle of His. On the other hand, ventricular arrhythmias have a wide QRS complex because there’s a slower spread of ventricular depolarization.

The first type of supraventricular arrhythmia includes those with sinus origin. All right, so first there’s sinus tachycardia, which is a heart rate above 100, with a regular rhythm and normal P waves before each QRS complex. It can be physiological, like during exercise, or pathological. Pathological sinus tachycardia happens when the heart needs to compensate for an acute decrease in stroke volume, like in acute heart failure, acute myocardial infarction or pulmonary embolism. It can also result from any overwhelming activation of the sympathetic nervous system, like in hyperthyroidism, or cocaine and amphetamine use. Now, the thing is that a fast heart rate decreases diastolic filling time, which actually further decreases the stroke volume. Additionally, over time, catecholamines are actually toxic to the myocytes, which results in a form of cardiomyopathy called tachycardia-induced cardiomyopathy. Very creative name.

Okay, on the other hand of the spectrum we have sinus bradycardia. Keep in mind that this can be completely physiological in athletes, who can have a resting heart rate between 40 and 60, and it’s also normal during sleep. Pathological causes of sinus bradycardia include hypothyroidism, anorexia nervosa and inferior wall myocardial infarctions. Another high-yield cause of bradycardia is the Cushing reflex, which includes the characteristic triad of bradycardia, hypertension and an irregular respiratory pattern. This reflex occurs as a consequence of increased intracranial pressure, which can manifest from a variety of pathologies like head trauma, strokes, and brain tumors. For your exams, note that Cushing triad may indicate impending brain herniation, and thus, it is a medical emergency. Other causes of sinus bradycardia include a bunch of medications like beta blockers, calcium channel blockers, and opiates, in which case the solution is discontinuing the medication if possible. Acute sinus bradycardia can be treated with IV atropine, while chronic or severe cases might need a pacemaker.

Another arrhythmia of sinus origin is... well... Sinus arrhythmia. This arrhythmia can occur naturally during inspiration and expiration. See, during inspiration, the heart rate increases, and during expiration it decreases. So on an ECG, the rhythm may appear irregular, but it’s in fact a totally normal variant.

Finally, sinus arrest or sinus exit block occur when the sinus node fails to fire. What you need to know is that on an ECG, there is simply a flatline pause. Fortunately, if the sinus node can’t press that reset button, somebody else like the AV node or virtually any other myocardial cell can take over.

Summary

An arrhythmia is any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse. Supraventricular arrhythmias are a group of cardiac arrhythmias that originate at or above the atrioventricular node and have a narrow QRS complex (<120 ms). Supraventricular arrhythmias include atrial fibrillation, atrial flutter, and supraventricular tachycardia.

Supraventricular arrhythmias can cause a patient's heart rate to become too fast (tachycardia) or too slow (bradycardia). They can also cause stasis of blood flow in the atrial compartment and increase the risk of clot formation, especially in the left atrial appendage. These clots can dislodge, and travel into the systemic circulation, causing potentially life-threatening pathologies like embolic strokes, acute limb ischemia, central retinal artery occlusion, or acute mesenteric ischemia.

Common symptoms seen in supraventricular arrhythmias include palpitations, dizziness, shortness of breath, and chest pain. Treatment for these arrhythmias usually involves medications like beta-blockers, calcium channel blockers, digoxin, and other antiarrhythmic drugs; or procedures like electrical cardioversion and catheter ablation. In some cases, lifestyle modifications may be recommended to reduce the risk of developing arrhythmias.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Josephson's Clinical Cardiac Electrophysiology" Lippincott Williams & Wilkins (2015)
  3. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  4. "Novel PRKAG2 Mutation Responsible for the Genetic Syndrome of Ventricular Preexcitation and Conduction System Disease With Childhood Onset and Absence of Cardiac Hypertrophy" Circulation (2001)
  5. "Josephson's Clinical Cardiac Electrophysiology" Lippincott Williams & Wilkins (2015)
  6. "Multifocal Atrial Tachycardia" New England Journal of Medicine (1990)
  7. "Risk Factors and Genetics of Atrial Fibrillation" Cardiology Clinics (2014)
  8. "Alcohol and Atrial Fibrillation" Journal of the American College of Cardiology (2016)