Ventricular arrhythmias: Pathology review

9,319views

Ventricular arrhythmias: Pathology review

dmid

dmid

Thymus histology
Spleen histology
Lymph node histology
Introduction to the immune system
Cytokines
Innate immune system
Complement system
T-cell development
B-cell development
MHC class I and MHC class II molecules
T-cell activation
B-cell activation, differentiation, and contraction
Cell-mediated immunity of CD4 cells
Cell-mediated immunity of natural killer and CD8 cells
Antibody classes
Somatic hypermutation and affinity maturation
VDJ rearrangement
Contracting the immune response and peripheral tolerance
B- and T-cell memory
Anergy, exhaustion, and clonal deletion
Vaccinations
Type I hypersensitivity
Type II hypersensitivity
Type III hypersensitivity
Type IV hypersensitivity
Sepsis
Neonatal sepsis
Abscesses
Food allergy
Anaphylaxis
Asthma
Immune thrombocytopenia
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Myasthenia gravis
Graves disease
Pemphigus vulgaris
Serum sickness
Systemic lupus erythematosus
Poststreptococcal glomerulonephritis
Graft-versus-host disease
Contact dermatitis
Transplant rejection
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
X-linked agammaglobulinemia
Selective immunoglobulin A deficiency
Common variable immunodeficiency
IgG subclass deficiency
Hyperimmunoglobulin E syndrome
Isolated primary immunoglobulin M deficiency
Thymic aplasia
DiGeorge syndrome
Severe combined immunodeficiency
Adenosine deaminase deficiency
Ataxia-telangiectasia
Hyper IgM syndrome
Wiskott-Aldrich syndrome
Leukocyte adhesion deficiency
Chediak-Higashi syndrome
Chronic granulomatous disease
Complement deficiency
Hereditary angioedema
Asplenia
Thymoma
Ruptured spleen
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Glucocorticoids
Bacterial structure and functions
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
Clostridium perfringens
Clostridium botulinum (Botulism)
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Corynebacterium diphtheriae (Diphtheria)
Bacillus anthracis (Anthrax)
Nocardia
Actinomyces israelii
Escherichia coli
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Pseudomonas aeruginosa
Enterobacter
Klebsiella pneumoniae
Shigella
Proteus mirabilis
Yersinia enterocolitica
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Serratia marcescens
Bacteroides fragilis
Yersinia pestis (Plague)
Vibrio cholerae (Cholera)
Helicobacter pylori
Campylobacter jejuni
Neisseria meningitidis
Neisseria gonorrhoeae
Moraxella catarrhalis
Francisella tularensis (Tularemia)
Bordetella pertussis (Whooping cough)
Brucella
Haemophilus influenzae
Haemophilus ducreyi (Chancroid)
Pasteurella multocida
Mycobacterium tuberculosis (Tuberculosis)
Mycobacterium leprae
Mycobacterium avium complex (NORD)
Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlamydia trachomatis
Borrelia burgdorferi (Lyme disease)
Borrelia species (Relapsing fever)
Leptospira
Treponema pallidum (Syphilis)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Gardnerella vaginalis (Bacterial vaginosis)
Viral structure and functions
Varicella zoster virus
Cytomegalovirus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Parvovirus B19
Human papillomavirus
Poxvirus (Smallpox and Molluscum contagiosum)
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Poliovirus
Coxsackievirus
Rhinovirus
Hepatitis A and Hepatitis E virus
Hepatitis D virus
Influenza virus
Mumps virus
Measles virus
Respiratory syncytial virus
Human parainfluenza viruses
Dengue virus
Yellow fever virus
Zika virus
Hepatitis C virus
West Nile virus
Norovirus
Rotavirus
Coronaviruses
HIV (AIDS)
Human T-lymphotropic virus
Ebola virus
Rabies virus
Rubella virus
Eastern and Western equine encephalitis virus
Lymphocytic choriomeningitis virus
Hantavirus
Prions (Spongiform encephalopathy)
Coccidioidomycosis and paracoccidioidomycosis
Histoplasmosis
Blastomycosis
Pneumocystis jirovecii (Pneumocystis pneumonia)
Candida
Mucormycosis
Aspergillus fumigatus
Sporothrix schenckii
Cryptococcus neoformans
Malassezia (Tinea versicolor and Seborrhoeic dermatitis)
Plasmodium species (Malaria)
Babesia
Giardia lamblia
Entamoeba histolytica (Amebiasis)
Cryptosporidium
Acanthamoeba
Naegleria fowleri (Primary amebic meningoencephalitis)
Toxoplasma gondii (Toxoplasmosis)
Trypanosoma brucei
Trypanosoma cruzi (Chagas disease)
Trichomonas vaginalis
Leishmania
Loa loa (Eye worm)
Toxocara canis (Visceral larva migrans)
Onchocerca volvulus (River blindness)
Ascaris lumbricoides
Anisakis
Angiostrongylus (Eosinophilic meningitis)
Ancylostoma duodenale and Necator americanus
Strongyloides stercoralis
Guinea worm (Dracunculiasis)
Wuchereria bancrofti (Lymphatic filariasis)
Trichinella spiralis
Enterobius vermicularis (Pinworm)
Trichuris trichiura (Whipworm)
Echinococcus granulosus (Hydatid disease)
Diphyllobothrium latum
Paragonimus westermani
Clonorchis sinensis
Schistosomes
Pediculus humanus and Phthirus pubis (Lice)
Sarcoptes scabiei (Scabies)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Mechanisms of antibiotic resistance
Integrase and entry inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Protease inhibitors
Hepatitis medications
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)
Neuraminidase inhibitors
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Advanced cardiac life support (ACLS): Clinical
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical
Heart failure: Clinical
Syncope: Clinical
Pericardial disease: Clinical
Valvular heart disease: Clinical
Chest trauma: Clinical
Shock: Clinical
Peripheral vascular disease: Clinical
Leg ulcers: Clinical
Aortic aneurysms and dissections: Clinical
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Loop diuretics
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
Positive inotropic medications
Antiplatelet medications
Blistering skin disorders: Clinical
Bites and stings: Clinical
Burns: Clinical
Diabetes mellitus: Clinical
Hyperthyroidism: Clinical
Hypothyroidism and thyroiditis: Clinical
Parathyroid conditions and calcium imbalance: Clinical
Adrenal insufficiency: Clinical
Neck trauma: Clinical
Insulins
Mineralocorticoids and mineralocorticoid antagonists
Abdominal pain: Clinical
Appendicitis: Clinical
Gastrointestinal bleeding: Clinical
Peptic ulcers and stomach cancer: Clinical
Inflammatory bowel disease: Clinical
Diverticular disease: Clinical
Gallbladder disorders: Clinical
Pancreatitis: Clinical
Cirrhosis: Clinical
Hernias: Clinical
Bowel obstruction: Clinical
Abdominal trauma: Clinical
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Blood products and transfusion: Clinical
Venous thromboembolism: Clinical
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Thrombolytics
Fever of unknown origin: Clinical
Infective endocarditis: Clinical
Pneumonia: Clinical
Tuberculosis: Pathology review
Diarrhea: Clinical
Urinary tract infections: Clinical
Meningitis, encephalitis and brain abscesses: Clinical
Skin and soft tissue infections: Clinical
Hypernatremia: Clinical
Hyponatremia: Clinical
Hyperkalemia: Clinical
Hypokalemia: Clinical
Metabolic and respiratory acidosis: Clinical
Metabolic and respiratory alkalosis: Clinical
Toxidromes: Clinical
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute kidney injury: Clinical
Kidney stones: Clinical
Stroke: Clinical
Seizures: Clinical
Headaches: Clinical
Traumatic brain injury: Clinical
Lower back pain: Clinical
Spinal cord disorders: Pathology review
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Osmotic diuretics
Opioid agonists, mixed agonist-antagonists and partial agonists
Opioid antagonists
Asthma: Clinical
Chronic obstructive pulmonary disease (COPD): Clinical
Acute respiratory distress syndrome: Clinical
Pleural effusion: Clinical
Pneumothorax: Clinical
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Pulmonary corticosteroids and mast cell inhibitors
Joint pain: Clinical
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Antigout medications
Pediatric allergies: Clinical
Kawasaki disease: Clinical
Congenital TORCH infections: Pathology review
Pediatric infectious rashes: Clinical
Pediatric bone and joint infections: Clinical
Sjogren syndrome: Clinical
Vasculitis: Clinical
Rheumatoid arthritis: Clinical
Seronegative arthritis: Clinical
Systemic lupus erythematosus (SLE): Clinical
Inflammatory myopathies: Clinical
ECG axis
ECG basics
Normal heart sounds
Abnormal heart sounds
Cardiac conduction system
Cardiac conduction velocity
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Vasculitis

Transcript

Watch video only

Clint is a 19 year old male that’s brought to the emergency department for acute chest pain. Upon examination, you notice that his heart rate is really fast, about 170 beats per minute. He has a history of depression, and is currently being treated with TCAs. He is otherwise healthy. A few minutes after arriving, Clint loses consciousness. His ECG shows this.

All right, so based on his presentation and ECG, Clint has some form of arrhythmia. The best way to approach arrhythmias is to one: know what a normal ECG looks like, and two: have a good classification system to narrow down the diagnosis. 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. It's also important to know that there is typically a delay in the 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 could be completely asymptomatic, and be picked up incidentally on an ECG. Arrhythmias can also present with palpitations, which is a sensation of your heart beating too hard or fast, fluttering, or skipping a beat. 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 muscles now demand 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 also 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 for your exams 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.

Okay, now the two types of ventricular arrhythmias are ventricular tachycardia and ventricular fibrillation. Ventricular tachycardia or VT for short originates from an ectopic focus located in the ventricle. The two main subtypes are monomorphic and polymorphic ventricular tachycardia. On ECG, both appear as wide QRS complexes at a rate ranging between 120 and 200 beats per minute.

“Monomorphic” means that all the QRS complexes look the same, and it’s classically a complication of myocardial scarring due to acute myocardial infarction. On the other hand, “polymorphic” means the QRS complexes have different shapes in each beat, as they come from different areas of the ventricle. This may occur due to acute myocardial ischemia causing the pacemaker cells to be stressed, and it’s not associated with myocardial scarring.

Another cause of polymorphic VT that is frequently tested in the exams is Brugada syndrome. This is a rare autosomal dominant condition characterized by genetic mutations hitting cardiac sodium channels. Now, the test question will typically describe a male of Asian descent, whose ECG pattern in V1 to V3 shows pseudo- right bundle branch block with the widened QRS presenting an RSR’ configuration, as well as ST elevations.

Now, some individuals affected may present this ECG pattern and yet be asymptomatic, while others may present symptoms like syncope. Regardless, they’re all at risk of developing polymorphic VT and sudden cardiac death, so treatment is primarily focused around prevention with implantable cardioverter-defibrillators.

Key Takeaways

An arrhythmia is any disturbance in the rate, rhythm, site of origin, or conduction of the cardiac electrical impulse. Ventricular arrhythmias are those that originate within the ventricles and have a wide QRS complex on ECG. These two types of ventricular arrhythmias are ventricular tachycardia and ventricular fibrillation.

Ventricular tachycardia can be monomorphic meaning that all the QRS complexes look the same, or polymorphic meaning the QRS complexes are different in each beat. A specific and very dangerous type of polymorphic ventricular tachycardia is Torsades de Pointes, which presents a twisting pattern of QRS complexes. This can rapidly progress to ventricular fibrillation, in which the whole PQRST ECG pattern breaks down completely, leaving just some random undulating waves. This is the most common cause of sudden cardiac death.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Monomorphic ventricular tachycardia as the primary presentation of an anterior STEMI" Clinical Case Reports (2019)
  3. "Drug induced QT prolongation and torsades de pointes" Heart (2003)
  4. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  5. "Pathophysiology of Heart Disease" Wolters Kluwer Health (2015)
  6. "Brugada syndrome: A general cardiologist's perspective" European Journal of Internal Medicine (2017)