Heart blocks: Pathology review

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Heart blocks: Pathology review

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
Cardiac conduction system
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
Seizures and 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)

Transcript

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Mikey is a 22 year old male college student from Vermont who was sent to the emergency department after passing out.

His vital signs show a heart rate of 40 beats per minute and a blood pressure of 90/50. On examination, there is an erythematous circular rash with central clearing.

His friends mention they recently went on a hiking trip. His ECG is as follows.

Natasha is a 60 year old female with chronic hypertension, diabetes, and peripheral vascular disease who comes to the emergency room complaining of sudden-onset, squeezing retrosternal chest pain accompanied by shortness of breath and sweating.

Her ECG is as follows. On laboratory evaluation, her troponin levels are significantly elevated.

Alright, so the normal electrical activity of the heart starts in the sinoatrial or SA node located near the opening of the superior vena cava into the right atrium.

Electrical activity is then conducted through the atrium 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.

Now, normally there is delay in conduction at the AV node and the Bundle of His, which gives some time for ventricular filling before the ventricle contracts.

A “heart block”, or AV block, occurs when conduction is delayed for too long at the AV node or the bundle of His. Also, electrical activity may be blocked at the level of the bundle branches, which are called bundle branch blocks.

Okay, on the ECG, the normal delay in the AV node is represented by the PR interval, which is normally less than 5 small boxes, or 200 milliseconds.

There are three main types of AV block.

1st degree AV block is technically not really a block, it’s more of a delay.

Every single atrial impulse eventually makes it to the ventricles.

The high yield concept here is that the only abnormality is a prolonged PR interval, and it’s usually asymptomatic, so it does not require treatment.

2nd degree AV block has two subtypes: Mobitz 1, and Mobitz 2. In Mobitz 1, each atrial impulse encounters a longer and longer delay until one of them does not make it through to the ventricles.

The high yield concept here is that on the ECG, this is reflected as the PR interval getting progressively longer and longer until all of a sudden, the heart drops a beat.

Like Mobitz 1, the heart also drops a beat in Mobitz 2, except this time, conduction through the AV node is all-or-nothing.

Either the atrial impulse goes through with no delay, or it doesn’t at all.

There is no progressive prolongation of the PR interval in Mobitz 2. On the ECG, Mobitz 2 shows a couple of normal PR intervals followed by a dropped beat.

Also, like 1st degree AV block, Mobitz 1 is usually benign and doesn’t require treatment unless it’s causing symptoms.

On the other hand, Mobitz 2 can be dangerous and may result in severe bradycardia and decreased cardiac output.

Therefore it requires treatment with a pacemaker.

Now, Mobitz 2 blocks can sometimes progress to our next type, the dangerous 3rd degree AV block.

In this type, none of the electrical impulses are conducted through the AV node, and that’s why it’s also called complete heart block.

Now remember that all cardiomyocytes are capable of starting their own electrical activity, a property called automaticity.

So in 3rd degree AV block, the ventricles recognize that they’re not getting any impulses, and respond by generating their own electrical rhythm called a ventricular escape rhythm, just to hang on to dear life.

Because the atria and the ventricles each have their own pacemakers, they now contract independent of one another, which is called AV dissociation. This desynchronization of the heart chambers can reduce cardiac output dramatically, leading to syncope or even sudden cardiac death.

On the ECG, the P-waves and QRS complexes have nothing to do with each other, each appearing at their own rates.

The atrial rate is 60 to 100 beats per minute, whereas the ventricular rate usually ranges between 30 to 45 beats per minute.

Because of how dangerous 3rd degree blocks are, anyone diagnosed with it needs a pacemaker.

Alright, a lot of things can cause the 3 types of AV block.

A myocardial infarction may involve the conduction pathway, causing a delay in electrical conduction.

This is especially common in right coronary artery occlusion because it gives off a small branch that supplies the AV node.

On the exam, a clue towards right coronary artery occlusion would be a case of inferior wall myocardial infarction, indicated by elevation of the ST segments in leads II, III and aVF.

Also, electrolyte disturbances like hyperkalemia can alter the membrane potential.

Then there are external causes like Lyme disease, medications such as beta-blockers, calcium channel blockers, adenosine, amiodarone and digoxin.

For your exams, remember that Lyme disease is typically associated with 3rd degree AV block.

Interestingly, congenital heart block is a complication of neonatal lupus, which could also show up on your exam.

Sources

  1. "Pathophysiology of Heart Disease" Wolters Kluwer Health (2015)
  2. "Chou's Electrocardiography in Clinical Practice" Saunders (2008)
  3. "Clinical electrophysiology of atrioventricular block" Cardiol Clin (1983)
  4. "Left Bundle Branch Block: Current and Future Perspectives" Circ Arrhythm Electrophysiol (2020)
  5. "2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society" J Am Coll Cardiol (2019)
  6. "Bradycardias and atrioventricular conduction block" BMJ. 2002 (2002)
  7. "Observations on second degree atrioventricular block, including new criteria for the differential diagnosis between type I and type II block" The American Journal of Cardiology (1972)