Heart blocks: Pathology review

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Heart blocks: 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
Fetal circulation
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 cycle
Cardiac work
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
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus 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
Persistent 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
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
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
Deep vein thrombosis and pulmonary embolism: 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
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
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Aortic aneurysms and dissections: Clinical
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Pulmonary hypertension
Raynaud phenomenon
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

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)