Heart Flashcards

1
Q

WPW affects between 0.3% and 1% in the population. Sudden cardiac death in people with WPW is rare (less than 0.6%), and is usually caused by the propagation of an atrial tachydysrhythmia (rapid and abnormal heart rate) to the ventricles by the accessory pathway.

A

Wolff–Parkinson–White syndrome

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2
Q

Disorders affecting the cardiomyocytes that make up the electrical conduction system of the heart are called heart blocks. Heart blocks are separated into different categories based on the location of the cellular damage. Damage to any of the conducting cells in or below the bundle of His are collectively referred to as “infra-Hisian blocks”. To be specific, blocks that occur in the right or left bundle branches are called “bundle branch blocks”, and those that occur in either the left anterior or the left posterior fascicles are called “fascicular blocks”, or “hemiblocks”. The conditions in which both the right bundle branch and either the left anterior fascicle or the left posterior fascicle are blocked are collectively referred to as bifascicular blocks, and the condition in which the right bundle branch, the left anterior fascicle, and the left posterior fascicle are blocked is called trifascicular block. Infra-hisian blocks limit the heart’s ability to coordinate the activities of the atria and ventricles, which usually results in a decrease in its efficiency in pumping blood.

A

Heart Block

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3
Q

Abnormal Wiring

A

Bundle of Kent

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4
Q

Abnormal Node

A

Node of Kent

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5
Q

carry the impulse to the heart apex and ventricular walls

A

Purkinje fibers

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6
Q

AV bundle splits into two pathways in the interventricular septum

A

Right and Left bundle branches

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7
Q

Impulse passes from atria to ventricles via the atrioventricular bundle

A

bundle of His

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8
Q

node delays the impulse approximately 0.1 second

A

Atrioventricular (AV)

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9
Q

node generates impulses about 60-80 times/minute in average adult

A

Sinoatrial (SA)

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10
Q

Atrioventricular conduction disease (AV block) describes impairment of the electrical continuity between the atria and ventricles. It occurs when the atrial depolarization fail to reach the ventricles or is conducted with a delay. It can result from an injury or be a genetically inherited disorder.

A

AV Block

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11
Q

The blood supply of the AV node is via the AV nodal artery. The origin of this artery is most commonly (about 90% of hearts) a branch of the right coronary artery, with the remainder originating from the left circumflex artery.[5][6][7] This is associated with the dominance of the coronary artery circulation. In right-dominant individuals the blood supply is from the right coronary artery while in left dominant individuals it originates from the left circumflex artery.

A

AV NODE- Arterial blood supply

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12
Q

decreases conduction velocity (negative dromotropy) at the AV node by decreasing the slope of phase 0 of the nodal action potentials. This leads to slower depolarization of adjacent cells, and reduced velocity of conduction. Acetylcholine, released by the vagus nerve, binds to cardiac muscarinic receptors, which decreases intracellular cAMP. Excessive vagal activation can produce AV block. Drugs such as digitalis, which increase vagal activity to the heart, are sometimes used to reduce AV nodal conduction in patients that have atrial flutter or fibrillation.

A

Parasympathetic (vagal) activationof AV Node

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13
Q

reduces the normal delay of conduction through the AV node, thereby reducing the time between atrial and ventricular contraction. The increase in AV nodal conduction velocity can be seen as a decrease in the P-R interval of the electrocardiogram.

A

Sympathetic activation of the AV node

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14
Q

The slow pathway typically crosses the isthmus between the coronary sinus and the tricuspid annulus; it has a longer conduction time, but a shorter effective refractory period. The fast pathway is commonly a superior route, emanating from the interatrial septum, and has a faster conduction rate but, in turn, a longer effective refractory period. Normal conduction during sinus rhythm occurs along the fast pathway, but higher heart rates and/or premature beats are often conducted through the slow pathway, since the fast pathway may be refractory at these rates.

A

Slow and Fast Pathways to AV node

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15
Q

posterior tract

A

Thorel’s

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16
Q

middle tract

A

Weckebach’s

17
Q

anterior tract

A

Bachmann’s bundle

18
Q

Occlusion of the arterial blood supply to the SA node (most commonly due to a myocardial infarction or progressive coronary artery disease) can therefore cause ischemia and cell death in the SA node. This can disrupt the electrical pacemaker function of the SA node, and can result in sick sinus syndrome.

Sick sinus syndrome is a relatively uncommon syndrome in the young and middle age population.
Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. It can also result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate).

A

Sinus Sick Syndrome

19
Q

The SA node receives blood supply from the SA node artery. Anatomical dissection studies have shown that this supply may be branch of the right coronary artery in the majority (about 60-70%) of hearts, and a branch of the left coronary artery (usually the left circumflex artery) in about 20-30% of hearts

A

SA NODE-arterial blood supply

19
Q

describes an irregular heartbeat caused by faulty electrical signals of the heart. When the heart’s sinoatrial node is defective, the heart’s rhythms become abnormal – typically too slow or exhibiting pauses in its function or a combination, and very rarely faster than normal

A

Sinus node dysfunction

20
Q

Connection between blood vessels that allow blood to flow to and away from tissues if a vessel gets blocked

A

ANASTAMOSIS

21
Q

(LUB-dup) are associated with closing of heart valves
First sound occurs as AV valves close and signifies beginning of systole (LUB)
Second sound occurs when SL valves close at the beginning of ventricular diastole (dup)

A

Heart Sounds

22
Q

occurs as AV valves close and signifies beginning of systole (LUB)

A

First sound

23
Q

occurs when SL valves close at the beginning of ventricular diastole (dup)

A

Second sound

24
Q

LUB

A

Tricuspid- fifth intercostal space right
Bicuspid- fifth intercostal space left

25
Q

DUP

A

Aortic- second intercostal space right
Pulmonary- second intercostal space left

26
Q

provides the origin for the pectinate muscles.

A

Crista terminalis

27
Q

a. Atria are the receiving chambers of the heart
b. Each atrium has a protruding auricle
c. Pectinate muscles mark atrial walls
d. Blood enters right atria from three sources
1. Superior venae cavae
2. Inferior venae cavae
3. Coronary sinus
e. Blood enters left atria from pulmonary veins

A

Atria of the Heart

28
Q

Vessels returning blood to the heart include:

A

Into Right Atrium
Superior venae cava
Inferior venae cava
Coronary sinus
b. Into Left Atrium
Right pulmonary vein
Left pulmonary vein

29
Q

Vessels conveying blood away from the heart include:

A

a. Pulmonary trunk
- which splits into
- right pulmonary artery
- left pulmonary artery
b. Ascending aorta (three branches)
– Brachiocephalic
- left common carotid
- Subclavian arteries (right and left)