Lecture 15 Flashcards

1
Q

Cardiac Cycle step 1

A

Contraction of atria
(AKA atrial systole)

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2
Q

Cardiac Cycle step 2

A

contraction of
ventricles (ventricular
systole)

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3
Q

Cardiac Cycle step 3

A

rest (diastole) when neither chamber is contracting

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4
Q

contraction name

A

systole (BP: 120)

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5
Q

relaxation name

A

diastole (BP: 80)

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6
Q

doctors are more interested in….

A

diastole because its the force by which the heart has to work against to eject blood against the contraction (diastole is period when heart fills back up with blood)

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7
Q

AFTERLOAD

A

diastolic arterial pressure, how hard heart has to work to overcome systolic pressure

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8
Q

strength and rate of heart contractions controlled by

A

Neural and Endocrine signals

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9
Q

sympathetic innervation (norepinephrine) causes

A

increased HR eg these signals released when doing excersize

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10
Q

parasympathetic innervation (acetylcholine) causes

A

decreased HR eg. these signals are released when sitting in a lecture

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11
Q

epinephrine causes

A

increased strength of heart contractions / how much blood is being ejected with each contraction

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12
Q

from rest to excersize:

A

HR can increase to nearly 200 bpm
cardiac output increases from 5 L/min to 25 L/min
(elite athletes: 40 L/min)

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13
Q

Max HR formula

A

220 - age

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14
Q

Electrical signal is propagated by: (3)

A

Nodes, Nerves, Intercalated disks (gap junctions)

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15
Q

Nodes

A

SA (sinoatrial) nodes, AV (atrioventricular) nodes

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16
Q

SA nodes are:

A

Heart’s natural pacemaker, electrical impulses generated here.

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17
Q

electrical impulse tells:

A

Heart to beat

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18
Q

Nerves

A

Bundle of His, Bundle branches, purkinge fibers
(All have lots of gap junctions)

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19
Q

Intercalated disks (gap junctions)

A

send signals between parts of heart, eg SA node sends signal to left atrium

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20
Q

Cardiac muscle consists of

A

individual cardiomyocytes connected by intercalated discs (GAP JUNCTIONS!) to work together as a single functional organ

21
Q

miscommunication usually results in

A

some kind of arrhythmia

22
Q

miscommunication is

A

something wrong with the sequential sequencing of the heart

23
Q

Abnormal sinoatrial node firing results in

A

tachycardia (fast), bradycardia (slow)

24
Q

Blocks can:

A

slow down or prevent signal propagation from atria to ventricles

25
blockages (eg at AV node)
can vary in terms of degree of the blockage
26
Ventricles can:
contract independently (bundle of His, 40 bpm)
27
Fibrillations
more serious, occur when cells depolarize independently
28
Atrial Fibrillations (A-Fib)
a quivering or irregular heartbeat (arrhythmia)
29
Ventricular fibrillation (V-fib)
the most serious cardiac rhythm disturbance. Must try and reset electrical signal
30
Atherosclerosis is
Narrowing of arteries due to calcified fatty deposits (plaque) and thickening of the wall
31
Atherosclerosis is triggered by
damage to arterial wall (inflammation)
32
Atherosclerosis can lead to
- heart attack or stroke - When this occurs in the arteries of heart muscle, it is called coronary artery disease
33
Factors contributing to Coronary Artery Disease:
Elevated blood lipids, hypertension, inflammatory mediators (C-reactive protein), Diet (sodium, potassium, saturated/trans fats, cholesterol), Smoking, physical inactivity, obesity/diabetes, Age, genetics
34
Treating Coronary Artery Blockages
Angioplasty, Bypass Surgery
35
Angioplasty
a catheter and balloon are threaded into the coronary artery to the point of blockage. Plaque is pushed to the outside of the artery walls and held there by stent.
36
Bypass Surgery
Vein taken from arm or leg; one end attached above the blockage and the other below
37
Hypertrophy
a sign of being “overworked”. The heart muscle will respond and hypertrophy just like your skeletal muscle would respond to weight-lifting
38
Endurance athletes
mostly an increase in LV chamber (need to increase cardiac output)
39
Weightlifters
mostly increased LV wall and septum thickness (need to overcome increased afterload – the amount of pressure needed to eject blood during ventricular contraction)
40
Enlargement of the Heart pros
Athlete's heart – an appropriate adaptation! Occurs in both endurance athletes and weightlifters! ☺
41
Enlargement of the Heart cons
Causes include high blood pressure and narrowing of aortic valve ... the heart must work harder to overcome these
42
Hypertension # stage 1
130-139/80-89
43
Hypertension # stage 2
140+/90+
44
Hypertensive crisis #
higher than 180/higher than 120
45
Vasoconstriction (artery hole gets smaller)
* Alpha-receptors are located on arteries. * Norepinephrine and epinephrine bind to 2 adrenergic receptors * This causes arteries to constrict (vasoconstriction) * This increases blood pressure * E.g. during exercise
46
Vasodilation (artery hole opened wider)
* Blood vessels in skeletal muscles lack alpha-receptors * Norepinephrine and epinephrine bind to b2 adrenergic receptors found in arteries of skeletal muscle * This dilates vessels of the skeletal muscles (vasodilation) so they can receive increased blood flow * E.g. also during exercise!
47
how much does Cardiac output increase during excersize
5x, 8x in elite athletes
48
why does BP not increase much during exercise
Distribution of blood does not increase proportionally. blood flow is diverted to where it is needed during exercise! The working muscles! Dilation of vessels to skeletal muscle and heart increases blood flow to muscles (β2 receptors and local metabolites). Constriction of vessels to the gut and kidneys decreases blood flow to these organs (B2 receptors). Dilating vessels in the muscle decreases resistance and we have a lot of muscle mass!
49
Resistance exercise (e.g. weightlifting) can cause
dramatic increases in blood pressure - up to 345/245 mmHg. Holding your breath – increases intrathoracic pressure during the lift – called the “Valsalva maneuver” Temporarily raises blood pressure and slows heart rate!