Lecture 15 Flashcards

1
Q

Cardiac Cycle step 1

A

Contraction of atria
(AKA atrial systole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cardiac Cycle step 2

A

contraction of
ventricles (ventricular
systole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cardiac Cycle step 3

A

rest (diastole) when neither chamber is contracting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

contraction name

A

systole (BP: 120)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

relaxation name

A

diastole (BP: 80)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AFTERLOAD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

strength and rate of heart contractions controlled by

A

Neural and Endocrine signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

sympathetic innervation (norepinephrine) causes

A

increased HR eg these signals released when doing excersize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

parasympathetic innervation (acetylcholine) causes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

epinephrine causes

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Max HR formula

A

220 - age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Electrical signal is propagated by: (3)

A

Nodes, Nerves, Intercalated disks (gap junctions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Nodes

A

SA (sinoatrial) nodes, AV (atrioventricular) nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SA nodes are:

A

Heart’s natural pacemaker, electrical impulses generated here.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

electrical impulse tells:

A

Heart to beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Nerves

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Intercalated disks (gap junctions)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

blockages (eg at AV node)

A

can vary in terms of degree of the blockage

26
Q

Ventricles can:

A

contract independently (bundle of His, 40 bpm)

27
Q

Fibrillations

A

more serious, occur when cells depolarize independently

28
Q

Atrial Fibrillations (A-Fib)

A

a quivering
or irregular heartbeat (arrhythmia)

29
Q

Ventricular fibrillation (V-fib)

A

the most serious cardiac rhythm disturbance. Must try and reset electrical signal

30
Q

Atherosclerosis is

A

Narrowing of arteries due to calcified fatty deposits (plaque) and thickening of the wall

31
Q

Atherosclerosis is triggered by

A

damage to arterial wall
(inflammation)

32
Q

Atherosclerosis can lead to

A
  • heart attack or stroke
  • When this occurs in the arteries of heart
    muscle, it is called coronary artery disease
33
Q

Factors contributing to Coronary Artery Disease:

A

Elevated blood lipids, hypertension,
inflammatory mediators (C-reactive protein), Diet (sodium, potassium, saturated/trans fats,
cholesterol), Smoking, physical inactivity, obesity/diabetes, Age, genetics

34
Q

Treating Coronary Artery Blockages

A

Angioplasty, Bypass Surgery

35
Q

Angioplasty

A

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
Q

Bypass Surgery

A

Vein taken from
arm or leg; one
end attached above
the blockage and
the other below

37
Q

Hypertrophy

A

a sign of being
“overworked”. The heart
muscle will respond and
hypertrophy just like your
skeletal muscle would respond to weight-lifting

38
Q

Endurance athletes

A

mostly an increase in LV
chamber (need to increase cardiac output)

39
Q

Weightlifters

A

mostly increased LV wall and septum thickness (need to overcome increased
afterload – the amount of pressure needed to eject
blood during ventricular contraction)

40
Q

Enlargement of the Heart pros

A

Athlete’s heart – an appropriate adaptation! Occurs in both endurance athletes and weightlifters! ☺

41
Q

Enlargement of the Heart cons

A

Causes include high blood pressure and narrowing of
aortic valve … the heart must work harder to overcome these

42
Q

Hypertension # stage 1

A

130-139/80-89

43
Q

Hypertension # stage 2

A

140+/90+

44
Q

Hypertensive crisis #

A

higher than 180/higher than 120

45
Q

Vasoconstriction (artery hole gets smaller)

A
  • 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
Q

Vasodilation (artery hole opened wider)

A
  • 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
Q

how much does Cardiac output increase during excersize

A

5x, 8x in elite athletes

48
Q

why does BP not increase much during exercise

A

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
Q

Resistance exercise (e.g. weightlifting) can cause

A

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!