Cardio-Resp 3&4 Flashcards

1
Q

Which is greater LV or RV?

A
  • LV performs more work by a factor of 5-7

- LV wall is thicker (8-10mm) vs RV (2-3mm)

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2
Q

Atria and ventricles are separated into ______ by ______ and ____

A

2 functional units
by connective tissue
and one way atrioventricular (AV) valves that preveent backflow to atria

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3
Q

AV valve between RA and RV

A

tricuspid valve

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4
Q

AV valve bewteen LA and LV

A

mitral valve or bicuspid

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5
Q

Valves located at origin of pulmonary artery and aorta are called…

A

one way semi-lunar valves

pump deoxy blood to lungs and pump oxy blood to body (respectively

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6
Q

Semilunar valves open as a response to…

A
  • the ventricles contracting. so that it can pump the blood out and through them
  • ventricles relax, semi-lunar valves shut so no backflow to into ventricles
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7
Q

How does blood travel from atria to ventricles?

A

-both atria fill with blood then contract simultaneously and send blood to ventricles
- then simultaneous contraction of ventricles (0.1-0.2 s) after
(one ventricle to pulmonary system - lungs; one ventricle to systemic system - body)

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8
Q

Stroke volume

A
  • ventricles contracting ejects 2/3 of blood contained

- the amount of blood coming from the ventricle in one heart beat

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9
Q

End systolic volume

A
  • the 1/3 of the initial blood volume in the ventricles
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10
Q

Diastole

A
  • filling of blood in ventricles (end diastolic - filled)
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11
Q

Systole

A
  • pumping of blood in ventricle (end systolic - pumped)
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12
Q

Cardiac output equation

A

CO = heart rate x stroke volume

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13
Q

Is the cardiac cycle equally split? Explain

A

at an average of 75bpm

  • the cycle lasts 0.8 seconds
  • diastole (atria contracted, ventricles relaxed - filling) = 0.5 s
  • systole = 0.3 seconds
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14
Q

3 regions of the heart that can spontaneously generate action potentials

A
  1. Sinoatrial node (SA node)
  2. AV node
  3. Purkinje fibers
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15
Q

SA node

A

sinoatrial node

  • functions as pacemaker
  • located in right atrium near opening of superior vena cava
  • vagus nerve innervates SA node, can adjust heart rate
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16
Q

Action potentials originate at ____

A

SA node

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17
Q

How do action potential spread to RA and LA?

A

spread to adjacent myocytes in RA and LA through gap junctions between cells

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18
Q

What do specialized myocardial cells in the AV node do?

A

Since the atria and ventricles are separate

- these cells are required to move impulse from atria to ventricles

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19
Q

Sequence of electrical activity of heart

A
  • SA node
  • AV node
  • AV bundle, “bundle of His”
  • descends down intraventricular septum, divides right and left with Purkinje fibers in ventricle wall
  • endocardium to epicardium
  • ventricles contract simultaneously
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20
Q

Impulse starts at SA node

A
  • SA node cells directly contact atrial muscle cells

- impulse spreads quickly (0.8 - 1.0 m/s)

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21
Q

Impulse moves to AV node

A
  • located in the posterior septal wall of the right atrium
  • conduction rate slows (0.03 to 0.05 m/s)
  • allows atria to contract and ventricles to fill
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22
Q

Impulse moves to the atrioventricular bundle (of His)

A
  • located between atria and ventricles
  • it is the only connection between atria and ventricles
  • conduction rate begins to increase
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23
Q

Impulse to Purkinje fibres (bundle branches)

A
  • conduction rate peaks
  • rapid conduction caused by more positive resting membrane potential and many gap junction
  • synapse directly with ventricular myocytes
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24
Q

Electrocardiogram (ECG)

A
  • recording of potential differences generated by heart
  • conducted to body surfaces and recorded by electrodes on skin
  • a recording of production and conduction of action potential in heart (not single action potential)
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25
Q

The sequence of ECG

A
  • P wave
  • PR segment
  • QRS complex
  • ST segment
  • T wave
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26
Q

P wave

A
  • right atrium with signal from SA node

- spreads across both atria, causing muscle cells to depolarize and contract (atrial systole)

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27
Q

PR segment

A
  • conduction after atrias contract, before ventricles contract
  • flatline
  • signal leaves atria and enters AV node before ventricles
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28
Q

QRS wave

A
  • down to Q: enters the bundle of His
  • up to R: spreads to bundle branch
  • downto S: spreading through Purkinje fibers along ventricle walls
  • contractile fibers contract rapidly and induce ventricular systole
  • atrial repolarization also occurs but not depicted on the diagram
29
Q

T wave

A
  • ventricular diastole

- ventricular repolarization

30
Q

ST segment

A

-ventricles are depolarized

31
Q

QT interval

A

-depolarization AND repolarization occurs

32
Q

How does a MI look on an ECG?

A
  • ST segment falls very low and has to curve up a lot to reach the T wave
  • -this is the signal heading out of the ventricles as they relax, heading to diastole (T wave)
  • but there is a problem with infact region that blocks them to do so
33
Q

Bradycardia is due to what?

A
  • right vagus innervates SA node and hyperstimulation causes bradycardia
  • the vagus nerve slows down HR
34
Q

Epinephrine

A
  • catecholamine from adrenal medulla

- activate in times of stress

35
Q

Epinephrine causes

A
  • increased heart rate, ionotropy
  • increased cardiac output
  • vasoconstriction of systemic arteries and veins
  • muscle and liver vasculatore
  • -low conc - vasodilation
  • -high conc. vasoconstriction
36
Q

Norepinephrine

A

-adrenal medulla catecholamine release, but most of it comes from sympathetic nerve spill over into the circulation

37
Q

Norepinephrine causes

A
  • increased heart rate, ionotropy
  • increased cardiac output
  • systemic vascular resistance therefore, increased arterial blood pressure
  • vasoconstriction in systemic arteries and veins
38
Q

Blockers

A

alpha and beta blockers

- one can alter response but another adrenoreceptor can still bind the catecholamine

39
Q

How does beta blockers treat cardiac function?

A
  • beta blockers are used to treat chronic heart failure
  • inhibits progressive deterioration of cardiac function
  • blocks sympathetic activation
40
Q

What does caffeine do to the heart?

A
  • stimulates the CNS
  • increases stroke volume (blood pumped from LV)
  • incr. blood pressure
  • incr. herat rate
41
Q

What are heart muscle cells called?

A

myocardial cells / myocytes

42
Q

Myocardial cell structure/components

A
  • actin filaments
  • myosin filaments arranged
  • striated
  • 2 organelles: mitochondria and sarcoplasmic reticulum (SR)
43
Q

What is the structure called of actin and myosin filaments?

A

sarcomeres

- contract via sliding mechanism

44
Q

How are myocytes connected?

A
  • gap junctions
  • stained as “intercalated discs”
  • located at the end of the myocardial cell
  • permits electrical impulses to be conducted cell to cell (synchrony)
45
Q

What is the main purpose of the SR?

A

Sarcoplasmic reticulum

-Ca2+ handling

46
Q

How does an electrical signal cause a heart muscle cell to contract?

A
  • action potential originates at SA node

- contraction from Ca2+ induced Ca2+ release

47
Q

How does Ca2+ induced Ca2+ release work?

A
  • Ca2+ enters myocyte cytoplasm through voltage gated channel
  • stimulates opening of Ca2+ release channel in sarcoplasmic reticulum SR
48
Q

Ca2+ from voltage gated channels serve as ______

A

a messenger for Ca2+ release channels (SR)

49
Q

How do heart muscles relax after contraction?

A

Ca2+ in cytoplasm is pumped back into the SR. (Sarcomeres located in cytoplasm).

50
Q

Excitation - Contraction Coupling in Cardiac muscle (5 steps)

A

Voltage gated calcium channels open and…

  1. Ca2+ diffuse ECF to cytoplasm
  2. Ca2+ release channels on SR open
  3. Ca2+ released from SR (2nd pool of calcium) binds to sarcomere
    - this stimulates contraction
  4. Ca2+ ATPase pump returns calcium back into SR
  5. Myocardial cell relaxes
51
Q

Heart cells are arranged into long, rod shaped organelles that are called

A

myofibrils

52
Q

What are Z discs?

A
  • proteins that anchor thin protein filaments (actin)

- separates each myofibril

53
Q

What is the section of fibre between Z-discs called?

A

Sarcomere

54
Q

What happens to the filaments when muscles contract?

A

thin filaments (actin)
thick filaments (myosin)
these slide past each other
Z dics move closer together

55
Q

What gives the striated pattern?

A

overlapping thin and thick filaments

56
Q

Recall the differences in the light and dark bands and zones within.

A
  • light bands: “I bands”
  • Z discs in middle of I band
  • dark bands “A bands”
  • “H zone” centre of A band where there is no actin present
57
Q

Myosin

A
  • thick filaments (TF)
  • rod shaped protein with angular head at one end
  • contraction causes swivel of head
58
Q

Tropomyosin

A

attached to actin

string like

59
Q

Troponin complex

A

3 subunit attached to tropomyosin

60
Q

How does myosin activation occur?

A
  • myosin head has actin binding site and ATP binding site
  • ATP to ADP (hydrolyzed); myosin head is activated and changes orientation
  • Ca2+ to troponin causes movement of troponin-tropomyosin complex
  • this exposes binding sites on actin
  • myosin cros bridge can now attach to actin and undergo power stroke

(contracting: ca2+ binds, Pi released from ATP, myosin binds actin)

61
Q

3 differences between cardiac and skeletal muscle contraction:
1. stimuli

A
  • skeletal need external stimuli by somatic motor nerves

- cardiac produces action potential automatically (SA nerve), involuntary

62
Q

3 differences between cardiac and skeletal muscle contraction:
2.

A
  • skeletal muscles are long and fibrous
  • myocardial are short, branched, interconnected; tubular cells; adjoined to adjacent myocardial cells by electrical synapses (gap junctions)
63
Q

3 differences between cardiac and skeletal muscle contraction:
3.

A
  • skeletal have direct excitation-contraction coupling between transverse tubules and SR (same pool of calcium)
  • cardiac havevoltage gated ca2+ channels in plasma membrane and Ca2+ release channels in SR do not directly interact
    (Ca2+ induced Ca2+ release)
64
Q

What is coronary artery disease?

A
  • 1 or more of 3 coronary arteries have plaque build up
  • partly restricts blood flow to heart causing chest pain/angina
  • build up of artherosclerosis causes MI/heart attack (death of heart muscle cells)
65
Q

Congestive heart failure

A
  • heart pumps inefficiently and cannot meet bodily needs for blood
  • ventricls (main heart pumps) cause insufficient flow
  • often caused by CAD or MI
66
Q

“congestive” congestive heart failure

A
  • back up of blood in veins leading to the ehart
  • causes the kidney to retain the fluid
  • symptoms: water retention or edema in legs/ankles
67
Q

Treatment to congestive heart failure

A
  • beta blockers to help heart pump
  • diuretics to remove salt and fluids
  • late stage surgery / heart transplant
68
Q

How do beta blockers work?

A
  • beta blockers target beta receptor
  • beta 1 adrenergic receptor (heart and kidneys) 1/3 beta receptors
  • beta receptors bind catecholamines and blockers block the binding
    = reduced heart rate
  • beta blockers also affect RAAS system of kidneys and dilate arteries
69
Q

Max heart rate _____ as age increases.

A

decreases