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BIOM 3200 > cardiovascular / cardiorespiratory system > Flashcards

cardiovascular / cardiorespiratory system Flashcards

1
Q

what are the 2 sides of the circulatory system

A

arteriole - carries blood away from the heart
venule - returns blood to the heart
- capillaries connect the 2 sides to exchange materials between blood and tissues

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2
Q

layers of the blood vessels

A
  • outer = tuneca externa: connective tissue
  • middle = tuneca media: smooth muscle
  • inner = tuneca interna: has its own 3 layers… endothelium, elastin, glycoproteins
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3
Q

characteristics of veins

A
  • most blood volume is held in the veins
  • returns blood from tissues to the heart
  • capacitance vessels - able to expand as they accumulate additional amounts of blood
  • less muscular than arteries
  • average pressure in veins is 2mmHg
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4
Q

what to venous valves do

A

ensure one-way flow of blood back to the heart

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5
Q

what does the skeletal muscle pump do for the venous system

A

helps veins of the lower limbs return blood to the heart - veins pass between skeletal muscle groups which provide contractions to help move blood back

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6
Q

how does venous blood from the abdominal regions get to thoracic regions

A
  • facilitated by breathing
  • contraction of the diaphragm and pressure in the abdomen from breathing squeezes the veins and helps blood return to the heart
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7
Q

what are varicose veins

A

when there is dysfunction of one way valves, more blood coagulates in the lower limbs
- blood pooling forms risk of clot formation which can lead to DVT - can’t deliver nutrients therefore get death of tissue

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8
Q

characteristics of arteries

A
  • brings blood from the heart to tissues
  • have numerous layers of elastin fibres between the smooth muscle cells of the tunica media
  • expand when the pressure of blood rises as a result of ventricle contraction
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9
Q

elasticity of arteries

A
  • arteries recoil like a rubber band when BP falls during relaxation of the ventricles
  • the elastic recoil drives blood during the diastolic phase when the heart is resting and not providing pressure
  • small arteries and arterioles are less elastic than large ones therefore their diameter only changes slightly
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10
Q

systolic pressure vs diastolic pressure

A

systolic: maximum pressure the heart exerts while beating (expanded)
diastolic: the amount of pressure in the arterioles between beats (relaxed)

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11
Q

vasoconstriction vs vasodilation

A

vasoconstriction: narrowing of blood vessels, decrease blood flow to capillary bed
vasodilation: widening of blood vessels, increases blood flow to capillary bed

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12
Q

walls of the capillary bed

A
  • composed of a single layer of endothelial cells
  • lack smooth muscle and connective tissue which make it easier to exchange material between blood and tissues
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13
Q

what keeps distribution of materials at capillary beds in a constant state of dynamic equilibrium

A

net filtration pressure at the artery end (difference in hydrostatic pressure) and net oncotic pressure at the vein end (difference in osmotic pressure)

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14
Q

exchange of nutrients at the capillary bed

A

at the arterial end of the capillary oxygen, nutrients, hormones etc. are brought to the capillary
- blood pressure forces fluid out of the capillary to the fluid surrounding tissue cells
at the venous end of the capillary carbon dioxide and wastes are removed from the capillary
- fluid is drawn back into the capillary by osmotic pressure

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15
Q

blood flow equations

A

flow = driving force/resistance
- the main driving force of blood flow is the pressure difference
- doesn’t deliver blood equally to tissues

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16
Q

poiseulle’s law

A

resistance depends on 3 major factors
1. tube/blood vessel radius
2. viscosity of the blood
3. tube/blood vessel length

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17
Q

how does vessel radius effect blood flow

A

decrease radius = increase resistance = decrease blood flow
- variable with the most impact on resistance
- regulated by smooth muscle contraction

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18
Q

how does blood viscosity effect blood flow

A

more viscous = more friction = more resistance = decrease blood flow
- “thickness of blood”
- won’t change in healthy people (unless dehydrated then more viscous)

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19
Q

what happens to blood viscosity if there is a blood clot

A

increase hematocrit = increase interactions between RBC = INCREASE CLOTS = decrease vessels radius = decrease blood flow

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20
Q

how does vessel length effect blood flow

A

increase length = increase friction = increase resistance = decrease blood flow
- length doesn’t change physiologically

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21
Q

pulmonary vein and pulmonary artery

A

have opposite O2 statuses than normal veins and arteries
- pulmonary vein carries oxygenated blood TO heart
- pulmonary artery carries deoxygenated blood AWAY from heart

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22
Q

what are the air passage ways of the body

A
  • nasal cavity
  • pharynx
  • larynx
  • oral cavity
  • trachea
  • bronchus
  • lungs
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23
Q

they pharynx and larynx

A
  • the nasal cavity leads to the pharynx (throat)
  • the pharynx is a muscular passage connecting the nasal cavity with the larynx
  • the larynx is where air is diverted toward the lungs and food towards the esophagus
  • the larynx also contains vocal cords (which are not actually cords by folds in the lining tissue of the larynx)
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24
Q

conducting zone and respiratory zone of the respiratory system

A

conducting zone: trachea, primary bronchus, terminal bronchioles
respiratory zone: terminal bronchiole, respiratory bronchioles and alveolar sacs
- gas exchange occurs at the respiratory bronchioles
- alveoli are air sacks that increase SA in the lungs to use for gas exchange
- the trachea warms and humidifies air

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25
Q

What are the physical properties of the lungs

A
  1. inspiration and compliance
  2. expiration and elasticity
  3. surface tension
  4. lunch volumes and capacities
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26
Q

what is lung compliance

A

compliance affects the ability of the lungs to expand during inspiration
- change in volume per change in trans pulmonary pressure
- lung disease reduces compliance - anything that produces a resistance to distension

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27
Q

what is intrapulmonary pressure

A

pressure in the alveoli and airways of the lungs

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28
Q

what is inspiration

A

breathing in (inhaling) - chest expands and diaphragm contracts
- for inspiration to occur, the lungs must be able to expand when stretched (must have high compliance)

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29
Q

what is expiration

A

breathing out (exhaling) - chest contracts and diaphragm expands
- for expiration to occur, the lungs must get smaller when tension is released (have elasticity)

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30
Q

what is lung elasticity

A
  • the tendency of a structure to return to its initial size after being distended
  • the lungs have a high content of elastin protein therefore are very elastic and resist distension
  • lungs are always in a state of elastic tension because they are normally stuck to the chest wall
  • tension is released by elastic recoil when
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31
Q

lungs need to be attached to the inner wall of the chest cavity to inflate

A
  • chest wounds prevent inflation, even if the individual continues to ventilate
  • there will be movement of air but not of the lungs
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32
Q

what can cause a lung to collapse

A

Pneumothorax
air enters the pleural space - increase in intrapleural pressure - trans pulmonary pressure is abolished

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33
Q

what keeps the lungs against the chest wall

A

intrapulmonary pressure > intrapleural pressure
(pressure inside > pressure outside)

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34
Q

what are pleural membranes

A

make up the outer lung surface and inner surface of the chest cavity
- visceral layer = attached to outside of lung
- parietal layer = attached to inside of chest

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35
Q

what is pleural fluid

A
  • a mucus-rich fluid produced by the PMs that lies between the 2 membranes
  • hold the 2 membranes together - holds lungs attached to the inner wall of the thoracic cavity
  • acts as a lubricant that allows the lungs to slide easily as they inflate and deflate
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36
Q

what causes surface tension of the lungs

A
  • exerted by fluid in the alveoli
  • created by attraction between water molecules in the fluid which pulls them tightly together
  • surface tension would cause the alveoli to collapse
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37
Q

what is sufficant

A

a mixture of phospholipids and hydrophobic sufficant proteins, secreted into the alveoli by type II alveolar cells
- lowers surface tension in alveoli - prevents them from collapsing during expiration

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38
Q

surfactant and babies

A
  • surfactant is produced in late fetal life, premature babies sometimes lack surfactant and their alveoli are collapsed as a result
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39
Q

what are the 4 types of lung volumes

A

tidal volume, inspiratory reserve, expiratory reserve, residual volume

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40
Q

what are the 4 types of lung capacities

A

total lung capacity, vital capacity, inspiratory capacity, functional residual capacity

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41
Q

tidal volume

A

volume of gas inspired or expired in an unforced respiratory cycle
- increase in tidal volume = increase in fresh air = increase in O2

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42
Q

inspiratory reserve

A

max volume of gas that can be inspired during forced breathing in ADDITION to tidal volume

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43
Q

expiratory reserve

A

max volume of gas that can be expired during forced breathing in ADDITION to tidal volume

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44
Q

residual volume

A

volume of gas remaining in the lungs after max expiration

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45
Q

total lung capacity

A

total amount of gas in the lungs after max inspiration

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46
Q

vital capacity

A

max amount of gas expired after max inspiration

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47
Q

inspiratory capacity

A

max amount of gas that can be inspired after normal tidal expiration

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48
Q

functional residual capacity

A

the amount of gas remaining in the lungs after a normal tidal expiration

49
Q

what is anatomical dead space

A

where no gas exchange occurs in the reparatory system (the conducting some)
- the conducting zone includes the nose, mouth, larynx, trachea, bronchi, bronchioles
- about 150mL

50
Q

what is the role of hemoglobin

A
  • holds most of the oxygen in the blood
  • Hb contains iron and is present in the cytoplasm of RBCs
  • Hb chemically combines with O2 and releases gas when cells need it
  • Hb acts as an O2 shuttle from the lungs to body tissue
  • Hb also has binding sites for CO2, acts as a CO2 shuttle from the body tissue to the lungs
51
Q

what is the Bohr effect

A

the acidity of the plasma determines whether O2 combines to form oxyhemoglobin or if O2 is released from oxyhemoglobin

52
Q

O2 and blood acidity

A

O2 combines with Hb = low acidity/higher pH
O2 released from Hb = high acidity/lower pH
- when O2 is not combined with Hb there are H+ ions present

53
Q

O2 uptake in the lungs

A
  • in the lungs O2 enters the blood and CO2 leaves
  • O2 dissolves in the lining fluid film of the alveoli, diffuses through the walls of the alveoli and capillaries into plasma
  • O2 then diffuses into RBCs and combines chemically with Hb to form oxyhemoglobin because acidity decreases
  • oxyhemoglobin formation occurs in the lungs because blood CO2 levels in lungs are low
54
Q

O2 release in the tissues

A
  • in the tissues O2 is used (taken up) and CO2 is produced
  • O2 is released from oxyhemoglobin and diffuses into body tissue
  • dissociation of Hb and O2 occurs in tissues because plasma CO2 in tissues is high (and pH decrease)
55
Q

CO2 transport in the blood

A
  • CO2 is a byproduct of metabolism - constant movement by diffusion from body cells into the blood plasma
  • CO2 has a low solubility and only very little can be carried in simple solution
  • 10% is dissolved molecular CO2, 20% is carried attached to Hb as carbamino compounds, majority diffuses into RBCs and is converted to bicarbonate ion by carbonic anhydrase
56
Q

CO2 in body tissues

A
  • constant CO2 production causes CO2 and H2O to react and form bicarbonate + H+
57
Q

CO2 in the lungs

A
  • Bicarbonate and H+ react to form H2O and CO2, causing CO2 being lost to the alveolar air sacs
58
Q

ventilation during exercise

A
  • there is a simultaneous increase in O2 consumption and CO2 production by muscles - matched with an increase in lung ventilation
  • 2 mechanisms explain increased ventilation: neurogenic and humeral
  • we are not good at maintaining venous levels during exercise
59
Q

neurogenic ventilation

A

explains immediate increase in ventilation when exercise begins
- sensory nerve activity from exercising limbs may stimulate respiratory muscles
- input from the cerebral cortex may stimulate the brain stem centers to modify ventilation

60
Q

Humoral ventilation

A

explains the continued rapid and deep ventilation after exercise has stopped
- PCO2 and pH in the region of chemoreceptors may be different from downstream regions
- variations cannot be detected by blood samples and still stimulate chemoreceptors

61
Q

what is the lactate threshold

A

the maximum rate of O2 consumption that can be attained before anaerobic metabolism produces a rise in blood lactate levels
- reached with continuous heavy exercise - rise in lactate levels due to aerobic limitations of the muscles

62
Q

why does the lactate threshold increase in athletes

A

CO2 is higher = higher rate go oxygen delivery to muscles
- skeletal muscles have more mitochondria and Kreb’s cycle enzymes

63
Q

how do changes in altitude relate to changes in ventelation

A
  • less O2 is available at higher altitudes so there is a decrease in oxyhemoglobin and O2 content of blood
  • the rate at which O2 can be delivered to cells after dissociating from Hb is decreased because max [O2] that can be dissolved in plasma decreases
64
Q

cardiac anatomy - major compartments of the heart

A

atria: receive blood from the venous system
ventricles: deliver blood into the arteriole system
septum: prevents mixture of blood from 2 sides of the heart

65
Q

pulmonary vs systemic circulation

A

pulmonary = right ventricle to left atrium
systemic = left ventricle to right atrium

66
Q

left vs right ventricle

A

the amount of work done by the left ventricle is much greater than the right ventricle
- left ventricle is 8-10mm thick
- right ventricle is 2-3mm thick

67
Q

One-way AV valves

A

prevent the back flow of blood into atria
- tricuspid valve: AV valve between the right ventricle and the atria (has 3 flaps)
- bicuspid valve: AV valve between the left ventricle and the atria (has 2 flaps)

68
Q

pulmonary artery vs aortic valve (aorta)

A

pulmonary valve: pumps deoxygenated blood to the lungs
aortic valve: pumps oxygenated blood to the body
- when the ventricles contract valves open so blood is pumped through them
- when ventricles relax valves close so blood doesn’t flow back through them

69
Q

end-diastolic volume

A

volume of blood in the ventricles at the end of diastole (right before ventricles contract)

70
Q

stroke volume

A

volume of blood pumped per beat by each ventricle - volume of the ejection fraction

71
Q

end-systolic volume

A

volume of the initial blood left in the ventricles following contraction - leftover after ejection fraction

72
Q

Systole

A

simultaneous contraction of both ventricles - one sends blood to lungs or pulmonary system, other sends blood to body or systemic system
- during contraction atria relaxed, ventricles contract and AV valves close
- ejection happens

73
Q

Diastole

A

80%: venous return fills the atria - increase in atrial pressure - AV valve opens - blood flows into ventricles
20%: both atria then contract simultaneously sending blood to ventricles
- during relaxation atria relax, ventricles relax, semilunar valves are closed
- rapid filling happens followed by atrial contraction

74
Q

what also occurs with an increased end-diastolic volume

A

increased stroke volume and contractility

75
Q

what is cardiac output

A

the volume of blood pumped per minute by each ventricle
stroke volume x heart rate
- average cardiac output is 5-5.5L/min

76
Q

average cardiac rate

A

60-100 bpm, but 70bpm is most common - each cycle lasts 0.8 seconds
- 0.5 seconds in diastole
- 0.3 seconds in systole

77
Q

electrical activity of the heart

A
  • electrical activity of the heart facilitates its pumping ability
  • myocardial cells interconnected by gap junctions (electrical synapses)
  • the entire mass of interconnected cells is the myocardium (functional syncytium)
78
Q

3 regions of the heart can spontaneously generate action potentials

A
  1. sinoatrial node (SA node)
  2. AV node
  3. purkinje firbers
79
Q

what happens when action potentials originate at the SA node

A
  • HCN channels allow spontaneous APs to occur
  • channels open in response to hypertension
  • allows entry of Na+ into the cell during diastole
    *pacemaker cells do not have a resting membrane potential
80
Q

spontaneous APs and muscle contractions of the heart

A
  • happen about every 0.8 seconds
  • APs spread to adjacent myocytes in the RA and LA through gap junctions between these cells
  • specialized cells (conducting tissue) are needed to move the impulse atria to ventricles since they are seperate
81
Q

timing of electrical activity of the heart beat

A
  1. impulses start at the SA node - spread in 0.8-1m/s
  2. impulse goes to the AV node - conduction rate slows for excitation between atria and ventricles to allow ventricles to fill with blood - AV valve has thinner myocytes and fewer gap junctions
  3. impulse continues through AV bundle (bundle of his) - conduction rate increases
  4. impulse descends down intraventricular septum and divides left and right with purkinje fibres in ventricle wall - conduction rate peaks
  5. spreads from endocardium to epicardium causing both ventricles to contract
82
Q

What is the electrodiagram

A

plotted results from the production and conduction of action potentials in the heart - potential differences are detected by electrodes placed on body surface

83
Q

components of the electrodiagram

A

P-wave: depolarization of atria in response to the SA node
PR interval: delay of AV node to allow filling of ventricle
QRS complex: depolarization of ventricles, triggers main pumping contractions
ST segment: beginning of ventricle repolarization, should be flat
T-wave: ventricular repolarization

84
Q

How is a heart attack classified

A

distorted ST segment in the ECD as a result of myocardial infract
- heath myocytes are more depolarized than the cells in the infarct region
- heartbeat is normally paced by SA node but is too slow or fast
- right vagus (ACh) innervates SA node hyper stimulation can lead to bradycardia

85
Q

catecholamines and ventricles

A
  • ventricles receive direct innervation from adrenergic neurone
  • activated in times of stress such as exercise, heart failure, pain etc.
86
Q

circulating epinephrine

A
  • released from the adrenal medulla
  • b-adrenergic receptors most sensitive (in myocardium)
  • increased heart rate snd contractility lead to increased cardiac output
  • binding causes VASODILATION of arterioles and relaxation and dilation of bronchioles
87
Q

circulating norepiephrine

A
  • released from cardiac sympathetic nerve endings, some from the adrenal medulla
  • a-adrenergic receptors are the most sensitive (in smooth muscle wall of blood vessels)
  • VASOCONSTRICTION in arteries and veins
  • overall increased systemic vascular resistance and increased arterial BP
88
Q

how do catecholamines “blockers” work

A
  • antagonists that block ligands (E and NE) from binding receptor
  • alpha-blocker (prazosin): may be used to treat high blood pressure (hypertension)
  • beta-blocker (propranolol): used to lower HR and BP
  • blocking one alone alters response but the other adrenoreceptor can still bind the catecholamine
89
Q

what causes heart failure

A

after cardiac injury or insult - cadiac contractility decrease - peripheral perfusion decreases (can’t send as much blood to systemic circulation - chronic SNS activation
SNS activation leads to…
- desensitization of B-adrenergic system
- apoptosis and necrosis
- fibrosis
- hypertrophy

90
Q

how are B-blockers used to treat heart failure

A
  • B-blockers limit chronic SNS activation - slow down deterioration
91
Q

heart muscle cells

A

-myocardial cells that have alternating actin and myosin filaments which make muscles striated
- actin and myosin filaments are arranged in the form of sarcomeres
- contract via a sliding filament mechanism

92
Q

what permits electrical impulses to be conducted cell to cell

A
  • myocytes are connected via gap junctions at the end of each myocardial cell
  • there gap junctions stain as intercalated discs
93
Q

myocytes are organized into fibres along with 2 major organelles…

A

mitochondria - for energy
sarcoplasmic reticulum - for calcium handling
- the SR is a special type of ER which regulates calcium by calcium

94
Q

Excitation: what happens when voltage-gated calcium channels open in heart muscle cells

A
  1. Ca2+ diffuses from ECF to the cytoplasm
  2. Ca2+ release channels on SR open
  3. Ca2+ released from SR binds to sarcomere (tropin), stimulates contraction
  4. Ca2+-ATPase pumps Ca2+ back into the SR
  5. myocardial cells relax
95
Q

cardiac action potentials and Ca2+ channels

A
  • originate in the SA-node (pacemaker)
  • APs cause membrane depolarization causing Ca2+ induced Ca2+ release
  • Ca2+ enters the myocyte through voltage water Ca2+ channels which stimulates opening of the Ca2+ release channels in the SR
96
Q

Ca2+ releases Ca2+…

A

Ca2+ from the voltage-gated channels serves as a messenger for Ca2+ release channels
- for heart muscles to relax, the Ca2+ in the cytoplasm must be pumped into the SR

97
Q

what are myofibrils

A
  • cardiomyocytes arranged into long, rod-shaped sub-units
  • separated into separate sections by z-discs
  • sarcomeres are the section of fibres between Z-discs
98
Q

what are z-discs

A
  • proteins that act as anchors for thin protein filaments
  • consist of actin and other proteins
99
Q

myosin and actin

A

myosin = thick filaments
actin = thin filaments

100
Q

Titin proteins

A
  • elastic proteins that run through the thick filaments and help stabilize them in position
  • begin in the middle of the sarcomere and anchor the thick filament to the Z-disc
  • help muscle return to resting length through elasticity
101
Q

types of bands within myofibrils

A

I-bands: the light bands, contain only actin
A-bands: the dark bands
Z-discs: lie in between the I-bands
H-bands: a narrow light band in the centre of the A-band, no actin overlap

102
Q

sliding filament theory of contraction

A
  • interactions between the thick myosin and thin actin filaments result in shortening of the sarcomere
  • shortening of the sarcomere - shortening of the myofibril - shortening entire muscle (contraction)
103
Q

what happens to each band in contractions

A
  • A-bands don’t shorten but move closer together
  • I-bands do shorten, but the thin filaments themselves don’t - thin filaments slide towards the H zone
  • H-band shortens or disappears
104
Q

tropomyosin and troponin

A

Tropomyosin: filamentous protein attached to actin and covers myosin binding sites in its resting state
troponin complex: complex of 3 subunits is attached to tropomyosin and has a high affinity binding site for Ca2+
- both facilitate in contraction

105
Q

relaxed vs contracted muscle - binding

A

relaxed: tropomyosin blocks the binding site for heads
contracting: myosin head binds to actin

106
Q

how does sliding between actin and myosin occur

A
  • thick filaments have an angular head at one end - the contraction of muscle is cause by swirling of the head
107
Q

how does contraction of cardiac muscle happen? - 8 steps

A
  1. resting myosin contains ADP and Pi
  2. Ca2+ released from SR will bind troponin
  3. this induces a conformational change in tropomyosin, revealing the myosin binding sites on actin
  4. attraction between myosin head and actin - binding (cross bridge) - release of Pi
  5. conformation change in myosin
  6. a power stroke occurs causing filaments to SLIDE across each other, shortening the sarcomere and releasing ADP
  7. a new ATP molecule binds the myosin head - release from actin
  8. the hydrolysis of ATP to ADP + Pi returns the myosin to its resting conformation
108
Q

how does contraction of cardiac muscle happen? - 6 steps

A
  1. resting fibre - cross bridge is not attached to actin
  2. cross bridge binds to actin
  3. Pi is released from myosin head, causing conformational change in myosin
  4. power stroke causes filaments to slide, ADP is released
  5. a new ATP binds to myosin head, allowing it to release from actin
  6. ATP is hydrolyzed and phosphate binds to myosin, causing cross bridge to return to its original orientation
109
Q

what is ultimately responsible for controlling heart contraction

A

calcium

110
Q

skeletal muscle vs cardiac muscle: generation of APs

A

skeletal: required external stimulation by somatic motor nerves
cardiac: produces APs automatically (SA node - HCN channels present in pacemaker cells)

111
Q

skeletal muscle vs cardiac muscle: anatomy/structure

A

skeletal: long, fibrous cells that are structurally and functionally separated
cardiac: short, branched, interconnected cells - tubular structure and joined by gap junctions

112
Q

skeletal muscle vs cardiac muscle: mechanism of excitation-contraction coupling

A

skeletal: direct excitation-contraction coupling between transverse tubules and SR volage-gated Ca2+ channels mechanically coupled to Ca2+ release channels
cardiac: voltage-gated Ca2+ channels in plasma membrane and Ca2+ release channels in the SR do not directly interact

113
Q

what is coronary artery disease

A
  • occurs when you have a plaque build-up in one or more of the coronary arteries
  • reduces radius = increase resistance = decrease blood flow
    when build-up of atherosclerosis is sufficient to completely block blood flow it causes myocardial infraction or heart attack
114
Q

What is angina

A
  • coronary artery disease can lead to pain in the left side of you chest known as angina
  • plaque build up partially restricts blood flow to the heart
  • can be treated with vasodilators such as nitroglycerin
115
Q

what is congestive heart failure

A
  • heart pumps ineffectively and can no longer meet the body’s needs for blood
  • often has to do with ventricles - caused by CAD, hypertension, congenital defects and MI
  • “congestive” part comes from a back-up of blood in the veins leading to the heart which causes kidneys to retain fluid
116
Q

symptoms and treatments for congestive heart failure

A

symptoms: water retention (edema) in legs and ankles
treatments: B-blockers to reduce stress on heart, diuretics to remove salts and fluids, surgery or heart transplant in late stages

117
Q

Beta-blockers and congestive heart failure

A
  • most common receptor in the heart is the B1-adrenergic receptor
  • B-blockers block the binding of catecholamines = reduced heart rate
  • also act on the RAA system of the kidneys and dilate arteries
118
Q

types of blood vessels - least to most pressure

A

large veins < venules < capillaries < small arteries and arterioles < large arteries

BIOM 3200 (7 decks)

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