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cardiovascular 1-5 Flashcards

1
Q

What are the names of the two circuits of the CV system?

A
  • pulmonary

- systemic

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2
Q

State the route of blood through circulation in the CV system.

(HInt - RAA CV)

A
  • RBC in suspension
  • arteries (away from the heart)
  • arterioles
  • capillaries (in lungs)
  • veins (back through the heart)
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3
Q

Where must each circuit of the double circulatory system begin/end and contain?

A
  • begin and end at heart (transport system pump)

- contains arteries, capillaries and veins

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4
Q

Describe circulation in terms of valves in the CV system.

Hint - 1-4. L-AS-A-SIC and 5-8. R-R-P-P

A
  1. left ventricle (aortic valve)
  2. aorta and systemic arteries
  3. arterioles (heart)
  4. superior vena cava, inferior vena cava, coronary sinus
  5. right atrium, deoxygenated blood (tricuspid valve)
  6. right ventricle (pulmonary valve)
  7. pulmonary trunk and pulmonary arteries
  8. in pulmonary capillaries, blood loses CO₂ and gains O₂ (lungs)
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5
Q

Where is the heart located?

A
  • mediastinum

- posterior to sternum and great vessels

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6
Q

Where are the sternum and great vessels connected to the heart?

A

to the base (superior end)

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7
Q

Where does the base of the heart sit posterior to, at what level is it and what is it formed by?

(Hint - not at vertebrae but at a CC)

A
  • posterior to sternum
  • at the level of 3rd costal cartilage
  • formed by atria
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8
Q

Where is the apex of the heart and what is it formed by?

A
  • pointed (bottom) tip of the heart

- formed by LV

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9
Q

Where does the heart extend to anteriorly and obliquely?

Hint - anteriorly in the back and between peparey, obliquely from ribs numbered according to that diet Philip did

A
  • anteriorly: vertebral column, first rib and between lungs

- obliquely: 12-14 cm from 2nd rib to 5th intercostal space

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10
Q

What does the heart divide by and how is it centred?

A
  • 2 unequal halves by the septum

- about 1.2cm to LHS

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11
Q

How many atria and ventricles are there and what do they do?

Hint - A collects then V gets rid

A
  • 2x atria - collecting chambers of the heart that contract to fill ventricles
  • 2x ventricles - muscular chambers which eject blood
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12
Q

What is systole?

Hint - s is later in the alphabet than d so think of the AV actions like that

A

ventricular contraction – atrial elongation

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13
Q

What is diastole?

A

ventricular relaxation and filling

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14
Q

From the vena cava, what is the flow of blood through the chambers and valves of the heart?

(Hint - R → L and A → V, for each ventricle it also passes through the nearest big vessels PA arteries)

A

1) RA and tricuspid AV valve (3 cusps)
2) RV and pulmonary artery
3) LA and biscupid/mitral AV valve (2 cusps)
4) LV and aorta

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15
Q

What are the 3 layers of the pericardium?

A
  1. epicardium (external)
    - visceral layer of serous (secretes lubricant) pericardium
  2. myocardium (middle)
    - 95% of the heart’s cardiac muscle (cardiomyocytes and fibroblasts)
  3. endocardium (innermost)
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16
Q

What is pericardium and the names of its 2 layers?

A
  • membrane surrounding and protecting heart
  • while allowing free movement
    1. fibrous pericardium
    2. serous pericardium
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17
Q

Describe the composition of the serous and fibrous pericardium.

A
  • serous pericardium: thinner membrane which forms a double layer around heart
  • fibrous pericardium: inelastic dense irregular CT which prevents overstretching and provides protection
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18
Q

What is the (inner) visceral layer of serous pericardium also called?

A

epicardium

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19
Q

Which fluid is found between parietal and visceral layers of serous pericardium what is its function?

A
  • pericardial fluid

- reduces friction

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20
Q

What are the two atrioventricular valves?

A
  • tricuspid valve

- bicuspid (mitral) valve

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21
Q

What are the two semilunar valves?

A
  • pulmonary valve

- aortic valve

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22
Q

What happens to AV valves when atria contract/ventricles relax?

A
  • cusps project into ventricle

- in ventricle, papillary muscles relax + chordae tendineae slac

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23
Q

What are the actions of AV valves when the atria relax/ventricles are contracted?

A
  • pressure drives cusps upward until edges meet and close opening
  • papillary muscles contract tightening chordae tendinae
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24
Q

What does the action of AV valves prevent?

A

regurgitation (backflow)

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25
Q

Compare cardiac muscle fibres to skeletal muscle fibres.

Hint - cells arrangement, number of energy-producing organelles and branching/stripes

A
  • muscle fibres shorter, less circular, branched, one, centrally-located nucleus
  • muscle fibres more mitochondria
  • single-branched striated muscle cells
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26
Q

Compare the similarities and differences in cardiac and skeletal muscle.

A
  • same arrangement of sarcomeres
  • same contraction mechanisms (sliding filament model)
  • different stimulus for contraction
  • different Ca sources
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27
Q

How are cardiomyocytes connected?

A

intercalated discs (= thickenings of sarcolemma)

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28
Q

Which three junctions make up an intercalated disc?

Hint - EA sports “For Da Game”

A
  1. fascia adherens or Z discs (anchoring sites for actin, connected to closest sarcomere)
  2. desmosomes (hold myocytes together)
  3. gap junctions (physical connections which propagate cell-to-cell electrical signalling)
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29
Q

Describe the unique banding pattern of striated/cardiac muscle.

A
  • two major contractile filaments actin and myosin arranged into myofibrils
  • each myofibril consists of sarcomeres (= contractile units)
  • each sarcomere separated by Z band/disc (thin line) in which:
  • thin actin filaments forming I-band attach Z-disc
  • darker A-band made of myosin filaments present between I bands
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30
Q

What happens to actin filaments when muscle contracts?

A
  • actin filaments of I band slide over myosin filaments of A band
  • Z discs move closer together
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31
Q

What are thin filaments made of?

A

actin

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32
Q

What protein forms thick filaments?

A

myosin

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33
Q

What is an action potential?

A

a characteristic apid rise and subsequent fall in voltage/p.d. across a cellular membrane

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34
Q

State the route of an action potential in the heart.

Hint - SABLP

A

SAN → AV node → AV bundle/bundle of His → L+R bundle branches → Purkinje fibres

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35
Q

State the 5 stages by which an action potential is conducted.

A
  1. stimulus → rapid change in voltage/AP above threshold
  2. depolarization →Na⁺ channels in cell membrane open and influx of Na⁺
  3. repolarization → rapid Na⁺ channel activation and large influx of K⁺ due to activated K⁺ channels
  4. hyperpolarisation → lowered membrane potential caused by K⁺ efflux ions and K⁺ channels closing
  5. resting state → return to RMP
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36
Q

During embryonic development of the heart, how many fibres become autorhythmic (heart pacemaker cells)?

A

1% of cardiac muscle fibres

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37
Q

State the 2 functions of autorhythmic fibres.

A
  1. pacemaker cells driving autorhythmic contractility activity of heart
  2. form specialised conducting system of muscle fibres to allow coordinated excitation of different regions of heart
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38
Q

How do SAN cells conduct action potentials?

A
  • no stable RMP → repeated spontaneous depolarization to threshold
  • current activates upon hyperpolarization at -40/-70 mV
  • pacemaker potential reaches threshold → triggers AP
  • AP from SAN → throughout both atria (via gap junctions of IC discs) → both atria simultaneously contract
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39
Q

Describe the 4 stages for conduction of action potentials in cardiac contractile fibres.

(NaCK)

A

(1) depolarisation - voltage-gated Na⁺ channels open, Na⁺ inflow, Na⁺ channels inactivated for short period
(2) plateau phase:
- maintained depolarisation due to Ca2⁺ inflow when slow Ca2⁺ channels open
- some K⁺ channels close
(3) repolarisation phase:
- K⁺ outflow as K⁺ channels open, Na⁺-K⁺ pump activated, cell repolarises
(4) refractory period:
- time period where muscle cell cannot fire 2nd AP

40
Q

State the 2 reasons for the importance of the refractory period?

A
  • ensures unidirectional stimulatory information

- prevents tetanic contraction (stimulation of 2nd contraction long, slow muscular before 1st has ended)

41
Q

What is an ECG and how is it measured?

A
  • (electrocardiogram) which represents measured compound cardiac potentials as they are propagated through heart
  • by an electrocardiograph
42
Q

What is einthoven’s triangle?

A

simplest form of ECG no longer used

43
Q

What is a modern ECG?

A
  • use 10 electrodes for 12-lead ECG

- 6 electrodes positioned on limbs and at 6 positions on chest

44
Q

What are bipolar limb leads?

A
  • 3 standard limb leads: I, II and III
  • use 2 leads to view heart
  • one carries +VE electrode and other carries -VE electrode which form Einthoven’ equilateral triangle
45
Q

For each lead state the areas connected and the angle measured from the heart:

a) Lead I (Lara)
b) Lead II (Llra)
c) Lead III (llaa)

A

a) Lead I: LA +VE, RA –VE = 0
b) Lead II: LL +VE, RA –VE II = 60 to Lead I
c) Lead III: LL +VE, LA –VE = 120

46
Q

For the 6 precordial (chest) leads (V1, V2, V3, V4, V5 and V6) which create transverse view of heart, state area in which they detect cardiac activity.

(Hint - Paired and SAL)

A
  • V1 and V2 = septal surface
  • V3 and V4 = anterior ventricular wall
  • V5 and V6 = lateral wall of LV
47
Q

What is represented by each wave?

a) a P wave? (Hint – P that comes at the start)
b) a QRS wave? (Hint – the P that comes in the middle)
c) a T wave? (Hint – 2 letters before T in the alphabet)

(AVV)

A

a) depolarisation of atria
b) depolarisation of ventricles
c) repolarisation of ventricles

48
Q

What is represented by each interval:

a) a P-Q interval? (Hint – Q is physics shorthand for charge - conduction)
b) a S-T interval? (Hint - just before atria become involved)
c) a Q-T interval? (Hint - de and re of part a)

A

a) conduction time between SAN and ventricular depolarisation
b) period where ventricular cells depolarised in plateau phase
c) ventricular depolarisation to repolarisation

49
Q

Which part of an ECG appears when cardiac AP arises in SA node and propagates throughout atrial muscle?

A

P wave appears

50
Q

Which part of an ECG appears when the AP enters AV bundle and out over ventricles (progresses down septum, upward from apex, outward from endocardial surface) before atrial systole and what does this mask?

A
  • QRS complex

- atrial repolarization (less obvious)

51
Q

Which part of an ECG appears during the contraction of ventricles/ventricular systole?

A

begins shortly after QRS complex appears and continues during S-T segment

52
Q

Which part of an ECG appears during the repolarisaton of ventricular fibres before ventricular diastole?

A

T-wave

53
Q

State the sequence of excitation of the heart related to the deflection waves of an ECG tracing.

A
  • start of P-wave - SAN atria excited
  • end of P-wave - AVN → where impulse delayed
  • start of Q-wave - impulse to apex where ventricular excitation occurs → bundle branches
  • QRS-wave - impulse reaches purkinje fibres → ventricular excitation complete
54
Q

Describe ECG tracings b)-d) and state the problem compared to healthy trace a).

A

(b) some P waves are not conducted through AV node, 2 P waves per cycle
(c) non-functional SAN, absence of P wave, paced by AV node (40-60 bpm)
(d) chaotic, irregular trace, seen in acute heart attacks; ventricles no longer pump blood and death occurs

55
Q

What is a dysrhythmia and for which 4 reasons can a dysrhythmia occur?

(Hint – herd)

A
  • disturbances of cardiac rhythm
    1. delayed after depolarisation - overstimulation of myocytes after normal AP as intracellular [Ca2+] increased beyond normal range
  1. re-entry
    - cardiac AP should die out in ventricles; unusual anatomical variations form conductive ring of cells/slow conducting pathways (often following myocardial damage) which re-enter into cardiac cycle which never finishes
  2. abnormal pacemaker activity
    - ectopic pacemakers develop elsewhere in heart
  3. heart block
    - AV node becomes electrically isolated
56
Q

In which 6 ways can ectopic pacemakers elsewhere in the body be induced by?

(Hint - HECENI)

A
  • excessive sympathetic stimulation
  • caffeine
  • nicotine
  • electrolytic imbalances
  • hypoxia
  • ischaemia → depolarisations due to decreased Na⁺ pump activity (cells maintained at low RMP)
57
Q

Which 3 forms can heart block take?

A
  • partial where for every 2/3 atrial contractions ventricle will contract
  • total where atria and ventricles independently contract
  • sporadic - total AV node-block with sudden periods of unconsciousness
58
Q

How can a dysrhythmia be treated?

A
  • bradycardia → pacemaker systems
  • tachycardia → surgical procedure or drugs (i.e. block voltage-sensitive Na⁺ channels, adrenoceptor-antagonists, refractory period elongates or Ca channel blockers)
59
Q

Describe the changes in pressure and actions in each stage of the cardiac cycle in the following diagram.

A
  1. atrial contraction begins
  2. atria eject blood into ventricles
  3. atrial systole ends - AV valves close
  4. isovolumetric ventricular contraction
  5. ventricular ejection occurs - now contract isotonically
  6. semilunar valves close - backflow of blood in aorta and pulmonary trunk + ventricular diastole
  7. isovolumetric relaxation occurs - all valves closed and ventricular myocardium relaxing
  8. AV valves open - A + V diastole and passive ventricular filling occurs before cardiac cycle ends
60
Q

What is a cardiac cycle, how long is one and what is the normal number of bpm for a healthy heart?

A
  • movement of heart throughout the period of 1 beat
  • 0.8 seconds
  • 75bpm
61
Q

What is auscultation and which 4 sounds should/shouldn’t be heard in a healthy heart?

A
  • simple method of cardiac assessment by listening to the heart using a stethoscope
  • S1 and S2 should be heard
  • S3 and S4 - faint and rarely audible in healthy adults
62
Q

What are heart sounds S1 and S2 and why do they occur?

A

• S1:
- 1st heart sound “lubb” and longer than S2
- start of ventricular contraction when AV valves close semilunar valves open
• S2:
- “dupp,” beginning of ventricular filling
- when semilunar valves close and AV valves open

63
Q

What do heart sounds S3 and S4 represent and when may they be heard?

A

• S3 - blood flowing into ventricles
• S4 - atrial contraction rather than valve action
- can be used to detect problems with papillary muscles/chordae tendineae
- heart valves may not properly close → AV valve regurgitation during ventricular systole

64
Q

What is the Sliding Filament Theory of muscle contraction?

Hint - HIZZA

A
  • when striated muscle fibre contracts, sarcomere:
    1. H-bands and I-bands of sarcomeres narrows
    2. zones of overlap widen
    3. Z-lines move closer together
    4. width of A-band remains constant
  • observations only make sense if thin filaments sliding toward the centre of each sarcomere, alongside thick filaments
65
Q

What are the 2 myofilaments of a sarcomere?

A
  1. myosin (A-band)
    - 2 identical heavy chains each bound to pair of light chains - tail forms helix with 2nd heavy myosin chain to form a dimer
  2. actin (I-band)
    - chain of globular actin molecules joined in helix each with a binding site for myosin head - coupled at every 7th molecule to proteins tropomyosin and troponin
66
Q

State the 4 stages of the cardiac contraction cycle.

(Hint - mason says goodbye, leaves on a bridge, then changes his mind and turns around, he makes it back just before the bridge breaks)

A
  1. myosin reactivation - myosin heads hydrolyse ATP and become reoriented and energised
  2. cross-bridge formation - myosin heads bind to actin, forming cross-bridges
  3. myosin head pivots - myosin heads rotate toward the centre of the sarcomere (= power stroke)
  4. cross-bridge detachment - myosin heads bind ATP, cross-bridges detach from actin
67
Q

How is cardiac contraction achieved?

(Hint - May is excited which excites her friend Cara, Cara connects with her friend TC which costs their friend Troy to be kicked out of the AB restaurant, ultimately this entire process was very energy-consuming)

A
  • excitation of myocyte results in the release of stored calcium from SR
  • calcium ions bind with troponin C resulting in movement of tropomyosin from actin-binding site
  • requires ATP breakdown
68
Q

State the stages of cardiac excitation-contraction coupling (ECC) using diagram in the notes if required.

TN
– troponin
ECC
– process whereby an AP triggers a myocyte to contract, followed by subsequent relaxation
SERCA
– sarco-endoplasmic reticulum calcium-ATPase

(Hint -

  1. Andy Parker accidentally caused the voltage to rise in the city
  2. his evil brother Dean Harry Parker his opens the city gates so that his Cronies can enter to cause chaos
  3. lots of cronies entering causes more cronies to be released from the City Centre
  4. the cronies are low on manpower so need to touch the TopazNeptune-Crystal can release the TopazNeptune-Indigo can open the portal for energy to be given to the cronies so they can slide so that MaryAnne can slide out of the way for the Saphire can continue expanding - this entire process depends on the continued presence of the cronies
  5. the number of cronies decreases because of the SERCA pump Andy Parker manages to bring in so TopazNeptune-Indigo can be closed and new good energy can save the day and the Sapphire can go back to normal and the cronies can be forced out)
A
  1. action potentials travel along with sarcolemma and T-tubule system to depolarize the cell membrane
  2. voltage-sensitive DHP receptors open and Ca2⁺ enters the cell
  3. Ca2⁺ influx triggers Ca2⁺ stored in SR to be released through Ca channels (increased intracellular [Ca])
  4. Ca binds to TN-C (conformational change) so TN-I exposes actin site that binds myosin ATPase so ATP hydrolysis occurs (energy)
    - myosin head and actin movement means filaments slide past each other shortening sarcomere; repeated as long as cytosolic [Ca] is elevated
  5. Ca entry into cell slows (isolated by SR by ATP-dependent calcium pump SERCA) lowering cytosolic [Ca] and some transported out of the cell by Na⁺-Ca2⁺ exchange pump
    - Ca unbinds from TN-C inducing conformational change in troponin complex so TN-I inhibition of actin-binding site
    - new ATP binds to myosin head displacing ADP and initial sarcomere length restored; repeats
69
Q

Using the following graph, complete the following information on each stage of the action potential:

(cause, duration, ends with)

a) rapid depolarisation
b) plateau phase
c) repolarization
d) refractory period

(Hint - NaCaK)

A

a)
cause: Na⁺ entry
duration: 3– 5 ms
ends with: closure of fast Na channels
b)
cause: Ca2⁺ entry
duration: 175 ms
ends with: closure of slow Ca channels
c)
cause: K⁺ loss
duration: 75 ms
ends with: closure of slow K channels
d)
cause: lag in K⁺
duration: 1-2 ms
ends with: Inactivation of Na and slow closure of K channels

70
Q

What are the 3 tunics (tissue layers) in all blood vessels?

Hint - EBM, ECS, EC

A
  1. tunica interna (intima)
    • epithelial inner lining
    - endothelium, BM (collagen) + internal elastic lamina
  2. tunica media - elastic (CT), circular SM and sometimes elastic lamina (external)
  3. tunica externa (adventitia) - elastic + collagen fibres → support and vasa vasorum
71
Q

What accounts for 5 types of vessels and differences among vessel types?

A

modification of basic structure

72
Q

Describe arteries and the two types.

A

• large arteries – propel blood while ventricles relax (pressure reservoir)
• medium arteries – transport blood over long distances without little drop in BP
- 3 layers
- tunica interna lined by squamous epithelium, a BM and internal elastic lamina and thick tunica media of SM cells

73
Q

Describe arterioles.

A
  • resistance vessels, fenestrated elastic lamina
  • tunica externa with elastic + collagen fibres
  • thin with tunica interna surrounded with few SM cells
  • smaller than arteries + close to capillaries
74
Q

How do arterioles influence peripheral resistance?

A

vasoconstriction and vasodilation

75
Q

What is:

a) a metarteriole? (Hint - “arteriole” missing a component)
b) a thoroughfare channel? (Hint - “channel” is like a secret passageway or a shortcut)

A

a) terminal end of the arteriole, distal end of vessel with no SM resembling capillary
b) provides direct route for blood from arteriole to venule, by-passing capillaries

76
Q

What is a metarteriole-capillary junction and what is formed here to monitor blood flow into capillaries?

A
  • proximal end of metarteriole

- most distal muscle cells form precapillary sphincter

77
Q

Complete the labels on the following capillary bed.

A 
A, G - SM fiber 
B - metarteriole 
C - precapillary sphincters (relaxed)
D - thoroughfare channel
E - precapillary sphincters (contracted)
F - endothelium
78
Q

Describe capillaries.

A
  • microscopic blood vessels found near all cells which connect arterioles to venules
  • only tunica interna
  • function → exchange vessels (fluid and metabolites) between blood circulatory system and tissues
79
Q

What are the 3 types of capillaries and which are most common?

A
  • sinusoid
  • continuous (most common)
  • fenestrated
  • in continuous - PM of endothelial cells forms continuous tube only interrupted by intracellular cleft
80
Q

For the metabolic rate of the tissue, state abundance of capillaries and give examples of tissues:

a) high metabolic rate
b) low metabolic rate

A

a) more/abundant - e.g. brain, liver, kidneys

b) fewer - e.g. lining epithelia, cornea, cartilage

81
Q

Describe venules.

Hint - walls, TE + TM and IS/nutrient function

A
  • walls porous
  • collect blood from capillaries
  • TE + TM = a few SM cells
  • function → sites for nutrient/waste exchange + migration of WBC’s
82
Q

Compare the size of arteries, capillaries and venules.

A
  • capillaries: 5-10μm
  • venules: 10-50μm
  • arteries: 100-10,000μm
83
Q

Describe veins.

Hint - TI + TM vs TE, thrombosis feature, blood direction, storage vessels, pressure levels

A
  • thin TI + TM → thicker TE layer
  • thin wall, large lumen and valves
  • take blood to heart
  • capacitance (low pressure) vessels
  • hold large blood volume → blood reservoirs
84
Q

For each blood vessel(s) state the % of body’s blood function:

a) veins/venules
b) systemic capillaries
c) arterioles and arteries
d) pulmonary vessels

(8 squared, add to make 20 then octagon)

A

a) 64%
b) 7%
c) 13%
d) 8-11%

85
Q

What is capillary exchange and which molecules are normally transported by transcytosis?

A
  • when substances enter/leave capillaries by diffusion, transcytosis (pinocytosis → exocytosis) and bulk flow
  • large hydrophilic molecules (i.e. hormone insulin)
86
Q

Where is body fluid derived from and where is ingested water stored?

A
  • in blood plasma (20%)

- in interstitial/EC fluid (80%)

87
Q

What does filtration depend on?

A
  1. blood hydrostatic pressure (BHP) - pressure generated by the blood pumping action of the heart
  2. interstitial fluid osmotic pressure (IFOP)
88
Q

What is reabsorption and what % of fluid filtered out of the capillaries is reabsorbed?

A
  • pressure-driven movement from interstitial fluid into blood capillaries
  • 85%
89
Q

Which 2 things does resorption of fluid in the blood depend on?

A
  1. blood colloid osmotic pressure (BCOP)
    – main pressure promoting reabsorption of fluid
  2. (less on) interstitial fluid hydrostatic pressure (IFHP)
90
Q

What does the NFP (flow of fluid from blood → tissues → blood) depend on and what does excess filtered fluid (+plasma proteins) from blood into interstitial fluid enter?

A
  • the balance between BCOP and IFHP forces

- enters lymphatic capillaries (becomes lymphatic fluid)

91
Q

How is NFP (net flow pressure) calculated and what is hydrostatic pressure? give an example of hydrostatic pressure.

A
  • difference between net hydrostatic pressure and net osmotic pressure
  • physical force exerted against a surface by a liquid
  • i.e. blood pressure
92
Q

What does a typical capillary have a BHP of at the:

a) arterial end,
b) venous end

A

a) 35mmHg

b) 16 mmHg

93
Q

What is the interstitial fluid hydrostatic pressure (IFHP) and what value does it take among all capillaries?

A
  • pressure in interstitial fluid (close to zero)

- we assume IFHP = 0 mmHg all along capillaries

94
Q

What is Blood Colloid Osmotic Pressure (BCOP) and what is its value for tissue fluid compared to blood plasma?

A
  • a force caused by the colloidal suspension of large plasma proteins (albumin)
  • less than 1/3rd the [protein] of blood plasma
    (BCOP is 26 mmHg; IFOP 0.1-5 mmHg )
95
Q

What is oncotic pressure, what does it tend to draw into capillaries and how?

A
  • differences between COP of blood and tissue fluid (BCOP – IFOP)
  • draw water into capillary
  • by osmosis opposing hydrostatic pressure
96
Q

Why is there a difference in osmotic pressure across capillary walls and when does reabsorption occur?

A
  • due to presence of plasma proteins (too large to pass through fenestrations between endothelial cells)
  • when blood colloid osmotic pressure pulls fluid into capillaries
97
Q

What is oedema, when does it occur and what is it caused by?

A
  • swelling caused by at least 30% increase in interstitial fluid volume
  • filtration&raquo_space;> reabsorption → water comes out
  • caused by increased capillary BP, increased capillary wall permeability to solutes, decrease in [plasma protein] and heart failure → inadequate reabsorption OR excess filtration

CRR (11 decks)

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