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CVS Flashcards

1
Q

What are the two circuits of blood flow in body?

A
  • Pulmonary circuit and systemic circuit
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2
Q

What is the pulmonary circuit?

A
  • right ventricle (ejects blood into pulmonary artery)

- goes into lungs (gas exchange), ejects blood into left atrium

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3
Q

What is the syswtemic circuit?

A
  • Starts with the LEFT VENTRICLE–> aorta—> arterioles–> capillaries–> exchange of nutrients and waste–> back to heart by main veins (vena cavae)
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4
Q

First, blood flows through the ____ circuit, then the __ circuit

A

Pulmonary circuit,m systemic circuit

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5
Q

In what 3 conditions will you have a fast death?

A
  • NO excitation
  • NO ventricular contraction
  • NO pulse
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6
Q

What are desmosomes?

A

Structural component of intercollated disks(the glue)

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7
Q

What do gap junctions allow for?

A
  • Spread of excitation of heart thus, NO contraction
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8
Q

Where is the excitation of the heart initiated?

A
  • SA node (sino atrial node)
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9
Q

What is the pathway of excitation of heart?

A
  • SA node–> internodal pathways–> Bundle of Hiss (in ventricular septum)–> apex–> purkinje fibres –> allows muscle to contract
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10
Q

What do the purkinje fibres do ?

A
  • transmit electrical impulses to ALL ventricular muscle cells AT SAME TIME so contract at SAME TIME
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11
Q

Approx how long does it take for depolarisation/excitation of atria?

A
  • approx 0.09 secs for depolarisation
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12
Q

Approx how long does it take for dwepolarisation/excitation of ventricles?

A

Approx 0.06 seconds

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13
Q

Where is there a significant slowing of rate of conduction?

A
  • getting through the AV node (atrioventricular node)
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14
Q

Roughly how long does it take to pass through the AV node?

A
  • 0.09 secs
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15
Q

How come it takes longer to pass through AV node?

A
  • Fewer gap junctions between AV node cells (thus slower to pass)
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16
Q

Why do we want slow conduction through the AV node?

A
  • So ventricles have ENOUGH time to FILL with blood before getting excited (and contracting) (i.e. ventricular filling needs to occur so pulse slows)
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17
Q

If an SA node (pacemaker cell) is isolated what happens?

A
  • It will generate APs by itself
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18
Q

What are the 3 features of ventricular Aps?

A
  • Have a plateu
  • Much more negative (MDP-maximum diastolic potential -90mV)
  • STABLE resting mempot
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19
Q

What are the 3 features of SA node APs?

A
  • much more positive MDP -65mV
  • No stable resting pacemaker potential
  • (no plateu)
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20
Q

What does aan Ena (nerst) of +70mV

A

If the cell was only permeable to sodium (Na+), it would come to rest at a mempot of +70mV

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21
Q

What source of excitation do ventricular muscle cells require?

A
  • External source (from K+, Ca2+, Na+)
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22
Q

What does TTX inhibit?

A
  • Fast Na+ channels

- Selective inhibitor

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23
Q

What will TTX do to a ventricular Ap?

A
  • NO AP occurs! Heart would stop= death
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24
Q

What will TTX do to pacemaker cells?

A

-NOTHING! Fast Na+ channels not involved in pacemaker AP

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25
Q

What causes pacemaker cells to have autonomous APs?

A
  • Contain an ‘f’ (funny) or ‘h’ (hyperpolarisation current
  • Known as pacemaker currnet
    SLOW inward flux of Na+ (SLOW Na+ channels)
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26
Q

What is special about the slow Na+ channel?

A
  • It is the only voltage dependent channel to be open during hyperpolarisation(negative) (others only during depolarisation)
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27
Q

What causes the upstroke in pacemaker AP?

A
  • Ca2+ (L-type)
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28
Q

What causes the upstroke in ventricular APs?

A
  • Na+
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29
Q

What causes repolarisation in pacemaker cells?

A
  • K+ moving out of cell
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30
Q

What is the sympathetic innervation of the heart?

A
  • post ganglionic: entire heart–> release NA (beta cells)
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31
Q

What are the arteries supplying the myocardium?

A
  • Coronary arteries
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32
Q

Where are the coronary arteries located?

A
  • Behind the aortic valve cusps (first part of aorta)
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33
Q

Where do the cardiac veins drain into?

A
  • Coronary sinus (large, single vein) –> empties into right atrium
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34
Q

What is the left AV valve also known as?

A
  • Mitral valve
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35
Q

What is electrical excitation of the heart coupled with?

A
  • Muscle contraction (Cardiac muscle)
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36
Q

What determines the heart rate?

A
  • The discharge rate of SA node(contractions per minute)
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37
Q

What does the delay of AP propagation through AV node allow?

A
  • Atrial contraction to finish before ventricles are excited
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38
Q

What is the only electrical connection between the atria and ventricles?

A
  • AV node and bundle of Hiss
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39
Q

Why does depolarisation in cardiac muscle cells continue for longer than in other cells of body?

A
  • K+ permeability lowers below resting value (K+ channels close that WERE open in resting state)
    AND increase in Ca2+ permeability
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40
Q

What does membrane depolarisation cause in myocardial cells? (ventricular muscle cells)

A
  • Ca2+ voltage gated channel to OPEN

- Ca2+ goes into cell

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41
Q

What are L-type Ca2+ channels?

A
  • L (long lasting)
  • Open slower than Na+ fast channels
  • Also known as: DHP (dihydroxypyridine) channels
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42
Q

What causes the membrane depolarised at plateu? (ventricular muscle cells)

A
  • Ca2+ ions into cel = K+ ions OUT OF CELL
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43
Q

In ventricular muscle cells, how does repolarisation eventualy occur?

A
  • Inactivation of L-type Ca2+ channels

- Opening of K+ channels (another type) (delayed rectifiers and close once current repolarised to -ve)

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44
Q

Are APs of atrial muscle cells similar to ventricular cells?

A
  • SHAPE of APs is similar

- Plateu duration SHORTER

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45
Q

What are the 3 contributors to the pacemaker POTENTIAL?

A
  1. K+ permeability lowers
  2. F type channels conduct depolarising Na+ current (only open in negative values)
  3. T-type Ca2+ channels (T for transient)
    - final depolarising boost to reach threshold (pacemaker)
    - channels open BRIEFLY
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46
Q

What is another name for F type channel?

A
  • Hyperpolarisation-activated Cyclic Nucleotide-gated channels (HCN)
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47
Q

Why do SA node cells initiate APs of the heart rather than AV node cells?

A

SA node cell threshoold reached more rapidly (determines pace of heart)

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48
Q

What is the pathway once threshold is reached for pacemaker cells?

A

AP occurs–> depolarisation (ca2+ influx via L-type (slow) Ca2+ channels–> Repolarisation (K+ exiting cell)–> PK+ increases –> PNa (f) increases
cycle starts again

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49
Q

Why do APs propagate slower along nodal cell membranes?

A
  • Inlfux of L-type (long lasting) Ca2+ channels so slow depolarisation occurs
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50
Q

What allows the SA node to have self excitation?

A
  • Pacemaker potential ( and 3 channels)
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51
Q

In what circumstances would you need a pacemaker?

A
  • When AV node isn’t working properly (reduce AP transmission atria–> ventricles)
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52
Q

What is myosin ATP-ase?

A
  • Enzyme (also ATP binding site) that catalyses ATP–> ADP
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53
Q

Does contraction always refer to shotening?

A
  • NO! Contraction is activation of force generating sites within muscle fibres (cross bridges form)
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54
Q

What does the cytosolic Ca2+ concentration determine?

A
  • Number of troponin sites occupied by Ca2+

- So number of actin sites for cross bridge binding

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55
Q

What is the EDV (End Diastolic Volume)?

A
  • When filling with blood, ventricle is RELAXED

- the amount of blood in ventricle at this time is EDV

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56
Q

What is the ESV (End Systolic Volume) ?

A
  • Amount of blood remaining in ventricle AFTER ejection
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57
Q

What is the formula for Stroke Volume?

A

EDV-ESV

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58
Q

What is stroke volume?

A
  • Amount of blood when ventricle is relaxed and filled VS. amount of blood in ventricle after ejection of blood
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59
Q

When does early diastole begin?

A
  • When ventricular muscle relaxes and ejection comes to an end
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60
Q

How is it good that most ventricular filling is completed during early diastole?

A
  • Makes sure filling happens properly when heart is beating very rapidly
  • So TOTAL filling time and duration of diastole reduced
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61
Q

Are the stroke volumes (SVs) of the L &RHS of ventricles the same??

A

YES!!

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62
Q

Do the left and right ventricles have different pressures?

A
  • YES! Right ventricular wall MUCH THINNER than left

- Left ventricular wall at much higher pressure

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63
Q

What is the ‘lub’ sound of the heart?

A
  • Closure of AV valves
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64
Q

What is the ‘Dub’ sound of the heart?

A
  • Onset of diastole (closing of aortic and pulmonary valves)
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65
Q

What occurs (generally) in heart murmurs?

A
  • Blood is turbulent instead of laminar (flow)
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66
Q

What is stenosis and what main symptom does it produce?

A
  • Abnormally narowed valve

- High pitched whistling murmur

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67
Q

What is ‘insufficiency’ and what main symptom doesit produce?

A
  • blood flowing backward through damaged, leaky valve

- Low pitched, gurgling murmur

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68
Q

What is a septal defect?

A

Blood flowing b/w two atria or two ventricels through small hole in septum

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69
Q

What is CO (cardiac output) and the formula?

A
  • VOLUME of blood that each ventricle pumps as a function of time (L/min)
  • CO= HR * SV
  • CO= HR * (EDV-ESV)
70
Q

Is cardiac output the same on both sides of the heart?

A

-YES! Because under the STEADY STATE, SV and HR are the same

71
Q

What is the effect of stroke volume (SV) and heart rate (HR) with blood loss?

A
  • SV DECREASES

- HR INCREASES

72
Q

What is the autonomous discharge rate of the SA node?

A
  • 100bpm

- Occurs without any nervous or hormonal regulation

73
Q

What effect does vagus stimulation have on heart rate?

A
  • REDUCES it
74
Q

What effect does sympathetic stimulation have on pacemaker potential?

A
  • Increases the SLOPE of pacemaker potential
75
Q

How does sympathetic stimulation increase the slope?

A
  • F-type (Na+) channel permeability increases
  • Faster depolarisation
  • SA node reaches threshold more rapidly –> HR increases
76
Q

How does an increase in parasympathetic current decrease the slope of the pacemaker potential?

A
  • Due to LESS INWARD CURRENT
  • threshold reached at slower rate
  • So HR decreases
  • SA node cell memb. hyperpolarised –> increases perm. to K+ (so potential starts from more negative value)
77
Q

What is a simpler explanation of stoke volume?

A
  • Vol. of blood each ventricle ejects during each contraction
78
Q

With each contraction of heart, do the ventricles empty completely?

79
Q

What would a more forceful contraction of the heart result in?

A
  • Increased SV

- More emptying of blood

80
Q

What can cause changes in force during ejection of stroke volume? (3 things)

A
  1. EDV changes (preload–> vol. of blood in ventricles just before contraction)
  2. Changes in amount of SYMP INPUT TO VENTRICLES
  3. Changes in afterload (arterial pressures that ventricles pump against )
81
Q

What is the Frank Starling Mechanism?

A
  • SV increases as EDV increases (given all other factors are in a STEADY STATE–> equal)
82
Q

What is EDV a determinant of?

A
  • How STRETCHED the ventricular sarcomeres are JUST BEFORE contraction.
83
Q

The greater the _____ the greater the stretch and more forceful the contraction

A

The greater the EDV, the greater the stretch, and the more forceful the contraction

84
Q

Is the normal point for cardiac muscle in resting person at optimal length of contraction?

A
  • NO! It’s on the rising phase of curve
85
Q

When do spaces between thick and thin filaments decrease in cardiac muscle?

A
  • When cardiac muscle is stretched towards optimum length (more crossbridging occurs–> twitch)
86
Q

From the Frank Starling mechanism, what does an increase in venous return cause?

A
  • Increase in C.O by increasing E.D.V (End Diastolic Volume) therefore stroke volume
  • Left and right cardiac outputs must be same though
87
Q

What will happen if the RHS of heart starts pumping more blood than LHS?

A
  • Increased blood flow (returning to left ventricle) will automatically produce increase in LEFT ventricular output (so blood doesn’t acculmulate in pulm, circulation
88
Q

What is ventricular contractility defined as?

A
  • Strength of contraction at any given EDV
89
Q

What does NA act on (which receptors of heart)?

A
  • Beta adrenergic receptors

- Increases ventricular contractility

90
Q

Does Adrenaline also increase contractility?

91
Q

Does the Frank Starling mechanism reflect increased contractility?

A
  • NO! Increased force of contraction + stroke volume from symp. stimulation or Adrenaline are INDEPENDENT of change in EDV –> so frank starling law doesn’t apply (Increased SV as EDV increases)
92
Q

How can we quantify contractility?

A
  • Ejection Fraction (EF)
93
Q

What is the ejection fraction equal?

94
Q

what does increased contractility equal?

A
  • Increased ejection fraction
95
Q

What is afterload?

A
  • How hard the heart must work to eject blood
96
Q

What does increased arterial pressure do to SV?

A
  • Increase it **
97
Q

DO the parasympathetic nerves have any significant effect on VENTRICULAR MUSCLE?

98
Q

A man comes into hospital with a pulse rate of 40 pulses/min. The ECG revealed an atrial rate of 90 contractions/min and a blockage of conduction through the AV node. Why was his pulse rate 40 pulses/min?

A
  • Pressure waves down arteries that reflect rate that ventricles are contracting –> Excited by purkinje fibres at lower rate: 40 pulses/min
99
Q

THE SA NODE IS IRREVERSIBLY DAMAGED:
(A) This is not a problem, the autonomic nerves are still stimulating the heart to beat
(B) This person foes not have long to live; without the SA node the heart cannot be excited
(C) The AV node will now initiate the excitation of the heart and the heart rate will be about 50beats/min
(D) The purkinje fibres will now initiate the excitation of the heart, and the heart rate will be about 40beats/min

A

(C) The AV node will now initiate the excitation of the heart, and the heart rate will be about 50 beats/min

100
Q

What is tachycardia?

101
Q

What is bradycardia?

102
Q

What type of cardiac innervation does a normal sedentary person have?

A
  • Symp and parasymp
103
Q

Why is blood flow out of the heart (left ventricle) intemittent?

A
  • Aortic valve closes after each contraction (BUT blood flow is continuous)
104
Q

When the heart is contracting and emptying, where does 2/3 of the blood go?

A
  • 2/3 of blood goes into stretching walls of arteries (aortic valve open)
105
Q

In systole, where does 1/3 of blood go?

A
  • 1/3 blood goes to arterioles (aortic valve shut)
106
Q

What is the dicrotic notch on the aortic pressure trace due to?

A
  • The closing of the aortic valve
107
Q

What is systolic blood pressure normally (SBP)

108
Q

What is disatolic blood pressure normally? (DBP)

109
Q

What does pulse pressure equal?

A

PP= SBP-DBP (40)

110
Q

What does MAP (Mean Arterial Pressure) equal?

A
  • MAP= DBP + 1/3 (PP)
111
Q

What is hypertension?

A
  • Higher than normal blood pressure

- CONSISTENTLY above approx. 140/90 (140 is systolic and 90 is diastolic)

112
Q

What is hypotension?

A
  • Lower than normal blood pressure

- CONSISTENTLY below approx. 100/60

113
Q

In the blood pressure (BP) profile (when wearing BP monitor), what is the drop in blood pressure over a period of time associated with?

114
Q

What do arterioles control?

A
  • Control proportional distribution of blood flow to different organs and tissues of body through changes in DIAMETER (alters resistance to flow)
115
Q

In a relaxed (dilated) arteriole, what is the flow and resistance like?

A
  • Flow INCREASES and resistance DECEREASES
116
Q

In a constricted arteriole, what is the flow and resistance like?

A
  • Flow DECREASES and resistance INCREASES
117
Q

What are the three factors that affect arteriolar radius?

A
  1. Neuronal
  2. Hormonal
  3. Local
118
Q

What happens in metabolic control (cardiac and skeletal muscle) of arterioles (autoregulation)?

A
  • Dilation of arterioles by H+, Adenosine, incrfeased CO2, decreased O2, K+ acting directly on smooth muscle cells
  • Blood flow increased
119
Q

What does the myogenic mechanism allow for?

A
  • Allows for organs to maintain CONSTANT blood flow despite changes in arterial pressure upstream
120
Q

Where in the body is the myogenic mechanism well developed?

A
  • In the brain -cerebral circulation
121
Q

Which two processes control the local needs of specific tissues and organs?

A
  • Metabolic and myogenic control
122
Q

What is the nerve supply to the arterioles?

A
  • Sympathetic (except for genitals)
123
Q

With reflex control of arterioles, what does NA act on and what does this lead to?

A
  • NA (released by sympathetic nerves) acts on arteriolar sm. muscle ALPHA adrenoceptors
  • Leads to SMOOTH muscle contraction =CONSTRICTION
124
Q

Is therer always a level of ‘resting’ sympathetic nerve activity to smooth muscle in arterioles?

A
  • YES!

- There is so the sm. msucle is aloway PARTIALLY contracted

125
Q

What does increased sympathetic activity to arterioles lead to?

A
  • Constrcition
126
Q

What does decreased sympathetic nerve activity to arterioles lead to?

127
Q

What effect does Adrenaline binding to alpha receptors on smooth muscle have?

A
  • Causes constriction of arterioles (contraction of smooth muscle)
128
Q

What effect does Adrenaline have when it binds to Beta2 Adrenergic receptors on smooth muscle or skeletal muscle?

A
  • Causes relaxation of muscle cells (smooth muscle in arterioles—> Dilation)
129
Q

Which two hormones involved in the renal system constrict arterioles?

A
  • Angiotensin II and Vasopressin (ADH)
130
Q

Which hormone in renal system dilates arterioles?

A
  • ANP (Atrial Naturietic Peptide)
131
Q

What effect does stress have on sympathetic nerve activity?

A
  • Leads to increase in symp. nerve activity

- Adrenaline secretion increases from adrenal medulla

132
Q

During stress, what happens to arterioles that have little sympathetic innervation and vascular smooth muscle alpha receptors (heart, liver, skeletal msucle) ?

A
  • Arterioles will be dilated

- Beta2 receptors have a dilating effect so adrenaline will bind and cause dilation

133
Q

During stress, what happens to arterioles with a dense symp. innervation and vascular sm. muscle alpha receptors (gut, kidney)?

A
  • Arterioles will CONSTRICT

- Alpha receptors have a contracting effect when adrenaline binds

134
Q

What is orthostatic hypotension (also specific BP values)?

A
  • Type of hypotension where person’s BP falls suddenly when standing up e.g. Yellow Wiggle
  • SYS BP: more than or equal to 20mmHg
  • DIA BP: more than or equal to 10mmHg
135
Q

Why is there a sudden drop in MAP with orthostatic hypotension? (In terms of SV EDV CO)

A
  • Venous return DECREASES
  • This casues EDV (vol. after filling) to decrease—> leads to SV decreasing —> leads to CO decreasing
    MAP= CO* TPR so big drop
136
Q

What is the total peripheral resistance (TPR) and how is this altered?

A
  • Sum of all vascular resistances of ALL tissues

- Changed by constricting or dilating blood vessels

137
Q

Would constriction of arterioles increase or decrease the TPR (total peripherals resistance)?

A
  • Constriction would cause INCREASED TPR
138
Q

What causes the MAP to rapidly increase back to normal after someone fainted with orthostatic hypotension?

A
  • Baroreceptor reflex (or Arterial baroreflex) -takes 5-10 seconds
139
Q

What are three ways the MAP can be increased in the body? (sort of three)

A
  1. Increase output of pump (CO) –> increase SV and HR
  2. Increase resistance (Increase in TPR)–> changing constriciton/dilation of blood vessels
  3. Combination of first two
140
Q

What are two ways in which HR is increased?

A
  1. Reducing parasympathetic activation of SA node

2. Increasing sympathetic activation of SA node

141
Q

How can the body increase SV? (which leads to increase in CO and MAP)?

A
  1. INCREASESympathetic activation of VENTRICLES –> increases amount of Ca2+ available for contraction–> more cross bridges–> increase in SV
  2. INCREASE sympathetic activation of VEINS
    - Increases VENOUS PRESSURE, VENOUS RETURN, EDV + SV
142
Q

How do we increase TRP (and MAP from this)?

A
  • Increase sympathetic activation of arterioles on ALPHA receptors
  • this increases arteriolar CONSTRICTION and TPR
143
Q

Which hormones are secreted from adrenal medulla in stress response ans what effect does this have?

A
  • A + NA
  • Increase CO (which increases HR and contractility/SV)
  • Increases TPR (vasoconstriction)
144
Q

What type of innervation does a normal sedentary person have?

A
  • Sympathetic and Parasympathetic
145
Q

What type of innervation does a receipient of a heart transplant have?

A
  • NO autonomic innervation
146
Q

What type of innervation does a quadriplegic have?

A
  • NO SYMPATHETIC

- Normal parasympathetic

147
Q

What 4 things is an ECG used to determine?

A
  1. Anatomical orientation of heart
  2. Disturbances in cardiac rhythm and conduction
  3. Effects of drugs or abnormal contractions of plasm. electrolytes (K+) on heart
  4. Location of ischaemic damage to myocardium and the extent
148
Q

When does the P wave occur in a normal ECG and what does it represent?

A
  • EXCITATION of the atria

- atrial depolarisation

149
Q

When does the QRS complex occur and in which phase?

A
  • Excitation of ventricles

- Ventricular depolarisation phase

150
Q

When does the T wave occur and in what does it represent?

A
  • Recovery (repolarisation) of ventricles

- Ventricular repolarisation stage

151
Q

Why is the T wave larger than P wave in aplitude?

A
  • More ventricular muscle cells thus more APs
152
Q

What are the 4 major causes of cardiac arhythmia?

A
  1. Pacemaker goes from SA node–> other pacemaking region (due to damage)
  2. Abnormal impulse formation in SA node (Sick sinus syndrome)
  3. Blocking or delay of conduction of impulse through heart
  4. Ventricular fibrillation (spontaneous generation of abnormal impulses)
153
Q

What are 4 conditions that can block the AV node?

A
  1. Ischaemia (not enough nutrients to heart, blockage of blood supply)
  2. Scarr tissue compressing AV-node
  3. inflammation of AV node (fever)
  4. Extreme stimulation of heart by vagus nerve (very rare)
154
Q

What can ventricular fibrillation be a consequence of ? -

A
  • Myocardial iscahemia and electrocution
155
Q

Does blood pressure increase or decrease with each ventricular systole?

A
  • Increases

- Left V ejects blood into aorta (p increases)

156
Q

What is microcirculation?

A
  • BLood flow from ARTERIOLE —-> venule
157
Q

What are capillaries the site of?

A
  • Site of exchange of nutrients and waste
158
Q

During exercise, do you get blood flow through the MAJORITY of the capillary bed in SKELETAL MUSCLE (are sphincters open)?

A
  • YES!

- To increase exchange of nutrients

159
Q

Do multiple RBCs pass adjacently through a capillary?

A
  • NO!!

- Capillaries are so small that they need to pass through in single file

160
Q

During exercise, do you get blood flow through the majority of the capillary bed in INTESTINES?

A

NO!!
- Sphincters are closed
(this is what can cause cramps if you’ve just eaten)

161
Q

Is pressure pulsatile at arterioles?

A
  • NO!

- Low pressure because thin walled vessels and don’t want to rupture

162
Q

What are 4 ways that materials can pass in/out of capillaries?

A
  1. Diffusion (O2, CO2)–> endothelial cells (lipid soluble)
  2. Diffuse through pores b/w endothelial cells (for hydrophillic substances e.g. glucose, aas)
  3. Bulk flow (H20)
  4. Vesicular transport (large molecules–> hormones)
163
Q

What must there be for flow?

A

-A pressure gradient (delta P)

164
Q

What is the only substance not to be filtered out of the capillary bed?

A
  • Plasma Proteins (too large)
165
Q

What factor drives filtration?

A
  • Hydrostatic pressure (blood pressure in capillaries)
166
Q

What opposes filtration and what is it due to?

A
  • Plasma osmotic (colloidal oncotic) pressure

- Due to plasma proteins having higher osmotic flow into capillaries (osmotic pressure)

167
Q

What is absorption in capillaries?

A
  • If movement is FROM interstitial fluids —> Plasma
168
Q

If osmotic pressure is HIGHER than hydrostatic pressure in capillaries, what happens?

A
  • RE-ABSORPTION will occur (movement from interstitial fluid to plasma)
169
Q

What is the role of the lymphatic system in capillary filtration/absorption and which vein does the lymph enter back into?

A
  • Drains solutes that capillaries filter

- Lymph enters back into subclavian vein and goes back into circulation

170
Q

What is an extracellular odema?

A
  • Failure to maintain correct distribution of body water

- thus excess acumulation of body fluid

171
Q

What can some causes of odema be?

A
  • Increased hydrostatic pressure (in capillaries) (heart failure)
  • Increased osmotic pressure (in capillaries)–> conditions altering plasma protein levels like kidney or liver failure
  • Lymphatics with cancerous growth blocking drainage
172
Q

What are the 3 mechanisms that venous return is influenced by? (e.g. in exercise)

A
  1. Pressure gradient
  2. Skeletal muscle ‘pump’
  3. Respiratory ‘pump’

BMS2031 (7 decks)

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