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VSC226 > Cardio > Flashcards

Cardio Flashcards

1
Q

What is the function of the cardiovascular system?

A

Transport of substances (oxygen and nutrients to cells, waste to liver and kidneys, hormones, immune cells, clotting proteins to specific target cells)

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2
Q

What are the 4 main components of the cardiovascular system?

A

Heart
Blood vessels
Blood - erythrocytes, leukocytes, platelets.
Lymphatics

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3
Q

What are the two portions of the cardiovascular system?

A

Pulmonary circulation - 9%

Systemic circulation - 91%

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4
Q

Which ventricle pumps to pulmonary circulation?

A

Right ventricle

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5
Q

Which ventricle pumps to systemic circulation?

A

Left ventricle

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6
Q

What order does blood flow into, through, and out of the heart? Include the valves.

A

Flows in via cranial and caudal vena cava, right atrium, tricuspid valve, right ventricle, pulmonary semilunar valves, pulmonary trunk, pulmonary artery, lungs, pulmonary veins, left atrium, bicuspid valve, left ventricle, aortic semilunar valves, aorta, body tissue.

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7
Q

What is the pericardium?

A

Double walled sac encircling the heart.
Superficial fibrous pericardium.
Serous pericardium - parietal layer on internal surface, visceral layer (epicardium) on external, fluid in between.

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8
Q

What are the 3 layers of heart tissue?

A

Epicardium - outer surface
Myocardium - cardiac muscle cell layer (contracts)
Endocardium - smooth inner surface of heart chambers.

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9
Q

What is the purpose of the atrioventricular valves? Which valves are they?

A

Ensure unidirectional blood flow through the heart - prevent back flow into atria when ventricles contract.
Lie between atria and ventricles - bicuspid (left atrioventricular/mitral) and tricuspid (right atrioventricular) valves.
Chordae tendineae anchor AV valves to papillary muscles.

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10
Q

What are the purpose of the semilunar valves? Which valves are they?

A

Prevent back flow into ventricles.
Aortic semilunar - lies between L ventricle and aorta.
Pulmonary semilunar - lies between R ventricle and pulmonary trunk.

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11
Q

Describe the action of AV valves.

A

When ventricles are relaxed, blood enters atria pushing the AV valve cusps down into the ventricles. This opens the valves.
As the ventricle contracts, blood presses against the valve, forcing it closed. Contraction of the papillary muscles tightens the chord tendineae, preventing the valves from being pushed into the atria.

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12
Q

Describe the action of semilunar valves.

A

As the ventricle contracts, blood presses against the valve cusps forcing them to open and allowing blood to flow into the aorta and pulmonary artery.
As the ventricle relaxes, blood in the aorta and pulmonary artery presses down against the valve cusps, pushing them closed.

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13
Q

What are heart sounds?

A

Turbulent blood flow

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14
Q

Which valves is the soft lubb sound made by?

A

Both AV valves, close simultaneously.

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15
Q

Which valves make the louder dubb sound?

A

Semilunar valves, close simultaneously.

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16
Q

What is coronary circulation?

A

Functional blood supply to the heart muscle itself.

Collateral routes ensure blood delivery to heart, even if major vessels are occluded.

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17
Q

What are the 3 cardiac muscle fibres?

A

Artial
Ventricular
Contractile fibres
Specialised excitatory (myocardium stimulates action potential) or conductive (conducts action potential to surrounding tissue).

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18
Q

What is cardiac syncytium?

A

Network of cardiomyocytes connected to each other by intercalated discs that enable the rapid transmission of electrical impulses through the network (gap junctions), enabling the syncytium to act in a coordinated contraction of the myocardium.
There is an atrial syncytium and a ventricular syncytium that are connected by cardiac connection fibres. Fibrous insulator prevents ventricle from contracting with the atrium.

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19
Q

What is the order of conduction in the heart?

A
  1. Sinoatrial node (SA, pacemaker)
  2. Atrioventricular node (AV)
  3. Atrioventricular bundle (bundle of his).
  4. Right and left bundle branches.
  5. Purkinje fibres.
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20
Q

What are cardiac contractions initiated by?

A

Action potentials in sinoatrial node.

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21
Q

What are the three pathways for spread of excitation?

A

Interatrial - SA node stimulates right atrium and left atrium.
Internodal - SA node stimulates AV node, both in right atrium.
AV node transmission - AV node transmits contraction to ventricles, slower than other two (0.1sec). Involves bundle of his and purkinje fibres.

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22
Q

What kind of event is an action potential?

A

Electrical event.

Always precedes mechanical event (contraction)

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23
Q

Which ions play a role in depolarisation and repolarisation of pacemaker cells?

A

Depolarisation - Sodium (via leaky/funny channels), Calcium (T or L type channels).
Repolarisation - Potassium

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24
Q

What are the different types of calcium channels. Explain them.

A

T-type: transient, rapid phase, pushes SA node to threshold by opening and allowing Ca movement into the cell.
L-type: Ligand gated/lag, slow phase, allows movement of Ca into the SA node during rapid depolarisation of action potential.

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25
Q

Which ions play a role in depolarisation and repolarisation of contractile cells?

A

Depolarisation - Sodium, Calcium (L type channels).

Repolarisation - Potassium

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26
Q

What are the phases of a contractile cells action potential?

A

0 - Rapid depolarisation - sodium channels open and it enters the cell.
1 - Small depolarisation - Sodium channels inactivate.
2 - Plateau - Potassium inward rectifier channels close, Ca channels open allowing Ca to enter cell.
3 - Repolarization - Potassium channels open and it exits cell, Ca channels close.
4 - Resting potential - Potassium channels still open, sodium and Ca channels closed.
Diagram lecture 1

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27
Q

Why is there no summation in cardiac muscle?

A

Due to long refractory period after stimulus - no fatigue.

During this time cardiac muscle cannot be re-excited.

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28
Q

What is each cardiac cycle initiated by?

A

spontaneous depolarisation of the SA node

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29
Q

What are the 4 periods of the cardiac cycle?

A 
Ventricular filling (Diastole) - relaxation, heart fills with blood. Pressure in atria higher than in ventricles-atrial contraction, AV valve open, semilunar valve closed.
Isovolumetric contraction (Systole) - ventricular contraction, increasing pressure.  No valves open.
Ventricular ejection (Systole) - pressure in ventricles greater than that in arteries, semilunar valves open.
Isovolumetric relaxation - ventricles relax, all valves closed, no blood entering or exiting ventricle.
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30
Q

What happens to the cardiac cycle when heart rate increases?

A

Duration of systole and diastole decreases.

Diastole more affected resulting in ventricular filling decreasing.

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31
Q

Provide details on the conduction pathway, specifically the path of the action potential, in the heart.

A
  1. Action potential initiated in SA node.
  2. Action potential conducted from SA node to atrial muscle.
  3. Action potential spreads through atria to AV node where conduction slows. (atrial depolarisation)
  4. Action potential travels rapidly down bundle of his to apex of the heart.
  5. Action potential travels upwards through ventricular muscles via purkinje fibres. (ventricular depolarisation)
  6. Heart returns to resting state, remaining there until another action potential is generated.
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32
Q

Does the PNS or the SNS maintain base HR?

A

PNS

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33
Q

What is an ECG and what does it do?

A

Electrocardiogram
Measures the electrical events of the heart in voltages from outside the heart.
Repeating waves (PQRST) represent sequence of depolarisation and depolarisation of the atria and ventricles.
Generally recorded at 25mm/s (increases with increased HR) with vertebral calibration of 1mV/cm.
Useful for diagnosing rhythm disturbances, changes in electrical conduction, myocardial ischaemia and infarction.

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34
Q

What causes an upwards deflection in an ECG?

A

Net current towards positive electrode

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35
Q

What causes downward deflection in an ECG?

A

Net current away from positive electrode.

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36
Q

What is the P wave representing?

A

Atrial depolarisation. Electrical event only - not contraction.

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37
Q

What is the QRS complex representing?

A

Ventricular depolarisation - not contraction (electrical event only). Atrial repolarisation occurs during this time too but is masked due to higher QRS peak.

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38
Q

What is the T wave representing?

A

Ventricular repolarisation

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39
Q

What is the PR interval?

A

Atrial depolarisation and AV node delay.

Passage of conduction through AV node, bundle of his, purkinje fibres.

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40
Q

What is the ST segment?

A

Isoelectric period of depolarised ventricles.

Ventricular contraction.

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41
Q

What is the QT interval?

A

Length of depolarisation plus depolarisation - corresponds to action potential duration.

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42
Q

What is the RR interval?

A

Interval between ventricular depolarisations.

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43
Q

How should electrodes be placed over the heart?

A

Negative near left shoulder, positive near sternum.

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44
Q

What is the Q wave representing?

A

depolarisation of the ventricular septum.

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45
Q

What is the R wave representing?

A

Bulk of the ventricles depolarise. Dominated by muscle mass of left ventricle.

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46
Q

What is the S wave representing?

A

Basilar portion of the ventricles depolarising.

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47
Q

What does the appearance of ECG traces depend on?

A

Location of recording electrodes on body surface.
Conduction pathways and speed of conduction.
Changes in muscle mass.

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48
Q

Which way does the net current of the heart always travel?

A

Towards the apex.
Creates upwards spike on ECG (traveling towards positive).
If current is travelling the other way it will create a downward spike on the ECG (traveling away from positive).

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49
Q

What are the three limb leads?

A

I - negative right arm to positive left arm
II - negative right arm to positive left leg
III - negative left arm to positive left leg.
Forms Einthoven’s triangle.

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50
Q

What are bipolar limb leads?

A

Means that the reading is being taken from two electrodes on the body.

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51
Q

What does Einthoven’s law state?

A

That the electrical potential of any limb is equal to the sum of the other two.

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52
Q

What does aVR, aVL, and aVF stand for?

A

Augmented unipolar limb leads.
R, L, F represents where the + lead should be placed.
Eg. aVR = positive lead on right arm.

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53
Q

Where does the mean electrical axis point towards?

A

Left ventricle due to larger muscle mass and therefore depolarisation.

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54
Q

Why is the horse ECG trace different?

A

Can’t lie a horse down to place electrodes so QRS shows as a dip rather than an apex. Recorded using base-apex lead.

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55
Q

Which period is shorter in the resting heart? Systole or diastole?

A

Systole

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56
Q

How do you determine cardiac output?

A

Volume of blood pumped/minute = Stroke volume x Heart rate (mL/min or L/min)

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57
Q

What is EDV?

A

End diastolic volume.
Volume of blood in ventricle at the end of diastole.
@135mL in humans

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58
Q

What is ESV?

A

End systolic volume.
Volume of blood in ventricle at the end of systole.
@70mL in humans

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59
Q

What is SV?

A

Stroke volume, volume of blood ejected from ventricles each cycle. SV = EDV-ESV (135-70=65)

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60
Q

What is ejection fraction and how can it be determined

A

Fraction of end diastolic volume ejected during a heart beat.
=SV/EDV

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61
Q

What is cardiac output? What is it influenced by?

A

Volume of blood pumped by each ventricle per minute.

Influenced by HR and SV

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62
Q

What factors affect heart rate?

A

Extrinsic regulation: Autonomic nervous system (PNS, SNS), hormonal control (Adrenaline, TH, glucagon).
No intrinsic regulation.

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63
Q

What factors affect stroke volume?

A

Extrinsic regulation: Autonomic nervous system (SNS), hormonal control (adrenaline, TH, glucagon).
Intrinsic regulation: Preload (frank starling mechanism), afterload (ventricular and aortic compliance).

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64
Q

Discuss innervation of the heart via the autonomic nervous system?

A

PNS - Vagus innervates SA node and AV node. Decreases HR.
SNS - Sympathetic efferents (cervicothoracic ganglion and sympathetic cardiac nerves) innervate SA, AV nodes, conduction fibres and ventricular myocardium. Increases HR

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65
Q

What is chronotropy?

A

Rate of firing of the SA node (heart rate - can be excitatory or inhibitory).

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66
Q

What is Inotrophy?

A

Contractility of myocardium.

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67
Q

What is dromotrophy?

A

Conduction velocity of AV node.

68
Q

What is Lusitropy?

A

Relaxation of the myocardium.

69
Q

What is the standard firing rate of the SA node?

A

100/min

70
Q

What kinds of receptors are present in cardiac tissue?

A

Sympathetic - beta 1 (adrenoreceptors) and beta 2, coupled G protein/cAMP signal transduction pathways. Alpha 1, G protein/IP3 pathway.
Parasympathetic - M2 (muscarinic), G protein/cAMP signal transduction pathways, acetylcholine.

71
Q

Discuss the mode of action of Sympathetic receptors within cardiac tissue.

A

Increased sympathetic activity (noradrenaline/adrenaline) –> Beta 1 receptors on SA node –> Increase open state of Na (funny) and Ca channels within SA node membrane –> Increase rate of spontaneous depolarisation –> Increase HR and contractility (SV).

72
Q

Discuss the mode of action of Parasympathetic receipts in cardiac tissue.

A

Increased parasympathetic activity (vagus nerve) –> Muscarinic cholinergic receptors in SA node –> Increase open state of K channels and closed state of Ca channels –> Decreased rate of spontaneous depolarisation and hyper polarise cell –> Decrease HR

73
Q

What effects does SNS and PNS innervation have on dromotropy?

A

Conduction velocity of AV node.
SNS - increases conduction velocity through node.
PNS - decreased conduction velocity through node.

74
Q

Is ventricular muscle innervated by the PNS?

A

No, only the SNS. Therefore no effect of PNS on SV.

75
Q

What is after load?

A

Aortic pressure and compliance.
Load against which the heart must contract to eject blood.
Amount of pressure sitting on semilunar valves before ventricular ejection can occur.

76
Q

What is preload?

A

End diastolic pressure and volume - venous return.

Initial stretching of the cardiomyocytes prior to contraction. Related to sarcomere length at end of diastole.

77
Q

What do preload and after load affect?

A

Ventricular contractility (inotropy) and therefore SV and CO

78
Q

Does the ventricular myocardium have vagal nerve efferent innervation?

A

No-vagal in PNS. Only SNS.

79
Q

Which hormones affect HR and SV? What are there effects?

A

Adrenaline; same effect as SNS.
Glucagon; Increases HR.
Insulin; Increases contractility
Thyroid Hormone; Increases HR and SV.

80
Q

What factors contribute to preload?

A 
Atrial pressure
Central venous pressure
Venous return
Ventricular compliance
Increased preload means increased SV and increased CO (via frank starling mechanism).
81
Q

What is the Frank Starling Mechanism?

A

Increase in venous return –> Increase in ventricular filling –> Myocardial fibres are closer to optimum length –> Greater strength of contraction –> Increased SV.

Increased stretch means increased recoil/contraction

82
Q

What factors affect after load?

A 
Aortic pressure
Aortic compliance (elasticity - lost with age)

Increased aortic pressure means increased after load and decreased CO.

83
Q

What is the mitral valve?

A

AV valve

84
Q

What is the effect of increased preload?

A

Increased stroke volume

85
Q

What is the effect of increased after load?

A

Decreased stroke volume

86
Q

What extrinsic factors (other than ANS and hormones) affect CO?

A 
Blood vessels and pressure
Blood volume and viscosity
Capillary exchange
Lymphatic return
Cardiovascular disease
87
Q

What factors affect myocardial oxygen consumption (MOC)?

A

HR
Inotrphy
Afterload
Preload - less than other factors.

An increase in all of these increases MOC

88
Q

Which vessels serve as reservoirs of blood?

A

Veins.

Can store a lot of blood with minimal increase in pressure.

89
Q

What is series blood flow?

A

Flow through a circuit/loop.
Eg. pulmonary and systemic circulation.
Aorta-arteries-arterioles-capillaries-venules-veins-vena cava

90
Q

What is parallel blood flow?

A

Blood flow to organs.
eg. Stomach, spleen, intestine, kidney.
Allows independent control of flow between tissues.

91
Q

In which vessel is the greatest blood pressure drop experienced?

A

Arterioles and capillaries

92
Q

What kind of blood pressure could you expect in the arterial tree?

A

High

93
Q

What king of blood pressure could you expect in veins?

A

Low

94
Q

True or false. Gravity increases actual blood pressure.

A

True

95
Q

Compare the pressure between pulmonary and systemic circulation.

A

Systemic has high pressure and high resistance.

Pulmonary has low pressure and low resistance.

96
Q

What cells make up blood vessels?

A

Endothelium

97
Q

Where is the velocity of blood flow the greatest?

A

Aorta.
Decreases as you go down the arterial tree.
Velocity = blood flow/cross sectional area

98
Q

How is flow (Q) through a blood vessel determined?

A

Pressure difference (triangle P)/resistance (R)
Increased pressure difference means increased flow.
Increased resistance means decreased flow.

99
Q

Compare laminar and turbulent blood flow.

A

Laminar - silent
Turbulent - high velocity, sharp turns, rough surfaces or rapid narrowing of vessels cause murmurs that can be heard via auscultation.

100
Q

What is blood pressure?

A

Force exerted by the blood against any unit area of vessel wall.

101
Q

How can resistance be calculated?

A

Change in pressure (triangle P)/flow (Q)

Decreased resistance = increased flow vice versa

102
Q

Does the pulmonary or systemic circuit have less resistance?

A

Pulmonary

103
Q

What is total peripheral resistance?

A

Combined resistance of all blood vessels within the systemic circuit.

104
Q

What effect does vasoconstriction have on blood flow?

A

Increases resistance, decreasing blood flow.

105
Q

What effect does vasodilation have on blood flow?

A

Decreases resistance, increasing flow

106
Q

What effect does increased Haematocrit have on blood flow?

A

Increases blood viscosity, increases vascular resistance and decreases flow.

107
Q

What is vascular capacitance?

A

Total quality of blood that can be stored in a given portion of the circulation for each mmHg (compliance).
Vein capacitance higher than arteries (this is because they are thin walled and have less muscle).
Vascular compliance Increase in volume/increase in pressure

108
Q

What are arteries?

A

Pressure reservoirs.

109
Q

What is systolic pressure?

A

Pressure created when the ventricles contract

@120mmHg

110
Q

What is diastolic pressure?

A

Pressure created by the recoil of the aorta and the closure of the aortic semilunar valve.
@80mmHg

111
Q

What is pulse pressure?

A

The difference between systolic and diastolic pressure.

@40mmHg

112
Q

What is dampening?

A

Intensity of pulsations becomes progressively less in smaller arteries due to increased cross sectional area.
Degree of dampening proportional to the resistance of small vessels and arterioles and the compliance of larger vessels.
Closer to the heart, less dampened the pulse.

113
Q

What effect does arterial compliance have on pulse pressure?

A

Increased compliance decreases pulse pressure.

114
Q

What factors affect mean pressure?

A

CO
Peripheral resistance.
Increased by constricting arterioles (increases TPR), constricting large vessels of circulation (increases venous return and CO), and increasing CO by increasing HR and contractility.

115
Q

What are the factors affecting pulse pressure?

A

Stroke volume - increases in SV cause increases in pulse pressure.
Arterial compliance - decreased compliance increases PP

116
Q

What is mean arterial pressure?

A 
Based on shape of aortic pulse pressure;
MAP = Pdias + 1/3(Psys-Pdias)
MAP = (CO x TPR) + CVP
TPR = total peripheral resistance
CVP = central venous pressure (normally 0mmHg)=pressure in (R) atrium
117
Q

Along with veins, which other organs serve as reservoirs for blood?

A

Spleen - aso special reservoir for RBC’s
Liver
Large abdominal veins
Venous plexus

118
Q

What factors affect central venous pressure (CVP)?

A

Blood volume
Venous tone (major factor)
Radius of arterioles
Cardiac function

Increases when blood volume and venous tone increase, arterioles dilate and cardiac function decreases.
Increased pressure here causes blood to back up into venous system thereby increasing venous pressure.

119
Q

What mechanisms help to keep blood pressure low in the legs?

A

Venous valves and venous pump.

Prevent back flow of blood into legs.

120
Q

How do you determine perfusion pressure?

A

Arterial pressure - venous pressure

121
Q

Discuss local control of blood flow.

A

Each tissue controls its own blood flow in proportion to its needs.
Tissue needs include - delivery of O2, nutrients, removal of CO2, H and other metabolites, and transport of various hormones and other substances.
Flow is closely related to metabolic rate of tissues.
Decreased O2 availability to tissues increases tissue blood flow.
Two major theories; Vasodilator theory, oxygen demand theory.

122
Q

What is active hyperaemia?

A

Increased blood flow in response to increased metabolic activity.
Increased metabolic activity generally causes vasodilation.
Factors can include increased CO2, lactic acid or adenosine.

123
Q

What is reactive hyperaemia?

A

Increased blood flow in response to a previous reduction in blood flow.
Eg. Blockage of blood flow to tissues -> metabolites increase and oxygen decreases -> vasodialtion -> release blockage -> increased blood flow due to lower resistance -> metabolites removed and oxygen delivered.

124
Q

What is auto regulation of blood flow?

A

Ability of a tissue to maintain blood flow relatively constant over a wide range of arterial pressures.
Prevents large fluctuations due to changes in MAP which can affect organ function if blood flow is decreased.
MAP remains fairly constant between the arterial pressures of 60 and 180mmHg.

125
Q

What are some common vasoconstrictors?

A

Noradrenaline, Adrenaline, Angiotensin, Vasopressin

126
Q

What are some common vasodilators?

A

Serotonin
Histamine
Prostaglandins
Nitric Oxide

127
Q

What is the Vasomotor centre (VMC)?

A

Present in brain (bilateral in reticular substance of medulla and lower third of pons), transmits impulses down through spinal cord to almost all blood vessels.
Composed of vasoconstrictor area, vasodilator area and sensory area.
Hypothalamus can exert powerful excitatory or inhibitory effect on VMC.

128
Q

Discuss short term regulation of MAP.

A

Seconds to minutes
Regulate CO and TPR.
Involves heart and blood vessels.
Primarily neural control (ANS).

129
Q

Discuss long term regulation of MAP.

A

Minutes to days
Regulates blood volume
Involves kidneys.
Primarily hormonal control.

130
Q

Discuss SNS innervation of blood vessels.

A

Innervate all vessels except capillaries.
Can increase vascular resistance in small arteries and arterioles.
Large veins and heart also SNS innervated.
Responsible for vasoconstriction.
High distribution in spleen, kidneys, gut and skin.
Not as important in brain or coronary circulation as they both require a constant supply.

131
Q

Discuss PNS innervation of blood vessels.

A

No present.

Important for control of HR via vagus nerve.

132
Q

What kind of ANS receptors are present in blood vessels?

A

SNS - alpha 1 (greatest affinity for noradr., G-protein/IP3 pathway, vasoconstricts arterioles/venoconstricts veins). Alpha 2; G protein/cAMP, constrictor, heart brain and kidneys. Beta 2; adrenoreceptor (adrenaline), dilator, primarily present in arterioles of coronary and skeletal tissue. Receive Adrenaline/noradrenaline.
PNS - M2, M3; muscarinic receptors, G protein/cAMP, acetylcholine, heart and arteries/arterioles, dilator.

133
Q

What are baroreceptors?

A

Nerve endings located in walls of carotid sinus and walls of aortic arch.
Carotid sinus transmits via Hering’s nerve to glossopharyngeal nerve.
Aortic arch transmits signals via vagus nerve.
Allows short term regulation of mean arterial pressure.

134
Q

How do baroreceptors respond to changes in arterial pressure?

A

Carotid sinus - responds between 60-180mmHg, most sensitive at 100mmHg.
As pressure increases, the number of impulses from carotid sinus increases resulting in; inhibition of vasoconstrictor, activation of vagal centre (decreased TPR, and HR).

135
Q

Moving from a supine to a standing position results in an….

A

increase in HR
increase in TPR
constriction of veins

136
Q

What are some of the functions of baroreceptors?

A

Maintain relatively constant pressure despite changes in body pressure.

137
Q

What role do chemoreceptors play in blood flow?

A

Chemosensitive cells sensitive to oxygen lack, CO2 excess, or H ion excess (decreased pH).
Located in carotid body and arch of aorta.
Activation results in excitation of vasomotor centre, increased SNS and increased BP.
Not stimulated until pressure falls below 80mmHg.

138
Q

What is the CNS Ischemic response?

A

Activated in response to cerebral ischemia.

Reduced cerebral blood flow causes CO2 buildup which stimulates vasomotor centre, increasing arterial pressure.

139
Q

What is the Bainbridge reflex?

A

Prevents damming of blood in veins, atria and pulmonary circulation.
Increase in atrial pressure increases HR.
Stretch of atria sends signals to VMC via vagal afferents to increase HR and contractility.

140
Q

What is respiratory sinus arrhythmia?

A

Increased SNS activity and increased HR during inspiration.

Increased PNS activity and decreased HR during expiration.

141
Q

How is long term blood pressure regulated?

A

Occurs through renal regulation of blood volume via changes in sodium and water retention.
Hormonal control of MAP - adrenaline, vasopressin, angiotensin II.

142
Q

What effect does vasopressin (ADH) have on blood volume and pressure?

A

Induces renal fluid reabsorption and vasoconstriction - increases blood volume and increases arterial pressure.

143
Q

What are the effects of Angiotensin II?

A

Indirect - stimulates aldosterone release, increases Na reabsorption, increases ADH secretion and water reabsorption.
Direct - stimulates vasoconstriction of arterioles (increases MAP), direct effect on kidney (decreased perfusion/vasoconstriction), water retention.

144
Q

Discuss capillary vessel area and velocity of blood.

A

Have greatest total cross-sectional area.

Have slowest velocity of blood flow, increasing exchange.

145
Q

What are the different types of capillaries?

A

Continuous - most common, small gaps between endothelial cells to allow small water molecules to move through.
Fenestrated - large gaps between endothelial cells forming pores/fenestrations. Allows proteins and in some cases blood cells to move through.
Sinusoidal/Discontinuous - irregular blood filled space with large fenestrations. Allow proteins, clotting factors, plasma and new RBC to enter circulation. Liver, bone marrow.

146
Q

Discuss local control of blood flow through capillary beds.

A

Local control of smooth muscle of arterioles, met arterioles and pre capillary sphincters.

147
Q

What is the interstitium?

A

Space between cells.
Fluid (gel) within this space is interstitial fluid.
Contains collagen fibres and proteoglycan filaments.

148
Q

What is the exchange between capillary and interstitial fluid dependant upon?

A

Distance
Surface area
Size of capillary pores
Property of the substance

149
Q

How does fluid move into and out of the capillary?

A

Via bulk flow (osmosis) based on pressure gradients.

Ficks Law - osmosis affected by pressure gradient, SA, permeability of membrane.

150
Q

What is filtration?

A

Movement from capillary into interstitial space

151
Q

What is absorption?

A

Movement from interstitial space into capillary

152
Q

What factors govern the movement of water and electrolytes?

A

Starling forces;

  1. Capillary hydrostatic pressure (Pc) tends to force fluid outward through the capillary membrane (FAVOURS FILTRATION).
  2. Interstitial fluid hydrostatic pressure (Pif) OPPOSES FILTRATION WHEN value is positive.
  3. Plasma colloid/Capillary oncotic pressure OPPOSES FILTRATION causing osmosis of water inward through the membrane.
  4. Interstitial fluid colloid oncotic pressure PROMOTES FILTRATION by causing osmosis of fluid outward through the membrane.
153
Q

What are the 4 determinants of net fluid movement across capillaries?

A

Capillary hydrostatic pressure (28mmHg)
Interstitial fluid hydrostatic pressure
Plasma colloid osmotic pressure
Interstitial fluid colloid oncotic pressure (10mmHg)

154
Q

What is the role of the lymphatic system?

A

Accessory route for fluid and proteins to travel from interstitial spaces to blood.
Prevents oedema.
Lymph derived from interstitial fluid that flows into lymphatics.
Major route for absorption of nutrients from GIT.
Role in immunity.

155
Q

What governs the degree of activity of the lymphatic pump?

A

Smooth muscle contraction (within lymph vessel).

External compression

156
Q

What is the average capillary exchange rate?

A

2mL/min

157
Q

What are the driving forces behind oncotic pressure?

A

75% driven by albumin, 25% by globulins (both plasma proteins).

158
Q

Where does the thoracic duct (lymphatics) drain to?

A

Cranial vena cava

159
Q

What is the major driver of capillary exchange?

A

Capillary hydrostatic pressure

160
Q

What happens if CHP is high but the 3 remaining factors are low?

A

Filtration into interstitial space occurs.

161
Q

What happens if IHP is high but the 3 remaining factors are low?

A

Absorption into capillary

162
Q

What are the components of blood?

A

Plasma - 55%
Buffy coat - leukocytes, platelets, <1%
Erythrocytes - 45%

163
Q

What are the components of plasma?

A

Water - 90%

Solutes - proteins including albumin and globulins, also fibrinogen and other (enzymes, hormones, etc), 8%

164
Q

What are the stages of RBC maturation/genesis?

A

Pronormoblast - basophil normoblast - polychromatophil normoblast - orthochromatic normoblast - reticulocyte - erythrocyte

165
Q

What is haematocrit?

A

Packed cell volume

% volume of blood that is red cells

166
Q

What is a leukocyte and what are some different forms?

A

WBC
Granulocytes (formed in bone marrow) - neutrophil, eosinophil, basophil.
Agranulocytes - monocytes, lymphocytes (formed in lymph tissue).

167
Q

What are platelets?

A

Cytoplasmic fragments derived from megakaryocytic (platelet in bone marrow), also called thrombocytes.
Colourless, cell fragments (no nucleus, has organelles).
Important for blood clotting.
Granules contain secretory products.

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