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Year 1 LSS 1 > Incomplete Cardiovascular System > Flashcards

Incomplete Cardiovascular System Flashcards

1
Q

How wide and long are ventricular cells?

A

100um long and 15um wide.

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2
Q

How far apart are T-tubules

A

2uM apart, lying alongside each Z-line of every myofibril.

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3
Q

How does an action potential cause excitation of cardiac muscle?

A

1) T-tubules experience depolarisation. L-type Ca channels open allowing Ca2+ to enter the cell
2) Ca2+ binds to the SR Ca release channels (Ryanodine receptors) on the sarcoplasmic reticulum
3) Ca2+ leaves the sarcoplasmic reticulum and causes contraction
4) CaATPase protein on sarcoplasmic reticulum pumps Ca2+ back onto sarcoplasmic reticulum
5) Na/Ca exchanger pumps Ca2+ outside cell

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4
Q

What underpins the relationship between muscle length and amount of force?

A
  • Increase in active force produced by actin-myosin interactions
  • increase of passive force produced by elastic element of the muscle
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5
Q

How does cardiac muscle relate to skeletal muscle in terms of compliance?

A

Cardiac muscle is less compliant than skeletal muscle.

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6
Q

When does cardiac muscle do isometric and isotonic contraction?

A

Isometric when pressure in both ventricles increase.

Isotonic is where blood is ejected from both ventricles.

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7
Q

What effect does increasing the pre-load have on a muscle?

A

Increases force of the muscle as it produces more passive force.

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8
Q

What effect does increasing the after-load have on a muscle?

A

Decreases force, as decreases the amount the muscle is able to shorten

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9
Q

What are the in-vivo correlates of pre-load and after-load?

A

Pre-load: around of blood that fills the ventricles.

After-load: the load against which the left ventricle ejects blood after the opening of the aortic valve.

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10
Q

What are the measures of cardiac pre-load and after-load?

A

Pre-load: end-diastolic pressure/volume, right atrial pressure
After-load: diastolic material blood pressure

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11
Q

What is starling’s law?

A

Increased diastolic fibre length increases ventricular contraction

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12
Q

What two factors explain starling’s law?

A
  • Changes in number of cross-bridges
  • Changes in Ca sensitivity of myofilament. Two theories for this: (A) Troponin C changes conformation as sarcomere length increases; (B) spacing between myosin and actin filaments decreases forming strong-binding cross-bridges.
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13
Q

What is stroke work?

A

Work done by the heart to eject blood under pressure into the aorta and pulmonary trunk. = SV x Pressure

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14
Q

What is the Law of Laplace?

A

When pressure within a cylinder is held constant, the tension of its walls increases with increasing radius.

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15
Q

How is the Law of Laplace applied to the ventricles?

A

Radius of curvature of the left-ventriclar wall is less than right-ventricle, allowing the left-ventricle to generate higher pressures with similar wall stress.

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16
Q

How is the heard beat divided and further divided?

A

Diastole (ventricular relaxation during which the ventricles fill with blood):

  • Isovolumetric ventricular relaxation
  • rapid filling of ventricles
  • late, slow filling
  • begin of atrial systole

Systole (ventricular contraction when blood is pumped into arteries):

  • Isovolumic ventricular contraction
  • Ventricular ejection
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17
Q

How is stroke volume calculated?

A

End-diastolic volume - End-systolic volume

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18
Q

What is the Ejection fraction?

A

SV / End-diastolic volume. Normally 65%

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19
Q

How do the pressure changes in the right side of the heart compare to those in the left side of the heart?

A

Follows same patterns except quantitatively lower.

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20
Q

Describe the points on a pressure-volume loop.

A

X1 marks the beginning of isovolumic contraction. The volume of the ventricles are high, but pressure is low. Pressure then shoots up to X2.
X2 to X3 represents ejection, as pressure increases and then decreases back to X2 level, while volume decreases.
X4 is isovolumic relaxation, as X4 to X1 represents ventricular filling and atrial systole.

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21
Q

How can SV be calculated by a pressure-volume loop?

A

X1 represents end-diastolic pressure while X3 represents end-systolic pressure.

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22
Q

How can the pressure-volume loops be changed?

A

Increasing pre-load widens PV loop. Increasing after load lengthens PV loop but flattens the loop as it decreases stroke volume (as less active force shortening can occur).
Increasing contractility will make the whole PV loop larger, increasing cardiac output.

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23
Q

How is Cardiac Output calculated?

A

CO = Stroke Volume x Heart Rate

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24
Q

Explain the origins of the heart sounds

A

S1 (lub) is due to closure of AV valves.
S2 (dub) is due to the closure of arctic and pulmonary valves.
S3 can signify turbulent ventricular filling.
S4 can be due to severe hypertension or mitral incompetence.

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25
Q

What ion in particular does the membrane potential depend on?

A

K+

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26
Q

What are the equilibrium potentials of K and Na?

A 
Ek = -80 mV
Ena = +66 mV
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27
Q

How long does a nerve and cardiac myocyte action potential last?

A

2ms for nerve

280ms for cardiac myocyte

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28
Q

Describe the three potassium currents during a cardiac myocyte action potential.

A

Transient Outwards K+ channels open straight after depolarisation causing a little bit of depolarisation.
Pk current more gradual and is caused by activation of K currents.
PK1 is a large current responsible for fully depolarising the cell. It flows during diastole, stabilising the resting membrane potential, reducing the risk of arrhythmias.

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29
Q

Give example of drugs that are Ca Channel antagonists

A

Nifedipine, Nitrendipine and Nisadipine

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30
Q

When has a full recovery time ended?

A

When a normal AP be elicited by a normal stimulus.

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31
Q

Why can the electrical properties of the heart be described as intrinsic?

A

Because it has independent generation and propagation of electrical activity.

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32
Q

Why is the AP shape of a sinoatrial node cell different to a ventricular cell?

A

It lacks K1 channels and has other currents at play.

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33
Q

How can the autonomic nervous system modulate the heart’s intrinsic beating?

A

Sympathetic: Noradrenaline/adrenaline makes the action potential steeper, allowing the threshold potential to be reached more easily and this increases heart rate.
Parasympathetic: Acetylcholine slows the gradient of the pacemaker potential, and so slowing the heart rate.

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34
Q

What are the main components of the heart’s conduction system?

A
  • Sinoatrial node
  • Inter-nodal fibres
  • Atrio-ventricular node
  • Bundle of His and Purkinje Fibres (ventricular bundles together)
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35
Q

Why is the AV node important?

A

It delays the action potential from reaching the ventricles, allowing blood time to fill the ventricles before systole.

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36
Q

What is notable about the Bundle of His and Purkinje fibres?

A

Bundle of His are very large and conduct the action potential ~6x velocity of ordinary cardiac muscle.
ensure contraction proceed upwards from the apex to the base.

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37
Q

What structure assists the propagation of AP through the cardiac muscle?

A

Intercalated disks

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38
Q

How does an electrocardiogram produce deflections?

A

When a wave of depolarisation travels towards the positive electrode, it causes an upwards deflection. Visa versa.

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39
Q

What are the two ECG configurations?

A
  • Limb lead configuration

- Chest lead configuration

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40
Q

What is a microcirculation?

A

The circulation of an individual tissue

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41
Q

What does a microcirculation consist of?

A

An arteroile branching out into a terminal arteriole, which supplies the capillary, eventually draining through the pericytic (post-capillary) venules and then venules.

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42
Q

What is Blood Flow Rare (F)?

A

The volume of blood passing through a vessel per unit time. F = (delta)P/R

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43
Q

How is the pressure gradient calculated in a microcirculation?

A

The difference between the pressure in the arteries and capillaries.

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44
Q

What is resistance?

A

Any hindrance to blood flow.

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45
Q

What is resistance influenced by?

A
  • VESSEL RADIUS (1/r^4)
  • Blood viscosity
  • Vessel length
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46
Q

What is the vascular tone?

A

The amount of constriction usually present in an arteriolar smooth muscle.

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47
Q

What are the ways microvessels respond to local needs?

A
  • Active hyperemia causes vasodilation
  • Change in temperature
  • Increase in blood pressure will cause myogenic vasoconstriction
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48
Q

How can Flow be applied to the entire circulation?

A

CO = MAPB/TPR

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49
Q

How does the cardiovascular control centre in the medulla control arterial blood pressure?

A

Controls vasoconstriction through activating alpha receptors or vasodilation by beta receptors.
Also through the release of vasopressin and increasing sympathetic activity leading to the release of adrenaline and noradrenaline.

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50
Q

How are capillaries ideally suited for diffusion?

A
  • minimise diffusion distance

- maximise surface area

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51
Q

What tissue is highly perfused, but only 10% of arteries are being used at rest?

A

Muscle

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52
Q

What are the types of gaps between endothelial cells?

A

Vast majority of capillaries are continuous, they have small water filled gaps between the cells.
Certain capillaries have fenestrae, which have slightly bigger holes on the endothelial cells.
A few capillaries are discontinuous, meaning they have large gaps.
In the brain, you don’t have water-filled gap junctions but tighter gap junctions.

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53
Q

What are the starling forces?

A
  • Hydrostatic pressure generated by the heart

- Osmotic pressure draws water into the capillaries

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54
Q

What is bulk flow?

A

The process of protein-free plasma filtering out of the capillary and mixing with surrounding interstitial fluid before being reabsorbed.

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55
Q

What happens when hydrostatic pressure is greater and lesser than oncotic pressure?

A

> causes ultrafiltration

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56
Q

Where do the lymphatics drain the excess interstitial fluid to?

A

right lymphatic duct
thoracic duct
and right/left subclavian veins

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57
Q

How much fluid do the lymphatics drain a day?

A

3L a day

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58
Q

What happens when the rate of fluid production > rate of fluid removal by lymphatics?

A

Oedema

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59
Q

What is elephantiasis?

A

Parasitic blockage of lymph nodes

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60
Q

What do the signals seen in an ECG represent?

A

The vector sum of all the action potentials in the heart.

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61
Q

Why does an ECG produce a useful reading?

A

Only particular zones of the heart are active at any given time
At these regions, the action potentials are synchronised and easily summable

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62
Q

What are the features of a 12-lead ECG?

A

10 wires/electrodes:

RA, LA, RF, LF + 6 chest leads (V1 to V6)

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63
Q

What views are facilitated through the 12-lead ECG?

A

Limb leads provides the frontal plane (sagittal)

Chest leads provides the horizontal plane (coronal)

64
Q

What are the normal settings on an ECG?

A

Speed of 50 mm/s and sensitivity of 10mm/mV. 1 small square = 0.04s as 1 large square =0.20s

65
Q

What causes the components of the PQRST wave?

A

P wave = atrial depolarisation
QRS complex = ventricular depolarisation
T wave = ventricular repolarisation

66
Q

What are the augmented leads?

A 
aVR = RA -> (LA + LF)
aVL = LA -> (RA + LF)
aVF = LF -> (RA + LA)
67
Q

Describe Einthoven’s triangle

A

Triangle using Right Arm (- -), Left Arm (+-) and Left Leg (++) with Right Leg as V=0
Lead 1 = LA -> RA
Lead 2 = LF -> RA
Lead 3 = LF -> LA

68
Q

What are normal and abnormal cardiac axis?

A

Normal: -30 to 90
+90 is right axis deviation
-30 is left axis deviation

69
Q

Where are the chest leads placed?

A

V1: Right 4th intra-costal space parasternal
V2: Left 4th intra-costal space parasternal
V3: Left midway between V2 and V4
V4: Left 5th ntra-costal space mid-clavicular line
V5: Left anterior axillary line (same plane as V4)
V6: Left Mid-axillary line (same plane as V4)

70
Q

What are three layers of the blood vessel wall?

A

Tunica intima - endothelium and basal lamina
Tunica media - predominantly smooth muscle cells
Tunica adventitia - contains blood supply, fibrous tissue, elastin and collagen

71
Q

What are the functions of vascular endothelium?

A
  • vascular tone management
  • thrombostasis
  • absorption and secretion
  • barrier
  • growth
72
Q

How do the 5 main molecules influence vascular endothelium?

A

NO: SM relaxation and inhibition of growth. Inhibits platelet aggregation.
PGI2 (prostacyclin): SM relaxation, inhibition of growth. Inhibits platelet aggregation.
TXA2 (thromboxane): SM constriction, platelet activation and aggregation.
ET-1 (Endothelin-1): SM contraction and growth.
ANGII (Angiotensin II): SM contraction and growth.

73
Q

How is NO production stimulated?

A

Activation of G-protein receptor, activating Phospholipase C. PIP2 -> IP3 and DAG.
IP3 stimulates endoplasmic reticulum to release Ca2+
Ca2+ upregulates eNOS (endothelial NO synthase) which catalyses:
L-argenine + O2 –> L-citruline + NO

74
Q

How does NO cause relaxation?

A

NO moves into the interstitial space from the endothelium and into the smooth muscle cells. It up regulates guanylyl cyclase to convert GTP into cGMP.
cGMP upregulates protein kinase G, which eventually causes relaxation.

75
Q

How can sheer stress cause vasodilation?

A

It can upregulate eNOS

76
Q

How is arachidonic acid produced?

A

Produced when phospholipase A2 converts a phospholipid into arachidonic acid.
DAG can also form arachidonic acid by enzyme DAG lipase.

77
Q

How is PGH2 made, and what is it a precursor to?

A

PGH2 is made by the conversion of arachidonic acid by COX1/2 enzymes. PGH2 is a precursor to thromboxane (TXA2), prostacyclin (PGI2) and other prostaglandins (such as PGD2, PGE2, PGF2)

78
Q

How can arachidonic acid lead to bronchoconstriction?

A

Arachidonic acid can be converted to LTD4 via lipoxigenase activity. LTD4 binds to LT receipts which causes bronchoconsriction.

79
Q

How does montoleukast work?

A

Inhibits LTD4, and can thus be used to treat asthma.

80
Q

How does prostacyclin cause relaxation?

A

Binds to IP receptors of smooth muscle cells causing adenyl cyclase to produce cAMP, which upregulates Protein Kinase A, leading to relaxation.

81
Q

How does thromboxane produce it’s effects?

A

Binds to TPbeta receptors in smooth muscle cells activating Phospholipase C, and so producing IP3. In smooth muscle cells IP3 does not lead to the production of NO, but instead leads to constriction.
Binds to TPalpha receptors on platelets leading to platelet activation and further thromboxane production (and this platelet aggregation).

82
Q

How is endothelin-1 produced?

A

Big-ET-1 is converted into ET-1 by endothelia converting enzyme on the endothelium surface membrane.

83
Q

How does endothelin-1 produce its effects?

A

ET-1 will bind to ETa receptors on smooth muscle cells activating Phospholipase C, and thus leading to IP3 causing constriction.
ETb endothelial receptors on endothelial cells will also activate Phospholipase C, but IP3 will upregulate eNOS, leading to smooth muscle relaxation.

84
Q

Where is ACE secreted?

A

Secreted by the endothelium of pulmonary vessels and renal vessels.

85
Q

What are the effects of angiotensin II?

A
  • Vasopressin secretion
  • Aldosterone secretion
  • Increases Na+ reabsorption directly.
  • Sympathoexitation
  • Arteriolar constriction
  • up regulates growth of vascular smooth muscle cells
86
Q

What does ACE do?

A
  • convert angiotensin I to angiotensin II

- degrade bradykinin

87
Q

What is the effect of bradykinin?

A

Stimulates phospholipase C on endothelial cells and this causes relaxation.

88
Q

What drugs increase levels/effects of NO and how?

A
  • ACh stimulates production of NO
  • GTN, nicrodramdil, ISMN donates ready to go NO
  • viagra prevents degradation of cGMP
89
Q

What are the biochemical effects of aspirin?

A

Inactivates COX-1 enzyme, and switches COX-2 enzyme to generate protective lipids.

90
Q

What are two subdivisions of adrenoreceptors and their main effects?

A

1) alpha-adrenoreceptor
- excitatory effects of smooth muscle mainly on blood vessels
2) beta-adrenoreceptor
- relaxant effects on smooth muscle
- stimulatory effects on the hear

91
Q

Where are alpha-adrenoreceptors located?

A

alpha-1 are located on post-synaptic effector cells, mainly on resistance vessels.
alpha-2 are located on the presynaptic nerve terminal membranes. Some alpha-2 receptors are also found in vascular smooth muscle cells.

92
Q

How do alpha-adrenoreceptors work?

A

alpha-1 receptors lead to IP3 production causing increased calcium in the sarcoplasm
alpha-2 receptors work to inhibit further transmitter release.

93
Q

Where are beta-adrenoreceptors located?

A

beta-1 receptors are found in cardiac muscle and smooth muscle of the GI tract.
beta-2 receptors are located on bronchial, vascular and uterine smooth muscle.
beta-3 receptors are found on fat cells.

94
Q

How do beta-adrenoreceptors work?

A

They are G-protein coupled receptors to Adenyl cyclase, which increase levels of cAMP, causing relaxation in smooth muscle, but excitation in cardiac muscle.

95
Q

What adrenoreceptors can be activated by the different catecholamines?

A 
Noradrenaline: a1, a2 and b1
Adrenaline: a1, a2, b1, b2
Dopamine: weak effects at a1 and b1
Isoprenaline: b1 and b2
phenylephrine: a1
96
Q

List the common cardiac arrhythmias

A
  • Bradycardia (100 bpm)
  • Cardiac conduction abnormalities
  • Supraventricular arrhythmias such as atrial fibrillation, atrial flutter, AVNRT
  • Ventricular arrhythmias such as ventricular tachycardia and fibrillation.
97
Q

What are the normal P wave, PR interval and QRS complex values?

A

P wave: duration

98
Q

What are the normal Q wave, QT interval and T wave values?

A

Q wave: duration

99
Q

What are the ECG properties of sinus tachycardia?

A
  • Abnormally fast heart rate coming from sinus node

- other waves/values normal

100
Q

What are the ECG properties of atrial fibrillation?

A
  • ‘Irregular irregular’ rhythm
  • no P-waves as atria are fibrillating and depolarisation isn’t happening synchronously.
  • normal QRS and T
101
Q

What are the ECG properties of atrial flutter?

A
  • saw tooth appearance
  • tachyarrhythmia
  • normal ventricular rhythm
102
Q

What are the ECG properties of atrioventricular reentrant tachycardia?

A
  • Regular QRS

- Hard to identify P wave as atrial and ventricles polarise at the same time

103
Q

What are the ECG properties of preexcitation syndrome?

A

Atrial conduction spreads through AVN and accessory pathway.
This causes short PR interval
Slurred upstroke

104
Q

What are the ECG properties of 1st degree AV block?

A
  • prolonged PR interval

- normal P wave and QRS complex

105
Q

What are the ECG properties of Mobitz Type 1 heart block?

A

Some of the beats of atrium does not enter ventricle. Gradual prolongation of PR interval until beat is skipped.

106
Q

What are the ECG properties of Mobitz Type 2 heart block?

A

Some atrial beats do not enter ventricle. Fixed PR intervals then drop beat.

107
Q

What are the ECG properties of 3rd degree heart block?

A

AV node not functioning
Ventricle starts beating at its own interval
Dissociated P waves and QRS complexes

108
Q

What are the ECG properties of RBBB?

A

1) QRS complex widens

2) QRS morphology shows bunny ears M in V1

109
Q

What are the ECG properties of LBBB?

A

1) QRS complex widens

2) QRS morphology shows W in V1

110
Q

What are the ECG properties of ventricular tachycardia?

A
  • ventricular tachyarrhythmia

- broad QRS

111
Q

What are the ECG properties of ventricular fibrilation?

A

Not compatible with life. Looks silly.

112
Q

What assumptions must be made for MBP = CO x TPR ?

A

Steady flow

113
Q

Why does blood pressure fall across the circulation?

A

Viscous (frictional) pressure losses.

114
Q

Compare the behaviours of laminar and turbulent flow

A

Laminar flow: each particle follows a smooth path, velocity of the fluid is constant at any rate.
Turbulent flow: irregular flow with tiny whirlpool regions associated with pathophysiological changes to the endothelial lining. The velocity if not constant at every point.

115
Q

Why does blood flow quicker in the middle than at the walls of the vessel?

A

Due to adhesive forces between the fluid and the surface.

116
Q

What is the sheer stress?

A

Sheer rate (velocity gradient) x viscosity

117
Q

What are the effects of high sheer stress?

A

Found in laminar flow, it promotes endothelial cell survival, vasodilation and anticoagulation.

118
Q

What are the effects of low sheer stress?

A

Found in turbulent flow, it promotes endothelial proliferation, apoptosis, vasoconstriction, coagulation and platelet aggregation.

119
Q

What are the two measures of blood pressure?

A

Pulse pressure = SBP - DBP

Mean blood pressure (MBP) = DBP + 1/3PP

120
Q

What does ventricular pressure drop more steeply in diastole in comparison to aortic pressure?

A

Due to ventricular pressure falling rapidly, but aortic pressure falling slowly after aortic valve closes. This is due to the elasticity of the aorta and large arteries, which buffer the change in pulse pressure.

121
Q

What is the Windkessel effect?

A

During ejection, blood enters the aorta and other arteries faster than it leaves them due to the elastic recoil of the arteries.

122
Q

Why does the WIndkessel effect decrease over time?

A

Arterial compliance decreases with age.

123
Q

What is the relationship between transmural pressure and vessel volume?

A

Compliance

124
Q

How does venous compliance compare to arteriolar compliance?

A

Venous compliance is 10-20x greater.

125
Q

What are the cardiovascular problems with standing?

A
  • Postural hypotension
  • Varicose veins caused by incompetent valves
  • Prolonged elevation of venous pressure causes oedema in feet.
126
Q

What affects venous volume distribution?

A
  • peripheral venous tone
  • gravity
  • skeletal muscle pump
  • breathing
127
Q

How is flow mainly determined?

A

By arteriolar constriction, which determines MABP.

128
Q

How do blood vessels compensate for changes in perfusion pressure? How do they sense this change?

A

Changing vascular resistance

There are two theories explaining how this change is sensed:

  • myogenic theory: smooth muscle fibres respond to tension in vessel wall
  • metabolic theory: as blood flow decreases, metabolites accumulate
129
Q

How does a blood vessel locally react to a drop in blood pressure?

A

Decrease resistance by increasing radius, and so increasing flow.

130
Q

What does atrial natriuretic peptide do?

A

cause systemic vasodilation, and has the opposite effect of aldosterone

131
Q

What part of the autonomic nervous system is important for controlling circulation? and heart rate?

A

Circulation: sympathetic

Heart rate: parasympathetic

132
Q

What blood vessels are innervated by sympathetic nerves?

A

All of them except capillaries.

133
Q

Describe the variability of sympathetic innervation to blood vessels

A

More innervate vessels supplying kidneys, gut, spleen and skin; fewer innervate skeletal muscle and brain.

134
Q

Where is the vasomotor centre located?

A

Bilaterally in the reticular substance of the medulla, and the lower third area of the pons.

135
Q

What parts make up the vasomotor centre?

A

Vasoconstricitor area, vasodilator area and cardioregularory inhibitory area.

136
Q

What does the vasomotor centre do in anticipation of exercise?

A

Increase heart rate and contractility

Increase ventilation rate

137
Q

What parts of the vasomotor centre control sympathetic tone?

A

The depressor (vasodilator) and pressor (vasoconstrictor) areas modulate sympathetic nerve activity.

138
Q

How does the sympathetic nervous system increase heart contractility

A

Noradrenaline binds to beta-1 receptors -> increase in cAMP -> increase in protein kinase A -> more uptake of Ca into intracellular stores.

139
Q

What can alter stroke volume?

A
  • Sympathetic activity and plasma adrenaline

- End-diastolic ventricular volume (starling’s law)

140
Q

Where are baroreceptors located and what is the afferent nerve?

A

Aortic arch - vagus nerve

Carotid sinus - glossopharyngeal nerve

141
Q

What ranges do baroreceptors detect pressure changes? What ranges are they most sensitive?

A

Detect pressure changes between 60-180mmHm. Most sensitive at 90-100mmHg.

142
Q

How does the autonomic nervous system react to an increase in baroreceptor activity?

A
  • Increase parasympathetic activity to heart

- Inhibit sympathetic activity to the heart, arterioles and veins.

143
Q

Why is moving from a supine to standing position challenging for a human?

A

Gravity forces all the blood downwards, causing blood to pool in veins (venous distension in lower limbs), and so reduced blood volume and blood pressure.
Gravity will also add to the hydrostatic pressure in the arteries causing more fluid to enter tissue, further reducing effective circulating blood, thus stroke volume and so transient hypotension.

144
Q

Describe the baroreceptor reflex to postural hypotension

A

Lower blood pressure decreases baroreceptor firing signals to the brain. This decreases inhibition of the sympathetic nervous system and increases inhibition of parasympathetic nervous system.
This means increased vasoconstriction and heart rate, and thus CO. This sees a rise in BP.

145
Q

What are the compensatory mechanisms involved with haemorrhage?

A
  • Baroreceptor reflex
  • Autotransfusion: decrease in hydrostatic pressure means more fluid leaves capillaries than enters.
  • Hormones such ADH, Angiotensin II and Aldosterone released to reduce urinary output.
146
Q

How does the body cope with loosing different percentages of blood?

A

30% (2l) loss will lead to shock

147
Q

How does the cardiovascular system respond to exercise?

A

A fall in blood pressure as vasodilation to increase blood flow. However this is compensated by anticipation of exercise allowing cardiovascular centre to increase sympathetic activity and decrease parasympathetic activity.

TPR will be balanced out by constricting blood flow to kidneys and GI tract.

Increased venous return increases stroke volume, and so contributing to increases CO (decrease in plasma volume through loss of water and salt by sweat opposes this).

The increase in CO is greater than the fall in TPR and so BP increases.

148
Q

How would you describe the distribution of blood pressure across the population?

A

Follows a normal distribution

149
Q

What is the current definition if hypertension?

A

more than 140/90 mmHg

150
Q

What is the distribution of primary against secondary hypotension?

A

Primary: 90-95%
Secondary: 5%

151
Q

What is secondary hypotension?

A

Has an identifiable cause: due to renal disease, tumours secreting aldosterone, catecholamines etc.

152
Q

What factors play a part in primary hypertension?

A
  • genetic

- environment: dietary salt, obesity, alchohol, pre-natal environment, pregnancy, other dietary factors

153
Q

What cardiovascular features is hypertension associated with?

A
  • increased TPR due to vasoconstriction, structural narrowing of arteries and loss of capillaries
  • reduced arterial compliance
  • normal CO
  • normal blood volume
154
Q

What is increased systolic hypertension?

A
  • where SBP is greater than 140, but DBP is less than 90

- due to increasing stiffness of medium/large arteries

155
Q

What are the consequences of hypertension?

A
  • CHD
  • Stroke
  • Periferal vascular disease
  • Heart failure
  • Atrial fibrillation
  • Dementia/cognitive impairment
  • Retinopathy

Year 1 LSS 1 (3 decks)

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