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Block 2 > Heart > Flashcards

Heart Flashcards

0
Q

Which vessels provide the most resistance to flow?

A

Resistance vessels - muscular arteries and arterioles

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1
Q

How much blood does each side of the heart pump out per minute?

A

5L

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2
Q

In which vessels will you find 67% blood volume at any one time?

A

Venues and veins

Capacitance vessels

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3
Q

How can MABP be estimated?

A

Diastolic blood pressure + 1/3 pulse pressure (SP-DP)

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4
Q

What is the relationship between velocity and cross sectional area of vessels?

A

v = Q/A
v is velocity
Q is flow
A is cross sectional area

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5
Q

What happens to the velocity of blood flow as it moves from aorta to arteries to capillaries?

A

Velocity decreases because the total cross sectional area of the vessels increases. Minimum velocity is in capillaries

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6
Q

What is the functional consequence of having low velocity of blood flow in capillaries?

A

Allows time for blood to exchange substances across capillary walls

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7
Q

What is the difference between laminar and turbulent flow?

A

Laminar - smooth, with parallel streams of fluid moving along tube. Flow is fastest in middle of tube so width of tube important determinant of resistance to flow
Turbulent - eddies and swirls with fluid moving in irregular patterns

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8
Q

Why does width of a tube so greatly affect the resistance it causes to flow?

A

Mean velocity is proportional to radius squared
Flow = v x A
Flow = r2⃣ x pie r2⃣
Flow is proportional to r4⃣
Resistance = 8x length x viscosity / pi radius 4⃣
Therefore 1/2 diameter of tube - 16 x resistance

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9
Q

What is the no slip condition?

A

In laminar flow, fluid closest to walls is motionless due to forces between wall and fluid

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10
Q

In laminar flow of blood, where do cells move?

A

Displaced to centre of tube, leaving marginal plasma layer which aids blood flow

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11
Q

What is Poiseuilles law?

A

Q = change in pressure x pi x radius 4⃣ / 8 x viscosity x length of tube

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12
Q

If flow is constant and the radius of vessel is halved, what happens to velocity and pressure?

A

Velocity increased x4

Pressure increased x16

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13
Q

Is pressure is constant and vessel diameter is halved, what happens to velocity and flow?

A

Velocity falls x4

Flow falls x16

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14
Q

Under what circumstances is flow likely to be turbulent?

A

High velocity
Low viscosity
Diameter of vessel is large

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15
Q

Why is higher pressure required to move a fluid during turbulent flow?

A

Some energy dissipated as heat and so heart has an increased workload

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16
Q

What is Reynolds number?

A

Determines whether a flow is laminar or turbulent.
Re = (velocity x diameter x density) / viscosity
Re below 2300 - laminar flow
Above 4000 - turbulent flow

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17
Q

What flow type do bruits indicate?

A

Turbulent

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18
Q

What can turbulent flow result in?

A

Damage to endothelium of blood vessels

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19
Q

Why are capillaries not the main source of resistance in the circuit?

A

Because they arranged in parallel so the overall resistance is reduced. In arteries and arterioles that are arranged in series, the resistance is much higher

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20
Q

What happens if resistance in arterioles is increased?

A

Stroke volume must be increased to maintain cardiac output

CO = MABP x TPR

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21
Q

What is transmural pressure?

A

Pressure acting across wall.
P intravascular - P extravascular
Tends to stretch the vessel as intravascular pressure is usually higher than extravascular

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22
Q

As blood vessels are not rigid, what effect does increasing pressure tend to have on resistance?

A

Resistance decreases with increasing pressure as vessel walls stretch

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23
Q

What would happen if intravascular pressure dropped to 0?

A

Vessel would collapse and flow would cease

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24
Q

What characteristics of blood vessels give them capacitance?

A

Distensibility, particularly veins

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25
Q

Why take most chest X-rays PA?

A

Size of heart most life size - near detector

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26
Q

What can mediastinal lymphadenopathy cause?

A

Dysphagia
Tracheal compression
Compression of left recurrent laryngeal nerve - hoarse voice

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27
Q

What sets the resting membrane potential of the heart?

A

Selective permeability to K+
Concentration gradient of K+
Na/K pump which maintains constant ionic concentrations

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28
Q

What happens during phase 0 of the ventricular myocyte action potential?

A

Na channels open and Na enters cell - depolarisation

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29
Q

What is Brugada syndrome?

A

Reduction in Na channel activity due to loss of function mutation
Altered spread of heart beat
Ventricular fibrillation
Ca channel function may also be affected

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30
Q

What is the refractory period?

A

Time when Na channels are inactivated and so it is not possible to fire another action potential in this time

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31
Q

Which channels are responsible for the plateau, phase 2 of the ventricular myocyte action potential?

A

L type Ca channels
Allow influx of Ca into cell and into T tubules
Prolongs action potential after Na channels are inactivated

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32
Q

What effect do adrenaline and noradrenaline have on Ca in the heart?

A

Ca entry from T tubules, sarcoplasmic reticulum and extracellular fluid is enhanced
Ca stores in sarcoplasmic reticulum are also enhanced

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33
Q

What is excitation contraction coupling?

A

Conversion of action potential to mechanical response - muscle contraction
Ca binds to troponin C on myofilaments
Cross bridges form - myosin heads and actin filaments
Myosin head hydrolyses ATP and cocks back so moving the filaments along each other and causing contraction

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34
Q

What is calcium induced calcium release?

A

Calcium enters L type calcium channels and binds to ryanodine receptors on sarcoplasmic reticulum
This causes release of calcium from SR - 80% Ca required for muscle contraction

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35
Q

Which channels are responsible for phase 3, repolarisation phase of the ventricular myocyte action potential?

A

K+ channels open allowing an efflux of K+

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36
Q

Which channels are responsible for the pacemaker potential in pacemaker tissue such as SA node?

A

Slow leak Na/K channels results in a drift of membrane potential towards threshold. Activated by negative voltages and binding cAMP. At threshold these channels close. Current is called If - funny current

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37
Q

What forms the main part of the action potential in pacemaker tissue?

A

T type Ca channels open at threshold

Close after around 100-150 ms

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38
Q

Which channels are responsible for hyper polarisation in pacemaker tissue?

A

K+ channels remain open to a little beyond resting membrane potential

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39
Q

What effect does noradrenaline have on pacemaker potential at the SA node?

A

B1 adrenergic receptors bind NA
Result in positive chronotropic effect - increase speed
Raises cAMP levels and so results in increased Na influx in funny current

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40
Q

What effect does ACh have on pacemaker potential at the SA node?

A

Pacemaker potential is slowed by acetylcholine acting at M2 muscarinic receptors
Negative chronotropic effect
Reduces cAMP levels so reduces Na influx and increases K efflux

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41
Q

Where does the mediastinum sit?

A

Between lungs

Extends from thoracic inlet to diaphragm

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41
Q

What separates superior and inferior mediastinum?

A

Sternal plane

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42
Q

Which part of mediastinum is thymus gland located in?

A

Superior and anterior

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43
Q

Where does the posterior mediastinum extend to?

A

Extends inferiorly to 12th thoracic vertebrae

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44
Q

Which part of mediastinum contains oesophagus?

A

Superior and posterior

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45
Q

Which arteries can be used for a coronary artery bypass graft?

A

Thoracic arteries

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46
Q

Which part of heart binds to central diaphragmatic tendon?

A

Fibrous pericardium

Middle mediastinum

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47
Q

What can be seen on a child’s chest x ray that is absent on an adults?

A

Sail sign - children have large thymus gland which decreases in size with age

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48
Q

What is the difference in position of the recurrent laryngeal nerves on left and right in the mediastinum?

A

Left - loops under aortic arch, near hilum of lunch

Right - loops under right subclavian artery

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49
Q

What form of imaging can be used to visualise the left atrium?

A

Transoesophageal cardiac ultrasound due to difficult position of left atrium at posterior/base of heart

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50
Q

What is the transverse sinus?

A

Passageway between arterial output and venous input
Posterior to aorta and pulmonary trunk
Superior to SVC
Remnant of the pericardial cavity formed when heart tube folds

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51
Q

What are the 3 layers of pericardium surrounding the heart?

A

Visceral
Parietal
Fibrous

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52
Q

What 3 parts make up the bicuspid and tricuspid valves of the heart?

A

Flap like cusps
Chordae tendinae
Papillary muscles

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53
Q

What can happen if papillary muscles are damaged?

A

Valve incompetence and cardiac murmur

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54
Q

What sits between atria and ventricles and prevents electrical conduction?

A

Fibrous tissue skeleton

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55
Q

How do semilunar valves work?

A

During diastole reverse-flowing blood catches in the pockets and closes the valve
Valve cusps are pushed toward vessel walls during ventricular systole

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56
Q

Where do the coronary arteries arise from?

A

Coronary sinus above cusps of aortic valve

Fill during diastole because cusp pockets are open allowing blood to flow into coronary arteries

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57
Q

What does dominance mean in reference to coronary arteries?

A

Dominance describes which coronary artery gives off posterior interventricular artery (PIVA). Eg right dominance, PIVA is a branch of RCA in 80% people

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58
Q

What does the right coronary artery usually supply?

A

Right atrium and ventricle
SA node
AV node
Posterior IV septum

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59
Q

What branches does the RCA give off (most of the time)?

A 
Sinoatrial nodal
Conus artery 
Anterior ventricular arteries
Marginal - reaches apex
Posterior interventricular
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60
Q

What branches does the left coronary artery give off?

A

Circumflex artery
Conus artery
Anterior interventricular (LAD)
Marginal artery

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61
Q

What does the LCA normally supply?

A

Left atrium and ventricle
Anterior IV septum
AV bundle
Right and left bundles

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62
Q

What are the surface marking boundaries of the heart?

A

2nd L CC
3rd R CC
6th R CC
5th L ICS - mid clavicular line

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63
Q

Where do you auscultate the valves of the heart?

A

Aortic - 2nd R ICS
Pulmonary - 2nd L ICS
Tricuspid - 4/5th L ICS
Mitral - 5th L ICS mid clavicular line

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64
Q

What are internal features of the right atrium?

A 
Fossa ovalis
Crista terminalis
SA node
AV node
Coronary sinus
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65
Q

What are internal features of the left atrium?

A

Fossa ovalis
Entrance of pulmonary veins x4
Auricle - rough walled

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66
Q

What is the smooth part of the left ventricle derived from?

A

Bulbus cordis

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67
Q

What are the rough appendages in the ventricles called?

A

Trabeculae carnae

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68
Q

What is the smooth part of the right ventricle called?

A

Conus arteriosus

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69
Q

What is the moderator band?

A

Septomarginal trabeculae - conduction system runs through here, right bundle branch. Provides shortcut

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70
Q

Which sit anterior, veins or arteries around heart?

A

Veins

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71
Q

What are the 3 branches that come off the arch of the aorta?

A

Brachiocephalic trunk –> R common carotid and R subclavian
L common carotid
L subclavian

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72
Q

What veins drain into the SVC?

A

L and R internal jugular
L and R subclavian
Drain to L and R brachiocephalic veins then to SVC

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73
Q

What is the ligamentum arteriosum a remnant of?

A

Ductus arteriosus - R to L shunt in foetus between pulmonary artery and aorta to bypass lungs

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74
Q

Where is the cardiac autonomic plexus?

A

Between aorta and trachea

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75
Q

Which parts of sympathetic chain supply heart?

A

T1-4 so descend through neck to heart

Visceral sensory fibres travel with these sympathetics so referred pain to this dermatome inc shoulder, arm, jaw etc

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76
Q

A wave of depolarisation away from an electrode will give what kind of deflection on a trace?

A

Negative

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77
Q

A wave of repolarisation towards and electrode will give what kind of deflection on a trace?

A

Negative

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78
Q

What does a lead II ECG record?

A

Bipolar limb lead between right arm and left leg

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79
Q

Describe where the precordial limb leads are placed on the body for an ECG

A

V1 - 4th intercostal space R sternal border
V2 - 4th intercostal space L sternal border
V3 - between leads 2 and 4
V4 - 5th L intercostal space in mid clavicular line
V5 - horizontally even with V4 but in anterior axillary line
V6 - horizontally even with V4 and V5 but in mid axillary line

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80
Q

Which electrode is the ground in an ECG?

A

Right leg

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81
Q

What are the augmented limb leads?

A

aVL - left arm
aVR - right arm
aVF - left leg

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82
Q

What change do you see from V1 to V6 ECG leads?

A

Progression of the R wave from negative to positive

Increase in thickness of the ventricular wall through V1-6

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83
Q

What is happening during the isolelectric portion of PR interval?

A

AV node being depolarised

84
Q

What is happening during the isolelectric portion of the ST segment?

A

Ventricular myocytes at plateau phase

85
Q

Why is the T wave broad?

A

Gradual repolarisation of ventricles

86
Q

What is the general direction of ventricular activation in the frontal plane called?

A

Axis

87
Q

At what speed does ECG paper normally run?

A

25mm/sec

88
Q

How much time does 1 small square on an ECG represent?

A

0.04 sec

89
Q

How do you calculate HR using big squares on an ECG?

A

300/number of big squares in RR interval

90
Q

What is the normal range of time of a PR interval?

A

120-200 ms

91
Q

What is the normal length of a QRS complex?

A

<120ms

92
Q

How long is a normal QT interval?

A

550ms

93
Q

What is the normal range of the axis of QRS in frontal plane?

A

-30 to 90 degrees

94
Q

What is ACS?

A

Acute coronary syndrome

Unstable angina, STEMI and NSTEMI MI

95
Q

When does angina occur?

A

When myocardial oxygen demand exceeds supply

96
Q

Describe the cellular changes associated with MI

A

Cardiac cell deprived of blood
Cell membrane increasingly permeable to K
K leaks out of injured region causing abnormal ventricular repolarisation
ST elevation and T wave peaking in ECG

97
Q

Someone with suspected MI, on ECG, no ST elevation, no cardiac markers. What is it?

A

Ischemia

98
Q

If STEMI is detected on lead II, III and aVF leads, which region is affected?

A

Acute inferior MI

99
Q

If STEMI is detected on two or more precordial leads, which area is affected?

A

Anterior

100
Q

What are the cardiac markers of an MI?

A

Troponin

Creatine kinase

101
Q

What is bivalirudin?

A

Clopidogrel and aspirin

Antiplatelet agent

102
Q

What is aspirin?

And what are its indicated uses in ACS?

A

COX inhibitor (irreversible)
Antiplatelet
Use for MI and ACS

103
Q

What is clopidogrel?

And what are its indicated uses?

A

Antiplatelet
Works by inhibiting binding of ADP to platelet receptor
Use in ACS, acute STEMI and in those with an aspirin allergy

104
Q

What are Ticagrelor and Brilique?

What are their indicated uses?

A

Anti platelet P2Y12 platelet receptor inhibitors

Use in ACS and acute MI

105
Q

What are Abciximab, Aggrastat, Integrilin and Eptifibatide?

What are their indicated uses?

A

gpIIb/IIIa inhibitors
Receptors undergo conformational change – inhibits fibrin binding – no platelet aggregation
Use in STEMI and ACS

106
Q

What is unfractioned heparin?

What are its indicated uses?

A

Antithrombotic
Unfractioned heparin binds to anti thrombin and activates it. This inactivates thrombin and factor Xa
Use in percutaneous coronary intervention and unstable angina

107
Q

What is enoxaparin?

What are its indicated uses?

A

Anti thrombotic, low molecular weight heparin
Anti Xa activity
Use in percutaneous coronary intervention and STEMI

108
Q

Why do you give B blockers to an MI patient?

A

Decrease HR, BP and myocardial contractility, improved coronary diastolic filling

109
Q

What is lisinopril and why would you give it to an MI or congestive heart failure patient?

A

ACE inhibitor
Inhibits ACE, which converts Angiotensin I to II
Less angiotensin II causes vasodilation, ↓ BP

110
Q

Which side of the heart sits anteriorly?

A

Right side

111
Q

Where do blood vessels develop in embryo?

A

Angiogenic cell clusters in extraembryonic mesoderm which forms part of placenta and umbilical cord

112
Q

When is blood present in foetal vessels during development?

A

Week 3

113
Q

At what point during development does the heart start beating?

A

Day 22-23

114
Q

When do heart tubes fuse?

A

During lateral folding in late week 3

115
Q

What is reversal in embryonic development?

A

Developing heart originally above head

Reversal occurs during folding and moves the heart to the future thoracic region

116
Q

What is the septum transversum?

A

Thick mass of cranial mesenchyme that gives rise to parts of thoracic diaphragm and ventral mesentery in development

117
Q

How many inflows and outflows does the developing heart tube have?

A

2 venous inputs

1 arterial outflow

118
Q

What is dorsal mesocardium?

A

Attaches heart tube to dorsal pericardial wall

During heart looping, it degenerates forming the transverse pericardial sinus

119
Q

Name the 5 dilations of the heart tube during development and what they give rise to in the adult

A

Sinus venosus - smooth wall of right atria
Atria - rough wall of both atria
Ventricle - ventricles
Bulbus cordis - outflow of ventricles
Truncus arteriosus - initial part of aorta and pulmonary trunk

120
Q

Where do the pulmonary veins originate?

A

Pulmonary veins grow out of the left atrial wall and branch x4. The proximal parts get absorbed into the atrial wall = smooth part

121
Q

What is the difference in origin of the smooth parts of the left and right atria?

A

Right smooth - originates from sinus venosus

Left smooth - growth into pulmonary veins

122
Q

Where do vascular shunts exist in embryo to bypass the lungs?

A

Between right and left atria - fossa ovalis

Between pulmonary trunk and aorta - ductus arteriosus

123
Q

Why does folding of heart tube occur?

A

Fixed positions of aortic arches and venous input

Growing tube cannot fit into space between without folding

124
Q

Which direction does the bulbus cordis move during folding of the heart tube?

A

Bulbus cordis grows rapidly & moves infero-anteriorly & right

125
Q

What direction do the atria and ventricles move during folding of the heart tube?

A

Ventricle moves left

Atria move postero-superiorly

126
Q

What is dextrocardia?

A

Heart ends up the wrong way around

Bulbus cordis moves left and ventricles move right during development

127
Q

What connects atria and ventricles in developing heart?

A

Atrioventricular canal

128
Q

What are endocardial cushions?

A

Endocardial cushions grow across atrioventricular canal from anterior to posterior
Cushions = swellings in mesenchyme
Meet in middle to separate left and right AV canals

129
Q

When does atrial septation occur?

A

Mid week 4 - week 5

130
Q

Describe the process of atrial septation

A

Septum primum grows down from top of atria towards endocardial cushion
Apoptosis at top of septum leads to formation of foramen secundum
Septum secundum grows down to the right of septum primum
Secundum is hard, primum is floppy and should close after birth

131
Q

Why is there a right to left shunt in utero?

A

Lungs fluid filled so high pulmonary vascular resistance
More blood entering right atrium than left
Blood shunted through foramen ovale

132
Q

Why is there a pressure shift post natally from right to left, to left to right?

A

Lungs drained and functional
Low pulmonary vascular resistance
Greater pulmonary blood flow so more blood in left atrium
Valve of foramen ovale closes

133
Q

When can a patent foramen ovale become a problem in an adult?

A

Valsava manoeuvre can briefly increase right-sided pressure over left
Can result in emboli passing from right-to-left
Increases possibility of transient ischaemic attack (TIA) & stroke

134
Q

Where can atrial septal defects occur?

A

Foramen/ septum secundum
Foramen/ septum primum
Endocardial cushion
Left to right shunt

135
Q

What clinical sign will be seen in a baby with an atrial septal defect?

A

Difficulty feeding

136
Q

What is the ventricular septum formed from?

A

Muscle, membrane and endocardial cushion

137
Q

Describe the muscular part of the ventricular septum

A

Grows toward endocardial cushions from ventricle floor
Crescent-shaped
Remains incomplete in cranial (upper) region

138
Q

When does ventricular septation occur?

A

Week 5-7

139
Q

What completes the ventricular septum in the cranial region?

A

Membranous down-growth of bulbar ridges

Endocardial cushion

140
Q

Where are ventricular septal defects most likely to occur?

A

In membranous part of septum

141
Q

What is the smooth part of the right ventricle called and where is it derived from?

A

Conus arteriosus

Develops from bulbus cordis

142
Q

What are the bulbar ridges derived from which contribute to the formation of the membranous ventricular septum?

A

Derived from neural crest mesenchyme

143
Q

How does partitioning of ventricular outflow occur?

A

A septum forms in the common ventricular (arterial) outflow

The septum spirals through 180º creating the aorta & pulmonary trunk

144
Q

What can failure of bulbar ridge formation result in?

A

Truncus arteriosus defect
Ventricular septal defect with overriding persistent truncus arteriosus
Cyanotic condition

145
Q

What can result from unequal division in truncus arteriosus?

A

Pulmonary stenosis/Aortic stenosis
Ventricular septal defect often present
Larger vessel often over-rides the VSD
Pulmonary stenosis may cause cyanosis

146
Q

How can transposition of great vessels occur?

A 
Failed development of conus arteriosus? 
Malformation of aorticopulmonary septum? 
2 isolated circulations 
Ductus arteriosus can help mix blood 
ASD & VSD often associated = beneficial
147
Q

What is a tetralogy of Fallot?

A

Pulmonary stenosis
RV hypertrophy
Over riding aorta
Ventricular septal defect

148
Q

Name 4 cyanotic defects

A

Transposition of great vessels
Tetralogy of Fallot
Truncus arteriosus defects
Critical pulmonary stenosis

149
Q

Name 3 non cyanotic heart defects

A

Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus

150
Q

What is a sarcomere?

A

Repeating unit of myofilaments in heart muscle between Z lines

151
Q

How does the heart muscle act as a syncytium?

A

Interconnection both mechanical and electrical
Cells branch and interdigitate
End to end membrane connections - intercalated discs

152
Q

Describe excitation contraction coupling

A

Action potential propagates along sarcolemma and enters cell via T tubule system
Causes Ca2+ to enter cells and intracellular Ca2 increases
More Ca2 released from sarcoplasmic reticulum
Calcium binds to troponin on thin filament
Causes tropomysin to move revealing actin binding site for myosin heads
Myosin heads attach themselves onto the actin filaments
Contraction + ‘walking along’

153
Q

What determines the strength of a cardiac contraction?

A

Dependent on Ca2+ concentration in extracellular fluid
At the end of the action potential Ca2+ flow reversed
Lowered Ca2+ concentration stops actin myosin interaction and relaxation ensues

154
Q

What effects do calcium channel antagonists have on the heart and vasculature?

A

Mostly work on the voltage dependent L-type calcium channels
3 broad groups - papaverines, dihydropyridines and benzothiazepines
All decrease systemic vascular resistance and central venous pressure by vasodilatation
Negative ionotropism
Decreased after load and contractility - decreases cardiac work and oxygen requirement

155
Q

What are verapamil, nifedipine and diltiazem?

A

Calcium channel blockers

156
Q

Which valvular disease is likely to be seen in an IV drug user due to endocarditis?

A

Tricuspid valve

157
Q

Which chamber of the heart is most likely to be affected by penetrative trauma?

A

Right ventricle because it is the most anterior chamber

158
Q

What are the 2 types of mitral valve disease?

A

Stenosis and regurgitation

159
Q

What are the heart sounds?

A

S1 - Closure of mitral and tricuspid valves
S2 - Closure of aortic and pulmonary valves
S3 - Ventricular filling
S4 - Atrial contraction under pressure

160
Q

What can be a result of aortic valve disease?

A

Left ventricular hypertrophy

161
Q

What would a mitral stenosis sound like?

A

Loud first heart sound
Low frequency diastolic rumble
Does not radiate
Palpable thrill at apex in severe disease

162
Q

What can cause mitral stenosis, and what can occur as a result?

A

Rheumatic fever
Area below 2cm2 causes reduction in flow and increase in ventricular filling time
Area below 1 cm2 causes pulmonary hypertension
LA increases in size
Increases tendency to develop atrial arrhythmia
These patients dependent on atrial kick to move blood through but if in AF, this doesn’t happen so can be a serious problem

163
Q

What can cause mitral regurgitation and what are clinical consequences?

A

Degenerative
Rheumatic
Congenital prolapse esp Marfans
MI and chordae tendinae rupture - acute emergency

164
Q

What signs suggest aortic stenosis and what are clinical consequences?

A

Restriction to forward flow into systemic circulation
Fixed cardiac output
Midsystolic murmur may radiate to carotid
ECG changes - left axis shift, larger QRS complex

165
Q

What are associated disorders with aortic regurgitation and what signs will be heard?

A

Incompetent valve causes back flow from aorta into ventricle
Associated with endocarditis, Marfan’s disease, ankylosing spondylitis, dissection,trauma
Early diastolic murmur, high pitched

166
Q

What effect will an increase in preload have on stroke volume?

A

Due to Starlings law - increase in end diastolic volume therefore increase stretch therefore increase in stroke volume

167
Q

What factors can increase contractility of the heart?

A 
Sympathetic stimulation
Adrenaline and noradrenaline
High intracellular calcium
High blood calcium 
Thyroid hormones
Glucagon
168
Q

What factors can increase after load?

A

Increased vascular resistance

Semi lunar valve damage

169
Q

What factors can increase preload?

A

Fast filling time

Increased venous return

170
Q

What factors can decrease contractility?

A

Parasympathetic stimulation
Acetylcholine
Hypoxia
Hyperkalaemia

171
Q

What factors can decrease preload?

A 
Decreased thyroid hormones
Decreased calcium ions
High or low potassium
High or low sodium 
Low body temp
Hypoxia
Abnormal pH
Drugs eg calcium channel blockers
172
Q

What is net filtration pressure?

A

NFP = (capillary hydrostatic pressure - ISF hydrostatic pressure) - (plasma osmotic force) - (ISF osmotic force)

173
Q

What fluid movement is present across capillaries in health?

A

10mmHg filtration at arterial end and 10mmHg absorption at venous end

174
Q

What is the clinical definition of heart failure?

A

Syndrome in which patients have typical symptoms (e.g. breathlessness, ankle swelling and fatigue) and signs (e.g. elevated jugular venous pressure, pulmonary crackles and displaced apex
beat) resulting from abnormality of cardiac structure of function

175
Q

What is the pathophysiological definition of heart failure?

A

Abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolising tissues

176
Q

What are the 2 types of heart failure?

A

HFREF - Heart Failure with Reduced Ejection Fraction (systolic)
HFPEF - Heart Failure with Preserved Ejection Fraction (diastolic)

177
Q

What 3 conditions does a diagnosis of HFREF require?

A

Symptoms typical of HF
Signs typical of HF
Reduced LVEF

178
Q

What conditions does a diagnosis of HFPEF require?

A

Symptoms typical of HF
Signs typical of HF
Normal or only mildly reduced LVEF and LV not dilated
Relevant structural heart disease (LV hypertrophy, LA enlargement) and or diastolic dysfunction

179
Q

What is the ejection fraction?

A

SV = end diastolic volume - end systolic volume

EF (%) = SV/ EDV

180
Q

What are the advantages and disadvantages of echocardiography?

A

Defines cardiac structure and function
Cheap and robust
Very subjective

181
Q

What can cause HFREF?

A

Affects contraction of the heart muscle
Myocardial Injury or Overload (↑ pre-load or afterload)
Regional (e.g heart attack) vs Global (e.g. Dilated CM)

182
Q

What are the short and long term effects after MI?

A

Short-Term:
↑ SNS ↑ Contractility↑ HR
Long Term:
Adverse Remodelling (ability of heart to deal with higher loads is decreased)

183
Q

What ventricular remodelling changes can occur in the heart after insult?

A

Myocardial Injury or chronic volume overload (pre-load) = ventricular dilation (systolic, HFREF)
Chronic pressure overload (after load) = hypertrophy (diastolic, HFPEF)

184
Q

Describe left sided congestive heart failure

A

Decreased CO - activity intolerance and decreased tissue perfusion
Pulmonary congestion - impaired gas exchange - cyanosis + hypoxia
pulmonary oedema - cough with frothy sputum, orthopnoea, paroxysmal nocturnal dyspnoea

185
Q

Describe right sided congestive heart failure

A

Congestion of peripheral tissues - oedema, ascites, liver congestion, GI tract congestion - anorexia, GI distress, weight loss, liver dysfunction

186
Q

How are levels of heart failure classified?

A

New York heart association classification

187
Q

Why do you get oedema in heart failure?

A

Venous end of capillary has higher hydrostatic pressure so the net absorption pressure is reduced and therefore some fluid is retained in the tissues

188
Q

What compensatory mechanisms occur in heart failure?

A

Decreased CO stimulates sympathetic nervous system so increased vascular tone, heart rate and contractility
Decreased renal blood flow so RAAS activation
Angiotensin II causes vasoconstriction
Aldosterone stimulates salt and water retention
Vasoconstriction increases after load
Salt and water retention increases preload

189
Q

What effects do natriuretic peptides have on cv system?

A

BNP and ANP – stimulated by myocardial wall stretch

Vasodilation, ↑Na secretion, ↓Cardiac Stress Counteract RAAS

190
Q

What effects do endothelins have on the CV system?

A

Powerful vasoconstrictor
Stimulated by aldosterone release (Na retention)
High concentrations in HF

191
Q

What are treatment options for acute decompensated HF?

A 
ABCDE 
O2 via  re-breath bag 
GTN (spray/ infusion)
Furosemide 
CPAP if needed 
Inotropes 
Rarely transplant
192
Q

What are treatment options for chronic HF?

A

B blocker, ACE inhibitor, implantable cardioverter defibrillator (ICD), HF education, anti coagulation, cardiac resynchronisation therapy (CRT)

193
Q

What is spironalactone?

A

Aldosterone antagonist, potassium sparing diuretic

194
Q

Which treatments are used in all categories of heart failure?

A

ACE inhibitors

B blockers

195
Q

What therapeutics are available to treat HFREF?

A

ACE inhibitors - opril
B blockers - olol
Aldosterone antagonist - spironalactone
Isosorbide dinitrate - vasodilator for angina
Diuretic - loop furosemide, thiazides, carbonic anhydrase inhibitor azolamide, osmotic mannitol
Angiotensin II receptor blocker - sartan
Digoxin

196
Q

What is end diastolic volume and end systolic volume?

A

Volume when heart is full - 140ml

Volume when heart is empty - 50ml

197
Q

What is cardiac output?

A

Volume of blood pumped by each ventricle per minute in litres per minute
CO = HR x SV

198
Q

What is stroke volume?

A

The volume of blood ejected from each ventricle during each ventricle contraction

199
Q

What factors affect heart rate?

A

Autonomic innervation
Hormones
Fitness levels
Age

200
Q

What factors affect stroke volume?

A 
Heart size
Fitness levels
Gender
Contractility
Duration of contraction
Preload (EDV)
After load (resistance)
201
Q

Describe the baroreceptor reflex

A

Baroreceptors in carotid sinus and aortic arch detect an increase in blood pressure
This causes firing of glossopharyngeal and vagus afferents to the vasomotor centre in the medulla
This causes increased firing of vagal efferents and decrease firing of sympathetics which results in decrease in HR, decrease in vasoconstriction and therefore decreases blood pressure

202
Q

Describe the atrial receptor reflex

A

Atrial stretch receptors detect increase in atrial pressure
This causes increase of firing of vagal afferents to the vasomotor centre in the medulla
This decreases parasympathetic efferent firing and increase sympathetic efferent firing which allows the heart to contract more forcefully and therefore eject the increased end diastolic volume

203
Q

Describe the chemoreceptor reflex

A

Carotid body and aortic arch chemoreceptors detect increase in CO2 and decrease in O2
This increases firing of glossopharyngeal and vagal afferents
Chemoreceptors in medulla can also detect the CO2 levels via pH
These all fire to the cardiac and the vasomotor centre in the medulla which then fires to increase sympathetic stimulation and decrease parasympathetic
This causes an increase in HR and contractility, and vasoconstriction in order to provide more oxygen and remove more CO2

204
Q

What is preload?

A

Initial stretching of the cardiac myocytes prior to contraction

205
Q

What factors increase preload?

A 
Increased atrial contractility
Decreased heart rate
Increased aortic pressure
Increased central venous pressure - venous return
Increased ventricular compliance
206
Q

What effect does the sympathetic nervous system have on starlings curve?

A

Shifts left - generates more force for a given EDV

207
Q

What is afterload?

A

Arterial pressure= load on the ventricle
Greater the load, the less the muscle fibres can contract
Example = Hypertension

208
Q

What effect does an increase in afterload have on starlings curve?

A

Shift right so decreased stroke volume for a given EDV

209
Q

Describe total peripheral resistance

A

Small arteries and arterioles
Key for generating resistance
Strongly influenced by hormones and ANS
Generates Afterload

Block 2 (9 decks)

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