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ESA 2 > CVS > Flashcards

CVS Flashcards

To cover most aspects of CVS for ESA 2. This is only for revision purposes, you'll need to do your own stuff. Everything contained is may be shit, use at your own risk. Note: You will still need to go through vital signs, ECG prep and embryology.

1
Q

Are arteries high resistance or low resistance vessels?

A

Low resistance

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2
Q

Define the term after-load on the ventricular myocardium

A

The force necessary to expel blood into the arteries

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3
Q

Define the term pre-load on the ventricular myocardium

A

When the ventricular myocardium is fully stretched and is exerting the same pressure as the venous pressure

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4
Q

Describe the response of the cardiovascular system to eating a meal

A

-Increased activity of the gut leads to the release of metabolites and local vasodilation -The total peripheral resistance falls, causing the arterial pressure to fall and the venous pressure to rise. -The rise in venous pressure and fall in arterial pressure causes a rise in cardiac output and heart rate. -The extra pumping of the heart reduces venous pressure and raises arterial pressure

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5
Q

How does the cerebral circulation meet the high demand of oxygen?

A

-High capillary density -High basal flow rate -High extraction rate

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6
Q

How is a secure cerebral blood supply created?

A

-Structurally - anastomoses between basilar and internal carotid artery -Functionally - brainstem regulates other circulations, myogenic autoregulation and metabolic factors

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7
Q

How might drugs be used to treat hypertension?

A

Drugs used in the treatment of hypertension act to reduce cardiac output and/or peripheral resistance. For example ACE-inhibitors, diuretics, adrenoceptor blocks and calcium channel blockers.

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8
Q

How would you work out the average pressure?

A

Diastolic pressure plus 1/3rd pulse pressure (Systole is shorter than diastole)

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9
Q

In the lungs what effect does an increase in the capillary pressure have on lymph?

A

More fluid to leave, oedema forming.

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10
Q

In the pulmonary circulation what pressures are found in the arteries and veins?

A

Arterial 12-15mmHg Venous 5 mmHg Capillaries in the middle

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11
Q

Is hypoplastic left heart syndrome compatible with life?

A

Without intervention this can be lethal.

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12
Q

List the five types of acyanotic heart defect.

A

-ASD -PFO -VSD -PDA -Coarctation of the Aorta

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13
Q

In pacemaker cells what causes the gradual depolarisation of the cells?

A

The funny (If) current carried by Na+ ions via slow Na+ channels that open as the potential goes very negative (repolarisation)

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14
Q

If there was no parasympathetic or sympathetic activity acting on the heart what would be the intrinsic heart rate? Why is the resting heart actually 60bpm?

A

100bpm however, the resting as there is lower as there is more parasympathetic activity acting on the heart than sympathetic

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15
Q

List the four types of cyanotic heart defect.

A

-Tetralogy of fallot -Tricuspid atresia -Transposition of the great arteries -Hypoplastic left heart

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16
Q

Suggest some vasodilators to increase capillary recruitment and vasodilation of capillaries.

A

-Adrenaline acts on B2 receptors causing vasodilation -K+ -Increased osmolarity -Adenosine -Inorganic phosphates -H+

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17
Q

What are inotropic drugs?

A

Drugs that affect the force of contraction of the heart

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18
Q

What are pericytes?

A

These cells are capable of dividing into muscle cells, or fibroblasts during angiogenesis, tumour growth and wound healing

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19
Q

What are the four abnormalities of tetralogy of fallot?

A

-VSD -Overriding aorta -Pulmonary stenosis -Right ventricular hypertrophy

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20
Q

What are the two heart sounds created by?

A

S1 - mitral and tricuspid S2 - aortic and pulmonary

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21
Q

What are the two layers which make up serous pericardium?

A

-Parietal layer (outside layer - next to fibrous) -Visceral layer (inner layer - adheres to heart)

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22
Q

What are the two circulations in the lungs?

A

-Bronchial -Pulmonary

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23
Q

What are the ways used to reduce the workload of the heart in angina?

A

-β-blockers -Ca2+ channel blockers -Organic nitrates

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24
Q

What are vasa vasorum? Where are they found?

A

Translated as “vessels of vessels” - little blood vessels that supply the big ones. They are found in the Tunica Adventitia of the vessels.

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25
Q

What are the two types of resistance vessels?

A

-Arterioles -Pre-capillary sphincters

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26
Q

What are VSDs?

A

VSDs are an opening in the interventricular septum (most commonly the membranous portion of the septum) can occur at any point. Since left ventricular pressure is much higher blood flows from left to right.

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27
Q

What can chronic hypoxia in the pulmonary circulation lead to?

A

-Increase in vascular resistance -Chronic pulmonary hypertension -Right ventricle pumps harder -Right ventricular heart failure

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28
Q

What conditions might cause an increased risk of thrombus formation?

A

-Atrial fibrillation -Valve disease

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29
Q

What conditions might first degree heart block be a sign of?

A

-Coronary artery disease -Acute rheumatic carditis -Digoxin toxicity -Electrolyte disturbances

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30
Q

What diuretic action do ACE inhibitors have?

A

Prevents release of angiotensin II and therefore prevents release of aldosterone from the zona glomerulsa. Usually aldosterone causes water retention, increasing blood volume so reducing it decreases blood volume and decreases pre-load to the heart.

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31
Q

What does coarctation of the aorta result in?

A

The narrowing of the aorta increases the afterload on the left ventricle and can lead to left ventricular hypertrophy.

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32
Q

What factors oppose vasomotor tone?

A

Vasodilator factors (H+, K+ and Adenosine)

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33
Q

What does coarctation of the aorta result in?

A

The narrowing of the aorta increases the afterload on the left ventricle and can lead to left ventricular hypertrophy.

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34
Q

What factors oppose vasomotor tone?

A

Vasodilator factors (H+, K+ and Adenosine)

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35
Q

What happens to the flow rate when the viscosity of a fluid is increased?

A

The middle layers will slow down so the mean velocity of flow decreases

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36
Q

What happens to the pacemaker potential to decrease the heart rate? How does this occur?

A

Makes the pacemaker potential less steep by acetylcholine acting on M2 receptors.

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37
Q

What are the four basic classes of anti-arrhythmic drugs?

A

-Drugs that block voltage gated Na+ channels -Antagonists of β-adrenoceptors -Drugs that block K+ channels -Drugs that block Ca2+channels

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38
Q

What happens to the pacemaker potential to increase the heart rate? How does this occur?

A

Makes the pacemaker potential more steep by noradrenaline targeting B1 receptors.

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39
Q

What is a paradoxical embolism?

A

A PFO can be the route by which a venous embolism reaches the systemic circulation if pressure on the right side of the heart increases even for a minute.

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40
Q

What is a patent ductus arteriosus?

A

It is the failure of the ductus arteriosus to close. This is a vessel that exists in the foetus to shunt blood from the pulmonary artery to the aorta before the lungs are functioning. It should close shortly after birth as the pressure in the pulmonary artery drops following perfusion of the lungs.

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41
Q

What is an acyanotic defect?

A

A defect that does not result in a lower than normal concentration of oxygen in the blood.

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42
Q

What are the three layers of a blood vessel called?

A

-Tunica Intima – Next to the lumen -Tunica Media – Intermediate -Tunica Adventitia – Outer layer

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43
Q

What is an atrial septal defect?

A

An ASD is an opening in the septum between the two atria, which persists following birth.

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44
Q

Other than their diuretic action what other action do ACE inhibitors have?

A

Prevent the formation of the vasoconstrictor angiotensin II, thus promoting vasodilation of arterioles and venous dilation. This decreases both afterload and preload to the heart.

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45
Q

What is coarctation of the aorta?

A

Narrowing of the aortic lumen in the region of the ligamemtum arteriosum (former ductus arteriosus)

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46
Q

What is contractility increased by physiologically?

A

An increased sympathetic activity which therefore makes the heart more susceptible to venous pressure.

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47
Q

Suggest 3 reasons why an arrhythmia might arise?

A

Ectopic pacemaker activity

After-depolarisations

Re-entry loop (normal spread disrupted by damaged area)

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48
Q

What is Cushing’s reflex?

A

Brain is in a rigid cranium, legions lead to an increase in intercranial pressure. Cushing’s reflex is where this increased pressure leads to reduced blood flow to vasomotor control regions in the brainstem which causes an increase in sympathetic vasomotor tone and therefore restores higher blood flow to brain.

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49
Q

What are after-depolarisations?

A

Abnormal depolarisations following the action potential, thought to be caused by high intracellular Ca2+ (leads to longer QT interval)

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50
Q

What is hypoplastic left heart syndrome?

A

The underdevelopment of the left ventricle and the ascending aorta. A PFO or ASD are also present and blood supply to the systemic circulation is via a ductus arteriosus.

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51
Q

What is hypoxia pulmonary vasoconstriction? Why is it important?

A

If the oxygen levels drop you get constriction of the blood vessels which diverts blood to the better alveoli, ensuring that perfusion matches ventilation.

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52
Q

What is meant by laminar flow?

A

In laminar flow, there is a gradient of velocity from the middle to the edge of the vessel. Velocity is highest in the centre, and fluid is stationary at the edge.

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53
Q

What is meant by the term viscosity? (in reference to flow)

A

The extent to which fluid layers resist sliding over one another.

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54
Q

State some specific features of cardiac muscle

A

Striations

Branching

Centrally positioned nuclei (1 or 2 per cell)

Intercalated discs

Adherens-type junctions

Gap junctions

The T tubules of cardiac muscle are inline with the Z bands and not with the A-I band junction

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55
Q

What is meant by turbulent flow?

A

As the mean velocity increases, flow eventually becomes turbulent. The velocity gradient breaks down as layers of fluid try to move over each other faster than physics will allow.

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56
Q

What is myogenic autoregulation in the cerebral blood flow?

A

Cerebral resistance vessels have a well developed myogenic response to changes in transmural pressure

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57
Q

What is pulmonary stenosis? What does it result in?

A

Narrowing of the right ventricular outflow tract, resulting in more right ventricular hypertrophy as it needs to force blood through the pulmonary artery a lot harder

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58
Q

How does the elastic nature of arteries acts to reduce arterial pressure fluctuation between systole and diastole?

A

Arteries have distensible walls, allowing them to stretch in systole. More blood flows in than out, so pressure does not rise so much. The arteries recoil in diastole and flow continues through the arterioles.

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59
Q

What is reactive hyperaemia?

A

Blood flow is cut off to an organ/ limb (ischaemia). The organ/limb continues metabolising and producing vasodilators during the period of no circulation. When the blood is returned, the vessels are massively dilated.

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60
Q

How long is the QRS complex normally?

A

0.12s (3 squares) or less

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61
Q

What is required for a patient with tricuspid atresia to survive?

A

Both an ASD (or PFO) AND a VSD (or PDA)

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62
Q

What is the average maximum cardiac output of a non athlete?

A

20-25 l/min

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63
Q

What is the benefit of a high NO production by the coronary endothelium?

A

Maintains high basal flow

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64
Q

What is the diastolic pressure?

A

The minimum arterial pressure affected by the systolic pressure and total peripheral resistance

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65
Q

What is the approximate volume of blood in the body?

A

5 litres

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66
Q

What is the diastolic pressure?

A

The minimum arterial pressure affected by the systolic pressure and total peripheral resistance

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67
Q

How is hypoplastic left heart syndrome caused?

A

If part of the endocardial tube gets pinched shut in a region that becomes the future ventricle, hypoplastic heart syndrome will occur.

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68
Q

What is the difference between a PFO and an ASD?

A

A PFO is not a true ASD as a flap still exists and is kept closed by the higher pressure of left atrium

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69
Q

What is the effect of exercise on pulmonary outflow?

A

-Increased cardiac output -Small increase in pulmonary arterial pressure -Opens apical capillaries -Transit time (time any red blood cells spends in the capillary) is reduced -Increased oxygen uptake by lungs

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70
Q

How does vasoconstriction occur?

A

Located in the outer tunic adventitia are unmyelinated nerve endings. Sympathetic nerve fibres stimulate vasoconstriction by releasing noradrenaline at the nerve endings and diffuses through fenestration in the external elastic lamina into the external tunica media to depolarise some of the superficial smooth muscle cells. Depolarisation is propagated to all cells of the tunic media via gap junctions.

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71
Q

What is the fibrous pericardium?

A

A tough connective tissue outer layer that defines the boundaries of the middle mediastinum.

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72
Q

What is the most common type of heart defect?

A

Ventricular Septal Defect (VSD)

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73
Q

What is the most distensible type of vessel?

A

Veins

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74
Q

How does angina occur?

A

When O2 supply to the heart does not meet its need. Ischemia of the heart tissue leads to chest pain, usually on exertion and relieved by rest. It is due to narrowing of the coronary arteries (atheromatous disease)

75
Q

What is the most distensible type of vessel?

A

Veins

76
Q

How do class III anti-arrhythmic drugs (Block K+ channels) work? Give an example of one of these drugs.

A

Prolong the action potential, by blocking K+ channels (responsible for repolarisation). The absolute refractory period is lengthened, preventing another AP from occurring too soon. Amiodarone

77
Q

What is the name given to the tonic (constant) contraction of smooth muscle in the vessels?

A

Vasomotor tone

78
Q

What is the normal PR interval?

A

0.12-0.2 seconds (3-5 small squares)

79
Q

What is the optimum ventilation perfusion ratio?

A

V/Q = 0.8

80
Q

How does a pacemaker cell repolarise?

A

Efflux of K+ ions

81
Q

What is the perfusion rate? State the normal range for the perfusion rate.

A

Rate of blood flow. Deliver between 5 and 25 L/min of blood to the body

82
Q

Describe the response of the cardiovascular system to standing up

A

-When you stand blood pools in the superficial veins of the legs due to gravity -Central venous pressure falls and causes cardiac output to fall (less going in) -Arterial and venous pressure are now falling -Baroreceptors detect falling arterial pressure and increase the HR -Total peripheral resistance increased to increase venous pressure

83
Q

What is the pulse pressure?

A

The difference between the systolic and diastolic pressure, commonly 40mmHg N.B. This gives a measure of how hard the heart is pumping

84
Q

How does the distensibility of blood vessels allow for blood flow to be increased?

A

Diameter of the lumen increases, so resistance falls and flow increases.

85
Q

What is the response of the cardiovascular system to a long term increase in blood volume?

A

-Blood volume increases, causes an increased venous pressure -Cardiac output rises and arterial pressure rises -More blood perfuses tissues which increases total peripheral resistance -Arterial pressure rises further and stays up N.B. Blood volume is controlled by the kidneys

86
Q

What is the significance of artereovenous anastomoses in apical (acral) skin?

A

Increase in core temperature leads to decreases sympathetic activity, pushing the hot blood through the low resistance venous shunt to the venous plexus -> reducing heat.

87
Q

What is the systolic pressure?

A

The maximum arterial pressure affected by how hard the heart pumps, the total peripheral resistance and the stretchiness of the arteries (compliance)

88
Q

How can the transposition of the great vessels be treated?

A

Initially a ductus arteriosus and/or an ASD can be maintained or created to allow for enough blood flow to support life. From this a full repair can take place, reconnecting the correct arteries.

89
Q

What is the tetralogy of fallout?

A

A group of 4 lesions placing the outflow portion of the interventricular septum too far in the anterior and cephalad directions

90
Q

How does excitation spread during systole?

A
  1. The SA node fires an action potential, which spreads over the atria causing atrial systole. The AP reaches the AV node, where it is delayed for about 120ms. 2. From the AV node, excitation spreads down the septum between the ventricles 3. Excitation spreads from inner (endocardial) to outer (epicardial) surface
91
Q

What is the total peripheral resistance?

A

The collective resistance of all the arterioles together

92
Q

What is the transposition of great vessels? Is it compatible with life?

A

The right ventricle is connected to the aorta and the left ventricle to the pulmonary trunk. This condition is completely incompatible with life.

93
Q

How does NO (nitric oxide) work as a vasodilator?

A

-Activates guanylate cyclase -Increasing cGMP -Lowering intracellular Ca2+ to cause relaxation of vascular smooth muscle

94
Q

What is tricuspid atresia?

A

The absence of the tricuspid valve

95
Q

How do organic nitrates work to treat angina?

A

Primary function - Venodilation to reduce the preload to the heart

Secondary function - Dilation of coronary arteries perfusing the heart more

They react with thiols (-SH groups) in vascular smooth muscle causing NO2- to be released. NO2- is reduced to NO, which is a powerful vasodilator.

96
Q

What is vasomotor tone mainly produced by?

A

The sympathetic branch of the ANS (α1 adrenoreceptors receptors)

97
Q

What level of blood flow to the brain should be maintained?

A

50-54 millilitres of blood per 100 grams of brain tissue per minute.

98
Q

What name is given to the narrow space created by the two layers of serous pericardium? What is contained in the narrow space?

A

Pericardial cavity - small amount of pericardial fluid

99
Q

What occurs at pacemaker cells when the funny current reaches its threshold value?

A

Ca2+ channels open, giving a relatively slow depolarisation. This is due to the deactivation of the fast Na+ channels.

100
Q

What part of the brain do baroreceptors send signals to?

A

Medulla oblongata

101
Q

How does adenosine act and what does it do?

A

Acts on A1 (adenosine receptors, not a1 adrenoreceptors) inhibiting adenylyl cyclase at the AV node. Increases K+ conductance and hyperpolarises cells of conduction tissue. it is anti-arrhythmic and resets the heart.

102
Q

What range of pressures are found in the left atrium?

A

1-10mmHg

103
Q

What range of pressures are found in the left ventricle in systole and diastole?

A

Systole 1-10mmHg Diastole - 100-140mmHg

104
Q

What range of pressures are found in the right atrium?

A

0-8mmHg

105
Q

What range of pressures are found in the right ventricle in systole and diastole?

A

15-30mmHg 0-8mmHg

106
Q

How do class IV anti-arrhythmic drugs (drugs that block Ca2+ channels) work? Give an example of one of these drugs.

A

Decreases slope of pacemaker action potential at SA node. Also decreases AV nodal conduction and decreases the force of contraction. (also causes some coronary and peripheral vasodilation) Drugs like verapamil

107
Q

What three factors affect the rate of diffusion?

A

-Area available for diffusion -Diffusion resistance - how difficult it is to move through a barrier -Concentration gradient how much is on either side

108
Q

What three factors affect the systolic pressure?

A

-Force of contraction -Total peripheral resistance -Compliance (stretchiness) of arteries

109
Q

What treatment would be given to treat the symptoms of pulmonary oedema? Explain how this works.

A

Diuretics as they lower blood volume

110
Q

How do class II anti-arrhythmic drugs (β-adrenoceptor antagonists) work? Give an example of one of these drugs.

A

Block sympathetic action by acting on β1 receptors in the heart, decreasing the slope of the pacemaker potential in the SAN. Inhibits adenyl cyclase, decreasing inotropy. (used after an MI) Beta blockers (propanolol, atenolol)

111
Q

What two divisions can the mediastinum be organised into?

A

-Superior Mediastinum -Inferior Mediastinum

112
Q

What is pulmonary stenosis? What does it result in?

A

Narrowing of the right ventricular outflow tract, resulting in more right ventricular hypertrophy as it needs to force blood through the pulmonary artery a lot harder

113
Q

What two factors affect the diastolic pressure?

A

-Systolic pressure -Total peripheral resistance

114
Q

How do class I anti-arrhythmic drugs (block voltage gated Na+ channels) work? Give an example of one of these drugs.

A

Na+ channels in the open/inactive state are blocked, but the drug dissociates quickly in time for the next action potential. As Na+ channels are blocked, after-depolarisations cannot trigger another AP. Lidocaine is an example.

115
Q

What two factors affect the mean velocity of flow?

A
  • Radius of the tube - Viscosity of fluid
116
Q

What is required for a patient with tricuspid atresia to survive?

A

Both an ASD (or PFO) AND a VSD (or PDA)

117
Q

What two factors determine the vasomotor tone?

A

-Sympathetic branch of autonomic nervous system increase vasomotor tone (vasoconstriction) -Vasodilator factors (like H+ and adenosine) decrease vasomotor tone (vasodilatation)

118
Q

What two sites in/around the heart are Baroreceptors located?

A

-Aortic arch -Carotid sinuses

119
Q

What type of ion is the cell membrane of myocardial cells mostly permeable to?

A

Potassium ions (K+)

120
Q

Explain what Starling’s law is…simply.

A

More you put in the harder it contracts. Harder it contracts, the higher the stroke volume.

121
Q

What type of noise is the first heart sound? Why is it created?

A

Mixed sound with a crescendo-descendo quality (lup) - produced by oscillations in structures as the AV valves close.

122
Q

How can the inferior mediastinum be organised?

A

-Anterior mediastinum -Middle mediastinum -Posterior mediastinum

123
Q

Describe the response of the cardiovascular system to haemorrhage

A

-Large amount of blood is lost -Reduced venous pressure leads to decreased cardiac output and therefore low arterial pressure -Baroreceptors detects decreased arterial pressure causing HR and resistance to rise leading to further decrease in venous pressure -Need to sort out venous pressure soon

124
Q

What type of noise is the second heart sound? Why is it created?

A

Sound of shorter duration, higher frequency and lower intensity than the first (dup) - produced by oscillations in structures as the Semilunar valves close

125
Q

Define the term stroke volume

A

The difference between end diastolic volume (amount left in after diastole) and systolic volume (amount left after systole)

126
Q

Define the the term venous return.

A

The rate of flow of blood back to the heart.

127
Q

What type of receptor and activity is responsible for vasoconstriction of vessels?

A

Sympathetic activity using α1 adrenoceptors

128
Q

What vasodilators in the cerebral blood flow are used to increase local flow?

A

-K+ -CO2 -Adenosine -O2

129
Q

What will happen to arterial and venous pressure if cardiac output rises?

A

Arterial pressure will rise and venous pressure will fall

130
Q

What will happen to arterial and venous pressure if the total peripheral resistance falls?

A

Arterial pressure will fall and venous pressure will rise

131
Q

Where are M2 muscarinic acetylcholine receptors found in the body and what is their function?

A

Found in the heart where they act parasympathetically to decrease the heart rate

132
Q

Where are M3 muscarinic acetylcholine receptors found in the body and what is their function?

A

Found in the airways and pupil of the eye where they act parasympathetically for contraction

133
Q

Where are α1 adrenoreceptors found in the body and what is their function?

A

Found in sweat glands and the pupil of the eye where they exert a sympathetic effect by localised secretion and dilation respectively.

134
Q

What part of the brain do baroreceptors send signals to?

A

Medulla oblongata

135
Q

Where are β2 adrenoreceptors found in the body and what is their function?

A

Found in the airways way they exert a sympathetic effect by relaxation of the airways

136
Q

Describe the distribution of blood volume over the major parts of the circulation (arteries, capillaries etc.)

A

-11% (0.55 L) in the Arteries and Arterioles -5% (0.25 L) in the Capillaries -17% (0.85 L) in the Heart and Lungs -67% (3.35 L) in the Veins

137
Q

Which three major elastic arteries arise from the Aortic arch?

A

-Brachiocephalic -Left common carotid -Left subclavian artery

138
Q

Which three types of drug may be described as antithrombotic? How do they work?

A

-Antiplatelet limit the migration/aggregation of platelets -Anticoagulants limit the ability of blood to clot -Thrombolytic drugs act to dissolve clots

139
Q

Why can blood vessels be described as having capacitance?

A

As vessels widen with increasing pressure, more blood transiently flows in than out. This allows distensible vessels to ‘store’ blood – They have capacitance.

140
Q

Define the term velocity of flow

A

The rate of movement of fluid particles along the tube N.B. how far, nothing to do with volume

141
Q

Define the term contractility.

A

. Contractility is not the force of contraction of the heart, rather the stroke volume you get for a given venous pressure

142
Q

Why does postural hypotension occur?

A

The baroreceptor reflex doesn’t function correctly meaning the arterial pressure stays low

143
Q

Why is tetralogy of fallot a cyanotic condition?

A

There is an increased pressure on the right side which causes deoxygenated blood to move through the VSD to left side and enter the aorta. The aorta is directly above the VSD (overriding aorta) so gets blood from both ventricles.

144
Q

Define the term central venous pressure.

A

The pressure in the great veins supplying the heart

145
Q

Why is the cardiac action potential so prolonged? (why does it take an age to repolarise)

A

The opening of voltage gated Ca2+ channels (which then leads to more Ca2+ being released from cellular stores causing contraction) and potassium ions flowing out

146
Q

Why is the cutaneous circulation significant?

A

-Balance heat loss/production -Vasoconstriction to increase blood flow in the systemic circulation (shock)

147
Q

Why is there a high vascular tone in skeletal muscle?

A

Permits a high amount of vasodilatation, means you can target it to specific requirements

148
Q

Why is there vasodilatation when there is ischaemia?

A

Muscles start to leak K+ which are a type of vasodilation metabolite. The ischaemia prevents this metabolite being removed by the blood so the metabolites cause vasodilatation

149
Q

Why isn’t the blood flow to the head and upper limb compromised?

A

The vessels usually emerge proximal to the coarctation i.e. brachiocephalic, carotid and subclavian go out before the narrowing

150
Q

Why might a patent ductus arteriosus become an issue?

A

The left to right shunt may be remodelled (pressures on the right go up) to form a right to left shunt which causes cyanosis.

151
Q

Are arterioles high resistance or low resistance vessels?

A

High resistance

152
Q

Why might class III anti-arrhythmic drugs not be used?

A

They can also be pro-arrhythmic… bad times

153
Q

Define the term flow

A

The volume of fluid passing a given point per unit of time

154
Q

Why might the PR interval be short?

A

-Atria have been depolarised close to the AV node -Abnormally fast conduction from atria to ventricles

155
Q

Why might there be chronic hypoxia in the pulmonary circulation?

A

-Emphysema -High altitudes

156
Q

Why might you get an increase in capillary pressure? Why might these lead to pulmonary oedema?

A

-Mitral valve stenosis -Left ventricular pressure Higher pressure in pulmonary circulation, more fluid leaving.

157
Q

Why would negatively inotropic drugs be used?

A

Reduce the workload of the heart (like after an MI) by reducing the O2 requirement of the heart and limiting further damage

158
Q

Why would positively inotropic drugs be used?

A

Used when the heart needs to beat harder like example cardiogenic shock or acute but reversible heart failure.

159
Q

What is the average pressure in the right atrium?

A

0-8mmHg with 4mmHg being the average

160
Q

What valve separates the right atrium and ventricle?

A

Tricuspid

161
Q

What is the average stroke volume of the heart?

A

75-80ml

162
Q

How would you calculate stroke volume?

A

End Diastolic Volume - End Systolic Volume

163
Q

Why don’t different pacemakers in the heart compete to initiate the rhythmn?

A

All other pacemaker fire at a slower rate than the SAN

164
Q

What proportion of ventricular filling occurs in the first 100 ms of diastole?

A

75-80%

165
Q

When do the mitral and tricuspid valves open?

A

Shortly after the beginning of diastole when the pressure in the ventricles falls below that of the atria

166
Q

What will happen if the mitral or tricuspid valve becomes incompetent i.e leaks? What will be heard on ausculation?

A

There will be turbulent backflow of blood giving rise to a systolic mummur on auscultation

167
Q

Which heart sound is affected by inspiration? Why?

A

The second as:

  • Delayed closure of pulmonary valve (increased right atrial pressure)
  • Early closure of aortic valve (decreased left atrial pressure?
168
Q

What would you expect to hear on auscultation of someone with a patent ductus arteriosus?

A

Machinery murmur - continous murmur through both systole and diastole

169
Q

What are the functions of the fibrous skeleton of the heart?

A
  • Prevent AV and semilunar valves from being overly distended
  • Provides attachment for leaflets of the valves
  • Electricle insulator - atria and ventricles contract independently (only AV node as a connection)
170
Q

In what circumstances will the bood become more viscous?

A
  • Increase in cells (polycythaemia - more red blood cells)
  • Increase in plasma proteins (fibrinogen)
  • Increase in immunoglobins (myeloma)
171
Q

Why is arterial pressure higher in the legs when people stand up? (as opposed to siiting down)

A

Addition of hydrostatic pressure - action of gravitational force on the column of hydrostatic fluid

172
Q

What about the structure of veins allows for them to distend?

A

They have a thin wall with a relatively small amount of smooth muscles (compared to arterioles)

173
Q

What is the relationship between central venous pressure and end diastolic volume?

A

As the central venous pressure increases so will the end diastolic volume

174
Q

What is the physiological range for central venous pressure?

A

1-10mmHg

175
Q

What receptor is atrophine an antagonist of?

A

Antagonist of the action of ACh at muscarinic receptors

176
Q

What effect might prolonged hyperkalaemia have on the availability of voltage-gate sodium channels?

A

It is held at a semi-deoplarised state so some sodium channels are inactivated.

177
Q

What effect might prolonged hyperkalaemia have on the pacemaker potential and heart rate?

A

Fewer channels are activated (as we aren’t at as negative a value) causing the potential to be slowed and the heart rate reduced - bradycardia

178
Q

What effect does a local anaesthetic (lidocaine) have on the cardiac action potential?

A

It only binds to the inactive/open channel so the cardiac action potential occurs and then it binds. It will then prevent further action potentials until it dissociates 600ms later.

179
Q

Why can local anaesthetics (lidocaine) be used to treat dysrhythmias/arrhythmias?

A
  • Prevention of premature ventricular action potentials
  • Suppress activity of tissue depolarised due to damage
180
Q

What mechanisms may be responsible for atrial fibrillation?

A

Re-entry loops due to overstretch of the aorta

181
Q

What complication might be associated with atrial fibrillation?

A

Thrombus formation

182
Q

Why would it be a bad idea to give someone suffering from chronic heart failure cardiac glycosides?

A

Make the damaged areas of heart work harder

183
Q

What will happen to the pressure in the left atrium as a patient breathes in and out?

A

The left atrial pressure decreases on inspiration because blood stays in the pumonary circulation

ESA 2 (5 decks)

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