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ESA Revision > CVS > Flashcards

CVS Flashcards

1
Q

Modifiable risk factors for atherosclerosis

A

Smoking, diabetes, hyperlipidaemia, hypertension.

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2
Q

Non-modifiable risk factors for atherosclerosis

A

Old age, family history, gender-male

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3
Q

Define atherosclerosis

A

Thickening and hardening of arterial walls as consequence of atheroma formation

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4
Q

Define atheroma

A

Accumulation of intracellular and extracellular lipid in intima and media of large and medium sized arteries

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5
Q

Define arteriosclerosis

A

Thickening of walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus

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6
Q

What is the most common cause of atrial fibrillation?

A

Re-entry loops

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7
Q

Why might atrial fibrillation lead to a stroke?

A

Uncoorodinated contraction of atrial muscle cells, resulting in the stagnation of blood in the atrium, can result in thrombus formation. This may dislodge into the systemic circulation, blocking a cerebral artery supplying the brain, causing an ischameic stroke.

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8
Q

Describe Virchow’s triad for thrombus formation

A

3 causes of thrombus formation: changes in blood vessel wall-, changes in blood flow- turbulence e.g. valve problems or stasis and changes in blood constituents- smoking, OCP.

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9
Q

Inferior MI: What leads would show abnormal complexes and which CA is most often responsible?

A

II, III and aVF, RCA

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10
Q

What area of heart does RCA supply?

A

Posterior and inferior

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11
Q

What area of heart does LCA suppy?

A

Lateral

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12
Q

Anteroseptal MI:What leads would show abnormal complexes and which CA is most often responsible?

A

V1-V2, LAD/ Anterior interventricular

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13
Q

Anteroapical MI: What leads would show abnormal complexes and which CA is most often responsible?

A

V3-V4, LAD(distal)

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14
Q

Anterolateral MI:What leads would show abnormal complexes and which CA is most often responsible?

A

V5-V6, I, aVL, Circumflex

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15
Q

Extensive anterior: What leads would show abnormal complexes and which CA is most often responsible?

A

V1-V6, I, aVL, Proximal LCA

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16
Q

Posterior: What leads would show abnormal complexes and which CA is most often responsible?

A

V1-V2 (tall R wave, not Q), RCA

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17
Q

V1-V6 electrode placement

A

V1- 4th IC space, R sternal border, V2- 4th IC space, L sternal border, V3- halfway between V2 and V4, V4- left 5th IC space, mid-clavicular line, V5- halfway between V4 and V6, anterior axillary line, V6- mid-axillary line.

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18
Q

Anterior interventricular/LAD supplies which heart areas?

A

R and LV, anterior 2/3 of IVS

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19
Q

SA nodal branch

A

SAN and pulmonary trunk if from RCA(60% of people), LA and SAN if from LCA

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20
Q

Circumflex

A

LA and LV

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21
Q

Left marginal

A

LV

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22
Q

Posterior interventricular

A

R and LV, posterior 1/3 of IVS

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23
Q

Right marginal

A

RV and apex

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24
Q

Formula for arterial blood pressure

A

CO x TPR

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25
Q

Pressure in RA

A

0-8mmHg

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26
Q

Pressures in RV

A

15-30mmHg/0-8mmHg

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27
Q

Pressures in pulmonary artery

A

15-30mmHg/4-12mmHg

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28
Q

Pressure in LA

A

1-10mmHg

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29
Q

Pressures in LV

A

100-140mmHg/1-10mmHg

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30
Q

Pressures in aorta

A

100-140mmHg/60-90mmHg

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31
Q

At what membrane potential does a ventricular myocyte AP begin and why?

A

-85mV as in diastole, membrane potential close to Ek as K+-selective channels open so membrane mostly permeable to K+ ions.

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32
Q

What is responsible for the long plateau phase in a ventricular myocyte AP?

A

The opening of L-type Ca2+ channels which have a slower activation and remain open for much longer compared to Na+ channels.

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33
Q

What does a long plateau phase in cardiac AP allow ventricular myocytes to do?

A

They have adequate time for contraction before onset of next AP and so can all contract simultaneously as cells still contracting when AP received in last cell.

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34
Q

Descrive calcium-induced-calcium-release during AP in a ventricular myocyte

A

Ca2+ influx from calcium voltage-gated channels activates release of calcium form intracellular stores e.g. SR, via ryanodine receptor- a non-classical ligand-gated ion channel, and this calcium is then responsible for cell contraction.

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35
Q

What would an ECG trace show within mins-hrs after a STEMI?

A

ST elevation, T wave upright

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36
Q

What would an ECG trace show within hrs-days 1/2 after a STEMI?

A

ST elevation, Twave decreases in height, R wave decreases in height, Q wave begins.

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37
Q

What would an ECG trace show within days 1/2 after a STEMI?

A

Q wave becomes deeper

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38
Q

What would an ECG trace show within days later after a STEMI?

A

ST normalises, T wave inverted, Q wave persists

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39
Q

What would an ECG trace show weeks after a STEMI?

A

ST and T normal, Q wave persists

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40
Q

Name 2 promoters of vasoconstriction

A

5-hydroxytryptamine and thromboxane A2

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41
Q

What do the letters MONA stand for in MI treatment?

A

Morphine, oxygen, nitrates and aspirin.

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42
Q

Describe the process of vascular smooth muscle cell contraction via alpha 1 adrenoceptors.

A

NA/adrenaline activate Gq, which is responsible for phospholipase C activation- cleaves PIP2 to IP3 and DAG. IP3 binds to ligand-gated ion channel on SR, causing Ca2+ efflux into cytoplasm, and this Ca2+ binds to calmodulin, activation MLCK. DAG activates protein kinase C which activates a protein which inhibits myosin phosphatase and so contraction promoted, causing vasoconstriction.

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43
Q

Describe how beta 2 adrenoceptors are responsible for vascular smooth muscle relaxation.

A

Gs- activate adenylyl cyclase- ATP converted to cAMP- inhibits MLCK so no phosphorylation of light chains in myosin so can’t form crossbridges with actin, so smooth muscle cell relaxation.

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44
Q

In a patient with suspected intermittent claudication, how could you determine how good their blood supply was?

A

Palpate pulses on both sides

45
Q

How might endothelial injury come about, initiating atherosclerosis?

A

Cigarette smoke, increased LDL, hypertension or haemodynamic stress e.g. shear stress where arteries bifurcate or branch.

46
Q

Describe the key stages in atheroma formation

A
  • Endothelial injury promotes monocyte and platelet adhesion-PDGF released-SMC proliferation and migration.
  • SMC take up LDLs-form foam cells-fatty streak.
  • SMCs also secrete collagen, elastin and proteoglycans, and continued collagen deposition allows simple plaque to form-becomes fibrotic- elasticity loss in arterial wall.
  • Macrophages and endothelial +SMCs produce oxidants-oxidise LDLs, and these are chemotactic for circulating monocytes-infiltrate intima-become macrophages-form foam cells.
  • Foam cells produce cytokines-further SMC migration into intima from media, proliferation + secretion of abnormal collagen amounts + other CT proteins, + recruitment of other inflammatory cells.
47
Q

What are venae comitantes?

A

Deep paired veins accompanying major arteries. Pulsations of artery aid venous return.

48
Q

What are vasa vasorum?

A

tiny arteries and veins which supply blood to the walls of large blood vessels, providing nutrients and removing waste products from the outer portion of arterial walls.

49
Q

RFs for a patent ductus arteriosus, and define the condition.

A
  • birth at high altitude
    -prematurity
    -maternal rubella infection in 1st trimester
    The ductus connecting the pulmonary artery and aorta, providing an essential foetal circulatory shunt, fails to close after birth.
50
Q

What a patent DA sound like on auscultation?

A

Constant machine-like murmur throughout systole and diastole.

51
Q

What happens the to heart with a patent DA, after birth?

A

Blood flows from the aorta into the pulmonary circulation as lower pulmonary vascular resistance, so pulmonary circulation, LA and LV become vol. overloaded, can lead to LV dilatation and L sided HF, where RH remains normal unless pulmonary vascular disease ensues, leading to Eisenmenger syndrome: deoxygenated blood enters systemic circulation with shunt reversal, so flow of desaturated blood to lower extremities, with peripheral cyanosis, but upper extremities not cyanotic as receive normally saturated blood from proximal aorta.

52
Q

What can be given to try and constrict the ductus?

A

Prostaglandin synthesis inhibitors.

53
Q

Define Ischaemic Heart Disease

A

Heart perfusion is inadequate to meet myocardial O2 demand

54
Q

What valve problem is associated with mitral facies and what type of heart murmur does this problem produce?

A

Mitral stenosis

Diastolic

55
Q

where do the R and L coronary arteries arise from?

A

the R and L aortic sinuses

56
Q

how do statins acts to reduce cholesterol?

A

inhibit endogenous cholesterol production via HMG COA reductase, AND upregulate LDL receptors so increase removal of LDLs from blood

57
Q

when can blood flow be heard?

A

when blood flow is turbulent

58
Q

key features of cardiac tamponade?

A

hypotension
raised JVP
distant, muffled heart sounds as they are masked by the excess fluid in the pericardial cavity
tachycardia- compensatory response for low CO as reduced diastolic filling

59
Q

mechanism behind cardiac tamponade?

A

fluid moves from pericardial capillaries into pericardial cavity. Fibrous pericardium restricts increase in volume of percardial cavity to reduce pressure, the heart is compressed and the pressure increases, limiting diastolic filling, pressure backs up into systemic circulation, CO is reduced, causing hypotension, leading to obstructive shock

60
Q

presentation of pericarditis?

A

sharp and pleuritic chest pain, releived by sitting forward
pericardial rub- rustling sound heard as fibrosed serous pericardium as inflamed
ECG shows ST elevation in all leads

61
Q

clinical importance of coronary arteries filling in diastole in angina?

A

angina is a central chest pain caused by inadequate perfusion of the myocardium. Occurs with exercise or exertion as during this period, diastole is shortened, and it is during diastole that the coronary arteries fill, and so coronary artery filling is reduced, and these arteries supply the myocardium, so the blood supply to the myocardium is reduced, causing myocardial ischaemia- this is the result of narrowing of coronary arteries by atheromatous plaques which restrict blood flow, and hence in exercise, blood flow is even more restricted because of reduced CA filling, hence causing ischamia as coronary arteries are end arteries- supply sole source of blood to particular area of heart and if occluded, have insufficient anastomoses to provide sufficient blood to that area of the heart.

62
Q

how can coarctation of the aorta be detected?

A

weak femoral pulses and radio-femoral delay

63
Q

where is a needle inserted for a pericardiocentesis in cardiac tamponade?

A

in pericardial space, just below xiphisternum to avoid damaging coronary vessels

64
Q

after hypovolaemia, how could you increase preload of heart?

A

blood transfusion

65
Q

drug used in anaphylaxis?

A

adrenaline- alpha 1 agonist so vasoconstriction to try and overcome hypotension

66
Q

ECG chnage indicating poor myocardial perfusion?

A

ST depression

67
Q

what is the foramen ovale?

A

opening between septum secundum and endocardial cushions in fetus, so passage between atrial cavities

68
Q

principle behind a defibrillator?

A

used in VF, electric current administered, all cells depolarised, put into refractory period so stops all electrical activity, aloowing coordinated electrical activity to restart

69
Q

how do local anaesthetics prevent VF?

A

prevent premature beats by blocking Na+ voltage-gated channels in open or inactivated state in depolarised myocardial ischaemic tissue

70
Q

what is the preload?

A

filling pressure of the heart

71
Q

what is SV influenced by?

A

preload, cardiac muscle force, and afterload- pressure heart has to pump against

72
Q

what does the EDV depend on?

A

the EDP and compliance of the ventricular wall

73
Q

Describe Starling’s law*

A

if EDP, hence EDV is increased, the force of the following contraction, and thus SV, increases, as muscle fibres are stretched more. Law states that the energy released during contraction depends on the initial fibre length

74
Q

why might you use a thiazide diuretic in hypertension?

A

inhibits the Na+-Cl- co-transporter in the DCT of the kidney, so increases Na+ and water excretion, hence reduces ECF and so circulating plasma volume, so decreases the CVP and preload on the heart, and therefore the SV and so the CO, thereby decreasing your arterial BP

75
Q

what will happen to the blood vessels of someone with hypertension for a long time?

A

weakening of the vessels, and atheroma formation

76
Q

where in the body could you directly visualise hypertension?

A

retina

77
Q

what structure enters the RA close to the SAN?

A

the SVC

78
Q

why can beta blockers be used in arrythmias?

A

reduce slope of pacemaker AP, so increase time between the APs hence slow the heart rate

79
Q

what does Starling’s law relate stoke volume to?

A

CVP

80
Q

why does a plateau occur on the frank-starling curve?

A

any further increase in CVP will NOT increase SV as the myocardial muscle fibres reach a critical length beyond which they are unable to contract efficiently

81
Q

how would the LV respond if more blood enters from pulm circulaton?

A

increased force of contraction as increased end-diastolic muscle fibre length

82
Q

why do R and L heart sides pump out same amount of blood per min?

A

Frank-Starling mechanism

83
Q

what is the risk to the heart of a severe or sudden hyperkalaemia?

A

the heart may stop in diastole as lack of voltage-gated Na+ channels to initiate the ventricular AP

84
Q

what heart problems is a patient with hypokalaemia at risk of?

A

increased slope of pacemaker AP as more If channels are available, and increased rate of spread of depolarisation between myocytes as more Na+ voltage-gated channels are available, hence risk of arrhythmias and ectopic beats as excitabilty of myocardium is increased

85
Q

how is Ca2+ that is moved into cardiac myocytes, moved into the SER for release by calcium induced calcium release?

A

SERCA

86
Q

adrenaline key action if given to a patient whose heart has stopped?

A

action at Beta 1 receptors to increase Ca2+ in IC stores

87
Q

main mechanism of action of nitrates for angina?

A

venodilation to reduce workload of the heart and hence myocardial O2 demand

88
Q

innervation of the pericardium?

A

fibrous and parietal layer of serous= phrenic nerve

viscerla layer of serous= autonomic= PNS from vagus and SNS from cervical ganglia and upper thoracic ganglia

89
Q

how can the sensitivity of the baroreceptor reflex be reduced?

A

ageing
hypertension
atherosclerosis, as all reduce the arterial wall compliance

90
Q

when an AP spreads from 1 myocyte to the next, why does retrograde conduction not normally occur?

A

original cell is refractory- sodium ion channels will be in an inactivated state

91
Q

what does being in sinus rhythm mean?

A

SAN located at junction of SVC and RA is initiating the heartbeat through AP generation

92
Q

in what pathological conditions might sinus tachycardia occur?

A

thryotoxicosis
heart failure
phaeochromocytoma
occurs when sympathetic tone elevated and so SAN firing is accelerated

93
Q

characteristic of ECG in 1st degree heart block?

A

wider than normal PR interval due to longer than normal delay at AV node, conduction slowed but all APs are conducted

94
Q

describe ECG appearance for Mobitz II heart block?

A

not all impulses conducted by AV node, so e.g. ventricular contraction only occurs for ever second atrial contraction, therefore only every 2nd P wave is followed by a QRS complex

95
Q

describe ECG appearance for Wenckebach phenomeonon- type of 2nd degree heart block?

A

PR interval progressively lengthens until AP not conducted by AV node from atria to ventricles so no QRS complex follows P wave, pattern then repeats itself

96
Q

what might cause 3rd degree heart block?

A

ischaemic damage to nodal tissue or bundle of His meaning that APs cannot be conducted from atria to ventricles

97
Q

what does a wide QRS complex indicate on an ECG?

A

slowed ventricular depolarisaton e.g. due to bundle branch block

98
Q

where is the PR interval on an ECG measured from?

A

start of P wave to start of QRS complex

99
Q

where is ECG ST segment measured from?

A

end of S wave to start of T wave

100
Q

where is ECG QT interval measured from?

A

start of Q wave to end of T wave

101
Q

normal length of PR interval?

A

0.12-0.2 s (3-5 small squares- each 0.04s)

102
Q

when might PR interval be lengthened?

A

1st degree heart block- delayed conduction by AV node

103
Q

what do large QRS complexes suggest?

A

ventricular hypertrophy e.g. due to hypertension or pulmonary vascular disease

104
Q

list 3 causes of AF?

A

IHD
thyrotoxicosis
hypertension

105
Q

2 causes of ST elevation?

A

acute MI

acute pericarditis- elevation in all leads

106
Q

effect of high calcium on QT interval?

A

shortened

107
Q

what does a relatively narrow QRS complex suggest?

A

ventricular rhythm originating from the conducting pathway

108
Q

how does aspirin function as an antiplatelet drug?

A

it acetylates cyclooxygenase, inhibiting the production of thromboxane A2 and so inhibits platelet aggregation

109
Q

how does clopidogrel inhibit platelet aggregation?

A

ADP receptor antagonist

may cause less gastric irritation than aspirin

ESA Revision (15 decks)

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