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Cardiovascular System (ESA 2) > Revision: CVS questions > Flashcards

Revision: CVS questions Flashcards

1
Q

fraction of blood flow into right atrium from i/svc

A

inferior: 80%, superior: 20%

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2
Q

pressure in r/atrium

A

0-8mmHg, avg=4mmHg

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3
Q

avg blood amount pushed from l/ventricle at rest

A

75-80ml

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4
Q

ejection fraction

A

ratio of stroke volume:end diastolic volume

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5
Q

time difference between the aortic and mitral valves opening/closing

A

aortic closes -> mitral opens 80 ms later

mitral closes -> aortic opens 40 ms later

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6
Q

jugular venous pressure

A

a -> atrial contraction

c -> transmission of increasing ventricular pressure, closing of tricuspid valve, possible also from transmission of neighboring carotid arteries

v -> venous return to right atrium when tricuspid valve is shut

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7
Q

inspiration/exhalation on right/left pressures of heart

A

inspiration: blood is drawn into the thorax, inc. r/ventricular pressure, closure of pulmonary valve is delayed
- l/ventricular SV falls, aortic valve closes early

opposite in expiration

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8
Q

mitral stenosis vs incompetence

A

sten. : fails to OPEN properly
incompetence: fails to CLOSE properly

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9
Q

equation linking flow, velocity, area

A

flow = velocity x area

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10
Q

blood components when flowing

A

cells tend to move out to the faster stream of blood flow in the centre

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11
Q

bruit

A

pronounced Broo-ee

unexpected audbile swishing sound/mumur heard over a vessel

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12
Q

what happens to the relationship between flow and driving pressure/pressure change if SMCs in tunica media contract

A

less flow at any given driving pressure

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13
Q

mean filling pressure

A

pressure in the arteries and veins when the heart stops

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14
Q

why does the starling curve fall at the top?

A

muscle fibres reach a critical length, beyond which they are unable to contract efficiently, largely due to passive stiffness of cardiac muscle fibres

NB. the length-tension curve is much steeper when rising and falling compared to skel. muscle due to an increase in Ca2+ sensitivity with increased sarcomere length and the passive stiffness of cardiac muscle fibres respectively

in the diagram, the active tension blue line is on the one we are interested in

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15
Q

normal range for CVP

A

central venous pressure, 1-10mmHg

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16
Q

contractility

A

force of contraction for a given fibre length

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17
Q

when might a sudden dangerous increase in PaSyNS activity occur, and why is it bad?

A

cold water, ice etc causes the heart rate to drop -> collapse, often a factor that leads to drowning

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18
Q

baroreceptors under long term high BP

A

they ‘reset’ so that they accept the high BP as the norm

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19
Q

duration, voltages of pacemaker potential

A

~1 second

lowest is ~ -60mv

peaks at ~+10mv

Threshold of Calcium VGCPs is ~ -40mV

20
Q

result of prolonged hyperkalaemia on steady state availability of Sodium VGCPs, also sudden severe hyperkalaemia

A

these are open only briefly during depolarisation and then shut again from inactivation, which they recover from at -ve membrane potentials

fewer VGCPs are open if the membrane is held depolarised by high EC potassium levels

also, the ion channels that make the funny current are activated at lower voltages (which is why they are ‘funny’) so fewer are available if pacemaker potential starts at a less -ve potential

severe: above 7mM -> medical emergency -> heart may stop due to lack of open sodium channels

21
Q

hypokalaemia

A

membrane potential -> likely to be more -ve -> inc. open sodium channels -> more pacemaker potentials etc (opposite of hyperkalaemia)

-also inc. excitability of myocardium -> ectopic beats and other arrhythmias

more complex than we need to know in CVS

22
Q

wider QRS indicates

A

associated with ventricular depolarisations that are not initiated by the normal conductance mechanism

23
Q

long P-R indicates

A

P-R is from start of P wave to start of Q

slow conduction from the atria to the ventricle (first degree heart block)

24
Q

ST segment alterations

A

should be isoelectric

raised -> STEMI, depressed -> NSTEMI, also can be a sign of ischaemia

25
Q

Prolonged Q-T interval

A

start of Q -> end of T

prolonged repolarisation of the ventricles, which can lead to arrhythmias as occurs in long QT syndrome.

may indicate a congenital long QT, rare, or more likely due to a pharmacological agent eg potassium channel blockers -> inc. length of AP

26
Q

Q wave is caused by

A

depolarisation of i/v septum from l/ to r/ - ie spread of excitation AWAY from electrode

27
Q

R wave caused by

A

spread of excitation down right and left bundles and through ventricular muscle mass

28
Q

S wave caused by

A

late ventricular depolarisation along rim of ventricular muscle

29
Q

finding the HR in an irregular beat

A

count for 30 large squares/6 seconds, multiply by 10

30
Q

normal values for P-R interval

A

0.12 – 0.2 seconds (3 – 5 small squares)

31
Q

how many large squares = 1 second

A

300 large squares -> 1 minute

therefore 5 large squares -> 1 second

32
Q

how do the views of chest leads compare to limb leads?

A

chest leads look at the transverse plane

limb leads look at the coronal plane

33
Q

how does a defibrillator work?

A

discharges a high voltage field which depolarise the whole heart allowing an organised rhythm to emerge, used in ventricular fibrillation

34
Q

why do pathological Q waves occur?

A

there is a dead region of myocardium of full thickness which acts like an ‘electrical window’ allowing a view through to the opposite side of the heart

35
Q

ECG of someone w/ hyper/okalaemia

A

tall tented (peaked) t waves/diminished t waves

36
Q

systolic/diastolic pressure in the pulmonary artery

A

15-30mmHg/4-12mmHg

37
Q

how to deal with someone who faints due to temporary reduction in cerebral blood flow

A

lie them down to reduce effects of gravity on circulation and maintain cerebral blood flow

38
Q

1 RCA, 2 SA nodal, 3 right marginal, 4 posterior interventricular, 5 AV nodal coronary arteries supply

A

1 RA, SAN and AVN, posterior part of IVS

2 pulmonary trunk, SAN

3 r/ventricle and apex of heart

4 r/ and l/ ventricles and posterior third of IVS

5 AVN

39
Q

1 LCA, 2 SA nodal, 3 anterior interventricular, 4 circumflex, 5 left merginal, 6 post. interventricular coronary arteries supply

A

1 most of left atrium and ventricle, IVS, AV bundles, can supply AVN

2 LA and SAN

3 r/ and l/ ventricles and ant. 2 1/3s of IVS

4 LA and L/ventricle

5 l/ventricle

6 r/ and l/ ventricles and post. third of IVS

40
Q

what causes the pattern of pain in an MI

A

most often to left arm, also to lower jaw, neck, right arm, back, and epigastrium

ischaemia -> triggers pain endings that enter in T1-4/5 and account for the chest pain

  • T1 accounts for pain in arm, also medial cutaneous nerve of arm often has branches from 2nd and 3rd intercostal nerves
41
Q

mechanism for unstable/crescendo angina

A

thrombosis on top of an atheromatous plaque, does not complete occlude artery so ischaemia occurs but not infarction

42
Q

pericarditis sign

A

pericardial friction rub from auscultation, sqeaky leather, sounds like grating/scratching/rasping, three components (1 systolic, 2 diastolic)

43
Q

how does smoking and alcohol cause ‘heartburn’?

A

smoking relaxes oesophago-gastric sphincter

alcohol causes gastritis and heartburn

44
Q

why might women of reproductive age be tired?

A

heavy periods -> iron deficiency -> anaemia

45
Q

equation linking mean arterial BP, CO and TPR

A

mean arterial BP=COxTPR

46
Q

COPD

A

name for a collection of lung diseases including chronic bronchitis, emphysema and chronic obstructive airways disease

People with COPD have difficulties breathing, primarily due to the narrowing of their airways, this is called airflow obstruction. Typical symptoms of COPD include: increasing breathlessness when active, a persistent cough with phlegm, frequent chest infections

Over many years, the inflammation leads to permanent changes in the lung. The walls of the airways thicken and more mucus is produced. Damage to the delicate walls of the air sacs in the lungs causes emphysema and the lungs lose their normal elasticity. The smaller airways also become scarred and narrowed. These changes cause the symptoms of breathlessness, cough and phlegm associated with COPD. Some cases of COPD are caused by fumes, dust, air pollution and genetic disorders, but these are rare

47
Q

ventricular fibrillation

A

abnormal rapid ventricular activity with loss of co-ordinated contraction

Cardiovascular System (ESA 2) (14 decks)

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