Revision: CVS questions Flashcards by Jack Hasler

fraction of blood flow into right atrium from i/svc

inferior: 80%, superior: 20%

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pressure in r/atrium

0-8mmHg, avg=4mmHg

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avg blood amount pushed from l/ventricle at rest

75-80ml

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ejection fraction

ratio of stroke volume:end diastolic volume

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time difference between the aortic and mitral valves opening/closing

aortic closes -> mitral opens 80 ms later

mitral closes -> aortic opens 40 ms later

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jugular venous pressure

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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inspiration/exhalation on right/left pressures of heart

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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mitral stenosis vs incompetence

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

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equation linking flow, velocity, area

flow = velocity x area

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blood components when flowing

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

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bruit

pronounced Broo-ee

unexpected audbile swishing sound/mumur heard over a vessel

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

less flow at any given driving pressure

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mean filling pressure

pressure in the arteries and veins when the heart stops

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why does the starling curve fall at the top?

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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normal range for CVP

central venous pressure, 1-10mmHg

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contractility

force of contraction for a given fibre length

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

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

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baroreceptors under long term high BP

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

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duration, voltages of pacemaker potential

~1 second

lowest is ~ -60mv

peaks at ~+10mv

Threshold of Calcium VGCPs is ~ -40mV

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

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

hypokalaemia

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

wider QRS indicates

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

long P-R indicates

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

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

ST segment alterations

should be isoelectric

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

Prolonged Q-T interval

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

Q wave is caused by

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

R wave caused by

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

S wave caused by

late ventricular depolarisation along rim of ventricular muscle

finding the HR in an irregular beat

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

normal values for P-R interval

0.12 – 0.2 seconds (3 – 5 small squares)

how many large squares = 1 second

300 large squares -\> 1 minute therefore 5 large squares -\> 1 second

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

chest leads look at the transverse plane limb leads look at the coronal plane

how does a defibrillator work?

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

why do pathological Q waves occur?

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

ECG of someone w/ hyper/okalaemia

tall tented (peaked) t waves/diminished t waves

systolic/diastolic pressure in the pulmonary artery

15-30mmHg/4-12mmHg

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

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

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

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

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

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

what causes the pattern of pain in an MI

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

mechanism for unstable/crescendo angina

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

pericarditis sign

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

how does smoking and alcohol cause 'heartburn'?

smoking relaxes oesophago-gastric sphincter alcohol causes gastritis and heartburn

why might women of reproductive age be tired?

heavy periods -\> iron deficiency -\> anaemia

equation linking mean arterial BP, CO and TPR

mean arterial BP=COxTPR

COPD

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

ventricular fibrillation

abnormal rapid ventricular activity with loss of co-ordinated contraction