Week 6 Flashcards

1
Q

Elastic arteries EAs

A

ABP reflects the driving pressure for blood flow
ABP determined in the elastic arteries
Rhythmic ejection of blood from ventricle leads to pulsatile pressure in aorta and large arteries
Functions of EAs:
- dampen the pulsatile pressure to ensure continuous flow into the circulation (‘dampening function’ Windkessel effect)
-ensures blood pressure is maintained during diastole (act as tubes to ensure flow to periphery ‘conduit function’)

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2
Q

Pulse pressure in the aorta

A

Systolic pressure peak -120mmHg
Diastolic pressure 80mmHg
Pulse pressure= SP-DP
Mean ABP= SP-DP/3 +DP

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3
Q

Windkessel effect

A

During systole elastic wall of aorta distends (energy converted to elastic energy)
Aortic wall recoils during diastole to propel blood forward (energy released)
Driving pressure sustained during diastole-> continuous blood flow
As blood is passed into aorta only 20-50% goes straight into peripheral circulation
Pressure wave progressively damped in smaller arteries
The mean pressure constantly dropping throughout peripheral circulation due to the resistance offered by different types of vessels
Blood renters heart at minimal pressure- central venous pressure- most of original energy lost due to friction and dissipated as heat

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4
Q

Effects of ageing on pulse pressure

A

Compliance= change in vol/ change in pressure
With age the elastic components of the aorta and its branches degenerate, collagen becomes more prominent and arteries stiffen
Ejection of same or even reduced SV leads to increased systolic pressure due to reduced elasticity
Reduced elastic recoil leads to lower diastolic pressure
So pulse pressure increases with age
Arteriosclerosis- loss of compliance and stiffening of arteries with age

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5
Q

Haemodynamics

A

Flow proportional to change in pressure
Flow inversely proportional to resistance
Change pressure= arterial pressure-venous pressure
Resistance to blood flow in single vessel determined by:
-vessel length
-blood viscosity can change due to proteins and RBCs and drop in temp can increase viscosity
-radius, main determinant
R a n xL/ pi x r^4. L= length n=viscosity r=radius
So small changes in radius can have very large effect on R

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6
Q

Poiseuille’s equation

A

Flow= change P x pi r^4/ n xL

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7
Q

Peripheral arterial occlusive disease PAOD

A

Atherosclerotic plaques in large and medium sized arteries (particularly lower limb)
Decrease radius increase resistance to flow
Ischaemia distal to stenosis
Particularly problematic and painful during exercise
Tissue hypoxia-> pain (intermittent Claudication)
Imbalance between oxygen supply and demand in increased metabolic demand eg in exercise it wont be met so get tissue hypoxia

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8
Q

Blood flow through vasculature

A

Poiseuilles equation only precisely applies if there’s laminar flow
Laminar flow: normal pattern of flow, highly efficient
-concentric layers blood, immobile layer at endothelium, flow is fastest in centre
Turbulent flow: occurs where flow velocity is high, inefficient , cannot apply Poiseuille’s law
-eg at large artery branches, pregnancy, exercise, anaemia, valve defects/arterial stenosis
-vibrations heard as sounds- murmurs, korotkoff sounds

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9
Q

Taking blood pressure korotkoff sounds

A

Cuff> 120mmHg stops flow brachial artery occluded:
-no sounds
Cuff 120-80mmHg pulsatile, turbulent flow:
-korotkoff sounds indicate level of systolic BP
Cuff <80mmHg laminar flow:
-no sounds diastolic pressure, artery filling, open

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10
Q

ABP

A

Level of arterial blood pressure is determined in elastic arteries and is the driving force for flow
Determined by:
-blood volume in the arterial system CO
-resistance to blood flow TPR
ABP= cardiac output x total peripheral resistance
ABP= CO x TPR

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11
Q

What determines SP

A

1.Stroke volume (anything that increases SV such as changes in cardiac filling and contractility will increase SP)
2. Aortic/arterial distensibility
3. Ejection velocity
4. DP of previous beat
Therefore increases in the following increase SP:
-EDV (preload)
-contractility
-decreased aortic compliance
-increased venous return
-exercise, circulating Catecholamines
-ageing

So SP gives information about cardiac output

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12
Q

What determines DP

A

Arteriolar resistance
Therefore the following increase DP:
-vasoconstriction
-arteriosclerosis
-atherosclerosis
HR: a very high heart rate increases DP because cardiac cycle is shorter so not enough time for the diastolic pressure to fall back down to normal level so DP increases

DP gives information about total peripheral resistance

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13
Q

Different components of ECG

A

An ECG provides a visual representation of the spread of electrical events through the heart. This electrical activity is detected on the surface of the body using recording electrodes. ‘Leads’ consisting of a pair of electrodes (one positive and one negative) are used to record the electrical activity
The shape of an ECG is dependent on which leads are used, and any abnormal conduction of electrical current. The convention is to use an idealised ECG shape to understand differences between the types of ECGs recorded, as well as differences within a person in different circumstances

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14
Q

Waves of ECG

A

P wave- atrial depolarisation
QRS complex- ventricular depolarisation
T wave- ventricular repolarisation
Approximate durations for heart rate 60bpm
P wave- 0.10s
PR interval- 0.12-0.20s
QRS complex- 0.08s
T wave- 0.16s
QT interval- 0.40s

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15
Q

ECG leads

A

A pair of electrodes forms what is known as an ECG lead. Theres 12 standard ECG leads
-3 standard limb leads, I, II, III
-3 augmented limb leads, aVR, aVL, aVF
-6 unipolar chest leads V1 to V6

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16
Q

Einthovens triangle

A

Lead I: Right arm to left arm
Lead II: right arm to left leg
Lead III: left arm left leg

17
Q

ECG records the summed electrical activity of heart described as electrical vector

A

Each lead has a positive pole and a negative pole and the difference in electrical potential between these poles is graphed over time
As a wave of electrical depolarisation moves through the heart if it moves towards positive pole of the lead positive deflection occurs , if it moves towards negative pole then negative deflection occurs
Isoelectric line is the resting line
The magnitude of these deflections is greatest when the vector is moving directly toward electrode
A vector that moves at right angle to axis of a lead produces little deflection on trace
Limb leads view the heart in the coronal plane where the chest leads view heart in transverse plane

18
Q

What does R-R interval on ECG represent

A

Time between 2 ventricular depolarisations, length of one cardiac cycle
HR= 60/R-R

19
Q

P-R interval represent

A

Time between atrial depolarisation and ventricular depolarisation, conduction of impulses of AV node
Change in P-R interval means slower or faster, conduction between atria and ventricles. Prolonged P-R interval- AV block which indicates delayed conduction through the AV node
This can occur in isolation or co-exist with other blocks (eg second degree AV block)

20
Q

Why is T wave positive if ventricular repolarisation

A

Endocardial cells depolarise first, wave of depolarisation from endocardial cells to epicardial cells. Overall direction between is base to apex same direction as lead II from negative to positive - depolarisation so seen as positive deflection
Action potentials in endocardial cells long, epicardial AP depolarise later and repolarise sooner, repolarisation in opposite direction from apex to base so still seen as positive deflection

21
Q

Absent P waves

A

The reason we get P wave because in short space of time all atrial cells depolarise as electrically coupled
If we start to lose electrical integrity across atria all cells start to depolarise at different times not then one deflection as a P wave dont get measurable P wave - atrial fibrillation

22
Q

QT interval

A

Measure of ventricular repolarisation time, really long action potentials, potential defect in potassium channels, high risk ventricular arrythmias