Cardiac system Flashcards

1
Q

K+ ionic movement

A

higher intracellular concentration
= moves out of the cell
= hyperpolarisation
= intracellular becomes more negative

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2
Q

Na+/Ca2 ionic movment

A

higher extracellular concentration
= moves into cell
= depolarisation
= intracellular becomes less negative

open Na+ channels = rapis deploarisation
open Ca2+ channels = sustained depolarisation

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3
Q

stroke volume =

A

the volume of blood ejected from the heart during each cycle

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4
Q

cardiac output =

A

the total volume of blood pumped by the ventricle per min

stroke volume x heart rate

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5
Q

cardiac muscle =

A

shorter, many branches

intercalated discs between cells allow depolarisation to rapidly spread throughout the myocardium

continuous rhythmic contraction

only one type of fibre, similar to I type

involuntary contraction triggered by a pacemaker, modulated by the nervous system

mostly aerobic, but will use anaerobic during ischaemia

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6
Q

moderate/submaximal exrecise -

A

uses approx. 80% of the energy supplied by free fatty acids (primary substrate)

aerobic

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7
Q

heavy exercise -

A

oxidising lactate can give a high percentage of ATP

anaerobic

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8
Q

trained athlete exercise -

A

will use aerobic free fatty acid metabolism to generate most ATP

aerobic

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9
Q

exercise following a meal -

A

glucose plays a larger role in ATP supply

anaerobic

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10
Q

ischaemia during exercise-

A

(inadequate blood supply to the heart)

largely anaerobic glycolysis

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11
Q

the spread of electrical activity in the heart:

A

1) sin-atrial node - generates action potential which spread across atria (atria contracts downwords)
2) non-conductive septum - stops the electrical impulse to ensure atria have finished contracting

delay

3) bundle of his - made of conductive purkyne fibres (penetrates non-conductive septum to pass on impulse)
4) atrioventricular node - ventricles contract upwards

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12
Q

p wave =

A

atrial depolarisation

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13
Q

QRS complex =

A

atrial repolarisaton and vetricular depolarisaton

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14
Q

T wave =

A

ventricle repolarisation

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15
Q

at rest…

A

parasympathetic activity + vagal stimulation

60-70 bpm

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16
Q

during exercise…

A

sympathetic activity - noradrenaline increase

= increased stroke volume, increased cardiac output and increased heart rate

140-180 bpm

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17
Q

vascular system:

A

heart -> artery -> arteriole -> capillary -> venule -> vein -> heart

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18
Q

the site of greatest regulation of BP =

A

arterioles - absorb the greatest pressure drop

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19
Q

resistance of the system =

A

viscosity of blood X length of vessel / radius (raised to the 4th power)

20
Q

blood flow =

A

change in pressure / resistance

21
Q

small inward diameter change =

A

increased resistance + increased pressure for a given flow

22
Q

vasomotor tone:

A

vascular smooth muscle does not fire action potentials

have significantly depolarised resting potential

23
Q

depolarisation =

A

contraction

24
Q

hyperpolarisation =

A

relaxation

25
Q

intrinsic mechanisms of blood pressure control:

A

metabolic regulation = dilation by vasoactiv metabolites (adenosine, K+, H+)

endothelial regulation = release of NO

myogenic regulation = constrictor response to increased pressure

26
Q

right side of heart:

A

deoxygenated blood

from systemic circulation (vena cava)

to lungs (pulmonary artery)

thinner myocardial wall ( only pumps nlood to lungs)

27
Q

left side of heart:

A

oxygenated blood

from pulmonary system (pulmonary vein)

to systemic circulation (aorta)

thicker muscular wall for pumping to the whole body

hypertrophy due to pressure load

28
Q

maximum heart rate during exercise =

A

208 - (0.7 x age)

29
Q

stroke volume depends on…

A

venous return

ventricular dispensability - how much it can fill

ventricular contractility - an inherent ability for ventricles to contract forcefully

aortic/ pulmonary arterial pressure - pressure against which ventricles contract

30
Q

Frank-starling mechanism:

A

the stroke volume increases in response to an increase in the volume of blood filling the heart (and end diastolic volume) when all other factors remain constant

more blood in ventricles = increased sympathetic activity= increased stretch = increased contraction to forcibly remove blood = increased actin and myosin cross bridges

31
Q

elite athletes are able to…

A

increase stroke volume more following training = increased cardiac output

32
Q

vasoactive metabolites -

A

cause decrease in vascular resistance = increased stroke volume

33
Q

blood pressure changes on exercise:

A

increase systolic BP due to sympathetic activity

no change to diastolic BP sue to vasoactive metabolites

34
Q

upper body exercise…

A

gives a gretaer BP response

35
Q

extreme heavy weightlifting…

A

can cause BP to transiently reach very high levles (480/350)

36
Q

cardiovascular system adaptations to training:

A

hypertrophy (increased left ventricle size)

incresed end diastolic volume

decreased vascular resistance

decreased overall heart rate - HRmax reached at a higher level of exercise

recovery more rapid

37
Q

QT interval =

A

duration of heart beat

  • long durations are arrhythmogenic = Long QT syndrome can cause sudden death in athletes
38
Q

ST segment elevation -

A

causes myocardial infarction (heart attack)

sign of ischaemia

39
Q

ECG changes in exercise:

A

slight increase in P wave amplitude

shortening of PR interval

shift to right of QRS axis

ST segment depression (small - 1mm)

decreased T wave amplitude

occasional ectopic (abnormal) contractions

40
Q

an exaggerated ST depression =

A

coronary heart disease

41
Q

exercise stress test…

A

can be used to detect problems with heart

42
Q

long QT syndrome -

A

caused by genetics or pharmacological

longer action potential
prolonged contraction
shorter diastole
responses to increased heart rate impaired

can cause degeneration of myocardial function
may have no obvious symptoms
often only occurs during heavy exercise
often causes sudden cardiac death

43
Q

Long QT syndrome 1:

A

Mutation in IKs = repolarisation reserve - important during exercise as without wouldn’t have increase in K+

44
Q

Long QT syndrome 2:

A

Mutation in IKr = main repolarising delayed rectifier

45
Q

hypertrophic cardiomyopathy:

A

cardiomyocytes are misaligned

genetic

abnormal thickening of the left ventricular wall

causes...
heart pumps inefficiently 
reduce stroke volume 
reduce cardiac output 
exacerbated by excessive training 
sudden death