Cardiac system Flashcards

(45 cards)

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 =

24
Q

hyperpolarisation =

25
intrinsic mechanisms of blood pressure control:
metabolic regulation = dilation by vasoactiv metabolites (adenosine, K+, H+) endothelial regulation = release of NO myogenic regulation = constrictor response to increased pressure
26
right side of heart:
deoxygenated blood from systemic circulation (vena cava) to lungs (pulmonary artery) thinner myocardial wall ( only pumps nlood to lungs)
27
left side of heart:
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
maximum heart rate during exercise =
208 - (0.7 x age)
29
stroke volume depends on...
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
Frank-starling mechanism:
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
elite athletes are able to...
increase stroke volume more following training = increased cardiac output
32
vasoactive metabolites -
cause decrease in vascular resistance = increased stroke volume
33
blood pressure changes on exercise:
increase systolic BP due to sympathetic activity no change to diastolic BP sue to vasoactive metabolites
34
upper body exercise...
gives a gretaer BP response
35
extreme heavy weightlifting...
can cause BP to transiently reach very high levles (480/350)
36
cardiovascular system adaptations to training:
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
QT interval =
duration of heart beat - long durations are arrhythmogenic = Long QT syndrome can cause sudden death in athletes
38
ST segment elevation -
causes myocardial infarction (heart attack) sign of ischaemia
39
ECG changes in exercise:
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
an exaggerated ST depression =
coronary heart disease
41
exercise stress test...
can be used to detect problems with heart
42
long QT syndrome -
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
Long QT syndrome 1:
Mutation in IKs = repolarisation reserve - important during exercise as without wouldn't have increase in K+
44
Long QT syndrome 2:
Mutation in IKr = main repolarising delayed rectifier
45
hypertrophic cardiomyopathy:
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 ```