Cardiac system Flashcards
K+ ionic movement
higher intracellular concentration
= moves out of the cell
= hyperpolarisation
= intracellular becomes more negative
Na+/Ca2 ionic movment
higher extracellular concentration
= moves into cell
= depolarisation
= intracellular becomes less negative
open Na+ channels = rapis deploarisation
open Ca2+ channels = sustained depolarisation
stroke volume =
the volume of blood ejected from the heart during each cycle
cardiac output =
the total volume of blood pumped by the ventricle per min
stroke volume x heart rate
cardiac muscle =
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
moderate/submaximal exrecise -
uses approx. 80% of the energy supplied by free fatty acids (primary substrate)
aerobic
heavy exercise -
oxidising lactate can give a high percentage of ATP
anaerobic
trained athlete exercise -
will use aerobic free fatty acid metabolism to generate most ATP
aerobic
exercise following a meal -
glucose plays a larger role in ATP supply
anaerobic
ischaemia during exercise-
(inadequate blood supply to the heart)
largely anaerobic glycolysis
the spread of electrical activity in the heart:
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
p wave =
atrial depolarisation
QRS complex =
atrial repolarisaton and vetricular depolarisaton
T wave =
ventricle repolarisation
at rest…
parasympathetic activity + vagal stimulation
60-70 bpm
during exercise…
sympathetic activity - noradrenaline increase
= increased stroke volume, increased cardiac output and increased heart rate
140-180 bpm
vascular system:
heart -> artery -> arteriole -> capillary -> venule -> vein -> heart
the site of greatest regulation of BP =
arterioles - absorb the greatest pressure drop
resistance of the system =
viscosity of blood X length of vessel / radius (raised to the 4th power)
blood flow =
change in pressure / resistance
small inward diameter change =
increased resistance + increased pressure for a given flow
vasomotor tone:
vascular smooth muscle does not fire action potentials
have significantly depolarised resting potential
depolarisation =
contraction
hyperpolarisation =
relaxation
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
right side of heart:
deoxygenated blood
from systemic circulation (vena cava)
to lungs (pulmonary artery)
thinner myocardial wall ( only pumps nlood to lungs)
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
maximum heart rate during exercise =
208 - (0.7 x age)
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
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
elite athletes are able to…
increase stroke volume more following training = increased cardiac output
vasoactive metabolites -
cause decrease in vascular resistance = increased stroke volume
blood pressure changes on exercise:
increase systolic BP due to sympathetic activity
no change to diastolic BP sue to vasoactive metabolites
upper body exercise…
gives a gretaer BP response
extreme heavy weightlifting…
can cause BP to transiently reach very high levles (480/350)
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
QT interval =
duration of heart beat
- long durations are arrhythmogenic = Long QT syndrome can cause sudden death in athletes
ST segment elevation -
causes myocardial infarction (heart attack)
sign of ischaemia
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
an exaggerated ST depression =
coronary heart disease
exercise stress test…
can be used to detect problems with heart
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
Long QT syndrome 1:
Mutation in IKs = repolarisation reserve - important during exercise as without wouldn’t have increase in K+
Long QT syndrome 2:
Mutation in IKr = main repolarising delayed rectifier
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
