Heart histology Flashcards
where is smooth muscle found
in walls of hollow contracting organs
blood vessels
urinary bladder
respiratory tract
digestive tract
reproductive tract
where is cardiac muscle found
heart
where is skeletal muscle found
large body muscles responsible for movement
structure of smooth muscle tissue
cells are short, spindle shaped and non striated
single central nucleus
function of smooth muscle
moves flood, urine and controls diameter of respiratory and blood vessels
structure of cardiac muscle
cells = short, branched, striated
single nucleus, cells are interconnected by intercalated discs
cardiac myocytes = branches
function of cardiac muscle
circulates blood
maintains BP
structure of skeletal muscle
cells = long, cylindrical , striated, multinucleate
functions of skeletal muscle
moves and stabilises the position of the skeleton, guards entrance and exits to digestive, respiratory and urinary tracts, generates heat, protects organs
physical association between T tubule and SR = excitation wave directly couple with SR where an excitation wave directly couple with the SR
PACE
preload
afterload
contractility
hEart rate
preload
volume of blood in heart prior to contraction
afterload
load against which the heart has to contract to eject the blood
contractility
the relative ability of the heart to eject a stroke volume (SV) at a given prevailing afterload (arterial pressure) and preload (end-diastolic volume; EDV).
Pressure - volume relationship of the left ventricle
- isovolumetric contraction
- LV ejection
- isovolumetric relaxation
- LV filing
stroke volume equation
volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction.
SV= EDV-ESV
end diastolic volume - end systolic volume
Increase end diastolic volume
increase stroke volume
increase contractility
more blood per contraction
myocardial infarction severity and contractility
Artherscelerotic plaque = lack of oxygen - scarring tissue after MI = hypertrophy - fibrosis
Severity and contractility link
increased severity = decreased ventricular contractility and compliance = risk of Heart failure
what are systolic contraction and diastole compliance determined by
determined by the structural properties of the cardiac muscle (e.g., muscle fibers and their orientation, and connective tissue) as well as by the state of ventricular contraction and relaxation.
flabby weak ventricle effect on systolic contraction, diastolic compliance and stroke volume
fall in contractility
systolic contraction decreases
therefore store volume falls
stiff fibrotic ventricle effect on systolic contraction, diastolic compliance and stroke volume
fal in compliance
diastolic compliance decreases
stoken volume falls
what is used to quantify contractility
ejection fraction
ejection fraction equation
EF = SV/EDV
stroke volume / end diastolic volume
normal EF
normally between 55-75% under resting conditions
EF of >75%
hypertrophic cardiomyopathy
EF of <40%
muscle is weakened and you may have heart failure.
how are experimental models used
measure contractility to understand myocyte damage/death and research for new therapies
mimic in vivi cardiomyocytes contraction
how are muscle fibres orientated and why
Multidirectional orientation
Different deep vs middle vs superficial
Different regions of heart = different strain patterns = take average = mimic within model
complex
to ensure efficient and directional movement of blood
strain
amount muscle is stretched
important to muscle function
how can we map myocardial strain patterns
map
through computer analysis
orientation of muscle fibres
multidirectional orientation
sinusoidal wave pattern
equal on both sides
muscle length over time
wave pattern
stretch proportional both sides
generates force = destretch
systolic and diastole force
net power
net power is area between on graph =
developed force (systole) (energy generated)
passive force (diastole) (energy lost)
change strain pattern = change net power of muscle
optimal strain pattern
12%
if strain amplitude is beyond 12% (+/-6)
power output reduces
passive force increases = structural proteins resist overstretching of myofibrils
length force relationship
increased starting muscle length = increases net power
until optimum = after that power decreases
change muscle length
until optimum level = starts to decrease again
more calcium = more contractility
resting HR in man
70-90 bpm (1.2-1.5Hz) at rest
max HR man
220 bpm - age (+/-) 10 bpm (3.7Hz)
max Power output and factors that alter power output
3,5Hz
muscle length, cycle frequency, strain amplitude
aged heart
age associated disease - ischemic heart disease
left ventricle thickening
increase cardiomyocyte size
loss of cardiomyocytes
increase extracellular matrix
decrease oxygen consumption
decreased max HR
reduce cardiac function
decrease EF
decrease responsiveness to adrenergic stimulation
why use certain models
In two different models by using ages vs normal = don’t get the same results = so important to select the right model - need to look at many aspects to see whether you are mimicking it as closley as possible
