lecture 13 Flashcards
how many times a day does the heart beat?
100 000 times
study of the heart
cardiology
apex
pointed tip that rests on the diaphragm
formed by most inferior point of left ventricle
base
formed by the atria
opposite of apex
pericardium layers (make up, facts, positions) 3
fibrous
- inelastic dense irregular CT
- fused with central tendon
- prevents heart form overstretching, anchors heart in position
serous
- deep to fibrous
- two layers, parietal and visceral serous pericardium
pericardial cavity
space between parietal and visceral layers
- filled withs serous fluid that reduced friction between the heart and its layers
heart wall
- deep to fibrous pericardium
- 3 layers: epicardium, myocardium, endocardium
epicardium
most superficial layer of heart wall
AKA visceral pericardium
- serous membrane, holds fat
- thicker over ventricles (left especially)
- rich with vessels (blood/lymph)
myocardium
intermediate layer of the heart wall
- made of cardiac muscle tissue
- 95% of the heart wall
- wrapped in endomysium and perimysium
endocardium
deepest layer of the heart wall
- made of endothelium
- lines chambers and valves
- continuous with blood vessel lining
- reduced friction
auricles
increase the volume of blood in each atrium
sulci
grooves that provide passage for the coronary arteries
right atrium receives blood from:
superior / inferior vena cava
coronary sinus
fibrous skeleton of the heart
four rings of dense CT encircle the heart valves and fuse at the interventricular septum
fibrous rings of the heart function
- prevent overstretching
- insertion points for cardiac muscles
- electrical insulation between atria and ventricles
how do valves work?
blood moves from high to low pressure.
when ventricles contract, papillary muscles pull the chordae tendineae tight. pressure of blood pushes the valves closed
how do the semilunar valves work?
during contraction, blood moves from high to low pressure. after contraction, pressure is higher in the arteries, which pushes the valves closed
coronary vessels
blood vessels that service the heart
coronary arteries
blood from ascending aorta after contraction flows into these
coronary veins
drains into coronary sinus which empties to right atrium
cardiac muscle tissue facts
- branched
- mononucleated
- striated
- lots of mitochondria
- intercalated discs
- autorhythmic
cardiac muscle compared to skeletal
cardiac
- more/bigger mitochondria
- less but bigger t tubules
- smaller sarcoplasmic R
- make calcium from Interstitial fluid
cardiac conduction system formation
1% of cardiac muscle cells become autorhythmic
how does cardiac conduction work? 5 steps
- sinoatrial node
- atrioventricular node
- action potential
- signal travels branches
- signal reaches purkinjie fibres
sinoatrial node
pacemaker of the heart
- generates spontaneous action potentials
- stimulates synchronous contraction of the atria
atrioventricular node
in interatrial septum
- receives slowly transmitted signal from SA node
why is the signal between heart nodes delayed
high resistance between SA and AV nodes
purkinjie fibres
end of the electrical fibres in the heart
AV bundle
below AV node
cardiac action potential phases (3)
depolarization
plateau
repolarization
depolarization
opens voltage gated sodium channels, membrane becomes positive (actually positive not just less negative)
also opens voltage gates calcium channels
plateau
unique to cardiac muscle
due to depolarization opening voltage gates calcium channels as well
rate of Ca2+ entry = rate of K+ exit = plateau of membrane potential
repolarization
once signal has passes, sodium and calcium channels close, and K+ is transported out of the cell, restoring membrane potential
refractory period
length of time that cell cannot response to another action potential
because at peak depolarization, sodium channels are plugged, even though the channel is open
longer than time of contraction to permit the heart to fill with blood before contracting again
tetanus
sustained muscle contraction (eg, lockjaw)
individual twitch contractions are not distinguishable from one another
cause by bacterial infection that secretes a toxin that blocks the release of neurotransmitters that promote the relaxation of muscles
how do cardiac muscle cells make ATP to contract and why
aerobic cellular respiration
they have lots and fucking huge mitochondria
systole
when the atria or ventricles contract
diastole
when the heart is relaxed
cardiac cycle
repeated systole and diastole
ECG and what it does
electrocardiogram
records changes in electrical currents due to action potentials in the heart muscles
ECG points of interest
P wave
P-Q interval
QRS complex
T wave
P wave
triggers atrial systole
- atrial muscle cells are in depolarization after being signalled by the SA node
- contraction of atria occurs AFTER the P wave
P-Q interval
time between P wave and QRS complex
- the time for action potential to travel from SA node to the AV node
- atrial systole is happening here
a longer P-Q interval could be due to:
heart damage
QRS complex
- measures rapid depolarization of ventricular muscle fibres
- once signal has moved to the septum, Q wave starts
- stimulates ventricular systole
T wave
- measures ventricular repolarization
- starts at the apex
- slower that depolarization
- leads to ventricular diastole
blood pressure
The force of blood on the walls of the cardiovascular system
auscultation
act of listening for heart sounds using a stethoscope
4 major heart sounds
s1 - as AV valve closes
s2 - as semilunar valve closes
s3 - ventricular filling
s4 - atrial filling
what are heart sounds?
blood turbulence
S1
Atrioventricular valve closing sound
S2
semilunar valves closing sound
S3
ventricular filling sound
may to too quiet to hear
S4
atrial filling sound
may be too quiet to hear
cardiac output
volume of blood pumped out of the ventricles per minute
stroke volume
volume of blood pumped by the ventricles per contraction
heart rate
the number of heart beats per minute
cardiac output (CO) calculation
CO = SV x HR
cardiac output = stroke volume x heart rate
L/min = L/beat x beats/min
do not forget to convert units if needed
cardiac reserve
difference between max cardiac output and cardiac output at rest in on person
avg = 4-5x resting value
elite = 7-8x resting
mainly controlled by heart rate (autonomic nervous system)
the heart must response to signals coming from: (2)
higher brain centres like the limbic system
sensory receptors
- proprioreceptors
- baroreceptors
- chemoreceptors
proprioreceptors
sense body movement
(eg. elevating heart rate during warm up)
baroreceptors
sense changes in blood pressure
(eg. changes in elevation)
chemoreceptors
sense chemical changes in blood
(eg. elevated CO2)
cardiac accelerator nerves
stimulate norepinephrine release
output pathway to heart
- increase rate of depolarization in SA/AV nodes - increases heart rate
or
increases contractility of atria and ventricles - increasing stroke volume
vagus nerves
stimulate acetycholine release
output pathway to heart
decreases rate of depolarization in SA/AV node - decreases heart rate
other things that effect heart rate (and therefore CO)
hormones (norepinephrine)
cation availability (ones required for cardiac muscle contraction)
age, gender, fitness, temperature
maximal heart rate formula
Max HR = 220bpm - age (years)
why is there a maximum heart rate at which CO stops increasing?
to allow the heart enough time to fill with blood
how is stroke volume regulated? (3)
preload
contractility
afterload
preload (and what effects it)
1 way SV is regulated
measure of stretching as the heart fills
two factors affect preload:
- length of diastole
- venous return
contractility
1 way SV is regulated
strength of myocardial contraction, given a set preload
two things change force of contractions:
- positive inotropic agents
- negative
positive inotropic agents
part of heart contractility
promote Ca2+ entry during action potentials
increase force of contractions
negative inotropic agents
part of heart contractility
increases K+ leaving the cell or decreases Ca2+ entering
decreases force of contraction
afterload
1 way SV is regulated
the pressure of blood required in the ventricles to push the semilunar valves open
hypertension
high afterload and decreased SV
blood left in the ventricles after systole
cardiac hypertrophy
enlarged heart
both athletes and fatasses may both experience cardiac hypertrophy, why?
athletes = training = sigma
fucking fat people = low cardiac reserve , heart has to work harder to keep their lazy asses alive because daily tasks are somehow difficult
