Lecture 15 Flashcards
Cardiac Cycle step 1
Contraction of atria
(AKA atrial systole)
Cardiac Cycle step 2
contraction of
ventricles (ventricular
systole)
Cardiac Cycle step 3
rest (diastole) when neither chamber is contracting
contraction name
systole (BP: 120)
relaxation name
diastole (BP: 80)
doctors are more interested in….
diastole because its the force by which the heart has to work against to eject blood against the contraction (diastole is period when heart fills back up with blood)
AFTERLOAD
diastolic arterial pressure, how hard heart has to work to overcome systolic pressure
strength and rate of heart contractions controlled by
Neural and Endocrine signals
sympathetic innervation (norepinephrine) causes
increased HR eg these signals released when doing excersize
parasympathetic innervation (acetylcholine) causes
decreased HR eg. these signals are released when sitting in a lecture
epinephrine causes
increased strength of heart contractions / how much blood is being ejected with each contraction
from rest to excersize:
HR can increase to nearly 200 bpm
cardiac output increases from 5 L/min to 25 L/min
(elite athletes: 40 L/min)
Max HR formula
220 - age
Electrical signal is propagated by: (3)
Nodes, Nerves, Intercalated disks (gap junctions)
Nodes
SA (sinoatrial) nodes, AV (atrioventricular) nodes
SA nodes are:
Heart’s natural pacemaker, electrical impulses generated here.
electrical impulse tells:
Heart to beat
Nerves
Bundle of His, Bundle branches, purkinge fibers
(All have lots of gap junctions)
Intercalated disks (gap junctions)
send signals between parts of heart, eg SA node sends signal to left atrium
Cardiac muscle consists of
individual cardiomyocytes connected by intercalated discs (GAP JUNCTIONS!) to work together as a single functional organ
miscommunication usually results in
some kind of arrhythmia
miscommunication is
something wrong with the sequential sequencing of the heart
Abnormal sinoatrial node firing results in
tachycardia (fast), bradycardia (slow)
Blocks can:
slow down or prevent signal propagation from atria to ventricles
blockages (eg at AV node)
can vary in terms of degree of the blockage
Ventricles can:
contract independently (bundle of His, 40 bpm)
Fibrillations
more serious, occur when cells depolarize independently
Atrial Fibrillations (A-Fib)
a quivering
or irregular heartbeat (arrhythmia)
Ventricular fibrillation (V-fib)
the most serious cardiac rhythm disturbance. Must try and reset electrical signal
Atherosclerosis is
Narrowing of arteries due to calcified fatty deposits (plaque) and thickening of the wall
Atherosclerosis is triggered by
damage to arterial wall
(inflammation)
Atherosclerosis can lead to
- heart attack or stroke
- When this occurs in the arteries of heart
muscle, it is called coronary artery disease
Factors contributing to Coronary Artery Disease:
Elevated blood lipids, hypertension,
inflammatory mediators (C-reactive protein), Diet (sodium, potassium, saturated/trans fats,
cholesterol), Smoking, physical inactivity, obesity/diabetes, Age, genetics
Treating Coronary Artery Blockages
Angioplasty, Bypass Surgery
Angioplasty
a catheter and balloon are threaded into the coronary artery to the point of blockage. Plaque is pushed to the outside of the artery walls and held there by stent.
Bypass Surgery
Vein taken from
arm or leg; one
end attached above
the blockage and
the other below
Hypertrophy
a sign of being
“overworked”. The heart
muscle will respond and
hypertrophy just like your
skeletal muscle would respond to weight-lifting
Endurance athletes
mostly an increase in LV
chamber (need to increase cardiac output)
Weightlifters
mostly increased LV wall and septum thickness (need to overcome increased
afterload – the amount of pressure needed to eject
blood during ventricular contraction)
Enlargement of the Heart pros
Athlete’s heart – an appropriate adaptation! Occurs in both endurance athletes and weightlifters! ☺
Enlargement of the Heart cons
Causes include high blood pressure and narrowing of
aortic valve … the heart must work harder to overcome these
Hypertension # stage 1
130-139/80-89
Hypertension # stage 2
140+/90+
Hypertensive crisis #
higher than 180/higher than 120
Vasoconstriction (artery hole gets smaller)
- Alpha-receptors are located on arteries.
- Norepinephrine and epinephrine bind to 2 adrenergic receptors
- This causes arteries to constrict (vasoconstriction)
- This increases blood pressure
- E.g. during exercise
Vasodilation (artery hole opened wider)
- Blood vessels in skeletal muscles lack alpha-receptors
- Norepinephrine and epinephrine bind to b2 adrenergic receptors found in arteries of skeletal muscle
- This dilates vessels of the skeletal muscles (vasodilation) so they can receive increased blood flow
- E.g. also during exercise!
how much does Cardiac output increase during excersize
5x, 8x in elite athletes
why does BP not increase much during exercise
Distribution of blood does not increase proportionally. blood flow is diverted to where it is needed during exercise! The working muscles!
Dilation of vessels to skeletal muscle and heart increases blood flow to muscles (β2 receptors and local metabolites). Constriction of vessels to the gut and kidneys decreases blood flow to these organs (B2 receptors). Dilating vessels in the muscle decreases resistance and we have a lot of muscle mass!
Resistance exercise (e.g. weightlifting) can cause
dramatic increases in blood pressure - up to 345/245 mmHg. Holding your breath – increases intrathoracic pressure during the lift – called the “Valsalva maneuver”
Temporarily raises blood pressure and slows heart rate!
