Chapter 18 - Heart Flashcards
the heart
beats and pumping
- Beats approx 100,000 times/day
- Pumping about 8000 L of blood/day
when you get old
first thing that happens is the heart
if heart is on the right side of body
you will die
the pressure near the chest is
the highest. the lower you get (legs), the lower it gets.
heart is inside a sack called
pericardium, has fluid.
Ligamentum arteriosum
keeps aorta and pulmonary artery together
everything that is returning is a
vein and everything that is leaving is an artery
Visceral layer of serous pericardium (epicardium)
- covers surface of the heart
- covered by pericardium
Myocardium
Cardiac muscle tissue
endocardium
Covers inner surfaces of heart
atrioventricular (AV) valves
Tricuspid and mitral valves
semilunar valves
- Pulmonary and aortic valves
- Prevent backflow of blood into ventricles
compared to the left ventricle, the right ventricle
Holds and pumps the same amount of blood
Has thinner walls bc it is the systemic circulation
Develops less pressure
Is more pouch-shaped than round
low blood pressure in old people
swollen feet. heart not pumping hard enough
we are using all our brains, but
we are never using all our heart capacity
if theres high blood pressure, the first place it is going to effect is the
is the coronary arteries
coronary circulation
Supplies blood to muscle tissue of heart
Coronary ischemia
blood doesn’t reach a tissue and the coronary arteries get blocked and the cells die
when coronary arteries are blocked, what do doctors do?
put in a stent
bypass. take arteries from other places
coronary artery disease
clot/plaque narrows pathway and reduces blood flow
- common cause of MI
- coronary thrombosis
Myocardial infarction (MI), or heart attack
- Part of coronary circulation becomes blocked
- Cardiac muscle cells die from lack of oxygen
- Infarct- Death of affected tissue creates a nonfunctional area
heart is only tissue that
uses anything as source of fuel
how to not get heart problems
- Stop smoking
- Treat high blood pressure
- Adjust diet to lower cholesterol and promote weight loss
- Reduce stress - cortisol affects heart
- Increase physical activity - heart becomes stronger
propranolol
block sympathetic stimulation
block norepinephrine
nitroglycerine
cause vasodilation
reduce blood pressure
calcium ion channel blockers
- Block calcium ion movement into muscle cells
- Relieve pain and help dissolve clots (in MI)
Pacemaker cells found in
- Sinoatrial (SA) node—in wall of right atrium
- Atrioventricular (AV) node—at junction between atria and ventricles
Conducting cells found in
- Internodal pathways of atria
- Atrioventricular (AV) bundle, bundle branches, and Purkinje fibers of ventricles
what do you need to depolarize a cell?
electricity. need Na channels.
Pacemaker potential
-Gradual depolarization of pacemaker cells
-Do not have a stable resting membrane potential
Rate of spontaneous depolarization
-SA node: 60–100 action potentials per minute
-AV node: 40–60 action potentials per minute
Parasympathetic stimulation slows heart rate
Purkinje fibers
pass electricity to the myocardium
impulse conduction through heart
- SA node activity and atrial activation begin
- Stimulus spreads across atria and reaches AV node
- Impulse is delayed for 100 msec at AV node
Atrial contraction begins
P wave
SA node fires, atria depolarization
QRS complex
Ventricular depolarization
Complex shape of spike due to different thickness and shape of the two ventricles
T wave
Ventricular repolarization and relaxation
Bradycardia—
abnormally slow heart rate
Tachycardia—
abnormally fast heart rate
Ectopic pacemaker
wire that goes to your SA node
Abnormal cells generate high rate of APs
Bypasses conducting system
Disrupts timing of ventricular contractions
Q wave
beginning of ventricular depolarization
P-R interval
conduction through AV node and AV bundle
membranes of adjacent junctions are
- Held together by desmosomes
- Linked by gap junctions
characteristics of cardiac contractile cells
1 central nucleus
Branching interconnections between cells
Intercalated discs
Action potential in cardiac contractile cells
- Rapid depolarization
Massive influx of Na+ through fast sodium channels. - Plateau
Extracellular Ca2+ enters cytosol through slow calcium channels. depolarization - Repolarization
K+ rushes out of cell through slow potassium channels
ACTH will
depolarize (voltage dependent channels) in the membrane and releases ca in cytoplasm
Ca 2+ Ca 2+ Na K HCN channels
L type T type fast slow slow
Refractory period
Absolute refractory period (200 msec)
Relative refractory period (50 msec)
Action potential in a ventricular contractile cell
- 250–300 msec
- 30x longer than that in skeletal muscle fiber
- Prevents summation and tetany
in the heart it is a
slow climbing of contraction and relaxation
energy for cardiac contractions
Aerobic energy
- From mitochondrial breakdown of fatty acids and glucose
- Cardiac contractile cells store oxygen in myoglobin
Cardiac cycle
- From start of one heartbeat to beginning of next
- alternating periods of contraction and relaxation
systole
contraction
diastole
relaxation
blood pressure in each chamber
Rises during systole
Falls during diastole
Blood flows from an area of higher pressure to lower pressure
- Controlled by timing of contractions
- Directed by one-way valves
cardiac cycle and heart rate
when heart rate increases?
-Cardiac cycle lasts about 800 msec
When heart rate increases
-All phases of cardiac cycle shorten, particularly diastole
phases of cardiac cycle
- start a atrial systole
blood is entering both atrials and ventricles. systemic-unoxygenated, right atria, right ventricle, enters lungs, gets oxygenated (arteries). pulmonary veins into left atria and left ventricle into systemic circulation
two main things that fills ventricles w blood?
- atria systole
- passive –> vacuum
first its atrial systole then
Atrial systole ends Atrial diastole begins -Ventricles contain maximum blood volume (called end-diastolic volume (EDV)) Ventricles contract and build pressure -Closing AV valves -Producing isovolumetric contraction
ventricular systole phase
ventricular diastole-early
Ventricular systole phase
-Ventricular pressure exceeds arterial pressure and opens semilunar valves, allowing blood to exit
Ventricular diastole-early
-Semilunar valves close as ventricular pressure falls
-Ventricles contain end-systolic volume (ESV)
-About 40% of end-diastolic volume
when the ventricles are filling that means
they are not contracting, they are relaxing
3 things that affect heart conditions
- males have bigger hearts
- age
- hormonal
after ventricular diastole-early is
Ventricular diastole- late
Isovolumetric relaxation
-All heart valves are closed
-Ventricular pressure is higher than atrial pressure (Blood cannot flow into ventricles)
AV valves open; ventricles fill passively
-Atrial pressure is higher than ventricular pressure
what can lead to heart failure?
ventricular damage
Individuals can survive severe atrial damage
cardiac output CO
Volume pumped by left ventricle in one minute
CO (mL/min) = HR (beats/min) × SV (mL/beat)
your heart pumps how many L per min?
5 liters. during exercise, 25-35 liters.
factors that affect heart rate?
- autonomic innervation
2. hormones (epinephrine and thyroxine)
factors that affect stroke volume?
- end diastolic volume
2. end systolic volume
Autonomic innervation
- Cardioacceleratory center-controls sympathetic neurons that increase heart rate
- Cardioinhibitory center-controls parasympathetic neurons that slow heart rate
cardiac reflexes
Cardiac centers
- Monitor blood pressure (baroreceptors)
- Monitor arterial O and CO2 levels (chemoreceptors)
Autonomic tone
-Fine adjustments meet needs of body
Effects on pacemaker cells of SA node
ACh
NE
Membrane potentials of pacemaker cells Are closer to threshold than those of cardiac contractile cells ACh released by parasympathetic neurons Decreases heart rate NE released by sympathetic neurons Increases heart rate
venous return
Amount of blood returning to heart through veins
-Stretch receptors in right atrium
Trigger increase in HR by stimulating sympathetic activity
HR increased by 3 factors
Epinephrine (E)
Norepinephrine (NE)
Thyroid hormone (T3)
Two factors affect EDV
Filling time
-Duration of ventricular diastole
Venous return
preload
Degree of ventricular stretching during ventricular diastole
Directly proportional to EDV
Affects ability of muscle cells to produce tension
frank starling
when edv increases, SV increases
afterload
Tension produced by ventricle to open semilunar valve and eject blood
increase in contractility is a
decrease in ESV
cardiac reserve
difference bw resting and maximal cardiac outputs
ejection fraction
SV/EDV
venous return controls
EDV, SV, CO
veins hold most of
blood. app. 70%
