Cardiac Cycle and Cardiac Output Flashcards
what is the cardiac cycle?
a single cardiac cycle includes all events associated with one heartbeat
describe the atria and ventricles during the cardiac cycle
atria and ventricles alternately contract and relax, forcing blood from area of high pressure to areas of low pressure
what happens as a chamber of the heart contracts?
the pressure within that chamber increases
compare and contrast the pressure, expelled blood volume, and pumping pattern on the right side of the heart compared to the left side of the heart
- pressure on right side of heart is much lower compared to the left side
- each ventricle expels the same volume of blood per beat
- the same pattern exists for both pumping chambers
how long does the cardiac cycle last when the heart rate is 75 bpm?
0.8 seconds
how long does atrial systole contract?
about 0.1 seconds
decribe the ventricles during atrial systole
ventricles relaxed
what causes atrial depolarization and what does this look like on a EKG?
depolarization of the SA node, is the P wave
what causes atrial systole?
atrial depolarization
what happens as atria contract? (2)
- as atria contract, they exert pressure on blood within
- this forces blood through open AV valves into the ventricles
what does atrial systole contribute to the ventricles?
atrial systole contributes the final volume of blood (25mL) to the blood volume already in the ventricles (120ml) for the overall 130mL in the ventricles at the end of systole
what is the end of atrial systole also?
end of atrial systole is also the end of ventricular diastole
what is end-diastolic volume? (EDV)
the amount of blood in each ventricle as the end of diastole (130mL)
what on an EKG marks the onset of ventricular depolarization/systole?
QRS complex
how long does ventricular systole last and what is happening?
lasts about 0.3 seconds; ventricles are contracting and atria are relaxed
what happens to AV valves as ventricular systole begins?
pressure rises inside ventricles and pushes blood up against AV valves, forcing them shut
what is the period of isovolumetric contraction?
for about 0.05 seconds at the end of ventricular systole, both SL and AV valves are closed; ventricular volume remains the same
why is isovolumetric contraction also called isovolumetric muscle contraction?
because cardiac muscle fibers are contracting and exerting force, but not shortening
what does the continued contraction of ventricles cause?
pressure inside chambers to rise sharply
when do both SL valves open?
when L ventricular pressure surpasses aortic pressure and R ventricular pressure rises above pulmonary trunk pressure
what is aortic pressure?
about 80 mmHg
what is pulmonary trunk pressure?
about 20 mmHg
what happens after the aortic and pulmonary trunk pressure is surpassed and both SL valves open?
ejection of blood begins
what is ventricular ejection? how long does it last?
the period when SL valves are open, lasts about 0.25 seconds
what happens in the ventricles during ventricular ejection
pressure in both ventricles continues to rise
L ventricle rises to about 120 mmHg
R ventricle rises to about 30 mmHg
how muhc blood does the L ventricle eject into the aortia during ventricular systole?
about 70 mL
what is end systolic volume?
the remaining volume of blood left in each ventricle at the end of systole; about 60 mL
what is stroke volume?
the volume ejected per beat from each ventricle
how do you calculate stroke volume?
stroke volume = end diastolic volume - end systolic volume
(SV = EDV - ESV)
what is stroke volume at rest?
about 70mL
what marks the onset of ventricular repolarization on EKG?
the T wave
what is the relaxation period? how long does it last?
when atria and ventricles are both relaxed; lasts about 0.4 seconds
what happens as heart beats faster to relaxation period and atrial and ventricular systole?
as heart beats faster, relaxation period becomes shorter, while atrial and ventricular systole shorten only slightly
what causes diastole?
ventricular repolarization
what happens as the ventricles relax?
pressure within the ventricles falls, and blood in the aorta and pulmonary trunk begin to flow back towards lower pressure in the ventricles
what causes the SL valves to close?
blood catches the cusps of the SL valves when flowing back into the ventricles
at what pressure does the aortic valve close?
about 100 mmHg
what does the dicrrotic wave on the aortic pressure curve represent?
the rebound of blood off closed cusps of aortic valve
what is isovolumetric relaxation?
the brief interval after SL valves close when ventricular blood volume does not change because all 4 valves are closed
what happens to the ventricles during isovolumetric relaxation and what is the result?
ventricles continue to relax and pressure falls quickly
what happens when ventricular pressure drops below atrial pressure?
AV valves open and ventricular filling begins
when does a majority of ventricular filling occur?
just after AV valves open
what happens to the blood that has been flowing into/building up in the atria during ventricular systole when the Av valves open?
rushes rapidly into ventricles
at the end of relaxation period, how full are the ventricles?
about 3/4 full
what happens on an EKG after the relaxation period and what does this signal?
P wave appears signaling beginning of another cardiac cycle
what is cardiac output?
the volume of blood ejected from the L or R ventricle into aorta or pulmonary trunk each MINUTE
how is cardiac output calculated?
cardiac output (mL/min) = stroke volume (mL/beat) x HR (beats/min)
what does cardiac output represent and what is it close to?
is close to the total blood volume, so cardiac output represents/ shows that your entire blood volume flows through tthe pulmonary and systemic circulation each minute
what normally increases caardiac output?
factors that increase stroke volume or heart rate, like exercise
what is cardiac reserve?
the difference between a persons max cardiac output and cardiac output at rest
compare an average persons cardiac reserve to their resting value
the average person has a cardiac reserve 4-5x their resting cardiac output
compare endurance athlete’s max cardiac reserve to their resting cardiac output
has a cardiac reserve 7-8x that of resting CO
describe the cardiac reserve of people with severe heart disease
may have little to no cardiac reverse; limits simple daily tasks
what happens to stroke volume if more blood returns to the heart during diastole?
more blood is ejected during the next systole
describe SV, EDV, and ESv at rest
at rest SV is 40-50% of EDV because 40-50% of blood remains in ventricles after each contraction (ESV)
what are the 3 factors that regulate stroke volume and ensure that L and R ventricles pump equal volumes of blood? describe
- preload: the degree of stretch of heart before it contracts
- contractility: forcefulness of contraction of individual ventricular muscle fibers
- afterload: pressure that must be exceeded before ejection of blood from ventricles can occur
what does a greater degree of preload do to muscle fibers?
a greater stretch on cardiac muscle fibers prior to contraction increases their force of contraction
what is the frank-starling law?
within limits, the more the heart fills with blood during diastole, the greater the forces of contraction during systole
what is preload proportional to?
preload is proportional to EDV
generally, the greater the EDV, what happens to the next contraction?
the greater the EDV, the more forceful the next contraction
what 2 key factors determine EDV?
- duration of ventricular diastole
- venous return to R ventricle
what 2 things can happen as HR increases in terms of EDV?
- duration of diastole is shorter and less filling time means smaller EDV so ventricles may contract before adequately filled
- when venous return increases, a greater volume of blood flows into ventricles, so EDV may increase
when happens to SV when HR exceeds 160 bpm and why?
SV typically declines because of short filling time
what happens to EDV preload as a result of rapid heart rate?
EDV is reduced and preload is lower
describe the resting SV of people with slow resting HR and why; include preload in your answer
people with slow resting HR usually have large resting SV because filling time is prolonged and preload is larger
what does the frank-starling law do?
equalized the output of R and L ventricles and keeps the same volume of blood flowing to both systemic and pulmonary circulations
according to the frank-starling law, what happens if the L side of the heart pumps a little more blood then the R side?
then the volume of blood returning to the R ventricle (venous return) will also increase
how does the frank-starling law work?
increased EDV causes least full ventricle to contract forcefully on the next beat, bringing both sides back into balance
what is contractility?
the strength of contraction at any given preload
what 2 factors affect stroke volume?
exercise and contractility
what are positive inotropic agents?
substances that increase contractility
for a constant preload, what happens to stroke volume when a positive inotropic agent is present?
stroke volume increases
what do positive inotropic agents usually do to increase contractility?
promote Ca2+ inflow during cardiac AP’s, which strengthens the force of the enxt contraction
what 3 things have positive inotropic effects?
- stimulation of the sympathetic division of the autnonomic nervous system hormones such as epinephrine and norepinephrine
2.increase of Ca2+ levels in interstitial fluid - the drug digitalis
where is the drug digitalis extracted from?
the foxglove plant
what is the active agent in digitalis? what does it do?
digoxin; inhibits Na+/K+ ATPase pumps and causes a rise in intracellular [Na+], so Na+ is not flowing out as much and the concentration gradient decrease across the cell membrane; this slows down the Na+/Ca2+ antiport (which usually brings Na+ in and pushes Ca2+ out), which means there is more Ca2+ remainingin cardiac muscle cells to increase contractility
what are negative inotropic agents?
substances that decrease contractility
what 5 things have negative inotropic effects?
- inhibition of sympathetic ANS
- anoxia
- acidosis
- some anaesthetics
- increases K+ levels in interstitial fluid
what is anoxia and how does it have negative inotropic effects?
reallow low O2; interferes with Na+ channels
how does high K+ have negative inotropic effects?
interferes with/blocks Na+ channels, slowing depolarization
what is afterload?
the pressure that must be overcome before the SL valves can open
when does ejection of blood from the heart begin?
when pressure in the R ventricle exceeds pressure in pulmonary trunk (approx 20mmHg) and when pressure in L ventricle exceeds pressure in aorta (approx 80mmHg) and the higher pressure in the ventricles can push open SL valves
what does and increase in afterload cause? what is the result?
increases in afterload cause stroke volume to decrease, so more blood remains in the ventricles at the end of systole
what 2 conditions can increase afterload?
- hypertension (electaed blood pressure)
- narrowing of arteries by atherosclerosis
what is congestive heart failure?
loss of pumping efficiency by heart
give 5 causes of congestive heart failure
- CAD
- congenital defects
- long term high blood pressure (increases afterload)
- MI (regions of dead heart tissue)
- valve disorders
what happens as the pumping of the heart becomes less effective in congestive heart failure? (2)
- more blood remains in ventricles at the end of each cycle
- gradually EDV (preload) increases
what happens initially in cingestive heart failure due to the Frank Starling law?
initialy, increased prelaod may promote increased force of contraction
describe the potentially lethal feedback loop of congestive heart failure
as preload increases further, the heart is overstretched and contracts less forcefully, and the less effective pumping leads to even lower pumping capability
what is the result of congestive heart failure?
one side of the heart usually fails before the other
what happens if the left ventricle fails first in congestive heart failure?
the heart can’t pump out all the blood it receives and as a result, blood backs up in the lungs and causes pulmonary edema
what is pulmonary edema?
fluid accumulation in the lungs that can cause suffocation if untreated
what happens if the right ventricle fails first in congestive heart failure?
blood backs up in systemic ceins and over time the kidneys cause increase in blood volume resulting in peripheral edema noticeable in the feet and ankles
what does cardiac output depend on? (2)
- heart rate
- stroke volume
what is important in short term control of cardiac output and blood pressure?
adjustments in heart rate
what happens in terms of cardiac output and why during exercise?
cardiac output increases to supply working muscles and other tissues with oxygen and nutrients
if the ventricular myocardium is damaged or if blood volume is reduced by bleeding, what may happen to stroke volume?
stroke volume may fall
in cases of exercise or decreased stroke volume, how do homeostatic mechanisms maintain adequate cardiac output? (2)
- increasing heart rate
- increase heart contractility
what are the 2 (of many) most important factors that contribute to heart rate regulation?
- ANS (sympathetic and parasympathetic)
- hormones released by adrenal medulla
where does nervous system regulation of the heart originate?
in the cardiovascular center of the medulla oblongata
what is the medulla oblongata?
a region of the brain stem that receives input from various sensory receptors and from the higher brain centers like the limbic system and the cerebral cortex
describe what the limbic system and cerebral cortex do
limbic system: emotional brain
cerebral cortex: analytical and logical
how does the cardiovascular center of the brain direct appropriate output?
by increasing or decreasing frequency of nerve impulses in sympathetic and parasympathetic branchers of ANS
why does your heart rate rise before physical activity begins in competitive situations?
limbic system sends nerve impulses to CV center
what takes over from the limbic system during exercise to keep heart rate up?
proprioceptors send nerve impulses at increased frequency to cardiovascular center
what ia a major stimulus for the fast increase in heart rate that occurs a the onset of exercise?
proprioceptor input
other than proprioceptors, what 2 other receptors send provide input to the cardiovascular center?
- chemoreceptors
- baroreceptors
where are important baroreceptors located? what do they do?
in the arch of the aorta and carotid arteries; detect changes in blood pressure and provide input to the cardiovascular center when it changed
what are the 4 E situations that increase sympathetic ANS stimulation?
- Excitement
- Emergency
- Exericse
- Embarassment
where do sympathetic neurons extend?
from the medulla into the spinal cord
what are the sympathetic neurons that extend from the thoracic region of the spinal cord called?
called cardiac accelerator nerves
where do cardiac accelerator sympathetic nerves extend to? (3)
- SA node
- AV node
- most portions of myocardium
what do impulses in cardiac accelerator nerves trigger?
release of norepinephrine that binds to beta-1 receptors on cardiac muscle fibers
what are the 2 effects of release of norepinephrine that binds to beta-1 receptors on cardiac muscle fibers?
- speeds rate of spontaneous depolarization in SA and AV nodes cause the pacemaker to fire more rapidly so HR increases
- in contractile fibers, enhanced Ca2+ entry through voltage-gated slow Ca2+ so contractility increases
why does a moderate increase in heart rate not cause stroke volume to decline?
the increased contractility offsets the decreased preload
under maximal sympathetic stimulation, what can HR reach in a young adult?
220 bpm
how do you calculate max heart rate?
220-age
what happens to stroke volume at max heart rate and why?
stroke volume decreases because of reduced filling time
what does max heart rate decline with?
age
how do parasympathetic nerve impulses reach the heart?
by L and R vagus nerve
where do vagal axon terminals terminate? (3)
- SA node
- AV node
- some in atrial myocardium
how do vagal axon terminal contribute to autonomic regulation of the heart rate?(3)
- release acetylcholine which decreases the HR by slowing the rate of spontaneous depolarization in autorhythmic fibers
- acetylcholine increases permeability of fiber membranes to potassium ions
- this causes hyperpolarization of cell
describe the balance of atunomic regulation of HR
continually shifting balance between sympathetic and parasympathetuc stimulation of the heart
at rest, what part of the ANS dominates?
parasympathetic
what 3 things are involved in chemical regulation of the heart rate?
- hypoxia, acidosis, alkalosis
- hormones
- ionic imbalances
how do hypoxia, acidosis, and alkalosis chemically regulate the heart rate?
all depress cardiac activity
what hormones are involved in chemical regulation of HR and where do they come from?
epinephrine and norepinephrine from the adrenal medulla
what do epinephrine and norepinephrine do to HR and contractility?
increase HR and contractility
what 3 things can cause the adrenal medulla to release more hormones? (epi and norepi)
- exercise
- stress
- excitement
what do thyroid hormones do to contractility and HR?
thyroid hormones enhance contractility and increase HR
what is a sign of hyperthyroidism?
tachycardia
how is the thyroid gland involved in chemical regulation of HR?
involved in overall metabolsim; affects receptors for epinephrine and norepinephrine and more receptors means more availability and a greater effect on the heart
what do ionic imbalances do?
can compromise the pumping effectiveness of the heart
what 3 ions in particular have large effects on the heart?
- K+
- Ca2+
- Na+
what do elevated blood concentrations of K+ or Na+ do to heart rate and contractility?
elevated blood concentrations of K+ or Na+ decrease HR and contractility
how does elevated blood concentrations of Na+ decrease contractility?
excess Na+ blocks Ca2+ infow during cardiac action potential, decreasing the force of contraction
how does elevated blood concentrations of K+ slow heart rate?
excess K+ blocks generation of action potential due to hyperpolarization making it hardder for the cell to reach the threshold to generate an action potential
what does a moderate increase in intersitital Ca2+, and therefor intracellular Ca2+ do to HR and contractility?
speeds HR and strengthens HR (increases contractility)
what is high Na+ called?
hypernatremia
what is high K+ called?
hyperkalemia
what is high Ca2+ called?
hypercalcemia
other than chemical regulation and ANS, give 4 factors in HR regulation
- age
- gender
- fitness
- body temperature
what is a newborn baby’s avg resting HR and why?
high, around 120 due to high metabolic rate and more sympathetic influence because have to grow a lot and real fast
why do adult females tend to have slightly higher resting heart rates than men?
females tend to have smaller hearts that have to beat faster
in a physically fit person, what can occur and why?
bradycardia (below 50bpm) because a slowly beating heart is more efficient
what does increased body temp do to HR and how?
increases heart rate because a higher temperature causes the SA node to discharge more quickly in an attempt to move blood and heat to the periphery away from the core
what does a decreased body temp dp to HR and contractility?
decreased body temp decreases HR and contractility because trying to keep the core warm
what is done to a person’s HR during heart surgery and why?
slow HR by hypothermia to slow metabolism to reduce the O2 need of tissues
