chapters 9-11 Flashcards
right side of the heart
receives blood from the peripheral organs and pumps it through the lungs
left side of the heart
receives oxygenated blood from the lungs and pumps it back to the peripheral organs
atria
primer pumps that fill the ventricles with blood
ventricles
contract and impart high blood pressure to the blood which is responsible for propelling the blood through the circulatory system.
Heart conduction
the heart has its own special conduction system that maintains its own rhythmicity and transmits action potentials throughout the heart.
Similarities between cardiac and skeletal muscle
- both are striated
- both have actin and myosin filaments that interdigitate and slide along each other during contraction
Unique characteristics of cardiac muscle
- has intercalated discs between cardiac muscle cells (these discs have very low electrical resistance allowing an action potential to travel freely between cardiac muscle cells)
- the cardiac muscle is a syncytium of many heart muscle cells in which the action potntial spreads rapidly from cell to cell
role of the A-V bundle
slowly conducts impulses from the atria to the ventricles
- this is an exclusive pathway because the atrial synctium and ventricular synctium are normally insulated from one another by fibrous tissue.
resting membrane potential of cardiac muscle
-85 to -95 millivolts
Action potential of cardiac muscle
105 millivolts
for how long does the membrane remain depolarized in the atria?
0.2 seconds
for how long does the membrane remain depolarized in the ventricles?
0.3 seconds
what causes an action potential in SKELETAL muscle?
entry of sodium through fast sodium channels which remain open for only a few 10,00ths of a second
what causes an action potential in CARDIAC muscle?
cardiac muscle also has fast sodium channels that open at the initiation of an action potential, but
cardiac muscle also has unique slow CALCIUM channels, or calcium-sodium channels
how do the slow calcium-sodium channels work?
calcium and sodium ions flow through the slow channels into the cell after the initial spike of the action potential, and they maintain the plateau.
Calcium that enters the cell through these channels also promotes cardiac muscle contraction
What else contributes to the plateau of the action potential in cardiac muscle? (prevents return of the membrane potential)
a decrease in the permeability of cardiac muscle cells to potassium ions
when the slow calcium-sodium channels close after 0.2 - 0.3 seconds, the potassium permeability increases rapidly and thus returns the membrane potential to its resting level.
what promotes cardiac muscle contraction?
diffusion of calcium into the myofibrils
the action potential spreads into each cardiac muscle fiber along the transverse (T) tubules, causing the longitudinal sarcoplasmic tubules to release calcium ions into the sarcoplasmic reticulum.
these calcium ions catylyze the chemical reactions that promote the sliding of the actin and myosin filaments along one another to cause muscle contraction.
What is an additional means of entry of calcium into the sarcoplasm that is unique to cardiac muscle?
the T tubules of cardiac muscles have 25x as great a volume as those in skeletal muscle
these t tubules contain large amounts of calcium that are released during the action potential.
the t tubules open directly into the extracellular fluid in cardiac muscle - so their calcium content is ver dependent upon extracellular calcium concentration
at the end of the plateau of the action potential, the influx of calcuim ions into the muscle fiber abruptly stops, and calcium is pumped back into the sarcoplasmic reticulum and T tubules, ending the contraction
cardiac cycle
the events that occur at the beginning of a heartbeat and last until the beginning of the next heartbeat are called the cardiac cycle.
how does each heart beat begin?
with a spontaneous action potential that is initiated in the sinus node of the right atrium near the opening of the superior vena cava
what happens after the action potential is initiated in the sinus node of the right atrium?
the action potential travels through both atria and the A-V node and bundle into the ventricles
what is the delay between atrial and ventricular contraction?
a delay of more than 1/10 of a second occurs in the A-V node and bundle, which allows the atria to contract before the ventricles contract.
when do the ventricles fill with blood?
during diastole
when do the ventricles contract?
during systole
electrocardiogram
a recording of the voltage generated by the heart from the surface of the body during each heartbeat
P wave
caused by spread of depolarization across the atria, which causes atrial contraction
atrial pressure increases just after the P wave.
QRS waves
appear as a result of ventricular depolarization
0.16 second after the onset of the P wave
this initiates ventricular contraction
ventricular pressure increases as a result
T wave
caused by repolarization of the Ventricle
what occurs during diastole before contraction of the atria?
about 75% of ventricular filling
when does the other 25% of ventricular filling occur?
during contraction of the atria
Atrial pressure wave (a wave)
caused by atrial contraction
atrial pressure wave (c wave)
occurs during ventricular contraction because of slight backflow and bulging of the A-V valves toward the atria.
atrial pressure wave (v wave)
caused by in-filling of the atria from venous return
What events occur just before and during diastole?
- during systole, the A-V valves are closed, and the atria fill with blood
- begining of diastole - isovolumic relaxation caused by ventricular relaxation; when ventricular pressure decreases below that of the atria, the A-V valves open.
- the higher pressure in the atria pushes blood into the ventricles during diastole
- the period of rapid filling of the ventricles occurs during the first 1/3 of diastole (this provides most of the ventricular filling)
- atrial contraction occurs during the last 1/3 of diastole and contributes about 25% of the filling of the ventricle (aka “atrial kick”)
What events occur during systole?
- at the begining of systole, ventricular contraction occurs, the A-V valves close, and pressure begins to build up in the ventricle. NO outflow of blood occurs during the first 0.2-0.3 seconds of ventricular contraction (period of isovolumic “same volume” (in the ventricles) contraction).
- when the left ventricular pressure exceeds the aortic pressure of about 80mm Hg and the right ventricular pressure exceeds the pulmonary artery pressure of 8mm Hg, the aortic and pulmonary valves open. Ventricular outflow occurs (“period of ejection”)
- most ejection occurs during the 1st part of this period (period of rapid ejection)
- this is followed by the period of slow ejection. during this period, aortic pressure may slightly exceed the ventricular pressure because the kinetic energy of the blood leaving the ventricle is converted to the pressure in the aorta, which slightly increases its pressure.
- during the last period of systole the ventricular pressures fall below the aortic and pulmonary artery pressures. The aortic and pulmonary valves close at this time.
Ejection Fraction
the fraction of the end-diastolic volume that is ejected.
- calculated by dividing the stroke volume by the end-diastolic volume
- has a value of about 60%
- the stroke volume of the heart can be doubled by increasing the end diastolic volume and decreasing the end-systolic volume.
end-diastolic volume
at the end of diastole, the volume of each ventricle is 110 - 120 mL
stroke volume
the amount of blood ejected with each beat (about 70mL)
end-systolic volume
the remaining volume in the ventricle at the end of systole (measures about 40-50 mL)
effect of ventricular ejection on the aorta
ventricular ejection increases pressure in the aorta to 120mm Hg (systolic pressure)
what happens when the ventricular pressure exceeds the diastolic pressure in the aorta?
the aortic valve opens and blood is ejected into the aorta.
Pressure in the aorta increases to about 120 mm Hg and distends the elastic aorta and other arteries.
what happens when the aortic valve closes at the end of ventricular ejection?
there is a slight backflow of blood followed by a sudden cessation of flow, which causes an incisurs, or a slight increase in aortic pressure.
During diastole, blood continues to flow into the peripheral circulation, and the arterial pressure dectreases to 80 mm Hg (diastolic pressure)
A-V valves (ticusped (right) and mitral (left) valves)
prevent backflow of blood from the ventricles to the atria during systole.
- have papillary muscles attached to them by the chordae tendineae
- during systole, the papillary muscles contract to help prevent the valves from bulging back too far into the atria
Semilunar valves (aortic and pulmonary valves)
prevent backflow of blood from the aorta and pulmonary artery into the ventricles during diastole
- these valves are thicker than the A-V valves and do not have any papillary muscles attached.
stroke work output of the ventricles
the output of energy by the heart during each heart beat
(the heart performs 2 types of work)
volume-pressure work of the heart
the work done to increase the pressure of the blood;
in the left heart, it equals stroke volume multiplied by the difference between the left ventricular mean ejection pressure and the left ventricular mean input pressure
the volume pressure work of the right ventricle is onlt about 1/6 that of the left ventricle because the ejection pressure of the right ventricle is much lower.
work to be done to supply kinetic energy to the blood
= MV 2/2
M = the mass of blood ejected
V = Velocity
what % of the work of the heart creates kinetic energy?
usualy only about 1%
upto 50% if there is severe aortic stenosis
Phases of the Cardiac Cycle (Phase I)
period of filling during which the left ventricular volume increases from the end-systolic volume to the end-diastolic volume, or from 45 mL to 115 mL (a 70 mL increase)
Phases of the Cardiac Cycle (Phase II)
Period of isovolumic contraction during which the volume of the ventricle remains at the end-diastolic volume but the intraventricular pressure increases to the level of the aortic diastolic pressure, or 80mm Hg
Phases of the Cardiac Cycle (Phase III)
Period of ejection during which the systolic pressure increases further because of additional ventricular contraction, and the ventricular volume decreases by 70 mL (which is the stroke volume)
Phases of the Cardiac Cycle (Phase IV)
period of isovolumic relaxation during which the ventricular volume remains at 45 mL, but the intraventricular pressure decreases to its diastolic pressure level
Preload - end-diastolic pressure
Afterload - the pressure in the artery exiting the ventricle (aorta or pulmonary artery)
what determines oxygen consumption by the heart?
cardiac work
mainly the volume-pressure type of work
this oxygen consumption has also been found to be proportional to the tension of the heart multiplied by the time the tension is maintained
wall tension in the heart is proportional to the pressure times the diameter of the ventricle. Ventricular wall tension increases at high systolic pressures or when the heart is dilated
what intrinsically regulates cardiac pumping ability?
the Frank-Starling Mechanism
Frank-Starling Mechanism of the heart
within physiological limits, the heart pumps all the blood that comes to it without allowing excess accumulation of blood in the veins.
- alternate wording- when venous return of blood increases, the heart muscle stretches more, which makes it pump with a greater force of contraction.
the extra stretch of the cardiac muscle during increased venous return, within limits, causes the actin and myosin filaments to interdigitate at a more optimal length for force generation
more stretch of the right atrial wall causes a reflex increase in the heart rate of 10% - 20% which helps the heart pump more blood
what happens to the heart when there is strong sympathetic stimulation?
the heart rate of an adult increases from a resting value of 72 beats per minute up to 180 - 200 beats per minute, and the force of the contractions of the heart increase dramatically
sympathetic stimulation therefore can increase cardiac output 2-3 fold
what happens to the heart when the sympathetic system is inhibited?
heart rate decreases and the force of contraction of the heart and cardiac output decreases
how does parasympathetic stimulation affect the heart?
it mainly affects the atria and can decrease the heart rate dramatically and the force of contraction of the ventricles slightly. The combined effect decreases cardiac output by 50% or more
what factors affect cardiac contractility?
- extracellular electrolyte concentrations - excess potassium in extracellular fluid causes the heart to become flaccid and reduces the heart rate, causing a large decrease in contractillity; excess calcium in the extracellular fluid causes the heart to go into spastic contraction; a decrease in calcium ions causes the heart to become flaccid
Heart and its rhythmical impulses
the heart has a special system for self-excitation of rhythmical impulses to cause repetitive contraction of the heart
this system conducts impulses through the heart and causes the atria to contract 1/6 of a second before the ventricles (allows extra filling of the ventricles before contraction)
Sinoatrial Node (Sinus Node)
initiates the cardiac impulse and controls the rate of beat of the entire heart
internodal pathway
conducts impulses from the sinus node to the atrioventricular node
A-V Node
delays impulses from the atria to the ventricles
- this allows the atria to empty their contents into the ventricles before ventricular contraction occurs
- a delay of .09 second occurs between the A-V node and the A-V bundle (slow velocity 1/12 that of normal cardiac muscle
- b/c 1) membrane potential is much less negative in the A-V node and bundle than in normal cardiac muscle and 2) few gap junctions exist between the cells in the A-V node and bundle, so the resistance to ion flow is great
A-V Bundle (bundle)
delays impulses and conducts impulses from the A-V node to the ventricles
Bundles of Purkinje Fibers (right and left)
conduct impulses to all parts of the ventricles
Sinus Node membrane potential
the membrane potential of a sinus node fiver is -55 to -60 millivolts compared with -85 to -90 millivolts in a ventricular muscle fiber
Action Potential in the Sinus Node
- fast sodium channels are inactivated at the normal resting membrane potential, but there is slow leakage of sodium into the fiber
- between action potentials the resting potential gradually increases because of this slow leakage of sodium until the potential reaches -40 milivolts
- then the calcium-sodium channels become activated, allowing rapid entry of calcium and sodium, but especially calcium (causes an action potential)
- greatly increased #s of potassium channels open within about 100-150 milliseconds after the calcium-sodium channels open, allowing potassium to escape from the cells. This returns the membrane potential to its resting potential, and the self-excitation cycle starts again (with sodium leaking slowly into the sinus nodal fibers)
what transmits pathways in the atrium?
internodal and interatrial pathways
Parts of the internodal pathway
- anterior internodal pathway
- middle internodal pathway,
- and posterior internodal pathway
- all carry impulses from the sinoatrial node to the A-V node.
- Small bundles of atrial muscle fibers transmit impulses more rapidly than the normal atrial muscle
- anterior interatrial band - conducts impulses from the right atrium to the anterior part of the left atrium
Rapid transmission of impulses throught the Purkinje System and Cardiac Muscle
the purkinje fibers lead from the A-V node, through the A-V bundle, and into the ventricles
- the A-V bundle lies just under the endocardium and receives the cardiac impulse first.
the A-V bundle then divides into the left and right bundles
Charachteristics of the purkinje system
- action potentials at 6 times the velocity found in cardiac muscle
- high permeability of gap junctions at the intercalated discs between the purkinje fiber cells likely causes the high velocity of transmission
Atrial and Ventricular Syncytia (separate and insulated from one another)
the atria and ventricles are separated by a fibrous barrier that acts as an insulator, forcing the atrial impulses to enter the ventricles through the A-V bundle.
spread of action potential to ventricular muscle
purkinje fiber lie just under the endocardiun, so the action potential spreads into the rest of the ventricular muscle from this area.
thente cardiac impulses travel up the spirals of the cardiac muscle and finally reach the epicardial surface
why is the sinus node the pacemaker?
it discharges faster than the other tissues in the cardiac conduction system
when the sinus node discharges, it sends impulses to the A-V node and Purkinje fibers and thereby discharges them before they can discharge intrinsically
the tissues and sinus node thenrepolarize at the same time, but the sinus node looses its hyperpolarization faster and discharges again before the A-V node and Purkinje fibers can indergo self-excitation
ectopic pacemaker
when some cardiac tissue develops a rhythmical rate faster than that of the sinus node
most common location of the new pace maker is the A-V node or penetrating portion of the A-V bundle
A-V Block (stokes-adams syndrome)
during A-V block, the atria beat normally, but the ventricular pacemaker lies in the purkinje system, which normally discharges at a rate of 15 to 40 beats per minute. After a sudden block, the Purkinje system doesn’t emit its rhythmical impulses for 5-30 seconds because it has been overdriven by the sinus rhythem.
during this time, the ventricles fail to contract, and the person may faint due to lack of cerebral blood flow
Stimulation of the parasympathetic (vagal) nerves to the heart releases what neurotransmitter?
acetylcholine
What are the effects of Acetylcholine?
- the rate of sinus node discharge decreases
- the excitability of the fibers between the atrial muscle and the A-V node decreases
Vagal Stimulation and Heart Rate
the heart rate decreases to 1/2 normal under mild or moderate vagal stimulation, but
- strong stimulation can temporarily stop the heart beat, resulting in a lack of impulses traversing the ventricles.
- under these conditions, the Purkinje fibers develop their own rhythem at 15-40 beats per minute (ventricular escape)
what are the mechanisms of vagal effects on the heart?
- Acetylcholine increases the permeability of the sinus node and A-V junctional fibers to potassium, which causes hyperpolarization of these tissues and makes them less excitable
- the membrane potential of the sinus nodal fibers decreases from -55 to -60 millivolts to -65 to -75 millivolts
the normal upward drift in membrane potential that is caused by sodium leakage in these tissues requires a much longer time to reach the threshold for self-excitation.
what are the effects of stimulation of the sympathetic nerves to the heart ?
- rate of sinus node discharge increases
- cardiac impulse conduction rate increases in all parts of the heart
- force of contraction increaeses in both atrial and ventricular muscle