The Heart (EXAM 2)

Ventricular Ejection Phase

-Blood movement: Form ventricles to the great vessel arteries -Ventricles are in systole -Atria are diastole -AV valves are closed to prevent black flow -SL valves: closed to open -Sounds: none -Volume: ESV; end-systolic volume (50mL)

Isovolumetric Relaxation Phase: Volume is not changing

-Blood movement: No net movement -Ventricle: diastole -Atria: diastole -AV valves: Closed -SL valves: open to closed -Sound: S2 -Volume: ESV

Describe the steps of an action potential in a pacemaker cell, including which ion channels are involved in each step.

1. Slow initial depolarization phase: more cations leak in than leak out through nonspecific cation channels in the plasma membrane, causing the membrane to slowly depolarize to threshold 2. Full depolarization phase: at threshold, voltage-gated Ca2+ channels open, and Ca2+ enter the cell, causing the membrane to fully depolarize 3. Repolarization phase: Ca2+ channels close and voltage-gated K+ channels open, causing K+ outflow and membrane repolarization 4. Minimum potential phase: K+ channels remain open, and the membrane hyperpolarizes. This opens nonspecific cation channels, and the cycle repeats

Based on what you already know about the effects of aldosterone, ADH, and ANP on blood volume, what would you expect the effects of each to be on cardiac output? Aldosterone: ADH: ANP:

Aldosterone: increase ADH: increase ANP: decrease

Cardiac muscle cells have lots of myoglobin (an O2-transporting protein) and many more mitochondria than skeletal muscle cells. Why do you think this might be?

Higher energy demand

Why is it important that the atria and ventricles don't contract at the same time? What electrophysiological phenomenon makes this possible?

So ventricles can fill with as much blood as possible before contracting AV node delay

Define autorhythmicity.

Setting own rhythm without a need for input from the nervous system.

Name the three populations of pacemaker cells that are part of the cardiac conduction system

Sinoatrial node (SA node) Atrioventricular node (AV) Purkinje Fiber System (atypical pacemakers)

Atrioventricular node (AV):

cluster of pacemaker cells located posterior and medial to the tricuspid valve. Intrinsic rate of 40 action potentials per minute

Explain why the atria and ventricles are not in systole at the same time.

The atria and ventricles are not in systole at the same time due to the AV node delay, which allows the ventricles to fill up with blood. The left and right ventricles are in systole at the same time and the left and right atria are in systole at the same time.

Afterload

against which the heart pumps as it contracts (involves ESV) -As afterload increases the stroke volume will decrease (inversely proportional)

Fibrillation

electrical activity in the heart essentially goes haywire, causing parts of the heart to depolarize and contract while others are repolarizing and not contracting

Bradycardia

is a heart rate under 60 beats per minute

Sinus tachycardia

is a regular but fast rhythm. The sinus bradycardia is a regular but slow rhythm.

Ventricular fibrillation

is immediately life threatening and is described as chaotic on an ECG. it is treated with defibrillation in which the SA node will resume pacing the heart.

R-R interval

is is the entire duration of a cardiac action potential. It can be measured to determine heart rate.

Atrial fibrillation

is not life threatening, and has an irregular rhythm with no p waves.

End systolic volume (ESV)

is the amount of blood in the ventricles after ventricular systole. The average volume is 50 mL of blood, which means about 70 mL is pumped from each ventricle. The ventricular ejection phase and the isovolumetric relaxation phase have an ESV volume.

Q-T interval

is the entire duration of a ventricular action potential.

End diastolic volume (EDV)

is the ventricular volume after ventricular diastole. The average volume is 120 mL of blood. The ventricular filling phase and the isometric contraction phase have an EDV volume.

Sinoatrial node (SA node):

located in upper right atrium slightly inferior and lateral to the opening of the superior vena cava. HAs the fastest intrinsic rate of depolarization, about 60 or more times per minute, a rate that is influenced from the sympathetic and parasympathetic nervous system.

Heart block at the AV node

makes the P-R interval on the ECG longer than normal, and there's more p waves (SA nodes are not being conducted through the AV node). Heart blocks can also widen the QRS complex.

The QRS complex

represent ventricular depolarization. Q and S are downwards deflections and R is a large upward deflection. Atrial repolarization is occurring during this time but it is masked by this complex. The QRS complex is larger than the p wave because the ventricles are larger.

P Wave

represents the atrial depolarization of the heart (except the SA node). The p wave is followed by a flat segment that represents the time period where the SA node depolarizes.

T wave

represents ventricular repolarization.

S-T segment

s flat and represents the ventricular plateau phase.

Stroke Volume (SV)

the amount of blood pumped in one heartbeat

P-R interval

the duration atrial depolarization and AV node delay, and the time it takes for the depolarization of the SA node to spread through the atria and ventricles.

Preload

the length or degree imposed on the heart before it contracts (involves EDV) -Increased preload= increased stroke volume

Ejection fraction

the percentage of blood (out of the total amount) that is ejected with each ventricular systole, and is equal to the stroke volume divided by the EDV.

Ventricular Filling Phase:

-Blood movement: from the atrium into the ventricles -Ventricle is relaxed/diastole -Atria, Start relaxed and when 80% of blood move passively then they will go into systole to push the last 20% to ventricle -AV: during is phase the valves switch from closed to open -SL: closed -Sounds: no hear sounds -Volume in ventricles at the end of the phase: maximum amount of blood; EDV: end-diastolic volume: when ventricles are done relaxing before they contract (120mL of blood)

Similarities of Skeletal and cardiac muscle cells

-Have striations (alternating light and dark bands) -transverse tubules and sarcoplasmic reticulum -Function to generate tension through the sliding-filament mechanism. -Voltage-gated sodium ion channels, calcium ion channels, and potassium ion channels.

Isovolumetric Contraction Phase: The volume doesn't change (shortest phase)

-No blood movement -ventricles are now in systole -atrium: are relaxed/ diastole -SL valves: closed -AV valves: go from open to closed -Heard sound: S1 -Volume: EDV

During how many of the phases of the cardiac cycle are the atria in systole? 1 2 3 4

1

Describe the steps of an action potential in a contractile cell, including which ion channels are involved in each step.

1. Rapid depolarization phase: voltage-gated Na+ channels activate and Na+ enter, rapidly depolarizing the membrane 2. Initial repolarization phase: Na+ channels are inactivated and some K+ channels open; K+ leak out, causing a small initial repolarization 3. Plateau phase: Ca2+ channels open and Ca2+ enter as K+ ext, prolonging the depolarization 4. Repolarization phase: Na+ and Ca2+ channels close as K+ continues to exit, causing repolarization

Trace an action potential from its origin in the sinoatrial node through the ventricles, including the names of all the intermediate conducting structures.

1. The SA node generates an action potential, which spreads via gap junctions to atrial cells and the AV node. 2. After the AV node delay, the action potential is conducted to the AV bundle and then to the right and left bundle branches 3. The action potential spreads from the bundle branches along the purkinje fibers to the contractile cells of the ventricles.

Your patient has a heart rate of 100 bpm, an EDV of 150 mL, and an ESV of 80 mL. What would their cardiac output be?

7000 mL/min

Define the AV node delay and explain its importance.

AV node delay is a slow conduction that last about 0.13 seconds. The time it takes for the action potential to spread from the SA node to the AV bundle allows the atria to depolarize (and contract) before the ventricles, giving the ventricles time to fill with blood. It also helps to prevent current from flowing backward into the atria. "ensures that the atria have ejected their blood into the ventricles first before the ventricles contract."

During which phase of the cardiac cycle do the AV valves close? What about the semilunar valves?

AV valves - isovolumetric contraction phase Semilunar valves - isovolumetric relaxation phase

Explain how the sympathetic and parasympathetic divisions of the autonomic nervous system affect cardiac output. Make sure to include whether each one is an inotropic agent, chronotropic agent, or both, and the mechanisms by which they each affect cardiac output.

An increase in the parasympathetic nervous system causes a decreases in cardiac output. The parasympathetic nervous system is a weak negative inotropic agent and a strong negative chronotropic agent. An increase in the sympathetic nervous system causes an increase in cardiac output. The sympathetic nervous system is a strong positive chronotropic agent and a strong positive inotropic agent.

Describe the overall importance of intercalated discs in terms of cardiac function.

Cardiac muscle cells also have intercalated discs which join pacemaker cells to contractile cells and contractile cells to one another. -Contain desmosomes: hold the cardiac muscle cells together -Gap junctions: allow ion to rapidly pass from one cell to another

Given the appropriate inputs, calculate stroke volume and cardiac output.

Cardiac output= heart rate x stroke volume Cardiac Output average= 72 bpm x 70 mL/b= 5L/min Stroke volume average= end diastolic volume - end systolic volume SV= 120 mL - 50 mL = 70 mL per beat

Differentiate between the functions of cardiac pacemaker and cardiac contractile cells.

Cardiac pacemaker cells coordinate the electrical activity of the heart. Will spontaneously and rhythmically generate action potentials that trigger contractile cells which contract in response.

Define diastole and systole.

Diastole: relaxation period Systole: contraction period

Describe how catecholamines, thyroid hormone, glucagon, aldosterone, ADH, and ANP affect cardiac output (e.g. will they increase or decrease it). Identify which aspect of cardiac output they will directly affect (e.g. heart rate, contractility, preload).

Epinephrine and Norepinephrine: increase HR and SV Thyroid hormone: increase HR and SV Glucagon: increase HR and SV Aldosterone & ADH: increase blood volume, preload, SV and cardiac input ANP: decrease blood volume, preload, SV and cardiac input

True or False? The initial depolarization of pacemaker cells is slower than in contractile cells because the potassium ion channels open slower.

False

Tachycardia

HR over 100 beats per minutes

Define heart failure, describe how heart failure would affect stroke volume and cardiac output, and give an example of a common side effect of heart failure.

Heart failure is anything that impairs the heart to function as a pump. Examples of heart failure include Myocardial infarctions, problems with the valves, or diseases of the heart muscles. Heart failure decreases stroke volume and cardiac output. A common side effect is edema, because the blood is pooling and not moving through the circuit very well. In the pulmonary circuit there will be edema in the lungs, and in the systemic circuit there will be buildup in the legs.

Given a combination of nervous system activity, hormones, and/or other physiological factors, predict the effects on cardiac output.

Hormones that cause retention from the kidneys: Increases preload, stroke volume and cardiac output Increase in sympathetic nervous system activity, positive inotropic and/or chronotropic hormones: increases contractility, stroke volume and cardiac output Increase body temp: increase heart temp and cardiac output Hormones that decrease fluid retention from the kidneys: decreases preload, stroke volume and cardiac output Increase parasympathetic nervous system activity: decrease heart rate and cardiac output Decrease body temp: decreases heart rate and cardiac output

Given a combination of increasing or decreasing preload, contractility, and afterload, predict how stroke volume would change as a result.

Increased preload= increased stroke volume / Decrease preload= decreased SV Increased contractility= increased SV / decrease contractility= decreased SV Increased afterload= decrease SV / Decreased afterload= increased SV

Define inotropic agent and chronotropic agent, and list examples of each.

Inotropic agents affect contractility, while chronotropic agents affect heart rate. The sympathetic nervous system is is a strong positive inotropic agent and the parasympathetic nervous system is a weak negative inotropic agent. The parasympathetic nervous system is a strong negative chronotropic agent and the sympathetic nervous system is a strong positive chronotropic agent.

Describe the Frank-Starling Law.

It is the relationship between preload and stroke volume. -The more the ventricular muscle cells are stretched, the more forcefully they contract. -Stretching causes a more optimal overlap of the actin and myosin filaments in the muscle cells, which enable a stronger contraction and a higher stroke volume. This relationship ensures that the volume of blood discharged from the heart is equal to the volume that enters it.

Which ventricle would face higher afterload on a regular basis?

Left ventricle

Why of the following ion channels was not found in cardiac contractile cells? A. Sodium B. Potassium C. Non-specific Cation D. Calcium

Non-specific Cation

List other physiological factors besides the nervous system and endocrine system that can affect cardiac output.

Other factors that affect cardiac output include the concentration of certain electrolytes in the extracellular fluid, body temperature, physical fitness, and age.

Which of the following populations of pacemaker cells would be unable to set the heart rate long-term? A. Sinoatrial (SA) node B. Atrioventricular (AV) node C. Purkinje fiber system

Purkinje fiber system

Explain how changes in pressure within the heart lead to the opening and closing of the heart valves, as well as movement of the blood within the heart and out of the heart into the great vessels.

Relaxed Left Ventricle -Pressure from the blood in the left atrium pushed the mitral valve open, allowing blood in the left atrium to drain into the relaxed ventricle -Pressure from the blood flowing backward in the aorta closes the aortic valve Contracted Left Ventricle -High pressure in the ventricle pushes the blood up to the mitral valve, closing it. -High pressure in the ventricle causes blood flow that pushes the aortic valve open

List the common heart sounds and identify the cause of each, including which valves are involved.

S1: AV valves close (mitral and tricuspid valves) S2: SL valves closing (pulmonary and aortic valve)

Cardiac output (CO):

The amount of blood pumped into the pulmonary and systemic circuit in 1 minute

Are signals from the sympathetic nervous system inotropic agents, chronotropic agents, or both? What about the parasympathetic nervous system?

Sympathetic: Strong agents for both Parasympathetic: Strong chronotropic agent, weak inotropic

Describe the two factors that influence EDV.

The length of time the ventricle spends in diastole The amount of blood returning to the right ventricle from the systemic circuit, a quality called venous return.

Identify whether pacemaker or contractile cells are more numerous in the heart.

There are more contractile cells in the heart (99%)

Compare the maximum pressures achieved by the right and left ventricles during the cardiac cycle, and explain why they are different.

The pressure in the pulmonary trunk varies between about 10 and 28 mm Hg. This means that the maximum pressure the right ventricle has to generate in order to push open the pulmonary valve and eject blood is about 28 mm Hg. The pressure in the aorta is considerably higher due to the higher overall blood pressure in the systemic circuit and ranges from 80-118mm Hg. For this reason the left ventricle has to squeeze significantly harder to generate the pressure needed to open the aortic valve and eject blood into the aorta.

Explain the importance of having a long refractory period in a contractile cell.

The refractory period is the period where the cells can't repolarize again. This is important because it allows the heart to relax and the ventricles is able to refill with blood again before they contract.

List the three factors that affect stroke volume

The three factors that affect stroke volume are preload, contractility and afterload.

Compare and contrast the types of ion channels found in pacemaker and contractile cells.

They both have channels for calcium and potassium. They both repolarize and depolarize. Repolarization is pretty quick in both. Pacemaker cells have a non specific cation channel Contractile cells have a sodium channels.

Why might it be important for cardiac contractile cells to have a long refractory period?

To allow time for the chambers of the heart to fill with blood

True or False? Pacemaker cells have no resting membrane potential, but contractile cells do.

True

Why do you think that the QRS complex is so much larger in magnitude than the P wave?

Ventricles are much larger than the atria

Describe how ventricular fibrillation and asystole are treated.

Ventricular fibrillation: treated by defibrillation and electric shock to the heart. The shock depolarizes all ventricular muscle cells simultaneously and throws the cells into refractory periods. The SA node will resume pacing the heart after the shock is delivered Asystole: is treated with CPR and pharmacological agents that stimulate the heart such as atropine and epinephrine

Four phases of the cardiac cycle

Ventricular filling Isovolumetric ventricular contraction Ventricular ejection Isovolumetric ventricular relaxation

Skeletal Muscle cells action potential

a rapid depolarization phase followed by a rapid repolarization phase. Skeletal muscles will go from a membrane potential of -85 to 20 and back to -85.

Contractility

ability to create tension (involve ESV) -The greater the ability of the heart to contract and pump the higher the stroke volume and cardiac output are

Heart block

blockage along the cardiac conduction system

Heart rate (HR)

cardiac cycles of beats per minute

Asystole

flat-lining

Cardiac pacemaker cells action potential

go from a membrane potential of -60 to -40 to 10 to -40 back down to -60. To start this action potential, the cell becomes hyperpolarized (-60) and then slowly begins depolarizing (-40). It then moves into its full depolarization phase (10) and repolarization phase (-40) but it is slower than in skeletal muscles. The cell then finishes by hyperpolarizing (-60).

Cardiac contractile cells action potential

similar to skeletal muscles because they have a rapid depolarization from a membrane potential of -85 to 20, but they differ after that. Cardiac contractile cells have an initial repolarization phase, followed by a plateau phase (called the refractory period) before the cell can repolarize.

Purkinje Fiber System (atypical pacemakers):

slowest cells that depolarize only about 20 times per minute. Their action channels rely on different ion channels and they function in a different way. There are three components: -AV bundle: penetrates the heart's fibrous skeleton in the inferior interatrial septum and the superior interventricular septum -The right and left bundle: course along the right and left side of the interventricular septum -Terminal branches: penetrate ventricles and finally come into contact with the contractile cardiac muscle cells