the heart Flashcards

1
Q
  1. Compare and contrast the microscopic anatomy of cardiac muscle vs. skeletal muscle fibers.
A

Both
- Striated and contract by the sliding filament mechanism

Cardiac muscle

  • Cells are short, fat, branched, and interconnected
  • Each fiber contains one or two large, pale, centrally located nuclei
  • Intercellular spaces are filled with a loose connective tissue matrix (endomysium) containing numerous capillaries - this matrix connects to the fibrous cardiac skeleton, which acts as a tendon and an insertion - gives cardiac cells something to pull or exert their force against

Skeletal muscle

  • Cells are long cylindrical, multinucleate - nuclei are just underneath the plasma membrane
  • Cells are all independent of each other both structurally and functionally
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2
Q
  1. Name and describe the special intercellular junctions present in cardiac muscle tissue.
A

Intercalated discs: contain desmosomes (prevent adjacent cells from separating during contraction) and gap junctions (allow ions to pass from cell to cell, transmitting current across the entire heart)

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3
Q
  1. What is the functional significance of these junctions (#16)?
A
  • The gap junctions allow ions to pass from, transmitting current across the entire heart
  • Desmosomes prevent adjacent cells from separating during contraction
  • The gap junctions electrically couple cardiac cells, therefore the myocardium behaves as a single coordinated unit/functional syncytium
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4
Q
  1. What is the significance of the large numbers of mitochondria and the rich blood supply to cardiac muscle tissue?
A

The large numbers of mitochondria make the cardiac cells highly resistant to fatigue

The rich blood supply to cardiac muscle tissue probably delivers O2 to the mitochondria to keep the cardiac muscle functioning - the heart relies almost exclusively on aerobic respiration, so cardiac muscle cannot operate effectively for long without oxygen → damage to myocardium would be from a lack of oxygen (therefore, need a rich blood supply)

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5
Q
  1. What is a functional syncytium? Identify the functional syncytia of the heart.
A

Functional syncytium: myocardium having as a single coordinated unit

Atrial syncytia and ventricular syncytia

Gap junctions tie cardiac muscle cells together to form a functional syncytium. This allows the wave of depolarization to travel from cell to cell across the heart. As a result, either all of the fibers in the heart contract as one unit or the heart does not contract at all

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6
Q
  1. Describe the three main functional differences between skeletal and cardiac muscle.
A

Means of stimulation

  • Certain cardiac muscle fibers exhibit autorhythmicity or automaticity. Some cardiac muscle cells are self excitable. The heart contains 2 kinds of myocytes, one being the contractile cardiac muscle cell responsible for the heart’s pumping activity. However, certain locations in the heart contain special noncontractile cells (pacemaker cells) that spontaneously depolarize. ← automaticity or autorhythmicity
  • Because heart cells are electrically joined together by gap junctions, these cells can initiate both their own depolarization and the rest of the heart. No neural input is required
  • Skeletal muscle fibers must be stimulated by a nerve ending to contract

Syncytium vs motor unit

  • All the fibers in the heart contract as a unit or the heart doesn’t contract at all
  • In skeletal muscle, impulses do not spread from cell to cell. Only skeletal muscle fibers that are individually stimulated by nerve fibers contract. The strength of contraction increases as more motor units are recruited
  • Such recruitment doesn’t happen in the heart because it acts as a single huge motor unit

Length of absolute refractory period

  • Absolute refractory period is the period of time during an action potential when another action potential cannot be triggered - ion channels are not prepared to open and thus cells cannot be excited
  • In skeletal muscle, the absolute refractory period is much shorter than the contraction, allowing multiple contractions to summate (tetanic contractions)
  • If the heart were to contract tetanically, it would be unable to relax and fill, therefore useless as a pump. To prevent this, the absolute refractory period in the heart is nearly as long as the contraction itself
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7
Q
  1. Identify (in order) the components of the heart’s conduction system.
A

The sinoatrial (SA) node generates the impulses → the impulses pause (0.1 s) at the atrioventricular (AV) node → the atrioventricular (AV) bundle connects the atria to the ventricles → the right and left bundle branches conduct the impulses through the interventricular septum → the subendocardial conducting network/Purkinje fibers depolarize the contractile cells of both ventricles

  1. The Sinoatrial (SA) node (in the right atrial wall) generates impulses and sets the pace for the heart as a whole (bc no other region of the conduction system or myocardium has a faster depolarization rate). This makes the SA node the heart’s pacemaker, and its characteristic rhythm (sinus rhythm) determines heart rate
  2. From the SA node, the depolarization wave spreads via gap junctions throughout both atria and via the internodal pathway to the atrioventricular (AV) node (in inferior portion of the interatrial septum). At the AV node, the impulse is delayed for about 0.1 seconds (allows the atria to respond and complete their contraction before the ventricles contract). Once through the AV node, the signaling impulse passes rapidly through the rest of the system
  3. From the AV node, the impulse sweeps to the atrioventricular (AV) bundle/bundle of His (in superior part of the interventricular septum). The AV bundle is the only electrical connection between the atria and ventricles (they are not connected by gap junctions).
  4. The AV bundle persists briefly, then splits into two pathways - the right bundle branches and the left bundle branches (course along the interventricular septum toward the heart apex)
  5. The subendocardial conducting network/Purkinje fibers (long strands of barrel-shaped cells with few myofibrils) completes the pathway through the interventricular septum, penetrates into the heart apex, and then turns superiorly into the ventricular walls. The right and left bundle branches excite the septal cells, but the bulk of ventricular depolarization depends on the large fibers of the conducting network and cell-to-cell transmission of the impulse via gap junctions between the ventricular muscle cells. Since the left ventricle is much larger than the right, the subendocardial conducting network is more elaborate in left ventricle than the right ventricle
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8
Q
  1. What are autorhythmic cells?
A

Autorhythmic cells are cardiac pacemaker cells - have the ability to depolarize spontaneously (their unstable resting potential that continuously depolarizes, drifting slowly toward threshold) and thus pace the heart

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9
Q
  1. What is a pacemaker potential? Why are pacemaker potentials important?
A

Pacemaker potentials are the spontaneously changing membrane potentials generated by cardiac pacemaker cells. Cardiac pacemaker cells have the special ability to depolarize spontaneously and thus pace the heart. Pacemaker cells have an unstable resting potential that continuously depolarizes, slowly drifting toward threshold ← pacemaker potentials

Pacemaker potentials initiate the action potentials that spread throughout the heart to trigger its rhythmic contractions

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10
Q
  1. How is a pacemaker potential generated (i.e., what ion channels are involved and at what point do the channels open/close)?
A
  1. In the sarcolemma, hyperpolarization at the end of an action potential both closes K+ channels and opens Na+ channels. The Na+ influx alters the balance between K+ loss and Na+, and the membrane interior becomes more positive (e.g. -60 mV to -40 mV)
  2. At threshold (about -40 mV), Ca2+ channels open, allowing entrance of Ca2+ from extracellular space. This influx of Ca2+ (rather than Na+) produces the rising phase of the action potential and reverses the membrane potential in pacemaker cells ← depolarization
  3. During the falling phase of action potential, Ca2+ channels inactivate. The falling phase of the action potential and repolarization reflect opening of K+ channels and K+ efflux from the cell, bringing the membrane potential back to its most negative voltage ← repolarization
  4. Once repolarization is complete, K+ channels close, K+ efflux declines, and the slow depolarization to threshold begins again
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11
Q
  1. What part of the myocardium normally has the fastest spontaneous depolarization rate?
A

SA node;

Bc it has the fastest spontaneous depolarization rate, it generates impulses and sets the pace for the heart as a whole

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12
Q
  1. What is the functional significance of the 0.1 second delay in impulse transmission at the AV node?
A

The 0.1 second delayed impulse allows the atria to respond and complete their contraction before the ventricles contract

This delay reflects the smaller diameter of the fibers here and the fact that they have fewer gap junctions for current flow → the AV node conducts impulses more slowly than other parts of the system (think cars forced to merge from 4 lanes to 2)

When the atria contract, blood gets pushed into the ventricles

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13
Q
  1. What is the function of the Purkinje fibers?
A

Purkinje fibers/subendocardial conducting network does the bulk of ventricular depolarization (and kind of ventricular contraction, b/c ventricular contraction happens almost immediately after the ventricular depolarization wave)

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14
Q
  1. What part of the heart is excited by the left and right bundle branches?
A

The septal cells of the interventricular septum

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15
Q
  1. What part of the conduction system serves as the sole electrical connection between the atria and the ventricles?
A

The AV bundle

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16
Q
  1. What is the normal pacemaker of the heart?
A

The SA node

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17
Q
  1. Compare and contrast the action potential of skeletal and cardiac muscle cells.
A

The action potential and contractile phase lasts much longer in cardiac muscle than in skeletal muscle. In skeletal muscle, the action potential typically lasts 1-2 ms, and the contraction for a single stimulus 15-100 ms. In cardiac muscle, the action potential lasts 200 ms or more because of the plateau, and tension development persists for 200 ms or more. This long plateau in cardiac muscle has 2 consequences…

  1. Ensures that the contraction is sustained so that blood is ejected efficiently from the heart
  2. Ensures that there is a long refractory period so that tetanic contractions can’t occur and the heart can fill again for the next beat
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18
Q
  1. In cardiac muscle, what are the sources of Ca2+ which trigger contraction?
A

10-20% of Ca2+ required for contraction come through the plasma membrane from the extracellular space. Once in the plasma membrane, this triggers Ca2+ influx → stimulates opening of Ca2+ ion release channels of the sarcoplasmic reticulum - SR is where the other 80-90% of Ca2+ comes from (and maybe mitochondria too)

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19
Q
  1. What produces the plateau phase of a cardiac muscle fiber’s action potential? What is the functional significance of the plateau phase?
A

First, depolarization opens a few fast voltage-gated Na+ channels that depolarize the cell very quickly. As Na+-dependent membrane depolarization occurs, the voltage change also opens channels (called slow Ca2+ channels) that allow Ca2+ to enter from the extracellular fluid. The Ca2+ surge across the sarcolemma prolongs the depolarization, producing a plateau in the action potential tracing. Not many voltage-gated K+ channels are open yet, so the plateau is prolonged

As long as Ca2+ is entering, the cells continue to
contract and be depolarized. Muscle tension develops during the plateau and peaks just after the plateau ends

Ensures that the contraction is sustained so that blood is ejected efficiently from the heart.

Ensures that there is a long refractory period, so that tetanic contractions cannot occur and the heart can fill again for the next heart beat.

20
Q
  1. How does the all-or-none law relate to cardiac muscle?
A

Can refer to the syncytium - all of a syncytium will either contract or not contract

21
Q
  1. When does the refractory period in cardiac muscle end? What is the functional significance of this long refractory period?
A

After about 200 ms due to slow Ca2+ channels closing and opening of slow K+ channels opening

Long refractory period prevents tetanic contractions → allows the heart to fill with blood for the next contraction

22
Q
  1. Define ECG.
A

An electrocardiogram/ECG is a graphic record of heart activity. An ECG is a composite of all the action potentials generated by nodal and contractile cells at a given time - NOT a tracing of a single action potential

23
Q
  1. Name the three important waves/deflections of a normal ECG tracing and describe what each represents.
A

P wave - small, lasts about 0.08 s and results from movement of the depolarization wave from the SA node through the atria. About 0.1 s after the P wave begins, the atria contract

QRS complex - large, results from ventricular depolarization and precedes ventricular contraction. It’s shape is complicated because the paths of the depolarization waves through the ventricular walls change continuously, producing corresponding changes in current direction. The time required for each ventricle to depolarize depends on its size relative to the other ventricle. The average duration of the QRS complex is 0.08 s. Q wave = depolarization of interventricular septum. R wave = depolarization of the main mass of the ventricles. S wave = the last stage of ventricular depolarization near the base of the heart.

T wave - caused by ventricular repolarization, typically lasts about 0.16 s. Repolarization is slower than depolarization, so the T wave is more spread out and has a lower amplitude (height) than QRS complex. Because atrial repolarization takes place during the period of ventricular excitation, the wave representing atrial repolarization is normally obscured by the large QRS complex being recorded at the same time

24
Q
  1. What is the duration of a normal PR interval? What might a prolonged P-R interval indicate?
A

The duration of a normal PR interval is about 0.16 s

P-R interval is the time from the beginning of atrial excitation to the beginning of ventricular excitation. The PR interval includes atrial depolarization and contraction as well as the passage of the depolarization wave through the rest of the conduction system

A prolonged PR interval would indicate AV node blockage

25
Q
  1. What is the duration of a normal QRS complex? What might a prolonged QRS complex indicate?
A

The duration of a normal QRS complex is about 0.08 s

Prolonged QRS= bundle branch block or hyperkalemia
because it increases K which slows down depolarization because it inactivates Na

26
Q
  1. What cardiac event/activity is represented by the S-T segment? What is the clinical significance of an elevated or depressed S-T segment?
A

The action potentials of the ventricular myocytes are in their plateau phases, the entire ventricular myocardium is depolarized

An ST segment that is elevated or depressed indicates cardiac ischemia (lack of blood flow and oxygen to the heart muscle)

27
Q
  1. Describe the pressure changes in the heart which cause the valves to open and close.
A

Atria starts to relax, so ventricles begin to contract → ventricular pressure rises sharply (b/c walls close in on the blood in ventricles due to contraction) → AV valves close (split-second period of time when ventricles are completely closed and blood volume in chambers remains constant as the ventricles contract (b/c AV valves are closed) = isovolumetric contraction phase) → ventricular pressure continues to rise until it exceeds the pressure in the large arteries (e.g. aorta and pulmonary trunk) → SL valves are forced open (this is when isovolumetric stage ends) → blood rushes from ventricles to aorta and pulmonary trunk (ventricular ejection phase)
During brief phase following the T wave, ventricles relax → ventricular pressure drops rapidly (b/c chambers are no longer compressed) and blood in aorta and pulmonary trunk flows back toward the heart → SL valves close

28
Q
  1. Identify the three main phases of the cardiac cycle.
A
  1. Atrial systole
  2. Ventricular systole
  3. Relaxation period of the heart
29
Q
  1. Describe the events associated with each of the above phases (#42), making note of changes in atrial & ventricular pressure, opening/closing of valves, ventricular volume changes, and correlation between cardiac events and the ECG.
A

Atrial systole
- At the beginning of atrial systole, the ventricles are filled to about 70% of their normal capacity due to passive flow of blood through the open AV valves. The AV valve flaps begin to drift close, setting the stage for atrial systole. At the end of P wave (depolarization), atria contracts, causing a slight rise in atrial pressure which pushes the residual blood from atria into the ventricles. At the end of atrial systole, ventricles hold ~120 ml of blood- this is called the end diastolic volume (max volume of blood ventricles contain in the cycle). Atria then relax and atrial diastole persists throughout the rest of the cycle while the ventricles depolarize (QRS complex)

Ventricular systole
- Begins as atrial systole ends. Atria start to relax → ventricles begin contracting and ventricular pressure rises. AV valves close when ventricular pressure becomes greater than atrial pressure—AV valve closure marker beginning of isovolumic contraction. The isovolumic contraction phase is when all the valves are closed and the ventricles are contracting/closing in on the blood in the ventricles and blood volume in chambers is constant. Ventricular contraction continues and pressure becomes greater than the pressure in the large arteries (aorta and pulmonary trunk) leaving the ventricles. SL valves open, marks the beginning of ejection phase. At the end of the ventricular contraction, the ventricles hold approx. 50 ml of blood aka the end systolic volume

Relaxation period
- As ventricles relax, ventricular pressure falls → SL valves close (to prevent blood from flowing out of aorta and pulmonary trunk back into heart), dicrotic notch (shown on pressure graph when back-flowing blood rebounds off of closed SL valves). When SL valves close, the period of isovolumic relaxation begins

30
Q
  1. Define and give a normal value for end diastolic volume (EDV), end systolic volume (ESV), and stroke volume (SV).
A

End diastolic volume (EDV): the maximum volume of blood the ventricles will contain in the cycle; 120 mL

End systolic volume (ESV): the blood remaining in the ventricles after they relax; 50 mL

Stroke volume (SV): the volume of blood pumped out by one ventricle with each beat; 70 mL

31
Q
  1. Which heart valves are open during isovolumic relaxation? during isovolumic contraction?
A

Isovolumic relaxation - none

Isovolumic contraction - none

32
Q
  1. Describe the first and second heart sounds. Which heart sound marks the beginning of ventricular diastole? ventricular systole?
A

S1

  • Occurs when AV valves close (b/c ventricular pressure is greater than atrial pressure)
  • Sound is louder, longer, more resonant
  • Marks the beginning of ventricular systole

S2

  • Occurs as the SL valves snap shut
  • Short, sharp sound
  • Marks beginning of ventricular diastole (relaxation)
33
Q
  1. What is the contribution of atrial contraction to ventricular filling?
A

During atrial contraction, there is a rise in atrial pressure, which compresses the blood in the atria and propels that blood out of the atria into the ventricles. This blood contributes to end diastolic volume

34
Q
  1. Define cardiac output and know how it is calculated.
A

Cardiac output (CO) is the amount of blood pumped out by each ventricle in 1 minute (L/min)

CO = HR (heart rate) * SV (stroke volume)

35
Q
  1. What is cardiac reserve?
A

Cardiac reserve is the difference between resting and maximal CO

36
Q
  1. How is stroke volume regulated?
A

Mathematically, SV represents the difference between end diastolic volume/EDV (the amount of blood that collects in a ventricle during diastole) and end systolic volume/ESV (the volume of blood remaining in a ventricle after it has contracted).

Preload, contractility, and afterload all alter EDV or ESV, therefore affecting SV

37
Q
  1. Define ejection fraction and know how it is calculated.
A

Ejection fraction is the percentage of blood leaving your heart each time it contracts
Ejection fraction = SV/EDV * 100%

38
Q
  1. Define the terms preload and afterload.
A

Preload: the degree to which cardiac muscle cells are stretched just before they contract (in a normal heart, the higher the preload the higher the SV)

Afterload: the pressure that the ventricles must overcome to eject blood

39
Q
  1. What is the relationship between stroke volume and venous return (i.e., preload)?
A

Cardiac muscle, like skeletal muscle, exhibits a length-tension relationship

Resting cardiac cells are normally shorter than optimal length. As a result, stretching cardiac cells can produce dramatic increases in contractile force. The most important factor that is stretching cardiac muscle is venous return - the amount of blood returning to the heart and distending (swelling?) its ventricles. Anything that increases venous return increases EDV and, consequently, SV and contraction force

Frank-Starling law = inc. venous return → inc. EDV (preload) → inc. SV → inc. CO

40
Q
  1. How does afterload influence stroke volume?
A

In healthy individuals, afterload isn’t a major determinant of SV b/c it’s relatively constant.

However, in people with hypertension, afterload is important because the high BP reduces the ability of the ventricles to eject blood. This results in more blood remaining in the heart after systole → inc. ESV and reducing SV

41
Q
  1. How does contractility influence stroke volume? How do changes in sarcoplasmic Ca2+ levels influence contractility?
A

Contractility: the contractile strength achieved at a given muscle length - independent of muscle stretch and EDV

More Ca2+ enters the cytoplasm from extracellular fluid and SR → contractility rises → enhanced contractility means more blood is ejected from the heart (greater SV), hence a lower ESV

42
Q
  1. What effects do the sympathetic and parasympathetic divisions of the ANS have on heart rate?
A

Sympathetic stimulation enhances contractility and speed relaxation. Does this by enhancing Ca movement in the contractile cells. Enhanced contractility lowers ESV, so SV does not decline as it would if only heart rate increased. When heart beats faster there is less time for ventricular filling and so lower EDV.

Parasympathetic division opposes sympathetic effects and effectively reduces heart rate when a stressful situation has passed. Parasympathetic initiated cardiac responses are mediated by acetylcholine which hyperpolarizes the membranes of its effect cells by opening K + channels. Because vagal innervation of the ventricles is sparse, parasympathetic activity has little effect on cardiac contractility.

43
Q
  1. What effect does the sympathetic division have on contractility?
A

Sympathetic stimulation enhances contractility

44
Q
  1. Identify other chemical and physical factors that influence heart rate.
A

Hormones

  • Epinephrine and norepinephrine - enhance heart rate and contractility
  • Thyroxine - in large quantities can cause a sustained increase in heart rate

Ions

  • Ca2+ - hypocalcemia depresses the heart while hypercalcemia increases heart rate and contractility
  • K+ - hyperkalemia alters electrical activity in the heart by depolarizing the resting potential and may lead to heart block and cardiac arrest. Hypokalemia causes the heart to beat feebly and arrhythmically

Age, gender, exercise, and body temp can also influence HR

45
Q
  1. Heart failure is a condition in which the pumping ability of the heart is low and, as a result, blood does not circulate effectively. Explain how heart failure can result in pulmonary edema.
A

Since the heart is a double pump, each side can pump or fail independently of each other. If the left side fails, pulmonary congestion occurs. The right side continues to propel blood into the lungs, but the left side does not adequately eject the returning blood into systemic circulation. Blood vessels in the lungs become engorged with blood → pressure in lungs increases → fluid leaks from the circulation into the lung tissue → pulmonary edema