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Organ Systems > Heart study questions > Flashcards

Heart study questions Flashcards

1
Q

Describe the structure and function of the serous pericardium

A

-Parietal layer: outer layer adhered to inner surface of fibrous pericardium
-Visceral layer: invests heart (also called epicardium)
bursa that reduces friction between heart and adjacent structures; Fist-in-a-balloon model.

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2
Q

Describe the fibrous pericardium and what it attaches to.

A

Thick CT surrounding heart

• Adhered to sternum and diaphragm

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3
Q

What are bulbospiral muscles and what do they do? How do they differ from trabeculae carneae?

A

spiral muscle that surrounds heart.
• Bulbospiral muscle “wrings out” blood
• Trabeculae carneae: thick ventricular cardiac muscle fibers on inner surface

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4
Q

What blood enters the right and left ventricles and where is it pumped after that?

A

(ignoring the atrium)
deoxygenated blood from body>Right ventricle> pumps deoxygenated blood to lungs
oxygenated blood from lungs>Left Ventricle> pumps oxygenated blood to body

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5
Q

Where and what is the fossa ovalis?

A

located inside right atrium. site of foramen ovale, a prenatal aperture that directs blood from right to left atrium, bypassing the lungs in utero.

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6
Q

Where is the opening of the coronary sinus?

What is its significance in coronary circulation?

A

located in the right atrium.

collects blood from heart muscle.

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7
Q

Describe the function of the tricuspid and bicuspid valves. Where are they located?

A

Tricuspid valve: conducts blood from right atrium into right ventricle.
Bicuspid (mitral) valve: conducts blood from left atrium into left ventricle.

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8
Q

How do the tricuspid and bicuspid relate to systole and diastole?

A

They are open during diastole and closed during systole

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9
Q

Describe the anatomy of the tricuspid valve.

A

– 3 cusps
– Papillary muscles attached to Chordae tendinae
– Moderator band (part of bundle of His)

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10
Q

Describe the anatomy of the bicuspid valve.

A
  • two cusps

- chordea tendinae attached to papillary muscles.

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11
Q

What are papillary muscles and how do they relate to trabeculae carneae?

A

Valve cusps are held in place by Chordae Tendineae attached to papillary muscles.
papillary muscles connect to trabeculae carneae on walls???
Trabeculae carneae – dense smooth muscle bundles in wall

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12
Q

What are pectinate muscles and auricles? What role do they play in circulation through the heart?

A

Pectinate (atrial) muscles and the vestigial auricle contract to push blood into ventricle

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13
Q

Which chamber has the thickest myocardium? Any idea why this is the case?

A

Left Ventricle due to pumping blood to the body instead of just to the lungs (Right V.)

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14
Q

Describe the anatomy and function of semilunar valves. Where are they located?

A

Semilunar valve cusps are in the bases of the pulmonary trunk and aorta
Aortic / pulmonary sinuses: spaces behind cusp catch blood during diastole making the cusps meet at central point

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15
Q

what produces the heart sound: how do they relate to valves and the stages of systole and diastole?

A

First Heart Sound (“Lub”) = SYSTOLE: closure of AV valves, opening of semilunar valves
Second Heart Sound (“Dub”) = DYSTOLE: closure of semilunar valves, opening of AV valves

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16
Q

Describe the origin and distribution of the major coronary arteries and veins.

A

Right & Left Coronary arteries stem from aortic sinuses and give off descending branches.
• Left coronary artery branches
– Anterior descending (interventricular)
– Circumflex (anastomoses with right coronary artery)
• Right coronary artery branches
– Marginal (inferior margin of heart)
– Posterior descending (interventricular)

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17
Q

What is collateral circulation of the heart? Is it helpful during an acute heart attack?

A

Gradual ischemia induce formation of collateral arteries that compensate for coronary artery occlusion
• Collateral formation is gradual over months to years in the case of advancing disease such as angina, but can be overwhelmed by rapid onset of major obstruction and myocardial infarction

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18
Q

Blood perfusion of the myocardium occurs during diastole – Why?

A

during diastole, ventricles relax. blood flows into the coronary arteries next to the semilunar valves. blood flow pressure into the coronary arteries depends on back pressure of blood against the semilunar valves.

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19
Q

What are the main features of angina pectoris in terms of coronary arteries?

A

partial blockage of coronary arteries causes pain or a squeezing sensation in the chest

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20
Q

Where are blood vessels for bypass surgeries taken from?

A

-Saphenous leg veins are used for smaller arteries, eg marginal
- Internal thoracic arteries are used for larger arteries, eg. anterior descending.
FYI: GORE-TEX is a common artificial vascular graft material. completely inert to the body.

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21
Q
  1. How does cardiac muscle differ from skeletal and smooth muscle in terms of cell structure and connections between cells?
A

IDFK

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22
Q

Describe the key features of the ventricular contraction AP and how they relate to the different ion channel activities

A

Contraction AP
• Myocardial contraction is triggered by long duration AP
• AP’s produced by Atria, Ventricles, & Purkinje fibers
– Extended plateaus
– Elicited by impulses conducted from
SA and AV nodes.
• Muscle contraction occurs in about the same time frame as the AP

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23
Q

How do calcium blockers function to reduce blood pressure in eg. hypertension?

A

Calcium blockers (nifedipine, verapamil, etc) block L type channels to reduce cardiac contractility.

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24
Q

Describe how the contractile AP causes the release of Ca from the SR. How does this mechanism differ from that of skeletal and smooth muscle?

A

• AP opens L-type Ca channels in T-tubule of myocardial cells
• Inward Ca flux binds with RyR “feet” and opens SR Ca channel in the terminal cisternae.
– Amount of Ca from L channels is too small to initiate contraction alone and serves solely to open the SR release of Ca.
– in both skeletal and cardiac muscle, it is the incoming AP that initiates release of SR Ca++

25
Q

How does the cardiac muscle cell relax after contraction?

A

Ca reabsorbed into SR via SERCA (sarcoendoplasmic reticulum calcium ATP-ase) and phospholambin

26
Q

What is the role of sympathetic activity in regulation of cardiac contractility

A

Sympathetic nervous system (NE and EPI) can enhance myocardial contraction via cAMP
• This is a mechanism in addition to that created by action potentials
• Both NE from sympathetic neurons & EPI from the adrenal medulla stimulate β1 (mostly) receptors
• β1 stimulates cAMP formation
• cAMP (via PKA) enhances opening of L-type Ca++ channels
• Ca++ influx triggers more Ca++ release from the SR and enhancing myocardial contraction

27
Q

In the atrium, how do sympathetic and parasympathetic activity work to regulate contractility?

A

Parasympathetic activity can decrease mostly atrial myocardial contraction
• Ach muscarinic receptors decrease cAMP synthesis via inhibitory G protein
• Decreased cAMP-PKA inhibits L-Ca++ channels and reduces Ca++ release from the SR
• Primary effect is in atrium. Far fewer parasympathetic nerves exist in ventricles.

28
Q

Describe the anatomy of the heart conduction system

A

SA (sinuatrial) node:
• junction of SVC and R atrium
• primary pacemaker of the heart; generates auto-rhythmic impulses
• AP’s trigger atrial contraction
AV (atrioventricular) node
• in base of right atrium
• regulator of conduction into ventricles
Bundle of His gives off right and left bundle branches.
• Conduction can be interrupted by necrosis caused by coronary artery occlusion

29
Q

What is the significance of the AV node in conduction from atrium to ventricle?

A

• AV node sends fibers through the CT ring surrounding the tricuspid valve to form the bundle of His
– CT rings surround the AV and semilunar valves
• bundle of His is the only conducting pathway between the atria and the ventricles

30
Q

Are any parts of the conduction system neural?

A

Nope, none. All the stuff you would expect to be neural are actually modified cardiac cells

31
Q

What impact does the slow conduction of the AV node have on the cardiac cycle?

A
  • AV conducting velocity is the slowest (100 msec delay) due to fewer gap junctions
  • Creates delay between atrial and ventricular contraction giving time for filling
32
Q

Describe the conduction AP and activity of ion channels. How does this differ from contraction APs?

A

The conduction AP is essentially passing the signal from the SA to the AV and bundle of His. It is the AP with the Slow type CA that triggers the K, which is turn triggers the funny Na channels

33
Q

What happens to the heart rate if there is a bundle block in the ventricle?

A

bundle of His is the only conducting pathway between the atria and the ventricles
Conduction can be interrupted by necrosis caused by coronary artery occlusion

34
Q

How does sympathetic activity impact heart rate

A

Sympathetic effects on nodal cells (slow action)
• NE (Sympathetic) and Epi (adrenal medulla) stimulate β1 receptors on:
– SA node to increase heart rate
– AV node to facilitate AV conduction.

35
Q

How does parasympathetic activity impact heart rate

A

Parasympathetic effects on nodal cells
• ACh stimulates M2 muscarinic receptors on:
– SA node to decelerate heart (right vagus)
– AV node to reduce AV conduction (left vagus)

36
Q

What receptors and ion channels are affected in sympathetic

A

β1 receptors increases the activity of both Ca++ and funny Na+ channels via cAMP and PKA
• Stimulation of funny Na+ is what increases heart rate by accelerating the depolarization toward threshold
• Sympathomimetics (eg ephedra) act on β1 receptors.

37
Q

What receptors and ion channels are affected in parasympathetic

A

Fast action
• M2 receptors hyperpolarize membrane by opening K+ channels
• slowing the depolarization by inhibiting T-type Ca++ & funny Na+ channels

Slow action
• M2 receptors activate inhibitory G proteins (Gi) that reduce cAMP synthesis
• Less cAMP inhibits funny Na+ channel; this reduces rate of membrane depolarization

38
Q

What is the difference between the fast and slow effects of parasympathetic activity?

A

Fast action exerts quick beat-by-beat control of SA and AV function
Slower process sets the “vagal tone” of the HR and competes with sympathetic acceleration of the heart

39
Q

What is vagal tone and what is its contribution to the resting heart rate?

A

Without vagal input, the SA node beats at an “intrinsic rate” of about 100/min (as in heart transplant). Vagal activity reduces this to about 70 for a resting heart rate.

40
Q

What is the relative contribution of the sympathetic activity to the resting heart rate?

A

Resting sympathetic activity is low and when stimulated generates a small (but still functionally significant) increase in HR compared to parasympathetic

41
Q

Describe the conduction events during the: Pwave, P-Q interval, R wave, S-T interval, T wave.

A

P wave: atrial depolarization initiated by the SA node causes the p wave
P-Q interval: with atrial depolarization complete, the impulse is delayed at the AV node
R wave: ventricular depolarization, atrial repolarization occurs.
S-T interval: ventricular depolarization is complete
T wave: ventricular repolarization begins at Apex causing the t wave

42
Q

When in the ECG is the ventricle fully repolarized?

A

After the T wave

43
Q

Differentiate between the mean electrical vector and the mean electrical axis. What is their significance? How are they impacted by right or left ventricular hypertrophy.

A

Mean electrical vector
• As the AP progresses from the SA node, it spreads as a wave of depolarization through heart tissue
• Where the AP is being produced, the cells are externally negative, ahead of them the cells are externally positive. This generates a positive polarity (dipole).
• Individual polarities along the wave sum to form the net or mean electrical vector

44
Q

During activity of a reentry pathway, would you expect to see a P wave? Why?

A

Wolff-Parkinson-White syndrome
Accessory pathway into ventricle can lead to:
• Extra ventricular depolarization (delta wave)
• Reentry activity can cause ventricular tachycardia
– Note late inverted P wave due to reverse atrial depolarization

45
Q

How does Hyperkalemia slow down the heart?

A

(ECG complex can evolve to a sinusoidal shape).
• Hyperkalemia depolarizes cardiac cells (why?) which in turn inactivates many sodium channels
• Bradycardia (slowed HR) is due to the sluggish conduction of the AP, associated with smaller P waves and widening of the QRS complex.
Peaked T waves (rapid onset and shorter duration):
• Elevated potassium increases the activity of voltage gated potassium channels and speeds membrane repolarization.

46
Q

Describe each phase of the cardiac cycle in terms of: ECG waves, ventricular, atrial and aortic pressures (where appropriate), isometric versus isotonic contraction, valve actions, heart sounds.

A

P wave: atrial systole
QR: Ventricular systole, isometric contraction, Heart sound 1, AV valves closed
ST: Late ventricular systole, isotonic contraction, semilunar valves open
T wave: end ventricular systole
post T wave: Diastole, heart sound 2, semilunar valves close, AV valves open, isovolumic

47
Q

In the ventricle, what is the difference between isovolumic contraction and isovolumic relaxation?

A

Isovolumic ventricular contraction
• Peak of R wave
• Pressure builds with all valves closed (isovolumic)
• First heart sound S1

Isovolumic relaxation
• Ventricle relaxes, pressure drops below aortic pressure and the aortic valve closes

48
Q

What is the difference between isovolumic contraction and ejection?

A

Isovolumic ventricular contraction
• Peak of R wave
• Pressure builds with all valves closed (isovolumic)
• First heart sound S1

Ejection: early phase
• ST phase
• Aortic valve opens when ventricular pressure exceeds aortic pressure
Ejection: later phase
• T wave
• Back pressure of aorta reduces ejection

49
Q

What is atrial systole and when does it occur? Would it be regulated by both sympathetic and parasympathetic activity?

A

P wave
• During slow heartbeat, pressure gradient from atrium into ventricle is adequate to fill the ventricle
– Blood is sucked into the ventricle
• In tachycardia (eg. exercise, dysfunction, etc), ventricular diastole is shorter and less blood enters ventricle
• To compensate, atrial contraction ejects blood into ventricle (“atrial systole”) to provide adequate filling

50
Q

What is cardiac output? Stroke volume?

A

CARDIAC OUTPUT is a measure of heart performance
• CO (ml/min) = SV stroke volume (ml) x HR heart rate (beats/min)
• Cardiac Output is the total volume ejected per unit time
Stroke Volume is the volume ejected in one beat (ml)
SV = (EDV, end-diastolic volume) - (ESV, end-systolic volume)

51
Q

What is Stroke volume?

A

STROKE VOLUME (SV) is determined by:
• Preload (initial, i.e. end-diastolic, volume)
• Afterload (aortic pressure)
• Contractility (inotropic state)

52
Q
  1. Describe preload in terms of ventricular muscle length, pressure changes, role of CT/elastic elements, length-tension relationship.
A

PRELOAD is the fiber length from which the muscle contracts.
• Diastolic filling stretches the myocardium to the end-diastolic volume, EDV
– Stops when intraventricular pressure is equal to the incoming atrial venous pressure.
– Filling in two stages: passive late diastolic filling and atrial systole
• Stretches muscle to generate passive tension (diastolic pressure)
• Sets the myofibrils for a given level of active tension (systolic pressure)

53
Q

What is the Frank Starling Law and how is it impacted by congestive heart failure?

A 
Increased preload (venous return) produces a commensurate increase in stroke volume
• SV increases because atrium stretches to accommodate incoming blood
• When an organ stretches out, its wall cannot sustain the internal pressure and so it needs to increase contractility to maintain integrity.
54
Q

Describe after load in terms of aortic pressure, myocardial contraction and valve actions

A

Afterload is the systolic pressure needed to overcome the blood pressure within the aorta in order to eject blood
• Increased aortic pressure (afterload) reduces the velocity of ventricular contraction. This reduces how much blood is ejected in a cycle.
• Decreased velocity is compensated by increasing contractility which increases the velocity of blood flow during ejection .

55
Q

How do preload and after load affect the velocity of ventricular contraction?

A

Increased venous pressure (preload) increases contractility which increases the velocity of blood flow

Increased aortic pressure (afterload) reduces the velocity of ventricular contraction. This reduces how much blood is ejected in a cycle.

56
Q

What is contractility and how is generated?

A

AP opens L-type Ca++ channel, triggering the release of Ca++ from the SR via the ryanodine, RyR, channel.
• Ca++ from the SR (not extracellular space) then binds to the troponin complex and activates the contractile apparatus

57
Q

How does sympathetic activity affect contractility in terms of onset, force level, relaxation time?

A

Sympathetic activity signals the ventricles to contract sooner, harder, and end earlier. It also triggers the atrial contraction to make up for the shortened filling time.

58
Q

How does sympathetic activity affect the cell signaling systems of contraction AP and SR activity?

A

Sympathetic activity causes the slow L-type calcium channels to be activated. This means it is easier open the channel, and the influx is greater. Sooner and great influx means an earlier and stronger contraction

59
Q

Account for the changes in latency, force and relaxation time. How does digoxin (digitalis) work to enhance contractility?

A
  1. increase vagal tone – low therapeutic dose
    • sensitization of baroreceptors
    • central vagal stimulation
    • facilitation of muscarinic transmission to the heart
  2. increase contractility – therapeutic dose
    • Digoxin increases contractility by inhibiting Na-K ATP-ase.
    • Cell gains sodium, decreasing Na+ concentration gradient
    • Ca/Na exchange is reduced
    • Ca++ accumulates within cell to initiate contraction.

Organ Systems (20 decks)

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