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Physiology (712) > Heart > Flashcards

Heart Flashcards

1
Q

Explain the 3-cog wheel depiction of the cardiovascular and vascular system.

A
  • The 3-cogs represent the connection between the tissues, heart, and airways/lungs.
  • If one clog is limited, this impacts the function of the others
  • You need to have all 3 of these working in sync to deliver O2 to the mitochondria
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2
Q

Explain what is meant by the “heart is composed of 2 parallel pumps”. What does this mean in terms of right and left ventricular stroke volume?

A
  • the R and L sides of the heart are separated by a continuous septum (atrial and ventricular)
  • they are parallel but separate → pump at the same time
  • atria contract synchronously, then the ventricles contract synchronously
  • if they lose independence → pathology
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3
Q

Where are the valves located in the heart? What is their function?

A
  • mitral/bicuspid AV valve (L): separates LA and LV
  • tricuspid AV valve (R): b/w RA and RV
  • pulmonary valve: b/w RV and pulmonary artery
  • aortic valve: b/w LV and aorta
  • ensure one-way blood flow and prevent backward/retrograde flow
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4
Q

Explain the impact of valvular dysfunction on both upstream and downstream CV physiology and anatomy.

A
  • valvular dysfunction leads to back flow being possible (upstream) and a reduction of blood flowing through the heart (downstream)
  • can allow for regurgitation and mixing of blood
  • especially bad in the heart itself bc you can have a mix of oxygenated + deoxygenated blood
  • chronic overfilling will lead to changes in anatomy at that chamber
  • the resulting “bad seal” will overtax cardiac muscles and overtime could cause CHF
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5
Q

What is the function of the papillary muscles and when in the cardiac cycle do they contract?

A
  • papillary muscles contract during ventricular contraction to oppose the pressure generated by the LV or RV
  • they push the leaflets of the valves backwards up into the respective atria
  • this prevents the backward flow of blood during ventricular contraction
  • function: contract to keep valves CLOSED during systole
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6
Q

List the layers of the heart

A
  • fibrous layer (fibrous pericardium)
  • parietal pericardium
  • pericardial cavity
  • epicardium (aka visceral pericardium)
  • myocardium
  • endocardium
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7
Q

Describe the positioning of the heart in the thoracic cavity.

A

The heart is located in the mediastinum lying underneath the sternum towards the left side

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8
Q

When first touching the heart in your cadaver, what layer are you most likely touching?

A
  • fibrous pericardium
  • made up of dense connective tissue
  • anatomic function = keep the heart from overfilling
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9
Q

What layers permit the heart to expand and contract with very little friction?

A
  • pericardial cavity
  • contains a small volume of fluid that allows parietal pericardium and visceral pericardium (epicardium) to easily move over one another
  • fluid reduces friction and pain with contraction
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10
Q

Blood cells flowing through the heart would come in contact with what layer of the heart?

A

endocardium

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11
Q

Explain the ramifications of the large aerobic capacity of the heart.

A
  • cardiac muscle cells require continuous O2 supply and constant blood flow
  • if heart isn’t getting O2, it literally can’t function
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12
Q

Explain how cardiac muscle grades contractile strength and intrinsic beat rate. During your last heartbeat, how many cardiac muscle cells actively contracted?

A
  • during any heartbeat: every cardiac muscle cell in the atria and the ventricles is contracted
  • the heart can regulate its own beat rate
  • HR can be regulated depending on workload of the heart
  • strength of contraction (contractility) → will increase when SNS is stimulated
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13
Q

How many cardiac myocytes contracted the last time you were suddenly scared? Describe the involvement of the autonomic nervous system in this response.

A
  • All of them
  • SNS activity: increase HR 3-fold, increase strength of contraction up to 2-fold, increase plasma epinephrine; net effect = increase CO
  • PNS: Activity of Parasympathetic nerves decreases HR
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14
Q

Define chronotropic. What is the impact of sympathetic innervation on the heart? Of parasympathetic innervation on the heart?

A
  • chronotropic = affecting the heart rate
  • Positive chronotropic effect → increases HR (sympathetic)
  • Negative chronotropic effect → decreases HR (parasympathetic)
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15
Q

Assume that a wave of depolarization starts at the SA node. Describe the pathway that the wave will follow as it moves across and “down” the heart. What cells conduct this wave in the LV? What structure allows the signal to move from the atria into the ventricles?

A
  • SA Node → AV Node → Bundle of His → R & L bundle branch → Purkinje Fibers
  • Purkinje Fibers conduct the wave in the LV (conduct AP into the interior of the myocardium)
  • AV Node allows the AP to move from atria to ventricles (slows down the signal to allow the completion of emptying the atria)
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16
Q

SA node has its own ____, so it allows for the heart to contract at its own rate, even without any outside ____

A

pacemaker; innervation

17
Q

Describe the action potential found in cardiac myocytes. How does it differ from that found in skeletal muscle cells?

A
  • Cardiac muscle: AP is conducted across the whole cardiac muscle due to intercalated disks, allowing the muscle to to act as one unit (longer, graded AP)
  • Skeletal muscle: uses a recruitment process (shorter, all or none AP)
  • Longer cardiac APs prevent tetanus (charlie horse) from happening in the heart
18
Q

What is the absolute refractory period and what is its role in the cardiac cycle?

A
  • time when another AP cannot be generated and heart cannot be induced to contract
  • how we get max HR
19
Q

What cardiac events are associated with the P, QRS, and T waves?

A
  • P wave: atrial contraction (atrial depolarization)
  • QRS complex: initiates contraction of the ventricle
  • T wave: relaxation of ventricles (repolarization)
  • EKG traces the currents of these waves
20
Q

Define systole

A
  • systole = contraction
  • every heart chamber (atria, ventricles) experiences this
  • smallest volume of blood in the heart here
21
Q

Define ventricular diastole

A
  • diastole = relaxation
  • heart chambers fill with blood
  • largest volume of blood in the heart here
22
Q

Define EDV

A
  • end diastolic volume
  • volume of blood in a heart chamber at the end of diastole
  • during diastole, chambers fill with blood, so EDV is as full as the chambers can get
23
Q

Define ESV

A
  • end systolic volume
  • volume of blood in the heart chamber at the end of systole (after the contraction)
  • heart is never completely empty during systole
24
Q

Define isovolumetric contraction

A
  • occurs during the first part of systole

- pressure is developing in each of the ventricles but no blood is flowing bc all the valves are closed

25
Q

EDV and ESV allow us to calculate ____

A
  • stroke volume

- SV = EDV - ESV

26
Q

What blood vessels supply blood to the heart?

A

right and left coronary arteries

27
Q

the heart has the most ____ cells in the body

A
  • focused

- myocytes (cardiac cells) aren’t replaced, which is why heart attacks are so damaging

28
Q

vagal (parasympathetic) stimulation of the heart regulates ____ more than ____ because vagal fibers are distributed mainly to ____

A

HR; contractility; SA and AV nodes

29
Q

at maximal exercise: ____ input is marginal and ____ input is maximal

A

parasympathetic; sympathetic

30
Q

explain the intrinsic HR

A
  • intrinsic ability of the heart to adapt changes in the volume of inflowing blood and to automatically accommodate to the blood that comes into it
  • heart can regulate its own rate because of the SA node
31
Q

Calculate CO for a heart rate of 140 BPM and a stroke volume of 80 mls. How hard is this individual working?

A
  • CO = volume of blood pumped per ventricle per minute = SV x HR
  • 80 m/s x 140 BPM = 11,200 ml/min = 11.2 L/min
  • average CO = 5-6 liters/min
  • This individual is working hard bc their CO is twice the average value
32
Q

how does preload influence CO?

A
  • preload = vol of blood in ventricles at end of diastole
  • Frank Starling Law: SV increases as ventricular vol increases due to the myocyte stretch, causing a more forceful systolic contraction
  • higher preload = greater SV = higher CO
  • dehydration → preload is decreased → CO is decreased
  • heart can compensate for this by increasing HR bc CO = SV x HR so if SV goes down, then HR going up will keep CO constant
33
Q

How does afterload influence CO and the workload of the heart?

A
  • afterload is the resistance left ventricle must overcome to circulate blood
  • less afterload → greater CO bc heart does not have to work as hard
  • increased afterload = lower SV
  • increased vol of LV due to ESV increasing
  • heart will have to work harder as afterload increases → hypertension
  • increased contractility
34
Q

How does contractility influence CO?

A
  • Contractility = force or strength of the contraction itself
  • As force of contraction (aka contractility) increases, the heart is able to pump more blood out per beat → increased stroke volume → increased cardiac output
35
Q

How does the Frank Starling mechanism ensure that the stroke volume is the same for the LV and RV?

A
  • Frank Starling Law says: as EDV increases, contractility increases
  • greater EDV = greater contractility = greater SV
  • increase on right = increase on left
36
Q

How is CO maintained in a patient who is dehydrated? In someone who is hypervolemic?

A
  • dehydration: decreased EDV, decreased stroke volume; HR will increase to maintain CO
  • hypervolemia:

Physiology (712) (9 decks)

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