Human heart structure & function Flashcards

4 chambers Arteries go away from heart Veins go towards heart Size of clenched fist

1
Q

how is Energy produced in the cardiac muscle

A

produces little of the ATP it needs by anaerobic cellular respiration. Instead, it relies on aerobic cellular respiration in its numerous mitochondria.
*Cardiac muscle fibers use several fuels to power mitochondrial ATP production. In a person at rest, the heart’s ATP comes mainly from oxidation of fatty acids and glucose.
*Like skeletal muscle, cardiac muscle also produces some ATP from creatine phosphate.
* One sign that a myocardial infarction is a rise in blood creatine kinase (CK), the enzyme that catalyzes transfer of a phosphate group from creatine phosphate to ADP to make ATP.

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2
Q

what are Cross striations in the cell?

A

myosin & actin fibres which bind to each other and shorten the length of the cell

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3
Q

how does a Cardiac Muscle Contraction Happen

A

The plasma membrane (sarcolemma) of an unstimulated muscle cell is polarized—the inside of the sarcolemma is negatively charged compared to outside.
* The unstimulated state of the muscle cell, called the resting potential, is created by the presence of large, negatively charged proteins and nucleic acids inside the cell.
* A balance between K + inside the cell and Na + outside the cell contributes to the polarization
* When they receive an electrical stimulation, rapid depolarization occurs when fast‐opening
Na + channels in the sarcolemma open and Na + ions rush into the cardiac muscle cell.
* Ca 2+ enters the cytosol from the sarcoplasmic reticulum (endoplasmic reticulum) within the cell and from outside the cell through slow‐opening Ca 2+channels in the plasma membrane.
* Within the cell, Ca 2+ binds to troponin, which in turn triggers the cross‐bridge binding that leads to the sliding of actin filaments past myosin filaments. The sliding of the filaments produces cell contraction.

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4
Q

what happens during in The Cardiac Action Potential

A

Unlike skeletal muscle, in response to a single action potential a cardiac muscle fibre develops a prolonged contraction.
* 10–15 times longer in duration than a skeletal muscle contraction due to a plateau phase.
* Cardiac muscle fibres also have a longer refractory period, and thus a new contraction cannot be initiated until muscle relaxation is well advanced. Thus, a maintained contraction (tetany) cannot occur in cardiac muscle.

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5
Q

blood supply to the heart

A

L +R coronary, LAD, circumflex

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6
Q

regulation of heart speed and force
Chemical regulators hormones

A

Adrenaline(Epinephrine) and noradrenaline (norepinephrine), from adrenal medullae increase heart’s pumping effectiveness by increasing heart rate and contraction force.
* Exercise, stress, & excitement cause adrenal medullae to release more hormones.
* Thyroid hormones also increase heart rate. One sign of hyperthyroidism (excessive levels of
thyroid hormone) is tachycardia (elevated resting heart rate).

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7
Q

regulation of heart speed and force
Chemical regulators ions

A

Elevated blood levels of K+ or Na+ decrease heart rate and contraction force.
* A moderate increase in extracellular and intracellular Ca2+ level increases heart rate and contraction force. When heart has stopped medics will sometimes inject calcium and adrenaline to try and improve output

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8
Q

what is a Cardiac cycle

A

A cardiac cycle is composed of all the events associated with one heartbeat
One cycle= 0.8 seconds
Heart pumps 5L of blood every minute at rest, but can increase massively during exercise

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9
Q

Cardiac cycle-pressure & ECG
changes

A

Semilunar valves= aortic + pulmonary valves
AV valves=tricuspid and mitral valve

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10
Q

pressure observed within cardiac chambers during systole and diastole

A

heart region=pressure(mmHg)
right atrium=0-4
right ventricle=25 systolic,4 diastolic
plumonary artery=25 systolic,10 diastolic
left atrium=8-10
left ventricle=120 systolic,10 diastolic
aorta=120 systolic,80 diastolic

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11
Q

important info aorta normal blood pressure and left ventricle

A

Normal blood pressure in aorta is 120/80 mmHg
The left ventricle must match this force to eject blood so highest pressure in left ventricle must be 120 mmHg

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12
Q

pulmonary artery pressure and right ventricle

A

Similarly, pulmonary artery pressure is 25/10
The right ventricle must match this to pump blood so highest right ventricle pressure must be 25 mmHg

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13
Q

how is the pressure during diastole

A

During diastole, the pressure in the atrium is just a bit higher than the ventricles to allow the blood to flow.

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14
Q

cardiac output

A

Cardiac output (CO) = Volume of blood ejected per minute from left ventricle into aorta
(same amount of blood ejected from right ventricle into pulmonary arteries)
Cardiac output determined by
(1) stroke volume (SV)= amount of blood ejected by left ventricle during each beat (contraction), and
(2) heart rate (HR)= number of heartbeats per minute. Cardiac output=stroke volume × heart rate

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15
Q

Factors that increase stroke volume or heart rate,

A

exercise, increase cardiac output.

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16
Q

regulation of stroke volume

A

the more blood that returns to the heart during diastole, the more blood ejected during the next systole

17
Q

what factors regulate stroke volume

A
  1. The degree of stretch in the heart before it contracts
  2. The forcefulness of contraction of individual ventricular muscle fibers
  3. The pressure required to eject blood from the ventricles
18
Q

regulation of stroke volume

A

the more the heart is stetched as it fills during diastole the greater the force of contraction during systole,known as the Frank -starling law of the heart.The more you stretch the heart,the more forcefully it contracts

19
Q

Stroke volume- EDV & venous return

A

Amount of blood within heart at end of diastole “stretch” (end diastolic volume EDV) affects amount of blood ejected (i.e., Starlings law).
* EDV is affected by venous return. If venous dilation occurs e.g., fainting, less blood may return to heart. If legs are raised above heart, more blood will return to heart
* EDV is influenced by heart rate. If heart rate goes quicker, less time to fill ventricles before next beat. When heart rate >160 beats/min, stroke volume/EDV declines due to short filling time
* Healthy people with slow resting heart rates usually have large resting stroke volumes because filling time is prolonged

20
Q

Regulation of Stroke volume 1

A

The forcefulness of contraction of individual ventricular muscle fibers.
Even at a constant stretch, the heart can contract more or less forcefully when certain substances are present.
* Increased contraction caused by sympathetic nerves, hormones such as adrenaline and noradrenaline, increased Ca2+ in tissue fluid, and the drug digitalis
* Decreased contraction is caused by inhibition of sympathetic nerves, low oxygen, acidosis, and increased K+ levels in the extracellular fluid.

21
Q

regulation of stroke volume 2

A

The pressure required to eject blood from the ventricles.
The aortic valve opens when pressure in left ventricle exceeds pressure in aorta. When aortic pressure is higher than normal or the valve is partly blocked, valves open later and close earlier so less blood is ejected

22
Q

Cardiac ultrasound

A

Cardiac ultrasound or echocardiography is a medical imaging procedure in which the goal is to generate a picture of the heart for the purpose of evaluating a heart condition or suspected heart problem

23
Q

Coronary angiography

A

Small tube inserted into groin, pushed up to coronary artery openings and dye injected

24
Q

How to spot a heart attack

A

Central crushing/pressing chest pain, can extend to neck or left shoulder
* Nausea,
* May have cold/sweaty skin
* Anxious

25
Q
A