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Human Physiology > Cardiovascular System Pt.1 > Flashcards

Cardiovascular System Pt.1 Flashcards

1
Q

What is the main function of the CV system

A

Transport of nutrients, water, gases, wastes, immune cells, and hormones

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2
Q

What are the 2 main circulatory paths

A

Pulmonary (heart-lungs-heart, deoxygenated to oxygenated) and systemic (heart-body/brain-heart, oxygenated to deoxygenated)

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3
Q

Where do arteries and veins move blood

A

Arteries move it away from the heart, veins carry blood towards the heart

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4
Q

What is blood composed of

A

Plasma (water, ions, amino acids, proteins, lipids, gases), and cellular components

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5
Q

What are the cellular components of blood

A

Erythrocytes (red blood cells), leukocytes (white blood cells), and platelets (cell fragments)

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6
Q

What is another word for cardiac muscle

A

Myocardium

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7
Q

What are cardiac muscle cells called

A

Cardiomyocytes (autorhythmic and contractile)

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8
Q

Where does the signal to contract in the heart originate

A

The sinoatrial (SA) node

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9
Q

How are cardiocytes connected

A

Electrically via gap junctions in intercalated disks and physically via desmosomes (keep cells from pulling apart)

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10
Q

What percent of myocytes are contractile

A

99%

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11
Q

What is the pacemaker potential in authorhythmic cells

A

I(f) channels open at -60 mV, permeable to potassium and sodium but net Na influx allows slow depolarization (slope determines HR)

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12
Q

What is the AP due to in voltage-gated Ca and K channels

A

Ca++ is what really depolarizes the cell

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13
Q

What are the 3 unique characteristics of contractile cell APs

A

2 types of K channels, voltage-gated Ca channels, and much longer duration/refractory period to prevent summation of twitches (so blood can pump properly)

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14
Q

What are the steps of contractile cell APs

A

Resting membrane potential about -90: 1) Na channels open, 2) Na channels close and fast K channels open, 3) Ca channels open, fast K close, some slow K open (causes plateau), 4) Ca channels close and more slow K channels open

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15
Q

How does the electrical signal get from the atria to the ventricles

A

From SA node via internodal pathways to atrioventricular (AV) node

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16
Q

What is the ventricular conducting system

A

AV bundle/bundle of His goes to bundle branches and then to Purkinje fibers (apex to base)

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17
Q

How is an electrocardiogram taken

A

Einthoven’s triangle

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18
Q

What is an electrocardiogam

A

Summed electrical activity of all heart cells

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19
Q

What are waves of ECGs

A

Deflections above or below the baseline (P,Q,R,S,T)

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20
Q

What are segments of ECGs

A

Sections between two waves (P-R, S-T, etc)

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21
Q

What are intervals of ECGs

A

Combinations of waves and segments (PR, QT)

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22
Q

What does the P wave correspond with

A

Atrial depolarization (tells atria to contract/systole)

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23
Q

What does the P-R segment correspond with

A

Conduction through the AV node and bundle

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24
Q

What does the QRS complex correspond with

A

Ventricular depolarization (tells ventricles to contract/systole)

25
Q

What does the T wave correspond with

A

Ventricular repolarization (tells ventricles to relax/diastole)

26
Q

When does atrial repolarization happen on an ECG

A

Not visible but during QRS complex

27
Q

What is bradycardia

A

Slower than normal HR

28
Q

What is tachycardia

A

Faster than normal HR

29
Q

What is a heart arrhythmia

A

Skipped or dropped beats, extra beats (premature ventricular contractions), and fibrillation (loss of coordinated electrical signaling and unorganized contraction)

30
Q

What is ischemia

A

Heart condition that leads to tissue damage as the result of lack of blood and oxygen flow

31
Q

What is a conduction block

A

Affects electrical signal conduction (slower than usual or not able to get through necessary tissues)

32
Q

What increases pressure in the heart

A

Contraction/systole

33
Q

What are the events of the cardiac cycle

A

1) Late diastole, 2) Atrial systole, 3) Isovolumic ventricular contraction, 4) Ventricular ejection, 5) Isovolumic ventricular relaxation

34
Q

What happens during late diastole in the heart

A

Both atria and ventricles are relaxed, blood fills the atria and ventricles via gravity (AV valves open)

35
Q

What happens during atrial systole

A

Last bit of blood is pushed into ventricles so they are filled with their EDV (end diastolic volume)

36
Q

What happens during early (isovolumic) ventricular contraction

A

Ventricular pressure rises, AV valves close, causing “lub” S1 sound

37
Q

What happens during ventricular ejection

A

Ventricles contract, pressure increases, SL valves open and blood is pushed into arteries, ESV (end systolic volume) left in ventricles

38
Q

What happens in ventricular relaxation

A

Ventricular pressure decreases, closing semilunar valves, and causing the “dup” S2 valve

39
Q

When do AV valves close

A

When pressure in the ventricles is greater than in the atria

40
Q

When do SL valves open

A

When ventricular pressure is greater than aortic pressure

41
Q

What is the dicrotic notch

A

Increased aortic pressure caused by backward suction from SL valves closing

42
Q

What is the equation for cardiac output

A

Stroke volume times HR

43
Q

What is cardiac output (CO)

A

Volume of blood pumped out by one ventricle (usually left) per minute

44
Q

What is stroke volume

A

Volume (mL) of blood pumped by a ventricle per contraction (EDV-ESV)

45
Q

What is heart rate

A

Number of heart beats per minute (bpm)

46
Q

How can the vagus nerve alter heart rate

A

Vagus nerve activates parasympathetic neurons, increasing K efflux and decreasing Ca influx, hyper polarizing cell, decreasing HR

47
Q

How does the sympathetic nervous system and adrenal medulla affect heart rate

A

SNS and adrenal medulla activate sympathetic neurons, release NE onto B-1 receptors of autorhythmic cells, increasing Na and Ca influx, increasing rate of depolarization, increasing HR

48
Q

What is stroke volume determined by

A

Force of contraction in ventricular myocardium

49
Q

What is the force of contraction in ventricular myocardium influenced by (for stroke volume)

A

Contractility and muscle fiber length at beginning of contraction (EDV)

50
Q

What is contractility

A

Forcefulness of contraction of individual ventricular muscle fibers (Ca interaction with troponin)

51
Q

What effect does sympathetic innervation have on contractility

A

Increases force of contraction in contractile cells due to Ca increase

52
Q

What does NE and E bind to in contractile cells

A

B-1 receptors

53
Q

What happens once B-1 receptors are bound to

A

cAMP 2nd messenger system is activated, phosphorylating voltage-gated Ca channels (increasing time they’re open) or phospholamban (increasing CA ATP-ase on SR and storing more CA in the SR)

54
Q

What is the Frank-Starling law

A

Stroke volume increases as EDV increases because of preload (degree of stretch)

55
Q

What is venous return

A

Amount of blood entering the heart through veins (influenced by skeletal muscle pump, respiratory pump, and venoconstriction)

56
Q

What is the skeletal muscle pump

A

As muscles contract, they compress veins and force blood back to the heart (valves prevent back flow)

57
Q

What is the respiratory pump

A

When the chest cavity decreases in volume, blood gets pushed into the heart

58
Q

What pathway is activated by B-1 receptors to cause venous constriction

A

PLC-IP3 pathway

Human Physiology (12 decks)

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