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Physiology > Lecture 1-Exam 3 (cardiac) > Flashcards

Lecture 1-Exam 3 (cardiac) Flashcards

1
Q

What does blood flow depend on?

A

on the pressure difference between arteries and veins and on how much resistance to flow is offered by the vascular system.

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2
Q

What vessels are the most significant point of control of the flow to capillary beds? Why?

A

Arterioles are most significant point of control of flow to capillary beds
* On proximal side of capillary beds and best positioned to regulate flow into the capillaries
* Outnumber any other type of artery, providing the most numerous control points
* More muscular in proportion to their diameter. Highly capable of changing radius

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3
Q

What is flow (Q) proportional and inversely proportinal to? Provide the equation

A
  • proportional to driving pressure gradient (ΔP) and
  • inversely proportional to resistance (R)
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4
Q

What is important when talking about rate of flow and pressure?

A

Rate of flow depends on the pressure difference, NOT the absolute pressure
* The greater the pressure difference between two points, the greater the flow; the greater the resistance, the less the flow

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5
Q

In our body with its anatomy, how do we have a nice driving pressure difference?

A

Coming out of the aorta, the P is 85mm (driving force) then the vena cava pressure is 0mm therefore pressure can go from high to low

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6
Q
  • When will the tube offer greater resistance (R)?
  • What law describes the determinants of resistance? (give equation)
A
  • length (L) increases or if the radius (r) is decreased and higher viscosity (η)= MORE RESISTANCE
  • Poiseuille’s law describes the determinants of resistance
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7
Q

What is the dominant varibale that determines resistance? Explain why

A

Radius is the dominant variable that determines resistance because radius is raised to the fourth power; for example, doubling the vessel radius increases flow by a factor of 16

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8
Q

Physiologic control of vascular resistance is achieved by what?

A

altering the blood vessel diameter through vasoconstriction and vasodilation

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9
Q
  • Vascular smooth muscle actively controls what?
  • Explain the new sock and old sock
  • What are the difference btw arteries and veins?
A
  • Vascular smooth muscle actively controls the diameter of arteries and veins
  • New sock: all the arteries, arteriole because of lots of smooth muscle+elasticity to stretch and recoil (maintain driving force)
    * Arteries are the blood pressure reservoir
  • Old sock: veins and venules because low pressure and will just take the volume of blood without most resistance.
    * Veins are the blood volume reservoir
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10
Q

What are the vascontrictors that are both nonreceptor mediated and receptor mediated with there mechanism of action?

A
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11
Q

What are the vasodilators that are direct and receptor mediated with their mechanism of action

A
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12
Q

The series and parallel arrangement of blood vessels within an organ affects what?

A

vascular resistance in the organ
* general rule of thumb; adding similar-sized arteries in parallel reduces resistance, whereas losing similar-sized arteries in series raises vascular resistance

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13
Q
  • Disease can cause loss of parallel flow cause what?
  • Long-term aerobic training such as distance running, in which the arteriolar and capillary network increase their numbers in parallel causes what?
A
  • Disease can cause loss of parallel flow thus increasing resistance
  • Long-term aerobic training such as distance running, in which the arteriolar and capillary network increase their numbers in parallel, thereby reducing resistance to blood flow
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14
Q

Explain the distribution of pressure, flow velocity and blood volume

A
  • Aorta: highest BP, velocity but low cross sectional area
  • Arteries: high BP and velocity but a little more cross sectional area than aorta
  • Arterioles: Biggest drop of pressure and velocity with an increase of cross section
  • Capillaries: have lower BP, velocity but the highest cross section
  • Venules: Lower BP, higher velocity and lower cross section than capillaries
  • Veins: Lower BP, higher velocity and lower cross section than venules
  • Vena cava: higher velocity but the lowest BP and cross section
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15
Q
  • Where is pressure the highest and lowest?
  • Why the largest pressure drop in arterioles?
  • What is the MAP and why?
A

Pressure is highest in the central arteries and lowest in the central veins. The largest pressure decrease occurs across the arterioles, indicating that they are the site of highest vascular resistance.

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16
Q

What is the regulation of MAP? (include equation)

A
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17
Q
  • Mean arterial pressure will increase when?
  • What does it also predict?
A
  • Mean arterial pressure will increase if the cardiac output, TPR, or both increase.
  • It also predicts that at a constant mean arterial pressure, blood flow through any portion of the vascular tree will increase if TPR decreases.
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18
Q

What are the other factors that influence resistance (and thus flow)? (3)

A
  • Vessel length
  • Blood viscosity
  • Vessel compliance
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19
Q

What happens with vessel length and BP+flow?

A
  • Blood pressure decreases over distance as potential energy is lost through friction between blood and blood vessel walls and between blood cells.
  • Pressure and flow decline with distance - arterial vs. venous pressure
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20
Q
  • What elevates viscosity the most?
  • What happens with increased and decreased viscosity?
A
  • RBC count and albumin concentration elevate viscosity the most
  • Decreased viscosity with anemia and hypoproteinemia speed flow
  • Increased viscosity with polycythemia and dehydration slow flow
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21
Q
  • What is compliance?
  • What if a structure has low complience? Where do we see this?
A
  • Compliance describes the distensibility of a structure and is defined as the volume change produced by a given pressure change
  • If a structure has low compliance (i.e., it is stiff), applying a normal pressure change (ΔP) will produce a small volume change (ΔV).
  • Vessel compliance is seen in certain heart diseases and also decreases with aging
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22
Q

What is the equation for complance? Explain how you would manipulate it

A
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23
Q
  • What do the pace markers cells have?
  • Cardiac cells have what? What does this allow?
A
  • Pace markers cells have automaticity and rhythmicity to initiate cardiac function
  • Cardiac cells have nexi (gap junctions to move ions) to have functional syncytium (to allow contraction together)
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24
Q

How can the ANS modulate the cardiac function?

A

.

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25
Q

What are the two major types of unique action potentials characterize electrical excitation of the heart?

A
  1. Those characteristics of ventricular and atrial muscle, as well as of Purkinje fibers, are called myocyte “fast response” action potentials
  2. Those observed in the sinoatrial (SA) node and atrioventricular (AV) node are called pacemaker “slow response” action potentials
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26
Q
  • Action potentials arriving at the ventricular muscle from the ventricular conducting system trigger what?
  • The ventricular muscle action potential has what?
A
  • Action potentials arriving at the ventricular muscle from the ventricular conducting system trigger the rapid spread of action potentials in all ventricular myocytes.
  • The ventricular muscle action potential has a very long duration (250 ms) with the following five phases 0 through 4
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27
Q

What is the intrinsic heart rate?

A
  • intrinsic=no neural input; heart beats on its own
  • 100 bpm

w/ no autonomic neural input

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28
Q

What is the SA node?

A

initial pacemaker region
origin of the cardiac action potential

this gives heart intrinis activity (heart can beat on its own)

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29
Q

What is the atrial ventricular node?

A
  • Passage of atrial AP to ventricular AP
  • Conductance slowed, enables atrium time to contract and fill ventricles
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30
Q

Does the pacemaker cells (SA node and Atrioventricular node) have fast or slow action potential?

A

SLOW it takes longer to dep bc slow action potential

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31
Q

Do conducting cells (atrial muscle, bundle branch, purkinje fibers, ventricular muscle) have fast or slow action potential and do the waves look the same

A
  • They have faster action potential
  • No, the waves are diff bv because of differences in expressed ion channels and their affect on “shaping” the AP waveform.

diffferences in wave shape bc of diff ion channels being expresses

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32
Q

Fast action potentials in ventricular cells
* Phase 0
* Phase 1
* Phase 2
* Phase 3
* Phase 4

A
  • Phase 0: depolarization
  • phase 1: early repolarization
  • phase 2: plateau
  • phase 3: final rep
  • phase 4: diastolic “resting potential
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33
Q

Ventricular muscle

What channels are open/closed/inactivated during phase 0 depolarization phase? What happens here?

A

open: Inward flux of Ina and Ica (other notes for Ca, Dr. H did not say Ca)
* the initial rapid upstroke that occurs immediately after stimulation
* Membrane potential moves from its resting value of about −90 mV to a peak of about +30 mV during phase 0.

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34
Q

Ventricular muscle

  • What channels are open/closed/inactivated in phase 1 partial repolarization?
  • What happens here?
A
  • Open: outward K flux (Ito 1 and 2)
  • inactivated: Na channels
  • is a partial repolarization of the membrane potential from its peak value of +30 mV to about 0 mV.

“transient outward”

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35
Q

Ventricular muscle

  • What channels are open/closed/inactivated in phase 2 plataeu?
  • What happens here?
A
  • Open: inward ICa and outward IKr IKs (delayed rectifier channels)-> counteract each other
  • also known as the plateau phase, is a dramatic slowing of repolarization.

inward Ca flux and outward K flux counteract each other

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36
Q

Ventricular muscle

  • What channels are open/closed/inactivated in phase 3 final repolarization?
  • What happens here?
A
  • Open: Outward K flux via IK1, IKr IKs
  • Inactive: Ca+ channels
  • is the repolarization of membrane potential back to the resting value

k1=inward rectifier K channels (goes outward tho)

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37
Q

Ventricular muscle

  • What channels are open/closed/inactivated in phase 4 diastolic “ resting” potential”?
  • What happens here?
A
  • open: Efflux K1
  • is the interval between action potentials when the ventricular muscles are at their stable resting membrane potential.

Ik1=inward rectifier K channels (goes outward tho)

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38
Q

Excitation-contraction coupling in cardiomyocytes:
* Cardiac muscle cells contract when?
* Pacemaker cells spontaneously generate what?
* AP are conducted along what? What does this cause?
* What is Ca2+-induced Ca2+ release?
* Almost all Ca2+ that interacts with what?
* Contraction occurs via what?

A
  • Cardiac muscle cells contract without nervous stimulation.
  • Pacemaker cells spontaneously generate action potentials, which spread through gap junctions.
  • Action potentials conducted along T tubules open voltage-gated Ca2+ channels causing entry of extracellular Ca2+ into the cells.
  • Ca2+-induced Ca2+ release is triggered from internal sarcoplasmic reticulum stores.
  • Almost all Ca2+ that interacts with troponin C to initiate contraction is derived from internal stores.
  • Contraction occurs via the same sliding filament mechanism as in skeletal muscle
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39
Q

What is effective/absolute refractory period?

A
  • Cells cant fire another action potentials between phase 0 and 2
  • Allows for necessary filling

caused by the inactivation state of na and/or ca channels, NOT CLOSED STATE

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40
Q

What is relative refractory period?

A
  • Cell can fire another action potential, but amplitude is reduced (b/w phase 3 and 4)
  • Epi or NE can cause an AP here

caused by the inactivation state of na and/or ca channels, NOT CLOSED state

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41
Q

Compare and contrast ventricular and pacemaker action potentials

A
  • Pacemaker cells has slower phase 0 (dep)
  • Pacemaker cells doesnt have a phase 1 (early rep)
  • Pacemaker cells doesnt have a phase 2 (plateau)
  • In pacemaker cells, Phase 4 is slowly dep while in ventricles it is completely in its resting state
42
Q

All pacemaker cells express what type of channel?

A
  • I(f) funny channel also called HCN channel for “hyperpol activated channel”
  • When the pacemaker potential reaches a threshold voltage of about −40 mV it opens these channels and it responsible for the automaticity

automaticity: initiates heartbeat
rhythmicity: regualr pacemaking activity

43
Q

Explain the phases of ionic currents mediating “slow” pacemaker cells.

A
  • Phase 0 depolarization: Inward Ca 2+ activated (slower bc Ca+ slower than Na+)
  • Phase 3 final repol: Efflux K activated
  • Phase 4 (slight, slow dep-resting state): IF “funny” cyclic gated nucleotide gated Na channel NECESSARY FOR AUTOMATICITY (bc activated by hyperpol)

nodal cells: only Ca channels, na channels not involved

44
Q

The maximum membrane potential difference in pacemaker cells is about? What is not present?

A

−60 mV, but there is no stable period of resting membrane potential.

45
Q

Action potential generation in the AV node is similar to the SA node but what is different?

A

but has a slower phase 4 depolarization

45
Q

When compared with ventricular muscle, phase 0 in the SA node what?

A

Is slow and the AP duration is shorter

46
Q
  • Nodal tissue does not contain what?
  • The AP is carried entirely by what?
A
  • Nodal tissue does not contain fast voltage-gated Na+ channels.
  • The action potential is carried entirely by slow, L- type voltage-gated Ca2+ channels.
47
Q

The SA is the normal pacemarker of the heart, why?
What happens when a person has a normal sinus rhythm?

A
  • The SA node is the normal pacemarker of the heart because it has the most rapid rate of phase 4 depolarization
  • A person is in normal sinus rhythm when cardiac excitation progresses from SA node through the entire conduction pathway
48
Q

What do endurance atheltes have? What is the result?

A

Have enhanced PNS tone which results in classic finding of a slow resting HR
* this is due to Ach on the nodal cells to cause hyperpol

49
Q
  • When does the AV node become the pacemarker?
  • What is their typical HR?
  • What is this called?
A
  • AV node becomes the pacemaker if the SA node fails or transmission to the AV node fails.
  • These patients are in nodal rhythm and typically have resting heart rates of 45–55 beats/min.
  • Ectopic pacemaker
50
Q
  • What is the bachmann’s bundle?
  • What direction of contraction do you need in order to have ejection of blood?
A
  • a thick muscular band that connects the right and left atria and is thought to allow for conduction of electrical impulses
  • Apex to superior aspect
51
Q
  • What does the noraml mechanical pumping cycle of the heart require?
  • What produces arrhythmias?
  • What happens if the ventricular rate is excessive?
  • Long refractory allows for what?
A
  • The normal mechanical pumping cycle of the heart requires a single excitation event.
  • Any additional action potentials spread rapidly through coupled myocardial cells and produce arrhythmias (inappropriate heart beats).
  • If the ventricular rate is excessive, there is insufficient time between beats for the ventricles to fill.
  • Long refractory = no tetany and allows for diastole
52
Q
A
53
Q
  • What is the cardiac cycle?
  • What is the cyctle of events in the heart?
  • Although “systole” and “diastole” can refer to what? What are they usually refered it?
A
  • Cardiac cycle: one complete contraction and relaxation of all four chambers of the heart
  • Cycle of events in heart: Systole=contraction and Diastole= relaxation
  • Although “systole” and “diastole” can refer to contraction and relaxation of either type of chamber, they usually refer to the action of the ventricles
54
Q
  • The cardiac cycle is what that occurs with each beat of the heart?
  • Electrical events precede what? What does this result from?
  • ECG waves can be correlated with what?
A
  • The cardiac cycle is the repetitive electrical and mechanical events that occur with each beat of the heart.
  • Electrical events precede mechanical events, which result from the entry of Ca2+ into the myocytes during cardiac action potentials.
  • ECG waves can be correlated with mechanical events
55
Q

What are the phases of the cardiac cycle?

A
56
Q

What are the seven phases of the cardiac cycle (wiggers diagram)

A
  1. Atrial systole
  2. Ventricular isovolumetric contraction
  3. Rapid ventricular ejection
  4. Slow ventricular ejection
  5. Ventricular isovolumetric relaxation
  6. Ventricular filling
  7. Diastasis
57
Q

What happens in phase 1c: atrial systole

A
  • P-wave: atrial depolarization precedes and triggers atrial contraction
  • A-wave: devloped atrial pressure
  • Blood moves from atrial chamber and fuether fills the ventricle (since AV valves are open)
  • A-V valves close: Causes 1st heart sound (d/t increase pressure)
58
Q

What happens in phase 2: isovolumic contraction?

A
  • QRS-wave: ventricular depolarization precedes and triggers rapid ventricular contraction
  • Contraction causes a rapid rise in developed ventricular pressure
  • With both input (A-V and output (aortic) valves closed, no blood moves
  • Aortic valve opens: ending phase 2
59
Q

What happens in phase 3: rapid ejection (ventricular ejection)?

A
  • With venticular pressure than the aortic pressure, the aortic valve opens and blood is rapidly ejected from the ventricle into the aorta, producing a rise in systolic aortic pressure
  • Ventricular contraction is transmitted mechanically to the atria profucing the c wave in atrial pressure
  • T wave: ventricular repolarization initiated ventricular relaxation, and ends phase 3
60
Q

What happens in phase 4: reduced ejection? (not in houstons slides)

A
  • Ventricular relaxation causes a decrease in ventricular pressure
  • Venticle slowly empties
  • Continuous return of venous blood begins atrial filling and increased atrial pressure
  • Aortic valve closes (causes 2nd heart sound)+ ending phase 4
61
Q

What is happening in phase 4: isovolumic relaxation?

A
  • Ventricular relaxation (and the empty venticular chamber) causes a rapid drop in ventricular pressure
  • Both input (AV) and output (aortic) valves are closed, no ventricular blood moves
  • AV valve opens: ending phase 5
62
Q

What is happening in 1a: ventricular filling (rapid flow)

A
  • Ventricular pressure is below atrial pressure, so with the opening of the AV valve, atrial blood rapidly flows into the ventricles
  • 3rd heart sound is caused by the rapid turbulant of flow (NOT VALVES)
63
Q

What happens in 1B: diastasis?

A
  • AV valve is open and venous blood is slowly filling both the atrial and ventricular chambers
  • Decreased, slow ventricular filling
  • Aortic pressure slowly declines as aortic blood is ditributed to the peripheral tissues
  • Atrial contraction (systole) ends
64
Q

How does the EDV, ESV, SV Correlate with left ventricular pressure?

A
65
Q

Explain the pressure volume loop (picture loop in head)

A
66
Q

What is cardiac output (include equation)?

A

Volume of blood ejected from each ventricle per minute

67
Q

What is stroke volume (include the equation)

A

Volume of blood ejected from each ventricle per beat

68
Q

What is EDV and ESV?

A

EDV: End Diastolic Volume
* Volume of blood in ventricle at the end of ventricular relaxation

ESV: End Systolic Volume
* Volume of blood in ventricle at the end of ventricular contraction

69
Q

Explain pathway

A
70
Q

What is the average CO for adults?

A

for adult is 5L/min because CO= (70ml X 70 beats/min)/ 1000 = 4.9L/min

71
Q

What is ejection fraction? (include the equation)

A

Ejection fraction is a simple measurement of ventricular performance and describes the fraction of end-diastolic volume ejected from the ventricle during systole

72
Q

Example: A healthy man of average size is found to have a resting end- diastolic volume of 140 mL and a resting SV of 80 mL, what is his ejection fraction?

A
73
Q

What are the levels of ejection fraction?

A
74
Q
  • What is the normal HR
  • What is tachycardia +causes?
  • What is bradycardia +causes?
A

Normative heart rate 60 – 90 bpm

Tachycardia: resting adult heart rate > 100 bpm
* Stress, anxiety, drugs, heart disease, or fever
* Loss of blood or damage to myocardium

Bradycardia: resting adult heart rate < 60 bpm
* In sleep, low body temperature, and endurance-trained athletes

75
Q
  • What does the ANS do and not do?
  • Cardiac centers are where? What do they do?
A
  • ANS does not initiate the heartbeat, but modulates rhythm and force
  • Cardiac centers in medulla oblongata initiate autonomic output to the heart
76
Q

What are several chemcial that affect the HR?

A
  1. Autonomic neurotransmitters (NE and Ach)
  2. Blood-borne adrenal catecholamines (NE and epinephrine) are potent cardiac stimulants
  3. Potassium and calcium (can increase or decrease HR depending on concentrations of chemical)
77
Q

Sympathetic postganglionic fibers are adrenergic, what do they do the heart?

A
  • release norepinephrine (NE)
  • Causes depolarization of SA node
  • By accelerating both contraction and relaxation, NE (via cAMP) can increase heart rate as high as 230 bpm
78
Q

Parasympathetic vagus nerves have cholinergic, what are their effects on the heart?

A

inhibitory effects on SA and AV nodes
* Acetylcholine (ACh) binds to muscarinic receptors
* Opens K gates in the nodal cells, causing hyperpolarization
* Cells fire less frequently, heart rate slows down
– Without influence from cardiac centers, the heart has an intrinsic firing rate of 100 bpm
– Vagal tone: holds down the heart rate to 70 to 80 bpm at rest

79
Q

Label the lines as normal (resting), neg chronotropic and pos chronotropic

A

(b) Representation of a normal pacemaker potential
(a) Effect of NE
(c) Effect of ACh

80
Q
  • The more rapidly rising phase 4 is because why?
  • he hyperpolarization and slower rise in phase 4 is because whY?
A
  • The more rapidly rising phase 4 in the presence of NE results from enhanced Na+ permeability.
  • The hyperpolarization and slower rise in phase 4 in the presence of ACh result from decreased Na+ permeability and increased K+ permeability, as a result of the opening of ACh-activated K+ channels.
81
Q

What does the frank starling principle describe?

A

Describes the relationship between SV and end-diastolic volume

82
Q
  • Increased diastolic filling produces what?
  • What are two mechanisms that causes this?
A

Increased diastolic filling produces greater stretch of heart muscle, resulting in a larger SV by two mechanisms:
* Optimizing overlap between the thin and thick muscle filaments.
* Increased sensitivity of troponin C to Ca2+.

83
Q

end-diastolic volume is the most important determinant of what?

A

determinant of SV in the healthy heart
* Increased contractility of ventricular muscle produces a left shift in the Frank-Starling relationship; decreased contractility produces a right shift.

84
Q

T/F: left and right heart outputs are equalized since output of one side becomes the venous return of the other side.

A

True: if this does not happen then you will have decrease blood coming back or congestion dt increase of vol coming back to heart

85
Q

Stroke volume is determined by three factors:

A
  1. Ventricular preload is the end-diastolic volume created by venous return. (increase pressure)
  2. Ventricular afterload is the sum of factors that oppose ejection of blood during systole.
  3. Contractility is the intrinsic vigor of muscle contraction related to the biochemical state of the cell.
86
Q

Preload is enhanced by several factors (5)

A
  1. Increased blood volume. (increase EDV= increased SV)
  2. Rhythmic skeletal muscle contraction, which propels blood toward the heart due to the presence of one-way valves in veins = increased venous return.
  3. Deep inspiration, which decreases intrathoracic pressure and increases abdominal pressure, promoting venous return to the thorax.
  4. Atrial systole.
  5. Venoconstriction, which reduces venous pooling and
    promotes the return of blood to the central circulation.
87
Q

In a healthy heart, increasing preload results in what?

A

Increased SV

88
Q

The major component of afterload is normally what?

A

the resistance to bloodflow created by small muscular arteries and arterioles.

89
Q

Aortic diastolic blood pressure is often used as what?

A

as an index of afterload because it is created by blood flow through vascular resistance

90
Q

What are other sources of afterload?

A

could be low compliance (stiffness) of the ventricle or great vessels, or stenosis of the semilunar valves.

91
Q

What are the effects of increased afterload on ventricular performance?

A

Dashed lines indicate the afterload slope, which becomes steeper when the ventricle develops more pressure but delivers a smaller stroke volume, reflecting higher impedance opposing blood flow (increased afterload).

92
Q

What is contractility?

A
  • A change in contraction force independent of preload or afterload.
  • A. Increased velocity of muscle shortening at zero muscle load (Vmax) in isolated muscle. B. Increased rate of pressure development in the left ventricle (dP/dt). C. Left shift of Frank-Starling relation. D. Elevation of the end-systolic pressure-volume point.
93
Q
  • Agents that increase contractility are called what?
  • Agents that decrease contractility are called what?
A
  • Positive inotropes
  • Negatice inotropes
94
Q

What is changed based on positive inotropic stimuli and negative inotropic stimuli

A

At any given combination of preload and afterload, isometric force generation of cardiac muscle is increased by positive inotropic stimuli and decreased by negative inotropic stimuli

95
Q
  • What are the most important physiological example of positive inotropes?
  • Catecholamines occypy what? What does this cause?
A
  • Catecholamines are the most important physiologic examples of positive inotropes.
  • Catecholamines occupy myocardial β1- adrenoceptors, causing the generation of intracellular cyclic adenosine monophosphate (cAMP) and activation of protein kinase A
96
Q
A
97
Q

Force of contraction in cardiac muscle can be altered by what?

A

intracellular calcium concentration: calcium-induced calcium release

98
Q

What are the mechanisms that increase myocardial contractility following B adrenergic stimulation

A
99
Q

What is the ANS effects on CO?

A
100
Q

fill in for factors that influence CO

A
101
Q
A

Physiology (11 decks)

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