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CV > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What drives blood flow?

A

Pressure gradient

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2
Q

Pulmonary wedge pressure

A

Measure of pressure in L atrium

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3
Q

How is stroke volume calculated?

A

End-diastolic volume minus end-systolic volume

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4
Q

How is ejection fraction calculated?

A

EF = SV / EDV

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5
Q

Why does the right ventricle have a shorter isovolumetric contraction than the left ventricle?

A

The RV doesn’t require as much pressure to open the pulmonary semilunar valve

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6
Q

More time spent in systole or diastole?

A

Diastole

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7
Q

L vs R ventricle: pressure and flow

A

Both sides eject same vol, (same CO and flow), but pressure and therefore velocity are higher from L side

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8
Q

How is left ventricular ejection fraction calculated?

A

Ejection fraction = stroke vol / end diastolic vol

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9
Q

What does the S1 heart sound indicate?

A

Closure of the tricuspid and bicuspid valves in response to ventricular contraction.

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10
Q

Which valve (tricuspid or bicuspid) closes first?

A

Bicuspid closes just before tricuspid

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11
Q

Why does the pulmonary valve open before the aortic valve?

A

Lower pressure required to open pulmonary valve than aortic valve. Therefore, R ventricle has shorter period of isovolumetric contraction.

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12
Q

Why does the aortic valve close before the pulmonary valve?

A

Greater pressure in the systemic circuit than the pulmonary circuit, which forces valve closed sooner.

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13
Q

What does the S2 heart sound indicate?

A

Closure of the aortic and pulmonary semilunar valves.

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14
Q

Which heart sound can have a normal physiologic split?

A

S2

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15
Q

Effect of inspiration on R heart

A

Increased negative intrathoracic pressure results in greater venous return to R atrium and ventricle, increased EDV, and greater R ventricular ejection volume. This delays closure of pulmonary valve (P2), increasing the splitting of S2.

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16
Q

Effect of inspiration on L heart

A

Increased negative intrathoracic pressure results in retention of blood in pulmonary vv, causing reduced venous return to L atrium/ventricle. This decreases EDV and ejection volume of L ventricle, reducing the duration of L ventricular ejection and accelerating closure of aortic valve (A2), which enhances split of S2.

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17
Q

What are the features of an S3 heart sound?

A

Occurs early in diastole, after S2

Called protodiastolic gallop

During rapid ventricular filling

Normal in younger people

May indicate ventricular enlargement or decreased compliance

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18
Q

What are the features of an S4 heart sound?

A

Occurs in late diastole, just before S1

Associated w/ unusually strong atrial contraction

Indicative of pathology

Presystolic gallop

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19
Q

Structural issues that can cause turbulence in heart

A

Thickening of valve leaflets

Narrowing (stenosis) of valve openings

Holes in chamber walls or septae between chambers

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20
Q

Characteristics of Mitral Insufficiency

A

Systolic murmur

Results in abnormally high L atrial pressure during ventricular contraction

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21
Q

Characteristics of Mitral Stenosis

A

Diastolic murmur

L atrial pressure is higher than normal because blood doesn’t move to L ventricle as easily

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22
Q

Characteristics of Aortic Stenosis

A

Systolic murmur

Much higher L ventricular pressure to overcome stenotic valve

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23
Q

Characteristics of Aortic Insufficiency

A

Diastolic murmur

Aortic pressure drops below normal level due to regurg of valve

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24
Q

Is valve opening/closing active or passive?

A

Passive

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25
Q

What is the dicrotic notch?

A

Pressure wave created in the aorta due to the closure of the aortic semilunar valve

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26
Q

Jugular venous pulse waves

A

A wave: atrial contraction pressure

C wave: pressure from ventricular contraction causing AV valve to bulge into atrium

V wave: increased atrial pressure de to passive filling with AV valve closed

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27
Q

What are large a waves indicative of?

A

Tricuspid stenosis

R heart failure

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28
Q

What are cannon a waves indicative of?

A

3º heart block

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29
Q

What does an absence of a waves indicate?

A

Atrial fibrillation

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30
Q

What does a large v wave indicate?

A

Tricuspid regurgitation

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31
Q

Effect of Skeletal Muscle “Pump” on Lower Extremity Venous Pressure

A

Standing: pooling of blood in lower extremity veins causes increased venous pressure in foot

Walking: mm contraction + valves promotes venous return to heart and decreases venous pressure in foot

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32
Q

Equation for work performed by the heart

A

Work = aortic pressure x change in volume

W = p · ΔV

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33
Q

Tension heat

A

Consumes the most energy in the heart

Results from splitting of ATP during isovolumetric contraction

No “work” being done because there is no movement

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34
Q

Major determinant of ventricular wall tension

A

Afterload

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35
Q

Major determinants of myocardial O2 demand

A

Wall tension

Heart rate

Contractility (inotropic state)

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36
Q

Key factors impacting stroke volume

A

Preload

Afterload

Contractility

37
Q

Preload

A

Effectively synonymous with end diastolic volume

Directly proportional to stroke volume (increased preload = increased SV)

38
Q

Afterload

A

A measure of the amount of force the ventricle needs to generate to overcome the pressure keeping the semilunar valves closed

Good indirect measure: MAP

Increased afterload results in decreased stroke volume

39
Q

Contractility (Inotropy)

A

Measure of force generation independent of preload

Increased inotropy will result in lower end systolic volume and therefore increased stroke volume

40
Q

How are wall tension, pressure, radius, and thickness related?

A

Wall tension is proportional to systolic pressure and radius of the chamber

Wall tension is inversely proportional to wall thickness

41
Q

What is the Frank-Starling law?

A

The stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant.

42
Q

Active tension in heart

A

Dramatic increase in active tension with increasing sarcomere length.

43
Q

How does heart failure affect the Frank-Starling relationship?

A

Failing heart will result in a shallower curve, since the chamber(s) become less able to pump the blood filling them

44
Q

How are cardiac output and venous return related?

A

Venous return must equal cardiac output

45
Q

Mean systemic filling pressure

A

Pressure exerted by the volume of blood itself on the system

X-intercept on venous return curve.

Depends upon the blood volume and compliance of vascular system.

46
Q

Molecular mimicry

A

Microbial epitope is similar enough to a self epitope that, when activated against the microbe, TH1 cells will react to self as well

47
Q

Epitope spreading

A

Local tissue damage leads to release of self Ag from tissues. These are picked up by APCs that further activate lymphocytes, leading eventually to further release of self-Ag.

48
Q

Bystander activation

A

Non-specific activation of self-reactive lymphocytes because factors necessary for activation happen to be present.

49
Q

Cryptic antigen model

A

Self-Ags that have been taken up by DCs are differentially processed. This uncovers epitopes that would otherwise be hidden. These epitopes activate self-reactive TH1 cells, leading to more damage.

50
Q

Group A Streptococcus

A

Gram-pos cocci

Beta hemolytic (uses heme as food source)

51
Q

M protein

A

Found in mucoid strains of strep (heavily encapsulated)

Can interact with the Vβ region of TCRs, making it a superantigen

Can result in polyclonal T cell expansion and cytokine storm

52
Q

How are Jones critera for ARF used?

A

Diagnosis requires two major manifestations or one major and two minor manifestations along with evidence of preceding S. pyogenes infection.

53
Q

Major manifestations of ARF

A

Carditis

Polyarthritis

Chorea

Erythema marginatum

Subcutaneous nodules

54
Q

Minor manifestations of ARF

A

Arthralgia

Fever

Elevated ESR or CRP

EKG evidence of prolonged PR

55
Q

Polyarthritis in ARF

A

Common finding, probability increases w/ reinfection

Occurs symmetrically in large joints

Synovial fluid is sterile but w/ high WBC

Tx: ASA and corticosteriods

Contributing virulence factor: hyaluronic acid capuse of microbe

56
Q

Carditis in ARF

A

Occurrence about 3 wks post infection

Pancarditis (involvement of whole heart)

Cardiomegaly

New onset of murmurs, most commonly apical systolic, and involving mitral valve

Contributing virulence factor: M protein

57
Q

Arthritis vs Arthralgia

A

Arthritis: painful joint, tender to touch, swollen

Arthralgia: painful joint w/o tenderness or swelling

58
Q

Types of receptor modulators

A

Full agonist

Partial agonist

Neutral agonist

Inverse agonist

59
Q

Full agonist

A

Fully mimics endogenous ligand

60
Q

Partial agonist

A

Does not fully induce endogenous response

May be a lower amplitude response, or only induce one of multiple effects of endogenous ligand

61
Q

Inverse agonist

A

Blocks or reduces constitutive activity

Also called competitive antagonists

62
Q

What is the NT used by all preganglionic ANS neurons?

A

ACh; cholinergic neurons

63
Q

What type of receptors are found in postganglionic receptors of the parasympathetic nervous system?

A

nAChR (primary type)

mAChR

64
Q

M2 subtype of mAChR

A

Found in heart and lungs

Is a GPCR that has Gαi/o domain

Inhibits adenylate cyclase pathway

65
Q

M3 subtype of mAChR

A

Found in lungs

Is a GPCR with a Gαq domain

Works in the PLC pathway to generate IP3 and DAG

66
Q

Nicotinic vs Muscarinic receptors

A

Nicotinic are ionotropic

Muscarinic are metabotropic (GPCRs)

67
Q

Major difference between cholinergic and adrenergic signal transduction

A

Cholinergic transduction terminated by enzymatic degradation (AchE)

Adrenergic signal transduction terminated by reuptake of NT

68
Q

What is the precursor for all catecholamines?

A

Tyrosine

69
Q

Are adrenergic receptors metabotropic or ionotropic?

A

Metabotropic

There are NO ionotropic adrenergic receptors

70
Q

Pathway of catecholamine synthesis

A
  1. Tyrosine is pumped into cell
  2. Tyrosine converted to Dopa in cell cytoplasm
  3. Dopa converted into Dopamine in cell cytoplasm
  4. Dopamine pumped into vesicle
  5. Dopamine converted into norepinephrine
  6. Norepinephrine converted to epinephrine (mainly in adrenal medulla)
71
Q

Na+-dependent tyrosine transporter

A

Transports tyrosine into nerve terminal

72
Q

Vesicular monoamine transporter (VMAT-2)

A

Transports Norepi, Epi, dopamine, and serotonin into vesicles

73
Q

Norepi transporter (NET)

A

Imports norepi into nerve terminal

74
Q

Metabolism of catecholamines

A

Modify catecholamines after reuptake

Monoamine oxidase (MAO)

Catechol-O-methyltransferase (COMT)

75
Q

What is the signaling pathway of α1 receptors?

A

Phospholipase C pathway

Cleaves PIP2 into IP3 and DAG, eventually activating PKC

76
Q

What is the signaling pathway of α2 receptors?

A

Gαi pathway

Inhibits adenylyl cyclase from forming cAMP

77
Q

What is the signaling pathway of the β receptors?

A

All work through Gαs to stimulate adenylyl cyclase to produce cAMP

78
Q

Rule of thumb for α1 receptors

A

stimulate contraction of all smooth muscle

Ex: causes vasoconstriction via contraction of vascular smooth muscle

79
Q

Rule of thumb for muscarinic receptors

A

Stimulate contraction of smooth muscle (different pathway than that of α1 receptors)

80
Q

Rule of thumb for β2 receptors

A

Relax smooth muscle

Ex: result in vasodilation

81
Q

How does sympathetic nervous system increase HR?

A

Norepi effects on β1 agonists results in:

Increased If (increased steepness of phase 4)

Increased ICa (increases slow depolarization rate and lowers threshold)

Decreased IK (increases steepness of phase 4)

Net result: faster depolarization to threshold, which increases HR

82
Q

How does parasympathetic nervous system decrease HR?

A

Agonistic ACh effects on M2

Decreased If (decreases slow depolarization rate)

Decreased ICa (decreased slow depolarization rate, increases threshold so it takes longer to get there)

Increased IK (decreases max diastolic potential)

Net effect: longer time for depolarization to reach threshold, decreases HR

83
Q

Factors that can promote increased EDV

A

Increased central venous pressure

Decreased HR

Increased ventricular compliance

Increased atrial contractility

Increased aortic pressure

Pathological conditions

84
Q

Factors that may reduce EDV

A

Decreased filling pressure

Increased HR

Decreased atrial contractility

Decreased afterload

Diastolic failure from decreased ventricular compliance

Mitral or tricuspid valve stenosis

85
Q

5 Positive Inotropic Agents

A

β1 adrenergic antagonists

Cardiac glycosides (digitalis derivatives)

Decreased ECF [Na+]

Increased ECF [Ca++]

Increased HR

86
Q

5 Negative Inotropic Agents (decreased contractility)

A

M2 muscarinic agonists

Decreased ECF [Ca++]

Ca++ channel blockers

Increased ECF [Na+]

Decreased affinity of troponin for Ca++ (ex. acidosis)

87
Q

What controls short term regulation of blood pressure?

A

Neural control

88
Q

What controls long term regulation of blood pressure?

A

Endocrine/paracrine control

89
Q
A

CV (4 decks)

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