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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
What is the dicrotic notch?
Pressure wave created in the aorta due to the closure of the aortic semilunar valve
26
Jugular venous pulse waves
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
27
What are large *a* waves indicative of?
Tricuspid stenosis R heart failure
28
What are cannon *a* waves indicative of?
3º heart block
29
What does an absence of *a* waves indicate?
Atrial fibrillation
30
What does a large *v* wave indicate?
Tricuspid regurgitation
31
Effect of Skeletal Muscle "Pump" on Lower Extremity Venous Pressure
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
32
Equation for work performed by the heart
Work = aortic pressure x change in volume W = *p* · ΔV
33
Tension heat
Consumes the most energy in the heart Results from splitting of ATP during isovolumetric contraction No "work" being done because there is no movement
34
Major determinant of ventricular wall tension
Afterload
35
Major determinants of myocardial O2 demand
Wall tension Heart rate Contractility (inotropic state)
36
Key factors impacting stroke volume
Preload Afterload Contractility
37
Preload
Effectively synonymous with end diastolic volume Directly proportional to stroke volume (increased preload = increased SV)
38
Afterload
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
Contractility (Inotropy)
Measure of force generation independent of preload Increased inotropy will result in lower end systolic volume and therefore increased stroke volume
40
How are wall tension, pressure, radius, and thickness related?
Wall tension is proportional to systolic pressure and radius of the chamber Wall tension is inversely proportional to wall thickness
41
What is the Frank-Starling law?
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
Active tension in heart
Dramatic increase in active tension with increasing sarcomere length.
43
How does heart failure affect the Frank-Starling relationship?
Failing heart will result in a shallower curve, since the chamber(s) become less able to pump the blood filling them
44
How are cardiac output and venous return related?
Venous return must equal cardiac output
45
Mean systemic filling pressure
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
Molecular mimicry
Microbial epitope is similar enough to a self epitope that, when activated against the microbe, TH1 cells will react to self as well
47
Epitope spreading
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
Bystander activation
Non-specific activation of self-reactive lymphocytes because factors necessary for activation happen to be present.
49
Cryptic antigen model
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
Group A Streptococcus
Gram-pos cocci Beta hemolytic (uses heme as food source)
51
M protein
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
How are Jones critera for ARF used?
Diagnosis requires two major manifestations or one major and two minor manifestations along with evidence of preceding *S. pyogenes* infection.
53
Major manifestations of ARF
Carditis Polyarthritis Chorea Erythema marginatum Subcutaneous nodules
54
Minor manifestations of ARF
Arthralgia Fever Elevated ESR or CRP EKG evidence of prolonged PR
55
Polyarthritis in ARF
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
Carditis in ARF
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
Arthritis vs Arthralgia
Arthritis: painful joint, tender to touch, swollen Arthralgia: painful joint w/o tenderness or swelling
58
Types of receptor modulators
Full agonist Partial agonist Neutral agonist Inverse agonist
59
Full agonist
Fully mimics endogenous ligand
60
Partial agonist
Does not fully induce endogenous response May be a lower amplitude response, or only induce one of multiple effects of endogenous ligand
61
Inverse agonist
Blocks or reduces constitutive activity Also called competitive antagonists
62
What is the NT used by all preganglionic ANS neurons?
ACh; cholinergic neurons
63
What type of receptors are found in postganglionic receptors of the parasympathetic nervous system?
nAChR (primary type) mAChR
64
M2 subtype of mAChR
Found in heart and lungs Is a GPCR that has Gαi/o domain Inhibits adenylate cyclase pathway
65
M3 subtype of mAChR
Found in lungs Is a GPCR with a Gαq domain Works in the PLC pathway to generate IP3 and DAG
66
Nicotinic vs Muscarinic receptors
Nicotinic are ionotropic Muscarinic are metabotropic (GPCRs)
67
Major difference between cholinergic and adrenergic signal transduction
Cholinergic transduction terminated by enzymatic degradation (AchE) Adrenergic signal transduction terminated by reuptake of NT
68
What is the precursor for all catecholamines?
Tyrosine
69
Are adrenergic receptors metabotropic or ionotropic?
Metabotropic There are NO ionotropic adrenergic receptors
70
Pathway of catecholamine synthesis
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
Na+-dependent tyrosine transporter
Transports tyrosine into nerve terminal
72
Vesicular monoamine transporter (VMAT-2)
Transports Norepi, Epi, dopamine, and serotonin into vesicles
73
Norepi transporter (NET)
Imports norepi into nerve terminal
74
Metabolism of catecholamines
Modify catecholamines after reuptake Monoamine oxidase (MAO) Catechol-*O*-methyltransferase (COMT)
75
What is the signaling pathway of α1 receptors?
Phospholipase C pathway Cleaves PIP2 into IP3 and DAG, eventually activating PKC
76
What is the signaling pathway of α2 receptors?
Gαi pathway Inhibits adenylyl cyclase from forming cAMP
77
What is the signaling pathway of the β receptors?
All work through Gαs to stimulate adenylyl cyclase to produce cAMP
78
Rule of thumb for α1 receptors
stimulate contraction of all smooth muscle Ex: causes vasoconstriction via contraction of vascular smooth muscle
79
Rule of thumb for muscarinic receptors
Stimulate contraction of smooth muscle (different pathway than that of α1 receptors)
80
Rule of thumb for β2 receptors
Relax smooth muscle Ex: result in vasodilation
81
How does sympathetic nervous system increase HR?
Norepi effects on β1 agonists results in: Increased *I*f (increased steepness of phase 4) Increased *I*Ca (increases slow depolarization rate and lowers threshold) Decreased *I*K (increases steepness of phase 4) Net result: faster depolarization to threshold, which increases HR
82
How does parasympathetic nervous system decrease HR?
Agonistic ACh effects on M2 Decreased *I*f (decreases slow depolarization rate) Decreased *I*Ca (decreased slow depolarization rate, increases threshold so it takes longer to get there) Increased *I*K (decreases max diastolic potential) Net effect: longer time for depolarization to reach threshold, decreases HR
83
Factors that can promote increased EDV
Increased central venous pressure Decreased HR Increased ventricular compliance Increased atrial contractility Increased aortic pressure Pathological conditions
84
Factors that may reduce EDV
Decreased filling pressure Increased HR Decreased atrial contractility Decreased afterload Diastolic failure from decreased ventricular compliance Mitral or tricuspid valve stenosis
85
5 Positive Inotropic Agents
β1 adrenergic antagonists Cardiac glycosides (digitalis derivatives) Decreased ECF [Na+] Increased ECF [Ca++] Increased HR
86
5 Negative Inotropic Agents (decreased contractility)
M2 muscarinic agonists Decreased ECF [Ca++] Ca++ channel blockers Increased ECF [Na+] Decreased affinity of troponin for Ca++ (ex. acidosis)
87
What controls short term regulation of blood pressure?
Neural control
88
What controls long term regulation of blood pressure?
Endocrine/paracrine control
89

CV (4 decks)

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