page 360-369 Flashcards

(52 cards)

1
Q

https://drive.google.com/open?id=0B8uJUY-tie8GUm5Zb0dwUFRLQkE

A

https://drive.google.com/open?id=0B8uJUY-tie8GcVV6R2JmN1dPRFE

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2
Q

ECG

A

Records the flow of electrical impulses through the heart.

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3
Q

To read ECG:

A

■ Remember that a single lead corresponds to an anatomic territory.

■ Look at multiple leads together for voltage abnormalities and axis

deviations.

■ Look at a single lead for arrhythmias.

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4
Q

https://drive.google.com/open?id=0B8uJUY-tie8GV0h3UGEwUUpadEk

A

https://drive.google.com/open?id=0B8uJUY-tie8GZEJRSnBnT3h6dFU

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5
Q

https://drive.google.com/open?id=0B8uJUY-tie8GYzRXOW52YWY0eGM

A

https://drive.google.com/open?id=0B8uJUY-tie8GLTJrRHMtU2lzYTA

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6
Q

https://drive.google.com/open?id=0B8uJUY-tie8GQUVQYm51djVYM1U

A

https://drive.google.com/open?id=0B8uJUY-tie8Ga3RGSHFLcV9CbHM

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7
Q

https://drive.google.com/open?id=0B8uJUY-tie8GaDFlaWhReks5ZDQ

A

https://drive.google.com/open?id=0B8uJUY-tie8GUGh6OEQ3WFhEUEE

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8
Q

Bainbridge Reflex

A

■ Stretch of atria (with ↑ blood volume) causes ↑ HR and, therefore, ↑ CO.

■ Mediated by stretch receptors in atria.

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9
Q

Receptor cells are sensitive to pressure and stretch.

■ Mediated by vagal (CN X) afferents to the medulla.

■ Efferent loop is slowing of vagal output

A

Bainbridge Reflex

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10
Q

Pumps more blood out of pulmonary system to the systemic system.

■ This helps prevent pulmonary edema.

A

Bainbridge Reflex

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11
Q

Baroreceptor

A

HR, BP

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12
Q

Chemoreceptor

A

Respiration > vasomotor

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13
Q

Baroreceptors

A

■ Modulate intravascular pressure and HR over a short time period.

■ Activated by ↑ BP.

■ Causes ↓ HR, vasodilation, ↓ BP

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14
Q

BARORECEPTOR REFLEX (VALSALVA )

A

■ ↑ BP/↑ stretch of baroreceptors → ↑ parasympathetic afferent output (CN

IX, X) → medulla → ↑ vagal efferent tone (CN X) (↓ sympathetic tone)

→↓HR, ↓ BP (vasodilation, venodilation) →↓CO.

■ Antagonist to Bainbridge reflex.

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15
Q

car sinus

A

Spindle-shaped dilation of receptors at

he common carotid artery bifurcation

(superior border of thyroid cartilage).

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16
Q

Afferent = CN IX.

A

carotid sinus

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17
Q

Afferent = CN X.

A

Aortic Arch Baroreceptora

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18
Q

Receptors in the aortic arch

A

Aortic Arch Baroreceptora

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19
Q

carotid sinus syndrome

A

Excessive stimulation of both carotid sinuses (eg, convulsive seizures) can

lead to momentary loss of consciousness because of vagal discharge, venodilation,

vasodilation.

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20
Q

RESPONSE TO SUDDEN STANDING

A

↓ BP in brain, upper body sensed by baroreceptors →

■ ↓ parasympathetic firing (CN IX, X); (sympathetic discharge → ↑HR,

↑ conduction velocity, ↑ cardiac contractility, ↑ peripheral resistance ↑

vasoconstriction), ↓ renal blood flow ↑a1 vasocontriction of afferent artery;

b1 on JGA →↑renin →↑angiotensin-II → aldosterone→↑blood back to

heart (↑preload because venoconstriction of large veins) → ↑ CO →

return/maintain BP.

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21
Q

HEMORRHAGE OR HYPOVOLEMIA

A

COMPENSATIONS :

■ Baroreceptor reflex (↑ sympathetic, ↓ parasympathetic tone).

■ ↑ epinephrine from adrenal medulla.

■ ↓ vagal output from medulla (↓ carotid sinus, ↓ aortic baroreceptor firing

22
Q

RAAS (Renin-Angiotensin-Aldosterone system). See renal also.

■ AT-II, aldosterone and increase in TPR

■ AT-II: On efferent arteriole to preserve GFR.

■ Aldosterone: On cortical collecting duct, increase Na+ reabsorption,

K+ excretion, H+ secretion by intercalated cells.

A

HEMORRHAGE OR HYPOVOLEMIA

23
Q

HEMORRHAGE OR HYPOVOLEMIA

A

ADH

■ Capillary fluid shift

■ Increases water reabsorption in CCD.

24
Q

Chemoreceptors

A

■ Detect changes in blood oxygen, carbon dioxide, and hydrogen ion

concentrations.

■ Modulate respiratory center in brain (regulate respiratory activity).

25
Afferent CN IX
Carotid Body
26
Afferent CN X
Aortic Body
27
CHEMORECEPTOR PATHWAY
↑ CO2, ↑ H+, and/or ↓ O2 → stimulates chemoreceptors (carotid, aortic bodies) → ↑ parasympathetic afferent output (CN IX, X) → medulla (respiratory center) → ↑ ventilation (to breathe down CO2) → (↑ BP, ↑ HR secondary to simultaneous secretion of catecholamines from the adrenal medulla). ■ Increase in sensitivity to CO2 and pH when \<60 mm Hg.
28
Mechanisms to meet ↑ demand to muscles during exercise (↑ supply). ■ ↑ CO because ↑ HR and ↑SV.
excersize
29
excersize
Sympathetic nervous system. ■ b2 adrenergic receptors in muscle/pulmonary tree ■ Vasodilate ■ ↑ Blood flow to muscles
30
excersize
b1 receptors in heart ■ ↑ HR ■ ↑ Contraction force (inotropic) (phospholumbar “releasing brake” on SERCA pump) ■ ↑ CO
31
excersize
a1 in other parts of body ■ Vasoconstriction ■ ↑ Arterial pressure
32
excersize
Enhanced venous return (↑ preload). ■ ↓ Venous compliance ■ Pumping effect of the skeletal muscle ■ Vasoconstriction
33
excersize
Local metabolites (released as O2 ↓ 0). ■ Adenosine, CO2, lactic acid ■ Vasodilate: ↓vascular resistance, ↑ blood flow
34
AUTOREGULATION OF BLOOD FLOW
As blood flow ↑ to muscles during exercise, the adenosine is washed out. ■ ↓ adenosine → arterioles and small arteries vasoconstrict → keeping blood flow at a normal rate (in face of ↑arterial pressure).
35
hematocrit
Percentage of RBCs in blood sample. ■ Normal: ■ Male: 44–46. ■ Female: 40–42.
36
Venous Hct is typically higher than arterial Hct because of xxx ■ More yyy in comparison to plasma. CO2 from tissues gets converted by zzz → HCO3 in RBC increases osmotic pressure →water rushes in →RBC greater volume
Venous Hct is typically higher than arterial Hct because of “chloride shift.” ■ More RBC mass in comparison to plasma. CO2 from tissues gets converted by carbonic anhydrase → HCO3 in RBC increases osmotic pressure →water rushes in →RBC greater volume
37
hb conc
Normal: ■ Male: 15–16 g/dL. ■ Female: 13–14 g/dL.
38
Severe anemia:
■ \<7.5 g/dL. ■ Hct = Hb °ø 3.
39
anemia
↓ Hct. ■ ↓ RBC and/or ↓ Hb concentration
40
Consequences of Anemia
■ ↓ oxygen transport in blood. ■ Fatigue, respiratory compensation, cardiac compensation. ■ Hypoxia in the tissues. ■ Causes small arteries and arterioles to dilate (so ↑ blood return to the heart [preload]). ■ Hypoxia in the pulmonary circulation results in vasoconstriction of those vessels (opposite to effect on other body tissues).
41
https://drive.google.com/open?id=0B8uJUY-tie8GbHk3T2wxVnc1bmM
https://drive.google.com/open?id=0B8uJUY-tie8GU0JJR195MTR4QlE
42
https://drive.google.com/open?id=0B8uJUY-tie8GQm9Bbnl1dXZObEE
https://drive.google.com/open?id=0B8uJUY-tie8GRnowaXEtQkhxT28
43
Carbon Monoxide Poisoning
■ CO competes with oxygen for Hb-binding sites and changes allosterics; CO has greater affinity (250°ø) ■ Normal Hb level ■ O2 content ↓ ■ Cherry red cheeks
44
Cyanosise
■ Deoxygenated hemoglobin in tissues gives the skin/mucous membranes a blue tint. ■ Does not occur in severe anemia because you need \>5 g of deoxygenated Hb per 100 mL of blood to appreciat
45
ERYTHROPOIETIN
■ Glycoprotein hormone produced in kidneys ■ ↑ RBC production by bone marrow ■ Acts at the hemocytoblast (pluripotent stem cell)
46
erythpoetin
↓ Erythropoiesis → anemia ■ ↑ Erythropoiesis → polycythemia ■ ↑ Blood viscosity, sluggish blood flow, ie, polycythemia vera (JAK2 mutation downstream of Epo Receptor)
47
Negative Feedback
■ ↓ O2 tension (anoxia/hypoxia) →↑erythropoietin (HIF) ■ ↑ O2→↓erythropoietin
48
Virchow’s Triad
■ Endothelial injury ■ Stasis ■ Hypercoaguability
49
hemostasis
■ Three parts: ■ Vasoconstriction ■ Platelet aggregation/plug (primary)—platelets bind wWF on damaged endothelium ■ Coagulation (secondary)—crosslinking with fibrin meshwork
50
Coagulation Intrinsic and extrinsic pathways
Prothrombin is cleaved to thrombin. ■ Converted by prothrombin activator (Factor Va). ■ Fibrinogen cleaved to fibrin. ■ Converted by thrombin. ■ Fibrin forms the clot and cross-links with the platelets.
51
https://drive.google.com/open?id=0B8uJUY-tie8GbWJ0Z0JSbHlCb1U
https://drive.google.com/open?id=0B8uJUY-tie8GdkpWdTRnN09ZT2c
52