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Physio > Exam 2 - CV Intro > Flashcards

Exam 2 - CV Intro Flashcards

1
Q

8 functions of cardiovascular system

A
  1. Gaseous exchange
  2. Removal of CO2, lactic acid, urea
  3. Delivery of major nutrients (building blocks)
  4. Delivery of micronutrients (vitamins, metals)
  5. Delivery of hormones
  6. Defense
  7. Thermal exchange
  8. Maintaining tissue hydration
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2
Q

3 hemostatic mechanisms to prevent blood loss

A
  • vascular spasm
  • formation of a platelet plug
  • coagulation (clotting)
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3
Q

CV system 4 important variables and what determines each

A
  • cardiac output (heart)
  • resistance (arterioles)
  • capacity (veins, venules)
  • blood volume (balance between fluid supply and fluid loss - kidneys)
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4
Q

what modulates gene expression in the intima of vascular endothelium?

A

shear stress

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5
Q

what three substances does the intima of vascular endothelium produce?

A
  • prostacyclin (PGI2) - vasodilator, inhibitor of platelet aggregation
  • NO - vasodilator, inhibitor of platelet aggregation and leukocyte-endothelial cell adhesion
  • endothelin - vasoconstrictor
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6
Q

describe structure of capillaries

A
  • just intima (no media or adventitia)

- surrounded by pericytes (Rouget cells)

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7
Q

functions of pericytes (5)

A
  • regulation of tight and adherens jxns
  • angiogenesis
  • regulation of ECM protein secretion
  • contractile - regulate capillary diameter/blood flow
  • phagocytosis
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8
Q

describe the structure/purpose of the media of vascular endothelium

A

smooth muscle - responsible for vasoconstriction and vasodilation

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9
Q

in general, what mainly controls vasoconstriction?

A
  • sympathetic nerve stimulation (a1 adrenergic receptors)
  • vasoconstrictors:
    • -thromboxane A2 (TXA2)
    • -vasopressin (ADH)
    • -angiotensin II
    • -endothelin
    • -epinephrine (adrenaline)
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10
Q

in general, what mainly controls vasodilation?

A
  • metabolically generated substances:
    • -H+
    • -CO2
    • -adenosine
  • vasodilators:
    • -prostacyclin
    • -NO
  • loss of sympathetic tone
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11
Q

in large vessels, where is the vasa vasorum contained?

A

within the adventitia

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12
Q

what are the three major bypasses that virtually remove the liver and lungs from fetal circulation?

A
  • ductus venosus (bypasses liver)
  • foramen ovale (shunt from RA -> LA)
  • ductus arteriosus (bypasses pulmonary circuit)
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13
Q

describe the changes in pressure that occur with birth

A

loss of placenta -> increase in systemic resistance -> increase in systemic and left heart pressure -> LA pressure increases -> foramen ovale closes

ventilation of lungs -> decrease in pulmonary resistance (availability of oxygen -> relieves hypoxic pulmonary vasoconstriction) -> pulmonary and right heart pressure decrease

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14
Q

describe the four structural changes that occur at/after birth

A
  1. ductus venosus closes -> ligamentum venosum
  2. higher pressure in LA closes foramen ovale -> fossa ovalis
  3. blood flow reverses through ductus arteriosus -> closes -> ligamentum arteriosum
    - -also bradykinin in high O2 conditions = vasoconstrictor
  4. LV increases in mass b/c pumping at higher pressure, while RV decreases in mass b/c pumping at lower pressure
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15
Q

post-ductal vs. pre-ductal coarctation of the aorta

A

post-ductal:

  • most common
  • stenosis past ductus arteriosus
  • normal flow reversal
  • live to about 40

pre-ductal:

  • stenosis before ductus arteriosus
  • flow reversal doesn’t always occur - fetal direction of flow persists and ductus arteriosus remains patent (here causes a right to left shunt though)
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16
Q

three congenital conditions that result in left to right shunts

A
  1. patent ductus arteriosus
    - except with pre-ductal coarctation
  2. VSD
  3. ASD (most common = patent foramen ovale)

(from left heart/aorta, which are normally high pressure, to the right heart/pulmonary trunk, which are normally low pressure)

17
Q

two congenital conditions that result in right to left shunts

A
  1. pre-ductal coarctation w/ patent ductus arteriosus
  2. Tetralogy of Fallot (blue baby syndrome; PROVE)
    -Pulmonary stenosis
    -RV hypertrophy
    -Overriding aorta
    -VEntricular septal defects
    (blood shunted from R -> L, bypassing lungs w/o getting O2)
18
Q

describe the relaxation of cardiac muscle

A
  • cAMP-dep PK phosphorylates Troponin I
  • SERCA pumps Ca2+ back into SR (activated when phospholamban is phosphorylated)
  • then Ca2+ is sequestered in SR by calsequestrin
  • some Ca2+ is pumped out of cell (Na-Ca exchanger, calcium ATPase)
19
Q

what is a positive lusitropic effect and what neurotransmitters can cause this?

A

= acceleration of cardiac muscle relaxation

catecholamines - phosphorylate phospholamban and phosphorylate troponin I

(during rapid HR, this allows rapid relaxation to still get adequate ventricular filling b/w pumps)

20
Q

what does the strength of cardiac muscle contraction depend on?

A

sarcoplasmic [Ca2+]

more Ca2+, stronger contraction

21
Q

effects of extracellular [Ca2+] on myocardial contractility

A

decreased EC Ca2+:
-decreased contractility -> arrests heart in diastole

increased EC Ca2+:
-increased contractility initially -> arrests heart in systole

22
Q

what are some positive inotropic agents and how do they work?

A
  • catecholamines (epi, norepi, dopa) - increase Ca2+ influx

- digitalis/digoxin - inhibit Na-K pump, which reduces Ca2+ efflux via Na-Ca exchanger

23
Q

what are some negative inotropic agents and how do they work?

A

-Ca-channel blockers - block Ca2+ entry

24
Q

what causes S1?

A

closure of the mitral and tricuspid valves

25
Q

what causes S2?

A

closure of the aortic and pulmonic semilunar valves

26
Q

what is the best indicator of RA pressure?

A

right internal jugular pressure

27
Q

what are some factors that increase central venous pressure?

A
  • decreased CO
  • increased blood volume
  • venous constriction
  • changing from standing to supine body posture
  • arterial dilation
  • forced expiration (Valsalva)
  • muscle contraction (abdominal and limb)
28
Q

four major determinants of CO

A
  • preload (inflow)
  • afterload (outflow)
  • HR
  • myocardial contractility
29
Q

what is heterometric autoregulation?

A

Starling Law
-the more the cardiac muscle can stretch, the stronger the contraction
(increasing preload will increase SV, and therefore CO)

30
Q

two factors that affect preload

A
  • blood volume

- venous capacity

31
Q

what is the mean filling pressure?

A

the pressure that the arteries and veins will equilibrate at if the heart stops and flow ceases

32
Q

does aortic valve stenosis cause HTN?

A

no - although it does increase afterload

Physio (12 decks)

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