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Anesthesia > Clinical cardiac and pulmonary physiology > Flashcards

Clinical cardiac and pulmonary physiology Flashcards

1
Q

equation: MAP

A

MAP = SVR x CO

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2
Q

equation: SVR

A 
80 x (MAP-CVP)/CO
*80 converts mmHg and L/min into dyne/s/cm^5
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3
Q

relationship between resistance and radius

A

resistance inversely proportional to r^4

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4
Q

Where is most resistance to blood flow?

A

arterioles (not capillaries bc large combined area)

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5
Q

equation: CO

A

HR x SV

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6
Q

normal EF and causes of change

A

60-70%
increased in hyperdynamic states (sepsis, liver failure)
decreased in poor cardiac function

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7
Q

measures of preload

A

EDV, LA pressure, PCWP (~LA), PA diastolic pressure

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8
Q

causes of low preload

A

hypovolemia, venodilation, tension ptx, pericardial tamponade

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9
Q

systolic pressure variation

A

changes in SBP with tidal breathing or ventilation that may be observed on arterial blood pressure tracing; extreme form is pulsus paradoxus

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10
Q

pulse pressure variation

A

analagous to SPV, calculated by computer

= (PPpeak-PPnadir)/PPavg

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11
Q

What shifts LV filling pressure vs. CO/SV curve down and to the right?

A

lower contractility or higher SVR

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12
Q

conditions associated with decreased myocardial contractility as a cause of hypotension

A

myocardial ischemia, anesthetic drugs, cardiomyopathy, previous MI, valvular heart disease (dec SV independent of preload)

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13
Q

What shifts cardiac cycle loop down and to left on systolic pressure-volume relationship curve?

A

decreasing SVR

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14
Q

Sympathetics effect on heart

A

stimulation: activates B1 receptors, increasing HR via AV node conduction; increases contractility

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15
Q

Parasympathetics effect on heart

A

stimulation: profoundly slowed heart rate via muscarinic ACh receptors in SA and AV nodes
suppression: increased HR, minor effect on contractility

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16
Q

location and activation of baroreceptors

A

carotid sinus and aortic arch
-increased systemic BP -> stretch receptors signal via vagus and glossopharyngeal to CNS -> parasympathetic-mediated dec in HR and decreased sympathetics = dec contractility and reflex vasodilatation

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17
Q

sensitivity of baroreceptors

A

varies; altered by longstanding HTN

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18
Q

Bainbridge reflex

A

atrial stretch -> increased HR, helps match CO to venous return

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19
Q

location and activation of chemoreceptors

A

carotid sinus
arterial hypoxemia -> sympathetic stimulation
prolonged hypoxemia -> bradycardia, possibly via central mechanisms

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20
Q

oculocardiac reflex

A

increased ocular pressure -> bradycardia

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21
Q

what reflex occurs with abdominal visceral stretch?

A

bradycardia

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22
Q

Cushing reflex

A

bradycardia in response to increased ICP

23
Q

effect of anesthetic drugs on cardiac reflexes

A

blunted cardiac reflexes in dose-dependent fashion

24
Q

percentage O2 extraction in coronary circulation

A

60-70% (vs 25% of body)

25
Q

backup mechanism of coronary circulation if O2 supply threatened

A

vasodilatation

-cannot increase extraction d/t baseline high level

26
Q

endogenous regulators of coronary blood flow

A

adenosine, nitric oxide, adrenergic stimulation

27
Q

critical coronary stenosis %

A

90%

-coronary compensatory vasodilatation downstream exhausted after this point

28
Q

determinants of perfusion pressure to left ventricle

A

DBP - LVEDP

*right ventricle has lower intramural pressure and is perfused in both systole and diastole

29
Q

Where is resistance to pulmonary blood flow?

A

larger vessels, small arteries, capillary bed

30
Q

CVP normal, high, pathologic pressures

A

nrl: 2-8 mmHg
high: >12
path: >18

31
Q

PAS normal, high, pathologic pressures

A

nrl: 15-30 mmHg
high: >30
path: >40

32
Q

PAD normal, high, pathologic pressures

A

nrl: 4-12 mmHg
high: >12
path: >20

33
Q

PAM normal, high, pathologic pressures

A

nrl: 9-16 mmHg
high: >25
path: >35

34
Q

PCWP normal, high, pathologic pressures

A

nrl: 4-12 mmHg
high: >12
path: >20

35
Q

How does increased PAP or CO affect pulmonary circulation?

A

distention and recruitment of capillaries, decreasing PVR by increased cross-sxl area

36
Q

How do lung volumes affect intra- and extra-alveolar vessels?

A

large lung volumes: intra are compressed, extra have lower resistance
small lung volumes: intra have lower resistance, extra may be compressed

37
Q

benefit of increased PVR at small lung volumes

A

divert blood flow from collapsed alveoli, e.g. one lung ventilation

38
Q

drugs that affect pulmonary circulation

A

nitric oxide, prostaglandins, phosphodiesterase inhibitors

39
Q

what is HPV

A

hypoxic pulmonary vasoconstriction; response to low PAO2 by diverting blood from poorly ventilated areas, decreasing shunt fraction
*normal lung can adapt, but globally hypoxic (apnea, high altitude) -> increased PAP

40
Q

How do anesthetic drugs affect HPV?

A

Inhaled anesthetics can impair response
No inhibition with opioids, propofol
*Clevidipine = arterial vasodilator

41
Q

Causes of pulmonary arteriolar thickening

A

certain long-standing congenital heart disease, idiopathic, cirrhosis (portopulmonary htn)

42
Q

change in height vs pressure difference

A

20cm change in height = 15 mmHg pressure difference

43
Q

lung zone 1

A

airway pressures > PAP & PVP
*No blood flow despite ventilation. Normally doesn’t exist, but with positive pressure ventilation or low PAP (blood loss, anesthesia) it may develop

44
Q

lung zone 2

A

PAP >= airway pressure > PVP

*Flow is proportional to difference between PAP and airway pressure

45
Q

lung zone 3

A

PAP, PVP > airway pressure

*normal blood flow pattern proportional to difference between PAP and PVP

46
Q

At what pressure does pulmonary edema develop?

A

PCWP >20 mmHg

  • If chronic, may tolerate to higher levels
  • May also occur at lower PCWP with capillary leak, as with lung injury (acid aspiration of gastric contents, sepsis, or blood transfusion)
47
Q

hypoxemia vs hypoxia

A

hypoxemia reflects pulmonary gas exchange

hypoxia is a more general term including tissue hypoxia and reflects circulatory factors

48
Q

What is P50 on oxyhemoglobin dissociation curve?

A

the PO2 at which Hgb is 50% saturated with O2

*normal in adult is 26.8 mmHg

49
Q

causes of left shift of oxyhemoglobin dissociation curve

A

P50 < 26.8 mmHg
alkalosis
hypothermia
decreased 2,3-DPG (stored blood)

50
Q

causes of right shift of oxyhemoglobin dissociation curve

A

P50 > 26.8 mmHg
acidosis
hyperthermia
increased 2,3-DPG (chronic arterial hypoxemia or anemia)

51
Q

consequence of left and right shifts of oxyhemoglobin curve

A

rightward: little change in O2 loading conditions but allows more O2 to dissociate into tissues, improving tissue oxygenation

52
Q

fetal hemoglobin characteristics

A

left shifted, to allow more O2 to be carried to fetus

53
Q

Haldane effect

A

The process of oxygen binding to hemoglobin and displacing carbon dioxide from the blood, making Hgb a stronger acid
Because of carbon dioxide being displaced from the blood, there is a downward shift in the carbon dioxide dissociation curve that takes place in physiologic settings with higher oxygen levels, such as the lungs. This facilitates the removal of carbon dioxide from the body.

Anesthesia (9 decks)

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