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Physiology I F2015 > 20. Perioperative HTN > Flashcards

20. Perioperative HTN Flashcards

1
Q

What components make up BP?

A
  1. Cardiac ejection
  2. Intravascular vol
  3. Vascular tone
  4. Vascular elasticity
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2
Q

(T/F) We lose vascular elasticity with age.

A

True.

Partially due to fibrotic tissue + atherosclerotic plaque –> large SBP + small DBP from lack of compliance + recoil

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3
Q

What is the most common way of measuring BP and how do we do it?

A

NIBP:

  1. Place cuff around + occlude brachial artery by inflating to supra-systolic level
  2. Deflate cuff + auscultate for korotkoff sounds
  3. Systolic BP = first sound we hear –> turbulent flow as artery allows flow through
    * *Diastolic BP** = absence of sounds
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4
Q

Describe what’s happening on an arterial waveform.

A
  • During systole, initial peak of BP propelling blood forward + stretching arterial walls
  • Dicrotic notch = point when aortic valve closes at end of cardiac ejection + artery recoils starts, giving second blip in arterial tracing
  • During diastole, PE will recoil walls back inwards bringing P’s down to diastolic values
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5
Q

(T/F) A BP of 120/70 is ideal.

A

False.

Borderline HTN, the lower the better w/ adequate perfusion, esp. to brain

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6
Q

What can happen as a result of continual HTN?

A
  • Places stress of arterial system, which all organs rely on for perfusion
  • Continual stress –> scarring + inflammation of arterial walls
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7
Q

What is the eq for MAP?

A

Mean arterial P = (2DBP + SBP)/3

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8
Q

If looking at normal blood vessel segment, how does incoming blood + resistance at organ beds affect flow?

A
  • Blood ejected from heart distends arterial walls + holding P’s until diastole begins + blood no longer flowing into arteries
  • Vascular system will meet resistance at other end of system from organ beds: increased vascular tone/resistance –> increased BP
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9
Q

If looking at an artery + we increase CO while maintain flow + vascular resistance, what happens to MAP? What can we do to keep things constant?

A

MAP increases. However, can maintain BP with vasodilation.

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10
Q

What affect does increased vascular resistance have on heart + BP?

A
  • Increased vascular resistance increases BP + forces heart to work harder (more resistance to push against)
  • Heart will continually adapt but can lead to…
    • Strain –> heart failure
    • Pushing at high P’s –> shear forces –> damaged endothelium + muscular layer of vessels –> accelerated atherosclerosis –> end organ dysfxn
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11
Q

If looking at an artery + see constriction of arterioles leading into organ beds, what happens to MAP?

A

Increased MAP.

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12
Q

What can cause pheripheral vasoconstriciton?

A
  • Phenylephrine
  • ANS sending sympathetic outflow via cathecholamines to cause vasoconstriction when acting on ɑ receptors
  • If constrict vessels to certain max. level, won’t have enough blood returning to heart to supply sufficient vol + maintain BP
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13
Q

What is eq for pulse pressure?

A
  • PP = SBP - DBP
  • Proportional to amt blood ejected during each cardiac cycle
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14
Q

What does higher PP indicate?

A
  • Increased SBP + maintenance of DBP
    • Increased ejection of blood
    • Vascular tone remains the same –> brings blood vessel back to same size
  • Decreased DBP + maintenance of SBP
    • Vasodilation (decreased resistance) to maintain SBP
    • Increased vascular pooling
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15
Q

What are pre-HTN BP values?

A
  • SBP > 120mmHg
  • DBP > 80mmHg
  • MAP > 93mmHg
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16
Q

What are HTN Stage I BP values?

A
  • SBP > 140mmHg
  • DBP > 90mmHg
  • MAP > 106mmHg
17
Q

What are hypertensive crisis BP values?

A
  • SBP > 180mmHg
  • DBP > 110mmHg
18
Q

When does HTN emergency occur?

A
  • When organ damage/dysfxn occurs
  • High P –> large stress on arteries –> rupture –> hematoma/bleeding (e.g. in brain)
  • Want to treat as much as possible but don’t want to drop BP too fast + risk poor organ perfusion –> cardiac ischemia + organ dysfxn
  • In emergency, may need to drop BPs faster to prev further organ damage
19
Q

What are 3 HTN categories?

A
  1. Essential HTN - most common, complex interaction b/w genes + environmental
  2. Chemical HTN - rel. to changes in fluid/electrolyte balances in body –> increased/decreased fluid vol/ vascular tone
  3. Renal-vascular HTN - caused by feedback in resp to decreased blood supply to renal organs –> release of hormones to maintain Na + water
20
Q

What is pheochromocytoma?

A

Adrenal gland has exaggerated release of catecholamines

21
Q

How does HTN affect response to surgical stimuli + admin of meds?

A
  • HTN causes exaggeraged BP + HR resp to stimuli
    • Non-HTN: BP increases 20-30mmHg + HR increases 15-20bpm
    • HTN: BP increases ~90mmHg + HR increases 40bpm
  • If pt gets treated before surgery for HTN, has much better response to stimuli
22
Q

What are consequences of labile BP?

A
  • Better for organ systems to experience less swings in HR/BP
  • Potential risks of inadequate perfusion
23
Q

What is autoregulation?

A
  • Maintenance of constant blood flow to organ despite changes in artery’s BP supplying organ
    • Increased vascular tone
    • Increased CO
  • Every organ has some degree of autoreg. to prev damage from excessive blood flow
  • Longterm HTN, body learns to autoregulate around BP to maintain flows
24
Q

Should you try to maintain “ideal BPs” for pt with chronic HTN?

A

No! If shift too much away from pt’s normal BP, risk of underperfusion due to autoregulation.

25
Q

Between what MAP values do organ perfusion remain same in normal, healthy pt?

A

50-150mmHg

26
Q

What happens to autoregulation curve when pt has HTN?

A
  • CBF vs MAP
  • Right-shift
  • When pt gets BP under control, shift curve back to normal –> more normal response + decreased surgical risk
27
Q

(T/F) HTN pt have increased risk of cardiac complications.

A

True.

  • Too high BP –> increased work for heart
  • Too low BP –> inadequate perfusion of heart
28
Q

At what BP values should you consider canceling case?

A

170/110

29
Q

What factors affect BP under anesthesia?

A
  1. Vasodilation (decreased SNS + volatiles)
  2. Cardiac depression –> decreased EF
  3. Baroreceptor blunting –> lack of feedback –> BP swings
  4. Sympathetic inhibition (narcotics) –> some pt have HTN due to sympathetic stim –> BP tanks
  5. Intravascular reduction (NPO, blood loss, vasodil)
30
Q

What happens to BP during induction?

A
  1. Tachycardia (noxious stim, e.g. intubation) –> fluctuations in vascular tone
  2. Vasoconstriction (noxious stim)
  3. PNS blockade
  4. SNS release
  5. Multifactorial stim
31
Q

What happens to BP during emergence?

A
  1. Pain
  2. Bladder distension
  3. Fluid overload (esp due to decreased venous capacitance)
  4. Agitation
  5. Hypoxia
  6. Hypercarbia
  7. Restoration of vascular tone

These sx caused increased sympathetic output + vascular tone

Physiology I F2015 (13 decks)

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