20. Perioperative HTN Flashcards
What components make up BP?
- Cardiac ejection
- Intravascular vol
- Vascular tone
- Vascular elasticity
(T/F) We lose vascular elasticity with age.
True.
Partially due to fibrotic tissue + atherosclerotic plaque –> large SBP + small DBP from lack of compliance + recoil
What is the most common way of measuring BP and how do we do it?
NIBP:
- Place cuff around + occlude brachial artery by inflating to supra-systolic level
- Deflate cuff + auscultate for korotkoff sounds
-
Systolic BP = first sound we hear –> turbulent flow as artery allows flow through
* *Diastolic BP** = absence of sounds
Describe what’s happening on an arterial waveform.
- 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
(T/F) A BP of 120/70 is ideal.
False.
Borderline HTN, the lower the better w/ adequate perfusion, esp. to brain
What can happen as a result of continual HTN?
- Places stress of arterial system, which all organs rely on for perfusion
- Continual stress –> scarring + inflammation of arterial walls
What is the eq for MAP?
Mean arterial P = (2DBP + SBP)/3
If looking at normal blood vessel segment, how does incoming blood + resistance at organ beds affect flow?
- 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
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?
MAP increases. However, can maintain BP with vasodilation.
What affect does increased vascular resistance have on heart + BP?
- 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
If looking at an artery + see constriction of arterioles leading into organ beds, what happens to MAP?
Increased MAP.
What can cause pheripheral vasoconstriciton?
- 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
What is eq for pulse pressure?
- PP = SBP - DBP
- Proportional to amt blood ejected during each cardiac cycle
What does higher PP indicate?
- 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
What are pre-HTN BP values?
- SBP > 120mmHg
- DBP > 80mmHg
- MAP > 93mmHg
What are HTN Stage I BP values?
- SBP > 140mmHg
- DBP > 90mmHg
- MAP > 106mmHg
What are hypertensive crisis BP values?
- SBP > 180mmHg
- DBP > 110mmHg
When does HTN emergency occur?
- 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
What are 3 HTN categories?
- Essential HTN - most common, complex interaction b/w genes + environmental
- Chemical HTN - rel. to changes in fluid/electrolyte balances in body –> increased/decreased fluid vol/ vascular tone
- Renal-vascular HTN - caused by feedback in resp to decreased blood supply to renal organs –> release of hormones to maintain Na + water
What is pheochromocytoma?
Adrenal gland has exaggerated release of catecholamines
How does HTN affect response to surgical stimuli + admin of meds?
- 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
What are consequences of labile BP?
- Better for organ systems to experience less swings in HR/BP
- Potential risks of inadequate perfusion
What is autoregulation?
- 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
Should you try to maintain “ideal BPs” for pt with chronic HTN?
No! If shift too much away from pt’s normal BP, risk of underperfusion due to autoregulation.
Between what MAP values do organ perfusion remain same in normal, healthy pt?
50-150mmHg
What happens to autoregulation curve when pt has HTN?
- CBF vs MAP
- Right-shift
- When pt gets BP under control, shift curve back to normal –> more normal response + decreased surgical risk
(T/F) HTN pt have increased risk of cardiac complications.
True.
- Too high BP –> increased work for heart
- Too low BP –> inadequate perfusion of heart
At what BP values should you consider canceling case?
170/110
What factors affect BP under anesthesia?
- Vasodilation (decreased SNS + volatiles)
- Cardiac depression –> decreased EF
- Baroreceptor blunting –> lack of feedback –> BP swings
- Sympathetic inhibition (narcotics) –> some pt have HTN due to sympathetic stim –> BP tanks
- Intravascular reduction (NPO, blood loss, vasodil)
What happens to BP during induction?
- Tachycardia (noxious stim, e.g. intubation) –> fluctuations in vascular tone
- Vasoconstriction (noxious stim)
- PNS blockade
- SNS release
- Multifactorial stim
What happens to BP during emergence?
- Pain
- Bladder distension
- Fluid overload (esp due to decreased venous capacitance)
- Agitation
- Hypoxia
- Hypercarbia
- Restoration of vascular tone
These sx caused increased sympathetic output + vascular tone
