HTN - Video Flashcards
T/F HTN is the leading factor for M + M
true
Nicotine raises BP by _ - _ mmHg
20-30mmHg
_ + drinks / day increases risk for HTN
3+
T/F Coffee raises BP significantly
false,
antioxidants cancel it out sorta
T/F K+ intake decreases BP
true
-acts like thiazide diuretic, decreasing Na+ reabsorption
T/F BP increases with BMI
true
Patho of SYSTOLIC HTN
overactive SNS
-teenagers/YA; men > women
Patho of isolated DIASTOLIC HTN
elevated diastolic, normal systolic
from increased SVR and NORMAL CO
-middle aged ppl
-can progress to systolic/diastolic if no tx
Patho of isolated SYSTOLIC HTN
widening of pressure from stiffened arteries from excess COLLAGEN > systolic increase thru years
-diastolic peaks at 55y then drops
-older adults
Immediate control of HTN within the body is regulated by:
ANS - baroreceptor reflex (carotid sinus reflex)
Describe the baroreceptor reflex response to HoTN:
low BP > increased SNS activation > increased adrenal secretion of epi and reduced vagal activity > increased vascular resistance, HR and contractility > increased BP
-low pressure > vasoconstriction + inhibition of vagal tone
Describe the baroreceptor response to HTN:
high BP > increased baroreceptor discharge > inhibition of systemic vasoconstriction and increased vagal tone
Why is baroreceptor reflex inadequate for long term BP control?
adaptation to BP changes occur over 1-2 days
What anatomical parts of the ANS sense BP changes?
centrally: hypothalamus + brainstem
peripherally: baroreceptors (wall of internal carotid aa and aorta)
Intermediate control of BP within body is determined by:
RAAS
Vasopressin
Interstitial fluid / capillary fluid balance (body pulls fluid intravascular from interstitial space to increase BP)
All VA depress the baroreceptor reflex in the heart but _ and _ depress it the least
Iso + Des
Chemoreceptors mainly regulate _ activity but also help with BP control. They are found in the _ _ and respond to low _ and high _ causing increased _ outflow > tachycardia and vasoconstriciton
respiratory
aortic bodies
O2
CO2
SNS
Renin-Angiotensin System
Finish sentences with the following words: ACE, angiotensinogen, angiotensin I, angiotensin II, renin, aldosterone, vasoconstriction
- Drop in BP and/or fluid volume > _ released from kidneys which interacts with _ released from the liver, forming _.
- _ release from the lungs and act on _ to form _.
- _ acts on the adrenal gland to stimulate the release of _ which then acts on the kidneys to stimulate reabsorption of Na and water. _ also directly acts on the blood vessels to stimulate _.
- renin, angiotensinogen, angiotensin I
- ACE, angiotensin I, angiotensin II
- Angiotensin II, aldosterone, angiotensin II, vasoconstriction
Long term factors controlling BP:
-RAAS (Aldosterone adjusts Na+ AND H2O reabsoprtion/excretion)
-Pituitary gland releasing ADH (vasopressin) > adjusts H2O absorption + secretion
-Atrial natriuretic peptides (ANP) from heart act on kidney to regulate renin secretion AND on pituitary gland to regulate ADH secretion
Primary HTN
-neural mechanisms (5)
- Baroreceptors
- Chemoreceptors
- Increased Angiotensin II
- Wt gain
- OSA
How do baroreceptors contribute to primary HTN?
inhibits INHIBITORY neural inputs; readjust to defend against higher BPs, lessening vagal response and vasodilation unless BP is higher and higher
ex) normally fire and help regulate at SBP 140 but after chronic HTN, won’t kick in until SBP >180
How do chemoreceptors contribute to primary HTN?
activation of EXCITATORY neural inputs from carotid body chemoreceptors > increased SNS activity or can be from inhibition of inhibitory factors from baroreceptors
-more r/t DEVELOPMENT of HTN than progression
How does increased angiotensin II contribute to primary HTN?
vasoconstriction + stimulates release of aldosterone (increased salt + water reabsorption)
How does weight gain contribute to primary HTN?
SNS burns fat but also increases HTN
-reflex sympathetic activity is a compensation the body uses to try burning excess fat but causes overactivity in vascular smooth muscle and kidneys > HTN
How does OSA contribute to HTN?
causes carotid chemoreceptors to reset to a new BP
-leads to increased SNS discharge and hypotension with repeated arterial desat during apneic periods, triggering chemoreceptor BP surges, causing the reflex to reset higher/more sensitive > when pt is awake and breathing normally, body interprets it as hypoxia > sustained increases in SNS activity and HTN
Renal mechanisms of HTN
-kidneys struggle to eliminate excessive salt in modern diet
-when pt chronically HTN, need a higher BP to trigger kidneys to begin excreting more Na+/water to reduce volume (increased volume > increased CO > autoreg response increasing SVR)
-retained Na+ > increased smooth muscle cx > sustained increase in SVR
How does renal sodium retention contribute to HTN?
sodium rtn > increased plasma volume > increased CO > increased SVR
How does sodium increasing smooth muscle cx contribute to HTN?
more smooth muscle cx > stronger vasoconstriction > end organ damage
Vascular mechanism of HTN
normally endothelial lining releases nitric oxidase synthetase > NO > vasodilation
when impaired, will not release NO but release proinflammatory, constricting, and pro-thrombotic factors instead
T/F RAAS is one of the most important mechanisms affecting endothelial cell function, vascular remodeling, and HTN. This system determines ECF volume, vascular resistance, and BP.
true
-hormonal mechanism
Non-pharm tx for HTN:
Baroreceptor activation therapy
-electrical stim of carotid baroreceptors > makes brain think pt is HTN > decreases SNS activity > peripheral vasodilation, reduced renin secretion, increases Na excretion, lower HR
Renal Denervation
-ablation of renal nerves > destroy both afferent and efferent nerves to stop vasoconstriction and renin release/ Na+water rtn (not a good option, kinda weak)
When is HTN usually treated?
stage 2 when SBP >140 or DBP >90
unless CV issues then at stage 1 (130s/80s)
Categories of BP in adults table:
-normal
-elevated
-HTN stage 1
-HTN stage 2
N: <120 / < 80
E: 120s / <80
Stage 1: 130s/ 80s
Stage 2: 140s+/90s+
HTN 1st line tx
- CCB
- RAAS inhibitors (ACEi or ARBs)
- Thiazide diuretics
Anesthesia fun facts about HTN treatments
-CCB
potentiate NMB and hemodynamic changes from IA
Anesthesia fun facts about HTN treatments
-ACEi
HTN/ labile BP when taken on DOS
Anesthesia fun facts about HTN treatments
-beta blockers
increased bradycardia, HoTN, bronchospasm risk
Anesthesia fun facts about HTN treatments
-diuretics
increased risk lyte imbalances, HoTN, arrhythmias
Sites of HTN med action:
-Blood vessels
ACEi
Alpha 1 receptor blockers
AT-1 receptor antagonists
CCB
Vasodilators
Sites of HTN med action:
Kidney
ACEi
Aliskrien
BB
Diuretics
AT-1 receptor antagonists
Sites of HTN med action:
Heart
BB
CCB
Sites of HTN med action:
CNS
BB
Alpha-2 agonists
Preop eval for HTN:
Assess for end organ damage
-vasculopathy, CV issues, renal issues, carotid bruits,
Assess daily meds and average BP
-DC ACEi + ARBs on DOS
-cancel if BP 180/110 or DBP > 110
Monitoring?
-NIBP ok for most unless CV or cerebral vascular issue > A-line
Anticipate goal BP range
-w/in 20% of average or MAP >65
When is it smart to cancel a case for HTN?
180/110 or DBP > 110
Intraop causes of HTN:
Intubation- if pt normotensive expect 20-25mmHg increase, much higher in HTN pt, if bad give Esmolol or Clonidine
Incision-anticipate!
Emergence-pain, excitement, be ready!
Other: hypoxia, pain, hypervolemia, full bladder
Acute postop HTN
-numbers
-when can it happen
-when will it resolve
20% above baseline or SBP > 110
within 1st 2 hr, resolving within hrs
Acute postop HTN
-risks
-causes
-tx
R: bleeding, anastomoses, MI, CHF, CVA, RAAS dysfunction, arrhythmias
causes: DCed HTN meds preop, stress, pain, emergence delerium
Tx: SA antihypertensives (esmolol/labetalol)
Why is M+M higher in pts with chronic HTN experiencing HoTN?
-decreased baroreceptor sensitivity bc used to higher pressure
-loss of vascular elasticity
-often volume depleted from NPO + thiazide diuretics
Pt with chronic HTN experiencing HoTN
tx
1st line = fluids
-then vaso, phenyl, ephedrine
Pt with chronic HTN experiencing HoTN
-regional considerations
-need more fluid preloading
-Tx: more fludis + phenyl, if refractory > vaso or methylene blue
What physiological mechanism/s regulate BP under GA and why?
RAAS stays intact
-IA depress baroreceptor reflex, the SNS, and cause dose-dependent decrease in BP
-again no bueno for pts taking ACEi and ARB bc this shoots down their main support
A HTN crisis is HTN + what?
end organ damage
-CVA, encephalopathy, SAH, MI, renal injury, HF, aortic dissection, etc
HTN crisis
-Tx timing
Guidelines = 10-20% within 1st hr then 5-15% in following 23hr
-too fast = blindness, MI, CVA
When should you NOT correct HTN and when should you correct it ASAP?
Don’t correct: acute ischemic stroke
-permissive <185/110, reperfusion tx <220/120
-need HTN bc perfusion is low to vessels distal to constricted vessel and rely on BP bc autoreg is disrupted
ASAP: acute aortic dissection
-get pressure down, SBP <110 to reduce shearing forces on aorta
HTN crisis Tx
-Nipride
arterial dilator
onset 1 min, effects gone in 10 min
0.25-0.5mcg/kg/min
-AVOID in preg
-MONITOR cyan tox
HTN crisis Tx
-CCBs
Clevedipine- fast onset, titratable, 1/2 life = 1 min
-risk reflex tachy
-CI in severe AS > risk for rapid HTN
Nicardipine - good but not titratable
