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Normal BP values
<120 / <80
120-139 / 80-89
stage 1 htn values
stage 2 htn values
≥160 / ≥100
What % of ppl with HTN don't know it or are untreated?
What percentage of ppl over age 55 will get HTN?
What normally happens to BP with advancing age?
Increases, but not necessarily to an acceptable level
Does SBP or DBP more accurately predict CV complications
SBP, in the past DBP was emphasized more
What factors influence systemic BP?
CO and peripheral rx
- CO= HR X SV
- Peripheral rx is affected by: circulating regulators (catecholamines, angio II), direct innervation (alpha1 and beta2 receptors), local regulators (NO), blood viscosity (Hct)
What 4 organs have major involvement in BP control?
Heart (contractility), BV themselves (SVR- tone), kidneys (regulate ECF (IV) volume), endocrine (hormones modulate the 1st 3)
What factors affect SV?
Venous return, venous tone (afterload), blood volume (renal function), contractility
What is autoregulation of ECF?
What occurs with increased ECF?
At what ABP does it occur at?
- -Autoregulation- local vasculature VC or VD to maintain constant blood flow.
- -With increased ECF vasoconstriction occurs, this increases TPR, which increases arterial pressure, which leads to increased urine output
- -Autoreg occurs btw 75-160 mmHg
How does increased ECF directly cause an increase in BP?
Increased ECF causes increased blood volume, increased preload, which increases CO
How does increased ECF indirectly cause an increase in BP?
Increased CO (direct effect) increases blood flow to all tissues, some vessels constrict to return blood flow back to normal, autoregulation causes an increase in TPR and an increase in BP
Does auto regulation effect GFR or renal blood flow?
No, minimal change only. Autoregulation is impaired in renal disease, so there are much larger changes
What is the effect of salt intake?
- ECF (plasma) osmolarity increases, this stimulates the thirst center and fluid intake increases.
- There is an increase in ADH secretion (released by hypothalamus), water pores are inserted, there is increase water reabsorption
What is pressure diuresis?
- -Increase in arterial pressure causes increased urine output (due to increased GFR)
- -There is also increased sodium excretion (pressure natriuresis)
In what 3 ways do the kidneys regulate intravascular volume?
- 1) urine output
- 2) decreased reabsorption
- 3) decreased angiotensin II (this further decreases reabsorption)
What occurs with increased volume to decrease renal tubular reabsorption (and thus decrease urine output)?
- -Increased volume causes increased BP, this causes increased peritubular capillary hydrostatic pressure, increased interstitial hydrostatic pressure, increased urine output
- -Increased BP means less angiotensin II, less reabsorption, increased UO
What effect does angiotension II have (2 major effects)? When is it released?
- -Causes vasoconstriction
- -Causes decreased excretion of salt water
- -Stimulates aldosterone which further enhances reabsorption
- -Released at low BP
Regardless of rx or CO the kidneys can return the BP to normal by decreasing IV volume, T or F?
Pts with chronic hypertension need a higher blood pressure (and capillary hydrostatic pressure) to excrete a given water and sodium load, why?
- -In the HTN pt, there are microvascular kidney injuries that impair Na+ excretion
- -Defective RAAS- hormonal problem
What occurs in stage 1 (acute phase) of volume loading HTN?
- -There is increased salt and water intake, this increases ECF and blood volume, CO increases (this is the basic cause of HTN)
- -BP rises, although slower due to baroreflex (BR takes a few days to adapt to new BP and can no longer prevent the rise in BP)
What occurs in stage 2 (secondary changes) in volume loading HTN?
- -Secondary changes occur over a few weeks
- -There is an increase in total peripheral rx (TPR) and a decrease in CO (due to autoregulation)
In what situation would volume-loading HTN occur?
Renal failure- there is an impaired ability of the kidneys to excrete excess ECF
Primary aldosteronism- excess aldosterone secreted by adrenals, increases rate of water and sodium reabsorption
What 2 factors decrease ECF and blood volume back to normal in the second stage of volume loading HTN?
- 1) Increased resistance in the arterioles decreases capillary hydrostatic pressure, fluid can now be reabsorbed from ISF back into the blood
- 2) With increased BP, the kidneys will excrete excess fluid
After weeks of volume loading would there be an increase or decrease in the following: BP, TPR, ECF volume, CO?
- -BP increased
- -TPR increased
- -Almost complete return of ECF volume and CO back to normal
Is the increased TPR found in volume loading HTN because of the HTN of a cause of the HTN?
Increased total peripheral resistance in volume loading HTN is secondary to the HTN, NOT a cause of it
What are common causes of death from chronic HTN?
- 1) MI- due to excessive cardiac workload
- 2) cerebral infarction- damage to cerebral vessels
- 3) renal failure- prolonged increase in hydrostatic pressures damages kidney blood vessels
What MAP is considered indicative of chronic hypertension?
- MAP > 110 mmHg
- Can occur with SBP > 135 and DBP > 90 mmHg
Where is renin stored?
In the juxtaglomerular cells of the kidney
In what form is renin stored as?
Stored in inactive form: prorenin
What causes renin release?
Is renin an enzyme or vasoactive substance?
It's an enzyme
Where is the juxtaglomerular apparatus?
In the kidney, near the ascending limb of the loop of Henle where it passes between the afferent and efferent arterioles
What are the 2 parts of the juxtaglomerular apparatus?
- 1) cells of the macula densa
- 2) juxtaglomerular cells in walls of afferent and efferent arterioles
BP decreases and the renin angiotensin system is activated, describe what happens.
- Prorenin splits
- Renin released
- Renin converts angiotensinogen to angio 1
- Lung converts angio 1 to angio 2
What is angiotensin I
A mild vasoconstrictor
What effects does angiotensin II have?
- 1) potent vasoconstrictor (increased TPR)
- 2) decreased excretion of water and salt
Net effect: increased BP and increased blood volume
Angiotensin II causes both vasoconstriction and decreased excretion of water and salt, which is longer term and more significant?
It's affect on blood volume
Angiotensin II direct and indirect effect on kidneys to retain salt and water.
Direct- acts directly on kidneys to cause salt and water retention
Indirect- causes adrenal glands to secrete aldosterone which increases salt and water reabsorption by the kidney tubules
How does angiotensin cause increased water and salt absorption at a cellular level?
It causes arteriolar constriction, this decreases renal blood flow, decreases GFR, decreases the pressure in the peritubular capillaries, this favors reabsorption from ISF back into the peritubular capillaries, and hence causes increased water and salt reabsorption
What percent of HTN cases are primary HTN?
What is primary HTN?
- -There is no identifiable cause for the HTN.
- -It's a diagnosis of exclusion.
- -Due to failure of normal homeostatic mechanisms due to acquired defect, possible genetic component
What supports the genetic component of primary HTN?
-More common in 1st degree relative and identical twins, uneven distribution among racial groups
How can obesity contribute to essential HTN?
- -Increased CO (more tissue to perfuse, increased metabolic demand)
- -Increased SNS activity (leptin released from adipose cells stimulates hypothalamus and affect vasomotor center- excitatory effect)
- -Increased angio II and aldosterone levels (due to increased SNS)
- -Impaired pressure natriuresis (kidneys won't excrete adequate amts of Na and water unless pressure high)
What is metabolic syndrome? What are other names for it?
-HTN, incr. triglyc., decr. HDL, cellular insulin rx, visceral obesity (around the abd)
-AKA ins rx syndrome or syndrome X
What percent of americans have metabolic syndrome?
How does insulin rx play a role in the essential HTN?
- -Impaired glucose transport into tissues, causes increased BG levels, causes pancreas to release more insulin, elevated insulin rx, HTN due to increased SNS activity
- -Also causes hypertrophy of tunica media leading to increased vascular rx
Essential HTN is associated with abnormalities in what systems?
- -Blood vessels
What abnormalities are associated with the heart in essential HTN?
-Increased SNS activity, increased HR in stressful situations (whitecoat syndrome), high CO
What abnormalities are associated with the blood vessels in essential HTN?
- -Contribute to TPR, constrict in response to increased SNS activity
- -Abnormal regulation of normal vascular tone by local factors (NO, endothelin)
What abnormalities are associated with the kidney in essential HTN?
- -volume based HTN due to water and salt retention
- -failure to regulate normal renal blood flow
- -should have decreased renin production but many have normal or increased renin production
T or F, even with malfunction of BV and heart for example, the kidneys should be able to prevent HTN by brining the BP to normal by ECF elimination?
What are characteristics of primary hypertension (age, severity, onset, family hx)?
- -Usually diagnosed between the ages of 20-50 yrs
- -Gradual onset
- -Family history
- -K normal
What are characteristics of secondary hypertension (age, severity, onset, family hx)?
- -Age of onset < 20 or > 50
- -Dramatic and acute onset
- -Abnormal K (low)
In looking for clues regarding diagnosis of primary vs. secondary HTN, what would a low K signal?
Possibility of primary aldosteronism or renovascular causes of secondary HTN
What are causes of secondary HTN?
- -chronic renal dz
- -primary aldosteronism
- -renovascular dz
- -coarctation of aorta
- -Cushing's syndrome
What are some exogenous causes of HTN?
- -Meds (OCP, glucocorticoids, erythropoitin)
What would one look at for clues regarding cause of HTN?
- -Labs (u/a, BUN/Cr, K, glucose, chol)
- -EKG (LVH could determine chronicity of HTN)
How can pheochromocytoma cause secondary HTN?
What percent of pt's with HTN have this?
- -Catechol secreting tumors usually in adrenal medulla
- -Release both NE and epi to cause HTN tachycardia (usually sustained)
- -0.2% of HTN its
Characteristics of pheochromocytoma pt with HTN?
- -Severe throbbing headache, profuse diaphoresis, palpitations
- -An attack of the ANS!!!
- -Wt loss
- -Episodic HTN (non sustained) in 1/3 of its
How can excess ACTH cause secondary HTN? IE what other diseases can it cause?
- -Primary aldosteronism increase in mineralocorticoids (aldosterone)
- -Cushing's syndrome increase in glucocorticoids (cortisol)
How can primary aldosteronism cause secondary HTN?
What percent of HTN pts have this?
- -adrenal adenoma (Conn syndrome)
- -bilateral hyperplasia
- -increased blood volume and reabsorption of Na+ (K+ excretion), hence decreased K is a clue!!
How can Cushing's syndrome cause secondary HTN?
What percent of HTN pts have this?
- -Excess cortisol secretion by adrenal cortex
- -Cortisol stimulates RAAS pathway and expands blood volume
How can hyperthyroidism cause secondary HTN?
What percent of hyperthyroid pts have HTN?
-SNS stimulation and cardiac hyperactivity
-1/3 have HTN
How can hypothyroidism cause secondary HTN?
What percent of hypothyroid pts have HTN?
- -Increased TPR, DBP HTN
How can renovascular disease cause secondary HTN?
What percent of HTN pts have this?
- -Or renal stenosis
- -1 or both renal arteries
- -usually due to arteriosclerosis, or external compression, emboli, or vasculitis
- -Decreased renal blood flow, decreased renal perfusion pressures, increased renin secretion, increased angio 2, increased aldosterone, VC
How can renal parenchymal disease cause secondary HTN?
What percent of HTN pts have this?
- -Increased intravascular volume damages nephrons and they can't excrete water and Na+
- -Can progress to ESRD
- -Excessive renin secretion can cause renal cell damage
How can coarctation of the aorta cause secondary HTN?
What percent of HTN pts have this?
- -Congenital aortic narrowing, just distal to left SC artery origin
- -Narrowing is beyond arterial branches to head and arms but before renal arteries
- -High pressure proximal of coarctation stiffens the aortic arch, accelerates artherosclerosis, and blunts the BR response to increased BP
What's a major clue to aortic coarctation as a cause of HTN?
BP higher in arms than in legs
What symptoms can identify HTN?
- -Most pts are symptomatic
- -Flushing, diaphoresis, blurred vision
What are the major organs affected by HTN?
- -Aortic and peripheral vascular system
How does HTN cause damage to the blood vessels?
- -Weakened vessel walls can accelerate artherosclerosis
- -Smooth muscle hypertrophy due to BV breakdown
- -Fatigue of elastic fibers
- -Disruption of normal protective mechanisms like NO
- -plaque can rupture or embolize and occlude distal vessels
Do young ppl usually have DBP HTN or SBP HTN?
Older pts more likely to have isolated SBP HTN
How does SBP vary throughout the lifespan?
- -SBP rises throughout life
- -DBP rises until age 50, then declines
What mechanisms are responsible for HTN in young ppl?
- -Increased CO, normal TPR
- -Called hyperkinetic phase of essential HTN
What mechanisms are responsible for HTN in older ppl?
- -Increased resistance due to hypertrophy of the blood vessels
- -CO has less of an effect
What is the hyperkinetic phase of EH?
- -Increased CO causes HTN
- -TPR is normal
- -Seen in young ppl
What is the major cardiac effect of HTN?
LVH and diastolic dysfunction
What type of hypertrophy develops with LVH?
-Concentric due to increased wall tension in the LV
Describe the changes in cardiac muscle that cause concentric hypertrophy
-New sarcomeres are added in parallel
-The wall becomes thicker, the wall radius does not change, diastolic function is impaired
What is the strongest predictor of cardiac morbidity?
LVH, the degree of hypertrophy correlates with CHF, MI, sudden cardiac death, and arrythmias
Does chronic pressure or volume overload cause concentric hypertrophy?
Does chronic pressure or volume overload cause eccentric hypertrophy?
Describe the changes in cardiac muscle that cause eccentric hypertrophy
- New sarcomeres are added in series
- Dilation occurs
- Radius increases
How can HTN cause CHF?
- Increase myocardial wall tension causes:
- -Increases myocardial O2 demand causing coronary insufficiency, and infarction or arrythmias
- both lead to CHF
What changes in SV, EDV, EDP, and filling (compliance) are seen with diastolic dysfunction?
- -Decreased SV
- -Increased EDP
- -Decreased EDV
- -Filling is impaired (decreased compliance)
What percent of pts who die from transmural MI have HTN?
What post MI complications does HTN put ppl at risk for?
CHF, ventricular wall rupture, LV aneurysm
What factor regarding HTN is mostly closely linked to CVAs?
magnitude of SBP
What do you need to consider when managing the HD status of a patient who is chronically hypertensive in terms of cerebral perfusion pressure?
Pt will need higher perfusion pressure to maintain cerebral blood flow. Should try to maintain them near their normal BP.
Explain why HTN is a major cause of CAD.
There is a combination of accelerated artherosclerosis in the coronary arteries, decreased O2 supply but increased O2 demand due to thick wall
T or F, LVH is compensatory at first, but later is unable to balance against continued HTN. The continued high BP leads to decreased ability of the LV to contract, and systolic function decreases.
What effects can HTN have on the aortic and peripheral arteries?
- -plaque formation
- -aortic dissection
What are the most common sites for plaque formation?
Aorta and major arteries to LE, neck, and brain
How does HTN contribute to aortic dissection?
- -Causes degenerative changes to the wall due to increased BP
- -Tears can occur as the wall is exposed to high pressure
- -Mortality rate is >90% unless surgically treated
What effects can HTN have on the kidneys?
- -fibrinoid necrosis
What's the only place where direct visualization of systemic arteries can be seen on PE?
What effect can HTN have on the retina?
What can papiledema be a sign of?
- Increased BP
- -Increased BP, cerebral autoregulation fails, high ICP, causes optic disc swelling, and papiledema
What clinical s/sx can be seen with hypertensive retinopathy?
- -Can be an asymptomatic clinical marker of severity and duration of HTN
- -Hemorrhage of small retinal vessels from acute malignant HTN
- -Blurred vision from optic nerve ischemia
Recommended Na+ intake
2.3- 2.5 g / day
What lifestyle changes can decrease BP
- -weight reduction
- -decreased ETOH
- -smoking cessation
- -relaxation therapy
Chronic ETOH use is associated with HTN and medication resistance, T or F?
Why is sodium rx to reduce BP controversial?
Because the kidneys should excrete excess sodium, however some ppl are salt sensitive and others are not
What occurs in ppl who are "salt sensitive"?
- -Their BP increases with an increase in Na+ intake
- -this is opposed to ppl who are not salt sensitive where an increase in Na+ intake does NOT cause increased BP
Is salt sensitivity an all or nothing phenomenon?
No, it's a continuum
What factors are associated with increased salt sensitivity?
- -African american race
- -age > 50 yo, salt sensitivity increases with age
Are Mg and Ca deficiency associated with HTN?
Yes, uncertain MOA
Is chronic caffeine use associated with HTN? What about right after drinking 2 cups of coffee?
- -Chronically there is no increase in BP.
- -After 2 cups of coffee there is a transient increase in BP by 5-15 mmHg
Do we use loop diuretics to treat HTN?
No, they are too potent and short acting
What classes of drugs are used to treat HTN?
- -RAAS antagonists (ACEIs and ARBs)
What types of HTNive pts benefit from diuretic therapy?
-Elderly, african americans, and salt sensitive ppl
What are examples of sympatholytics used to treat HTN?
BB, alpha blockers, and alpha2 agonists
How do BB decrease BP?
- -Decrease CO, HR, and contractility
- -Decrease renin and angiotensin II, decreased rx
What's an example of an alpha 2 (??? alpha 1) blocker? Who would benefit from this?
- -alpha 1 has minimal cardiac effects
- Men with HTN and BPH
What are examples of alpha 2 agonists and how do they work?
- -Clonidine and methyldopa
- -Decrease SNS outflow to the heart, BV, and kidneys
What are examples of rapidly acting mechanisms of BP control? How long does it take for them to work?
- -Baroreceptor, CNS ischemic response, chemoreceptor mechanism
- -Secs to mins
What are examples of intermediate acting mechanisms of BP control? How long does it take for them to work?
- -Stress-relaxation of vasculature (with increased BP blood vessels stretch to buffer pressure back to normal)
- -Fluid shift (to and from ISF to readjust blood volume PRN)
- -Mins to hours
What are examples of long acting mechanisms of BP control? How long does it take for them to work?
- -renal blood volume control can return BP almost back to normal if kidneys are working properly
- -also involves RAAS and aldosterone
- -days to yrs
In our pre-anesthesia evaluation, what factors are we looking at regarding HTN?
- -adequacy of control
- -end organ damage
- -current anti-hypertensives
What can we expect in terms of intraop BP in a poorly controlled HTN pt?
What can we expect in terms of intraop BP in the general HTN pt?
How might we control intraop HTN?
- -Increase anesthetic depth
- -Esmolol or labetalol
How might we control intraop hypotension?
What effect does spinal anesthesia have on BP?
Hypotension due to SNS blockade
What's a benefit of using clonidine?
It also causes sedation
How can we blunt the response to laryngoscopy?
- 1) IV lido or LTA lido (squirt onto VC), dose is 1.5 mg / kg, do NOT do both due to risk of toxic dose
- 2) Front load with opiates before induction, this will also decrease the amount of induction agent needed.