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What is normal BP?
systolic <120 and diastolic <80
what is a pre-hypertensive BP?
systolic 120-139 OR diastolic 80-89
What is a stage I HTN BP?
systolic 140-159 OR diastolic 90-99
What is a stage 2 HTN BP?
systolic ≥ 160 OR diastolic ≥ 100
According to the Framingham heart study, what percent of people over age 55 will develop HTN during their lifetime?
90%--MAJOR public health problem!
HTN puts you at risk for what?
- Renal disease
- Peripheral vascular disease
_____ of hypertensive people don't know they have HTN or if they've been told they aren't being treated
2/3--this is a huge problem! Screening is a HUGE part of preventative medicine
BP increases or decreases w/age?
Risk factors increase _________ with an increase in BP
Now, there is more emphasis on the ________ blood pressure than the ________
- systolic; diastolic
- Systolic more accurately predicts CV complications.
What is essential HTN?
primary HTN, no exact cause
What is secondary HTN?
due to some other co-morbidity or cause that ultimately results in increased BP
What TWO factors are involved in regulation of BP?
CO and Peripheral Resistance
What 4 organs are involved in BP control?
- 1. Heart- contractility is job of heart.
- 2. Blood vessels themselves- responsible for SVR or tone.
- 3. Kidneys regulate ECF fluid volume, IV volume in particular.
- 4. Endocrine system-hormones (really modulate the 1st three -the heart as a pump, blood vessels and their tone, & the regulation of IV fluid volume managed by the kidneys)
If we increase ECF, we increase BP. In what TWO ways does this happen?
Direct: increased volume will increase BP by increased preload (venous return) which will increase SV and CO
Indirect: increased resistance
Explain the concept of autoregulation with ECF volume and BP.
the local vasculature responds by constricting or vasodilating to maintain a constant blood flow. (goal to maintain a constant blood flow w/changes in pressure). So CO increases w/increase ECF volume, BP in all tissues will increase. To compensate for that, some vessels will constrict in order to return blood flow back to normal so this constriction will increase total peripheral resistance. So consequently, (two things happen w/increase ECF, increase preload and increase CO & indirect effect because of CO increase in flow, resistance will increase which will also increase BP
Autoregulation works between_____-_______mmHG
What is the effect of salt intake on ECF volume?
- ↑ osm of ECF →↑ stimulation of thirst center → ↑ fluid intake
- by stimulating osmoreceptors in hypothalamus
- ↑ ADH secretion →↑ water reabsorption (insertion of water pores, more water will be absorbed)
- So now not just excess salt but excess water driven by the excess salt intake
TRUE or FALSE. Salt is a major determinant of ECF volume
Usually with autoregulation there are minimal changes in renal blood flow and GFR, but what happens with renal disease?
autoregulation is impaired in renal disease so you see much larger changes in BP
What is pressure natiuresis
if salt goes up, we're excrete more Na+
It is tempting to think about HTN as isolated CV problem. However, no matter how high the CO or the resistance, the _______s really still have ability to return BP to normal by decreasing
what is pressure diuresis?
- ↑ BP causes two things:
- 1. ↑ urine output due to ↑ GFR
- 2. ↓ renal tubular reabsorption
- -↑ peritubular capillary hydrostatic pressure →↑interstitial hydrostatic pressure →↑ u/o
- - ↓ angiotensin II → ↓ reabsorption → ↑ u/o
Provided the kidneys are healthy, if BP goes up, what will they kidneys do?
Excrete both more volume (of urine) and sodium in that urine, which will then return BP back to normal. (Pressure diuresis and pressure natiuresis)
A decrease in renal tubular absorption help decrease BP, how?
- increase in peritubular capillary hydrostatic pressure. So that causes a decrease in reabsorption from interstitial fluid (get increased u/o) Consequently there's less reabsorption from interstitum the hydrostatic pressure in interstitum is also high.
- And a decrease in Angiotensin II (more on another card)
What is the role of Angiotensin II have with renal tubular absorption?
Role of Angiotensin II is that it will cause an increase in Na+ reabsorption by the tubules (What is does normally) also stimulates aldosterone secretion which further enhances Na+ reabsorption.
Normally w/angiotensin II so setting of increase BP and increase in u/o due to increase GFR decrease tubule reabsorption (influence of peritubular capillary hydrostatic pressure and a decrease in angiotensin II) which will decrease reabsorption. So all of this will continue until BP normalizes
What happens to pressure diuresis and natiuresis with chronic HTN? Why?
higher pressures are needed to excrete a given Na+ and H20 load.
- A few reasons why:
- 1. HTN patient may have micro vascular injury to the kidneys that impairs Na+ excretion.
- 2. There may be a defect in RAAS system (hormonal problem) - HTN is sometimes treated w/meds that work along the RAAS pathway.
If total peripheral increases acutely and kidneys function normally, BP should return to normal (d/t pressure diuresis and natiuresis). However if the increase in resistance alters renal blood flow, what will happen??
the kidneys will be affected and things will not resolve as they would w/patient w/normal kidneys. Kidneys must function to manage excess ECF volume (and Na+).
What are the TWO sequential stages of volume loading HTN?
- Stage 1 (Acute phase):
- a. ↑ salt & water intake → ↑ ECF &
- blood volume → ↑ CO
- b. ↑ BP (slower rise due to baroreflex) but that only works for a few days then no longer effective at preventing increased BP
- Stage 2 (Secondary changes):
- a. ↑ total peripheral resistance
- b. ↓ CO (because of autoregulation)
There are 2 things that will return ECF and blood volume to normal together w/a decrease in CO, what are they?
- 1. Increase in resistance in arterioles, that will decrease capillary hydrostatic pressure which then allows the fluid to be reabsorbed from interstitial space back into the circulation.
- 2. With an increase in BP the kidneys (if working normally) will excrete the excess fluid. So after weeks of volume loading (excess salt and water intake) the result in HTN, increase in resistance, however almost complete return of ECF volume, blood volume, and CO back to near normal.
Is the increase in total resistance a cause of HTN in the setting of volume loading HTN?
NO! it occurs after the HTN developed, not as a cause of it, sort of a result of it.
Secondary to HTN rather than being a cause of it.
What are the causes of volume loading HTN?
- Renal failure:
- a. Dialysis maintains ECF fluid volume
- Primary Aldosteronism:
- a. Excess aldosterone secretion by adrenals (steroid hormone that’s secreted by adrenal cortex zone of glomerulus specifically)
- b. Increases rate of renal sodium and water reabsorption (Aldosterone causes Na+ and H2O reabsorption and K+ secretion. If we make excess aldosterone, get more HTN)
If we get excess aldosterone, doe BP Increase or decrease?
what is the definition of HTN (Chronic)?
- Mean arterial pressure greater than upper limit of normal.
- Mean greater than 110 is considered HTN diastolic greater than 90 and systolic greater than 135
What are some increased BP common terminal events?
- 1. Myocardial infarction (excessive workload of heart-HF, CAD, MI)
- 2. Cerebral infarction (damage to major cerebral blood vessels)
- 3. Renal failure (prolonged hydrostatic pressure in blood vessels of kidney leads to tissue destruction)
- ***Volume-loading hypertension from
- impaired ability of the kidneys to excrete any excess ECF
What is renin?
It's a protein enzyme that is part of the RAAS
Renin is synthesized and stored in an inactive form called what? Where is it stored?
- Stored in the juxtaglomerular cells of the kidneys
Explain where the juxtaglomerular apparatus is located and it's parts according to Gutyon.
- located where the ascending limb of loop of Henle passes between the afferent and
- efferent arterioles.
- 2 parts:
- 1. Cells of macula densa
- 2. Juxtaglomerular cells in walls of afferent and efferent arterioles
What happens when BP falls decreasing GFR...(in the kidneys-2 effects to return GFR back to normal)?
1. ↓ resistance of afferent arterioles→ ↑ glomerular hydrostatic pressure- ↑ GFR to normal
2.↑ renin →↑ angiotensin I → ↑ angiotensin II → vasoconstriction of efferent arterioles → ↑ glomerular hydrostatic pressure returning GFR to normal
Explain the detailed version of the RAAS when BP falls
Prorenin molecules in juxtaglomerular cells will split & release renin. Renin converts angiotensinogen (plasma protein) to angiotensin I. Angiotensin I is a mild vasoconstrictor. Then in the lungs angiotensin I is converted to angiotensin II (caused by ACE, angiotensin converting enzyme). Angiotensin II is a powerful vasoconstrictor. Remember the arterioles are resistance vessels, it really effects arterioles causing vasoconstriction and increasing total peripheral resistance. Works somewhat in veins as well, causes mild constriction in veins that will increase preload (increasing venous return). The other thing angiotensin II does, it will cause decreased secretion of salt and water by the kidneys. So consequently that will increase ECF volume, Blood volume, and BP.
Angiotensin II can increase blood volume and cause acute vasoconstriction. Which is more significant long term?
The effect it has on blood volume is more significant than the effect of acute vasoconstriction. Does both but effect on volume is more significant in the long term than the effect on vasoconstriction.
what does decrease GFR do at the loop of Henle?
↓ GFR → ↓ flow via L of H → ↓ NaCl concentration at macular densa (↑ reabsorption)
Is the RAAS significant in acute blood loss?
If we hemorrhage enough to decrease MAP to 50mmHg, what increase will we see in MAP if intact RAAS?
- brings pressure back to about 80mmHg
- BUT w/out intact RAAS, goes from 50mmHg to only 60mmHg
How long does the RAAS system take to become active w/acute hemorrhage?
~20minutes to become fully active (much slower than ANS and baroreflex)
What is the angiotensin mechanism for salt and water retention?
Direct action on kidneys
(causes arteriolar constriction, which will also ↓ renal blood flow, which ↓GFR so less water going out. So ↓ renal blood flow, ↓ pressure in tubular capillaries, that favors reabsorption from interstitial fluid back into the peritubular capillaries. Then angiotensin will directly cause the intertubular endothelial cells to increase both water and salt reabsorption
- Stimulation of adrenal cortex to secrete aldosterone which increases water & salt
what % of cases are essential HTN?
How do you diagnose essential HTN?
Diagnosis of exclusion
What is the epidemiology and genetics of HTN?
- No specific genetic markers
- Likely several loci (but there are loci that have association)
- More common in first-degree relatives
- More common in identical vs. dizygotic twins
- Uneven distribution among racial groups
What is the autosomal dominant contributer to HTN?
Defects within the renal Na+ channels (that is the genetic portion). Also there are genes that involve abnormalities of the RAAS.
There is a specific association of HTN and what three things?
obesity, insulin resistance, and diabetes.
What is the lifestyle connection to HTN?
- Obesity and sedentary lifestyle.
- Weight loss and increased activity are 1st line tx for HTN
What are the characteristics of obese sedentary patients who have HTN? (there are 4)
- ↑ CO (more tissue to perfuse, increased in metabolic demand-even adipose is metabolically active)
- ↑ SNS activity
- (Cause not totally understood,believed to be from hormone leptin that is released form adipose cells, that directly stimulates hypothalamus, which has excitatory effect on vasomotor center of the medulla)
- ↑ Angiotensin II & aldosterone levels
- (increased 2-3x, partly d/t increase in SNS activity causes increase release of renin)
- impaired pressure natriuesiskidneys won’t secrete adequate
- amount of Na+ and water unless the pressure is high or the kidney function is
- improved, increase in SNS and increase in angiotensin II for multiple reasons the untreated HTN will result in kidney loss of function
What are metabolic syndrome risk factors?
- ↑ Triglycerides
- ↓ HDL
- Cellular insulin resistance
- Glucose intolerance
- Visceral obesity
- Excess adipose tissue in abdomen
What are some other names for metabolic syndrome?
Insulin resistance syndrome or syndrome X.
What % of Americans have metabolic syndrome?
How is obesity DIRECTLY related to HTN?
release of angiotensin, augmented blood volume (From large body mass) and increase in blood viscosity.
Insulin is also thought to play a role in the development of essential HTN. How does this work?
(particularly in obese and type II diabetic) impaired transport of glucose into tissues because of insulin resistance. Blood glucose levels rise, causes the pancreas to release more insulin, and get elevated insulin levels which will contributed to HTN d/t SNS . Also see hypertrophy of tunica media of vessels will contribute to increase vascular resistance.
What are the cardiac abnormalities associated with essential HTN?
- ·Many HTN patients and 1st degree relatives have increase SNS (increase HR during stressful situations) results in ↑ CO based HTN.
- ·Blood vessels naturally are also involved here and they’re contribution to total Peripheral resistance HTN, constrict in response to SNS activity.
- ·Abnormal regulation of vascular tone by local factors (↓NO secretion, ↑ endothelin, naturetic peptide).
- ·There are some ion channel defects in the contractile smooth muscle, K+ or Na/K channel defects.
- -Also exaggerated medial hypertophy
What are the CNS abnormalities associated with essential HTN?
- -Increased basal sympathetic tone
- -abnormal stress response
- -abnormal response to signals from signal receptors and arterial-baro receptors
What are the five systemic abnormalities associated with essential HTN?
- Adrenal (hormone secretion)
- **Comes back to statement that
- w/out some sort of renal dysfunction the malfunction in other systems wouldn't
- produce a sustained HTN because the normal kidney should manage the ECF volume and bring the BP back to normal.
What are the renal abnormalities associated with essential HTN?
- Induce volume based HTN by retention of water and Na+. That can be d/t failure to regulate normal renal blood flow. Again d/t ion channel defects like Na & K ATPase pump which will then cause Na retention.
- Dysfunction of RAAS in the kidneys. Usually ↑ BP means less renin secretion, but
- w/essential HTN the renin levels are normal in 60% and high in 10-15% so they’re only decreased in about 25% of patients.
Normally the renin level should decrease with essential HTN. Renin secretion is abnormal is many patients w/essential HTN. It is normal is ____%, it is high in ___% and decreased in only about _%.
- Normal 60%
- High in 10-15%
- Decreased in 25%
When does HTN usually begin?
typically after young adulthood and INCREASES with increasing age
_____ of Americans over 60yr are HTN
The ______ (systolic or diastolic) increases throughout life
The ______ (Systolic or diastolic) increases until about age 50 when it begins to decline
__________ (systolic or diastolic) HTN is more common in young people
- But a significant number of pt. over age 50 have isolated systolic HTN w/normal diastolic numbers
In younger people the increase in BP tends to be driven by _______. sometimes referred to as the hyperkinetic phase of essential HTN
Increased Cardiac Output in the setting of normal total resistance (is the primary abnormality in young people)
As age increases, the effect of CO decreases, what is the increased in BP driven by?
- CO decreases because maybe overtime LV hypertrophy develops, LV gets stiff, decreased diastolic filling, decreases SV and CO. Hypertrophy in the blood vessels, that
- contributes to increase in total peripheral resistance. Hypertrophy of smooth muscle in blood vessels from prolonged exposure to high pressure. Old people its increase in total resistance as major abnormality.
What are some clues to causes of HTN?
- Age (of onset, 20-50=essential)
- Severity (if dramatic = secondary)
- Onset (gradual vs acute- acute = secondary)
- Associated signs & symptoms (ex: renal artery bruit)
- Family history (essential more common in 1st degree relatives, secondary is more patchy and sporadic)
Why is it important to look for clue to causes of HTN? (3 reasons)
- 1. Although we’re not prescribing TX for
- HTN, the TX will vary if primary or secondary cause for HTN.
- 2. If we find a potential secondary cause & TX that, we may cure the HTN.
- 3. If there is an underlying cause, that may have additional anesthesia implications we need to prepare for.
Secondary HTN is more likely if the age of onset is before ___ and after _____
before 20 years old and after 50 years old
(20-50 is the usual age range for diagnosis of essential HTN)
Essential HTN is what % and what are the clues?
- Clues: age of onset 20-50yrs, family hx, normal serum K+, u/a
Chronic renal disease HTN is what % and what are the clues?
- 2-4 %
- Clues: Increased creatinine, abnormal u/a
Primary aldosteronism causes HTN, what % and what are the clues?
- <2%-15% (varies by screening methods)
- Clues: decreased Serum K+
Renovascular causes HTN, what % and what are the clues?
- Clues: abnormal bruit, sudden onset (age >50 or <20), decreased serum K+
Pheochromocytoma causes HTN, what % and what are the clues?
- Clues: Palpitations, diaphoresis, headache
- Weight loss, Episodic htn in 1/3 of pts
Coarctation of the Aorta causes HTN in what % and what are the clues?
- BP in arms > legs, or right arm > left arm
- Mid-systolic murmur between scapulae
- CXR: aortic indentation, rib notching d/t
Cushings syndrome is what % of HTN and what are the clues?
- Clues: "Cushingoid” appearance
When doing a patient evaluation for HTN, what do you look at?
- Detailed H & P looking for “clues”
- Laboratory studies
- --Renal function tests
- EKG (look for LVH)
- Exogenous causes
- --Medications (oral contraceptives, glucocorticoids, erythropoietin, sympathetic drugs (often in OTC) NSAIDs)
When is the serum K low (what types of HTN)
- renal vasculature
What are the three secondary causes of HTN and give examples of each
- Renal causes
- Renal parenchymal disease
- Renovascular disease
- Mechanical causes
- Coartation of the aorta
- Endocrine causes
- ACTH excess
- Thyroid hormone abnormalities
Renal causes of secondary HTN include renal parenchymal disease, describe this
(Cells themselves are damaged) Accounts for 2-4% of HTN patients that can result from many different things. Underlying mechanism for HTN though is increased in volume. Damaged nephrons can’t excrete the normal amount of NA+ and water This is on a continuum, mild parenchymal damage, then renal perfusion pressure then still excreted adequate amount of Na and water but then goes to renal disease then malignant HTN. Also part of parenchymal damage is excessive renin secretions.
Renal causes of secondary HTN include Renovascular disease, describe this.
(renal artery stenosis). Accounts for about 1%. I can be one or both renal arteries (both kidneys) usually d/t atherosclerosis but can be d/t emboli or vasculitis or even some external compression. Mechanism is that there is decrease in renal blood flow because of renal vascular disease, because of the decrease in renal blood flow, there will be lower renal perfusion pressure, cause an increase in renin secretions, and then we go down pathway until we get vasoconstriction and sodium retention from angiotensin II (Na retention from angiotensin II & aldosterone)
A mechanical cause of secondary HTN is coarctation of the Aorta, describe this
Rare congenital narrowing of aorta just distal to the L subclavian artery. Two things happen. 1st is decreased blood flow to kidneys, so there you go off on RAAS. 2nd is there are high pressures proximal to the coarctation. That will stiffen the AoArch there will be accelerated atherosclerosis, and all oft this will blunt the normal aroreflex response to an elevation in BP.
Pheochromocytoma is an endocrine cause of secondary HTN. Describe this
- catecholamine secreting tumor (usually in adrenal medulla, but can be outside of the adrenal gland)
- Account for very small # (0.2%) of HTN pts.
- Release both epi and norepi cuases tachycardia as well as HTN.
- Both the increase HR and HTN, can be chronic or intermittent.
- Patient can describe characteristic severe throbbing headache, profuse diaphoresis and palpitations.
- Autonomic attack, attack on SNS.
- Most will have sustained HTN but some can be normotensive between attacks.
True or False, most pheochromocytomas are malignant.
FALSE! Most pheos are benign. About 10% re found to be malignant.
How do you treat a pheochromocytoma?
Tx involves both alpha and beta blockade and surgical removal. Think just anatomically if surgery involves adrenal gland, just manipulation can cause release of hormones. If having adrenalectomy sue always wants to think about pheo.
Excessi amounts of Adrenalcorticotropic hormone. (ACTH) is an endocrine cause of seconday HTN. Describe this.
- Adrenal cortex will secrete both mineralocorticoid (aldosterone, influences Na+ which is a mineral) and glucocorticoids (cortisol)
- If there is an excess of either, then HTN will result. Aldosterone increases blood volume, reabsorption of Na+ in exchange for K+ (so causes secretion of K+). So if we look at labs, hypokalemia is clue about mineralocorticoid excess.
- Glucocorticoids can be implicated in ↑ BP. This is again volume expansion from stimulation of RAAS pathway. About 80% of patient w/cushing syndrome have some degree of HTN. Lost of causes of excess glucocorticoids
What are a few causes of primary alodsteronism
d/t an adrenal adenoma(which is also referred to Conn syndrome) or from simple bilateral hyperplasia. Hyperplasia is usually the cause.
Primary aldosteronism can be found in ____%of HTN.
About _____% of patient w/cushing syndrome have some degree of HTN
Thyroid hormone abnormalities can be a cause of secondary HTN. Describe this
Thyroid hormones are very similar in structure tocatecholamines (epinephrine). The fact that hypothyroid patient are HTN is surprising They demonstrate more diastolic HTN and increase in peripheral vascular resistance. As opposed to hyperthyroidism, their HTN is more related to hyper cardiac activity (from blast of SNS)
About ____ of pt. who are hyperthyroid and ____ of pt. who are hypothyroid will havesignificant HTN
- 1/3 of hyperthyroid
- 1/4 of hypothyroid
What are the classic s/s of HTN?
What are the more useful s/s of HTN?
- Classic: Headache, Epistaxis, & Dizziness
- Useful: Flushing, Diaphoresis, & Blurred vision
True or False. Most patients who are HTN have symptoms.
FALSE! Most hypertensive patients are asymptomatic
A consequence of HTN is organ damage. What are the organs most likely to be damaged?
- Cerebral vascular system
- Aorta and the peripheral vascular system
If untreated ___% of HTN patients will die of CAD or CHF, about ___% from stroke, and ______% from complications of renal failure.
- CAD/CHF 50%
- Stroke 33%
- Complications of Renal Failure 10-15%
Organ damage reflects the degree of chronic BP elevation. What can it be attributed to?
- Increase workload of the heart.
- Damage to the blood vessels.
- ---Arterial damage from both the increase in BP (weakened vessel walls) and accelerated atherosclerosis.
- ---Blood vessels breakdown, get smooth muscle hypertrophy.
- ---Endothelial cells will be dysfunction, no normal vasodilation/constriction going on. Elastic fibers will fatigue.
- Accelerated atherosclerosis is d/t disrupting natural protective mechanisms (like NO).
- If vessel gets lined w/plaque that plaque can thrombose it can embolize and occlude more distal blood vessels. If talking about a large vessel in atherosclerosis then there is
- also the risk of rupture of an aneurysm
What are the major cardiac effects of HTN?
- LVH & diastolic dysfunction
- ↑ afterload & concentric hypertrophy (increase wall tension in the LV. What the LV does now to deal w/that wall tension is it will hypertrophy)
- ↑ LV filling pressures
- (concentric hypertrophy deceases diastolic filling)
- Pulmonary congestion (from ↑ LV filling pressures)
- Strong predictor of cardiac morbidity
What is concentric hypertrophy?
where new sarcomeres get added in parallel so wall gets thicker, no increase in size of chamber it’s the wall itself gets thicker and stiffer. Because it gets thicker and stiffer, it impairs diastolic filling so diastolic function declines
What are some physical findings you'll see with LVH and diastolic dysfunction?
- heaving in LV impulse on chest palpation from increased muscle mass
- 4th heart sound as LA contracts into the stiff LV
TRUE or FALSE. LVH is one of the strongest predictors of Cardiac morbidity in HTN patients.
- Degree of hypertrophy will correlate w/development of CHF, angina, arrhythmias, myocardial infarction and sudden cardiac death
Can hypertrophy happen w/regular physical exercise?
- YES. Hypertophy is a normal physiologic response to increased stress (why we do strength training)
- Normal physiologic adaptation, Athletes may develop LVH in response to that training. But that type of ypertrophy is really reversible, non pathologic. Upon evaluation you can see if they have LVH, have them stop exercising for a bit and see if goes down, if it does it’s normal
Concentric hypertophy is from chronic _____ overload and with eccentric hypertrophy it’s a chronic ______ overload.
- Concentric = pressure overload
- Essentric = volume overload
In concentric hypertrophy, is diastolic or systolic function impaired?
Describe how eccentric hypertrophy happens?
Volume overload. So you can picture the cavity is filled more w/volume, so new sarcomeres are added in series. Dilation, systolic failure, because the ventricle dilates. If we look at difference in terms of cavity. Concentric the internal radius remains the same or is smaller. W/eccentric hypertrophy there is usual an increase in radius as well as the wall itself dilates.
Describe the pathway for hypertension induced CHF
The increase in wall tension (Association w/HTN) we have a thicker ventricular wall, we have an increase myocardial demand, along w/concentric hypertrophy of the ventricle. So more wall to perfuse, more oxygen required, that leads to coronary insufficiency, infarction, dysrhythmias, and ultimately that can result in HF. The LVH itself resulting stiff ventricles, impaired diastolic filing and HF. Get to HF in a few ways in HTN patient.
what is this showing?
Pressure volume loop for concentric hypertrophy. Again red loop is concentric hypertrophy (white is normal)
Compliance of ventricle is decreased, that increases slope of relationship between filling pressure and volume. ↓ EDV. ↑ EDP ↓ SV.
What are the THREE major cardiac effects of HTN and give examples
- Systolic dysfunction
- --↓ CO
- --Pulmonary congestion
- Coronary artery disease
- --↓ oxygen supply
- --↑ oxygen demand
- Cerebrovascular disease
- --Hemorrhagic stroke
- --Thromboembolic stroke (more common)
What % of pt. who die from transmural MI have a hx of HTN?
- FYI: Transmural infarction = associated w/atherosclerosis involving a major coronary artery
Although ______ pressure is important it's the magnitude of __________pressure that’s
been linked closely to CVAs
diastolic pressure; systolic pressure
TRUE or FALSE. Presence of isolated systolic HTN more than doubles the risk for a stroke
Why are we concerned about keeping the blood pressure within a certain range for EACH patient (so HTN pt get the BP to where it NORMALLY is)?
- Patient may not have a stroke but have cerebral disease d/t HTN.
- Generalization for collateral blood flow for these patient, need higher perfusion pressure. So for us, if BP drops abruptly, worry bout that. Want to keep BP near where they are usually, what range is acceptable for THIS patient. Don’t’ want to decrease BP for bleeding etc. if chronic HTN.
How does HTN effect the Aorta & peripheral vessels?
- Plaque formation (can occur in other arteries other than heart. Common sites are aorta
- and major arteries to lower extremities, the neck and the brain)
- Aneurysm formation (LV and abdominal aorta)
- Aortic dissection (Degenerative changes in wall of Aorta in chronic HTN so the wall that’s degenerating is continuously exposed to high pressure and can start to tear and blood dissects into tunica media)
Triple A (abdominal aortic aneurysm) usually develops where? When is there a high risk of rupture?
- below the level of the renal arteries.
- Greater than 6cm in diameter have high risk of rupture within 2 years if not corrected.
What is the mortality rate of an aortic dissection?
greater than 90% unless its emergently treated w/surgical repair.
How does chronic HTN effec the kidneys?
- Fibrinoid necrosis
- HTN induced renal disease-leading cause of renal failure. Hypertrophy of smooth muscle in blood vessels. Decrease in vascular supply. Renal tubules can become ischemic. If mild HTN, that doesn't’ cause too much of a problem, we have more nephrons than we need as long as there aren't any other insults to kidney but malignant HTN can progress to chronic renal failure. If chronic renal disease, can't get rid of excess it needs to and get chronic HTN.
How does HTN effect the Retina?
- Hypertensive retinopathy
- It’s the only place where systemic arteries can directly be visualized on physical exam. Seen as asymptomatic clinical marker for severity and duration of the HTN. The pt may be unaware of it if the damage is extensive then vision can be compromised. Pt. may be completely unaware of it but benefit to diagnostician to see those vessels.
- Acute malignant HTN can cause small retinal vessels to burst causing hemorrhage.
- If there is ischemia of optic nerve the patient may develop blurred vision.
- If the BP reaches really high levels and cerebral autoregulation fails, there can be a high intercranial pressure and swelling of the optic disc (papilledema).
Lifestyle changes are the 1st line tx for BP. Describe these changes
- 1. Weight reduction
- 2. Exercise
- 3. Diet
- a) Sodium
- b) Potassium
- c) Alcohol
- d) Other
- 4. Smoking cessation
- 5. Relaxation therapy
The kidneys should secrete any excess Na+, but some do not, what % of HTN patients are salt sensitive?
50% of pt w/essential HTN are salt sensitive, they have a defect in natiuresis
Describe this graph
Two curves meant to show two patients w/essential HTN (red represents someone not sensitive to Na intake & blue is sensitive to Na+ intake) The pt. that’ is sensitive, the BP will show substantial increase w/high salt diet. May be structural or functional difference in kidneys.
Does salt sensitivity increase with age?
YES! It’s a continuum (not all or nothing things) salt sensitivity increases w/age after 50yrs. More likely to be salt sensitive as we age (even if we weren't initially)
What patient population (race) appears more salt sensitive?
Na+ _____mg/day is recommended.
Which is 1/3 less than average salt consumption
What types of patients are deficient in K+?
- Tend to occur w/low fruit /veggie diet
- K+ wasting diuretics
- No benefit to giving K+ to normal kalemic individuals. (won’t counteract the Na)
How does alcohol consumption affect BP?
- Chronic alcohol consumption is r/t hypertension and resistance to anti-HTN agents.
- SBP can rise acutely after alcohol intake.
- Mechanism for this is unclear
- Chronic alcoholism is assoc. w/cardiomyopathies
- If pt. decreases alcohol will decrease BP
How does Ca+ and Mg+ effect BP?
Ca+ intake and Mg-deficiency have been associated with HTN but the mechanisms and recommendations are unclear.
Caffeine will transiently increase BP ______mmHg (after a few cups) routine use doesn’t contribute to chronic elevation
When is relaxation therapy useful?
essential HTN w/exaggerated SNS response
How does smoking effect BP?
- transiently ↑ BP
- Nicotinic Ach receptors in autonomic ganglionic, ganglionic blocking medications (Trimethofan) will ↓ BP (blocker)
- Smoking is risk factor for developing sustained HTN.
- The effect of smoking on the blood vessels may contribute to the development of renovascular HTN.
What are the 4 types of pharmacological treatments for HTN?
- Renin-angiotensin-aldosterone system antagonists
When are diuretics useful for controlling HTN?
- mild to moderate HTN w/normal renal function.
- Just as salt sensitivity would indicate, they're good for AA or elderly pts. (who are salt sensitive)
- Thiazide and K+ sparing diuretics. Will promote Na secretion in distal nephron.
- Loop diuretics are too potent and too short acting so not utilized for this purpose.
How do sympatholytics help control HTN?
- Beta blockers & central alpha adrenergic blockers.
- BB ↓ CO and HR and contractility, & ↓renin secretion, ↓ Angiotensin II, ↓ resistance.
- Centrally acting alpha 2 (agonist) like methyldopa and clonidine, ↓ SNS outflow to heart, blood vessels, the kidneys
- Alpha 2 blockers sometimes utilized, Prazosin, this is sometimes used for men w/HTN who also have benign prosthetic hypertrophy.
- (works for both)
- Ca+ channel blockers
Alpha 2 blockers are useful of pheochromocytoma. Not used for chronic essential but are of particular use in that
What is a vasodilator used to control HTN?
- Hydralazine, hydralazine get ↑ HR which can be problematic (maybe combo w/Beta blockers is helpful)
- Vasodilators have effect on other tissues not just kidneys
All drugs effect the RAAS pathway in some form, but what are some drugs that work specifically on the RAAS pathway.
- ACE I & ARBs
- ARBs help to avoid some SE like the cough
- pt. gets on the ACE i.
- *think about drug interaction, right drug for right patient.
what is this showing
- RESPONSE TIME for different BP control mechanisms
- Rapid, intermediate, and long acting
Rapid acting mechanisms for BP control work within seconds to minutes. Describe these mechanisms
For acute change in BP. These are mostly neuro system based Baroreflex, the CNS ischemic response, and the chemoreceptor mechanism.
- So we’re in the OR, within seconds of acute drop BP the smooth muscle in tunica
- media of veins constrict, increase venous return, HR and pumping capacity increase constriction.
The intermediate acting mechanisms for BP control work within minutes to hours, describe these mechanisms
Kicks in when rapid not working so effectively anymore.
- These mechanisms are RAAS, the stress relaxation of vasculature, if BP becomes
- too high the blood vessels will stretch, that will buffer the pressure back to normal.
Also the shift of fluid
occurs to and from the interstitial fluid to readjust blood volume as needed
Long term mechanism for BP control will act within days to years, describe this mechanism
Really the renal blood volume, BP control. Few hours to even begin taking effect but again if the kidneys are working properly this will bring BP almost all the way back to normal. Again this involves aldosterone, RAAS.
What three things are we assessing during the pre-anesthesia evaluation regarding HTN?
- Adequacy of control (normotensive pre-op decreases risk of ischemia during op)
- End organ damage
- Current anti-hypertensives
Are HTN more likely to exhibit HYPOtension during anesthesia?
YES! however increases BP occurs regardless of the degrees of pre-op BP control in pt. w/essential HTN. What we see is that pt. w/dx of HTN, they’re just going to be more labile for use.
How do we assess for end organ damage during the pre-anesthesia eval?
- CV system, cerebral vascular system, kidneys, EKG, renal function tests, any other labs that seem appropriate.
- Think in terms of possibility of ischemic heart disease or possibility of previous episodes of CHF.
- Have a degree on some level of shifted auto regulation
Why do we care what current anti-HTN meds they are on during the pre-anesthesia eval?
Continuing Beta blockade = good thing, d/c beta blockade get rebound HTN, not a good thing. But if the patient is on some of these meds, be mindful of degree of beta blocker, can’t compensate for acute blood loss, can’t increase HR.
Meds alpha 2 agonist may also produce sedation which is additive to anesthesia. (clonidine)
Diuretics, unless K+ sparing, may be hypokalemic and if on something that regulates RAAS may be hyperkalemia.
Combo of beta blocker and ACE-I or ARB are more likely to be labile intra-op. sometimes ACE-I & ARB are held day of surgery, but need heightened awareness and be ready to treat.
What are our concerns for the HTN patient during induction?
- Adjunctive medications
How does our technique effect induction of HTN patients??
- Does pt. need rapid sequence? Can we/should we give medications slow? Keep the dose low, titrating just to effect so selection of induction meds involves not only the drug but the dose we want to give. less is often more.
- Establish what we find acceptable range for HR and BP for THIS patient, and how we’ll TX it. Don't wait for 3-5 min cycle, retake if BP off and get drug to give.
- Minimize the time of direct laryngoscopy
- incorporate it into plan , realize you’re putting that stress on the patient.
What can we give (Front load) for induction so we won't have to give so much of the induction drug (which effects BP)
- Give opioids prior to induction drug that way we can achieve the same thing, lower amount of induction drug and blunt response to laryngoscopy.
- We can also use lidocaine, Can be give IV lido (1.5mg/kg) and if we give this before the propofol, no sting!
- Also can administer topical lidocaine, Can give laryngotracheal lidocaine to squirt directly on vocal cords. But doing that we’re visualizing vocal cords so that’s already stimulating. Don’t’ want to do both. Be mindful that everything is additive.
What kind of drug could we give if our patient is HYPOtensive during induction while still maintaining an adequate depth of anesthesia
In using non depolarizer (time to take effect 2-2.5min or so) need to maintain adequate depth of anesthesia. Hypotensive w/induction drug itself, turn on inhalation agent with a squirt of phenylephrine. Keep pt. anesthetized and BP up.
If our patient is hypertensive and we have used enough opioids/volatiles/etc. so they are adequately anesthetized, what drug(s) could we give?
- Esmolol and labetalol.
- Esmolol is pretty good because it has short duration of action, be aware that the duration of the labetalol may be greater than the duration of the stimulus we’re trying to block. You bought the drug for a greater period of time, the stimulus is now gone and now no longer hypertensive, they’re hypotensive because we gave them some labetolol.
What four things must do during maintenance phase of anesthesia for our HTN patient?
- Treatment of intraoperative hypertension
- Treatment of intraoperative hypotension
During anesthesia, we need to have a goal for HD and a plan to achieve that goal. What is the general plan to do this?
Bear in mind need to maintain anesthetic depth. Can adjust anesthetic (volatiles and propofol are vasodilators) BUT a better way is to use anesthetics for anesthesia and the vasoactive for HD.
How often should you check the BP in the OR?
Standard is BP at least Q5min or more frequent. Recheck BP before TX (esp. if dramatic difference) after TX always check BP (after it’s circulated-if too soon TX old #) to see if TX worked or trending up or down.
What types of things should we keep in mind when picking type of anesthesia can we do for HTN patients? (GA, TIVA, etc)
- TIVA or primary inhalation technique is appropriate for HTN patient but effect HD
- Regional is also ok, as we saw spinal anesthetic results in sympathetic blockade so get ↓ BP.
What may be the plan for tx of hypertension intra-op?
- increasing the depth of anesthetic or we can also use esmolol or labetalol.
- Think of contraindications for those drugs. If reactive airway disease, don’t give non selective beta blocker.
What could be our general plan for tx of hypotension intra-op
- ephedrine or phenylephrine
- Increasing preload w/crystalloid or colloid
What are our concerns during emergence of the hypertensive patient?
- Assessment & management of postop HTN
- a) BP and HR will increase particularly in HTN pt. (really in everyone) because antimuscurinic medications used for part of NM blockade reversal.
- b) Think are they in pain? Where do we think they are in analgesia?
- c) One source of discomfort is a full bladder. (If gave a lot of volume, think of that)
- d) SNS stimulation can see as HTN and HR, can result from hypercarbia and hypoxemia. Can get SNS stimulation when not adequate ventilation.