3. Objectives:
• At the end of this session, the students will be able to:
§ Define Hypertension
§ Classify HTN
§ Explain the Pathophysiology of HTN
§ Discuss the general treatment of HTN
§ Explain the perioperative management of hyprtensive
pts
§ Discuss the complications of HTN
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4. Introduction:
§ Hypertension is extremely common, affecting over one
billion people worldwide
§ It is responsible for over seven million deaths annually.
§ The presence of hypertension increases the risk of:
üMyocardial infarction,
üHeart failure,
üRenal failure and
üStroke
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5. Introduction...
§ Hypertension (high or raised blood pressure): is a
condition in which the blood vessels have persistently
raised pressure. (WHO)
vBP >140/90 mmHg at least on 2 occasions measured
weeks apart
§ Most common circulatory derangement affecting 25% of
adults in US, 20.6% in Ethiopia.
§ The incidence increases progressively with age
§ Higher in African American population
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8. Pathophysiology of HTN:
§ Essential/primary Vs Secondary hypertension
vEssential:
§ No identified cause
vSecondary:
§ Identifiable cause is present
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9. Pathophysiology of HTN...
vEssential hypertension
§ Accounts for more than 95% of all cases of hypertension
§ Characterized by a familial incidence and inherited
biochemical abnormalities
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10. Pathophysiology of HTN...
= X
COP
BP SVR
HR SV
Blood volume (strongly
influenced by sodium
and fluid handling
abilities of the kidneys
Dependent on: blood
vessels (wall thickness
and vasomotor tone),
metabolic factors, local
environment, and
humeral
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11. Pathophysiology of HTN...
§ Blood pressure are regulated by: baroreceptor reflex and
RAAS
vNeurally mediated Baroreceptor reflex mechanism:
minute-to-minute regulation of blood pressure
§ Initiated by: stretch
receptors within the
aortic arch and
carotid bodies
§ SNS output § SVR, COP
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12. Pathophysiology of HTN...
vHormonally regulated RAAS mechanism: long-term
control of BP
• Stimulated by:
• Reduced COP, renal
perfusion, sodium
intake
• Angiotensin II, ADH
(vasopressin)
• Increase SVR, Na+
and H2O retention
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14. Pathophysiology of HTN...
§ Pathophysiology of arterial hypertension: an increase in
cardiac output, an increase in SVR, or both; due to:
üIncreased SNS activity in response to stress,
üOver production of sodium-retaining hormones and
vasoconstrictors (renin, aldosterone..)
üHigh sodium intake, and inadequate dietary intake of
potassium and calcium,
üDeficiencies of endogenous vasodilators such as
prostaglandins and nitric oxide (NO), and
üThe presence of medical diseases such as diabetes mellitus
and obesity
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15. Pathophysiology of HTN...
§ Hypertension, insulin resistance, dyslipidemia, and
obesity often occur concomitantly
§ About 40% of persons with hypertension also manifest
hypercholesterolemia
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16. Pathophysiology of HTN...
§ Alcohol and tobacco use is associated with essential
hypertension
§ OSA causes temporary increases in blood pressure
üIt leads to sustained hypertension; independent of known
confounding factors such as obesity
üIn deed, ~30% of hypertensive patients manifest OSA
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17. Pathophysiology of HTN...
ØComplications of hypertension:
vLeft ventricular hypertrophy and coronary artery disease.
§ Pressure overload
Concentric:
§ Increase in muscle
mass and wall
thickness,
§ But not ventricular
volume
Ø Impairs diastolic
function: slowing
ventricular
relaxation and
delaying filling
§ Hypertension
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18. Pathophysiology of HTN...
vCoronary artery disease:
§ Chronic arterial hypertension, leading to myocardial
ischaemia and myocardial infarction.
§ Due to a pressure related increase in oxygen demand and
a decrease in coronary oxygen supply resulting from
associated atheromatous lesions.
§ Hypertension is a significant risk factor for death from
coronary artery disease.
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20. Pathophysiology of HTN...
vHeart failure: chronic pressure overload=> diastolic
dysfunction and progresses to overt systolic failure with
cardiac congestion.
vStrokes: result from thrombosis, thrombo-embolism, or
intracranial haemorrhage.
vRenal disease: initially revealed by micro-albuminaemia
may progress slowly and becomes evident in later years
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23. Pathophysiology of HTN...
vClinical signs suggesting end organ damage from
hypertension:
üIschemic heart disease,
üAngina pectoris,
üLeft ventricular hypertrophy,
üCongestive heart failure,
üCerebrovascular disease,
üStroke,
üPeripheral vascular disease, and/or
üRenal insufficiency
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24. Pathophysiology of HTN...
vLab investigations:
üBUN and serum creatinine
üSerum electrolytes (specially K+)
üFBG
üECG
üCXR
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25. Pathophysiology of HTN...
ØSecondary hypertension:
§ Accounts for less than 5% of all cases of systemic
hypertension
§ Secondary hypertension has a demonstrable cause
§ Reno vascular hypertension due to renal artery stenosis is
the most common cause:
üHyperaldosteronism, Pheochromocytoma, Cushing's
syndrome, Pregnancy-induced hypertension, drugs, pain,
aging, thyrotoxicosis,…
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26. Treatment of Hypertension:
§ The goal is to decrease BP:
üLower than 140/90
ü<130/80 if DM and renal disease
§ Lowering BP is important for:
üDecreasing the incidence of CVA
üDecreases the morbidity and mortality associated with
IHD
üIt slows or prevents progression to a more severe stage
of hypertension and
üDecreases the risk of congestive heart failure and renal
failure
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27. Treatment of HTN..
§ Patients with concomitant risk factors and evidence of
target organ damage are most likely to benefit from early
pharmacologic antihypertensive therapy.
§ Pts with no these risk factors may benefit from a trial of
lifestyle modification and subsequent re evaluation before
initiation of pharmacologic therapy.
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32. Treatment of HTN..
vPharmacologic therapy
§ Initiation of drug therapy should occur in tandem with
lifestyle modification
§ Once drug therapy is started patients are seen every 1 to 4
weeks
§ Then every 3 to 4 months once the desired degree of BP
control has been achieved
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33. Treatment of HTN..
§ All anti-hypertensive drugs: act by decreasing the cardiac
output, the peripheral vascular resistance, or both.
§ The classes of drugs most commonly used include:
üThe thiazide diuretics,
üB-blockers,
üACE inhibitors, angiotensin II receptors antagonists,
üCalcium channel blockers,
üa-adrenoceptor blockers,
üCombined a- and b-blockers,
üDirect vasodilators,
üSome centrally acting drugs (a2-adrenoceptor agonists
and imidazoline I1 receptor agonists).
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34. Treatment of HTN..
• Commonly used Long-term management drugs
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35. Treatment of HTN..
§ Use of long-acting drugs is preferable
§ Thiazide diuretics are recommended as initial therapy for
uncomplicated hypertension
üCan also increase the efficacy of multidrug regimens
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36. Treatment of HTN..
§ For hypertensive pts with co morbid conditions, specific
class of anti-hypertensive drugs may be indicated.
§ ACE inhibitors for hypertensive pts with heart failure
§ If mono therapy is unsuccessful, a second drug is added
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38. Treatment of HTN..
vTreatment of secondary hypertension:
§ Treatment of secondary hypertension is often surgical
§ Pharmacologic therapy is reserved for pts in whom
surgery is not possible
§ Certain disease entities may require a combined approach
for optimal outcome
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39. Treatment of HTN..
§ Surgical therapy is reserved for identifiable causes of 2ry
hypertension
üCorrection of renal artery stenosis
üAdrenalectomy for adrenal adenoma or
pheochromocytoma
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40. Treatment of HTN..
§ Pharmacologic therapy:
üACE inhibitors +/- diuretics if renal artery
revascularization is not possible
üSpironolactone/amiloride for primary aldosteronism
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41. Treatment of HTN..
vHypertensive crisis:
§ Typically presents with a BP >180/120
§ Categorized as:
üHypertensive urgency
üHypertensive emergency
§ Pts with chronic hypertension are more likely to present
with urgencies rather than emergencies.
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42. Treatment of HTN..
vHypertensive emergency
§ Patients with evidence of acute or ongoing target organ
damage require prompt therapy to lower SBP
§ Encepalopathy develops when DBP exceeds 150mmHg in
chronic hypertensive pts
§ In parturients it can develop with DBP <100mmHg
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43. Treatment of HTN..
§ A parturient with a DBP >109 mmHg is considered a
hypertensive emergency and requires immediate
management
§ The goal of treatment is to decrease DBP promptly but
gradually
üMAP is reduced by 20% in the 1st hour
üThereafter, the BP can be reduced to 160/110 over the
next 2 to 6 hours
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44. Treatment of HTN..
vHypertensive urgency
§ Situations in which BP is severely elevated, but the patient
is not exhibiting evidence of target organ damage
§ These patients can present with headache, epistaxis, or
anxiety
§ Selected patients may benefit from oral antihypertensive
therapy
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45. Treatment of HTN..
ØPharmacologic therapy:
§ For most hypertensive emergencies:
üNitroprusside: 0.5 to 10 µg/kg/min intravenously is a
drug of choice
üNicardipine infusion is another option and may
improve both cardiac and cerebral ischemia
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46. Treatment of HTN..
ØTx of hypertensive emergencies:
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47. Anesthesia management of HTN:
§ Why is hypertension a headache for Anesthetists:
üCommon disorder
üHigh risk factor for CVD
üEnd organ damage – heart, brain, kidney
üAlteration in cerebral and renal blood flow
üSignificantly affected by perioperative happenings
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48. Anesthesia management of HTN..
§ There are no universally accepted guidelines for
postponement of elective surgery in HTN patients, But:
§ The decision to delay elective surgery in hypertensives
should be based on risk:
üBP >180/110mmHg or DBP: 100 to 115 mm Hg
üEvidence of end organ damage
üMultiple risk factors (DM, smoking, resting ischemia,
elevated cholesterol..)
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49. Anesthesia management of HTN..
§ In such patients, surgery should be deferred :
üAdmit the patient
üInvestigate
üAll risk factors should be controlled aggressively
üRe schedule four to six weeks
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50. Anesthesia management of HTN..
ØPre op evaluation
§ Hypertensive patients should be made normotensive
prior to elective surgery...B/C:
üIncidence of intraop hypertension & MI increases in
hypertensive pts.
üIntraop BP fluctuation is more common in pts with
uncontrolled BP before induction.
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51. Anesthesia management of HTN..
§ No evidence that the incidence of increased post op
complication when hypertensive pts undergo elective
surgery (as high as DBP: 110)
§ However, increased incidence of myocardial re infraction
in hypertensive pts with history of MI
§ In hypertensive pts who exhibit signs of target organ
damage, postponement of an elective procedure is
justified
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52. Anesthesia management of HTN..
§ Patients with ‘white coat syndrome’ are more likely to
have exaggerated presser response and to develop
perioperative MI.
§ Hypertensive pts should be evaluated for presence of end
organ damage preoperatively:
üAngina pectoris, left ventricular hypertrophy,
congestive heart failure, cerebrovascular disease, stroke,
peripheral vascular disease, renal insufficiency
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53. Anesthesia management of HTN..
§ Pts with chronic hypertension are presumed to have
ischemic heart disease until proven otherwise.
§ Renal insufficiency secondary to chronic hypertension is a
marker of a widespread hypertensive disease process.
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54. Anesthesia management of HTN..
§ Review the pharmacology and potential side effects of the
drugs being used for antihypertensive therapy.
§ There is a risk that hemodynamic instability and
hypotension will occur during anesthesia in patients
receiving ACE inhibitors.
§ Discontinue ACE inhibitors 24 to 48 hours preoperatively
in patients at high risk of intraoperative hypovolemia and
hypotension.
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55. Anesthesia management of HTN..
§ Hypotension requiring vasoconstrictor treatment occurs
more often after induction of anesthesia in patients
continuing ARB treatment
§ ARBs better be discontinued on the day before surgery
§ Diuretics???
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56. Anesthesia management of HTN..
vPreop evaluation summary
§ Determine adequacy of BP control
§ Review pharmacology of drugs being administered to
control BP
§ Evaluate for evidence of end-organ damage
§ Continue drugs used for control of BP
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57. Anesthesia management of HTN..
ØInduction of Anesthesia
§ Induction of anesthesia can result in an exaggerated
decrease in BP due to=>
üPeripheral vasodilatation in the presence of a decreased
intravascular fluid volume.
üMore noticeable in patients continuing ACE inhibitor or
ARB therapy up until the time of surgery
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58. Anesthesia management of HTN..
§ Laryngoscopy and tracheal intubation can produce=>
significant hypertension.
§ IV induction drugs do not predictably suppress the
circulatory responses evoked by tracheal intubation
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59. Anesthesia management of HTN..
§ Suppress tracheal reflexes and blunt the autonomic
responses to tracheal manipulation:
üDeep inhalation anesthesia or
üInjection of an opioid, lidocaine, β-blocker, or
vasodilator
üLimit laryngoscopy duration to <15 seconds
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60. Anesthesia management of HTN..
ØSummary of concerns during induction:
§ Anticipate exaggerated BP response to anesthetic drugs
§ Limit duration of direct laryngoscopy
§ Administer a balanced anesthetic to blunt hypertensive
responses
§ Consider placement of invasive hemodynamic monitors
§ Monitor for myocardial ischemia
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61. Anesthesia management of HTN..
ØMaintenance of anesthesia
§ The hemodynamic goal is to minimize wide fluctuations
in BP.
§ Management of intraoperative BP instability is very
important.
§ RA can certainly be used in hypertensive patients.
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62. Anesthesia management of HTN..
vIntra operative hypertension:
§ Light anesthesia & pain is most common cause
§ Volatile anesthetics are useful in attenuating sympathetic
nervous system activity response
§ There is no evidence that one volatile anesthetic drug is
preferable to another
§ A volatile–opioid technique can be used for maintenance
of anesthesia
§ Pancuronium can modestly increase blood pressure, but
not contraindicated
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63. Anesthesia management of HTN..
ØIntra operative hypotension
§ Common in pts who has been treated with ACE inhibitors
or ARBs
§ Can be treated with:
üDecreasing the depth of anesthesia, and/or
üBy increasing fluid infusion rates
üSympathomimetic drugs such as ephedrine or
phenylephrine
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64. Anesthesia management of HTN..
vMonitoring
§ Routine monitoring
§ ECG is particularly useful in recognizing the occurrence
of myocardial ischemia during periods of intense painful
stimulation
§ Invasive monitors if extensive surgery or evidence of
significant end-organ damage
üArterial monitoring
üCVC/PAC
üTransesophageal echocardiography
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65. Anesthesia management of HTN..
vPost op management
§ Postop hypertension is common in chronic hypertensive
patients.
§ It requires prompt assessment and treatment to decrease
the risk of MI, cardiac dysrhythmias, CHF, stroke, and
bleeding.
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66. Anesthesia management of HTN..
§ Hypertension that persists despite adequate treatment of
postop pain may necessitate administration of an iv
antihypertensive medication such as labetalol.
§ Gradually, conversion can be made to the patient's usual
regimen of oral antihypertensive medication.
§ Anticipate periods of systemic hypertension
§ Maintain monitoring of end-organ function
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