2. DEFINITION
Sustained systolic blood
pressure above 140 mmHg
or a diastolic pressure
above 90mmHg
ESSENTIAL HYPERTENSION:It
can be defined as a rise in blood
pressure of unknown cause that
increases risk for cerebral,cardiac
and renal events.
SECONDARY
HYPERTENSION:Rise in blood
pressure due to an identifiable
cause.
3. ISOLATED SYSTOLIC HYPERTENSION:SBP≥140 mmHg and
DBP<90 mmHg
WHITE COAT HYPERTENSION:High Bp in the physician's office
with normal BP at rest or while ambulatory
HYPERTENSIVE
URGENCY:Diastolic BP>120mmHg.Distinguished from
hypertensive emergencies by lack of acute progressive target
organ damage.
5. PATHOPHYSIOLOGY
• AUTONOMIC NERVOUS SYSTEM
Normal – Integration of input from cardiac stretch
receptors, vascular baroreceptors and peripheral
chemoreceptors with central regulatory processes
and emotional stress. These control the cardiac
output, vascular resistance and blood volume.
Abnormal – Hypertension associated with
dysregulation of baroreceptors and chemoreflex
pathways both peripherally and centrally
New concepts – Evidence for a novel renin –
angiotensin system within the brain. Activation of this
pathway in response to oxidative stress and
inflammation increases sympathetic nervous system
output and arginine vasopressin release and inhibits
baroreflex regulation.
6. New concepts: • Local production of angiotensin II occurs in various tissues including fat, blood vessels,
heart, adrenals, and brain. AII cleavage by non-ACE enzymes including the serine protease chymase • A
recently described counterregulatory renin-angiotensin pathway that decreases blood pressure and target
organ damage
Abnormal: Dysregulated renin release leads to elevated renin levels, angiotensin II overproduction,
increased aldosterone, and hypertension.
Normal – : acute and sustained control of extracellular fluid volume, peripheral resistance, and blood
pressure based largely on peripheral sensors and effectors. Renin released from the kidney in response to
decreased blood pressure hydrolyzes angiotensinogen → angiotensin I that is then cleaved to angiotensin II
by angiotensin-converting enzyme (ACE) located on vascular endothelium in the lung. Angiotensin II →
vasoconstriction, adrenal release of aldosterone → kidney reabsorption of salt and water.
CLASSICAL RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
7. ENDOGENOUS VASODILATOR/VASOCONSTRICTOR BALANCE
Normal: The vascular endothelium produces a range of vasoactive substances in response to
pressure and the shear force imparted by pulsatile blood flow. Nitric oxide (dilation) and endothelin
(constriction/dilation) in particular are major regulators of vascular tone. Other vasoactive
substances include the peptides atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and
urodilatin. ANP and BNP are released from myocardium, and urodilatin is renal in origin. These
peptides exert vasodilation along with natriuresis and blunting of reninangiotensin-aldosterone
responsiveness by activation of the NP receptors.
Abnormal: With hypertension, oxidative stress in particular has been linked to impaired endothelial
function, leading to “feedforward” changes in vascular tone, vascular reactivity, and coagulation and
fibrinolytic pathways. Disruption of NP release or receptor response may be present.
New concepts: • The NPs are degraded by the enzyme neprilysin, and endothelin-1 formation
requires endothelin-converting enzyme. • Therapy directed toward neprilysin inhibition in
combination with an endothelin-converting enzyme inhibitor or angiotensin receptor blocker may
promote vasodilator/natriuretic effects of the natriuretic peptides while reducing the deleterious
vasoconstrictor/proinflammatory effects of endothelin 1 and angiotensin II.
8. CAUSES OF SECONDARY HYPERTENSION
DRUG INDUCED
ESTROGEN OCPs
NSAID IBUPROFEN, COX-2 Inh, NAPROXEN
STEROID PREDNISOLONE, METHYL PRED
PSYCHIATRIC BUSPIRONE, CARBAMAZEPINE,
CLOZAPINE, FLUOXETINE, LITHIUM,
TCA
ILLICIT COCAINE, AMPHETAMINES
HERBAL EPHEFRA, GINSENG, MA HUANG
9. CAUSES OF SECONDARY HYPERTENSION
AGE DEPENDENCE / NON - DRUG INDUCED
AGE GROUP % M/C ETIOLOGY
CHILDREN ( UPTO 12 YRS) 70 - 85 RENAL PARENCHYMAL DISEASE
COARCTATION PF AORTA
ADOLESCENTS (12 – 18 YRS) 10 - 15 COA
YOUNG ADULTS (19 – 39) 5 THYRPOID DYSFUNCTION,
FIBROMUSCULAR DYSPLASIA
RENAL DISEASE
MIDDLE AGED ( 40 – 64) 8 – 12 ALDOSTERONISM, THYROID
DYSFUNCTION, OSA, CUSHING’S,
PHEOCHROMOCYTOMA
OLDER ( > 65) 17 ARTHEROSCLEROTIC RAS, RENAL
FAILURE, HYPOTHYROIDISM
10. HYPERTENSIVE EMERGENCY
• Marked hypertension with acute target organ damage like
hypertensive encephalopathy,intracerebral hemorrhage or
inf,unstable angina pectoris or acute myocardial infarction,acute
left ventricular failure with pulmonary edema,dissecting aortic
aneurysm,eclampsia of pregnancy
11. EFFECTS OF PERIOPERATIVE
HYPERTENSION
CVS EFFECTS:
• Increased BP Increased afterload and myocardial oxygen
demand myocardial oxygen supply and demand imbalance
• Chronic increased BP myocardial hypertrophy myocardial
oxygen supply and demand imbalance
• Hypertrophied myocardium decreased compliance abnormal
diastolic filling
12. • Diastolic dysfunction especially apparent during
stress,important during surgey and acute recovery interval
• Hypertensive patients more dependent on preload and atrial
contribution towards filling for maintainance of cardiac output
• Maintain preload and nomal sinus rhythm
13.
14. • CNS EFFECTS:
• Increased risk of stroke
• Chronic hypertension causes a shift to the right in cerebral autogulation
• Decrease in cerebral blood flow and cerebral ischemia occur at higher blood
pressures than in normotensive patients
• Long term therapy:autoregulation curve shifts leftward normal
• Treatment of hypertension significantly reduces the incidence of stroke
• Impaires cerebral autoregulation
• EFFECTS ON RENAL FUNCTION:
Effective control of BP prevents renal dysfucntion
40. METHODS TO BLUNT THE SYMPATHETIC RESPONSE
IV ESMOLOL(1-2mg/kg,
IV
LIGNOCAINE(1.5mg/kg,
90 Sec before
intubation/extubation
Short acting
narcotics(FENTANYL 2-
3mcg/kg,SUFENTANIL
0.3-0.5mcg/kg
Increased concentration
of inhalational agents
IV NTG IV LABETALOL
41. Preoperative use of Beta
blockers or clonidine
smoothen intraoperative
blood pressure
Choice of anesthetic
techniques and medications
on the basis of presence of
comorbid disease and type
of surgery(Avoid Ketamine)
Hypertensive patients
treated with diuretics or
having LVH more
susceptible to vasodilatory
effects of inhaled
anesthetics and neuraxial
blockade
42. POSTOPERATIVE CONCERNS
POSTOPERATIVE
HYPERTENSION:Arbitrarily
defined as SBP>190 mmHg
and/or DBP≥100 mmHg on
two consecutive readings
following surgery.
IMPLICATIONS: Risk of hemorrhage
Distruption of vascular or
cardiac suture lines
Cerebral edema
Increased myocardial wall
stress and oxygen
consumption
43. CAUSES...
• Preoperative hypertension
• Withdrawl of antihypertensive
medications
• Pain
• Emergence delerium
• Hypoxia
• Hypercarbia
• Hypothermia
• Hypervolumia
• Type of surgery
44. MANAGEMENT
• Life style modifications
• Antihypertensive medications
• Aggressive pain management
• Correction of causes
49. • Resistant hypertension, defined as uncontrolled blood
pressure despite three or more antihypertensive drugs of
different classes, including a non potassium-sparing diuretic,
or the need for four or more drugs to achieve control is
present in 10%–15% of the hypertensive population.
• Refractory hypertension, defined as uncontrolled blood
pressure on five or more drugs, is present in 0.5%. Even
more common is intolerance to antihypertensive drugs or
simple noncompliance
