Transcript Slide 1

‫سورة طه آيه ‪114‬‬
By
Dr. Mohamed Sayd Shorbagy
1.
Patient
marked
planned
for
hypertension
urgent
surgery
preoperatively,
with
blood
pressure should be maintained intraoperatively
in the range of:
a) 100/60
b) 130/80
c) 150/90
2. Most fatal hypertensive crisis to
be diagnosed preoperatively is:
a) Acute porphyria
b) Hyperthyroidism
c) Pheochromocytoma
3. Most important drug to be continued
till the time of surgery is:
a)
Calcium channel blocker
b)
β blocker
c)
Diuretics
4. Patients with essential hypertension
are usually:
a)
Hypovolemic
b)
Normovolemic
c)
Hypervolemic
5. Fenoldopam is a:
a) Dopamine receptor agonist
b) Angiotensin receptor blocker
c) Brain natriuretic peptide
Classification
 The prevalence of hypertension (HTN) is about 2025% of the general population, making it the most
common preoperative co-morbidity.
 Isolated Systolic Hypertesion (ISD) is the most
common subtype of hypertension
affecting
predominantly individuals older than 60 years of age
with approximately half of these individuals having
very wide pulse pressure (>65 mmHg) or pulse
pressure hypertension (PPH).
 Isolated diastolic hypertension (IDH) is most
prevalent in indiviuals younger than 50 years and is
an important marker of coronary heart disease.
Etiology
 Essential hypertension. Unkown etiology.
 Renal, Acute and chronic glomeruloephritis,
renovascular stenosis.
 Endocrine. Adrenal-Cushing’s syndrome,
pheochromocytoma, hyperthyroidism.
 Neruogenic.
Pshychogenic,
increased
intracranial pressure, spinal cord section.
 Miscellaneous.
Coarctation
of
aorta,
pregnancy-induced
hypertension,
acute
porphyria, acute stress including surgery.
Pathophysiology
 The underlying mechanism of essential hypertension
is unkown may due to abnormal sympathetic nervous
system activity, altered renin-angiotensin system
regulation.
 The characteristic hemodyanmic changes:
1. Increased systemic vascular resistance with normal
COP.
2. Markedly increased sympathetic response to stress
such as endotracheal intubation.
3. A greater increase in blood pressure with
vasoconstriction and greater decrease in BP with
vasodilation.
End organ damage
1. Cardiac: left ventricular hypertrophy,
infarction, arrhythmias and congestive
heart failure.
2. Eye : hypertensive retinopathy.
3. Renal: Nephropathy.
4. Cerebral: stroke or transient ischemic
attack.
Some investigators have shown that patients
with untreated, poorly controlled or labile
preoperative hypertension are at increased risk for
perioperative blood pressure lability, dysrhyrthmias,
myocardial ischemia and transient neurologic
complications.
Left ventricular hypertrophy, which signifies
long-standing poorly controlled hypertension, can
increase the risk of myocardial ischemia from
imbalances of myocardial oxygen supply and
demand regardless of the presence or absence of
coronary artery disease.
In hypertensive patients, autoregulation of
cerebral blood flow is reset to a higher range than
normal, and although it protects the brain against
sudden increase in pressure, it makes it more
vulneranle to hypotension. Therefore, when blood
pressure is lowered acutely, hypertensive patients
will show signs of cerebral ischemia at a higher level
of BP than normotensive patients.
So, if marked hypertension (>180/120 mmHg)
is present preoperatively, arterial blood pressure
should be maintained in the high normal range (150140/90-80mmHg).
The following figure shows the renin-angiotensin
systems and the mechanism of action of
antihypertensive drugs:
Diuretics:
 They include thiazides (e.g., hydrochlorothiazide),
loop diuretics (e.g., furosemide, ethacrynic
acid),and potassium sparing agents (e.g.,
spironolactone, triametrene). All direutics initially
lower the pressure (BP) by increasing urinary
sodium excretion and by reducing plasma volume,
extracellular fluid volume, and cardiac output. For
patient with ST segment changes and evidence of
pulmonary edema and hypertension or with
increased intracranial cerebral pressure and
hypertension, intravenous furosemide maybe
appropriate.
Antiadrenergic agents:
1. Centrally acting drugs: clonidine, dexmedetomidine
and mivazerol. Stimulation of 2 receptors in the
vasomotor centers of the brain reduces sympathetic
outflow.
2. Peripherally acting drugs:
 1
and
2
receptors
phenoxybenzamine
(dibenzyline), phentolamine (regitine).
 1 receptor
(cardura).
prazosin
(minipress)
doxazosin
By blocking -mediated vasoconstriction, these
drugs induce a fall in peripheral resistance with both
arteriolar and venous dilation.
 -receptor
blockers
atenolol
(tenormin),
metoprolol (lopressor), nadol (corgard),pindolol
(visken),propranolol
(inderal),
esmolol
(breviblock). These drugs lower the BP by
decreasing
heart rate, contractility, cardiac
output, and renin levels.
 - and receptor blockers – labetalol (trandate)
 Endothelin receptor antagonist:
bosentan
(receptor A and B antagonist) and sitaxenstan
(receptor A antagonist) are examples of a few of
this class of agents used in the m¬anagement of
pulmonary hypertension and less so for
hypertension related heart failure.
Cardiovascular effects of calcium
channel blockers
Verapamil Dilatiazem Nifedipine Nicardipine
Heart rate




Nodal
conduction


 or-
- or-
Myocardial
depression


- or
-
Vasodilation




, more increase; , more decrease;  increase; , decrease; -, no change.
Dopaminergic agonists:
 Fenoldopam, dopamine receptor (DA1 selective)
agonist, a systemic and renal vasodilator, offers
significant advantages as a parenterally administered
agent for the management of BP in hypertensive
emergencies and in the periopertive setting.
Angiotensin converting enzyme inhibitors:
 They include captopril, enalapril, lisinopril,
quinapril, and ramipril. These drugs inhibit the
conversion of the inactive decapeptide angiotensin I
to the active octapeptide angiotensin II.
Angiotensin II receptor blockers
 Blockade of the action of angiotensin II leads of elevation in
plasma levels of renin, angiotensin I, and angiotensin II.
However, this build up of precursors does not overwhelm the
receptor blockade, as evidenced by a persistent fall in both
blood pressure and plasma aldosterone levels.
Vasodilators
Direct vasodilators:
 They include hydralazine, nitroprusside, nitroglycerin, and
calcium channel blockers. These drugs directly relax the
smooth muscle of resistance and capacitance vessels to
different degrees.
Other vasodilators:
 They include brain natriuretic peptides such as nestiritide that
is primarily used in acute exacerbation of heart failure to
improve forward flow and reduce symptoms and signs of heart
failure.
Anesthetic Management Of HTN
 Careful control of the hemodynamic responses to
noxious stimuli such as endotracheal intubation,
surgical incision and manipulation, and emergence
from anesthesia is essential.
 The anesthetic goal is to minimize:
1. Cerebral hypoperfusion from hypotension.
Cerebral hemorrhage and hypertensive
encephalopathy resulting from hypertenison.
2. Renal failure from renal hypoperfusion.
3. Myocardial ischemia from
hypertension or hypotension.
tachycardia,
Preoperative evaluation and preparation
 In addition to the routine systemic preoperative
physical examination and history, special attention
should be paid to the following: etiology and
severity of hypertension, the subtype of
hypertension, current therapy (hypokalemia and
hypomagnesemia with diuretics) and the end-organ
damage by chronic hypertension (for cardiac
evaluation: ECG and Echo, for renal evaluation:
serum creatinine and blood urea nitrogen).
 Failure to diagnose a pheochromocytoma
preoperatively, may prove fatal crisis.
Elective surgery should be delayed for
patients with severe hypertension (diastolic BP>
115 mmHg) or with severe isolated systolic
hypertension (ISH) (systolic BP> 200 mmHg)
until the BP is below 180/110 mmHg. If time
permits, The blood pressure should be lowered
over 6 to 8 weeks to less than 140/90 mmHg.
Acute control within several hours is
inadvisable before elective surgery, because this
practice may put the cerebral circulation at risk
for ischemia.
 Current opinion generally favors continuation of
antihypertensive medication, especially β-blockers,
up to the time of surgery. The withdrawal syndrome
of beta blocker is characterized by an enhanced
sensitivity to sympathetic stimulation due to
increased β-receptor density.
Preoperative control of hypertension:
1. A single dose of clonidine, 5μg
hours
before
surgery
per kg orally, 2
significantly
decreases
anesthetic requirements and hemodynamic lability
in patients with mild-to-moderate hypertension.
2. A single small oral dose of a β-adrenergic blocking
agent such as labetalol. Atenolol, or oxpernolol
given preoperatively to untreated, asymptomatic
mildly hypertensive patients.
3. The premedication with diazepam, lorazepam, or
midazolam can be regulated to have the patient
arrive in the operating room sedated.
Controlled hypotensive technique for
hypertensive patients:
 Uncontrolled or untreated severe hypertension is a
contraindication to controlled hypotension.
Intraoperative management
Regional anesthesia:
 These patients should have intravascular fluids given
prior to the regional anesthetic, regional blocks should
be administered to an adequately medicated and
sedated patient to prevent stress-related release of
catecholamines.
Monitoring:
1. Electrocardiogram (ECG). Simultaneous leads V5 and II,
multiple leads ST analysis
2. Blood pressure (BP).
3. Pulse oximeter.
4. End-tidal CO2 analyzer.
Induction:
 Deeper anesthesia with potent inhalation agents to
attenuate tachycardia and hypertension should be
done with caution because of higher incidence of
hypotension arising from both vasodilatation and
cardiac depression.
Intubation:
 Laryngoscopy time should be 15 seconds or less to
minimize BP elevation. Other measures are
described as follows:
1. lidocaine, 1.5 mg per kg is given 2 minutes before
intubation and using it in topical airway anesthesia.
2. Esmolol, 2 mg per kg.
3. Labetalol, 0.15 to 0.45 mg per kg.
4. Nicardipine, 1 mg intravenously 2 minutes before
tracheal intuabtion.
Hypotension after induction of anesthesia
usually can be easily corrected by volume replacement
and simultaneous titration of vasopressors such as
ephedrine 5 to 10 mg or phenylephrine in 0.1 mg
inrements.
Maintenance of anesthesia:
 Potent inhalation anesthetices or narcotics should
be titrated to the desired level of central nervous
system depression while the blood pressure (BP) is
monitored continuously.
The combination of nitrous oxide and low to
moderate doses of narcotics and potent
inhalation agents may provide the most stable
intraoperative couuse.
Fluid therapy:
 Patients with essential hypertension are usually
hypovolemic because of vasoconstriction and
diuretic therapy.
 Overhydration should be avoided because it may
contribute to postoperative hypertension when the
vasodilating effects of anesthetics are gone. Careful
estimation of fluid intake and output is essential.
Intraoperative hypertension (causes and management):
Differential diagnosis of intraoperative hypertension:
Related to Chronic hypertension, increased intracranial pressure,
preexisting
aortic dissection, early acute myocardial infarction.
disease
Related to
surgery
Prolonged tourniquet time, post-cardiopulmonary bypass,
aortic cross-clamping, postacarotid endarerectomy.
Pain, inadequate depth of anesthesia, catecholamine
release, malignant hyperthermia, shivering, hypoxia
Related to
hypercarbia, hypothermia, hypervolemia, improperly
anesthetic sized (too small) blood pressure cuff, intra-arterial
transducer positioned too low.
Rebound hypertension (from discontinuation of clonidine,
Related to
btea blockers, or methyldopa), systemic absorption of
medication vasoconstrictors intravenous dye (e.g, indigo carmine)
Others
Bladder distention, hypoglycemia.
Postoperative management:
 The
causes
of
postoperative
hypertension include pain, emergence
excitement, hypoxemia, hypercarbia,
reaction to endotracheal tube, full
bladder,
hypothermia,
relative
hypervolemia from intraoperative
administration of excess fluids. The
most common cause of postoperative
hypertension is incisional pain.