I.Brain :
a.Cerebral metabolism may not be at usual levels during
hypotensive period if the blood pressure is very low and
the patient is in the head up position.
b.When the blood pressure is reduced below 60 torr,
additional cerebrovasodilatation is not possible.
Therefore lower levels of blood pressure may be
accompanied by a reduction in cerebral blood flow.
c.Oxygen consumption does not change significantly.
d.Mental function may be altered to a minor degree in the
post operative period however this usually transient.
II.Heart and blood vessels :
a.Coronary perfusion remain adequate.
b.There is no permanent myocardial damage although
there may be some transient myocardial ischemia in
erderly patients or those with hypertension if the blood
pressure is allowed to fall below 60 torr.
In those patients,a systolic pressure of at least 80 torr
should be maintained at all times.
c.Cardiac output changes vary with the agent or tehnique
utilized :
1.Trimetaphan causes slight changes in cardiac output.
2.With pentholinium (Ansolysen) changes in cardiac output
are rate dependent.
3.High spinal block and deep general anesthesia yield
a significant decrease in cardiac output.
4. Nitropruside causes no change in cardiac output if
blood pressure is maintained above 80 torr and all
other conditions are stable.
III.Lungs :
a.Physiological dead space is increased.
b.Vital capacity is increased.
IV.Kidney :
a.Urine formation:
Renal filtration is reduced with a fall in systolic blood
pressure. Below 60 torr, urine formation ceases,
however this does not mean that kidney damage is
occured.
b.Renal blood flow:
Initially depressed,it then returns to preoperative
levels. It is maintained as the systollic blood pressure
falls,through a compensatory vasodilatation.
This mechanism will start to fail when blood pressure
goes below 60 torr.
V.Liver :
a.Due to the physiology and anatomy of the liver's blood
supply,it is subject to a higher critical level of
hypotension.
b.There are two sources of blood to liver :
1.The hepatic artery supplies 20% of total supply,at high
oxygen tension (95% saturated) and,
2.The portal vein supplies 80% of the hepatic blood
supply at 74% oxygen saturation.
c.When the systolic blood pressure below 60 torr,the liver
become cyanotic and turgid.
d.When the liver is subjected to anoxia:
1.It can't form urea from ammonium salts or amino acids.
2.It also can't inactivate vasodepressor substances.
PRACTICAL TECHNIQUE OF INDUCED HYPOTENSION:(2,4,5)
The requirement of surgery fall into three broad groups and no single agent is capable of providing ideal condition for all of them.
The first group, requires relatively slow onset and sustained moderate hypotension with a slow return to normal pressure, this is the case is most plastic,maxillo
facial and ear,nose and throat surgery when rapid return to normal pressures may cause reactionary haemorrhage.
In the second group requires where massive blood loss is anticipated moderate sustained hypotension together with a reduction in heart rate is probably all that is required.
The third group comprises some operations are not only impossible without profound hypotension but also short period of very low pressure such as during clipping of a cerebral aneurysm.
Further indications include resection of aortic coarctation where rapid fluctuation in blood pressure necessitate immediate control.
In all cases a background anesthetic against which hypotension can be induced is essential,the principles of balanced anesthesia dictating that it is better to employ individual agents to achieve spesific effect rather than to persue the toxic properties of an agent such as halothane in the production of hypotension by myocardial depression.
Perhaps the best background anesthesia sequence consist first omiting atropine in premedication since this induces tachycardia but using generous sedation or analgesic. It is important to avoid preoperative anxiety and the release of adrenaline as the effects take some time to abate under anesthesia, heavy premedication will continue to extent an effect during anesthesia.
Induction of anesthesia with thiopenthone or propofol
fentanyl and a long acting non depolarizing muscle relaxant which does not induce tachycardia should be employed.
Following topical anesthesia of the larynx,intubation is performed.
Moderate hyperventilation with nitrous oxide and oxygen together with low concentration of one of the volatile anesthetics as then the background technique against which hypotensive agents can be used.
Of those currently available, 0,5-1% isoflurane is probably now the agent of choice.
Under these stable conditions,spesific hypotensive drugs can be employed with the minimum of side effects such as tachycardia or excessive hypotension.
The mean arterial pressure(MAP) is not usually reduced below 50 mmHg in normotensive individuals and chronically hypertensive patients may require a higher MAP (systolic is best kept greater than the preoperative diastolic value and should be reduced to no more than 50 mmHg less than the normal pressure.
Even more modest reductions in BP of no more than 20-30 mmHg are advisable in patients who have anemia,fever,
cerebral hematoma,occlussive cerebrovascular disease and the probablity of prolonged retractor pressure.
Harp and Wollman also pointed out long ago that the con-
comittent use of hyperventilation and hypotension may decrease cerebral blood flow sufficiently to increase the risk focal ischemia significantly.
Consequently patients should be normocarbic during the period of induced hypotension.
During hypotension a mentioned earlier the inspired oxygen concentration may be increased to 40% or even 50% if very low pressure are being employed over a short period as during neurosurgery.
DRUGS AND METHODS :
1.NITROPRUSIDE(NP) :(1,2,3)
a.NP is a potent,rapid acting,hypotensive drug adminis
tered by intravenous infusion.
b.Its effects are achieved by peripheral vasodilatation
and decreased peripheral resistance.
c.Its mechanism is direct action on blood vessel walls,
independent of the autonomic innervation.
d.Shortly after administration of the drug is slowed down
or discontinued and the blood pressure(BP) begins to
rise; it returns to the preoperative level within 1-10
minutes.
e.The prepared stock solution is sodium nitropruside
dehydrate 50 mg.
Sodium nitropruside(SNP) should be diluted in 5%
dextrose to produce a 0,01% solution to 0,02%
depending on the age and physical status of the
patient.
When infused at an initial rate 30-40 mcg per min,
it will produce a fall in BP within 30-40 seconds.
f. Degradation of SNP occurs in the presence of light
and/or low pH, and yields sodium ferrocyanide and
cyanide.Thus cyanide poisoning is possibility.
1.The presence of these compounds can be detected
by a change in color of the solution from normal
brown pink to an abnormal dark brown or blue;
either of these colors indicates the preparation is
chemically unfits for use.
2.This fotosensitive breakdown can be prevented by
either storing SNP in amber-colored vials or
wrapping opaque.
g.SNP should be administered by an infusion pump or
by microdrip regulator and BP should be recorded
directly via a radial artery cannula.
h.Although SNP is a good hypotensive agent-rapidly
reversible and predictable in the action-it can have
an adverse metabolic effect if administered in a dose
over 3 mg per kg of body weight.
In high doses severe hypotension and/or methhemog
lobinaemia have been reported.
I.The average dose of SNP is 3 mcg/kg/min (range of
0,5-8 mcg/kg/min). On vial (50 mg)of SNP is diluted in
500 ml of 5% D/W; each ml contains 100 mcg.
Infusion rate initially with 0,5 mcg/kg/min and is
increased slowly.
The infusion is discontinued if the target MAP is not
achieved with 10 mcg/kg/min,within the first 10-15
min,to preclude the possibility of cyanide toxicity.
j.The deterious effects of SNP include cyanide and
thiocyanate toxicity, intracranial hypertension,
rebound hypertension, abnormalities coagulation,
increased pulmonary shunting,hypothyroidism,
mitochodrial damages and decreases in myocar
dial,liver and skletal muscle oxygen reserves.
Cyanide is a metabolit of SNP.
Toxic blood levels of greater than 100 mcg/dl
develop when 1 mg/kg SNP is administered within
2,5 hours, or when more than 0.5 mg/kg per hour is
administered within 24 hours.
SNP may increase the ICP of patients who have a
decrease in intracranial compliance because of its
dilatation of capacitance and resistance vessels.
Patients who have space occupying lesion are at even
greater risk since venous return could be impeded by
the mass with a resultant increase in cerebral blood
volume and ICP and compromise in regional cerebral
perfusion.
Even after the cranium is opened and ICP equals
atsmospheric pressure the SNP-induced cerebral
vasodilatation may cause cerebral swelling and
disturbance in perfusion in area under retraction.
to be continued
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