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ANESTHETIC IMPLICATIONS OF
HTN,CAD,ANAEMIA
Presented by- Dr. Kamal Prakash Sharma
ModeratorDr. Manoj Kumar Panwar
HYPERTENSION
Hypertension is most frequent preoperative abnormality in surgical
patients, with an overall prevalence of 20–25%.
Definition: defined as two or more BP readings >140/90.
Diagnosis of HTN cannot be made only by one preoperative reading
but also requires confirmation by history of raised BP.
BP also affected by posture, day time or night, emotional state, recent
activity, drug intake, equipment and technique used.
Thus preoperative anxiety, pain often produces some degree of
hypertension even in normal patients but patients with a history of HTN
have greater preoperative elevations in blood pressure.
Degree of end organ damage, morbidity and mortality correlates with
duration and severity of HTN.
Long standing uncontrolled hypertension accelerates atherosclerosis
and hypertensive organ damage.
Hypertension is a major risk factor for Cardiac, Cerebral, Renal, and
Vascular, Ocular disease.
Complications include Myocardial infarction, LVH, Congestive
Heart failure, Stroke, Renal failure, Peripheral occlusive disease,
and Aortic dissection.
The presence of left ventricular hypertrophy (LVH) and carotid
bruits—even in the absence of symptoms is an important predictor of
cardiac mortality.
CLASSIFICATION OF BLOOD PRESSURE
Category
Systolic pressure
Normal
<130
High normal
130-139
Hypertension
Stage 1/Mild
140-159
Stage 2/Moderate
160-179
Stage 3/Severe
180-209
Stage 4/Very severe
>210
Diastolic pressure
<85
85-89
90-99
100-109
110-119
>120
ETIOLOGY:1)Primary /Essential hypertension
2)Secondary hypertension
Renal HTN
Vascular
Pyelonephritis, glomerulonephritis
Diabetic nephropathy
Endocrinal HTN
Phaeochromocytoma
Cushing’s disease
Primary aldosteronism
Vascular
Coarctation of aorta
Pregnancy induced hypertension
DRUG THERAPY
Drug therapy has been shown to decrease progression of HTN, CAD,CHF and renal
damage.
Drug therapy also can reverse some pathophysiological changes like LVH and altered
cerebral autoregulation.
ORAL ANTIHYPERTENSIVE AGENTS
1)DIURETICS-
Thiazide type
Loop type
Potassium sparing
2)SYMPATHOLYTICS –
Adrenergic receptor blockers
Central alfa-2 agonists
Postganglionic blockers
3)VASODILATORS-
Calcium channel blockers
ACE inhibitors
Angiotensin receptor blockers
4)DIRECT VASODILATORS- Hydralazine
Minoxidil
Most patients with mild hypertension require only single-drug
therapy, which may consist of a thiazide diuretic, ACE-inhibitor, ARB,
beta-adrenergic blocker, or calcium channel blocker.
The Joint National Committee on Hypertension recommends low doses
of a thiazide diuretic for most patients. However, concomitant illnesses
should influence drug selection.
An ACE inhibitor is considered an optimal first-line choice for patients
with left ventricular dysfunction or heart failure.
ACE inhibitor or ARB is considered an optimal initial single agent in
the setting of hyperlipidemia, chronic kidney disease or diabetes.
Beta-blocker or less commonly, a calcium channel blocker is used as a
first-line agent for patients with CAD.
ACE inhibitors, ARBs & adrenergic blockers are generally less
effective than diuretics and calcium channel blockers in black patients.
Patients with moderate to severe hypertension require a second or
third drug.
Preoperative Management
It is generally recommended that elective surgery be delayed for severe HTN
until BP is less than 180/110 mm Hg.
If severe end organ damage is present, the goal should be to normalize BP as
much as possible before surgery.
Effective lowering of risk may require 6-8 weeks of therapy to allow
regression of vascular and endothelial changes.
If surgery can’t be postponed, the goal is not to decrease chronically
increased BP too rapidly, as too rapid lowering of BP may increase risk of
cerebral, coronary ischemia.
Thus decision to delay or to proceed with surgery should be
individualized, based on the severity of HTN, coexisting myocardial
ischemia, ventricular dysfunction, cerebrovascular or renal
complications, surgical procedure (whether major surgically induced
changes in cardiac preload or afterload are anticipated).
History
 Severity and duration of the hypertension
 Drug therapy currently prescribed
 Compliance with the drug regimen.
 Presence or absence of hypertensive complications like myocardial
ischemia, ventricular failure, impaired cerebral perfusion, or peripheral
vascular disease.
Adverse effects of current antihypertensive drug therapy
Physical Examination & Laboratory Evaluation
BP measurement and auscultation
Ophthalmoscopy
Electrocardiogram
Chest radiograph
Echocardiography
Renal function
Serum electrolyte levels
Premedication
Premedication reduces preoperative anxiety and is highly desirable in
hypertensive patients.
Mild to moderate preoperative hypertension often resolves following
administration of an anxiolytic agent, such as midazolam.
 Preoperative antihypertensive agents should be continued as close to
schedule as possible and can be given with a small sip of water.
Intraoperative Management
The overall anesthetic plan for a hypertensive patient is to maintain an
appropriate stable blood pressure range.
Blood pressure should generally be kept within 10–20% of
preoperative levels.
Patients with borderline hypertension may be treated as normotensive
patients.
Those with long-standing/poorly controlled HTN have altered
autoregulation of cerebral blood flow, higher than normal MAP may be
required to maintain adequate cerebral blood flow.
Monitoring includes NIBP, ECG, SpO2, EtCO2, IBP, Urine output.
Induction
Induction of anesthesia and intubation are often a period of
hemodynamic instability for hypertensive patients.
Regardless of the level of preoperative blood pressure control, patient’s
with HTN display an accentuated hypotensive response to induction,
followed by an exaggerated hypertensive response to laryngoscopy and
intubation.
Propofol, barbiturates, benzodiazepines, and etomidate are equally safe
for induction in most hypertensive patients.
Ketamine is contraindicated.
Short duration laryngoscopy ≤15 seconds .
One of several techniques may be used before intubation to attenuate the
hypertensive response:
1) Deepening anesthesia with a potent volatile agent for 5–10 min.
2) Administering a bolus of an opioid .
3) Administering lidocaine 1.5 mg/kg intravenously or intratracheally.
4) Achieving adrenergic blockade with esmolol 0.3–1.5 mg/kg, propranolol 1–
3 mg or labetalol 5–20 mg.
5) Using topical airway anesthesia.
Anesthesia may be safely continued with volatile agents (alone or with
nitrous oxide), a balanced technique (opioid + nitrous oxide + muscle relaxant)
With the possible exception of large boluses of pancuronium, any muscle
relaxant can be used routinely.
Hypertensive patients display an exaggerated response to both endogenous
catecholamines (from intubation or surgical stimulation) and exogenously
administered sympathetic agonists.
Intraoperative Hypertension
Causes include light anaesthesia, hypoxemia & hypercapnia due to hypoventilation,
CO2 insufflation during laproscopic procedures, excessive CO2 production.
Cause of HTN should be sought and treated first before using antihypertensive agent
Some parenteral agents for acute treatment of HTN
Agent
Nitroprusside
Nitroglycerine
Esmolol
Labetalol
Propranolol
Nicardipine
Nifedipine
Fenoldopam
Dosage Range
0.5-10 ug/kg/min
0.5-10 ug/kg/min
0.5mg/kg over 1min
f/b 50-300 ug/kg/min
5-20 mg
1-3 mg
0.25 -0.5 mg
10 mg
0.1-1.6 mg/kg/min
Onset
Duration
30-60 s
1 min
1-5 min
3-5 min
1 min
1-2 min
1-2 min
1-5 min
5-10 mg
5 min
12-20 min
4-8 h
4-8 h
3-4 h
4 hour
5 min
Postoperative Management
Postoperative hypertension is common and should be anticipated in
patients who have poorly controlled hypertension.
Close blood pressure monitoring should be continued in both the
recovery room and the early postoperative period.
In addition to myocardial ischemia and congestive heart failure,
marked sustained elevations in blood pressure can contribute to the
formation of wound hematomas and the disruption of vascular suture
lines.
Postoperative HTN may be due to pain, volume overload,
hypoxemia, hypercapnia, bladder distention, hypothermia &
shivering.
Cause should be corrected and parenteral antihypertensive agents given
if necessary.
When the patient resumes oral intake, preoperative medications should
be restarted.
CORONARY ARTERY DISEASE
The overall incidence of CAD in surgical patients is estimated to be between 5% and
10%.
Major risk factors for CAD
Hyperlipidemia
Hypertension
Diabetes
Cigarette smoking
Increasing age
Male sex
Positive family history
Obesity
History of cerebrovascular or peripheral vascular disease
Menopause
Use of high-estrogen oral contraceptives
Sedentary lifestyle
CAD may be clinically manifested by symptoms of myocardial ischemia (usually
angina), necrosis (infarction), arrhythmias(sudden death) or ventricular dysfunction
(congestive heart failure).
Treatment of Ischemic Heart Disease
The general approach in treating patients with ischemic heart disease is 5-fold:
1) Correction of coronary risk factors in the hope of slowing disease progression.
2) Modification of the patient's lifestyle to eliminate stress and improve exercise
tolerance.
3) Correction of complicating medical conditions that can exacerbate ischemia,
such as hypertension, anemia, hypoxemia, thyrotoxicosis, fever, infection, or
adverse drug effects.
4) Pharmacological manipulation of the myocardial oxygen supply–demand
relationship(nitrates, beta blockers, calcium channel blocker, aspirin)
5) Correction of coronary lesions by percutaneous coronary intervention or PCI
(angioplasty with or without stenting, or atherectomy) or coronary artery bypass
surgery.
PREOPERATIVE THERAPY:OBJECTIVE
To increase O2 supply to myocardium by
maintaing diastolic BP
Hb concentration
maintaining O2 saturation
To decrease determinants of myocardium O2 demand
HR
Contractility
Ventricular wall tension
Improved plaque stabilisation
DRUGS PRESCRIBED
To continue beta blockers.
Vasodilation with nitroglycerine, nitroprusside, prazosin in order to
decrease ventricular wall tension.
Allaying fear, anxiety and pain preoperatively are desirable goals in
patients with CAD to prevents sympathetic activation, which affects
myocardial oxygen supply–demand balance.
A benzodiazepine alone or in combination with a opioid is commonly
used. Concomitant administration of oxygen helps avoid hypoxemia
following premedication.
Preoperative Rx like statins, antihypertensives should generally be
continued until the time of surgery.
ASPIRIN
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INTRAOPERATIVE MANAGEMENT
The basic challenges during induction and maintenance of anesthesia in
patients with ischemic heart disease are
(1) To prevent myocardial ischemia by optimizing myocardial oxygen
supply and reducing myocardial oxygen demand.
(2) To monitor for ischemia.
(3) To treat ischemia if it develops.
Intraoperative Events That Influence Myocardial Oxygen
supply-demand relationship
Decreased Oxygen Delivery
Decreased coronary blood flow
Tachycardia
Diastolic hypotension
Hypocapnia (coronary artery vasoconstriction)
Coronary artery spasm
Decreased oxygen content
Anemia
Arterial hypoxemia
Shift of the oxyhemoglobin dissociation curve to the left
Increased Oxygen Requirements
Sympathetic nervous system stimulation
Tachycardia
Hypertension
Increased myocardial contractility
Increased afterload
Increased preload
Choice of Anesthesia
Regional Anesthesia
Regional anesthesia is often a good choice for procedures involving the
extremities, the perineum & possibly the lower abdomen.
Precipitous decreases in blood pressure should be rapidly treated with
small doses (25–50 ug) of phenylephrine or similar agent to preserve
coronary perfusion pressure until sufficient intravenous fluid can be
given.
Marked hypotension can usually be avoided by prior volume loading.
Small doses of ephedrine (5–10 mg) may be preferable in the presence
of bradycardia.
Hypotension not responding to phenylephrine or ephedrine may be
treated with small doses of epinephrine (2–10 ug).
 Patchy/incomplete surgical anesthesia/excessive sedation during
regional anesthesia defeats the purpose of selecting a regional technique,
unnecessarily stresses the patient & may precipitate myocardial ischemia
General Anesthesia
Induction should have
minimal hemodynamic effects.
produce reliable loss of consciousness.
provide sufficient depth of anesthesia to prevent a vasopressor
response to intubation.
Induction with small incremental doses of the selected agent usually
avoids the precipitous decreases in blood pressure that can be seen
following a large bolus.
Titration of the induction agent—first against loss of consciousness
and then to an acceptable decrease in blood pressure.
Moreover, sufficient anesthetic depth for intubation can be achieved
with less cardiovascular depression than that caused by the bolus
technique.
Administration of a muscle relaxant (as soon as the eyelid reflex is
lost) & controlled ventilation ensure generally adequate oxygenation
throughout induction.
Endotracheal intubation is performed once sufficient anesthetic depth
is reached or arterial blood pressure reaches its lowest acceptable limit.
Blood pressure, heart rate and the ECG should be repeatedly assessed
with each step during induction.
Induction Agents
 Propofol, barbiturates, etomidate, benzodiazepines, opioids, and
various combinations of these drugs are often used.
High-dose opioid anesthesia had previously been used widely for
patients with significant ventricular dysfunction.
Opioids used as sole agents may not be complete anesthetics because
of high incidence of intraoperative awareness, hypertension, prolonged
respiratory depression, chest wall rigidity following this technique & is
unsuitable for most noncardiac operations.
Myocardial ischemia may accompany the sympathetic nervous system
stimulation that results from direct laryngoscopy and tracheal intubation.
Short-duration direct laryngoscopy (≤15 seconds) is useful in reducing
the magnitude & duration of the circulatory changes associated with
tracheal intubation.
If the duration of direct laryngoscopy is not likely to be brief or if
hypertension already exists, it is reasonable to consider administering
drugs to minimize the pressor response.
Maintenance of Anesthesia
Tachycardia & HTN are likely to develop in response to intense
stimulation, as during direct laryngoscopy or painful surgical stimulation.
Controlled myocardial depression using a volatile anesthetic may be
useful in such patients to minimize the increase in sympathetic nervous
system activity.
The volatile anesthetic may be administered alone or in combination
with nitrous oxide.
Use of a nitrous oxide–opioid technique with the addition of a volatile
anesthetic is equally acceptable to treat any increases in blood pressure
that accompany painful surgical stimulation.
Volatile anesthetics may be
beneficial in patients with ischemic heart disease by virtue
of decreasing myocardial oxygen requirements & preconditioning the
myocardium to tolerate ischemic events
detrimental because of decrease in BP and associated
decreases in coronary perfusion pressure.
Patients with severely impaired left ventricular function may not
tolerate anesthesia-induced myocardial depression.
Opioids may be selected for these patients & addition of nitrous oxide,
benzodiazepine or low-dose volatile anesthetic may be needed because
total amnesia cannot be ensured with an opioid alone, but the addition of
nitrous oxide/volatile anesthetic may be associated with myocardial
depression.
Choice of Muscle Relaxant
The choice of muscle relaxant in patients with ischemic heart disease is
also influenced by their impact on myocardial oxygen demand supply
relationship.
Muscle relaxants with minimal or no effect on HR & BP (vecuronium,
rocuronium, cisatracurium) are choices for patients with ischemic heart
disease
Histamine release and the resulting decrease in BP caused by
atracurium are less desirable.
Myocardial ischemia has been described in patients with ischemic
heart disease given pancuronium, presumably because of increase in HR
and BP produced by this drug.
Reversal of muscle paralysis with standard agents does not appear to
have any detrimental effects in patients with CAD. Use of glycopyrrolate
decrease the likelihood of transient tachycardia
INTRAOPERATIVE MONITORING
 Perioperative monitoring is influenced by the complexity of the
operative procedure and the severity of the ischemic heart disease.
 An important goal when selecting monitors is to select those that
allow early detection of myocardial ischemia.
 Most myocardial ischemia occurs in the absence of hemodynamic
alterations.
1) NIBP, SpO2, EtCO2
2) ELECTROCARDIOGRAPHY
The diagnosis of myocardial ischemia focuses on changes in the ST
segment characterized as depression or elevation of at least 1 mm.
T-wave inversion and R-wave changes can also be associated with myocardial
ischemia, although other factors such as electrolyte changes can also produce
such changes.
The degree of ST-segment depression parallels severity of ischemia.
Traditionally, monitoring two leads, II and V5, has been the standard, but it
appears that monitoring three leads improves the ability to detect ischemia.
Leads II, V4, and V5 or V3, V4, and V5 are the sets of three leads
recommended. There is a predictable correlation between the lead of the ECG
that detects myocardial ischemia and the anatomic distribution of the diseased
coronary artery.
3) INTRAARTERIAL PRESSURE monitoring is advisable for all patients
with severe CAD and with major or multiple cardiac risk factors.
4) CENTRAL VENOUS or PULMONARY ARTERY PRESSURE
monitoring during prolonged or complicated procedures involving large
fluid shifts/blood loss. Monitoring of pulmonary artery pressure may be
desirable for patients with significant ventricular dysfunction (ejection
fraction < 40–50%).
5) TRANSESOPHAGEAL ECHOCARDIOGRAPHY
The development of new regional ventricular wall motion
abnormalities is the accepted standard for the intraoperative diagnosis of
myocardial ischemia.
These regional wall motion abnormalities seen before ECG changes
occur.
Intraoperative Management of Myocardial Ischemia
Treatment of myocardial ischemia should be instituted when there are
1-mm ST-segment changes on the ECG.
 Prompt, aggressive pharmacologic treatment of changes in heart rate
and blood pressure is indicated.
A persistent increase in heart rate can be treated by intravenous
administration of a β-blocker such as esmolol.
Nitroglycerin is a more appropriate choice when myocardial ischemia
is associated with a normal to modestly elevated blood pressure.
 In this situation, the nitroglycerin-induced coronary vasodilation and
decrease in preload facilitate improved subendocardial blood flow but
the nitroglycerin-induced decrease in afterload does not decrease
systemic blood pressure to the point that coronary perfusion pressure is
jeopardized.
Hypotension is treated with sympathomimetic drugs to restore
coronary perfusion pressure.
 In addition to vasoconstrictor drugs, fluid infusion can be useful to
help restore blood pressure.
Regardless of the treatment, prompt restoration of blood pressure is
necessary to maintain pressure-dependent flow through coronary
arteries narrowed by atherosclerosis.
In an unstable hemodynamic situation, circulatory support with
inotropes may be necessary.
 It may also be necessary to plan for early postoperative cardiac
catheterization.
Postoperative Management
The goals of postoperative management are the same as those for
intraoperative management: prevent ischemia, monitor for myocardial
injury and treat myocardial ischemia/infarction.
Intraoperative hypothermia may predispose to shivering on awakening,
leading to abrupt and dramatic increases in myocardial oxygen
requirements.
Pain, hypoxemia, hypercarbia, sepsis & hemorrhage also lead to
increased myocardial oxygen demand. The resulting oxygen
supply/demand imbalance in patients with ischemic heart disease can
precipitate myocardial ischemia, infarction or death.
Although most adverse cardiac events occur within the first 48 hours
postoperatively, delayed cardiac events (within the first 30 days) can also
occur.
Prevention of hypovolemia and hypotension is necessary
postoperatively & not only intravascular volume but also an adequate
hemoglobin concentration must be maintained.
Continuous ECG monitoring is useful for detecting postoperative
myocardial ischemia, which is often silent.
 Postoperative myocardial ischemia should be identified, evaluated and
managed aggressively, preferably in consultation with a cardiologist.
ANAEMIA
Definition: A qualitative or quantitative decrease in the number of red blood
cells (RBC's) or hemoglobin, resulting in a lower ability for the blood to carry
oxygen to body tissues.
In adults, anemia is usually defined as Hb concentrations less than 11.5 g/dL
(hematocrit, 36%) for women and less than 12.5 g/dL (hematocrit, 40%) for
men.
CAUSES OF ANAEMIA
A) Physiological anaemia of pregnancy
B) Acquired:
a. Nutritional- Iron deficiency, folate deficiency, B-12 deficiency, etc.
b. Infections- Malaria, hookworm infestation, etc
c. Haemorrhagic- Acute or chronic blood loss
d. Bone marrow suppression- Aplastic anaemia,drugs, etc.
e. Renal disease
f. Haemolytic
C) Genetic - haemoglobinopathies – sickle cell disease, thalassaemia, etc
PATHOPHYSIOLOGY OF ANAEMIA
Oxygen is carried in the blood in two forms as:
1) Physical solution in plasma (dissolved form).Arterial blood contains
only 0.3 mL of O2, in each 100 mL of blood at a PO2 of 100 mm Hg
and temperature of 37’C
2) Reversible chemical combination with haemoglobin/Oxyhaemoglobin
Hb reversibly binds to four molecules of O2 which equals to 1.37-1.39
mL/g of Hb. O2 content of the blood is calculated from the equation:
CaO2= Hb × 1.37 × SaO2 + 0.0034 × PaO2 mm Hg
Total quantity of O2 in arterial blood delivered to tissues is a function
of cardiac output (CO). Therefore,
Oxygen delivery= CaO2 × Cardiac Index × 10mL/min/m2
Whenever anemia occurs, i.e., CaO2 decreases, CO increases as a
compensatory mechanism to maintain O2 delivery to tissues.
O2 delivery is also affected by the relationship between the Hb
saturation (SaO2) & the partial pressure of O2 in the blood, described as
oxygen dissociation curve (ODC).
Thus in an anemic pregnant patient various compensatory mechanisms
get activated:
1. Increase in CO
2. Rightward shift of ODC
3. Decrease in blood viscosity
4. Increase in 2,3-DPG concentration in RBC
5. Release of renal erythropoietin leading to stimulation of erythroid
precursors in bone marrow
Thus, in physiological or chronic anaemia tissue oxygenation is not
impaired as a result of compensatory mechanisms.
May be compromised in severe or acute onset anaemia leading to
serious consequences like right heart failure, angina, tissue hypoxemia.
ANAESTHETIC CONSIDERATIONS
Preoperative assessment
Clinical assessment should focus at assessment of the cause, type and
severity of anemia and adequacy of compensatory mechanisms.
History suggestive of poor tissue perfusion can manifest as tiredness,
easy fatigability in mild anemia to SOB/dyspnoea, palpitations, angina
in moderate to severe anemia.
Signs of high CO like tachycardia, wide pulse pressure, systolic
ejection murmur are essential for planning the mode of anaesthetic
management.
Investigations should include a complete haemogram, reticulocyte
count, peripheral smears and blood grouping.
Other investigations include ESR, blood urea nitrogen levels, S.
creatinine, bilirubin levels, S. proteins, S. Iron, total iron-binding
capacity, B12 and folate levels, Hb electrophoresis and ECG for any
evidence of myocardial ischaemia, etc.
Minimal acceptable level of Hb and need for preoperative
transfusion
A ‘minimum acceptable haemoglobin level’ does not exist.
A healthy myocardium compensates for the low Hb or Hct levels (7-8
gm/dL of Hb or 21-24% Hct)in order to optimize O2 delivery.
 In patients with overt or silent episodes of myocardial ischaemia, a
level of < 10 gm/dL carries risk of decompensation.
Many task force guidelines recommend that RBC transfusions should
not be dictated by a single Hb trigger”; instead, it should be based on the
patient’s needs and risks of developing complications of inadequate
oxygenation.
The American College of Surgeons recommends RBC transfusions to
normovolemic patients with anemia only if symptoms are present.
 An Hb level of 8 g/dL was suggested as a “transfusion trigger” by the
Transfusion Practice Committee of the American Association of Blood
Banks
A threshold of 7 g/dL was suggested by the National Institutes of
Health Consensus Conference on Perioperative Blood Transfusion.
The decision to transfuse should be made on basis of symptoms,
coexisting medical conditions, continuing blood loss or threat of
bleeding
Benefits from replenishing O2-carrying capacity by transfusion must
always be balanced against transfusion-associated risks like pulmonary
edema, immune suppression.
Choice of anaesthesia
Depend on the severity, type of anaemia, extent of physiological
compensation, concomitant medical conditions, type and nature of
procedure and anticipated blood loss.
The main anaesthetic considerations in chronic anaemia are to
minimize factors interfering with O2 delivery, prevent any increase in O2
consumption and to optimize the partial pressure of O2 in the arterial
blood.
The following measures need to be diligently adhered to in the peri
operative period
A. Avoidance of hypoxia
a. Preoxygenation is mandatory with 100% O2.
b. Oxygen supplementation should be given in the perioperative period.
c. Maintenance of airway is important to prevent fall in FiO2 due to
airway obstruction, difficult intubation, etc. Hence measures and
expertise to secure a definitive airway should be available immediately.
d. Spontaneous ventilation technique with High FiO2 (40-50%) to
overcome effects of hypoventilation is suitable only for short procedures.
e. Aggressively treat and avoid conditions that increase the O2 demands
like fever, shivering,acute massive blood losses.
f. Nitrous oxide should be used cautiously in patients with folate and
Vitamin B-12 deficiency.
B. Minimize drug-induced decreases in CO
a. Intravenous induction of anaesthesia should be slowly titrated to
prevent precipitous fall in CO.
b. Careful positioning of the patient to minimize position associated
volume shifts.
c. Mild tachycardia and wide pulse pressure may be physiological and
should not be confused with light anaesthesia.
C. Factors leading to left shift of ODC should be avoided
a. Avoid hyperventilation to minimize respiratory alkalosis. Hypocapnia
also decreases CO. Maintain normocapnia.
b. Hypothermia should be avoided –
i. ensure normal core body temperatures
ii. IV fluids and blood products if any should be warmed
D. Monitoring:- aimed at assessing the adequacy of perfusion and
oxygenation of vital organs.
ECG, NIBP, EtCO2, Temperature monitoring, Pulse oximetry, urine
output
CVP, IBP monitoring, ABG analysis and measurement of mixed
venous PvO2 in severe anemia where in major blood losses are
anticipated.
Serial Hb and Hematocrit values can guide us to monitor ongoing
blood losses.
E. Regional anaesthesia is preferred for peripheral limb surgery as they
are associated with reduced blood loss
F. Central neuraxial blocks using either a low-dose spinal anaesthesia
along with adjuvants or an intermittent dosing, continuous epidural.
Advantages:good analgesia
ability to provide supplemental O2
decreased blood loss with stable haemodynamics.
Disadvantages:- hypotension
haemodilution and subsequent heart failure
pulmonary edema on the return of vascular tone.
 It is advisable to use vasoconstrictors to sustain blood pressure.
Regional anaesthesia can also be implicated in the worsening of
symptoms of subacute degeneration of spinal cord and hence should be
avoided inVitamin B12 deficiencies with neurological symptoms.
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