M.Sc RESEARCH PROPOSAL
DEPARTMENT OF PHYSIOLOGY
CHAPTER ONE
INTRODUCTION
•
Over the years,
several studies have reported that hypertensive patients during general
anaesthesia are more predisposed to intraoperative haemodynamic instability
than normotensive patients (1).
•
Hypertension is
one of the most common worldwide diseases afflicting humans and is a major risk
factor for stroke, myocardial infarction, vascular disease, and chronic kidney
disease.
•
Despite extensive
research over the past several decades, the etiology of most cases of adult
hypertension is still unknown and control of blood pressure is suboptimal in
the general population. (4).
•
Chobanian AV et
al (2003) Based on the recommendation of the joint national committee on
prevention, detection, evaluation and treatment of high blood pressure.
the classification of blood pressure expressed in mm Hg for
adults 18yrs or older is as follows:
Normal
: systolic 120- 139mm Hg
diastolic lower than 80mm Hg
Pre
hypertension : systolic 120-139mm Hg
diastole 80- 89mm Hg
Stage
1 :systolic 140-159mm Hg
diastolic 90-99mm Hg
Stage
2 : systolic 160mm Hg or greater
: diastolic 100mm Hg or
greater
CHAPTER TWO
OBJECTIVE OF THE STUDY
To investigate during general Amaesthesia the
contribution of preoperative pulse pressure on intraoperative haemodynamic
instability in hypertensive patients.
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CHAPTER
THREE
LITERATURE
REVIEW
The Pathogenesis of essential hypertension is
multifactorial and highly complex (8).
Multiple factors modulate the blood pressure (BP) for
adequate tissue perfusion and include humoral mediators, vascular reactivity,
circulating blood volume, vascular caliber, blood viscosity, cardiac output,
blood vessel elasticity and neural stimulation.
A possible pathogenesis of essential hypertension been
proposed in which multiple factors including genetic predisposition, excess dietary
salt intake and adrenergic tone, may interact to produce hypertension, although
genetics appears to contribute to essential hypertension, the exact mechanism
has not been established. Environmental factors include obesity, alcohol
intake, sodium intake and stress (8).
Secondary hypertension is where blood pressure
elevation is the result of specific and potentially treatable cause. They
include –renal disease, endocrine causes, congenital cardiovascular causes,
drugs and pregnancy (Kumar and Clark 2005).
Cerebrovacular
disease and coronary artery disease are the most common cause of death,
although hypertensive patients are also prone to renal failure and peripheral
vascular disease.
Especially severe of hypertension, or hypertensive
crises, are defined as a blood pressure of more than 180/120mmhg and may be
further categorized as hypertensive emergencies or urgencies.
Hypertensive emergencies are characterized by evidence
of impeding or progressive target organ dysfunction, whereas hypertensive
urgencies are those situations without progressive target organ dysfunction(5).
•
Hypertension may
be primary, which may develop as a result of environmental or genetic causes,
or secondary which has multiple etiologies, including renal, vascular and
endocrine causes.
Primary or essential hypertension accounts for 90- 95%
of adult cases, and a small percentage of patients (2- 10%) have a secondary
cause. (7)
•
The difference
between the systolic and diastolic pressure is termed the pulse pressure, about
40mmHg in the healthy young adult with blood pressure of 120/80mm Hg.
Two major factors affect the pulse pressure viz: the
compliance of the arterial tree, the stroke volume output of the heart and a
third less important factor is the ejection from the heart during systole.
(Guyton & hall 2000)
•
Safer et al
(2003) found out that at a given stroke volume, arterial stiffness and wave
reflections are the main determinants of increased pulse pressure.
•
Ceravilo .r. et
al (2003) deduced from their research that endothelial dysfunction and
inflammation factors may also contribute to increased pulse pressure.
•
Blood pressure
and flow are largely controlled by the autonomic nervous system and are also influenced
by surgery and anaesthetic drugs. (berne Rm et al, cardiovascular physiology
2008 missouri mosby).
•
Anaesthetic drugs
like halothane may depress the rate of depolarization of the sinoarterial node
and the atrioventicular node may become the pacemaker of the heart.
Moreover surgical procedures can cause vagal
stimulation and produce severe bradycardia.
•
Examples include
pulling on the mesentery of the bowel, anal dilatation or pulling on the
external musles of the eye.
Pulse pressure has been widely studied as a
cardiovascular risk marker, especially when it is above 60mm Hg. (9)
•
In a study done
by balick weber cc et al (2011) in guadeloupe on the impact of pulse pressure
on intraoperative haemodynamic instability, result showed that there was an increased
intraoperative haemodynamic instability
in hypertensive subjects with increased preoperative pulse pressure.
CHAPTER FOUR
RESEARCH
METHODOLOGY
§ Location: Federal Teaching Hospital Abakaliki Ebonyi State.
•
Subjects: A
total of 100 patients between 35-60yrs of age undergoing surgeries under
general anaesthesia will be used.
•
Fifty
hypertensive subjects and fifty normotensive subjects
•
Approval for the
study will obtained from the hospital ethical committee, also written consent
will be obtained from each patient.
•
Inclusion criteria: subjects will be between 35-60yrs age bracket, subjects will be
classified as hypertensive based on world health organisation criteria for
hypertension. And surgeries done under general anaesthesia.
•
Exclusion criteria: subjects scheduled for regional anaesthesia, renal transplantation,
surgery for phoechromocytoma or conn adenoma will not be included in the study.
•
Also subjects
with congestive heart failure or known left ventricular ejection
fraction <40%, idiopathic hypertrophic cardiomyopathy, arrhythmia,
significant heart valve disease, sickle cell disease. Will also be excluded.
•
Blood pressure measurement: blood pressure will be measured- in millimeteres of
mercury-with a mercury column sphygmomanometer and a cuff of appropriate size
applied to the sitting subjects left arm at heart level after a sufficient
sedentary period, systolic and diastolic blood pressure will be determined by
korotkoff phase 1 and v respectively.
Intraoperative
haemodynamic parameter (heart rate and blood pressure) will be measured by an
automatic oscillometric arm cuff device set to measure every 5 minutes[BENEVIEW
T5 MINDRAY]. Automated blood pressure monitors electronically measures the
pressure at which the oscillation amplitude changes, a microprocessor derives
systolic, mean, and diastolic pressures using algorithm.
Experimental
procedure
Premeditations shall be given
intravenously few minutes before the induction of anesthesia and consisted of
benzodiazepam (diazepam) 10mg and an anticholinergic atiopine 0.02mg/kg to
reduce salivary and bronchial secretions.
General anastheic shall be induced
with thiopentone sodium and orotracheal intubation facilitated by
succinylcholine (100mg). Ancestheisa is to be maintained with (1-2) % end tidal
halothane.
A long acting muscle relaxant
(pancuronium) 4mg shall be used if muscle relaxation is required for a longer
period of time and reversal of neuromuscular blockade will be performed when
indicated crystalloids shall be infused during operation at a basal rate of
10ml/kg/h.
Inspired oxygen fraction will be set
at 50% in halothane and minute ventilation should be adjusted to maintain end
tidal co2 below 40.
An anaesthetic chart shall be set up to record
haemodynamic parameters displayed on the automated machine every 5 minutes, and
all therapeutic interactions shall be recorded as well.
Therapeutic intervention will be quantified by the use
of a therapeutic index defined as
Therapeutic
index = 1 – (no of hypo and hyper episodes – no of therapeutic
intervention
Number
of hypo and hyper episodes
In order to take into account the difference
anesthetic durations, the number of hypotensive or hypertensive episodes will
be divided by the duration of anaesthesia in minuets.
Data/ statistical analysis
•
The data will be
collected on forms designed from the study
•
Data will be
entered in SPSS version 10, it will be presented in form of table and figures
and expressed as mean
•
Statistical
association will be determined using CHI-square test and student T –test.
•
P < 0.05 will
considered significant
References
•
1) Goldman .L.
caldera DL (1979) Risks of general anaesthesia and elective operation in
hypertensive patients. Anaesthesiology 50:285-292
•
2) Howell
.S.J.sear JW.foex p (2004), hypertension, hypertensive heart disease and
perioperative cardiac risk. Br J Anaesth 92-570
•
3) Beyer k, tappe
p. halton p. pittet v. pichard s.et al (2009) Hypertention and intraoperative
incidents : a multicentric study of 125,000 surgical procedures in swiss
hospitals. Anesthesia 64 :494-502.
•
4) Roger VL, GO
AS, Lioyd-jones, DM, et al. Heart disease and stroke statistics- 2012 update :
a report from the American heart association, circulation Jan 3 2012, 125(1)
:e2-e220
•
5)Chobanian Av,
Bakris GL, Black HR, Cushman Wc, Green LA, 1220 JLJR, et al. seventh report of
the joint national committee on prevention, detection, evaluation and treatment
of high blood pressure. Hypertension. Dec 2003., 42 (6) :1206-52
•
6) Institute for
clinical systems. Improvement (ICSI). Hypertension diagnosis and treatment.
Bloomington, minn: ICIS 2010.
•
7) Rhodes R,
planzer R, Human physiology 3rd. Fort worth, tx :saunders college publishing
1996.
•
8) Gandhi SK,
Powers JC, Nomeir AM, Fowle K, Kitzman DW, Rankin KM, et al. the pathogenesis
of acute pulmonary edema associated with hypertension. N. Engl J. Med. Jan 4 2001; 344(1): 17-22.
•
9) Safer ME, LEVY
BL, stuijker- Boudier H(2003), current perspective on arterial stiffness and
pulse pressure in hypertensive and cardiovascular diseases, circulation 107
:2864-2869.
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