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

To investigate during general Amaesthesia the contribution of preoperative pulse pressure on intraoperative haemodynamic instability in hypertensive patients.   


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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.

§  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     


      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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