Blood pressure (BP) is the pressure exerted by circulating blood upon the walls of blood vessels and is one of the principal vital signs.
During each heartbeat, BP varies between a maximum (systolic) and a minimum (diastolic) pressure.
The mean BP is a function of pumping by the heart and resistance to flow in blood vessels; it decreases as the circulating blood moves away from the heart through arteries (1,2).
Physiology Principles
Mean arterial pressure (MAP) is the average pressure over a cardiac cycle and is determined by the cardiac output (CO), systemic vascular resistance (SVR), and central venous pressure (CVP); it can be calculated by the equation MAP = (CO × SVR) + CVP.
Pulse pressure (PP) is the difference between systolic and diastolic BP which results from the pulsatile nature of cardiac output. PP = SBP - DBP.
BP regulation is modulated by several reflexes on a minute-to-minute basis.
Arterial baroreflex is mediated by stretch-sensitive sensory nerve endings located in the carotid sinuses and the aortic arch. The rate of firing of these baroreceptors increases with arterial pressure, and the net effect is a decreased sympathetic outflow, resulting in decreased arterial pressure and heart rate.
The reninangiotensinaldosterone system contributes to the regulation of arterial pressure primarily via the vasoconstrictor properties of angiotensin II and the sodium-retaining properties of aldosterone (3).
Chemoreceptors located in the carotid and aortic bodies regulate BP by monitoring blood pO2, pCO2, and pH.
Diastolic BP plays an important role in coronary perfusion pressure. Coronary perfusion pressure (CPP) is the difference between the aortic diastolic pressure and left ventricular end-diastolic pressure (LVEDP). CPP = DBP - LVEDP.
Manual intermittent measurement techniques: Auscultation remains the most widely used and was originally described by Nikolai Korotkoff in 1905. A sphygmomanometer, cuff, and stethoscope measure BP by auscultating sounds generated by turbulent arterial flow beyond the partially occluding cuff. The first sound is heard at the systolic pressure (phase I). Its character progressively changes (phases II and III), becomes muffled (phase IV), and is finally absent (phase V). Diastolic pressure is recorded at phase IV or V.
Automated intermittent measurement techniques: Most automated noninvasive BP devices are based on oscillometry, where variations in cuff pressure resulting from arterial pulsations during cuff deflation are sensed. The pressure at which the peak amplitude of arterial pulsations occurs corresponds closely to MAP; systolic and diastolic pressures are derived from proprietary formulas that examine the rate of change of the pressure pulsations.
Direct measurement techniques of arterial BP: Arterial cannulation with continuous pressure transduction and waveform display remains the accepted reference standard for BP monitoring. It is invasive, more costly, and requires technical expertise to perform (4).
Physiology/Pathophysiology
Acute hypertension is a risk factor for myocardial ischemia, stroke, and bleeding from the surgical sites.
Chronic hypertension doubles the risk of cardiovascular disease including coronary heart disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal failure, and peripheral arterial disease. Because most patients with long-standing hypertension are assumed to have some element of coronary disease and cardiac hypertrophy, excessive BP elevations are undesirable.
Uncontrolled hypertension (>180/120 mm Hg) and/or clinical signs and symptoms of hypertensive emergency warrant cancellation of elective surgery until the BP is optimized. Patients should receive emergency medical care and not simply be sent home. Warning signs and symptoms of hypertensive emergency include:
Headache
Confusion
Visual changes
Seizures
Focal neurologic changes
Nausea and vomiting
Papilledema
Exudative hemorrhages
Shortness of breath
Chest pain
Azotemia, oliguria, and proteinuria
Perioperative Relevance
In the operative setting, systolic and diastolic pressures should generally be kept within 1030% of preoperative levels (5).
The systolic BP (generated from myocardial ventricular contraction) helps estimate the risk for a heart attack or stroke according to the Framingham study. Intraoperatively, systolic BP correlates with the amount of surgical bleeding.
MAP is commonly referred to during cardiac surgery (particularly during bypass) and is a determinant of cerebral perfusion pressure (CPP = MAP ICP). Cerebral blood flow is autoregulated between MAPs of 60 and 180 mm Hg; should the MAP fall below 60 mm Hg, the cerebral blood flow becomes severely decreased. In hypertensive patients, the autoregulation curve is shifted to the right (6).
Severe intraoperative hypotension is an anesthetic emergency, and treatment is vital to ensure adequate organ blood flow, particularly to the brain, heart, kidneys, and the placenta in pregnancy. Consequences of hypotension can include stroke, myocardial infarction, acute tubular necrosis, fetal compromise, acidosis, and death. Because hypotension can be harmful, this symptom is often treated before the cause has been ascertained. Hypotension can result from abnormalities in preload, contractility, afterload, heart rate, cardiac rhythm, intravascular volume, or SVR. Common causes of hypotension include:
Hypovolemia can reduce preload and may be due to hemorrhage, vomiting, diarrhea, burns, or sepsis.
Increased intrathoracic pressure, as seen with positive pressure ventilation and tension pneumothorax, can reduce preload.
Spinal and epidural anesthesia cause vasodilatation and decreased preload due to sympathetic block; if the block is above T4, it may also result in decreased myocardial contractility and bradycardia.
Excessive anesthesia: General anesthetics (both inhalation and intravenous) may cause hypotension by reducing CO and SVR.
Obstruction of major vessels can increase afterload and cause pump failure. Causes include pulmonary embolism or aortocaval compression by tumor or pregnancy.
Decreased myocardial contractility, as from beta-blockers, cardiac arrhythmias, cardiac tamponade, and myocardial infarction
Bradycardia, as from heart block or vagal overtone
Shock, as from spinal, cardiogenic, or anaphylaxis shock or sepsis
Treatment of intraoperative hypotension often precedes treating the cause:
Optimize preload: Administer an intravenous fluid bolus.
Elevate legs or head down tilt to improve venous return.
Reduce anesthetic agent if appropriate.
Use sympathomimetic drugs.
Causes of intraoperative hypertension include:
"Light" anesthesia or pain
Hypercarbia
Medication error (inadvertent administration of pressors)
Preeclampsia/eclampsia
Acute increase in intracranial pressure
Volume overload
Full bladder
Pheochromocytoma
Autonomic hyperreflexia
Decreased vascular compliance (arteriosclerosis)
Disorders with increased cardiac output (aortic regurgitation, thyrotoxicosis)
Renal parenchymal diseases
Aortic coarctation
Medications (such as monamine oxidase inhibitors, cocaine, or methamphetamine)
Autonomic hyperreflexia or dysreflexia (AD) is a life-threatening condition which occurs most often in individuals with spinal lesions above the T6 spinal cord level. At this level, the lesion is cephalad to the sympathetic cell bodies in the spinal cord and is believed to disrupt descending CNS impulses that normally regulate sympathetic outflow. AD is a reaction of the autonomic (involuntary) nervous system to overstimulation which is characterized by severe hypertension, (reflex) bradycardia, profuse sweating, vasodilation above the level of the lesion (including flushing of the skin, nasal stuffiness, severe headaches), apprehension, anxiety, and occasionally cognitive impairment. AD is believed to be triggered by afferent stimuli originating below the level of the lesion, which increase BP via sympathetically mediated vasoconstriction in muscle, skin, and splanchnic vascular beds (7). The stimuli that trigger AD often result from the distension of a viscous such as the bladder or intestine.
Graphs/Figures
Table 1. Drugs used for intraoperative hypotension
Drug
Receptor
Dose
Phenylephrine
1
50100 mcg bolus (adult)
0.150.75 mcg/kg/min
Norepinephrine
1,2; 1
0.010.1 mcg/kg/min
Epinephrine
1,2;
0.010.03 mcg/kg/min
Ephedrine
1; 1,2
510 mg bolus (adult)
Dopamine
; ; D1
210 mcg/kg/min
Dobutamine
1,2
230 mcg/kg/min
Table 2. Drugs used for intraoperative hypertension
Drug
Peak effect
Duration
Dose
Esmolol
25 min
25 min
50200 mcg/kg/min
Labetalol
515 min
26 hrs
1020 mg bolus over 2 min
Hydralazine
1520 min
34 hrs
510 mg bolus every 15 min, up to 40 mg
Nitroprusside
Immediate
25 min
0.31.0 mcg/kg/min
Nitroglycerine
Immediate
25 min
5100 mcg/kg/min
Nicardipine
560 min
2040 min
2.5 mg over 5 min, infusion 515 mg/hr
Diltiazem
330 min
3 hrs
1020 mg/hr
References⬆⬇
Health and Life. Normal blood pressure range adults. Available at: http://healthlifeandstuff.com/2010/06/normal-blood-pressure-range-adults/
RohrigR, JungerA, HartmannB, et al.The incidence and prediction of automatically detected intraoperative cardiovascular events in noncardiac surgery. Anesth Analg. 2004;98(3):569577.
Additional Reading⬆⬇
MorganGE, MikhailMS, MurrayMJ.Anesthesia for patients with cardiovascular diseases. In: Clinical Anesthesiology, 4th ed., McGraw Hill, 2005, chapter 20.
See Also (Topic, Algorithm, Electronic Media Element)
Maintaining an adequate BP is essential to maintain perfusion to vital organs. BP should be maintained within 1030% of the patient's baseline.
The consequences of hypotension are sufficiently serious to potentially warrant treatment even before the cause of the hypotension is ascertained. Intraoperative hypotension most commonly reflects "deep" anesthesia, hypovolemia, or the use of specific drugs or anesthetic techniques.
Uncontrolled hypertension is associated with an increase in perioperative morbidity and mortality. Elective cases should be cancelled when a patient demonstrates signs of a hypertensive emergency. Anesthesiologists are often faced with the decision to cancel or proceed with uncontrolled BPs exceeding 180/110 mm Hg.
Titrating therapies to traditional endpoints such as blood pressure does not ensure that the microvascular bed is being adequately perfused. for example, a normal or high blood pressure may be a vasoconstrictive response to a low cardiac output state.