Importance: The arteries carry blood away from the heart to the tissues. The aorta branches toward periphery until blood reaches the arterioles and finally, the capillaries. The arterioles are the main site of resistance to the pumping function to the heart (accounting for approximately 50%) and also control blood flow into the capillaries. The mean arterial pressure - (MAP) is the product of cardiac output (CO) by the total peripheral resistance (TPR). Many anti-hypertensive drugs change one or both of these two parameters trying to lower blood pressure levels.
Defining Terms: Whenever the left ventricle ejects blood into the aorta, some energy derived from contraction is actually stored in the arterial walls in the form of potential energy. This latter accounts for the elastic recoil of the arteries that keeps capillary forward blood flow. This is an intrinsic property of the arteries: if their walls were build up of rigid tubes, one should expect no flow during diastole and pressure would fall to zero levels. The heart work in this way would be twice than the normal. Thus, the arterial system works like a hydraulic filter and lessens the excessive cardiac work of intermittent pumping.
Mean Arterial Pressure: It is the average pressure reached inside the arteries. The area under the arterial pulse curve (see below) is calculated by means of an integral function which yields the MAP. For the sake of simplicity, the MAP is nearer the levels of diastolic pressure than the systolic ones and can be estimated by the formula: MAP = Pd + (Ps - Pd)/3, where Pd and Ps are the diastolic and systolic pressure respectively, which are the minimum and maximum pressure levels reached in the arteries at a single cardiac cycle. Normal values of MAP varies widely but usually ranges between 77-97 mmHg.
Compliance is defined as the slope of the pressure-volume family curves ( C=dV/dP). An old patient will show a right shifted, flattened curve comparing to a young person, whose curve will be sigmoidal and left-shifted. Therefore, dV/dP generally is higher in this group than in the older s. Grossly speaking, compliance refers to the capacitance of the arterial system to accommodate volume in a specific level of pressure. In anyone with decreased arterial compliance, the heart at systole will eject blood into the rigid system slower than into a more compliant one, and peak arterial pressure will occur late in systole.
Pulse pressure is the difference between systolic and diastolic pressure and is mainly dependent on stroke volume and arterial compliance. If the first increases, the pulse pressure increases proportionally. The relationship is inverse regarding to compliance: as this one diminishes, the pulse pressure rises. As far as we travel along the arterial tree, the pulse pressure becomes higher - the systolic pressure in the radial artery may exceeds that of the aorta by 30%. However, MAP tends to be similar.
The Arterial Pulse Curve. Whenever the ventricles contract and eject blood into the great arteries, a pulse wave is generated and is transmitted along the arterial system. This wave has a finite velocity, far higher than blood velocity. The palpable pulse is the tactile sensation of this wave. As one travels along the system, the pulse wave becomes more distorted and the high frequency incisors disappears. A diastolic hump may be seen. Whenever the pulse wave reaches branching points in the system, some is returned back, like a mirror reflecting images. Actually the pulse wave is a mechanical event originated from the ventricular contraction, which travels along the arteries, and is influenced mainly by the stroke volume and the intrinsic elastic properties of the arteries.
Putting all together: Keeping otherwise variables constant, the arterial pressure will vary in a proportional fashion to the volume increments inside the vessels. This volume increment, at each cardiac cycle, depends upon the rate of inflow into the arteries (Qi - cardiac output) and rate of outflow (Qo - peripheral run-off). At equilibrium, Qi and Qo should be similar and so would be the volume increment (V2 - V1). Therefore, in this model, V1 relates to the diastolic pressure, V2 to the systolic pressure and the Vm to the MAP. The variation of volume with time is: (1) dV/dT = Qi - Qo Qo is dependent on the peripheral resistance, according to the Ohm’s law: (2) R= MAP / Qo By definition of compliance: (3) C = dV/dP => dV=C.dP Therefore, C.dP / dT = Qi - Qo which yields: (4) dP/dT = Qi - Qo / C
According to the equation (4) above, if at anytime Qi exceeds Qo, arterial pressure (Pa) will rise until equilibrium is reached (Qi=Qo). The height to which Pa will rise is independent of the arterial wall compliance (C). This one will determine only the rate at which Pa values will be reached. Therefore, the greater the compliance the slower will be the rise.
If the resistance rises, Qo will be lower, according to the equation (2) and Pa will rise until Qo equals Qi again reaching the new equilibrium value.
Therefore the arterial pressure will be a function of Qi and Qo variations over the time. As Qo varies mainly with the resistance, one should conclude from the present discussion that:
The mean arterial pressure is dependent only on the cardiac output and the peripheral resistance. Actually, this is the Ohm’s law applied to the entire cardiovascular system: MAP = CO x TPR.
Regulation of blood pressure - 1) Rapid-acting mechanisms - are achieved by the baroreceptors, localized mainly in the carotid sinus. Whenever the carotid wall is stretched, the Hering or carotid sinus nerve, which is a branch of the glossopharyngeal nerve (IX pair), discharges and will stimulate inhibitory areas of the vasomotor center, and the autonomous system will down-regulate blood pressure via efferent vagal (X pair) pathways. The baroreceptors are only sensitive to MAP variations and they adapt in 1 to 3 days to whatever blood pressure they are exposed to. Vasomotor or Traube-Hering waves are cyclic increases and decreases in blood pressure probably due to the oscillations of baroreceptors activity over the time.Atrial reflexes - when atrial walls are distended, reflex vasodilatation and tachycardia occur.
2) Moderately rapid-acting mechanisms - refers to the actions of the circulating hormones as catecholamines, endothelins, prostaglandins, nitric oxide, angiotensin and others.
3) Long-term regulation - differs from the rapid-acting because this is a non-adaptive mechanism, providing a sustained regulatory effect. The Kidney is the main site for this regulation, controlling the volemia through the reabsorption of sodium (Na+) and water, this one being influenced by the renin-angiotensin-aldosterone system (RAA).
Measurement of Arterial Pressure is routinely made in ambulatory or home devices. The sphygmomanometer consists of a cuff which is wrapped and inflated around the patient’s arm until the systolic pressure is overcome. At this moment, the brachial artery will be occluded. With the stethoscope positioned over the brachial artery area, one should release gradually the pressure from the bag (3 mmHg each heartbeat) and listen carefully for the Korotkoff sounds, which indicates the systolic blood pressure level, until they muffle or disappear (diastolic pressure).
The normal levels cannot be accessed accurately because blood pressure vary widely during the day (circadian pattern) and is influenced by many factors and one cannot diagnosis arterial hypertension with only one measure (see below).
The blood pressure (BP) lacks diagnostic specificity: decreased BP occurs in circulatory decompensation while increased pressure may indicate improved circulatory function, adrenal stress response or excessive vasopressor therapy. The pulse pressure increases with age due to decreased compliance, mostly by the cost of the systolic levels. The average of this increment is 100 plus the age, in mmHg. (eg., a 60 years old person may have systolic pressure of 160 (100 + 60) mmHg. Normal levels of blood pressure usually are 120/80 mmHg with the pulse pressure ranging from 40 to 50 mmHg. Young adults (especially teenage girls) may normally have BP as low as 90/60 mmHg. It is important to know the patient’s baseline, pre-illness pressures. Decreased pulse pressure may be an early sign of hypovolemia
Intra-arterial blood pressure is more accurate and may exceed cuff measured values by 2 to 8 mmHg (in critical patient this difference may exceed 30 mmHg). The method consists of a system of catheter connected to an artery, and pressures transducers which transmits signs to a monitor which displays the arterial BP waveforms, the systolic and diastolic pressures and the MAP. Intra-arterial measurement is indicated in shock, critically-ill patients and intra operative and postoperative monitoring in patients undergoing extensive and/or life-threatening surgeries.
Pathological Pulse Waves
Pulsus paradoxus - is defined as an exaggerated decrease in systolic pressure of 8-10mmHg or more during inspiration. It was described by Kusmaull who gave the name paradoxus because the pulse of his patient was not felt by him whenever the patient inspirated, despite the yet existing heartbeats. Inspiration increases venous return therefore increasing the right heart output transiently, according to the Frank-Starling’s law. Blood will be “sequestered” in the pulmonary circulation and the left heart output will be reduced transiently, accounting for the normal (< 8-10mmHg decrease) lower systolic pressure during this phase. Right ventricle contracts more vigorously during this phase and may bulge mechanically the interventricular septum toward the left ventricle, reducing its size and also may account for the lower systolic levels. Conditions likely to cause pulsus paradoxus are: Cardiac tamponade, severe COPD and mechanical positive pressure ventilation.
Pulsus alternans - is an alternating weak and strong contractions causing a similar alteration in the strength of the peripheral pulse. It may be found in severe heart failure and heart block.
Watter hammer pulse - is the bounding pulse (+4/+4) felt in severe aortic regurgitation where the pulse pressure is wide. This name is derived from a toy that produced similar boundings when managed.
Pulsus parvus et tardus - is the classical aortic stenosis pulse and feels like a “caress” under the examiner’s fingers in contrast to the tapering pattern of the normal pulse. In aortic stenosis, the stroke volume is reduced but the rapid ejection phase is prolonged because of the high pressure gradient. The volume increment inside the aorta will be less pronounced and delayed, producing this pulse pattern.
Pulse deficit or weak and threading pulse - is the weak pulse (+1/+4) of the shock syndromes, reflecting an underlying circulatory insufficiency
Arterial Hypertension can be of systemic or pulmonary origin. More than 90% of systemic arterial hypertension are idiopathic (essential) and no specific cause can be determined. Most of these cases do have a genetic and hereditary basis and many theories try to determine a specific cause though it may be multifactorial. Probably, the most common cause of systemic hypertension in white people is insulin resistance, which indirectly causes sodium retention. The renin angiotensin system also plays a role. The severity of the disease can be accessed by grading the diastolic pressure. This classification can vary from some authors but usually, diastolic levels greater than 90 mmHg are the upper limit that one diagnosis hypertension. Levels above 120 mmHg are defined as severe hypertension. The definitive diagnosis must be made carefully, with repeated measures in different days (at least 3 measures). Non-pharmacological treatment is life style changing (aerobic exercises, biofeedback, weight reduction) and decreased salt intake. Drugs (B-blockers,diuretics, ACE inhibitors, vasodilators) are used to lower CO and/or TPR, thereby deceasing MAP.
1) Cardiovascular Physiology - Berne&Levi, 1977, Mosby
2) Handbook of Pharmacology & Physiology in anesthetic Practice - Robert K.Stoelting - 1995, Lippincott - Raven.
3) Clinical Cardiology - Sokolow, 1990 - Lange.
4) Invasive and Nonivasive Physiologic Monitoring - William C.Shoemaker in Textbook of Cirtical Care Medicine, 1995
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